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YR1 - Pharmacology SEM 2 > 17. Clinical Pharmacology of Hypertension > Flashcards

17. Clinical Pharmacology of Hypertension Flashcards

1
Q

What does Hypertension lead to an increased risk of? (4)

A

Elevated Blood Pressure/Hypertension

  • It may lead to an increased risk of:
    1. Stroke
    2. Heart failure
    3. Myocardial infarction
    4. Renal failure
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2
Q

How is arterial BP measured/recorded as?

What is Pulse Pressure?

A

BP = Systolic BP/Diastolic BP

Pulse pressure = the difference between the systolic and diastolic pressures

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3
Q

What is considered a normal BP?

high normal?

Mild/Moderate/Severe hypertension?

A

Blood Pressure - Traditionally it was said that:

  • Normal = <120/80 mm Hg
  • High Normal =120/80 to l39/89
  • MILD hypertension = 140/90 to 159/99
  • MODERATE hypertension = 160/100 to 179/109
  • SEVERE hypertension = >180/110
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4
Q

What is the target BP for a hypertensive patient?

A

Blood Pressure Targets

  • At present blood pressure treatment targets vary among Australian and international guidelines
  • Generally for patients who require BP lowering therapy the aim is to reduce blood pressure to <140/90 mmHg
  • This target may be difficult to achieve in some patients, even with combination drug therapy, but movement towards this level, even if it is not reached, is likely to be beneficial in reducing CVD risk
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5
Q

What are the 2 types of hypertension?

Causes of both?

A

Hypertension

  1. Primary or essential hypertension (95% of cases) - no single definable cause → homeostatic mechanism set it at this level
  2. Secondary hypertension - cause can be identified:
    1. Phaeochromocytoma = tumour of adrenal medulla = ↑adrenaline + ↑noradrenaline = ↑BP
    2. Primary aldosteronism
    3. Renal disease
    4. Some medications
      • e.g. NSAIDS, oral contraceptives, corticosteroids
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6
Q

What are 7 non-pharmacological treatments for hypertension?

A

Non-pharmacological Treatment of Hypertension

Non-pharmacological measures should be instituted first, and at times may be the only intervention necessary. These include:

  1. Regular physical activity (aerobic exercise)
  2. Weight reduction in overweight patients
  3. Reduction of alcohol intake
  4. Moderate sodium restriction
  5. Healthy eating plan
  6. Management of obstructive sleep apnoea
  7. Smoking cessation (reduces cardiovascular risk)
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7
Q

What are 5 drug groups used to treat elevated blood pressure/hypertension including

A

Pharmacological Treatment of Hypertension

There are several drug groups used to treat hypertension including:

  1. Angiotensin converting enzyme inhibitors (ACE inhibitors)
    • 1st drug available + thus most data collected
  2. Angiotensin ll receptor antagonists (A II antagonists)
    • not associated with cough
    • GP prescribing preferences
  3. Calcium channel blocking agents
  4. Thiazide diuretics
  5. Beta adrenoceptor antagonists (beta blockers)
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8
Q

What is the RAAS system and what 3 things does it control?

A

Renin-Angiotensin-Aldosterone System (RAAS)

  • The Renin-Angiotensin-Aldosterone System is a major regulatory system within the body involved in homeostasis
  • It helps regulate a number of functions including:
  1. Blood pressure
  2. Fluid volume
  3. Electrolyte levels e.g. sodium and potassium
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9
Q

What is Angiotensinogen?

What is Renin?

Where are they produced?

A

RAAS

  • Angiotensinogen = a glycoprotein (alpha 2 globulin) produced by the liver and released into the circulation
  • Renin = an enzyme secreted by the juxtaglomerular apparatus in the kidneys which hydrolyses angiotensinogen to produce angiotensin l
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10
Q

What are 2 factors affecting renin release?

A

RAAS - Renin

Factors affecting renin release include:

  1. a drop in renal blood flow/blood pressure
  2. a fall in sodium concentration in renal tubules
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11
Q

What is Angiotensin I

What is ACE?

A

RAAS

  • Angiotensin l = a decapeptide which is thought to be inactive
  • Angiotensin converting enzyme (ACE) = an enzyme found in many tissues, particularly the lungs. It converts angiotensin l to angiotensin II. It is identical to Kinase II
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12
Q

What are 5 effects of Angiotensin II?

A

RAAS - Angiotensin II = an octapeptide which exerts a number of effects including:

  1. vasoconstriction
  2. the release of aldosterone
  3. increase in blood pressure
  4. vascular and cardiac cell growth (hypertrophy)
  5. thirst and release of ADH (vasopressin)
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13
Q

What is Aldosterone?

