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Hypertension and antihypertensive drugs Flashcards

1
Q

What is BP?

A
  • Driving force to perfuse organs with blood
  • Not uniform throughout body
  • Commonly measure and report systolic and diastolic
  • Cyclical
  • Physiological variable
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2
Q

How do we calculate mean arterial blood pressure?

A
  • Cardiac output x total peripheral resistance
  • DBP + ((SBP-DBP)/3)
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3
Q

How is blood pressure regulated by the sympathetic nervous system?

A
  • Decrease in blood pressure
  • Increased sympathetic activity
  • Activation of B1 adrenoceptors on heart causes increased cardiac output
  • Activation of A1 adrenoceptors on smooth muscle causes increased venous return and increased peripheral resistance
  • Activation of B1 adrenoceptors on kidney leads to increased renin
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4
Q

How is blood pressure regulated by the kidneys?

A
  • Decreased renal blood flow increases renin production
  • Leads to increase in angiotensin II
  • Decreased glomerular filtration increases sodium and water retention
  • Results in increased aldosterone and increased blood volume
  • Increased aldosterone leads to increased angiotensin II
  • Angiotensin II causes increased peripheral resistance
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5
Q

How is peripheral resistance changed?

A
  • Smooth muscle tone changes TPR
  • Vasoconstriction causes increased peripheral resistance
  • Requires increased BP to drive blood through systemic circulation
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6
Q

Outline the pathophysiology of hypertension

A
  • Cause still not completely understood
  • Leads to vascular changes including remodelling, thickening, hypertrophy
  • Increased vasoactive substances including ET-1, AngII
  • Vascular remodelling also occurs as a result of local salt sensitivity
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7
Q

What do hyperinsulinaemia and hyperglycaemia lead to?

A
  • Endothelial dysfunction
  • Increased reactive oxygen species
  • Nitric oxide signalling reduced
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8
Q

What is the ultimate result of hypertension?

A
  • Permanent medial hypertrophy of vasculature
  • Increased TPR
  • Decreased compliance of vessels
  • End organ damage (renal, peripheral vascular disease, aneurysm, vascular dementia)
  • Hypertensive heart disease causes left ventricular hypertrophy and dilated cardiac failure
  • Increased morbidity and mortality
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9
Q

How is hypertension defined?

A
  • BP of 140/90 is defined as hypertension
  • A reduction in BP (both systolic and diastolic) reduces cardiovascular risk
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10
Q

What are some different causes of hypertension?

A
  • Essential/primary/idiopathic hypertension - 90% of cases
  • Secondary hypertension - to other pathology
  • Pre hypertension
  • Isolated systolic/diastolic hypertension
  • White coat/clinic
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11
Q

How can we increase awareness of hypertension?

A
  • Screen those at risk
  • Increase public awareness of risk factors
  • Appropriate lifestyle changes to limit risk
  • Reliable measurements based on clinical guidelines
  • Regular monitoring and refinement of medication once initiated
  • Hypertension is a silent killer
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12
Q

How is a clinical diagnosis of hypertension made?

A
  • Sitting, relaxed and arm is supported
  • Both arms
  • If >15 mmHg difference, repeat measurement and use arm with higher reading
  • Take measurements over a period of visits
  • Can also do ambulatory BP and home BP measurements
  • Determine whether emergency treatment is required
  • Cardiovascular disease risk and end organ damage need to be assessed
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13
Q

What are some target blood pressures for different categories of patients?

A
  • <140/90 in <80 years old, including type II diabetes
  • <150/90 > 80 years old
  • <135/85 type 1 diabetes
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14
Q

Outline stage 1 hypertension

A
  • Clinic BP ranging from 140/90 mmHg to 159/99 mmHg
  • ABPM/HBPM average reading >135/85 mmHg
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15
Q

Outline stage 2 hypertension

A
  • Clinic BP ranging from 160/100 mmHg to 180/120 mmHg
  • ABPM/HBPM average reading >150/95 mmHg
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16
Q

Outline stage 3 hypertension

A
  • Clinic systolic BP of 180 mmHg or higher
  • Or clinic diastolic BP of 120 mmHg or higher
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17
Q

How can we prevent prehypertension from developing into hypertension?

