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Cross-linking of collagen restricts perfusion of local capillary beds.They may be alive, but they can no longer function.Without oxygen, the nerve cells lose 95% of their energy.Our cells are like the fish, their lake is the extracellular fluid, and modern life supplies the acidity in all the forms just listed.That is why fish die from acid rain.The invention of agriculture, emphasizing grains which were mere survival foods, I believe was mothered by necessity due to global ecological change following the retreat of the last ice age and the global flood, leaving much of the earth's terrain covered in sediments which were then colonized by early species such as the grain grasses before other food species could thrive. The cultures then developed according to the consciousness of the grain they served... corn, wheat, rice... And as the spirit minerals in those soils have become depleted along with the biological nutrient minerals, the souls of those cultures languishes... crying out in thirst, like Christ facing the cross, thirsting for the life of the spirit, the water of life that forever quenches that deepest of needs. ~~~~~~~ ### Neuroprotection [go to Table of Contents] Nerve damage occurs by specific chemical pathways. While there are probably thousands of different triggers, including many different neurotoxins, like pesticides and heavy metals, they all have some things in common that makes it easier to deal with when it comes to prevention and healing. Causal pathways converge on key deficiency states like oxidation (electron deficiency), which is contributed to by hypoxia (oxygen deficiency), which is exacerbated by acidity (alkaline macromineral deficiency). The alkaline minerals are used up over time to buffer the acid effects of environmental toxins, pharmaceuticals, endotoxins produced in the gut, and excitotoxins resulting from stress and the modern diet. In an acid state, oxygen becomes bound and unavailable. That is why fish die from acid rain. Our cells are like the fish, their lake is the extracellular fluid, and modern life supplies the acidity in all the forms just listed. Without oxygen, the nerve cells lose 95% of their energy. They may be alive, but they can no longer function. Cross-linking of collagen restricts perfusion of local capillary beds.The swelling of acidic tissue further contributes to ischemia.At this point the cause and effect can go round and round, resulting in a chronic state of ill health in the affected nerve cells.
Two different approaches have been implemented, namely, single voxel spectroscopy (SVS) and chemical shift imaging (CSI).It has been demonstrated that this technique provides with biochemical information, which can be useful in differentiating normal from abnormal brain tissue and in a certain extent provide information that might be important for differential diagnosis.The drop in the concentration of the paramagnetic deoxyhemoglobin leads to a focal signal increase in the affected tissue using T2*-weighted sequences [19, 45]. This effect is known as BOLD effect and was first used to show functionally activated brain regions as result of sensory or motor stimulation [46]. In order to depict the BOLD effect, echo planar sequences must be used due to a very short time window of the BOLD effect and the reduced sensitivity to motion that EPI sequences may provide with. BOLD imaging can be useful for many applications such as: localization of neural activities in the brain, display areas of the brain activate by sensory or motor activation (Fig. 2.18), and as a noninvasive tool for the presurgical mapping of cortical function in patients with intracranial tumors [47–49] (Fig. 2.19). Therefore, functional MRI can contribute to more efficient surgical removal of both benign and malignant brain tumors with an increase in patient survival and a decrease in surgical morbidity [50]. Fig. 2.18 Motor cortex activation during a finger tapping experiment in a patient with a high-grade tumor. Areas of activation are superimposed on axial T2-weighted images Fig. 2.19 Language centers activation with fMRI in a patient with a high-grade tumor. Activation areas are evident both in Wernicke (yellow arrow) and Broca (blue arrow) areas Proton magnetic resonance spectroscopy (1H-MRS) is a noninvasive method to study various chemical compounds found on human brain tissue. It has been demonstrated that this technique provides with biochemical information, which can be useful in differentiating normal from abnormal brain tissue and in a certain extent provide information that might be important for differential diagnosis. Two different approaches have been implemented, namely, single voxel spectroscopy (SVS) and chemical shift imaging (CSI).In the second technique, multiple voxels are utilized either in a plane (2D CSI) or in a volume (3D CSI); therefore,it is possible to study larger areas with a single experiment.Metabolic maps can be calculated based on the information derived from each voxel.
In what follows, we assume the reader has had an initial exposure to basic neural components such as dendrites, soma (cell body), axons and synapses, and the propagation of spikes down the branches of an axon to reach synapses on other neurons or on muscles or other effector organs.Connections of the amygdala with hippocampus and cerebral cortex provide the possible basis for enrichment of "behavioral emotion" by episodic memory and cognitive state. ## 1.5 Neurons and Neural Networks Nicolas Brunel introduces "Basic Neuron and Network Models" in chapter 2, which provides some sense of how models capture aspects of the workings of neurons that will help us understand the potential functionality of neural circuitry. Jonathan Rubin and John Rinzel then survey the treatment of "Neurons and Neuronal Networks as Dynamical Systems" (chapter 3) with the emphasis on the way in which the mathematics of nonlinear systems can use such notions as equilibria, stability, and oscillations to illuminate general properties of neural system dynamics. There is something of a chicken-and-egg problem between chapters 2 and 3 in that some of the terminology of dynamical systems theory is needed for the exposition of basic neuron and network models, but it is only with some understanding of such models that one can appreciate the deeper application of dynamical systems theory to neuroscience. There are radically different types of neurons in the human brain, and endless variations in neuron types of other species. In brain theory, the complexities of real neurons are abstracted in many ways to aid in understanding different aspects of neural network development, learning, or function. In what follows, we assume the reader has had an initial exposure to basic neural components such as dendrites, soma (cell body), axons and synapses, and the propagation of spikes down the branches of an axon to reach synapses on other neurons or on muscles or other effector organs.Output of a neuron may be characterized by spike trains (i.e., viewing the output of each neuron as a time series, defined in continuous time, of when the action potential at the axon hillock passes threshold for axonal propagation) or by firing rate (some measure of the rate at which spikes have been generated in a recent time interval).
However, some fibromatoses, especially those superficially located, are negative for this marker and the diagnosis should be based on careful clinicopathological correlation.The former tend to display nuclear β-catenin positivity, while the latter are usually negative or display cytoplasmic positivity only [15].Hyalinized collagen bundles are often present and may display a keloidal appearance. At the periphery, compact bundles of fibroblasts and capillaries probe the fascial planes and may infiltrate fat or skeletal muscle. It is not surprising that this histological picture is relatively often confused with that of a malignant tumour. Variants of nodular fasciitis include those with metaplastic bone (ossifying fasciitis); a variant that involves the periosteum (periosteal fasciitis); a variant that involves the scalp and tends to occur in children (cranial fasciitis) [6]; and a variant within the lumen of a blood vessel (intravascular fasciitis) [7, 9]. A rare variant of intradermal nodular fasciitis has also been described [10, 11]. Intra-articular location may also be seen [12]. Tumour cells are variably positive for smooth muscle actin and calponin [13] and usually negative for smooth muscle markers including desmin and h-caldesmon [14]. The histological diagnosis may be very difficult, especially in small biopsies. Confusion with a sarcoma or with fibromatosis are major pitfalls, with obvious detrimental consequences. **Figure 137.4** Typical tissue culture-like appearance of nodular fasciitis with prominent myxoid background. Immunohistochemistry may be useful in the distinction between fibromatosis and nodular fasciitis. The former tend to display nuclear β-catenin positivity, while the latter are usually negative or display cytoplasmic positivity only [15]. However, some fibromatoses, especially those superficially located, are negative for this marker and the diagnosis should be based on careful clinicopathological correlation.Lesions like this with a self-limited life and a distinctive clonal genetic translocation have been referred to as transient neoplasms [16].###### Clinical features [1, 2, 3, 4] ###### History and presentation The majority of tumours appear as tender rapidly growing masses beneath the skin.The average size is 1–3 cm in diameter.
Severe flu-like symptoms appear dose-related.##### ADVERSE EFFECTS/TOXIC REACTIONS Hypersensitivity reactions occur rarely.**Rare:** Confusion, leg cramps, back pain, gingivitis, flushing, tremor, anxiety, eye pain.**Occasional:** Dizziness, pruritus, dry skin, dermatitis, altered taste.Chronic Hepatitis C **IM, Subcutaneous:** **ADULTS:** 3 million units 3 times/wk for up to 6 mos. For pts who tolerate therapy and whose ALT level normalizes within 16 wks, therapy may be extended for up to 18–24 mos. May be used in combination with ribavirin. **CHILDREN, 3–17 YRS (WITH HIV CO-INFECTION):** 3–5 million units/m2 3 times/wk with ribavirin for 48 wks. Chronic Hepatitis B **IM, Subcutaneous:** **ADULTS:** 30–35 million units weekly, either as 5 million units/day or 10 million units 3 times/wk for 16 wks. **Subcutaneous:** **CHILDREN 1–17 YRS:** 3 million units/m2 3 times/wk for 1 wk, then 6 million units/m2 3 times/wk for 16–24 wks. **Maximum:** 10 million units 3 times/wk. Malignant Melanoma **IV:** **ADULTS:** Initially, 20 million units/m2 5 times/wk for 4 wks. **Maintenance:** 10 million units subcutaneously 3 times/wk for 48 wks. Follicular Non-Hodgkin's Lymphoma **Subcutaneous:** **ADULTS:** 5 million units 3 times/wk for up to 18 mos. Dosage in Renal Impairment Do not use when combined with ribavirin. Dosage in Hepatic Impairment No dose adjustment (see Contraindications). ##### SIDE EFFECTS **Frequent:** Flu-like symptoms (fever, fatigue, headache, myalgia, anorexia, chills), rash (hairy cell leukemia, Kaposi's sarcoma only). **Pts with Kaposi's sarcoma:** All previously mentioned side effects plus depression, dyspepsia, dry mouth or thirst, alopecia, rigors. **Occasional:** Dizziness, pruritus, dry skin, dermatitis, altered taste. **Rare:** Confusion, leg cramps, back pain, gingivitis, flushing, tremor, anxiety, eye pain. ##### ADVERSE EFFECTS/TOXIC REACTIONS Hypersensitivity reactions occur rarely. Severe flu-like symptoms appear dose-related.INTERVENTION/EVALUATION Offer emotional support.Monitor all levels of clinical function (numerous side effects).Encourage PO intake, particularly during early therapy.Monitor for worsening depression, suicidal ideation, associated behaviors.PATIENT/FAMILY TEACHING • Clinical response occurs in 1–3 mos.• Flu-like symptoms tend to diminish with continued therapy.
Migraine 6.Preeclampsia 4.Eclampsia 3.CVA 2.You suspect: 1.Vital signs are HR: 110, BP: 158/92, RR: 18, and SpO2: 97%.She also notes blurred vision in her right eye.A 37-year-old female who is 36 weeks pregnant calls the ambulance because she has an intense headache and is dizzy.Ventricular septal foramen 5.Hepatic portal system 4.Ductus venosus 3.Foramen ovale 2.Maintains the corpus luteum, which stimulates the production of estrogen and progesterone. 3. Turns the ruptured follicle into the corpus luteum after ovulation. 4. Stimulates the development, production, and release of milk from the mammary glands. 2. A sexually active, 35-year-old female presents with a 2-day history of increasing RLQ pain. She states that she has a history of tubal ligation reversal 4 months ago and has been actively trying to get pregnant with her new husband. She has not taken a pregnancy test and denies fever. Assessment reveals rebound tenderness and spotting vaginal bleeding. All of the following could cause the patient's symptoms EXCEPT: 1. Ectopic pregnancy. 2. Ovarian torsion. 3. Ruptured appendix. 4. Ruptured ovarian cyst. 3. A 27-year-old female complains of diffuse lower abdominal pain. She complains of an associated fever and chills and this morning noted that the pain worsened when she walked. She takes birth control pills and rarely uses condoms despite having multiple partners. She is conscious and alert. Which option indicates the most likely cause of the patient's symptoms? 1. Endometriosis 2. Uterine pregnancy 3. Toxic shock syndrome 4. PID 4. In fetal circulation, most of the blood bypasses the lungs of the fetus by going through which of the following? 1. Foramen ovale 2. Ductus venosus 3. Hepatic portal system 4. Ventricular septal foramen 5. A 37-year-old female who is 36 weeks pregnant calls the ambulance because she has an intense headache and is dizzy. She also notes blurred vision in her right eye. Vital signs are HR: 110, BP: 158/92, RR: 18, and SpO2: 97%. You suspect: 1. CVA 2. Eclampsia 3. Preeclampsia 4. Migraine 6.External, visible bleeding can be profuse.2.Commonly caused by external blunt trauma.3.The placenta covers or partially covers the cervical os.4.Should be suspected with a late-term pregnancy in a person with hypotension.7.Which of the following events takes place during the 2nd stage of labor?1.The infant is born.2.The placenta is delivered.3.The bag of waters breaks.4.
The goal of current research efforts at several laboratories has been to establish the cognitive and neural bases for the representation of semantic knowledge and to define the set of cognitive processes and neural structures that support semantic memory in communication and thought.**neurodegenerative disorder** A disorder characterized by progressive deterioration of brain systems from a healthy baseline state, often marked by the presence of gliosis. **neurodevelopmental disorder** A disorder caused by abnormal development of specific neural structures. **paranoid** A common subtype of schizophrenia characterized by delusions, especially of persecution, a preponderance of auditory hallucinations, and few negative or disorganized symptoms. **positive symptoms** Symptoms present in patients with schizophrenia and absent from healthy individuals, including delusions, hallucinations, and disorganized thought and behavior. **tardive dyskinesia** A disorder characterized by abnormal, involuntary hyperkinetic movements that can develop in patients on long-term neuroleptic treatment. Semantic Memory Murray Grossman, Phyllis L. Koenig University of Pennsylvania, USA This work was supported in part by funding from the U.S. Public Health Service (AG15116, NS35867, and AG17586) and the American Health Assistance Foundation. **Semantic memory is the long-term representation of mean** ingful information and the processes we use to make this information available for a multitude of cognitive tasks. Unlike episodic memory, we cannot necessarily recall the specific experiences associated with the acquisition of information represented in semantic memory. Semantic memory allows us to recognize a fork as a tined implement used for transferring food (without having to recall how we learned what a fork is) and to know that an apple is a sweet, red fruit with a pitted core that grows on trees in moderate climates (apart from our memory of the last time we ate one). The goal of current research efforts at several laboratories has been to establish the cognitive and neural bases for the representation of semantic knowledge and to define the set of cognitive processes and neural structures that support semantic memory in communication and thought.We focus on results that have contributed to our understanding of the neural substrate for semantic knowledge and associated processes.
The paralysis of the gastrocnemius-soleus complex with preservation of the deep posterior compartment, the intrinsic foot musculature, and the tibialis anterior causes the hindfoot cavus.#### Residual Poliomyelitis The character of poliomyelitis-induced cavus foot deformity is hindfoot cavus with dramatically high calcaneal pitch.Type X is found in 10-20 % of all CMT cases and is X-linked inheritance pattern. CMT-4 is quite rare and is autosomal dominant. Symptom onset and progression of the deformity are not uniform and usually begin in late childhood or early adulthood. Typically, it happens first in the intrinsic foot muscles, followed by lateral compartment (peroneus), anterior compartment (extensors), and lastly by the calf muscles and the posterior tibialis muscle. The diagnosis is based on the symptoms, neurologic assessment, family history, electromyography, nerve conduction velocity studies, and DNA testing. DNA testing and biopsy of the nerve are ultimate diagnostic tests for CMT disease [15, 16], but not all the genetic markers for CMT are identified. The electromyographic study demonstrates decreased velocity of nerve impulse conduction and increased charging time of the nerve. #### Idiopathic Cavus Foot Idiopathic type can be considered a deformity caused by a neurologic disorder not able to be diagnosed specifically. Lelievere asserted that idiopathic cavus foot is caused by a neurologic disorder in which the only symptoms are in the cavus foot. Although the degree of deformity overall seems less severe compared with the neurogenic cavus foot, the idiopathic type is also a complex deformity with similar features [17]. The idiopathic type is commonly symmetric and shows mainly hindfoot cavus. #### Residual Poliomyelitis The character of poliomyelitis-induced cavus foot deformity is hindfoot cavus with dramatically high calcaneal pitch. The paralysis of the gastrocnemius-soleus complex with preservation of the deep posterior compartment, the intrinsic foot musculature, and the tibialis anterior causes the hindfoot cavus.The ankle and foot fracture malunion (talar neck fracture, intraarticular calcaneal fracture) can also arouse fixed cavus foot deformity.The differential diagnoses for cavus foot deformity are shown in Table 11.2.## Diagnosis ### Clinical Features The hallmark of a cavus deformity is progressive ankle and foot deformities that are cosmetically disturbing.
The body responds to this with initiation of several neuroendocrine responses including activation of the sympathetic nervous system and renin-angiotensin-aldosterone chain.### **PATHOLOGIC CONDITIONS** #### **Cardiomyopathy** Cardiomyopathy is a disease involving destruction of the cardiac muscle fibers, causing impairment of myocardial function and decreased cardiac output (CO).Tracy CM, Epstein AE, Darbar D. 2012 ACCF/AHA/HRS focused update of the 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. _Circulation._ 2012;126:1784-1800. Wagner GS, Macfarlane P, Wellens H, et al. AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: part VI: acute ischemia/infarction: a scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society. _Circulation_. 2009;119:e262-e270. ## 19 ADVANCED CARDIOVASCULAR CONCEPTS _**Barbara Leeper**_ * * * **KNOWLEDGE COMPETENCIES** 1. Describe the etiology, pathophysiology, clinical presentation, patient needs, and principles of management of: • Cardiomyopathy • Valvular disease • Pericarditis • Aortic aneurysm • Cardiac transplantation 2. Compare and contrast the pathophysiology, clinical presentation, patient needs, and management approaches of: • Cardiomyopathy • Valvular disease • Pericarditis • Aortic aneurysm • Cardiac transplantation 3. Identify indications for, complications of, and nursing management of patients receiving intra-aortic balloon pump and ventricular assist device therapy. ### **PATHOLOGIC CONDITIONS** #### **Cardiomyopathy** Cardiomyopathy is a disease involving destruction of the cardiac muscle fibers, causing impairment of myocardial function and decreased cardiac output (CO). The body responds to this with initiation of several neuroendocrine responses including activation of the sympathetic nervous system and renin-angiotensin-aldosterone chain.This process contributes to remodeling of ventricular myocytes and the downward spiral of cardiomyopathy.The cause of cardiomyopathy is often unknown.Cardiomyopathies are commonly classified into three types: dilated, hypertrophic, and restrictive (Figure 19-1).**Figure 19-1.** Types of cardiomyopathies.**(A)** Dilated (cardiac dilatation and impaired contractility).
They are called the _10-percent tumor_ because approximately 10 percent are bilateral, 10 percent are extra-adrenal, and 10 percent are malignant.These chromaffin tumors secrete catecholamines and usually are located in the adrenal medulla, although 10 percent are located in sympathetic ganglia.Only 0.1 percent of hypertensive patients have a pheochromocytoma.Feigenberg and associates (2008) found cortical bone mass reductions using ultrasound in young primiparas in the puerperium compared with nulligravid controls. Rarely, some women develop idiopathic osteoporosis while pregnant or lactating. Its incidence is estimated to be 4 per million women (Hellmeyer and colleagues, 2007). The most common symptom of osteoporosis is back pain in late pregnancy or postpartum. Other symptoms are hip pain, either unilateral or bilateral, and difficulty in weight bearing (Dunne and colleagues, 1993; Smith and associates, 1995). In more than half of women, no apparent reason for osteopenia is found. Some known causes include heparin, prolonged bed rest, and corticosteroid therapy (Cunningham, 2005; von Mandach and co-workers, 2003). In a few cases, overt hyperparathyroidism or thyrotoxicosis eventually develops. Treatment is problematical, but most clinicians recommend calcium and vitamin D supplementation. Long-term follow-up indicates that although bone density improves, these women, as well as their offspring, may have chronic osteopenia (Carbone and colleagues, 1995). ### **ADRENAL GLAND DISORDERS** Pregnancy has profound effects on adrenal cortical secretion and its control or stimulation. These interrelationships are discussed in detail in Chapter 5 (p. 129). #### **Pheochromocytoma** These tumors are common findings at autopsy but are infrequently diagnosed. Only 0.1 percent of hypertensive patients have a pheochromocytoma. These chromaffin tumors secrete catecholamines and usually are located in the adrenal medulla, although 10 percent are located in sympathetic ganglia. They are called the _10-percent tumor_ because approximately 10 percent are bilateral, 10 percent are extra-adrenal, and 10 percent are malignant.Symptoms are usually paroxysmal and manifest as hypertensive crisis, seizure disorders, or anxiety attacks.Hypertension is sustained in 60 percent of patients, but half of these also have paroxysmal crises.Other symptoms during paroxysmal attacks are headaches, profuse sweating, palpitations, chest pain, nausea and vomiting, and pallor or flushing.
But doing so is fundamental to recovering from an illness, as Bernie Siegel pointed out in _Love, Medicine & Miracles._ Dysfunctional relationships put us in a state of chronic stress in part because we tend to "internalize" emotions that arise from these unhealthy relationships.Numerous other studies have shown that social isolation is associated with adverse health outcomes and that self-expression, education, and a sense of community can lower levels of stress hormones, improve quality of life, and enhance immune function. People who are socially isolated often have an overactive stress response. In fact, social isolation alone has been identified as an independent, major risk factor for all causes of mortality. Social connection, on the other hand, has been shown to positively influence disease outcomes including: all-cause mortality, depression, heart disease, disease susceptibility, diabetes mellitus, and survival from breast cancer (even metastatic breast cancer). The study done on the last of these is absolutely fascinating. Researchers surveyed 6,900 participants about their contact with friends and relatives, church membership, membership in clubs or groups, and marriage, and then followed them for 17 years. Those without close ties or frequent social contact had an overall death rate that was 3.1 times higher than those who did have those contacts. Of course, not just any relationship will do the trick. Stressful relationships have been linked to a number of adverse outcomes, ranging from cardiovascular disease to cancer. They also have an impact on digestive disease. Despite the importance of relationships, establishing them and repairing those that are broken are two of life's most challenging tasks. But doing so is fundamental to recovering from an illness, as Bernie Siegel pointed out in _Love, Medicine & Miracles._ Dysfunctional relationships put us in a state of chronic stress in part because we tend to "internalize" emotions that arise from these unhealthy relationships.When you are angry, a profound stress response is set off that is measurable biochemically, and it impacts your health on a number of levels.# ADAM'S STORY _Adam was a 35-year-old entrepreneur who was in the process of planning his wedding.
The classification of parasomnias is changing as new information emerges.58 They include REM parasomnias and periodic limb movements.They are sometimes mistaken for epileptic seizures.### Parasomnias Parasomnias are disorders that manifest around or during sleep.During an attack, patients retain self-awareness and long-term memory and can perform familiar tasks or navigate a familiar environment, but they appear unable to lay down any new memories and appear amnesic of all recent events during the attack. Once an attack is over, patients regain some memory about the event but remain amnesic for the central period of the episode. Attacks are usually isolated, but there is a 6% recurrence rate. The clinical presentation is usually so characteristic that, once seen, it is not easily mistaken for epilepsy. There is no evidence to support an epileptic cause or transient arterial ischemic events.56 A popular hypothesis is that of venous congestion in bilateral temporal lobes as a result of internal jugular vein valve insufficiency and sudden rises in intrathoracic pressure.57 If attacks are recurrent, have associated features (e.g., automatisms), and result in symptoms of memory impairment afterward, the diagnosis of TEA should be considered. ### Psychogenic Amnesia Psychogenic amnesia or dissociative fugue is rare and typically triggered by stressful or adverse life events. Careful clinical evaluation may reveal inconsistencies in the presentation that alert the practitioner to a conversion disorder. Features include extensive loss of autobiographic memories (including self-identity) in the context of preserved new learning, absence of repetitive questioning, and the ability to continue normal activities of daily living. ### Parasomnias Parasomnias are disorders that manifest around or during sleep. They are sometimes mistaken for epileptic seizures. The classification of parasomnias is changing as new information emerges.58 They include REM parasomnias and periodic limb movements.Occasionally video monitoring can be helpful.### Transient Ischemic Attacks TIA symptoms tend to be negative (i.e., a loss of function).Epileptic seizures invariably produce positive symptoms.One rare exception is that of apparent focal motor seizures caused by critical cortical ischemia from carotid artery stenosis, or shaking limb TIA (SLTIA) (Figure 58-2).
– Disorders may alter lab results: Hyperthyroidism and diabetes will increase serum ACE level.ACE inhibitors will lower serum ACE level.• Serum ACE inhibitors elevated in >75% of patients but is not diagnostic or exclusionary – Drugs may alter lab results: Prednisone will lower serum ACE and normalize gallium scan.• ~30% of patients have extrapulmonary manifestations (2)[C], which may include the following: – Uveitis – Other eye findings: conjunctival nodules, lacrimal gland enlargement, cataracts, glaucoma, papilledema – Cranial nerve palsies – Salivary gland swelling – Lymphadenopathy – Arrhythmias – Hepatosplenomegaly – Polyarthritis – Rashes (7)[B] Maculopapular of nares, eyelids, forehead, base of neck at hairline, and previous trauma sites Waxy nodular of face, trunk, and extensor surfaces of extremities Plaques (lupus pernio) of nose, cheeks, chin, and ears EN (component of Löfgren syndrome) Atypical lesions DIFFERENTIAL DIAGNOSIS • Sarcoidosis is a diagnosis of exclusion. • Infectious granulomatous disease, such as tuberculosis and fungal infections • Hypersensitivity pneumonitis • Lymphoma • Other malignancies associated with lymphadenopathy • Berylliosis (1)[B] DIAGNOSTIC TESTS & INTERPRETATION No definitive test for diagnosis, but diagnosis is suggested by the following: • Clinical and radiographic manifestations • Exclusion of other diagnoses • Histopathologic detection of noncaseating granulomas Initial Tests (lab, imaging) • CBC: Anemia/leukopenia ± eosinophilia can be seen. • Hypergammaglobulinemia can exist. • LFTs: Abnormal liver function and increased alkaline phosphatase can be encountered with hepatic involvement. • Calcium: Hypercalciuria occurs in up to 10% of patients, with hypercalcemia less frequent. • Serum ACE inhibitors elevated in >75% of patients but is not diagnostic or exclusionary – Drugs may alter lab results: Prednisone will lower serum ACE and normalize gallium scan. ACE inhibitors will lower serum ACE level. – Disorders may alter lab results: Hyperthyroidism and diabetes will increase serum ACE level.Routine CXRs are staged using Scadding classification.– Stage 0 = normal – Stage 1 = bilateral hilar adenopathy alone – Stage 2 = bilateral hilar adenopathy + parenchymal infiltrates – Stage 3 = parenchymal infiltrates alone (primarily upper lobes) – Stage 4 = pulmonary fibrosis (8)[C] • Chest CT scan may enhance appreciation of lymph nodes.
