DRUGS USED TO TREAT DISEASES OF THE BLOOD

Question 1

• essential metallic component of heme

Answer 1

IRON

Question 2

Transport protein of Iron

Answer 2

Transferrin

Question 3

Storage protein of Iron?

Answer 3

Ferritin

Question 4

most common type of anemia

Answer 4

microcytic hypochromic anemia caused by iron deficiency

Question 5

Laboratory Picture of Iron deficiency?

Answer 5

Laboratory picture: ↓ Iron, ↓ Ferritin, ↑ TIBC

Question 6

megaloblastic anemias are caused by

Answer 6

a deficiency of vitamin B12
or folic acid

Question 7

Most common type of megaloblastic anemia?

Answer 7

Pernicious Anemia

Question 8

Cause of pernicious anemia?

Answer 8

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

Question 9

Iron Hematopoietic growth factors oral preparations?

Answer 9

FERROUS SULFATE, Ferrous gluconate,
Ferrous fumarate, Ferrous carbonate

Question 10

Iron Hematopoietic growth factors parenteral preparations?

Answer 10

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

Question 11

most prominent SE for oral iron

Answer 11

GI Distress

Question 12

Most notable SE of Dextran-containing parenteral iron

Answer 12

Anaphylaxis and allergic reactions

Question 13

Treatment of Iron intoxication?

Answer 13

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

Question 14

state of chronic iron overload that da

Answer 14

CHRONIC IRON INTOXICATION: HEMOCHROMATOSIS

Question 15

Triad of hemochromatosis?

Answer 15

Triad: CIRRHOSIS, DIABETES MELLITUS, SKIN PIGMENTATION

Question 16

Treatment of chronic iron intoxication: hemochromatosis?

Answer 16

o Phlebotomy
o chronic administration of DEFEROXAMINE or DEFERASIROX

Question 17

Heavy Metal Chelators? (3)

Answer 17

DEFEROXAMINE, DEFERASIROX, DEFERIPRONE

Question 18

what vitamin is required for normal DNA synthesis

Answer 18

Folate

Question 19

Folate is absorbed in what part of the intestine?

Answer 19

proximal jejunum

Question 20

• deficiency usually presents as megaloblastic anemia

Answer 20

FOLIC ACID DEFICIENY

Question 21

What vitamin deficiency causes neurologic defects?

Answer 21

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

Question 22

Where is vitamin B 12 absorbed?

Answer 22

absorbed in the distal ileum in the presence of intrinsic factor

Question 23

main stimulus for the production of EPO?

Answer 23

Hypoxia-inducible factor 1

Question 24

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

Answer 24

EPO

Question 25

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

Answer 25

Myeloid Growth Factors

Question 26

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

Answer 26

Thrombopoietin

Question 27

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

Answer 27

Megakaryocyte growth factor

Question 28

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

Answer 28

ELTROMBOPAG

Question 29

4 mechanisms of Hemostasis?

Answer 29

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

Question 30

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

Answer 30

Arterial thrombosis

Question 31

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

Answer 31

Nonselective, irreversible COX 1&2 inhibitor

Question 32

SE of COX inhibitors?

Answer 32

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

Question 33

* Associated with Reye syndrome in children * Do not use as NSAID for gout

Answer 33

ASPIRIN

Question 34

SAMTER TRIAD?

Answer 34

Asthma, ASA Sensitivity, Nasal Polyps

Question 35

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)

Answer 35

Abciximab, Eptifibatide, Tirofiban

Question 36

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

Answer 36

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

Question 37

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

Answer 37

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

Question 38

SE of TICLOPIDINE?

Answer 38

Thrombotic thrombocytopenic purpura

Question 39

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

Answer 39

MOA Cilostazole, Dipyridamole

Question 40

used only in refractory intermittent claudication in patients with PAD.

Answer 40

CILOSTAZOL

Question 41

2 major types of anticoagulants:

Answer 41

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

Question 42

Antidote of Heparin?

Answer 42

Protamine

Question 43

Antidote of warfarin?

Answer 43

Vitamin K, FFP

Question 44

In pregnancy, heparin or warfarin?

Answer 44

Heparin

Question 45

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

Answer 45

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

Question 46

Pathophy of HEPARIN-INDUCED THROMBOCYTOPENIA

Answer 46

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

Question 47

Management of Heparin Induced Thrombocytopenia?

Answer 47

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

Question 48

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

Answer 48

Warfarin

Question 49

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

Answer 49

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.

Question 50

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

Answer 50

Warfarin Skin Necrosis

Question 51

Management of warfarin-Skin Necrosis?

Answer 51

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

Question 52

LEPIRUDIN, BIVALIRUDIN, Desirudin, ARGATROBAN, DABIGATRAN MOA?

Answer 52

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

Question 53

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

Answer 53

Dabigatran is PO while all the rest are parenteral

Question 54

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

Answer 54

IDARUCIZUMAB

Question 55

HEPARIN MOA?

Answer 55

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

Question 56

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

Answer 56

Heparin

Question 57

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

Answer 57

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

Question 58

ENOXAPARIN Advantage over regular heparin is

Answer 58

higher bioavailability and t½

Question 59

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

Answer 59

Inhibit Factor Xa in the final common pathway

Question 60

Antidote for Apixaban, Rivaroxaban

Answer 60

andeXAnet alfa

Question 61

MOA WARFARIN [X], DICUMAROL, ANISINDIONE

Answer 61

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

Question 62

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

Answer 62

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

Question 63

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

Answer 63

Antidote is AMINOCAPROIC ACID

Question 64

Competitively inhibits plasminogen activation by inhibiting tPA

Answer 64

TRANEXAMIC ACID

Question 65

Tranexamic Acid contraindication?

Answer 65

DIC

Question 66

Prevention of hemorrhagic diatheses in newborns

Answer 66

VITAMIN K1 (PHYTONADIONE), VITAMIN K2 (MENAQUINONE)

Question 67

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

Answer 67

ADH/vasopressin V2 receptor agonist

Question 68

Uses of Desmopressin, vasopressin, terlipressin

Answer 68

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