← Pathology I Test 1 Export Options Alphabetize Word-Def Delimiter Tab Comma Custom Def-Word Delimiter New Line Semicolon Custom Data Copy and paste the text below. It is read-only. Select All What does Bursa do? Cushions areas of joints that are subject to friction during movement. What is the primary function of the tonsils and adenoids? To protect the entry into the respiratory system. What is the function of bone marrow? Produces blood cells. What is the primary function of lymphocytes? Play important role in immune reactions. What is the primary functin of the adnexa of the eye? Accessory structures that provide extrnal protection and allow the eyes to move. What is the function of the middle ear? It transmits sound waves to the inner ear. What are the functions of sebaceous glands? Secrete sebum to lubircate the skin and discourage the growth of bacteria on the skin. What is the function of hair? It aids in controlling the loss of body heat. What is the primary function of the adrenal glands? Regulate electrolyte levels, influence metabolism, respond to stress. What is the function of pancreatic Islets? Control blood levels and glucose metabolism. What is the function of the Pineal gland? Influences the sleep-wakefulness cycle. What is the function of the pituitary gland? Secretes hormones that control the activity of the other endocrine glands. What is the function of the thyroid gland? Stimulate metabolism, growth, and activity of the nervous system. What is hypertrophy? Enlargment due to increase in size not number of cells. Hypertrophy is often combined with what? Hyperplasia (abnormal multiplication of cells). Hypotrophy is what and it is AKA? A wasting of tissues, organs, or entire body. Aka atrophy. What causes endometrial hyperplasia? Estrogen. What is metaplasia? The reversible replacement of one differentiated cell type with another mature differentiated cell type. What is anaplasia? A change in the structure of cells and a change in their orientation to each other. What is aplasia? The defective development or congenital absence of an organ or tissue. What is dysplasia? Abnormal tissue growth with loss of cell orientation, shape, and size Dysplasia is always what? pre-cancerous. When is cell injury reversible and when is it irreversible? Reversible- when the abnotmal stress/stimuli persists for a short period of time. Irreversible- when the stress/stimuli persists or is severe. What will swelling be like for reversible damage? It will be generalized. What is a bleb? A bubble or blister. What type of cells will have bleb's ones with reversible or irreversible damage? Reversible. What type of cells will have damage to the plasma membrane ones with reversible or irreversible damage? Irreversible. What type of cells will have swelling of the ER ones with reversible or irreversible damage? Both but irreversible damge has contiunued swelling of ER. Cells with both reversible and irreversible damage have swollen mitochondria, but what is the difference in cells with irreversible damage? They have vacuolization which is a Ca 2+ influx. What happens to the nucleus in cells with reversible or irreversible damage? Reversible- chromatin clumps. Irreversible- Nuclear condensation, fragmentation and dissolution. What is the pH like for cells with reversible or irreversible damage? Reversible has low intracelluar pH. Irreversible- continued low intracellular pH. What type of cells have calcification ones with reversible or irreversible damage? Irreversible. What happens to reversible damaged cells when looking at them with light microscope? They have fatty changes (steatosis). What is the difference between necrosis and apoptosis? Necrosis- common after ischemia and chemical injury CELL SWELLING. Apoptosis- is programmed cell death and CELL SHRINKAGE. What happens to the plasma membrane during necrosis and apoptosis? Necrosis- it is disrupted. Apoptosis- Intact/altered. What happens with the cells contents with necrosis and apoptosis? Necrosis- enzymatically digested. Apoptosis- intact. What type of adjacent inflammation is present with necrosis and apoptosis? Necrosis- frequent adjacent inflammation. Apoptosis- no adjacent inflammation. What causes necrosis and apoptosis? Necrosis- invariably pathologic. Apoptosis- Often physiological. Cells get injured due to what 2 types of deprivation? 1. Hypoxia- inadequate oxygenation. 2. Ischemia- loss of blood supply. Give an example of a genetic derangement that causes cell injury? Sickle cell anemia. Mitochondrial damage that causes cell injury is due to what? Increased Ca2+, oxidative stress, activated phospholiapase A2. Aerobic respiration gives us how much ATP? 36 atp What do we get from anareboic respiration? 2 ATP, and lactic acid. Where will Vitamin E be doing free radical protection? In the membranes. Glutothione is stored mostly where to do what? Stored in the retina to protect against all redox reactions. Why is homogenated milk bad for us? Xanthine oxidase is better absorbed in body. What is the role of P-450? Detox. It is enzymes that increase the solubility of compounds and help excrete them. What is the down side of P-450? While detoxing it can make some reactive oxygen intermediates which can injure cells. Where are the P-450 enzymes found at? In the Smooth ER of hepatocytes. Free radical injury is induced through what? membrane lipid peroxidation, protein modification, DNA breakage. How are free radicals degraded? Through enzymes, spontaneous decay, and antioxidants. Reperfusion after anoxia (an abnormally low amount of oxygen in the body tissues) induces what? Free radical production. What is thrombolytic therapy? Use of drugs to break up clotts. What commonly happens after thrombolytic therapy? Reperfusion after anoxia and often causes injury through free radical production. Name 3 types of oxygen radicals? 1. Hydrogen peroxide. 2. Superoxide. 3. Hydroxyl radical. The P-450 detoxes what? Barbiturate. What will lysosomal catabolism do with a subcellular response to injury? heterophagy and autophagy. What are 2 types of toxic cell injury? 1. Direct toxin. 2. Indirect toxin. Give an example of a direct toxin? Heavey metals like mercury. How will heavy metals like mercury be toxic to cells? It disrupts the S-S bonds. Give an example of an Indirect toxin? CCl4 it is metabolized in the liver to CCl3 and this is more toxic. What leaks from damaged mitochondria? Ca2+. What happens to the mitochondria with subcellular injury? Increased number with cellular hypertrophy and decreased number with cellular atrophy. Also mitochondria may assume extreme large and abnormal shapes. What is damaged subcellularly that will interfere with organelle and molecular transport, cell architecture, cell-to cell signals, cellular mobility and phagocytosis? Cytoskeletal abnormalities. What are chaperones? Heat shock protiens (HSP). What will HSP (heat shock proteins) respond to? They respond to a variety of chemical/physical stimuli. What are the 3 roles of HSP? 1. Protein folding. 2. Disaggregation of protein-protein complexes (unclumping). 