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142 Cards in this Set
- Front
- Back
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What is and what causes steatosis of the liver
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reversible accumulation of triglycerides in the liver
"fatty metamorphosis" can be caused by alcohol |
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what is and what is one cause of mallory's hyaline
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the aggregation of cytokeratin filaments w/in cell - is permanent and may lead to cell death
can be caused by chronic alcoholism |
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a genetic disease that results in abnormal accumulation of iron in tissues
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hemochromatosis
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abnormal accumulation of iron in tissue due to any cause (ie. may be due to local injury such as old hemorrhage
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hemosiderosis
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removing red blood cells to treat hemosidersosis
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phlebotomy
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e.g of a disease where there is cell death due to apoptosis
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Burkitt Lymphoma - malignancy of B lymphocytes with apooptotic cell death of malignant cells and phagocytosis of apoptotic bodies by macrophages
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two mechanisms for boeth intrinsic and extrinsic apoptosis
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Intrinsic: injury (radiation) or withdrawel of growth factors
Extrinsic: receptor ligand interactions, cytotoxic T-lymphocytes |
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refers to the lightly stained marcrophages with apoptotic bodies surrounded by dense infiltrate of malignant lymphocytes - seen in burkitts lymphoma
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"starry sky pattern"
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what is one way ischemia can cause the reversible deposition of lipid.
what is one reversible way that proteins are digested? |
occlusion - ischemia - decrease in oxidative phosphorylation - decrease ATP - detachment of ribosomes - decrease in protein synthesis - lipid deposition
decrease in ATP also leads to increase in glycolysis which decreases glycogen and pH - activates intracellular lysosymes - causing nuclear changes, protein digestion |
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ischemia can eventually lead to irriversible damage in cells. The decrease in pH accompanying the increase in glycosis leads to increase in degradation in internal structures by lysosymes -
the break down of phopholipids affects mitochondria how |
increase in mitochondrial membrane - Ca influx - increase in Ca is toxic.
mitochondria also swells |
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why is there edema w/ ischemia
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cells loose ability to regulate Na/K pump and cell swells
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the increase in cytosolic Ca has what four effects
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decrease in ATP
decrease in Phospholipids (phospholipidase) Disruption of membrane (protease) endonulclease - nucleus chromatin damage |
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is one of the earliest morphologic changes of cell death
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mitochondrai change
becomes porous, and enters a low energy state - ultimately it loses enzymatic systems and cannot recover normal function they swell and Ca ppt |
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the commonest form of necrosis in which denaturation of protein dominates the picture
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coagulative necrosis
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infarction is an example of what kind of necrosis
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coagulative necrosis
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usually necrosis with extensive acute inflammation (e.g bacterial or fungal infections) resulting in fairly complete digestion of tissue
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liquifative necrosis
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an abscess and cerebral infarction are common examples of what kind of necrosis
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liquifactive necrosis
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shape of renal infarct
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wedge shaped - the kidney has end arterial circulation - the infarction is narrow at the medulla and widens towards the cortex
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red infarcts occur when
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when blood is still passes into necrotic tissue
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necrotizing fungal pneumonia is an example of what kind of necrosis
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liquifactive
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a type of necrosis that may be part of acute pancreatitis
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enzymatic fat necrosis
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a combonation of coagulative and liquifactive necrosis
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caseus necrosis - seen in TB - seen in the middle of a granuloma
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how does enzymatic fat necrosis occur?
