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81 Cards in this Set
- Front
- Back
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Reversible cellular changes |
1- Physiological- uterine enlargement 2- Pathological- Myocardial hypertrophy 2 to systemic HTN 3- If stress become persistent or excessive adaptation lead to |
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Hypertrophy |
1- Increase in cell size 2- Increase structural proteins and organelles |
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Hyperplasia |
1- Increase in number of cell 2- Controlled proliferation of stem cells and differentiated cells |
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Atrophy |
1- Decrease in cell size and number 2- Apoptosis, disuse, denervation, loss of blood supply, loss of hormonal stimulation, poor nutrition |
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Metaplasia |
1- Change from one cell type to another 2- Reprogramming of stem cells |
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Dysplasia |
Disordered cell growth |
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Why 2 pathologic processes usually precede dysplasia |
Persistent metaplasia Pathological hyperplasia |
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What is the major difference between metaplasia and dysplasia |
Metaplasia- Change in cell type Dysplasia - Change in cell structure |
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What type of metaplasia that can occur after trauma |
Myositis ossificans (formation of bone within muscle after trauma) |
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Reversible cell injury |
1- Decrease ATP- Decrease Ca and Na/k pump- Cellular swelling and mitochondrial swelling 2- Ribosomal/Lysosomal detachment- Decrease protein synthesis 3- Plasma membrane changes- blending 4- Nuclear changes 5- Rapid loss of function 6- Myelin figures |
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Irreversible cell injury |
1- Breakdown of plasma membrane - Cytosolic enzyme leak outside of cell, influx of Ca- activation of degradative enzyme be 2- Mitochondria damage/dysfunction- loss of electrons transport chain- Decrease ATP 3- Cytoplasmic vacuolization and programmed cell death 4- Rupture of lysosomes 5- Nuclear degradation 6- Amphoteric inclusions in mitochondria |
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Pyknosis vs karyothexis vs karyolysis |
Pyknosis- nuclear condensation Karyorrhexis- nuclear fragmentation Karyolysis- nuclear dissolution |
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What is the earliest morphologic manifestation of reversible cell injury |
Cellular swelling |
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Apoptosis |
1- ATP dependent programmed cell death 2- Two pathways intrinsic and extrinsic both involve the release of caspases(cytosolic protease) cellular breakdown include cell shrinkage, chromatin condensation, plasma membrane blending and formation of apoptotic bodies that are phagocytosed 3- Characterized by deeply eosinophilia cytoplasm, basophils nucleus, pyknosis, karyorrhexis. Cell membrane remain intact without significant inflammation 4- DNA laddering (fragments in multiples of 180) significant indicator of apoptosis |
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Intrinsic pathway of apoptosis |
1- Occurs in tissue remodeling in embryogenesis Occurs when a regulator factor is withdrawn from a proliferative effector cell or exposure to injurious stimuli 2- Regulated by Bcl-2 family BAX and BAK are proapoptotic and Bcl-2 and Bcl-xl are antiapoptotic 3- BAX and BAK for pores in mitochondrial membrane causing the release of cytochrome C from mitochondrial membrane into cytosplam causing activation of caspases 4- Bcl- 2 keep mitochondrial membrane impermeable preventing cytochrome C release Bcl-2 over expression - decrease caspases activation- tumerogenesis |
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Extrinsic pathway of apoptosis |
1- Ligand receptor interaction (FASL binding to FAS(CD59) or TNF-alph) 2- Immune complex (T-cell release from progeria of granozymes B) 3- FAS-FASL interaction is necessary for Thymic medullary negative selection 4- FAS mutation increase number of circulation self reaction lymphocytes due to failure of clinic deletion 5- Defects in FAS-FASL interaction cause autoimmune lymphoproliferative syndrome |
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Chromosome location of Bcl -2 |
Chromosome 18 on heavy chain of antibody |
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Types of necrosis |
1- Coagulative 2- Liquefactive 3- Caseous 4- Fat 5- Fibrinoid 6- Gangrene |
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Necrosis |
1- Exogenous injury 2- Plasma membrane damage 3- Enzyme degradation and Protein denaturing 4- Intracellular cell leakage 5- Local inflammatory reaction |
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Coagulative necrosis |
1- Seen in ischemic/infarcts of most tissues (except brain) 2- Due to ischemia or infarction of tissues- enzyme degradation proteolysis blockage 3- Histology 1- Preserve cellular architects 2- Nuclear disappear 3- Increase cytoplasmic binding
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Liquefactive necrosis |
1- Seen in Bacterial abscess and Brain in fact 2- Due to neutrophils reals lysosomal enzymes that digest tissue 3- Histology early 1- Cellular debris and macrophages Late cystic space and cavitation (brain) Neutrophils and cellular debris (bacterial) |
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Caseous necrosis |
1- Seen in TB and systemic fungal infection 2- Due to macrophages wall of infectious microorganisms- granular debris 3- Histology Fragmented cells and debris surrounded by lymphocytes and macrophages |
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Fat necrosis |
1- Seen in enzymatic- acute pancreatitis (soaponification of peripancreatic fat) Non-enzymatic Trauma (injury to breast tissue) 2- Due to damaged pancreatic cells release lipase that break down triglycerides to fatty acids that bind to calcium (soaponification) 3- Histology Dead fat cell without peripheral nucleus dark blue on H&E stain |
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Fibrinoid necrosis |
1- Seen in immune- vascular reaction (PAN) non-immune - vascular reaction (hypertensive emergency and Pre-eclampsia) 2- Due to immune mediated deposition type 3 hypersensitivity and/or plasma protein leakage from damaged vessels 3- Histology - Vascular wall thick and pink |
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Gangrene necrosis |
1- Seen in distal digits and GI tract due to chronic ischemia 2- Due to Dry- ischemia Wet- superinfection 3- Histology- Dry- Coagulative necrosis Wet- Liquefactive necrosis with superimposed Coagulative |
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Ischemia |
1- Inadequate blood supply to meet demand 2- Decrease arterial perfusion (artherioschlorosis, vasospasm and decrease cardiac output) 3- Decrease venous drainage( testicular and ovarian torsion, bud chiarri syndrome) |
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Areas most vulnerable to hypoxia/ischemia and subsequent infarction |
Brain- ACA, MCA, PCA boundary area Heart- Subendicardium of LV Kidney- Straight segment of proximal tube (medulla) and thick ascending limb of medulla Liver- Area around central vein zone 3 Colon- splenic flexure (Griffith’s point) Rectosigmoid junction (Sudeck point) |
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Watershed areas border areas |
Recurve blood supple from the most distal branched of 2 arteries with limited collateral vascularity These area are susceptible to ischemia from hypo-perfusion |
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Nerves vulnerable to hypoxia/ischemic insults |
Purkinje cell of cerebellum Pyramidal cells of the hippocampus and neocortex (zone 3,5,6) |
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Types of infarcts |
Red infarct Pale infarct |
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Red infarct |
1- Occurs in 1- venous occlusion 2- Tissue with multiple blood supple 3- Reperfusion- after angioplasty 2- Reperfusion injury due to damage by free radicals |
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Pale infarct |
1- Occur in solid organs with single blood supple (Heart and kidney) |
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Free radicals |
1- Damage cells via membrane lipid perioxidation, protein modification and DNA breakage |
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Initiation of free radicals |
1- Radiation (cancer therapy) 2- Redox reaction 3- Transitional metals 4- Metabolism of drugs - phase 1 5- Nitric oxide (inflammation) 6- WBC 7- Oxidative burst |
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Elimination of free radicals |
1- Scavenger enzymes (catalase, superoxide dismutase and Gluthione perioxidase 2- Spontaneous decay 3- Antioxidant ( vitamin A,C and E) 4- Curtain metal carting protein- transferin, ceruloplasmin) |
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Examples of free radical oxygen toxicity |
1- Retinopathy of prematurity (abnormal vascularization) 2- Bronchopulmonary dysplasia 3- Reperfusion injury after thrombotic therapy |
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Examples of free radical Drug/chemical toxicity |
1- Acetaminophen overdose (hepatotoxicity) 2- Carbon tetrachloride (convert cytochrome P 450 to CCl free radical- Fatty liver (cell injury - Decrease apolipoprotein synthesis- Fatty changes) Centri-lobular necrosis |
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Example of free radical metal storage disease |
Hemochromatosis (iron) Wilson disease (copper) |
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Types of calcification |
Dystrophic Metastatic |
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Dystrophic calcification |
1- Seen in abnormal tissue (disease tissues 2- Extent- localized 3- Associated condition 1- TB and other granulomatous disease 2- Liquefactive necrosis of chronic abscess 3- Fat necrosis 4- Infarct 5- Thrombosis 6- Schistosomiasis 7- Congenital CMV 8- Toxoplasmosis 9- Rubella 10- Psammoma bodies 11- CREST 12- Atherosclerotic plaque 4- Etiology- 2 to injury or necrosis 5- Serum Ca- normal |
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Metastatic calcification |
1- Seen in normal tissue 2- Extent- widespread 3- Associated conditions- Predominantly in intestinal tissue in lung, kidney or Gut ( decrease acid secretion which increase pH favor Ca deposition) 2- Nephrocalcinosis of collecting tubules leading to nephrogenic diabetes insipidus and renal failure 4- Etiology- 1- 2nd Hypercalcemia (1 hyperparathyroidism, sarcoidosis and hypervitaminosis D) 2- high calcium phosphate product level ( chronic renal failure from 2nd hyperparathyroidism, long term dialysis, calciphylasxis and multiple myeloma) 4- Serum calcium- Abnormal |
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Lipofuscin |
1- A yellow brown wear and tear pigment associated with normal aging 2- Composed of polymers of lipid and phospholipid complexed with protein 3- May be derived through lipid perioxidation of polyunsaturated lipid of subcellular membrane 4- Autopsy of elder revelease deposition in eyes, heart, liver, kidney colon and other organs 5- Lipid containing residues of lysosomal degradation |
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Too much lipofuscin |
Macular degeneration Neurodegeneration |
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Ionizing radiation |
1- Induced cellular and DNA damage 2- Affects rapidly regenerating tissues |
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Acute radiation full exposure on the skin |
1- Hair loss 2- Erythema 3- Desquamation 4- Ulcer/necrosis |
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Acute radiation full exposure on neurovascular |
1- Ataxia 2- Cognitive impairment 3- Impaired reflex 4- Seizure 5- Papiloedema |
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Acute radiation full exposure on gastrointestinal |
1- Stomatitis 2- Abdominal pain 3- Nausea 4- Vomiting 5- Diarrhea 6- GI bleeding |
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Acute radiation full exposure on hemotopoetic cells |
Myelosuppression |
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Acute radiation partial exposure on skin gonads eyes |
Skin- blister Gonads- 1- Sterility 2- Decrease spermatozoa Eyes- cataract |
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Radiation induced fibrosis head and neck |
1- Truisms 2- Mucosal fibrosis 3- Ulceration 4- Fistula |
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Radiation induced fibrosis Lungs |
Pulmonary fibrosis |
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Radiation induced fibrosis GI |
1- Ulceration 2- Fistula 3- Obstruction |
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Radiation induced fibrosis GU |
1- Uretral and ureteric stenosis 2- Fibrotic bladder construction 1- azospermia 2- Fistual of ovaries, Vulva and vagina 3- Obstructive uropathy
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Radiation induced fibrosis GU |
1- Uretral and ureteric stenosis 2- Fibrotic bladder construction 1- azospermia 2- Fistual of ovaries, Vulva and vagina 3- Obstructive uropathy
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Radiation fibrosis of the skin |
1- Induration 2- Thickness 3- Shrinkage 4- Loss of elasticity 5- Lymphodemia |
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Radiation related malignancy thyroid |
Papillary thyroid carcinoma |
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Radiation related malignancy hematopoietic |
1- Myelodisplastic syndrome 2- Lymphomas and leukemia (CML, AML, ALL) |
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Radiation related malignancy skin bone and others |
Skin- angiosarcoma Bone- osteosarcoma Others- solid tumor (breast, ovaries and lungs) |
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How does ionizing radiation induce cellular and DNA damage directly |
Via particles or photons |
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How does ionizing radiation induce cellular and DNA damage indirectly |
Via release of reactive oxygen species |
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How does ionizing radiation lead to tissue damage |
Progressive inflammation |
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Amyloidosis |
1- Abnormal aggregation of protein in beta platted linear sheets- Insoluble fibrils- Cellular damage and apoptosis 2- Amyloid deposits visualize with Congo red stain (red/orange with non-polarized light) apple green with polarized light 3- Tubular basement membrane enlarged under light microscope |
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Primary amyloidosis |
1- AL (from Ig light chain) 2- Seen in Plasma cell disorders ( multiple myeloma) |
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Primary amyloidosis |
1- AL (from Ig light chain) 2- Seen in Plasma cell disorders ( multiple myeloma) |
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Secondary amyloidosis |
1- Serum Amylod A (AA) 2- Seen in chronic inflammatory conditions |
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Primary amyloidosis |
1- AL (from Ig light chain) 2- Seen in Plasma cell disorders ( multiple myeloma) |
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Secondary amyloidosis |
1- Serum Amylod A (AA) 2- Seen in chronic inflammatory conditions |
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Dialysis related amyloidosis |
1- Beta 2 microglobulin 2- Seen in patients with ESRD and/or on longer term dialysis |
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Manifestation of amyloidosis |
1- Nuerological- neuropathy 2- Cardiac- restrictive cardiomyopathy 3- GI- macroglosia and Hepatomegaly 4- Kidney- nephrotic syndrome 5- Hematological - easily brushing and splenomegaly 6- MSK- carpal tunnel syndrome |
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Localized amyloidosis |
1- Alzheimer’s disease 2- Type 2 diabetes Mellitus 3- Medullary thyroid cancer 4- Isolated atrial amyloidosis 5- Systemic denial (age related) amyloidosis |
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Localized amyloidosis |
1- Alzheimer’s disease 2- Type 2 diabetes Mellitus 3- Medullary thyroid cancer 4- Isolated atrial amyloidosis 5- Systemic denial (age related) amyloidosis |
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Alzheimer’s disease and amyloidosis |
1- Beta amyloid plaque 2- Cleave from amyloid precursor protein (APP)on chromosome 21 |
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Type 2 diabetes Mellitus and amyloidosis |
1- Islet amyloid polypeptide (IAPP) 2- Deposition of amylin in pancreatic islet |
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Medullary thyroid cancer and amyloidosis |
Calcitonin |
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Isolated atrial amyloidosis |
1- ANP 2- Normal in aging increase risk of atrial fibrillation |
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Systemic senile (age related) amyloidosis |
1- Normal with aging Tranthyretin (TTR) 2- Seen predominately in cardiac ventricle 3- Cardiac dysfunction more insidious than in AL amyloidosis |
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Hereditary amyloidosis |
Familial amyloid cardiomyopathy Familial amyloid neuropathy |
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Hereditary amyloidosis |
Familial amyloid cardiomyopathy Familial amyloid neuropathy |
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Familial amyloid cardiomyopathy |
1- Mutated Tranthretin (ATTH) 2- Ventricular endomyocardium deposition- Restrictive cardiomyopathy and arrhythmia 3- 5% of African American are carriers of muted alleles |
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Familial amyloid polyneuropathy |
1- Mutated Transthyretin (ATTR) 2- Due to transthyretin gene mutation |
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Familial Mediterranean fever |
1- Dysfunction of neutrophils AR Occurs in persons of meditation origin 2- Frequent episodes of fever and serous inflammation 3- Serum amyloid A deposit as AA amyloid |
