Drugs for IHD and Heart Failure Flashcards
Core Drug: Digoxin: Mechanism of Action:
- inhibits the Na+/K+ ATPase channel
- binds to the extracellular K+ binding site
- increases intracellular Na+
- Na+ and Ca2+ exchange through
exchanger (Na+ out, Ca2+ in) - increased intracellular Ca2+
- increased ionotropy
- increases force of contraction and
contractility of the heart
Core Drug: Digoxin: What tissues/organs it acts on?
- SA node
- AV node
- cardiac muscle
Core Drug: Digoxin: Physiological effects:
- slows the heart rate
- increases contractility
Core Drug: Digoxin: side effects:
- DOES NOT DECREASE BP
- arrhythmias especially with hypokalaemia
- xanthopsia = colour vision deficiency,
mostly see yellow - anorexia
Core Drug: Digoxin: Interactions:
- many drugs increase toxicity
Core Drug: Digoxin: Pharmacokinetics:
- orally active
- requires loading dose
- half life c. 36 hours
- narrow therapeutic window
Core Drug: Digoxin: Clinical Use:
- end stage heart failure sometimes
- to slow heart rate in atrial fibrillation, very
commonly
Core Drug: “Digoxin Effect”:
reverse tick on ECG
not necessarily toxic
Core Drug: Digoxin: specific antidote:
Digibind
for too much digixin causing toxicity
Digoxin is from which plant
foxglove
Core Drug: digoxin: Mechanism of action diagram:
Heart Failure Pathophysiology:
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Therapeutic Targets for heart Failure Drugs:
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Therapeutic Targets for angina drugs:
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Core Drug: Furosemide: Mechanism of action:
- blocks Na+/K+/Cl co transporter in the thick ascending limb of the loop of henle
- blocks the Cl- channel of the cotransporter
- increased loss of: Na+, K+, Cl- and WATER
Core Drug: Furosemide: clinical uses:
- much more powerful than other diuretics
- used to clear peripheral oedema
- used intravenously for acute pulmonary
oedema
Core Drug: Furosemide: Pharmacokinetics:
- “Lasix” = lasts for 6 hours
- route of administration?
- therapeutic window?
Core Drug: Furosemide: Side Effects:
- dehydration
- renal impairment
- hypokalaemia
- hyponatraemia
- hypomagnesaemia
- hyperuricaemia (high uric acid, causes
gout) - auditory nerve damage (especially high
doses and renal impairment)
Core Drug: Ramipril: mechanism of action:
- ACE inhibitors (improves prognosis,
mortality and quality of life) - blocks conversion of angiotensin I to
angiotensin II - and blocks break down of Bradykinin
(vasoactive peptide) - hence decrease in angiotensin II and increase in bradykinin peptide
Core Drug: Ramipril: Physiological effects:
- arteriolar dilation:
- decreases after load, left
ventricle has to pump more, increases
speed of contraction - venodilation:
- decreases preload
- descending LA pressure - decrease in aldosterone and ADH, hence
decrease in fluid retention
Core Drug: Ramipril: clinical uses:
- most commonly used drug to treat heart
failure - also used for hypertension
Core Drug: Ramipril: side effects:
- dry cough (bradykinin accumulation in
lungs) - renal impariment
- hyperkalaemia: commonly given with a
diuretic
Core Drug: Ramipril: pharmacokinetics:
- route of administration?
- dosage: once daily dosage
- therapeutic window?
- half life?
Core Drug: Losarten/Candesarten: mechanism of action:
- blocks action of angiotensin II on the
angiotensin I receptor