NMS phisrebiberkotch.gq - Ebook download as PDF File .pdf), Text File .txt) or read book online. NMS Pathology (National Medical Series for Independent Study). Home · NMS 79MB Size Report. DOWNLOAD PDF NMS Review for USMLE Step 2 CK. NMS Pathology Virginia A. LiVolsi MD, Maria J. Merino MD, John S.J. Brooks MD, Scott H. Saul MD, John E. Tomaszewski MD.

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The abdominal examination was unremarkable for acute findings but showed an appreciable increase in liver volume. The base of the right lung was dull with normal fremitus. Arterial blood gases were: PaO 2 Supportive therapy was immediately started with infusion of fluids, electrolytes, and antibiotics ceftazidime 2 g three times a day.

To reduce the high fever, metamizole 1 g IV along with ice packing was repeatedly used. In the next four days, fever remained elevated, muscular tone increased, and level of consciousness decreased.

A progressive decrease in blood platelet content, together with an elevation of fibrin degradation products D-dimer: The abdomen of the patient was evaluated during a surgical consult but, because of the general increase in muscular tone, it was not possible to reach an acceptable diagnosis. Seven days after admission, the patient had a massive hematemesis, his blood pressure decreased to 60 mmHg and, in spite of standard resuscitation therapy, he died.

At autopsy, gastric and duodenal ulcers were found, together with an acute necrotizing enterocolitis and an acute purulent peritonitis.

Pulmonary edema was the considered immediate cause of death. Previous reports have shown that death occurs because of cardiovascular collapse, pulmonary embolism, aspiration pneumonia, or renal failure due to rhabdomyolisis Kaufmann and Wyatt Other serious complications in these patients are myocardial infarction, sepsis, and disseminated intravascular coagulation Pelonero et al Case 2 had massive liver damage and signs of blood loss, possibly due to intravascular coagulation, while case 3 had clear laboratory signs of intravascular coagulation that probably contributed to the development of intestinal perforation and massive loss of blood.

There are also a number of pharmacological reasons that could explain why gastrointestinal bleeding was frequent in our patient series. The most obvious is probably the use of nonsteriodal antiinflammatory drugs NSAIDs to reduce body temperature. This is a commonly accepted procedure for the treatment of elevated fever Kaufmann and Wyatt in spite of the fact that NSAIDs inhibit prostaglandin synthesis, thus decreasing epithelial mucus formation and mucosal resistance to injury.

NSAIDs may cause lesions not only in the stomach, but in the duodenum, ileum, and colon Wolfe et al In our clinical records, NSAID administration was associated with that of the H 2 receptor antagonist ranitidine, a procedure that was obviously not sufficient to prevent tissue damage and bleeding.

NMS Pathology 3rd Edition

NSAIDs inhibit both cyclooxygenase COX 1 a constitutive enzyme present in most of the cells, including platelets, and COX 2, an inducible enzyme particularly abundant in neutrophils and in macrophages Vane et al Inhibition of platelet function could certainly have facilitated bleeding in NMS patients Patrono et al Dantrolene was another drug administered to NMS patients. It has been previously observed that patients treated with this drug may suffer a number of side effects including gastric irritation, abdominal cramps, and constipation Patrono et al These side effects are not surprising since dantrolene inhibits calcium flux across the sarcoplasmic reticulum and may inhibit the depolarization-induced contraction of smooth muscles thus changing gastrointestinal and colon motility Ward et al Dantrolene administration may also cause important liver damage Utili et al ; Donegan et al , and its use may certainly be involved in causing the massive liver necrosis of case 2.

All the patients also received agents able to stimulate dopamine receptors. Dopamine receptor agonists were administered on the assumption that they could facilitate recovery.

