Pharmacology - Autonomics IV-V-VI Flashcards Preview

MS 2 - Unit 2 > Pharmacology - Autonomics IV-V-VI > Flashcards

Flashcards in Pharmacology - Autonomics IV-V-VI Deck (96):
1

Effect of alpha-1 adrenergic receptor

increase in IP3, DAG
smooth muscle contraction

2

Effect of beta-1 adrenergic receptor

increase force and rate of contraction of heart
increase cAMP
increased renin secretion in kidney

3

Effect of beta-2 adrenergic receptor

increase cAMP
smooth muscle relaxation

4

Effect of beta-3 adrenergic receptor

increase cAMP
lipolysis

5

What is the primary mechanism for reducing/terminating the effects of NE?

re-uptake;
repackaged for future release

6

Monoamine oxidase (MAO) and Catechol-O-Methyltransferanse break down what?

NE, Epi, exogenous adrenergic drugs ie tyramine
major metabolic enzymes;
prominent in liver

7

Elevated levels of plasma metanephrine is an indicator of:

Pheochromocytoma
Metanephrine is a metabolite of NE/E

8

Non-selective beta-1 and 2 antagonist

Propranolol

9

Non-selective beta-1 and 2 agonist

Isoproterenol
**most potent agonist of beta-1 and 2

10

Beta-2 agonist

Albuterol

11

D1 agonist

Fenoldopam
dopamine receptor agonist
**does not cause NE release - just acts on D1

12

Alpha-2 selective agonist

Clonidine
**most potent agonist of alpha-2

13

Alpha-1 selective agonist

Phenylephrine

14

Alpha-1 antagonist

Prazosin

15

Beta-1 antagonist

Atenolol

16

Vasculature have both alpha-1 and beta-2 receptors. Which dominates?

Effects of alpha-1 (constriction) are dominant

17

Dopamine acts on what receptors?

DA
alpha-1
beta-1

18

What is the most potent stimulator of alpha-2?

Epinephrine

19

Tyramine and amphetamine are what kinds of adrenergic drugs?

Indirect agonists - cause release of NE

20

Ephedrine and Hydroxyamphetamine are what kinds of adrenergic agents?

Mixed (direct and indrect effects) agents

21

Uses: Fenoldopam

to treat a hypertensive emergency, anuria
to increase blood flow at renal, mesenteric and cerebral arteries;
to lower blood pressure (hypertensive emergencies)

22

Uses: Epinephrine

control hemorrhage;
vasoconstriction in dental procedures
alpha-1

***anaphylactic shock*** alpha and beta activation - vasoconstriction, bronchodilation and decrease histamine release from mast cells (beta-2)

23

Uses: Ephedrine, Phenylephrine

Nasal decongestions
alpha-1

24

Uses: Dopamine

treat hypotension ie to replace adrenal catecholamines like with spinal anesthesia, following pheochromocytoma surgery

25

Class: Ergotamine

Ergot alkaloid
alpha-adrenergic blocker BUT alpha-agonist??

26

Class: Ergonovine

Ergot alkaloid
alpha-adrenergic blocker BUT alpha-agonist??

27

Use: Ergonovine

to treat post-partum hemorrhage
"oxytocic"

28

Use: Ergotamine

to treat prodrome of migraines

29

Side Effects: Ergot alkaloids

Hallucinations (like LSD)

30

Use: Bromocriptine

Treat hyperprolactinemia;
Treat Parkinsonianism
DA2 agonist

31

Beta-1 selective agonist for cardiac stimulation

Dobutamine
also used during cardiac stress test

32

first generation beta blocker
non-selective

propranolol
non-seletive

33

second generation beta blocker
beta-1 selective

metoprolol
atenolol

34

third generation beta blocker
non-selective with additional actions

carvedilol
labetalol

35

third generation beta blocker
beta-1 selective with additional actions

betaxolol

36

plasma half life of metoprolol

about 4 hours
Metoprolo is a beta-1 selective 2nd generation beta blocker

37

plasma half life of atenolol

about 6-8 hours
Atenolol is the least lipid soluble beta blocker, thus not in CNS;
beta-1 selective second generation beta blocker

38

Use: Labetolol

to treat hypertension
lowers TPR with little tachycardia
3rd generation - beta blocker with additional actions (ie some alpha-1 antagonism)

39

Use: Carvedilol

to treat HTN and CHF;
3rd generation - beta blocker with additional actions (ie some alpha-1 antagonism)

40

Third generation beta blocker "additional actions" include:

NO production
beta-2 agonism
Ca entry blockade
alpha-1 antagonism
K channel opening
antioxidant activity

41

Therapeutic uses of beta-blockers in general include:

Cardiac arrhythmias
Angina
Glaucoma
Migraine
Anxiety/stage fright
Heart failure
HTN

42

Use ONLY what kind of beta-blockers to treat heart failure?

2nd and 3rd generation

43

Too much stimulation of what receptor may precipitate an asthma attack?

Beta-2

44

Phentolamine
Phenoxybenzamine
Prazosin
these drugs are all:

alpha receptor antagonists

45

What are the major side effects of alpha-reeptor antagonists?

tachycardia;
postural hypotension

46

Which alpha-receptor antagonist covalently binds to alpha-1 receptors?

Phenoxybenzamine
therefore, long-acting

47

Which alpha-receptor antagonists are nonselective, in that they affect alpha-1 and alpha-2?

Phentolamine
Phenoxybenzamine

**Prazosin is selective for alpha-1

48

Therapeutic use: Prazosin

HTN
Peripheral vascular disease (including Raynaud's and frostbite and atherosclerosis)
BPH

49

Therapeutic use: Phenoxybanzamine

Pheochromocytoma;
Peripheral vascular disease (including Raynaud's and frostbite);

50

Phentolamine and Phenoxybenzamine have what unfortunate sexual side effect?

Inhibit ejaculation

51

Therapeutic use: Phentolamine

Pheochromocytoma;
Peripheral vascular disease (including Raynaud's and frostbite);

52

Beta-2 blockers may not be appropriate for which patient population?

Diabetics
bc there can be a decrease in glycogenolysis and lipolysis in response to hypoglycemia

53

MOA: alpha-methyltyrosine

blocks synthesis of DA and NE by inhibiting tyrosine hydroxylase

54

Use: alpha-methyltyrosine

Mgmt of pheochromocytoma
Side effects are "many and serious"

55

MOA: Reserpine

Release of empty vesicles (NE is not taken into vesicles b/c it binds uptake transporter and stops it)

56

Class:
alpha-methyltyrosine
reserpine
guanethidine

nerve ending blocker

57

MOA: guanethidine

False neurotransmitter (vesicles become full of guanethidine rather than NE)
--CNS shooting blanks essentially

58

Use: guanethidine

HTN
Side effects are "many and serious"
not commonly used clinically

59

What is one major side effect of Reserpine and a reason it is not commonly used clinically?

depression/suicide

60

MOA: cocaine

prevents NE uptake

61

Use: cocaine

Local anesthetic, vasoconstrictor

62

Side effects: cocaine

insomnia
anxiety
arrhythmia

63

NE acts on what receptors?

alpha-1
alpha-2
beta-1

64

Therapeutic use: NE

treat hypotension

NE vasoconstricts, increases BP and HR

65

Epinephrine acts on what receptors?

alpha-1
alpha-2
beta-1
beta-2

66

Therapeutic use: Epinephrine

anaphylactic shock;
glaucoma

Epinephrine increases HR and contractility, BP

67

Use: Isoproterenol

non-selective beta agonist:
asthma
shock
heart block

Isoproterenol decreases resistance, increases CO, increases HR and bronchodilates

68

Side effects: Isoproterenol

Palpitations
tachyarrhymias
headache

69

Therapeutic uses: dobutamine

cardiac decompensation
shock
heart block

Dobutamine increases contractility, increases HR directly and indrectly

70

Side Effects: Dobutamine

Tachyarrhythmia
HTN

71

beta-2 selective agonists, name 2:

albuterol
terbutaline

72

Therapeutic uses:
Albuterol
Terbutaline

asthma
COPD

Albuterol and Terbutaline relax bronchial and uterine smooth muscle

73

Side Effects:
Albuterol
Terbutaline

Tachycardia
Muscle tremor

74

Uses: Phenylephrine

Nasal congestion
Postural hypotension

Phenylephrine is a vasoconstrictor

75

Side effects: Phenylephrine

Reflex bradycardia
HTN

76

Therapeutic use:
Clonidine
alpha-methyldopa (prodrug)

HTN
shock
withdrawal from drug dependence

Actions: decrease sympathetic outflow from CNS, decrease resistance

77

Side effects:
Clonidine
alpha-methyldopa (prodrug)

Sedation

78

Side effects: Fenoldopam

Posturalhypotension

79

Uses: amphetamine

ADHD
Narcolepsy
recreational

CNS stimulation, increase BP, increase HR

80

Side effects: amphetamine

Insomnia
HTN
anxiety
arrhythmias

81

MOA: amphetamine

indirect acting release of NE

82

Uses: Dopamine

shock
renal failure
hypotention

Actions:
vasodilation, increase GFR, increase HR, increase BP

83

Side effects: dopamine

vasoconstriction at high doses

84

Give the agonist and antagonist for beta-1 receptor:

Agonist: Dobutamine
Antagonist: Atenolol

85

Give the agonist and antagonist for non-selective beta-1 and 2 receptors:

Agonist: Isoproterenol
Antagonist: Propranolol

86

An alternative to propranolol, that is also a non-selective beta antagonist, is:

Timolol

87

Uses:
Propranolol
Timolol

HTN
Angina
Arrythmias

88

Side effects:
Propranolol
Timolol

Bradycardia
Bronchoconstriction
sexual dysfunction

89

Give the agonist and antagonist for alpha-1 receptor:

Agonist: Phenylephrine
Antagonist: Prazosin

90

Therapeutic use: Betaxolol

CHF
HTN

Side effects: bradycardia

91

MOA Terazosin

vasodilatory effect via block of a1 receptors, leading to a reflex tachycardia

92

MOA Atropine

Atropine would lead to block of cholinergic M3 receptors

93

BPH is often managed with:

BPH is often managed with alpha blockers
ie Prazosin
Terazosin

94

MOA alpha-methyltyrosine

Alpha-methyltyrosine blocks tyrosine hydroxylase and would cause a depletion of norepinephrine (and dopamine and epinephrine) stores. This effectively produces a chemical sympathectomy, resulting in post-synaptic receptor up-regulation; thus, producing a
denervation supersensitivity.

95

Labetalol is:

a non-selective beta-blocker with additional α1 antagonist properties.
"third generation"

96

Therapeutic Use: Ipratroprium

COPD, asthma
antimuscarinic