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Module 103, Theme 3: Physiology of the CVS: principles of pathology, diagnosis and treatment of CV diseases. > Anti-hypertensives > Flashcards

Anti-hypertensives Flashcards

1
Q

Hypertension

A

Blood pressure that is persistently higher than the normal: 150/95 mm Hg

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2
Q

Normal BP

A

150/ 95 mm Hg

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3
Q

Regulation of stroke volume

A

Carried out by the ventricles

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4
Q

Regulation of heart rate

A

Carried out by SAN regulation

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5
Q

Regulation of total peripheral resistance

A

Controlled by arteriole constriction in the peripheries.

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6
Q

Factors that increase cardiac output

A

Increase in:

Preload
Cardiac force of contraction
Frequency of heart beats
Release of NADR

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7
Q

Extrinsic regulation of CO

A

Autonomic nervous system

Sympathetic- increases heart rate and contractility.

Parasympathetic: decreases heart rate and contractility.

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8
Q

Sympathetic effect on cardiac output

A

Acts on Beta-1 receptors

Causes an increase in cAMP—-> Increases Ca2+ released —> increases the rate and contractility in the heart.

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9
Q

Parasympathetic effect on cardiac output

A

Acts on M2 receptors:

Decreases cAMP—> less Ca2+ —> decreases rate and contractility.

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10
Q

Sympathetic effect on total peripheral resistance

A

System releases noradrenaline from adrenal medulla.

Acts on alpha-1 receptors— Increase IP3—-> Increase Ca2+ released —-> Causes vasoconstriction in arterioles.

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11
Q

Effect of angiotensin II on BP

A

Acts on AT1- R - causes vasoconstriction and arterio-constriction

Venoconstriction = increase in preload

Arterioconstriction= increase in afterload

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12
Q

Arterioconstriction

A

A factor that increases afterload, thus blood pressure.

Trigger by angiotensin II acting of AT1-R

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13
Q

AT1-R

A

Angiotensin II Type 1 receptor.

Angiotensin II is an agonist that triggers arterioconstriction and venoconstriction.

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14
Q

Regulation of BP by the kidneys

A

Kidneys sense an increase in blood flow and triggers the RAS.

Release of aldosterone and angiotensin increase preload and afterload= increase in BP

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15
Q

Effect of aldosterone on BP

A

Release is triggered when RAS is activated from an increase in renal blood flow.

Aldosterone is released from adrenal cortex and acts on AT1-R.

This causes more Na+ retention, thus more H20 retention.

This increases preload= increase in BP

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16
Q

Regulation of TPF by angiotensin II

A

Angiotensin II is made in the lungs via ACE.

Triggers an increase in IP3— > increase in Ca2+

When this occurs in arteriole muscular walls, causes vasoconstriction.

This increase TPR= increase in BP.

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17
Q

Aldosterone effect on aldosterone-sensitive distal nephron

A

Aldosterone binds to cytoplasmic receptors and activates them.

The activated receptor binds to the nucleus and triggers increased expression of Na= channels= increases water retention = increase BP.

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18
Q

Factors that determine what antihypertensive is given

A

Age

Race

Co-existing diseases

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19
Q

Using age to determine what antihypertensive is given

A

If patient is <55:
ACE inhibitor/ ARB is given

If patient is >55:
Ca2+ channel blocker is given

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20
Q

Using race to determine what antihypertensive is given

A

If the patient is Black African/American/Caribbean:

Ca2+ is given despite the age. They respond less to ACE inhibitors and beta-blockers

21
Q

Side effects/ contraindications of ACE inhibitors

A

Dry cough

1st dose hypotension

Contraindication with bilateral renal artery stenosis

May cause hyperkalaemia

22
Q

Dry cough with ACE inhibitors

A

ACE inhibitors prevent the breakdown of bradykinin.

ACE breaks down bradykinin in CNS/PNS/ SP/ BKergic neurone.

This prevents bradykinin to be converted to an inactive peptide. This triggers coughing response- too much bradykinin in system.

23
Q

1st dose hypotension with ACE inhibitors

A

Side effect of ACE inhibitors

Due to an overstimulation of inhibiting the RAAS

24
Q

Contraindication of ACE inhibitors

A

Bilateral renal artery stenosis

The kidney is already hypoperfused due to narrower efferent arteriole

ACE inhibitor dilates the efferent arteriole whilst decreasing/ keeping the afferent arteriole the same.

This decreases perfusion even more.

25
Q

ARB

A

Angiotensin receptor blockers

Antagonises AT1-R, blocking the action of Angiotensin II

Example: Losartan

26
Q

Losartan

A

An ARB

27
Q

Spironolactone

A

Aldosterone antagonist- a diuretic, potassium sparing.

Blocks epithelial sodium channel (ENaC)- less absorption of Na+ in the blood.

28
Q

Ca2+ channel antagonist

A

Blocks Ca2+ channels:

Dihydropyridines act on blood vessel smooth muscles.

Phenylalkylamines and benzothiazepines action on cardiac cells.

29
Q

Dihydropyridines

A

Ca2+ channel antagonists that target L-type Ca2+ channels on smooth muscle of blood vessels.

Example: amlodipine.

Used to treat hypertension

30
Q

Amlodipine

A

Dihydropyridine

Targets L-type Ca2+ channels on blood vessels.

Used to treat hypertension

31
Q

Phenylalkylamines

A

Ca2+ antagonists that target L-type channels in the heart

Decreases heart rate and contractility.

Example: Verapamil

32
Q

Benzothiazepines

A

Ca2+ antagonists that target L-type Ca2+ channels in the heart.

Decreases heart rate and contractility.

Example: Diltiazem

33
Q

Verapamil

A

Phenylalkylamine that blocks L-type Ca2+ channels in the heart.

Decreases HR and contractility.

34
Q

Diltiazem

A

Benzothiazepine that decreases HR and heart contractility.

35
Q

Side effects and contraindications of Ca2+ channel antagonists.

A

Flushing and headaches

Combination of antagonists not recommended.

Action enhanced by grapefruit juice.

Peripheral oedema.

36
Q

Peripheral oedema as a side effect of Ca2+ channel antagonists.

A

With specifically dihydropyridines:

-Preferential dilation of precapillary arteriole.
Impairment of pre-capillary sphincter.

This increases HP across the capillary- forcing liquid out into surrounding tissues.

37
Q

Thiazide and thiazide-like diuretics.

A

Acts on distal convoluted tube to initiate diuretic action.

Blocks reabsorption of Na+ and Cl- back into the blood.

Activates Katp in blood vessel smooth muscle which dilates arterioles.

Example: Indapamide

38
Q

Indapamide

A

Thiazide-like diuretic.

Prevents the release of K+ from Katp, which increases Ca2+ in smooth muscle cells.

This hyperpolarises the cell- causing dilation of arterioles= decreases TPR and BP.

39
Q

Side effects and contraindications of thiazide and thiazide-like diuretics.

A

Hypokalaemia

Increase in urate, glucose and blood lipids.

40
Q

Bendroflumethiazide

A

A thiazide diuretic, treats high BP.

41
Q

Side effects and contraindications of beta-blockers

A

Bronchoconstriction

Vasoconstriction- B2 receptor

Fatigue

Increase in blood lipids

Hypoglycaemia

CNS side effects

Not efficacious in Black people.

42
Q

Beta blockers and vaso/bronchoconstriction

A

If the inhibit Beta-2 receptors, prevents the formation of cAMP.

This prevents the relaxation of smooth muscles in the airways and peripheral arterioles.

43
Q

Beta blockers and hypoglycaemia

A

Low blood glucose usually triggers the release of adrenaline.

This is inhibited by beta-blockers.

This keeps blood glucose low.

Therefore beta-blockers are contraindicated in diabetics.

44
Q

Non-selective beta-blockers

A

Acts on both beta-1 and beta-2 receptors

Example: propranolol

45
Q

Propranolol

A

Non-selective beta-blocker

46
Q

Bisoprolol

A

Selective beta-1 antagonist.

47
Q

Alpha-1 antagonists

A

Act as vasodilators

Blocks NADR from binding to Alpha-1 receptors.

Prevents release of IP3—> Ca2+ —-> vasoconstriction

examples: Doxazosin

48
Q

Doxazosin

A

Alpha-1 antagonist used to treat hypertension in patients with benign prostatic hypertrophy.

49
Q

Minoxidil

A

Vasodilator that opens K+ channels.

Hyperpolarises the smooth cell muscle cells- leading to vasodilation.

Module 103, Theme 3: Physiology of the CVS: principles of pathology, diagnosis and treatment of CV diseases. (20 decks)

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