Results showed considerable _in vitro_ antibacterial efficacy against _Escherichia coli, Shigella dysenteriae, Shigella sonnei, Shigella flexneri, Vibrio_ _cholerae, Salmonella typhi, Salmonella typhimurium, Pseudomonas putida, Bacillus subtilis,_ and _Staphylococcus aureus._ Antioxytocic action of saponin isolated from _A.recemosus_ were given in concentrations of 50, 100, and 150 μg/ml.**_32.7.2.11 Asparagus recemosus_** _Asparagus recemosus_ was tried in menopausal syndrome for relieving symptoms like hot flashes, excessive sweating, tiredness, and sleep disturbances in a study conducted by Government Ayurveda College, Trivandrum, India. The report reads that the treatment was effective. No further details were available about the author, dosage, and or duration. In another study,50, 53–55 _A. recemosus, T. cordifolia, W. somnifera,_ and _Picrorhiza kurrooa_ were tested on the functions of macrophages obtained from mice treated with the carcinogen ochratoxin A (OTA). At the end of 17 weeks of treatment, the chemotactic activity of murine macrophages was significantly decreased with OTA compared with controls. Production of interleukin-1 (IL-1) and tumor necrosis factor (TNF) was also markedly reduced. OTA-induced suppression of chemotactic activity and production of IL-1 and TNF-alpha by macrophages was significantly inhibited with the treatment with _A. racemosus,_ _T. cordifolia, W. somnifera,_ and _P. kurroa._ It was also noted that _W. somnifera_ treated macrophage chemotaxis and _A. recemosus_ -induced excess production of TNF-alpha when compared with controls. Mandal et al.56 studied the antibacterial activity of _A. racemosus_ and compared it with chloramphenicol. The methanol extract of the roots of _A. recemosus_ were given in concentrations of 50, 100, and 150 μg/ml. Results showed considerable _in vitro_ antibacterial efficacy against _Escherichia coli, Shigella dysenteriae, Shigella sonnei, Shigella flexneri, Vibrio_ _cholerae, Salmonella typhi, Salmonella typhimurium, Pseudomonas putida, Bacillus subtilis,_ and _Staphylococcus aureus._ Antioxytocic action of saponin isolated from _A.Similar studies58,59 on the lactogoggue effect of _Asparagus recemosus_ showed positive effects, but details were not available.## **References** 1.Carlson, K.J.and Ziporyn Terra, E.S., _Harvard Guide to Women's Health_ , Harvard University Press, Cambridge, 1996.2.Kjerulff, K.H., Erickson, B.A., et al.
In one study, dogs with neoplasms <10 cm2 survived 584 days while those with neoplasms >10 cm2 survived only 292 days.1 Dogs with hypercalcemia have shorter survival (256 days) than dogs that are normocalcemic (584 days).Reported survival times vary from 0 to 1873 days.1 Size may be associated with prognosis.##### Growth and metastasis This tumor is usually occult to the owner and clinical veterinarian and therefore by the time it is recognized approximately 80% of the cases will have tumor in the pelvic canal, metastases to the sacral and internal iliac lymph nodes (70%), and have induced hypercalcemia (30% of cases) with clinical signs such as polyuria and polydipsia. The rate of growth is variable, generally it is slow but metastasis occurs in the majority of cases, as high as 90% in some series. The most common sites of distant metastasis are the lungs, spleen, and liver. In a proportion of cases, primarily those neoplasms that are small and discovered on physical examination, the neoplasm may be amenable to surgical excision. However, larger masses or those cases that have clinical disease, either a perineal mass or signs associated with hypercalcemia, often have peripheral infiltration of the soft tissue and perianal muscles by the neoplasm with a desmoplastic response and metastasis to regional lymph nodes. Hypercalcemia and hypophosphatemia may return to reference ranges following excision and when these laboratory abnormalities subsequently return it indicates the neoplasm has recurred or metastasized and the prognosis is poor. Reported survival times vary from 0 to 1873 days.1 Size may be associated with prognosis. In one study, dogs with neoplasms <10 cm2 survived 584 days while those with neoplasms >10 cm2 survived only 292 days.1 Dogs with hypercalcemia have shorter survival (256 days) than dogs that are normocalcemic (584 days).
1850;24(5-35):172–214._Arch Gén Méd_.Aran F. Recherches sur une maladie non encore décrite du système musculaire (atrophie musculaire progressive).2.1831;7:231–233._London Med Gazette_.Cases of a peculiar species of paralysis.Darwall J.# References 1.Recent data indicate that both C9ORF72 and TARDBP are involved in axonal transport.135 There is no evidence for genetic causes of sporadic ALS, which has shown a steadily increased mortality frequency throughout the century,136 still rising.12 This increase is of a magnitude that excludes genetic migration and has been interpreted from epidemiologic data alone to support an environmental etiology.6 A recent very large meta-analysis137 of genome-wide associations in ALS largely failed in associating risk gene variants with sporadic ALS. One locus at 1p34.1 modulating age of ALS onset was however identified. Considerable genetic heterogeneity seems to be present within the clinical ALS phenotype. The genetic influences on sporadic ALS can be described as weak.137 To what extent the specific protein functions associated with C9ORF72, SOD1, and TARDBP expressions interact with effects of metal exposure remains to be elucidated, and opens new and exciting avenues for future research in the intersections between genetic expression and environmental metal toxicity. ## Concluding Remarks Metal toxicity contributing to ALS pathogenesis has remained a viable hypothesis since mid-nineteenth century. Metals with neurotoxic properties have been detected in tissues and fluids from ALS patients. Disturbed metal homeostasis and various metal exposures can be suspected to contribute to ALS. Combined information from spatial clustering, occupational exposures, and conjugal cases further support this view, although precise mechanistic knowledge is still lacking. Modern analytical techniques and reliable sampling methods are needed to clarify the role of metals in ALS pathogenesis providing an incentive for preventive action. # References 1. Darwall J. Cases of a peculiar species of paralysis. _London Med Gazette_. 1831;7:231–233. 2. Aran F. Recherches sur une maladie non encore décrite du système musculaire (atrophie musculaire progressive). _Arch Gén Méd_. 1850;24(5-35):172–214.Charcot J-M. Amyotrophies spinales deuteropathiques sclérose latérale amyotrophique & Sclérose latérale amyotrophique._Bureaux du Progrès Médical_.1874;2:234–266.4.Ayton S, Lei P, Bush AI.Biometals and their therapeutic implications in Alzheimer's disease._Neurotherapeutics_.2015;12(1):109–120.5.Kiernan MC, Vucic S, Cheah BC, et al.Amyotrophic lateral sclerosis._Lancet_.2011;377(9769):942–955.6.
Stress reduction techniques or correcting sleep deprivation may be critical.For still others, the cortisol pathway is dominant.Changing meal timing or intermittent fasting may be most beneficial.For others, the main problem may be insulin resistance.Low-carbohydrate diets may work best here.For some patients, sugar or refined carbohydrates are the main problem.Other foods do not need to be restricted: kale or broccoli, for instance. Others have erroneously concluded that "it's all about calories." Actually, it's nothing of the sort. Calories are only a single factor in the multifactorial disease that is obesity. Let's face the truth. Low-calorie diets have been tried again and again and again. They fail every single time. There are other answers that are not really answers. These include, "There is no best diet" or "Choose the diet that suits you" or "The best diet is one you can follow." But if supposed experts in nutrition and disease don't know the right diet, how are you supposed to? Is the Standard American Diet is the best diet for me because it's the one I can follow? Or a diet of sugared cereals and pizza? Obviously not. In cardiovascular disease, for example, "Choose the treatment that suits you" would never be considered satisfactory advice. If the lifestyle factors of stopping smoking and increased physical activity both reduce heart disease, then we would strive to do both, rather than try to choose one or the other. We would _not_ say, "The best lifestyle for heart disease is the one you can follow." Unfortunately, many so-called experts in obesity profess this exact sentiment. The truth is that there are multiple overlapping pathways that lead to obesity. The common uniting theme is the hormonal imbalance of hyper-insulinemia. For some patients, sugar or refined carbohydrates are the main problem. Low-carbohydrate diets may work best here. For others, the main problem may be insulin resistance. Changing meal timing or intermittent fasting may be most beneficial. For still others, the cortisol pathway is dominant. Stress reduction techniques or correcting sleep deprivation may be critical.Most diets attack one part of the problem at a time.But why?In cancer treatment, for example, multiple types of chemotherapy and radiation are combined together.The probability of success is much higher with a broad-based attack.In cardiovascular disease, multiple drug treatments work together.
** Evidence of malnutrition includes decreased food intake, significant unintentional weight loss, decreased albumin and prealbumin levels, and thin appearance.What additional evidence from AJ's physical examination could be used to assess his nutritional status prior to initiating parenteral nutrition?**3.List AJ's likely medical problems demonstrated by his overall clinical picture. ** * Bowel obstruction as evidenced by distended loops of small intestine and a lack of air in the rectum on abdominal X-rays and feculent fluid obtained from the nasogastric tube. * Possible mesenteric thrombosis,considering his past medical history of stroke. * Severe electrolyte imbalance demonstrated by hyperkalemia, elevated BUN and creatinine. * Possible bilateral pneumonia * Unintentional weight loss and severe malnutrition. **2. What are the possible etiologies of AJ's bowel obstruction? ** In a compilation of the various causes of intestinal obstruction (both small and large bowel), taken from 13 reported series comprising a total of 12,731 adult patients, hernia accounted for 40 percent of the causes of the obstruction; adhesions 29 percent, intussusceptions 12 percent, and cancer 10 percent. However, in elderly patients, the main cause of large intestinal obstruction is colon cancer (70 percent of the cases), followed by diverticulitis (5 percent), and volvulus (10 percent). The symptoms are often insidious, though in most cases acute obstruction is the direct reason for a surgical consultation. Diarrhea, with the passage of blood and mucus, may result from an ulceration of the bowel. The occurrence of diarrhea may lead patients to assert that their bowel is functioning, but the looseness is secondary to the irritation caused by constipation as in AJ's case. **3. What additional evidence from AJ's physical examination could be used to assess his nutritional status prior to initiating parenteral nutrition? ** Evidence of malnutrition includes decreased food intake, significant unintentional weight loss, decreased albumin and prealbumin levels, and thin appearance.As negative acute phase reactants, these hepatic proteins can be falsely depleted during situations that result in a systemic inflammatory response (acute or chronic), such as trauma, surgery, or infection.It is helpful to simultaneously evaluate other markers of inflammation, such as temperature, white blood cell count or C-reactive protein.
Nonsurgical management of dysrhythmias includes oxygen therapy, drug therapy, temporary pacing, cardioversion, CPR, defibrillation, and catheter ablation.#### Nonsurgical Management.D. Monitor blood pressure and urine output.C. Monitor respiratory status for shortness of breath.B. Assess for pulmonary edema.A. Assess for cyanosis of the hands and feet.• Provide antidysrhythmic therapy according to unit policy (e.g., antidysrhythmic medication, cardioversion, or defibrillation), as appropriate. • Monitor and document patient's response to antidysrhythmic medications or interventions. • Monitor appropriate laboratory values (e.g., cardiac enzymes, electrolyte levels). • Monitor the patient's activity tolerance and schedule exercise/rest periods to avoid fatigue. • Observe for respiratory difficulty (e.g., shortness of breath, rapid breathing, labored respirations). • Promote stress reduction. • Offer spiritual support to the patient and/or family (e.g., contact clergy), as appropriate. Assess the patient's apical and radial pulses for a full minute for any irregularity, which may occur with problems such as premature beats, atrial fibrillation (AF), and second-degree heart blocks. If the apical pulse rate differs from the radial pulse rate, a pulse deficit exists and suggests that _the heart is not pumping adequately to perfuse the body._ Clinical manifestations of sustained tachydysrhythmias and bradydysrhythmias are summarized in Chart 36-1. Review the interpretation of the patient's 12-lead ECG and other diagnostic assessment. Nclex Examination Challenge Physiological Integrity What is the most appropriate assessment for the nurse to evaluate whether a client has adequate cardiac output and tissue perfusion? A. Assess for cyanosis of the hands and feet. B. Assess for pulmonary edema. C. Monitor respiratory status for shortness of breath. D. Monitor blood pressure and urine output. #### Nonsurgical Management. Nonsurgical management of dysrhythmias includes oxygen therapy, drug therapy, temporary pacing, cardioversion, CPR, defibrillation, and catheter ablation.Many types of drugs are given to manage dysrhythmias (see the Evidence-Based Practice box on at right).Evidence Based Practice What are the Latest Recommendations for Preventing Medication Errors?**Michaels, A.D., Spinler, S.A., Leeper, B., Ohman, E.M., Alexander, K.P., Newby, L.K., et al.(2010).
The electron-density of these granules is similar to the electron-densityof heterochromatin (H) in the nuclei.+ve reaction) and how one can discern the crystalline core in the insulin granules.Note how densely the neuroendocrine granules (arrows) in theislet cells have stained (i.e.Granules in exocrine and endocrine pancreatic cells are compared here.If sufficient numbers of neuroendocrine granules are present in the specimen, there is usually no difficulty in deciding what one is looking at, but when very few 'dense granules' are present, the distinction between a neuroendocrine granule and say for example, a lysosome, a lipid droplet or a rather small serous secretory granule becomes difficult or impossible. In such instances, immunohistochemistry (light microscopy) or immunocytochemistry (electron microscopy) may help (by demonstrating specific peptides or neurotransmitter substances or neuron specific enolase) or one can try the uranaffin reaction† (Payne _et al._ , 1983, 1984) ( _Plates 162_ and _163_ ) The uranaffin positive structures (which stain with uranium and hence appear electron-dense) include nuclei (chromatin DNA) and nucleolus (RNA), ribosomes (RNA) and neuroendocrine granules (staining thought to be due to high concentrations of adenosine triphosphate (ATP), diphosphate (ADP) or monophosphate (AMP) in these granules). Other structures such as exocrine secretory granules and lysosomes are uranaffin negative ( _Plate 162_). It is fortunate that ribosomes stain with this reaction for one can use them as an inbuilt control ( _Plate 163_). A positive granule is one which is as electron-dense as a ribosome, any granule showing less density is negative. Plate 162 Uranaffin reaction on a dog pancreas. Granules in exocrine and endocrine pancreatic cells are compared here. Note how densely the neuroendocrine granules (arrows) in theislet cells have stained (i.e. +ve reaction) and how one can discern the crystalline core in the insulin granules. The electron-density of these granules is similar to the electron-densityof heterochromatin (H) in the nuclei.In contrast to these uranaffin +ve structuresare the zymogen granules (Z) which are much less electron-dense (i.e.− ve reaction).× 8000 Plate 163 Uranaffin reaction on a carcinoid of ileum.(Same case as _Plates 170_ and _172_ ).The neuroendocrine granules are intensely stained (thick arrows), so are the polyribosomes (arrowheads), heterochromatin (H) and perichromatin granules (thin arrows).
Pilo-erection ("goose-bumps") is often associated with opioid withdrawal, especially when drug is stopped suddenly ("cold turkey").The opioid withdrawal syndrome is characterized by the patient feeling dysphoria, craving another dose of opioid, being irritable, and having signs of autonomic hyperactivity such as tachycardia, tremor, and sweating.At and above pain-relieving doses, the opioids induce euphoria, which is the main reinforcing property of the opioids. Opioids can also induce a very intense but brief euphoria, sometimes called a "rush," followed by a profound sense of tranquility which may last several hours, followed in turn by drowsiness ("nodding"), mood swings, mental clouding, apathy, and slowed motor movements. In overdose, these same agents act as depressants of respiration, and can also induce coma. The acute actions of opioids can be reversed by synthetic opioid antagonists, such as naloxone and naltrexone, which compete as antagonists at opioid receptors. When given chronically, opioids readily cause both tolerance and dependence. Adaptation of opioid receptors occurs quite readily after chronic opioid administration. The first sign of this is the need of the patient to take a higher and higher dose of opioid in order to relieve pain or to induce the desired euphoria. Eventually, there may be little room between the dose that causes euphoria and that which produces toxic effects of an overdose. Another sign that dependence has occurred and that opioid receptors have adapted by decreasing their sensitivity to agonist actions is the production of a withdrawal syndrome once the chronically administered opioid wears off. The opioid antagonists, such as naloxone, can precipitate a withdrawal syndrome in opioid-dependent persons. The opioid withdrawal syndrome is characterized by the patient feeling dysphoria, craving another dose of opioid, being irritable, and having signs of autonomic hyperactivity such as tachycardia, tremor, and sweating. Pilo-erection ("goose-bumps") is often associated with opioid withdrawal, especially when drug is stopped suddenly ("cold turkey").Thus, what may have begun as a quest for euphoria may end up as a quest to avoid withdrawal.Clonidine, an α2-adrenergic agonist, can reduce signs of autonomic hyperactivity during withdrawal and aid in the detoxification process.Opioid receptors can readapt to normal if given a chance to do so in the absence of additional intake of an opioid.
Ciprofloxacin was also compared to placebo in a study conducted by Arnold et al.The authors found similar response rates 56 % versus 55 % among patients who received ciprofloxacin versus those who received mesalamine as assessed by improvements in CDAI scores [11].Ursing and Kamme described the use of metronidazole in five patients with Crohn disease and reported a response in four of them [9]. In the first double-blinded comparative study involving antibiotics, metronidazole was compared to sulfasalazine in active Crohn disease in 78 patients. Patients were randomized to receive either metronidazole or sulfasalazine for 4 months and then crossed over to receive the alternate drug for an additional 4 months. The authors found that metronidazole was slightly more effective than sulfasalazine in treating active Crohn disease based on improvements in the Crohn Disease Activity Index (CDAI) [3]. Further double-blinded studies, including one performed by Sutherland et al., evaluated two doses of metronidazole (20 and 10 mg/kg) versus placebo. One hundred and five patients were randomized, and 56 completed the 16-week study. The authors found significant reductions in disease activity index scores and serum orosomucoid levels among the groups receiving metronidazole versus those who received placebo. The authors also found that patients with both large and small disease responded better to therapy than those with isolated small bowel disease [10]. Few randomized trials have been published evaluating the use of ciprofloxacin as monotherapy in active Crohn disease. In a randomized study conducted by Colombel et al., 40 patients with mild to moderate active Crohn disease received either ciprofloxacin or mesalamine for 6 weeks. The authors found similar response rates 56 % versus 55 % among patients who received ciprofloxacin versus those who received mesalamine as assessed by improvements in CDAI scores [11]. Ciprofloxacin was also compared to placebo in a study conducted by Arnold et al.Significant decreases in CDAI were observed in the ciprofloxacin-treated group 187–112 versus 230–205 in the placebo-treated group [12].Several studies conducted in adults have evaluated the use of combination therapy with ciprofloxacin and metronidazole in active Crohn disease.
medial geniculate body, one of a pair of areas on the posterior dorsal thalamus that relay auditory impulses from the lateral lemniscus to the auditory cortex.medial fibroplasia, the most common of the various nonatherosclerotic lesions characterized on an angiogram by the string-of-beads sign (areas of the artery wall having protruding aneurysms alternating with stenosis and thinning).medial calcaneal nerve, a nerve that is often multiple and originates from the tibial nerve near the ankle and descends onto the medial side of the heel. It innervates skin on the medial surface and sole of the heel. medial calcific sclerosis. See Mönckeberg's arteriosclerosis. medial cerebellar nucleus. See fastigial nucleus. medial circumflex femoral artery, an artery that passes medially around the shaft of the femur and near the margin of the adductor brevis, giving off a small branch, which enters the hip joint through the acetabular notch and anastomoses with the acetabular branch of the obturator artery, then divides into two major branches deep to the quadratus femoris muscle. One of these branches ascends to the trochanteric fossa and connects with branches of the gluteal and lateral circumflex femoral arteries. The other branch passes laterally to participate with other arteries to form an anastomotic network of vessels around the hip. medial cuneiform bone, the largest of three cuneiform bones of the foot, situated on the medial side of the tarsus, between the scaphoid bone and the first metatarsal. It serves as the attachment for various ligaments, the tendons of the tibialis anterior, and the peroneus longus. It articulates with the scaphoid, the intermediate cuneiform, and the first and second metatarsals. Also called internal cuneiform bone. medial fibroplasia, the most common of the various nonatherosclerotic lesions characterized on an angiogram by the string-of-beads sign (areas of the artery wall having protruding aneurysms alternating with stenosis and thinning). medial geniculate body, one of a pair of areas on the posterior dorsal thalamus that relay auditory impulses from the lateral lemniscus to the auditory cortex.medial labial frenulum, a fold of mucosa on the inner surface of both lips that connects the lip to the adjacent gum.medial malleolus, the rounded process of the tibia forming the internal surface of the ankle joint.Also called internal malleolus.medial palpebral arteries, small branches of the ophthalmic artery that supply the medial area of the upper and lower eyelids.
These substances include numerous biochemicals that can activate serotonin and dopamine receptors and produce euphoria and hallucinations in large enough doses.### Some natural psychoactive substances Naturally occurring psychoactive substances have been used in religious rituals and shamanism for thousands of years.Increasing serotonin that is naturally released appears to produce better results than increasing the concentration systemically. Some currently used serotonin enhancers include the following (trade names are in parentheses): fluoxetine (Prozac), paroxetine (Paxil), and sertraline (Zoloft). ### Drugs affecting dopamine Dopamine is a catecholamine neurotransmitter that has five known receptors types (D1, D2, D3, D4, and D5). Dopamine is produced in the substantia nigra and the ventral tegmental area. Attempts to supply dopamine to make up for its loss in the substantia nigra, as in Parkinson's disease, failed because dopamine does not cross the blood brain barrier if administered into the blood stream. However, its precursor in the pathway for its synthesis in cells, L-dopa, does. This treatment can mitigate Parkinson's symptoms for several years but eventually becomes ineffective. Moreover, in the course of treatment, patients may develop motor control syndromes called _dyskinesias._ The ineffectiveness is probably because of the loss of receptors for dopamine or the death of the cells dopamine normally activates. Dopamine is also the reinforcement neurotransmitter for the reward system of the brain. It is released in the prefrontal cortex in response to food, sex, and neutral stimuli to which pleasurable stimuli have become associated. Drugs such as cocaine, nicotine, and amphetamines lead to an increase of dopamine in the brain's reward pathways and can hijack and overwhelm the natural reward system, leading to addiction. Many anti-anxiety medications target dopamine receptors, particularly the D2 receptor, as discussed previously. ### Some natural psychoactive substances Naturally occurring psychoactive substances have been used in religious rituals and shamanism for thousands of years. These substances include numerous biochemicals that can activate serotonin and dopamine receptors and produce euphoria and hallucinations in large enough doses.Psilocybin is noted for its frequent effect of inducing religious-like experiences and is actually rarely a drug of abuse.Naturally occurring cholinergic antagonists from plants such as the deadly nightshade and mandrake are hallucinogenic.Cannabinoids found in marijuana activate receptors called CB1 and CB2 that are involved in the brain's pain and immune control systems.
Ideal blood sugar level at bedtime is <140 mg/dl (7.7 mmol/l).• Test at bedtime.Ideal blood sugar two hours after meals is <140 mg/dl (7.7 mmol/l).• Test two hours after each meal.Ideal blood sugar before meals is <120 mg/dl (6.7 mmol/l).Guidelines for Self-Monitored Blood Glucose • Test on awakening and just before each meal.Every type 2 diabetic should own a blood glucose monitor and become familiar with its use. Even those diabetics whose blood glucose is well controlled through diet, lifestyle, and supplements should measure their blood glucose regularly. Numerous dietary factors, supplements, exercise, stress, and illness can all have a significant impact on blood glucose control. Becoming aware of how all these factors influence diabetes will help motivate type 2 diabetics to make positive changes, and monitoring will provide immediate feedback about the results of any changes. Diabetics who have a more serious case of disease, with diminished pancreatic insulin production, may benefit from efforts to establish consistently near-normal blood glucose control using intensive insulin therapy similar to that of type 1 diabetics. A C-peptide blood test can provide an estimate of how much insulin type 2 diabetics are producing and is one way to help determine the appropriateness of using insulin (discussed below). If diabetics are placed on an intensive insulin therapy program, they must self-monitor their blood glucose as frequently as type 1 diabetics on intensive insulin therapy (usually before and two hours after each meal). One way to achieve optimal blood glucose in these individuals is to give a daily injection of long-acting insulin (Lantus), which provides a smooth, continual release of insulin for 24 hours, in addition to diet and medication. Diabetics on this type of program definitely need to measure blood glucose frequently. Guidelines for Self-Monitored Blood Glucose • Test on awakening and just before each meal. Ideal blood sugar before meals is <120 mg/dl (6.7 mmol/l). • Test two hours after each meal. Ideal blood sugar two hours after meals is <140 mg/dl (7.7 mmol/l). • Test at bedtime. Ideal blood sugar level at bedtime is <140 mg/dl (7.7 mmol/l).This assessment can greatly influence treatment, especially in a diabetic hoping to avoid or cease using insulin.The level of pancreatic insulin production can also partially determine the types of medication or natural health products that are more likely to be effective.
