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Pharmacology > Hypertension > Flashcards

Hypertension Flashcards

1
Q

Name the major risk factors for cardiovascular disease (CVD)

A 
Diabetes mellitus
Hypertension
Obesity
Smoking
Dyslipidemia
Family hx of primary hypertension or premature CVD in men <55yo and women <65yo
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2
Q

Name examples of target organ damage (TOD) seen in hypertensive disease

A

Left ventricular hypertrophy
Microalbuminuria
Elevated creatinine levels

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3
Q

Name associated clinical conditions (ACC) of hypertensive disease

A 
Ischaemic heart disease
- angina
- prior myocardial infarction
Heart failure
Stroke/TIA
Chronic kidney disease
Retinopathy
Peripheral arterial disease
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4
Q

What is the cause of a treatment-resistant state in hypertensive disease?

A

Vascular damage

Renal damage

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5
Q

Each 2mmHg rise in SBP is assoc with increased risk of mortality due to?

A

7% from heart disease

10% from stroke

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6
Q

Complications of hypertension

A 
Stroke (60-70%)
Heart failure (50%)
Heart attack (25%)
Kidney failure (20%)
Dementia
Sexual dysfunction
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7
Q

Epidemiology of hypertension

A

Influenced by age + lifestyle factors
50% of those over 60yo have HT
As population ages, HT and required treatment increases

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8
Q

Clinical signs of high blood pressure?

A 
Fatigue
Decreased activity tolerance
Dizziness
Palpitations
Angina
Dyspnoea
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9
Q

Organs that undergo target organ damage from hypertensive disease?

A

CVS (heart and blood vessels)
Kidneys
Nervous system
Eyes

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10
Q

Definition of primary hypertension

A

AKA essential hypertension
95% of hypertensive cases
Idiopathic

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11
Q

Definition of secondary hypertension

A 
Secondary to other potentially rectifiable causes
Less common (5%)
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12
Q

Lifestyle change recommendations to reduce blood pressure and/or cardiovascular risk factors in hypertensive disease

A

Salt intake (restrict 5-6g/day)
Moderate alcohol intake (limit to 20-30g/day men OR 10-20g/day women)
Increase vegetables, fruit
Low fat dairy intake
BMI (<25kg/m2)
Waist circumference (men <102cm/40in; women<88cm/34in)
Exercise (>30min/day 5-7 days/week)

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13
Q

Hypertension pharmacotherapy options

A 
Central agents
Catecholamine inhibitors
Vasodilators
Aldosterone blockers
Diuretics
ACE inhibitors
Angiotensi-1 receptor blockers
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14
Q

Factors influencing pharmacotherapy choice to treat hypertension

A

Concomitant diseases
Patient’s ethnicity
Drug profile S/E
Allergy

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15
Q

Thiazides
Type
Examples
Mechanism of action

A

Low ceiling diuretics
Hydrochlorothiazide, chlorthalidone

Main: Inhibit Na+ and Cl- transporter in distal convoluted tubules -> increased Na+ and Cl- excretions
Other:
a) weak inhibitors of carbonic anhydrase -> increased HCO3- excretion
b) increased K+/Mg2+ excretion
c) decreased Ca2+ excretion

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16
Q

Thiazides
Type
Examples
Mechanism of action

A

Low ceiling diuretic
Hydrochlorothiazide, chlorthalidone, chlorothiazide, indapamide, metozalone

Main: Inhibit Na+ and Cl- transporter in distal convoluted tubules -> increased Na+ and Cl- excretions
Other:
a) weak inhibitors of carbonic anhydrase -> increased HCO3- excretion
b) increased K+/Mg2+ excretion
c) decreased Ca2+ excretion

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17
Q

What is the brand name of hydrochlorothiazide?

A

Microzide

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18
Q

What is the brand name of chlorothiazide?

A

Diuril

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19
Q

Name potential side effects of thiazides

A 
Hypokalemia
Hypovolemia
Hyperuricemia
Metabolic adverse drug reaction (ADR) -> mostly after high dose -> impaired glucose tolerance + dyslipidaemia
Erectile dysfunction
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20
Q

Aldosterone receptor blockers
Type
Examples
Mechanism of action

A

Potassium sparing diuretics
Spirinolactone

Binds and blocks aldosterone receptors -> reduce Na+ and water reabsorption -> decreased SVR -> decreased BP

Considered a weak diuretic
Often used on cinjunction w/ more potent K+ depleting diuretics

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21
Q

Name potential side effects of aldosterone receptor blockers

A 
If patient has renal impairment, uses ACE drugs or potassium supplement -> MONITOR CLOSELY for hyperkalemia
Gynecomastia
Amenorrhoea
Post-menopausal bleeding
Dizziness
Cramps
Nausea
Diarrhea
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22
Q

Calcium channel blockers
Examples
Mechanism of action

A

Amlodipine, nifedipine, verapamil

Act on voltage dependent Ltype Ca2+ channels -> reduce Ca2+ influx -> smooth muscle relaxation + vasodilation
Effectively treat systolic HT
Potentially superior to other antiHT for stroke prevention
Effective in patient’s with comorbid conditions e.g Reynaud’s, migraine
Particularly effective in the elderly and african americans

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23
Q

Which class of antihypertensive drug is particularly effective in the elderly and african americans?

A

Calcium channel blockers

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24
Q

Which class of antihypertensive drug effectively treats systolic hypertension?

A

Calcium channel blockers

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25
Q

Which class of antihypertensive drug is the potentially superior antiHT drug for stroke prevention?

A

Calcium channel blockers

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26
Q

Which class of antihypertensive drug is effective in patient’s with comorbid conditions e.g Raynaud’s, migraine?

A

Calcium channel blockers

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27
Q

Classification of calcium channel blockers

A

Phenylalkylamines
Benzothiazepines
Dihydroxypyridines

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28
Q

Classification of calcium channel blockers

Phenylalkylamines

A

Verapamil

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29
Q

Classification of calcium channel blockers

Benzothiazepines

A

Diatezem

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30
Q

Classification of calcium channel blockers

Dihydropyridines

A 
1st generation
- nifedipine
2nd generation
- isradipine
- nicardipine
- felodipine
3rd generation
- amlodipine
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31
Q

Cardiovascular effects of diatezem

A 
Calcium channel blocker (benzothiazepines)
Vasodilation +++
Suppression of cardiac contractility ++
Automaticity suppression (SA node) +++++
Conduction suppression (AV node) ++++
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32
Q

Cardiovascular effects of verapamil

A 
Calcium channel blocker (phenylalkylamines) Vasodilation ++++
Suppression of cardiac contractility ++++
Automaticity suppression (SA node) +++++
Conduction suppression (AV node) +++++
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33
Q

Cardiovascular effects of nifedipine

A 
Calcium channel blocker (dihydropyridines)
Vasodilation +++++
Suppression of cardiac contractility +
Automaticity suppression (SA node) +
Conduction suppression (AV node) 0
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34
Q

Cardiovascular effects of amlodipine

A 
Calcium channel blocker (dihydropyridines)
Vasodilation +++++
Suppression of cardiac contractility +
Automaticity suppression (SA node) +
Conduction suppression (AV node) 0
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35
Q 
Which of the following drugs results in the most vasodilation?
Verapamil
Diatazem
Nifedipine
Amlodipine
A

Nifedipine
Amlodipine
(the dihyropyridines)

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36
Q 
Which of the following drugs results in the least vasodilation?
Verapamil
Diatazem
Nifedipine
Amlodipine
A

Verapamil

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37
Q 
Which of the following drugs results in the most suppression of cardiac contractility?
Verapamil
Diatazem
Nifedipine
Amlodipine
A

Diatazem

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38
Q 
Which of the following drugs results in the least suppression of cardiac contractility?
Verapamil
Diatazem
Nifedipine
Amlodipine
A

Nifedipine

Amlodipine

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39
Q 
Which of the following drugs results in the most automaticity suppression?
Verapamil
Diatazem
Nifedipine
Amlodipine
A

Verapamil

Diatzaem

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40
Q 
Which of the following drugs results in the least automaticity suppression?
Verapamil
Diatazem
Nifedipine
Amlodipine
A

Nifedipine

Amlodipine

41
Q 
Which of the following drugs results in the most conduction suppression?
Verapamil
Diatazem
Nifedipine
Amlodipine
A

Diatazem

42
Q 
Which of the following drugs results in the least conduction suppression
Verapamil
Diatazem
Nifedipine
Amlodipine
A

Nifedipine

Amlodipine

43
Q

What are potential side effects of dihydropyridines?

A 
Peripheral oedema 
Reflex tachycardia
Flushing
Headache
Hypotension
44
Q

What are potential side effects of non-dihydropyridines?

A

Constipation

Conduction abnormalities

45
Q

Angiotensin converting enzyme (ACE) inhibitors
Examples
Mechanism of action

A

Enalapril, benazepril, captopril, lisinopril, fosinopril, quinapril, ramipril, moexipril, trandolapril, perindopril
Prevents conversion of angiotensin I -> angiotensin II -> prevents vasoconstriciton + aldosterone release

46
Q

What are advantages of using ACE inhibitors?

