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4th year passmedicine by topic > Anti-Hypertension/Anti-Anginal Drugs > Flashcards

Anti-Hypertension/Anti-Anginal Drugs Flashcards

1
Q

ACEi mechanism of action

A

inhibit the conversion angiotensin I to angiotensin II

ACE inhibitors are activated by phase 1 metabolism in the liver

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2
Q

ACEi S/E

A

cough
angioedema: may occur up to a year after starting treatment
hyperkalaemia
first-dose hypotension: more common in patients taking diuretics

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3
Q

ACEi is OK in pregnancy & breastfeeding

A

false

avoid in both

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4
Q

ACEi specialist advice should be sought before starting ACE inhibitors in patients with potassium >/5mmol/l

A

true

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5
Q

ACEi cautions/contraindications

A

pregnancy/breastfeeding
renovascular disease - may result in renal impairment
aortic stenosis - may result in hypotension
hereditary of idiopathic angioedema

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6
Q

ACEi and what significantly increases the risk of hypotension

A

high-dose diuretic therapy (more than 80 mg of furosemide a day)

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7
Q

ACEi rise/fall in creatinine and potassium may be expected after starting ACE inhibitors

A

rise

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8
Q

ACEi acceptable changes are an increase in serum creatinine

A

30% from baseline

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9
Q

ACEi acceptable changes potassium

A

increase in potassium up to 5.5 mmol/l.

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10
Q

Voltage-gated calcium channels are present in which cells

A

myocardial cells, cells of the conduction system and those of the vascular smooth muscle

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11
Q

Calcium channel blockers: Which one is VERy negatively inotropic

A

Verapamil - VERy negatively inotropic

Should not be given with beta-blockers as may cause heart block

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12
Q

Calcium channel blockers: Nifedipine, amlodipine, felodipine affect the myocardium more than peripheral vascular smooth muscle

A

false

other way round

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13
Q

Calcium channel blockers:

Nifedipine, amlodipine, felodipine result in worsening heart failure

A

false
Affects the peripheral vascular smooth muscle more than the myocardium and therefore do not result in worsening of heart failure

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14
Q

Calcium channel blockers: Diltiazem Less negatively inotropic than verapamil

A

true

caution should still be exercised when patients have heart failure or are taking beta-blockers

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15
Q

Calcium channel blockers:

S/E

A

Verapamil: Heart failure, constipation, hypotension, bradycardia, flushing

Diltiazem: Hypotension, bradycardia, heart failure, ankle swelling

Nifedipine, amlodipine, felodipine
(dihydropyridines): Flushing, headache, ankle swelling

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16
Q

Angiotensin II receptor blockers are generally used in situations where patients have not tolerated an ACE inhibitor, usually due to the development of a cough.

A

true

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17
Q

Angiotensin II receptor blockers examples

A

candesartan
losartan
irbesartan

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18
Q

Angiotensin II receptor blockers:

should be used with caution in patients with

A

renovascular disease

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19
Q

Angiotensin II receptor blockers:

SE

A

hypotension and hyperkalaemia.

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20
Q

Angiotensin II receptor blockers:

mechanism

A

block effects of angiotensin II at the AT1 receptor

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21
Q

Angiotensin II receptor blockers: shown to reduce/increase progression of renal disease in patients with diabetic nephropathy

A

reduce

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22
Q

Angiotensin II receptor blockers: evidence base that losartan reduces CVA and IHD mortality in hypertensive patients

A

true

23
Q

Thiazide diuretics:

mechanism

A

inhibiting sodium reabsorption at the beginning of the distal convoluted tubule (DCT) by blocking the thiazide-sensitive Na+-Cl− symporter.

24
Q

Thiazide diuretics: Potassium is lost as a result of

A

Potassium is lost as a result of more sodium reaching the collecting ducts.

25
Q

Thiazide diuretics: electrolyte abnotmalities

A

hyponatraemia, hypokalaemia, hypercalcaemia

hypocalciuria, which may be useful in reducing the incidence of renal stones

26
Q

Thiazide diuretics: common adverse effects

A 
dehydration
postural hypotension
gout
impaired glucose tolerance
impotence
27
Q

Thiazide diuretics: rare adverse effects

A

thrombocytopaenia
agranulocytosis
photosensitivity rash
pancreatitis

28
Q

Loop diuretics:

mechanism

A

inhibiting the Na-K-Cl cotransporter (NKCC) in the thick ascending limb of the loop of Henle, reducing the absorption of NaCl.

29
Q

Loop diuretics: exaples

A

Furosemide and bumetanide

30
Q

Thiazide diuretics: examples

A

bendroflumethiazide

31
Q

Loop diuretics:

There are two variants of NKCC; loop diuretics act on

A

NKCC2, which is more prevalent in the kidneys.

32
Q

Loop diuretics: indications

A

heart failure: both acute (usually intravenously) and chronic (usually orally)
resistant hypertension, particularly in patients with renal impairment

33
Q

Loop diuretics: electrolyte abnormalities

A

hyponatraemia
hypokalaemia, hypomagnesaemia
hypocalcaemia

hypochloraemic alkalosis

34
Q

Loop diuretics: cause hypoglycaemia

A 
false
hyperglycaemia (less common than with thiazides)
35
Q

Loop diuretics: adverse effects

A

hypotension
ototoxicity
gout

36
Q

beta-blockers improve both symptoms and mortality in heart failure

A

true

37
Q

beta-blockers are rate-control drug of choice in atrial fibrillation

A

true

38
Q

propranolol is/is not lipid soluble

A

Lipid soluble therefore crosses the blood-brain barrier

39
Q

Beta-blockers s/e

A 
bronchospasm
cold peripheries
fatigue
sleep disturbances, including nightmares
erectile dysfunction
40
Q

Beta-blockers contraindications

A

uncontrolled heart failure
asthma
sick sinus syndrome
concurrent verapamil use: may precipitate severe bradycardia

41
Q

Beta-blocker overdose

Features

A

bradycardia
hypotension
heart failure
syncope

42
Q

Beta-blocker overdose mx

A

if bradycardic then atropine

in resistant cases glucagon may be used

43
Q

Ivabradine mechanism

A

works by reducing the heart rate. It acts on the If (‘funny’) ion current

44
Q

If (‘funny’) ion current is located where

A

highly expressed in the sinoatrial node, reducing cardiac pacemaker activity.

45
Q

Ivabradine adverse effects

A

visual effects, particular luminous phenomena, are common
headache
bradycardia, heart block

46
Q

Nicroandil is

A

Vasodilatory drug

potassium-channel activator with vasodilation is through activation of guanylyl cyclase which results in increase cGMP.

47
Q

Nicroandil adverse effects

A

headache
flushing
skin, mucosal and eye ulceration
gastrointestinal ulcers including anal ulceration

48
Q

Nicroandil contraindications

A

left ventricular failure

49
Q

Nitrates Mechanism of action

A

nitrates cause the release of nitric oxide in smooth muscle, activating guanylate cyclase which then converts GTP to cGMP, which in turn leads to a fall in intracellular calcium levels

50
Q

Nitrates work in angina by?

A

in angina they both dilate the coronary arteries and also reduce venous return which in turn reduces left ventricular work, reducing myocardial oxygen demand

51
Q

Nitrates s/e

A

hypotension
tachycardia
headaches
flushing

52
Q

many patients who take nitrates develop tolerance and experience reduced efficacy

A

tru

53
Q

Nittrates advises that patients who develop tolerance should

A

take the second dose of isosorbide mononitrate after 8 hours, rather than after 12 hours.

This allows blood-nitrate levels to fall for 4 hours and maintains effectiveness

this effect is not seen in patients who take modified release isosorbide mononitrate

4th year passmedicine by topic (96 decks)

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