Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Mini II > Adrenergic Drugs > Flashcards

Adrenergic Drugs Flashcards

1
Q

What receptors are activated for epinephrine?

A

alpha-1, alpha-2
beta 1,2,3

B1 = B2 = B3 > a2

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

what receptors are activated for NE?

A

alpha1, alpha2, beta 1

Alpha&raquo_space;> Beta

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

What receptor is activated for Phenylephrine?

A

alpha-1

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

What receptors are activated for Clonidine and Apraclonidine?

A

alpha-2

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

What receptors are activated for Isopreternol?

A

Beta 1,2,3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What receptor is activated in Dobutamine?

A

Beta 1 selective agonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What receptor is activated for Albuterol/Salmeterol

A

Beta 2 selective agonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What receptors are activated for Dopamine?

A

D1, D2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Ephedrine (dopamine)

A

direct and indirect acting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Tyramine, Methyldopa, Cocaine, Amphetamine

A

Indirect-acting (mainly, but is mixed)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the MOA Indirect- acting adrenergic drugs?

A

1) stimulation of release of catecholamines from adrenergic nerve endings
a. facilitated exchange diffusion
b. false-transmitter concept

2) inhibition of re-uptake of catecholamines already released (some indirect acting adrenergic drugs inhibit the re-uptake of NE by blocking the amine transport system)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Role of Reflex Homeostatic adjustments– Epinephrine:

Systolic BP
Diastolic BP

A

Increases Systolic BP

Decreases Diastolic BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Role of Reflex Homeostatic adjustments– Epinephrine:

Direct action on cardiac rate

A

Increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Role of Reflex Homeostatic adjustments– Epinephrine:

Reflex action on cardiac rate

A

Decresaed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Role of Reflex Homeostatic adjustments– Epinephrine:

Final effect on cardiac rate

A

Increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Role of Reflex Homeostatic adjustments– NE

Systolic BP
Diastolic BP

A

Increases both

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Role of Reflex Homeostatic adjustments– NE

Direct action on cardiac rate

A

Increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Role of Reflex Homeostatic adjustments– NE

Reflex action on cardiac rate

A

DECREASES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Role of Reflex Homeostatic adjustments– NE

Final effect on cardiac rate

A

decreases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Role of Reflex Homeostatic adjustments– ISO

Systolic BP
Diastolic BP

A

Increases Systolic

Decreases Diastolic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Role of Reflex Homeostatic adjustments– ISO

Direct action on cardiac rate

A

increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Role of Reflex Homeostatic adjustments– ISO

Reflex action on cardiac rate

A

increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Role of Reflex Homeostatic adjustments– ISO

Final effect on cardiac rate

A

INCREASES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Pharmacodynamics EPI (Heart)

A

cardiac = B1 (mostly) some B2

Increased HR
Increased conduction
Increased contractility
DECREASED cardiac efficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Pharmacodynamics EPI (Vessels):

Vasoconstriction predominates where?
Vasodilation predominates where?

A

Vasoconstriction: Cutaneous, GI, Renal Vessels (alpha-1)

Vasodilation: Skeletal muscle & Liver (Beta-2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Pharmacodynamics EPI (Blood Pressure):

Low doses EPI cause increase or increase in bp?

A

Decrease (Vasodilation B2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Pharmacodynamics EPI (Blood Pressure):

Intermediate doses EPI cause increase or increase in bp?

A

Systolic BP increases (due to rise in CO)

Diastolic BP decreases (B2 receptor mediated vasodilation usually predominates)

Mean BP is usually slightly elevated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Pharmacodynamics EPI (Blood Pressure):

High doses EPI cause increase or increase in bp?

A

both systolic and diastolic BP INCREASE (B1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Pharmacodynamics EPI (Respiratory Sys):

Effects on smooth muscle, mucociliary clearance?

A

bronchial smooth muscle relaxation

INCREASED mucociliary clearance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Pharmacodynamics EPI (GI)

effects on smooth muscle, peristalsis, sphincters?

A

Relaxation of smooth muscle (a2 on cholinergic reduces ACh release, activaiton of b2 receptors directly relaxes smooth muscle)

decreased GI peristalsis

Contraction of sphincters (a1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Pharmacodynamics EPI (GU)

A

contraction of trigone and internal sphincter, relaxation of pregnant uterus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Pharmacodynamics EPI (CNS):

A

lacks direct central effects (bc epi doesnt enter CNS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Pharmacodynamics EPI (Eye):

does EPI cause mydriasis or ____.

Does it decrease or increase intraocular pressure?

A

contraction of radial muscle of iris –> mydriasis

DECREASED intraocular pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Pharmacodynamics EPI (skeletal muscle)

causes what in skeletal muscle?

