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Pharm > Test 2 Lectures 2-4 > Flashcards

Test 2 Lectures 2-4 Flashcards

1
Q

Which is the craniosacral vs. thoracolumbar division of the spinal cord? Which has longer post- or pre-ganglionic neurons?

A
  1. Sympathetic - thoracolumbar division (short pre-ganglionic cells and long-post
    ganglionic cells)
  2. Parasympathetic - craniosacral division (long pre-ganglionic cells and short
    post-ganglionic cells)
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2
Q

A .Pre-ganglionic fibers release __________.
B. Post-ganglionic parasympathetic fibers release _________.
C. Post-ganglionic sympathetic fibers release _________.
D. Adrenal medulla releases _________and ________ (to a lesser extent) into
the circulation
E. Exceptions: Post-ganglionic sympathetic fibers that innervate sweat glands
and some skeletal muscle blood vessels that release _________.

A
  • ACh
  • ACh
  • NE
  • Epi, NE
  • ACh
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3
Q

Is accommodation regulated by symp or parasymp?

A

Parasymp

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4
Q

Describe the 4 autonomic influences on the eye (symp vs. parasymp and their function)

A

Dilator: constrict it to open the pupil (symp)
- Could prevent aqueous humor from draining effectively or to visualize eye
Sphincter contraction would release pressure (parasymp)
- Parasymp agonists help flatten iris–aqueous humor drainage
Ciliary mm. (parasymp)
- Helps change of lens to promote accommodation
- Also helps w/promoting drainage!
Ciliary epithelium (symp)
- Makes aqueous humor

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5
Q

How does sympathetic activation affect HR? (what currents are affected and how?) (what phase # does this take place during?)

A

Sympathetic activation increases inward calcium current and the funny current to promote faster spontaneous depolarization during phase 4 of sinoatrial node action potential and lower threshold for activation

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6
Q

How does sympathetic activation affect heart contractility?

A

Sympathetic activation also stimulates greater calcium influx into myocytes during depolarization culminating in greater contractile force of the heart.

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7
Q

What enzyme converts dopamine to NE in vesicles?

A

Dopamine beta-hydroxylase

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8
Q

What are the 3 routes of termination of an action potential in a sympathetic neuron?

A

1) re-uptake into nerve terminals or post-synaptic cell
2) diffusion out of synaptic cleft
3) metabolic transformation

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9
Q

Where are alpha-1 receptors expressed?

What are the effects?

A
  1. Most vascular smooth muscle
  2. Pupillary dilator muscle
  3. Contracts (^ vascular resistance)
  4. Contracts (mydriasis)
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10
Q

Where are alpha-2 receptors expressed?

What are the effects?

A
  1. Adrenergic and cholinergic nerve terminals (pre-synaptically)
  2. Some vascular smooth muscle (like alpha-1)
  3. Inhibits NT release
  4. Contracts (^ vascular resistance)
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11
Q

Where are beta-1 receptors expressed?

What are the effects?

A
  1. Heart
  2. Juxtaglomerular cells
  3. Stimulates rate and force
  4. Stimulates renin release
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12
Q

Where are beta-2 receptors expressed?

What are the effects?

A
  1. Respiratory, uterine, and vascular smooth muscles
  2. Somatic motor nerve terminals (voluntary muscle)
  3. Relaxation (unlike alpha-1/2)
  4. Causes tremor
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13
Q

Where are dopamine-1 receptors expressed?

What are the effects?

A
  1. Renal and other splanchnic blood vessels

1. Relaxes (reduces resistance)

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14
Q

Eye – activation of dilator muscle causes ___________ (mydriasis vs miosis), innervation of ciliary epithelium
regulates production of ____________.

A
  • mydriasis

- Aqueous humor

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15
Q

Constricting pupillary dilator muscle __________ drainage, while relaxation __________ drainage.