Both Drs.These particles are antigenic [material that causes immune reactions] and may set up an allergic or antibody response that the child will never outgrow."The immature cells lining the intestines will allow foreign food particles to pass through undigested."Their intestines are not meant to digest anything other than breast milk.(AYURVEDA), N.D. See Allergies, Hearing and Ear Disorders, Pregnancy and Childbirth. ### Diet and Nutrition Proper nutrition not only helps create a strong defense against illness, it is crucial to a child's well-being. Dr. Smith notes that a majority of early childhood illnesses and infections are due to food allergies, especially from the early introduction of cow's milk or other allergy-producing foods into a child's diet. Breast-feeding: Breast-feeding decreases the likelihood of developing allergic sensitivities to certain foods later in life, according to Dr. Sodhi. "Children who are breast-fed not only take in vital nutrients from the mother's milk, but they also receive the antibodies necessary to protect them against childhood illnesses such as ear infections and measles." Human breast milk contains nutrients that are easily digested, contribute to healthy brain development, and provide immunity to infectious agents that the infant will encounter in the environment. It contains anti-inflammatory substances that infants cannot manufacture on their own; stimulates the production of antibodies, which can neutralize a substance foreign to the body before it becomes an allergen; and populates the child's immature intestinal barrier with beneficial microflora. Dr. Smith emphasizes that nursing for at least 8-10 months contributes to the child having fewer allergies, better jaw formation, good teeth, and a good dental arch. "If babies are given anything other than breast milk in the first few months of life, food sensitivities may develop," says Dr. Smith. "Their intestines are not meant to digest anything other than breast milk. The immature cells lining the intestines will allow foreign food particles to pass through undigested. These particles are antigenic [material that causes immune reactions] and may set up an allergic or antibody response that the child will never outgrow." Both Drs.Solid Foods: Dr. Smith notes that when a child is ready to eat solid foods, usually sometime around 4-6 months old, parents can introduce fresh fruits and vegetables, grains and legumes, and low-fat proteins like chicken and fish.
Many individuals with mild disabilities are able to manage their medical needs independently or with minimal assistance from a primary health care provider, whereas others require frequent and even continuous interactions with the health care system.Regardless of the definition used, patients with disabilities will have a wide spectrum of health care needs.Although most caregivers are adept at handling many of their children's emergencies, caregivers seek help for a variety of reasons, including the need for respite, equipment malfunction, an overwhelming medical problem, or help with transport to the child's home hospital. In contrast to the pediatric population, there is no universally recognized definition for adults with special health care needs. The Institute of Medicine (IOM) has used several different definitions for disability, including an "inability or limitation in performing socially defined activity and roles expected of individuals within a social and physical environment. "6 The number of adults who meet this broad definition is difficult to calculate. Current estimates indicate that as many as 50 million U.S. residents have some type of disability.7 Estimates come from various national surveys that vary in their definitions, questions, and target populations. Even more importantly, of 18 different national surveys reviewed by the IOM Committee on Disability in America, only four include institutionalized individuals.7 Given the large number of surveillance groups, the IOM has recommended adoption of the World Health Organization's International Classification of Functioning, Disability and Health, which is currently being used in many countries as a standardized assessment tool for both individuals and populations. Regardless of the definition used, patients with disabilities will have a wide spectrum of health care needs. Many individuals with mild disabilities are able to manage their medical needs independently or with minimal assistance from a primary health care provider, whereas others require frequent and even continuous interactions with the health care system.Many of the childhood conditions that are associated with special health care needs, such as cerebral palsy, will persist into adulthood.The relative incidence of traumatic injury is highest among adolescents and young adults, making traumatic brain and spinal cord injuries a significant contributor to both physical and cognitive disability.
2 = Some effort against gravity; limb cannot get to or maintain (if cued) 90 (or 45) degrees, drifts down to bed, but has some effort against gravity.1 = Drift; limb holds 90 (or 45) degrees, but drifts down before full 10 seconds; does not hit bed or other support.Motor (Arm)** | Right arm: ______ Left arm: ______ 0 = No drift; limb holds 90 (or 45) degrees for full 10 seconds.**5.Specific patient manifestations depend on the extent and location of the ischemia and the arteries involved (Chart 47-3). TABLE 47-3 NIH STROKE SCALE CATEGORY AND MEASUREMENT | SCORE* ---|--- **1a. Level of Consciousness (LOC)** | ______ 0 = Alert; keenly responsive. 1 = Not alert; but arousable by minor stimulation to obey, answer, or respond. 2 = Not alert; requires repeated stimulation to attend or is obtunded and requires strong or painful stimulation to make movements (not stereotyped). 3 = Responds only with reflex motor or autonomic effects or totally unresponsive, flaccid, and areflexic. **1b. LOC Questions** | ______ 0 = Answers two questions correctly. 1 = Answers one question correctly. 2 = Answers neither question correctly. **1c. LOC Commands** | ______ 0 = Performs two tasks correctly. 1 = Performs one task correctly. 2 = Performs neither task correctly. **2. Best Gaze** | ______ 0 = Normal. 1 = Partial gaze palsy; gaze is abnormal in one or both eyes, but forced deviation or total gaze paresis is not present. 2 = Forced deviation, or total gaze paresis not overcome by the oculocephalic maneuver. **3. Visual** | ______ 0 = No visual loss. 1 = Partial hemianopia. 2 = Complete hemianopia. 3 = Bilateral hemianopia (blind including cortical blindness). **4. Facial Palsy** | ______ 0 = Normal symmetrical movements. 1 = Minor paralysis (flattened nasolabial fold, asymmetry on smiling). 2 = Partial paralysis (total or near-total paralysis of lower face). 3 = Complete paralysis of one or both sides (absence of facial movement in the upper and lower face). **5. Motor (Arm)** | Right arm: ______ Left arm: ______ 0 = No drift; limb holds 90 (or 45) degrees for full 10 seconds. 1 = Drift; limb holds 90 (or 45) degrees, but drifts down before full 10 seconds; does not hit bed or other support. 2 = Some effort against gravity; limb cannot get to or maintain (if cued) 90 (or 45) degrees, drifts down to bed, but has some effort against gravity.4 = No movement.Untestable = Amputation or joint fusion.**6.Motor (Leg)** | Right leg: ______ Left leg: ______ 0 = No drift; leg holds 30-degree position for full 5 seconds.1 = Drift; leg falls by the end of the 5-second period but does not hit bed.2 = Some effort against gravity; leg falls to bed by 5 seconds, but has some effort against gravity.
Compare electronarcosis.Electrosleep therapy is said to be beneficial for patients with anxiety, depression, gastric distress, insomnia, personality disorders, and schizophrenia.The procedure is repeated from 5 to 30 times.The current, which is discharged for 15 to 20 minutes, produces a tingling sensation but does not always induce sleep.electroporation /-pôrā″shən/ , a type of osmotic transfection in which an electric current is used to produce temporary holes in cell membranes, allowing the entry of nucleic acids or macromolecules (a way of introducing new deoxyribonucleic acid into the cell). See also transfection. electroresection /-risek″shən/ [Gk, elektron \+ L, re, again, secare, to cut] , a technique for the removal of bladder tumors or prostate tissue by electrocautery. A wire is guided to the site through the urethra with the aid of an optic probe. Electricity is passed through the wire when the wire is properly located in the tissue to be destroyed. The procedure is performed after administration of an anesthetic. electroshock [Gk, elektron \+ Fr, choc] , a condition of shock caused by accidental contact with an electric current. The symptoms are similar to those of shock produced by thermal burns, trauma, or coronary thrombosis. electroshock therapy, (Obsolete) now called electroconvulsive therapy. electrosleep therapy [Gk, elektron \+ AS, slaep \+ Gk, therapeia, treatment] , a technique designed to induce sleep, especially in psychiatric patients, by administering a low-amplitude pulsating current to the brain. The cathode is placed supraorbitally, and the anode is placed over the mastoid process. The current, which is discharged for 15 to 20 minutes, produces a tingling sensation but does not always induce sleep. The procedure is repeated from 5 to 30 times. Electrosleep therapy is said to be beneficial for patients with anxiety, depression, gastric distress, insomnia, personality disorders, and schizophrenia. Compare electronarcosis.electrostimulation /-stim′yəlā″shən/ , the application of electric current to stimulate muscle tissue for therapeutic purposes, such as facilitation of muscle activation and muscle strengthening.See also electric muscle stimulator.
Take diabetes.Most of us use traditional cures for minor aches and pains, but doctors at top research institutions now realize that they also work for some of our most serious health threats."I haven't had a serious cold since—and no sinus infections at all," she says.Her friend, a family physician, told her to start taking echinacea at the first sign of sniffles.All those drugs in your medicine cabinet? At least 25 percent of them contain active ingredients that are similar or identical to those found in plants. The active substance in aspirin—one of the world's most popular medications—was originally derived from white willow bark. The decongestant ephedrine is based on chemicals in the ephedra plant. The heart drug digitalis is derived from the foxglove. The cancer drug taxol comes from the Pacific yew tree. In fact, big drug makers continually send teams of scientists to remote locations to scour the countryside for medically promising chemicals. ### Finding What Works In current medical practice, traditional healing techniques are sometimes neglected, but with luck they're never forgotten. Physical therapists use the same hot and cold treatments that were popular among Native American tribes—treatments that often work better than aspirin, with none of the side effects. Kitchen cuts certainly heal better when you apply a dab of triple antibiotic. But guess what? A slathering of honey does the same thing, and may help the cut heal faster. Molly Hopkins, a 60-year-old landscape designer in Albuquerque, New Mexico, discovered first-hand that traditional treatments are sometimes superior to their conventional counterparts. "I used to get sinus infections every time I got a cold, and then I had to take antibiotics," she says. Her friend, a family physician, told her to start taking echinacea at the first sign of sniffles. "I haven't had a serious cold since—and no sinus infections at all," she says. Most of us use traditional cures for minor aches and pains, but doctors at top research institutions now realize that they also work for some of our most serious health threats. Take diabetes.Those who also eat a clove of garlic daily may naturally lower blood sugar and with it their doses of medicine.Depression is another condition that frequently requires medication, yet studies show that the herb St. John's wort may be just as effective as drugs for mild to moderate cases.
Biceps reflex testing (Seidel et al, 2011) Bichat's membrane /bishäz/ [Marie F.X.See also deep tendon reflex.biceps reflex, a contraction of a biceps muscle produced when the tendon is tapped with a percussor in testing deep tendon reflexes.See biceps brachii.Biceps femoris biceps flexor cubiti.It is one of the hamstring muscle group and lies on the posterior, lateral side of the thigh.bicarbonate therapy, a procedure to increase a patient's stores of bicarbonate when there are signs of severe acidosis. It is usually performed only in certain cases, and with extreme caution, as a stopgap measure to neutralize acidosis partially when the patient's blood pH has fallen to levels that may be hazardous to the survival of vital tissues. bicarbonate transport, the route by which most of the carbon dioxide is carried in the bloodstream. Once dissolved in the blood plasma, carbon dioxide combines with water to form carbonic acid, which immediately ionizes into hydrogen and bicarbonate ions. The bicarbonate ions serve as part of the alkaline reserve. bicellular /bī·sel′yo̅o̅·lər/ [L, bis, twice + cella, storeroom] , made up of two cells, or having two cells. biceps, (Informal) a muscle having two heads; frequently used to refer to the muscles that flex and supinate the forearm. biceps brachii /bī″seps brā″kē·ī/ [L, bis, twice, caput, head, bracchii, arm] , the long fusiform muscle of the upper arm on the anterior surface of the humerus, arising in two heads from the scapula. It flexes the arm and the forearm and supinates the hand. Also called biceps, biceps flexor cubiti. Compare brachialis, triceps brachii. Biceps brachii (Patton, 2016) biceps femoris [L, bis, twice, caput, head, femoris, thigh] , one of the posterior femoral muscles. It has two heads at its origin. The biceps femoris flexes the leg and rotates it laterally and extends the thigh, rotating it laterally. It is one of the hamstring muscle group and lies on the posterior, lateral side of the thigh. Biceps femoris biceps flexor cubiti. See biceps brachii. biceps reflex, a contraction of a biceps muscle produced when the tendon is tapped with a percussor in testing deep tendon reflexes. See also deep tendon reflex. Biceps reflex testing (Seidel et al, 2011) Bichat's membrane /bishäz/ [Marie F.X.bichromatic analysis /-krōmat″ik/ [Gk, bios \+ chroma, color] , the spectrophotometric monitoring of a reaction at two wavelengths.It is used to correct for background color.Bicillin C-R /bi-sil′in/ , combination preparation of two antibiotics.Brand name for penicillin G benzathine and penicillin G procaine.
**c.** Have client remain in waiting room or office for at least 30 minutes after the injection to monitor for adverse effects.** Record the date and time for follow-up site reading.**b.** Record the site, date, and time of the test.** Postprocedure interventions **a.**3.** Obtain informed consent.**b.** Anti-nuclear antibody (ANA) titer determination **1. ** The ANA titer determination is a blood test used for the differential diagnosis of rheumatic diseases and for the detection of anti-nucleoprotein factors and patterns associated with certain autoimmune diseases. **2. ** The test is positive at a titer of 1:20 or 1:40, depending on the laboratory. **3. ** A positive result does not necessarily confirm a disease. **4. ** The ANA titer is positive in most individuals diagnosed with systemic lupus erythematosus (SLE); it may also be positive in individuals with systemic sclerosis (scleroderma) or rheumatoid arthritis. **5. ** An ANA titer result can be false positive in some individuals. **B. ** Anti-dsDNA antibody test **1. ** The anti-dsDNA (double-stranded DNA) antibody test is a blood test done specifically to identify or differentiate DNA antibodies found in SLE. **2. ** The test supports a diagnosis, monitors disease activity and response to therapy, and establishes a prognosis for SLE. **3. ** Values **a. ** Negative: Lower than 70 units by enzyme-linked immunosorbent assay (ELISA) **b. ** Borderline: 70 to 200 units **c.** Positive: Higher than 200 units **C.** See Chapter 11 for testing related to acquired immunodeficiency syndrome (AIDS). **D.** Skin testing **1. ** Description **a. ** The administration of an allergen to the surface of the skin or into the dermis **b. ** Administered by patch, scratch, or intradermal techniques **2. ** Preprocedure interventions **a. ** Discontinue systemic corticosteroids or antihistamine therapy 5 days before the test as prescribed. **b. ** Obtain informed consent. **3. ** Postprocedure interventions **a. ** Record the site, date, and time of the test. **b. ** Record the date and time for follow-up site reading. **c.** Have client remain in waiting room or office for at least 30 minutes after the injection to monitor for adverse effects.70-1).FIGURE 70-1 Interpretation of intradermal test results, based on the size of the wheal after 15 to 30 minutes.(From Monahan F, Sands J, Neighbors M, Marek J, Green C: _Phipps' medical-surgical nursing: Health and illness perspectives,_ ed 8, St. Louis, 2007, Mosby.)**e.** Measure flare along with the wheal and document the size and other findings.
This product, in tandem with Notatum 4X, often tests positive after dental surgery, since the Aspergillus assists in bone and soft-tissue healing and the Mucor aids blood flow and reduces the effects of bruising. Other commonly used microbial isopathics include Mucor 4X drops (used alone when the Aspergillus does not test positive) to reduce bleeding and bruising after dental cavitation surgery and Roqueforti/Candida 3X rectal suppositories to help treat vaginal yeast, prostatitis, or intestinal dysbiosis associated with appendix and genital focal infections. However, practitioners should be aware that suppositories, and sometimes even the tablets and capsules, occasionally have strong healing effects, even with SanPharma's gentler production methods. Therefore, the milder drop form of these medications is often more suitable for weaker patients, especially at the beginning of treatment when the goal is to simply reduce inflammation and reintegrate the estranged focus with the body. When capsules or suppositories are indicated, they often need to be prescribed in conjunction with an effective drainage protocol, using the more potent gemmotherapy remedies described in chapter 2. Finally, it should be noted that the most important step that practitioners can make to reduce the possibility of potentially strong healing effects is to receive thorough training in the use of these remedies before prescribing them.IV NEURAL THERAPY WITHOUT NEEDLES MASSAGE PROTOCOL This neural therapy massage protocol can mitigate 70 to 100 percent of the (often silent) nerve and tissue irritation generated from a scar, and it can be performed in the privacy of your own home.Since all the scars on the body resonate together in one sheet of skin, it is important to remember to include _all_ scars in your treatment—from your first scar, the belly button or umbilicus, to the smallest arthroscopic surgical scar to acne and stretch mark scars and even ear-piercing scars.
The investigators suggested that interventions based on diet that could alter the composition of microbiota could be considered as an option for managing the metabolic syndromes.This coincided with significantly lower methylation of CpGs in the promoter region of the FFAR3 gene in the obese and type 2 diabetic individuals (Remely et al., in press).How the commensal bacteria contribute to DNA methylation is an interesting question that deserves investigation. It was speculated that the symbionts might alter expression or modification of factors that recruit DNA methyltransferases to specific sequences on the genes involved in modulation of immune responses (Takahashi et al., 2011). There are lines of evidence pointing to the involvement of the gut symbionts metabolic end products in the epigenetic effects. For example, folate derivatives produced by microbiota act as cofactors in one-carbon (C1) transfer reactions utilized in the synthesis of a variety of essential compounds that contribute to DNA methylation (reviewed in Nagy-Szakal & Kellermayer, 2011). In addition, short-chain fatty acids are presumably involved in epigenetic regulation of inflammatory responses mediated by free fatty acid receptors (FFARs) (Pegorier, Le May, & Girard, 2004). In a recent study, it was shown that the composition of the gut microbiota differs in obese and type 2 diabetic individuals with the diversity of the microbiota being significantly lower in these two groups of patients compared to normal-weight individuals. This coincided with significantly lower methylation of CpGs in the promoter region of the FFAR3 gene in the obese and type 2 diabetic individuals (Remely et al., in press). The investigators suggested that interventions based on diet that could alter the composition of microbiota could be considered as an option for managing the metabolic syndromes.The effect of gut microbiota in the development of the immune system and its association with the perinatal programming of asthma has also been documented (Azad & Kozyrskyj, 2012).Accordingly, delayed colonization or altered profile of the microbiota may facilitate development of chronic allergies in infants.
Rituximab was efficacious in inducing remission of relapsing disease.At 6 months, 64 % in the rituximab group achieved remission without the use of prednisone at 6 months, as compared to 53 % in the control group.Both groups received one to three pulses of methylprednisolone (1000 mg each), followed by tapering dose of prednisone.The European Vasculitis Study Group (EUVAS) compared IV pulse cyclophosphamide (15 mg/kg every 2 weeks for three pulses, followed by pulses at 3-week intervals until remission, and then for another 3 months) with daily oral cyclophosphamide (2 mg/kg/day) for induction of remission [29]. They showed that the time to remission and proportion of patients in remission at 9 months was similar in both groups. The cumulative dose of cyclophosphamide in the daily oral group was twice that in IV group (15.9 g vs. 8.2 g; P < 0.001), and the latter had lower rate of leukopenia. A meta-analysis of nonrandomized studies showed that pulse cyclophosphamide was significantly more likely to induce remission and had a lower risk of infection and leukopenia. Pulse cyclophosphamide dosing may, however, be associated with a greater risk of relapses, exposing patients to further immunosuppression [30]. The dose of oral and IV cyclophosphamide is 2 mg/kg/day and 500–750 mg/m2 respectively. The dose should be adjusted to maintain a nadir leukocyte count, 2-weeks' post treatment, of 3000–4000/cu mm. B cell depletion with rituximab is emerging as an important component of induction therapy. It has been used successfully in patients with refractory lupus nephritis and in granulomatosis with polyangiitis [31]. The Rituximab in ANCA-Associated Vasculitis (RAVE) trial compare rituximab with standard therapy for inducing remission in patients with ANCA associated vasculitis [32]. Patients received either rituximab (375 mg/m2/week for 4 weeks) or cyclophosphamide (2 mg/kg/day). Both groups received one to three pulses of methylprednisolone (1000 mg each), followed by tapering dose of prednisone. At 6 months, 64 % in the rituximab group achieved remission without the use of prednisone at 6 months, as compared to 53 % in the control group. Rituximab was efficacious in inducing remission of relapsing disease.The RITUXVAS study randomized patients with ANCA associated vasculitis to receive a standard steroid regimen plus either rituximab (375 mg/m2/week for 4 weeks) with two IV cyclophosphamide pulses (n = 33), or IV cyclophosphamide for 3–6 months followed by azathioprine (n = 11) [33].There was no significant difference in the rate of remission, severe adverse events and death in the two groups.
Other regions activated by painful stimuli include dorsolateral prefrontal cortex, striatum, cerebellum, hypothalamus, amygdala, and periaqueductal gray.In addition, in many studies activation is also observed in the primary and secondary somatosensory areas.The axons of spinothalamic lamina V cells ascend in the anterior spinothalamic tract and constitute another major pathway conveying tactile and pain-related activity; these axons terminate in VPI and also in conspicuous patches in the main somatosensory relay nuclei (VPM and VPL) around immunohistochemically distinct (calbindin-positive) cells, where WDR nociceptive neurons can be identified. In contrast to most sensory thalamocortical pathways, these neurons seem to project to the superficial layers of the primary somatosensory cortical region (SI) in the postcentral gyrus. Nociceptive WDR cells have been recorded in SI, and clusters of nociceptive-specific cells have been recorded in area 3a. There are also other multisynaptic pathways that may provide ancillary pain information to the forebrain. Nociceptive spinothalamic cells in the spinal intermediate zone, especially at upper cervical segments, project bilaterally to the medial thalamus and to motor-related thalamic nuclei. Spinomedullary lamina X neurons that project to the dorsal column nuclei or the nucleus solitarius may be important for visceral pain. A spinoreticulothalamic pathway by way of the dorsal medulla may provide a substrate for widespread activation of supragranular frontal cortex. The main regions of the human cerebral cortex that are activated by painful stimuli in functional imaging (PET, fMRI) and laser-evoked potential studies are the insula (limbic sensory cortex) and the anterior cingulate (limbic motor cortex). In addition, in many studies activation is also observed in the primary and secondary somatosensory areas. Other regions activated by painful stimuli include dorsolateral prefrontal cortex, striatum, cerebellum, hypothalamus, amygdala, and periaqueductal gray.Some of these areas may subserve distinguishable roles in pain perception, which are currently being vigorously investigated.
Many clinics prescribe tetracycline, 500 mg orally four times daily for 5 days after the procedure, as presumptive treatment for _Chlamydia._ Rh immune globulin should be given to all Rh-negative women following abortion.Prophylactic antibiotics are indicated for surgical abortion; for example, a one-dose regimen of doxycycline, 200 mg orally can be given 1 hour before the procedure.Rates of morbidity and mortality rise with length of gestation. In the United States, more than 60% of abortions are performed before 9 weeks, and more than 90% are performed before 13 weeks' gestation; only 1.2% are performed after 20 weeks. If abortion is chosen, every effort should be made to encourage the patient to seek an early procedure. In the United States, while numerous state laws limiting access to abortion and a federal law banning a rarely used variation of dilation and evacuation have been enacted, abortion remains legal and available until fetal viability, between 24 and 28 weeks' gestation, under _Roe v. Wade_. Complications resulting from abortion include retained products of conception (often associated with infection and heavy bleeding), uterine perforation, and unrecognized ectopic pregnancy. Immediate analysis of the removed tissue for placenta can exclude or corroborate the diagnosis of ectopic pregnancy. Women who have fever, bleeding, or abdominal pain after abortion should be examined; use of broad-spectrum antibiotics and reaspiration of the uterus are frequently necessary. Hospitalization is advisable if acute salpingitis requires intravenous administration of antibiotics. Complications following illegal abortion often need emergency care for hemorrhage, septic shock, or uterine perforation. Prophylactic antibiotics are indicated for surgical abortion; for example, a one-dose regimen of doxycycline, 200 mg orally can be given 1 hour before the procedure. Many clinics prescribe tetracycline, 500 mg orally four times daily for 5 days after the procedure, as presumptive treatment for _Chlamydia._ Rh immune globulin should be given to all Rh-negative women following abortion.There is growing evidence to support the safety and efficacy of immediate postabortal insertion of IUDs.Mifepristone (RU 486) is approved by the FDA as an oral abortifacient at a dose of 600 mg on day 1, followed by 400 mcg orally of misoprostol on day 3.This combination is 95% successful in terminating pregnancies of up to 9 weeks' duration with minimum complications.
Initially, the bone achieves its increase in size and shape through growth (increase in size) and a complicated process known as skeletal modeling.Bone tissue is continuously formed and remodeled throughout life.In addition, bone is a major source of inorganic ions, and actively participates in the body's calcium/phosphate balance.In late childhood and adulthood there is continuous renewal of the skeleton via a process termed remodeling. Both modeling and remodeling require two separate processes namely bone resorption and bone formation to occur simultaneously to be effective. This requirement is known as "coupling". Keywords Runx-2 (runt-related transcription factor 2)cbfa-1 (core binding factor alpha1)Pebp2aA (Polyoma enhancer binding protein 2aA)Osterixcleidocranial dysplasiaosteopontinLeptinosteoblast specific factor-1, N-syndecanosteoblast/osteocyte factor-45 (OF45)dentin matrix protein 1fibroblast growth factor 23sclerostinSclerosteosisSOST geneosteocyteosteoclastogenesisparathyroid hormone1, 25 dihydroxyvitamin D3 transforming growth factor alphaepidermal growth factortartrate resistant acid phosphataseosteoprotegerinintegrinsintegral membrane proteinsfibronectincollagen type Ibone sialoprotein IIosteopontinsuppressor of cytokine signaling-1osteoclast-associated receptorappositiongrowth platedrosophilasarcolemmamyofilamentsmotorend platesomitesskeletogenesisosteoactivinbiglycandecorincalcitonincalcitriolbone morphogenetic proteinsconnective tissue growth factor ## Introduction The skeleton serves as an internal structural support system for vertebrates. It has mechanisms to grow and change in shape and size to suit varying stressors including the ability to resist the mechanical forces. In addition, bone is a major source of inorganic ions, and actively participates in the body's calcium/phosphate balance. Bone tissue is continuously formed and remodeled throughout life. Initially, the bone achieves its increase in size and shape through growth (increase in size) and a complicated process known as skeletal modeling.Both modeling and remodeling require two separate processes namely bone resorption and bone formation to occur simultaneously to be effective.This requirement is known as "coupling".Overview Bone forms the skeletal framework of all vertebrates.It is a composite tissue consisting of organic matrix, inorganic minerals, cells, and water.