It is indeed widely accepted that when dopamine is locally injected in the pre-optic anterior hypothalamus it reduces body temperature Cox et al , while neuroleptic injected into the basal ganglia may cause muscular rigidity and generate heat Adnet et al Dopamine interacts with at least 5 receptor subtypes Emilien et al and it is not clear which of them is involved in human thermoregulation. It is known, however, that dopamine receptor agonists including dopamine, bromocriptine, and apomorphine affect gastric and intestinal secretion and motility often leading to emesis Morris ; Parkes Thus it is reasonable to assume that systemic administration of dopamine agents could increase secretion of the gastrointestinal tract, cause alteration of the peristalsis and contribute to the fatal outcome of cases 1 and 3.

Finally, all the patients with fatal outcome had been treated for prolonged periods years and were under treatment, at the appearance of NMS symptoms, with drugs able to antagonize muscarinic receptors.

Case 1 had received chlorpromazine together with orfenadrine, case 2 received levomepromazine and amitryptiline, and case 3 had received chlorpromazine, zuclopenthixol, and carbamazepine.

All these agents have a significant affinity for muscarinic receptors Costa et al ; Kwok and Mitchelson It is widely accepted that these receptors play a key role in the control of gastrointestinal motility and secretion Stockbrugger ; Nelson et al ; Ehlert et al , and that a prolonged treatment with muscarinic receptor antagonists causes supersensitivity of these receptors. This supersensitivity may be easily observed as an abstinence syndrome in patients treated for prolonged periods with antidepressants.

Vomiting and diarrhea together with perspiration are the main signs of this pathology Dilsaver and Greden It is therefore reasonable to assume that withdrawal of muscarinic antagonists contributed to an increase in gastrointestinal motility and secretion in cases 1 and 3 who died with gastrointestinal bleeding. The three fatal cases described suggest that the mortality rate is still elevated in patients with severe NMS. They also suggest that in the management of these patients it may be useful to: Finally, the elevated mortality rate in our patient series in which all the patients received dantrolene and dopamine receptor agonists suggest that further clinical studies are necessary before assuming that the administration of these agents is a useful therapeutic procedure.

National Center for Biotechnology Information , U. Ther Clin Risk Manag. Author information Copyright and License information Disclaimer.

All rights reserved. Abstract Background Neuroleptic malignant syndrome NMS is a rare side effect of antipsychotic therapy characterized by fever, muscular rigidity, altered mental status, increased level of serum creatinine phosphokinase, and increased number of white blood cells.

NMS pathology.pdf

Results Eight patients presented with this neurological disorder. Conclusion Our results suggest that gastrointestinal bleeding is a frequent cause of death in NMS patients. Introduction Neuroleptic malignant syndrome NMS is a rare, potentially fatal complication of antipsychotic therapy and may occur in patients treated with either typical or atypical neuroleptic agents Shalev et al ; Robb et al ; Stanfield and Privette Methods We examined the clinical records of patients admitted to the Toxicology Unit of Florence University Hospital between and Table 1 Criteria used for diagnosis of neuroleptic malignant syndrome.

Chronic antipsychotic treatment 2. Altered mental status 4. Rigidity and tremors 5. Published on Nov 12, SlideShare Explore Search You. Submit Search.

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Start on. Show related SlideShares at end. WordPress Shortcode. Reduced venous return results in decreased preload and hence decreased myocardial work or oxygen consumption accounting for a significant component of mechanism of action of these agents.

Unlike agents such as sildenafil, GTN does not affect phosphdiesterase V and indeed concomitant use of sildenafil with GTN is contraindicated to avoid potential excessive vasorelaxation that may be associated with reflex tachycardia and myocardial contractility. In this regard, it is apparent that GTN does not interfere with baroreceptor reflex pathways.

Although the evidence is somewhat contradictory, it appears that GTN does not directly relax resistance coronary arteries but may favorably enhance perfusion of collateral vessels. Although GTN may have application in the treatment of congestive heart failure, it does not inhibit Na-K ATPase as is apparent in agents such as digitalis. The infection is transmitted by the fecal—oral route and takes hold very quickly. The virus replicates in the gastrointestinal tract and is shed in the feces during the incubation and acute phases of the disease.

