Cardio Drugs Flashcards
Give examples of ACE Inhibitors (ACE Is)
“pril”
Ramipril, Lisinopril and Quinapril
MoA of ACE Is
Inhibit ACE from converting angiotensin I into angiotensin II (a vasocontrictor)
Effect of ACE Is
Vasodilate, causing a reduce in blood pressure
Give examples of Angiotensin Receptor Blockers (ARBs)
“sartan”
Valsartan, Losartan and Eprosartan
MoA of ARBs
They are antagonists to angiotensin II (a vasoconstrictor)
Effect of ARBs
Vasodilate, causing a reduce in blood pressure
Give examples of Beta 1 Blockers (BBs)
“olol”
Atenolol, Bisoprolol, Metropolol
Give examples of Nonselective Beta Blockers (BBs)
“olol”
Propanolol
MoA of B1Bs
They block B1 adrenoceptors
Effect of B1Bs
- Decrease the force of contraction of the heart
- Decrease the HR
MoA of Nonselective BBs
They block both B1 and B2 adrenoceptors
Effect of Nonselective BBs
Basically blocks sympathetic responses:
- Decreases the HR (reduced SA-AV node conduction)
- Decreases force of contraction of the heart
- Have an antiarrhythmic effect
- Reduce Renin, so decrease BP
Give examples of Calcium Channel Blockers (CCBs)
Smooth Muscle selective: “dipines”
Amlodipine, Nifedipine and Felodipine
Cardio selective: Verapamil
Others: Diltiazem
MoA of CCBs
Block L-type Ca2+ channels in Smooth muscle
Effect of CBBs
- Vasodilation (Coronary and peripheral), so reduces BP
- Reduces myocardial oxygen consumption rate
Give examples of Anti-Arrhythmic drugs?
Digoxin, Adenosine, Amiodarone, Verapamil, Magnesium Sulphate
MoA of Digoxin
Blocks Na+/K+ pump, slowing AV node conduction
MoA of Verapamil
Blocks L-type Ca2+ channels, slowing AV node conduction
MoA of Adenosine
Stimulates adenosine receptor that inhibits adenyl cyclase, therefore inhibiting Ca2+ influx.
It hyperpolarises the AV node, suppressing conduction.
MoA of Amiodarone
Slows conduction of the SA and AV nodes
Give examples of Alpha Blockers
“zosin”
Prazosin and Doxazosin
MoA of A1 Blockers
Block A1 receptors
Effects of A1 Blockers
Vasodilation
Give examples of Nitrates
Short acting: Glyceryl trinitrate (GTN)
Long acting: Isosorbide mononitrate
MoA of Nitrates
They metabolise to produce NO, increasing cGMP, activating kinase A causing relaxation.
Also keeps K+ channels open.
Effect of Nitrates
Vasodilation
MoA of Ivabradine
It inhibits the funny channel and therefore inhibits the pacemaker activity of the SA node
Effect of Ivabridine
Decreases the HR
Give examples of Diuretics
Thiazide: Bendroflumethiazide
Loop: Furosemide
Others: Spironolactone
MoA of Spironolactone
- It is a competitive inhibitor of aldosterone
- It targets the distal nephron
MoA of Loop Diuretics
Inhibits reabsorption of NaCl in the Loop of Henle
MoA of Thiazides
Inhibit reabsorption of NaCl in the distal tubule
Give examples of Fibrinolytics
Streptokinase and tissue plasminogen activator (tPA)
MoA of Fibrinolytics
Oppose the anticoagulation cascade via activation of plasminogen
Effect of Fibrinolytics
“Clot busters”
Re-open occluded arteries by dissolving clots
Give examples of Anticoagulants
“Blood thinning”
“rin”
Warfarin, Heparin, LMWH,
“an”
Rivaroxiban, Apixaban, Dabigatran
MoA of Warfarin
Prevents Vitamin K conversion
MoA of Heparin
Inactivates Xa and thrombin IIa
MoA of LMWH
Inactivates Xa
MoA of Rivaroxiban and Apixaban
Inhibits Xa
MoA of Dabigatran
Direct thrombin inhibitor
Give examples of Antiplatelets
Aspirin,
“grel”
Clopidogrel, Prasugrel, Ticagrelor
MoA of Aspirin
Prevents platelet aggregation via prevention of thromboxane A2 production
MoA of Clopidogrel, Prasugrel, Ticagrelor
They inhibit adenosine diphosphate receptors
Give examples of Potassium Channel Openers (PCOs)
“dil”
Nicorandil and Minoxidil
MoA of PCOs
They open K+ channels, causing hyperpolarisation of L-type Ca+ channels
Effect of PCOs
They cause relaxation of arterial smooth muscle
Give examples of Statins
“statin”
Simvastatin and Atorvastatin
MoA of Statins
They competitively inhibit HMG-CoA reductase, reducing cholesterol production
Effect of Statins
Reduce cholesterol, LDLs and triglycerides
Give examples of Fibrates
Bezafibrate and Gemfibrozil
MoA of Fibrates
They activate PPAR Alpha, that stimulate lipid metabolism
Effect of Fibrates
Reduce triglycerides, LDLs and HDLs
Side effect of BBs
- Bronchospasm (never give to asthmatics)
- Bradycardia
- Aggravates heart failure
- Masks a hypo
- Impotence + libido (decreased sex drive)
- Cold peripheries
- Dangerous in hypotension
Side effects of Digoxin
A lot of really bad shit
- Disturbances of colour vision
- Bradycardia
- Tender breasts
- Can cause heart block
- Is toxic in hypokalaemia
Side effects of Nitrates
- Can develop tolerance (give 8 hour free window)
- Headaches
Side effects of Loop Diuretics
Hypo everything
Side effects of CCBs
- Ankle Oedema
- Don’t give with BBs as will cause severe bradycardia (especially verapamil)
Side effects of ACE Is
Never use in pregnancy
- Dry cough
- Angioedema (in afro-Caribbeans)
- hyperkalaemia
- first dose hypertension (if on diruetics)
Side effects of ARBs
Never use in pregnancy
-Hyperkalaemia
Side effects of Anticoagulants
Risk of haemorrhage
Side effect of PCOs
NaCl and water retention
Give an example of an Anti-Muscarinic
Non-selective: Atropine
MoA of Atropine
Inhibit the parasympathetic nervous system (M1, M2, M3) and so increased SA node conduction
Effects of Atropine
Increased HR
Side effects of Atropine
Dry mouth and pupil dilation
Give an example of a B1 receptor agonist
Dobutamine
MoA of Dobutamine
Stimulation of B1 receptor
Effects of Dobutamine
Increases AV node conduction
Side effects of Statins
Don’t give in pregnant woman
- Myopathy
- Renal Failure
Side effects of Fibrates
Myositis
Side effects of Antiplatelets
- Haemorrhage
- Peptic ulcer (high dose aspirin)
Side effects of Spironolactone
- Gynecomastia
- Hyperkalaemia