3. Protein transport to cell organells. What happens to albumin C with increased temperatures? It denatures. Where will proteins mostly break down at? At sistein where the s-s bridges are. Coagulative necrosis happens with necrosis to what areas? Heart, liver, and kidney. Coagulative necrosis is a result of what? Protein denaturation. What will coagulative necrosis look like? Preservation of basic cell outline for several days. Liquefactive necrosis happens where? Brain. Liquefactive necrosis is characteristic of what 2 things? 1. Bacterial infection. 2. CNS stroke. Liquefactive necrosis is a result of what? Enzymatic digestion. Gangrenous necrosis is associated with what area? Limbs and GI tract. Gangrenous necrosis is usually a limb with loss of blood and what? Coagulation necrosis. What is wet gangrene? Coagulation necrosis with liquifactive action of bacterial infection and attracted leukocytes. Caseous necrosis occurs where? It is seen in tuberculosis infections. What is the appearance of caseous necrosis? Cheesy white appearance. What is the tissue architecture like with caseous necrosis? It is obliterated. Fat necrosis occurs where? In the pancreas What will fat necrosis look like? Chalky area. Is fat necrosis a typical necrosis pattern? No. What will fat necrosis look like under microscope? Foci of shadowy outlines of fat cells with basophilic calcium deposits surrounded by inflammatory reaction. Coag. necrosis is stimulated by what? Hypoxia and toxins. Histologicaly what will coag. necrosis look like? cellular swelling, organelle disruption. What happens to DNA with coag. necrosis? Random diffuse from tissue damage and membrane injury. What is the tissue reaction of coag. Necrosis? Inflammation. What is the stimulus for apoptosis? Mainly physiologic but can be pathologic. What will cells undergoing apoptosis look like histologically? Cellular shrinkage, chromatin condensation, apoptotic bodies. What happens to DNA with apoptosis? It breaks down by internucleosomal (between the nucleosome.) What is the tissue reaction like during apoptosis? No inflammation phagocytosis of ABs Give an example of a pathologic pathway that could lead to apoptosis? Injurious stimuli like radiation or hypoxia. What will Apoptosis look like when in agarose gel culture cells? It will look like a ladder pattern of DNA fragment. What will necrosis or coag. Necrosis look like when in agarose gel culture cells? It will look like diffuse smearing of DNA. What is the receptor and the ligand that will signal apoptosis? Ligand- FAS. Receptor- TNF When a cell undergoes apoptosis what will leak out of the mitochondria? Cytochrome C When apoptotic cells breakdown they break down into what? Apoptotic bodies. What happens to apoptotic bodies and how? They are phagocytosed and they have ligands on them for phagocytic receptors. What wil execution caspases do? Once a cell is told to undergo apoptosis from: injury, withdrawal from growth factors, ligand FAS and receptor TNF, or cytotoxic T cells then the execution caspases start the degradation of cytoskeleton and nuclear proteins. The FAS ligand brings what together in close proximity? Several FAS death domains. With several FAS death domains in proximity what happens? Autocatalysis of caspase and this leads to apoptosis. Where is the brain of a cell? The membrane. What are 2 catagories of intracellular accumulations? 1. Exogenous material. 2. Endogenous metabolites. What is hemosiderin? An endogenous metabolite that is an accumulation of iron from RBC. What is anthracosis? Accumulation of a pigment that blackens the lings and the involved lymph nodes. Give 2 examples of endogenous metabolites without using hemosiderin? 1. Lipids. 2. Pigment from tattoos. What is steatosis? Abnormal accumulation of triglycerides in parenchynmal cells also it is a fatty change. Where will steatosis usually happen at? The liver, but can happen in the heart, muscles, and kidneys. Steatosis can be caused by what? Alcohol abuse, toxins, protein malnutrition, Diaetes M., Obesity, and anorexia. What will alcohol dehydrogenase do with alcohols? It converts them into aldehydes or ketones. What will alcohol dehydrogenase do with methanol and ethylene glycol? Methanol- converts it to formaldehyde. Ethylene glycol- converts it to oxalic acid. Under a microscope what will intracellular accumulations of Cholesterol and cholesterol esters look like? Foamy appearance. What is an intracellular accumulation of cholesterol and cholesterol esters in arteries called? Atherosclerosis. What are xanthomas? Intracellular accumulations of cholesterol in the skin and tendon masses. What are reabsorption droplets? Intracellular accumulations of protein in proximal renal tubles. What are russell bodies? excess secretory protein synthesis which leads to intracellular accumulations of protein that leads to a distended ER with large eosinophilic inculsions. What is amyloidosis? Aggregation of abnormal proteins. What are some neuro diagnosis of Intracellular accumulations of protein? Alzheimer's, Huntington's, parkinsons's, Maybe Diabetes M. Type II. What will help protect agains intracellular accumulations of proteins? GSH. What is the pattern of hyaline cartilage intracellular accumulation? There is no specific pattern of accumulation due to the variety of alteration. What will hyaline cartilage accumulations look like in a microscope? Homogenous GLASSY pink appearance. What are some examples of intracelluar hyaline accumulations? reabsorption droplets, russel bodies, Mallory alcoholic hyalin. Where will intracellular accumulations of glycogen be found at? In clear vacoules within the cytoplasm. What causes intracellular accumulations of glycogen? Glucose metabolism disorders like Diabetes M., and Genetic disorders that lead to glycogen storage disease. Glycogen accumulations have Numbers like GSD type I-V and these are associated with an enzyme deficiency and a type of disease for the next five questions give the enzyme deficiency and type of disease for the numbers given. OK GSD Type I? Glucose-6-phosphatase, Von gierke's disease. GSD Type II? acid maltase, Pompe's disease. GSD Type III? Glycogen debrancher, cori's disease or Forbe's disease GSD Type IV? Glycogen branching enzyme, Andersen disease. GSD Type V? Muscle glycogen phosphorylase, McArdle disease. What is Lipofuscin? An endogenous intracellular accumulation of a brown pigment. What is melanin? A black pigment. Hemosiderin is what? A accumulation of Iron from RBC and it is considered an endogenous intracellular accumulation of a golden-brown pigment. What does dystrophic mean? Bad growth or abnormal growth. What is dystrophic calcification? Abnormal growth of calcium. Dystrophic calcification deposition occurs where? Only locally in dying tissue. Dystrophic calcifications happens under what serum levels of calcium? Under normal serum calcium levels. What calcium metabolsim pathology is present with dystrophic calcification? None. Dystrophic calcification effects arteries and hearts how? Arteries- atherosclerosis, heart- damaged heart valves. What will pull Ca2+ out of body? EDTA. Besides pulling Ca2+ out of the body what else will EDTA pull out of the body? Heavy metals. Metastatic calcifcation deposits calcium where? IN otherwise normal tissues. What is blood serum like during metastatic calcification? The Calcium levels in serum are high it is also high in tissues. Metastatic calcification is usually due to what? Secondary hypercalcemia. What is the most common cause of hypercalcemia? Hyperparathyroidism. What are the 4 pricipal causes of metastatic calcification? 