what is one histological landmark? |
pancreatic lipases
fatty acids released and Ca saponification and chalky yellow droplets w/in the necrosis |
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type of necoriss that is really the consequence of bacterial colonization of tissue which has already undergone necrosis - usually due ot ischemia
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gangrenous
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a pattern of necrosis which is liquifactive superimposed on pre-existing coagulative necrosis
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gangrenous
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biologically active chemical that is not "us"
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xenobiotic
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a chemical which terminates pepide chain synthesis prematurely resulting in toxic, incomplete toxins
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puromycin - antibiotic that is so toxic it is not used clinically
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strangulation, asphyxia, drowning cause what
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systemic anoxia
anoxia is NO oxygen - hypoxia is reduced oxygen |
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chemical that blocks oxidative phosphorylation in the mitochondria
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cyanide
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Chemical that binds to hemoglobind and causes cellular anoxia by reducing the O2-carrying capacity of RBC
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carbon monoxide poisoning
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CCL4 is metabolized to what in liver -
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free radicals - regarded as major mediator of damage ot cell membranes resulting in swelling, disruption of protein synthesis, and in severe cases loss of mitochondrial function, leakage of lysosome, influx of Ca blah blah blah
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hydroxyl free radicals react with what 3 things
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1. unsaturated lipids (lipid peroxidation)
2. DNA 3. proteins |
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vitamin E, ascorbic Acid, and glutathione are all
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antioxidant - protect against free radical damage
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cisPlatinum is used in
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chemotherapty for cancer
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what are the two limiting toxicities of cisPlatinum
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Diarrhea
Renal fairlure |
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forms covalent bonds w/ variety of macromolecules (e.g DNA) and is toxic to tissue which need DNA synthesis
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cisPlatinum
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how might you counter act the cytotoxicity seen in cisPt
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keep pt well hydrated - give cisPt as prolonge infusion, treat for a day and then rest the patient
alater the chemical fom of cisPT |
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acetaminophen is metabolized by what - to what
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by p450 to NAPQI
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w/ acetaminophen - it is the rise in what that reacts with hepatic proteins
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rise in NAPQI which is normally metabolized to mercapturic acide by glutathione untill that system is overwhelmed
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a general term for a analog of molecule normally active in cellular metabolism may block pathway or shift equilibrium
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antimetabolite
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inorganic Hg injures cells how
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combines with -SH and inactivates many enzymes
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the replacement of one adult cell type by another adult cell type
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metaplasia
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literally "disordered growth"
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dysplasia
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what cell change is seen in normal lactational change in the breast
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epithelial hyperplasia w/in lobule
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heart failure and venous obstruction may cause edema through what mechanism
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increased intravascular hydrostatic pressure
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burns, inflammation, and chemical injury may cause Edema by what mechanism
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increased permeability of vessel walls
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neoplasia, post-surgery, parasites might cause edema by what mechanism
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lymphatic obstruction or destruction
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increased volume of blood w/in a specific vascular bed
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hyperemia
syn: congestion |
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active hyperemia
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increased flow to an area
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passive hyperemia
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decreased outflow of blood from area
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flow of blood from the vascular compartment
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hemorrhage
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3 factors determining the clinical significance of a hemorrhage
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volume of blood
rate of bleedin site where the hemorrhage occurs |
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blood during a hemmorrhage may accumulate as a what in an organ
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hematoma
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minute hemorrhages in skin and mucous membranes
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petechiae
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a little larger thatn petechiae
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purpura
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larger than purpura - bruise
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ecchymosis - bruise
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couphing up blood from larynx, trachea, bronchi
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hemoptysis
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vomiting blood
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hematoemesis
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esophageal varices will result in what - couphing or vomiting blood
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hematemesis - vomiting blood
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will a sudden loss of blood leave a pt anemia
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no - they will be hypovolemic and hypotensive but until fluid portion of the blood is replaced the red cell concentration is diluted
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difference between hypoxia and anoxia
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hypoxia - low O2
anoxia - no O2 |
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gross morphology of a bland infarct
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tissue is pale, "anemic", white
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Hemorrhagic infarct
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bleeding into dead tissue
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what kind of necrosis is the hallmark of infarction
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coagulative
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what are some changes seen in infarction
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cells become eosinophilic, nuclei shrink, become hyperchromatic, less distinct, and then break up
neutrophils infilrate to digest dead tissue, Macrophages scarring may result |
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pulmonary infact caused by ischemia is most often due to
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embolus - and usually wedge-shaped
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backward heart failure is do to? also called?
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failure to pump blood out of veins and often called congestive failure
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forward heart failure occurs do to what?
