Ward Prep: Brs Ch 3 Hemodynamic Dysfunction

Front 1

Define hematoma

Back 1

type of hemorrhage (blood escapes vasculature). accumulation of blood in tissue or organ

Front 2

Define ecchymosis

Back 2

type of hemorrhage (Blood escapes vasculature) bruise, accumulation of blood in skin/subcutaneous tissue. Ecchymosis > purpura > ecchymosis

Front 3

Define hyperemia

Back 3

localized inc volume of blood

Front 4

clinically distinguish between hemorrhage and hyperemia

Back 4

hemorrhage doesn't blanche w/ pressure

Front 5

Where do hemorrhagic infarcts occur and why

Back 5

1) lung and GI tract. Dual blood supply (brochial + pulmonary; multiple anastomosing branches of the mesenteric artery) when 2nd source is insufficient to save tissue 2) volvulus, incarcerated hernias, post operative adhesions (venous occlusion)

Front 6

what is virchow's triad

Back 6

factors leading to thrombosis: 1) hypercoagulabliity 2) abnormal flow 3) endothelial injury

Front 7

what does von willebrand factor do

Back 7

bridges glycoprotein receptors on platelets and exposed collagen on injured endothelium

Front 8

what is gp2b3a? Function?

Back 8

gp on platelet surface. Fibrinogen bridges gp2b3a complexes on adjacent platelets, promoting cohesion

Front 9

steps of platelet function in thrombosis

Back 9

1) adhesion: gp Rs - vWF - collagen 2) Release rxn = degranulation => comformational ∆ exposes PL => COAGULATION CASCADE. Also TXA2 production. 3) cohesion. G2b3a crosslinked by fibrinogen 4) stabilization by fibrin 5) limitation:prostacyclin (PGI2), fibrin split products

Front 10

how are endothelial cells involved with thromboresistance

Back 10

1) produce heparin-like molecules => ATIII (inhibits intrinsic pathway and 10 and 2) 2) produce tissue plasminogen activator 3) produce thrombomodulin => modulates thrombin => activates protein C => inhibits 5 and 8 (with protein S) 4) produces protein S 5) prostacyclin (PGI2) 5) produces NO

Front 11

draw the coagulation cascade

Back 11

nice. See p38 in BRS for how 12a activates coagulation, fibrinolysis, complement sys, and kinin system

Front 12

how does heparin work? Which factors are inhibited

Back 12

heparin activates ATIII which inhibits 12, 11, 9, 10, 2 (intrinsic pathway => inc PTT)

Front 13

how does LMWH work? Which factors are inhibited?

Back 13

LMWH activates ATIII but only inhibits 10.

Front 14

how does coumadin work? Which factors are inhibited

Back 14

coumadin/warfarin inhibits vitamin k epoxide reductase which restores vitamin k, which is req for gamma carboxylation of 9, 7, 10, 2 => inc PT. also dec prot C, S

Front 15

What's the most important fibrynolytic protease? How is it activated? How does it function?

Back 15

plasminogen, activated to plasmin indirectly by 12a and directly by tPA (endo cells). (12a inc Kallikrein which activates plasmin which activates C3a. Kallikrein also activates bradkinin). It splits fibrin into fibrin split products.

Front 16

Who gets herditary thrombophilias and where do the thrombi form?

Back 16

young women, venous thrombosis leading to thromboemboli.

Front 17

Name 3 diseases that are hereditary thombophilias. Which is the most common?

Back 17

1) Factor V Leiden. *MC*. Mutation prevents inactivation by Activated Protein C. 2) Prothrombin 20210A transition. 2nd mc. UTR mutation => elevated plasma prothrombin (facor 2) levels. 3) Methylene Tetrahydrofolate Reductase mutation => Inc homocysteine => arterial + venous thrombosis. Rx: folic acid, B6, B12. 4) other: inc 8, 9, 11 or fibrinogen; or dec ATIII, C, S

Front 18

Pathophysiology of antiphospholid antibody syndrome? Lab finding?

Back 18

Antibodies vs. PL/antigen complexes => recurrent arterial/venous thromboemboli + fetal loss + thrombocytopenia. Mechanism unclear, maybe direct activation of platelets. Antibodies include anti-cardiolipin (FP VDRL syphilis test) and ant-phostphatidylcholine. Paradoxical elevated PTT b/c antibody binds to the PL reagent

Front 19

What is lupus anticoagulant

Back 19

An anti-phospholid antibody in the setting of lupus = 2° antiPL syndrome.

Front 20

Pathophysiology of heparin-induced thrombocytopenia? Timescale?

Back 20

Type 1: not autoimmune. Direct platelet aggregating affect. Type 2: heparin binds platelet protein => antibody binds complex => platelet activation/aggregation => thrombosis and thrombocytopenia. 1-2 weeks after initiation of tx. Earlier if sensitized

Front 21

What is a saddle embolus?

Back 21

large pulmonary emoblus that obstructs the bifurcation of the pulmonary artery.

Front 22

Multiple medium pulmonary emboli leads to

Back 22

pulmonary hypertension or acute RH failure

Front 23

Left atrial mural thrombus a/w

Back 23

Atrial fibrillation w/ mitral stenosis

Front 24

Left ventricular mural thrombus is caused by

Back 24

MI

Front 25

Arterial emboli passing trhough the carotid artery most frequently lodge in

Back 25

middle cerebral artery

Front 26

3 common locations for arterial thrombi to lodge

Back 26

1) branches of the carotid (middle cerebral artey) = cerebral infarction 2) branches of mesenteric artery => hemorrhagic infarction of intestine 3) branches of renal artery => wedge-shaped pale infarct of renal cortex

Front 27

What is a paradoxical emboli? What happens

Back 27

Venous thrombosis emoblizes gains access to the arterial circulation through a right to left shunt: patent foramen ovale or atrial septal defect

Front 28

Fat emboli syndrome. Cause and px

Back 28

Cause: severe/multiple fx => fatty intraosseuous tissue enters cirtulation => lodge at capillary beds. Px 1) respiratory distress (ARDS) 2) Petechiae 3) neurological mainfestations. ARDS = pulmonary edema + low PaO2/FiO2 w/o elevated LAP

Front 29

Air Emboli. Causes.

Back 29

Introduction of air intro circulation. Epnetrating chest injury, criminal abortion, decompression sickness (the bends/caisson disease): return to surface => N2 comes out of solution => small infarcts.

Front 30

Amniotic fluid emboli causes what

Back 30

Amniotic fluid escapes into maternal circulation => coagulation => disseminated intravascular coagulation (=> maternal death)

Front 31

What is anasarca

Back 31

generalized edema (heart failure, liver failure or kidney failure)

Front 32

Define shock

Back 32

hypotension + hypoperfusion

Front 33

Name 4 types of shock and describe them

Back 33

1) hypovolemic shock: shock (hypotension+perfusion) dec in blood volume (hemorrhage, burn, vom/diarrhea) 2) cardiogenic shock (usu MI) 3) septic shock: LPS => direct endothelial injury (DIC) + induce TNF, IL1, 6, 8 (vasoD). superantigens (staph aureus => toxic shock syndrome). sepis = shock + bacteremia. 4) neurogenic shock (severe tauma => reactive peripheral vasodilation)

Front 34

what does shock do to acid/base balance

Back 34

hypoperfusion => metabolic imbalance => lactic acidosis => metabolic acidosis

Front 35

What happens to kidneys in shock

Back 35

acute tubular necrosis