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General Principles
General Definitions and Concepts + Biochemistry
| Question | Answer | |
|---|---|---|
| Irreversible injury hypoxia | membrane/ mitochondrial damage | Increase cytosolic Ca2+ activates phospholipase, proteases, endonuclease |
| Mitochondrial damage | release cytochrome c activates apoptosis | |
| Free radicals | unpaired electron in outer orbit | damage cell membranes and DNA |
| What are some common free radicals? | Superoxide, hydroxyl, peroxide, drugs (acetaminophen) | |
| Superoxide dismutase | neutralizes superoxide | |
| Glutathione | Neutralizes peroxide | |
| Catalase | Neutralizes peroxide | |
| Lipofuscin | Indigestible lipid of lipid peroxidation | brown pigment increased in atrophy and FR damage |
| Reperfusion injury in heart | Superoxide FRs + calcium | |
| Mitochondrial injury | cytochrome c in cytosol initiates apoptosis | |
| What substances can cause SER hyperplasia? | alcohol, barbiturates, and phenytoin | |
| What are complications of SER hyperplasia? | Increases drugs metabolism | Low vitamin D |
| Chediak-Higashi | membrane protein defect in transferring lysosomal enzymes to phagocytic vacuoles | AR; giant lysosomes |
| I cell disease | absent enzyme made in Golgi apparatus (mannose 6-phosphate) | empty lysosomes |
| Rigor mortis | stiff muscles after death due to ATP depletion | |
| What is the MCC of Fatty Liver? | Alcohol (increases NADH) | |
| Fatty change in liver | VLDL pushes nucleus to side | DHAP ---> G3P -----> TG |
| What are causes of fatty change? | Increase synthesis of TG/FAs, beta-oxidation of FAs, synthesis apoproteins/release VLDL | |
| Fatty change in Kwashiorkor | Decrese synthesis of apoproteins | |
| Ferritin | Primary iron storage protein | soluble in blood; serum level reflects marrow storage iron |
| Hemosiderin | Insoluble ferritin degradation product visible with Prussian blue stain | |
| Atrophy | Reduction in cell/tissue mass by either loss or cell shrinkage | |
| Brain atrophy | Ischemia | |
| What neurological condition is associated with brain atrophy? | Alzheimer's | |
| Exocrine gland atrophy in CF | duct obstruction by thick secretions | |
| Labile cells | stem cells | Skin, bone marrow, GI tract |
| Stable cells | in G0 phase | Smooth muscle and hepatocytes |
| Permanent cells | cannot replicate | Cardiac/striated muscles; neurons |
| Hypertrophy | increase in cell size | |
| LVH | - Increase preload (valve regurgitation), - Increase afterload (HTN, aortic stenosis) | |
| RVH | Pulmonary hypertension | |
| Bladder smooth muscle hypertrophy | Prostate hyperplasia constricts urethra | |
| Removal the kidney causes | Hypertrophy of remaining kidney | |
| Hyperplasia | Increase number of cells | |
| Endometrial Hyperplasia | Unopposed estrogen | |
| What are some associated conditions with UNOPPOSED estrogen? | Obesity, exogenous estrogen | |
| RBC hyperplasia | Increased EPO | Blood loss, ectopic secretion, high altitude |
| Prostate hyperplasia | increased DHEA | |
| Gynecomastia | Hyperplasia male breast tissue; | normal in newborn, adolescent, elderly |
| Metaplasia | one adult cell type replaces another cell type | |
| Squamous metaplasia in bronchus | smoking | |
| Intestinal metaplasia in stomach is associated with? | Paneth cells, Goblet cells | H. pylori chronic atrophic gastritis |
| Squamous metaplasia bladder | Schistosoma haematobium infection | |
| Barrett's esophagus | glandular metaplasia of distal esophagus; due to GERD | |
| Dysplasia | atypical hyperplasia and metaplasia are precursors for cancer | |
| Squamous dysplasia in cervix | Human papillomavirus | |
| Squamous dysplasia in bronchus is mostly caused by ___________________. | Smoking | |
| Necrosis | death of group of cells | |
| Coagulation necrosis | preservation of structural outline | |
| What is the cause of coagulation necrosis? | Increased to lactic acid | |
