Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacy CPS Flashcards > CARDIOLOGY > Flashcards

CARDIOLOGY Flashcards

1
Q

differences between STEMI and NSTEMI

A

STEMI: ST elevation +elevated troponin. Complete occlusion of blood vessels resulting in necrosis of myocardium

NSTEMI: ST depression + elevated troponin, partial occlusion of blood vessels resulting in necrosis of myocardium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

differences between stable and unstable angina

A

stable: exercise induced, no minimal ECG changes with no changes in troponin
unstable: often occurs while resting, sleeping or minimal physical activation. ST depression with no changes in troponin. Can lead to heart attack

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

symptoms of angina

A

chest heaviness, pressure, pain and discomfort.

chest symptoms may radiate to upper body, last <5 mins and received by rest or nitroglycerin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

symptoms of ACS

A

same as angina but

lasting > 5 mins and not relieved by nitroglycerin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

treatment for stable angina

A

chronic:
BB and/OR
NTG and/ OR
DPH ( long acting)

decreasing mortality:
anti platelet ( ASA or clopidogrel) statin
ACE-I or ARB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

how many total dose of NG spray can u administer

A

total 3 doses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what condition does ACS compromise of

A

unstable angina
NSTEMI
STEMI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is TIMI risk score ?

A

estimates mortality, recurrent MI or severe recurrent ischemia requiring urgent revascularization for patients with unstable angina and NSTEMI

high risk if TMI >/3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what medication to start post MI

A

A= ACE-I,
B- BETA BLOCKER
C- cholesterol - statin
D: DUAL ANTIPLALET

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

know treatment algorithms for UA/NSTEMI

A

SEE PIC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

when would you choose fibrinolytic vs PCI

what is the absolute CI?

A

fibrinolytic: <1 hr presentation, when PCI is not an option, delay to invasive strategy

PCI: skilled PCI lab available, high risk STEMI, , late presentation >3 hrs, diagnosis in doubt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

MOA of fibrinolytic?

CI?

A

altepase, tenecteplase

conversion of plasminogen to plasmin in the presence of of fibrin, resulting in fibrinolysis

any suspected hemorrhage or bleeding, known vascular lesion, or ischemic stroke within 3 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

know algorithm to STEMI

A

See pic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Which heparin should be used? how long should they be one this ?

A

UFH: STEMI patient receiving fibrinolytic.
LMWF ( enoxaparin has been shown to be superior to UFH in patients treated with tenecteplase

Heparins should be continued for a minimum of 48 hours ( or until PCI) and use can be extended in patients with high-risk features.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is the MOA of UFH? AND AE?

A

potentiates antithrombin, inhibits factor Xa and IIa

AE: bleeding, HIT , osteoporosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

when should we initiate beta blocker ? what should the HR be?

A

BB in the first 24 hrs to all patient without contraindications,

Titrate to resting HR: 55-65 bpm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

know duration of DAPT THERAPY

A

DAPT 1 year , if not at high risk of bleeding, continue DAPT for 3 years

if high risk after 1 year, SAPT ( ASA 81mg once daily or Clopidogrel 75 mg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

when should be hold DAPT therapy for surgery

A

BMS: at least 1 month after PCI
DES: 3 months after PCI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

switching between ticagrelor and prasugel?

A

prasugel to ticagrelor: no loading dose, ticagrelor 90 mg BID is recommended

Ticagrelor to prasugel: LD of 60 prasugel mg followed by 10 mg daily

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

switching from clopidogrel to ticagrelor or prasugel

A

clopidogrel to ticagrelor: LD ticagrelor of 180 mg followed by 90 mg BID

clopidogrel to prasugel: LD of 60mg followed by 10 mg regardless of timing of clopidogrel dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

when should u delay CABG surgery in patient taking ASA, clopidogrel , ticagrelor or prasugel?

