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Adrenergic Flashcards

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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
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)

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
Study These Flashcards
A

Phenylephrine

25
``` 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 ```
Milirone
26
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
Vasopressin
27
What is the drug of choice for pregnant women to increase bp?
Methyldopa
28
Drop BP by reducing sympathetic tone Effective antihypertensive Class effect = sedation
Alpha 2 selective agonists
29
Rapid CNS uptake Stimulant Effects mediated by NE and DA
Amphetamine
30
``` Amphetamine variant Similar effect and abuse potential Use: ADD-spectrum Caution - UDS ```
Methylphenidate (Ritalin)
31
``` Psychostimulant Totally different from amphetamine NE, DA reuptake inhibition NE, DA, 5-HT3, glutamate increase; GABA decrease Use: narcolepsy ```
Modafinil (Provigil)
32
``` Selective NE reuptake inhibition No CV effects Clonidine-like effect Use: ADD ```
Straterra
33
``` Local anesthetic, peripheral sympathomimetic Reuptake inhibition, especially dopamine Excited delirium Avoid concurrent beta- blockade Use: epistaxis ```
Cocaine
34
``` _____ agonism Key to management of acute asthma Common “allergy” in dentistry7.9% Triggered by allergens, stress, food, drugs Angioedema = similar but different ```
Beta 2 agonism
35
The following drugs are ______: Albuterol Levalbuterol Terbutaline
Short term control Short acting beta agonists (SABA)
36
``` 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 ```
Longer term control | Long acting beta agonists (LABA)
37
``` 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 ```
Asthma pts
38
``` 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) ```
Asthma pts
39
What drugs should be avoided for asthma pts?
No ASA or NSAIDS Avoid histaminic drugs Avoid antihistamines Avoid cholinergics
40
______ alpha antagonists Concentration dependent Duration dependent on t1/2
reversible
41
______ alpha antagonists Body has to generate new receptors Drug effect can persist even after drug is cleared -Phenoxybenzamine
Irreversible
42
``` _____ drugs pharm effects Cardiovascular α1 blockade blocks vasoconstriction Orthostatic hypotension Other Miosis, nasal stuffiness Decreased resistance to urinary flow ```
Alpha blockers
43
____ is the most common issue with alpha blockers | -vasoconstriction is inhibited
Orthostatic hypotension
44
``` Blocks α1 and α2 Decreased PVR and cardiac stimulation Can lead to CV adverse reactions - Uses: treats extravasated drugs ```
Phentolamine
45
``` What 3 drugs? Selective α1 Arterial and venous vascular smooth muscle relaxation and prostate relaxation 50% bioavailabilityFirst pass effect Uses: BPH ```
Prazosin Terazosin Doxazosin
46
``` Competitive α1 blocker High bioavailability More specific to prostate Less orthostatic hypotension ```
Tamsulosin
47
Antagonize effects of catecholamines and beta agonists Differ in affinity for β1 and β2 β1 specificity decreases as dose increases End in -lol
Beta blockers
48
What are the 6 B1 specific beta blockers?
``` Betaxolol Esmolol Acebutolol Metoprolol Atenolol Nebivolol ```
49
``` Beta-1 selective Short t1/2 Quick onset Requires central line for administration Great for tight BP control ```
Esmolol
50
``` 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 ```
Labetalol
51
T/F: for cocaine users, don't use beta blockers
True
52
____ specific drugs are safer for asthmatic pts?
B1
53
Should you use non-specific B-blockers and epi on asthmatic pts?
No

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