A
  • Prevents

- Promotes

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16
Q

Describe the pharmacological mechanism of action of alpha-1 adrenergic receptors produces smooth m. contraction.

A

Binding -> Gq -> PLC -> PIP2 -> DAG + (soluble) IP3 -> Ca2+ release -> smooth m. contraction

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17
Q

Describe the pharmacological mechanism of action of alpha-2 adrenergic receptors reduce presynaptic NT release.

A

Binding -> Gi -> inhibits AC/cAMP/PKA -> reduced P’lation of presynaptic N-type Ca2+ channel -> reduced Ca2+ release -> reduced NT release (presynaptically)

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18
Q

Describe the pharmacological mechanism of action of beta-1 adrenergic receptors produce their effects on the heart.

A

Binding -> Gs -> AC/cAMP/PKA -> increased Na+ (funny current) and P’lation of L-type Ca2+ channels -> increased sarcoplasmic Ca2+ storage + release -> chronotropy (SA node cells) and inotropy (cardiomyocytes)

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19
Q

Describe the pharmacological mechanism of action of beta-2 adrenergic receptors reduce smooth m. contraction in the uterus, bronchioles, and vascular smooth m.

A

Binding -> Gs -> AC/cAMP/PKA -> P’lates (and inhibits) MLCK -> reduced affinity for Ca/calmodulin -> decreased P’lation of myosin -> reduced smooth m. contraction.

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20
Q

Describe the pharmacological mechanism of action of alpha-2 adrenergic receptors produce peripheral vasoconstriction.

A

Binding -> Gi -> inhibits AC/cAMP/PKA -> decreased P’lation of MLCK -> increased affinity for Ca/calmodulin -> P’lation of myosin -> smooth m. contraction

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21
Q

What are the 3 endogenous ligands for adrenergic receptors?

A

NE, EPI and dopamine (DA)

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22
Q

Recall: what degrades each of the catecholamines (NE, epi, DA) after their release?

A

COMT: Epi, NE, DA
MAO: NE, DA

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23
Q

Give the relative affinity for the alpha1 adrenergic receptor of NE, EPI, and isoproterenol

A

Epi ≥ NE&raquo_space; isoproterenol (negligible binding)

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24
Q

Give the relative affinity for the alpha2 adrenergic receptor of NE, EPI, and isoproterenol

A

Epi ≥ NE&raquo_space; isoproterenol (negligible binding)

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25
Q

Give the relative affinity for the beta1 adrenergic receptor of NE, EPI, and isoproterenol

A

Isoproterenol > epi&raquo_space; NE

NE lacks ability to relax smooth m.

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26
Q

Give the relative affinity for the beta2 adrenergic receptor of NE, EPI, and isoproterenol

A

Isoproterenol > epi = NE

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27
Q

MAP =

A

CO x TPR

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28
Q

CO =

A

HR x SV

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29
Q

TPR has a predominant effect on __________ (systolic/diastolic) pressure, while CO has a predominant effect on ___________ (systolic/diastolic) pressure.

A
  • diastolic

- systolic

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30
Q

What adrenergic receptors does epi have affinity for?

A

alpha1, alpha2, beta1, beta2

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31
Q

What are the BP effects of epi at LOW doses? (explain)

What are the BP effects of epi at HIGH doses? (explain)

A
  • Epi has higher affinity for beta2 relaxing receptors (vs. alpha1 constrictors)
  • Therefore, TPR slightly decreases at low dose, decreasing BP
  • At high dose, there is still some beta2 receptor binding, but there are way more alpha1 (and alpha2) receptors
  • Leads to robust increase in TPR and hence, BP
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32
Q

What are the CO effects of epi at low and high doses? (explain)

A
  • Low dose: although TPR slightly decreases, increased Na+ (funny) and L-type Ca2+ channel release leads to increased Beta1 activation, increased chronotropy, as well as inotropy, leading to increased CO
  • High dose: further increase BP (due to alpha1/2 activation) leads to further increase in CO thru same mech as above
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33
Q

Briefly state the bronchiolar effects of epi and what receptor they are due to.

