alpha/beta antagonists

Question 1

alpha 1 actions

Answer 1

1. post synaptic

2. vasoconstriction, midriasis, GI relaxation, contraction of GI and bladder sphincters

Question 2

alpha 2 action (post synaptic)

Answer 2

1. hyperpolarization of CNS cells (decreased MAC)

2. platelet aggregation

Question 3

alpha 2 (presynaptic)

Answer 3

1. inhibition of NE release (negative feedback loop)

Question 4

beta 1 (post synaptic)

Answer 4

• increased cardic conduction, automaticity and contractility

Question 5

beta 2 post synaptic

Answer 5

vasodilation, bronchodilation, GI, uterine & bladder relaxation; glycogenolysis and (lipolysis=beta 3)

Question 6

beta 2 (presynaptic)

Answer 6

causes norepinephrine release

Question 7

alpha antagonists:
phentolamne-
1. action
2. effects
3. uses

Answer 7

• (regitine)
  1. nonselective alpha blocker
  2. vasodilation, decreased systemic BP, increased HR d/t baroreceptor reflex, blocks alpha 2 leading to increased NE
  3. treatment of hypertensive crisis, prevent sloughing after extravisation of sympathiomimetic drugs (pressors)

Question 8

phentolamine

1. onset
2. peak
3. duration
4. dose

Answer 8

1. o: 1-2 minutes,
2. p: 2 minutes
3. dur: 10-15 min
4. dose:
   - hypertension-0.05-0.1 mg/kg IV followed by infusion of 0.1-1.0
   mg/min
   -antisloughing-5-10mg (0.1-0.2 mg/kg) injdecte in and or around the IV

Question 9

alpha antagonist:
Phenoxybenzamine:
1. class/action
2. side effects
3. onset
4. uses
5. what might you want to add to this medication?

Answer 9

1. nonselective alpha blocker
2. vasodilation, orthostatic hypotension
3. very slow onset
4. use for control of blood pressure from pheochromocytoma (adrenal tumor of chromaffin cells), treatment for Raynauds.
5. a beta blocker due to unopposed beta

Question 10

pheochromocytoma

1. what is it?
2. s/s (what is the diagnostic triad/quadrad)?
3. testing
4. what is clonidine suppression test?

Answer 10

1. tumor that secretes catecholamines (usually adrenal)
2. triad/quadrad= HTN, tachycardia, diaphoresis & headache
3. MRI,CT, catacholamine levels, vanylmandilic acid (metabolite of catecholemine breakdown) levels, clonidine supression test
4. clonidine is a central acting alpha 2 agonist, it mimics catecholamines in the brain causing innervation to adrenal medula to cause decrease in adrenal catecholamines. it does not reduce catecholamines if the patient has Pheochromocytoma

Question 11

yohimbine:

1. action:
2. uses:

Answer 11

1. selective presynaptic alpha 2 blocker (central & periph acting)
2. used to reverse sedatives (think precedex), used for idiopathic orthostatic hypotension, erectile dysfunction

Question 12

yohimbine:

1. peripheral effect:
2. central effect:
3. why abuse risk?
4. effect on MAC?

Answer 12

1. peripheral effect is decreased alpha 2 adrenergic activity
2. central effect is stimulation of mood and mild antidiuretic effect
3. possible drug abuse risk d/t dissociative state similar to PCP
4. since alpha 2 agonists decrease MAC by acting on receptors in cns, yohimbine may increase MAC by

Question 13

beta antagonists:
propanolol:
1. \_\_\_ beta blocker:
2: \_\_\_ \_\_\_ of beta blockers:
3. what type of antagonism (beta 1 or 2)?
4. metablism
5. protein binding:
6. thererfore, does what with other protein bound meds?

Answer 13

1. original; first beta blocker introduced
2. the “gold standard” of beta blockers
3. equal antagonist of beta 1 and beta 2 (contraindicated in asthmatics).
4. well absorbed in GI but has extensive first pass metabolism
5. extensively protein binding (90-95%).
6. competes with them for binding sites (could effect coumadin levels etc.).

Question 17

esmolol

1. drug class
2. onset and acting
3. use in laryngoscopy
4. main use
5. use in ECT

Answer 17

breviblock

1. selective beta 1 (beta 2 at high doses)
2. rapid onset, short acting
3. dull sympathetic response to laryngoscopy
4. management of periopertive hypertension and SVT
5. prevention of HTN from ECT (therapy)

Question 18

esmolol:

1. why does it burn on injection?
2. why is duration so short?
3. how much is excreted unchanged in urine?
4. metabolites? active or inactive?
5. how long do effects last?

Answer 18

1. because the pH is 5 (acidic)
2. it is rapidly hydrolyzed in the blood by plasma esterase (NOT plasma cholinesterase though)
3. less than 1% excreted unchanged in urine
4. inactive metabolites
5. takes 15 minutes for HR to return to pre drug rate

Question 19

esmolol:

1. onset:
2. peak:
3. duration:
4. doses:
   a) pre induction
   b) hypertension
   c) svt

Answer 19

1. 1-2 minutes
2. 5 minutes
3. 10-30 min
4. a)pre induction: 100-200 mg IV prior to laryngoscopy
   b) htn: 0.5-2 mg/kg followed by infusion of 50-300 mcg/kg/min
   c) svt: 500 mcg/kg loading dose, followed by 200 mcg/kg/min

Question 20

Labetolol

1. trade names:
2. ratio of alpha to beta?
3. alpha and beta affected but which ones?

Answer 20

1. normodyne, trandate
2. 3:1 for p.o.; 7:1 from IV
3. combined alpha 1, beta 1 & 2 (alpha 2 are spared; negative feedback from NE stimulation intact)

Question 20

propanolol:

1. action:
2. what are 2 beta 2 side effects?
3. why doesn’t this cause a problem?

Answer 20

1. decreases HR and contractility reducing cardica output
2. beta 2 causes increased coronary vascular resistance and PVR (peripheral vascular resistance), but o2 sparing effects of decreased HR and contractility predominate

Question 21

labetolol

1. metabolism
2. excretion
3. elimination half time? what prolongs it?
4. why is it good for stroke patients?

Answer 21

1. conjugate in liver by glucoronic acid
2. 5% unchanged in urnie
3. elimination half time is 5-8 hours (prolonged in liver issues, but not affected by renal issues)
4. cerebral blood flow and ICP are unchanged (does not lower)

Question 21

propanolol:
metabolism:
1. where metabolized? completely?
2. does it alter the effects of any medications?

Answer 21

1. in liver; active metabolites
2. a)causes decreased clearance of amide local anesthesia
   b) decreases pulmonary uptake of fentanyl (gives one higher circulating levels).

Question 22

1. limits of autoregulation are?

2. what is the shift if someone is normally hypotensive?

Answer 22

1. 60-150 map
2. shift to the right
   3.

Question 22

propanolol:
pharmacodynamics:
1. onset:
2. peak:
3. duration:
4. dose:
5. also used for?  what is the dose?

Answer 22

1. iv< 30 sec
2. iv< 1 minute; po varies
3. 1-6 hrs IV, 6-12 hrs po
4. htn or arrhythmia: 0.5-3 mg iv to max of 6-10 mg.
5. migraines; 20-80 mg p.o.

Question 23

labetolol:
pharmakodynamics:
1. onset/ 
2. peak:
3. duration:
4. dose:
5. infusion dose:

Answer 23

1. 2-5 minutes
2. 5-15 min
3. 2-4 hours
4. 2.5-20 mg iv slow push
5. (not often used as a drip ) 0.5-2 mg/min

Question 24

labetolol:

1. side effects:
2. uses:
3. alternative uses: why better than nipride?
4. what should you be aware of if giving for alternative use?

Answer 24

1. hypotension, bradycardia, CHF, bronchospasm
2. management of HTN
3. deliberate hypotension during surgery (10 mg iv intermittenly not associated with increases in HR or shunting like nipride)
4. beware of duration (2-4 hours) vs. duration of surgery

Question 25

alpha and beta questions:

1. how much phentolamine would you give if your IV push epi went SQ?
2. what are 2 possible uses for phenoxybenzamine
3. when might one see reflex tachycardia?
4. what does yohimbine block (what is physiological cause)?

Answer 25

1. 5-10 mg in & around the IV
2. pheochromocytoma tx & raynauds
3. phentolamine (regitine) is a non selective alpha blocker that increases HR d/t stimulating of baroreceptor reflex and blocking alpha 2 which leads to increased NE
4. presynaptic alpha 2 (increases mood, good for erectile dysfunction) also post synaptic alpha 2 block which increases NE (tx for orthostatic hypotension)