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pharm 2 > HEME AND ANTI PLATELET AND ANTI COAGULANT > Flashcards

HEME AND ANTI PLATELET AND ANTI COAGULANT Flashcards

1
Q

what group are GM-CSF and G-CSF part of?

A

myleoid growth factros –> they stimulate one more more myleiods subtypes such as neutrophils, monocytes, eosinophils

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2
Q

whats an example of recombinant GM-CSF?

A

Sargramostim given IV or subQ

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3
Q

what is the famous S/E for sargramostin? what group is it part again? what other s/e are there ?

A

GM-CSF, myeloid growth factors

CAPILLARY LEAK SYNDROME - widepspread edema
other: bone pain, flu sx, diareehha, supraventricular arrhythmias,

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4
Q

when should you give sargramostin GM-CSF?

A

marrow transplation duh
**chemotherapy **since they wipe out of myleiod lineage
and **neutropenia **

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5
Q

what group is filgrastim and PEGfilgrastim past of?

A

G-CSF, myloid growth factors
diff between G-CSF and GMCSF is that G-CSF is peygalated so theres an extra sugar attacked to the molecule

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6
Q

when would you give filgrastin or PEGfilgrastin? again what group?

A

Group: G-CSF, myloid growth factors
give for marrow transplation, chemotherapy, neutropenia - the SAME THING as GM-CSF

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7
Q

what is the S/E for filgrastim/PEGfiltragasimt - G-CSE?

A

they DO NOT HAVE CAPILLARY LEAK SYNDROME ONLY GM-CSF (sargramostim)
S/E: bone pain, splenomeaglay, sickle crissi

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8
Q

what group is interleukin 11 part of?

A

Thrombo growth factors

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9
Q

what group is eltrombopag part of? when would you give it?

A

eltrombopag –> thrombo GF
given for ITP, CA chemotherapy, various myeloiddisplastic syndromes
**liver dz/hepatitis **- since Thrombo GF are made in the liver, if your liver is fucked up then you wont make any GF

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10
Q

what group is romiplostin part of ? describe the molecular structure

A

romiplostin is part of thrombo GF - it is a small peptide grafted on the AA globulim –> will bind to thrombo receptor

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11
Q

when would you give romiplostin?

A

mainly for ITP

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12
Q

what group is oprelvekin part of ?

A

recombinnat IL-11 (part of thrombo GF)

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13
Q

when would you give oprelvekin? what is a S/E?

A

**CA chemotherapy **–> you would give it wtih eltrombopag
S/E: **fluid retention ** - u fix it with diuretics

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14
Q

what group is epoetin alfa and darbepoetin part of?

A

recombinant erythropotein made in the kidney

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15
Q

what is the diff between epoetin and darbepoetin?

A

epoetin - shorter LIFE SPAN 4-5HRS
Darbepoetin - LONGER life span 1-1.5days

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16
Q

which erythoprotein recombinant is BETTER for CKD?

A

darbepotin since it has a longer half life

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17
Q

when would you give epoetin or darbepoetin?

A
  1. surgery - when you know youll lose alot of blood or going into surgery
  2. CKD - makes sense since kideny cant make their own eythropotein
  3. chemotherapy - make sense everything is wiped out
  4. **AIDS, ahteltes **- helps give them a booster
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18
Q

what are the S/E to eopeotin/darbepoetin?

A
  1. iron def - the marrow makes ALOT of RBCs so the irons stores wont be able to release quickly enouh so YOU HAVE TO GIVE IRON SUPPLEMETS
  2. CV event - excessive RISE to hematocrit
  3. HTN - RISE in hematocrit since you have more red cell volume pushing agasint the cell vessles

remember : if theres a INC of 4x in hematocrit in a two week period, then D/C

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19
Q

when would you give ferrous sulfate?

A
  1. gravid - 15-30mg
  2. iron deficency - 200mg
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20
Q

what is the efficacy of giving iron PO?

A
  1. reticulocyte count will increase a week after
  2. Hgb/Hct will improve weeks after with an inc of 2g/dL or more by 3-4 weeks :)
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21
Q

what are the S/E to ferrious sulfate? how would you tx the s/e?

A
  1. GI SX
  2. poisoning - mostly with GI SX
  3. you would TX the S/E with deferoxamine which will remove the iorn from the blood from ferratin but it doesnt do anything to hemoglobin
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22
Q

when would you give parental iron?