| Infarction | pale; hemorrhagic; | dry gangrene |
| Liquefactive necrosis | Brain infarct, bacterial infections | wet gangrene |
| Caseous necrosis | variant coagulation necrosis | granulomas due to TB/systemic fungi |
| Granulomas | activated macrophages (epithelioid cells) | multinucleated giant cells |
| Granulomas are formed by ________ (+) ____cells. | CD4 TH1 cells | |
| Epithelioid cells | Gamma-interferon released by CD4 T cells activates macrophages | |
| Multinucleated giant cells | fusion of epithelioid cells | |
| Granulomas are associated with type ______ hypersensitivity. | IV | |
| Enzymatic fat necrosis | associated with pancreatitis | soap formation (Ca2+ fatty acids) |
| Fibrinoid necrosis | necrosis of immune reactions | |
| Example conditions that produce fibrinoid necrosis. | Immune vasculitis and endocarditis | |
| Postmortem necrosis | autolysis; no inflammatory reaction | |
| Dystrophic calcification | calcification of damaged tissue with normal serum calcium | Pancreatitis; atherosclerotic plaque |
| Metastatic calcification | calcification of normal tissue | increased serum calcium or phosphorus |
| Nephrocalcinosis | Metastatic calcification of collecting tubule basement membranes | |
| Signs and symptoms of Nephrocalcinosis | Polyuria due to nephrogenic DI + renal failure | |
| Apoptosis | gene regulated individual cell death | |
| Signals activating apoptosis | Mullerian inhibitory factor (MIF), TNF, and hormone withdrawal | |
| Signal modulator of apoptosis | TP53 suppressor gene, BCL-2 genes | |
| BCL-2 genes | anti-apoptosis gene | prevents cytochrome c from leaving mitochondria |
| Caspases | responsible for enzymatic cell death in apoptosis | proteases and endonucleases |
| Markers of apoptosis | Eosinophilic cytoplasm, pyknotic (ink dot) nucleus | |
| Apoptosis | Loss Mullerian epithelium in male fetus | Thymus involution; killing cancer cells |
| Histamine | key chemical in acute inflammation | mast cell; arterioles vasodilation; increase in venular permeability |
| Rubor acute inflammation | rednes | arteriole vasodilation (histamine) |
| Calor acute inflammation | Heat; arteriole vasodilation (histamine) | |
| Tumor acute inflammation | swelling; Increase vessel permeability | |
| Dolor acute inflammation | Pain; bradykinin, PGE | |
| Acute inflammation | Neutrophil dominant | Increased levels of IgM |
| Initial vessel evetns | transient vasoconstriction --> arteriolar vasodilation --> Increase venular permeability | |
| Neutrophil rolling acute inflammation | due to selectins | |
| Integrins | neutrophil adhesion molecules | C5a and leukotriene B, activate; neutrophil margination |
| CD11/CD18 | markers for integrins | |
| Endothelial cell adhesion molecules | activated IL-1 and TNF | |
| ICAM | intercellular adhesion molecule | |
| VCAM | vascular cell adhesion molecule leukocyte adhesion molecule defect | |
| Activation neutrophil adhesion molecules | neutropenia; endotoxins | Neutrophilic leukocytosis; corticosteroids |
| Chemotaxis | directed moventem | C5a and LTB4 |
| Opsonizing agents | IgG, C3b | enhance phagocytosis |
| Neutrophils, monocytes, macrophages | receptors for IgG, C3b | |
| O2-dependent MPO system | most potent microbicidal system | neutrophils and monocytes |
| Production of superoxide from O2 | NADPH oxidase with NADPH cofactor | produces respiratory burst |
| Nitro blue tetrazolium (NBT) | Test for respiratory burst | |
| Superoxide dismutase | converts superoxide to peroxide | |
| Myeloperoxidase | lysosomal enzyme that combines peroxide + Cl to form bleach (HOCl) | |
| Microbicidal defects | chronic granulomatous disease childhood (XR), myeloperoxidase deficiency (AR) | |
| Chronic granulomatous disease | absent NADPH oxidase | No respiratory burst |
| Anaerobic glycolysis | ATP synthesis in hypoxia | Lactate decreases intracellular pH, and denatures proteins |
Created by:
rakomi
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