Cardiovascular

Question 1

Beta-blockers

Answer 1

Bsp: propranolol, metoprolol, bisoprolol
some block all β-receptors, others are selective for β1 (= cardioselective BBs), β2, or β3
β1: heart, kidneys vs. β2: lungs, GIT,..

MOA: competitive antagonism at ß-receptors (they are
normally activated by epinephrine & norepinephrine)
(= adrenergic = fight-or-flight response)
→ antiadrenergic effects (“feed, breed, pee, poo“):
1. lower heart rate
2. lower heart contraction
3. lower renal renin production (→ vasodilation + less H2O retention → lower blood pressure)

IND:

• cardiology: hypertension, tachycardias, atrial fibrillation, …
• glaucoma (as eye drops), migraine prophylaxis
• symptomatic control in anxiety (tachycardia, tremor)
• performing-enhancing im sports and music

CI: asthma, bradycardia, diabetes, many more

ADR:

• hypotension, bradycardia, sexual dysfunction, …
• BB-induced hypoglycaemia unawareness
• bronchospasms/dyspnoea (if non-cardioseletive BBs used)

Question 2

ACE-Inhibitor

Answer 2

RAAS Blocker

MOA: peptid mimetics that inhibit ACE =
blocking the conversion of AT-I to AT-II
→ less vasoconstriction + less aldosterone
→ lower RR

Question 3

Sartans

Answer 3

= AT1-Receptor Blocker (ARB)

RAAS blockers:
competitive Inhibition on Angiotensin-I-Receptor (AT1-R.)
→ keine Wirkung von Angiotensin II (= weniger Aldosterone, weniger periphere Vasokonstriktion, weniger H2O resorption über ADH)

Question 4

Ca2+ Channel Blockers

Answer 4

Bsp: Amlodipine

MOA: antagonism at L-type Ca2+ channels in muscle cells (“angioselective effect”)
→ lower Ca2+ influx
→ inhibition of smooth muscle cell contraction (= vasodilation)
→ lower vascular resistance without decrease of cardiac output

nice side effect: prevention of excessive constriction
in the coronary arteries

important IA: Amlodipine (CYP3A4-Inh.) + Simvastatin zeigt “Statin Intoleranz”

Question 5

Loop Diuretics

Answer 5

eg. furosemide

MOA: inhibition of Na+-K–2Cl- Co-transporter in the loop of Henle
→ higher excretion of Na+, K+, Cl-
→ osmotic driving force of water → higher urine volume

Diuretics general:
IND: - hypertension, heart failure, poisonings, edema, ascites
- abused by people with eating disorders

antihypertensive effect due to…
… lower blood volume (→ decreased preload)
+ other mechanisms (some diuretics only)

ADR (= CI)

1. electrolyte imbalances (hypokalemia, hyponatremia)
2. hypovolemia/dehydration (higher blood viscosity → risk of thrombosis) 3. higher concentration of “everything” (hyperuricaemia, dyslipidaemia)

Question 6

Potassium-sparing Diuretics

Answer 6

eg. spironolactone

MOA: MR antagonism
→ higher excretion of Na+
→ osmotic driving force of water → highe urine volume

Diuretics general:
IND: - hypertension, heart failure, poisonings, edema, ascites
- abused by people with eating disorders

antihypertensive effect due to…
… lower blood volume (→ decreased preload)
+ other mechanisms (some diuretics only)

ADR (= CI)

1. electrolyte imbalances (hyperkalemia, hyponatremia)
2. hypovolemia/dehydration (higher blood viscosity → risk of thrombosis) 3. higher concentration of “everything” (hyperuricaemia, dyslipidaemia)

Question 7

Thiazides

Answer 7

Hydrochlorothiazide, HCT

MOA: inhibition of Na+-Cl-Symporter in the distal tubule
→ higher excretion of Na+, Cl-
→ osmotic driving force of water → higher urine volume

Diuretics general:
IND: - hypertension, heart failure, poisonings, edema, ascites
- abused by people with eating disorders

antihypertensive effect due to…
… lower blood volume (→ decreased preload)
+ other mechanisms (some diuretics only)

ADR (= CI)

1. electrolyte imbalances (hypokalemia, hyponatremia)
2. hypovolemia/dehydration (higher blood viscosity → risk of thrombosis) 3. higher concentration of “everything” (hyperuricaemia, dyslipidaemia)