The partial pressure of a gas is proportional to the fractional concentration of the gas and total gas pressure. Predictably, PO2 would decrease from the normal range of 97 to mm Hg to approximately 67 mm Hg following decreases in alveolar PO2.

This decrease is partially due to water vapor pressure, which remains constant at 47 mm Hg, and PCO2 , which may decrease slightly due to stimulation from ventilation. This modest decline in PO2 would not be associated with a decrease in oxygen saturation of arterial hemoglobin. A compensatory response would shift the oxyhemoglobin dissociation curve to the right because of the production of 2,3diphosphoglycerate 2,3-DPG ; however, this response usually takes more time than the average plane flight.

Antibodies are not involved in this type of immune response. Neutrophils and mast cells are part of the nonspecific immune response, so they would not be major mediators of the specific response to the tuberculin test.

Therefore, these cells would not be part of the type IV response. IL-2 stimulates not suppresses the activated T cells to proliferate, as well as to differentiate to effector T cells. IL-2 has no effect on somatic cells of the body or on macrophages.

Although other T cell cytokines can influence the type of antibody made by plasma cells e. Although he is being treated, this patient has already progressed to the late stages of the disease, and he is now displaying the classic signs of cirrhosis. The bleeding is most likely the result of ruptured esophageal varices.

Portal hypertension causes the development of several collateral circulations; these other vessels offer less resistance to flow, and they enlarge over time to accommodate the increased volume. The rectal and esophageal veins dilate to become varices, which may allow significant blood loss if they tear. The caput medusae vascular pattern over the abdomen indicates enlargement of another collateral circulation.

Portal hypertension also causes blood flow to back up in the spleen, which results in splenomegaly. Hemoglobin synthesis is limited by iron availability. A hemochromatosis patient has excess iron and will probably not be hemoglobin deficient.

Protein C is an anticoagulant whose exact mechanism of action remains unknown. Deficiency of protein C has been demonstrated in some cases of disseminated intravascular coagulation.

Although neither eroded gastric ulcer nor bronchogenic carcinoma is excluded by hemochromatosis, hemochromatosis does not predispose to either of those conditions. Additional symptoms of visual problems may be secondary to space-related lesions of tumor mass.

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Prolactinomas are the most frequent secretory tumors. Computed tomography CT or magnetic resonance imaging MRI examination can be used to reveal micro- or macroadenomas and distinguish hyperprolactenima that is idiopathic or secondary to other types of mass lesions compressing stalk and interfering with dopamine inhibition.

Galactorrhea is a result of direct effect of PRL on breast tissue. Radiation therapy may be an alternative.

Although prolactin levels may increase in hypothyrodism due to decreased clearance of prolactin, increased levels of estrogen, or enhanced TRH receptors in lactotrophs , hyperthyroidism is not associated with elevated levels of PRL or the physical symptoms described above. Galactorrhea can indeed be drug-induced but agents that interfere with dopamine effects such as psychotropic agents that are dopamine antagonists rather than dopamine agonists like bromocryptine may produce such symptoms.

Diabetes insipidus is a disorder of posterior pituitary involving insufficiency in arginine vasopressin and does not cause symptoms in reproductive tissues.

Thus, in developed countries, the regulation of iron homeostasis requires absolute control of absorption. Unfortunately, the normal mechanisms of regulation are not well understood.

The iron buildup seen as a physiologic response to anemia is almost entirely confined to phagocytic cells of the reticuloendothelial system. Yet, in hemochromatosis patients, parenchymal cells of the liver, pancreas, and heart accumulate large amounts of iron, whereas phagocytes remain normal. Thus, although there is clearly a regulatory problem at the absorptive stage, the reticuloendothelial system is also functioning improperly.

Patients with various erythropoietic difficulties and a resultant physiologically normal iron accumulation almost never have the extensive pathology seen in patients with primary hemochromatosis.

Involvement of the pancreas commonly leads to diabetes mellitus, and skin pigmentation is a routine finding. Grossly, these tumors are hemorrhagic. Microscopically, as shown in this photograph, they are characterized by two main cellular components: stromal cells and giant cells.