And over two dozen of these emergent strains posed life-threatening crises to humanity, having outwitted most commonly available antibiotic treatments.In fact, by 1993 nearly every common pathogenic bacterial species had developed some degree of clinically significant drug resistance.Super-strains of staph that were resistant to huge numbers of potential drugs existed naturally by 1990. For example, an Australian research team treated a patient infected with a strain that was resistant to cadmium, penicillin, kanamycin, neomycin, streptomycin, tetracycline, and trimethoprim. Since each of these drugs operated by specific biochemical mechanisms that were used by a host of related drugs, the Australian staph could resist, to varying degrees, some thirty-one different drugs. In a series of test-tube studies the Australians showed that these various resistance capabilities were carried on different plasmids that could be separately passed from one bacterium to another. The most common mode of passage was conjugation: one bacterium simply stretched out its cytoplasm and passed plasmids to its partner. Using PCR genetic fingerprinting techniques to trace back in time over 470 MRSA strains, a team of researchers from the New York City Health Department discovered that all of the MRSA bacteria descended from a strain that first emerged in Cairo, Egypt, in 1961. By the end of that decade the strain's descendants could be found in New York, New Jersey, Dublin, Geneva, Copenhagen, London, Kampala, Nairobi, Ontario, Halifax, Winnipeg, and Saskatoon. A decade later they were seen planet-wide. Fortunately, staph wasn't resistant to vancomycin. Not yet, anyway. Staphylococcus wasn't the only bacterial organism that was successfully using plasmids, jumping genes, mobile DNA, mutations, and conjugative sharing of resistance factors to overcome whatever drugs Homo sapiens threw at them. In fact, by 1993 nearly every common pathogenic bacterial species had developed some degree of clinically significant drug resistance. And over two dozen of these emergent strains posed life-threatening crises to humanity, having outwitted most commonly available antibiotic treatments."Unless currently effective antimicrobial agents can be successfully preserved and the transmission of drug-resistant organisms curtailed, the post-antimicrobial era may be rapidly approaching in which infectious disease wards housing untreatable conditions will again be seen."NIH senior scientist Richard Krause labeled the bacterial situation "an epidemic of microbial resistance."
#### **BERBERIS VULGARIS** ###### BARBERRY Barberry has been in use as a healing herb for thousands of years.**•** Do not give celery seed to children under two years old.**•** Pregnant women should not take celery seed without a physician's approval because of its strong diuretic properties.If you are experiencing a stomach upset or diarrhea while taking celery seed, discontinue use.**•** Do not use with hypertension or heart disease. **•** Angelica can increase photosensitivity; use a sunscreen if spending time outdoors. **•** Pregnant women should avoid angelica because of its history as an abortifacient. #### **APIUM GRAVEOLENS** ###### CELERY SEED _Ajwan_ Celery seed, or ajwan, grows wild in India all year round. Traditional Ayurvedic practitioners prescribe celery seed to reduce high vátha states—indigestion, nervous stomach, and ungrounded emotions. In aromatherapy, celery seed oil can be used to counteract jet lag and exposure to smog and toxic environments. ##### PROPERTIES Celery seed has pungent, salty qualities, and a heating/moisturizing effect. It is used as a stimulant, expectorant, antispasmodic, and lithotrophic. **Part of Plant Used** The bulb. **Conditions Treated** The common cold, coughs, sinus congestion, respiratory infections, bronchitis, laryngitis, arthritis, digestive problems, high blood pressure, insomnia, diseases of the liver and spleen, and irregular menstruation. **Form Taken** As a food, a tea or infusion, steam, powder, massage oil, or gargle. **Used with Other Herbs? ** Basil, black pepper, camphor, eucalyptus, sandalwood. HOW TO USE **• Celery seed reduces kapha and vátha, and increases pitta. ** **• It is most commonly used as a diuretic, since fluid retention aggravates high blood pressure, congestive heart conditions, premenstrual syndrome, arthritis, and gout. ** **CAUTION** **•** Celery seed may cause minor discomfort in some people. If you are experiencing a stomach upset or diarrhea while taking celery seed, discontinue use. **•** Pregnant women should not take celery seed without a physician's approval because of its strong diuretic properties. **•** Do not give celery seed to children under two years old. #### **BERBERIS VULGARIS** ###### BARBERRY Barberry has been in use as a healing herb for thousands of years.##### PROPERTIES Barberry is a stimulant, a respiratory aid, and is antibiotic, antibacterial, and antifungal.It decreases heart rate, shrinks tumors, stimulates intestinal movement, and enlarges blood vessels.**Part of Plant Used** The berries, roots, and ground bark.
However, most placebo-controlled trials found no significant improvement in endothelium-mediated vasodilation when postmenopausal women were supplemented with up to 80 mg/day of soy isoflavones– or up to 60 g/day of soy protein containing isoflavones.– Arterial stiffness is another measure of arterial function. Measurements of arterial stiffness assess the distensibility of arteries, and a strong association between arterial stiffness and atherosclerosis has been observed. In placebo-controlled clinical trials, supplementing the diet of postmenopausal women with 80 mg/day of a soy isoflavone extract for 5 weeks significantly decreased arterial stiffness, as did supplementation of men and postmenopausal women at 40 g/day of soy protein, providing 118 mg/day of soy isoflavones for 3 months. Although most studies have not found supplementation with soy protein or isoflavones to improve endothelium-mediated vasodilation, preliminary research suggests that soy isoflavone supplementation may decrease arterial stiffness. However, a recent randomized, controlled, crossover trial in hypertensive individuals found that supplementation with soy protein containing 118 mg/day of isoflavones for 6 months did not improve measures of arterial function, including arterial stiffness. More research is needed to determine whether supplementation with soy isoflavones improves arterial function. #### Hormone-Associated Cancers ##### Breast Cancer The incidence of breast cancer in Asia, where average isoflavone intakes from soy foods range from 25 mg/day to 50 mg/day, is lower than breast cancer rates in the Western countries where average isoflavone intakes in non-Asian women are less than 2 mg/day., However, many other hereditary and lifestyle factors could contribute to this difference.A few studies suggest that a higher soy intake during adolescence may lower risk of developing breast cancer later in life., See Chapter 3 for more information about soy consumption and breast cancer risk.At present, there is little evidence that taking soy isoflavone supplements decreases the risk of breast cancer.
following commencement of insulin therapy).#### Acute (painful) sensory neuropathy This is predominantly seen in male patients and is associated with poor glycaemic control or rapid improvement in glycaemic control (e.g.Topical capsaicin may also be tried.carbamazepine, gabapentin and pregabalin) may help with symptom relief.Continued aggressive management of cardiovascular risk factors is mandatory, as this is the major cause of morbidity and mortality in this group of patients. ### Neuropathy * More common in patients with a long history of DM (males > females), especially in those with poor glycaemic control. * Multifactorial, reflecting a combination of metabolic and vascular factors. #### Distal symmetrical polyneuropathy ('sensory peripheral neuropathy') This is the most common form of diabetic neuropathy (characterised by loss of both myelinated and unmyelinated nerve fibres) and typically affects the longest fibres first – hence the so‐called 'glove and stocking' distribution. Symptoms include dysaesthesia (numbness and tingling), often worse at night, progressing to chronic pain (stabbing/burning/shooting) with time. Examination reveals absent ankle jerks, diminished vibration sense in the lower limbs, and an inability to feel the standard 10‐g monofilament. Reduced pain and temperature sensation follow, with muscular wasting and weakness late features. Affected individuals are at high risk of developing diabetic foot complications (neuropathic/neuro‐ischaemic ulcers, Charcot arthropathy). Optimal diabetic control is central to the prevention of distal symmetrical polyneuropathy. Tricyclic antidepressants (e.g. amitriptyline), duloxetine (a serotonin and noradrenaline reuptake inhibitor) and various anticonvulsants (e.g. carbamazepine, gabapentin and pregabalin) may help with symptom relief. Topical capsaicin may also be tried. #### Acute (painful) sensory neuropathy This is predominantly seen in male patients and is associated with poor glycaemic control or rapid improvement in glycaemic control (e.g. following commencement of insulin therapy).Various cranial nerves (e.g.third, fourth and sixth), the ulnar nerves and the lateral common peroneal nerves are most commonly affected, and more than one nerve can be involved at any given time (i.e.mononeuritis multiplex).It is often transient and spontaneous recovery of function usually occurs over a period of months, but can be variable.
However, we found a significant difference between the history of a previous transurethral resection of prostate that was associated with lower values for both end points."We observed no significant differences for DRT related to the consumption of cranberry compared with apple juice._A flavonoid fraction from cranberry extract inhibits proliferation of human tumor cell lines._ Ferguson PJ, Kurowska E, Freeman DJ, Chambers AF, Koropatnick DJ. J Nutr. 2004 Jun;134(6):1529-35. **Key Finding:** "Cranberry press cake (the material remaining after squeezing juice from the berries) when fed to mice bearing human **breast tumor** MDA-MB-435 cells, was shown previously to decrease the growth and metastasis of tumors. Further studies were undertaken to isolate the components of cranberry that contributed to this anticancer activity and determine the mechanisms by which they inhibited proliferation. Using standard chromatographic techniques, a warm-water extract of cranberry press cake was fractionated and an acidified methanol eluate (Fraction 6, or Fr6) containing flavonoids demonstrated antiproliferative activity. The extract inhibited proliferation of 8 human tumor cell lines of multiple origins. The androgen-dependent **prostate** cell line LNCaP was the most sensitive of those tested (10 mg/L Fr6 inhibited its growth by 50%.) Other human tumor lines originating from **breast** (MCF-7), **skin** (SK-MEL-5), **colon** (HT-29), **lung** (DMS114), and **brain** (U87) had intermediate sensitivity to Fr6." _A randomized trial of cranberry versus apple juice in the management of_ **_urinary symptoms_** _during external beam radiation therapy for_ **_prostate cancer._** Campbell G, Picles T, D'yachkova Y. Clin Oncol (R Coll Radiol). 2003 Sep;15(6):322-8. **Key Finding:** "One hundred and twelve men with prostate cancer were randomized to either 354 ml cranberry juice or apple juice a day. We observed no significant differences for DRT related to the consumption of cranberry compared with apple juice. However, we found a significant difference between the history of a previous transurethral resection of prostate that was associated with lower values for both end points."2002 Dec 4;50(25):7449-54.**Key Finding:** "Phytochemicals, especially phenolic, in fruits and vegetables are suggested to be the major bioactive compound for the health benefits associated with reduced risk of chronic diseases such as **cardiovascular disease** and **cancer.
In addition, the risk of small blood vessel complications (eyes, kidneys, nerves) is much lower than the spectrum of problems now called frailty.Several factors are involved, including some we've already mentioned: multiple medications, muscle weakness, previous strokes (which if they are small events may not have been recognised as strokes – see Chapter 9), neuropathy (less ability to feel the feet and an additional cause of muscle weakness – see Chapter 11), blood pressure falling when standing up, and visual impairment (for example due to diabetic retinopathy, cataracts or age-related macular degeneration). Insulin treatment, especially if it results in overall low blood glucose levels (HbA1c under 7.0%, or 53 mmol/mol) is a risk for falls. Many of these factors can be managed positively to reduce the risk. ### _Social factors_ Good care of Type 2 diabetes is collaborative, and often involves life partners. Illness or the death of a partner can be a terrible additional burden in managing diabetes, especially for people taking insulin. In many cases, partners have been giving injections for years, as well as monitoring blood glucose levels, and they often show wonderful skill and intuition – after all, they know their partners better than anyone. The loss of someone so dedicated to the care of diabetes can be a major blow. Hospital and general practice teams are often in a good position to identify these difficulties, though replacing the round-the-clock skills of someone who may have been helping with diabetes for decades is a huge challenge. #### Summary Maintaining 'tight' blood glucose control in old age isn't as important as in younger people, not because of elder discrimination but because it isn't as important as other diabetes-related matters – for example, maintaining meticulous blood pressure and low cholesterol levels. In addition, the risk of small blood vessel complications (eyes, kidneys, nerves) is much lower than the spectrum of problems now called frailty.In addition, older people need to maintain good nutrition with higher protein and fat intake and do as much exercise as possible to try and avoid the muscle wasting of age (sarcopenia).Chapter 13 # Psychology and Type 2 diabetes #### Key points * Managing Type 2 is as much a matter of managing the mind as medication and diet.
Most of the foods that contain these compounds contain other additives as well, such as preservatives, and dyes.Food Emulsifiers and Stabilizers Various compounds are used to emulsify and stabilize many commercial foods to ensure that the solids, oils, and liquids do not separate out.If so, supplementation (200 mcg per day) may be beneficial.Molybdenum deficiency may produce sulfite sensitivity.Typically, 15% of patients with chronic hives test positive to oral challenge with BHT. The use of chewing gum containing BHT was enough to induce hives in one patient. Sulfites. Like tartrazine, sulfites have been shown to induce asthma, hives, and angioedema in sensitive individuals. Sulfites are ubiquitous in foods and drugs. They are typically added to processed foods to prevent microbial spoilage and to keep them from browning or changing color. The earliest known use of sulfites was in the treatment of wines with sulfur dioxide by the Romans. Sulfites are used to preserve many foods, especially dried fruit, prepared salads, items at salad bars, wine, and beer. Wine and beer drinkers typically consume up to 10 mg sulfites per day even with moderate drinking (two to three glasses of wine or beer). Sulfites are also used as preservatives in many pharmaceuticals. Sulfites can cause asthma as well as hives. Normally, the enzyme sulfite oxidase metabolizes sulfites to safer sulfates, which are excreted in the urine. Those with a poorly functioning sulfoxidation system, however, have an increased ratio of sulfite to sulfate in their urine. Sulfite oxidase is dependent on the trace mineral molybdenum. Although most nutrition textbooks list molybdenum deficiency as uncommon, an Austrian study of 1,750 patients found that 41.5% were molybdenum deficient. Molybdenum deficiency may produce sulfite sensitivity. If so, supplementation (200 mcg per day) may be beneficial. Food Emulsifiers and Stabilizers Various compounds are used to emulsify and stabilize many commercial foods to ensure that the solids, oils, and liquids do not separate out. Most of the foods that contain these compounds contain other additives as well, such as preservatives, and dyes.#### Infections Infections are a major cause of hives in children.In adults, immunological tolerance to many microorganisms apparently occurs owing to repeated antigen exposure.The role of bacteria, viruses, and yeast (Candida albicans) in hives is briefly reviewed below.Chronic trichomonas infections have also been found to cause hives.
A fracture of the humeral head, neck, or greater tuberosity can occur at the same time.It is the most common shoulder dislocation experienced after a traumatic event.B** Anterior dislocation is almost always traumatic and is usually from falls.**.Neurologic and vascular examinations of the upper extremity should be performed completely.The nurse should palpate for crepitus, pain, or muscle spasm, the presence of a pulse, and interruption in bone integrity. **. D** Proper immobilization includes immobilization above and below the level of injury. This technique provides the best stabilization of the extremity. Immobilization devices should be checked frequently for effectiveness, the extremity monitored for swelling, and to ensure splints are padded appropriately to prevent further injury. Immobilizing the actual injury can cause further damage to the site. **. B** The nurse should notify the physician of the need for pain management so that proper irrigation and cleansing can be performed with the patient as comfortable as possible. The initial wound care includes removal of gross contaminates from the wound and covering exposed bone or tissue with a sterile saline dressing. The patient should be informed of the importance of cleaning the debris and the significance of treatment and infection prevention; however, pain is the fifth vital sign and should be addressed. A significant complication of fractures is infection, therefore antibiotics are indicated, but the wound still requires appropriate cleansing. **. A** If there is vascular or nerve involvement associated with a humeral fracture, it usually is caused by the axillary nerve or axillary artery. Rarely, the brachial artery, brachial plexus, or radial artery are involved with a shoulder injury. Identification of an anterior or posterior bulge may suggest a dislocation. Tenderness and swelling often are diffuse, making it difficult to detect clear point tenderness. Neurologic and vascular examinations of the upper extremity should be performed completely. **. B** Anterior dislocation is almost always traumatic and is usually from falls. It is the most common shoulder dislocation experienced after a traumatic event. A fracture of the humeral head, neck, or greater tuberosity can occur at the same time.This injury may be seen in violent seizure activity.Inferior, superior, and intrathoracic shoulder dislocations can also occur but are extremely rare.**.D** Distal pulses may still be present because of the extensive collateral flow of the arm.The arm would be cool to the touch and have absent axillary pulses.There is usually a hematoma present in the axillary region.
Companies initially attempted to play down the evidence that ulcers were linked to a bacterium that could be eliminated, because this information wasn't good for business.A second reason things are different now is that unlike other industrial processes, many of which have led to tangible benefits, the logic of healthcare marketing may block real benefits.Why should we expect anything less than comparable improvements in medical care—especially as we seem to hear of ever more medical breakthroughs in the media? There are a few reasons why things are different now. One is that drugs and other services in the medical market physically act on the stuff of which we are made and may reconfigure us quite dramatically in ways we are not told about. Unlike short courses of antibiotics, which do not substantially change us, chronic courses of treatments aimed at managing risk factors do change us. Whether it be a cholesterollowering statin, an anti-inflammatory such as Celebrex, a treatment for osteoporosis such as Actonel, or a psychotropic cocktail, these drugs do not just have the action we are told about but often have much greater effects throughout the body than the one the company markets, potentially leading to an increased risk of dementia in the case of Vioxx and Celebrex, an enduring susceptibility to heart attacks in the case of Fosamax and Actonel, or changes in our ability to make love in the case of Paxil, Cymbalta, or Zoloft. Beyond these specific problems, the indiscriminate actions of many of these drugs on our physical constitution quite probably alter both our susceptibility to various diseases and our personalities too in subtle ways. A second reason things are different now is that unlike other industrial processes, many of which have led to tangible benefits, the logic of healthcare marketing may block real benefits. Companies initially attempted to play down the evidence that ulcers were linked to a bacterium that could be eliminated, because this information wasn't good for business.As a result some of us are now dying earlier than we should, and many more are suffering needlessly.By taking us away from productive work any premature deaths and incapacity come at a cost to the economy, and so it is in the interest of all of us to pay attention to the medical care each of us gets.
Most medicines given to infants and young children are liquids.Beyond these relatively "simple" difficulties are potential problems that many parents may not be aware of, such as accurately measuring liquid doses.### The Art of Giving Medicine to Children All parents know the difficulties of giving medicine to infants and children.However, some _can_ be serious. When the benefits to children of some medications or supplements are not proven, then the risks are greater than the benefits. Examples include OTC antidiarrheal medicines and many supplements (see chapter 3 for more information). _This is a very important concept to understand and appreciate_. Studies of pediatric medication adverse effects are described later in this chapter. #### As Needed, or Every Day? An important distinction to know about your child's medicine is whether it should be given on a regular daily schedule or only as needed. Medicines for fever, such as acetaminophen (Tylenol) and ibuprofen (Motrin, Advil), are typically given as needed, when your child is uncomfortable or has a high body temperature. Other medicines should _not_ be given only as needed, and are most effective when given daily, even if the child feels well and has no apparent symptoms from the illness. Examples of medications scheduled for every day administration are many asthma medicines, such as Flovent (fluticasone) or Singulair (montelukast), and many medicines for seizure disorders, such as Tegretol (carbamazepine) or Dilantin (phenytoin). It is easy to confuse some asthma medicines, such as some metered dose inhalers (Proair [albuterol] or Proventil [albuterol]), which are mostly given as needed when the child has difficulty breathing. Other metered dose inhalers, such as Flovent (fluticasone), should be used every day, whether or not the child has breathing difficulty, and are not effective when used only as needed. ### The Art of Giving Medicine to Children All parents know the difficulties of giving medicine to infants and children. Beyond these relatively "simple" difficulties are potential problems that many parents may not be aware of, such as accurately measuring liquid doses. Most medicines given to infants and young children are liquids.Beyond accurately measuring a dose of liquid medicine comes the "art" of getting your infant or young child to take the medicine.Color, texture, smell, and, perhaps most important, taste of the liquid medicine all come into play.What can be done to entice your child to take his or her medicine?
Treatment is also provided for a range of metabolic and toxic syndromes, including autism, heavy metal exposure, diabetes, obesity, and poly-cystic ovary syndrome.Among the digestive disorders treated are celiac sprue, Crohn's disease, food allergies and sensitivities, irritable bowel syndrome, and ulcerative colitis.Your liver is the one of the keys to your energy and stamina. Consider using the suggestions in this chapter to enhance your diet and supplements with the support of your liver in mind. If you suspect that you have any type of liver problem, we encourage you to be seen by an integrative physician and seek functional-medicine liver testing. We consider this one of the most frequently overlooked and underappreciated aspects of good health. **Trent W. Nichols, M.D.,** is a board certified internist, nutritionist and gastroenterologist who is a fellow of the American College of Physicians and American College of Nutrition. He additionally is an active physician/scientist involved in pharmaceutical, nutritional, and bioelectromagnetic research. He is a graduate of the University of Denver with a BS in Chemistry and of the Northwestern University Medical School. His residency in internal medicine and gastroenterology fellowship were also at Northwestern University. He is a member of the Institute of Functional Medicine, the Bioelectromagnetic Society, Tissue Engineering Society International, the Society for Neuroscience, and is vice president of the North American Academy of Magnetic Therapy. Dr. Nichols has been in private practice in Hanover for over 26 years. He was recently selected as one of America's Top Physicians by Consumers' Research Council of America, 2004-5. **The Center for Nutritional and Digestive Disorders** is a functional-medicine practice dedicated to helping patients with chronic disorders. The center sees patients with gastrointestinal disorders and those with other types of chronic conditions. Among the digestive disorders treated are celiac sprue, Crohn's disease, food allergies and sensitivities, irritable bowel syndrome, and ulcerative colitis. Treatment is also provided for a range of metabolic and toxic syndromes, including autism, heavy metal exposure, diabetes, obesity, and poly-cystic ovary syndrome.12 Damage from Free Radicals JEFFREY BLAND, PH.D.The cascade of events that begins in the digestive tract and culminates in the liver can generate a particular kind of risk due to reactive and destructive molecules called free radicals.If these dangerous reactions are not detoxified, they can ricochet through the cellular materials of the body.
**Action:** _Tonify:_ Regulate intestinal function._Clear:_ Push from the web to the tip 100–500 times.**Technique:** _Tonify:_ Push from the tip to the web 100–500 times.#### **L ARGE INTESTINE MERIDIANDA CHANG JING (LI)** **Location:** Edge of the index finger that faces the thumb, from the tip to the web.**Indications:** Cough, diarrhea, abdominal distension, food stagnancy, vomiting, labored breathing (phlegm), dyspepsia, loss of appetite, chest oppression, vexation, restlessness. #### **I NNER PALACE OF LABORNEI LAO GONG (P 8)** **Location:** Center of the palm; a flexed middle finger will touch the point. **Technique:** Press Rotate 50–300 times _or_ Rotate Push 30–100 times. **Action:** Clear heat, relieve exterior symptoms, stop convulsions. **Indications:** Fright, convulsions, common-cold fever, excess heat patterns, deficient heat patterns, heart fever, vexation, internal heat, thrush, gum erosion, high fever, twitching. #### **K IDNEY LINESHEN WEN** **Location:** Root of the little finger, crease at the palm. **Technique:** Press Rotate 100–500 times _or_ Press 100–300 times. **Action:** Expel wind, brighten eyes, disperse lumps and stagnation, clear stagnant heat, lead fire outward. **Indications:** Red eyes, thrush, toxic heat patterns, conjunctivitis, internal heat with external cold. #### **K IDNEY MERIDIANSHEN JING (K)** **Location:** Little fingertip pad. **Technique:** _Tonify:_ Press Rotate 100–500 times. _Clear:_ Push tip toward palm. **Action:** _Tonify:_ Strengthen kidneys and yang qi. _Clear:_ Purge stagnant heat in lower abdomen. **Indications:** Congenital deficiencies, postillness weakness, morning diarrhea, bed-wetting, cough, asthma, frequent or difficult urination, convulsions, epilepsy, toothache, paralysis aftermath. #### **L ARGE INTESTINE MERIDIANDA CHANG JING (LI)** **Location:** Edge of the index finger that faces the thumb, from the tip to the web. **Technique:** _Tonify:_ Push from the tip to the web 100–500 times. _Clear:_ Push from the web to the tip 100–500 times. **Action:** _Tonify:_ Regulate intestinal function.**Indications:** Diarrhea, dysentery, constipation, abdominal pain, anal swelling and redness.#### **L ARGE TRANSVERSE LINEDA HENG WEN** **Location:** Palm side of the wrist crease.**Technique:** 1.Press Rotate 100–500 times.2.Push Apart 80–300 times.**Action:** 1.Expel wind, depress adverse rising qi, balance yin yang, remove food stagnation.2.
