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Hem/Onc > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What is the main stimulus for EPO production?

A

Hypoxia

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2
Q

Where in the fetus and real human is EPO made?

A

Fetus- liver
Human- birth

(lol am i stirring some opinions)

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3
Q

These are the molecules that stimulate the activity of T cells an dmacrophages.

A

Interleukins and interferons

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4
Q

Which molecule prevents the overproduction of platelets and sensitizes them to the effects of thrombin and collagen?

A

Thrombopoietin (TPO)

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5
Q

What are the 2 pathologies in which EPO is used?

A

Chronic kidney disease and cancer

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6
Q

What is the sstructural difference between rhEPO and darbepoietin (NESP)?

A

The # of sialic acid groups attached to the protein (NESP has 2 extra)

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7
Q

The extra sialic acid groups on NESP does what to the lifespan?

A

has a 3-fold longer 1/2 life than EPO (and thus a higher potency)

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8
Q

What happens if Hb levels in EPO-treated pts exceedes 12 g/dL?

A

Death, serious CV evetns, and stroke

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9
Q

5-azacytidine, decitabine, hydroxyurea, and butryates are all used to treat what condition?

A

Sickle cell anemia

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10
Q

For the sickle cell drugs, what is the main MOA to treat the condition?

A

↑ HbF production

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11
Q

Which sickle cell drug does this describe?

Relatively safe for long-term administration
Slower induction of HbF but effective in 60% of pts
↓ the frequency of painful crises by 50% and # of tranasfusions required

A

Hydroxyurea

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12
Q

Filagastrim (recombinant human G-CSF) and PEG-filagastrim are used to treat what condition?

A

cancer-induced and chemo-induced neutropenia

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13
Q

What is the main MOA for filagastrim?

A

dose-independent increase in absolute neutrophil count

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14
Q

PEG-filagastrim is basically the same as filagastrin but what’s the difference?

A

It’s metabolized slower –> less injections

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15
Q

What is the ONLY drug for chemo-induced thrombocytopenia?

A

rhIL-11 (oprelvekin)

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16
Q

What is the major drawback to rhIL-11?

A

It has to be administerd prophylactically because there is a 1-2 week delay from administration to a clinically significant increase in platelet count

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17
Q

What is the main immune complication to heavily bioengineered variants of TPO?

A

excess risk of anti-TPO autoantibodies, which could supress antural platelet production

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18
Q

So if heavily engineered TPO can cause problems, what type of TPO should u use to prevent neutralzing antibodies?

A

Lightly bioengineered variant (rhTPO)

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19
Q

What are the 2 new TPO agonists?

A

Eltrombopag

Romiplastim

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20
Q

What condition are eltrombopag and Romiplasmin approved for?

A

ITP

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21
Q

What are the problems with rhIL-11 (oprelvekin)?

A

fatigue, fluid retention, A-fib

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22
Q

What is the condition that tretinoin (all-trans retinoic acid/ATRA) is used for?

A

Acute promyelocytic leukemia

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23
Q

In acute promyelocytic leukemia, what ruses to the PML gene, which blocks differentiation?

A

RARa

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24
Q

How does ATRA cause more normal granulocytes?

A

Stimulates differentiation

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25
Q

However, what is the life-treatening problem with ATRA treatment?

A

Overproduction of WBCs

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26
Q

What is the most common parasitic infection in the world?

A

Malaria

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27
Q

How many species cause malaria?

A

5 plasmodial parasites: P. falciparum, P. vivax, P. ovale, P. malariae, and P. knowlesi.

The most serious type is P. falciparum.

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28
Q

What is the most important Sx of malaria?

A

Fever

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29
Q

Why is fever an important manifestation of malaria?

A

It’s caused by intravascular lysis of erythocytes and release of merozoites into the blood

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30
Q

What is the main problem with older agents used to treat malaria?

A

Resistance

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31
Q

Since old drugs like chrolorquine, primethamine and sulfadoxine have resistance, what is the new DOC for malaria?

A

Artemisinin dereivative

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32
Q

How does chloroquine kill the malaria parasite?

A

Prevents the detoxification of the a toxic product of Hb (ferriprotoporphyrin IX)

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33
Q

What is the main MOA of arteminisin for the Tx of malaria?

A

when activated by Fe, is forms a ROS –> aklylate many proteins and heme –> toxic to plasmodia

(iron pulls the pin on the arteminisin grenade)

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34
Q

What is one advantage of artemisinin over other anti-malarial agents?

A

it’s better tolerated than most other antimalarial agenets

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35
Q

What is the main CNS complication of artmisinin?

A

Brainstem neuropathy (potentially lethal) and auditory impairment

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36
Q

Since artemisinin has a short half life and resistance could occur, what should it be used with?

A

A secondary drug

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37
Q

This is the malarial drug that is an electron carrier in the respiratory chain and severely disrupt the metabolic processes of plasmodial mitochondria.

A

Quinone

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38
Q

What 2 malaria spp is primaquine used, which causes haptic malaria?

A

P. vivax and P. ovale

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39
Q

Which 2 pts should not be given primaquine as it can cause fatal hemolysis?

A

G6PD deficient pts

Pregnant chicks

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40
Q

What is the MOA of atovaquone for malaria?

A

Inhibits the interaction btwn reduced ubiquinone and the cytochrome bc1 complex and disrupts electron transport.

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41
Q

Why is stopping electron transport a good wat to kill malaria?

A

They require it to regenerate oxidixed DHOD –> used for DNA replication

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42
Q

Which subunit does doxy bind to?

A

30s

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43
Q

Can u use doxy in pregnant ladies?

A

No

44
Q

Which subunit does clindamycin bind to?

A

50s

45
Q

Can u use clindamycin in pregnant ladies?

A

No

46
Q

Since sulfadoxine is a PABA analogue, which enzyme does it inhibit, which is an essential encyme in the folic acid synthesis pathway?

A

DHP synthase

“s”ulfa for “s”ynthase

47
Q

Which drug is a folate analogue that competitively inhibits parasite DHF reductase for the Tx of malaria?

A

Pyrimethamine

48
Q

Sulfonamide-pyrimethamine inhibit which stage of P. falciparum?

A

Schizont stage

49
Q

Is Sulfonamide-pyrimethamine used in other strains of malaria, other than P. falciparum?

A

No

50
Q

The sensitivity of Metronidazole is directly related to the activity of what?

A

PFOR

51
Q

Which organisms is PFOR selective for?

A

protozoa ONLY

so its used for ameba and anaerobic organisms

52
Q

What is the pharmacokinetic reasons why Iodoquinol and paromomycin are effective against intraluminal amebae?

A

They’re poorly absorbed in the Gi tract –> reach high concentrations in the lumen of the colon

53
Q

Protozoa, anaerobic bacteria, and helminths are all parasites in which what drug has activity against?

A

Nitrazoxamide

54
Q

What is the MOA for Nifurtimox to treat Chagas disease?

A

Creates toxic intracellular ROS in the parasite

55
Q

What are the 2 first-line drugs against Leishmania?

A

Sodium stibogluconate and Melglumine antimonate

56
Q

What do mammals have in their nervous systems that helminthes dont, which makes helminthes more susceptible to neurotoxins?

A

Myelin

57
Q

Since Ivermectin does NOT kill adult filarial worms, what is it’s MOA, which causes it to be used every 6-12 months for 5-10 years?

A

Prevents the production and release of new microfilariae

58
Q

What is the DOC for schistosomiasis?

A

Praziquantel

59
Q

What is the DOC for certain filarial infections, which KILLS ADULT filarial worms, and is thus a curative agent?

A

Diethylcarbamazine (DEC)

60
Q

Which coag factors does warfarin inhibit?

A

VII, IX, IXa, X, and II

61
Q

Which coag factors does heparin inhibit?

A

Xa, IIa

62
Q

t-PA stimulates which reaction?

A

Plasminogen –> plasmin

63
Q

UFH and LMWF serve as a catalytic surface to which what 2 molecules bind?

A

Antithrombin III

Serine proteases

64
Q

Which factor does UFH and LMWH inhibit, indirectly by activating antithrombin III?

A

Xa

65
Q

UFH is good at inhibiting Xa and what other coag factor?

A

thrombin

66
Q

What is the MOA of lepirudin?

A

Direct thrombin inhibitor

67
Q

What is the disease that herudin/lepirudin used to treat?

A

Heparin-induced thrombocytopenia

68
Q

What is the drug that is also a direct trhombin inhibitor that binds to both the activa sir and exosite of thrombin, and is used in anticoagulation in pts undergoing coronary angioplasty/graphy?

A

Bivalirudin

69
Q

What is the direct thrombin inhibitor that is used for heparin-induced thrombocytopenia, and binds ONLY to the active site of thrombin?

A

Argatroban

70
Q

Waht is the anticoagulant that prevents the activation of vitamin K?

A

Warfarin

71
Q

How long does it take warfarin to have its effects?

A

18-24hrs

72
Q

Warfarin is given to prevent thrombosis in pts undergoing what other drug therapy?

A

Heparin

73
Q

Which form of heparin is at risk for bleeding and HIT?

A

UFH

74
Q

What is the problems with hirudin/lepirudin?

A

bleeding and a small percentage of patients may develop anti-hirudin antibodies, limiting the long-term effectiveness of this agent as an anticoagulant

75
Q

The reactivation of what coag factor is a problem with bivalirudin?

A

thrombin

76
Q

What pts cant u give bivalirudin?

A

Renal insufficiency pts

77
Q

Why is argatroban super sweet?

A

No adverse rxns

78
Q

What is the most serious and predictable toxicity for warfarin?

A

Bleeding

79
Q

For severe hemorrhage, what is the rapid thing u should give for warfarin problems?

A

FFP

80
Q

Should u give warfarin to pregnant ladies?

A

No

81
Q

What are the drugs that diminish warfarins anticoagulant effect?

A

Cholestyramine
Barbiturates, carbamazepine, phenytoin, rifampin
Vitamin K (reduced)

82
Q

What are the drugs that enhance warfarins anticoagulant effect?

A

Chloral hydrate
Amiodarone, clopidogrel, ethanol (intoxicating dose), fluconazole, fluoxetine, metronidazole, sulfamethoxazole
Broad-spectrum antibiotics
Anabolic steroids (testosterone)

83
Q

What is the MOA of streptokinase to degrade clots?

A

forms a stable complex with plasminogen –> cleavag eof palsminogen –> plasmin

84
Q

What are the 2 clinical indications for streptokinase?

A

STEMI

PE

85
Q

What are the 2 adverese effects of streptokinase?

A
  1. capable of producing antigenic responses with repeated administration
  2. systemic fibrinolysis
86
Q

Waht are the 3 clinical indications for recombinant t-PA (Alteplase)?

A
  1. STEMI
  2. PE
  3. CVA
87
Q

What is the generitcally engineered variant of t_PA with a longer half life and increased specificity for fibrin, and can be administeres as a double bolus?

A

Reteplase

88
Q

This variant of t-PA has an increased fibrin specificity and increases its resistance to plasminogen activator inhibitor 1, and has a long 1/2 life?

A

Tenecteplase

89
Q

This antiplatelet agent irreversibly inhibits the ADP-pathway of platelet activation.

A

Clopidogrel

90
Q

What are the clinical indications for using clopidogrel with ASA?

A

Coronary intervention

Prevention in pts with recent MI, stroke, or PVD

91
Q

Is clopidogrel more or less favorable (as fase as adverse effects) than ticlopidine?

A

More

92
Q

Waht are the 3 major adverse effects of ticlopidine?

A

Neutropenia
Thrombocytopenia
TTP

93
Q

Which GpIIb/IIIa receptor blocker isa monoclonal Ab and reduces both logn and short-term ischemic events in pts undergoing high-risk percutaneous coronary intervention?

A

Abciximab

94
Q

Which GpIIb/IIIa receptor blocker is a synthetic peptide, and is used to ↓ ischemic events undergoing percutaneous coronary intervention, unstable angina, and for NSTEMI?

A

Eptifibatide

95
Q

Which GpIIb/IIIa receptor blocker is a nonpeptide tyrosine analogue that reversible antagonizes fibrinogen binding to the GpIIb/IIIa receptor, and is used for acute coronary syndromes?

A

Tirofiban

96
Q

This is a receptor of platelet PDE, which inhibits cAMP degredation, and is used with other drugs?

A

Dipyridamole

97
Q

Dipyridamole + warfarin are used for which pts?

A

inhbit thrombus formation on prosthetic heart valves

98
Q

Dipyridamole + ASA are used to reduce liklihood of thrombus formation in which pts?

A

Thrombotic diathesis (bleeding tendency)

99
Q

What are the adverse effects of Dipyridamole, as a result of the coronary steal phenomenon?

A

Angina in CAD pts

100
Q

enoxaparin, dalterparin, and tinzaparin all belong to which anticoagulant?

A

UFH and LMWH

101
Q

Fondapurinux belongs to which class of anticoagulants?

A

Xa inhibitors

102
Q

Lepirudin, bivalirudin, argatroban, dabigatran belogn to which anticoagulant class?

A

Direct thrombin inhibitors

103
Q

Which condition is recombinant activated protein C (r-APC) used in?

A

severe sepsis

104
Q

Which factors are synthesized by vitamin K?

A

II, VII, IX, and X

also protein C and S

105
Q

What is the Moa of aminocaproic acid to reduce perioperative bleeding during coronary artery bypass grafting?

A

Inhibits plasminogen and plasmin

106
Q

What is the MOA of Aprotinin to to decrease perioperative bleeding & erythrocyte transfusion requirement in pts treated w/ aprotinin during cardiac surgery?

A

Inhibiting fibrinolysis

Inhibiting thrombin to promote platelet activity by preventing hyperstimylation

107
Q

Which drug increases the risk of post-op acute renal failure?

Aminocaproic acid or Aprotinin

A

Aprotinin

Hem/Onc (5 decks)

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