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CardioPulm Final > Biochemistry > Flashcards

Biochemistry Flashcards

1
Q

What is the normal range of platelets?

A

150,000 to 300,000 ul3

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2
Q

Where are platelets derived from?

A

thrombocytes -> megakaryocytes -> platelets

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3
Q

What vasoconstrictors do platelets contain?

A

granules contain serotonin (5-HT) and COX1 -> generates thromboxane A2

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4
Q

What can be found on platelet cell membranes?

A

glycoproteins/phospholipids (prevents them from sticking to each other); receptors for collagen/laminin (exposed when endothelial cells are damaged); receptor for released signal molecules

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5
Q

What controls platelet production?

A

thrombopoietin (TPO) which is produced by kidney and liver continuously

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6
Q

What happens to TPO in high platelet #s?

A

TPO bound to c-MPL receptor on platelets/megakaryocytes ->i internalized -> degraded

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7
Q

What happens to TPO in low platelet #s?

A

doesn’t bind to c-MPL receptor; free TPO triggers platelet production

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8
Q

What is the difference between TPO and EPO?

A

EPO is selective to RBCs; TPO will increase all blood cell production

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9
Q

What is the purpose of vasospasm?

A

collapses vessel to disrupt blood flow and avoid further blood loss

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10
Q

What is the most important factor contributing to vasospasm?

A

myogenic response - smooth muscle cells respond to damage by releasing chemicals and and contracting (some reflex involved)

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11
Q

What other factors contribute to vasospasm?

A

platelet factors (5-HT, thromboxane A2) and neuronal reflex (not required)

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12
Q

What is von Willenbrand factor (vWF) and what is its function?

A

released from damaged vessel cells and initiates binding between collagen and platelets (used as an intermediate to bind between collagen and platelets)

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13
Q

What happens to platelets when activated?

A

they swell and retract to extend podocytes; retraction also releases granules of thromboxane A2, ADP, and 5-HT)

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14
Q

What is formed by the activation of platelets? How effective is it?

A

activated platelets stick to vessel wall and each other to form platelet plug; may be all that is needed to stop bleeding of small breaks (nosebleeds, cuts on skin)

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15
Q

Difference between primary and secondary hemostasis?

A

Primary = localized platelet plug as site of injury (temporary patch)

Secondary = enlarged platelet plug by adding fibrin via clotting cascade

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16
Q

What are the vitamin K dependent factors?

A

factor II, VII, IX, X, protein C, and protein S

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17
Q

What triggers the extrinsic pathway and what factors are involved?

A

activated by external trauma (cut on skin); involves the activation of factor VII through tissue factor (III) released from damaged cells

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18
Q

What triggers the intrinsic pathway and what factors are involved?

A

activated by trauma inside the vascular system and involves factors XII, XI, IX, and VIII

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19
Q

Describe the extrinsic pathway

A

tissue factor (III) comes into contact w/ factor VII and the 2 bind to Ca which makes a trimolecular complex that cleave factor X -> Xa

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20
Q

What factor starts off the intrinsic pathway and what is its cofactor in activation?

A

XII (hageman factor) -> XIIa through HMWK as cofactor

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21
Q

What converts prekallirein to kallirein and what is its purpose?

A

Factor XIIa helps in the conversion which accelerate conversion of XII -> XIIa through positive feedback

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22
Q

What factor does factor XIIa cleave?

A

factor XI -> XIa

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23
Q

What does factor XIa cleave in the intrinsic pathway?

A

cleaves factor IX (christmas factor) -> IXa (a protease)

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24
Q

What cleaves factor VIII to factor VIIIa?

A

thrombin (IIa)

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25
Q

What cleaves factor X -> Xa in the intrinsic pathway?

A

IXa, VIIIa, Ca and phospholipids (forms tenase)

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26
Q

What is the purpose of the common pathway and what factors are involved?

A

Common pathway results in a stable fibrin clot (secondary hemostasis); involves factors I, II, V, X, and XIII

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27
Q

What cleaves factor V to Va?

A

thrombin (IIa)

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28
Q

What makes up the prothrombin activator (prothrombinase) and what is the result?

A

Xa, Va, Ca, and phospholipids form prothrombinase; acts on prothrombin (II) to form thrombin (IIa)

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29
Q

Thrombin converts fibrinogen into what?

A

Fibrin which is then polymerized into fibrin fibers in the presence of Ca

30
Q

What is needed to create cross-linked fibrin?

A

Thrombin and Ca help convert Factor XIII (fibrin stabilizing factor) to XIIIa which stabilizes fibrin into cross-linked “net”

31
Q

Describe all the roles of thrombin (factor II)

A 
Prothrombin -> thrombin
Factor V -> Va
Factor VIII -> VIIIa
activation of platelets
Fibrinogen -> fibrin
XIII (fibrin stabilizing factor) -> XIIIa -> cross-linked fibrin
32
Q

What is used to activate Protein C?

A

Thrombin combines w/ thrombomodulin on endothelial cells to activate protein C

33
Q

What does protein C do?

A

inactivates t-PA inhibitor that is floating in the blood

34
Q

What is t-PA and where does it come from?

A

tissue plasminogen activator is released by damaged tissue; used to convert plasminogen to plasmin

35
Q

Describe the steps to breaking down a clot

A

t-PA released by damaged tissues; thrombin binds to thrombomodulin on endothelial cells to activate protein C (instead of creating fibrin); activated protein C inhibits t-PA inhibitor floating in blood so that t-PA can activate plasminogen -> plasmin which then lysis the fibrin in the clot

36
Q

Explain how atherosclerosis activates intrinsic pathway

A

plaque can rupture through endothelium and activate clotting cascade; clot can develop and occlude the rest of the artery (causing MI or stroke)

37
Q

What does prothrombin time (PT) test?

A

tests extrinsic and common pathways

38
Q

What is the normal range of PT and what could cause prolonged PT?

A

10-13 seconds; may be prolonged w/ vitamin K deficiency, Coumadin (warfarin) therapy, DIC, or liver disease (would have normal PTT)

39
Q

What does partial thromboplastin time (PTT) test?

A

intrinsic and common pathways

40
Q

What is the normal range of PTT and what could cause prolonged PTT?

A

25-35 seconds; may be prolonged w/ heparin therapy or overdose, DIC, or hemophilia

41
Q

What is the function of vitamin K?

A

allows factors (II, VII, IX, X, protein C and S) to bind to phospholipid membranes through y-glutamyl carboxilation; puts factors in a place where they can be activated

42
Q

How is vitamin K activated?

A

must be reduced from quinone -> quinoa form in liver through 2,3 epoxide reductase and quinone reductase

43
Q

What is the MOA of Coumadin (Warfarin)?

A

inhibits the enzyme epoxide reductase and prevents activation of vitamin K -> prevents activation of dependent factors in cascade

44
Q

Which form of warfarin is more pharmacologically active?

A

S-warfarin; must be free floating and not bound to anything

45
Q

What are the half-lives for the vitamin K dependent factors?

A 
II = 60 hrs
VII = 4-6 hrs
IX = 24 hrs
X = 40-60 hrs
46
Q

What happens w/ protein C deficiency?

A

significant risk for venous thrombosis b/c thrombin is not activating protein C and is still activating Va and VIIIa in the clotting cascade

47
Q

What factor is deficient in hemophilia A? What factor do you test for?

A

factor VIII; they will lack factor Xa so test for that

48
Q

Describe the 3 basic structures of lipids

A

monoacyglycerol (MAG) - 1 fatty acid attached
diacylglycerol (DAG) - 2 fatty acids attached
triacylglycerol (TAG) - 3 fatty acids attached

49
Q

What is the source of TAG synthesis in intestinal cells?

A

dietary TAGs digested in small intestine by pancreatic lipases

50
Q

What lipoprotein is made in intestinal cells? Where is it released?

A

chylomicron - largest and least dense lipoprotein; released into lymphatics and enters blood through lymphatic duct

51
Q

What is the source of TAG synthesis in the liver?

A

glucose or glycerol (promoted by excess carbohydrates)

52
Q

What enzyme is specific to the liver and what does it do?

A

glycerol kinase -> used to transform glycerol into glycerol 3-P

53
Q

What is the source of fatty acids in the liver?

A

acetyl CoA (forms new fatty acids in hepatocytes)

54
Q

What lipoprotein is made in the liver? What does it hold besides TAGs?

A

VLDL - very low density lipoprotein; holds TAGs and cholesterol

55
Q

What is source of TAG synthesis in adipocytes?

A

glucose (promoted by excess carbohydrates and fats)

56
Q

What is the fatty acid source in adipocytes? How do they enter adipocytes?

A

chylomicrons and VLDL; broken down in capillaries by capillary lipoprotein lipase (CLPL) and fatty acids enter adipocytes

57
Q

What is the major enzyme involved in breaking down TAGs in adipocytes? What activates and inhibits the enzyme?

A

hormone sensitive lipase (HSL)
activated by glucagon, Epi, and NE (hunger, exercise)
inhibited by insulin (fed status)

58
Q

How do broken down fatty acids leave adipocytes?

A

short chain (< 6C) are released into blood; long chain fatty acids are combined w/ albumin (carrier) before entering blood

59
Q

What is perilipin and how is it regulated?

A

protein that coats lipid droplets (prevents access by HSL); regulated by PKA (phosphorylation allows association w/ HSL)

60
Q

What is the function of lipoproteins?

A

serve as vehicles for transporting hydrophobic substances through vessels and serve as ligands to help internalize lipoproteins

61
Q

What are the 5 types of lipoproteins?

A

chylomicrons - intestinal cells; least dense; largest
VLDL - hepatocytes
IDL
LDL - “bad cholesterol”; majority is cholesterol
HDL - “good cholesterol”; smallest; most dense (majority is proteins)

62
Q

Describe the functions for each of the following apolipoproteins: ApoB-48, ApoC-II, ApoE, ApoB-100

A

ApoB-48 - facilitates transport
ApoC-II - activates CLPL
ApoE - facilitates uptake into liver
ApoB-100 - facilitates uptake into cells

63
Q

On what lipoproteins would you find ApoB-48?

A

chylomicrons

64
Q

On what lipoproteins would you find ApoC-II?

A

chylomicrons and VLDL (sources of fatty acids for adipocytes) and HDL

65
Q

On what lipoproteins would you find ApoE?

A

chylomicrons, VLDL, IDL, and HDL

66
Q

On what lipoproteins would you find ApoB-100?

A

VLDL, IDL, LDL

67
Q

What is the function of ApoA-1 and where would you find it?

A

found on HDL; activates LCAT enzyme that converts cholesterol to cholesterol ester

68
Q

What is Type I Hperlipoproteinemia and how would you dx?

A

inability to hydrolyze TAGs in chylomicrons and VLDL either due to deficiency in CLPL (infancy) or ApoC-II (post-adolescence); plasma TAG levels > 1000 mg/dL

69
Q

What is Type II Hyperlipoproteinemia and how would you dx?

A

defects in uptake of LDL and impaired ability to recognized ApoB-100
Normal cholesterol - 130-200 mg/dL
Heterozygous – 300-500 mg/dL
Homozygous - >800 mg/dL

70
Q

How does high LDL cause atherosclerosis?

A

High LDL influx in arterial wall causes it to be converted to oxidized version by ROS; unregulated uptake by macrophages that become foam cells and burst (cause platelet adhesion)

CardioPulm Final (8 decks)

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