Drugs Used In Hypertension Flashcards

1
Q

What is the single biggest cause of death worldwide?

A

Hypertension

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2
Q

What is the first line treatment for hypertension in patients below the age of 55? 2

A
  1. Angiotensin converting enzyme (ACE) inhibitors

2. Angiotensin receptor blockers (ARBs)

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3
Q

Where is renin produced?

A

Juxtaglomerular cells

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4
Q

What does renin do?

A

Renin convert angiotensinogen into angiotensin I

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5
Q

Where is ACE found?

A

On the surface of the epithelial cells in the capillaries

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6
Q

What ACE do?

A

Converts angiotensin I into angiotensin II

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7
Q

Describe the functions of angiotensin II 5

A
  1. Causes vasoconstriction in blood vessels; increases resistance
  2. Stimulates the pituitary gland to release ADH (increasing water reabsorption); increased SV
  3. Stimulates the adrenal gland to release aldosterone (increasing Na reabsorption; increased SV
  4. Increases Na/H2O reabsorption in the kidneys; increased stroke volumes
  5. Increased resistance and increased SV increases BP
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8
Q

Why don’t we use ACE inhibitors and ARBs in patients over the age of 55?

A

Over the age of 55 the renin-angiotensin system isn’t as functional. We therefore use calcium channel blockers.

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9
Q

Describe the MOA of thiazide and other diuretics? 4

A
Diuretics cause a decrease in
1. Blood volume
2. Venous return 
3. Cardiac output 
 Which leads to a decrease in blood pressure
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10
Q

Explain a possible theory for diuretics causing vasodilation 3

A
  1. Diuretics result in the reduction in smooth muscle Na
  2. This may result in a secondary reduction of intracellular Ca
  3. Muscle may therefore be less responsive to vasoconstriction
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11
Q

What are the side effects of diuretics? 3

A

Diuretics may result in :

  1. Hypokalaemia
  2. Diabetes mellitus
  3. Gout
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12
Q

Who is thiazide diuretics useful in?

A

Thiazide diuretics is particularly useful in older patients (>55 )

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13
Q

Give two examples of thiazide like diuretics 2

A
  1. Hydrochlorothiazide

2. Indapamide

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14
Q

Give an example of a potassium sparing diuretic

A

Amiloride

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15
Q

Explain the effects of β adrenoceptor antagonist 2

A
  1. β blockers initially reduce BP by decreasing CO.
  2. It is also suggested that β blockers, antagonize β1 receptors in the juxtaglomerular cells, inhibiting the release of renin
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16
Q

What are the disadvantages of β blockers?7

A
  1. Cold hands
  2. Fatigue
  3. Provocation of asthma
  4. Heart failure
  5. Conductance block
  6. Raise serum triglyceride levels
  7. Decrease high density lipoprotein levels
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17
Q

How can some of the side effects of β blockers be prevented?

A

We can use cardio-selective hydrophillic drugs (drugs without liver metabolism or brain penetration) such as atenolol.

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18
Q

How does the body increase BP? 3

A
  1. Stimulation of β1 receptors increases CO
  2. Stimulation of α1 receptors causes vasoconstriction in smooth muscle of blood vessels increasing resistance
  3. Increased renin -> increased angiotensin II -> increased aldosterone
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19
Q

How do α1 blockers reduce BP?3

A
  1. α1 receptors cause vasoconstriction in vascular smooth muscle
  2. Inhibition results in vasodilation
  3. Decreased SVR -> decreased BP
20
Q

Give 2 examples of α1 blockers

A
  1. Doxazosin

2. Prazosin

21
Q

Hoe do selective β blockers decrease BP?

A
  1. β1 receptors in the heart stimulate an increase in heart rate and increase strength of contraction
  2. β1 antagonists would result in decreased CO
  3. Decreased CO -> BP
22
Q

Give 2 examples of selective β blockers

A
  1. Atenolol

2. Bisoprolol

23
Q

Describe how non selective β blockers decrease BP 2

A
  1. Antagonize both β and α receptors

2. Therefore, decrease CO (β) and SVR (kidneys β1; VSM α1)

24
Q

Name a non-selective β adrenoceptor antagonist

A

Propanolol

25
Q

Name a non selective α & β blocker

A

Carvedilol

26
Q

Name an α2 adrenoceptor agonist

A

Methyldopa

27
Q

What is the MOA of methyldopa? 4

A
  1. Methyldopa is converted into methyl epinephrine
  2. Methylepinephrine stimulates α2 receptors in the medulla
  3. Result in decreased sympathetic outflow decreased SVR
  4. Decreased CO and SVR decreases BP
28
Q

What are the 2 classes of calcium channel blockers?

A
  1. Dihydropyridines

2. Non-dihydropyridines

29
Q

What do dihydropyridine calcium channel blocks inhibit?

A

L type calcium channels

30
Q

Discuss how dihydropyridines work 4

A
  1. L type caclium channels allow calcium to enter the cell
  2. When calcium enters the cell, muscle contracts causing vasoconstriction-> increasedSVR
  3. Dihydropyridines selectively block calcium channels on VSM
  4. Blocking the channel results in vasodilation-> decreasing BP
31
Q

Name 2 dihydropyridines

A
  1. Amlodipine

2. Nifedipine

32
Q

What are the side effects of dihydropyridines? 5

A

All side effects are related to systemic vasodilation and include:

  1. Dizziness
  2. Headaches
  3. Flushing
  4. Peripheral oedema
  5. Swelling of gums (gingival hyperplasia)
33
Q

How do non-dihydropyridines work 5

A
  1. No dihydropyridines are non-selective calcium channel blockers
  2. Block calcium channels in VSM and cardiac cells
  3. Decreased AV node and SA node
  4. Decreased contractility, HR and conduction
  5. Anti-arrhythmic properties
34
Q

List 2 non-dihydropyridines

A
  1. Dilitiazem

2. Verapamil

35
Q

What are the side effects of non-dihydropyridines

A
  1. Excessive bradycardia
  2. Cardiac conduction abnormalities
  3. Verapimil can inhibit the calcium channels in the gut leading to constipation
36
Q

Describe the 3 classes of diuretics

A
  1. Loop diuretics
  2. Thiazide diuretics
  3. Potassium sparing diuretics
37
Q

Explain loop diuretics

A
  1. Reduces the reabsorption of sodium chloride in the kidneys
  2. Increased diuresis
  3. Decreased volume is the vascular system results in decreased volume returning to the heart
  4. Decreased BP -> decreased CO
38
Q

Give an example of a loop diuretic

A

Furosemide

39
Q

Explain how thiazide diuretics work 3

A
  1. Reduce sodium reabsorption in the kidneys to a lesser extent than loop diuretics. Decreased sodium reabsorption-> increased diuresis -> decreased CO. Short term effect
  2. Long term effects are thought to be produced by thiazide induced vasodilation
40
Q

Give an example of thiazide diuretics 1

A

Hydrochlorothiazide

41
Q

Explain how potassium sparing diuretics work

A
  1. Interrupts the actions of aldosterone (Na reabsorption and K excretion)
  2. Used in conjunction with loop or thiazide diuretics
42
Q

What do ACE inhibitors do? 3

A
  1. Angiotensin converting enzyme converts angiotensin I into its active form angiotensin II
  2. Inhibition of ACE results in decreased angiotensin II
  3. ACE inhibitors up-regulate bradykinin -> vasodilation
43
Q

Name 2 ACE inibitors

A
  1. Captopril

2. Ramipril

44
Q

How do angiotensin receptors blockers function? 2

A
  1. Angiotensin II binds to angiotensin type I receptors (AT1) which results in vasoconstriction and activation of aldosterone release
  2. ARBs antagonistically bind to AT1 resulting in vasodilation and inhibition of aldosterone release
45
Q

List 2 ARBs

A
  1. Losartan

2. Valsartan

46
Q

List side effects of ACE inhibitors and ARBs

A
  1. Inhibition of aldosterone-> hyperkalaemia
  2. Dry couch
  3. Angiooedema (increased levels of bradykinin and substance P)