Term
Three abnormalaties that lead to thrombus formation
(virchows triad)
What are they |
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Definition
Endothelial injury
Stasis or turbulent blood flow
Hypercoagulability of blood |
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Term
Hypercoagulability of Blood
Effect of:
Leiden mutation
Homocysteine
Prothrombin Gene
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Definition
Leidein Mutation: Mutation in Factor 5 that makes it resistant to cleavage by protein C. Increases DVT
Elevated levels of homocysteine in arterial and venous thrombosis
Mutated thrombin has decreased binding affinity for antithrombins |
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Term
Heparin-induced thrombocytopenia(HIT) syndrome
Unfractionated heparin causes what?
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Definition
Unfractionated heparin may induce antibodies that bind to platelets
Binding of antibodies causes activation, aggregation and consumption of platelets(thrombocytopenia)
Platelets and endothelial damage combine to produce a prothrombotic state
May lead to DIC |
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Term
Lines of Zahn
What do they indicate about a thrombus? |
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Definition
Lines of zahn indicate that a thrombus formed in flowing blood.(that the patient was alive when it formed)
Most apparent when formed in Heart or aorta |
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Term
Life cycle of thrombi
Name and describe the 4 stages. |
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Definition
Propagation: Accumulate platelets and fibrin
Embolization: Thrombi Dislodge and travel
Dissolution: result of finbrinolysis. t-PA effective in first hours when thrombi are still small.
Organization and recanalization: Old thrombi have ingrowth of endothelial, smooth muscle and fibroblasts |
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Term
Pulmonary Embolism(PE)
Where are they commonly from?
What is a saddle embolus?
Multiple emboli will cuase what? |
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Definition
Most come from DVT and are silent(incorporated)
Saddle embolus blocks main pulmonary artery causing sudden death
Multiple emboli can cause pulmonary hypertension adn right ventricular failure
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Term
Fat and Marrow Embolism
Where do they come from?
Symptoms? |
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Definition
Fat and marrow embolism come from Fractures of long bones
Symptoms: Tachypnea, dyspnea, tachycardia
Diffuse petechial rash related to thrombocytopenia |
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Term
Amniotic Fluid Embolism
Incidence and fatality?
Symptoms?
What Causes?
Histology?
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Definition
Low incidence, high fatality
Sudden dyspnea, cyanosis, shock
Pulmonary edema and DIC follow
Cause: Squamous cells shed from fetal skin, lanugo hair, mucin from fetal respiratory tract
Histology: Laminated swirls |
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Term
White Infarct
vs
Red Infarct |
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Definition
Red infarct: venous occlusions where blood can collect in infarcted zone, dual circulation.
White infarct: Arterial occlusoins in solid organs with end-arterial circulation(heart, spleen, kidney) and where tissue density limits seepage of blood from adjoining capillary beds into necrotic area |
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Term
Cardiogenic SHock
vs
Hypovolemic SHock
What causes each?
What is the clinical appeareance?
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Definition
Cardiogenic shock:
low cardiac output due to myocardial pump failure
(infarcation, arrtheymias, Cardiac tamponade, PE)
Hypovolemic Shock
Low cardiac output due to loss of blood or plasma volume
(massive hemorrhage or fluid loss from severe burns)
Both have hypotension; weak rapid pulse; tachypnea and cool clammy cyanotic skin |
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Term
Septic Shock
Clinical sign?
Clotting problems? |
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Definition
Vasodilation and peripheral pooling of blood as part of an immune reaction to infection (skin warm and flushed)
Complement & cytokine prodction activate endothelial cells
↑ TF productoin ↑PAI-1 Factor 12 also activates coagulation
Thrombosis, increased vascular permeabiliby, vasodilation
Causes DIC in half of septic patients
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Term
Septic Shock
What casues?
(what activates mononuclear cells and what do they release)
Metabolic Abnormalities? |
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Definition
Most cases are endotoxin gram - bacilli. LPS & O antigen
LPS binds CD14 → Activation of mononuclear cells →
TNF/IL-1: Systemic vasodilation, wide spread endothelial injury and activation
Septic patients have insulin resistance and hyperglycemia
Waterhouse-friderichsen syndrome:
Usually caused by neisseria meningitides
Adrenal necrosis due to DIC
Defecit in glucocorticoid production
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Term
Stages of Cardiogenic & Hypovolemic shock
Non-progressive?
Progressive?
Ireversible?
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Definition
Non-progressive phase/ Compensatory
Neurohormonal mechanisms maintain cardiac output and BP. Catecholamine release/sympathetic, rennin-angiotensin
Tachycardia, peripheral vasocostriction, renal conservation of fluid
Progresive Stage
Tissues go hypoxic→ anaerboic glycolysis → Lactic acidosis
Arterioles dilate and blood begins to pool in microcirculation(increase in BP -> edema)(DIC)
Irreversible Stage
Tissue and cell injury so severe that even if hemodynamic defects are corrected survival is not possible. (Adenosine has leaked out of cells so no ATP)
Lysosomal enzyme leakage, myocardial function worsens(NO synthesis)
Acute tubular necrosis(kidney) |
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Term
Chronic Thrombocytopenic Purpura(ITP)
What cuases?
Typical Hx?
PT & PTT & bleeding time?
Whats the difference from Acute immune thrombocytopenic purpura? |
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Definition
Autoantibodies to platelet glycoproteins IIB-IIa, usually IgG
Adult woman, history of easy bruising, nosebloods, hemorrhages form minor trauma.
PT & PTT are normal (Both measure clotting factors, so any thrombocytopenia will not effect)
Bleeding time will be increased.
Acute immune thrombocytopenic purpura usually occurs in children after a viral illness or heparin therapy. |
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Term
Thrombotic Microangiopathies:
What is it?
Hemolytic Uremic SYndrome, Causes?
TTP, Causes? |
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Definition
Thrombosis in cappilaries and arterioles that lead to thrombocytopenia.
Hemolytic uremic syndrome: E. Coli infeciton.
Thrombotic thrombocytopenic purpura(TTP): Defect in ADAMTS12(vWF metalloprotease) Degrades high molecular weight multimers of vWF |
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Term
Factor 8 and vWF
What is their relationship?
Ristocetin agglutination test? |
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Definition
Factor 8 binding to vWF stabilizes factor 8
vWF function assesd using ristocetin agglutination
Defective vWF will not bind risocetin and will not cause agglutination
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Term
Von willebrand Disease
CLotting Tests?
Defect?
Types?
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Definition
Defect in vWF
Most common bleeding disorder
PTT prolonged(because vWF stabilies factor 8)
Type I and III vWD have reduced circulating quanitity of vWF
Type II is qualitative defects in vWF |
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Term
Hemophilia A
What factor is mutated?
Genetics?
Blood tests? |
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Definition
Hemophilia A is a factor 8 defect
X-linked recessive(males have it)
Most severe is inversion X chromosome that stops synthesis
Petechiae are absent
Prolonged PTT(intrinsic) and normal PT |
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Term
Hemophillia B
(christmas disease)
Mutation in what?
Genetics?
Tests? |
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Definition
Mutation in factor 9
(factors 8 & 9 activate 10)
X-linked recessive(Males get it)
PTT(Intrinsic) is prolonged and pt is normal |
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