A

ASA- continue

ticagrelor: 48-73 hrs (2-3 days) before CABG
clopidogrel: 48-73 hrs (2-3 days) before
prasugel: 5 dyas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

patient with AF without high risk features who undergo elective PCI:

A

AGE < 65 AND CHAD2=0

ASA+ clopidogrel: at least 1 moth for BMS and 3 months for DES and up to 12 months

Age >/ 65 OR CHAD2>/1
OAC + clopidogrel ( 1 month for BMS and 3 months for DES)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

AF + PCI FOR ACS or high risk elective PCI

A

AGE < 65 and CHAD2=0

ASA+ P2Y2 Inhibitor2 ( ticagrelor or prasugrel preferred over clopidogrel for ACS )- up to 12 months

AGE >/ 65 OR chads>/1

reduced OAC+ ASA+ Clopidogrel
ASA stop 1 day post PCI or anytime up to 6 months
followed by: clopidogrel + OAC up to 12 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

ACE-I and ARB AE

A

hypotension ( dizziness, headache), dry couch, hyperkalemia

ARB: similar to ACE but less dry cough and less angioedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

ACE- CI

A

pregnancy, bilateral renal artery stenosis, history of angioedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

list BB that are non-selective, selective , alpha blocking activity

A

non -selective: TPN ( Timolol, propanolol, nadolol)

B1 selective: Nebivolol, ABM (metoprolol, bisoprolol, atenolol) -

Non selective + ISA : pinolol

Selective + ISA: acetbutolol

with alpha blocking activity: labetalol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what the difference b/w different types of BB

A

B1 selective- less non cardiac AE due to B1 selectivity

alpha blocking activity: additional AE ( dizziness, edema, nasal congestion, postural hypotension)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

DHP- CCB AE ?

A

hypotension, headache, peripheral edema, flushing, gingival hyperplasia ( amlodipine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

why is nifedipine not recommended

A

avoid short acting nifedipine because it increases risk of MI and death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

NON-DHP CCB MOA and AE

A

Blocks voltage-gated calcium channels but are more cardio-selective than DHP-CCBS

constipation ( verapamil), anorexia, dizziness, bradycardia; heart bock, new or worsening heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

DI for NON-DHP CCB

A 
strong CYP3A4 Inhibitors 
BBS 
antiarrhythmics ( digoxin, amiodarone) 
anti-hypertensives
CYP3A4 substrates ( simvastatin) 
Verapamil can also increase digoxin levels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

AE of clopidogrel? MOA?

A

MOA: P2Y12 inhibitor

diarrhea, rash, bleeding, purpura

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

AE of prasugel and CI?

A

increased bleeding risk, headache, nausea, dizziness
hypercholesterolemia, atrial fibrillation

CI: >75 years < 60kg, history of ischemic stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what are symptom of atrial fibrillation

A

palpitation, tachycardia, SOB, light headedness, syncope, decreased exercise capacity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

describe different classification of atrial fibrillation ( paroxysmal, persistent, permanent/chronic )

A

paroxysmal: episodes lasting less than 30 seconds, terminating within 7 days ( spontaneous)

Persistent: lasting longer than 7 days up to 1 year
sinus rhythm restored by cardioversion or medications

permanent: continuous episode longer than 1 year, decision made not be pursue sinus rhythms restoration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what factors is included in CHADS-65 SCORE?

what is the score use for

A 
CHF ( 1 POINT ) 
HTN ( 1 POINT 
AGE >/ 65 
DIABETES 
STROKE (2 POINTS)

estimates risk of stroke in patient with afib

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

when would anti platelet be considered in AFIB?

A

< 65 YEARS, CHADS-65 <0 with CAD or PAD`

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

when would DOAC be preferred over warfarin?

A

NVAF: DOAC recommended

AF+ mechanical prosthetic valve or moderate mitral stenosis: warfarin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

BB preferred in the presence of : LV dysfunction, hypertension, CAD

A

LV dysfunction: bisoprolol or carvedilol
hypertension: atenolol or metoprolol
CAD: atenolol, propanolol or metoprolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

which DOAC can be dose down to 15 ml/min

A

apixaban

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

DOAC that has high risk of dyspepsia

A

dabigatran

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

DOAC that is dose once daily

A

rivaroxaban and edoxaban

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

when will u dose apixaban 2.5mg BID

A

A: age > 80
B: body weight <60 mg
C: serum creatinine> 133mmol/ L

meet 2/3 criteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

MOA of warfarin

A

inhibitors VKORC1

affect factors 2,7,9,10 and protein C and S

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

when is rhythm control preferred

A 
recently diagnosed AF ( within a year) 
highly symptomatic  significant QOL impairment 
multiple recurrences 
difficult to achieve rate control 
arrthymia-induced cardiomyopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

treatment for paroxysmal AF

A

low recurrence burden: observation + pill in pocket

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

which agent for rhythm control

A

Heart failure:
LVEF < 40%: amiodarone
LVEF > 40% amiodarone or sotalol

CAD : Amiodarone, dronedrone, sotalol

No HF or CAD: amiodarone, dronedrone, flecainide, propafenone, sotalol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

WHICH BB is preferred in AF and LVEF < 40%

A

bisoprolol, carvedilol, metoprolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

can we used ND-CCB in LVEF < 40%

A

NO, you can used LVEF >40% ( diltiazem or verapamil)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

CI of NDHP-CCB

A

pre-excitation, CHF, or LV dysnfuction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

which AAD needs to be combine with AV-nodal blocking agent, why?

A

flecainide, propafenone, both can decrease the refractory period of the AV node, thereby increasing the ventricular rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what is the pill in pocket strategy

A

flecainide or propafenone can be taken intermittently or as booster dose as outpatient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

AE of digoxin

A

anorexia, N/V, weakness, dizziness, visual changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

explain virchow’s triad

A

hemodynamic changes: alteration in blood flow, blood stasis or turbulence

Hyper coagulable state: change in clotting functions that can be inherited of acquired

vascular injury: damage to the blood vessels’ endothelium, activates the coagulation cascade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

treatment of HIT

A

start alternative agent: Lepirudin, fondaparinux, argatroban transition to warfarin once patient stabilized and platelets >100 000 /mm3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

difference between LMWH and UFH

A

potentiates anti thrombin III inactivating thrombin ( as well as Xa) and preventing
conversion from fibrinogen to fibrin

more predictable anticoagulation dose response than UFH, decreased incidence of HIT, decrease need for routine monitoring and decrease major bleeding compared to heparin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

antidote for UFH and LMWH

A

protamine sulphate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

when is UFH preferred over LMWH

A

UFH in severe renal impairment, those at high risk of bleeding who may require rapid reversal and patient who have very recently received thrombolytic therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

what is the role of fondaparinux

A

selective factor Xa inhibitor
better efficacy over heparins
does not require routine coagulation monitoring
** can be used in patient with current of history of HIT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

treatment for VTE with dabigatran

A

cannot be used as initial therapy- use full dose of LMWH or hepairin for 5-10 days before switching to dabigatran 150mg PO BID

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

switching heparin, LMWF or warfarin to DOAC

A

No need to bridge with heparin or LMWF
for warfarin, start DOAC when INR <2 ( dabigatran and apixaban) or when INR <2.5 ( edoxaban) or INR < 2.5-3 ( rivaroxaban)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

what are statin indicated conditions

A

LDL > 5.0 mol/ L

diabetes: age >40 years old, age >30 and DM x>/ 15year duration (Type 1 DM)
microvascular disease
CKD

Atherosclerotic cardiovascular disease ( ASCVD)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

when should we initiate statin for primary prevention

A

(1) all high-risk patients (≥ 20% 10-year risk); or (2) intermediate-risk patients (10%-19.9%) when LDL-C is ≥ 3.5 mmol/L (or ApoB ≥ 1.05 g/L or non-HDL-C ≥ 4.2 mmol/L). among intermediate-risk individuals men 50 years of age or older or women 60 years of age or older with 1 additional risk factor including low HDL-C, impaired fasting glucose, increased waist circumference, cigarette smoking, hypertension)

then statin indicated conditions

64
Q

should u start statin on patient on dialysis

A

no, but if they are already on statin at that time, it can be continue

65
Q

when should we consider PCSK9 ihbitiors

A

alirocumba and evolocumab
considered in very high-risk individuals (patients with familial hypercholesterolemia or in secondary cardiovascular prevention) whose lipid targets have not been reached with maximally tolerated lipid-lowering medication
has greater LDL lowering than statin

66
Q

MOA of statin: AE?

CI?

A

inhibit HMG CoA reductase

Myalgia, GI, headache, dizziness, increased CK and transaminases

CI: pregnancy, active liver disease

67
Q

can statin be used in pregnancy or breast feeding

A

no

68
Q

MOA of ezetimibe , AE

A

inhibits intestinal cholesterol absorption

AE: back pain, arthralgia, diarrhea, abdominal pain, fatigue, dizziness, headache.

69
Q

MOA of fibres and AE?

A

increased activity of PPARa which results in an increased of lipid metabolism

AE: Upper GI disturbances (nausea, abdominal pain, flatulence), myalgias.

70
Q

MOA of cholesteramine, AE?

conselling points?

A

binds to bile acids in the GI tract

constipation (>10%), bloating, abdominal fullness, flatulence

counsel: Administer other drugs 1 h before or 4–6 h after resin to limit possible reduced absorption in the GI tract.

71
Q

when is fenofibrate useful

A

high TG >2.3 mmol and low HDL-C

72
Q

what is 3 types heart failure

A

impaired inability to fill with ( diastole) or eject ( systole) blood

1: HF with preserve LVEF ( diastolic dysfunction): filling problems due to HTN ( LVEF >/50%)
2: HF with midrange EF ( LVEF 41-49%)
3: HF with reduced LVEF ( systolic dysfunction): pumping problems ( <40% )

73
Q

to compensate for decrease CO, body respond with 4 mechanisms

A

1: stimulation of RAAS: retains water and constricts blood vessels ( increase after load and preload)
2: increased SV ( stroke volume) to increase CO ( increase preload)

3: enlarging ventricular walls to increase Force of contract ( hypertrophy)
4: Increased HR to increased CO ( preload and after load)

74
Q

symptoms of hF

A

hypotension, dyspnea, systemic congestion, peripheral edema

75
Q

non-pharm treatment for HF

A 
salt restriction ( <2-3 g of Na+/day) 
fluid restriction: 2L/ day from all sources 
monitor weight 
treat risk factors: HTN, diabetes ( risk of HF reduced by 50% by managing HTN along :)
76
Q

know NYHA function classification of HF

A

I: No symptoms with ordinary activity

II: Symptoms occur with ordinary activity ( SOB)

III: Symptoms occur with less than ordinary activity

IV: Symptoms occur at rest or with minimal activity

77
Q

What is treatment for midrange and persevere EF

A

symptomatic relieve: diuretic for congestion and managing risk factors

78
Q

treatment for HF-rEF

A

ACE-I OR ARB OR ARNI
BB ( metoprolol, carvedilol and bisoprolol)
MRNA
SGLT2I ( dapa and empa)

79
Q

what is the role of ivabradine?

A

sinus rhythm with a resting heart rate ≥77 bpm

80
Q

what is the role of nitrates/ hydralazine

A

reduces mortality and morbidity in black patients with NYHA class III–IV HF and is recommended in addition to standard therapy (ACE inhibitor, beta-blocker with or without MRA) in this settin

81
Q

which ARBs showed decreased in mortality with HF

A

candesartan and valsartan

82
Q

switching from ACE-I to ARNI

A

washout period of 36h required when switching from ACE to ARNI but no washout required when switching from ARB

83
Q

what is the role of digoxin in HF? what is the usual dose range

A

** does not reduce mortality

considered in Ventricular rate control in patient with AF not controlled on BB or who cannot tolerate BB

0.0625–0.25 mg daily

84
Q

target trough levels for digoxin and when should we measure them

A

Measure trough serum concentrations at least 8 hours after administration and adjust the dose to maintain the serum concentration between 0.6 and 1.2 nmol/L

85
Q

which drug do not show reduce mortality in HF

A

diuretics ( furosemide)

digoxin

86
Q

what is systolic and diastolic BP

A

systolic: heart muscles contract causing elevated BP since blood is pumped out of the heart
diastolic: heart muscle relaxes and decrease BP as blood fills the heart

87
Q

know values for:
isolated systolic HTN
hypertensive emergency
hypertensive urgency

A

isolated: >140/ <90 mmhg
emergency: >180/120 mmHg with organ damage
hypertensive urgency: >180/120 mmhg and no organ damage

88
Q

what is blood pressure?

A

BP= cardiac output (CO) x systemic vascular resistance ( SVR)

89
Q

explain the RAAS system

A

kidney releases renin in response to hypotension, sympathetic stimulation and decreased blood flow to the kidneys
angiotensin II: increased cardiac contractility and CO
increased aldosterone synthesis–> increased Na/H20
vasoconstriction –> increased SVR ( systemic vascular resistance)

90
Q

resistant hypertension

A

bp above target while on 3 or more BP at optimal doses

91
Q

what is defined as hypertension HIGH RISK patient

A

50 years old AND SBP 130-190 AND one or more of the following:
clinical or sub clinical cardiovascular disease OR CKD OR estimated 10-year global cardiovascular risk >/ 15% OR 75 years old

92
Q

threshold for intitation of antihypertensive therapy

hypertension high risk patient AND Treatment target

A

> 130/ N/A

target <120/ N/A

93
Q

threshold for intitation of DM patient AND Treatment target

A

threshold: >/ 130/ 80

goal <130/ 80

94
Q

threshold for intitation of moderate-to-high risk patient and LOW risk AND Treatment target

A

moderate-high risk
threshold: >/140/ 90
goal < 140/90

low risk
threshold >160/100
goal: <140/ 90

95
Q

1st line HTN treatment in patient without other compelling indications

A 
thiazide /thiazide like diuretics 
ACEI
ARB
LA-CCB
BB
96
Q

HTN+ DM+ (microalbuminaria, renal disease, CVD Or other CV risk: 1st and 2nd line

A

1st: ACEI-ARB
2ND: addition of of DHP-CCB over thiazide/ thiazide like diuretic

97
Q

HTN in African american patient

A

ACEI/ARB not preferred unless other compelling indications ( kidney production or HF)

98
Q

HTN and pregnancy?

A

1st: methyldopa, labetalol, long acting nifedipine, and other BB
2nd: hydralazine, clonidine or other thiazide diuretics PO

99
Q

Difference between TIA and stroke

A

TIA: disruption in blood flow to the brain resulting in damage
neurological deficit lasting <24 hr ( usually <30 mins) and may be reversible

Stroke: same as TIA but neurological deficit lasting >24 hrs and may be irreversible

100
Q

treatment of stroke?

A

alteplase

100
Q

what is the criteria for administering alteplase

A

administer alterplase within 4.5 hrs of symptoms onset

d\

101
Q

what is Alteplase CI

A

any source of active hemorrhage or any condition that could increase the risk of major hemorrhage after altepase

102
Q

what is the dose of apletplase

A

0.9 mg/kg to max of 90mg infused over 60 mins

103
Q

target door to alteplase

A

less than 60 mins

104
Q

When would u administer ASA

A

Administered ASA 160mg at least 24 hrs AFTER tPA once CT excludes intracranial hemorrhage

105
Q

would u aggressive lower BP in stroke>

what should BP be after alteplase

A

no, it will cause hypo-perfusion

BP should be lowered and maintained below 185/110 before altephase and kept below 180/105 mmHg for the next 24 hrs after

106
Q

What is the single most important modifiable risk factor for stroke

A

BP

107
Q

1st line treatment for raynaud phenomenons

A

DHP- CCB
60 mins before exposure to the cold
Alpha 1 adrenergic prazosin
Regular usage to avoid syncope/orthostasis

Alternative:
PDE5

108
Q

Treatment for supra ventricular arrthymia

A

procainamide

109
Q

what is orthostatic hypotension

A

drop in systolic BP >20mmHg or diastolic BP >10 mmHg when sitting to an upright position.

110
Q

Treatment for Orthostatic hypotension

A

midodrine, fludrocortisone

111
Q

warfarin INR range

A

2-3

mechanical valvue 2.5-3.5

112
Q

when should u check INR after dose adjustment

A

no earlier than 2-3 days ( INR change normally 3-7 days)

113
Q

factors that can change INR

A

1) antibiotics, azole antifungals, synthroid dose changes can increase INR

vitamin K rich foods ( green leafy vegetables, soy, avocado)

alcohol
current fever, diarrhea, flu, recent cold

Liver Disease can increase INR

114
Q

when should u stop warfarin for preoperative which does require bridging

A

stop 5 das pre- op and obtain INR value on POD-1, use therapeutic LMWH for about 3 days pre-op, last pre-op LMWF dose should be 24 hrs Pre op

115
Q

MOA of thiazide and AE?

A

MOA: Na+ CI- co- transporter inhibition in the kidney tubules

AE: diuresis, hypokalemia ( decrease Cl, mg,
increase Ca, hyperuricemia

116
Q

MOA of loop diuretics and AE

A

bumetanide, furosemide

AE: hypokalemia, increased urinary frequency and dehydration

117
Q

Which drug belongs to vasodilators and AE

A

Hydralazine, isosorbide, nitroglyerin,
Dilation of blood vessels and smooth muscle relaxation

AE: headache, fushing, hypotension and syncope,

118
Q

what are significant drug interactions with vasodilators

A

PDE-5 inhibitors ( sildenafil drugs)

119
Q

what is the MOA of doxazosin, prazosin, and terazosin? AE?

A

peripheralalpha 1 adrenergic receptors inhibitors

AE: postural hypotension, headache & palpatations,

120
Q

MOA of methyldopa?

A

stimulation of central alpha adrenergic receptors

121
Q

MOA of ivabradine?

A

inhibition If which results in decrease heart rate

122
Q

HR has to be what to administer ivabradine

A

HR > 70 BPM

123
Q

MOA of digoxin and AE

A

inhibits Na-K ATpase

GI (N/V/D)
fatigue and dizziness
Bradycardia; AV blocks

124
Q

which BB also belong to CLASS III antiarrythmic

A

sotalol

125
Q

disadvantage of UFH which limits its used

A

narrow therapeutic range, need for lab monitoring and increased risk of HIT

126
Q

if patient previous had HIT, which alternative drug can be used

A

fondaparinux due to lack of immune mediated effect on platelets, always still use with caution

127
Q

antidote for UFH and LMWH

A

Protamine sulphate

128
Q

what the loading dose of clopidogrel should be in a patient with ST-elevation myocardial infarction (STEMI).

A

300-600mg

129
Q

Which of the following drugs are NOT recommended in ST-elevation myocardial infarction (STEMI)?

A

Calcium channel blockers increase morbidity and mortality in patients with STEMI and are not recommended. They may be used cautiously to relieve ischemia or to achieve rate control in patients with atrial fibrillation if beta-blockers are contraindicated.

130
Q

what is the MAX dose tenecteplase

A

The recommended total dose should not exceed 50 mg and is based upon patient weight.

131
Q

Which of the following laboratory tests is MOST indicative of myocardial injury?

A

troponin

132
Q

what are important contraindication of BB

A

severe bradycardia ( <50bpm)
2nd and 3rd degree AV block
severe hypotension

**ASTHMA is not a CI

133
Q

(LMWHs) have the Health Canada approved indication for the treatment of acute ST-segment elevation myocardial infarction (STEMI)?

A

enoxaparin

134
Q

Which of the following lab values should be monitored every 6-12 months for patients taking direct oral anticoagulants (DOACs)?

A

Serum creatinine (SCr). It is prudent for patients who are receiving a DOAC to have an assessment of kidney function, hemoglobin and platelet count every 6-12 months and with any acute medical illness, since worsening of renal function may warrant a change in the dose of a DOAC,

135
Q

Which of the following oral anticoagulants has a once daily dosing regimen for stroke prevention in non-valvular atrial fibrillation?

A

Rivaroxaban

136
Q

pre-operative management of DOAC and post operative

A

in low-moderate bleeding risk: give last dose 2 days before procedure
in high risk: give last dose 3 days before surgery ** except for dabigatran, give last dose 5 days before surgery

resume on day after surgery ** 24 hrs post operative

137
Q

what does HAS-BLED stand for

A 
H: hypertension 
A: abnormal liver/ renal function 
S: stroke history 
B: bleeding 
L: labile INR 
E: elderly ( >./ 65) 
D: drug/alcohol usage
138
Q

what important DI should we be aware of with DOAC

A

Drugs that inhibit P-gp can INcrease systemic exposure to DOACs and increase risk of bleeding. Concomitant use of the strong P-gp inhibitors (e.g., ketoconazole) and apixaban, dabigatran and rivaroxaban is contraindicated.

139
Q

is regular lab work required for LMWH

A

no

140
Q

which type of diet will ELEVATE or DECREASE INR with warfarin

A

elevate: cranberry juice
decrease: food high in vitamin K including green leafy vegetables

141
Q

what would be considered a good TTR ( time to therapeutic range)

A

> 60%

142
Q

can acetaminophen affet iNR

A

yes, increase in dose >1-2 g/day

143
Q

The ability of the left ventricle to return blood to the systemic circulation is expressed via:

A

EF ( ejection fraction)

144
Q

which drug should we avoid in HF

A

Avoid diltiazem and verapamil in patients with HFrEF because of their negative inotropic effects, and felodipine and nifedipine because of the lack of data

145
Q

list the most potent to least potent diuretics

A

furosemide? metalozone > HCTZ> spironolactone

146
Q

what is the role of nitrates and hydralazine ( H-ISDN in HF)

A

unable to tolerate an ACEI, ARB, or ARNI because of hyperkalemia, renal dysfunction

addition to standard guideline-directed medical therapy at appropriate doses for black patients with HFrEF and advanced symptoms

147
Q

Which of the following medications have been shown to reduce hospitalizations in patients with heart failure with preserved ejection fraction (HFpEF)?

A

ARB

148
Q

Which of the following laboratory finding(s) indicates fluid overload in a patient with heart failure?

A

BNP

149
Q

Most common cause of HF

A

CAD ( ischemic)

150
Q

what is the benefit of spironolactone ins patient with post MI

A

Spironolactone has been shown to reduce mortality in post-MI patients with severe LV dysfunction.

151
Q

How long should dual antiplatelet therapy (DAPT) be used after a medically managed ST-elevation myocardial infarction in the absence of contraindications to ASA or a high risk of bleeding?

A

14 DAYS

** Whereas, DAPT is indicated for 12 months when percutaneous intervention is used to manage a STEMI or NSTEMI.

Don’t think this slide is right..

152
Q

How long should dual antiplatelet therapy (DAPT) be used after a medically managed NSTEMI n the absence of contraindications to ASA or a high risk of bleeding?

A

1 MONTH

153
Q

What is the most common cause of cardioembolic stroke?

A

aFIB

154
Q

switching from DOAC to warfarin

A

stop apixaban, edoxaban and rivaroxaban and use bridging agent ( enoxaparin) with warfarin until iNR is achieved

** there has been guidlines which mentioned overlapping dabigatran with warfarin until INR achieved

155
Q

When should we initiated icosapent ethyl

A

TG> 1.5 to 5.6 mmol/L

156
Q

Which agent is most potent in decreasing TG

A

Fibrates

Pharmacy CPS Flashcards (27 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions