Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

142 Cards in this Set

  • Front
  • Back
What is and what causes steatosis of the liver
reversible accumulation of triglycerides in the liver
"fatty metamorphosis"

can be caused by alcohol
what is and what is one cause of mallory's hyaline
the aggregation of cytokeratin filaments w/in cell - is permanent and may lead to cell death

can be caused by chronic alcoholism
a genetic disease that results in abnormal accumulation of iron in tissues
abnormal accumulation of iron in tissue due to any cause (ie. may be due to local injury such as old hemorrhage
removing red blood cells to treat hemosidersosis
e.g of a disease where there is cell death due to apoptosis
Burkitt Lymphoma - malignancy of B lymphocytes with apooptotic cell death of malignant cells and phagocytosis of apoptotic bodies by macrophages
two mechanisms for boeth intrinsic and extrinsic apoptosis
Intrinsic: injury (radiation) or withdrawel of growth factors
Extrinsic: receptor ligand interactions, cytotoxic T-lymphocytes
refers to the lightly stained marcrophages with apoptotic bodies surrounded by dense infiltrate of malignant lymphocytes - seen in burkitts lymphoma
"starry sky pattern"
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
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
why is there edema w/ ischemia
cells loose ability to regulate Na/K pump and cell swells
the increase in cytosolic Ca has what four effects
decrease in ATP
decrease in Phospholipids
Disruption of membrane (protease)
endonulclease - nucleus chromatin damage
is one of the earliest morphologic changes of cell death
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
the commonest form of necrosis in which denaturation of protein dominates the picture
coagulative necrosis
infarction is an example of what kind of necrosis
coagulative necrosis
usually necrosis with extensive acute inflammation (e.g bacterial or fungal infections) resulting in fairly complete digestion of tissue
liquifative necrosis
an abscess and cerebral infarction are common examples of what kind of necrosis
liquifactive necrosis
shape of renal infarct
wedge shaped - the kidney has end arterial circulation - the infarction is narrow at the medulla and widens towards the cortex
red infarcts occur when
when blood is still passes into necrotic tissue
necrotizing fungal pneumonia is an example of what kind of necrosis
a type of necrosis that may be part of acute pancreatitis
enzymatic fat necrosis
a combonation of coagulative and liquifactive necrosis
caseus necrosis - seen in TB - seen in the middle of a granuloma
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
type of necoriss that is really the consequence of bacterial colonization of tissue which has already undergone necrosis - usually due ot ischemia
a pattern of necrosis which is liquifactive superimposed on pre-existing coagulative necrosis
biologically active chemical that is not "us"
a chemical which terminates pepide chain synthesis prematurely resulting in toxic, incomplete toxins
puromycin - antibiotic that is so toxic it is not used clinically
strangulation, asphyxia, drowning cause what
systemic anoxia

anoxia is NO oxygen - hypoxia is reduced oxygen
chemical that blocks oxidative phosphorylation in the mitochondria
Chemical that binds to hemoglobind and causes cellular anoxia by reducing the O2-carrying capacity of RBC
carbon monoxide poisoning
CCL4 is metabolized to what in liver -
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
hydroxyl free radicals react with what 3 things
1. unsaturated lipids (lipid peroxidation)
2. DNA
3. proteins
vitamin E, ascorbic Acid, and glutathione are all
antioxidant - protect against free radical damage
cisPlatinum is used in
chemotherapty for cancer
what are the two limiting toxicities of cisPlatinum
Renal fairlure
forms covalent bonds w/ variety of macromolecules (e.g DNA) and is toxic to tissue which need DNA synthesis
how might you counter act the cytotoxicity seen in cisPt
keep pt well hydrated - give cisPt as prolonge infusion, treat for a day and then rest the patient

alater the chemical fom of cisPT
acetaminophen is metabolized by what - to what
by p450 to NAPQI
w/ acetaminophen - it is the rise in what that reacts with hepatic proteins
rise in NAPQI which is normally metabolized to mercapturic acide by glutathione untill that system is overwhelmed
a general term for a analog of molecule normally active in cellular metabolism may block pathway or shift equilibrium
inorganic Hg injures cells how
combines with -SH and inactivates many enzymes
the replacement of one adult cell type by another adult cell type
literally "disordered growth"
what cell change is seen in normal lactational change in the breast
epithelial hyperplasia w/in lobule
heart failure and venous obstruction may cause edema through what mechanism
increased intravascular hydrostatic pressure
burns, inflammation, and chemical injury may cause Edema by what mechanism
increased permeability of vessel walls
neoplasia, post-surgery, parasites might cause edema by what mechanism
lymphatic obstruction or destruction
increased volume of blood w/in a specific vascular bed