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failure to pump blood into the arteries with sufficient pressure to perfuse the organs - can cause ischemia
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global heart failure
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failure having elements of both backward and forward failure
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heart failure can often cause congestion in what two organs
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lungs, liver
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heart failure causes what kind of edema
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pitting edema as well as edema in lungs and liver
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chronic congestion of the liver is one result of of what kind of heart failure
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right sided heart failure (backward heart failure)
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"nutmeg liver" refers to
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congested liver
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what is the difference between thrombus and clot
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clot is coagulated blood outside the vascular system - anywhere
thrombus is coagulated blood w/in the vascular system |
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Virchow's triand includes
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1. injury to vessel wall
2. increased blood coagulability 3. decreased flow |
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the most important factor in thrombosis
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endothelial injury
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injury to the endocardium and or decreased flow following myocardial infarction may lead to what kind of thrombosis
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ventricular mural thrombosis
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this type of thrombosis may occur due to endothelial injury (i.e bacterial) or hypercoagulbility states
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thrombosis of heart valves
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two types of venous thrombosis
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phlebothrombosis (statis)
thrombophlebitis (inflammation) |
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thrombosis caused by statis of blood in uninflammed veisn and the most clinically significant form of thrombosis
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phlebothrombosis
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thrombosis in inflammed veins is referred to as thrombophlebitis and can be what two kinds
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sterile (due to trauma, radiation, or chemicals) and septic (due to bacteria)
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four outcomes of thrombosis
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1. lysis (dissolution) = resolution
2. organization 3. propagation towards the heart 4. embolization to the lungs |
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a detached intravascular solid, liquid or gaseous mass that is carried by the blood to a distant site from its point of origin
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embolus
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how might the outcome of a pulmonary thromboemboli differ depending on the size of the artery
report for small medium large arteries |
small artery: silent unless septic
med artery: wedge shaped infarct lg artery: RH failure sudden death, cardiogenic shock |
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loss of blood plasma causes what kind of shock
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hypovolemic
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cardiac pump failure causes what kind of shock
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cardiogenic
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loss of vascular tone results in what kind of shock
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neurogenic
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systemic vasodilation results in what kind of shock
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anaphylactic
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how does cardiogenic and septic shock differ interms of CO
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CO is down in cardiogenic and up in septic
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systemic thromboemboli is usually caused by
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left heart failure or mural thrombi
consequence is down stream infarction but depends on collaterol supply note: mural thrombus is a thrombus attached to a large vessel wall. usually heart or aorta. common causes of mural thrombi are myocardial infarction, myocarditis, aneurysms |
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fat embolism results from
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trauma to fat tissue, burns
causes pulmonary insificiency, neurologic symptoms, anemia etc. |
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air embolism occurs under what two circumstances
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1. acute decompressio sickness (high to low pressure)
2. chronic decompression sickness (caissen disease - persistant gas bubbles) |
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a decreased systemic perfusion of tissue caused by decreased effective ciculating blood volume or decreased cardiac output
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shock
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foam cells , often times at the root of the aorta, seen in children ages 5-9
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fatty streaks
precurser to atheroma in subendothelium |
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6 stages of therosclerosis
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1. Fatty Dot (isolated foam cells)
2. Fatty Streaks 3. Intermediate 4. Atheroma 5. Fibroatheroma 6. Complicated Plaques |
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fibroatheroma involves what
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atheroma + collagen proliferating around fat, cholest, CE
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atheroma includes what layers
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extends into media
center tends to undergo necrosi, usually asymptomatic, covered by fibrous cap facing the lumen of vessel. |
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what age - atheroma
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ages 30s to 40s
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in what stage of atherosclerosis does fibrous cap occur
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atheroma
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atherosclerosis is a type of
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arteriosclerosis (hardening of the arteries)
atherosclerosis is a chronic inflammatory disease of the large arteries marked by intimal thickening and lipid accumulation |
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the four possible clinical manifestations of atherosclerosis
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1. calcification
2. ulceration 3. thrombosis (may separate due to increase in hemodynamic stress e.g exercise) 4. Hemorrhage into Plaque - could result in aneurysm |
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localized abnormal dilation of blood vessell or wal of heart which ruptures and causes hemmorrhage
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aneurysum
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more than 50% of all deaths are due to
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atherosclerosis
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key processes in atherosclerosis
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intimal thickening and lipid accumulation
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stenosis
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narrowing of the vessel lumen
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occlusion due to atherosclerosis could happen by what three mechanisms
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1. thrombosis on plaque
2. Hemorrhage into plaque 3. atheroembolus which all result in mI, cerebral infarct, gangrene |
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what is the injury hypothesis which explains pathogenesis of atherosclerosis
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atherosclerosis is a chronic inflammatory response to the arterial wall initiated by injury to endothelium
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2 aspects to homeostats
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1. maintain blood in a clot free, fluid state
2. induce rapid and localized hemostatic plug at the site of vessel injury |
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four stages of hemostasis
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1. vessel wall: vasoconstriction-neurogenic
2. Primary Hemostatis - platelets (adh, act, aggre) 3. Secondary hemostasis (coagulation cascade) 4. thrombus and Anti-thrombic events |
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3 main procoagulative things that endothelial cell does
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1. storage and release of VWF-FVIII
2. Vasocontstriction (endothelin) and vasodilation (NO, prostacyclin) 3. Secretes FVIII |
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VWF binds what on the platelet
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GP1b
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VWF binds what on Endothelial cell
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FVIII (which degrades rapidly when no bound to VWF)
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what activates VWF
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thrombin, Fibrin, Histamine
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VWF binds what on the subendothelium
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collagen
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platelet aggregation is due to what binding
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platelet (GPIIb/IIIa - fibrinogen - GPIIb/IIIa etc)
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what is deficient in Glanzmanns Thrombasthenia
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GPIIb/IIIa
no fibrinogen bridging! |
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what is missing in Bernard-Souler syndrome
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GP1b (on platelet) binds VWFand is important in primary hemostatis
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what two factors activate/increase platelet aggregation
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ADP and TxA2
activates GPIIb/IIIa - VWF |
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actomyosis
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when platelets contract and decrease injury site
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platlets are measured what two ways
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1. platelet aggregation
2. Bleeding time test |
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Aspirin inhibits irreversible
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Cox-1
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inhibition of inappropriate platelet aggregation can prevent stroke, ischemia is what theory
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anti-platelet theory
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selectins bind
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glycoproteins
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Immunoglobulin binds
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Integrins
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what effect does plasmin have on fibrinogen and fibrin
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cleavage
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Factor XIIIa does what
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stabalizes fibrin clot by crosslinking lysine and glutamine side chains of Alpha and gamma chains -
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Quaternary Complex
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exzyme activated co-factor which is assembled on surface by Ca ions and improves the efficeiency of VIIIa + Ca which helps IXa convert X to Xa
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K dependent factors
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2,7,9,10
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PECAM1, ICAM-1, and VCAM-1 are all
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in the immunoglobulin superfamily
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Factor V Leiden mutation
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FActor V cannot be destroyed by aPC
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DDAVP works to treat vWF defects by
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mimicking vasopresson and increasing the release of vWF+ FVIII
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prothrombin 2010 mutation results in
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increase in prothrombin (factor II) due to increase in mRNA stability
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Ab binds platelet factor 4 which then binds heparin which increases thrombin due to platelet activation of endothelial cell
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Heparin-induced thrombocytopenia
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what is one anticoagulant factor which decreases the synthesis of procoagulant factors
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oral vit K antagonist e.g comadin
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anti-coagulant atht inhibits the action of thrombin (and factor Xa)
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Heparin derivitives, R-huidin
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coagulation cascade happens during the primary or secondary hemostatis ?
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secondary
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how does heparin work
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anti-thrombin III binds heparin
conf change in anti-thrombin (active site exposed) inhibits factos 9-12 |
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what is the Protein C pathway
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Thrombin binds Thrombomodulin (EC)
activates Protein C Protein C plus Protein S inhibit FVa, FVIIIa and inhibit the oagulation cascade |
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protein C is what dependent
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Vit K dependent - so Vit K deficieciency may cause thrombosis
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is important in remodeling clot and opening up occluded vessels
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Fibronolytic system
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where is vWF, FV, HMWK, PF4, fibrinogen, PDGF, TFG located w/in the platelet
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Alpha granule
note: ADP, ATP, serotonin, calcium are located int he dense body |
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life of platelet in circulation
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10
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