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19 Cards in this Set
- Front
- Back
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atheromatous plaque changes associated with acute coronary syndromes
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ulceration of the plaque surface
thrombosis hemorrhage into the plaque substance intermittent platelet aggregation |
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two main hypotheses of atherosclerosis disease mechanism
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1 intima cell proliferation
2 repetitive formation and reorganization of thrombi these hypotheses are combined to form the response-to-injury hypothesis--> atherosclerosis is a chronic inflammatory and healing response of the arterial wall to endothelial injury. Lesion progression: interaction between modified lipoproteins, monocyte-derived macrophages and T lymphocytes |
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progression of pathogenic events in atherosclerosis
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endothelial injury--> accumulation of lipoproteins--> monocyte adhesion to the endothelium--> transformation to foam cells--> platelet adhesion--> factor release--> smooth muscle recruitment/proliferation--> ECM production--> lipid accumulation
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Causes of endothelial injury in atherosclerosis
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most important: hemodynamic factors & high cholesterol
HTN hyperlipidemia toxins from cigarette smoke homocysteine infection immune reactions |
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components of atherosclerotic plaque
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cells- smooth muscle, macrophages, T lymphocytes
ECM- collagen, elastic fibers, proteoglycans lipid- intracellular and extracellular |
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presentation of rheumatic heart disease of mitral valve
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slowly worsening congestive heart failure
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presentation of serous pericarditis
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chest pain not related to exercise, not relieved by nitroglycerin
fibrinous pericarditis also has a friction rub |
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presentation of restrictive cardiomyopathy
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heart failure without chest pain
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presentation of calcific aortic stenosis
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slow valve closing leads to increasing LV pressure (up to 200mm Hg)--> pressure overload (concentric) LV hypertrophy--> increased ischemic heart disease
once symptoms (angina, CHF, syncope) occur, outcomes are bleak |
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presentation of 75% coronary atherosclerosis
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exertional chest pain
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presentation of viral myocarditis
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pain may be present at rest, lasts only several weeks
wide variety of symptoms from asymptomatic to heart failure symptoms- fatigue, dyspnea, palpitations, precordial discomfort, fever |
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causes of serous pericarditis
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non-infectious inflammatory diseases:
rheumatic fever SLE scleroderma tumor uremia |
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causes of fibrinous/serofibrinous pericarditis
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acute MI
postinfarction (Dressler syndrome) uremia chest radiation rheumatic fever SLE trauma |
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types of pericarditis
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serous (non-infectious inflammation)
fibrinous/serofibrinous purulent/suppurative (microbial) hemorrhagic (neoplasm) caseous (TB or fungal) |
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causes of neutropenia due to ineffective granulopoiesis
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1 aplastic anemia
2 myelophthisic anemia (tumor, granuloma, fibrosis) 3 drugs (chlorpromazine) 4 megaloblastic anemia 5 kostman sydrome |
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causes of neutropenia due to accelerated destruction/removal of neutrophils
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1 immunologic disorders (SLE)
2 drugs (aminopyrine, thiouracil, sulfonamides- Ab mediated destruction) 3 spleomegaly 4 overwhelming bacterial, fungal or rickettsial infection (increased peripheral utilization) |
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most common cause of agranulocytosis
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drug toxicity- cancer drugs (alkylating agents and antimetabolites)
aminopyrine, chloramphenicol, sulfonamides, chlorpromazine, thiouracil, phenylbutazone |
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causes of neutrophilic leukocytosis
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acute bacterial infection
tissue necrosis (MI or burns) |
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morphologic changes to neutrophils that accompany sepsis and sever inflammatory disorders (Kawasaki)
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1 Dohle bodies- dilated ER that appear as sky blue puddles
2 toxic granulations- coarser and darker than normal granules (abnormal azurophilic primary granules) 3 cytoplasmic vacuoles |
