2.4 cardiovascular pharmacology Flashcards

1
Q

Please give an overview of the five major drug classes used for the treatment of hypertension

A
  • Beta-Blockers (propranolol, bisoprolol): competetive anatagonsim at Beta-Receptors (supressing the effects of the sympatic nervous system)
  • ACE-Inhibitor: peptid mimetic inhibtis ACE in RAAS system
  • AT1 receptor blocker: antagonism at the AT1 receptor
  • Calcium Channel blockers (amlodipine): antagonists as L-type Ca2+ channels in arterial smooth muscle cells
  • Diuretics (loop (furosemide), thiazides (hydrochloridethiazemide, HCT), potassium-sparing (spironolactone)):
    higher production of urine through ionic (na,K,Cl) excretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the rationale for using combination therapies as initial therapies of hypertension?

A

synergistic (low dose) combination of drugs is more effective and better tolerated than high-dose monotherapy

arterial pressure is the result of cardiac output x peripheral resistance, which are two different target systems –> intended drug-drug interaction

When deciding which drug to start with,
one has to consider…
 individual contraindications
 individual comorbidities (= preferential
use of some drugs from some conditions)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Explain the MOA of beta blockers

A
  • Beta-Blockers (propranolol, bisoprolol): competetive anatagonsim at Beta-Receptors in the sympatic nervous system which are normally activated by (nor)epinephrine
    –> adrenergic effects turned off (fight or flight) (–> feed, breed, pee, poop),
    decraesed heart rate, decreased heart contraction, decreased renal renin production (vasodilation + decreased H2O retention)
    cardioselective beta1 blocker or unspecific ones (beta1-3)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Explain the MOA of RAAS blockers

A
  • ACE-Inhibitor: peptid mimetic inhibtis ACE in RAAS system and therefore blocks the conversion of Angiotension I to Angiotensin II leading to less vasoconstiction and aldosterone production and therefore lowering BP
  • AT1 receptor blocker: antagonism at the AT1 receptor, on blood vessels, heart tissues, adrenal gland –> decreased production of aldosterone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Explain the MOA of Ca2+ channel blockers

A
  • Calcium Channel blockers (amlodipine): antagonists as L-type Ca2+ channels in arterial muscle cells (decerased Ca2+ influx across cell membranes)
  • -> leading to vasodilation and therefore less vascular resistance (withour decrease of cardiac output)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Explain the MOA of diuretics and name the different subgroups

A
  • loop diuretics (furosemide) inhibition of Na/K/Cl co-transporter at loop of henle
  • thiazides (hydrochloridethiazemide, HCT) inhibition of the na/cl symporter at the distal tubule
  • potassium-sparing (spironolactone) mineralocorticoid receptor antagonism, increased excretion of Na

–> Higher production of urine through ionic (na,K,Cl) excretion (transport mostly inhibited before) leads to decrease in osmotic force of water and therefore more urine –> lowering of blood volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly