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13 Cards in this Set

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importance of knowledge of the natural history of a disease
prognosis can be determined by established knowledge of natural history treatment decisions guided in part by natural history important in planning approaches to disease prevention
1
infections: manifestations, causes of manifestations
Causes of manifestations: a. Products of the inflammatory response (cytokines, peptides) b. Products of the infectious agent (toxins, other peptides) c. Host response directed to specific foreign antigens Manifestations: a. Systemic symptoms such as fever malaise, night sweats, and weight loss (constitutional, or B symptoms) b. pain and swelling at sight of infection c. Destruction of affected organ, in whole or in part d. Disseminated intravascular coagulation (DIC), due in some cases to release of endotoxin and/or coagulants e. Shock and/or death (due to organ destruction, fluid loss, altered vasomotor tone, DIC) f. immune deficiency (HIV)
2
Neoplasm manifestation causes
1. Mass effect (pain, pressure, obstruction, bleeding) 2. Organ failure due to replacement by primary or metastatic growth, or as an effect of treatment 3. Tumor products (hormones, peptides, coagulants) causeing various abnormalities (i.e ACTH from lung carcinoma, erythropoietin from kidney carcinoma) 4. Generalized wasting and/or malaise
3
Types of immunological diseases
1. Hypersensitivity reactions: Manifestations include rashes, itching, asthma, renal insufficiency, anaphylaxis (generalized allergic reaction w/ vasodilation, possible shock), death 2. Autoimmune diseases: immune reactions to self-antigens, often associated with "autoantibodies", localized tissue dammage, systemic manifestations (such as fever) b/c inflammatory response 3. Immunodeficiencies: Primary (genetic) and secondary (acquired) deficiencies of the immune system. Manifestations related to susceptibility to infection.
4
reversible ischemic injury
1. diminished oxidative phosphorylation in mitochondria w/ subsequent decrease in ATP
2. loss of contractility after 2 min
3. cell switches to anaerobic glycolysis, pH decrease from lactic acid
4. Increase in oxy radicals, damage membrane, abnormal Na/K pumping, intracellular edema
5. mitochondria show clearing of matrix, disrutpion of cristae, dilation of endoplasmic reticulum in myocardium after 30 min
5
irreversible ischemic injury
1. necrosis occurs 2. occur in myocardium after 60 min 3. mitochondria show more clearing of matrix, cristae disruption, amorphous densities 4. intracellular edema indicated by separation of myolfilaments 5. changes in inner cell membrane, release of sequestered calcium into cytosol, phospholipase activation, phospholipid degradation w/ further loss of Ca barrier 6. chromatin margination
6
Light microscopic changes of acute ischemic injury
1. mycocytolysis characterized by cells that appear vacuolated b/c of intracell edema. 2. cytoplasm opque and hypereosinophilic from denatured protein and \u2193 pH 3. Nuclei may be lsed or appear pyknotic 4. at border of ischemia and normal myocardium, cells may die contracted, giving appearance of contraction bands
7
Methods of reperfusion of ischemic myocardium
1. lyse the clot biochemically, using streptokinase, urokinase, or other new thrombolytic agents 2. Mechanical dissolution of the clot, as with angioplasty 3. bypass of the occluded segment by coronary artery bypass 4. current investigation of oxygen radical scavengers to minimize injury
8
Apoptosis: morphology by EM
0 1. condensation of nuclear chromatin to form dense, circumscribed masses at the nuclear envelope 2. loss of cell cohesion 3. decrease in cell volume and increase in cell density 4. splitting of nucleus 5. formation of cytoplasmic blebs, followed by their seperation to form membrane bound cytoplasmic bodies 6 phagocytosis of apoptotic bodies, followed by lysosomal degradation
9
Apoptosis morphology by light microscopy
cells are shrunken and convoluted (shrinkage necrosis) and apoptotic bodies appear as round cytoplasmic masses with eosinophilic or basophilic material
10
Biochemistry of apoptosis
1. rapid regular nuclear dna fragmentation 2. cytoplasmic proteinases (such as caspases) casue cell changes 3. Apoptosis dependent on gene activation 4. Apoptosis genes include bcl-2 oncogene, c-myc oncogene, bax, p53 tumor suppressor
11
physiologic and pathologic events caused by apoptosis
1. programmed cell death in embryogenesis 2. cell deletion in proliferating tissue (i.e. intestinal epithelium) 3. hormone dependent involution and pathologic atrophy of cells 4. cell death in tumors 5. death of immune cells 6. cell death from injurious stimuli (virus, thermal injury, radiation)
12
key events in ischemic cardiac myocytes
0 2 min: loss of contractility 10 min: atp to 50% normal 20-40 min: irreversible cell injury
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