Anti-Hypertension/Anti-Anginal Drugs Flashcards
ACEi mechanism of action
inhibit the conversion angiotensin I to angiotensin II
ACE inhibitors are activated by phase 1 metabolism in the liver
ACEi S/E
cough
angioedema: may occur up to a year after starting treatment
hyperkalaemia
first-dose hypotension: more common in patients taking diuretics
ACEi is OK in pregnancy & breastfeeding
false
avoid in both
ACEi specialist advice should be sought before starting ACE inhibitors in patients with potassium >/5mmol/l
true
ACEi cautions/contraindications
pregnancy/breastfeeding
renovascular disease - may result in renal impairment
aortic stenosis - may result in hypotension
hereditary of idiopathic angioedema
ACEi and what significantly increases the risk of hypotension
high-dose diuretic therapy (more than 80 mg of furosemide a day)
ACEi rise/fall in creatinine and potassium may be expected after starting ACE inhibitors
rise
ACEi acceptable changes are an increase in serum creatinine
30% from baseline
ACEi acceptable changes potassium
increase in potassium up to 5.5 mmol/l.
Voltage-gated calcium channels are present in which cells
myocardial cells, cells of the conduction system and those of the vascular smooth muscle
Calcium channel blockers: Which one is VERy negatively inotropic
Verapamil - VERy negatively inotropic
Should not be given with beta-blockers as may cause heart block
Calcium channel blockers: Nifedipine, amlodipine, felodipine affect the myocardium more than peripheral vascular smooth muscle
false
other way round
Calcium channel blockers:
Nifedipine, amlodipine, felodipine result in worsening heart failure
false
Affects the peripheral vascular smooth muscle more than the myocardium and therefore do not result in worsening of heart failure
Calcium channel blockers: Diltiazem Less negatively inotropic than verapamil
true
caution should still be exercised when patients have heart failure or are taking beta-blockers
Calcium channel blockers:
S/E
Verapamil: Heart failure, constipation, hypotension, bradycardia, flushing
Diltiazem: Hypotension, bradycardia, heart failure, ankle swelling
Nifedipine, amlodipine, felodipine
(dihydropyridines): Flushing, headache, ankle swelling
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.
true
Angiotensin II receptor blockers examples
candesartan
losartan
irbesartan
Angiotensin II receptor blockers:
should be used with caution in patients with
renovascular disease
Angiotensin II receptor blockers:
SE
hypotension and hyperkalaemia.
Angiotensin II receptor blockers:
mechanism
block effects of angiotensin II at the AT1 receptor
Angiotensin II receptor blockers: shown to reduce/increase progression of renal disease in patients with diabetic nephropathy
reduce
Angiotensin II receptor blockers: evidence base that losartan reduces CVA and IHD mortality in hypertensive patients
true
Thiazide diuretics:
mechanism
inhibiting sodium reabsorption at the beginning of the distal convoluted tubule (DCT) by blocking the thiazide-sensitive Na+-Cl− symporter.
Thiazide diuretics: Potassium is lost as a result of
Potassium is lost as a result of more sodium reaching the collecting ducts.
Thiazide diuretics: electrolyte abnotmalities
hyponatraemia, hypokalaemia, hypercalcaemia
hypocalciuria, which may be useful in reducing the incidence of renal stones
Thiazide diuretics: common adverse effects
dehydration postural hypotension gout impaired glucose tolerance impotence
Thiazide diuretics: rare adverse effects
thrombocytopaenia
agranulocytosis
photosensitivity rash
pancreatitis
Loop diuretics:
mechanism
inhibiting the Na-K-Cl cotransporter (NKCC) in the thick ascending limb of the loop of Henle, reducing the absorption of NaCl.
Loop diuretics: exaples
Furosemide and bumetanide
Thiazide diuretics: examples
bendroflumethiazide
Loop diuretics:
There are two variants of NKCC; loop diuretics act on
NKCC2, which is more prevalent in the kidneys.
Loop diuretics: indications
heart failure: both acute (usually intravenously) and chronic (usually orally)
resistant hypertension, particularly in patients with renal impairment
Loop diuretics: electrolyte abnormalities
hyponatraemia
hypokalaemia, hypomagnesaemia
hypocalcaemia
hypochloraemic alkalosis
Loop diuretics: cause hypoglycaemia
false hyperglycaemia (less common than with thiazides)
Loop diuretics: adverse effects
hypotension
ototoxicity
gout
beta-blockers improve both symptoms and mortality in heart failure
true
beta-blockers are rate-control drug of choice in atrial fibrillation
true
propranolol is/is not lipid soluble
Lipid soluble therefore crosses the blood-brain barrier
Beta-blockers s/e
bronchospasm cold peripheries fatigue sleep disturbances, including nightmares erectile dysfunction
Beta-blockers contraindications
uncontrolled heart failure
asthma
sick sinus syndrome
concurrent verapamil use: may precipitate severe bradycardia
Beta-blocker overdose
Features
bradycardia
hypotension
heart failure
syncope
Beta-blocker overdose mx
if bradycardic then atropine
in resistant cases glucagon may be used
Ivabradine mechanism
works by reducing the heart rate. It acts on the If (‘funny’) ion current
If (‘funny’) ion current is located where
highly expressed in the sinoatrial node, reducing cardiac pacemaker activity.
Ivabradine adverse effects
visual effects, particular luminous phenomena, are common
headache
bradycardia, heart block
Nicroandil is
Vasodilatory drug
potassium-channel activator with vasodilation is through activation of guanylyl cyclase which results in increase cGMP.
Nicroandil adverse effects
headache
flushing
skin, mucosal and eye ulceration
gastrointestinal ulcers including anal ulceration
Nicroandil contraindications
left ventricular failure
Nitrates Mechanism of action
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
Nitrates work in angina by?
in angina they both dilate the coronary arteries and also reduce venous return which in turn reduces left ventricular work, reducing myocardial oxygen demand
Nitrates s/e
hypotension
tachycardia
headaches
flushing
many patients who take nitrates develop tolerance and experience reduced efficacy
tru
Nittrates advises that patients who develop tolerance should
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