syn: congestion
active hyperemia
increased flow to an area
passive hyperemia
decreased outflow of blood from area
flow of blood from the vascular compartment
3 factors determining the clinical significance of a hemorrhage
volume of blood
rate of bleedin
site where the hemorrhage occurs
blood during a hemmorrhage may accumulate as a what in an organ
minute hemorrhages in skin and mucous membranes
a little larger thatn petechiae
larger than purpura - bruise
ecchymosis - bruise
couphing up blood from larynx, trachea, bronchi
vomiting blood
esophageal varices will result in what - couphing or vomiting blood
hematemesis - vomiting blood
will a sudden loss of blood leave a pt anemia
no - they will be hypovolemic and hypotensive but until fluid portion of the blood is replaced the red cell concentration is diluted
difference between hypoxia and anoxia
hypoxia - low O2

anoxia - no O2
gross morphology of a bland infarct
tissue is pale, "anemic", white
Hemorrhagic infarct
bleeding into dead tissue
what kind of necrosis is the hallmark of infarction
what are some changes seen in infarction
cells become eosinophilic, nuclei shrink, become hyperchromatic, less distinct, and then break up

neutrophils infilrate to digest dead tissue, Macrophages
scarring may result
pulmonary infact caused by ischemia is most often due to
embolus - and usually wedge-shaped
backward heart failure is do to? also called?
failure to pump blood out of veins and often called congestive failure
forward heart failure occurs do to what?
failure to pump blood into the arteries with sufficient pressure to perfuse the organs - can cause ischemia
global heart failure
failure having elements of both backward and forward failure
heart failure can often cause congestion in what two organs
lungs, liver
heart failure causes what kind of edema
pitting edema as well as edema in lungs and liver
chronic congestion of the liver is one result of of what kind of heart failure
right sided heart failure (backward heart failure)
"nutmeg liver" refers to
congested liver
what is the difference between thrombus and clot
clot is coagulated blood outside the vascular system - anywhere

thrombus is coagulated blood w/in the vascular system
Virchow's triand includes
1. injury to vessel wall
2. increased blood coagulability
3. decreased flow
the most important factor in thrombosis
endothelial injury
injury to the endocardium and or decreased flow following myocardial infarction may lead to what kind of thrombosis
ventricular mural thrombosis
this type of thrombosis may occur due to endothelial injury (i.e bacterial) or hypercoagulbility states
thrombosis of heart valves
two types of venous thrombosis
phlebothrombosis (statis)
thrombophlebitis (inflammation)
thrombosis caused by statis of blood in uninflammed veisn and the most clinically significant form of thrombosis
thrombosis in inflammed veins is referred to as thrombophlebitis and can be what two kinds
sterile (due to trauma, radiation, or chemicals) and septic (due to bacteria)
four outcomes of thrombosis
1. lysis (dissolution) = resolution
2. organization
3. propagation towards the heart
4. embolization to the lungs
a detached intravascular solid, liquid or gaseous mass that is carried by the blood to a distant site from its point of origin
how might the outcome of a pulmonary thromboemboli differ depending on the size of the artery
report for
large arteries
small artery: silent unless septic
med artery: wedge shaped infarct
lg artery: RH failure sudden death, cardiogenic shock
loss of blood plasma causes what kind of shock
cardiac pump failure causes what kind of shock
loss of vascular tone results in what kind of shock
systemic vasodilation results in what kind of shock
how does cardiogenic and septic shock differ interms of CO
CO is down in cardiogenic and up in septic
systemic thromboemboli is usually caused by
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
fat embolism results from
trauma to fat tissue, burns

causes pulmonary insificiency, neurologic symptoms, anemia etc.
air embolism occurs under what two circumstances
1. acute decompressio sickness (high to low pressure)
2. chronic decompression sickness (caissen disease - persistant gas bubbles)
a decreased systemic perfusion of tissue caused by decreased effective ciculating blood volume or decreased cardiac output
foam cells , often times at the root of the aorta, seen in children ages 5-9
fatty streaks

precurser to atheroma
in subendothelium
6 stages of therosclerosis
1. Fatty Dot (isolated foam cells)
2. Fatty Streaks
3. Intermediate
4. Atheroma
5. Fibroatheroma
6. Complicated Plaques
fibroatheroma involves what
atheroma + collagen proliferating around fat, cholest, CE
atheroma includes what layers
extends into media

