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48 Cards in this Set
- Front
- Back
- 3rd side (hint)
Describe the action of the following endothelial anti-coagulation factors:
Thrombomodulin, Heparin-like molecule, Thrombin receptor, tissue Plasmin activator. |
Thrombomodulin (receptor)-->binds Thrombin--> + Protein C.
Heparin-like molecule (receptor)-->binds Antithrombin III---| Xa, IXa. Thrombin receptor --> Endothelial effects--> Prostacyclin (PGI2), NO, ADP --> inhibit aggregation tPA --> Fibrinolytic cascade |
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A thrombotic mass that forms on a cardiac valve
(less commonly, on cardiac mural endocardium) is known as _____. |
A vegetation .
(may produce thromboemboli: Rt heart - embolus to lungs, Lt heart - embolus to brain, spleen, kidney) Frequently seen w/ infective endocarditis |
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What is a paradoxical embolus?
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When a right-sided cardiac thrombus crosses a patent Foramen Ovale and enters systemic arterial circulation.
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Define Trouseeaus' syndrome:
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Hypercoagulable state w/ malignant neoplasms--> arterial & vanous thromboses.
(also seen in some Cancer pts) |
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Define Adenocarcinoma.
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A malignant neoplams arising from glandular epithelium --> forms a mass lesion
(endocardial metastases rare) |
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Where would you find an atheroma?
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Typically form in Arteries
(not in heart valves) |
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Define "Chronic passive congestion"
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capillary, sinusoidal, or venous stasis of blood w/in an organ. (i.e. lung, liver)
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Also called "Nutmeg Liver"
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Define "Mural Thrombus"
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Thrombi that form on the surfaces of the heart or LARGE arteries.
(not trombotic lesions on cardiac valves) |
May include cardiac chamber, dilated aorta, or major aorta branch.
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Define Petechiae
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Pin-point hemorrhage.
Remember the scale: Petechia<Purpura<Echymoses<Hematoma (Dr. Knollman) |
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Where would you likely see "Phlebothromboses"?
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In Large Veins
(LV stasis --> phlebothrombosis; swelling w/ pain and tenderness of LE) |
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Pulmonary Edema
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Ccommon clinical problem. Typically from Left-ventricular failure.
Also: Renal failure, acute resp. distess syndrome, P. infections, hypersensitivity rxns. |
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1-3 days following Long bone fracture, pt presents w/ dyspnea & tachycardia.
Name the respiratory complication. |
Fat embolism.
Microscopic fat globules enter blood (delayed) from fractured long-bone marrow. (Cause both mechanical & chem damage) |
May present w/ thrombocytopenia
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61 y/o pt presents w/ incr. serum AST, ALT; lower leg swelling; prominent JVD; nut-meg liver. What's underlying condition?
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Congestive Heart failure = Rt side.
(with liver necrosis & chronic passive congestion |
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Cholestasis can commonly arises from what?
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Biliary tract obstruction.
(seen w/ icterus) |
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Define Icterus
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Jaundiced
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Name the most common cause of DVT.
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Vascular stasis (from immobility)
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What is the role of Nitric Oxide (NO) in clotting?
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Platelet aggregation INHIBITOR
(also a vasodilator... & microbicidal) |
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What is role of Aspirin in clotting?
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Aspirin INHIBITS platelet functioning.
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What is role of Calcium in clotting?
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Calcium is a cofactor in coagulation pathway.
But hypercalcemia --| minimal effect on clotting. |
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25 y/o woman presents w/ m.status change w/in 24 hrs; rt temporal hemorrhagic infarction (mid Cerebral A occluded). Hx includes pulmonary embolism, miscarriage, false-pos test for syphilis. Also: increased PTT; normal platelets. Likely cause?
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A hypercoagulability. Pt has anti-phospholipid-protein antibodies (lupus anticoagulant). Seen both with and w/o SLE. Ab binds cardiolipin (syphilis indicator).
Sx: recurrent arterial, venous thrombosis & miscarriages. |
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Define Von Willebrand disease.
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Platelet adhesion deficit Gp1b receptor on platelet has nothing to bind to --> minimal platelet aggregation -->tendancy to bleed
(not thrombotic) --vWF produced by normal endothelium (NOT post injury)-- |
vWF produced by normal endothelium (NOT post injury)
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Define: Factor V (Leiden)Mutation
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Coagulation problem.
(PT, PTT normal) Not cleaved; by Protein C. |
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Name mechanism of Tissue plasminogen activator.
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Thrombolytic agent: generates Plasmin -> cleaves fibrin to dissolve clots.
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Name Heparin's mechanism of action on clotting
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Heparin prevents thrombosis by activating anti-thrombin III...
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49 y/o man stablized following ant. left ventricle infarction. 3 days later, develops severe SOB and decreased Ejec Fraction; dies 2 hrs later. Which microscopic changes likely seen in lungs?
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See congestion of alveolar capillaries w/ transudate in alveoli.
(acute Left heart failure-->backed up pulmonary vein --> incr. hydrostatic pressure in capillaries) |
a- fibrin+neutrophils in lungs?
b- congestion in alv. capillaries w/ transudate in alveoli c- alveolar fibrosis w/ hemosiderin macrophages d-purulent exudate in pleural space |
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What happens (expected) in "Decompression Sickness"
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dissolution of Nitrogen (ascending from deep scuba dive) in blood--> forms gas bubbles--> occludes arterioles.