A

its for MOM AND DAD

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23
Q

what group is iron dextran part of ?

A

parental iron

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24
Q

what group is ferric gluconate part of ?

A

parental iron

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25
Q

what group is iron sucrose part of?

A

parental iron

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26
Q

out of the three parenteeral irons, which one has a S/E of anaphylasis and CDK?

A

iron dextran - can casue analphylaxis
iron sucrose - cause CKD

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27
Q

what are the S/E of parenteral irons?

A

analphylaxis - iron dextrose
arthralgia - those with RA and gets IV iron? RA will flare up
normal S/E - HA, malaise, fever, lymphadenopathy, urtricaria

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28
Q

what is the S/E for B12 and the danger about it?

A

B12 S/E - neuro issues
Danger - unpredicatable absoprtion –> when you tx megaloblsatic anmeia, you give B12 and folate but enough folate corrects the hematolgic issues but you have absorbed enough b12

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29
Q

what drug interfers with folate?

A

antiepileptic drugs like phenobarbitral or phenytoin

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30
Q

EASY: what are the duties for PG12, thromboxane, ADP, llb/lla receptors, PAR and what drugs inhibits each of them ?

A
  1. PG12 - plaelletes aggregation
  2. TXA2 - works to activate the platelets, ASA inhibits it
  3. ADP - DEC cAMP, clopidogrel inhibits
  4. llb/lla receptor - allows plaelltes to stick tg, abciximab inhibits it
  5. PAR - F2A (thrombin) works on the PAR receptors, vorapaxar inhibits it
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31
Q

what is the MOA for asprin?

A

remember that ASA inhibits TXA2
MOA:
1. normally arachnoid acid enters a catalytic pocket in the COX1 enzyme. Arachnoid acid –> prostaglandin –> TXA2 –> plaelelte activation
2. but ASA will work by going into the pocket and acetlying the serine group thats already here which wil IRREVERSIBLY ACETYLATE THE COX1 ENZYME
3. this will prevent arachoind acid from going in –> no more TX2 –> no activation of plaletes

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32
Q

why wont other NSAIDS do the same MOA?when it comes to ASA MOA

A

other NSAIDS does not covalently desotry the COX enzymes so SOME TXA is made but with ASA theres no TXA2 made so aspirn is the best !

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33
Q

what meds would you give for stroke/MI?

A

give clopidrogel(inhibits adp) with asprin which will inhibit plaeltes

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34
Q

whats anotehr drug you would give for stroke/MI?

A

vorapaxar(inhibits PAR) with asprin for stroke/MI

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35
Q

what drugs would you give for STROKE pt ONLY?

A

you would give dipyridamole with asprin

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36
Q

what are the S/E to asprin?

A

becasue you are inhibting paleltles, the S/E you will get are:
1. BLEEDING
2. GI ulceration - prostaglandin turns off their PP so you have excess acid production
3. tinituts - only at HIGH dose
4.**tachy, resp alkalosis, met acidosis **

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37
Q

whats another name ofr ADP receptor?

A

P2Y12 antagonists

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38
Q

how does clopidogrel work?

A

it will bind to the ADP receptor and there WONT BE a dec in cAMP so cAMP will INCREASE and this will prevent palelte activation

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39
Q

what enzymes is clopidrogel activated by?

A

CYP2C19 in the liver

40
Q

when would you give clopidrogel? what group is it part of?

A

ADP group - P2Y12 antagonist
1. **prevention of stroke/MI **
2. coronary STENT placement to prevent palelte from sticking tg
3. drug drug interaction - be careful since **PPI inhibits 2C19 **

41
Q

what group is prasugrel part of?

A

**P2Y12 antagonist **

42
Q

what group is ticagrelor part of ?

A

**P2Y12 antagonist **

43
Q

what group is cangrelor part of?

A

**P2Y12 antagonist **

44
Q

what are the S/E for prasugrel? again, what group is it part of?

A

Group: P2Y12 antagonist
S/E: less incidence for stent thrombosis than clopidogrel but THERES INC risk of BLEEDING than clopidrogel

45
Q

what group and S/E do ticagrelor have?

A

group: P2Y12 antagonist
S/E: high chance of bleeding than clopidogrel

46
Q

out of the three P2Y12 antaognist, which is given IV that he told us about?

A

Cangrelor given IV

47
Q

what are PDE, phsiphodiesteranse antagonist?