1. Increased PTH from a primary tumor on the parathyroid glands. 2. Bone destruction. 3. Vitamin D related. 4. Renal failure leading to increased phosphate retention leading to secondary hyperparathyroidism. Metastatic calcification principally affects what? Interstitial tissue of the vasculature, kidneys, lungs, gastric mucosa. What is a pathologic calcification? Multiple myeloma. What is multiple myeloma? Widespread lucencies in the bone. Increased PTH leads to what? Increased serum calcium. Increased Calcitonin leads to what? decreased serum calcium and increased bone calcium. What is inflammation? Reaction of blood vessels leading to accumulation of fluid and leukocytes in the extravascular tissues. What 3 thing will inflammation do? 1. Eliminate microbes and toxins. 2. Eliminate necrotic cells and tissues. 3. prepare for tissue repair. What are the components of acute and chronic inflammatory responses? Circulating cells, portiens, blood vessel cells, and proteins of extracellualr matrix. With inflammation what is the major WBC? Neutrophil. With inflammation there are how many more neutrophils than lymphocytes? there are 2 neutrophils for every lymphocyte. Neutrophil does what with inflammation and turns into what? It is the first responder that works on bacterial or fungal infections and deaths turns them into pus. A lymphocyte becomes what in tissue? Plasma cells. Lymphocytes work during what? Chronic inflamation. Monocytes do what are? What are they called in tissues? They present pathogens parts to T cells, and they are called macrophages in tissue. Eosinophils do what? They work with parasite and allergic responses. Basophils are what in tissues? Mast cells. Basophils do what? releasing histamines in response to allergic and antigen responses. What is the Lifespan of a RBC? 120 days. What is the lifespan of a WBC? Days to years. What is the lifespan of platelets? 8 days. With acute inflammation what is the main WBC? Neutrophils. Which one is faster onset chronic or acute inflammation? Acute. Which one lasts longer chronic or acute inflammation? Chronic. With chronic inflammation what is the main WBC? macrohpages and lymphocytes. What are the 5 signs and symptoms of acute inflammation? 1. Redness. 2. Heat. 3. Swelling. 4. Pain. 5. Loss of function. With acute inflammation what happens to blood flow? Vascular dilation and increased blood flow. What is edema like with acute inflammation? deposition of plasma fluid and proteins. What will accumulate at the injury site of an acute inflammation? Leukocytes. Normal arteriol blood pressure is 32 mmHg what will it be during acute inflammation? 50 mm Hg. The normal venous blood pressure is 25 mm Hg what will it be during acute inflammation? 30 mm Hg. What is the net result of fluid flow with acute inflammation? Net is an excess of extravasated fluid. What is oncotic pressure? Pulling in because concentration of proteins is higher in vasculature. What is Rouleaux? Stacking of RBC. What is margination? RBC go to center and White blood cells go to margins. What is pavementing? Rolling, tight binding, diapedisis What will TNF and IL-1 do? They are adhesion molecules for leukocytes. Leukocytes can phagocytosis particles as they bind to what surface binding proteins? Fc C3b. Production of microbicidal reactive oxygen intermediates happens where? Within phagocytic vesicles. What are the 2 major mediators of inflammation? Plasma derived and cell derived. Histamine is released from what 2 cells? Platelets and mast cells. What is the action of histamine? Stimulates retraction of endothelial cells of the venules which increases gaps and increases permeability. How long will histamine action last and why? Short action because it is inactivated by histaminase. What Vitamin can stabilize Mast cells? Vitamin C 2-3 grams. What is bradykinin? A hormone that causes inflammation. Bradykinin has a similar action as what? Histamine. Bradykinin induces what? Pain. Name the liver (the other would be cellular) derived chemical mediators of inflammation? kinin system which is bradykinin, coagulation/ fibrionlysis system, anaphylatoxins, membrane attack complex. The complement system is a group of what? plasma proteins produced by the liver that circulate in an inactive form. How is the complement system activated? Through classical or alternative pathways. Activation of the complement system leads to what? formation of biologically active fragments, intermediate complexes, and terminal membrane attack complexes. What are the 4 main functions of the activated complement derivatives? 1. Opsonization- facilitated phagocytosis of bacteria. 2. Anaphylaxis- histamine release with increased vessel wall permeability. 3. Chemotaxis- migration of leukocytes. 4. Cell lysis- through the action of MAC. Activation of the complement system by different pathways leads to cleavage of what? C3. The functions of the complement system are mediated by breakdown of what? C3 and other complement proteins, and by membrane attack complex. What is the first step of the complement system? phagocytosis bacteria. What is the second step of the complement system? Attachment of the opsonized bacterium to the PMN. What is the third step of the complement system? Formation of phagocytic vacuole. What will cleave C3? C3 convertase. What is the classical complement pathway aka? Mannose-binding lectin (MBL). The classical and alternative complement pathways converge into what? C3 cleavage. What happens to C3 when it is cleaved? it becomes Ca and then Cb. Factor XII is aka? Hageman factor. The 4 plasma mediator systems are triggered by what? Activation of factor XII aka hageman factor. Thrombin induces inflammation how? By binding to protease-activated receptors on platelets, endothelium, smooth muscle, and other cells. Arachidonic acid is derived from what? Phospholipids through the action of phospholipases. What 2 pathways is arachidonic acid metabolized into? 1. Lipoxygenase. 2. Cyclooxygenase. The cyclooxygenase is aka? Cox pathways. What is leukotrienes? an arachidonic acid derivative that does chemotaxis, vascular permeability, bronchospasm. What is lipoxins? an arachidonic acid derivative that does vasodilation, inhibition of neutrophil chemotaxis, monocyte adhesion. What is thromboxane? An arachidonic acid derivative that does platelet aggregation, thrombosis. What is prostacyclin? An arachidonic acid derivative that opposes the effects of thromboxane. What is prostaglandins? An arachidonic acid derivative that does smooth muscle contraction. What type of oil is good for conversion to arachidonic acid? Animal fat. What type of oil is not good for conversion to arachidonic acid, but good for omega 3? Fish oils. In general arachidonic acid derivatives do what? Inflammation. TNF and IL-1 will do what during acute inflammation? fever, increased sleep, decreased appatite, increase acute-phase proteins, hemodynamic affects (shock), neutrophilia (increase neutorphils). TNF and IL-1 do what to endothelial cells? Increase leukocyte adherence, increase PGI synthesis, Increse procoagulant activity, decrease anticoagulant activity, increase IL-1, Il-8, IL-6,PDGF. TNF and IL-1 do what to fibroblasts? Increase proliferation, increase collagen synthesis, increase collagenase, increase protease, increase PGE synthsis. TNF and IL-1 do what to leukocytes? Increse cytokine secretion (IL-1, IL-6). Long term TNF production leads to what? Cachexia- waisting. What will NO (nitric oxide) do in blood vessels and macrophages? Causes vasodilation and toxic free radicals are produced. How is NO (nitric oxide) produced? By 2 synthase enzymes. What is a sign of good cardiovasular health? An A.M. erection. What is larger primary or secondary neutrophil granules? Primary. What are the other names of primary and secondary neutrophil granules? Primary- azurophil, secondary- specific. What happens to vasculature with chronic inflammation? Angiogenesis. When acute or chronic inflammation is healed by fibrosis what happens? Loss of function. When acute inflammation is healed by resolution what happens to the vasculature? It returns to normal. How is extra fluid from edema drained when inflammation is healed by resolution? Into lymphatics or by pinocytosis into macrophages. What happens to neutrophils when acute inflammation is healed by resolution? Phagocytois and apoptosis. Who plays the central role in resolution healing of an acute inflammation? Macrophages. What is the last step of resolution healing of an acute inflammation? Disposal of macrophages. What is the early stage of most inflammation? Serous inflammation. Serous inflammation is what type> A pathological form of inflammation. Joint swelling in rheumatoid arthritis is what type of inflammation? Serous inflammation. Name 3 skin types of serous inflammation? viral infection like herpesvirus, excyma, skin burn. Fibrinous pericarditis is a pathologic inflammation that does what? Deposits fibrin in pericardium. What type of pathological inflammation is purulent inflammation? Pus. What is an abscess? A blocked off region. What is a sinus? a narrow passage leading to an abscess or the like. What is a fistula? a narrow passage or duct formed by disease or injury, as one leading from an abscess to a free surface, or from one cavity to another What type of inflammation happens with abscess, sinus, and fistula? Purulent inflammation. Granuloma is seen in what? Tuberculosis. The granuloma consists of what? Lymphocytes, epithelioid cells, multinucleated giant cells. What type of inflammation is found with a peptic ulcer? both acute and chronic. How are macrophages activated? by cytokines from immune-activated T cells. Or by nonimmunologic stimuli such as endotoxin. How can an activated macrophage lead to tissue injury? from toxic oxygen metabolites, proteases, neutrophil chemotactic factors. Chronic inflammation of the lungs shows what 3 histological characteristics? 1. Collection of chronic inflammatory cells. 2. Destruction of parenchyma. 3. Replacement by connective tissue. What fills the alveolar spaces in acute inflammation? Neutrophils and blood vessels. What is the most important part of having the macrophages accumulate in the tissues? Continued recruitment. Chronic inflammation is inflammation that lasts for how long? Longer than 1 month. What increases with chronic inflammation? increased Lymphocytes and increased neutrophils (less than lymphocytes). What are 2 cytokines that signal activated macrophages where to go? TNK and IL-1. What are granuloma's? focal accumulation of activated macrophages which often develop into epithelial-like appearance. Chronic inflammation heals how? Fibrosis. Regeneration of stable tissue is done how? Compensatory growth. Regeneration of renewing tissue is done how? Regrowing. What leads to commitment of stem cells to differentiate into specific cells? Activation of key regulatory proteins by growth factors and cytokines. Transduciton systems require what? Cell-surface receptors. Transduction system that has tyrosine kinase receptors bind to what? Growth factor. What happens when growth factor binds to a tyrosine kinase receptor? Dimerization and autophosphorylation of tyrosine residue. With a partial hepatectomy what happens during DNA replication? incorporation of tritiated thymidine. What happens with a partial hepatectomy? Remaining part enlarges. The missing part is not replaced. What are the 3 stages of activating something to undergo enlargment? 1. Priming. 2. Proliferation. 3. Growth inhibition. What signals the priming stage? Cytokines: TNF, IL-6, others. What will activate the proliferation stage? Growth factors: HGF, TGF-alpha, others. What will inhibit growth? TGF-Beta, Activin, others. What are the adjuvants (helpers) of the proliferation phase? Norepinephrine, insulin, thyroid hormone, growth hormone. What are the major components of the ECM? Collagen, proteoglycans, and adhesive glycoproteins. What vitamin is needed for HO-ization? Ascorbic acid. What is fibronectin? 2 glycoprotein chains held by disulfide bonds. What binds ECM components and interacts with the cytoskeleton at focal adhesions complexes? Integrin. Angiogenesis by mobilizatin of ____ from the bone marrow. EPCs. EPC's from the bone marrow migrate to where? Site of injury or tumor growth. What do EPC's do at sights of injury? They differentiate and form a mature network of vessels. What are MMP's? Matrix metalloproteinase. They help degrade collagen and other ECM proteins. MMP's are dependent on what? Zinc. What are the 4 mechanisms of MMP regulation? 1. regulation of synthesis by growth factors or cytokines. 2. Inhibition of synthsis by corticosteroids or TGF-beta. 3. secreted in inactive form. 4. Blockage of the enzymes by specific tissue inhibitors of metalloproteinase. The inflammation phase of wound healing lasts how long? 3 days. The granulation tissue phase of the healing process takes place when? 0.3 days until 10 days. The wound contraction phase of the healing process takes place when? 3 days to 30 days. What will clean up an injured site after the healing process? Macrophages. What type of scaring occurs with primary and secondary and tertiary intention healing? Primary- minimal scarring. Secondary- broader scar. Tertiary- wound is purposely left open. What type of injury is primary intention healing? Little tissue loss. Most surgical wounds heal by which intention? Primary inention healing. A primary intention wound is closed how? By sutures, staples or adhesive. What is allowed to happen to the wound with secondary intention healing? It is allowed to granulate. Why can the healing process be slower with secondary intention healing? Due to the presence of drainage from infection surgeons may pack the wound with gauze or use a drainage system. How long will a tertiary intention scar be left open? 4-5 days. What is Keloid? Excess collagen deposition in the skin forming a raised scar. Stimulus from chronic inflammation activates what? Macrophages and lymphocytes. Activated macrohages and lymphocytes in chronic inflammation areas lead to what? Production of growth factors, cytokines. Growth factors cytokines in a chronic inflammation lead to what? Increased collagen synthesis. Increased collagen synthesis in a chronic inflammation leads to what? Fibrosis. Activated macrohages and lymphocytes in chronic inflammation do what to MMP's? They decrease their activity. What happens in chronic inflammation when MMP's decrease their activities? IT will decrease the collagen degradation. When collagen is not degraded or is allowed to be synthesised in chronic inflammation what happens? Fibrosis. What happens with an injury when the stimulus that caused the acute injury is removed? Parenchymal cell death. Parenchymal cell death with superficial wounds leads to what? Regeneration- restitution of normal structure. Parenchymal cell death with deep wounds leads to what? Healing- scar formation organizatin of exudate. What is neoplasia? New growth. What is a tumor? Formation of masses. What is Cancer? tissue invasion appearance like crawling crab. What is oncology? The branch of science dealing with neoplasia. Will a tumor always be a neoplasia? yes. Is a neoplasia always a tumor? No. What is hyperplasia? Increase in number of cells. What is metaplasia? 1 adult cell type is replaced by another. What is dysplasia? abnormal growth with loss of cellular orientation, shape. What is anaplasia? An IRREVERSIBLE abnormal cell lacking differentiation. What is irreversible neoplasia? a clonal proliferation of cells that is uncontrolled and excessive. What is desmoplasia? REVERSIBLE fibrous tissue formation in response to neoplasm. What are the 2 clinical classifications of tumors and what are they like? 1. Benign- good. 2. Malignant- BAD. What is the name of a slow and a fast growing tumor? slow- bening. Fast- malignant. Which type of tumor has metastases (transfer to other parts of the body)? Malignant. What is the external surface of benign and malignant tumors? Benign- smooth, malignant- irregular. What type of tumor will have a capsule? Benign. What type of tumor will show necrosis? Malignant. What type of tumor will have hemorrhage? Malignant. Tumors can get up to how big before they need a new blood supply? 10mm. How will large tumors get new blood supply? They release chemotaxic factors that induce angiogenesis. What will the benign and malignant tumors look like microscopically? Benign- look like normal tissue of origin. Malignant- does not resemble normal tissue of origin. What will benign and malignant tumor cells look like microscopically? Benign- well differentiated. Malignant- poorly differentiated. What will benign and malignant tumor cell nuclei look like microscopically? Benign- normal size and shape also uniform. Malignant- variable shape (Pleomorphic). What will tumor cells mitoses be like for benign and malignant tumors? Benign- few. Malignant- Many and irregular. How many normal chromosomes do we have? 23 pairs. what do we look for in a vaginal smear? Nuclear to cytoplasmic ratio. What does metastasis mean? Change positions. What are the 4 main pathways of metastasis? 1. Lymphatics. 2. Blood. 3. Seeding surface of body cavity (transcoelomic spread). 4. Intraepitheilal. What is the first step in the metastatic cascade? a primary tumor. What is the second step in the metastatic cascade? Metastatic clone evolves. What is the third step in the metastatic cascade? Proliferation of the clone and invasion of vessel. What is the 4th step in the metastatic cascade? Transport by circulation. What is the 5th step in the metastatic cascade? Emboilization (getting caught). Where wil emboilization most commoly take place? At areas where vasculature gets funneled. What is the 6th step in the metastatic cascade? Invasion What is the 7th step in the metastatic cascade? New tumor formation at the site of metastasis. What is a clone? A distinct subpopulation. What is the biological role of tumor-induced angiogenesis? TO overcome limitations of nutrient and oxygen delivery. Seeding surfaces of body cavities is a direct seeding and what is the problem? There is no plain of resistance to spreading. What is mesenchyme? cells of mesodermal origin that are capable of developing into connective tissues, blood, and lymphatic and blood vessels. Mesenchymal tumors are named how (both benign and malignant? Benign- use cell of origin + oma. Malignant- cell of origin + sarcoma Epithelial tumors are named how (both benign and malignant? Benign- use terms like adenoma and papilloma. Malignant- use terms like carcinoma. Carcinoma implies what? Epithelial origin but malignant Sarcoma implies what? It is of mesenchymal origin but malignant. What would a benign and malignant tumor of fibroblast cells be called? B- Fibroma. M- Fibrosarcoma. What would a benign and malignant tumor of fat cells be called? B- Lipoma M- Liposarcoma. What would a benign and malignant tumor of blood vessels? B- hemangioma. M- Hemangiosarcoma. What would a benign and malignant tumor of smooth muscle cells? B- Leiomyoma. M- Leiomyosarcoma. What would a benign and malignant tumor of striated muscle be called? B- rhadbomyoma. M- Rhabdomyosarcoma. What would a benign and malignant tumor of cartilage cells be called? B- Chondroma. M- Condrosacroma. What would a benign and malignant tumor of squamous skin cells be called? B- Epithelioma. M- Squamouse cell carcinoma. What would a benign and malignant tumor of transitional epithelium be called? B-Transitional cell papiloma. M- transitional cell carcinoma. What would a benign and malignant tumor of glandular ducts in epithelium be called? B- adneoma. M- adenocarcinoma. What would a benign and malignant tumor of neuroendocrine cells be called? B- carcinoid. M- oat cell carcinoma. What would a benign and malignant tumor of Liver cells? B- liver cell adenoma. M- Liver cell carcinoma. What would a benign and malignant tumor of kidney cells be called? B- renal cell adenoma. M- renal cell carcinoma. What would a benign and malignant tumor of white blood cells? No benign. M- luekemia. What would a benign and malignant tumor of lymphoid cells? No benign. M- Lymphoma. What would a benign and malignant tumor of plasma cells? No bening. M- multiple myeloma. What would a benign and malignant tumor of neuroblasts be called? B- ganglioneuroma. M- Neuroblastoma. What would a benign and malignant tumor of glial cells? No benign. M- Glioma. What would a benign and malignant tumor of meningeal cells? B- menigioma. No malignant. What would a benign and malignant tumor of schwann cells be called? B- Schwannoma. M- Malignant schwannoma. What would a benign and malignant tumor of embryonic cells be called? B- teratoma. M- Teratocarcinoma. What will adenoma of colon look like microscopically? Uniform appearance. sarcoma looks like what? Flesh-like appearance. What will sarcoma look like microscopically? Elongated cells that resemble fibroblast. What will carcinoma look like microscopically? Neoplastic cells are surrounded by non-specific stroma. What will renal cell carcinoma look like in a nephrectomy? Spongy yellowish. What type of tumor is a blastoma? Malignant tumors composed of embryonic cells from embryonic primordia. What type of a tumor is a teratoma? They are derived from germ cells and contain mixed tissues from all 3 germ layers and can have any type of tissues like teeth. Teratoma is the benign form what is the malignant form? Teratocarcinoma. What are eponymic tumors? They have the names of the doctors that discovered them. What is Hodkin's disease? An eponymic tumor of the lymph nodes. What is Ewing's sarcoma? An eponymic tumor of the bones. What is Kaposi's sarcoma? An eponymic tumor of the skin. What should be look for with Kaposi's sarcoma? It is a Hugh clue of Aids. What are the different ways to classify tumors? Grading and staging. What are the different ways of staging tumors? TNM, Overall stage groupings. Tumor staging is based on what? Clinical assessment during GROSS examination as to the extent of SPREAD. Tumor grades are based on what? Histologic examination. Tumor staging using the TNM system will accounts for what? T- size of the tumor. N- presence of lymph Node metastases. M- Distant metastases. The T or size of the tumor is ranked how? 0-4. N or presence of lymph node metastases is ranked how? 0-4. M or metastases of tumors is ranked how? 0-1. 