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127 Cards in this Set
- Front
- Back
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hemothorax
hemopericardium hemoperitoneum hemarthrosis |
hemorrhage in the:
pleural cavity pericardial sac peritoneal cavity synovial space |
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petechial hemorrhages
petechiae purpura |
small, punctate hemorrhages in the:
skin mucous membranes serosal surface |
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ecchymosis
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diffuse hemorrhage in skin and subcut tissue
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define: hyperemia
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localized increase in the volume of blood in capillaries and small vessels
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define: active hyperemia
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e.g. blushing, inflammation
- localized arteriolar dilation |
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define: passive hyperemia/ passive congestion
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- obstructed venous return, or increased back pressure from CHF
1. acute passive congestion 2. chronic passive congestion |
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acute passive congestion
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seen in shock, acute inflammation, or sudden RHF
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chronic passive congestion of the lung
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- caused by LH failure or MS
1. congestion and distention of alveolar capillaries -> capillary rupture 2. phagocytosis of RBCs -> intra-alveolar hemosiderin-laden macrophages: heart failure cells 3. long standing congestion -> fibrosis and hemosiderin deposition -> 'brown induration' of lung |
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when do you get brown induration of the lung?
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- long standing lung congestion
- due to fibrosis and deposition of hemosiderin |
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what are heart failure cells?
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- hemosiderin laden macrophages seen in chronic passive congestion of the lung
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chronic passive congestion of the liver and lower extremities
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caused by RH failure
- nutmeg liver can occur |
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nutmeg liver
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- caused by chronic passive congestion of the liver (RH failure)
- produced by dilated, congested central veins and the surrounding brownish-yellow, fatty liver cells |
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what is an infarct?
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- necrotic tissue from ischemia
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anemic infarcts
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- white or pale infarcts
- caused by arterial occlusions in the heart, spleen and kidney |
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hemorrhagic infarcts
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- red infarcts: RBCs ooze into the necrotic area
- occur in lung and GI tract b/c of arterial occlusion. These sites have redundant blood supplies -> hemorrhage into the infarct - can also be caused by venous occlusion |
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what are venous occlusion hemorrhagic infarcts associated with?
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- venous infarcts contribute to volvulus, incarcerated hernias, and postoperative adhesions
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define: volvulus
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twisting of the stomach or large intestine.
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what predisposes a patient to thrombosis?
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- venous stasis
- CHF - polycythemia - sickle cell disease - visceral malignancies - OCPs with smoking |
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define: polycythemia
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increase in red blood cells in the body. The disease has three forms. Polycythemia vera involves over production of red blood cells, white blood cells, and platelets. Secondary polycythemia is a complication of diseases or factors other than blood cell disorders. Stress polycythemia involves decreased blood plasma.
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platelet functions
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1. maintain integrity of the vascular endothelium
2. endothelial repair by making PDGF 3. platelet plugs 4. coagulation cascade through the platelet phospholipid complex |
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platelet adhesion
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vessel injury exposes subendothelial collagen -> platelet adhesion -> interaction of platelet specific surface glycoprotein receptors and subendothelial collagen (mediated by vW factor)
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what does von Willebrand factor do?
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- mediates the interaction of surface platelet specific glycoprotein receptors and subendothelial collagen
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platelet release reaction
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- after adhesion to the subendothelial surface, platelts release:
- ADP - 5-HT - histamine - PDGF - other platelet granule constituents |
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list the throbogenesis 'cascade'
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1. platelet activation
2. platelet release reaction 3. activation of coagulation cascade 4. Arachidonic acid metabolism 5. Platelet aggregation 6. Stabilization of platelet plug 7. limitation of plug formation |
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how do platelets activate the coagulation cascade?
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- conformational change in the platelet membrane makes platelet phospholipid complex available -> coagulation cascade -> thrombin
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platelets and arachadonic acid metabolism
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- once the platelet membrane phospholipase is exposed, arachidonic acid becomes thromboxane A2 (TxA2) via the COX pathway
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what is TxA2 derived from?
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arachadonic acid via the COX pathway
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what effector action does TxA2 have?
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- potent vasoconstrictor and platelet aggregant
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what is the difference between platelet aggregatin and adhesion?
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- aggregation: stick to each other
- adhesion: stick to subendothelium |
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what happens during platelet aggregation?
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- platelets stick to each other
- additional platelets are recruited from blood to produce initial plut - mediated by glycoprotein IIb-IIIa complex |
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what does the glycoprotein IIb- IIIa complex do?
