Anti-Hypertension/Anti-Anginal Drugs

Question 1

ACEi mechanism of action

Answer 1

inhibit the conversion angiotensin I to angiotensin II

ACE inhibitors are activated by phase 1 metabolism in the liver

Question 2

ACEi S/E

Answer 2

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

Question 3

ACEi is OK in pregnancy & breastfeeding

Answer 3

false

avoid in both

Question 4

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

Answer 4

true

Question 5

ACEi cautions/contraindications

Answer 5

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

Question 6

ACEi and what significantly increases the risk of hypotension

Answer 6

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

Question 7

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

Answer 7

rise

Question 8

ACEi acceptable changes are an increase in serum creatinine

Answer 8

30% from baseline

Question 9

ACEi acceptable changes potassium

Answer 9

increase in potassium up to 5.5 mmol/l.

Question 10

Voltage-gated calcium channels are present in which cells

Answer 10

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

Question 11

Calcium channel blockers: Which one is VERy negatively inotropic

Answer 11

Verapamil - VERy negatively inotropic

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

Question 12

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

Answer 12

false

other way round

Question 13

Calcium channel blockers:

Nifedipine, amlodipine, felodipine result in worsening heart failure

Answer 13

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

Question 14

Calcium channel blockers: Diltiazem Less negatively inotropic than verapamil

Answer 14

true

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

Question 15

Calcium channel blockers:

S/E

Answer 15

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

Diltiazem: Hypotension, bradycardia, heart failure, ankle swelling

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

Question 16

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.

Answer 16

true

Question 17

Angiotensin II receptor blockers examples

Answer 17

candesartan
losartan
irbesartan

Question 18

Angiotensin II receptor blockers:

should be used with caution in patients with

Answer 18

renovascular disease

Question 19

Angiotensin II receptor blockers:

SE

Answer 19

hypotension and hyperkalaemia.

Question 20

Angiotensin II receptor blockers:

mechanism

Answer 20

block effects of angiotensin II at the AT1 receptor

Question 21

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

Answer 21

reduce

Question 22

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

Answer 22

true

Question 23

Thiazide diuretics:

mechanism

Answer 23

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

Question 24

Thiazide diuretics: Potassium is lost as a result of

Answer 24

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

Question 25

Thiazide diuretics: electrolyte abnotmalities

Answer 25

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

Question 26

Thiazide diuretics: common adverse effects

Answer 26

``` dehydration postural hypotension gout impaired glucose tolerance impotence ```

Question 27

Thiazide diuretics: rare adverse effects

Answer 27

thrombocytopaenia agranulocytosis photosensitivity rash pancreatitis

Question 28

Loop diuretics: | mechanism

Answer 28

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

Question 29

Loop diuretics: exaples

Answer 29

Furosemide and bumetanide

Question 30

Thiazide diuretics: examples

Answer 30

bendroflumethiazide

Question 31

Loop diuretics: | There are two variants of NKCC; loop diuretics act on

Answer 31

NKCC2, which is more prevalent in the kidneys.

Question 32

Loop diuretics: indications

Answer 32

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

Question 33

Loop diuretics: electrolyte abnormalities

Answer 33

hyponatraemia hypokalaemia, hypomagnesaemia hypocalcaemia hypochloraemic alkalosis

Question 34

Loop diuretics: cause hypoglycaemia

Answer 34

``` false hyperglycaemia (less common than with thiazides) ```

Question 35

Loop diuretics: adverse effects

Answer 35

hypotension ototoxicity gout

Question 36

beta-blockers improve both symptoms and mortality in heart failure

Answer 36

true

Question 37

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

Answer 37

true

Question 38

propranolol is/is not lipid soluble

Answer 38

Lipid soluble therefore crosses the blood-brain barrier

Question 39

Beta-blockers s/e

Answer 39

``` bronchospasm cold peripheries fatigue sleep disturbances, including nightmares erectile dysfunction ```

Question 40

Beta-blockers contraindications

Answer 40

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

Question 41

Beta-blocker overdose | Features

Answer 41

bradycardia hypotension heart failure syncope

Question 42

Beta-blocker overdose mx

Answer 42

if bradycardic then atropine | in resistant cases glucagon may be used

Question 43

Ivabradine mechanism

Answer 43

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

Question 44

If ('funny') ion current is located where

Answer 44

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

Question 45

Ivabradine adverse effects

Answer 45

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

Question 46

Nicroandil is

Answer 46

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

Question 47

Nicroandil adverse effects

Answer 47

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

Question 48

Nicroandil contraindications

Answer 48

left ventricular failure

Question 49

Nitrates Mechanism of action

Answer 49

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

Question 50

Nitrates work in angina by?

Answer 50

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

Question 51

Nitrates s/e

Answer 51

hypotension tachycardia headaches flushing

Question 52

many patients who take nitrates develop tolerance and experience reduced efficacy

Answer 52

tru

Question 53

Nittrates advises that patients who develop tolerance should

Answer 53

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