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Pharmacology > Adrenergic > Flashcards

Adrenergic Flashcards

1
Q 
\_\_\_\_\_\_ nervous system
-Regulates all organ systems and blood pressure
Organ systems, blood pressure
Hormone vs. neurotransmitter
Adrenal medulla
A

Sympathetic nervous system

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2
Q

Does NE get broken down right away?

A

No; ACh does

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3
Q

What enzyme reuptakes NE in pre-synaptic scenarios?

A

Monoamine oxidase

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4
Q

What enzyme reuptakes NE in postC-synaptic scenarios?

A

Catechol-O-Methyltransferase

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5
Q

____ sympathetic agonists:

Route
Affinity
Expression of receptor subtypes

A

Direct

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6
Q

____ sympathetic agonists:

Catecholamine displacement
Amphetamines
Decreased NE clearance
Reuptake inhibition

A

Indirect

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7
Q 
\_\_\_\_ receptors:
α1 α2 
β1  β2 
Dopamine
Sympathomimetic vs sympatholytic
A

Adrenergic receptors

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8
Q 
\_\_\_\_\_\_ receptors
Can be downregulated / desensitized
Congestive Heart Failure (CHF)
Acidosis
Hypoxia
A

Adrenergic receptors

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9
Q 
Vasoconstriction
Blood pressure increased
Mydriasis
Urinary sphincter constriction
Peripheral vascular beds
Excitatory
A

Alpha 1

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10
Q 
In the vasculature
Inhibition of NE and ACh 
Decreased sympathetic tone
Decreased BP
Sedation
Inhibitory
A

Alpha-2

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11
Q 
Cardiac excitation
Increased rate, contractility, 
conduction
-Excitatory
-Heart
A

Beta-1

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12
Q

Are beta and alpha 1s excitatory or inhibitory?

A

Excitatory

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13
Q

Are beta and alpha 2s excitatory or inhibitory?

A

Inhibitory

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14
Q 
Bronchodilation
Smooth muscle relaxation
Skeletal muscle vasodilation
Decreased vascular resistance
-Inhibitory
A

B2

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15
Q 
Resistance vessel vasodilation
Renal
Splanchnic
Coronary
Cerebral
A

Dopamine

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16
Q

What are the endogenous catechloamines?

A

epi
NE
dopamine

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17
Q

Where does dopamine get released from?

A

Brain and kidney

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18
Q

Where does NE get released from?

A

Sympathetic nerve endings

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19
Q

Where does epi get released from?

A

adrenal medulla

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20
Q 
Endogenous
Primary neurotransmitter at sympathetic nerve endings
Maintenance of sympathetic tone
BP 
No cardiac output changes
Minimal chronotropic changes
Increased coronary blood flow
Caution with prolonged infusions
Uses:
- increase bp in super sick pts
A

NE

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21
Q 
Endogenous
Only released by adrenal medulla
Stress preparation
coronary blood flow
Caution prolonged infusions
Uses:
-B2 action in low dose for anaphylaxis
-Vasoconstriction in nerve block
A

Epi

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22
Q 
Endogenous
NE precursor
Dose-specific effects
Low dose (0.5 – 3 mcg/kg/min)
Intermediate (3 – 10 mcg/kg/min)
High (10 – 20 mcg/kg/min)
Uses:
-Increases bp and significantly increases HR
-Increase risk of ventricular arrthmias
A

Dopamine

23
Q

Synthetic
Augments myocardial contractility
Dose-dependent increase in stroke volume (SV) and cardiac output (CO)
Alpha agonist AND antagonist
Beta-mediated vasodilation (low dose)
High dose increases myocardial O2 consumption
Uses:
-cardiac stress test
-INcrease contraction with smooth muscle dilation (HF pts)

A

Dobutamine

24
Q 
Synthetic
All alpha, no beta
Not a catechol derivative, not 
metabolized by COMT
Can lead to baroreceptor-mediated 
decrease in HR
Push dose pressor
Uses:
-increases bp
-Only taken up in pre-synaptic neuron by MOT
A

Phenylephrine

25
Q 
Phosphodiesterase-3 inhibitor
Inhibits breakdown of cAMP
Positive inotropy
Potent vasodilator
Increased diastolic relaxation
Reduced preload and afterload
Good in the setting of receptor 
downregulation
Uses:
- increase force of contraction
-MOre likely to elicit B2 effect than dobutamine
-More likely to cause hypotension
A

Milirone

26
Q

AKA: antidiuretic hormone
Stored in posterior pituitary
Released when plasma osmolality increases or BP drops
V1 and V2 receptor agonist
Neutral to negative impact on CO
Dose dependent SVR and vagal tone increase
Not affected by pH
Uses:
- Decreases urination to get osmolarity of blood back to normal

A

Vasopressin

27
Q

What is the drug of choice for pregnant women to increase bp?