By an intuitive leap—the sort of which only the human brain is capable—Cade decided to give lithium salts to several agitated and manic patients who were under his care.Lithium, when combined with uric acid, made the latter nicely soluble in water, and during extensive experiments injecting this compound into guinea pigs, Cade noticed that the animals became quiet without falling asleep.These ionic shifts are responsible for maintaining the electrical charge—the action potential—of the neurons, and dampening their movement reduces the speed at which the neurons can recover after transmitting pulses of information. Thus, the excitability of a whole network can be reduced and, as a result, the progression of epileptic seizures or the fermentation of manic excitement is contained. The anticonvulsants, as these drugs are appropriately named, have become a valuable addition to the treatment of bipolar illness. Divalproex sodium, better known in America by its trade name of Depakote, is as effective in treating acute mania as lithium is, and it is more useful in those complicated, and rapidly changing, mood states where the symptoms of depression and mania are mixed together. The usefulness of lithium in mania, in contrast to the logical analysis that has determined the value of anticonvulsants, was stumbled upon in the late 1940s almost entirely by accident. John Cade, an Australian psychiatrist, while seeking a toxic agent in the urine of psychotic patients, was investigating uric acid and urea, both by-products of protein metabolism, as possible candidates. Lithium, when combined with uric acid, made the latter nicely soluble in water, and during extensive experiments injecting this compound into guinea pigs, Cade noticed that the animals became quiet without falling asleep. By an intuitive leap—the sort of which only the human brain is capable—Cade decided to give lithium salts to several agitated and manic patients who were under his care.And yet within three weeks he was "enjoying the unaccustomed and quite unexpected amenities of a convalescent ward," and after three months he was so improved that he left the hospital to return to work and to his family.Doctor Cade had made a miraculous discovery that would revolutionize the pharmacological treatment of manic-depressive illness.
Even when zoos transport and relocate their animals for breeding, most don't routinely screen for STDs.Nor does yearly population tracking of Yukon caribou end with the females in stirrups and the vet chitchatting while warming up an Arctic-chilled speculum.Wildlife veterinarians don't regularly count the genital warts on tundra swan penises when they radio-collar them for migration surveys.An international survey of physicians once ranked afflictions by their level of prestige. Brain tumors, heart attacks, and leukemia were the top three. Diseases that strike below the belt were dead last. And medical advances of the past half century have made it even easier to look away from sexual infections. In developed countries, most of us have the luxury of thinking of STDs as being essentially curable—or, at worst, treatable, chronic diseases requiring daily medication. (Think of antiviral medication for herpes or, in a more extreme case, daily drug cocktails for HIV.) What's more, pervasive and effective "safe sex" education has given the strong message—true in some cases—that barrier methods and abstinence can make you practically impervious to STDs. But for animals, safe sex isn't a choice. In fact, when you think about it, unprotected sex is the only kind nonhuman animals have. Without access to condoms and abstinence pledges, not to mention antibiotics and vaccines, nonhuman animals have to cope and survive and reproduce somehow, regardless of what infections come their way. When you consider the amount of "unsafe" sex going on, 24/7, in a mere square mile of wilderness, it seems remarkable that animals aren't 100 percent infected at all times with STDs. Veterinarians, like physicians, often give animal STDs scant attention, compared to other health concerns. Wildlife veterinarians don't regularly count the genital warts on tundra swan penises when they radio-collar them for migration surveys. Nor does yearly population tracking of Yukon caribou end with the females in stirrups and the vet chitchatting while warming up an Arctic-chilled speculum. Even when zoos transport and relocate their animals for breeding, most don't routinely screen for STDs.Like most patients and physicians, I wasn't exactly clamoring to hear more about STDs.But we all should pay attention, because STDs are remarkably deadly.HIV/AIDS is the world's sixth biggest cause of death.When you combine those numbers with cancer deaths from sexually spread viruses such as human papilloma virus (HPV) and hepatitis B and C, the mortality climbs even higher.
Other functions are not fully understood because response appears to vary with species, context, and cell type | Susceptibility to viral infections NLRX1 | Unknown | Activates NF-κB and ROS through JNK pathway, negatively regulates RIG-I-mediated IFN response and LPS-elicited TRAF6-IKK signaling pathways | Susceptibility to chronic hepatitis B infection, gastric cancer PYD | NLRP1 | Muramyl dipeptide, _Bacillus anthracis_ lethal toxin | Inflammasome assembly resulting in caspase-1 activation and production of active IL-1β and IL-18 | Skin autoimmune disorders, vitiligo, Addison's disease, diabetes, celiac disease, autoimmune thyroid disorders, systemic lupus erythematosus, systemic sclerosis, giant cell arteritis, congenital toxoplasmosis, Alzheimer's disease, corneal intraepithelial dyskeratosis, arthritis NLRP2 | Unknown | | Beckwith–Wiedemann syndrome, GVHD NLRP3 | Crystals (monosodium urate, calcium pyrophosphate dihydrate, cholesterol, asbestos, silica, hydroxyapatite), amyloid β, mitochondrial DNA, cardiolipin, ceramides, ATP, ROS, RNA viruses, bacterial toxins | Inflammasome assembly resulting in caspase-1 activation and production of active IL-1β and IL-18 | Gout, Cryopyrin-associated periodic fever syndromes (CAPS), diabetes, celiac disease, psoriasis, inflammatory bowel diseases, Alzheimer's disease, atherosclerosis NLRP4 | Unknown | Unknown, possible suppressor of NF-κB | NLRP5 | Unknown | Unknown | Familial biparental hydatidiform moles NLRP6 | Unknown | Unknown, possible negative regulator of NF-κB and IL-1β, an NLRP6 inflammasome has been proposed in mouse colonic epithelial cells | Metabolic syndrome-associated abnormalities, colitis, and colon cancer NLRP7 | Bacterial acylated lipoproteins (acLP) | Unknown, possible negative regulator of IL-1β, inflammasome assembly in response to bacterial acLP | Familial biparental hydatidiform moles, abnormal pregnancies and embryonic development, testicular and endometrial cancer NLRP8 | Unknown | Unknown | Alzheimer's disease, colorectal cancer NLRP9 | Unknown | Unknown | Abnormal embryonic development NLRP10 | Unknown | Negatively regulates caspase-1 activation, regulation of DC emigration from inflamed tissues in mice | Atopic dermatitis NLRP11 | Unknown | Unknown | NLRP12 | Unknown | Negatively regulates NF-κB activation | Hereditary fever syndromes, dermatitis NLRP13 | Unknown | Unknown | Abnormal embryonic development NLRP14 | Unknown | Unknown | Familial biparental hydatidiform moles, spermatogenic failure BIR | NAIP | Type III secretion system needle proteins | Formation of a large oligomeric complex with NLRC4 resulting in caspase-1 activation and production of IL-1β | Spinal muscle atrophy The current paradigm for NLR activation is self-oligomerization followed by recruitment of adaptor proteins that mediate activation of downstream effectors.This in turn culminates in activation of the IκB kinase (IKK) complex, IκBα phosphorylation followed by its degradation and activation of NF-κB (Windheim _et al._ , 2007; Abbott _et al._ , 2007; Figure 2).
Thompson, Massey University.)(Image courtesy of K.G.Peripheral (basilar) epithelial cells are palisaded and nonbasilar cells may keratinize as shown in the epithelium on left.It is arranged in a trabecular anastomosing pattern and is supported by dense mature fibrous stroma.(B) Odontogenic epithelium comprises the majority of the tumor.#### Incidence and clinical presentation Uncommon in domestic animals, ameloblastomas have been reported most frequently in dogs, but have also been described in cats, horses, sheep, and cattle.7,8 In dogs, neither breed nor age preference has been identified, but the mandible is more commonly affected than the maxilla.9 Cats with ameloblastoma are middle‐aged to older without breed or sex bias and both jaws are affected with approximately equal frequency.7Ameloblastomas are more commonly located centrally in bone than peripherally within the gingiva and protrude from the site of origin into the oral cavity. Expansion into surrounding structures can occur especially of ameloblastomas originating in the upper dental arcade (Figure 13.28A). A sinunasal tumor was reported to be consistent with an ectopic ameloblastoma in a horse.10 Ameloblastomas generally grow slowly. They can be discrete or infiltrative with infiltrative neoplasms resulting in poorly defined peripheral osteolysis and possible recurrence after resection. Keratinizing ameloblastoma has been rarely associated with high levels of serum parathyroid hormone‐related peptide (PTHrP) and hypercalcemia, which resolved after tumor removal.11 **Figure 13.28** Ameloblastoma, sheep. (A) Transverse section shows expansion of the white, multilobular ameloblastoma into oral and nasal cavities. (B) Odontogenic epithelium comprises the majority of the tumor. It is arranged in a trabecular anastomosing pattern and is supported by dense mature fibrous stroma. Peripheral (basilar) epithelial cells are palisaded and nonbasilar cells may keratinize as shown in the epithelium on left. (Image courtesy of K.G. Thompson, Massey University.)In follicular ameloblastoma, nonbasilar epithelial cells may recapitulate stellate reticulum or may be spindle‐shaped, basaloid, or acanthomatous and in people are subclassified according to these morphological differences (spindle cell, basal cell, or acanthomatous ameloblastoma).13 Granular ameloblastoma has not been described in domestic animals.
Hospitalization may be needed if the doctor believes that people are dangerous.A good doctor-patient relationship helps.Most people are able to remain employed.However, people may become progressively more involved with their delusion.Prognosis and Treatment Delusional disorder does not usually cause severe impairment.How well different antipsychotic drugs block different types of neurotransmitters varies. Every effective antipsychotic drug known blocks dopamine receptors. The new antipsychotic drugs (clozapine, olanzapine, quetiapine, risperidone, and ziprasidone) also block serotonin receptors. Experts thought that this property might make these drugs more effective. However, recent brain imaging studies have not supported this view. Clozapine, which blocks many other receptors, is clearly the most effective drug for psychotic symptoms. But it is underused because of its side effects and the need for monitoring with blood tests. Symptoms A delusional disorder may arise from a preexisting paranoid personality disorder (see Cluster A: Odd or Eccentric Behavior). Beginning in early adulthood, people with a paranoid personality disorder have a pervasive distrust and suspiciousness of others and their motives. Early symptoms of delusional disorder may include feeling exploited, being preoccupied with the loyalty or trustworthiness of friends, reading threatening meanings into benign remarks or events, bearing grudges for a long time, and responding readily to perceived slights. Diagnosis After ruling out other specific conditions that are associated with delusions, a doctor bases the diagnosis largely on the person's history. The doctor must assess the degree of dangerousness, particularly the extent to which the people are willing to act on their delusions. Prognosis and Treatment Delusional disorder does not usually cause severe impairment. However, people may become progressively more involved with their delusion. Most people are able to remain employed. A good doctor-patient relationship helps. Hospitalization may be needed if the doctor believes that people are dangerous.A long-term treatment goal is to shift the person's focus away from the delusion to a more constructive and gratifying area, although this goal is frequently difficult to achieve.CHAPTER 135 Sexuality Sexuality is a normal part of human experience.However, the types of sexual behavior that are considered normal vary greatly within and among different cultures.
Arrhythmia is converted to sinus rhythm.Anticoagulation therapy is performed.| Ventricular rate is controlled.Blood pooling in atria places patient at risk for thrombus formation and embolization to the brain and other organs.If ventricular response is rapid, patient experiences manifestations of decreased cardiac output and is at risk for heart failure and myocardial ischemia.Atrial fibrillation Arrhythmia in which chaotic ectopic atrial foci cause the atria to quiver rather than contract Atrial rate >400 beats/ min | Pacemaker site: many ectopic foci in atrial tissue Rhythm: irregular Rate: atrial rate—>400 beats/min P waves: presence of chaotic F waves QRS complex: normal Intervals: lack of P waves, irregular R-R interval | In healthy people, possible association with stress or excessive alcohol consumption Chronic atrial fibrillation in patients with heart failure, mitral valve disease, rheumatic heart disease, hypertension, and hyperthyroidism Relationship with atrial reentry mechanism Only a few impulses from AV node pass through to the ventricle | Signs and symptoms are related to rate of ventricular response. If ventricular response is rapid, patient experiences manifestations of decreased cardiac output and is at risk for heart failure and myocardial ischemia. Blood pooling in atria places patient at risk for thrombus formation and embolization to the brain and other organs. | Ventricular rate is controlled. Anticoagulation therapy is performed. Arrhythmia is converted to sinus rhythm.Symptoms include manifestations of decreased cardiac output.| Pharmacologic management is used to increase heart rate.Temporary pacemaker may be inserted.Underlying cause is identified and treated.
Follow-up studies have yielded mixed results.Additional screening for this mutation turned up no additional observations in 4,296 control chromosomes, leading to a significant association with TS (p = 0.0056) (State, 2011).Verkerk and colleagues reported a complex rearrangement in a father with TS as well as his affected children, disrupting the gene encoding Contactin-Associated Protein-like 2 (CNTNAP2), which is also associated with a rare recessive form of autism and epilepsy and is thought to contribute to common forms of social disability, language delay, and possibly schizophrenia. Lawson-Yuen et al. reported a family with tics and TS transmitting an exonic deletion of the Neuroligin 4, X-linked (NLGN4X), in which rare mutations also cause autism (State, 2011). These studies point to the now well-established phenomenon of rare variants in a single gene or region leading to highly divergent developmental and neuropsychiatric phenotypes, as has been demonstrated for autism, schizophrenia, epilepsy, and intellectual disability (Malhotra and Sebat, 2012). As discussed in the following, recent studies of structural variation in TS lead to the same conclusion, that variants in the same genes or genomic regions can lead both to TS and other neuropsychiatric conditions. A third cytogenetic finding has garnered attention because it was the first to lead to the identification of a protein-disrupting rare mutation in a nearby gene. A de novo chromosome 13 inversion was identified in a simplex family with TS to a region upstream of the gene SLITRK1 (Slit and Trk-like Family Member 1). Sequencing of a cohort of 179 unrelated affected individuals revealed a frame-shift deletion in the gene in a small pedigree segregating TS and trichotillomania. In addition, two independent instances of a single, very rare single base mutation (var321) were identified in the 3′ untranslated region (UTR) corresponding a micro-RNA (miR-189) binding site. Additional screening for this mutation turned up no additional observations in 4,296 control chromosomes, leading to a significant association with TS (p = 0.0056) (State, 2011). Follow-up studies have yielded mixed results.Two candidate gene studies of common variation at the SLITRK1 locus have supported association, but as noted, neither this locus nor any others reached genome-wide significance in GWAS studies of TS.
During this time he has focused on the immunotherapy of cancer and has conducted numerous clinical trials involving a variety of vaccines and immunotherapy.Since 1991 he has been professor of oncology at St. George's, University of London.He was awarded the Joshua Lederberg Award in 2011 in recognition of this work.She received her bachelor's degree with honors at University of California at San Diego (UCSD) in biochemistry and cell biology. She received her medical degree from UCSD School of Medicine. She is board certified in internal medicine and is a diplomate of the American Board of Holistic Integrative Medicine. She has twenty years of internal medicine experience and is currently in private practice in Poway, California. Dr. Angus G. Dalgleish Dr. Angus G. Dalgleish trained at University College Hospital, where he earned an intercalated degree in anatomy with Professor J. Z. Young. Following house jobs, he took a position with the Royal Flying Doctor Service of Australia for one year and stayed on to train in internal medicine and oncology at hospitals in Brisbane and Sydney. He returned to the United Kingdom in 1984 and undertook a thesis on retroviruses with Robert Weiss. He was then appointed as senior clinical scientist at the MRC Clinical Research Centre in Northwick Park, London, where he pursued his interests in HIV pathogenesis and the potential of thalidomide to treat chronic diseases. His suggestion that analogs of thalidomide could lead to enhancement of therapeutic activity and reduction of side effects was co-opted by David Stirling of Celgene, and this partnership led to the licensing of Revlimid (lenalidomide) and Pomalyst (pomalidomide) for myeloma and lymphoma. He was awarded the Joshua Lederberg Award in 2011 in recognition of this work. Since 1991 he has been professor of oncology at St. George's, University of London. During this time he has focused on the immunotherapy of cancer and has conducted numerous clinical trials involving a variety of vaccines and immunotherapy.He is on numerous scientific advisory boards involving the development of vaccines and immunotherapy, including Celgene, Immodulon, CureVac, and Bionor Pharma.
Causalgia and reflex sympathetic dystrophy.Suggested Reading Baron R., Levine J.D., Fields H.L.**sensitization** A process that decreases the stimulus intensity required for a nociceptive response or that increases the magnitude of the nociceptive response elicited by a given nociceptive stimulus.It is thus clear that continued exploration of the detailed molecular properties of nociceptors and their peripheral and central projections should be highly profitable from both the scientific and therapeutic points of view. # See Also the Following Articles Migraine; Opiates; Pain; Peripheral Nervous System # Glossary **A _δ_ -fiber** A sensory neuron whose axon in the peripheral nerve is lightly myelinated. These axons have the lowest conduction velocity among myelinated axons. **allodynia** The pain elicited by a normally nonpainful stimulus after inflammation or damage to peripheral or central neurons. **C-fiber** A sensory neuron whose axon in the peripheral nerve is unmyelinated. These axons are the slowest conducting in the peripheral nerves. **dorsal horn** The region of spinal cord gray matter in which nociceptive neurons terminate. This region is generally divided into laminae (laminae I–V). Lamina I is also known as the marginal zone, lamina II as the substantia gelatinosa, and laminae III–V, as nucleus proprius. **dorsal root ganglion** The location of cell bodies of sensory neurons innervating the body. A corresponding ganglion for the face is the trigeminal or gasserian ganglion. **dorsal root ganglion cell** A sensory neuron consisting of a cell body in the dorsal root ganglion, a peripheral process innervating the peripheral tissues (skin, muscle, etc. ), and a central process projecting into the spinal cord to synapse on postsynaptic neurons. **hyperalgesia** The increase in perceived intensity of a normally painful stimulus after injury. **nociceptor** A class of sensory neuron responding selectively to tissue damage in its receptive field. **sensitization** A process that decreases the stimulus intensity required for a nociceptive response or that increases the magnitude of the nociceptive response elicited by a given nociceptive stimulus. Suggested Reading Baron R., Levine J.D., Fields H.L. Causalgia and reflex sympathetic dystrophy.Muscle Nerve, 1999;22:678–695.Basbaum A.I., Woolf C.J.Pain._Curr.Biol._.1999;9:R429–431.Belmonte C., Cervero F., eds.The Neurobiology of Nociceptors.New York: Oxford University Press, 1996.Dubner R., Gold M., eds.Colloquium on the Neurobiology of Pain.Proc.Natl.Acad.Sci.USA, 96.1999:7627–7755.Fields H.L., Rowbotham M., Baron R. Postherpetic neuralgia.Irritable nociceptors and deafferentation.
In contrast, after 12 days in culture, cells cultured in the three-dimensional DegraPol-foam showed higher ALP activity than on the two-dimensional TCPS.Osteoblasts cultured on TCPS demonstrated up to day 8 higher alkaline phosphatase (ALP) activity than on the three-dimensional DegraPol-foam.Similar results were obtained in our group [4].Hepatocytes cultured in dishes coated with crude liver membrane preserved their liver-specific functions and xenobiotic metabolism in cultures with tissue oxygen tension for up to 9 days [10]. Using these culture conditions, it was further demonstrated that hepatocytes, in combination with the glucoregulatory hormones insulin and glucagon, adapt their glucose metabolism to that of the corresponding liver region. Glucagon stimulates gluconeogenesis predominantly in the periportal region and insulin supports glycolysis at higher capacity in the pericentral region. The pericentral zone is exposed to a higher insulin/glucagon ratio than the periportal zone [8–10]. 13.8 Seeding Density After reaching optimal cell density by serial passages and phenotype confirmation, in vitro cell tests can be performed. In general, seeding density is important for normal cell function, especially if cell–cell communications must be established, either by direct cell–cell contacts or via the paracrine secretion of trophic factors by the cells. It is well known that cells seeded at high cell density preserve their phenotype at higher levels than cells seeded at low cell density and the proliferation capacity is reduced at high cell density. Many cell types exhibit an inverse relationship between growth and differentiation in vitro [3]. Investigations of osteoblast developmental stages [4] indicate that, proliferating osteoblasts express decreased levels of their typical phenotypic activities during periods of rapid growth as well as cell replication slowed down, the cells began to produce more ALP and other markers of osteoblastic phenotype. Similar results were obtained in our group [4]. Osteoblasts cultured on TCPS demonstrated up to day 8 higher alkaline phosphatase (ALP) activity than on the three-dimensional DegraPol-foam. In contrast, after 12 days in culture, cells cultured in the three-dimensional DegraPol-foam showed higher ALP activity than on the two-dimensional TCPS.The optimal cell density depends on the biological endpoints to be measured.If one intends to measure effects of a drug on the metabolic activity of the cells, then it is important to use cells at high cell density (nearly 100% confluence).In contrast, nonconfluent cultures have to be used in case we intend to assess mitogenic/carcinogenic effects of a test pharmaceutical.
At the megakaryocyte level, plasma proteins can be adsorbed and packaged into platelet granules (see Chapter 13).They also have a role in inflammation since they contain many growth factors.They play a central role in hemostasis as they contain many hemostatic cofactors and inhibitors in their granules.Eosinophils Eosinophils are characterized by their prominent orange-reddish (refractile) granules seen on Wright–Giemsa stain (Atlas Figure 6). Eosinophils usually have bilobed nuclei. Eosinophils increase in reaction to foreign protein and thus are seen in parasitic infection (especially larva of roundworms, helminths), allergic conditions, cancer and certain drugs. Granules contain several proteins, most notably major basic protein (MBP). Normally eosinophils constitute 0–2% of WBC differential cell count. 5. Basophils Basophils are equally colorful with very dark, bluish prominent granules following Wright–Giemsa stain (Atlas Figure 7). Granules contain: histamine, heparin, and hyaluronic acid. Histamine release (basophil degranulation) is part of the allergic reaction. Normally basophils are 0–1% of WBC differential blood count. They are often increased in patients with chronic myelogenous leukemia and other myeloproliferative disorders. Mast cells which are tissue basophils also have prominent granules and play a role in host defenses against parasites. 6. Platelets (Thrombocytes) Platelets bud off from the cytoplasm of the bone marrow megakaryocytes. The "mega" karyocyte in the bone marrow is recognized by its large size. Uniquely, the cell doubles its nuclear and cytoplasmic material but does not divide. Megakaryocyte growth and platelet segmentation is regulated by thrombopoietin. Platelets are anucleated cell fragments that contain remnant mRNA. They have a 7–10 day half-life and their first 1–2 days are spent in the spleen. Platelets can be entrapped by an enlarged spleen as seen in congestive and inflammatory disorders. They play a central role in hemostasis as they contain many hemostatic cofactors and inhibitors in their granules. They also have a role in inflammation since they contain many growth factors. At the megakaryocyte level, plasma proteins can be adsorbed and packaged into platelet granules (see Chapter 13).The mononuclear phagocytic system is also called the reticuloendothelial (RE) system.These cells are found in bone marrow, thymus, lymph nodes, spleen, serosal surfaces, adrenal cortex, Peyer's patches, and Waldeyer's ring.They function as a "clean-up system" for circulating debris, microorganisms and aged, defective or antibody-coated RBC.
Cysticercosis is acquired by humans who eat undercooked pork containing the larval cysts.: Cysticercosis is caused by the larval form of _Taenia solium,_ a common central nervous system (CNS) pathogen in many tropical areas.#### Cysticercosis Principles of Disease.Corticosteroids, including dexamethasone, provide no benefit and can worsen outcome in cerebral malaria.Signs and symptoms also include massive hepatosplenomegaly, neutropenia, and weight loss.10 The patient who has amebic liver abscesses from _Entamoeba histolytica_ infection presents with high fevers, right upper quadrant pain, and elevated white blood cell count.11 ### Neurologic Symptoms Cerebral Malaria Principles of Disease and Clinical Features. : Cerebral malaria is a common, life-threatening complication of _P. falciparum_ infection. Parasitized RBCs express malarial cell surface glycoproteins called knobs that are sticky. They adhere to capillary walls, causing sludging in the cerebral microvasculature, localized ischemia, capillary leak, and petechial hemorrhages. Clinical manifestations include fever, altered mentation including obtundation, coma, and occasionally seizures. A careful history and early diagnosis and therapy are essential to prevent severe morbidity and death. Management. : Treatment of cerebral malaria consists of intravenous quinine, quinidine, or artemisinin (if it is available); supportive care, including mechanical ventilation for comatose patients and patients with noncardiogenic pulmonary edema; antiepileptics; and correction of acidosis and hypoglycemia (associated with quinine use and cerebral malaria). The mortality rate is high, especially in children, but if the patient recovers, neurologic sequelae are rare. Corticosteroids, including dexamethasone, provide no benefit and can worsen outcome in cerebral malaria. #### Cysticercosis Principles of Disease. : Cysticercosis is caused by the larval form of _Taenia solium,_ a common central nervous system (CNS) pathogen in many tropical areas. Cysticercosis is acquired by humans who eat undercooked pork containing the larval cysts.They are trophic for the CNS, muscle, and soft tissue.Clinical Features.: In the brain, the cluster of larvae of _T.solium_ forms an expanding cyst that induces an intense immunologic reaction from the host, including inflammation, fibrosis, and ultimately calcification.Neurologic abnormalities develop when neural tissue cannot accommodate the enlarging cyst.
