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Pharmacology > CV block 5 > Flashcards

CV block 5 Flashcards

Cardiovascular Block 5

1
Q

what are cardiac stimulants?

A

stimulate heart function. stronger, faster

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2
Q

Cardiac Stimulants drugs

A

Adrenergic Agonists, Cardiac Glycosides

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3
Q

Antihypertensives – reduce blood pressure

A

Adrenergic Blockers, Calcium Channel Blockers, ACE/angiotensin II inhibitors, diuretics, vasodilators, alpha2 agonists, nitrates

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4
Q

how does antihypertensive drugs work?

A

reduces workload of the heart

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5
Q

Drugs to reduce vascular occlusions

A

anticoagulants, antiplatelets, thrombolytics.

Improve blood supply

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6
Q

Drugs to reduce atherosclerotic potential

A

lipid lowering drugs

-reducing plasma cholesterol and triglyceride levels

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7
Q

what is Inotropic effect?

A

where there is a change in the contractile force in the heart

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8
Q

what is chronotropic effect?

A

where there is a change in the heart rate.
- slow beat
+ fast beat

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9
Q

what is dromotropic effect?

A

where there is a change in the conduction speed of electrical impulses in the heart

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10
Q

examples of sympathomimetics drugs?

A

adrenaline, dopamine, dobutamine

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11
Q

what is the clinical use of adrenaline/epinephrine?

A

used in circulatory shock, hypotension and cardiac arrest

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12
Q

how does adrenaline acts?

A

acts on B1-receptors in heart for + inotropic and chronotropic effect

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13
Q

How’s adrenaline administered?

A

IV or IM

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14
Q

Adrenaline adverse effect?

A

nausea, hypertension, constipation, tachycardia

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15
Q

what does dopamine do to the body?

A

produces positive inotropic effects on the heart, reducing its workload and maintains renal blood flow.

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16
Q

how dopamine administered?

A

IV

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17
Q

common adverse effect of dopamine

A

increase HR, vasoconstriction, hypotension tolerance, nausea/vomiting

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18
Q

Dobutamine

A

Has positive inotropic effect by stimulating the b1-receptors

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19
Q

how does dobutamine works?

A

Less vasoconstriction in the peripheries so if an IV line - less likely to cause tissue damage

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20
Q

onset and life of dobutamine

A

action in 5 minutes and short half life.

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21
Q

use of digoxin

A

is no longer the first choice for congestive heart failure, but can still be useful in patients who remain symptomatic despite proper diuretic and ACE inhibitor treatment.

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22
Q

effectivity and ineffectively of digoxin

A
  • ineffective at decreasing long term morbidity and mortality in Congestive Heart Failure.
  • increase quality of life in short/medium term.
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23
Q

Digoxin clinical application

A

CHF and atrial fibrillation

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24
Q

How is digoxin eliminated from the body?

A

via kidney

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25
Q

what is the half life of digoxin?

A

40 hours
5 x 40 hrs – 6 x 40 hrs
= 200 hrs – 240 hrs
= 8.3 -10 days

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26
Q

therapeutic index of digoxin?

A

narrow therapeutic index drug

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27
Q

adverse effects of digoxin?

A

Loss of appetite, nausea and vomiting, and abdominal

distress may indicate digoxin toxicity.

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28
Q

GI disturbances of digoxin?

A

s (anorexia; diarrhoea); nausea and vomiting

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29
Q

CNS effects of digoxin?

A

disorientation, visual disturbances, confusion, hallucinations

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30
Q

digoxin interaction with potassium

A
  • high K+ levels= decreased digoxin activity

- low K+ levels = increased digoxin activity

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31
Q

drug interaction of digoxin

A
  • cause hypokalaemia=Loop diuretics, Corticosteroids, Lithium,
  • Calcium channel blockers, ACE inhibitors, antacids..
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32
Q

digoxin care

A
  • monitor K levels
  • monitor toxicity
  • check renal function
  • HR, need to be 60+
  • monitor serum digoxin levels
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33
Q

what is the antidote for digoxin?

A

digibind IV

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34
Q

Which is NOT a sympathomimetic

agonist?

A

acetylcholine

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35
Q

Digoxin has which of the following effects on the

heart?

A

positive inotropic and negative chronotropic

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36
Q

peripheral vasodilators clinical applications

A

angina, CHF, hypertension

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37
Q

use of peripheral vasodilators

A

to reduce workload on the heart.

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38
Q

Peripheral Vasodilators acts on veins: nitrates

A

reduce preload; so decrease cardiac

output and tissue perfusion

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39
Q

peripheral vasodilators act on arterioles: hydralazine, nitroprusside

A

reduce cardiac afterload; so decrease cardiac workload and increase cardiac
output and tissue perfusion

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40
Q

nitrate mode of action

A
  1. Nitrates are converted into nitric oxide (NO).
  2. NO increases the intracellular levels of cGMP
  3. cGMP causes decrease in calcium ions within
    the muscle cells.
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41
Q

result of nitrate MOA

A

the blood vessels (veins) dilate, relax. This venodilation means that preload is reduced.