A

tremor (B2 accelerates sequestration of cystolic Ca and enhances discharge of muscle spindles)

increased K+ uptake into cell (B2 activation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Pharmacodynamics EPI (metabolic effects):

epinephrine causes hyper or hypoglycemia?

A

hyperglycemia:

1) inhibition of insulin secretion
2) stimulation of glycogenolysis and gluconeogenesis
3) stimulation of glucagon secretion
+
increased lipolysis (B3)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the Route of Administration for Epinephrine?

A

Parenteral ONLY! (0% oral bioavailability)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the half life of epinephrine?

A

2 minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are the adverse effects of EPI in the CNS?

A

restlessness, throbbing HA, dizziness, tremors, weakness, dyspnsea

cerebral hemorrhage (rare- from increased BP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are the adverse effects of EPI in CVS?

A

HPT, pallor

anginal pain (in patients with CHD), sinus tachy, ventricular arrhythmias

pulmonary edema (rare)

40
Q

Therapeutic uses of Epinephrine

A

serious acute hypersensitivty rxn (anaphylaxis, angioedema)

Cardiac arrest (a1 receptor activation)

prevention of surgical bleeding (given topically for superficial wounds)

to retard absorption of local anesthetics

41
Q

in cardiac arrest what receptor does epi activate to increase venous return?

A

alpha 1

42
Q

What is the final effect of NE on the heart?

A

decrease in HR

43
Q

What is NE action on the Vessels?

A

Vasoconstriction predominates in all vascular beds (except coronary and pulmonary where autoregulatory actions override direct vasoconstrition effect of NE)

44
Q

Is BP increased or decreased when EPI is given?

A

increased (but pulse pressure doesn’t change)

45
Q

therapeutic uses of NE?

A

hypotension and vasodilatory shock (due to spinal trauma, spinal anesthesia, sepsis)

with local anesthetics (to retard their absorption)

46
Q

What is the MOA and pharmacological effect of dopamine at low doses?

A

activation of D1 receptors

vasodilation in kidney, mesenteric and coronary beds

inhibition of Na+ reabsorption in PCT

(overall –> increased diuresis!)

47
Q

What is the MOA and pharmacological effect of dopamine at intermediate doses?

A

activation of B1 receptors + release of NE from nerve terminals

increased stroke volume and HR

48
Q

What is the MOA and pharmacological effect of dopamine at high doses?

A

activation of a1 and d2

increased systemic vascular resistance, nausea, and vomiting

49
Q

what is the route of administration of dopamine?

A

IV infusion only

50
Q

half life of dopamine

A

2 mins

51
Q

therapeutic uses of dopamine

A

cardiogenic, neurogenic and septic shock

52
Q

mechanism of action of a1 receptor agonist

A

Gq –> PLC

1) IP3 –> inc. Ca2+ –> Increased contraction of vascular smooth muscle
2) DAG –> Protein kinase C –> Inc. Ca+ –> increased contraction of vascular smooth muscle

53
Q

effects on cardiovascular system of alpha1 agonist

A

increase in blood pressure associated with bradycardia because of activation of baroreceptor reflex

54
Q

which class of drugs can cause rebound congestion (when used as nasal decongestant) as an adverse effect?

A

phenylephrine (a1 agonist)

55
Q

therapeutic uses of alpha 1 agonists

A

aka. phenylephrine

postural hypotension

nasal or ocular decongestant

mydriatics

local vasoconstrictor (i.e in epistaxis)

to prolong action of local anesthetics

56
Q

drugs that act on a2 and imidazoline receptors

A

clonidine

apraclonidine

57
Q

drugs that act on a2 receptors

A

Guanfacine

Tizanidine

58
Q

MOA of clonidine

A

1) activation of PREsynaptic a2 receptors located in nucleus of tractor solitarius in rostral ventrolateral medulla
2) activation of non-adrenergic binding sites– imidazoline receptors

Overall– decreased firing of reticulospinal tract which decreases central adrenergic tone (main antihypertensive MOA of clonidine)

59
Q

effects of a2 selective agonists on CVS

A

i. e. clonidine
1) low/intermediate– hypotension
2) high– Hypertension

60
Q

effects of a2 agonists on CNS

A

i.e. clonidine

craving-reducing effects in addicts
sedative effects
analgesic effects

61
Q

half life clonidine

A

12 hours

62
Q

therapeutic uses of a2 agonists

A

i.e. clonidine

1) HTN (second choice drugs)
2) open angle glaucoma
3) withdrawal from tobacco, alc or opiods
4) preanesthetic medication to induce preoperative sedation and reduce requirement for anesthetic
5) severe pain
6) diabetic neuropathy
7) neuropsychiatric disorders (Tourettes, ADHD, autism)

63
Q

effects of B-agonists on the Heart

A

i.e. Isoproterenol

Increased HR (tachycardia)

