Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

MedChem > LaVoie - medchem Adrenergic pt. 2 > Flashcards

LaVoie - medchem Adrenergic pt. 2 Flashcards

1
Q

What compound has the greatest alpha 1 potency, a primary amino group, and has both alpha 1 and beta 1 agonist activity?

A

NE

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

Rank potency of alpha 1 agonists

A

NE = > E&raquo_space; ISO

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

Rank potency of Beta 1 agonists

A

E > ISO > NE

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

Rank potency of Beta 2 agonists

A

ISO > E > NE

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

Primary amines:

A

Have both alpha + beta agonist activity

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

Secondary amines:

A

Have Beta agonist activity, with larger alkyl on the N (particularly B1 agonist activity). If the alkyl group has >3 C units (like ISO), then it will have high B2 agonist activity. There are some exceptions, like dobutamine

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

Tertiary amines:

A

Have poor agonist activity. However, they may have NE releasing (NER) activity

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

Imidazoline:

A

Can have alpha agonist + alpha antagonist activity. Has a pKb = 3, pKa = 11 - so at physiological pH (pH = 7) imadazoline will be highly protonated and will NOT penetrate the BBB well

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

Alpha 1 agonists. Draw structure and state what X stands for -

A 
X = H: Xylometazoline; Otrivin
X = OH; Oxymetazoline; Afrin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Alpha-Adrenoreceptors high –> low affinity

A

NE > E > ISO

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

Beta-Adrenoreceptors high –> low affinity

A

ISO > E > NE

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

Alpha-2 receptors:

A
  • Located on presynaptic neuron site
  • When NE binds to Alpha-2 receptor, A2 will stop production of cAMP –> inhibit release of NE
  • Controls NE release/activity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Alpha-1 receptors:

A
  • Located on postsynaptic neuron site

- When NE binds to A1 receptors, it will increase second messengers in the neuron, increasing/potentiating NE signaling

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

A1 - receptor activity (table):

A
  • Vasoconstriction
  • Increase peripheral resistance
  • Increase BP
  • Mydriasis
  • Increase closure of internal sphincter of bladder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

A2-receptor activity (table):

A
  • Inhibit NE release
  • Inhibit ACh release
  • Inhibit insulin release
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

B1-receptor activity (table):

A
  • Tachycardia (increase HR)
  • Lipolysis
  • Increase myocardial contractility (increase heart force)
  • Increase renin release (this + increase HR + HF = increase BP)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

B2-receptor activity (table):

A
  • Vasodilation
  • Decrease peripheral resistance
  • Bronchodilation
  • Increase muscle + liver glycogenesis
  • Increase glucagon release
  • Relax uterine SM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Adrenaline, Noradrenaline

A
  • Alpha 1: stimulating SM contraction
  • Alpha 2: Stimulate SM contraction, inhibit NTS release
  • Beta: increase heart contractility, increase SM contraction (vasodilation + bronchodilation), increase glycogenolysis to increase blood glucose levels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

A1 receptors + actions at those tissues

A
  • Most vascular smooth muscle (innervated) - contraction

- Prostate - Contraction

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

A2 tissue + actions

A
  • Adrenergic + cholinergic terminals - inhibit release of NTS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

B1 Tissue + actions

A
  • Dominantly heart - increase HR + heart force
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

B2 tissue + actions

A
  • Respiratory, uterine, and vascular SM - Promotes SM relaxation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

B3 tissue + actions

A
  • Fat cells - increases lipolysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

D1 cells

A
  • SM - dilation of renal blood vessels

- Dopaminergic receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Phenylephrine: | Draw structure
- Has Beta-hydroxyl group + monophenol --> is direct-acting agonist - Small group on amino group --> A1 receptor agonist
26
Ephedrine: | Draw Structure
- Has Beta-hydroxyl group --> Direct-acting Beta Agonist - No phenol --> NE releaser (NER) - Have mixed effect
27
B-receptor affinity; compounds that have affinity from highest to lowest
- Larger alkyl groups on amino group = greater affinity for Beta receptors - ISO > E > NE
28
Dopamine
- A1 direct-acting agonist
29
Epinephrine for pulse, BP, and peripheral resistance
- Increases heart force + rate - bc B1 agonist - Increases systolic pressure, Decreases diastolic pressure - Peripheral resistance Decreases - indicates it also acts on B2 receptors
30
NE for pulse rate, BP, and peripheral resistance
- Increase in systolic + diastolic pressure = bc potent A1 agonist - Increase in peripheral resistance significantly - potent A1 agonist - Decrease in heart force + rate = works on carotid baroreceptors in the heart, which are reflex bradycardia receptors that counteract (or try to counteract) high BP by lowering it. So will try to lower the BP that peripheral resistance + increases in BP is causing
31
ISO for pulse rate, BP, and peripheral resistance
- Decreases peripheral resistance (strong vasodilator) - potent B2 agonist - Increase in heart rate + contractility - even though it is a strong vasodilator, it causes an increase in heart contractility and HR, which increases systolic pressure - Increase in systolic pressure, decrease in diastolic pressure - decrease in diastolic pressure bc of decrease in peripheral resistance - Stimulates both B1 + B2, but B2 activity is dominant - Also causes broncho-dilation
32
Dopamine
- B1 stimulant (agonist) - Acts on dopaminergic receptors - Increases HR + heart force = increases CO - Causes dilation of BVs in kidneys
33
Pathway to make E?
Tyrosine --> Dopa --> Dopamine --> NE --> E
34
Major pathway for inactivation of E?
COMT + MAO A
35
Major pathway for inactivation of NE?
MAO A + COMT
36
Major pathway for inactivation of Dopamine?
MAO B + COMT
37
Use of LABAs in asthma?
LABA MONOtherapy --> Contraindicated for asthma: increases asthma-induced death LABA+ICS combo therapy --> Approved for asthma + COPD treatment
38
Advair Diskus
Fluticasone (ICS) + Salmeterol (LABA)
39
Advair HFA
Fluticasone (ICS) + Salmeterol (LABA)
40
Airduo Respiclick
Fluticasone (ICS) + Salmeterol (LABA)
41
Breo Ellipta
Fluticasone (ICS) + Vilanterol (LABA)
42
Dulera
Mometasone (ICS) + Formoterol (LABA)
43
Symbicort
Budenoside (ICS) + Formoterol (LABA)
44
Anoro Ellipta
Vilanterol (LABA) + Umeclinidium Br (LAMA)
45
Trellegy Ellipta
Vilanterol (LABA) + Umeclinidium Br (LAMA) + Fluticasone (ICS)
46
Brevo Ellipta
Fluticasone Furoate (ICS) + Vilanterol (ICS)
47
Breztri
Vilanterol (LABA) + Umeclinidium Br (LAMA) + Budenoside (ICS)
48
LABA monotherapy for long-term control of asthma
CONTRAINDICATED - can never be used alone, esp for long-term persistent asthma NOT approved for treating acute asthma exacerbations nor acute asthma symptoms
49
LABA + ICS use?
Approved for long-term control use for asthma + COPD
50
Should LABAs be added to treatment regimen for pts who have adequately controlled asthma using low-medium dose ICS?
No - contraindicated
51
When should LABAs be added onto therapy for asthma pts?
When pts are currently taking a long-term asthma control medication like ICS but can't control their asthma
52
Do you ever stop using LABAs once on it? And if you do, when?
Yes, at some point pts can stop using LABAs. Once asthma control is reached and achieved, perform regular check-up intervals and consider stepping down (discontinue LABA) without losing asthma control. Continue pt on long-term asthma control medication (ICS)
53
When are SABAs used? Examples of SABAs
- Albuterol + Levalbuterol - Drug of choice as quick reliever for asthmatic symptoms and asthma exacerbations; helps prevent EIB - More PRN
54
