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#‼️PHARMACOLOGY > V - BLOOD AND COAGULATION > Flashcards

V - BLOOD AND COAGULATION Flashcards

1
Q

Required for the biosynthesis of heme and heme containing proteins, including hemoglobin and myoglobin; For Iron deficiency anmia, iron supplementation

A

Ferrous sulfate, Ferrous gluconate, Ferrous Fumarate, Iron dextran, Sodiun Ferric Gluconate complex, Iron sucrose (TOPNOTCH)

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2
Q

Chelates excess iron; For acute and chronic iron poisoning

A

Deferoxamine, Deferasirox (TOPNOTCH)

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3
Q

Cofactor required for essential enzymatic reactions that form tetrahydrofolate, convert homocysteine to methionine and metabolize methymalonyl-CoA; For vitamin B12 deficiency, megaloblastic anemia

A

Cyanocobalamin, Hydroxocobalamin (TOPNOTCH)

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4
Q

Precursor of an essential donor of methyl groups used for synthesis of amino acids, purines and deoxynucleotide; For Megaloblastic anemia, prevention of neutral tube defects(spina bifida), prevention of coronary artery disease

A

Folic acid (TOPNOTCH)

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5
Q

Agonist of erythropoietin receptors expressed by red cell progenitors; For Anemia, associated with chronic renal failure, cancer, HIV infection and prematurity

A

Epoetin Alfa, Darbepoetin alfa, Methoxy Polyethylene Glycol- Epoetin Beta (TOPNOTCH)

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6
Q

Binds receptors on myeloid progenitors and stimulates cell maturation and proliferation ; Accelerates neutrophil recovery and reduces incidence of infection; For neutrophenia associated with chemotheraphy, myelodysplasia, and aplastic anemia

A

(G-CSF) Filgrastim, Sargamostim (GM-CSF), Pegfilgrastim (TOPNOTCH)

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7
Q

Recombinant form of an endogenous cytokine; activates IL -11 receptors ; For secondary prevention of thrombocytopenia in patients undergoing chemotheraphy

A

Megakaryocyte growth factor OPRELVEKIN (IL-11), THROMBOPOIETIN, ELTROMBOPAG, ROMIPLASTIM

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8
Q

nhibits rate-limit in enzyme in cholesterol biosynthesis (HMG-CoA reductase), Increased hepatic cholesterol uptake, Increased high affinity LDL receptors which leads to decreased LDL levels

A

Simvastatin, Atorvastatin, Rosuvastatin, Fluvastatin, Pravastatin, Lovastatin, Pitavastatin, Cerivastatin (TOPNOTCH)

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9
Q

DOC for hypercholesterolemia(high LDL), decrease risk of acute coronary syndromes, ischemic stroke

A

Simvastatin, Atorvastatin, Rosuvastatin, Fluvastatin, Pravastatin, Lovastatin, Pitavastatin, Cerivastatin (TOPNOTCH)

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10
Q

Prominent SE of statins: ____

A

Hepatoxicity, Myopathy, Rhabdomyolysis (TOPNOTCH)

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11
Q

Increased risk of myopathy and rhabdomyolysis when statins are used with

A

Fibrates (TOPNOTCH)

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12
Q

non-absorbable polyemers that bind bile acids and similar steroids in the intestines preventing their reabsorption, increases cholesterol utilization for replacement, modestly lowers LDL levels by increasing hepatic LDL receptors

A

Bile Acid Binding Resin (TOPNOTCH)

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13
Q

Bile Acid Binding Resin

A

Colesevelam, Colestipol, Cholestyramine (TOPNOTCH)

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14
Q

SE: Constipation, Bloating, Gritty taste, Gallstone formation, steatorrhea, malabsortion of fat soluble substances (vitamin k, folate)

A

Colesevelam, Colestipol, Cholestyramine (TOPNOTCH)

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15
Q

Selective inhibitor of the NCP1L1 transporter decreasing intestinal absorption of cholesterol and other phytosterols, decreases cholesterol hepatic pool, increases hepatic LDL receptors

A

Sterol Absorption Blocker: EZETIMIBE

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16
Q

NPC1L1 transporter inhibitor

A

Ezetimibe (TOPNOTCH)

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17
Q

Cholesterol analog, takes the place of dietary and billiary cholesterol, decreasing intestinal absorption of cholesterol and other phytosterols

A

Sterol absorption blocker: SITOSTEROL

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18
Q

Decreases VLDL synthesis and LDL cholesterol concentrations, decreases hormone-sensitive lipase activity leading to decreased LDL levels, Increases HDL cholesterol by decreasing its catabolism

A

Niacin * Decreases catabolism of apoA-I. Decreases VLDL synthesis and secretion from the liver. Decreases LDL cholesterol concentrations. Increases HDL cholesterol

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19
Q

DOC for increasing HDL levels

A

Niacin (TOPNOTCH)

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20
Q

SE: Flushing, nausea, vomiting, Pruritus, Acanthosis nigricans, Rashes, Gastrointestinal irritation, Hepatoxicity (mild), Hyperuricemia, Impaired glucose tolerance, Arrythmias, Amyblopia

A

Niacin *Harmless flushing associated to niacin intake is addressed by Naproxen 200 mg or Aspirin

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21
Q

Activates PPAR-alpha and increases expression of lipoprotein lipase and apolipoproteins (apoA-I, apoA-II) leading to enhanced clearance of TG-rich lipoproteins, Lowers triglycerides, Increases HDL

A

Fibrates (TOPNOTCH)

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22
Q

DOC for hypertriglyceridemia

A

Fibrates (TOPNOTCH)

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23
Q

Fibrates

A

Gemfibrozil, Fenofibrate, Bezafibrate (TOPNOTCH)

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24
Q

Fibrates have higher risk of gallstone formation if given together with ____

A

resins (TOPNOTCH)

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25
Q

Nonselective, irreversible COX 1&2 inhibitor. Reduces platelet production of thromboxane A2, temporarily inhibit Prostacyclin synthesis

A

Aspirin (TOPNOTCH)

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26
Q

Uncoupler of oxidative phosphorylation, associated with Reye syndrome in children

A

Aspirin (TOPNOTCH)

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27
Q

Reversbily inhibits the binding of fibrin and other ligands to the platelet GPIIb-IIIa receptor

A

GPIIb-IIIa inhibitor: Tirofiban , Abciximab, Eptifibatide Review: GP IIb-IIIa is a receptor found on the surface of platelets that bind to FIBRINOGEN for PLATELET AGGREGATION. Deficiency of GPIIb-IIIa: GLANZMANN THROMBASTENIA. Presents with normal Platelet count.

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28
Q

For prevention or arterial thrombosis (MI, TIA, CVD), Inflammatory disorders (rheumatic fever, juvenile rheumatoid arthritis, kawasaki disease)

A

Aspirin (TOPNOTCH)

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29
Q

Inhibits phosphodiesterase III and increases cAMP in platelets and blood vessels, Inhibits platelet aggregation and causes vasolidation

A

Antiplatelet drug; PDE inhibitor: Dipyridamole, Cilostazol * Cilostazol used only in refractory intermittent claudication in patients with PAD. * Usually anticoagulant is added with dipyridamole. Example in cases of patient prosthetic heart valves.

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30
Q

additional MOA: inhibit uptake of adenosine by endothelial cells and RBC, thus increasing adenosine levels leading to inhibition of platelet aggregation

A

PDE III inhibitor: Dipyridamole, Cilostazol (TOPNOTCH)

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31
Q

Irreversibly inhibits binding of ADP to platelet receptors,thus reducing platelet aggregation

A

Antiplatelet drug (Thienopyridine): ADP inhibitors CLOPIDOGREL [B], TICLOPIDINE [B], PRASUGREL [B], TICAGRELOR [C]

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32
Q

Activates antithrombin III which Inactivates thrombin or factor IIa, factor IXa & factor Xa by forming stable complexes with them

A

Anticoagulant (indirect thrombin inhibitor): Heparin

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33
Q

SE: Bleeding, transient Heparin-induced thrombocytopenia, Osteoporosis with chronic use

A

Heparin (TOPNOTCH)

34
Q

DOC for anticoagulation during pregnancy ; administered IV or SC ; Monitor with aPTT,

A

Heparin (TOPNOTCH)

35
Q

Antidote for heparin toxicity

A

Protamine Sulfate (TOPNOTCH)

36
Q

Binds and potentiates effect of antithrombin III on factor Xa (more selective for Xa)

A

Anticoagulant (indirect thrombin inhibitor): LMWH ENOXAPARIN [B], DALTEPARIN [B], TINZAPARIN [B], DANAPAROID [B], FONDAPARINUX [B], NADROPARIN [B]

37
Q

LMWH

A

Enoxaparin, Dalteparin, Tinzaparin, Danaparoid, Fondaparinux (TOPNOTCH)

38
Q

Does not require aPTT monitoring, Protamine sulfate is only partially effective in reversing effects

A

LMWH: Enoxaparin, Dalteparin, Tinzaparin, Danaparoid, Fondaparinux (TOPNOTCH)

39
Q

Binds to thrombin’s ative site and inhibits its enzymatic action

A

Direct Thrombin Inhibitors: Lepirudin, Desirudin, Bivalirudin, Argatroban, Dabigatran (TOPNOTCH)

40
Q

bind to free and bound factor Xa

A

Direct Oral Factor Xa inhibitor: Rivaroxaban, Apixaban (TOPNOTCH)

41
Q

Inhibits vitamin K epoxide reductase (responsible for y-carboxylation of the vitamin K- dependent clotting (factors II, VII, IX, X, Protein C & Protein S)

A

Warfarin (TOPNOTCH)

42
Q

For chronic anticoagulation (DVT, atrial fibrillation, valve replacement)

A

Warfarin (TOPNOTCH)

43
Q

SE: Bleeding, Teratogen (bone defects, hemorrhage), warfarin-induced skin necrosis (transient hypercoagulability)

A

Warfarin 1st Tri: Chondrodysplasia 2nd Tri: CNS Malformations 3rd Tri: Bleeding Diatheses

44
Q

Monitor effects with PT-INR

A

Warfarin (TOPNOTCH)

45
Q

Antidote forwarfarin toxicity

A

Vitamin K or FFP (TOPNOTCH)

46
Q

Chemical antagonist of heparin. Reverses excessive anticlotting activity of unfractionated heparin

A

Protamine Sulfate (TOPNOTCH)

47
Q

Tissue plasminogen activator analog. Converts plasminogen to plasmin, which degrades the fibrin and fibrinogen, causing thrombolysis

A

Alteplase, Anistreplase, Reteplase, Streptokinase, Tenecteplase, Urokinase (TOPNOTCH)

48
Q

Tx should be done within 6 hrs, better if within 3hrs ; Antidote is AMINOCAPROIC ACID

A

Alteplase, Anistreplase, Reteplase, Streptokinase, Tenecteplase, Urokinase (TOPNOTCH)

49
Q

Competitively inhibits plasminogen activation thus inhibiting fibrinolysis

A

Tranexamic acid (TOPNOTCH)

50
Q

For Vitamin K deficiency, Antidote to warfarin, prevention of hemorrhagic diatheses in newborns

A

Vitamin K1, K2 (Phytonadione, Menaquinone) (TOPNOTCH)

51
Q

Vasopressin V2 receptor agonist, Increases factor VIII activity of patients with mild hemophilia A or VWD

A

Desmopressin (TOPNOTCH)

52
Q

low doses undergo first order kinetics while high doses undergo zero order reaction ; Long term use reduces the risk of colon cancer

A

Aspirin

Review:

  • FIRST-ORDER ELIMINATION: rate of elimination is proportionate to the concentration; most common; constant PROPORTION is eliminated
  • ZERO-ORDER ELIMINATION / SATURABLE / MICHAELISMENTEN KINETICS: rate of elimination is constant regardless of concentration; constant AMOUNT is eliminated
53
Q

NSAID (Highly COX-2 selective)

A

CELECOXIB, ETORICOXIB, PARECOXIB, ROFECOXIB, VALDECOXIB

*Rofecoxib and Valdecoxib withdrawn due to increased incidence of thrombosis. MELOXICAM is a PREFERENTIALLY COX2 selective inhibitor

54
Q

NSAIDs that can be used to close PDA

A

Ibuprofen and Indomethacin (TOPNOTCH)

55
Q

has significant analgesic effect but not anti-inflammatory effect

A

Ketorolac (TOPNOTCH)

56
Q

SE: Gastrointestinal toxicity, pancreatitis, Nephrotoxicity, Serious hematologic reactions, BM suppression

A

Indomethacin (TOPNOTCH)

57
Q

Selective COX-2 inhibitor

A

Celecoxib, Etoricoxib, Parecoxib (TOPNOTCH)

58
Q

Rofecoxib and Valdecoxib withdrawn due to

A

increased incidence of thrombosis (TOPNOTCH)

59
Q

Selectively inhibits COX-3 in the CNS, Weak COX-1 and COX-2 inhibitor in the periphery, Inhibits prostaglandin synthesis

A

Paracetamol (Acetaminophen) (TOPNOTCH)

60
Q

Inhibits AICAR transformylase and thymidylate snythetase, with secondary effects on polymorphonuclear chemotaxis

A

Methotrexate (TOPNOTCH)

61
Q

DMARD of choice for Rheumatoid arthritis

A

Methotrexate (TOPNOTCH)

62
Q

Rescue agent for Methotrexate toxicity

A

Leucovorin (Folinic acid) (TOPNOTCH)

63
Q

Binds to TNF-a and prevents it from activating TNF-a receptor

A

“InCAGE”

DMARD: INFLIXIMAB [B], CERTOLIZUMAB [B], ADALIMUMAB [B], GOLIMUMAB [B], ETANERCEPT

Side Effects: Bacterial infections (URTIs), Reactivation of latent tuberculosis, Lymphoma, Demyelination, Reactivation of hepatitis B, Autoantibody formation (ANA, antidsDNA), Infusion reactions, hepatoxicity, hematotoxicity, cardiotoxicity

64
Q

SE: Bacterial infections (URTIs), reactivation of latent tuberculosis, lymphoma, Demyelination, Reactivation of Hepatitis B, Auto antibody formation (ANA, anti dsDNA), infusion reactions, hepatoxicity, hematotoxicity, cardiotoxicity

A

TNF-a inhibitor: Infliximab, Adalimumab, Etanercept (TOPNOTCH)

65
Q

Antidote for paracetamol toxicity

A

N-acetyl cysteine (TOPNOTCH)

66
Q

Forms 6-thioguanine, suppressing inosinic acid synthesis, B-cell and T-cell function, Immunoglobulin production and interleukin-2 secretion

A

DMARD: Azathioprine (TOPNOTCH)

*Cannot give Allopurinol with azathioprine (allopurinol reduces xanthine oxide catabolism of purine analogs, increasing 6-thioguanine nucleotides, leading to severe leukopenia)

67
Q

Cannot give _______ with azathioprine (the drug reduces xanthine oxide catabolism of purine analogs, increasing 6-thioguanine nucleotides, leading to serve leukopenia)

A

Allopurinol (TOPNOTCH)

68
Q

Suppression of T-lymphocyte leading to decreased leukocyte chemotaxis, stabilization of lysosomal enzymes, inhibition of DNA and RNA synthesis, trapping of free radicals

A

Chloroquine, Hydroxychloroquine (TOPNOTCH)

69
Q

T or F: Chloroquine, Hydroxychloroquine are safe for pregnant patients

A

TRUE (TOPNOTCH)

70
Q

Forms phospharamide mustard, which cross links DNA to prevent cell replication, Supresses T-cell and B-cell function

A

Cyclophosphamide (TOPNOTCH)

71
Q

SE: hemorrhagic cystitis

A

DMARD, Cancer Chemotherapeutic Drug: Cyclophosphamide

Rescue agent is MESNA

72
Q

Rescue agent for Cyclophosphamide toxicity

A

MESNA (TOPNOTCH)

73
Q

Inhibits interleukin-1 and iterleukin-2 receptor production and secondarily inhibts macrophage-T-cell interaction and T-cell responsiveness

A

DMARD: Cyclosporine (TOPNOTCH)

74
Q

anti-IBD drug, Active metabolite (sulfapyridine) inhibits the release of inflammatory cytokines

A

DMARD: Sulfasalazine (TOPNOTCH)

75
Q

Inhibits microtubule assembly and LTB4 production leading to decreased macrophage migration and phagocytosis

A

Microtubule assembly inhibtor: Colchicine

* diarrhea is the adverse effect which signals toxicity from colchicine

76
Q

adverse effect which signals toxicity from colchicine

A

diarrhea (TOPNOTCH)

77
Q

are weak acids that compete with uric acid for reabsorption in the PCT leading to increased uric acid excretion

A

Uricosuric agent: Probenecid, Sulfinpyrazone (TOPNOTCH)

78
Q

may be given together with antimicrobial agents (particularly Pens) to prolong therapeutic effect by inhibiting renal tubular secretion of antibiotics

A

Probenecid (TOPNOTCH)

79
Q

Active metabolite (alloxanthine) irreversibly inhibits xanthine oxidase and lowers production of uric acid

A

Xanthine oxidase inhibitor: Allopurinol, Febuxostat (TOPNOTCH)

80
Q

1st line treatment of chronic gout, tumor lysis syndrome

A

Xanthine oxidase inhibitor: Allopurinol, Febuxostat (TOPNOTCH)

81
Q

T or F: Allopurinol is more effective than Febuxostat

A

FALSE

Febuxostat is more effective than Allopurinol

#‼️PHARMACOLOGY (31 decks)

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