HTN, part II

Question 1

MOA of Minoxidil

Answer 1

• K+ channel regulator
• opens potassium channels and stabilizes the membrane
  
  • cells become hyperpolarized -> relax -> vasodilate
• dilates arterioles but not veins

Question 2

adverse effect of Minoxidil

Answer 2

hypertrichosis: excessive hair growth

Question 3

MOA of Fenoldopam

Answer 3

• specific agonist on D1 receptors
  
  • causes relaxation of arteriolar smooth muscle

Question 4

indications of Fenoldopam ? route of administration

Answer 4

• used for emergency hypertensive situations
• IV; half life 5 min

Question 5

What are Dihydropyridines

Answer 5

• calcium channel blockers
• Nifedipine, Nimodipine; (-dipines)

Question 6

MOA of calcium channel blockers

Answer 6

• bind to L-type channels in the myocardium and vascular smooth muscle which causes channels to close
  
  • get long lasting relaxation of vascular smooth muscles
  • decreased cardiac contractility, automaticity, and conduction

Question 7

which systems are effected by calcium channel blockers

Answer 7

• will relax all smooth muscles
  
  • vascular smooth muscle is the most sensitive, but bronchiolar, GI, and uterine are also relaxed
  • arterioles are more sensitive than veins

Question 8

what are the major cardiac effects of CCBs

Answer 8

• negative inotropic effect due to decreased contractility
• reduced impulse generation in SA node
• slowed AV node conduction

Question 9

Diltiazem and Verapamil fall under what drug class

Answer 9

calcium channel blockers

Question 10

Differentiate between Nifedipine, Verapamil, and Diltiazem

Answer 10

• Nifedipine: strongest vasodilator (inc HR due to reflex tachycardia)
• Verapamil: strongest cardiac effects (dec HR)
• Diltiazem: in between

Question 11

CCB

• route of administration
• excretion
• half-life

Answer 11

• oral
• renal excretion
• half life 3-5 hrs

Question 12

which CCB is the most likely to produce reflex tachycardia

Answer 12

• Nifedipine
  
  • highest vasodilation -> marked hypotension -> reflex tachycardia

Question 13

which CCB is the most likley to cause depressed SA and AV node function

Answer 13

verapamil

Question 14

adverse effect of dihydropyridines

Answer 14

• cause the most vascular side effects: HA, flushing, dizziness, peripheral edema
• gingival hyperplasia

Question 15

what is the most common side effect of verapamil

Answer 15

constipation

Question 16

Dihydropyridines should be used cautiously in patients with what condition

Answer 16

hypertensive patients with CHF

Question 17

Verapamil and Diltiazem are contraindicated in patients with

Answer 17

• SA or AV node abnormalities
• CHF

Question 18

explain RAAS

Answer 18

1. angiotensinogen is made by liver, freely flowing i nblood
2. rate limiting step: release of renin
   
   • renin converts angiotensinogen -> angiotensin I
3. angiotensin I comes into contact with ACE in the lungs and it is converted to Angiotensin II
   
   • Ang II -> vasoconstriction and aldosterone secretion

Question 19

what is another function of ACE besides converted Ang I to Ang II

Answer 19

ACE is responsible for bradykinin degradation; bradykinin effects Prostaglandins and causes vasodilation so ACE causes vasoconstriction

Question 20

Effect os ACE-inhibitors

Answer 20

• drop BP
  
  • reduce vasoconstriction by ang II
  • reduce release of aldosterone
  • cause vasodilation through bradykinin
• does not not reflex sympathetic activation (tachycardia) because of baroreceptor resetting

Question 21

ACE-I are most effective in what patient popuations

Answer 21

white, young

Question 22

ACE-I are the DOC for treatment of hypertensives with what conditions

Answer 22

• DM
• **diabetic nephropathy
• CKD
• left ventricular hypertrophy (CHF)

Question 23

why are ACE-I often combined with diuretics

Answer 23

• enhance antihypertensive efficacy of diuretic drugs
  
  • inhibit aldosterone so natriuresis is unopposed
• balance adverse effects on potassium of diuretics

Question 24

adverse effects of ACE-I

Answer 24

• will cause severe hypotenstion in hypovolemic patients
• hyperkalemia
• cough
• angioedema
• acute renal failure in patients with bilat renal artery stenosis

Question 25

contraindications of ACE-I

Answer 25

• pregnancy -> teratogenic
• with K+ sparing diuretics -> hyperkalemia
• with NSAIDS -> will cause decreased vasodilation

Question 26

MOA of Angiotensin receptor blockers (ARB)

Answer 26

• block AT1 receptors without affecting AT2
• effects are similar to ACE-I
  
  • except no cough or angioedema (no effect on bradykinin)