A
  1. Bronchodilation (beta2)

2. Decreased bronchial secretions (alpha1)

34
Q

Toxic effects of epi? (1)

A

Arrhythmia

35
Q

Therapeutic uses of epi? (3)

A
  • Anaphylaxis
  • Cardiac arrest
  • Bronchospasm
36
Q

What adrenergic receptors does NE have affinity for?

A

Alpha1, alpha2, beta1

37
Q

Is NE’s half-life long or short? How is it therefore administered?

A
  • Short half-life

- Give by controlled infusion.

38
Q

Explain the CV effects of NE.

A
  • Primarily alpha1 receptor activation, leading to vasoconstriction and increased TPR (*more than w/epi because there is no vasodilating beta2 activation)
  • Also inotropic and chronotropic effects due to beta1 activation
  • Large increase in TPR leads to baroreceptor reflex (sinuses) that slows HR, but still overall increase in MAP
39
Q

Toxicity of NE? (1)

A

Arrhythmia

40
Q

Therapeutic use of NE? (1)

A

Vasodilatory shock

41
Q

Contraindications of NE? (1)

A

Pre-existing ischemia

42
Q

What receptors does DA bind?

A

(Looks like NE, but also binds its own receptors)

- D1, D2, alpha1, alpha2, beta1

43
Q

Explain the physiological effects of DA at low, medium, and higher doses.

A
  • Low: D1 activated, decrease in TPR
  • Medium: Beta1 activated, increased contractility and HR
  • High: Alpha receptors activated, further increasing BP and TPR
44
Q

Dopamine:

Toxicity, therapeutic uses, and contraindications?

A
  • Tox: hypotension (at low infusion rates), ischemia (at high infusion rates)
  • Uses: Cardiogenic shock
  • Contra: Tachyarrhythmias
45
Q

What drug category is isoproterenol?
What degrades it?
Explain its effects.

A
  • Non-selective beta-adrenergic agonist
  • COMT
  • Peripheral vasodilation (beta2), diastolic
  • Transient increase in systolic BP due to positive inotropy and chronotropy (beta1, but offset by beta2 effects above)
  • Bronchodilation (beta2)
46
Q

Isoproterenol:

Toxicity, therapeutic uses, and contraindications?

A
  • Tox: Tachyarrhythmias
  • Uses: not often used
  • Angina w/arrhythmias
47
Q

What drug category is Dobutamine?
What degrades it?

Explain its effects.

A
  • Selective beta1-adrenergic receptor agonist
  • Rapidly degraded by COMT, must be infused
  • Increased CO
48
Q

Dobutamine:
Toxicity and therapeutic uses? (no contraindications)
Relative 1/2-life?

A
  • Tox: hypotension

- Uses: short-term tx for CHF (1/2-life 2-3 min) or cardiogenic shock

49
Q

What drug category are terbutaline and albuterol?

Explain their effects.

A
  • Selective beta2-adrenergic agonists

- Bronchodilation (+ uterine relaxation in late pregnancy)

50
Q

Terbutaline and albuterol:

Toxicity and therapeutic uses? (no contraindications)

A
  • Tox: tachycardia (B1), muscle tremor (B2), tolerance (B2)

- Uses: bronchospams, chronic obstructive airway dz tx

51
Q

What drug category is phenylephrine?
Explain its effects.
1/2-life?

A
  • Selective alpha1-adrenergic agonist
  • Increase TPR and BP
  • Baroreceptor reflex decreases HR
  • Dilates pupils
  • Decreased bronchial and upper airway secretions
  • 1/2-life less than 1 hr
52
Q

Phenylephrine:

Toxicity, therapeutic uses, and contraindications?

A
  • Tox: HTN
  • Uses: Paroxysmal SVT, mydriatic agent, nasal decongestant (constricts leaky sinuses)
  • Contra: HTN, V-tac
53
Q

What drug category is clonidine?

