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51 Cards in this Set
- Front
- Back
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what is the difference between edema and effusion |
edema is accumulation in the tissues, effusion is accumulation of fluids in the cavities |
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What are the altered pressures that are associated with the movement of fluid outside of the vessels |
elevated hydrostatic pressure and diminished colloid osmotic pressure |
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how do you distinguish between the fluids of inflammatory and non inflammatory edema |
inflammatory edema- protein rich exudate
noninflammatory edema- protein poor transudate |
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what occurs almost immediately after vascular injury? |
arteriolar vasoconstriction to limit blood flow to injured area |
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what is exposed during vessel injury that begins the process of primary hemostasis |
vWF and collagen which promote platelet adeherence and activation. The clumping platelets release their own factors that recruit further platelets to form the primary hemostatic plug |
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what characterizes secondary hemostasis |
the deposition of fibrin
tissue factor binds and activates factor VII and culminates with thrombin generation.
thrombin converts fibrinogen to fibrin which results in a fibrin clot formation |
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how are clots stabablized and resorbed? |
contraction of fibrin clot to form a permenant plug.
when sufficient time has passed counter-regulatory mechanisms (t-PA) dissolve the clot and tissue is repaired |
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GpIb and vWF binding facilitates what clotting process |
GpIb is expressed on the surface of the platelet and binds to exposed vWF on the injured vessel to adhere platelet to injury site |
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what is the shape of platelets before and after adhesion |
before- smooth disk
afterwards - spiky "sea urchin" |
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what is TxA2? how can we pharmacologically manipulate it? |
TxA2 is released by activated platelets to recruit more platelets to injury site
it is a prostoglandin which is produced from Arachadonic acid via cyclooxygenase (COX). COX is irreversibily inhibited by asprin. Therefore asprin will lower TxA2 levels and produce a minor anticoagulant effect. |
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what test in lab assesses the integrity of the extrinsic pathway? what factors are involved in this pathway? |
PT prothrombin time.
factor VII leads to factor X activation (factor X is the initiator of the common coagulation pathway)
factor VII is activated by exposure to tissue factor which is a sign of vascular damage |
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what test in lab assesses the integrity of the intrinsic pathway? what factors are involved in this pathway? |
PTT (XII, XI,IX,VIII) activated factor 9 activates factor 10 which is initiator of common pathway. Factor 10 activates prothrombin
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How does thrombin affect its upstream products? |
thrombin activates XI, and 2 very important co-factors V and VIII these amplify the coagulation cascade |
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what inactivates Va and VIIIa and what does it require to do it? What activates it |
Protein C, it requires protein S. Protein C is activated by thrombomodulin |
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In addition to activating the coagulation cascade thrombin also is a mediator of _______________ and _______________________ |
platelet activation and pro-inflammatory effects such as monocyte, lymphocyte activation, as well as neutrophil adhesion |
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What important factors circulate to prevent platelet activation |
ADPase PGI2 NO |
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How do heparin like molecules affect coagulation |
heparin binds and activates AT-III which then goes on to inhibit thrombin and many other factors involved in the clot cascade. |
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what is a petechiae? a purpura? what deficits of primary hemostasis can result in the presense of them |
1-2 mm microhemorrhages (pupura >3mm)
platelet defecits and most commonly vWF disease |
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what condition will occur if blood loss exceeds 20% of total blood volume |
hemorrhagic (hypovolumic) shock |
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what 3 primary abnormalities characterize the virchow triad |
endothelial injury stasis/turbulent blood flow hypercoagulability
together predispose individual to thrombosis |
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What can activated cytokines do that could push someone toward thrombosis |
downregulated thrombomodulin resulting in prolonged effect of activated thrombin |
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How does turbulent flow push an individual toward thrombosis (3) |
promotes endothelial activation due to endothelial injury
pushes platelets toward endothelium
prevents washout and dilution of activated clotting factors |
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what is a common primary hypercoagulability stated that is inherited |
factor V leiden |
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how does the factor V leiden mutation create a hypercoaguable state |
makes factor V resistant to inactivation by activated protein C (which is activated by thrombomodulin when thrombin is present. usually limits formation of clots) |
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what is a benefit of using LMW-heparin |
less likely to induce HIT because it is more specific in its target (just heparin) |
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describe the pathogenesis of antiphospholipid antibody syndrome |
antibodies attack plasma glycoprotein B2-glycoprotein1 which induces hypercoaguable state.
this is often seen in systemic lupis |
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where are lines of zahn seen? what are they useful for distinguishing? |
in thrombi. if you see them it means the thrombi formed in flowing blood (ie: before death) |
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what do you cal a thrombi that occured in the heart chambers or aortic lumen |
mural thrombus |
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what is a vegetation? |
thrombus that occurs on a heart valve |
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what systemic disease is associated with libman-sacks endocarditis and develobment of vegetations |
lupus erythematosus |
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how do thrombi cause clinical issues |
occlusion at primary site or embolization to secondary occlusion site. phleboembolism from DVT often results in a PE |
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where do pulmonary emboli most often originate from |
leg DVT's (deep vein thrombosis) |
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what is a saddle embolus |
a pulmonary embolus that straddles the pulmonary bifurcation |
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if 60% of the the pulmonary circulation is obstructed cor pulmonale can occur. what is that? |
sudden right sided heart failure |
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where do most systemic emboli arise? |
mural thrombi (mostly ventricular wall deficits) |
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what is strange about a paradoxical embolism |
it originates in the venous system and makes it to the arterial system. This can only happen if there is an intra-atrial or intra-ventrcular deficit. |
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when do you often see a fat or marrow embolism? |
after fractures of long bones |
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what is an air embolism? |
gas bubles in circultion that can culminate with frothy masses forming that obstruct flow and cause distal infarct |
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what type of thrill-seekers can experience air emboli? |
scuba divers who are coming back up and fighter pilots undergoing rapid ascent.
any rapid increase in pressure can cause gases that are dissolved in the blood to to leave solution.
this is commonly refered to as "the bends" |
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What type of embolism is the 5th leading cause of maternal mortality? how does it arise? |
amniotic fluid embolism
it arises from infusion of amnionic fluid into maternal circulation often via tear of the placental membrane or uterine veins surrounding the placenta |
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what 2 causes underlie the vast majority of infarctions |
arterial thrombosis or arterial embolism |
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what is the appearance of a red infarct? where do you see it |
red hemorrhagic infarcts that often appear wedge shaped
loose spongy tissues, tissues with dual circulation, venous occlusions... |
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where do white infarcts occur |
solid organs, points of end circulation
they have solid borders, as tissue density limits seepage of additional blood into necrotic area |
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what type of necrosis occurs in the brain |
liquefactive |
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how long can neurons be derived of blood before they are irreversibly damaged |
3-4 minutes |
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how long can myocardial cells be derived of blood before they are irreversibly damaged |
20-30 minutes |
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define cardiogenic shock |
low cardiac outupt due to myocardial pump failure |
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define hypovolemic shock |
low cardiac output due to low blood volume |
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systemic inflammation is often associated with shock. what are some conditions that cause systemic inflammation |
microbial infections, burns, trauma, pancreatitis |
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what organisms most commonly trigger shock |
gram + bacteria gram - bacteria fungi |
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What are PAMPS? how can they initiate a shock response |
Pathogen associated molecular patterns. They are recognized by toll like receptors which trigger inflammatory cascade.
Counterregulatory mechanisms can oscillate a balance between TH1 (pro inflammatory) and TH2 (anti-inflammatory immunosupressed) states throughout clinical course |