A

Reduce mortality in left ventricular dysfunction
Prevent progressive post-infarct cardiac failure
Reduce cardiovascular outcomes in high risk patient
Reno-protective in diabetics + renal disease w/ proteinuria
Lack deleterious effect on glucose tolerance + blood lipids

47
Q

What are side effects of using ACE inhibitors?

A 
Dry cough
Angioedema
Hyperkalemia
First dose hypotension
Reversible taste disturbance
48
Q

What are contraindications for using ACE inhibitors?

A

Renal artery stenosis

Pregnancy

49
Q

When must one take caution when using ACE inhibitors?

A

Pre-existing eGFR <20

50
Q

ACE-inhibitors versus angiotensin receptor blockers (ARB)

A

ARBs do not prevent bradikinin inactivation -> less dry cough + angioedema
75% ACE-I vs 95% AB RAAS blockade
No difference in clinical endpoints
Choice of therapy guided by cost + tolerability

51
Q

Angiotensin receptor blockers

Examples

A

Losartan, valsarta, irbesartan, telmisartan, candesartan, eprosartan

52
Q

Direct vasodilators

A

Hydralazine
Minoxidil
Sodium nitroprusside
Diazoxide

53
Q

Direct vasodilators

Mechanism of action of hydralazine

A

Dilates arterioles but not veins

54
Q

Direct vasodilators

Mechanism of action of minoxidil

A

Opens K+ channels in smooth muscles with its active metabolite

55
Q

Direct vasodilators

Mechanism of action of sodium nitroprusside

A

Increases intracellular GMP ad dilates both aa and vv

56
Q

Direct vasodilators

Mechanism of action of diazoxide

A

Stimulates opening of K+ channels

57
Q

Which direct vasodilator is a powerful vasodilator for treatment of hypertensive emergencies? And an alternative to this?

A

Sodium nitroprusside

Can also use diazoxide

58
Q

Centrally acting agents
Examples
Mechanism of action
Side effects

A

Alpha agonists, adrenergic receptor blockers
Stimulates central alpha 2 receptors which results in inhibiting efferent sympathetic activity
Should be used 3rd/4th line
Can be addictive (e.g clonidine, methyldopa)
Sedation, orthostatic hypotension

59
Q

Centrally acting agents
Clonidine
Mechanism of action
S/E

A

Alpha-2 agonist -> reduces norepinephrine production w/o stimulating sympathetic nervous system -> vasodilation -> decreased BP
S/E sedation, dry mouth, Na+ retention, water retention

60
Q

Centrally acting agents
Alpha-methyldopa
Mechanism of action
S/E

A

Alpha-methylnorepinephrine stored in neurosecretory vesicles instead of NE -> released -> alpha-receptor agonist
S/E sedation, lassitude, nightmares, lactation (due to dopaminergic neuron inhibition)

61
Q

Examples of beta 1 selective adrenergic receptor blockers

A

Atenolol, bisoprolol, metoprolol

62
Q

Examples of beta 1 + 2 adrenergic receptor blockers

A

Propanolol (lipophilic)

63
Q

Examples of alpha, beta 1 and beta 2 receptor blockers

A

Carvedilol (lipophilic), labetolol

64
Q

What is the name of the active metabolite of alpha-methyldopa?

A

Alpha-methylnorepinephrine

65
Q

What is the significance of a lipophilic adrenergic receptor blocker?

A

Can cross the blood brain barrier

66
Q

Name mortality reducing beta blockers

A

Carvedilol
Bisoprolol
Nebivilol
Metoprolol

67
Q

Atenolol
Class
Caution
Contraindications

A

4th line antihypertensive - ONLY use in pt with comorbid angina or uncontrolled hypertension
Cardioselective beta blocker (least lipophilic)
Caution: elderly, renal failure
Contraindications: asthma, symptomatic cardiac failure, Av block, bradycardia

68
Q

When is the only time you give atenolol as antihypertensive treatment?

A

ONLY use in pt with

(1) comorbid angina or
(2) uncontrolled hypertension

69
Q

Why do you take caution when prescribing atenolol to an elderly or renal failure patient?

A

Excreted unchanged in urine

Can accumulate if low GFR

70
Q

How is carvedilol excreted?

A

Via bile

71
Q

What is the use of beta blockers in COPD patient with severe hypertension?

A

Benefit versus risk assessment

Little reversibility + not severe COPD -> carvedilol benefit outweighs bronchospasm risk

72
Q

Definition and classification of severe hypertension

A

SBP>180mmHg and DBP >110mmHg

  1. Asymptomatic severe
  2. Hypertensive urgency
  3. Hypertensive emergency
73
Q

Definition of asymptomatic severe hypertension

A

SBP>180mmHg and DBP >110mmHg
Asymptomatic
No TOD
No ACC

74
Q

Definition of hypertensive emergency

A

SBP>180mmHg and DBP >110mmHg

Assoc w/ acute and ongoing damage to kidneys, brain, heart, eyes or vascular system

75
Q

What grade retinopathy qualifies as TOD during hypertensive emergency

A

Grade 3/4

76
Q

Definition of hypertensive urgency

A

SBP>180mmHg and DBP >110mmHg
Severe headache, SOB, oedema
No immediate life-threatening neuro, renal, eye or cardiac complications

77
Q 
Glyceryl trinitrate
Drug class
Mechanism of action
Side effects
Contraindications
A

Organ nitrates
Venodilation -> decrease preload via coronary vasodilation
SE: hypotension, headache
CI: hypertrophic obstructive cardiomyopathy (HOCM)

78
Q

Which common drug does glyceryl trinitrate interact with?

A

Sildenafil (potentiates vasodilation)

PDE5 inhibitor with tadalafil, verdenafil

79
Q 
Furosemide
Drug class
Mechanism of action
Side effects
Caution
A

High ceiling loop diuretic
Inhibits Na+ and Cl- reabsorption in the ascending limb of Henle -> venodilation -> decreased venous return
IV is very fast acting
SE:: hypotension, hypovolemic shock, ototoxicity if given in large IV doses therefore give slow at 4mg/min

80
Q

Why must you give furosemide slowly at 4mg/min?

A

Can cause hypotension, hypovolemic shock, ototoxicity if given in large IV doses

81
Q

How does decreased renal function affect furosemide treatment?

A

Patient requires a higher dose

82
Q

What site do organic acids compete with drug transport for?

A

Lumen side of ascending limb of Henle

83
Q

Special populations to consider in antihypertensive treatment

A 
Africans
Left ventricular hypertrophy (LVH)
Elderly
Pregnancy
Children/adolescents
84
Q

What is important to remember when providing african patients with anti-hypertensive treatment?

A

Response to diuretics + CCB > ACE-I, ARB, beta blockers

Angioedema 2x-4x more

85
Q

What is important to remember when providing elderly patients with anti-hypertensive treatment?

A

Isolated systolic hypertension
Same general principles
Thiazide/CCB may be better tolerated

86
Q

What is important to remember when providing pregnant patients with anti-hypertensive treatment?

A

Methyldopa, beta-blockers + vasodilators (hydralazine) are options
Avoid ACE-Is and ARBs

87
Q

What is important to remember when providing left ventricular hypertrophy patients with anti-hypertensive treatment?

A

Aggressive BP control allows LVH to regress but NOT w/ hydralazine or minoxidil

88
Q

What is important to remember when providing children/adolescent patients with anti-hypertensive treatment?

A

Avoid ACE-I or ARBs in pregnant or sexually active girls

89
Q

Safest anti-hypertensive options for pregnant woman with pre-existing hypertension?

A

Methyldopa
Nifedipine
Labetalol
Diuretics + beta blockers still C/I from 2nd trimester because of fetal growth retardation and electrolyte imbalances

90
Q

Pre-eclampsia
Time of onset
Clinical presentation
Treatment

A

Usually after 20 weeks of pregnancy
Hypertension, oedema, proteinuria,hyperuricemia
Bed rest + antiHT

91
Q

Pre-eclampsia

Complications

A 
Convulsions
Cerebral haemorrhage
Abruptio placentae
Pulmonary oedema
Renal failure
92
Q

Recommended anti-hypertensives in heart failure

A

Diuretic
Beta blocker
ACE-I
ARB

93
Q

Recommended anti-hypertensives in post MI

A

Beta blocker

ACE-I

94
Q

Recommended anti-hypertensives in high coronary disease risk

A

Diuretic
Beta blocker
ACE-I
CCB

95
Q

Recommended anti-hypertensives in diabetes

A

Diuretic
ACE-I
ARB
CCB

96
Q

Recommended anti-hypertensives in chronic kidney disease

A

ACE-I

ARB

97
Q

Recommended anti-hypertensives in recurrent stroke prevention

A

Diuretic

ACE-I

98
Q

“Compelling indications” for a drug means?

A

Literature has proven it superior treatment in that medical situation

Pharmacology (32 decks)

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