Explain its effects.

A
  • Selective alpha2-adrenergic agonist
  • Peripherally, clonidine causes mild vasoconstriction and slight increase in BP
  • Crosses BBB to cause reduced symp outflow, reducing vasoconstriction and BP
54
Q

Clonidine:

Toxicity and therapeutic uses? (no contraindications)

A
  • Tox: Dry mouth, hypertensive crisis (following acute withdrawal due to symp sensitization from the inhibition)
  • Uses: HTN (when due to symp activation)
55
Q

What are the 2 classes of indirect sympathomimetics?

A
  1. Releasing agents

2. Reuptake blockers

56
Q

Name the 6 indirect sympathomimetic drugs that are known as “releasing agents”

A
  • Amphetamine
  • Methamphetamine
  • Methylphenidate
  • Ephedrine
  • Pseudoephedrine
  • Tyramine (in food)
57
Q

Recall: when does tyramine cause its damaging effects?

How long is it’s 1/2-life?

A

Highly susceptible to degradation (Very short 1/2-life) by MAO and thus has little effect unless pt is taking MAO inhibitor (then NE builds up)

58
Q

How do the 6 amphetamine-like drugs (releasing agents) work?

A

Amphetamine-like drugs are taken up by re-uptake proteins and subsequently cause reversal of the re-uptake mechanism resulting in release of NT in a Ca2+ independent manner.

(amphetamines P’late transpoter)

59
Q

What are the CV effects of amphetamine, methamphetamine, methylphenidate,
ephedrine, pseudoephedrine, and tyramine?

A
  • Increased TPR and diastolic BP (alphas)
  • Positive inotropic and chronic tropic effects (beta1), increase systolic BP
  • CNS: stimulant + anorexia
60
Q

Amphetamine, methamphetamine, methylphenidate, ephedrine, pseudoephedrine, and tyramine:
Toxicity, therapeutic uses, and contraindications?

A
  • Tox: Tachycardia (B1)
  • Uses: ADHD, narcolepsy, nasal congestion (pseudoephedrine in sudafed)
  • Contra: Tx w/MAOI in past 2 weeks
61
Q

Name the drugs that are non-selective beta-blockers (B1 and B2), cardioselective beta blockers (B1), and partial agonists (B1 and B2)

A
  • Non-selective: propranolol, timolol, nadolol
  • Cardioselective: atenolol, metoprolol
  • Partial agonists: Pindolol

(comes up again later)

62
Q

Effects on HR/contractility of non-selective beta-blockers (B1 and B2), cardioselective beta blockers (B1), and partial agonists (B1 and B2)

A
  • Non-selective: decrease
  • Cardioselective: decrease
  • Partial agonists: decrease, but less because of partial agonism
63
Q

Effects on TPR of non-selective beta-blockers (B1 and B2), cardioselective beta blockers (B1), and partial agonists (B1 and B2)

A
  • Non-selective: increase (unopposed constriction by alpha1)
  • Cardioselective: little effect (beta2 still work to vasodilate)
  • Partial agonists: may be slight decrease
64
Q

Effects on renin release of non-selective beta-blockers (B1 and B2), cardioselective beta blockers (B1), and partial agonists (B1 and B2)

A
  • Non-selective: decrease
  • Cardioselective: decrease
  • Partial agonists: decrease
65
Q

Effects on bronchioles of non-selective beta-blockers (B1 and B2), cardioselective beta blockers (B1), and partial agonists (B1 and B2)

A
  • Non-selective: bronchoconstriction (particularly in asthmatics)
  • Cardioselective: less bronchoconstriction (but still not recommended)
  • Partial agonists: Asthmatics have a reduced
    capacity to dilate bronchioles.
66
Q

Effects on glucose metabolism of non-selective beta-blockers (B1 and B2), cardioselective beta blockers (B1), and partial agonists (B1 and B2)

A
  • Non-selective: masks sx of hypoglycemia (due to epi release)
  • Cardioselective: little effect
  • Partial agonists: reduced response to epi (since partial response)
67
Q

What drug category are propranolol, nadolol, and timolol?

Explain their effects.

A
  • Non-selective beta-blockers
  • Decreased HR and contractility
  • Reduced renin release (therefore reduced vasoconstriction)
  • Inhibition of aqueous humor production
68
Q

Propranolol, nadolol, and timolol:

Toxicity, therapeutic uses, and contraindications?

A
  • Tox: Bronchospasm, masks sx of hypoglycemia (blocks epi), bradycardia, increased triglycerides
  • Uses: HTN, angina, glaucoma, early to mod heart failure, arrhythmia
  • Contra: Bronchospasm during asthma, sinus bradycardia, 2nd and 3rd degree heart block, cardiogenic shock
69
Q

What drug category are metoprolol, atenolol, esmolol?
Explain their effects.
Which is short-acting?

A
  • Cardioselective beta1 blockers (reduced resp side-effects)
  • Decrease HR and contractility
  • Reduced renin release
  • Decreased symp activation
  • Esmolol is short-acting (emergent use)
70
Q

Metoprolol, atenolol, esmolol:

Toxicity, therapeutic uses, and contraindications?

A
  • Tox: Hypotension, bradycardia
  • Uses: HTN, angina, arrhythmia
  • Contra: sinus bradycardia, 2nd/3rd degree heart block, cardiogenic shock
71
Q

What drug category is pindolol? (when would you use it over other beta-blockers?)
Explain its effects.

A
  • Partial agonist beta-blocker (*used when symp activity is high)
  • Decrease BP
  • Decrease contractility
  • Reduced renin release
  • Decreased symp activation
72
Q

Pindolol:

Toxicity, therapeutic uses, and contraindications?

A
  • Tox: hypotension
  • Uses: HTN
  • Contra: sinus bradycardia, 2nd/3rd degree heart block, cardiogenic shock
73
Q

What drug category are phentolamine and phenoxybenzamine? (how are they different)
Explain its effects.

A
  • Non-selective alpha-blockers (phentolamine is reversible, phenoxybenzamine is irreversible)
  • Decrease BP (alpha blockage + unmasks beta effects)
  • Increased chronotropy and inotropy
74
Q

Phentolamine and phenoxybenzamine:

Toxicity and therapeutic uses? (No contraindications)

A
  • Tox: prolonged HTN, reflex tachycardia

- Uses: HTN associated w/pheochromocytoma, vasoconstrictor-induced extravasation

75
Q

What drug category are prazosin, doxazosin, and terazosin?

Explain its effects.

A
  • Selective alpha1-receptor blockers
  • Inhibit vasoconstriction (less cardiac stimulation than non-selective alpha-blockers cuz alpha2 still works)
  • Prostate smooth m. relaxation
76
Q

Prazosin, doxazosin, and terazosin:

Toxicity and therapeutic uses? (No contraindications)

A
  • Tox: Orthostatic HTN

- Uses: HTN, BPH

77
Q

List the two adrenergic receptors that are expressed on the pre-synaptic membrane of both noradrenergic and non-noradrenergic nerve terminals and describe how their activation influences NT release

A
  • Alpha2 (inhibits NT release)

- Beta2 (causes tremor)

78
Q

What are the relative 1/2-lifes of the catecholamines?

A

All short

79
Q

How do the 1/2-lives of propranolol, nadolol, and timolol differ?

A

Propranolol and timolol: 4 hrs

Nadolol: 20-24 hrs

80
Q

What’s another name for ephedrine?

What is the relative 1/2-life of ephedrine/norephedrine?
What degrades them?

A

Adrenaline chloride

  • Relatively short 1/2-life
  • COMT for ephedrine, COMT and MAO of norephedrine

Pharm (32 decks)

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