The stromal cells probably are the neoplastic component. These tumors may be locally aggressive, and metastasis is rare. If completely excised or curetted, however, they usually have a benign clinical course. Both T cells and B cells develop in the bone marrow.

B cells also mature in the marrow, whereas T cells migrate to the thymus for maturation. Gut-associated lymphoid tissue, bronchial-associated lymphoid tissue, and other mucosal-associated lymphoid tissues are peripheral lymphoid tissues. The gut-associated lymphoid tissue collects any antigens entering the body through the gastrointestinal tract, and the proper immune response may begin.

The spleen is the site of filtration of antigens in the blood and of red blood cell destruction. Most plasma cells migrate to the bone marrow, making it the site for most antibody production. Germinal centers are sites for B cell proliferation after they encounter antigen in the context of the proper cytokines. In addition to reducing hemoglobin saturation, carbon monoxide reduces the ability of oxyhemoglobin to deliver oxygen to the periperhy by shifting the dissociation curve to the left not right.

Carbon monoxide can also inhibit other heme-containing proteins such as cytochromce oxidase and cytochrome P, but the significance of such inhibition in pathophysiological conditions is unclear. They are characterized by a proliferation of stromal cells associated with a similar proliferation of ductal cells.

Visible at low magnification are slit-like spaces, some having a leaf-like configuration, that are lined by hyperplastic ductal epithelium with a surrounding cellular stroma.

Malignant lesions that mimic fibroadenomas include phyllodes tumors.

The Fab for antigen binding portion binds specifically to one antigen. If the antibody is attached to the immature B cells that synthesized it, binding of the antigen to the Fab portion can lead to activation of the B cell. Free antibodies in the blood can bind to bacteria or their toxins. Then macrophages or other cells can ingest the antibody—antigen complexes using Fc receptors for recognition. The Fc for constant portion is responsible for the effector functions of antibodies.


It binds to Fc receptors on neutrophils or macrophages to trigger phagocytosis of the antibody—antigen complex. Bound antibodies that cross-link their Fc portions can trigger the classical complement pathway. Antibody-dependent, cell-mediated cytotoxicity occurs when antibodies attach to specific antigens on tumor cells or other cells recognized as foreign and designate those cells to be killed by either natural killer NK cells or macrophages.

The NK cells and macrophages have Fc receptors that allow them to identify the cells that are to be killed. Smooth muscle cells lack the sarcomeres of skeletal muscle and are innvervated by the autonomic nervous system rather than the somatic nervous system. In some smooth muscles, basal cytosolic calcium is sufficient to maintain a contractile state in the absence of external stimuli e.

In addition, some smooth muscle cells can generate action potentials without external stimuli and hence manifest pacemaker activity. Many types of smooth muscle have an intrinsic property in which mechanical stretch produces contraction. On physical examination, a delayed upstroke of the carotid pulse may be noted, as well as a late-peaking systolic ejection murmur and soft A2 on auscultation. Over time, left ventricular hypertrophy may develop, leading to an S4 gallop and ECG abnormalities.

Aortic stenosis may be differentiated from mitral stenosis and aortic regurgitation by the systolic murmur rather than the diastolic murmurs caused by these two lesions. Similarly, the murmur heard in mitral regurgitation is holosystolic rather than ejection type, and it does not vary with changes in the cardiac cycle length.

However, mitral regurgitation intensity does vary with the administration of amyl nitrite, a vasodilator that causes decreased intensity of the murmur.

Complete heart block is associated with a narrow QRS.A native of Roslyn, N. The book is 12 tests each containing 50 questions. Dopamine receptor down-regulation is condition] APA Clin Exp Neurol. As the name implies, this is an acute, not chronic, syndrome. Dopamine interacts with at least 5 receptor subtypes Emilien et al and it is not clear which of them is involved in human thermoregulation.

All the patients also received agents able to stimulate dopamine receptors. Table 1 Criteria used for diagnosis of neuroleptic malignant syndrome.

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