Brainscape's Knowledge GenomeTM

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


See full index

PHARMACOLOGY > CHAPTER 6: ADRENERGIC AGONISTS > Flashcards

CHAPTER 6: ADRENERGIC AGONISTS Flashcards

direct acting, indirect acting, mixed acting, beta specific, and alpha specific

1
Q

catecholamines vs. non-catecholamines

A

catecholamines: sympathomimetic amines that contain 2 OH on benzene rings
- high potency
-rapid inactivation by COMT
- poor penetration into CNS

non-catecholamines: lack catechol group
- poor substrate for MAO—> prolonged duration of action
- greater access to CNS

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

how does the affinity for B2 receptors increase?

A

as the group on the amine nitrogen gets larger, the affinity increases

ex: isoproterenol has more methyl groups than epinephrine on the amine

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

what is a natural endogenous drug? which drugs are natural endogenous drugs?

A
  • naturally made in the body
  • epinephrine and norepinephrine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

mechanism of action: adrenergic agonists
- direct
- indirect
- mixed action

A

DIRECT: directly on a and B receptors
-epi, NE, isoproterenol, phenylepi

INDIRECT: block uptake of NE or ENHANCE release of NE from vesicles
- amphetamine, cocaine, tyramine

MIXED: mixed activity, acts both directly and indirectly
- ephedrine, pseudoephedrine

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

effect of adrenergic agonists on: HEART

A
  • inotropic effect
  • chronotropic effect
  • dromotropic effect
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is inotropic effect? pos and neg?

A
  • contractility of myocardium, depends on ions to contract

positive: drug increases strength of contractility
negative: drug dec strength of contractility

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

what is chronotropic effect? pos and neg?

A
  • rate of contraction

positive: drug inc rate of contraction
negative: drug dec rate of contraction

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

what is dromotropic effect? pos and neg?

A
  • rate of condution through AV node/ how fast the electrical signal goes to allow AV contraction
    dromo=circuit

pos: drug inc rate of conduction
neg: drug dec rate of conduction

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

diastolic vs. systolic BP

A

systolic: contraction of vessels, a1 activation
diastolic: ventricular filling, BP slightly reduced, b2 receptors

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

EPINEPHRINE:
-mechanism of action (MOA)

A

-interacts with BOTH a and B
receptors
both receptors still engaged, both effects stimulated, but BALANCE each other

-LOW DOSES: B effects on vascular system (vasodilation)
-HIGH DOSES: a effects predominate (vasoconstriction)

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

epinephrine:
- actions

A

CARDIOVASC: inc cardiac output (B1)
RESPIRATORY: bronchodilation (B2)
HYPERGLYCEMIA: inc glycogenolysis in liver/ inc blood glucose (B2), inc release glucagon (B2), dec insulin release (a2)
LIPOLYSIS: stimulation B2 in adipose tissue

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

what does epinephrine do to peripheral resistance? inc or dec?

A

SLIGHTLY DECREASES peripheral resistance
why not increase? bc yes the alpha receptors are being activated (HIGH DOSE), BUT so are beta (LOW DOSE) so periph resistance will still be decreased.

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

epinephrine:
-therapeutic uses/indications

A
  • bronchospasm
  • anaphylactic shock
  • cardiac arrest
  • local anesthetics
    - ADJUVANT to induce vasoconstriction
    - allows prolonged anesthetic effect at area of
    administration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

epinephrine:
- pharmacokinetics

A
  • RAPID onset
  • BRIEF duration of action (rapid degradation)
    ROUTES: IM anaphylaxis, IV emergencies, SC, endotracheal, inhalation

RAPIDLY metabolized by MAO and COMT enzymes, metabolites excreted in urine

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

epinephrine:
- adverse effects

A

CNS: anxiety, fear, tension, headache, tremor
CV: cardiac arrhythmias (especially if receiving DIGOXIN-cardiac disease drug)
- pulmonary edema due to inc afterload caused by vasoconstrictive properties of the drug
- inhalation anesthetics sensitize heart, lead to tachycardia

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

NOREPINEPHIRNE (NE):
- MOA

A
  • neurotransmitter, NE stimulates ALL adrenergic receptors
  • a receptor most affected in therapeutic doses
    inc affinity for a1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

norepinephrine:
- actions

A

little B1, NO B2
CARDIOVASCULAR:
- intense vasoconstriction (a1)
- baroceptor reflex/ vagal stimulation:
inc peripheral resistance, sends a message to brain that BP increased, response is REFLEX bradycardia

  • tachycardia with atropine pretreatment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

norepinephrine:
- therapeutic uses/indications

A
  • septic shock (last stage of sepsis)
19
Q

what is septic shock?

A

the last stage of sepsis, there is a generalized infection in the body w/ extremely low BP

  • NE will inc the BP in this type of patient
20
Q

norepinephrine:
- pharmacokinetics

A
  • RAPID onset via IV (1-2 min DOA)
  • metabolized by MAO and COMT, urine excretion
21
Q

norepinephrine:
- adverse effects

A
  • CNS disturbances
  • cardiac arrhythmias
  • pulmonary edema
  • blanching to necrosis of skin IF extravasation occurs
22
Q

what is extravasation?

A

veins constrict at the site of injection, and fluid (drug or vesicant fluids) leaks from vein into surrounding tissue

23
Q

ISOPROTERENOL:
- MOA

A
  • stimulates BOTH B1 and B2
  • non-selectivity is a DISADVANTAGE/ rarely used therapeutically
24
Q

isoproterenol:
- actions

A

CV: inc HR, contractility, and cardiac output (B1)
- dilate arterioles of skeletal muscle (B2)—->
DEC peripheral resistance (vasodilation)

RESPIRATORY: potent bronchodilator (B2)

25
Q

isoproterenol:
- adverse effects

A

similar to B-receptor related side effects of EPINEPHRINE

26
Q

DOPAMINE:
- MOA

A

can activate a and B
- HIGH DOSE: vasoconstriction (a1)
- LOW DOSE: stimulate B1 cardiac receptors

  • D1 and D2 dopaminergic receptors: in peripheral mesenteric and renal vasc beds—-> VASODILATION, inc blood flow
  • D2 on presynaptic adrenergic neurons, activation interferes w NE release
27
Q

dopamine:
- actions

A
  • CV (pos inotropic and chronotopic)
  • renal and visceral—> INC blood flow to kidneys and viscera
28
Q

dopamine:
- therapeutic uses/indications

A
  • cardiogenic shock and septic shock
  • hypotension
  • severe congestive heart failure
29
Q

dopamine:
- pharmacokinetics

A

rapidly metabolized by MAO and COMT enzymes

30
Q

dopamine:
- adverse effects

A

SNS stimulation due to overdose
- short-lived effects: nausea, hypertension, arrhythmias

31
Q

ALPHA specific direct-acting:
actions and list which drugs

A
  • therapeutic effects from stimulation of a receptors within SNS
  • phenylephrine, midodrine, clonidine, oxymetazoline
32
Q

alpha specific: phenylephrine

A
  • primarily a1
  • cold and allergies, supraventricular tachycardia, hypotension
33
Q

alpha specific: midodrine

A
  • primarily a1
  • orthostatic hypotension
    ( when changing body position, you feel dizzy, hard time adjusting BP, pressure inc in vessels)
34
Q

alpha specific: clonidine

A
  • centrally on a2 (presynaptic rec, dec NE, dec SNS)
  • hypertension, withdrawal symptoms from opiates and benzodiazepines
35
Q

alpha specific: oxymetazoline

A
  • BOTH a1 and a2
  • nasal congestion, eye redness
36
Q

BETA specific direct acting:
SABAs and LABAs

A

SABAs: short-acting B2 agonists
LABAs: long-acting B2 agonists

37
Q

SABAs: list which, indications, adverse effects

A

albuterol, metaproterenol, terbutaline
- manage acute asthma symptoms
- adv effects: tremor, tachycardia (B1), anxiety

38
Q

LABAs: list which, indications

A

salmeterol, formoterol, indacaterol
- manage respiratory diseases (asthma, COPD)

39
Q

INDIRECT ACTING: MOA, list which

A

MOA: release, inhibit reuptake, or inhibit degradation of epinephrine OR norepinephrine
-amphetamine, cocaine, tyramine

40
Q

indirect-acting: amphetamine

A
  • inc non vesicular release of catecholamines (dopamine, NE) from nerve terminals
  • INC BP (a1), stimulate B1 effects on heart
41
Q

indirect-acting: cocaine

A
  • block NE transporter needed for cellular reuptake of NE into adrenergic neuron by staying in synaptic cleft
  • enhance SNS activity
42
Q

indirect-acting: tyramine

A

found in fermented food (cheese and wine)

43
Q

MAOA and MAOB- tyramine metabolism in small intestine

A
44
Q

MIXED ACTION

A

ephedrine:
- not catechol, poor COMT and MAO substrate, LONG duration of action
- good absorption orally, penetrate CNS
- unchanged in urine
- raise systolic and diastolic BP by vasoconstriction/cardiac stim, bronchodilation
- stimulate CNS mildly: alertness, dec fatigue, prevent sleep

pseudoephedrine:
- not catechol, poor COMT and MAO substrate, LONG duration of action
- fewer CNS effects
- incomplete hepatic metabolism before elimination in urine
- used orally, treat nasal and sinus congestion, congestion of eustachian tubes
(vessels are constricted=less congestion)

PHARMACOLOGY (29 decks)

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