A
  • Promotion of regular exercise
  • Modified healthy/balanced diet
  • Reduction in stress and increased relaxation
  • Limited/reduced alcohol intake
  • Discourage excessive caffeine consumption
  • Smoking cessation
  • Reduction in dietary sodium
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18
Q

What is prehypertension defined as?

A
  • > 120/80 but <140/90 mmHg
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19
Q

What are the primary hypertension therapeutic agents?

A
  • Angiotensin converting enzyme inhibitors
  • Angiotensin receptor blockers
  • Calcium channel blockers
  • Diuretics (thiazide and thiazide like)
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20
Q

Where is ACE found?

A
  • Found on luminal surface of capillary endothelial cells
  • Predominantly in lungs
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21
Q

What is the function of ACE?

A
  • Catalyses conversion of angiotensin I to potent, active vasoconstrictor
  • Angiotensin II
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22
Q

How does angiotensin II exert its effects?

A
  • Angiotensin II affords action through AT1 (and AT2 receptors)
  • AT1 receptor typical of classic angiotensin-II actions e.g. vasoconstriction
  • Stimulates aldosterone (acts at distal renal tubule)
  • Cardiac and vascular muscle cell growth
  • Vasopressin (ADH) release from posterior pituitary
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23
Q

How do angiotensin II and aldosterone increase BP?

A
  • Vasoconstriction
  • Increasing circulating blood volume
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24
Q

How do ACE inhibitors work?

A
  • Inhibits circulating and tissue ACE
  • Causes reduction in angiotensin II activity
  • Vasodilation
  • Reduced aldosterone release
  • Reduced ADH release
  • Reduced cell growth and proliferation
  • Contribute to antihypertensive effects
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25
Q

Do ACE inhibitors prevent all production of angiotensin II?

A
  • No
  • Angiotensin II also produced from angiotensin I independently of ACE via chymases
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26
Q

Give some examples of ACE inhibitors?

A
  • Lisinopril
  • Ramipril
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27
Q

What are some adverse side effects of ACE inhibitors?

A
  • Hypotension
  • Dry cough
  • Hyperkalaemia (lower aldosterone leads to increased [K+])
  • Cause or worsen renal failure (especially renal artery stenosis)
  • Angioedema
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28
Q

Why do ACE inhibitors cause a dry cough?

A
  • Bradykinin is also a substrate for ACE
  • Use of ACE inhibitors prevents breakdown of bradykinin
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29
Q

What are the contraindications of ACEi?

A
  • Renal artery stenosis
  • AKD
  • Pregnancy
  • Idiopathic angioedema
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30
Q

What are the drug interactions of ACEi?

A
  • Increases activity of K+ drugs due to reduced aldosterone
  • NSAIDs disrupt renal function through action on efferent arteriole and ion imbalance
  • Other antihypertensive agents
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31
Q

Give some examples of angiotensin II and receptor antagonists

A
  • Candesartan
  • Losartan
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32
Q

What are the adverse side effects of ARBs?

A
  • Hypotension
  • Hyperkalaemia (low aldosterone increases K+)
  • Cause or worsen renal failure
33
Q

What are the pros and cons of using ARBs over ACEi?

A
  • No effect on bradykinin
  • Less effective in low-renin hypertensive patients
  • Dry cough and angioedema much less likely
  • Directly target AT1 receptors - more effective at inhibiting Ang-II mediated vasoconstriction
34
Q

What are the contraindications of ARBs?

A
  • Renal artery stenosis
  • AKD
  • Pregnancy
  • CKD
35
Q

What are the drug interactions of ARBs?

A
  • Increase activity of K+ drugs
  • NSAIDs
36
Q

How do calcium channel blockers work?

A
  • L-type calcium channels allow inward Ca2+ flux into cells
  • Expressed throughout body - including vascular smooth muscle cells and cardiac myocytes plus SA and AC node
  • CCBs target calcium-initiated smooth muscle contraction
  • Prevent smooth muscle contraction to reduce BP
37
Q

What are the 3 classes of calcium channel blocker?

A
  • Dihydropyridines
  • Non-dihydropyridines - phenylalkylamines and benzothiazepines
  • Have different selectivity for vascular smooth muscle or myocardium
38
Q

What are dihydropyridines selective for?

A
  • Peripheral vasculature
  • Have little chronotropic or inotropic effects
  • Cerebral vs peripheral selectivity dictates which are used for hypertension
39
Q

What are phenylalkylamines selective for?

A
  • Depresses SA node
  • Slows AV conduction
  • Negative inotropy
40
Q

What are benzothiazepines selective for?

A
  • Somewhere between peripheral vasculature and cardiac targets
41
Q

When are CCBs primary choice antihypertensive?

A
  • In low renin patients
42
Q

Give some examples of dihydropyridines

A
  • Amlodipine - has long half life
  • Nifedipine
  • Nimodipine - selective for cerebral vasculature
43
Q

What are the adverse side effects of dihydropyridines?

A
  • Ankle swelling
  • Flushing
  • Headaches (vasodilation)
  • Palpitations (compensatory tachycardia)
44
Q

What are the contraindications for dihydropyridines?

A
  • Unstable angina
  • Severe aortic stenosis
45
Q

Which drugs interact with dihydropyridines?

A
  • Amlodipine and simvastatin (increased effect of statin)
46
Q

Give an example of phenylalkylamines?

47
Q

What are phenylalkylamines used for?

A
  • Arrhythmia
  • Angina
  • Due to hypertension
48
Q

Outline the properties of the phenylalkylamines

A
  • Class IV antiarrhythmic agent
  • Prolongs action potential/effective refractory period
  • Less peripheral vasodilation
  • Negative chronotropic and inotropic effects
49
Q

What are some adverse side effects of phenylalkylamines?

A
  • Constipation
  • Bradycardia
  • Heart block
  • Cardiac failure
50
Q

What are the contraindications of phenylalkylamines?

A

Poor LV function (caution)
- AV nodal conduction delay

51
Q

What are the drug interactions of phenylalkylamines?

A
  • B blockers (cardiologist use only
  • Caution with other antihypertensive and antiarrhythmic agents
52
Q

What are benzothiazepines?

53
Q

Give some examples of thiazide and thiazide-like diuretics

A
  • Bendroflumethiazide
  • Indapamide
54
Q

Outline the action of thiazide and thiazide-like diuretics?

A
  • Inhibit Na+/Cl- co-transporter in distal convoluted tubule
  • Lead to decreased Na+ and H2O reabsorption
  • Long term effects mediated by sensitivity of vascular smooth muscle to vasoconstrictors
  • Useful over CCB in oedema
55
Q

What are the adverse side effects of thiazide and thiazide-like diuretics?

A
  • Hypokalaemia
  • Hyponatraemia
  • Hyperuricemia (gout)
  • Arrhythmia
  • Increased glucose (especially with beta blockers)
  • Small increase in cholesterol and triglyceride
56
Q

What are the contraindications for thiazide and thiazide-like diuretics?

A
  • Hypokalaemia
  • Hyponatraemia
  • Gout
57
Q

What are the drug interactions of thiazide and thiazide-like diuretics?

A
  • NSAIDs
  • Decreased K+ drug such as loop diuretics
58
Q

Which different patient groups are given different treatment for hypertension?

A
  • Hypertension with type 2 diabetes
  • Hypertension without type 2 diabetes:
    1. Age <55 and not of black African/Afro-Caribbean family origin
    2. Age 55 or over
    3. Black African or African-Caribbean family origin
59
Q

Outline how we treat hypertension with type 2 diabetes

A
  • Step 1: ACEi or ARBs
  • Step 2: CCB/thiazide-like diuretic
    -Step 3: ACEi/ARB + CCB + thiazide diuretic
  • If treatment still fails, confirm resistant hypertension
60
Q

Outline how we treat hypertension in people aged <55 and not of black African or African-Caribbean origin

A
  • Step 1: ACEi or ARB
  • Step 2: ACEi/ARB and CCB/thiazide-like diuretic
  • Step 3: ACEi/ARB and CCB and thiazide-like diuretic
  • If treatment fails confirm resistant hypertension
61
Q

Outline how we treat hypertension in people age 55 or over

A
  • Step 1: CCB
  • Step 2: CCB and ACEi/ARB/thiazide-like diuretic
  • Step 3: ACEi/ARB and CCB and thiazide-like diuretic
62
Q

Outline how we treat hypertension in Black African or African-Caribbean people?

A
  • Step 1: CCB
  • Step 2: CCB and ACEi/ARB/thiazide-like diuretic
  • Step 3: ACEi/ARB and CCB and thiazide-like diuretic
63
Q

What is the 2 pronged approach for treating hypertension with type 2 diabetes?

A
  • Two-pronged approach
  • Decreased peripheral vascular resistance
  • Leads to decreased BP and dilation of efferent glomerular arteriole
  • Leads to reduced intraglomerular pressure
64
Q

How do we treat resistant hypertension?

A
  • If BP not controlled after ACE-i/ARB + CCB +Thiazide-like diuretic
  • Give spironolactone and alpha/beta blockers
  • Spironolactone acts as an aldosterone receptor antagonist
65
Q

What should we consider before adding extra drugs to treat resistant hypertension?

A
  • Check that BP is measured accurately
  • Check patient adherence/concordance to treatment
  • Check for any secondary causes of hypertension
66
Q

What are the adverse side effects of spironolactone?

A
  • Hyperkalaemia
  • Gynaecomastia
67
Q

What are the contraindications for spironolactone?

A
  • Hyperkalaemia
  • Addison’s disease
68
Q

What are the drug interactions of spironolactone?

A
  • Increase activity of K+ drugs
  • Pregnancy
69
Q

When do we consider alpha and beta blockers instead of spironolactone?

A
  • If high K+ concentration
70
Q

Give some examples of beta adrenoceptor blockers used to treat hypertension

A
  • Labetalol
  • Bisoprolol
  • Metoprolol
71
Q

Outline the action of B-adrenoceptor blockers?

A
  • Decrease sympathetic tone
  • Block noradrenaline
  • Reduce myocardial contraction
  • Reduced cardiac output
72
Q

What are the adverse side effects of B-adrenoceptor blockers?

A
  • Bronchospasm
  • Heart block
  • Raynaud’s
  • Lethargy
  • Impotence
  • Mask tachycardia - sign of insulin induced hypoglycaemia
73
Q

What are the contraindications of B-adrenoceptor blockers?

A
  • Asthma
  • COPD
  • Haemodynamic instability
  • Hepatic failure
74
Q

What are the drug interactions of B-adrenoceptor blockers?

A
  • Non-dihydropyridine CCBs (verapamil and diltiazem)
  • Can lead to asystole
75
Q

What is the action of alpha adrenoceptor blockers?

A
  • Selective antagonism of alpha-1 adrenoceptors
  • Reduce peripheral vascular resistance
  • Relatively safe in renal disease
  • Also used to treat benign prostatic hyperplasia
76
Q

What is an example of an alpha adrenoceptor blocker?

77
Q

What are the adverse side effects of alpha adrenoceptor blockers?

A
  • Postural hypotension
  • Dizziness
  • Syncope
  • Headache and fatigue
78
Q

What are the contraindications for alpha adrenoceptor blockers?

A
  • Postural hypotension
79
Q

What are the drug interactions of alpha adrenoceptor blockers?

A
  • In patients affected by dihydropyridine CCB
  • Causes increased oedema

CPT (22 decks)

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