1 if present and 0 if not present. How many tumor overall stage groups are there? 0, I, II, III, IV. What will stage 0 mean? Carcinoma in situ (situated in original position). what will stage I mean? Cancers are localized to one part of the body. What will stage II mean? Cancer is locally advanced and lymph nodes on only one side of the diaphragm have metastisis. What will stage III mean? Lymph nodes above and below the diaphragm have metastisis. What will stage IV mean? Cancers have spread to other organs or throughout the body. How many tumor grading levels are there? I, II, III. Tumor Grade I is what? well differentiated. Tumor grade II is what? Moderately well differentiated. Tumor grade III is what? Undifferentiated. Which method of classifying tumors is more predictive in value staging or grading? Staging. The difference between normal and malignant cells is mostly what? Quantitative. What type of cells are less differentiated? Cancer cells. What type of cells are more adapt to survive under unfavorable conditions? Cancer cells. What will cancer cells contain less of? Mitochondria, RER, specialized enzymes. Why will cancer cells contain less Mitocondria, RER, and specialized enzymes? They are less differentiated and don't complete a normal function and therefore don't need to maximize energy production. Tumor cells may acquire embryonic/fetal features due to what? tumor cell regression. What is fetal protein? A product of fetal hepatocytes. What is fetal protein in adults a marker for and why? A marker for a tumor because the tumor cell regressed into making a fetal protein. Where is embryonic glycoproteins made at? by large intestine adenocarcinoma and normal fetal intestines. What type of cells are anchoreged dependent? Normal cells. Cancer cells show a lack of contact inhibition. What type of cells can be passaged from one flack to another? How often can this happen? Cancer cells. Indefinitely (immortal). Can normal cells grow in soft agar and roller bottles? No, but cancer cells can. Do cancer cells need growth factors? No because they are dependent on autocrine stimulation. What are 2 causes of cancer generally? 1. Exogenous causes. 2. Endogenous. Name a type of biologic exogenous cause of cancer? Virus. Name 2 types of endogenous causes of cancer? 1. Oncogenes. 2. Tumor suppressor genes. Name 5 major chemical carcinogens? polycyclic aromatic hydrocarbons, aromatic amines, nitrosamines, steroid hormones, metals and inorganic compounds. Where will polycyclic aromatic hydrocarbons come from? Tobacoo tar. How can we get cancer from polycyclic aromatic hydrocarbons and what type of cancer will it cause? Inhalation- Carcinoma of lungs, Skin contact- Skin cancer, Metabolic- Liver cancer. Where will aromatic amines come from and how will it cause cancer and what type? From dye and rubber industry, it is excreted in urine and causes bladder cancer. Where will nitrosamines come from and how will they cause cancer and what type? From food additives (smoked food), it is a bacrial conversion in the gut and it leads to intestinal cancer. Where will Steroid hormones come from and how will they cause cancer and what type? Ovary/adrenal, from stimulation of endometrium, causes endometrial carcinoma. Where will Metals and organic compounds come from and how will they cause cancer and what type? Pesticides, from skin contact, skin cancer, AND ore, from inhalation, nasal cancer. Alfatoxins come from what? Mold. Alfatoxins mode of action to cause cancer is what? Ingestion/metabolism. What type of cancer will alfatoxins cause? Liver. Where will asbestos come from and how will they cause cancer and what type? Industrial, inhalation, lung. Where will CCL4 come from and how will they cause cancer and what type? dry cleaning, solvent, refrigerant, contact, liver cancer. Where will Vinyle chloride come from and how will they cause cancer and what type? Many sources, inhalation, Liver. 85% of aniline derivatives are used to make what? Methylene diphenyl diisocyanate (MDI) which is used to make POLYURETHANE. What is 3rd hand smoke? Chemicals will remain on areas that smoke touches like clothes and anything it gets on like houses. Chemical carcinogens are absorbed in what form? Procarcinogen. What happens to procarcinogens? They are transformed into the active carcinogen. What are the 5 steps that carcinogen undergoes? 1. Initiation. 2. Promotion. 3. Conversion. 4. Progression. 5. Clonal expansion. What will initiation do? Irreversible genetic changes. What is promotion? Stimulation to proliferate. What is converision? New cell type able to self proliferate. What is progression? acquisition of new genetic feature. What is clonal expansion? identical and divergent. What type of carcinogen would UV light, X-rays, radioactive isotopes and atomic bombs be called? Physical carcinogens. When UV light damages DNA what usually happens? It is repaired. Unrepaired DNA that was damaged by UV light can cause what? Basal cell carcinoma, squamous cell carcinoma, melanoma. Where is cancer from UV light prevalent at? Southern US and Australia. What is shistosoma haematobium? A parasite that acts as a urinary bladder carcinogen. What is opisthorchis sinesis? A chinese live fluke that acts as a bile duct and liver carcinogen. How can a virus cause cancer in DNA? It integrates in the DNA. Speaking of viral carcinogens what is transduction? acute transforming RNA viruses in the form of cellular oncogenes. Speaking of viral carcinogens what is insertion? Slow transforming oncogenic RNA viruses; insert into the genome and activate a latent cellular oncogene, which is then capable of transforming the normal cell into a malignant cell. Human papilloma virus aka HPV is what and what are the 2 types? Invasive cervical carcinoma types 16, 18. Epstein-Barr virus can be what type of carcinogen? Burkett's lymphoma, nasopharangeal. Hepatitis B and C viruses are what type of carcinogen? Liver. Kaposi's sarcoma is associated with what? HIV/aids, herpsesvirus. What type of carcinogen is kapsoi's sarcoma? Skin cancer. What are RNA viruses that are carcinogenic? Human T-cell leukemia/lymphoma virus (HTLV-1), Adult T cell leukemia which is in HIV group. What are the 2 types of human oncogenes? viral and cellular. What is an oncogene? A gene that is the cause of cancer. An oncogene has gained what? function and becomes a cancer-inducing agent. How many alleles need to be damaged for a gene to become an oncogene? only 1. A proto-oncogene transformes into an oncogene by going through what 4 steps? 1. point mutation. 2. Gene amplification. 