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- found on the surface of platelets
- mediates linking of platelets during aggregation by fibrinogen bridges |
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what promotes aggregation?
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- ADP
- thrombin - TxA2 - collagen - epi - platelet activating factor |
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how are platelet plugs stabilized?
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- by fibrinogen bridges
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what limits platelet plug formation?
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- I class prostacyclin (PGI2)
- synthesized by endothelial cells through COX pathway - PGI2 is an antagonist to TxA2 - fibrin degredation products also limit platelet aggregation |
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what do intact endothelial cells do?
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- work to oppose coagulation after injury by thromboresistance
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list some functions of endothelial cells
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1. produce heparin-like molecules
2. secrete TPA 3. degrade ADP 4. inactivate and clear thrombin; synthesize thrombomodulin 5. make protein S, PGI2, and NO |
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what are heparin-like molecules?
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- made by intact endothelial cells
- are endothelial proteoglycans that activate antithrombin III, which neutralizes throbin, IXa, and Xa |
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define: plasminogen
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an inactive form of plasmin that occurs in plasma and is converted to plasmin by organic solvents
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define: plasmin
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an enzyme that dissolves the fibrin of blood clots
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what is thrombomodulin?
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a cell surface protein that binds thrombin and coverts it to an activator of protein C
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what does protein C do?
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- a vit K dependent plasma protein
- activated protein C (APC) cleaves Va and VIIIa -> inhibits coagulation |
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what does protein S do?
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- is a cofactor for APC (activated protein C)
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describe the extrinsic clotting cascade
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- initiated by tissue factor
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what is tissue factor?
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Tissue factor, also called thromboplastin, factor III or CD142 is a protein present in subendothelial tissue, platelets, and leukocytes necessary for the initiation of thrombin formation from the zymogen prothrombin.
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what does factor XIII do?
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prothrombin mediated cleavage of fibrinogen results in a firbin monomer.
- factor XIII polymerizes and stabilizes this monomer -> fibrin clot |
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how is the action of tissue factor-factor VIIa limited by?
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the tissue factor pathway inhibitor
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how do you evaluate the extrinsic pathway?
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prothrombin time (PT)
- a measure of II, V, VII, X, and fibrinogen |
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intinsic clotting cascade
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- contact activation with contact factors:
- XII (Hageman factor) - prekallikrein - high molecular weight kininogen - factor XI |
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how else might the intrinsic clotting cascade be activated?
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- most likely initiated by tissue factor-factor VIIa complex
- possibly by the platelet phospholipid complex |
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how do you evalute the intrinsic pathway?
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partial thromboplastin time (PTT)
- measure of II, V, VIII, IX, X, XI, XII, and fibrinogen |
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fibrinolysis
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1. proenzyme plasminogen -> plasmin
2. plasmin splits fibrin |
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what is so special about factor XII to XIIa activation?
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- links the fibrinolytic, coagulation, completment and kinin system
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what are some antithrombotic diseases?
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1. hemophilia
2. Christmas disease 3. von Willebrand disease |
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list the hereditary thrombophilias
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1. factor V leiden
2. prothrombin 20210A transition 3. methylene tetrahydrofolate reducatse mutation |
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general notes about hereditary thrombophilias
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- prothrombotic
- occurs in adolescents and young women - recurrent venosu thrombosis and thromboembolism |
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what can cause hereditary thrombophilias?
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- deficiency in:
antithrombin III protein C protein S |
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Factor V Leiden
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- most freq cause of hereditary thrombophilia
- abnormal factor V protein -> altered cleavage site targed by APC -> prevents inactivation of Va |
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prothrombin 20210A transition
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- second most common cause of hereditary thrombophilia
- a G to A mutation in the 3' untranslated region of the prothrombin gene - associated with elevated plasma prothrombin levels and an increase in venous thrombosis |
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methylene tetrahydrofolate reducatase mutation (MTHRF C677T)
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- increase in serum homocysteine -> arterial and venous thrombosis
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how do you treat MTHRF C677T?
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- can reduced the increase in homocystein by dietary supplementation with folic and vit B6 (pyridoxine) and B12 (cobalamin)
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what sort of birth defects are associate with MTHRF?
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neurla tube defects
- possibly a range of neoplasms |
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which factors, when increased, are also associated with venous thrombosis?
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- factor VIII
- factor IX - factor XI - fibrinogen |
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antiphospholipid antibody syndrome
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- prothrombotic disorder
- autoantibodies (aPl) directed against protein antigens complexed to phospholipids |
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what are the clinical symptoms of antiphospholipid antibody syndrome?
