IHL I - Bilirubin Metabolism and Platelet Function Flashcards

0
Q

activity of aspirin?

A

inhibits platalet activity

through COX pathway (prostaglandins)

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1
Q

petechiae

A

pinpoint hemorrhages under skin

subQ bleeds

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2
Q

aspirin action of COX?

A

irreversible inhibition

due to acetylation of the enzyme

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3
Q

COX activity?

A

catalyzes production of TXA2 in arachidonic acid pathway

TXA2 and ADP promote platelet recruitment and aggregation to form platelet plug

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4
Q

TXA2

A

potent vasoconstrictor

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5
Q

abciximab

A

inhibit the GPIIb/IIIa receptors on platelets

no platelet aggregation

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6
Q

daibigatan

A

inhibits thrombin

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7
Q

therapeutic use of aspirin

A

antiplatelet therapy

cardiovascular disease, angine, CAD, post-MI

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8
Q

aspirin long term affects?

A

can develop a resistance to aspirin after a long time

variable among patients

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9
Q

PTT

A

pro thromboplastin time

measures the intrinsic pathways

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10
Q

Vit K requiring factors

A

2, 7, 9, 10

**liver disease - vit K goes down

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11
Q

platelet function assays

A

can measure protein activity

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12
Q

ristocetin cofactor assay

A

measure vWF activity

**ristocetin is an antibiotic leading to thrombocytopenia

induces platelet agglutination but only in the presence of vWF

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13
Q

platelet aggregometry

A

checks for aggregation of platelets
-if they aggregate, they are functioning correctly

shine a light through sample
-if light visible through test tube you can identify aggregation

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14
Q

hemophilia A

A

factor VIII deficiency

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15
Q

hemophilia B

A

factor IX deficiency

16
Q

vWF deficiency

A

cant form platelet plug

also a decrease in factor VIII

17
Q

type O blood type and vWF?

A

have lowest levels

AB has highest

18
Q

purpura

A

subQ bleeding

19
Q

treatment of vWF

A

dDAVP (desmopressin nasal spray)

type I vWD treatment

stimulates release of endogenous vWF from endothelial cells

also for hemophilia A (bc vWF activates factor VIII)

20
Q

less at risk from thrombosis if vWF disease?

A

maybe

21
Q

normal range of bilirubin?

A

< 2 mg/dL

22
Q

source of bilirubin?

A

senescent RBCs broken down (120 days)

23
Q

main site of RBC breakdown?

A

occurs extravascularly

in the spleen

24
Q

heme oxygenase

A

breaks down heme to biliverdin

produces O2 and ferric iron (Fe3+)

requires NADPH

25
Q

conjugated bilirubin formation?

A

enzyme: UDP-GT

adds glucuronic acid (or xylose or ribose)

26
Q

stercobilin

A

oxidized from stercobilinogen in the large intestine

*presence of O2

27
Q

crigler najjar

A

deficient UDP-GT

increased levels of indirect bilirubin (very high)

death early age

28
Q

prehepatic jaundice

A

because of excess production of bilirubin following hemolysis

excess RBC lysis
Rh-ABO incompatibility
sickle cell disease

29
Q

intrahepatic jaundice

A

impaired uptake, conjugation, or secretion of bilirubin

reflects a generalized liver dysfunction

congenital: Gilbert’s, Crigler-Najjar, Dubin-Johnson, Rotor

30
Q

Posthepatic jaundice

A

obstruction of biliary tree

cholestasis

31
Q

intrahepatic cholestasis

A

failure of excretion at the cellular level

-due to swelling of hepatocytes and edema

32
Q

extrahepatic cholestasis

A

due to obstruction at any point in tract distal to the bile canaliculi

plasma bilirubin is conjugated
also pale-colored stool and dark urine

33
Q

autoimmune disease of prehepatic jaundice?

A

Rho incompatibility

34
Q

intrahepatic congenital diseases?

A

gilbert, crigler-najjar, dubin-johnson, rotor

35
Q

posthepatic jaundice?

A

extrahepatic bile duct blockage

ex/ gall stones

36
Q

direct coombs test

A

for incompatibility of blood tests

positive shows presence of antibody on blood cells

37
Q

phototherapy treatment?

A

converts trans to cis isomer

makes it more water soluble

38
Q

amylase and lipase

A

from the pancreas

elevated if problem in the pancreas