test 5 part 2 Flashcards

1
Q

Adrenergic Antagonists

A
▪ Smypatholytics
▪ Adrenoreceptor antagonists
▪ Adrenergic blocking agents
▪ These drugs block “fight or flight” response
–α Blockers
–β Blockers
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2
Q

α Blockers

A
  • profoundly affect BP
  • blocks the binding of the ligand to the receptor
  • end up with vessel dilation
  • causes reflex tachycardia
  • baroreceptors respond to decrease in BP so parasympathetic output decreases and sympathetic outflow increases
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3
Q

types of α Blockers

A

▪ Non Selective α Blockers
▪ Selective α1 Blockers
▪ Selective α2 Blockers

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4
Q

what does α1 do

A

– Increased vascular tone

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5
Q

what does α2 do

A

– Control release of norepinephrine

– Inhibitory autoreceptors

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6
Q

Phenoxybenzamine (Dibenzyline) uses

A
  • Pheochromocytoma which is a tumor in the adrenal gland which causes too much catecholomine release (body has higher levels of epi and NE => sympathetic stimulation
  • phenoxybenzamine blocks all of the receptors that the catecholomines are acting at
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7
Q

Phentolamine (Regitine) uses

A

– Short term treatment of pheochromocytoma
– Locally to prevent dermal necrosis when NE given peripherally
– Given locally post NE extravasation
– Epinephrine reversal

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8
Q

Nonspecific α Blocker Side Effects

A
  • Orthostatic hypotension (lying down you feel fine then when you stand up and get really light headed)
  • Dizziness and headache
  • Tachycardia
  • Sexual dysfunction
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9
Q

Selective α1 Blockers

A

▪ Competitive
▪ Decrease PVR and lower BP
▪ Minimal changes in cardiac output
▪ First dose may produce orthostatic hypotension

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10
Q

β Adrenergic Blockers “-olol”

A
▪ Competitive antagonists 
▪ Vary in
        – Selectivity
        – Intrinsic sympathomimetic activity
        – CNS effects
        – Vasodilatory effects
        – Pharmacokinetics
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11
Q

β Adrenergic Blockers dosing

A

▪ Choice depends on side effects, patient compliance and preference
▪ Dosing must be individualized due to differences in base catecholamine levels, receptor density and variable cellular responses

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12
Q

β Adrenergic Blockers used to treat

A
▪ Hypertension
▪ Angina
▪ Cardiac arrhythmias
▪ Myocardial infarction
▪ Heart failure
▪ Hyperthyroidism
▪ Glaucoma
▪ Migraine prophylaxis
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13
Q

Blockade of the β1 Receptors

A
  • Decreases force of heart
  • decreases HR
  • Decreases renin secretion
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14
Q

Blockade of the β2 Receptors

A
  • Increase airway resistance

- Increase vascular resistance

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15
Q

β Adrenergic Blockers types

A

▪ Nonselective β blockers
▪ Selective β blockers
▪ Antagonists and partial agonists
▪ β and α blockers

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16
Q

Propranolol Cardiac Effects

A

▪ Negative inotrope
▪ Negative chronotrope
▪ Reduces cardiac output, workload, and oxygen consumption

17
Q

Propranolol Vascular Effects

A

▪ Prevents β2 mediated vasodilation in skeletal muscles
▪ PVR increases
▪ CO reduction triggers reflex peripheral vasoconstriction
▪ PVR returns to normal or decreases with long term use

18
Q

Propranolol Bronchial Effects

A

▪ Blockade of β2
receptors causes constriction of bronchial smooth muscle
▪ Contraindicated in patients with asthma or COPD!

19
Q

Propranolol Glucose effects

A

▪ Decreased glycogenolysis
▪ Decreased glucagon secretion
▪ Hypoglycemia

20
Q

Propranolol Drug Interactions with Isoproterenol (nonselective β1 and β2 agonist)

A

▪ Blocks the action of Isoproterenol
– No cardiac stimulation (β1)
– No reductions in MAP and diastolic BP (β2)

21
Q

Propranolol Drug Interactions with epinephrine

A

▪ Blocks some actions of Epinephrine
– No cardiac stimulation (β1)
– No reductions in MAP and diastolic BP (β2)
– Still get vasoconstriction (α1)

22
Q

Propranolol Therapeutic Uses for hypertention

A

– Decreased cardiac output
– Inhibition of renin release (don’t have angiotensin)
– Decrease in total PVR with long term use
– Decreased sympathetic outflow from CNS

23
Q

Propranolol Therapeutic Uses for long term angina

A

– Decreases oxygen requirement of the heart muscle

24
Q

Propranolol Therapeutic Uses for Myocardial infarction

A

– Protective effect for future MI
– Reduces infarct size and hastens recovery
– Reduces sudden death post MI

25
Q

Propranolol Therapeutic Uses for migraine

A

– Prophylactically

– Enters CNS

26
Q

Propranolol Therapeutic Uses for hyperthyroidism

A

– Blunts the widespread sympathetic stimulation

27
Q

Propranolol Adverse Effects

A
▪ Bronchoconstriction
▪ Arrhythmias
▪ Sexual impairment
▪ Metabolic disturbances
▪ CNS effects
28
Q

Propranolol Adverse Effects: Bronchoconstriction

A
  • blocks β2 receptors not allowing them to bronchodilate

- don’t use with asthma or COPD

29
Q

Propranolol Adverse Effects: Arrhythmias

A

– Long term use leads to receptor up-regulation
– Abrupt discontinuation can lead to severe arrhythmias and worsen angina or hypertension
- NEVER STOP ABRUPTLY

30
Q

Propranolol Adverse Effects: Metabolic disturbances

A

– Hypoglycemia β2
– Increased LDL
– Increased triglycerides β3 in the fats so it is not breaking down
– Decreased HDL

31
Q

Propranolol Adverse Effects: CNS effects

A
– Depression 
-Dizziness 
-Lethargy 
-Weakness
– Visual disturbances 
-Hallucinations 
-Vivid dreams 
-Short term memory loss
32
Q

Selective β1 Blockers

A

▪ Minimize the unwanted bronchoconstriction

▪ Cardioselectivity lost at high doses and start to block the β2 receptor

33
Q

Selective β1 Blockers

Therapeutic Uses

A

▪ Lower blood pressure in hypertension
▪ Increase exercise tolerance in angina
▪ Chronic stable angina therapy
▪ Chronic heart failure management

34
Q

Acebutolol (Sectral) therapeutic uses

A

– Hypertension with bradycardia

▪ Further decrease in heart rate is less pronounced

35
Q

Nonselective β Blockers with α1 Blocking Actions

A

▪ Produce peripheral vasodilation (block α1)
– Other β blockers produce an initial increase in PVR
▪ Reduce blood pressure

36
Q

Nonselective β Blockers with α1 Blocking Actions Therapeutic Uses

A

▪ Pregnancy induced hypertension

▪ Hypertensive emergencies (IV)