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Cath Sap 5 board prep > Pharma > Flashcards

Pharma Flashcards

1
Q

Why not higher doses of asa and what trial helped with this?

A

Higher dose is higher bleeding risk seen w cure trial

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2
Q

Vorapaxar moa and when is it given why not used more widely

A

Reduction in ischemic endpoints but sig bleeding with asa Studied in its with cad and pad Moa is par inhibitor and thromboxane a2 Traced acs was asa + plavix+ vorapaxar stopped early bc of ich Trap 13 percent reduction in ischemic events with a 66 percent increase in bleeding risk

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3
Q

3 steps to platelt mediated thrombosis and pharma targets?

A
  1. Adhesion - Vwf, endothelial damage, collagen (no approved antiplt agents in this category 2. activation - ADP (most antiplts), TXA2, TXA 3. Aggregation - GIIb/IIIa links together - this is the final common pathway so is very potent.
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4
Q

why are GIIb/IIIa so potent

A

final common pathway for clotting so very potent.

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5
Q

ASA trials need to know

A
  1. Lancet 1988 with stemi ASA + SK 8% vasc death comared to 13% in placebo and 10.7% w asa a;pme amd 1-/4 wotj SL a;pme/ 2/ Caorms MEJM in 1985 50% RRR with ASA over no ASA in MI or cardiac death.
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6
Q

PCI w/o ASA

A

meta-analysis 2013 worse ischemica events (not looking at other adjunctive therapies)

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7
Q

Stemi load ASA

A

325 chewed. load

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8
Q

MOA of P2Y12 differnt MOAs ****

A
  1. Clopidogrel - P2y12 2 step esterification and then oxiadtion with CYP45 3A 2. Prasugrel one step oxifation to active form 3. Ticag CPTP active drug All block ADP from binding P2Y12 and starting the Gi@ coupled receptor to activate platelets.
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9
Q

MOA of the 3 P2Y12 differnt MOAs ****

A
  1. Clopidogrel - P2y12 2 step esterification and then oxiadtion with CYP45 3A 2. Prasugrel one step oxifation to active form 3. Ticag CPTP active drug All block ADP from binding P2Y12 and starting the Gi@ coupled receptor to activate platelets.
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10
Q

General MOA of P2Y12/CPTP

A

block ADP inteactoin with P2Y12 recpetor preventing platelet activation.

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11
Q

first p2y12 study

A

STARS - (leon MB) ticlopidine + asa ten either asa alone or asa + warfarin in reducing ST after BMS. rate of 30 day STent trhombosis. 2.9 with ASA alone, 2.7 with ASA + coumadin, 0.5 with asa + ticlopidine.

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12
Q

STARS trial

A

0.5 % with ticlopidine + ASA , 2.9 % ASA alone, 2.7% with ASA + Coumadin

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13
Q

1st clopidogrel trial

A

CURE and PCI-cure reduction with clopidogrel.

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14
Q

cyp for clopidogre

A

cyp450 3a

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15
Q

current oasis 7

A

600 with UA/NSTEMI or STMEI and early invasive very slight reduction in CV death/MI stroke after PCI

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16
Q

Prasugrel Trial ST Bleeting?

A

Triton timi 38 2.4 % vs. 1.1% ST (definite 0.8 vs 2.0% p < 0.0001) 12K pts. increased bleeding and black box warning > 75, low body weight < 60 g , hx of stroke (and 7 days of surgery

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17
Q

3 times when cant use prasugre

A

increased bleeding and black box warning > 75, low body weight < 60 g , hx of stroke (and 7 days of surgery

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18
Q

Prasugrel 5?

A

trilogy ACS , 75 years of age (same as clopidogrel if allergy)

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19
Q
  1. Why dyspnea with ticagrelor?
  2. Frequency of dyspnea plavix vs. ticag
  3. daily asa dose
A
  1. bc of adenosine reuptake is blocked by ticagrelor.
  2. 7.8% vs. 13,8%
  3. 81 mg, ticag used this to explain the North american group
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20
Q

Delayed absorption of antiplatets in STEMI

A

up to 6 hours even with the more potent agents, exacerbated by opiates.

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21
Q

Guidline strength for patients not at high risk for bleeding w/ ticag and prasugrel over clopidogrel

A

IIa

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22
Q

Updated guidelines 2016/2017 for duration of dapt

SIHD?

ACS?

A

SIHD - 6 month HBR 3 mo

ACS 12 mon HBR 6 mo

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23
Q

Does PCI complexity favor longer dapt

What are the complex features?

A

Yes if complex features consdier >=12 mo DAPT

3:2:1 (3 vessels,3 stents, 3 lesions, bifurcation with2 stents, length greater than 60 or cto

3 vessels treated

>= 3 stents placed

>= 3 lesions

Bifurcation with 2 stents

stent lenght > 60 mm

CTO

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24
Q

After CABG if ACS event what is dapt rec

Non ACS CABG DAPT

A

Should have plavix added to complete 12 mo of dapt.

IIb for clopidogrel after SIHD CABG

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25
Q

3 mo dapt when based on guidelines

A

HBR and SIHD

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26
Q

Plavix binding to P2Y12

Clopidogrel is first or second gent

Abs CI for Prasugrel

A

irreversible

seocnd I guess

prior TIA or stroke

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27
Q

when load with tigcag in setting of cangrelor

crushed ticag/prasugrel

A

any time bc both reversible

beneficial

28
Q

Broad classification of vasodilators

A

endothelium dependent–> need to bind to a receoptor leading to the release of Nitric oxide—> Ach, serotonin,

endothelium independent –> Nitroprusside, nitroglycerine (needs o2)

29
Q

Draw basic pathway of NO synthesis

A

Nitric diffuses across cell or endothelial dependent vasodilators bind recepto to rellease NO—> GTP —> G-cyclase–> cGMP –> relaxation

30
Q

How dose ACh work

A

binds muscarinic receptor–> if healthy vasodil effect, if diseased vasoconstr can be used to assess endothelial dysfunction (research tool)

31
Q

3 common drugs for no reflow

A
  1. Verapamil
  2. Adenosine
  3. Nitroprusside
32
Q

Pressor summary chart based on pressor type

A

DA Alpha1, beta 1 , DA

Dobutamine b1, B2

Epi Alpaa, B1, B2

Isoproternol B1, B2

pehnyl Alpa

Vasopressin v1 v2 on smooth muscle and vaodilate

33
Q

vasoreceptors and function

A

DA vasodil kidney

Alpha vasoconstrict peripheral

B1 increases heart rate and onctractility

B2 vasolilates sm in lung

V1 vasocon periperhal v2 free water retention

34
Q

trail of CV shock

A

SOAP II de backer nejm NE betther than DA (also the case in septic shock)

DA more arrhtythmia.

35
Q

concious sedation def

A

drug induced depression of consciousness during which patients respond purposefully to verbal commands either along or accomanied by tactile stim

36
Q

ASA class?

Benzos and opiates have ____ effects

Minimum recovery time after concious sedation

A

Approprate for 1-3

Class I is normal and health,

Class II is mild systemic dz

Class III is severe systemic dz, nondecomp

Class IV severe systemic dz, decompensated

Class V moribund, survival unlikel

Synergistic

2 hours.

37
Q

Reversal agents and dosages

A

Naloxone (Narcan) 0.4 mg duration 30 min

Flumazenil 1 mg duration 30 min

38
Q

Severe MS awaiting procedure and bp drops what medication do you give

A

Phenyl (works rapdily and dont want to increase HR which will worsenen the gradients)

39
Q

Two class one medications for monoVT

A

bb and amio (also good for polymorphic)

40
Q

Gusto mod bleeding HR

Gusto Severe (5g)

A

~2

3.2

41
Q

RR reduction for heparin + asa in ACS

A

0.67 HR (so 1/3 RR or 30%)

42
Q

Metanalysis of medical rx heparin vs. enox

STEEPLE

Synergy

A

20% RRR combination of Essence and timi 11b

Lovenox in elective PCI (IV) vs. heparin, Montalescot et al NEJM 2006 no difference with higher bleeidng in heparin.

STEMI/NSTEMI loaded with heparin vs. enox –> no difference but if switched it was bAD

43
Q

study showing if switched from lovenox to heparin it was bad

A

Synergy trial

44
Q

***What do guidelines say about those receiving lovenox prior to PCI

A

if only had one dose of neox or received dose 8 to 12 hours prior to pci then give 0.3 mg/Kg IV at the time of PCI.

It also says dont switch to UFH if received lovenox (no one listens to this).

45
Q

Patient had 2 doses of enox with last dose 7 hours prior do you need to give more IV

A

no. Need to give 0.3 mg/kg IV if 8 to 12 hours from last dose and only had one dose. This is some bs that will be on the test.

46
Q
  1. Heparin, LMWH, fonda all act on what
  2. All bival trials basically show what?
  3. Exception
A

basically Xa (via thrombin 3)

vs. Heparin + GPI no diff in ischemia with much less bleeding

Except in ISAR react 3 which shwoed no differ in either but was vs heparing alon as GPIs were left off.

47
Q

More recent Bival vs. Heparin trials and prolems (3)

A

EUomax Heat PPCI, Matrix

increased ST

48
Q

problem with bival recnt trials compared to heparin

A

more ST.

49
Q

ATLAS II TIMI 51

A

ACS added riva (to whatever rx on for ACS), 2.5 mg or 5 mg–> reduction in MACE at 2 years…. (still 20% reduction, with 3x riksk of bleeding and 4x increased risk for 5 mg–> FDA did not give an indiaction for this which is why we dont really do.

50
Q
  1. Study of riva added to DAPT
  2. If patient come to lab after receivn fonda in ED what do you give as far as UFH
A

Atlas timi 51 –> 2x increased risk of bleeding.

85 IU/kg heparin IV and only 60 IU/kg if on IIb/IIIa

51
Q

Anticoagulation with lysis key points

A
  1. UFH 1.5 to 2 x upper limit of lab x 48 hrs or until revasc
  2. Enoxaparin admin according to age weight and cr clearance given as an iv bolus followed in 15 min by SC dose, continue up to 8 days or revasc
  3. fonda admin with inital IV dose followed in 24 hours by daily SC injuectio as long as GFR > 30 continue up to 8 days or revasc
52
Q

Bival dosing in PCI

A

for those who had UFH wait 30 min the 0.75 g/kg lad then 1.75 mg/kg.h infusion

if already on the infusion give an additional 0.5 mg.gkand increase infusion to 1.75 mg/kg/h

53
Q

Goal ACT heparin

hepain load

A

250-300 hemotc and 300-350 hemochron unless on GPI then go for 200-250 on hemotec

no GPI 70-100 /kg

GPI 50-70 U/kg

54
Q

If use fibrinolsysi need ___ x 48 hours or if….

incidence of hit in LMWH

Severe bleeding incidence in current trials (gusto maj hb 5 untis

A

antithrombotic x 48 hours or if go to cath lab and reperfuse can stop.

<1% in LWMH

<1 %

55
Q
  1. 3 IIB/IIIa inhibitors
  2. Mol weight
  3. potency
  4. clearance
  5. t/12
A

eptifibatide (integralin) - comnetitive, 800, 1/2, renal, 2 hrs

tirofibran (aggrestate) competifiv, 500, 1/2, renal, 2 hrs

abciximab reopro - high affinity, 50,000, 1/2, proteolysi, 24 hrs

56
Q

Which GIIb/IIIat type gives disaggregation of clots

dosing?

A

all of them.

Abciximab - 0.5mg. kg then 0.125 mg/kg/min for 12 hours after PCI no renal adju

Tirofiban aggrestat 25 mcg (10 mcg bolus in a trial was inferior so increased) maintenc 0.1 for 18 hours need to dose reduce by 50% if GFR < 60). one with the high bolus

Eptibifibatide (extrasylabal so double bolus) 180 mcg/kg followed by 180 mcg/kg bolus followed by a maintence dose of 2.0 mcg/kg. min reduce by 50% 18-24 hours

57
Q

Worst SE of GPIIb/IIA

How long to stop prior to surgery

When give IIB/IIIa guidelines

A

tCP worse with abcicimab (can transfuse bc irrevs.)

4hrs for small mol 24 hours for apiximab

if not preloaded class I, otherwise only the highest risk for Mi.

58
Q

Type I indicationfor IIb/IIIa

A

none

59
Q

Cangrelor binds?

Board question

A

CTPT direct P2Y12 agonist. superior to clopdiogrel in 1 trial (champion pheonix)

if preloaded doesnt help. (not discussed in guidelnies)

Give clopdiogrel/prasugrel at end of infusion. pro drug short half life so will get metobolized off. (irreversible)

60
Q

dont give bival w/

A

gibb/iiia

61
Q

GL recommendation on preloading in NSTEMIU?

Why ticlopdinine go away

A

says to do it.

agranulocytosis (needed cbc q2weeks)

62
Q

PRU associated with adverse outcomes

other association with this ?

What polymorpms is assocaited with stnet thrombosis

general recommendations for testing

A

> 208

Bleeding is less.

homeozygote for cyp2c19 –> note the carrier status is common *2–>east asian–> black box warning for this.

not really recommended even thought its a moraker of fecresed risk.

63
Q

trial looking at PPI

Genetic testing Guidlines

A

cogent was negative (liberal) –> use pantoprazole

IIb or C.

64
Q

FDA recs for length of rx for dapt stoppage prior to sugery?

A

prasugrel 7 days

Ticag 5 days

plavix 5 days

65
Q

3 surgeries were bleeding risk too high for DAPT operation

A

intracranial

spinal

post chamber eye

66
Q
A

Cath Sap 5 board prep (12 decks)

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