A

MOA: PDE normally breaks cAMP but antagonist wont break cAMP so there will be INC of cAMP
(we like dec cAMP

48
Q

what group is dipyridamole part of?

A

PDE antagonist - it will prevent the dec of cAMP so we will have HUGE CONC. of cAMP

49
Q

what are the S/E of dipyridamole?

A

vasodilation, smooth musucle relaxaation

50
Q

when would yo ugive dipyridamole?

A

valve replacement surgery or stent replacement surgery **ONLY WITH ASPRIN FOR STROKE PREVENTION **

51
Q

what are PAR1 antagonists?

A

thrombin F2 will bind to PAR receptors and activate platles so with PAR1 antaognist they will not activate platleltes

52
Q

what group is vorapaxar part of?

A

PAR1 antagonists

53
Q

what is MOA for vorapaxar? S/E?

A

MOA - bind to thrombin receptor and inhibit it!
remember: it is used with ASA to present MI/stroke

S/E: bleeding
drug drug interaction CYP3A4
- inhibtior = keto, inducer = rifampin

54
Q

what group is abciximab part of?

A

GP 2b/3a inhibitors

55
Q

what group is eptifibatide part of?

A

GP 2b/3a inhibitors

56
Q

what are the half lives of abciximab and eptifibatide ?

A

abciximab - lives 30 mins
eptifibatide - lives 15 mins

57
Q

what is the MOA for GP 2a/3b inhibitors?

A

they block the 2b/3a receptors –> prents fibrin and VwF from crossing linking the plaletes

58
Q

when should u give GB 2a/3b inhibators?

A

GIVE IT DURING PROCEDURES so plaletes cannot cross link with each other
- perioperative procedures like stent placement, angioplasty

it is OFTEN COMBINED WITH HEPRAIN

59
Q

what are the S/E to GP 2b/3a inhibators?

A

bleeding, thombocytopenia

60
Q

which factors turn off the coag cascade?

A

protein C protein S

61
Q

which factors do antithrombin neutrialize?

A

F2a, F7a, F9a, F10a, F11a, F12a

62
Q

what kind of molecule is unfractionaed heprain?

A

unfractionaed heprain is a glycosamide glycan that is found in the liver

63
Q

explain the MOA of unfractionated heparin

A

heprain contains a pentasaccharide which is rich in sulfate groups –> it binds to ANTI THROMBIN –> casues change and allows for INACTIVATION OF F10a

unfractionaed heprain also has a polysaccride LONG TAIL –> which will wrap around the anti thrombin molecule and push thrombin –> accelerate the rate of **inactivation of F2a **

64
Q

what ratio do unfractinaed heprain have ?

A

1:1
anti 10a:anti 2a

65
Q

what group does enoxaprin belong to?

A

LMWH - low molecular weight heparin

66
Q

what is so unique about enoxaprin?

A

it has a SHORTER TAIL compared to unfractionazed heprain

67
Q

what is the effect of having a short tail for LMWH?

A

since it has a short tail it cannot inactivate F2, it can still inactivate F10 but not F2

68
Q

what is the ratio for LMWH?

A
  • Anti- Xa:IIa 2-3:1
69
Q

what group does fondaparinux belong to? what is the improtance?

A

fonaparinux - heparin group
importance: it has NO TAIL its just a pentasaccride that will bind to anti thrombin and inactivate F10 but NOT F2 since there is NO TAIL

70
Q

explain the method of heprain resistance? also how is heprain cleared by?

A
  1. cleared by macrophags
  2. heprain has production of endogenous peptide which will want to bind to antithrombin and heprain wont work –> peptides likes to work in the acute phases in humans –> so if someoen has chronic inflammatory or cancer, heprairn will not work as well
71
Q

how is LMWH and fondaparinux cleared by?

A

remember that heparin is cleared by macrophages
LMWH and fondaparinux - cleared by renal but it can accumlate in those with kidney dz

72
Q

when would you give heparin?

A
  1. DVT, PE - to prevent clot formation
  2. MI - prevents re thrombosis and embolization of vessels
  3. unstable angina - with ASPIRN
73
Q

what are the S/E to heparin?

A
  1. bleeding duh
    - TX with** protamine sulfate **- prevents hemorrahages
  2. LFT - inc LFT only problamatic if someoen has liver dz
  3. Osteroporosis - only worrisome in those peri-post menopausal women
  4. HYPERK - heprain inhibits aldosterone which can increase K levels
74
Q

what are the contradindication of heprain?

