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3.23 > Lecture 5: Pharmacology of the Medicines used in treating hypertnsion > Flashcards

Lecture 5: Pharmacology of the Medicines used in treating hypertnsion Flashcards

1
Q

What is the goal of treating hypertension?

A

To achieve and maintain systolic blood pressure below 140 mmHg and diastolic blood pressure 90 mmHg

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2
Q

What is the first line of treatment for hypertension?

A

Lifestyle modifications

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3
Q

What are the lifestyle modifications required for the treatment of hypertension?

A
  • Weight reduction
  • Regular physical exercise
  • DASH eating plan (lots of fruit and veg, little meat)
  • Reduction of dietry sodium intake
  • Moderation of alcohol intake
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4
Q

What are the pharmacological treatments for hypertension?

A
  • Diuretics
  • Sympatholytics
  • Calcium channel blockers
  • Direct acting vasodilators
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5
Q

How do diuretics work?

A

Indirectly prevent the reabsorption of water in the kidneys, most of them by preventing the reabsorption of sodium

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6
Q

What do ACE inhibitors lead to?

A
  • less angiotensin II
  • more bradykinin
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7
Q

What is first line treatment for hypertension?

A

ACE inhibitor

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8
Q

Where do diuretics have their effect?

A

Collecting duct

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9
Q

What are the different classes of diuretics?

A
  • Loop diuretics
  • Thiazides
  • Potassium sparing diuretics
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10
Q

Name loop diuretics

A

Furosemide supplemented with spironolactone or amiloride

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11
Q

Where is the sight of action of furosemide?

A

Proximal convolated tubule

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12
Q

Where is the sight of action of thiazides?

A

Early distal convoluted tubule

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13
Q

Where is the sight of action of potassium sparing?

A

Tubule and collecting duct - distal nephron

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14
Q

What is the mechanism of action of diuretics?

A

Loop diuretics act principally by inhibiting the Na/K/2Cl co-transporter

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15
Q

What is a major problem with loop diurectics?

A

Hypokalaemia

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16
Q

What are the most commonly used diurects?

A

Thiazide

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17
Q

How do thiazide diuretics work?

A

Inhibit the sodium-chloride transporter in the distal tubule

18
Q

What drugs act on RAAS?

A

Angiotensin converting enzyme:
- Captotril
- Enalapril
- Lisinopril
- Other ACE inhibitors

Angiotensin II receptors
- Losartan
- Valsartan
- Other ARBs

19
Q

What inhibits renin production?

A
  • B1 antagonists
  • Aliskiren - not recommended for use
20
Q

What do ACE inhibitors have thier effect on?

A

Lung

21
Q

Give examples of ACE inhibitors (3)

A
  • Catopril
  • Lisinopril
  • Enalapril
22
Q

What does a decrease in angiotensin II result in?

A
  • Vasodilation
  • Decreased blood volume
  • Decreased cardiac and vascular remodelling
  • Potassium retention
  • Fetal injury
23
Q

What does an increase in bradykinin result in?

A
  • Vasodilation
  • Cough
  • Angioedema (rare)
24
Q

How do ACE inhibitors work?

A

Block the action of the ACE, to prevent the conversion of angiotensin I to angiotensin II
- Reduces peripheral vascular resistance (afterload), so lowers blood pressure
- Dilates the efferent glomerular arteriole, which reduces intra-glomerular pressure
- Reduces aldosterone levels which promotes sodium and water excretion, helps reduce preload

25
Q

Name some angiotensin II receptor blockers (3)

A
  • Losartan
  • Valsartan
  • Candesartan
26
Q

How do ARBs work?

A

Block the action of angiotensin II on the angiotensin I receptor

27
Q

Name aldosterone antagonist (3)

A
  • Spironolactone
  • Eplerenone
  • Potassium sparing diuretics
28
Q

How do aldosterone antagonists work?

A
  • Competitively bind to aldosterone receptor
  • Promote Na and H20 excretion in the collecting tubule and duct
29
Q

What are the sympatholytics (Antiadrenergics)? (5)

A
  • Beta blockers
  • Alpha 1 blockers
  • Centrally acting alpha 2 antagonists
  • Adrenergic neuron blockers
  • Ganglionic blockers
30
Q

What are the actions of beta-adrenergic blockers in hypertension?

A
  • Blockage of cardiac beta-1-receptors cause a decrease in heart rate and contractility, so a decrease in CO
  • Improve efficiency
  • Suppress reflex tachycardio caused by vasodilators
  • Blockage of beta 1 receptors in JG in kidneys, decrease in renin release, decrease in RAAS mediated vasoconstriction ( angiotensin II) and volume expansion (aldosterone)
31
Q

What does long term use of beta-adrenergic blockers cause?

A

A decrease in peripheral vascular resistance

32
Q

What are non selective beta adrenergic blockers?

A

When the beta adrenergic blocker blocks both beta 1 and beta 2 receptors

33
Q

What are cardioselective beta adrenergic blockers?

A

Beta adrenergic blockers that have greater affinity for beta 1 than beta 2

34
Q

What do partial agnosists have?

A

Intrinsic sympathomimetic activity

35
Q

Name calcium channel blockers - Dihydropyradines? (2)

A
  • Nifedipine
  • Amlodipine
36
Q

How do calcium channel blockers work?

A
  • Block calcium channels in arterioles
  • Dilation of peripheral vessels, leading to a decreased blood pressure
  • Dilation of coronary arteries, increase in coronary perfusion
37
Q

Do calcium channel blockers block cardiac Ca channels at therapeutic doses?

A

No

38
Q

How do nifedipine and amlodipine increase heart rate and contractility?

A
  • Lowering blood pressure acts on the baroreceptor reflex, this stimulates the medulla to increase the firing of SNS to beta receptors in the heart
  • Nifedipine lacks direct cardiosuppressant actions, cardiac suppression is unopposed, so an increase in heart rate and an increase in contractility.
39
Q

Name non dihydropyradines calcium channel blockers

A
  • Verapamil
  • Diltiazem
40
Q

How do non dihydropradine CCBs work?

A

Act on the heart to slow conduction and decrease contractility

41
Q

Where do diuretics have their effect?

A

Collecting duct

42
Q

What is first line treatment for hypertension?

A

ACE inhibitor

3.23 (26 decks)

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