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PLE_PHARMA > DRUGS USED TO TREAT DISEASES OF THE BLOOD > Flashcards

DRUGS USED TO TREAT DISEASES OF THE BLOOD Flashcards

1
Q
  • essential metallic component of heme
A

IRON

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2
Q

Transport protein of Iron

A

Transferrin

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3
Q

Storage protein of Iron?

A

Ferritin

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4
Q

most common type of anemia

A

microcytic hypochromic anemia caused by iron deficiency

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5
Q

Laboratory Picture of Iron deficiency?

A

Laboratory picture: ↓ Iron, ↓ Ferritin, ↑ TIBC

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6
Q

megaloblastic anemias are caused by

A

a deficiency of vitamin B12
or folic acid

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7
Q

Most common type of megaloblastic anemia?

A

Pernicious Anemia

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8
Q

Cause of pernicious anemia?

A

caused by a defect in the synthesis of intrinsic factor or
by surgical removal of that part of the stomach that
secretes intrinsic factor

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9
Q

Iron Hematopoietic growth factors oral preparations?

A

FERROUS SULFATE, Ferrous gluconate,
Ferrous fumarate, Ferrous carbonate

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10
Q

Iron Hematopoietic growth factors parenteral preparations?

A

IRON DEXTRAN, Iron sucrose,
Sodium ferric gluconate complex
All are Preg Cat A

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11
Q

most prominent SE for oral iron

A

GI Distress

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12
Q

Most notable SE of Dextran-containing parenteral iron

A

Anaphylaxis and allergic reactions

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13
Q

Treatment of Iron intoxication?

A

TREATMENT
o removal of unabsorbed tablets from the gut
o correction of acid-base and electrolyte abnormalities
o parenteral administration of DEFEROXAMINE, which
chelates circulating iron

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14
Q

state of chronic iron overload that da

A

CHRONIC IRON INTOXICATION: HEMOCHROMATOSIS

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15
Q

Triad of hemochromatosis?

A

Triad: CIRRHOSIS, DIABETES MELLITUS, SKIN PIGMENTATION

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16
Q

Treatment of chronic iron intoxication: hemochromatosis?

A

o Phlebotomy
o chronic administration of DEFEROXAMINE or DEFERASIROX

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17
Q

Heavy Metal Chelators? (3)

A

DEFEROXAMINE, DEFERASIROX, DEFERIPRONE

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18
Q

what vitamin is required for normal DNA synthesis

A

Folate

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19
Q

Folate is absorbed in what part of the intestine?

A

proximal jejunum

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20
Q
  • deficiency usually presents as megaloblastic anemia
A

FOLIC ACID DEFICIENY

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21
Q

What vitamin deficiency causes neurologic defects?

A

vitamin B12 deficiency (NOT folic acid deficiency) causes
neurologic defects (subacute combined degeneration)

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22
Q

Where is vitamin B 12 absorbed?

A

absorbed in the distal ileum in the presence of intrinsic factor

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23
Q

main stimulus for the production of EPO?

A

Hypoxia-inducible factor 1

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24
Q

stimulates the differentiation and maturation of erythroid
progenitor cells within the bone marrow

A

EPO

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25
Q

DRUG CLASS OF FILGRASTIM (G-CSF),
Sargramostim (GM-CSF)
Pegfilgrastim, Plerixafor, Lenograstim

A

Myeloid Growth Factors

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26
Q

glycoprotein made primarily in the liver that stimulates the
formation of megakaryocytes

A

Thrombopoietin

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27
Q

Drug Class of OPRELVEKIN (IL-11), Thrombopoietin,
Eltrombopag, Romiplastim
MOA Recombinant form

A

Megakaryocyte growth factor

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28
Q

Small-molecule thrombopoietin (TPO)-
receptor agonist that interacts with
human TPO receptor

A

ELTROMBOPAG

29
Q

4 mechanisms of Hemostasis?

A
  1. Vasoconstriction
  2. Platelet plug formation
  3. Formation of clot via blood coagulation
  4. Fibrous Organization
30
Q

is the most common cause of acute
myocardial infarction (MI), ischemic stroke, and limb gangrene

A

Arterial thrombosis

31
Q

MOA OF ASPIRIN (Acetylsalicylic acid, ASA), Salsalate, Sodium salicylate

A

Nonselective, irreversible COX 1&2 inhibitor

32
Q

SE of COX inhibitors?

A

Gastrointestinal toxicity, Tinnitus, Hypersensitivity,
Hyperventilation, HAGMA, Increased bleeding time,
Nephrotoxicity (AKI and Interstitial Nephritis)

33
Q
  • Associated with Reye syndrome in children
  • Do not use as NSAID for gout
A

ASPIRIN

34
Q

SAMTER TRIAD?

A

Asthma, ASA Sensitivity, Nasal Polyps

35
Q

MOA: Inhibits platelet aggregation by interfering with GPIIb/IIIa
binding to fibrinogen and other ligands

MNEMONICS: GPIIB-IIIa mnemonic: May 2 to 3 pack Abs yung mga taga FIBA (basketball)

A

Abciximab, Eptifibatide, Tirofiban

36
Q

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

A

CLOPIDOGREL, TiCLOPidine, PrasuGREL, TicaGRELor

Mnemonic:

ADP Inhibitors: Read ADP as “A Dip” – A dip in the pool with Cupid (sounds
like Clopid). Just remember CLOPIDoGREL here, the rest either have GREL
or CLOPID in their name

37
Q

What drug is used for Prevention and treatment of arterial thrombosis
(stroke,TIA, unstable angina), Prevention of restenosis
after PCI, Acute coronary syndromes

A

As part of the ACS regimen, a loading dose of 300mg Clopidogrel can
reduce platelet activity by 80% within 5hrs of administration.

38
Q

SE of TICLOPIDINE?

A

Thrombotic thrombocytopenic purpura

39
Q

Inhibits phosphodiesterase III and increases cAMP in
platelets and blood vessels. Inhibits platelet aggregation
and causes vasodilation

A

MOA Cilostazole, Dipyridamole

40
Q

used only in refractory intermittent
claudication in patients with PAD.

A

CILOSTAZOL

41
Q

2 major types of anticoagulants:

A

o Indirect thrombin inhibitors: heparin, enoxaparin (LMWH),
coumarin derivatives (warfarin),
o Direct thrombin inhibitors: Lepirudin

42
Q

Antidote of Heparin?

A

Protamine

43
Q

Antidote of warfarin?

A

Vitamin K, FFP

44
Q

In pregnancy, heparin or warfarin?

A

Heparin

45
Q

What laboratory tests will you request to assess the extrinsic and
intrinsic coagulation pathways?

A

PiTT = PTT for intrinsic pathway
PeT = PT for extrinsic pathway

46
Q

Pathophy of HEPARIN-INDUCED THROMBOCYTOPENIA

A

Pathogenesis involves opsonization of the heparin-platelet
complex. Heparin is immunogenic, leading to its own
phagocytosis and a decrease number of platelet.

47
Q

Management of Heparin Induced Thrombocytopenia?

A

The key here is to replace heparin with a Low molecular weight
heparin just like Fondaparinux or a Direct Thrombin
Inhibitor like Lepirudin.

48
Q

inhibits Vitamin K epoxide reductase (which is responsible for
carboxylation reactions to activate the clotting factors II, VII, IX,
X, Protein C and S)

A

Warfarin

49
Q

In patients requiring anticoagulation, why is an overlap between
heparin and warfarin usually done?

A

Heparin rapidly inhibits the already activated factors, while
Warfarin inhibits the activation process of the clotting
factors X, IX, VII and also inhibits Protein C and S (effect on
Protein C and S is faster). Protein C and S are anti-clotting.
o The initial inhibition of Protein C and S ultimately results in
a temporary proclotting state.

50
Q

due to
initial pro-clotting effect of warfarin
o Blood clots block the blood
vessels and cause necrosis,
where an area of skin is
destroyed

A

Warfarin Skin Necrosis

51
Q

Management of warfarin-Skin Necrosis?

A

Heparin-Warfarin bridging is done to prevent this: You must
start first with Heparin to address the activated factors and
gradually introduce warfarin.

52
Q

LEPIRUDIN, BIVALIRUDIN,
Desirudin, ARGATROBAN, DABIGATRAN MOA?

A

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

53
Q

Which is Per ORem? LEPIRUDIN, BIVALIRUDIN,
Desirudin, ARGATROBAN, DABIGATRAN

A

Dabigatran is PO while all the rest are parenteral

54
Q

is a monoclonal antibody used for
reversal of Dabigatran toxicity (needs dose adjustment for
renally impaired patients)

A

IDARUCIZUMAB

55
Q

HEPARIN MOA?

A

Activates antithrombin III
(inactivates thrombin or Factor IIa, Factor IXa & Factor Xa
by forming stable complexes with them)

56
Q

DOC for anticoagulation during pregnancy, given with
thrombolytics for revascularization procedures, given with
GPIIb-IIIa inhibitors for angioplasty and stent placement

A

Heparin

57
Q

MOA ENOXAPARIN, Dalteparin, Tinzaparin, Danaparoid,
Nadroparin, FONDAPARINUX

A

Binds and potentiates effect of antithrombin III on
factor Xa (more selective). Less effect on thrombin

58
Q

ENOXAPARIN Advantage over regular heparin is

A

higher bioavailability
and t½

59
Q

rivaroXaBAN [C], ApiXaBAN, BetriXaban, EdoXaban MOA?

A

Inhibit Factor Xa in the final common pathway

60
Q

Antidote for Apixaban, Rivaroxaban

A

andeXAnet alfa

61
Q

MOA WARFARIN [X], DICUMAROL, ANISINDIONE

A

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

62
Q

STREPTOKINASE, ALTEPLASE,
Anistreplase, Reteplase, Tenecteplase, Urokinase MOA?

A

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

63
Q

ANTIDOTE for STREPTOKINASE, ALTEPLASE,
Anistreplase, Reteplase, Tenecteplase, Urokinase

A

Antidote is AMINOCAPROIC ACID

64
Q

Competitively inhibits plasminogen activation
by inhibiting tPA

A

TRANEXAMIC ACID

65
Q

Tranexamic Acid contraindication?

A

DIC

66
Q

Prevention of hemorrhagic diatheses in newborns

A

VITAMIN K1 (PHYTONADIONE),
VITAMIN K2 (MENAQUINONE)

67
Q

MOA DESMOPRESSIN [B], Vasopressin [C], Terlipressin

A

ADH/vasopressin V2 receptor agonist

68
Q

Uses of Desmopressin, vasopressin, terlipressin

A

Hemophilia A, von Willebrand’s disease, Central
diabetes insipidus

69
Q
A

PLE_PHARMA (16 decks)

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