In GGR damage is recognized by XPE and/or XPC, whilst in TCR the photoproducts cause RNA polymerase II to stall and damage recognition is done by CSA and CSB.Nucleotide excision repair has two subpathways: global genome repair (GGR) and transcription coupled repair (TCR) in which repair is selectively directed at the actively transcribing strand [16, 17].The basic principle of DNA repair in the skin is the recognition of the photolesion that is to be removed and replaced with a new base(s) followed by ligation to give intact DNA. Faithful DNA repair is critical for genomic integrity. The insertion of an incorrect base in proliferating epidermal cells may result in mutations that give rise to skin cancer. ##### Nucleotide excision repair The most important repair process in human skin is nucleotide excision repair (NER). This process is dependent on a large group of enzymes with specific roles in the recognition and excision of DNA photolesions, and the repair of DNA using the opposite strand as a template. NER is triggered by the activation of p53 protein that occurs in response to cellular stress including DNA damage, oncogenic stimulation and hypoxia. This triggers a G1/S cell cycle arrest and transcriptional activation of NER genes. NER is also called unscheduled DNA synthesis (UDS), as opposed to scheduled DNA synthesis that is observed in cells undergoing mitosis. Failure to repair DNA by the lack of one or more repair proteins may have catastrophic consequences exemplified by patients with xeroderma pigmentosum (XP) who are extremely prone to skin cancer (see Chapter 78) [16]. Studies on cell cultures from XP patients have greatly increased our understanding of DNA repair and indeed many of the DNA repair proteins are described by the XP prefix. Nucleotide excision repair has two subpathways: global genome repair (GGR) and transcription coupled repair (TCR) in which repair is selectively directed at the actively transcribing strand [16, 17]. In GGR damage is recognized by XPE and/or XPC, whilst in TCR the photoproducts cause RNA polymerase II to stall and damage recognition is done by CSA and CSB.Assessment of GGR in human epidermis _in vivo_ shows that repair of 6-4(PP) is relatively rapid and more or less complete within 6 h. In contrast, the half-life for the removal of the CPD is about 30 h [18].This difference may be because the 6-4(PP) causes a more significant distortion in the double helix than the CPD, which may result in more rapid recognition and repair.
Vital capacity (VC)_ _3–3.Inspiratory capacity (IC)_ _h.Inspiratory reserve volume (IRV)_ _g.Tidal volume (V T)_ _f.Total lung capacity (TLC)_ _e.Expiratory reserve volume (ERV)_ _d.Residual volume (RV)_ _c.Functional residual capacity (FRC)_ _b.What is the effect on each of the following standard lung volumes and capacities of changing from a supine to an upright position?_ _a.The loss of alveolar surface area and decreased pulmonary capillary blood volume result in a decreased pulmonary diffusing capacity, which will be discussed in Chapter 6. This can also contribute to a progressive decrease in arterial oxygen tension with aging. * * * ### **KEY CONCEPTS** _**Alveolar ventilation** is less than the volume of air entering or leaving the nose or mouth per minute (the minute volume) because the last part of each inspiration remains in the conducting airways ( **the anatomic dead space** )_. _Alveoli that are ventilated but not perfused constitute **alveolar dead space**_. _The **physiologic dead space** is the sum of the anatomic dead space and the alveolar dead space_. _At constant carbon dioxide production, alveolar P CO2 is approximately inversely proportional to alveolar ventilation; alveolar PO2 must be calculated with the **alveolar air equation. **_ _At or near the functional residual capacity, alveoli in lower regions of the upright lung are relatively better ventilated than those in upper regions of the lung_. * * * ### **CLINICAL PROBLEMS** _3–1. Which of the following conditions are reasonable explanations for a patient's functional residual capacity that is significantly less than predicted?_ _a. Third trimester of pregnancy_ _b. Pulmonary fibrosis_ _c. Obesity_ _d. Emphysema_ _e. All of the above_ _f. a, b, and c_ _3–2. What is the effect on each of the following standard lung volumes and capacities of changing from a supine to an upright position?_ _a. Functional residual capacity (FRC)_ _b. Residual volume (RV)_ _c. Expiratory reserve volume (ERV)_ _d. Total lung capacity (TLC)_ _e. Tidal volume (V T)_ _f. Inspiratory reserve volume (IRV)_ _g. Inspiratory capacity (IC)_ _h. Vital capacity (VC)_ _3–3.A volume of 1 L of gas is measured in a spirometer at 23°C (296 K; PH2O is 21 mm Hg), and barometric pressure is 770 mm Hg_._a.What would the volume be under STPD conditions?_ _b.What would the volume be under BTPS conditions?_ _3–5.A subject starts at her FRC and breathes 100% O2 through a 1-way valve.The expired air is collected in a very large spirometer (called a Tissot spirometer).
Merkel cells (see Commentary 1.3 ) in the basal epidermis of the skin store neuropeptides, which they release to associated nerve endings or other cells in a neuroendocrine role, in response to pressure and possibly other stimuli (Lucarz and Brand 2007).2.6), similar to the neurotransmitter vesicles seen in some types of neuronal terminal. The group includes cells described as chromaffin cells (phaeochromocytes), derived from neuroectoderm and innervated by preganglionic sympathetic nerve fibres. Chromaffin cells synthesize and secrete catecholamines (dopamine, noradrenaline (norepinephrine) or adrenaline (epinephrine)). Their name refers to the finding that their cytoplasmic store of catecholamines is sufficiently concentrated to give an intense yellow–brown colouration, the positive chromaffin reaction, when they are treated with aqueous solutions of chromium salts, particularly potassium dichromate. Classic chromaffin cells include clusters of cells in the suprarenal medulla; the para-aortic bodies, which secrete noradrenaline; paraganglia; certain cells in the carotid bodies; and small groups of cells irregularly dispersed among the paravertebral sympathetic ganglia, splanchnic nerves and prevertebral autonomic plexuses. The alimentary tract contains a large population of cells of a similar type (previously called neuroendocrine or enterochromaffin cells) in its wall. These cells act as sensory transducers, activating intrinsic and extrinsic primary afferent neurones via their release of 5-hydroxytryptamine (5-HT, serotonin). The neonatal respiratory tract contains a prominent system of neuroendocrine cells, both dispersed and aggregated (neuroepithelial bodies); the numbers of both types decline during childhood. Merkel cells (see Commentary 1.3 ) in the basal epidermis of the skin store neuropeptides, which they release to associated nerve endings or other cells in a neuroendocrine role, in response to pressure and possibly other stimuli (Lucarz and Brand 2007).A number of descriptions and terms have been applied to cells of this system in the older literature (see online text for details).
Located inferior to the thalamus and superior to the pituitary gland, the hypothalamus is a collection of many tiny nuclei that contribute to the regulation of the body's homeostasis.The hypothalamus is considerably smaller than the thalamus, but it exerts powerful effects on autonomic, endocrine, and emotional functions.Elsevier, New York._Principles of Neural Science_ , 3rd ed., p. 291.Thus, somatosensory information from the body and face reach the VPL and ventral posterior medial (VPM) nuclei, respectively, and taste fibers also project to the VPM nucleus. Visual projections from the optic nerve synapse in the lateral geniculate nucleus and auditory fibers in the medial geniculate nucleus. The ventral anterior and ventral lateral nuclei receive fibers from the cerebellum and in turn send projections to the basal ganglia, so that they contribute to the motor system. The dorsal medial nucleus and the pulvinar are the major association nuclei, connected with the frontal and the parietal–temporal–occipital cortices, respectively. The anterior nucleus has a role in the limbic system (see following discussion). Finally, the intralaminar nuclei, the two largest of which are the centromedian and the parafascicular, receive input from the ARAS in the brain stem and then relay this general information rostrally to activate the cerebrum as a whole. Figure 10 The thalamus, with its many nuclei depicted. These nuclei act as relay stations for information traveling to and from the cortex. Reprinted with permission from Kandel, E. R., Schwartz, J. H., and Jessell, T. M., Eds., (1991). _Principles of Neural Science_ , 3rd ed., p. 291. Elsevier, New York. The hypothalamus is considerably smaller than the thalamus, but it exerts powerful effects on autonomic, endocrine, and emotional functions. Located inferior to the thalamus and superior to the pituitary gland, the hypothalamus is a collection of many tiny nuclei that contribute to the regulation of the body's homeostasis.The autonomic nervous system is divided into the parasympathetic branch, which is generally associated with the anterior regions of the hypothalamus, and the sympathetic branch, which is associated with posterior sites.Endocrine function is also governed by the hypothalamus by virtue of its strong neural and vascular connections with the two lobes of the pituitary gland.
Turn off all electronic devices 1 hour before bedtime.Practicing good sleep hygiene will help.Start by getting at least 7 to 8 hours of sleep a night on a regular basis.This is one of those things that everyone dismisses but that can kill you a decade sooner than your family and friends, if you ignore it.That's why sleep apnea can take more than 10 years off your life. Literally. When your blood oxygen levels drop in the night, your body becomes desperate for air. In a state of alarm, your microglia activate. Your adrenals panic, kicking out cortisol—the stress hormone—to wake you up. Maybe you fluff your pillow and go back to sleep. Maybe you go to the bathroom. Either way, you start breathing, which is what your body needs. But when you go back to sleep, the cycle starts all over again. Some people experience it as restlessness. Others find themselves getting up several times at night. None of them is getting the good night's sleep that is so vital to our health and survival. Considering how hard it is on the body, it's no surprise that sleep apnea causes hypertension, weight gain, type 2 diabetes, and stroke. It is associated with PTSD, anxiety disorders, depression, and chronic pain. It also upregulates microglia, causing inflammation. People with sleep apnea often snore loudly and never feel rested, even after regularly getting 8 to 9 hours of sleep. Anyone, even children, can suffer from sleep apnea, though men are somewhat more likely than women to develop it. Smoking and being overweight are risk factors, since both can inhibit the ability to breathe well. Anything that obstructs the airway in the throat can create bouts of sleep apnea, from enlarged tonsils to the collapse of the soft tissue walls of the throat during sleep. Of course, there are a lot of reasons for waking up in the night and even more for feeling tired all day. Complaining about lack of sleep is almost as common as complaining about the weather, but that doesn't mean it's not serious. This is one of those things that everyone dismisses but that can kill you a decade sooner than your family and friends, if you ignore it. Start by getting at least 7 to 8 hours of sleep a night on a regular basis. Practicing good sleep hygiene will help. Turn off all electronic devices 1 hour before bedtime.Using relaxation or meditation tapes can also be useful.If you still sleep poorly—snoring, getting up in the night, tossing and turning, or waking up feeling tired—recognize that it is an unnecessary health problem that needs to be addressed.If you suspect you have sleep apnea, the simplest diagnosis is the home WatchPAT test (see Resources), which I use with my patients.
auditory ossicles [L, audire \+ ossiculum, little bone] ,the malleus, the incus, and the stapes, three small bones in the middle ear that articulate with each other.See vestibulocochlear nerve.auditory nerve.Also called auditory canal.It contains the eighth cranial nerve.auditory amnesia [L, auditorius, hearing; Gk, amnesia, forgetfulness] ,a loss of memory for the meaning of sounds. Also called word deafness. auditory area [L, auditorium, hearing] ,the sound perception area of the cerebral cortex. It is located in the floor of the lateral fissure and on the dorsal surface of the superior temporal gyrus. auditory brainstem response (ABR),an electrophysiological test used to measure hearing sensitivity and evaluate the integrity of ear structures from the auditory nerve through the brainstem. It is also used to screen hearing of newborns. auditory canal. See auditory meatus. auditory cortex. See acoustic center. auditory epilepsy,a reflex form of epilepsy provoked by sounds. Also called audiogenic epilepsy. auditory figure-ground,the ability to focus on a particular sound, such as a voice, without being distracted by background sounds in the environment. auditory hair [L, audire, to hear; AS, haer] ,one of the cells with hairlike processes in the spiral organ of Corti. The hairs, or cilia, function as sensory receptors. Also called acoustic hair cell, cell of Corti. auditory hallucination [L, audire, to hear, alucinari, a wandering mind] ,commonly seen in schizophrenia. It is a subjective experience of hearing voices or other sounds despite the absence of an actual reality-based external stimulus to account for the phenomenon. auditory meatus [L, audire, to hear, meatus, passage] ,1. the external auditory meatus, a tubelike channel of the external ear extending from the auricle to the tympanum of the middle ear.2. the internal auditory meatus, a short channel extending from the petrous part of the temporal bone to the fundus near the vestibule. It contains the eighth cranial nerve. Also called auditory canal. auditory nerve. See vestibulocochlear nerve. auditory ossicles [L, audire \+ ossiculum, little bone] ,the malleus, the incus, and the stapes, three small bones in the middle ear that articulate with each other.Auditory ossicles (Waugh and Grant, 2014) auditory system assessment,an evaluation of the patient's ears and hearing and an investigation of present and past diseases or conditions that may be responsible for an auditory impairment.
Nocturnal dyspnea that is relieved by sitting up and dangling the legs suggests heart failure.Evaluation Sometimes the symptoms suggest a cause to the doctor.In coronary artery disease, shortness of breath usually occurs during physical activity, but in people with severe disease, it may occur during minimal activity or during rest.Causes Any disorder that upsets the normal, delicate balance between the body's oxygen supply and oxygen requirement can cause shortness of breath. It is a common symptom of lung disorders, including infections, asthma, and allergies. Shortness of breath can also occur in people who have a disorder of the respiratory muscles, a disorder of the nervous system that interferes with breathing, or too few red blood cells to carry oxygen to tissues (anemia). Shortness of breath is also a common symptom of heart disorders, mainly heart failure (Heart Failure) and coronary artery disease (Coronary Artery Disease). In heart failure, shortness of breath results from fluid seeping into the air spaces of the lungs—a condition called pulmonary congestion or pulmonary edema. Ultimately, this process is similar to drowning. In the early stages of heart failure, shortness of breath may occur only during physical activity. As heart failure worsens, shortness of breath occurs with less and less activity and eventually occurs at rest. Shortness of breath at rest occurs mostly when people lie down because fluid seeps throughout the lung tissue. This symptom often occurs at night and is then called nocturnal dyspnea. When people sit up and dangle their legs, gravity causes fluid to collect at the base of the lungs, reducing symptoms. Consequently, people with nocturnal dyspnea usually sleep propped up by pillows to avoid lying flat. In coronary artery disease, shortness of breath usually occurs during physical activity, but in people with severe disease, it may occur during minimal activity or during rest. Evaluation Sometimes the symptoms suggest a cause to the doctor. Nocturnal dyspnea that is relieved by sitting up and dangling the legs suggests heart failure.Shortness of breath with cough and fever suggests a lung infection.Shortness of breath that seems to be triggered by exposure to something in the environment, such as smoke or animal hair, suggests asthma or an allergic disorder.If the cause is not obvious, tests are usually done.
Fig.The internal iliac artery supplies the pelvis.).The latter becomes the femoral artery, which is the main artery of the leg (see Chap.The common iliac arteries split into the internal and external iliac arteries.It is one of the arteries that feed the pelvis.The median sacral artery varies.The standard MPMCTA usually does not visualize the spinal arteries.Both arcades can serve for collateral circulation in case of obstruction of a feeding vessel. Their dilatation indicates increased blood flow. The inferior mesenteric artery feeds the left colic artery, the sigmoid arteries (two or three), and the superior rectal artery (see Fig. 14.7). A missing inferior mesenteric artery is often the result of ligation in colic surgery. In this case, the remaining colon is fed either via the superior mesenteric artery or via the iliac artery, and the latter may show arcades connecting via the rectal arteries with the inferior mesenteric arteries. The phrenic arteries supply the diaphragm (see Fig. 14.5a, b). Superimposition limits visualization, as is also the case for the suprarenal arteries. Often, only one of the suprarenal arteries is opacified because the contralateral one is not present or is miniscule. The renal arteries (see Figs. 14.5a, b and 14.8) vary. Additional arteries are common. Furthermore, the inferior suprarenal arteries may originate from the renal arteries. Sometimes, this also applies to the gonadal arteries. The lumbar arteries correspond to the intercostal arteries. One of them may be larger than the others. In general, this larger artery may be the main vessel for the arterial blood supply of the spine. The obstruction of these larger vessels by ligation during surgery, by stent placement in the abdominal aorta, or by aortic dissection may have induced paraplegia in the living. Therefore, detailed analysis is necessary when such complications are known from the patient's history or MPMCTA indicates such outcomes. The standard MPMCTA usually does not visualize the spinal arteries. The median sacral artery varies. It is one of the arteries that feed the pelvis. The common iliac arteries split into the internal and external iliac arteries. The latter becomes the femoral artery, which is the main artery of the leg (see Chap. ). The internal iliac artery supplies the pelvis. Fig.Reconstruction following the vessels.Arterial phase, MIP.(b) Renal arteries (16) and renal veins (44).Axial display.Descending thoracic aorta (3), abdominal aorta (4), common hepatic artery (11), splenic artery (12), superior mesenteric artery (14), testicular artery (28), inferior caval vein (41), portal vein (50), splenic vein (52) and intercostal arteries (36) Fig.
An ANOVA determines whether the means of the normal distributions are identical.Therefore, one may use many types of multivariate analyses, such as a multiple regression analysis, logistic regression, or Cox hazard function.D) Multivariate analysis When many factors can affect an outcome variable, all of them must be examined.In this case, there are eight values; the median is the average of the fourth and fifth data points, i.e., (15 + 15)/2 = 15. D) 40 The number of false positives is equal to the number of patients who had positive results on the screening test but did not actually have glaucoma. The chart below further illustrates the patients' disease status of whether or not they have glaucoma versus their results on the new screening test. Test Results | Glaucoma | No Glaucoma ---|---|--- Positive | 10 (True positive) | 40 (False positive) Negative | 5 (False negative) | 45 (True negative) A) 67%, 53% Sensitivity is the percentage of patients who have the disease but have normal results. Specificity is the percentage of patients who do not have the disease but have ­abnormal results. Sensitivity = TP/(TP + FN) = 10/(10 + 5) = 67% Specificity = TN/(TN + FP) = 45/(45 + 40) = 53% Positive predictive value = TP/(TP + FP) Negative predictive value = TN/(TN = FN) A) Type I error Errors may be made regarding the null hypothesis (H0), which states that no ­difference exists between the control group and the intervention group. If one ­rejects the null hypothesis when in fact the results occurred by chance, this is called a _type I error_ or _a error._ If one accepts the null hypothesis when in fact there really was a difference, this is called a _type II error_ or _b error_. Sampling error is bias of the data secondary to the use of a nonrepresentative population. The power of the study is β (i.e., the ability to detect a difference when a difference is present). D) Multivariate analysis When many factors can affect an outcome variable, all of them must be examined. Therefore, one may use many types of multivariate analyses, such as a multiple regression analysis, logistic regression, or Cox hazard function. An ANOVA determines whether the means of the normal distributions are identical.A χ2 test determines whether more than two sampled populations can be considered equal.C) Case-controlled study Two types of studies exist: retrospective (observational) and prospective (experimental).Within the _retrospective_ , or _case-control_ variety, either a case report or a case series may be employed.
* Computed tomography (CT).* Plain radiographs.##### Diagnosis * Palpation of the stifle.* Bilateral patella luxations may have a _knock-kneed_ conformation.* Bilateral medial patella luxations may have a _bow-legged_ conformation.* Pain – most evident in acute luxation.##### Clinical signs * Lameness – intermittent or continuous.* Presentation may be bilateral.The medial meniscus is most often affected as relatively more weight passes through the medial meniscus when the animal ambulates. Bilateral cruciate disease may also become evident. This may be related to the extra strain placed on the contralateral pelvic limb. The patient may also develop changes in the lumbar spine related to abnormal gait pattern and uneven loading through the limbs. This may be seen as muscle tension over the lumbar spine with associated trigger points and lumber spine stiffness on palpation. #### Patella luxation The patella is a sesamiod bone located within the patella ligament. Luxation occurs when the patella rides outside the femoral groove when the stifle is flexed. It can be classified as medial or lateral; medial luxation is most common. Each time the patella luxates the associated cartilage is at risk of damage, resulting in inflammation and leading to secondary osteoarthritis and pain. ##### Aetiology * It can be traumatic (rare). * It often relates to a shallow femoral groove. * Muscle imbalance and poor limb alignment may result in patella luxation. * Or it may be multifactorial in nature. ##### Incidence * Often found in small dogs (poodle, Yorkshire terrier, Chihuahua). * Presentation may be bilateral. ##### Clinical signs * Lameness – intermittent or continuous. * Pain – most evident in acute luxation. * Bilateral medial patella luxations may have a _bow-legged_ conformation. * Bilateral patella luxations may have a _knock-kneed_ conformation. ##### Diagnosis * Palpation of the stifle. * Plain radiographs. * Computed tomography (CT).If the luxation is medial the groove can be deepened on the lateral side.**Table 1.3** Patella luxation grades.
Injuries to the extremities are the most common, but 33% of injuries involve the eyes, head, face, or neck.65 In one study of pediatric patients presenting to a trauma center with non-powder firearm injuries, 57% sustained serious injuries, with 30% requiring operative treatment and 7% dying.66 The most significant injuries are intracranial penetration in the region of the orbit or thin regions of the skull. Non-powder firearm injuries are a common cause of blindness in adolescent boys; other less well known complications include remobilization and lead poisoning. Penetration of the heart and aorta occasionally results in death. Overall, non-powder firearm injuries are more numerous and less severe than powder firearm injuries, but head, chest, and abdominal wounds from these weapons may be erroneously regarded as trivial, with catastrophic results.62 ## Prevention Strategies for Youth Violence Children and adolescents lack judgment and experience and cannot be expected to avoid violence and injury on their own.67 Risk factors for youth violence include history of violence victimization, exposure to violence, access to weapons, substance abuse, antisocial beliefs, low parental involvement, low income, poor academic performance, social rejection, low levels of community participation, and high levels of community transience.To decrease youth violence, physicians and other health care providers should urge the media to do the following: decrease the violence, use of weapons, and pain and suffering depicted in the media; accurately portray the true consequences of violent acts; and decrease the amount of violent lyrics and violent scenes in music videos and video games.
## Immunosuppression In the early years of the AIDS epidemic placement of dental implants was ill advised since affected patients developed major life-threatening oral infections.In general, these undesirable effects are greatest in patients who take high doses of the drugs for long periods of time.In such patients, local bleeding after the placement of dental implants can usually be well controlled by conventional hemostatic methods. The risk of developing life-threatening bleeding or bleeding that cannot be controlled using local measures following placement of dental implants is so low that there is no need to stop oral anticoagulant therapy (Beirne 2005). Therapeutic levels of an anticoagulant drug such as warfarin are measured by the international normalized ratio (INR) which is the patient's prothrombin time (PT) divided by the mean normal PT for the laboratory (i.e. PTR). The PTR is then adjusted for the reagents used to arrive at a standardized INR value that will be comparable anywhere in the world. A higher INR reflects a higher level of anticoagulation with an attendant increased risk of hemorrhage (Herman _et al_. 1997). Although there are insufficient data to draw any evidence-based conclusions, placement of single implants is regarded as safe when the INR target values are 2.0–2.4 (Herman _et al_. 1997). ### Immunosuppressive agents Any medication that interferes with wound healing or suppresses components of innate and adaptive immunity can theoretically increase the risk of implant failure. Corticosteroids are a good example. They are potent anti-inflammatory agents that are widely used for the management of a wide variety of ailments. These drugs can interfere with wound healing by blocking key inflammatory events needed for satisfactory repair. In addition, through their immunosuppressive effects on lymphocytes, they can increase the rate of post-operative infections. In general, these undesirable effects are greatest in patients who take high doses of the drugs for long periods of time. ## Immunosuppression In the early years of the AIDS epidemic placement of dental implants was ill advised since affected patients developed major life-threatening oral infections.There have been no controlled studies dealing with the risk of dental implant failures in HIV-positive individuals.However, several case reports suggest that placement of dental implants in HIV-positive patients is not associated with elevated failure rates (Rajnay & Hochstetter 1998; Baron _et al_.2004; Shetty & Achong 2005; Achong _et al_.2006).Low T-helper (CD4) cell counts (i.e.
These women may need to hold their weight at the pre-pregnancy level or lose some weight (see Table 8.2).There are no additional recommendations for obesity levels II (BMI 35–39.9) and III (BMI > 40); or for women with additional problems such as breathing difficulties, diabetes, high blood pressure and high cholesterol.These foods are good for protein, calcium and B vitamins. Breastfeeding women will need at least six portions a day (1,250–1,350 mg/day calcium). * Fruit and vegetables – at least five portions a day. These foods are good for vitamins, such as vitamin C (pregnancy 50 mg/day, lactation 70 mg/day) and folic acid (400 µg/day). Pregnant and lactating women should have at least three portions of fruit and two portions of vegetables a day. The fruit or vegetables may be fresh or frozen. * Fatty foods and sugary foods – avoid these foods. Many of these only provide empty calories and have very little nutritional value. Drinks Women should drink often during the day, to have at least 2,000 ml/day(8–10 cups) of alcohol-free fluid. In addition, they should avoid drinking tea with meals or supplements because this affects the body's ability to use the iron. Body Weight The expected weight gain for women with a BMI between 19.6 kg/m2 and 24.9 kg/m2 is 11.5–16 kg. Most of this weight gain will occur during the third trimester. This is associated with the lowest risk of complications during pregnancy and labour and with a reduced likelihood of having a low birth weight infant (IOM, 2009). To meet the energy costs of pregnancy, a modest increment of 200 kcal/day above the estimated average requirement (EAR) is suggested in the third trimester only (DH, 1991). There are no additional recommendations for obesity levels II (BMI 35–39.9) and III (BMI > 40); or for women with additional problems such as breathing difficulties, diabetes, high blood pressure and high cholesterol. These women may need to hold their weight at the pre-pregnancy level or lose some weight (see Table 8.2).Safe Exercising in Pregnancy The Royal College of Obstetricians and Gynaecologists advise that: * All women should be encouraged to participate in aerobic and strength-conditioning exercise as part of a healthy lifestyle during their pregnancy.
