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RCS > L6, L8- Adrenergic Drug Overview > Flashcards

L6, L8- Adrenergic Drug Overview Flashcards

1
Q

list some disorders that are treated with adrenergic agonists or antagonists

A
  • HTN
  • HF, angina, arrhythmias
  • asthma
  • migraine
  • anaphylactic reactions
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2
Q

describe the effect of epinephrine at low and high doses in skeletal muscle vasculature

A

Low: β2 more sensitive than α1, therefore physiological concentrations of epinephrine => vasodilation

High: α1/β2 activated, α1 predominates => vasoconstriction

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3
Q

describe the effects of epinephrine at low and high concentrations in terms of adrenergic activation

A

Low: mainly β1/β2 receptors are activated

High: α1 effects are more pronounced

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4
Q

list the general effects of epinephrine

A
  • inc HR + contractile force => inc CO (inc myocardium O2 demand) (β1)
  • inc renin release (β1)

-skin and viscera arterial vasoconstriction (α1)

  • skeletal muscle BVs vasodilate (β2)
  • bronchodilation (β2)
  • inc liver glycogenolysis, inc α-cell glucagon release (β2)

-inc lipolysis (β1/β2)

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5
Q

describe the effects of epinephrine on BP at high doses (given IV)

A

Net inc in MAP:

  • inc ventricular contraction (β1)
  • inc HR (β1): may be opposed by baroreceptor reflex
  • vasoconstriction (α1)
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6
Q

describe the effects of epinephrine on BP at low doses (given IV)

A

No net inc in MAP:
-inc ventricular contraction + inc HR (β1) => inc systolic pressure
-dec peripheral resistance, vasodilation (β2 more sensitive than α1) => dec diastolic pressure
[no change in MAP = no baroreceptor reflex]

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7
Q

describe the cardiovascular effects of NE

A

(Note- very little if any β2 activation)
Inc peripheral vascular resistance, SP, DP –> inc MAP + dec HR:
-peripheral vasoconstriction (α1)
-inc cardiac contractility (β1- CO is unchanged/decreased)
-inc MAP –> bradycardia via baroreceptor reflex

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8
Q

describe baroreceptor reflex in response to vasoconstriction / increased BP

A
  • carotid sinus –> inc PSNS activity, dec SNS activity
  • inc PSNS + dec SNS => dec HR
  • dec SNS => dec cardiac force of contraction
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9
Q

describe baroreceptor reflex in response to vasodilation / decreased BP

A
  • carotid sinus –> inc SNS activity, dec PSNS activity
  • inc SNS + dec PSNS => inc HR
  • inc SNS => inc cardiac force of contraction
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10
Q

the main cardiovascular effect of NE proceeding atropine administration is….

A

tachycardia

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11
Q

list in order of highest affinity the receptors DA binds to (in SNS)

A

D1 > β1 > α1

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12
Q

describe the cardiovascular effects of low dose dopamine

A

Mainly D1 in renal and other vascular beds are activated:

  • vasodilation
  • inc GFR, renal blood flow, Na excretion
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13
Q

describe the cardiovascular effects of intermediate dose dopamine

A
  • more β1 receptors activated in heart inc CO (very little for β2)
  • inc NE release from nerve terminals –> contributes to cardiac effects
  • inc systolic BP, no change in diastolic => inc MAP, PVR unchanged
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14
Q

describe the cardiovascular effects of high dose dopamine

A

-more α1 receptors activated in vasculature => vasoconstriction –> inc BP
-TPR may be increased
(Note- these are the therapeutic or clinical doses used)

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15
Q

describe the effects of isoproterenol

A

(β agonist)

  • β1: inc HR (potentiated by baroreceptor reflex), contractility, CO
  • β2: skeletal muscle arteriole dilation –> dec PVR + bronchodilation
  • dec diastolic, inc systolic pressure => dec MAP
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16
Q

dobutamine is a (1) type adrenergic drug that exhibits (2) type effect on the heart with (3) effects as the end result. It also has (4) effects on vasculature

A

1- β1 agonist
2- inotropic (mild chronotropic)
3- mild inc in HR and PVR
4- mild vasodilation

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17
Q

list the adverse effects of β2 agonists

A
  • tremor, restlestness, apprehension, anxiety, tachycardia

- less likely in inhalation than with parenteral or oral therapy

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18
Q

describe the cardiovascular effects of phenylephrine

A

α1 vasoconstriction –> inc PVR –> inc diastolic/systolic BP + MAP => baroreceptor reflex leading to dec HR

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19
Q

clonidine works by activating on (1) receptors which leads to (2) in order to reduce (3); its adverse effects are (4)

A

1- pre-synaptic α2 receptors
2- reduce SNS outflow
3- reduce BP
4- lethargy, sedation, xerostomia

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20
Q

methyldopa is converted to (1) in order to act on (2) receptors, and results in (3) overall; its adverse effects are (4)

A

1- α-methylnorepinephrine (within noradrenerigic neurons)
2- central α2 receptors
3- dec BP
4- sedation, impaired mental concentration, xerostomia

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21
Q

what is the general mechanism of adrenergic releasing agents

A

inc in NE release from presynaptic terminals –> potentiates effects of endogenous NE

22
Q

(1) is commonly found in fermented foods like cheese and wine (Chianti). It is oxidized by (2), therefore consumption of (1) is avoided in (3) patients as it can result in (4)

A

1- tyramine
2- MAO
3- MAOI patients (anti-depressants)
4- precipitate serious vasopressor episodes