A
  1. ANY active bleeding
  2. hemophilla
  3. intracranila hemorrhage
  4. known GI lesion
  5. recent lumbar puncture
  6. history of HIT - heprain induces thombocytopenia
75
Q

is heparin save or unsafe in gravidity?

A

SAFE - ‘HEPARIN LEAVES BABY HAPPY’

76
Q

what is the MOA of warfarin ?

A
  1. glutamyl carboxlase is needed to to make VIT K
  2. reduced VIT K will be converte to oxidaized VIT K
  3. oxideid VIT K will then be converte to reduced VIT K and the cycle can repeast
  4. IF OXIDED VIT K CANNOT TURN INTO REDUCED VIT K –> THEN theres no VIT K to carboxylate the VIT K DEPENDEANT CLOTTIGN FACTORS (2 7 910 C S)
  5. warfrin inhibits the VIT K reductase enzyme (whcih goes from oxidied vit K to reduced version)
77
Q

know the major half life for 2 10 9 S C 7 in that oder

A

50 > 36 > 24 > 24 >8 > 6

78
Q

what is the importance of the half life for each of the collecting factors?

A

if someone is prone to get a clot and you put them on warfarin, they will lose Protein C (1/2 of8) and S (1/2 of 24) but F2 will stay for 50hours so coagulation will STILL happen ode
* “initially pro coagulation EARLY ON since it inhibits C and S“

79
Q

explain the bridge method wiht warfrin medication

A

if someone is being tx w heparin and are at risk of thrombosis –> u CANT start on warfarin, you NEED TO START on heparin (fast onset, short duration) TO NEUTRALIZE EVERYTHING  then put on warfarin to monitor INR which WILL WORK

80
Q

what is wafrin metabolzied by? 4x

A
  • CYP2C99, 1A1, 1A2, and 3A4
81
Q

what are the indication for warfrin?

A
  1. DVT/PE - after you give heprain, bridge for five days before giving warfrin
  2. stroke prevention - direct F10 inhibators are PERFED when treating AFIB
82
Q

what type of drug is perfers when treating AFIB?

A

F10 inhibaitors

83
Q

what are the S/E for warfrin?

A
  1. BLEEDING
    inr 2-3 = less risk of bleeding, first sign of bleeding = RED URINE
    inr 4-10 = hold warfrin recheck INR then restart
    inr 10+ = hold drugm, give PO VIT K, once inr normal restart
  2. hemorrhages - tx w clotting factors, fresh frozen plasma, VIT K depdenant factors
84
Q

what are the other s/e for warfrin? and what about gravid?

A
  1. GI
  2. skin necrosis
  3. toe discoloration
  4. drug drug interaction

GRAVID- BAD - warfin decares wars on baby

85
Q

whats the MOA for direct factor 10a inhibators?

A

directly inhibits F10a, doesnt need checkup with INR

86
Q

what group does rivaroxaban belong to?

A

adirect F10ai

87
Q

what group does apixaban belong to?

A

direct F10ai

88
Q

what group does edoxaban belong to?

A

direct F10ai

89
Q

what F10ai is metabolzied by CYP3A4?

A

Rivaroxaban and apixaban

90
Q

when would you use direct F10ai?

A
  1. stroke prevention - AFID
  2. acute DVT, PE - alterntive to heprain or warfrn
91
Q

what are the s/e to direct F10ai?

A
  1. bleeding - if it leads to hemorrage then tx with andexnet alpha
    andexnet –> prevents hemmorages its a deocy drug that will bind to the drug itself and PREVENT from binding to F10a
92
Q

what is andexenet alpha used for ?

A

to prevent hemorrage since its a decoy drug that prevents the drug from binding to F10a

93
Q

what are the three fibrinolytic drugs?

A

these are t-PA drugs
1. alteplase
2. reteplase
3. tenecteplase

94
Q

what is the MOA for tPA drugs?

A

tPA are fibrinolytic drugs
MOA - TPA is released from damanged endothelil cells –> which converts plasminogen to pasmin –> which will degrade fibrin and clot

95
Q

what are the indication and S/E for tPA-fibronolytics?

A

indication: PE, ischemia stroke, AMI
S/E: mucosal bleeidng or severe bleeding in brain vessels

96
Q

what group is ε-Aminocaproic acid part of?

A

PRO-coagulants

97
Q
A

pharm 2 (3 decks)

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