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the bends
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39 y/o woman presents w/ 3-cm carcinoma in left breast. Left breast is slightly enlarged & overlying skin is thickened, reddish-orange, and pitted. What's with the skin?
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Lymphatic obstruction. w/ "peau d'orange" appearance
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venous thrombosis?
lymphatic obstruction? Ischemia? Chronic passive congestion? Chronic inflammation? |
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Pt presents w/ hx of frequent nose-bleeds and increased menstural flow. petechiae & purpura present on skin of lower extemities. Normal PT, PTT, platelet count. Decreased vonWillebrand Factor activity.
Which clotting step affected? |
Platelet adhesion.
Decr vWF affects adhesion step only. |
where's that picture from lecture?
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Define Factor V (leiden) mutation; list incidence.
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Most common genetic hypercoagulability.(2-15% population)
=Factor V mutation resistant to cleavage (Va) by Protein C. --> unchecked coagulation= freq. emboli. (Disorder of 50% of DVT pts) |
(Disorder of 50% of DVT pts)
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How does cigarette smoking affect clotting?
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Forms atherosclerotic plaques on Arterial walls.
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Describe DIC
(Disseminated Intravascular Coagulation) |
Sudden onset of widespread fibrin thrombi in microcirculation...eventually reverses (fibrolytic) --> severe systemic bleeding.
(consumption coagulopathy; present w/ thrombocytopenia) |
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What is simple causes of gangrene?
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ARTERIAL Obstruction
(not venous) |
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Describe interplay between Thromboxane (TxA2) and prostacyclin (PGI2) in platelet aggregation.
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TxA2 (synthesized -COX- from platelets) vasoconstricts and favors platelet aggregation. PGI2 vasodilates and inhibits platelet aggregation.
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What are the 4 stages of normal hemostasis?
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1) Reflex Vasoconstriction
2) Primary Hemostasis (platelet recruitment, adhering) 3) Secondary hemostasis =coagulation cascade. (Thrombin activation) 4) Thrombus/Antithrombotic events (tPA, thrombomodulin release) |
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Describe Shock (cardiovascular collapse)
List the 3 categories |
Systemic hypoperfusison & Hypotension. Decr Cardiac output or blood volume. Affects ==> Brain, Heart, Lungs, Kidney, Adrenals, GI.
1) Cardiogenic - heart "pump failure" 2)Hypovolemic shock - blood/plasma loss 3) Septic shock - mostly by gram-neg infections > gram-pos / fungal |
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Most common cause of Arterial Thrombosis?
Of Venous thrombosis? |
Arterial Thrombosis = Atherosclerotic damage to v endothelium.
Venous = Stasis of blood |
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Dense alpha granules in Platelets contain/release what?
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Primarily ADP. Also: fibrinogen, factor V, extra vWF (besides that on healthy endothelial cells), and factor IV (recruit more platelets)
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Describe Glanzmann's thromboasthenia.
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Deficieny of GPIIb-IIIa: the platelet receptor that binds/cross-links fibrinogen forming platelet aggregates.
"Fibrinogen Glanzes off platelets" lol. |
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What is the function of Thrombomodulin?
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Present on intact endothelium, it binds thrombin & activates Protein C (to inhibit coagulation by cleaving Va & VIIIa)
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What is the role (if any) between diabetes and atherosclerosis?
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Diabetes mellitus accelerates and worsens atherosclerosis.
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Define "Organization & Recanalization" as it pertains to hemostasis.
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The boring of new channels/lumens through a non-dissolved thrombus to allow some blood flow.
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Describe the clinical terms for sizes of hemorrage.
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Petechia (pinpoint)
Purpura (3 mm) Echymosis (1-3 cm) Hematoma (space/cavity-filling) Congestion - occurs w/ vascular dilation/pooling within an organ. |
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A pt w/ 15 yr hx of recurrent thromboses develops septicemia; dies of multiple organ failure. Which organ is spared ischemic injury? (Brain, liver kidney, heart, spleen)
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Liver: it has a dual blood supply (hepatic artery + portal vein)
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In which organs could a "hemorrhagic infarct" be seen?
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Those with dual blood-supply: Lungs, Liver, GI tract...
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What is Aspirin's mechanism of action on clotting?
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Aspirin --| COX --> TxA2 --> platelet aggregation
Aspirin blocks cyclooxygenase pathway of AA metabolism & eicosanoid production --including Thromboxane A2, which causes vasoconstriction, promotes platelet aggregation. |
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Define: anasarca
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generalized edema into subQ connective tissue
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An otherwise healthy woman delivering her full-term infant suddenly turns dyspnic, cyanotic, hypotensive. Seizure & coma follow. What happened? Expected findings?
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Amniotic Fluid Embolism; placental/uterine vein tears at delivery;
Amniotic fluid--> maternal circulation; embolus -->lungs. May see fetal squam. cells, lanugo in maternal pulmonary microcirculation. |
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Describe what PTT tests.
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Patial trhromboplastin time. Screens INTRINSIC path & adequacy of all factors except XIII & VII.
(25-30 sec =normal); Panic >60 sec. Incr w/: lupus anticoagulant, inhibitors (heparin), vWF disease (sometimes), hemophilia A/B, DIC. |
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