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Human Pharmacy > Antihypertensive Drugs > Flashcards

Antihypertensive Drugs Flashcards

1
Q

How is blood pressure regulated? (physiologically)

A

Sympathetic Nervous system –> inc cardiac output, Beta-1 activation

Kidneys

vasoactive substances produced in blood vessel wall (NO, prostacyclin, aldosterone, etc.)

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2
Q

What influences PVR?

A

Alpha-1 adrenoceptor stimulation = vasoconstriction

Vasopressin, Angiotensin (AT) II, Aldosterone = vasoconstriction

Locally released substances = adenosine, serotonin, endothelin, prostaglandins

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3
Q

What are the categories of antihypertensives?

A

Reduce PVR = vasodilators (inc NO), alpha-1 blockers, AT receptor blockers, centrally acting sympatholytic, ACE inhibitors,

Reduce CO = Beta1-adrenoceptor blockers

Target Na secretion and dec BV = Diuretics

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4
Q

What suffix helps identify ACE inhibitors?

A

-pril

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5
Q

What suffix helps identify ARBs?

A

-sartan

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6
Q

What is the MOA of ACE inhibitors?

A

Block the conversion of angiotensin I to angiotensin II through inhibition of angiotensin converting enzyme.

Also inhibit bradykinin

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7
Q

List the relevant ACE inhibitors

A

Captopril, enalapril, fosinopril, lisinopril, perindopril, ramipril

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8
Q

What effects (NOT ADRs) will ACE inhibitors have?

A

Reduce AT-II induced vasoconstriction, Na retention, aldosterone release

Reduce effect of AT-II on sympathetic NS activity and growth factor

Cause accumulation of bradykinin

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9
Q

Name and explain some ADRs of ACE inhibitors

A

Dry cough = due to bradykinin inhibition, irritating the airways and causing vasodilation

Hypotension, headache, dizziness = drop in blood pressure

Hyperkalaemia = reduced aldosterone secretion

Angioedema, rash (esp captopril), diarrhoea, photosensitivity, psoriasis

Elevated hepatic aminotransferase = start of liver damage

Hyponatraemia = aldosterone inhibition –> reduced Na retention

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10
Q

Explain the cough associated with ACE inhibitors

A

Type of cough = persistent, non-productive cough, mild-tolerable

  • Cough is not dose dependent and occurs days-months after treatment has started
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11
Q

How long does the ACE inhibitor cough take to subside?

A

Improves within 1-4 weeks after stopping medication

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12
Q

How long after commencing treatment of ACE inhibitors could angioedema appear?

A

First week of treatment (possible months to years later)

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13
Q

Are ACE inhibitors recommended in diabetic patients?

A

Yes! It is recommended in patients with albuminuria or inc. serum creatinine

ACE inhibitors have a renoprotective effect

They do carry the risk of renal failure with bilateral renal artery stenosis

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14
Q

Why do ACE inhibitors increase the risk of renal failure in patients with Bilateral renal artery stenosis?

A

Due to the renal stenosis, there is already a reduced GFR/blood entering the glomerulus.

ACE inhibitors will act to further decrease this GFR due to inhibition of ACE, preventing an increase in GFR and ATII formation.

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15
Q

What are the targets of angiotensin? (what are the receptor functions)

A

AT1 Receptor = contract vascular smooth muscle, secrete aldosterone (adrenal cortex), increase Na+ reabsorption from PCT, increased NA release, stimulation of cell growth in arteries and heart.

AT2 Receptor= influences bradykinin

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16
Q

What is the MOA of Sartans?

A

Competitively blocks the binding of ATII to the AT1 receptor with relative selectivity.

Causes a reduction in ATII-induced vasoconstriction, Na reabsorption and aldosterone release.

Also produced reduced ATII effect on sympathetic NS activity and growth factors.

17
Q

Do sartans pose the same cough risk as ACE inhibitors?

A

Like ACE inhibitors, Sartans will still cause a cough.

Sartans pose a lower cough risk

18
Q

Name the relevant Sartans

A

candesartan, eprosartan, irbesartan, losartan, olmesartan, telmisartan, valsartan

19
Q

Name and explain some ADRs of Sartans

A

dizziness, headache

hyperkalaemia = due to inhibition of aldosterone –> blocks the insertion of Na transporters in the collecting duct –> prevent Na/K exchange –> inc K+ retention

First dose hypotension, rash, renal impairment, dyspepsia, muscle cramps, diarrhoea, decreased heamoglobin, nasal congestion, insomnia, angioedema

Cough = due to accumulation of bradykinin

20
Q

Name the main diuretic classes used as antihypertensives (give some examples)

A

Thiazide and Thiazide like diuretics = hydrochlorothiazide (most common), indapamide, chlorthalidone

Loop diuretics = frusemide, bumetanide, ethacrynic acid

Potassium sparing diuretics = spironolactone, eplerenone, amiloride, triampterene

21
Q

What are the benefits of thiazide/-like diuretics in hypertension treatment

A

Well tolerated first line drug (>65 yrs old)

Low dose = maximal antihypertensive w/ minimal hypokalaemia

22
Q

What are some things to be mindful of when using thiazides as antihypertensives?

