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D2, Fall Quarter > BMS Exam III > Flashcards

BMS Exam III Flashcards

1
Q

activated clotting factors

A

serine proteases

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2
Q

factor VIII deficiency

A

hemophilia A

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3
Q

tissue factor

A

thromboplastin

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4
Q

Warfarin/coumarin affects:

A

extrinsic pathway - blocks VKOR (vitamin K exposide reductase

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5
Q

Vitamin K, required cofactor

A

GLUTAMATION RXN for factors 2, 7, 9, 10 & Proteins C&S; post-translational MODIFICATION of several coagulation factors necessary for Ca+2 binding

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6
Q

reduced Vit K + clotting factors

A

γ-carboxyglutamate (GLA) = has high affinity binding site for Ca+2, which binds to coagulation factor

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7
Q

Anti-thrombin III (endogenous inhibitor)

A

inhibits all clotting factors (2, 7, 9, 10) that need factors that need Ca+2

HEPARIN activates anti-thrombin III

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8
Q

Protein C&S (endogenous inhibitor) inhibits

A

Va & VIIIa

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9
Q

TFPI (endogenous inhibitor)

A

inhibits TF-7A (similar to anti-thrombin III) = factors 2, 7, 9, 10 are inactivated

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10
Q

Intracellular PO4

A

intermediary metabolism in cells

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11
Q

Extracellular PO4

A

essential matrix mineralization

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12
Q

HIGH Ca+2 and PO4 in blood

A

CaPO4 = limited solubility – precipitate in soft tissue

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13
Q

1α-hydroxylase synthesizes (in kidneys)

A

calcitriol/vitD3 – rate limiting step: renal failure = major problem ; PTH simulates 1α-hydroxylase!

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14
Q

24-hydroxylase

A

deactivates vitD3 into calcitroic acid (regulation)

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15
Q

Ca+2 movement in intestine

A

paracellular + transcellular (Ca+2 channels)

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16
Q

Vitamin D deficiency

A

osteomalacia in adults, rickets in children

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17
Q

Vit D receptors

A

nuclear receptors = increase efficiency of translation

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18
Q

PTH

A

maintains plasma Ca+2 via GPCR signaling (Gs –> cAMP –> decreasing Gq, increaseing PLC

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19
Q

LOW plasma Ca+2

A

INCREASE in PTH release –> INCREASE plasma Ca+2 –> directly INCREASE bone resoprtion; DECREASE plasma PO4 because of PO4 excretion in urine (via Vit D)

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20
Q

PTH GPCR signaling

A

Uniquely DECREASES PTH release (negative feedback)

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21
Q

Majority Iron stored as

A

Ferritin (marcrophages + hepatocytes) – good indicator of iron levels

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22
Q

When iron is LOW in cells, IRP binds

A

mRNA binds 5’ to block translation of Ferritin (down regulation); binds 3’ end to increase synthesis of transferrin receptors

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23
Q

IRP bind 5’

A

down regulation = block Ferritin translation

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24
Q

IRP bind 3’

A

up regulation = increases transferrin receptors

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25
Q

IDA (Iron Deficiency Anemia)

A

Low serum ferritin, high level of transferrin – tx: ferrous sulfate + ascorbic acid

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26
Q

Anemia of Chronic Disease (ACD)

A

Cytokines stimulation hepcidin (inhibit ferroportin = down regulates intestinal absorption + releases Fe from macrophages) + inhibits erythropoiesis (decreased RBC production)

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27
Q

HIGH ferritin

A

ACD

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28
Q

Hemochromatosis

A

HFE defect, too much iron uptake inside cells; hepcidin cannot inhibit ferroportin

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29
Q

First substrates of heme metabolism

A

Succinyl CoA + glycine in mitochondria

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30
Q

First heme biosynthesis enzyme

A

ALA synthase

31
Q

Acute Intermittent Porphyria (most common)

A

Defective PBG deaminase = neuropsychiatric symptoms + abdominal – TX: Hemin = repress ALA synthase

32
Q

Porphyria cutanea tarda

A

Defective uroporphyrinogen decarboxylase – uroporphyrinogen build-up = photosensitivity

33
Q

Heme Catabolism via macrophages in spleen, liver + red bone marrow

A

RBC –> hemoglobin –> heme –> biliverdin –> bilirubin –> (conjugated, more soluble) –> binds bile –>urobilinogen –> sterecobilin –> excreted in feces

34
Q

Unconjugated (indirect) hyperbilirubinemia

A

Neonatal jaundice = UDP-glucuronyltransferas deficiency; Gilbert syndrom; hemolysis

35
Q

Conjugated (direct) hyperbilirubinemia

A

Hepatobiliary disease + bile stones (bile duct obstruction)

36
Q

G6P dehydrogenase

A

Rate limiting step in nucleotide metabolism in PPP

37
Q

Two PPP defects

A

G6PD deficiency = cannot produce NADPH, gluthathion not reduced&raquo_space; build up of H2O2&raquo_space; hemolytic anemia (associated with Type I hypersensitivity)

38
Q

Anti-coagulant Drugs

A

Heparin; Thrombin II & Factor X Inhibitors (dabigatran or rivaroxaban = not better than heparin); Coumarin/Warfarin

39
Q

Hemophilia B

A

Factor IX deficient

40
Q

Heparin (IV, parenteral)

A

Bind anti-thrombin III (interferes with all steps of coagulation) –> inactiavtes thrombin (HMW, long) and factor Xa (LMW, short + HWM, long) — tx: venous thrombosis, pulmonary embolism, myocardial infarction, unstable angina — sf(x): bleeding, heparin induced thrombocytopenia (HIT anemia) = low platelet count

41
Q

Reverse Heparin

A

Protamine (binds Heparin)

42
Q

Warfarin *increases coagulation risk for first 3 days

A

Inhibits Vit K Epoxide Reductase (VKOR) – interferes w/ clotting factor production in liver… bleed out; DDI = aspirin + preggo women b/c vitamin K for bone development (teratogen) – tx: venous thrombosis, ishemic stroke, pulmonary embolism – sf(x): increases coagulation risk for first 3 days… prevent via heparin bridge or thrombosis due to protein C deficiency

43
Q

Reverse Warfarin

44
Q

aPTT

A

Monitor bleeding time on pts on heparin or thrombin II inhibitor (dabigatran)

45
Q

PT, INR

A

Monitor bleeding for Warfarin

46
Q

Lepirudin

A

Alternative to heparin – Thrombin (Factor IIa) + prothrombin (Factor X) inhibitor – sf(x): bleeding (aPTT)

47
Q

RivaroXaban MOA

A

Factor X (prothrombin) inhibitor – clincal use: nonvalvular atrial fibrillation; sf(x): bleeding

48
Q

DabigaTran MOA

A

Factor IIa (thrombin) inhibitor

49
Q

Anti-Platelet Drugs

A

Aspirin + Clopidogrel, blocks platelet activation and aggregation

50
Q

Aspirin MOA

A

Blocks TXA2 (platelet AGGREGATION) –> reduces production of platelets

51
Q

Clopidogrel (Plavix)

A

Prevents ADP from binding to receptor on platelets (blocks platelet ACTIVATION) – tx: acute coronary syndrome, prevents restenosis after percutaneous coronary intervention (PCI), arterial thrombosis

52
Q

Prevent + tx of atererial thrombosis

A

Aspirin + Clopidogrel

53
Q

Abciximab (parenterally, IV)

A

Anti-Platelet Drug, interferes with GP IIb/IIIa – binding to fibrinogen and other ligands

54
Q

Percutaneous coronary intervention (PCI)

A

Abciximab – only given parenterally – sf(x): bleeding, thrombocytopenia (anemia)

55
Q

Fibrinolytic drugs

A

Urokinase or tPA; Alteplase, Reteplase, Streptokinase – tx: coronary artery thrombosis, ischemic stroke, pulmonary embolism

56
Q

tPA, MOA

A

plasminogen –> plasmin (cleaves fibrin = reverses blood clot) – sf(x): cerebral hemorrhage – ANTIDOTE: Aminocarproic acid

57
Q

Vitamin D supplements

A

Cholecalciferol, ergocalciferol, calcitriol – tx: osteoporosis, rickets/osteomalacia, renal failure, malabsorption

58
Q

Vitamin D

A

inhibits PTH, increases Ca+2 and PO4 serum, prevents excretion?

59
Q

Calcidiol

A

produced in liver, measurable levels of vitamin D

60
Q

Vit D toxicities

A

Hypercalcemia, hypercalciuria (excretion of Ca+2)

61
Q

Osteoclast action, vit D and PTH

62
Q

Furosemide

A

For hypercalcemia = inhibition of the Na/K/2Cl transporter in the ascending loop of Henle → (↑) Ca+2 excretion, (↑) urine Ca+2 and Mg – sf(x): hypokalemia, ototoxicity, hyperuricemia, hypomagnesmia

63
Q

Ototoxicty

A

Furosemide

64
Q

Bisphosphonate, MOA

A

Suppreses bone resorption (inhibits osteoclast activity via inhibition of farnesyl pyrophosphate synthesis) – tx: Paget’s disease, osteoporosis, hypercalcemia, bone metastasis – sf(x): GI irritation, renal failure, osteonecrosis of jaw

65
Q

Bisphosphonates = “dronate”

A

*Fosomax = Alendronate, Risendronate, Ibandronate, Zolendronic acid

66
Q

Raloxifene (SERM)

A

Selectively interacts w/ estrogen receptors = bone (agonist), breast + endometerium (antagonist) = Used for osteoporosis, reduces vertebral fracture risk – sf(x): thromboembolism, hot flashes

67
Q

Calcitonin (nasal spray)

A

Hormone that acts via cognate GCPR = tx: osteoporosis + hypercalcemia

68
Q

Denosumab (monoclonal Ab, given subcutaneous injection every 6 months)

A

Blocks bone resorption (binds RANKL = stimulates osteoclast) – tx: osteoporosis – sf(x): increased risk of infection

69
Q

Terparatide (PTH, not parathyroid hormone) via subcutaneous injection

A

Amino acid 1-34 or all 84 PTH, regulates Ca+2 and PO4 metabolism in bone + kidney. Stimulates bone turnover –> net bone formation!

70
Q

Side effects of Terparatide (PTH)

A

Prolonged use can match bone formation and resorption, hyper calcemia, hypercaluria

71
Q

Sulfonamide, MOA

A

Block folate production, targets bacterial PABA

72
Q

Trimethoprim

A

Anti-folate: selectively inhibits DHFR

73
Q

Metrotrexate

A

Blocks DHFR –> interferes with biosynthesis of dTMP and purines == tx: inflammatory bowel disease, rheumatoid disease, cancer chemotherapy

74
Q

5-FU (flurodeoxyuryidale)

A

Blocks thymidylate synthase so blocks dUMP → dTMP

D2, Fall Quarter (3 decks)

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