A

Methyldopa

28
Q

Drop BP by reducing
sympathetic tone
Effective antihypertensive
Class effect = sedation

A

Alpha 2 selective agonists

29
Q

Rapid CNS uptake
Stimulant
Effects mediated by NE and DA

A

Amphetamine

30
Q 
Amphetamine variant
Similar effect and abuse 
potential
Use: ADD-spectrum
Caution - UDS
A

Methylphenidate (Ritalin)

31
Q 
Psychostimulant
Totally different from 
amphetamine
NE, DA reuptake inhibition
NE, DA, 5-HT3, glutamate 
increase; GABA decrease
Use: narcolepsy
A

Modafinil (Provigil)

32
Q 
Selective NE reuptake 
inhibition
No CV effects
Clonidine-like effect
Use: ADD
A

Straterra

33
Q 
Local anesthetic, peripheral 
sympathomimetic
Reuptake inhibition, 
especially dopamine
Excited delirium
Avoid concurrent beta-
blockade
Use: epistaxis
A

Cocaine

34
Q 
\_\_\_\_\_ agonism
Key to management of acute asthma 
Common “allergy” in dentistry7.9%
Triggered by allergens, stress, food, drugs
Angioedema = similar but different
A

Beta 2 agonism

35
Q

The following drugs are ______:
Albuterol
Levalbuterol
Terbutaline

A

Short term control
Short acting beta agonists
(SABA)

36
Q 
The following are \_\_\_\_:
Formoterol
Salmeterol
Blocks receptors 12-18h
NOT FOR ACUTE ATTACKS
Have to be used with steroids
Advair = salmeterol + fluticasone
Symbicort = formoterol + budesonide
Dulera – formoterol + mometasone
A

Longer term control

Long acting beta agonists (LABA)

37
Q 
For \_\_\_\_ pts: 
Minimize likelihood of 
exacerbation
Talk to your patient to learn 
their management strategies
Instruct pt. to bring albuterol 
inhaler to all appointments
Decrease stressors
A

Asthma pts

38
Q 
For \_\_\_\_ pts: 
Drug considerations
No ASA or NSAIDS
Avoid histaminic drugs
Avoid antihistamines
Avoid cholinergics
In an emergency
Supplemental O2
Consider epinephrine
0.3 mg IM (or use EpiPen)
A

Asthma pts

39
Q

What drugs should be avoided for asthma pts?

A

No ASA or NSAIDS
Avoid histaminic drugs
Avoid antihistamines
Avoid cholinergics

40
Q

______ alpha antagonists
Concentration dependent
Duration dependent on t1/2

A

reversible

41
Q

______ alpha antagonists
Body has to generate new receptors
Drug effect can persist even after drug is cleared
-Phenoxybenzamine

A

Irreversible

42
Q 
\_\_\_\_\_ drugs pharm effects
Cardiovascular
α1 blockade blocks 
vasoconstriction
Orthostatic hypotension
Other
Miosis, nasal stuffiness
Decreased resistance to 
urinary flow
A

Alpha blockers

43
Q

____ is the most common issue with alpha blockers

-vasoconstriction is inhibited

A

Orthostatic hypotension

44
Q 
Blocks α1 and α2
Decreased PVR and 
cardiac stimulation
Can lead to CV adverse 
reactions
- Uses: treats extravasated drugs
A

Phentolamine

45
Q 
What 3 drugs?
Selective α1
Arterial and venous vascular smooth muscle relaxation and prostate relaxation
50% bioavailabilityFirst pass effect
Uses: BPH
A

Prazosin
Terazosin
Doxazosin

46
Q 
Competitive α1 blocker
High bioavailability
More specific to prostate
Less orthostatic 
hypotension
A

Tamsulosin

47
Q

Antagonize effects of catecholamines and beta agonists
Differ in affinity for β1 and β2
β1 specificity decreases as dose increases
End in -lol

A

Beta blockers

48
Q

What are the 6 B1 specific beta blockers?

A 
Betaxolol
Esmolol
Acebutolol
Metoprolol
Atenolol
Nebivolol
49
Q 
Beta-1 selective
Short t1/2 
Quick onset
Requires central line for 
administration
Great for tight BP control
A

Esmolol

50
Q 
Beta and alpha blockade
3:1 oral
7:1 IV
Dose dependent duration of 
action
up to 20 hours
- minimum effect on alpha
-for cocaine users, dont use beta blockers
A

Labetalol

51
Q

T/F: for cocaine users, don’t use beta blockers

A

True

52
Q

____ specific drugs are safer for asthmatic pts?

A

B1

53
Q

Should you use non-specific B-blockers and epi on asthmatic pts?

A

No

Pharmacology (12 decks)

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