Where does it act in the nephron?

Effects?

A

RAAS

  • Aldosterone = a hormone released from the adrenal cortex which acts on the distal convoluted tubule and collecting duct
  1. increases the reabsorption of sodium and water (returned to the body)
  2. increases the excretion of potassium (excreted out of the body)
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14
Q

How does Angiotensin II cause an increase in BP?

A

RAAS

Angiotensin II increases blood pressure:

  1. Produces vasoconstriction (vascular smooth muscle contraction) and an increase in peripheral vascular resistance
    • ↑ resistance = ↑BP
  2. Causes the release of aldosterone from the adrenal cortex which acts on the kidney to conserve sodium and water
    • ↑ volume = ↑BP

Both effects produce an increase in blood pressure

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15
Q

Which 2 receptors does Angiotensin II work on?

A

RAAS - Angiotensin lI

Acts on two different receptor types:

  1. angiotensin II type 1 receptors (AT1 receptors)
  2. angiotensin II type 2 receptors (AT2 receptors)
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16
Q

What are 4 effects of angiotensin II produced by stimulation of AT1 receptors?

A

Angiotensin lI

  • Effects of angiotensin II produced by stimulation of AT1 receptors include:
  1. Vasoconstriction
  2. Release of aldosterone
  3. Cell growth in heart and blood vessels
  4. Thirst and release of vasopressin
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17
Q

What do ACE inhibitors do?

3 examples?

A

Angiotensin Converting Enzyme Inhibitors (ACE Inhibitors)

  • Examples include
    • Enalapril
    • Perindopril
    • Ramipril
  • ACE inhibitors inhibit angiotensin converting enzyme (ACE), the enzyme which converts angiotensin l to angiotensin ll

Effects

  • Reduce angiotensin II levels (inhibit production)
  • Increase bradykinin levels (inhibit breakdown)
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18
Q

How do ACE inhibitors produce a drop in BP?

(3 ways)

A

Angiotensin Converting Enzyme Inhibitors (ACE Inhibitors)

Produce a drop in blood pressure by:

  1. Inhibiting the production of angiotensin ll leading to vasodilation and a drop in peripheral resistance
  2. Reducing the secretion of aldosterone leading to diuresis and sodium loss
  3. Increasing bradykinin levels leading to vasodilation and a drop in peripheral resistance (actual contribution to drop in blood pressure?)
19
Q

What are 6+ adverse effects of ACE inhibitors?

A

ACE Inhibitors - Adverse Effects

  1. Dizziness, orthostatic (postural) hypotension, rash, angioedema
  2. Hyperkalaemia (stop potassium supplements)
  3. Cough
  4. Pregnancy (Category D)
  5. Renal artery stenosis
  6. Drug interactions
20
Q

Why should people on ACE inhibitors stop taking potassium supplements?

A

ACE inhibitor - Adverse Effects = Hyperkalaemia

21
Q

How can ACE inhibitors produce a cough?

A

ACE Inhibitors - Adverse Effects

May produce a cough in some patients

  • persistent, dry, non-productive, often worse at night
  • up to 20% of patients
  • more common in females
  • thought to be due to a build up of bradykinin
22
Q

Can ACE inhibitors be taken during pregnancy?

A

ACE Inhibitors and Pregnancy (Category D)

  • Post-marketing experience with all ACE inhibitors suggests that exposure in utero may be associated with hypotension and decreased renal perfusion in the foetus.
  • Have also been associated with foetal death in utero.
  • When ACE inhibitors have been used during the 2nd and 3rd trimesters of pregnancy, there have been reports of neonatal hypotension, renal failure, skull hypoplasia and death
  • Oligohydramnios (reduced amniotic fluid = less protection to baby) has also been reported, presumably resulting from decreased foetal renal function; oligohydramnios has been associated with foetal limb contractures, craniofacial malformations, hypoplastic lung development and intrauterine growth retardation
23
Q

Why are ACE inhibitors contraindicated in bilateral renal artery stenosis?

A

Renal Artery Stenosis

  • In renal artery stenosis glomerular afferent arteriolar blood flow and pressure are reduced by the narrowed vessel
  • Glomerular perfusion pressure is maintained by the vasoconstrictor effect of angiotensin II on efferent arterioles
  • ACE inhibitors reduce the synthesis of angiotensin II, reduce the vasoconstrictor effect of angiotensin II on efferent arterioles and their use can result in renal failure
24
Q

What are 3 examples of Angiotensin ll Receptor Antagonists?

A

Angiotensin ll Receptor Antagonists

Examples include:

  1. Candesartan
  2. Irbesartan
  3. Telmisartan
25
How do Angiotensin ll Receptor Antagonists work?
**Angiotensin ll Receptor Antagonists** * Act as competitive antagonists of angiotensin ll at angiotensin ll type one (AT1) receptors * Do not antagonise the effects of angiotensin II produced by the stimulation of angiotensin ll type two (AT2) receptors * Do not block the production of angiotensin II
26
How do Angiotensin ll Receptor Antagonists produce a fall in blood pressure?
**Angiotensin ll Receptor Antagonists** Produce a fall in blood pressure by: * Inhibiting angiotensin ll induced vasoconstriction leading to vasodilation and a drop in peripheral resistance * Inhibiting the secretion of aldosterone leading to diuresis and sodium loss * Do NOT increase bradykinin levels (they do not inhibit ACE) * Produce similar drops in BP to ACE inhibitors
27
What are 6+ adverse effects of Angiotensin ll Receptor Antagonists (ARBs)?
**Angiotensin ll Receptor Antagonists - Adverse Effects** 1. Dizziness, orthostatic (postural) hypotension, rash, angioedema 2. Hyperkalaemia (stop potassium supplements) 3. Pregnancy (Category D) - same as ACE inhibitors 4. Renal artery stenosis - same as ACE inhibitors 5. Cough - same as placebo (do not block ACE and do not increase bradykinin levels) 6. Drug interactions
28
How can Angiotensin ll Receptor Antagonists ​produce hyperkalaemia?
**Angiotensin ll Receptor Antagonists - Hyperkalaemia**
29
What are the 2 types of Calcium channel blockers and 2 examples of each?
_Calcium Channel Blocking Agents_ 1. **Dihydropyridines**: examples include: 1. amlodipine 2. felodipine 2. **Non-dihydropyridines**: examples include: 1. diltiazem 2. verapamil
30
How does calcium enter cells? Which type of channel is most important in cardiovascular disease prevention/hypertension control?
_Calcium Channel Blocking Agents_ * Calcium can enter cells in a number of ways * Voltage-gated calcium channels allow calcium to enter the cell whenever the membrane is depolarised * There are 5 different subtypes of voltage- gated calcium channels, namely L,T,N,P/Q and R * **L type channels** are an important calcium source for contraction of smooth and cardiac muscle
31
How do Calcium Channel Blocking Agents work?
**Calcium Channel Blocking Agents** * Bind to the alpha1 subunit of the voltage- gated L type calcium channels and block the entry of calcium into the cell * Block the entry, not the intracellular actions of calcium * In blood vessels reduced calcium levels result in vascular smooth muscle relaxation (vasodilation), a reduction in peripheral vascular resistance and a drop in blood pressure
32
What are 2 examples of Dihydropyridines and how do they work?
_Calcium Channel Blocking Agents_ **Dihydropyridines** * Examples include: * amlodipine * felodipine * Primarily inhibit calcium entry into vascular smooth muscle cells of blood vessels (arterioles) * ↓Ca2+ in blood vessels specifically = ↓contractions = ↓vasconstriction = ↑vasodilation = ↓Peripheral resistance * Used to treat hypertension and angina
33
What are 2 examples of Non-dihydropyridines and how do they work?
_Calcium Channel Blocking Agents_ **Non-dihydropyridines** * Examples include * diltiazem * verapamil * Inhibit calcium entry into vascular smooth muscle cells of blood vessels, as well as cells in the heart and gastrointestinal tract * Wider spectrum of activity * Used to treat hypertension, angina and some cardiac dysrhythmias (arrhythmias) * Reduced heart contractility
34
What are 5 adverse effects of calcium channel blocking agents?
**Calcium Channel Blocking Agents - Adverse Effects** 1. Hypotension, headache, flushes, reflux 2. Bradycardia e.g. diltiazem, verapamil * Will slow the heart = reduced electrical conductance * Don’t use in pts with heart failure due to bradycardia 3. Peripheral oedema (ankle) - arteriole dilation and increased permeability of post capillary venules (does not respond to diuretics) 4. Constipation e.g. verapamil * GIT SM blocked = reduced peristalsis 5. Drug interactions
35
What are Thiazide Diuretics? Example? Mechanism of Action?
**Thiazide Diuretics** * Example = hydrochlorothiazide (Dithiazide) * Inhibit the reabsorption of sodium and chloride in the early distal convoluted tubule of the nephron * ↑Na+/H2O loss = Diuretic = ↓ blood volume = ↓BP * EARLY → Diuretic * LATER → Vasodilation * Produce vasodilation and reduce peripheral resistance - longer term reduction in BP (debate as to how vasodilation is produced)
36
What are 5+ adverse effects of thiazide diuretics? What are 2 diseases that can be precipitated by thiazide diuretics?
**Thiazide Diuretics - Adverse Effects** 1. Dizziness, orthostatic (postural) hypotension, rash, photosensitivity 2. Frequency and urgency 3. Electrolyte disturbances e.g. hypokalaemia, hyponatraemia 4. May produce hyperuricaemia and precipitate gout (effect on transporters of both uric acid reabsorption and secretion in the renal tubule) 5. May produce hyperglycaemia and precipitate diabetes (debate as to the mechanism)
37
What is Indapamide? Adverse effects?
**Antihypertensives - Indapamide** * Indapamide is a thiazide like drug used to treat hypertension * AEs → Dizziness, orthostatic (postural) hypotension, rash, impotence, frequency and urgency * Electrolyte disturbances e.g. hypokalaemia, hyponatraemia * May produce hyperuricaemia → gout * May produce hyperglycaemia → diabetes
38
What are the 2 types of Beta Adrenoceptor Antagonists (Beta Blockers) used for Hypertension?
_Beta Adrenoceptor Antagonists (Beta Blockers) - 2 Types:_ 1. **Non-selective** * Some beta blockers are nonselective beta adrenergic receptor antagonists * They are competitive antagonists at all beta receptors * They competitively antagonise the actions of adrenaline and noradrenaline at β1, β2 and β3 adrenergic receptors * Example = propranolol 2. **Selective** * **​​**Some beta blockers are selective beta adrenergic receptor antagonists * They are competitive antagonists of adrenaline and noradrenaline at β1 receptors on the heart * They are known as selective, or cardio- selective, beta blockers * Examples = atenolol and metoprolol * It is important to note that their selectivity is not absolute, and in high doses they may also block β2 and β3 adrenergic receptors
39
What are 10 medical conditions Beta blockers can be used to treat?
**Beta Adrenoceptor Antagonists (Beta Blockers)** * Not the 1st drug of choice for hypertension * Beta blockers are used to treat a number of important medical conditions * These include 1. Hypertension 2. Angina 3. Heart failure 4. Myocardial infarction 5. Cardiac dysrhythmias 6. Glaucoma 7. Migraine 8. Tremor 9. Thyrotoxicosis 10. Anxiety
40
What are 3 theories as to how Beta Blockers reduce blood pressure?
**Beta Adrenoceptor Antagonists (Beta Blockers)** Mechanism of action in reducing BP is not fully elucidated: 1. Reduced renin release (block of β1 receptors on the juxtaglomerular cells of the kidney) 2. Reduced cardiac output (block of β1 receptors in heart) 3. Reduction in peripheral resistance (central effect reducing sympathetic outflow)
41
What are 4+ adverse effects of beta blockers?
**Beta Blockers - Adverse effects** 1. Wheezing and acute asthmatic attacks in patients who have asthma (includes cardio- selective β1 blockers) 2. Bradycardia, fatigue, reduced exercise tolerance 3. Cold extremities and aggravation of Raynaud’s disease 4. Sleep disturbances, nightmares, impotence
42
Why should Beta Blockers not be stopped abruptly?
**Beta Blockers - Adverse Effects** * Abrupt withdrawal of beta blocker therapy may be dangerous in some patients * Abrupt withdrawal can result in severe angina, cardiac dysrhythmias (arrhythmias) and myocardial infarction * Therapy should not be stopped abruptly * Where necessary reduce dose gradually according to guidelines
43
For patients with uncomplicated hypertension, which agents should you begin mono-therapy with?
**Hypertension - Drug Treatment** For patients with uncomplicated hypertension, begin mono-therapy with any of these agents: 1. Angiotensin converting enzyme (ACE) inhibitors 2. Angiotensin II receptor antagonists 3. Dihydropyridine calcium channel blocking agents 4. Thiazide diuretics (not in younger patients)
44
Why are Thiazides not recommended as first-line therapy in younger patients? Why are Beta-blockers no longer recommended as first line therapy in uncomplicated hypertension?
**Hypertension - Drug Treatment** * Thiazide diuretics have been associated with an increased risk of new onset diabetes and are not recommended as first-line therapy in younger patients * Beta-blockers are no longer recommended as first line therapy in uncomplicated hypertension because they * are not as effective as the first line drugs in reducing the risk of stroke * maybe associated with an increased risk of developing diabetes * However, always consider what other conditions the patient has e.g. angina, heart failure

YR1 - Pharmacology SEM 2 (8 decks)

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