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Hypertension and antihypertensive drugs Flashcards

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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
Do ACE inhibitors prevent all production of angiotensin II?
- No - Angiotensin II also produced from angiotensin I independently of ACE via chymases
26
Give some examples of ACE inhibitors?
- Lisinopril - Ramipril
27
What are some adverse side effects of ACE inhibitors?
- Hypotension - Dry cough - Hyperkalaemia (lower aldosterone leads to increased [K+]) - Cause or worsen renal failure (especially renal artery stenosis) - Angioedema
28
Why do ACE inhibitors cause a dry cough?
- Bradykinin is also a substrate for ACE - Use of ACE inhibitors prevents breakdown of bradykinin
29
What are the contraindications of ACEi?
- Renal artery stenosis - AKD - Pregnancy - Idiopathic angioedema
30
What are the drug interactions of ACEi?
- Increases activity of K+ drugs due to reduced aldosterone - NSAIDs disrupt renal function through action on efferent arteriole and ion imbalance - Other antihypertensive agents
31
Give some examples of angiotensin II and receptor antagonists
- Candesartan - Losartan
32
What are the adverse side effects of ARBs?
- Hypotension - Hyperkalaemia (low aldosterone increases K+) - Cause or worsen renal failure
33
What are the pros and cons of using ARBs over ACEi?
- 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
What are the contraindications of ARBs?
- Renal artery stenosis - AKD - Pregnancy - CKD
35
What are the drug interactions of ARBs?
- Increase activity of K+ drugs - NSAIDs
36
How do calcium channel blockers work?
- 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
What are the 3 classes of calcium channel blocker?
- Dihydropyridines - Non-dihydropyridines - phenylalkylamines and benzothiazepines - Have different selectivity for vascular smooth muscle or myocardium
38
What are dihydropyridines selective for?
- Peripheral vasculature - Have little chronotropic or inotropic effects - Cerebral vs peripheral selectivity dictates which are used for hypertension
39
What are phenylalkylamines selective for?
- Depresses SA node - Slows AV conduction - Negative inotropy
40
What are benzothiazepines selective for?
- Somewhere between peripheral vasculature and cardiac targets
41
When are CCBs primary choice antihypertensive?
- In low renin patients
42
Give some examples of dihydropyridines
- Amlodipine - has long half life - Nifedipine - Nimodipine - selective for cerebral vasculature
43
What are the adverse side effects of dihydropyridines?
- Ankle swelling - Flushing - Headaches (vasodilation) - Palpitations (compensatory tachycardia)
44
What are the contraindications for dihydropyridines?
- Unstable angina - Severe aortic stenosis
45
Which drugs interact with dihydropyridines?
- Amlodipine and simvastatin (increased effect of statin)
46
Give an example of phenylalkylamines?
- Verapamil
47
What are phenylalkylamines used for?
- Arrhythmia - Angina - Due to hypertension
48
Outline the properties of the phenylalkylamines
- Class IV antiarrhythmic agent - Prolongs action potential/effective refractory period - Less peripheral vasodilation - Negative chronotropic and inotropic effects
49
What are some adverse side effects of phenylalkylamines?
- Constipation - Bradycardia - Heart block - Cardiac failure
50
What are the contraindications of phenylalkylamines?
Poor LV function (caution) - AV nodal conduction delay
51
What are the drug interactions of phenylalkylamines?
- B blockers (cardiologist use only - Caution with other antihypertensive and antiarrhythmic agents
52
What are benzothiazepines?
- Diltiazem
53
Give some examples of thiazide and thiazide-like diuretics
- Bendroflumethiazide - Indapamide
54
Outline the action of thiazide and thiazide-like diuretics?
- 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
What are the adverse side effects of thiazide and thiazide-like diuretics?
- Hypokalaemia - Hyponatraemia - Hyperuricemia (gout) - Arrhythmia - Increased glucose (especially with beta blockers) - Small increase in cholesterol and triglyceride
56
What are the contraindications for thiazide and thiazide-like diuretics?
- Hypokalaemia - Hyponatraemia - Gout
57
What are the drug interactions of thiazide and thiazide-like diuretics?
- NSAIDs - Decreased K+ drug such as loop diuretics
58
Which different patient groups are given different treatment for hypertension?
- 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
Outline how we treat hypertension with type 2 diabetes
- 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
Outline how we treat hypertension in people aged <55 and not of black African or African-Caribbean origin
- 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
Outline how we treat hypertension in people age 55 or over
- Step 1: CCB - Step 2: CCB and ACEi/ARB/thiazide-like diuretic - Step 3: ACEi/ARB and CCB and thiazide-like diuretic
62
Outline how we treat hypertension in Black African or African-Caribbean people?
- Step 1: CCB - Step 2: CCB and ACEi/ARB/thiazide-like diuretic - Step 3: ACEi/ARB and CCB and thiazide-like diuretic
63
What is the 2 pronged approach for treating hypertension with type 2 diabetes?
- Two-pronged approach - Decreased peripheral vascular resistance - Leads to decreased BP and dilation of efferent glomerular arteriole - Leads to reduced intraglomerular pressure
64
How do we treat resistant hypertension?
- 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
What should we consider before adding extra drugs to treat resistant hypertension?
- Check that BP is measured accurately - Check patient adherence/concordance to treatment - Check for any secondary causes of hypertension
66
What are the adverse side effects of spironolactone?
- Hyperkalaemia - Gynaecomastia
67
What are the contraindications for spironolactone?
- Hyperkalaemia - Addison's disease
68
What are the drug interactions of spironolactone?
- Increase activity of K+ drugs - Pregnancy
69
When do we consider alpha and beta blockers instead of spironolactone?
- If high K+ concentration
70
Give some examples of beta adrenoceptor blockers used to treat hypertension
- Labetalol - Bisoprolol - Metoprolol
71
Outline the action of B-adrenoceptor blockers?
- Decrease sympathetic tone - Block noradrenaline - Reduce myocardial contraction - Reduced cardiac output
72
What are the adverse side effects of B-adrenoceptor blockers?
- Bronchospasm - Heart block - Raynaud's - Lethargy - Impotence - Mask tachycardia - sign of insulin induced hypoglycaemia
73
What are the contraindications of B-adrenoceptor blockers?
- Asthma - COPD - Haemodynamic instability - Hepatic failure
74
What are the drug interactions of B-adrenoceptor blockers?
- Non-dihydropyridine CCBs (verapamil and diltiazem) - Can lead to asystole
75
What is the action of alpha adrenoceptor blockers?
- Selective antagonism of alpha-1 adrenoceptors - Reduce peripheral vascular resistance - Relatively safe in renal disease - Also used to treat benign prostatic hyperplasia
76
What is an example of an alpha adrenoceptor blocker?
- Doxazosin
77
What are the adverse side effects of alpha adrenoceptor blockers?
- Postural hypotension - Dizziness - Syncope - Headache and fatigue
78
What are the contraindications for alpha adrenoceptor blockers?
- Postural hypotension
79
What are the drug interactions of alpha adrenoceptor blockers?
- In patients affected by dihydropyridine CCB - Causes increased oedema

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