Beta Blockers
ACE Inhibitors
Diuretics
Combinations
Miscellaneous
100

What effect do beta blockers have on chronotropy (HR), inotropy (contractility), dromotropy (conduction velocity) and lusitropy (rate of relaxation of myocardium)?

Chronotropy: Decreased (lower HR)
Inotropy: Decreased (weaker contraction)
Dromotropy: Decreased (slower conduction)
Lusitropy: Decreased (slower relaxation)

i.e decreases all of them

100

What does ACE stand for?

Angiotensin Converting Enzyme


Converts Angiotensin I to Angiotensin II

100

What impact do diuretics have on blood pressure?

Decrease BP

(due to additional loss of fluid)

100

What class of cardiac drugs should not be paired with ACE Inhibitors? 

Angiotensin Receptor Blockers (ARBs)

100

What adrenoreceptor type (e.g α1, β2, etc) is the main one in the heart? 

β1

200

Beta blockers end with the suffix "-____"

"-olol" (e.g propranolol, esmolol, atenolol, etc)

200

Names of ACE Inhibitors end with the suffix "_____"

"-pril" (e.g benazepril, zofenopril, perindopril, and trandolapril)

200

What are the most and least potent classes of diuretics, respectively?

Loop diuretics and Potassium-sparing diuretics

200

ACE Inhibitor + Thiazide diuretic combo is used to treat

Heart failure or post-stroke

200

What adrenoreceptor type (e.g α1, β2, etc) is the main one in vascular smooth muscle cells?

α1

300

Beta blockers prevent _______ and _______ from binding to beta adrenergic receptors

Epinephrine and Norepinephrine (Adrenaline and Noradrenaline)

300

A persistent dry ____ is a common side effect of ACE inhibitors due to increased bradykinin 

Cough.

Note: Patients who experience this side effect are often switched to ARBs

300

Loop diuretics, thiazide diuretics, and aldosterone antagonists have the suffixes "-____", "-____", and "-____", respectively

Loop: "-ide" (e.g furosemide)

Thiazide: "-thiazide" (e.g hydrochlorothiazide)

Aldosterone antagonists: "-actone" (e.g spironolactone)

300

ACE Inhibitor + beta blocker is used to treat

Post MI or patients with heart failure

300

Agonising β1 and β2 receptors in the SA node causes ____ to be released to increase the rate of spontaneous depolarisation and, therefore, the frequency of action potentials (increased chronotropy)

cAMP

400

Beta blockers are competitive antagonists at receptors which are [Gi/Gq/Gs] GPCRs

Gs 

400

Which electrolyte should you be most worried about becoming elevated due to ACE inhibitors?

Potassium

ACE Inhibitors decrease aldosterone and, therefore, slow the secretion of Potassium. This can lead to hyperkalaemia. 

400
How do aldosterone antagonists spare Potassium?

Aldosterone stimulates the reabsorption of Sodium via Na/K transporters, which reabsorb 3 Na+ in exchange for secreting 2 K+

Hence, by blocking aldosterone, we block the secretion of Potassium

400

Which type of diuretic (Loop, Thiazide, Aldosterone antagonists) would present a risk of hyperkalemia when combined with ACE inhibitors?

Aldosterone antagonists (aka one of the types of Potassium-sparing diuretics)

400

What sarcoplasmic reticulum receptor is activated by β1 agonism in cardiomyocytes?

SERCA2a

500

Beta blockers shouldn't be combined with _______ because of a risk of heart block

Verapamil (Calcium channel blocker)

500

Which organ should you be most concerned about when prescribing ACE inhibitors?

Kidneys

Renal dysfunction can occur due to a drop in renal perfusion pressure and, therefore, a decrease in GFR. This is due to ACE inhibitors' preferential vasodilation of the renal efferent arteriole, which impairs the kidneys' ability to compensate for low perfusion states

500

How do Loop diuretics work? (action, target, location of target)

Loop diuretics inhibit the Na-K-2Cl symporter in the thick ascending limb of the Loop of Henle

500

Which class of cardiac drugs would you combine with ACE inhibitors (or ARBs) when treating lipid abnormalities?

Calcium channel blocker

500

β2 receptor agonism causes vasodilation via vascular smooth muscle relaxation by what mechanism?

(will give full points if you get at least half of it right)

Adrenaline/Noradrenaline binding (agonism) → ↑ intracellular cAMP → inhibition of MLCK → ↓ MLC phosphorylation → dephosphorylated MLC does not bind actin → ↓ myosin-actin cross bridge formation → relaxation

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