STEMI generally occurs in the presence of extensive coronary and systemic atherosclerotic plaque, which may serve as the site for the formation of platelet aggregates—a sequence suggested as the initial step in the process of coronary thrombosis, coronary occlusion, and subsequent MI.Hematologic Alterations Platelets.Plasma and urinary 17-hydroxycorticosteroids and ketosteroids, as well as aldosterone, rise markedly in patients with STEMI. Their concentrations correlate directly with the peak level of serum CK, thus implying an association between the stress imposed by larger infarcts and greater secretion of adrenal steroids. The magnitude of the elevation in cortisol correlates with infarct size and mortality. Glucocorticosteroids also contribute to impaired glucose tolerance. Thyroid Gland. Although patients with STEMI are generally euthyroid clinically, serum triiodothyronine (T3) levels can decrease transiently, a fall that is most marked on approximately the third day after the infarct. A rise in reverse T3 usually accompanies this fall in T3, with variable changes or no change in thyroxine (T4) and thyroid-stimulating hormone levels. The alteration in peripheral T4 metabolism appears to correlate with infarct size and may be mediated by the rise in endogenous levels of cortisol that accompanies STEMI. Renal Function. Both prerenal azotemia and acute renal failure can complicate the marked reduction in cardiac output that occurs in cardiogenic shock. On the other hand, an increase in circulating atrial natriuretic peptide occurs following STEMI and correlates with the severity of LV failure. An increase in natriuretic peptide also occurs when RV infarction accompanies inferior wall infarction, thus suggesting that this hormone may contribute to the hypotension that accompanies RV infarction. Hematologic Alterations Platelets. STEMI generally occurs in the presence of extensive coronary and systemic atherosclerotic plaque, which may serve as the site for the formation of platelet aggregates—a sequence suggested as the initial step in the process of coronary thrombosis, coronary occlusion, and subsequent MI.Elevated levels of serum fibrinogen degradation products, an end product of thrombosis, as well as release of distinctive proteins when platelets are activated (such as platelet factor 4 and beta-thromboglobulin), occur in some patients with STEMI.Fibrinopeptide A (FPA), a protein released from fibrin by thrombin, is a marker of ongoing thrombosis and increases during the early hours of STEMI.
#### Management Imatinib, a tyrosine kinase inhibitor that specifically blocks the enzymatic action of the BCR-ABL fusion protein, is first-line treatment for the chronic phase.The Ph chromosome and the _BCR-ABL_ oncogene are shown by cytogenetics and reverse transcriptase polymerase chain reaction (RT-PCR).ALL has a propensity to involve the CNS, so treatment also includes prophylactic intrathecal drugs, methotrexate or cytosine arabinoside (cytarabine). Cranial irradiation is used in those at very high risk or in those with symptoms. The prognosis in children with ALL is excellent with almost all achieving complete remission and with 80% being alive and disease free at 5 years. The results in adults are not so good, the prognosis getting worse with advancing years. Overall about 70–80% achieve complete remission with only about 30% being cured. ### Chronic myeloid leukaemia #### Clinical features CML occurs most commonly in middle age and is characterized by the presence of the Philadelphia (Ph) chromosome. There is an insidious onset, with fever, weight loss, sweating and symptoms of anaemia. Massive splenomegaly is characteristic. Untreated, this chronic phase lasts 3–4 years. This is usually followed by blast transformation, with the development of acute leukaemia (usually acute myeloid) and, commonly, rapid death. Less frequently, CML transforms into myelofibrosis, death ensuing from bone marrow failure. #### Investigations Blood count usually shows anaemia and a raised white cell count (often >100 × 109/L). The platelet count may be low, normal or raised. Bone marrow aspirate shows a hypercellular marrow with an increase in myeloid progenitors. The Ph chromosome and the _BCR-ABL_ oncogene are shown by cytogenetics and reverse transcriptase polymerase chain reaction (RT-PCR). #### Management Imatinib, a tyrosine kinase inhibitor that specifically blocks the enzymatic action of the BCR-ABL fusion protein, is first-line treatment for the chronic phase.Event-free, and overall, survival appear to be better than for other treatments.Imatinib can be continued indefinitely.In the acute phase (blast transformation) most patients have only a short-lived response to imatinib, and other chemotherapy as for acute leukaemia is used in the hope of achieving a second chronic phase.
Specific criteria for defining each of the categories of SSI infection can be found in the CDC's Guidelines for Prevention of Surgical Site Infection.The classification scheme defines the following two categories of SSI based on location: incisional SSI (subdivided into superficial and deep) and organ/space SSI (Figure 1).Yang, Z, Zheng, Q, Wang, Z. Meta-analysis of the need for nasogastric or nasojejunal decompression after gastrectomy for gastric cancer. _Br J Surg_. 2008; 95:809–816. # Surgical Site Infections Laura H. Rosenberger, MD, MS and Robert G. Sawyer, MD ## Overview Surgical site infections (SSIs) are a common surgical complication that affects between 2% and 5% of the 30 to 40 million operations that occur in the United States per year. SSIs are the most common nosocomial infection among surgical patients and are consistently the second most common healthcare-associated infection overall. Mortality rates after SSI are markedly higher when compared with patients without an SSI, as are the patient's length of stay (mean, 7 days), hospital readmission rates, and direct patient costs ($500 to $3000 per infection). ## Definition Controversy and ambiguity continue to exist in the definition of an SSI. Experts may disagree about the appearance of an incision in regards to SSI, particularly in the presence of surrounding cellulitis or wound drainage. In 1970, the Centers for Disease Control and Prevention (CDC) established the National Nosocomial Infections Surveillance (NNIS) system (now part of the National Healthcare Safety Network [NHSN]) in part to create criteria defining SSI and to standardize the definition for accurate surveillance and reporting. Currently, it is the national standard by which medical personnel and researchers consistently define SSI. By definition, SSIs occur within the first 30 days after the operation if no implant is placed or within 1 year if an implant remains. The classification scheme defines the following two categories of SSI based on location: incisional SSI (subdivided into superficial and deep) and organ/space SSI (Figure 1). Specific criteria for defining each of the categories of SSI infection can be found in the CDC's Guidelines for Prevention of Surgical Site Infection.## Risk Factors Development of an SSI requires microorganism contamination at the surgical site.During an operative procedure in which skin is incised, endogenous skin flora, the most common source of pathogens, are introduced into the exposed tissue.
Most _Trichosporon_ species are inhibited by cycloheximide, so this antibiotic should be excluded from the culture medium.The hyphae segment into arthroconidia 2–4 μm in diameter, and budding blastoconidia may also be seen (Figure 32.6).There may be extensive growth within the hair, giving rise to characteristic nodular swellings on the hair shaft.###### Causative organisms Until 1994, the aetiological agent of white piedra was considered to be the basidiomycetous yeast _Geotrichum_ ( _Trichosporon_ ) _beigelii_ , but genetic analysis has now determined that this name covered a complex of different species [9]. The agent of white piedra in head hair is now considered to be _T. ovoides_ , while organisms reported from crural white piedra include _T. inkin_ , _T. asahii_ and _T. mucoides_. ###### Clinical features ###### Presentation This infection is asymptomatic. White piedra is characterized by the presence of soft, white or light brown nodules. The infection is more common on the hairs of the beard, moustache and genital areas than the scalp [4, 5]. The fungus grows both within and outside the hair shaft, and the hair shaft may be weakened and break off. The nodules are transparent, easily detached from the hair and vary in size from microscopic to 1 mm in diameter. The underlying skin is not affected and there is no fluorescence under Wood's light. ###### Differential diagnosis The presence of pruritus and the distinctive shape of egg cases of pediculi should serve to distinguish pediculosis from piedra, but microscopical examination is desirable. ###### Disease course and prognosis If not treated this is a chronic infection. ###### Investigations The nodules of white piedra are in the form of a sheath, which may extend around the hair shaft. There may be extensive growth within the hair, giving rise to characteristic nodular swellings on the hair shaft. The hyphae segment into arthroconidia 2–4 μm in diameter, and budding blastoconidia may also be seen (Figure 32.6). Most _Trichosporon_ species are inhibited by cycloheximide, so this antibiotic should be excluded from the culture medium.**Figure 32.6** White piedra.Hair mounted in KOH, bright field.The gelatinous nodules formed by various _Trichosporon_ species surround the hair.(Courtesy of the Department of Medical Mycology, St John's Institute of Dermatology, King's College London, London, UK.)**_Trichosporon_ species**.
If meningitis accompanies meningococcemia, focal neurologic signs as well as seizures may occur but are less common than with pneumococcal meningitis.Renal failure is common secondary to impaired renal perfusion; acute tubular necrosis may develop.It is also likely that intrapulmonary DIC contributes to the pulmonary edema, and patients frequently require mechanical ventilation.They are typically admitted for fever and a nonblanching rash and no other specific findings. If they are untreated, meningitis or fulminant septicemia and shock can develop.74 Chronic Meningococcemia. : This syndrome is characterized by fever, rash, and arthritis in conjunction with a positive blood culture for _N. meningitidis_. Headache and upper respiratory symptoms are often present. This is the rarest form of meningococcal disease, accounting for 1 to 2% of cases. It may progress to meningitis, endocarditis, or fulminant meningococcemia regardless of treatment.69 #### Complications Myocarditis with congestive heart failure is a common complication of meningococcemia and is the primary cause of death in more than half of patients. Many of the inflammatory mediators released during sepsis cause myocardial dysfunction, and the severity of sepsis is related to the degree of impairment of myocardial contractility. The acidosis, hypoglycemia, hypokalemia, hypocalcemia, hypophosphatemia, and hypoxia that accompany meningococcemia also contribute to the myocardial dysfunction. Treatment with cardiac glycosides is beneficial,69 but patients may become unresponsive to positive inotropic medications. Acute respiratory failure occurs from capillary leak in the patient who requires volume resuscitation. It is also likely that intrapulmonary DIC contributes to the pulmonary edema, and patients frequently require mechanical ventilation. Renal failure is common secondary to impaired renal perfusion; acute tubular necrosis may develop. If meningitis accompanies meningococcemia, focal neurologic signs as well as seizures may occur but are less common than with pneumococcal meningitis.
Although each involves osteoclasts and osteoblasts, the coordinated outcomes differ greatly.## ORGANIZATION AND FUNCTION OF BONE CELLS ### Intermediary organization of the skeleton In what he termed the intermediary organization (IO) of the skeleton, Frost [1] described four discrete functions of bone cells: growth, modeling, remodeling, and fracture repair.39. Agrawal K, Bhadada S, Mittal BR, et al. Comparison of 18F‐FDG and 68Ga DOTATATE PET/CT in localization of tumor causing oncogenic osteomalacia. Clin Nucl Med. 2015;40(1):e6–10. # 39 Bone Histomorphometry in Clinical Practice _Robert R. Recker 1 and Carolina Aguiar Moreira2_ _1 Division of Endocrinology, Osteoporosis Research Center, Creighton University School of Medicine, Omaha, NE, USA_ _2 Department of Medicine & Section of Endocrinology (SEMPR), Federal University of Parana, Laboratory PRO, Fundacao Pro Renal, Curitiba, Paraná, Brazil_ ## INTRODUCTION Histological examination of undecalcified transilial bone biopsy specimens is a valuable and well‐established clinical and research tool for studying the etiology, pathogenesis, and treatment of metabolic bone diseases. In this chapter, we will review the underlying organization and function of bone cells; identify a set of basic structural and kinetic histomorphometric variables; outline an approach to interpretation of findings, with examples from a range of metabolic bone diseases; describe techniques for obtaining, processing, and analyzing transilial biopsy specimens; identify clinical situations in which bone histomorphometry can be useful; and relate histomorphometric measures to data from other methods for assessing bone properties and bone physiology. ## ORGANIZATION AND FUNCTION OF BONE CELLS ### Intermediary organization of the skeleton In what he termed the intermediary organization (IO) of the skeleton, Frost [1] described four discrete functions of bone cells: growth, modeling, remodeling, and fracture repair. Although each involves osteoclasts and osteoblasts, the coordinated outcomes differ greatly.The remodeling IO, which predominates during adult life, is the focus of this chapter.Coordinated groups of bone cells (ie, osteoclasts, osteoblasts, osteocytes, and lining cells—see Chapters 3 and ) comprise the basic BMUs that carry out bone remodeling.Basic structural units (BSUs) are the packets of new bone that BMUs form [2].
** Acyclovir initiated within 72 hours after acute vesiculation; pain control with analgesics, gabapentin, or tricyclic antidepressants #### **BACTERIAL SKIN INFECTIONS** **What is cellulitis?**What is the treatment of herpes zoster?** You cannot give someone zoster, but you can transmit primary varicella from an active cutaneous lesion to a susceptible individual.** Emollients, topical corticosteroids, topical retinoids, calcipotriene, classical tar **What type of therapy should be considered in widespread psoriasis? ** Phototherapy with ultraviolet light, oral retinoids, methotrexate, and immunomodulatory drugs (eg, etanercept, efalizumab) #### **HERPES ZOSTER** **Herpes zoster, or shingles, is a reactivated form of what virus from the sensory ganglia? ** Varicella-zoster virus **What does herpes zoster look like? ** Grouped clear vesicles on an erythematous base in a dermatomal distribution **Where does herpes zoster most commonly occur? ** The trunk **What are risk factors for herpes zoster? ** History of varicella, age >50 years, immunocompromise **How does herpes zoster present in the prodromal, acute, and chronic stages? ** Prodromal (2-3 weeks): stabbing/pricking pain in the involved dermatome Acute (3-7 days): new crops of lesions from papules → vesicles → pustules → crusts Chronic (months-years): post-herpetic neuralgia usually resolves within 12 months **What percentage of patients with herpes zoster will develop post-herpetic neuralgia (PHN)? ** 10%-15%. Incidence increases with age. **How can the diagnosis of herpes zoster be confirmed? ** Tzanck smear, viral culture, or direct fluorescent antibody test **What is a Tzanck smear? ** Scrape the base of a fresh blister and then spread on a glass slide stained with Giemsa or Wright stain to look for typical multinucleated giant cells **Can herpes zoster be spread? ** You cannot give someone zoster, but you can transmit primary varicella from an active cutaneous lesion to a susceptible individual. **What is the treatment of herpes zoster? ** Acyclovir initiated within 72 hours after acute vesiculation; pain control with analgesics, gabapentin, or tricyclic antidepressants #### **BACTERIAL SKIN INFECTIONS** **What is cellulitis?** _Staphylococcus aureus_ and _Streptococci pyogenes_ **What part of the body is most commonly affected in cellulitis?** Lower legs **A young, otherwise healthy person presents with cellulitis of the arm.What should you suspect?** IV drug use **What should you think of in a patient with bilateral lower leg cellulitis?** Venous stasis dermatitis **What are the risk factors for cellulitis?
ADDITIONAL ESSENTIAL NUTRIENTS Sulfur deficiency may lead to pain and inflammation in the body, slow metabolism, brittle hair or nails, fatigue, blood sugar problems, and aggravation of allergies.Vomiting will often occur with single doses of 225 mg or greater.Copper deficiency can also occur from excessive intake.Mild gastrointestinal upset has been reported at doses greater than 50 mg per day.A healthy prostate contains significantly more zinc than a diseased or enlarged prostate. This concentration of zinc in the prostate suggests zinc plays a critical role in prostate health. However, there appears to be a finite range before zinc may cause more harm than good to the prostate. Daily high doses of 80 mg or more may increase the progression of prostate enlargement. Conversely, reasonable doses—less than 40 mg—of zinc may help to reduce the size of the prostate in benign prostate hypertrophy. Zinc helps restore damage to the stomach mucosal lining after peptic ulcers., It is a treatment for sickle cell anemia and used both topically and orally for acne. Zinc can also be effective for attention deficit hyperactive disorder (ADHD) because research suggests children with ADHD may have lower levels of zinc in relation to children without ADHD. Other therapeutic uses of zinc include fungal infections of the scalp, herpes simplex virus,, and to foster oral health. Preferred Form(s): | Zinc Amino Acid Chelate ---|--- Adult RDA: | Males—11 mg; Females—8 mg; Pregnancy—11 mg; Lactation—12 mg Adult Optimal Range: | 15–20 mg Tolerable Upper Limit: | 40 mg Safety Concerns: | Zinc is generally safe and non-toxic. Mild gastrointestinal upset has been reported at doses greater than 50 mg per day. Copper deficiency can also occur from excessive intake. Vomiting will often occur with single doses of 225 mg or greater. ADDITIONAL ESSENTIAL NUTRIENTS Sulfur deficiency may lead to pain and inflammation in the body, slow metabolism, brittle hair or nails, fatigue, blood sugar problems, and aggravation of allergies.Sulfur is essential to the body's detoxification systems, immune function, and the proper function of some enzymes.Sulfur helps the body detoxify through the elimination of environmental chemicals, food toxins, drugs, and the normal by-products of hormones.It is involved in collagen formation, thus the reason it is often combined with glucosamine and chondroitin in joint health formulas.
Infectious diseases can dramatically increase morbidity and mortality in emergency situations, particularly in situations involving DPs.The risk of infectious disease transmission increases with overcrowding, poor environmental conditions, poor sanitation, water of inadequate quantity and quality, and poor overall state of health of the affected population.The rates in Sub-Saharan African countries are somewhat higher at 1.14/10,000/day. When the baseline of the children under 5 mortality rate (U5MR) is unknown, health agencies should aim for a U5MR below 2.0/10,000/day. A higher rate should be thoroughly investigated and addressed, and a rate twice the norm should be considered an emergency situation. Remember that in an emergency the critical task is to decrease the mortality rate, as it reflects a range of stress on the population. It will also be a measure by which the relief effort will be judged. The following is the procedure for calculating mortality rates. **Example** : 52 deaths in 2 weeks in an affected population of 40,000 people **Under-5 Mortality Rate:** The number of under-5 deaths per 10,000 under-5 children per day **. ** **Example** : 40 deaths in under-5 kids in 1 week in a population with 25,000 children under 5 years in age #### (2) Morbidity Rate While mortality rates measure deaths, **morbidity rates** measure the frequency of illness within specific populations. Unlike mortality rates, which are always an incidence, morbidity may be reported as an incidence or prevalence (see the previous section of definitions). Incidence is the preferred count for diseases of short duration, such as measles, mumps, and rubella. Prevalence is useful for chronic diseases of longer duration such as malnutrition. Time and place must always be specified. #### **3. Prevention and Control of Infectious Diseases** #### _**a. Introduction**_ In an emergency, priority should be given to prevention and control of infectious diseases. The risk of infectious disease transmission increases with overcrowding, poor environmental conditions, poor sanitation, water of inadequate quantity and quality, and poor overall state of health of the affected population. Infectious diseases can dramatically increase morbidity and mortality in emergency situations, particularly in situations involving DPs.Other diseases of significance in emergencies include typhoid, hepatitis A, sexually transmitted infections including HIV/AIDS, tuberculosis, diphtheria, meningococcal meningitis, influenza, anthrax, SARS, polio, guinea worm, filariasis, schistosomiasis, scabies, and emerging infections of unknown etiology.Attention should be paid to patterns of antimicrobial resistance in common pathogens.
Although Purkinje neuron loss or dysgenesis could occur prenatally along with olivary dysgenesis and the migration errors in the inferior cerebellar peduncle, observations of intact cerebellar lamina seem to argue against a massive dysgenesis or loss of Purkinje neurons before the final phases of granule cell proliferation and migration.Decreased Purkinje neuron number is not accompanied by empty basket cells, which is indicative of early rather than later developmental age at the time of loss. Since the decrease in Purkinje number is evident regardless of history of seizures or seizure medication, the age of onset and cause of cell loss are not explained by seizure onset or seizure treatment. Also, cerebellar folia do not show signs of atrophy (mutant mice with developmental loss of Purkinje cells show cerebellar hypoplasia, not atrophy). In several autism cases, the inferior olives (which are developmentally, structurally, and functionally intimately involved with cerebellar Purkinje neurons) are maldeveloped and neuronal migration errors appear in the inferior cerebellar peduncles. In one postmortem autism case, Purkinje neurons were irregularly aligned, which could not caused by some later postnatal event. The dysplastic olives and migration errors are clear signs of first trimester events but have only been seen in three autism postmortem cases. The developmental ramifications of dysplasia and migration defects are unknown. Despite the reduced number of Purkinje neurons, cerebellar cortex in autism has clearly defined cortical lamina (granule, Purkinje, and molecular layers), even in cases with large distances between single surviving Purkinje neurons. Although Purkinje neuron loss or dysgenesis could occur prenatally along with olivary dysgenesis and the migration errors in the inferior cerebellar peduncle, observations of intact cerebellar lamina seem to argue against a massive dysgenesis or loss of Purkinje neurons before the final phases of granule cell proliferation and migration.# V Potential Etiologies Autism is currently thought to be etiologically heterogeneous.Many ideas about the etiology of autism have been presented in the literature; for example, mitochondrial DNA mutation and toxin exposure have been cited as possible causes of autism.Although intriguing, these do not yet account for subsets of persons with autism.
_Topical_.Gargle with fresh juice for sore throat.**Uses**.Anti-inflammatory.**Action**.Ananas comosus_._Ananassa sativa.**PINEAPPLE** (Juice).Zinc.C. D. E. Iodine.B17.B6._Supplements_ : Pantothenic acid.Ginseng, Kelp, Safflower, Wild Indigo._Also relative to pineal disorders_.In water, or honey, thrice daily.Tinctures: 1-2 teaspoons.Liquid Extracts: 30-60 drops.Dose: powders 500mg.Practitioner use only. _Tea_ : half a teaspoon dried herb to each cup boiling water; infuse 10 minutes: sips hourly for oedema and water retention. _Liquid Extract_ : 30-60 drops, in water. _Powder_ : 1-4g. _Poultice_ : for bite of mad dog, other animal or snake bite. GSL **PIMPLE**. A spot. A small papule or pustule usually appearing on the face. Treatment as for ACNE. **PINE BUDS**. _Pinus sylvestris L. German_ : Gemeine Kiefer. _French_ : Pin Silvestre. _Italian_ : Pino salvatico. _Parts used_ : needles, shoots, resin. **Action**. Antiseptic, antiviral, expectorant, antipruritic, alterative. **Uses**. Traditional remedy for pulmonary tuberculosis and upper respiratory disorders. _External_ : ointment for skin disorders and hair loss. **Preparations**. _Tincture_ : 1 part to 20 parts 90 per cent alcohol; macerate 14 days, strain. Dose: 5-10 drops in water thrice daily. _Cough mixtures_ : ingredient of. _Powder, capsules_ : (200mg). 6 to 8 capsules daily between meals. ( _Arkocaps_ ) Or in a stable base, powder is used as an ointment for eczema. **PINEAL GLAND**. A small gland behind the third ventricle of the brain: the 'third eye'. It secretes a hormone, melatonin that regulates little known body cycles such as the 'biological clock'. Light sensitive, melatonin production is high when daylight is poor. It acts on the brain, deeply influencing behaviour and mood. Jet-lag may be due to disrupted melatonin production. Disorders manifest as sleeplessness and disorientation. _Formula_. Horsetail 1; Gotu Kola 1; Guaiacum quarter. Dose: powders 500mg. Liquid Extracts: 30-60 drops. Tinctures: 1-2 teaspoons. In water, or honey, thrice daily. _Also relative to pineal disorders_. Ginseng, Kelp, Safflower, Wild Indigo. _Supplements_ : Pantothenic acid. B6. B17. C. D. E. Iodine. Zinc. **PINEAPPLE** (Juice). _Ananassa sativa. Ananas comosus_. **Action**. Anti-inflammatory. **Uses**. Gargle with fresh juice for sore throat. _Topical_.In the morning the foot is soaked in hot water and debris scraped away; 2-3 applications may be necessary.**PINK DISEASE**.See: ACRODYNIA.**PINKROOT**.Carolina pink._Spigelia marilandica L. German_ : Indianisches Wurmkraut._French_ : Spigelie anthelminthique._Spanish_ : Spigelie._Italian_ : Spigelia.Root.Practitioner use only._Constituents_ : spigeline, tannin, oil.
She also complains of a 2-year history of dyspareunia, which is now becoming more severe.Previously, she had no peri-menstrual pain.**A 24-year-old woman is evaluated for worsening pelvic pain just prior to and during menses for the past 5 months.If bleeding persists and is known to be due to combined OCPs, a short course of oral estrogen can be used for management.They are often associated with painful, suppurative, unilateral inguinal lymph nodes that may rupture (bubo). Lastly, Giemsa or Wright staining which reveals Donovan bodies (choice d) is used to diagnose granuloma inguinale (Donovanosis). These ulcers are typically painless with an ulcer base that is clean but with friable margins that easily bleed and are beefy red in appearance. **A 24-year-old female comes to your office concerned that she is having bloody spotting in between her menstrual periods for the past 2 months. She denies abdominal or pelvic pain. She does not believe she is pregnant as she started combined oral contraceptive pills (OCPs) approximately 2 months ago. What is your next step in management**? **a. Order a vaginal ultrasound now to assess for endometrial hyperplasia**. **b. Order a urine β-hCG test now to assess for pregnancy**. **c. Reassure patient that intermenstrual bleeding is common in the first 3 months after starting OCPs and does not require further evaluation**. **d. Perform a speculum examination now to examine for any cervical or endometrial infections**. Answer: c Intermenstrual ("breakthrough") spotting and bleeding occur in approximately 25% of women during the first 3 months of use. Patients should be counseled to anticipate breakthrough bleeding (choice c). When intermenstrual bleeding occurs after 3 months of use, the patient should be evaluated for causes of bleeding unrelated to oral contraceptive use, including cervical or endometrial infection (choice d), neoplasia (choice a) and pregnancy (choice b). If bleeding persists and is known to be due to combined OCPs, a short course of oral estrogen can be used for management. **A 24-year-old woman is evaluated for worsening pelvic pain just prior to and during menses for the past 5 months. Previously, she had no peri-menstrual pain. She also complains of a 2-year history of dyspareunia, which is now becoming more severe.She has no history of sexually transmitted infections, pelvic inflammatory disease, abnormal Pap smears or pregnancies.Her physical examination reveals tenderness to palpation in the lower quadrants, with no rebound or guarding.Her external genitalia are normal, and the cervix appears healthy.There is no cervical motion tenderness, but pain is felt on uterine motion.
exhale.See expiration.Exfoliative dermatitis (Bolognia et al, 2014) exhalation.Treatment is individualized, but care is essential to prevent secondary infection, avoid further irritation, maintain fluid balance, and stabilize body temperature.Known causes include drug reactions, scarlet fever, leukemia, lymphoma, and generalized dermatitis.The cause is unknown in about half of cases.exercise tolerance, the level of physical exertion an individual may be able to achieve before reaching a state of exhaustion. Exercise tolerance tests are commonly performed on a treadmill under the supervision of a health professional who can stop the test if signs of distress are observed. exeresis /ekser″əsis/ [Gk, ex \+ eresis, removal] , (Obsolete) the surgical excision of a part, organ, or body structure. exertional headache /igzur″shənəl/ [L, exserere, to stretch out; AS, heafod \+ acan, headache] , an acute headache that occurs during strenuous exercise. It usually recedes when the level of effort is reduced, when an analgesic medication is taken, or both. exfoliation /eksfō′lē·ā″shən/ [L, ex \+ folium, leaf] , peeling and sloughing off of tissue cells. This is a normal process that may be exaggerated in certain skin diseases or after a severe sunburn or may be be done deliberately, such as with microdermabrasion. See also desquamation, exfoliative dermatitis. −exfoliative, adj. exfoliative cytology /eksfō″lē·ətiv/ , the microscopic examination of desquamated cells for diagnostic purposes. The cells are obtained from lesions, sputum, secretions, urine, and other material by aspiration, scraping, a smear, or washings of the tissue. Compare aspiration biopsy cytology. exfoliative dermatitis, any inflammatory skin disorder characterized by excessive peeling or shedding of skin. The cause is unknown in about half of cases. Known causes include drug reactions, scarlet fever, leukemia, lymphoma, and generalized dermatitis. Treatment is individualized, but care is essential to prevent secondary infection, avoid further irritation, maintain fluid balance, and stabilize body temperature. Exfoliative dermatitis (Bolognia et al, 2014) exhalation. See expiration. exhale.exhaustion /igzôs″chən/ [L, exhaurire, to drain away] , a state of extreme loss of physical or mental abilities caused by fatigue or illness.Multiple causes are possible, including extreme cases of mania.Exhaustion can be life-threatening.