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- recurrent venosu and arterial thromboembolism
- fetal loss - thrombocytopenia - neurologic manifestations |
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why is antiphospholipid antibody syndrome a misnomber?
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the target antigen of aPL is not phospholipids but actually plasma proteins that bind to phopholipids (eg: [[β2-glycoprotein 1]] or prothrombin).
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how is antiphospholipid antibody syndrome often diagnosed?
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- prolonged PTT
- it's paradoxical, b/c prologned PTT is usually associated with antithrombotic syndromes - instead, antiphospholipid antibodies bind with the phospholipid reagent used in the PTT test -> prolonged PTT |
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what is antiphospholipid antibody sydrome sometimes associated with?
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- SLE
- thus, an antiphospholipid antibody that prolongs PTT is often called the 'lupus anticoagulant' |
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what is a antiphospholipid antibody associated with SLE?
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- anticardiolipin antibody. can caused false positive serologic test for syphilis
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Disseminated intravascular coagulation (DIC)
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- both a prothrombotic and antithrombotic disorder characterized by widespread thrombosis and hemorrhage
- caused by consumption of platelets and coagulation factors |
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heparin induced thrombocytopenia (HIT) syndrome
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- heparin-induced thrombocytopenia and thrombosis
- a consequence of therapy with high molecular weight heparin - caused by antibodies to the complex of heparin and platelet factor 4 (PG4) |
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describe arterial thrombi
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- formed in areas of active blood flow
- when they mature -> lines of Zahn - eventually liquify and disappear, or become recannalized |
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describe venous thrombi
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aka. phlebothrombosis
- formed in areas of less active blood flow - predisposed by stasis - dark red color, with higher concentration of RBCs than arterial thrombi - no lines of Zahn (or barely seen) - associated with venous inflammatory changes: thrombophlebitis |
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what is thrombophlebitis?
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- inflammation of veins with thrombus formation
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postmortem clots
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- appear soon after death
- not true thrombi- are not attached to vessel wall |
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describe the appearance of postmortem clots
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- two layered appearance from RBC settling:
1. in RBC-rich layer: currant jelly appearance 2. in RBC-poor layer: chicken fat apperance |
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where do venous thrombi most often occur?
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- veins of the lower extremities
- perprostatic veins - other pelvic veins |
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thromboembolism
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- fragments of thrombi
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pulmonary emboli
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- cause sudden death
- usually occur in immobilized patients or those in CHF |
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what are saddle emboli?
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- a type of PE that is so large that it obstructs the bifurcation of the pulmonary artery
- can cause suddent death |
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what do intermediately sized emboli do?
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- cause pulmonary hypertension and acute right ventricular failure
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describe hemorrhagic pulmonary infarcts
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- wedge shapebed
- located just beneath the pleura - cuased by pulmonary infarction |
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where do arterial emboli originate from?
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- mural thrombus
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what is a mural thrombus?
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- a thrombus that adheres to one wall of a heart chamber or major artery
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what are mural thrombi of the left atrium associated with?
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- mitral stenosis
- atrial fibrillation |
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what are mural thrombi of the left ventricle caused by?
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- MI
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what do thrombi at the junction of the internal and external carotid arteries cause?
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- thrombotic brain infarcts
- can also be the origin of emboli |
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where are arterial emboli arrested?
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1. branches of the carotid artery
2. branches of the mesenteric artery 3. branches of the renal artery |
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what happens when arterial emboli are arrested at the branches of the carotid artery?
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- most frequently, at teh midle cerebral artery (a branch of the carotid artery)
- causes cerebral infarction |
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what happens when arterial emboli are arrested at the branches of the mesentery artery?
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- leads to hemorrhagic infarction of the intestine
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what happens when arterial emboli are arrested at the branches of the renal artery?
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- produces the wedge-shaped pale infarct of the renal cortex
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what are paradoxical emboli?
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- left sided emboli that originate in the venous circulation, but go to the arterial circulation through a right to left shunt.
- need a patent foramen ovale or an ASD |
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what are fat emboli?
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- particles of bone marrow and fatty intraosseous tissue that enter the blood stream
- caused by severe fractures |
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where do fat emboli lodge themselves?
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- in lungs, brain, kidneys and other organs
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what are the symptoms of fat emboli?
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- potentially fatal FAT EMBOLISM syndrome: pulmonary distress, cutaneous petechiae, and neurological manifestations
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what are air emboli?
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- introduction of air intot he circulation
- caused by penetrating chest injury or clumsy abortion - can occur as decompression sickness |
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what is decompression sickness?
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- seen in deep sea divers that come up too fast.
- bubbles of relatively insoluble N come out of solution and obstruct the circulation -> the 'bends' and 'caisson disease' in the CNS and bones |
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what are the 'bends'?
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- musculoskeletal pain felt in decompression sickness
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what is caisson disease?
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- small infarcts seen in decompression sickness
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why are obese people more at risk for decompression disorder?
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- nitrogen has an affinity for adipose tissue
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amniotic fluid emboli
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- caused by the escape of amniotic fluid into the maternal circulation
- can activate the coagulation process -> DIC - can cause maternal death |
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name some misc sources of emboli
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- atherosclerotic plaques
- inflammed, infected tissue - tumor fragments |
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CHF and edema
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1. RH failure: peripheral edema
2. LH failure: pulmonary edema |
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when do you have increased capillary permeability?
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- during inflammation
- or during injury to capillary endothelium (burns) - causes edema |
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list the causes of edema
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1. increased hydrostatic pressure (CHF)
2. increased capillary permeability 3. decreased oncotic pressure 4. increased Na retention 5. blocked lymphatics |
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how does decreased oncotic pressure cause edema?
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- decreased oncotic pressure can come from hypoalbuminemia from:
1. loss of protein (nephrotic syndrome) 2. decreased production (cirrhosis) |
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describe the causes of sodium retention
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1. primary: associated with renal disorders
2. secondary: associated with CHF - decreased CO -> decreased RBF -> activates renin-angiotensin system -> aldosterone -> increased Na retention |
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what is lymphedema?
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- caused by blockage of lymphatics
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define anasarca
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generalized edema
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define hydrothorax
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accumulation of fluid in plerual cavity
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define hydropericardium
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accumulation of fluid in pericardial cavity
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define hydrperitoneum
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aka ascites
- accumulation of fluid in peritoneal cavity |
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define transudate
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- NONINFLAMMATORY edema from altered intrvascular hydrostatic or osmotic pressure
- low protein content - specific gravity < 1.012 |
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define exudate
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- results from increased vascular permeability caused by INFLAMMATION
- high protein content - specific gravity > 1.012 - many inflammatory leukocytes - low glucose |
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what are the causes of shock
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1. decreased CO (hemorrhage, or severe LV failure)
2. widespread peripheral vasodilation (from sepsis, trauma. includes hypotension) |
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name the 4 types of shock
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1. hypovolemic shock
2. cardiogenic shock 3. septic shock 4. neurogenic shock |
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hypovolemic shock
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- circulatory collapse from recution in blood volume:
1. severe hemorrhage or fluid loss (burns) 2. loss of fluid through GI (vomiting, diarrhea) |
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cardiogenic shock
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- circulatory collapse caused by pump failure in the LV
- often caused by massive MI |
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septic shock
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- associated with gram- neg infections, that cause gram negative ENDOTOXEMIA
- can also occur with gram-positive infection |
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describe the mechanism behind septic shock
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1. initial vasodiatlion leads to peripheral poology of blood -> hypovolemia and impaired perfusion
2. LPS from gram neg -> cytokine cascade and kinin system -> complement activation -> direct injury to vessels 3. endothelial injury -> coagulation pathways and DIC |
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which cytokines participate in septic shock?
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- TNF
- IL-1 - IL-6 - IL-8 |
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how do superantigens produce shock?
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- produce septic shock like manifestations
- TSS is associated with staph aureus infection |
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neurogenic shock
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- associated with severe trama and reactive peripheral vasodiation
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stages of shock
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1. nonprogressive (early)
2. progressive 3. irreversible |
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nonprogressive shock
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- compensatory mechanisms (increased HR, TPR) maintain perfusion of vital organs
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progressive stage of shock
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- tissue hypoperfusion and onset of circulatory and metabolic imbalance (e.g. metabolic acidosis) from lactic acidemia
- compensatory mechs are no longer adequate |
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irreversible stage of shock
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- organ damage and metabolic disturbances are so severe that SURVIVAL IS NOT POSSIBLE
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morphologic manifestations of shock
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* acute tubular necrosis of kidney (potentially reversible)
- necrosis in brain - centrilobular necrosis in liver - fatty chages in heart and liver - patchy mucosal hemorrhages in colon - depletion of lipid in adrenal cortex - pulmonary edema |
