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Module 103: The Heart, Lungs and Blood > Theme 3: Lecture 11 - Drug treatments for CVD 2 > Flashcards

Theme 3: Lecture 11 - Drug treatments for CVD 2 Flashcards

1
Q

What are the 5 classes of anti-hypertensive drugs

A
  • ACE inhibitors and Angiotensin receptor blockers.
  • Calcium channel antagonists
  • Diuretics
  • Beta Blockers
  • Vasodilators
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2
Q

What is first line anti-hypertensive treatment to someone under 55

A

ACE inhibitors or angiotensin receptor blockers

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3
Q

What is first line anti-hypertensive treatment to someone over 55 or a black person of African or Caribbean family origin of any age

A

Calcium channel blocker

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4
Q

What is second line anti-hypertensive treatment

A

ACE inhibitors and Calcium channel blockers

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5
Q

What is third line anti-hypertensive treatment

A

ACE inhibitors and calcium channel blockers and Thiazide like diuretics

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6
Q

What is fourth line anti-hypertensive treatment

A

ACE inhibitor and calcium channel blockers and thiazide like diuretics and consider further diuretics or alpha blocker or beta blocker

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7
Q

What are the side affects of ACE inhibitors

A
  • Dry cough (number 1 reason why these drugs aren’t tolerated)
  • 1st dose hypotension
  • Renal impairment (therefore contraindicated in bilateral renal artery stenosis)
  • May cause hyperkalaemia
  • No effect on serum glucose or lipids
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8
Q

Why can ACE inhibitors cause a dry cough

A
  • ACE inhibitors also inhibit the breakdown of Substance P and Bradykinin into inactive peptides
  • Substance P and Bradykinin are irritants that cause respiratory tract sensitivity leading to this dry cough
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9
Q

Why do ACE inhibitors cause first dose hypotension

A
  • Angiotensin is meant to keep BP high, if we suddenly reduce the amount of it, BP is going to plummet quite dramatically
  • Over time body will adapt to ACE inhibitors and hypotension stops becoming a problem
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10
Q

What is hyperkalaemia

A

high blood K+ levels

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11
Q

Give an example of an ACE inhibitor

A

Ramipril

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12
Q

What is the suffix to all ACE inhibitors

A

-pril

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13
Q

How do ACE inhibitors cause renal impairment

A
  • Normally if blood flow is reduced going into Bowman’s capsule, this is sensed by the kidneys
  • Renin is produced which eventually produces angiotensin II
  • This acts on AT1 receptors present in the blood vessel leaving Bowman’s capsule causing it to constrict
  • The pressure in the glomerulus will build up improving filtration
  • This doesn’t happen if the patient is on ACE inhibitors
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14
Q

Give an example of an angiotensin receptor blocker (ARB)

A

Losartan

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15
Q

How do Angiotensin receptor blockers work (ARB)

A

Block the actions of angiotensin II on AT1 receptors

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16
Q

What are the side affects of ARBs

A

minimal side effects

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17
Q

Give an example of an aldosterone antagonist

A

Spironolactone

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18
Q

How are aldosterone antagonists used

A

As an add on for resistant hypertension

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19
Q

When do aldosterone antagonists become frontline treatment

A

For hypertension in patients with primary aldosteronism

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20
Q

What is primary aldosteronism

A

a hormonal disorder that leads to high blood pressure. It occurs when your adrenal glands produce too much aldosterone

21
Q

What are the 3 main classes of Ca2+ channel blockers

A
  • Dihydropyridines
  • Phenylalkylamines
  • Benzothiazepines
22
Q

What do dihydropyridine Ca2+ channel blockers target

A

L-type calcium channels on smooth muscle arterioles

23
Q

Which is the main type of Ca2+ channel blocker used to treat hypertension

A

dihydropyridines

24
Q

What do phenylalkylamines Ca2+ channel blockers do

A

Target L-type Ca2+ channels in the heart and decrease the frequency and force of contraction

25
Q

What do benzothiazepine Ca2+ channel blockers do

A

Target L-type Ca2+ channels in the heart and decrease the frequency and force of contraction

26
Q

Name a dihydropyridine calcium channel blocker

A

Amlodipine

27
Q

Name a phenylalkylamine calcium channel blocker

A

Verapamil

28
Q

Name a benzothiazepine calcium channel blocker

A

Diltiazem

29
Q

Describe the regulation of smooth muscle contraction in arterioles

A
  • Calcium enters the cell and combines with the protein calmodulin
  • Calcium and calmodulin will stimulate MLCK
  • MLCK is inhibited by cAMP
  • MLCK uses ATP to phosphorylate the myosin light chain of a protein, this allows actin and myosin to interact and muscle to contract
  • Phosphatase dephosphorylates the myosin light chain
30
Q

Side affects of calcium channel blockers

A
  • Peripheral oedema

- Flushing and headaches

31
Q

Contraindications of calcium channel blockers

A
  • Combinations of Ca2+ channel antagonists not recommended

- Grapefruit juice inhibits action (CYP3A4) - calcium channel blockers are broken down by this cytochrome P450 enzyme

32
Q

Why do you get peripheral oedema when taking calcium channel blockers

A
  • Pre capillary sphincters have L type calcium channels on them
  • Preferential dilation of precapillary arteriole and impairment of the function of the pre-capillary sphincter increases hydrostatic pressure across the capillary and reducing fluid reabsorption.
33
Q

How do thiazide and thiazide like diuretics work

A
  • Some diuretic action. Work on the distal convoluted tubule to block the Na+,Cl- cotransporter
  • also acts via activation of ATP K+ channel in smooth muscle of blood vessel to dilate arterioles and decrease BP
34
Q

How does Indapamide work

A

hyperpolarises smooth muscle cells causing a relaxation/dilation of the arteriole and a decrease in total peripheral resistance

35
Q

Name two thiazide or thiazide like diuretics

A
  • Indapamide

- Bendroflumethiazide

36
Q

Side effects of thiazide and thiazide like diuretics

A
  • Hypokalaemia
  • Increase in urate
  • Increase in glucose
  • Increase in blood lipids
37
Q

Contraindications of thiazide like diuretics

A

diabetes

38
Q

Why is diabetes a contraindication of thiazide like diuretics

A
  • After a meal, glucose levels are elevated and will enter beta cells of the pancreas
  • They become metabolised, generate ATP and ADP, which would close the ATP K+ channel
  • This acts to depolarise the cell which leads to Ca2+ being able to enter the cell through voltage dependant calcium channels (VDCC)
  • The Ca2+ causes release of insulin into the bloodstream
  • Thiazide like diuretics will open the ATP K+ channel which inhibits Ca2+ coming into the cell so insulin isn’t released leading to a rise in blood glucose
39
Q

Side effects of beta blockers

A
  • Fatigue
  • Vasoconstriction
  • Bronchoconstriction
40
Q

What do beta blockers do

A

Lower the heart rate and contractility

41
Q

Why do patients on beta blockers feel fatigued

A

Patient’s can’t get the oxygen and nutrients that they need when exerting themselves because the heart rate and contractility won’t increase as the receptors are blocked

42
Q

Why are beta blockers contraindicated in diabetics

A
  • Low blood glucose activates the release of adrenaline, mobilises glucose release from liver.
  • Leads to tremor, palpitations and sweats
  • Blocked by Beta Blockers i.e the symptoms are removed so patients won’t know that their blood sugar is low
43
Q

What are the types of beta blocker

A
  • Non selective (beta 1 and beta 2)

- Selective beta 1 antagonist

44
Q

Name a non selective beta blocker

A

propranolol

45
Q

Name a selective beta 1 antagonist

A

bisoprolol

46
Q

What are vasodilators (which receptor do they bind to)

A

alpha 1 antagonists

47
Q

Name a vasodilator

A

Doxazosin

48
Q

What are vasodilators used to treat

A

Used to treat hypertension in patients with benign prostatic hypertrophy

49
Q

Name a vasodilator that will open K+ channels

A

Minoxidil

Module 103: The Heart, Lungs and Blood (51 decks)

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