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82 Cards in this Set
- Front
- Back
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when you have high arterial pressure, you have ________ venous pressure. this drives fluid and solutes out of ______
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high venous pressure; drives fluid and solutes out of capillary and into interstitium
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most of fluid going back into vessels does so b/c of ________
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plasma colloid osmotic pressure; some interstitial fluid moves into lymphatics
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what are the vascular pressures?
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venous bed: 10 mmHg
arterial bed: 25 mmHg R atria: 1-3 mmHg R ventricle: 25 mmHg L atria: 10 mmHg L ventricle: 80-120 mmHg |
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when do you have increased hydrostatic Pressure?
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when increase Pressure load in capillaries or veins
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what happens to the tissues in congestive heart failure?
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edema!
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what happens to the vascular pressures in congestive heart failure?
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go up! arterial bed stays same and L ventricle stays same
venous bed: 30 mmHg arterial bed: 25 mmHg R atria: 30 mmHg R ventricle: 30 mmHg L atria: 30 mmHg L ventricle: 80-120 mmHg |
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how do you get edema in tissues when congestive heart failure?
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pressure in L atria inc --> inc R ventricle pressure --> inc R atria pressure --> inc venous bed pressure --> edema
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what conditions do you see increased hydrostatic pressure in?
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*congestive heart failure: right and left sided
*constrictive pericarditis: dec filling *venous obstruction/decreased flow |
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what are diseases w/ venous obstruction/dec flow?
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liver cirrhosis: ascites
portal vein obstruction thrombosis- venous obstruction mass- venous obstruction lower extremity inactivity (bedrest)- venous stasis |
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what's the problem in left sided CHF?
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DECREASED cardiac output
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what's the etiology of left sided CHF?
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myocardial dysfunction
atherosclerosis infarcts hypertension aortic/mitral valve diseases myocarditis constrictive pericarditis |
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what's the etiology of right sided CHF?
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left sided failure
pulmonary hypertension pulmonary/tricuspid valve disease myocarditis |
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what are the findings in L sided CHF?
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dec tissue perfusion
reactive vasoconstriction (inc vascular tone) peripheral and pulmonary edema organ congestion: liver, spleen, kidneys, GI effusions: pleural |
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what are the findings in R sided CHF?
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dec tissue perfusion
reactive vasoconstriction (inc vascular tone) peripheral edema organ congestion: liver, spleen, kidneys, GI effusions: pleural *NO PULMONARY EDEMA |
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what really leads to CHF edema?
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dec CO --> dec arterial blood flow
--> dec GFR --> INC absorption of Na+ + H2O INC aldosterone *also INC central venous pressure and INC capillary pressure |
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what's constrictive pericarditis? result?
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fibrinous pericarditis w/ att to pericardial sac that restricts heart expansion --> DEC cardiac output
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what's alveoli filled w/ in pulmonary edema?
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fluid/transudate w/ few extravasated RBCs
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what are circumstances w/ reduced plasma colloid osmotic/oncotic pressure?
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protein losing states
cirrhosis/malnutrition |
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what sp diseases do protein losing states and cirrhosis/malnutrition result in decreased plama colloid osmotic/oncotic pressure?
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protein losing states: nephrotic syndrome, glomerulonephritis, protein losing enteropathies (albumin loss)
cirrhosis/malnutrition: dec albumin production |
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what's the effect of reduced plasma colloid osmotic/oncotic pressure?
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*non-dependent edema, periorbital /facial
*effusions: ascites (peritoneal), pleural *peripheral edema |
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what is the result of sodium and H2O retention?
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inc plasma volume
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what are the diseases ass w/ sodium and H2O retention?
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*acute/chronic renal failure
*abnormal renin-aldosterone |
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what main categories result in lymphatic obstruction?
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neoplasms, infections, post-surgery, post rad tx
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what are sp diseases from lymphatic obstruction?
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lymphomas- neoplasms
filarisis- infection mastectomy- post surgery abdominal lymph node of obstruction: rad tx |
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what are localized diseases that fall under lymphatic obstruction?
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inflammation
vessicle/bullae injury |
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what are the localized and diffuse causes of cerebral edema?
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localized- trauma, infections/abscess
diffuse- hypertensive crisis, venous obstruction, CSF obstruction, trauma |
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what are the effects of cerebral edema?
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decreased mental status
tissue destruction, infarct, paralysis brain stem herniation: death |
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what are exs of active and passive congestion?
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active: inflammation
passive: CHF |
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what is an inc amt of blood in capillaries, venules?
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congestion
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what's increased blood flow to area due to inflamm or vascular control?
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active congestion
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what are the reasons you can get active congestion?
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inflammation
exercise heat |
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why do you get congestion in inflamm, exercise, and heat?
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inflamm: vasodilation, inc vascular permeability
exercise: inc muscle tissue blood flow heat: inc skin blood flow |
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what does passive congestion lead to?