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42
Q

nitrates adverse effects

A

– headache, facial flushing,

hypotension, rebound tachycardia

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43
Q

use of morphine

A 
a venodilator (useful in pulmonary oedema due to reducing pulmonary hypertension)
-decreases BP, therefore workload on the heart
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44
Q

Glyceryl trinitrate (GTN) is a critical component of:

A

dynamite

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45
Q

Nitrate vasodilators act mainly on:

A

veins

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46
Q

For patients with diabetes or chronic renal disease this is

lower:

A

130/80 mmHg

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47
Q

normal BP

A

below 140/90 mmHg

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48
Q

For patients with heart failure (or post MI) a lower blood pressure is desirable

A

110/70

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49
Q

Drugs Used to Treat Hypertension

A

-A is for ACE inhibitors,
ARBs (Angiotensin II-Receptor Blockers), alpha antagonists, alpha2 agonists
-B is for b-blockers
-C is for CCBs (calcium channel blockers) & Combined action drugs
-D is for Diuretics

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50
Q

Alpha Blockers drugs

A

terazosin & doxazosin

51
Q

Mode of Action Alpha Blockers

A

block the a1-receptor sites and reduces sympathetic nervous system response. stops neurotransmitters binding.

52
Q

Adverse effects of alpha blockers

A

postural hypotension, nasal congestion, fatigue, inhibition of ejaculation, lack of energy

53
Q

Clinical Application of alpha blockers

A

control of hypertension, peripheral vascular disease, urinary retention.

54
Q

how is alpha blockers administered?

A

orally

55
Q

Beta-Blockers has 4 useful actions in hypertension.

A
  • Block beta receptors in the heart- decrease heart rate and contractility therefore decreases cardiac output and BP
  • Suppress reflex tachycardia caused by vasodilator
  • Reduce the release of renin by the kidneys, hence less fluid retention
  • Long term use reduces peripheral vascular resistance
56
Q

Beta-Blockers drugs

A

metoprolol, atenolol, carvedilol

57
Q

Beta-Blockers clinical applications

A

cardiac disease, hypertension, angina, migraine prophylaxis

58
Q

Beta-Blockers mode of action

A

: block β-1 receptors in the heart muscle therefore decreases cardiac output and BPdecreases.

59
Q

Beta-Blockers administration

A

orally

60
Q

Non-selective drugs

A

labetalol

61
Q

Non-selective drugs blocks

A
  • Blocks a1 and b-receptors.

* Can be used for pregnancy induced hypertension

62
Q

how are Non-selective drugs administered

A

orally or IV

63
Q

Selective b-blockers drugs

A

target b1-receptors which
predominate in the heart eg. atenolol (Tenormin),
metoprolol (Lopressor)

64
Q

What are the inotropic and

chronotropic effects of beta blockers?

A

negative

65
Q

Do not discontinue β-blocker therapy quickly as it

could cause?

A

rebound hypertension, angina, dysrhythmia and MI.

66
Q

Contraindication of Beta-Blockers

A

-COPD, asthma
-Bradycardia (45-50 bpm)
-Cardiogenic or hypovolaemic shock
-Severe hypotension
-Should be avoided in diabetes (especially
nonselective adrenergic blockers)

67
Q

a2-Agonists drugs

A

methyldopa, clonidine

68
Q

adverse effects of a2-agonists drugs

A

fatigue, hypotension,
inhibition of ejaculation,
nasal congestion

69
Q

Calcium Channel Blockers (CCBs) drugs

A

amlodipine, felodipine, diltiazem

70
Q

Calcium Channel Blockers (CCBs) clinical applications.

A

angina, hypertension

71
Q

Calcium Channel Blockers (CCBs) MOA.

A

blocks calcium channel and
stops calcium entering into the vascular and
cardiac cells.

72
Q

What are the inotropic and chronotropic effects of

calcium channel blockers?

A

Negative!!

73
Q

Adverse effects - CCBs

A

decreased BP, headache, abdo discomfort, peripheral edema, decreased HR

74
Q

CCBs - Drug Interactions

A

• β-blockers
• Digoxin
• Inhibitors of CYP3A4
(e.g. erythromycin, grapefruit juice)

75
Q

what is Nimodipine

A

selective for cerebral blood vessels

76
Q

how Nimodipine affects the brain?

A

will increase cerebral blood flow particularly to damaged areas of the brain.

77
Q

antidote for Overdosing nimodipine

A

Treat with activated charcoal and whole bowel irrigation

78
Q

ACE inhibitors drugs

A

captopril, enalapril

79
Q

Angiotensin II antagonists (ARBs) drugs

A

losartan

80
Q

diuretics drugs

A

aprinox, frusemide (lasix), spironolactone

81
Q

Angiotensin Converting EnzymeInhibitors (ACE Inhibitors) drugs and clinical application

A
  • cilazapril, quinapril (prodrugs)

- hypertension

82
Q

how ACE inhibitors administered?

A

orally.• Usually given in combination with diuretics

83
Q

What is a prodrug?

A

-administered in an inactive (or significantly less active) form. once administered, the prodrug is metabolised
into an active metabolite

84
Q

Adverse Effects - ACE Inhibitors

A

hypotension, unproductive cough, taste disturbances, headache, GI upset, hyperkalaemia

85
Q

ACE inhibitors Drug Interactions

A

diuretics, lithium, NSAIDs

86
Q

Angiotensin Receptor Blockers (ARBs) drugs (ends with sartans)

A

losartan, candesartan

87
Q

Angiotensin Receptor Blockers (ARBs) clinical application

A

hypertension, heart failure.

88
Q

Angiotensin Receptor Blockers (ARBs) can be combined with?

A

diuretics

89
Q

What are the

adverse effects ARBs?

A

ARBs block AT1 receptors
-headache, hypotension,
dizziness, GI disturbances

90
Q

Angiotensin Receptor Blockers (ARBs)

A
  • Generally well tolerated
  • NO unproductive cough
  • reduced risk of hyperkalaemia
  • maximum effect seen 4-6 weeks
91
Q

what does diuretics do?

A
  • reduce circulating fluid
  • reduce blood pressure and oedema by increasing urine production.
  • All diuretics enhance water and sodium excretion
92
Q

Thiazides drugs

A

bendroflumethiazide, hydrochlorothiazide

93
Q

Clinical Application of thiazides?

A

drug of choice for management of

hypertension [mild to moderate].

94
Q

mode of action of thiazides

A

act on distal convoluted tubule of nephron and decreases sodium reabsorption, increases
concentration of fluid entering collecting ducts and induces diuresis

95
Q

adverse effects of thiazides

A

dehydration, hyponatraemia,

hypokalaemia, hyperglycaemia

96
Q

Loop Diuretics drugs

A

frusemide (lasix)

97
Q

clinical application of loop diuretics

A

states of oedema: CHF

98
Q

mode of action of loop diuretics

A

nhibit reabsorption of sodium and

chloride ions from Loop of Henle into interstitial fluid.

99
Q

adverse effects of loop diuretics

A

: dehydration, hyponatraemia, hypokalaemia, dizziness, headaches, deafness

100
Q

loop diuretics drug interactions?

A

increase digoxin and lithium toxicity

101
Q

Potassium Sparing Diuretics types include

A
  • Spironolactone

- Amiloride

102
Q

Spironolactone [aldosterone antagonist]

A

Inhibits the action of aldosterone in the distal tubule leading to sodium loss and potassium being retained.

103
Q

Amiloride

A

acts directly on K+/Na+ interchange in the distal tubule causing Na+ loss and K+ retention

104
Q

Potassium Sparing Diuretics clinical application

A

used mainly in the prevention of potassium loss from the use of other diuretics.

105
Q

Osmotic Diuretics drugs

A

Mannitol —— Administered by IV only

106
Q

Clinical application of Osmotic Diuretics

A

states of oedematous (e.g.
glaucoma, elevation of intracranial pressure); CHF;
emergency situations.

107
Q

Mode of Action of Osmotic Diuretics

A

expand extracellular fluid and plasma volume which increases blood flow to kidney, increases osmolarity of blood and renal filtrate and promotes diuresis.

108
Q

Adverse effects of Osmotic Diuretics

A

electrolyte imbalance, dehydration,

hypovolaemia

109
Q

Characteristics of Mannitol:

A
  • Relatively non-toxic
  • Excreted quickly
  • Is not reabsorbed from glomerular filtrate
  • Water soluble or hydrophili
110
Q

Antihypertensives- An annoying adverse effect of ACE inhibitors is:

A

a dry, unproductive cough

111
Q

Examples of Angiotensin receptor blockers are:

A

Losartan & candesartan

112
Q

An example of an osmotic diuretic is:

A

mannitol

113
Q

Anticoagulants drugs

A

Heparin, Warfarin, Dabigatran

114
Q

Antiplatelet drugs

A

Aspirin

115
Q

Thrombolytics drugs

A

Streptokinase, Urokinase, TPA*

116
Q

what is heparin?

A

occurs naturally in the body and is found i mast cells. acts by augmenting the function Antithrombin III, a natural inhibitor of coagulation

117
Q

how is heparin administered?

A

IV fast action or SUBCUT slower action.

118
Q

adverse effect of heparin

A

haemorrhage. others include hypersensitivity and thrombocytopenia
- safe in pregnancy

119
Q

what to do when there’s too much heparin

A

discontinue treatment when haemorrhaging occur. administer Protamine Sulphate slowly-severe bleeding

120
Q

other heparin drugs- low molecular weight heparin (fragmin)

A

longer half-life, can be used by outpatients post-MI, easily be self administered

121
Q

what is warfarin?

A

long term anticoagulant therapy. it inhibits epoxide reductase which oxidises Vit K for reuse

122
Q

warfarin compared to heparin

A

slower onset of action 12-24
longer duration of action 3-5
narrow therapeutic index

123
Q

food high in Vit K

A

cabbage, cauliflower, broccoli, brussel sprouts, spinach, parsley, onions, liver

124
Q

antiplatelets -aspirin

A

platelets bind to damaged endothelial walls, blocked by aspirin, thromboxane produced= vasoconstrictor, further platelet aggregation, promotes clot formation

Pharmacology (7 decks)

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