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PPE - Pharmacology > Treatment for Hypertension and Heart Failure > Flashcards

Treatment for Hypertension and Heart Failure Flashcards

1
Q

What is the physiological control of blood pressure?

A

Autonomic Nervous system
Renin-Angiotensin system

Others:

  • Bradykinin
  • Endothelin
  • Nitric Oxide
  • Atrial Natriuretic Peptide
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2
Q

What happens when blood pressure goes down to increase it?

A

Decrease in Renal perfusion:

  • Decrease in Urinary output
  • Increase in Blood volume
  • RAS system increases (Increase in blood volume)
  • Increase in vasoconstriction
  • Increase in peripheral resistance

Change sensed by baroreceptors:

  • Decrease parasympathetic nervous system
  • Increase in Sympathetic nervous system (Activates RAS)
  • Increase in cardiac output

All lead to an increase in BP

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3
Q

What happens when blood pressure goes up to reduce it?

A

Increase renal perfusion:

  • Increase in urinary output
  • Decrease in blood volume
  • Decrease in RAS system (decreases blood volume)
  • Decrease in vasoconstriction
  • Decrease in peripheral resistance

Change sensed by baroreceptors:

  • Increase parasympathetic nervous system
  • Decreases sympathetic nervous system
  • Decrease cardiac output

Decrease in blood pressure

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4
Q

Describe the Renin-Angiotensin-Aldosterone system.

A 
Angiotensinogen is created in the liver
Renin from the kidney Converts it into
Angiotensin I
ACE (angiotensin II then converts that into
Angiotensin II

Angiotensin II The has 3 major effects:

  • Increase in Aldosterone production
  • Retention of salt and water (Aldosterone also promotes this)
  • Vasoconstriction

All this leads towards an increase in blood pressure

ACE also converts Bradykinin into inactive kinins

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5
Q

How can a higher blood pressure lead to morbidity and mortality?

A 
Higher blood pressure
\/
Increased arterial thickening
\/
Smooth muscle cell hypertrophy
Accumulation of vascular matrix
Loss of arterial compliance
\/
Target Organ Damage
\/
Heart - Kidneys - Brain - Eyes

\/

CV morbidity and mortality

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6
Q

Does hypertension treatment improve mortality and morbidity?

A

Yes

In a study Done it showed that against a placebo hypertensive treatment improves mortality and morbidity

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7
Q

What is defined as hypertension?

A

Defined 140/90mmHg

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8
Q

What are causes of hypertension?

A

Primary (essential) hypertension

  • High BP without any single evident cause
  • 90% hypertensive population

Secondary hypertension

  • High BP with a discrete, identifiable underlying cause
  • 10% hypertensive population
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9
Q

How do we treat hypertension?

A

Identify and treat underlying cause if present

Identify and treat other cardiovascular risk factors or co-morbidities

Lifestyle advice/non-pharmacological therapy

Pharmacological therapy

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10
Q

What are some lifestyle therapies to reduce hypertension?

A 
Patient education
Maintain normal body weight (BMI 20-25)
Reduce salt intake to 30 min/day
consume >5 portions of fresh fruit/vegetables daily
Reduce intake of total and saturated fat
(Smoking cessation)
(Relaxation therapies)
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11
Q

What is the 1st line pharmacological therapy of hypertension?

A

A - Angiotensin Converting Enzyme (ACE) inhibitors
- Angiotensin Receptor Blockers (ARB)
C - Calcium channel blockers
D - Diuretics (thiazide)

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12
Q

What do ACE Inhibitors do?

A

Competitive inhibitors of Angiotensin Converting Enzyme (ACE)

Reduction in formation of angiotensin II
Mainly arteriolar vasodilators
Some venodilation
Circulating aldosterone reduced

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13
Q

Tell me about ACE inhibitors.

A

Lisinopril, ramipril
Inhibit ACE activity
Prevents generation of Angiotensin II
Potentiates the action of bradykinin

Main side effect - dry cough (10-15%)
Important side effects:
- Angio-oedema (rare, more common in black pop.)
- Renal failure (incl. renal artery stenosis)
- Hyperkalaemia

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14
Q

Tell me about Angiotensin Receptor Blockers.

A 
Losartan, Valsartan
Bind to angiotensin AT1 receptor
Inhibit vasoconstriction and aldosterone stimulation caused by angiotensin II
Well tolerated few side effects
Important side effects:
- Renal failure
- Hyperkalaemia
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15
Q

Tell me about calcium channel blockers.

A

Bind to specific alpha subunit of L-type calcium channel, reducing cellular calcium entry

Vasodilates peripheral, coronary and pulmonary arteries
No significant effect on veins

Short acting dihydropyridines - baroreflex mediated tachycardia

Verapamil depresses SA node and slows A-V conduction

3 main groups:

  • Dihydropyridines (Nifedipine, Amlodipine)
  • Benzothiazepines (Diltiazem)
  • Phenylalkylamines (Verapamil)
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16
Q

Tell me about dihydropyridine calcium channel blockers

A

Amlodipine, Nifedipine

Properties:
Good oral absorption
Protein bound >90%
Metabolised by the liver
Few have active metabolite
Adverse effects:
Sympathetic nervous system activation - tachycardia and palpitations
Flushing, sweating, throbbing headache
Oedema
Gingival hyperplasia (rare
Amlodipine - gynaecomastia
17
Q

Tell me about Phenylalkylamines.

A

Verapamil

Properties:
Impedes calcium transport across the myocardial and vascular smooth muscle cell membrane
Class IV anti-arrhythmic agent/prolongs the action potential/effective refractory period
Peripheral vasodilation and a reduction in cardiac preload and myocardial contractility

Adverse effects:
Constipation
Risk of bradycardia
Reduce myocardial contractility (negative inotrope) - can worsen heart failure

18
Q

Tell me about benzothiazepines.

A

Diltiazem (not really used in hypertension)

Properties:
Impedes calcium transport across the myocardial and vascular smooth muscle membrane
Prolongs the action potential/effective refractory period
Peripheral vasodilation and a reduction in cardiac preload and myocardial contractility

Adverse effects:
Risk of bradycardia
Less negative inotropic effect than verapamil - can worsen heart failure

19
Q

Tell me how thiazide/thiazide like diuretics work.

A

E.g. Bendroflumethiazide

Reduce distal tubular sodium reabsorption
Sustained action

Blood pressure reduction - complex
Several mechanisms
- Initial blood volume decrease
- Later - total peripheral resistance falls

Dose-blood pressure response curve flat

20
Q

What are the adverse effects of Bendroflumethiazide?

A

Hypokalaemia
Increased urea and uric acid levels
Impaired glucose tolerance (especially with beta-blockers)
Cholesterol and triglyceride levels increased

Activates renin angiotensin system

21
Q

What is the BHS and NICE pharmacological treatment guideline?

A

Step 1:
Younger than 55 years - A
55 years or older/black patients - C or D

Step 2:
A + C or A + D

Step 3:
A + C + D

Step 4
Add further diuretic therapy
or
Alpha-blocker
or
Beta-blocker
Consider seeking specialist advice
22
Q

Give an indication, caution, contraindication of thiazide/diuretics.

A

Elderly, ISH (Isolated systolic hypertension), Heart failure

No caution

Gout

23
Q

Give an indication, caution, contraindication of Beta-blockers

A

MI/Angina

Heart failure, PVD, diabetes (except with CHD)

Asthma, COPD, heart block

24
Q

Give an indication, caution, contraindication of CCB (dihydropyridines

A

Elderly, ISH

25
Q

Give an indication, caution, contraindication of CCB (rate limiting)

A

Angina

Combination with beta-blockade

Heart block, heart failure

26
Q

Give an indication, caution, contraindication of ACE inhibitors.

A

Heart failure, LV dysfunction, MI, Diabetes (Type 1), nephropathy

Renal impairment, PVD

Pregnancy, renovascular hypertension

27
Q

Give an indication, caution, contraindication of ARBs

A

ACE inhibitor intolerance, hypertension with LVH, type 2 DM

Renal impairment, PVD

Pregnancy, renovascular hypertension

28
Q

Give an indication, caution, contraindication of alpha blockers.

A

Benign prostatic hyperplasia

Postural hypotension, heart failure

Urinary incontinence

29
Q

What are some other anti-hypertensive drugs?

A

Alpha adrenoceptors blockers

Beta adrenoceptors blockers
Direct renin inhibitors (new class) - Aliskirin

Centrally acting agents

  • Methyl Dopa
  • Clonidine
  • Moxonidine

Vasodilators

  • Hydralazine
  • Minoxidil
  • Sodium nitroprusside
30
Q

Tell me about alpha blockers.

A 
Properties:
-Selective antagonism at post-synaptic alpha-1 adrenoceptors and antagonise the contractile effects of noradrenaline on vascular smooth muscle
Reduce peripheral vascular resistance
More effect in upright position
Benign effect on plasma lipids/glucose
Safe in renal disease
Adverse effects:
Postural hypotension
Dizziness
Headache and fatigue
Oedema (especially if combined with dihydropyridines)
31
Q

Tell me about beta blockers.

A

E.g. Atenolol, bisoprolol, nebivolol
Developed for angina but found to lower blood pressure
Reduce heart rate and cardiac output
Inhibit renin release
Inhibit renin release
Initially TPR increases later falls to normal

Adverse effects:
Lethargy, impaired concentration
Reduced exercise tolerance
bradycardia
Cold hands - Raynaud's
Impaired glucose tolerance
Contraindication - asthma
32
Q

What are some of the treatments for heart failure?

A

Prognosis may be improved by:

RAS antagonism:

  • ACE inhibitors/ARB
  • Aldosterone blockade

Beta blocker

33
Q

What are the physiological effects of beta-blockers?

A 
Reduce heart rate (cardiac beta receptor)
Reduce BP (Reduced CO)

Reduced myocardial oxygen demand

Reduce mobilisation of glycogen
Negate unwanted effects of catecholamines

PPE - Pharmacology (24 decks)

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