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PathExam1
Path Exam 1 "Things To Know"
| Question | Answer |
|---|---|
| Amyloid | Group of fibrillar proteins w/ a common physical conformation (beta-pleated sheet) |
| Amyloidosis | Extracellular accumulation of an amorphous eosinophilic (hyaline) substance |
| Atrophy | A decrease in the size and/or number of cells usually with consequent decrease in the size of an organ or tissue and a decrease in function |
| Dysplasia | Disordered cell growth and maturation |
| Dystrophic calcification | Deposition of calcium in necrotic or damaged tissue |
| Hemochromatosis | Marked accumulation of iron with damage/impairment of function |
| Hemosiderin | Aggregates of ferritin micelles |
| Hemosiderosis | Mild accumulation of iron with no damage or impairment |
| Hyperplasia | Increase in the NUMBER or cells in an organ or tissue |
| Hypertrophy | Increase in the SIZE of cells with consequent increase in the size of an organ or tissue |
| Metaplasia | Replacement of one mature cell type by another mature cell type |
| Metastatic calcification | Deposition of calcium in normal tissues |
| Primary (genetic) hemochromatosis | Due to gene mutation (short arm of chromosome 6) that results in excessive intestinal absorption of iron |
| Coagulative necrosis - Change in cytoplasm | Increased eosinophilia |
| Coagulative necrosis - Changes in nucleus | Pyknosis - Karyorrhexis - Karyolysis |
| Do cells shrink or swell when ATP is depleted? | Cells swell b/c Na-K ATPase no longer functions -> Na+ diffuses in and K+ diffuses out -> net gain of solute -> osmotic swelling |
| Extrinsic pathway of apoptosis | Receptor-mediated - Important for the control of inflammation - Tumor Necrosis Factor (TNF) or Fas ligand (FasL) interact with their receptors -> receptors activate intiator caspases |
| Fat necrosis - Gross Images | Chalky white areas |
| Fat necrosis - Micro Images | Necrotic fat cells associated with calcium deposits |
| How does cell size change due to necrosis or apoptosis? | Cell swells in necrosis - Cell shrinks in apoptosis |
| Intrinsic pathway of apoptosis | Stree-mediated - Important for the removal of damaged cells - DNA damaged by free radicals or increased mitochondrial permeability -> Cytochrome c or other pro-apoptoic mediators like p53 released -> initiator caspases activated |
| Karyolysis | Loss of sustainable nuclear material |
| Karyorrhexis | Fragmentation of the nucleus |
| Pyknosis | Shrinkage of the nucleus with increased basophilia |
| Sources of free radicals | Exogenous sources (neutrophils during acute inflammation ) - Generation within affected cells (ionizing radiation : metabolism of exogenous chemicals and drugs : abnormal accumulation of iron or copper : NO production by some cells) - Reperfusion injury |
| What are the 2 hallmarks of reversible cell injury? | Cell swells - Ribosomes dissociate from ER |
| What are the 3 hallmarks of irreversible cell injury? | Irreversible mitochondrial dysfunction - Membrane damage - Nuclear damage (pyknosis - karyorrhexis - karyolysis) |
| What should think if you see a bunch of gram positive cocci in a micro image? | Liquefactive necrosis - Lung abssess as a result of infection |
| What type of necrosis results from a lung infarct? | Coagulative necrosis (lung infection -> absess/liquefactive ::: TB -> granulomatous) |
| What's saponification and what's it associated with? | Free fatty acids combine with calcium to form chalky white deposits - Occurs in fat necrosis |
| Average lifespan (ALS) | Steadily increasing - More old, old people |
| Biological age | Reflects the progressive accumulation of age-associated changes in tissues and organs - Modified by diet, socio-economic factors and the environment |
| Cellular quiescence | Withdrawal from the cell cycle into G0 |
| Chronological age | The time elapsed since birth |
| Maximum lifespan | Has not increased significantly over time - Hypothetical maximum is approx 110-120 years |
| Progeria | Lamin A gene mutation |
| Replicative cell senescence | Cells cannot be stimulated to re-enter the cell cycle |
| Werner's syndrome | WRN gene mutation |
| Alpha1-antitrypsin | Acute phase protein - A proteinase inhibitor |
| Alpha2-macroglobulin | Acute phase protein - A proteinase inhibitor |
| C3 | Acute phase protein - Complement component |
| Ceruloplasmin | Acute phase protein - Binds copper |
| Coagulation system | Plasma protease |
| Complement system | Plasma protease |
| C-reactive protein (CRP) | Acute phase protein - Involved in opsonization - Secreted rapidly by the liver in response to inflammation - Elevation persists as long as there is inflammation - Levels decrease when inflammation resolves |
| Erythrocyte Sedimentation Rate (ESR) | An increased "sed" rate is considered non-specific evidence of an inflammatory process - Rouleaux of RBCs (stack of coins) sediments more rapidly than dispersed individaul RBCs - RBC rouleauxs involved in blood stasis in vascular response causing inflamma |
| Fibrinogen | Acute phase protein - Involved in coagulation |
| Fibrinolytic system | Plasma protease |
| Haptoglobin | Acute phase protein - Binds hemoglobin |
| Histamine | Vasoactive amine |
| IL-1 | Cytokine that causes fever |
| IL-6 | Cytokine that causes fever |
| Interferons | Cytokine that causes fever |
| Kinin system | Plasma protease |
| Leukotrienes | Arachidonic acid metabolite |
| Lipoxins | Arachidonic acid metabolite |
| Prostaglandins | Arachidonic acid metabolite |
| Serotonin | Vasoactive amine |
| Serum Protein Electrophoresis (SPEP) - How do you interpret its results? | Albumin followed by other acute phase proteins and lastly Ig - 1 big spike is normal (albumin) - 1 big spike (albumin) with other smaller spikes in the middle means acute inflammation - 2 big spikes (albumin and Ig) with smaller spikes in between means ch |
| TNF-alpha | Cytokine that causes fever |
| What 3 chemical mediators of inflammation cause fever? | TNF-Alpha - IL-1 - IL-6 |
| What 3 chemical mediators of inflammation cause leukocytosis? | TNF-Alpha - IL-1 - CSFs increase the number of circulating immature neutrophils or "band"cells (LEFT SHIFT) |
| What 3 chemical mediators of inflammation cause pain? | Bradykinin - PGE2 - Substance P |
| What do you think of a micro image where everything is teal except a couple random black dots?? | Stained Yeast (Histoplasma) - Infections cause granuloma formation - GRANULOMATOUS INFLAMMATION |
| What do you think of a micro image with gram-negative cocci and cells with kidney-shaped nuclei? | Acute inflammation - Weird nuclei are neutrophils!! |
| What is trichrome stain and when do you see it? | Stains collagen BLUE - Seen in micro images of chronic inflammation with FIBROSIS |
| What type of cell is prevalent in purulent exudate? | Neutrophils - look for the bilobed nuclei |
| bFGF | Stimulates cell division and angiogenesis |
| Collagen | Provides tensile strength to support epithelial cells and it surrounds connective tissue cells |
| EGF = TGF-Alpha | Stimulates cell division for many cell types and angiogenesis - Binds to the epidermal growth factor receptor on the cell surface |
| Elastic fibers | Provides tissue with recoil ability |
| Fibronectin | Adhesive glycoprotein that binds other stuff together - Early stabilizer of wonds - Regulates cell migration (chemotactic for fibroblasts and macrophages) |
| Fibroplasia | AKA Fibrosis - Process characterized by the proliferation of fibroblasts and consequent deposition of extracellular matrix (predominately collagen) by the fibroblasts |
| Granulation tissue | Know this for histological images!! Repair tissue composed of activated fibroblasts and proliferating small blood vessels along with extracellular matrix and variable numbers of inflammatory cells |
| Heparan sulfate proteoglycan | Helps tissue retain water |
| How long does it take the epithelium to reach normal thickness in a primary wound? | Approximately 5 days or less |
| IL-8 | Chemotactic to neutrophils - Stimulates angiogenesis - Produced by macrophages |
| Laminin | Part of the basement membrane |
| Name 2 genetic defects that affect collagen | Ehler-Danlos and Osteogenesis imperfecta |
| Organization | IMPAIRED FUNCTION AFTER REPAIR - The reparative process characterized by fibrosis. It typically occurs in tissue that has been injured sufficiently to destroy the stromal framework and/or regenerative capacity of the parenchymal tissue |
| PDGF | Stimulates production of IL-1 and bFGF - Chemotactis - Stimulates collagen synthesis |
| Proteoglycans | Organizes ECM |
| Regeneration | New growth or repair of tissues lost due to disease or injury |
| Resolution | NORMAL FUNCTION AFTER REPAIR - The return of a tissue to its normal state following a pathologic condition such as inflammation - Typically characterized by the enzymatic digestion of an exudate followed by removal of the breakdown products |
| TGF-Beta | Chemoattractive from fibroblasts - Stimulates collagen synthesis - Inhibits proliferation of some cell types ( leukocytes and most epithelial cell types) |
| Thrombospondin | Involved in cell-cell and cell-matrix binding - Inhibits angiogenesis |
| Type IV collagen | Part of the basement membrane |
| VEGF | Stimulates: division of endothelial cells - angiogenesis - transcytosis |
| What 2 factors contribute to wound strength and what percent of normal is it during the first week following primary injury? | Due to fibrin and repithelization - Strength is 5-10% of original |
| What 2 things characterize a 1 month old primary wound? | Scant/Absent inflammation - Decreased vascularity |
| What 3 things characterize a 2-3 week old primary wound? | Fibroplast proliferation - Collagen accumulation - Decreases inflammation |
| What does a primary wound look like after 1 year? | A hypocellular hypovascular scar |
| What percent of normal is a primary wound after one month and what factor coorelates with the amount of strength? | 15-20% of the original strength - Strength coorelates with the increase in collagen content |
| When do neutrophils appear after a primary wound? | By day 2 |
| When do neutrophils appear after a primary wound? | Within 24 hrs they begin to infiltrate the margins |
| When do neutrophils leave and macrophages are the only ones left in a primary wound? | By day 5 |
| When does collagen begin to bridge a primary wound? | By day 5 |
| When does granulation tissue begin to invade a primary wound? | By day 3 |
| When is epithelial continuity restored after a primary wound? | By day 2 |
| Wound contraction | Reduction in the size of the wound - Up to 70-80% |
| Congestion | PASSIVE increased volume of blood in the vessels of a tissue |
| Congestive heart failure (CHF) | Cardiac output is inadequate to meet the metabolic demands of the body |
| Contusion | Bruise - A hemorrhage within tissue following rupture of small blood vessels by blunt force injury |
| Ecchymoses | Large blotchy hemorrhages |
| Edema | Accumulation of excess fluid in the interstitial space |
| Hemarthrosis | Hemorrhage into joint space |
| Hematoma | Accumulation of blood within a tissue or space |
| Hemopericardium | Hemorrhage into pericardial sac |
| Hemoperitoneum | Hemorrhage into peritoneal cavity |
| Hemophilia = | "Easy bleeder" |
| Hemorrhage | The escape of blood from the cardiovascular circuit |
| Hemothorax | Hemorrhage into pleural cavity |
| Hyperemia | ACTIVE increased volume of blood in the vessels of a tissue |
| Left-sided heart failure | Results in pulmonary congestion and edema and reduced renal perfusion. Consequences of reduced renal perfusion: Impaired secretion of nitrogenous wastes (pre-renal azotemia) - activation of the renin-angiotensin-aldosterone system - retention of sodium an |
| Petechiae | Minute (1-2 mm) hemorrhages |
| Purpura | Medium-sized (up to about 1 cm) hemorrhages |
| Right-sided heart failure | Results in systemic and portal venous congestion. Manifests as: edema - effusions within body cavities - impairment of organ function (especially the liver). Associated with: pulmonary hypertension - primary myocardial disease - diseases that cause left |
| Shock | A state of inadequate perfusion characterized by a disproportion between the circulating blood volume and the volume of the circulating system that needs to be filled (in other words, there is an inadequate effective circulating blood volume) |
| Activated Partial Thromboplastin Time (aPTT) | Assesses intrinsic and common pathways - Used to monitor heparin therapy |
| Alpha2-antiplasmin | Primary inhibitor of plasmin |
| Annexin V | Inhibits tissue factor |
| Anticoagulants | Prostacyclin (PGI2) - Thrombomodulin - Tissue factor pathway inhibitor (TFPI) |
| Antithrombin | Inhibits all serine proteases except factor 7a - Heparin binds to it and increases its activity |
| Aspirin | An "anti-platelet" agent - Inhibits cyclo-oxygenase activity irreversibly - Prolongs bleeding time |
| Blood clot | Gel-like matrix that includes: water - fibrin - other plasma proteins - platelets - WBCs - RBCs |
| Christmas disease/Hemophilia B | Factor 9 deficiency |
| Classic hemophilia/Hemophilia A | Factor 8 deficiency |
| Coagulation | Clot formation - The goal is fibrinogen -> cross-linked fibrin |
| Does liver disease increasing bleeding or clotting? | It causes increased bleeding even though it decreases production of both coagulation and anti-coagulation facts |
| Embolus | Clot material that has relocated to a site distant from that at which it formed |
| Factor V Leiden | People with this mutation get blood clots!! Most common hereditary thrombosis syndrome - Mutant form of factor V CANNOT be degraded by protein C and protein S (anti-coagulants that regulate the clotting cascade) |
| Fibrinolysis | Clot dissolution - The goal is cross-linked fibrin -> fibrin degradation products - Mediated primarily by plasmin |
| Heparin | Binds to antithrombin and increases its activity (inhibits serine proteases especially 2a and 10a) |
| Plasmin | Primary mediator of fibrinolysis |
| Plasminogen activator inhibitor-1 (PAI-1) | Converts fibrin to fibrinogen - Inhibits factors 5 and 8 |
| Plasminogen activator inhibitor-1 (PAI-1) | Inhibits tPA and uPA |
| Platelets | Add mechanical strength to clots - membrane promotes activation of clotting factors - Granule contents mediate vasoconstriction and angiogenesis |
| Procoagulants | Include von Willebrand factor (vWf) |
| Profibrinolytics | Include tissue plasminogen activator (tPA) |
| Prostacyclin (PGI2) | Vasodilator - Inhibits platelet aggregation |
| Proteins C and S | Inactivate factor 5 and 7 - Enhance fibrinolysis |
| Proteins S and C | Inactivate factors 5 and 8 - Enhance fibrinolysis |
| Prothrombin Time (PT)/International Normalized Ration (INR) | Assesses extrinsic and common pathways - Used to monitor warfarin therapy |
| The 1 clotting cascade matrix protein | Fibrinogen |
| The 1 clotting cascade transglutimase | Factor 13 - Crosslinks soluble fibrin into insoluble fibrin strands |
| The 2 clotting cascade factors that are encoded on the X-chromosome | Factors 8 and 9 (the one's associated with Classic Hemophilia and Christmas disease) |
| The 4 clotting cascade co-factors | High molecular weight kininogen (HMWK) - 5 - 7 - Tissue factor |
| The 4 main regulators of fibrinolysis | tPA - uPA - PAI-1 - Anti-plasmin |
| The 7 serine protease clotting factors | Prekallikrein - 2 - 7 - 9 - 10 - 11 - 12 |
| Thrombin | Converts factor 13 to its active form so that it can cross-link fibrin |
| Thrombomodulin | An endothelial receptor for thrombin - binding causes activation of protein C which cleaves factors 5a and 8a so they can not longer promote coagulation |
| Thrombophilia = | Predisposed to thrombosis - Inherited or acquired |
| Thromboxane A2 (TXA2) | Vasoconstrictor - Enhanced platelet aggregation |
| Thrombus | A blood clot that remains at its site of formation |
| Tissue factor pathway inhibitor (TFPI) | Anti-coagulant - Binds to factor 10a and inactivates the 8a:tissue factor complex |
| Tissue plasminogen activator (tPA) | Anti-coagulant - Activates plasminogen to release plasmin |
| Urinary-type plasminogen activator (urokinase = uPA) | Like tPA - Converts plasminogen to plasmin |
| Virchow's Triad | The 3 factors that promote thrombus formation -Endothelial injury - Abnormal blood flow (either stasis or turbulence) - Blood hypercoagulability |
| Vitamin K dependent clotting factors | Factors 2 - 7 - 9 - 10 and proteins C and S |
| von Willebrand factor (vWf) | Promotes platelet adhesion by binding to their gp 1b receptors - Complexes with factor 8:C (a procoagulant factor) to prevent its degradation - synthesized by endothelial cells and stored platelet alpha granules - deficiency causes bleeding disorder |
| Warfarin | Inhibits all Vit K-dependent clotting factors |
| What is the only acceptable anticoagulant for use in collection of blood for coagulation testing? | Citrate - It chelates Ca2+ |
| Which begins to act more quickly heparin or warfarin? | Heparin b/c it inhibits prothrombin (factor 2) which has the longest half-life (3-4 days) - Heparin can increase the activity of antithrombin immediately |
| Which clotting factors have the longest and the shortest half-lives? | Fibrinogen t1/2 is longest (3-4 days) - Factor 7 t1/2 is shortest (4-6 hours) |
| Which coagulation test should be used to monitor Heparin Tx? | aPTT - intrinsic and common pathways |
| Which coagulation test should be used to monitor Warfarin (Coumadin) Tx? | PT/INR - extrinsic and common pathways |
| Angelman syndrome | Due to deletion of the maternal chromosome at the 15q11-13 locus. Symptoms: hyperactivity - inappropriate laughter - severe mental retardation |
| Cystic fibrosis | Autosomal recessive |
| Down syndrome | Chromosomal abnormality |
| Duchenne muscular dystrophy | X-linked recessive |
| Fragile X syndrome | X-linked recessive |
| Gaucher Disease | Autosomal recessive |
| Genetic imprinting | Imprinted allele in biologically inactive. Disease results if the non-imprinted allele is deleted or mutated. |
| Klinefelter syndrome | Chromosomal abnormality |
| Mitochondrial disease | Disease that can only be inherited from the mother |
| Multifactorial inheritance | Diseases that result from multiple genes as well as the environment. Examples: hypertension - atherosclerosis - congenital anomalies - diabetes |
| Neurofibromatosis-1 | Autosomal dominant |
| Phenylketonuria | Autosomal recessive |
| Polycystic kidney disease | Autosomal dominant |
| Prader-Willi syndrome | Due to deletion of the paternal chromosome at the 15q11-13 locus. Symptoms: hypotonia - obesity - hypogonadism - mental retardation |
| Turner syndrome | Chromosomal abnormality |
| A critical lack of protein results in… | Kwashiorkor |
| An overall lack of calories results in… | Marasmus |
| Beriberi | B1 (Thiamine) deficiency. Often seen with alcoholism. Wet: High-output CGF and dilated cardiomyopathy (tachycardia and edema). Dry: Peripheral neuropathy with muscular atrophy and diminished sensations and reflexes. |
| Iron deficiency | Caused by: Blood loss - inadequate dietary intake. Causes: Hypochromic microcytic anemia and developmental abnormalities in toddlers. |
| Kwashiorkor | Total protein malnutrition with enough calories overall |
| Marasmus | Total calorie malnutrition |
| Protein deficiency | Causes Kwashikwor or Marasmus (depending on whether or not there is total calorie deficiency as well) |
| Selenium deficiency | ASSOCIATED WITH CONGESTIVE CARDIOMYOPATHY. Usually seen in the context of unsupplemented TPN. |
| Thiamine deficiency | Beriberi and Wernicke-Korsakoff Syndrome |
| Vitamin A deficiency | Causes night blindness, xerophthalmia and Bitot's spots. Stored in the liver where RESERVES ARE SUFFICIENT FOR MANY MONTHS OF DEPRIVATION. |
| Vitamin C deficiency | Scurvy |
| Vitamin E deficiency | Associated with diseases that cause fat malabsorption. Causes: Neurologic damage (degeneration of the posterior column) - pigmented retinopathy - skeletal muscle disease |
| Wernicke-Korsakoff syndrome | CNS effects of thiamine (vitamin B1) deficiency |
| What causes necrosis of the mamillary bodies? | Thiamine (vitamin B1) deficiency - Wernicke-Korsakoff syndrome |
| What characterizes "dry" Beriberi? | Peripheral neuropathy |
| What characterizes "wet" Beriberi? | Cardiomyopathy and high-output CHF |
| What vitamin deficiency does keratomalacia result from? | Vitamin A |
| What vitamin maintains ferrous iron in the reduced state? | Vitamin C |
| Zinc deficiency | CAUSES A RASH ESPECIALLY IN INFANTS!!! May be seen in the context of unsupplemented TPN. Autosomal recessive condition involving metal ion transport (acrodermatitis enteropathica). |
| Alpha-fetoprotein (AFP) | Tumor marker for liver and germ cell cancers |
| Bevacizumab (Avastin) | Humanized antibody directed against VEGF |
| CA 125 | Tumor marker for ovarian cancer |
| Carcinoembryonic antigen (CEA) | Tumor marker for GI and breast cancers |
| Cetuximab (Erbitux) | Monoclonal antibody directed against the extracellular domain of EGFR |
| Familial breast cancer | Mutations in BRCA-1 and BRCA-2 genes |
| Familial polyposis | APC mutation |
| Hereditary Nonpolyposis Colorectal Cancer (HNPCC) | DNA mismatch repair gene defects |
| hMSH2 | DNA mismatch repair gene that is mutated in HNPCC |
| Human chorionic gonadotropin (hCG) | Tumor marker for trophoblastic and germ cell tumors |
| Imatinib mesylate (Gleevec) | Tyrosine kinase inhibitor that targets bcr-abl |
| Methods to detect minimal residual cancer cells | Histologic or cytologic study of tissues or fluids - Flow cytometry - FISH - Molecular studies (PCR) - Tumor markers |
| Most common cancers in men | Lung -> Prostate -> Colon |
| Most common cancers in women | Lung -> Breast -> Colon |
| Prostate-specific antigen (PSA) | Tumor marker for prostate cancer |
| Tumor suppressor genes - mutator type | Genes that function in DNA repair or regulation of apoptosis |
| What is the 2 hit hypothesis? | 1 allele has germline mutation, and 2nd allele is mutated through somatic mutation |
| What's the result of mutator gene mutation? | Leads to loss of genomic stability and more mutations |
| What's the result of tumor suppressor gene mutation? | Leads to activation of cell cycle, despite possible DNA damage, passing defects on to progeny |
| Xeroderma pigmentosum | Mutation in genes involved in nucleotide excision repair of pyrimidine-pyrimidine dimers caused by ultraviolet damage |
| Aflatoxin B1 | Exposure increases risk of hepatocellular carcinoma |
| Diffuse interstitial fibrosis especially in lower and peripheral lung is indicative of… | Asbestosis |
| Insulation Construction and Demolition and Shipbuilders associated with… | Asbestosis |
| I've been working in a ship yard and smoking like a chimney. I may be at risk for…. | Asbestosis. Diffuse interstital fibrosis. 87x relative risk of lung cancer vs. no exposure and no smoking. |
| What kind exposure causes globus pallidus necrosis? | Carbon monoxide poisoning!! |
| What does Tylenol toxicity cause and how long between OD and effect? | Centrolobular hepatic necrosis 3-5 days later |
| What type of lesion is associated with hypersensitivty pneumonitis? | Chronic exposure causes granulomatous interstitial pneumonia with interstitial fibrosis |
| What are the two enzymes that are inhibited by lead and what are the effects of their inhibiton? | d-ala dehydrase (causes a buildup of d-ala) and ferrochetalase (causes a buildup of porphyrins in the blood and these are toxic to the liver) |
| Form of mercury that is absorbed by the respiratory system and affects the brain | Elemental Hg |
| Aflatoxin B1 | From Aspergillus flavus (mold) often in warm moist peanuts or grains. Broken down by mixed function oxidases in the liver. Results in epoxides that can covalently bind to DNA. If cell division occurs before the DNA can be repaired, carcinogenesis may o |
| What enzyme is depleted in Tylenol toxicity? | Glutathione |
| Overall, what is the product that lead inhibits the synthesis of? | Heme |
| Themophilic actinomycetes - True molds - Animal antigens … associated with… | Hypersensitivty pneumonitis = Extrinsic allergic alveolitis |
| Form of mercury that is absorbed by the GI tract and skin and affects the kidney | Inorganic Hg |
| What are the effects of lead toxicity in children vs. those in adults? | Kids get brain damage (acute changes include edema and vasculopathy both chronic changes are often subtle). Adults get peripheral neuropathy (demyelinization and axonal degeneration) often causing drop foot. |
| What would cause drop foot in an adult? | Lead toxicity |
| What could causes a combination of (1) anemia (2) kidney tubular necrosis and interstitial nephritis and (3) abdominal pain? | Lead toxicity but more likely to see the peripheral neuropathy and brain effects on exam |
| What cell type plays a large role in the effects of asbestosis? | Macrophages. They secrete growth factor (IL-1) -> fibroblast proliferation and lysosomal enzymes and free radicals -> tissue injury. Both ultimately cause fibrosis. |
| Pneumoconioses | Non-neoplastic lung diseases due to inhalation of dust particules. Generally restricted to inorganic dusts. |
| Form of mercury that is absorbed by the GI tract and skin and affects the brain | Organic Hg |
| Collagenous nodules in upper lung is indicative of… | Silicosis |
| Miners Stonecutters and Sandblasting associated with… | Silicosis |
| Unique characteristic amongst tumor suppressors? | Defect in DNA repair and apoptosis. Dominant negative (p53 forms dimers) effect. |
| What is a key difference in the cellular changes due to cancer promoter vs. cancer initiators? | In contrast to the effects of initiators the changes resulting from promoters do not affect DNA and are reversible |
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