Her work combines behavioral and neuroimaging techniques to investigate speech input and output processes in the human brain.**Carolyn McGettigan** , MA (Cantab), Ph.D. (London), neuroscientist and Research Associate at the Institute of Cognitive Neuroscience, University College London, London, UK.Over the last decade developments and research in the Logothetis laboratory have contributed to our understanding of the neurophysiological mechanisms underlying the functional magnetic resonance imaging (fMRI) signal. **Jennifer L. Long** , MD, Ph.D., is an Otolaryngology-Head and Neck Surgery resident at University of CaliforniaLos Angeles, CA, USA. Her special interests are in clinical laryngology and voice, vocal fold development and function, and tissue engineering approaches to treating laryngeal disorders. **James P. Lund** , BDS, Ph.D., FCAHS, dentist and neuroscientist and Professor in the Faculty of Dentistry and Alan Edwards Centre for Research on Pain at McGill University, Montréal, Canada. He is also a member of the Groupe de Recherche sur le Système Nerveux Central of the Université de Montréal. He works on the central patterning of rhythmical jaw movements and their modification by sensory inputs, particularly pain. He is also part of a group that carries out clinical trials to improve function in people who have lost teeth. **Alanna Maltby** , BSc, is a Ph.D. student at the Institute of Zoology, Zoological Society of London and University College London, UK, researching the evolution and diversity of echolocation calls in bats. **Marta B. Manser** , Ph.D., MSc, zoologist, Professor of Animal Behaviour at Zürich University, Zürich, Switzerland. Her main research interest is in communication and cognition in social mammals in their natural habitat, in particular a comparative approach on vocal communication, group decision-making and spatial orientation in several mongoose species with different social structures, but living in similar ecological habitats. **Carolyn McGettigan** , MA (Cantab), Ph.D. (London), neuroscientist and Research Associate at the Institute of Cognitive Neuroscience, University College London, London, UK. Her work combines behavioral and neuroimaging techniques to investigate speech input and output processes in the human brain.**Walter Metzner** , Ph.D., neurobiologist, Professor at the University of California, Los Angeles, USA.
This is expressed in olfactory neurons and inhibits further neurogenesis by upregulating production of the Cdk inhibitor p27kip1.Another well-documented chalone-like molecule is GDF11 (Growth and Differentiation Factor 11) in the olfactory system.Note the considerable muscle mass.19.8 A Belgian Blue bull.Fig.The original control of regional specification in the discs during development lies with morphogen gradients, especially that of Decapentaplegic (Chapter 17), which also has a strong growth-promoting function. However, normal discs grow uniformly, not in a manner corresponding to the Decapentaplegic gradient. This is probably because the gradient activates different downstream systems at different concentrations and these have different local effects on the growth rate such that the overall growth is fairly uniform. ### Mammals The best-characterized example of chalone action in vertebrates is the control of muscle growth exerted by the TGFβ superfamily member myostatin (= Growth and Differentiation Factor 8; GDF8). This is secreted by developing muscle cells and it reduces both the cell division of myoblasts and the enlargement of myofibers. The Myostatin knockout mouse has a two to threefold increase in muscle mass, arising from the presence of both more and larger myofibers. Some breeds of domestic cattle, such as the Belgian Blue, have been shown to carry hypomorphic alleles for Myostatin, indicating that traditional animal breeding has already anticipated rational genetic modification in this area (Fig. 19.8). In the embryo Myostatin is expressed in the central part of the dermomyotome, in between the epaxial and hypaxial myoblast-generating areas, and is later expressed in the limb buds, both by the myoblasts and some other mesenchymal tissue. The early expression in tissues neighboring the developing muscle indicates that it may have a role in defining the boundaries of the myogenic areas as well as the later negative-feedback regulation. Fig. 19.8 A Belgian Blue bull. Note the considerable muscle mass. Another well-documented chalone-like molecule is GDF11 (Growth and Differentiation Factor 11) in the olfactory system. This is expressed in olfactory neurons and inhibits further neurogenesis by upregulating production of the Cdk inhibitor p27kip1.Interestingly, both myostatin and GDF11 belong to the same subgroup of TGFβ-like factors, and both are inhibited by follistatin.This suggests that there could be global controls that modulate the behavior of a number of tissue-specific negative-feedback mechanisms.
One of the major reasons to biopsy ulcerating or nodular lesions in the small bowel remains assessment for lymphoma because this may change the management from surgical to medical.These allow classification of the lymphoma and ultimately determine optimal treatment and prognosis.T-cell lymphomas of the small intestine are more common than B-cell lymphomas and are typically associated with celiac disease. Most enteropathy-associated T-cell lymphomas (EATL) are located in the proximal small intestine. The diagnosis of small bowel lymphoma should be entertained in celiac patients who do not improve on a gluten-free diet or who develop recurrent gastrointestinal symptoms, anemia, or weight loss. Finally, patients with human immunodeficiency virus and low CD4 count are at risk for developing B-cell gastrointestinal lymphomas, which often have a high grade of malignancy and a poor prognosis. ### Clinical Presentation The clinical presentation of patients with lymphoma of the small intestine differs according to the histologic tumor type. Abdominal pain is the most frequent symptom of all types, occurring in approximately two thirds of patients. Other symptoms include gastrointestinal (GI) bleeding, intestinal obstruction or perforation, or a palpable abdominal mass. Patients with EATL often present with acute bleeding, obstruction, or perforation. ### Diagnosis Radiographic evaluation may include a CT scan, which characteristically demonstrates multiple, large tumors and bowel wall segments with homogenous thickening and a normal or enlarged lumen (Figure 4). Diagnosis of lymphoma requires a tissue biopsy so that studies including immunohistochemistry, flow cytometry, and cytogenetic and molecular genetic evaluation can be performed. These allow classification of the lymphoma and ultimately determine optimal treatment and prognosis. One of the major reasons to biopsy ulcerating or nodular lesions in the small bowel remains assessment for lymphoma because this may change the management from surgical to medical.FIGURE 4 Lymphoma involving the ileum.The Ann Arbor staging system used for most lymphomas is considered to be inadequate for the staging of GI lymphoma since it does not incorporate information on the depth of tumor invasion, that is known to affect prognosis.Several other staging systems have been proposed, and the most widely accepted is the Lugano staging system (Table 2).
Yes.Can lowering blood cholesterol level reduce the progression and clinical expression of atherosclerosis?By the early 1950s it had been established that blood cholesterol levels in humans could be experimentally lowered by substituting dietary polyunsaturated fats for saturated fats as a single variable in metabolic ward studies (8;9).Yes.## ATHEROSCLEROSIS IN EXPERIMENTAL ANIMALS (CHAPTER 2) The fact that rabbits could be made hypercholesterolemic just by feeding them pure cholesterol and that their arteries then showed lesions closely resembling those of human atherosclerosis was beautifully demonstrated in 1913 by Anitschkow and Chalatov (4). Over the following decades it was shown that atherosclerosis can be produced in virtually any experimental animal provided a way can be found to elevate the blood cholesterol sufficiently. ## HYPERCHOLESTEROLEMIA AS A CAUSATIVE FACTOR IN THE HUMAN DISEASE (CHAPTER 3) Can the findings from experimental atherosclerosis in animals be extrapolated to humans? Yes. In 1939, an astute clinician in Oslo, Carl Müller, pulled together many case reports on the rare syndrome of hereditary xanthomatosis and concluded that the marked hypercholesterolemia in these cases was the cause of both the skin lesions and the lesions in the coronary arteries (5). Can the findings in these rare and extreme examples of hypercholesterolemia be extrapolated to the general population? Yes. The classic studies of Keys _et al._ (6) and the NIH-sponsored Framingham study (7) showed that coronary heart disease risk was proportional to blood cholesterol levels in the population at large, i.e. _not_ limited to those with rare genetic defects. Can anything be done to lower an elevated blood cholesterol? Yes. By the early 1950s it had been established that blood cholesterol levels in humans could be experimentally lowered by substituting dietary polyunsaturated fats for saturated fats as a single variable in metabolic ward studies (8;9). Can lowering blood cholesterol level reduce the progression and clinical expression of atherosclerosis? Yes.He showed that substitution of a polyunsaturated fat for the saturated fat-rich, butter-cream-venison diet favored by the Norwegians reduced their blood cholesterol by about 17 percent and kept it down.The number of secondary coronary events in the treated group was reduced by about one-third and the result was significant at the _p_ < 0.03 level (10).
### Virilization: Normal in Males, Abnormal in Females In males, androgens stimulate the embryo to increase the length and diameter of the penis and to develop the prostate and scrotum.When an embryo is about six weeks old, these hormones kick-start gender identity.Androgens are a group of sex hormones that strongly affect your liveliness, libido, mood, and self-confidence.When you've got your estrogen levels in balance, life feels joyous and right again. ### Signs of Estrogen Balance • You have regular periods (estrogen and progesterone work together on this one). If you're postmenopausal, you'll notice the other signs. • Your joints and vagina feel well lubricated. • Orgasm regains its central role in your libidinous life, and that sense of dullness is a distant memory. • You roll with the punches; you don't feel so stressed and overwhelmed. • Sleep is a crucial part of your self-care regimen, and restores your energy, although you don't prefer it to sex with your partner. • Your mood is stable throughout your menstrual cycle. • You have improved brain function: the fog lifts, your memory and recall improve. ## CHAPTER 8 ## EXCESS ANDROGENS: DO YOU HAVE PIMPLES, OVARIAN CYSTS, AND ROGUE HAIRS? Listen up: the combination of excessively high androgens is the most common hormone problem of women in their fertile years, and perhaps even before puberty. After menopause, high androgens are associated with serious health problems, such as heart disease, stroke, mood problems, and cancer. High androgens wreak havoc hormonally for women from the embryo to maturity. Androgens are a group of sex hormones that strongly affect your liveliness, libido, mood, and self-confidence. When an embryo is about six weeks old, these hormones kick-start gender identity. ### Virilization: Normal in Males, Abnormal in Females In males, androgens stimulate the embryo to increase the length and diameter of the penis and to develop the prostate and scrotum.In females, lack of androgens causes the embryo's ambiguous genitalia to commit to a female pattern, as a default setting.
Implantation is performed under general anaesthesia.The Edwards SAPIEN device is a bovine pericardial valve mounted inside a balloon expandable stainless steel stent (length, 16 mm; diameter, 23/26 mm).Other devices have early human data or are in preclinical investigation._Circulation_ 2003; **108** :319–24. Roques F, Nashef SAM, Michel P. The EuroSCORE Study Group. Risk factors for early mortality after valve surgery in Europe in the 1990s: lessons from the EuroSCORE pilot program. _J Heart Valve Dis_ 2001; **10** :572–8. Schwartz F, Baumann P, Manthey J, _et al_. The effect of aortic valve replacement on survival. _Circulation_ 1982; **66** :1105–10. Vahanian A, Baumgartner H, Bax J, _et al_. Guidelines on the management of valvular heart disease: the Task Force on the Management of Valvular Heart Disease of the European Society of Cardiology. _Eur Heart J_ 2007; **28** :230–68. ### **Percutaneous intervention** The last decade has seen substantial progress in the development of percutaneous therapies for structural heart disease. #### **Transcatheter aortic valve implantation** Many patients who could benefit from aortic valve replacement are treated conservatively because of their high operative risk. Balloon valvuloplasty does not provide sustained clinical benefit or improve survival and is only considered as a bridge to surgery in selected cases. The introduction of transcatheter aortic valve implantation (TAVI), however, will alter our threshold for intervention. ##### _Procedure_ Currently two devices, the Edwards SAPIEN valve (Edwards Life Sciences, Irving, CA) and Corevalve (Medtronic, Minneapolis, MN) have the CE mark and are the subject of clinical trials. Other devices have early human data or are in preclinical investigation. The Edwards SAPIEN device is a bovine pericardial valve mounted inside a balloon expandable stainless steel stent (length, 16 mm; diameter, 23/26 mm). Implantation is performed under general anaesthesia.The calcified valve is pre-dilated and the device delivered using a steerable catheter (22/24F).Fluoroscopy, aortography, and transoesophageal echocardiography (TOE) are used to assess position.Left ventricular flow is then briefly arrested by rapidly pacing the right ventricle (200 bpm) and the device is deployed.
Nevertheless, it is generally more appropriate to reconstruct the mandible with non-vascularized autogenous bone.31.2 A fractured reconstruction plate used to span a segmental defect, which had not received a bone graft.Fig.Subsequent soft tissue grafting is often necessary to supply attached mucosa for denture or implant insertion. This is often carried out by means of a split-thickness skin graft, and normally done as a secondary procedure following incorporation of the bone graft. Fig. 31.1 A marginal resection of the mandible for a fibro-osseous lesion (a) reconstructed with an iliac crest bone graft mortised into place intraorally at the time of the primary resection (b) and secondarily skin grafted and implants inserted and an implant supported restoration placed (c, d). ## Segmental Resection Segmental resection of the mandible with loss of mandibular continuity may be necessary for benign or malignant lesions, as well as for chronic infection. Temporary immediate reconstruction is often carried out by means of a reconstruction plate, but these are rarely satisfactory for long-term use. The usual history is for the plate to either exteriorize itself and become secondarily infected, or for screw loosening and mobility to occur. Depending on the forces placed on it, these problems will normally occur after some 18 months or 2 years. Plate fracture has also been reported (Fig. 31.2). In particular, reconstruction plates fail most frequently in the anterior mandible, but can survive in the long-term in the body and posterior parts of the mandible, particularly if these have adequate soft tissue coverage, which may have to be in the form of a soft tissue flap, such as a pectoralis major flap. Fig. 31.2 A fractured reconstruction plate used to span a segmental defect, which had not received a bone graft. Nevertheless, it is generally more appropriate to reconstruct the mandible with non-vascularized autogenous bone.Immediate segmental reconstruction with non-vascularized autogenous bone from an intraoral approach has been associated with a high failure rate, although it was recommended by Obwegeser amongst others.The reasons for failure are generally wound breakdown intraorally and contamination of the wound with saliva, or primary infection due to oral contamination.
spano-, prefix meaning "scanty or scarce": _spanogyny, spanomenorrhea, spanopnea._ sparfloxacin, an antiinfective.See **cantharis**.Spanish fly.See **air sickness**.space sickness.**Metered dose inhaler with spacer** _(Potter et al, 2011)_ space regainer, a fixed or removable appliance for moving a displaced secondary tooth into its normal position in a dental arch.space adaptation syndrome, the ability to accommodate changes in cardiac function, bone mineral changes, and muscle atrophy while in the weightless state of a space traveler. space maintainer, a fixed or removable appliance for preserving the space created by the premature loss of one or more teeth. It can be unilateral or bilateral. Types include band-loop, crown-loop, and lingual arch. See also **separator**. **Space maintainer** _(Bird and Robinson, 2005)_ space medicine, a branch of medicine concerned with the effects of travel in space, beyond the atmosphere and pull of gravity, including weightlessness, motion sickness, and restricted physical activity. space obtainer, an appliance for increasing the space between adjoining teeth. spacer /spās′ r/ L, _spatium,_ space], on a metered dose inhaler, a chamber between the inhaler canister and the patient's mouth where droplets of medication can slow down and evaporate so that there is less direct impact on the oropharynx, with more medication delivered to the lower respiratory tract instead of being lost in the mouth. This is especially helpful for children. See also [**metered dose inhaler**. **Metered dose inhaler with spacer** _(Potter et al, 2011)_ space regainer, a fixed or removable appliance for moving a displaced secondary tooth into its normal position in a dental arch. space sickness. See **air sickness**. Spanish fly. See **cantharis**. spano-, prefix meaning "scanty or scarce": _spanogyny, spanomenorrhea, spanopnea._ sparfloxacin, an antiinfective.ADVERSE EFFECTS: Life-threatening effects are leukopenia and pseudomembranous colitis.Other adverse effects are eosinophilia, anemia, flatulence, diarrhea, QT interval prolongation, vasodilation, rash, pruritus, and photosensitivity.Common side effects are headache, dizziness, insomnia, nausea, vomiting, and abdominal pain.
Similar changes commonly occur in the tonsils and lymphoid tissue of the oropharynx.The T-cell proliferation is sometimes so exuberant that it is difficult to distinguish the nodal morphology from that seen in malignant lymphomas.B-cell areas (follicles) may also show mild hyperplasia.In hosts with acquired defects in cellular immunity (e.g., AIDS, organ transplantation), reactivation of EBV can lead to B-cell proliferation, which can progress through a multistep process to EBV-associated B-cell lymphomas. EBV also contributes to the development of some cases of Burkitt lymphoma (Chapter 13), in which a chromosomal translocation (most commonly an 8 : 14 translocation) involving the MYC oncogene is the critical oncogenic event (Fig. 8-13). Morphology The major alterations involve the blood, lymph nodes, spleen, liver, CNS, and, occasionally, other organs. The peripheral blood shows absolute lymphocytosis; more than 60% of white blood cells are lymphocytes. Between 5% and 80% of these are large, atypical lymphocytes, 12 to 16 µm in diameter, characterized by an abundant cytoplasm containing multiple clear vacuolations, an oval, indented, or folded nucleus, and scattered cytoplasmic azurophilic granules (Fig. 8-14). These atypical lymphocytes, most of which express CD8, are sufficiently distinctive to strongly suggest the diagnosis. Figure 8-14 Atypical lymphocytes in infectious mononucleosis. The lymph nodes are typically discrete and enlarged throughout the body, particularly in the posterior cervical, axillary, and inguinal regions. On histologic examination the most striking feature is the expansion of paracortical areas due to activation of T cells (immunoblasts). A minor population of EBV-infected B cells expressing EBNA2, LMP1, and other latency-specific genes can also be detected in the paracortex using specific antibodies. EBV-infected B cells resembling Reed-Sternberg cells (the malignant cells of Hodgkin lymphoma, Chapter 13) may be found. B-cell areas (follicles) may also show mild hyperplasia. The T-cell proliferation is sometimes so exuberant that it is difficult to distinguish the nodal morphology from that seen in malignant lymphomas. Similar changes commonly occur in the tonsils and lymphoid tissue of the oropharynx.It is usually soft and fleshy, with a hyperemic cut surface.The histologic changes are analogous to those of the lymph nodes, showing an expansion of white pulp follicles and red pulp sinusoids due to the presence of numerous activated T cells.These spleens are especially vulnerable to rupture, possibly in part because the rapid increase in size produces a tense, fragile splenic capsule.
One cancer drug's story is particularly instructive.Because normally you can do a cancer study on as few as thirty or forty patients."You have to understand how incredible that is.During the 1980s and '90s, three companies showed interest in antineoplastons: Sigma Tau Pharmaceuticals of Italy, Chugai Pharmaceuticals of Japan, and Elan Pharmaceuticals of Ireland. One by one they dropped away. The medical director of Sigma Tau wrote, "Dr. Burzynski was informed on January 31, 1991, that Sigma Tau did not intend to proceed with the development of the antineoplastons. We have studied antineoplastons A10 and AS2.1... in human and [mouse] tumor cell lines.... On the basis of these results the project has been discontinued." Burzynski saw the rejections as a conspiracy among cancer doctors willing to lie to save their careers. "Most of the oncologists—I'm talking about reputable oncologists—they work for pharmaceutical companies," said Burzynski. "They work in clinical trials; they receive various types of incentives from pharmaceutical companies. They will do everything they can to lie.... We have a lot of evidence about some of these doctors who are dishonest, who are liars, who cheat." In truth, it's not that hard to prove that new cancer therapies work. Paul Goldberg, editor of _The Cancer Letter_ —a Washington, D.C.–based publication covering cancer research and drug development—has commented on the strange case of Stanislaw Burzynski. "Drug approval is a technical, time-consuming, and costly process," he said. "Nonetheless, thousands of anticancer compounds have been shown to be effective—or dismissed as ineffective—over the decades since Dr. Burzynski initiated his experiments." Henry Friedman, the oncologist from Duke University who had independently reviewed Burzynski's data, agreed: "Despite thousands of patients treated with antineoplastons, no one has yet shown in a convincing fashion... that the therapy works. You have to understand how incredible that is. Because normally you can do a cancer study on as few as thirty or forty patients." One cancer drug's story is particularly instructive.Investigators reasoned that a drug that blocked the protein made by this gene could work.In response, a small biotech company in Berkeley, California, called Plexxikon—not much bigger than the Burzynski Research Institute—took an interest.
For example, patients may take St. John's wort for depression rather than be evaluated for possible psychotherapy and/or drug therapy.In some cases, herbal preparations are self-administered to treat a serious health problem that could more effectively be treated by conventional medicine, potentially resulting in a delay of diagnosis and treatment._Teach patients that because an herb is labeled as "natural," it does not mean that the herb is safe. Because it may be safe does not mean that it is effective._ Some dietary and herbal supplements have pharmacoactive effects that can be serious or deadly, as in cases of overuse, inappropriate use, supplement toxicities, and supplement-drug and supplement-supplement interactions. Considerations for Older Adults Older adults in the community often overuse dietary and herbal supplements to help prevent potentially life-threatening health problems and promote quality of life. For example, older women may take too much calcium because they want to prevent osteoporosis. As a result, excess calcium can deposit in kidneys as renal calculi (stones). Teach women the importance of collaborating with their health care provider to monitor serum calcium levels and kidney function before and during calcium supplementation. Older adults who live in independent and assisted-living communities often self-administer a variety of supplements without telling their nurses or primary care providers. Nurses working in these settings need to talk with their residents about the safety and efficacy of CAM therapies. To prevent toxicities and supplement-drug interactions, encourage residents to inform the health care team about which supplements they are taking (Moquin et al., 2009). In some cases, herbal preparations are self-administered to treat a serious health problem that could more effectively be treated by conventional medicine, potentially resulting in a delay of diagnosis and treatment. For example, patients may take St. John's wort for depression rather than be evaluated for possible psychotherapy and/or drug therapy.As a result, they may take conventional drugs and natural products to treat the same condition.The resulting drug-supplement interactions may be harmful or life threatening.Nursing Safety Priority Drug Alert When caring for patients in any health care setting, ask them if they use herbs or nutritional supplements and, if so, for what purpose.
Five of the twenty-two patients in the study were able to completely discontinue their medications, maintaining control solely with gurmar.Diabetic patients who did not require insulin also benefited from gurmar, showing a reduction in their blood sugar levels and a reduced need for their oral diabetic medicines.Gurmar may be another useful agent in therapy of this prevalent illness. Studies in animals have shown that gurmar has many different effects on the metabolism of sugar. One of the most consistent findings is the reduction of glucose absorption from the digestive tract in animals given gurmar. Chemicals in gurmar inhibit the uptake of sugar from the small intestines resulting in a lowering of blood sugar levels., In addition to blocking sugar absorption, gurmar extracts have also been shown to inhibit the absorption of oleic acid, a building block of fat in the body. Gurmar has other interesting effects on glucose metabolism. Components of gurmar slow the uptake of glucose into muscles and inhibit the storage of glycogen in the liver., Absorption of cholesterol is also reduced. The net effect of these various actions is better sugar tolerance. Diabetic rats fed daily doses of gurmar extracts showed lower blood sugar levels, higher insulin levels, and a doubling in the number of cells in the pancreas responsible for producing insulin. If these findings are applicable to people, gurmar could be an important advance in the treatment of diabetes mellitus. Although formal studies in human beings are limited, initial reports are encouraging. Patients with insulin-dependent diabetes given a daily dose of a gurmar extract had a reduction in their insulin requirements and a lowering of their fasting glucose levels. Diabetic patients who did not require insulin also benefited from gurmar, showing a reduction in their blood sugar levels and a reduced need for their oral diabetic medicines. Five of the twenty-two patients in the study were able to completely discontinue their medications, maintaining control solely with gurmar.Another application for this herb is in the treatment of obesity.Neurophysiological studies have found that when gurmar is present on the tongue, taste nerves fail to send the information about sweetness to the brain.