3. Chromosomal rearrangement. 4. Insertion of viral oncogene. How will the MYC oncogene be activated in Burkitt's lymphoma? 8 switches with 14. What gene is associated with CML? abl. What gene is associated with burkitt's lymphoma? c-myc What gene is associated with follicular and undifferentiated lymphomas? bcl-2 What gene is associated with breast, ovarian, and gastric carcinomas? erb-B2 What gene is associated with colon cancer? ras. What gene is associated with a lung tumor? L-myc What gene is associated with neuroblastoma? N-myc What gene is associated with herebitary papullary renal cancer? met What gene is associated with multiple endocrine neoplasia (MEN) types II and III? ret What gene is associated with GI stomal tumor? c-kit. What do tumor suppressor genes do? They protect genes against activated or newly acquired oncogenes. What happens when a tumor suppressor gene has lost function? it is no longer a cancer-inhibiting agent. With tumor suppressor genes how many allels must be lost for expression of disease? Both. Name 2 of the best tumor suppressor genes? p53, retinoblastoma gene (rb-1). Retinoblastoma gene protects against what? eye cancer. p53 protets against what type of tumor? Numerous like brest and colon. What type of tumor suppressor genes protect neurofibromatosis 1 and 2? NF-1 and NF-2. Wilms tumor (kidney) is protected by what tumor suppressor gene? WT-1. Familial adenomatous polyposis coli (intestine) is protected by what tumor suppressor gene? APC. Breast carcinoma and ovarian carcinoma is protected by what tumor suppressor gene? BRCA1 Breast carcinoma is protected by what tumor suppressor gene? BRCA2 Melanoma is protected by what tumor suppressor gene? p16 pancreatic cancer is protected by what tumor suppressor gene? DPC Colon cancer is protected by what tumor suppressor gene? DCC What is the generic way of naming Tumor suppressor genes? D___ C. stands for deleted __name of area___ cancer Name 5 types of hereditary cancers? 1. Neurofibromatosis type I. 2. Familial adenomatous polyposis coli. 3. Wilms tumor. 4. skin tumors in xeroderma pigmentosum. 5. Chromosomal fragility syndromes. TNF does what? Activates white blood cells. Some cancers do what under the influence of immune factors? Involute spontaneously. What is used for treatment of bladder cancer? BCG. Tumor vaccines are used for treatment of what type of carcinomas? Melanoma and renal cells. Tumor antigens may be used for what? as tumor markers. What should tumor markers be used for? Not as primary diagnosis, but to confirm a diagnosis and to monitor therapy. What is the tumor marker used to screen for prostate carcinoma? PSA What is the tumor marker used to screen for pancreatic cancer? CEA What is the tumor marker used to screen for testies? alpha-fetoprotein What is the tumor marker used to screen for moles, and gestational trophoblastic tumors? Beta-hCG What is the tumor marker used to screen for ovarian, and malignant epithelial tumors? CA-125 What is the tumor marker used to screen for melanoma, neural tumors, and astrocytomas? S-100. What is the tumor marker used to screen for metastases to bone? alkaline phosphatase. What is the tumor marker used to screen for neuroblastoma, lung, and gastric cancer? Bombesin. What is the tumor marker used to screen for hairy cell leukemia? TRAP What is the tumor marker used to screen for pancreatic adenocarcinoma? CA-19-9 What is the tumor marker used to screen for thyroid cancers? Tg. Leukemias and lymphomas cause what type of paraneoplastic syndrome? gout, urate nephropathy. Hypercalcemia is a paraneoplastic syndrome caused by what types of cancers? squamous cell carcinoma of the lung, breast, renal A venous thrombosis is a paraneoplastic syndrome caused by what type of cancer? pancreatic What are the 7 warning signals of cancer? CAUTION= Change on bowel or bladder cancer, A sore that doesn't heal, Unusual bleeding or discharge, Thickening or lump in breast or elsewhere, Indigestion or difficulty swallowing, Obvious change in wart or mole, Nagging cough or hoarseness. Psammos means what? Sand How are psammoma bodies seen? with a microscope. Psammoma bodies are seen with several cancers and appear as what? Laminated, concentricm calcific spherules. psammoma bodies are though to arise from what? infarction and calcification of papillae tips. And calcification of intralymphatic tumor thrombi. Deaths from lung cancer is on the rise or fall for males and females. Plateaued in males and is rising for females. What is the first and second leading cause of death in the USA? 1. Heart disease. 2. Cancer. What is incidence? The number of new cases at a defined time. What is prevalence? All cases new and old at a defined time. What is mortality? Deaths attributed to something. What is the most common sign of colon cancer? Blood in stool What is the most important risk factor for colon cancer? Family Hx What is the most important risk factor for breast cancer? Family Hx What is the most common sign of cervix cancer? Vaginal bleeding. What is the most important risk factor with cervix cancer? STD What is the most common sign of uterus cancer and what is the most important risk factor? Vaginal bleeding, and hormonal imbalance. What is the most common sign of skin cancer and what is the most important risk factor? Skin lesion, sun expsoure. What cancer has the most incidence ( New cases) amoung Males and Females? Males- 1. Prostate 2. Lung. 3. Colon. Females- 1. Breast. 2. Lung. 3. Colon. For males and females what cancers have the highest mortality rate? Males- 1. Lung. 2. Prostatic. 3. Pancrease. Females- 1. Lung. 2. Breast. 3. Pancrease. Cancers often metasis to what 4 areas? liver, lung, brain, bone. List the tumors that metasis to the liver in order of highest to lowest? colon, stomach, pancrease, breast, lung. What percentage of brain cancers are from metastases? 50%. What percentage of liver cancers are from metastasis? More than primary tumors. What percentage of bone tumors are from metastasis? More than primary tumors. Name the 3 body fluid compartments? intracellular, interstitial, intravascular. How much fluid is taken in a day? 2.5 liters. How much fluiid is let out in a day and how? 2.5 liters. 0.1 in stool, 0.9 in respiration/sweat, 1.5 in urine. What are the 2 forms of edema? 1. Exudate. 2. Transudate. Which type of edema is typical of inflammation? Exudate. Exudate is rich in what? Protein and blood cells. Transudate contains less proteins and fewer cells and is typical of what? Hydrostatic or osmotic pressure pathology. Transudate is what? An ultra-filtrate of plasma fluid. Name 4 pathogenesis of edema? 1. Increased hydrostatic pressure. 2. Increased wall permeability. 3. decreased oncotic pressure. 4. Lymphatic obstruction. What is hydrostatic pressure? Blood pressure pushing fluid out of capillaries. What is oncotic pressure? Plasma proteins that are in capillaries want to be diluted and pull fluid back into the capillary. Transudate edema has a specific gravity higher or lower than 1.012? Lower. Transudate edema is due to what? Increased hydrostatic pressure, incresed oncotic pressure, Na retention. Exudate edema is due to what? Lymphatic obstruction. Hydrostatic pressure causes edema and is caused by what 2 things? hypertension, heart failure (increased venous backpressure). Oncotic pressure when low causes edema and is caused by what? decreased protein synthesis, proteinuria (loss of proteins in urine). Obstructions that cause edema are usually caused by what? Tumors or chronic inflammation, also parasites like filaria which causes elephantiasis. What is hypervolemic? High levels of blood. Hypervolemic causes edema and is due to what? Na and H2O retention. What is anasarca? Extreme generalized edema. What is hydrothorax, hydropericardium, and hydroperitoneum? Clincal forms of edema that are in cavities. Low blood pressure leads to what type of edema? Pulmonary edema. Elephantiasis is caused by what? Lymph blockage from a parasite. Heart problems will show edema where? lower extremitiesm or back if supine. Kidney problems will show edema where? Diffuse edema. Liver problems will show edema where? ascites (fluid in peritoneal cavity). Hyperemia is what? Excess blood flow. Active hyperemia is what? Dialation of arterioles like when blushing, exercise, inflammation. Passive hyperemia is what? Venous backpressure Passive hyperemia is associated with what? hydrosatic edema, cyanosis, and heart failure. Chronic passive congestion of lungs leads to what? edema and RBC extravasation into alveoli. Chronic passive congestion of the lungs is accompanied by what? Anoxia (low oxygen in blood), and pulmonary fibrosis. With chronic passive congestion of the lungs macrophages take up RBC and degrade hemoglobin and this causes what? Hemosiderin accumulation. Cardiac hemorrhage is often what? Fatal. What will arterial hemorrhage look like? Bright red pulsating/squirting. Capillary hemorrhage does what to venous pressure? increases it. Skin hemorrhages are what? Bruises What is a purpura? A skin hemorrhage that is between 1mm and 1 cm. What is ecchymosis? A skin hemorrhage that is large blotch bruises What is petechia? Skin hemorrhages that are less than 1mm. What is hemoptysis? Respiratory tract hemorrhage What is epistaxis? Nose bleeds. What is hematemesis? Vomiting blood. What is hematochezia? Anorectal bleeding. What is melena? Passage of black blood in stool from upper GI tract. What is hematuria? Blood in urine. What is metrorrhagia? Bleeding not related to normal monthly menses. What is menorrhagia? Profound menstrual bleeding. How much blood can we lose and be ok? Less than 500 ml What happens if we lose 1000- 1500 ml of blood? Circulatory shock. How much blood loss is lethal? 1500 ml or more. What is hematoma? Compression of tissues. What happens with intracerebral hemorrhage? Stroke, death. Slow chronic hemorrhage leads to what? Iron deficiency anemia. What type of hemorrhage has slower onset subdural or epidural and why? Subderal because the lower pressure veins bleed more slowly than arteries. Thrombosis is what? Clotting. Thrombosis takes place how? transformation of fluid blood into a solid aggregate encompassin gRBCs and fibrin. Thrombosis forms what? A thrombus. What are the 3 principle components of a intravascular coagulation? 1. Coagulation factors. 2. Platelts. 3. Endothelia cells. What are the 2 pathways for coagulation factors? Endogenous (intrinsic) and exogenous (extrinsic). What 2 things will platelets do? neutralize haparin and other cnticoagulant factors, and secrete thromoxane which stimulates coagulation. Endothelial cells normaly have what? Antithrombotic properties. How will endothelia cells help with coagulation if they have antithromboit proterties? IL-1 and TNF activate them and ehy lose their negative charge and antithrombitic properties. Endothelial damage uses which coagulation factor pathway? Intrinsic. Tissue damage uses which coagulation factr pathway? Extrinsic. What is the first step in forming a thrombi? Defect is covered with fibrin and platlets. What is the second step in forming a thrombi? Fibrin meshwork anchors RBCs into nascent thrombus. What is the thrid step in forming a thrombi? Fully formed thrombi consists of layers of fibrin and RBCs Intramural thrombi of the heart causes what? overlying Myocardial infarct. Valvular thrombi of the heart causes what? mimic endocarditis. arterial thrombi causes what? atherosclerosis when attached to the walls. When is a venous thrombi found? in dialated veins. Where are microvascular thrombi found at? Arterioles, capillaries, and venules. Deep venous thrombosis can lead to what? Pulmonary embolism Deep venous thrombosis is predisposed by Virchow's triad which is what 3 things? 1. Stasis. 2. Hypercoagulability. 3. endothelial damage. Who is at risk for deep venous thrombosis? Elderly people on transcontinental flights. What are lines of zahn? Distinct layering of cellular elements and fibrin that occur in atrial and venous thrombi. Occlusion of the lumen from a thrombi is called what? Infarct. Lysis of the thrombus is called? reperfusion. Recanalization of a thrombus leads to what? reestablished blood flow. What is embolizatin of a thrombi? Breaking off of a clot. What is an embolus? Undissolved materials like thrombus in blood. Name 4 types of embolisms? thromboemboli, liquid emboli, gaseous emboli, solid particle emboli. Amniotic fluid emboli can lead to what? DIC, especially postpartum. Pulmonary embolus clinically present with what? Chest pain, tachypnea, dyspnea. 95% of pulmonary emboli arise from what? Deep leg veins. Name the 3 origins of venous thromboemboli? saddle, lung, venous thrombi. Name 6 origins for arterial thromboemboli/ brain infarct, kidney, spleen, Intestinal, ventricular, extremity infarct. A white infarct is typical of what? Arterial occlusion in solid organs with single blood supply. Red infarct is typical of what? Venous obstruction like intestines and testies twisting. The fate of infarcts depends on what? Their anatomical site, type of cells forming the tissue, circulatory status , extent of necrosis. White infarcts ________ areas. Rimmed Volvulus equals what? Twisting. What type of infarct is ween with volvulus? Red infarct. What are 3 possible causes of shock/ 1. Pump failure of the heart. 2. Loss of fluid from circulation. 3. Loss of peripheral vascular tone. Pump failure leads to what type of shock? Cardiogenic shock. Loss of fluid from circulation lead to what type of shock? Hypovolemic shock. Loss of peripheral vascular tone leads to what type of shock? Hypotensive shock. Loss of blood, myocardial or valvular disease, or vasodilation leads to what? Heart failure heart failure leads to what? Decreased cardiac output. Decreased cardiac output leads to what? Decreased blood to tissues. Decreased blood to tissues leads to what? Cell anoxia. Cell anoxia leads to what? Shock and edema Shock leads to what? Coma, renal failure, lung failure, death, gi bleeding. What are the 3 clinical stages of shock/ 1. early or compensated shock. 2. Decompensated but reversible shock. 3. Irreversible shock. What happens with the heart during compensated shock? Tachycardia (beats faster). What else happens with compensated shock? Vasoconstriction of arterioles and reduced urine production. What happens with decompensated reversible shock? hypotension, tachypnea and shortness of breath, oliuria, acidosis. What happens with irreversible shock? 1. Circulatory collapse. 2. marked hypoperfusion of vital organs. 3. Loss of vital functions.