Biochem

Question 1

activation of extrinsic vs intrinsic

Answer 1

extrinsic : external trauma

intrinsic: trauma inside the vascular system

Question 2

extrinsic pathway is mediated by factors

Answer 2

VII

Question 3

intrinsic pathway is mediated by

Answer 3

factors XII, XI, IX, VIII

Question 4

extrinsic and intrinsic pathways converge at factor

Answer 4

X

Question 5

factor IIa is also known as

Answer 5

thrombin (II is prothrombin)

Question 6

main function of thrombin

Answer 6

converts fibrinogen to fibrin

Question 7

primary vs secondary hemostasis

Answer 7

primary = weak platelet plug 
secondary = stronger reinforced by fibrin clot

Question 8

thrombin is essential to which level of hemostasis

Answer 8

secondary hemostasis

Question 9

major actions of thrombin besides conversion of fibrinogen to fibrin (4)

Answer 9

activate factor XIII (cross-links fibrin)
Self-activation
activation of platelets
Activates factor V and VIII

Question 10

function of factor XIII

Answer 10

cross links fibrin, activated by thrombin

Question 11

MoA of anticoagulants like warfarin

Answer 11

Vitamin K inhibition (epoxide hydrolase) - prevents formation of the gamma-carboxyglutamate AA utilized in Factors II, VII, IX, X and proteins S and C

Question 12

Coagulation factors that contain gamma-carboxyglutamate AA

Answer 12

Factors II, VII, IX, X and proteins S and C

Question 13

which form of vitamin k is active form

Answer 13

quinol form in the liver

Question 14

why do patients with liver disease tend to have issues with hemostasis

Answer 14

cannot form coagulation factors (II, VII, IX, X and proteins S and C) that are formed in the liver

Question 15

primary reversal agent for warfarin

Answer 15

vitamin k

Question 16

warfarin inhibits the enzymes

Answer 16

vitamin k 2,3-epoxide reductase and vitamnin K quinone reductase

Question 17

vitamin K quinone converted to quinol by what enzyme

Answer 17

vitamin K quinone reductase

Question 18

genetic protein C deficiency causes

Answer 18

significantly increased risk of venous thrombosis because it plays a role in inactivate factor Va and VIIa (intrinsic factors) and therefore limits thrombin formation
common mutation

Question 19

hemophilia a is a deficiency in what

Answer 19

factor VIII

Question 20

hemophilia b is a deficiency in what

Answer 20

factor IX

Question 21

hemophilia is a defect in what pathway

Answer 21

intrinsic pathway

Question 22

in the extrinsic pathway, what activates factor VII

Answer 22

Tissue factor (thromboplastin)

Question 23

PT evaluates

Answer 23

extrinsic factors

Question 24

PTT evaluates

Answer 24

intrinsic factors and common clotting pathways

Question 25

PT is always _____ than PTT

Answer 25

faster

Question 26

PT: prolonged PTT: normal ===

Answer 26

liver diseasd: decreased vitamin K, decreased factor VII (or defective) chronic low grade disseminated intravascular coagulation (AC drug warfarin therapy)

Question 27

why is there a 48 hour interval between discontinuing warfarin therapy and establishing a normal PT?

Answer 27

time required for activation of coagulation pathway

Question 28

if a patient presents with a stroke, what is the most appropriate immediate treatment

Answer 28

facilitation of the conversion of plasminogen to plasmin (this is the mechanism of action of thromobolytics, which are used to treat strokes) warfarin has a slower action plasmin breaks down fibrin

Question 29

a deficiency in what factor would elevate PT without affecting PTT?

Answer 29

factor VII (only one that is unique to extrinsic)

Question 30

what are the two paths to DHAP in the liver

Answer 30

``` glycolysis glycerol kinase (only present in the liver, can get from Glycerol to G3P) --> DHAP by glycerol 3P Dehydrogenase (the glycerol kinase mechanism is not present in adipocytes) ```

Question 31

fatty acyl coa synthetase is the rate limiting step in

Answer 31

FA synthesis

Question 32

how are are TAGs transported in the blood

Answer 32

chylomicrons

Question 33

enzyme that catalyzes the breakdown of TAGs in adipocytes

Answer 33

hormone sensitive lipase

Question 34

activating and inhibiting factors of hormone sensitive lipase

Answer 34

+ - glucagon, norepi and epi | - = insulin

Question 35

how is hormone sensitive lipase activated

Answer 35

7tm receptor --> AC --> cAMP --> protein kinase signals to the cell that energy is low glucagon binds a 7transmembrane receptor

Question 36

what are the energy levels in the body when cAMP is high

Answer 36

ATP:ADP ratio is low

Question 37

FA and glycerol are transported by what in the blood

Answer 37

albumin

Question 38

what mediates transfer of acyl-CoA into the mitochondria

Answer 38

carnitine shuttle

Question 39

what inhibits carnitine acyl transferase from transporting Acyl-CoA into the mitochondria

Answer 39

malonyl-CoA

Question 40

xanthoma

Answer 40

cutaneous manifestation of hyperlipidemia

Question 41

type I familial hyperchylomicronemia is caused by

Answer 41

deficiency in apoC-II or defective lipoprotein lipase | causes an increase in chylomicrons and TAGs

Question 42

an increase in TAGs and chylomicrons would be associated with

Answer 42

Type I familial hyperchylomicronemia

Question 43

type II a and b hypercholesterolemia is caused by

Answer 43

a defective LDL receptor is completely (IIa) or partially (IIb) defective causes an increase in cholesterol, LDL VLDL and TAGs in IIb

Question 44

patient presents with abdominal pain, acute pancreatitis, and cutaneous eruptive xanthomas. Which is more likely - type I or type II hyperlipoproteinemia?

Answer 44

type I

Question 45

what causes type II hyperlipoproteinemia

Answer 45

defects in uptake of LDL via LDL receptor (cause increases in cholesterol in blood and subsequent athersclerosis)