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reduced venous return/obstruction
edema common w/ CHF |
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what type of congestion is this:
edema, extravasated RBC's, interstitial thickening (chronic), "heart failure cells" = hemosiderin laden macs |
lung congestion
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what type of congestion is this: centrilobular congestion, centrilobular necrosis/fibrosis (chronic, i.e. cardiac cirrhosis)
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liver congestion
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what congestion: splenomegaly, fibrosis (chronic)?
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spleen congestion
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what category does lung congestion, liver congestion, spleen congestion and localized, venous thrombosis go under?
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passive congestion
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in liver congestion, where do you see more congestion around?
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central vein
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how is bleeding vs clotting controlled?
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dynamic equilibrium
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what are actions of primary hemostasis?
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vascular seal = platelets
vasoconstriction platelet adhesion platelet aggregation |
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what are actions of secondary hemostasis?
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coagulation pathway
endothelial/platelet activation coagulation cascae |
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what falls under category of thrombolytic/fibrinolytic elements?
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regulatory factors for clotting vs clot lysis
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what are steps in primary hemostasis?
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1-platelet adhesion
2-shape change 3- granule release (ADP, TXA2) 4- recruitment of more platelets 5-aggregation : hemostatic plug |
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if there's a deficiency in von Willebrand's factor, what disease?
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von Willebrand's disease
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if deficiency of GpIb, what disease?
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Bernard-Soulier syndrome
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if deficiency of GpIIb-IIIa complex, what disease?
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Glanzmann's thrombasthenia
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what do you see in inadequate primary hemostasis (platelet)?
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petechiae
purpura hemorrhage |
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what's a pinpoint loss of blood into tissues ex: skin?
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petechiae
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what's larger loss of blood into tissues ex: skin?
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purpura
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what's severe bleed (brain, GI)?
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hemorrhage
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what are steps in secondary hemostasis?
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1- tissue factor
2- phospholipid complex expression 3- thrombin activation 4- fibrin polymerization |
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if VIII and IX deficient, what disease?
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hemophilia
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what factors interact to make active thrombin?
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Xa, V and thrombin
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what activates Xa?
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IXa + X
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what's result when trauma/injury /diseases of larger vessels?
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hemorrhage
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what are traumatic hemorrhage exs?
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ecchymosis, contusion, hematomas, pleural/peritoneal hemorrhages
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what results in GI bleeding?
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ulcers
GI lesions hemorrhoids |
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what results from platelet function/# defect?
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internal hemorrhage, petechiae, purpura, ecchymosis
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what are coagulation defects?
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internal hemorrhage:
-factor VIII and IX deficiencies (hemophilia) -disseminated intravascular coagulopathy (DIC) |
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how big are ecchymosis subq hemorrhages?
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> 1-2 cm hemorrhages
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what activates platelets?
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exposed collagen, vWF
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what makes platelets aggregate?
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ADP, thromboxan A2
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what tissue factor there when tissue injury?
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thromboplastin
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what are activated factors during procoagulant time?
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XIIa, XIa, IXa, Xa, VIIa, IIa
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what are anti-fibrinolytic factors during clotting time?
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plasminogen activator inhibitors
alpha-2-antiplasmin |
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what is involved in times of pro-coagulation?
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platelet activation
platelet aggregation factors thromboplastin activated factors: XIIa, XIa, IXa, Xa, VIIa, IIa anti-fibrinolytic factors |
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what are anti-coagulation factors?
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antithrombin III (ATIII)
protein C + Protein S thrombomodulin |
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what does antithrombin III do?
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binds w/ heparin in blood and on endothelial cells
inactivates Xa, IXa, IIa |
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what does protein C + protein S do?
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inactivates Va, VIIIa
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what does thrombomodulin do?
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works w/ thrombin to activate Protein C
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what are clot lysis factors?
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tissue plasminogen activator --> activates plasminogen --> plasmin --> degrades fibrin
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what factors involved in thrombis? inhibit thrombis?
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favor thrombis: vWF
inhibit thrombis: Antithrombin III, Protein C, Xa, IXa, PGI2, NO and ADP |
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what do fibrin D dimers indicate?
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active breakdown process or clotting process
-measured to rule out emboli |
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what activates fibrinolytic pathway?
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alpha 2-antiplasmin
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what's thrombin's effect on thrombosis?
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*fibrinogen to fibrin rxn
*activates XIII to cross link fibrin *activates VIII, V *stimulates platelet aggregation and secretion *endothelial leukocyte adhesion molecules |
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what's thrombin effect on anti-thrombosis?
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*tissue plasminogen activator (tPa): used during heart attacks to help patient
*vasoactive- NO, PGI2 (inhibits platelet aggregation) *cytokines (platelet derived growth factor) |
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what does the combination of heparin + antithrombin III do?
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inhibits thrombin
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when do you want to give tPa?
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soon- before XIII crosslinks w/ clot
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if have excess of factors, what disease?
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clotting one!
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what does prothrombin time measure?
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extrinsic pathway: sensitive to 2, 7, 9, 10... made by liver and vitamin K dependent
tx: Warfarin, pumadin |
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what does partial thromboplastin time measure?
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*increases sensitivity to whole cascade w/o VII
*monitors heparin |
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*know clotting cascade
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hey it could happen!
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