For peds pts (adolescents and children), if a LABA is added to their ICS, what is recommended?
It is recommended to have them use a combo product to increase adherence to regimen
55
What does the FDA say about LABA + ICS?
If the guidelines for LABA uses and the labels are followed, it improving asthma symptoms and the benefits significantly outweigh the risks in reducing # of severe exacerbations and death from asthma
56
Pseudoephedrine: dose, DOA, formulation
PO - 60mg - q4-6hrs PO-SR - 120mg - 12 hrs --> long DOA Very effective orally
57
Phenylephrine: dose, DOA, formulation
Topical - 1-2 sprays or a few drops - q3-4hrs Recently used orally
58
Epinephrine: dose, DOA, formulation
Topical spray ONLY | - Max 1ml/15min
59
Oxymetazoline: dose, DOA, formulation
Topical spray - 2-3 sprays - BID --> Long DOA
60
Xylometazoline: dose, DOA, formulation
Topical drops - 2-3 sprays - q8-10 hrs --> Long DOA
61
Propylhexedrine: dose, DOA, formulation
Topical inhalant - 2 inhalations through each nostril - For PRN use; avoid xs use
62
Tetrahydrozoline: dose, DOA, formulation
Topical drops - 2-4 drops - q3hrs Topical spray - 3-4 sprays - q3hrs
63
Bioavailability of phenylephrine vs. pseudoephedrine
Phenylephrine - undergoes major 1st pass metabolism; only 63% bioavailability Pseudoephedrine - 90% bioavailability
64
Ephedrine: dose, DOA, formulation
Topical drops - 2-3 drops - q4hrs
65
Desoxyephedrine: dose, DOA, formulation
Topical inhalant - 2 inhalations each nostril - q2hrs
66
Naphazoline
Topical drops - 2 drops - q3hrs
67
NE as an ___ causes ___
a1 agonist; mydriasis
68
Anti-muscarinic vs. B3 agonists for OAB MOA:
Anti-muscarinic: blocks M3 receptors, preventing muscle contraction of bladder. Delays need for voiding (decreases urinary frequency + urgency) B3 agonist: binds to B3 receptors on detrusor muscles and causes relaxation of bladder muscle. Increases urine capacity. Delays need for voiding (decreases urinary frequency + urgency)
69
Onset + DOA of bronchodilation for: E, ISO, albuterol, salmeterol, metaproterenol, terbutaline
E, ISO: quick onset, short DOA - have catechol, so quickly inactivated by COMT Albuterol: quick onset, short DOA (Albuterol > ISO >> E). SABA Salmeterol: slow onset, long DOA. LABA Metaproterenol, terbutaline: quick onset, short DOA (Albuterol > Metaproteronl > terbutaline > ISO >> E)
70
Side effects of adrenergic agonists
``` Arrhythmias Headaches Hyperactivity Insomnia - seen w/ pseudo bc of CNS stimulation Nausea Tremors ```
71
Pheochromocytoma
- Rare tumor of adrenal gland | - Xs release of NE + E --> high BP
72
Raynaud's disease
- Rare BV disorder affecting fingers + toes - Poor blood circulation to extremities - When cold or stressed: BVs narrow --> skin at surface turns white + blue
73
Adrenergic alpha 1 antagonists effects
- a1 abundant on prostate + bladder neck - Affects SM tone mediated by sympathetic NS of A1 receptors - Block a1 receptors: relaxes bladder neck and prostate, allowing better urinary flow and reduce symptoms for BPH pts
74
Alpha antagonist side effects
- Dizziness - Orthostatic hypotension (lose reflex vasoconstriction when standing) - Headache - Reflex tachycardia (especially with non-selective alpha blockers) - Nasal congestion (dilation of mucosal arterioles)
75
Nonselective alpha blockers
- More reflex tachycardia than selective a1 blockers - Phentolamine relaxes systemic vasculature --> hypotension - Hypotension sensed by baroreceptor --> increase sympathetic signaling --> increase NE release - B3 receptors increase HR + force --> offset drop in BP - Also inhibits A2 receptors (manages presynaptic negative feedback for NE release) --> less NE regulation --> further BP drop
76
All quinazoline A1 antagonists:
Cause vasodilation and increases in HR. eventually attenuates to returns to normal after few wks of treatment
77
Route of elimination by liver + kidneys for antagonists:
Liver: Propranolol, Carvedilol, Metoprolol, Betaxolol, Labetolol, penbutolol > Timolol Both Liver + kidney: Pindolol, Bisprolol, Nebivolol Kidney: Atenolol, Nadolol, Sotalol, Carteolol > Acebutolol

MedChem (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions