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competency 10/11 > cardio: CAD > Flashcards

cardio: CAD Flashcards

1
Q

etiology of IHD

A

primarily caused by coronary atherosclerotic plaque formation -> imbalance between oxygen supply and demand -> myocardial ischaemia

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2
Q

types of IHD

A
  1. stable angina: significant fixed lesion, atheromatous obstruction
  2. unstable angina: unstable plaque that leads to rupture (recurrent platelet rich, non-occlusive thrombi) -> acute MI
  3. vasospastic angina: transient spasm of localised portions of vessels
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3
Q

factors that increase risk of death in IHD

A
  1. number of coronary vessels obstructed
  2. presence of heart failure
  3. smoking
  4. left main or left main equivalent coronary artery disease
  5. diabetes
  6. prior MI
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4
Q

during systole,

A

heart pumps blood throughout the body oxygen and nutrients

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5
Q

during diastole,

A

blood supply to the heart occurs via the arteries which arise from the aorta

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6
Q

oxygen supply

A
  1. coronary blood flow
  2. oxygen extraction (heart unable to extract oxygen from blood itself)
  3. oxygen availability: Hb concentration, o2 saturation
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7
Q

oxygen demand

A
  1. heart rate
  2. contractility
  3. intramyocardial wall tension
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8
Q

reduced coronary blood flow results from

A
  1. formation of atherosclerotic plaque in coronary (most common)
  2. coronary vasospasm (sudden tightening: triggers may include drug, smoking, cold weather, extreme stress or exertion) or dissection (when there is a cut in the inner diameter of the coronary blood vessel, a clot may form inside the wall that blocks blood flow, hence reduction of flow to heart)
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9
Q

diameter of coronary blood vessels: <50% obstruction

A

usually pain free even at exertion

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10
Q

diameter of coronary blood vessels: >= 70% obstruction

A

found in most coronary artery stenoses, linear decrease in coronary flow as plaque occupies more arterial lumen

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11
Q

diameter of coronary blood vessels: >= 80% obstruction

A

high-grade obstruction, loss of linear decrease between coronary flow and plaque size

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12
Q

diameter of coronary blood vessels: >= 95% obstruction

A

absence of blood flow

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13
Q

clinical presentation of angina

A

location: in the chest, may radiate to epigastrium, lower jaw, teeth, between the shoulder blades, or in either arm to the wrist and fingers
character: pressure, tightness, heaviness, sometimes strangling/constricting/burning
duration: brief =< 10 minutes
symptoms increase with exercise and other precipitating factors (eating, emotions, extreme temp), relieved quickly by sublingual nitrates

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14
Q

CTA

A

coronary computed tomography angiography - visualises coronary artery lumen and wall using an iv contrast agent

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15
Q

antianginal drugs

A

nitrates, bb, ccb, ranolazine, ivabradine

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16
Q

vasculoprotective drugs

A

aspirin/clopidogrel, statin, acei/arb

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17
Q

non-modifiable risk factors of IHD

A

age, gender (male), family history

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18
Q

modifiable risk factors of IHD

A

smoking, htn hld, dm, physical inactivity, obesity, stress

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19
Q

b1 receptor

A

heart -> hr

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20
Q

b2 receptors

A

lungs -> bronchodilation
systemic circulation -> vasodilation

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21
Q

incr HR -> incr arterial wall stress -> ?

A

-> release of endothelin, angiotensin, etc. resullting in incr atherosclerosis: chronic stable angina
-> incr risk of coronary plaque rupture: acute coronary syndromes

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22
Q

decr HR -> incr diastole

A

incr coronary perfusion time -> incr blood flow -> incr o2 supply -> decr o2 demand/supply mismatch -> decr angina

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23
Q

decr HR -> decr myocardial work

A

decr o2 demand -> decr o2 demand/supply mismatch -> decr angina

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24
Q

mortality benefits of bb are not demonstrated in which group of patients?

A

only patients with chronic stable angina
- decr morbidity and mortality in patients with HTN, acute MI and/or HF

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25
Q

which is the best tolerated: BB, nitrates, CCBs?

A

BB

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26
Q

b1 selective bb

A

Bisoprolol (2.5-10 OD)
Atenolol (25-100 OD)
Metoprolol (80-240 OD for LA, 50-150 BD)
Nebivolol

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27
Q

bb with b1, b2 and a1 blockades

A

Carvedilol (6.25-50 BD)
Labetalol (200-800 BD)

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28
Q

bb with b1 and b2 blockades

A

Propranolol (80-240 OD for LA, BD)

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29
Q

cardioselectivity results in

A

reduced adverse effects

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30
Q

lose cardioselectivity at

A

higher doses

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31
Q

avoid bb with ISA

A

eg. acebutolol
- partially simulate beta receptors
- not as effective due to minimal decr in HR, resulting in small decr in MVO2
- generally reserved for patients with low resting HR, who experience angina with exercise

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32
Q

lipophilicity is a/w

A

more cns side effects

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33
Q

adr of bb

A

fatigue, bronchospasm, bradycardia, weakness, dizziness, sleep disturbance, loss of libido
- may mask hypoglycemic sx, hence use with caution in insulin-dependent DM

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34
Q

DHP CCBs

A

selective vasodilators: only act on peripheral and coronary vessels (vasculature)
- potential reflex incr in HR, myocardial contractility, and o2 demand
- amlodipine, nifedipine

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35
Q

non-DHP CCBs

A

equipotent for cardiac tissue (HR moderating) and vasculature
- verapamil, diltiazem

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36
Q

CCB on o2 supply

A

vasodilation of coronary arteries:
- decr coronary vascular resistance
- incr coronary blood flow

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37
Q

CCB on o2 demand

A

vasodilation of systemic arteries:
- decr systemic vascular resistance and arterial BP
non-DHP also decr myocardial contractility and conduction thru AV node, thereby decr HR

38
Q

short-acting DHP CCBs

A

nifedipine
- powerful peripheral vasodilator effect, precipitates exaggerated reflex tachycardia, incr o2 demand

39
Q

potential ddi of ccb

A
  • high first-pass metabolism by cyp3a4
  • profound adr on hr and contractility when in combi with bb
40
Q

amlodipine dosing

A

2.5-10mg OD

41
Q

nifedipine ER dosing

A

30-180mg OD

42
Q

verapamil IR dosing

A

30-120mg TDS-QDS

43
Q

verapamil SR dosing

A

120-240mg BD

44
Q

diltiazem SR dosing

A

60-180mg BD

45
Q

nitric oxide activates

A

solute guanylate cyclase, to increase intracellular conc of cyclic guanosine monophosphate -> vasorelaxation

46
Q

nitrates MOA on IHD

A

incr o2 supply: dilation of large epicardial coronary arteries and collateral vessels in area with or without stenosis
decr o2 demand: vasodilation by stimulating incr cGMP production

47
Q

SA nitrates are used for

A

acute relief of anginal attacks

48
Q

LAN used for

A

prophylaxis

49
Q

ddi of nitrates

A

PDEi
- sildenafil and verdenafil: within 24 hours
- tadalafil: within 48 hours

50
Q

nitrate tolerance

A

reduction or loss of antianginal effects with continuous use

51
Q

strategies to minimise nitrate tolerance

A
  • maintain a nitrate free interval (approx 10-12 hours per day)
  • lower doses of nitrate
  • use LA»>SA
52
Q

S/L SAN tab
- duration of action
- onset of action
- usual dosage
- shelf life

A
  • duration of action: 10-30min
  • onset of action: 1-3min
  • usual dosage: 0.5mg/tab
  • shelf life: 3-6months upon opening of the bottle, depending on brand
53
Q

S/L SAN spray
- duration of action
- onset of action
- usual dosage
- shelf life

A
  • duration of action: 10-30min
  • onset of action: 2-4min
  • usual dosage: 0.4mg/spray
  • shelf life: 3 years
54
Q

ISDN
- duration of action
- onset of action
- usual dosage

A
  • duration of action: 2-6hr
  • onset of action: 15-40min
  • usual dosage: 10-60mg Q4-6H
55
Q

ISDN SR
- duration of action
- onset of action
- usual dosage

A
  • duration of action: 4-8hr
  • onset of action: 15-40min
  • usual dosage: 40-80mg Q6-8H
56
Q

ISMN
- duration of action
- onset of action
- usual dosage

A
  • duration of action: 7-8hr
  • onset of action: 30-60min
  • usual dosage: 10-20mg BD (am and midday), titrate to 20-40mg BD
57
Q

ISMN SR
- duration of action
- onset of action
- usual dosage

A
  • duration of action: 8-12hr
  • onset of action: 30-60min
  • usual dosage: 60mg OD, titrate to 30-120mg OD
58
Q

transdermal patch LAN
- duration of action
- onset of action
- usual dosage

A
  • duration of action: 4-8hr
  • onset of action: 30min
  • usual dosage: 0.2-0.4mg/hr
59
Q

ISDN usually dosed

A

TDS before meals

60
Q

ISMN is a ___ of ISDN

A

major active metabolite
- 100% bioavailable, no first pass metabolism

61
Q

Transdermal nitrate patch: Area should be clean, dry, and hairless. If hair
is likely to interfere with patch adhesion or
removal, it can be ____

A

clipped but not shaved

62
Q

ACEi use in IHD

A

vasculoprotective
- reduce LV and vascular hypertrophy, atherosclerosis progression, plaque rupture, and thrombosi

63
Q

antiplatelet use in IHD

A

vasculoprotective
- inhibit platelet activation and aggregation -> prevent coronary thrombosis
- balanced against risk of bleeding

64
Q

_____________ should be used in all patients with acute and chronic IHD, with or without manifest sx in the absence of contraindications

A

aspirin 75-162mg OD

65
Q

for secondary prevention of MI and death, which antiplatelet (aspirin or clopidogrel) was superior?

A

clopidogrel, but the magnitude of difference was small
- acceptable alternative to aspirin
- combi with aspirin beneficial in high risk patients

66
Q

MOA of ranolazine

A

inhibits late phase of inward Na channel in ischemic cardia myocytes
-> prevents Na+ overload -> prevents Ca2+ overload -> prevents electrical and mechanical dysfunction

67
Q

ranolazine dose

A

375mg BD, titrate to 500mg BD after 2-4 weeks according to patient’s response, max 750mg BD

68
Q

adr of ranolazine

A

dizziness, headache, constipation, nausea, qtc prolongation

69
Q

c/i of ranolazine

A
  1. hepatic cirrhosis
  2. renal impairment, crcl<30
  3. concomitant adm with potent cyp3a4 inhibitors eg. ketoconazole and other azoles, clarithromycin, telithromycin. nefazodone, hiv protease inhibitors
  4. preexisiting qtc prolongation and concomitant qtc prolonging drugs ef. class 1a/3 antiarrhythmics
70
Q

MOA of trimetazidine

A

inhibits 3-ketoacyl coA thiolase (3-KAT, fatty acid oxidation) -> improves myocardial glucose utilisation -> decrease o2 demand

71
Q

trimetazidine dose

A

20mg TDS or 35mg BD (MR)
- dose adj for renal impairment

72
Q

adr of trimetazidine

A

mainly GI (abdominal pain, nausea, vomiting, diarrhea), dizziness, headache

73
Q

c/i of trimetazidine

A
  • PD and motion disorders (tremor/shaking, muscle rigidity, walking disorders, RLS)
  • renal impairment, crcl<30
74
Q

ivabradine MOA

A

sinus node funny channel inhibitor -> prolongs diastole, decr HR -> decr o2 demand

75
Q

ivabradine should only be used in chronic stable angina patients with

A

normal sinus rhythm and hr>= 70bpm

76
Q

ivabradine dose

A

5mg BD, incr to 7.5mg BD after 3-4 weeks if resting sx persist and HR>60bpm
- elderly: initial dose of 2.5mg BD

77
Q

avoid use of ivabradine if renal function <

A

15ml/min (lack of data)

78
Q

when should we discontinue use of ivabradine?

A

if sx does not improve within 3 months after start of treatment

79
Q

adr of ivabradine

A

bradycardia, blurred vision, luminous phenomena (transiently enhanced brightness in a limited area of the visual field)

80
Q

warnings and precautions for ivabradine

A
  1. animal fetal toxicity - not reco in pregnancy, use contraception
  2. atrial fibrillation
  3. not reco in patients with 2nd deg AV block
81
Q

ivabradine c/i

A
  1. acute decompensated HF
  2. BP <90/50mmHg
  3. sick sinus syndrome, sinoatrial block or 3rd deg AV block (unless a functioning demand pacemaker is present)
  4. resting HR <70bpm prior to treatment
  5. severe renal/hepatic impairment
  6. pacemaker dependence (HR maintained exclusively by the pacemaker)
  7. in combi w cyp3a4 inhibitors
82
Q

standard therapy for CAD

A

BB or CCB -> BB + DHP-CCB -> add 2nd line drug

83
Q

compelling indication: high HR > 80bpm

A

BB or non-DHP CCB -> BB + CCB -> BB + ivabradine

84
Q

compelling indication: low HR < 50 bpm

A

DHP-CCB -> switch to LAN -> DHP-CCB + LAN -> add nicorandil, ranolazine, trimetazidine

85
Q

compelling indication: LV dysfunction or HF

A

BB -> BB + LAN or BB + ivabradine -> add another 2nd line drug

86
Q

compelling indication: low BP

A

low-dose BB or low-dose CCB -> switch to ivabradine, ranolazine or trimetazidine -> combine two 2nd line drugs

87
Q

PCTA

A

percutaneous transluminal coronary angioplasty
- involves dilation of a coronary artery obstruction with balloon catheter
- balloon inflation are repeated until the plaque is compressed and blood flow resumes
- use of intraluminal stent to prevent restenosis

88
Q

BB is not used in ____ angina

A

vasospastic

89
Q

why are nitrates and ccbs used in vasospastic angina?

A

aside from decreasing myocardial o2 requirement, they redistribute coronary flow to ischaemic tissue and incr myocardial o2 deliver

90
Q

nitrate-induced endothelial dysfuction

A

excess nitrates stimualte the oxidase system -> peroxynitrite produced, resulting in endothelial dysfunction

91
Q

protection from nitrate-induced endothelial dysfunction by:

A
  1. carvedilol: BB with additional prevention of free radical generation
  2. nebivolol: BB with b3 agonism, incr nitric oxide synthase expression and NO (aka nitric-oxide potentiating vasodilatory effect - decr demand and incr supply)
  3. hydralazine: vasscular smooth muscle relaxant
  4. ACEi (captopril) and ARB (telmisartan)
  5. vit c (antioxidant)
  6. high doses of atorvastatin: reduces oxidative stress
92
Q

adr of vastarel

A

nausea, vomiting, fatigue, dizziness, and myalgia
- increase parkinsonian symptoms: extrapyramidal rigidity, bradykinesia, and tremor

competency 10/11 (31 decks)

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