Therapeutics Iii Exam 6- Acute Coronary Syndrome

Front 1

non modifiable risk factors for ACS (3)

Back 1

male (gender)
age
genes

Front 2

modifiable risk factors for ACS (8)

Back 2

diabetes
htn
hyperlipidemia
smoking
obesity
sedentary lifestyle
diet
hyperhomocysteinemia

Front 3

5 etiologies (or pathophys..) for ACS
like what is happening that can cause it

Back 3

CAD- plaque disruption
then platelets aggregate
can be vasospasm (cocaine)
thrombosis
inflammation (hs-CRP)
or a combination

Front 4

pathophys of ischemia

Back 4

imbalance between O2 supply and demand

Front 5

imbalance of supply/demand slide

Back 5

review- listen to lecture again...

Front 6

signs of MI- are there definitive signs?

(5 signs)

Back 6

there are no characteristic signs- varies a lot

often see HF with JVD and S3 sounds
ECG changes or arrhythmias
hypotension
hypertension
leukocytosis (due to demargination off of vessel walls after acute MI or ACS- also due to stress)
increase in biomarkers if it's MI

Front 7

6 sx of MI

Back 7

midline anterior chest discomfort
arm, back or jaw pain
dyspnea
diaphoresis
N/V
anxiety- feeling of doom

Front 8

3 risk factors for silent MIs

Back 8

diabetics - can't feel things
women - present in weird ways
elderly

Front 9

ACS presenting with normal EKG or other ischemic changes (that aren't ST elevation) (2)

how to differentiate?

Back 9

non-STEMI
unstable angina

non-STEMI will have elevated troponins (hours after)

Front 10

other things that can lead to weird EKGs (2) how to resolve

Back 10

Hypoxia, dehydration can lead to ischemia- fix underlying issue and recheck EKG

Front 11

STEMI- what is it? how to handle/treat?

Back 11

complete occlusion-->will lead to death if not reversed

Clot buster meds if unable to get immediate surgery (then air lift for surgery- not that effective) --> best choice is angioplasty, cath lab

Front 12

cardiac biomarkers for ACS (4)

Back 12

troponins
CK-MB
LDH1-2
AST

Front 13

role that troponin can play in assessing ACS (2)

Back 13

1) it can rule out MI- if after 3 troponin tests, it still has not elevated, we can probably rule it out

2) if the patient has an elevated troponin we can keep taking the levels to get a "peak" which is correlated to how much dmg was done to the heart

Front 14

troponin- peak, how is it typically ordered
remains elevated for how long (not at peak just above normal limits)
clearance

Back 14

peaks in 12-20 hours
ordered q8h x3 to rule out MI
remains elevated for up to 10 days
is renally cleared

Front 15

CK-MB- normal range
diagonstic range
when does it return to baseline
when does it peak

Back 15

CK-MB is 5% of total CK
>5% CK-MB is diagnostic of MI
peaks in 6-24 h
returns to normal in 48 h (shorter than troponin- can be used for assessing reinfarction)

Front 16

when does AST peak during MI?

Back 16

1-2 days

Front 17

4 ways to dx acute MI

Back 17

1) elevated cardiac biomarker lvls > 99th percentile of UNL with one of the following: ischemic sx, ECG changes suggestive of new ischemia, Q-wave development (i guess...abnormal q waves), hypomotility/abnormality of wall motion on imaging

2) sudden death w/ cardiac arrest/ECG change
3) elevated cardiac biomarkers > 3x UNL after PCI
4) biomarkers > 5x ULN after CABG
(these are higher limits due to screwing with heart in surgery releases these biomarkers anyway)

Front 18

4 therapeutic goals for AMI

Back 18

minimize infarct
salvage ischemic myocardium
prevent or minimize complications
decrease m/m

Front 19

3 ways to salvage ischemia in ACS pt

Back 19

medical (drugs)
PCI (percutaneous coronary intervention)
open heart surgery (CABG- coronary artery bypass grafting)

Front 20

PCI examples (3)

Back 20

PTCA (percutaneous transluminal coronary angioplasty) or balloon angioplasty
stents
atherectomy

Front 21

TIMI risk - the points (7)

Back 21

age >=65 yo
>= 3 risk factors for CAD (smoking, DM, HTN, HLP, FH)
known coronary artery stenosis of >50%
ST seg deviation on EKG
>= 2 episodes of angina in last 24 h
use of aspirin within preceding 7 days (marker for risk)
elevated biomarker lvls

Front 22

TIMI score interpretation - when to admit, blahblah

Back 22

6-7? Or 5, 6-7?- cath lab-->early invasive strategy
0-1, 2- outpatient management- probably not a huge deal
3-4- grey zone- at least admitted to step down /telemetry unit , consider EI

Front 23

general treatment strat for NSTEMI/UA (2)

Back 23

1) antiischemic and antithrombotic therapy
2) then select: EI or EC (selectively invasive)

Front 24

EI vs EC

Back 24

EI- immediately do diagnostic coronary angiography and revascularization within 2-3 days of sx onset

EC- is catheterization and revasc only if ischemia recurs or is unresolved (i.e use meds unless shit blows up)

Front 25

when is EI indicated? (3)

Back 25

EI most strongly supported in pt with EKG changes, elevated troponin and/or >=3 TIMI risk factors

Front 26

supportive care for STEMI/UA (and NSTEMI) (4)

Back 26

MONA
morphine
oxygen
nitrates
aspirin

Front 27

morphine dosing

Back 27

1-4 mg IV q5-15 min prn

Front 28

3 purposes of morphine

Back 28

analgesic
anxiolytic
preload reduction due to histamine related vasodilation (relieves pulmonary edema)

Front 29

O2 "dosing" and when to give
purpose

Back 29

4L/min if O2 sat still <90%
route in ALL pt for at least the first 6 h
may limit ischemic myocardial injury

Front 30

dosing of nitroglycerin- 2 steps
when to give the second step

Back 30

0.4 mg SL x3 doses prn
if still persistent pain after 3 doses, or if HTN/HF:
do nitro 5 mcg/min infusion, increasing by 5-10 mcg/min q5-10 min up to 200 mcg/min

Front 31

why give ASA to suspected AMI

Back 31

risk of death decreases by 23% in suspected AMI

Front 32

dosing of ASA upon admit
outpatient

Back 32

325 mg STAT (as in, chew if they aren't already taking it)

as an outpatient-->81 mg qd 4 LYFE

Front 33

higher chronic dosing of ASA (higher than 75-162 mg) whachu think

Back 33

not really more beneficial and you get increased risk of bleeds, esp if used with plavix

Front 34

goal of giving anticoag (like the heparins)

Back 34

anticoag goal: prevent total occlusion of infarct related artery

Front 35

4 options for anticoagulation

Back 35

UFH gtt
LMWH
fondaparinux
bivalirudin (if they are going to cath lab)

Front 36

when to start anticoag for NSTEMI/UA

when to stop (2)

Back 36

start anticoag if troponin+ or ongoing chest pain that's unrelieved by SL NTG

STOP if troponins negative and chest pain resolved
OR
post-cath (presume the lesion has been fixed at this point)

Front 37

heparin- binding site...?

Back 37

30% of molecules contain pentasaccharide high affinity binding site for AT III

Front 38

3 things to monitor for heparin
and frequency (for one of them)

Back 38

monitoring: q6h aPTT until therapeutic (1.5-2.5x control)
then aPTT q12-24h

H/H to assess for bleeding (idk how frequent...)

platelets for HIT

Front 39

LMWH MoA

monitoring test

Back 39

LMWH- MoA: less effect on thrombin due to shorter length (primarily acts on Xa)

NO APTT- have to use anti factor Xa

Front 40

UFH vs. LMWH (3) benefits and AEs

Back 40

lower 30 day incidence of death or nonfatal MI with LMWH vs UFH
similar bleed rates
LMWH consistently provided benefits to EC strat patients

Front 41

enoxaparin dosing
renal dosing

Back 41

1 mg/kg q12h

unless renally compromised: CrCl < 30, then it is q24h

Front 42

2 options for LMWH

Back 42

enoxaparin
dalteparin

Front 43

fondaparinux MoA

monitoring

Back 43

synthetic heparin pentasaccharide- binds to AT leading to conformational change that increases its affinity for Xa

thus no APTT monitoring (anti Xa)

Front 44

fondaparinux contraindication

Back 44

CrCl < 30

Front 45

fondaparinux vs. LMWH

Back 45

equivalent to enoxaparin in outcomes but with less bleeding (this is better tolerated)

Front 46

fondaparinux- downside

Back 46

increased catheter related thrombi so must use supplemental UFH if giving PCI

Front 47

MoA of bivalirudin (and all rudins)

Back 47

direct thrombin inhibitor-->inhibits thrombin mediated platelet activation

Front 48

renal dosing for bivalirudin

Back 48

renally dosed (decrease to 1mg/kg/h if < 30 CrCl)

Front 49

indication for bivalirudin

Back 49

alternative to hep/LMWH in EI strategy ONLY- no data for EC

Front 50

thienopyridine MoA

Back 50

adenosine diphosphate receptor antagonists (important in platelet activation)

Front 51

3 thienopyridines (3)

Back 51

ticlodipine (not used anymore due to neutropenia)
clopidogrel
prasugrel

Front 52

clopidogrel- dosing for NSTEMI/UA

Back 52

300-600 mg load (usually see 300 mg) then 75 mg QD

Front 53

prasugrel dosing for NSTEMI/UA

Back 53

60mg load (more potent) then 10 mg QD

Front 54

uses (indications and durations of therapy) for thienopyridines in NSTEMI/UA (3)

Back 54

in place of asa if allergic
in ADDITION to asa for up to 9 months if EC
in addition to asa for up to 12 months if after PCI

Front 55

when NOT to give plavix

how to handle if situation occurs where you did take it

Back 55

if CABG planned, do not give
increases risk of bleeding- wait 5 days before surgery if they have been giving plavix

Front 56

loading does of plavix for PCI and when to give

Back 56

300-600 mg load > 6 h before PCI

Front 57

duration of plavix therapy if pt is on med management for his NSTEMI/UA

Back 57

>=1 month if medically managed. ideal is 1 year

Front 58

duration of plavix therapy if pt has BMS

Back 58

>= 1 month following bare metal stents (ideal 1 year)

Front 59

duration of plavix therapy if pt has DES

Back 59

ONE YEAR following DES (drugs are usually anti cell proliferating so prevent endothelial cells from covering the metal- which = MORE CLOTZ if off of anticoag)

Front 60

restenosis- what it do
results in what

Back 60

stent gradually narrows or get obstructed by tissue ingrowth
this results in return of angina

Front 61

incidence of restenosis in BMS vs DES

Back 61

15% in BMS
6% in DES

(just...know it's less in DES)

Front 62

properties of prasugel (3)

Back 62

1) 3rd gen thienopyridine
2) more consistent platelet inhibition than with plavix
3) Cmax occurs in 30 min vs. 2hr with plavix (faster Cmax)

Front 63

prasugel activation (2 steps)

Back 63

converted by intestinal esterases to inactive form (prodrug- same with plavix)

CYP metabolism to active metabolite

Front 64

prasugel activation enzymes (2)

Back 64

CYP3A4/2B6

Front 65

prasugel metabolism (2)

Back 65

S-methylation
cysteine conjugation

Front 66

plavix CYP enzymes (bioactivaiton) (2)

Back 66

plavix- 2C9/2C19

Front 67

prasugel- differences in AUC in what 3 pops (3)

Back 67

higher in asians and
pt >= 75 yo
<60 kg (highest AUC)

Front 68

prasugel dosing adjustments (2)

Back 68

none in renal/hepatic
5 mg qd if < 60 kg (not studied prospectively)

Front 69

prasugel vs plavix

Back 69

major bleeding unrelated to CABG with prasugel

Front 70

prasugel usage in ACS- evidence?

Back 70

no studies in medical management of ACS

Front 71

relative CI for prasugel (2)

Back 71

avoid concurrent NSAIDS and warfarin
generally not rec'd if >= 75 yo unless diabetic or prior MI (in which case benefit > risk)

Front 72

contraindications for prasugel

Back 72

contraindicated if prior TIA/CVA

Front 73

prasugel dosing prior to CABG- how long to hold?

Back 73

hold >= 7 days prior to CABG