A

Prolonged use = elevated glucose, uric acid (be mindful of this in gout), and lipid derangement

May produce compensatory RAAS production

Osteoprotective = decreased Ca2+ excretion

23
Q

True or False

Loop diuretics are more effective as antihypertensives in comparison to Thiazides?

A

FALSE

Loop diuretics are less effective but are very effective in congestive heart failure

24
Q

Which potassium-sparing diuretic has a lesser anti-androgenic effect?

A

Eplerenone has a lesser anti-androgenic/anti-testosterone effect compared to spironolactone

25
Q

What are the benefits of eplerenone use?

A

Fewer endocrine effects (less anti-androgenic)

Reduces left ventricular hypertrophy in HTN patients

reduces microalbuminuria in type II diabetes

26
Q

True or False

K+ sparing diuretics are commonly used as monotherapies in hypertension

A

FALSE

K+ sparing diuretics are commonly used in combination with thiazide and loop diuretics to reduce K+ secretion.

27
Q

Name some centrally acting antihypertensive drugs

A

Clonidine

Methyldopa

28
Q

What is the general MOA of centrally acting antihypertensives?

A

Partial alpha-2 receptor agonist –> reduces sympathetic outflow from CNS –> reduces PVR —> reduces blood pressure

Note: Cardiac output will be slightly reduce or unchanged

29
Q

What are things to be mindful of with methyldopa use as antihypertensive?

A

Causes immunological effects = causes methyldopa sensitisation —> immune effects —> Coombs +ve haemolytic anaemia and autoimmune hepatitis

Pregnancy = it does not harm the fetus

30
Q

What are some things to note with centrally acting anti-hypertensives?

A

Cause more ADR’s, primarily CNS related ones compared to other anti-hypertensives

They should not be stopped abruptly = greatly exacerbate the effect/condition that the drug was attempting to treat

Rebound hypertension may occur with abrupt stopping of clonidine

31
Q

What is the role of Hydralazine in treatment of hypertension?

A

Strong, non-specific vasodilator

MOA = potential dec of Ca2+ –> direct relaxation of vascular SM (arteries mainly)

ADRs = tachycardia (reflex compensation), oedema (global dilation –> blood pools —> fluid leaks), peripheral neuritis, systemic lupus

32
Q

What is the role of sodium nitroprusside in treatment of hypertension?

A

Strong, non-specific vasodilator

MOA = stimulates NO release –> relaxes both arterial and venous smooth muscle

ADRs = dizziness, excessive sweating, blurred vision, ataxia, tinnitus, metabolic acidosis, hypotension, muscle twitching

33
Q

Name some common drugs that interact with Thiazide/-like and loop diuretics

A

Lithium = increases serum lithium levels

NSAIDs = dec renal blood flow –> dec effectiveness of diuretic

34
Q

Name some common drugs that interact with potassium-sparing diuretics

A

ACE inhibitors = inc K+ concentration —> increased risk of hyperkalaemia

Potassium supplements = inc risk of hyperkalaemia

35
Q

Name some common drugs that interact with alpha1-adrenoceptor antagonists (-sin drugs)

A

other anti-hypertensives (e.g. beta-blocker, diuretics, etc.) = inc risk of hypotension

36
Q

Name some common drugs that interact with beta-blockers

A

Beta-blocker (dec HR) = diltiazem, verapamil —> inc cardiovasc depression

NSAIDs = dec hypotensive effect

37
Q

Name some common drugs that interact with ACE-inhibitors

A

Lithium = causes inc lithium levels

K+-sparing diuretics and K+ supplements = inc risk of hyperkalaemia

NSAIDs = dec hypotensive effect

38
Q

Explain the ‘triple whammy’ drug effect

A

Triple whammy drug effect occurs when a patient is given an ACE-inhibitor (or ARB), an NSAID, and a diuretic.

NSAID + ACE-inhib (or ARB) + diuretic = dec glomerular blood flow —> dec GFR —> detrimental effects on kidney function

Further explanation:
NSAIDs = block prostaglandin production —> dec glomerular blood flow

Diuretics = dec blood vol —> reduce glomerular blood flow

ACEI or ARBs = efferent arteriole dilation —> dec GFR

39
Q

What are the long term effects of thiazide diuretics?

A

Decreased Na content of SM, dec SM sensitivity to vasopressors, dec PVR

dec BP

Human Pharmacy (11 decks)

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