center tends to undergo necrosi, usually asymptomatic, covered by fibrous cap facing the lumen of vessel.
what age - atheroma
ages 30s to 40s
in what stage of atherosclerosis does fibrous cap occur
atherosclerosis is a type of
arteriosclerosis (hardening of the arteries)

atherosclerosis is a chronic inflammatory disease of the large arteries

marked by intimal thickening and lipid accumulation
the four possible clinical manifestations of atherosclerosis
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
localized abnormal dilation of blood vessell or wal of heart which ruptures and causes hemmorrhage
more than 50% of all deaths are due to
key processes in atherosclerosis
intimal thickening and lipid accumulation
narrowing of the vessel lumen
occlusion due to atherosclerosis could happen by what three mechanisms
1. thrombosis on plaque
2. Hemorrhage into plaque
3. atheroembolus

which all result in mI, cerebral infarct, gangrene
what is the injury hypothesis which explains pathogenesis of atherosclerosis
atherosclerosis is a chronic inflammatory response to the arterial wall initiated by injury to endothelium
2 aspects to homeostats
1. maintain blood in a clot free, fluid state
2. induce rapid and localized hemostatic plug at the site of vessel injury
four stages of hemostasis
1. vessel wall: vasoconstriction-neurogenic
2. Primary Hemostatis - platelets (adh, act, aggre)
3. Secondary hemostasis (coagulation cascade)
4. thrombus and Anti-thrombic events
3 main procoagulative things that endothelial cell does
1. storage and release of VWF-FVIII
2. Vasocontstriction (endothelin) and vasodilation (NO, prostacyclin)
3. Secretes FVIII
VWF binds what on the platelet
VWF binds what on Endothelial cell
FVIII (which degrades rapidly when no bound to VWF)
what activates VWF
thrombin, Fibrin, Histamine
VWF binds what on the subendothelium
platelet aggregation is due to what binding
platelet (GPIIb/IIIa - fibrinogen - GPIIb/IIIa etc)
what is deficient in Glanzmanns Thrombasthenia

no fibrinogen bridging!
what is missing in Bernard-Souler syndrome
GP1b (on platelet) binds VWFand is important in primary hemostatis
what two factors activate/increase platelet aggregation
ADP and TxA2

activates GPIIb/IIIa - VWF
when platelets contract and decrease injury site
platlets are measured what two ways
1. platelet aggregation
2. Bleeding time test
Aspirin inhibits irreversible
inhibition of inappropriate platelet aggregation can prevent stroke, ischemia is what theory
anti-platelet theory
selectins bind
Immunoglobulin binds
what effect does plasmin have on fibrinogen and fibrin
Factor XIIIa does what
stabalizes fibrin clot by crosslinking lysine and glutamine side chains of Alpha and gamma chains -
Quaternary Complex
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
K dependent factors
PECAM1, ICAM-1, and VCAM-1 are all
in the immunoglobulin superfamily
Factor V Leiden mutation
FActor V cannot be destroyed by aPC
DDAVP works to treat vWF defects by
mimicking vasopresson and increasing the release of vWF+ FVIII
prothrombin 2010 mutation results in
increase in prothrombin (factor II) due to increase in mRNA stability
Ab binds platelet factor 4 which then binds heparin which increases thrombin due to platelet activation of endothelial cell
Heparin-induced thrombocytopenia
what is one anticoagulant factor which decreases the synthesis of procoagulant factors
oral vit K antagonist e.g comadin
anti-coagulant atht inhibits the action of thrombin (and factor Xa)
Heparin derivitives, R-huidin
coagulation cascade happens during the primary or secondary hemostatis ?
how does heparin work
anti-thrombin III binds heparin

conf change in anti-thrombin (active site exposed)

inhibits factos 9-12
what is the Protein C pathway
Thrombin binds Thrombomodulin (EC)

activates Protein C
Protein C plus Protein S
inhibit FVa, FVIIIa and inhibit the oagulation cascade
protein C is what dependent
Vit K dependent - so Vit K deficieciency may cause thrombosis
is important in remodeling clot and opening up occluded vessels
Fibronolytic system
where is vWF, FV, HMWK, PF4, fibrinogen, PDGF, TFG located w/in the platelet
Alpha granule

note: ADP, ATP, serotonin, calcium are located int he dense body
life of platelet in circulation