23
Q

describe the general mechanism of mixed-acting adrenergic agonists

A
  • induces NE release

- activates adrenergic receptors

24
Q

the general mechanism of α-adrenergic blockers is…

A
  • SNS control of vasculature mainly due to α1

- blockade of α1 => reduces sympathetic tone (vasodilation) => dec PVR, BP

25
Q

list the 2 non-selective α anatagonists

A
  • phenoxybenzamine (irreversible)

- phentolamine (reversible)

26
Q

to reverse the vascular effects of epinephrine, _____ can be used, explain

A

α antagonist (phenoxybenzamine): blocks α1 vasoconstriction –> β2 receptors remain unblocked, epinephrine binds => vasodilation
(w/o α-blocker there is inc MAP, w/ α-blocker there is slight dec MAP)

27
Q

selective α1 antagonists act in order to (1) in HTN and (2) in BPH

A

1- relaxes arterial/venous smooth muscle

2- relaxes smooth muscle in bladder neck, prostate capsule, prostatic urethra

28
Q

describe dosing with α1 antagonists

A
  • must taper / titrate doses up (and down), start with 1/4-1/3 of normal dose
  • 1st dose => exaggerated hypotensive response => syncope
29
Q

non-selective β antagonists will have a ______ effect on the heart

A
  • slow HR

- dec myocardial contractility

30
Q

non-selective β antagonists will have a ______ effect on the lungs

A

blocking β2 receptors => respiratory crisis in COPD/asthma patients (recommended to use selective β antagonists)

31
Q

non-selective β antagonists will have a ______ metabolic effect

A
  • dec glycogenolysis

- dec glucagon secretion

32
Q

(1) are selective β1 antagonists used to treat HTN in (2) and (3) patients

A

1- atenolol, metoprolol
2- impaired respiratory function (COPD, asthma)
3- DM patients receiving insulin / oral hypoglycemic agents

33
Q

list the 10 uses for β antagonists

A

1) HTN
2) glaucoma
3) migraine
4) hyperthroidism
5) angina pectoris
6) AFib
7) MI
8) primary prevention of bleeding from esophageal varices in cirrhosis
9) performance anxiety
10) essential tremor

34
Q

β-blockers treat HTN by….

A

lowering CO

35
Q

β-blockers treat glaucoma by….

A

(mainly timolol)

diminishing intraocular pressure

36
Q

β-blockers treat migraine by….

A

given prophylactically for prevention

37
Q

β-blockers treat hyperthyroidism by….

A

blunts SNS stimulation that occurs in hyperthyroidism

38
Q

β-blockers treat angina pectoris by….

A
  • dec O2 requirements in heart muscle

- used only in CHRONIC management of stable angina, no acute use

39
Q

β-blockers treat AFib by….

A

controlling ventricular contraction rate

40
Q

β-blockers treat MI by….

A

protective effect on myocardium

41
Q

β-blockers are the common or preferred drug of choice for the following 3 symptoms / conditions….

A
  • prevent bleeding from esophageal varices in cirrohosis (nonselective β-blockers: propanolol, nadolol)
  • performance anxiety
  • essential tremor via postural / action tremors
42
Q

list the 4 general adverse effects of β-antagonists

A
  • bronchoconstriction (non-selective, use selective β1-blockers in COPD/asthma)
  • hypoglycemia (non-selective, use selective β1-blockers in DM)
  • lipid metabolism (inc TG, reduce HDL)
  • CNS effects
43
Q

describe hypoglycemia in terms of β-blocker use

A
  • non-selective β-blockers, use selective for β1
  • blockade of β2 receptors in liver impairs hypoglycemia recovery in insulin dependent diabetics
  • they will mask tachycardia seen in hypoglycemia (an important warning sign)
44
Q

describe the adverse effects of β-blockers on lipid metabolism

A

(both non-selective and selective β1 blockers; usually unaffected with labetalol, pindolol)

  • prevents release of free FAs from adipocytes
  • inc TG, dec HDL
45
Q

describe the adverse CNS effects with use of β-blockers

A
  • sedation
  • dizziness
  • lethargy, fatigue
46
Q

what are the 2 main warnings / precautions taken with β-blocker use and why

A
  • do not withdraw abruptly; particularly with CAD patients
  • gradually taper on and off to avoid acute tachycardia, HTN, ischemia

-this is due to up-regulation of β-receptors, w/o blockers the normal effects would overshoot

47
Q

list the 4 different ANS receptors in the eye and their associated functions

A
  • α1: pupillary dilator / radial muscle in iris, mydriasis
  • M3: pupillary constrictor / sphincter muscle in iris, miosis
  • M2: ciliary muscle, lens adaptation (contraction for near, relaxation for far)
  • β2: ciliary epithelium, aqueous humor production
48
Q

describe the iris muscles

A
  • Radial (pupillary dilator) muscle responds with α1 receptor, contraction pulls iris out => mydriasis
  • Sphincter (pupillary constrictor) muscle responds to M3, contractions squeezes iris => miosis
49
Q

what are the muscarinic effects on the eye (+ uses)

A
  • miosis
  • ciliary muscle contraction for near sight
  • facilitates aqueous humor outflow into canal of Schlemm –> reduces intraocular pressure in glaucoma
50
Q

what are the adrenergic effects and effects of blocking adrenergic receptors in the eye

A
  • Stimulation: mydriasis, facilitates aqueous humor secretion (NO cycloplegia)
  • Blocking: miosis, less aqueous humor secretion –> reduces intraocular pressure in glaucoma

RCS (29 decks)

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