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127 Cards in this Set

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