64
Q

effects of B-agonists on vessels

A

i.e. isoproterenol

b2 mediated vasodilation predominates in all vascular beds

65
Q

effects of B-agonists on BP

A

i.e. Isoproterenol

systolic BP remains unchanged or increases

Diastolic BP decreases sharply

Mean BP usually falls

66
Q

administration of isoproterenol

A

IV infusion only

67
Q

therapeutic uses of isoproterenol

A

emergency situations where heart contractility is low and HR is slow yet peripehral resitance is high (i.e. Cardiac surgery)

Torsade de Pointes (polymorphic Vtach)

68
Q

MOA of increased cardiac contractility of B1 receptor agonist:

A

(i.e. Isoproterenol)

Gs –> Adenylyl cyclase –> inc. cAMP –> Protein Kinase A:

1) increased phosphorylation of troponin C
2) inc. opening of voltage gated Ca2+ channels
3) inc. Ca2+ reuptake by SR

69
Q

MOA of increased cardiac conduction by B1 receptor agonist

A

Gs –> adenylyl cyclase –> inc. cAMP –> protein kinase A –> opening Na+ channels –> depolarization of cell membranes of SA node, AV node and Ventricular conduction system

70
Q

pharmacological effects of dobutamine on the heart

A

b1 agonist

increase contractility and conduction

71
Q

therapeutic uses of dobutamine?

A

b1 agonist

Iv infusion to patients with cardiac failure or cardiogenic shock

72
Q

effects of albuterol/salmeterol on respiratory system

A

b2 agonist

bronchodilation, enchanced mucociliary clearance, suppression of release of inflammatory mediators (leukotrienes, histamine), reduction of microvascular permeability

73
Q

administration of albuterol/salmeterol

A

inhalation (main route), po, sc

74
Q

MOA of smooth muscle relaxation by B2 receptor agonists

A

i.e. albuterol

Gs –> adenylyl cyclase –> inc. cAMP –> protein kinase A:

1) Inc. Ca2+ efflux –> decreased smooth muscle contraction
2) inc. inactivation of myosin-light-chain kinase –> dec. phosphorylation of myosin light chains –> decreased smooth muscle contraction

75
Q

adverse effect of B2 receptor agonist on CNS

A

tremor, muscle cramps

76
Q

Therapeutic uses of albuterol/salmeterol

A

b2 agonist

1) asthma
2) COPD
3) Hyperkalemia
4) premature labor

77
Q

Tyramine

direct or indirect adrenergic drug?

A

Indirect acting adrenergic drug

78
Q

MOA of tyramine

A

false transmitter taken up by adrenergic neurons where it is transformed into octopamine

79
Q

Pharmakokinetics of tyramine

A

normal byproduct of tyrosine metabolism in body

inactive if ingested because of a very large fisrt-pass effect

80
Q

clinical uses of tyramine

A

localize lesion of sympathetic nerves

81
Q

MOA of Methyldopa

A

(indirect adrenergic drug)

false NT which is taken up by adrenergic neurons where it is transformed into methylnorepinephrine (a2 receptor agonist)

activation of central a2 receptors by methylnorepinephrine reduces central adrenergic tone

82
Q

MOA of amphetamines

A

indirect acting adrenergic drug

stimulation of release of monoamines (NE, dopamine, serotonin)– peripherally and centrally

83
Q

MOA of cocaine

A

indirect-acting adrenergic drug

blockade of reuptake of monoamines (NE, dopamine, and serotonin)

84
Q

Ephederine MOA

A

activation of a1, a2, b1 and b2 receptors
enhanced release of NE from adrenergic neurons

it is an over the counter ingredient in decongestants

85
Q

what drugs would you give for cardiogenic shock?

A

dobutamine, dopamine

86
Q

what drugs would you give for vasodilatory shock (i.e. neurogenic, septic?)

A

NE, Phenylephrine, dopamine

87
Q

What drugs would you give for anaphylactic shock, CPR?

A

epinephrine

88
Q

what drug would you give for torsade de pointes?

A

isoproterenol

89
Q

what drug would you give for HTN?

A

clonidine or methyldopa

90
Q

what drugs would you give for local anesthesia (to cause local vasoconstriction?)

A

epinephrine, NE

91
Q

what drugs would you give for asthma, copd?

A

b2 selective agonists or epinephrine

92
Q

what drugs woudl you give for anaphylaxis or angiodema?

A

epinephrine

93
Q

what drug would you give for open anlge glaucoma?

A

apraclonidine

94
Q

what drug woudl you give for narcolepsy, ADHD, weight reduction?

A

amphetamines and congeners

95
Q

what drug woudl you give for withrdawal from tobacco, alcohol or opiods? or Tourettes syndrome, ADD, etc.

A

clonidine

Mini II (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions