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Advanced Pharmacology > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Briefly describe the autonomic nervous system and what are its subdivisions?

A

Contains systems not under our concious control including: symapathetic, parasympathetic, and enteric.

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2
Q

What are is the “fight or flight” mode and its responses?

A

Activation of the sympathetic nervous system that increases HR and BP, dilates bronchioles, and shunts blood to needed muscles.

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3
Q

What is the ergotropic response?

A

Movement related response that requires energy during sympathetic activation.

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4
Q

What is the “rest and digest” mode and its responses?

A

Activation of the parasympathetic nervous system leads to energy conservation and shunting blood to endocrine, GI, and urogenital organs.

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5
Q

What is trophotropic response?

A

Means leading to growth. Describes parasympathetic response.

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6
Q

Where are the pre and postganglionic fibers located in the sympathetic nervous system?

A

In the thoracolumbar region. The preganglionic fibers terminate in the paravertebral chain ganglia. The postganglionic fibers innervate the affected organs.

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7
Q

Where are the pre and postganglionic fibers of the parasympathetic nervous system located?

A

In the craniosacral region.The preganglionc fibers leave the CNS through the cranial nerves and sacral spinal roots (there is no chain ganglion)

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8
Q

What is the differences between the cell bodies of the somatic nervous system and autonomic nervous system?

A

In the SNS the cell bodies are located within the brain/spinal cord and called nuclei. In the ANS they are located outside the brain/spinal cord and clusterd together to form ganglia.

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9
Q

Describe the nerve fibers in the sympathetic nervous system?

A

The preganglionc fibers are short while the postganglionic fibers are long. The fibers form a chain so that activation will activate the entire pathway. The ganglia are close to the spinal cord.

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10
Q

Describe the nerve fibers in the parasympathetic nervous system?

A

The preganglionc fibers are long and the postganglionic fibers are short. The ganglia are in the effector organs.

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11
Q

What is the length of effects of the parasympathetic nervous system? why?

A
  • They are short lived
  • Once the intended effect is reach, there is no more need to keep effect going

Ex: HR is 120 PNS brings down to 70 and then shuts off.

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12
Q

What are the effector organs of the autonomic nervous system?

A

Cardiac muscle, smooth muscle, and glands (not skeletal)

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13
Q

What do all preganglionic fibers of the ANS release?

A

Aceytlcholine

Both sympathetic and parasympathetic

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14
Q

What do the postganglionic fibers of the ANS release?

A

Both ACh and norepiniphrine to either stimulate or inhibit.

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15
Q

What are sympathomimetics and the different types?

A
  • Drugs that mimic the action of norepinehrine
    -Inotropy, chronotropy, vasoconstriction, bronchodilation
  • Direct or indirect.

Direct: epinephrine, isoproterenol, albuterol
Indirect: Ephedrine and amphetamines.

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16
Q

What are sympatholytics and the different types?

A
  • Block the effects of the sympathetic nervous system
  • Beta and alpha blockers
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17
Q

What are the different receptors in the autonomic nervous system? What ligand do they respond to?

A
  • Cholinergic - respond to aceytlcholine
    -Muscarinic
    -Nicotinic
  • Adrenergic - respond to norepinephrine/epinephrine
    -Alpha
    -Beta
    -Dopamine
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18
Q

What are the muscarinc receptor subtypes? Define if excitatory or inhibatory.

A
  • Muscarinic M1 - Excitatory
  • Muscarinic M2- Inhibitory
  • Muscarinc M3- Excitatory
  • Muscarinic M4- Inhibitory
  • Muscarinc M5- Excitatory
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19
Q

What are the nicotinic receptor subtypes?

A
  • Nicotinic Nn (neuronal)
  • Nicotinic Nm (muscular)
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20
Q

What are the alpha adrenoreceptor subunits? What is their signal transduction pathway?

A
  • Alpha 1 - activates Gq GPCR which acivates phospholipase C and IP3/DAG as 2nd messengers.
  • Alpha 2 - activates Gi GPCR that inhibits adenylate cyclase which decreases cAMP production
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21
Q

What are the beta adrenoreceptor subunits? What is their signal transduction pathway?

A
  • Beta 1, 2, 3 - all activate Gs GPCR that stimulates adenylate cyclase and increases cAMP production.
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22
Q

Describe the pathway of norepinephrine activated alpha 1 receptors?

A
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23
Q

Describe the pathway of B1/B2 stimulation in a cardiac myocyte?

A

Alpha 2 is inhibitory and prevents the release of norepinephrine

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24
Q

Describe the pathway of Beta 2 stimulation in peripheral smooth muscle?

A

cAMP inhibts MLCK (myosin light chain kinase) and leads to relaxation

alpha 1 consticts in vascular smooth muscle and beta 2 dilates peripheral smooth muscle = more blood flow to muscles during fight or flight

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25
Q

Describe the pathway of cholinergic receptor binding by ACh?

A
  • M1,M2, M3 - activate Gq and activate phospholipase
  • M2, M4 - activate Gi and inhibit adenylate cyclase
  • Nicotinc- Bind to ion channels
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26
Q

Describe the autonomic and hormonal feedback loops that regulate changes in MAP?

A
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27
Q

What is the function of chain ganglia?

A

They allow multiple organs to be effected by the stimulation of one neuron. Happens during fight or flight

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28
Q

Define heteroreceptors and autoreceptors? What are the types of autoreceptors?

A

Heteroreceptors - receptors on the neuron that can bind to molecules other than the released neurotransmitter.
Autoreceptors - bind to the neurotransmitter released by the neuron.
* can be inhibitory (negative feedback) or excitatory (positive feedback)
* Inhibitory = a2 receptor on noradrenergic nerve terminal
* Excitatory = B receptor on noradrenergic nerve terminal

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29
Q

What is the effects of stimulation of sympathetic and parasympathetic activity in the heart?

A
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30
Q

What is the effects of stimulation of sympathetic and parasympathetic activity in the blood vessels?

A
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31
Q

What is the effects of stimulation of sympathetic and parasympathetic activity in the bronchioles?

A
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32
Q

What is a cholinomimetic (parasympathomimetic)?

A

A drug that mimics the actions of acetylcholine

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33
Q

What is a parasympatholytic (antimuscanaric)?

A

A drug that inhibts the effects of Ach and the parasympathetic nervous system.

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34
Q

What types of receptors are involved in skeletal muscle blood vessels? What is there effect when stimulated? What is the normal skeletal circulating blood volume when at rest and stimulated?

A

At rest 20%, up to 80% during fight or flight

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35
Q

What is the structure of a neuron?

A
  • Information is recieved in the dendrites
  • The cell body decides whether or not to send a signal
  • The axon hillock generates the action potential
  • The signal reaches the telondendrion
  • The neurotransmitter is relased from the synaptic bouton
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36
Q

What is the structure of the synapse?

A
  • Comprised of the presynpatic and postsynaptic terminals
  • Neurotransmitters are stored in secretory vesicles that will bind with the presynaptic membrane and enter the synaptic space where it can ineract with receptors on the postsynaptic membrane
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37
Q

What are the 3 types of synapses?

A
  • Chemical - release neurotransmitters
  • Electrical - gap junctions
  • En passant - synapses connect to the middle of the axon
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38
Q

What are the 4 fates of neurotransmitters in the synapse?

A
  • Diffuses away from synapse
  • Degraded by enzymes (acetylcholinesterase)
  • Uptake into pre-synaptic cell
  • Uptake into surrounding cell
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39
Q

What are the 6 main neurotransmitter classes and examples of each?

A

1.Esters - Acetylcholine (R-COOR)
2.Monamines - Norepinephrine, serotonin, dopamine
3.Amino Acids - GABA, glutamate
4.Purines - Adenosine, ATP
5.Peptides - Substance P, endorphins
6.Inorganic gases - Nitric oxide (not stored, made as needed)

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40
Q

What are the 3 neurotransmitters involved in emotion?

A
  • Norepinephrine
  • Dopamine
  • Serotonin
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41
Q

What are examples of excitatory and inhibitory NT?

A
  • Excitatory - Glutamate
  • Inhibitory - GABA and glycine

Remember: excitatory leads to depolarization; inhibitory leads to hyperpolarization

42
Q

What is the pathway for ACh release and degradation?

A

Dependent on extracellular calcium
- Action potential reaches terminal
– Triggers Ca2+ influx
– Ca2+ destabilizes storage vesicles
– Fusion of vesicle with terminal membrane
– Exocytosis – release of contents into synaptic cleft
– ACh plus cotransmitters (ATP, peptides)
– ACh broken down by AChE

42
Q

Where and how is ACh synthesized? Where is stored?

A
  • Made in the cytoplasm
  • Acetyl-CoA and Choline turned into ACh by Choline acetyltransferases (ChAT)
  • Stored in vesicles in quanta by VAT (1000-50,000 per vesicle)
43
Q

How is acetylcholine transported into the cell? Into the vesicle?

A
  • CHT (choline transporter) - into neuron
  • VAT (vesicular acetylcholine transporter) - into vesicle

Ach pnemonic: CHT ChAT VAT

44
Q

How is the vesicle anchored (docked)?

A
  • SNARE complex:
  • Syntaxin
  • SNAP - 25
  • VAMP = vesicular associated membrane protein
45
Q

What is priming of a vesicle?

A

-It is ATP dependent and allows for rapid exocytosis
-Similar to cocking a gun

46
Q

Draw out the entire pathway for ACh to be released into the synapse.

A
47
Q

What are some targets for cholinergic inhibition in the synapse and examples?

A
  • Voltage gated ion channels - Calcium channel blockers
  • Acetylchoinesterase inhibitor - Sarin nerve gas (atropine is treatment), neostigmine, pyridostigmine
  • Botox - inhibits vesicle release from storage proteins by cleaving SNAP
48
Q

What is the precursor to adrenergic neurotransmitters?

A
  • Tyrosine - can be converted to dopa, dopamine, epinephrine, or norepinephrine
49
Q

How is norepinephrine taken back up into the neuron?

A

NET - norepinephrine transporter

50
Q

How is NE degraded in the synapse?

A

MAO (mono-amine oxidase)

51
Q

Draw the entire pathway of NE release from a neuron.

A
52
Q

What are some targets for adrenergic inhibition in the synapse and examples?

A
  • Metyrosine - inhibits conversion of tyrosine
  • Resperine - inhibits VMAT
  • Cocaine & tricyclic antidepressants - inhibit NET (as well as serotonin reuptake)
  • MAOIs - Inhibit NE degradation
53
Q

What is the difference in signaling between muscarinic and nicotinic cholinocepters?

A
  • Muscarinic - GPCR
  • Nicotinic - Ion channels
54
Q

What are the direct acting cholinomimetic groups? Examples of each?

A
  • Esters of choline (permanently charged, do not cross barriers well) - succinylcholine, carbachol (decrease IOP), methacholine (diagnosis of asthma)
  • Alkaloids -Pilocarpine, nicotine (lipid soluble), arecoline (betel nut)
55
Q

What are some effects of cholinomimetic agonists in the eye?

A

Causes pupil constriction which increases intraocular drainage

56
Q

What are some effects of cholinomimetic agonists in the CV system?

A
  • Reduction in peripheral vascular resistance
  • Vasodilation = lowering of BP, reflexive HR increase
  • bradycardia in overdose
57
Q

What are some effects of cholinomimetic agonists in the lungs?

A
  • Bronchial smooth muscle contraction
  • Tracheobronchial mucosa secretion increased

We want a normal tone in our bronchioles; decreases flow and increases surface area to remove foreign particulate
This can be bad for asthmatics

58
Q

What are some effects of cholinomimetic agonists in the GI system?

A
  • Increase motor and secretory activity
  • Salivary and gastric gland stimulation
  • Sphincters relax
59
Q

What are some effects of cholinomimetic agonists in the brain?

A

Nicotine has alerting response and causes release of dopamine (addiction), serotonin, GABA, NE

In large doses can causes toxicity and death

60
Q

What are the different types of glaucoma?

A
  • Open angle - drainage into canal of schlemm partially blocked leading to increased IOP
  • Narrow angle - iris is bulged forward and narrowed, partially blocking the canal of schlemm
61
Q

What drug is contraindicated in closed angle glaucoma? Why?

A

Atropine - it causes relaxation of ciliiary smooth muscle causing complete obstruction of drainage of aqueous humor (medical emergency)

62
Q

How do indirect acting cholinomimetics work?

A

They block or inhibit acetylcholinesterase

63
Q

What are examples of indirect cholinomimetics?

A
  • Alcohols - Edrophonium
  • Carbamates - Neostigmine, pyridostigmine
  • Organophosphates - Echothiophate (covalent bond formed, somewhat irreversible)

Note the difference in durations of action!!!

64
Q

What drugs can be used to diagnose and treat myasthenia gravis?

A
  • Cholinesterase inhibitors - edrophonium used as diagnostic (short half life); can be treated with neostigmine or pyridostigmine to increase the amount of ACh in the synapse
65
Q

How are acetylcholinesterase inhibitors used in surgical anesthesia?

A

We can use a drug like neostigmine to reverse the effects of NMB (pancuronium)

66
Q

What are the symptoms of organophospate posioning (pesticides)? What is the treatment?

A
  • SLUDGE - M: Salivation, Lacrimation, Urination, Defecation, GI upset, Emesis, Miosis
  • Atropine or pralidoxime
67
Q

Be able to describe this pathway

A
68
Q

What are the symptoms of nicotine toxicity?

A

Headaches, nausea, dizziness, collapse, breathlessness, loss of conciousness

69
Q

How does pralidoxime treat organophosphate toxicity?

A

It prevents aging of the organophosphate and regenerates acetylcholinesterase

70
Q

What is atropines MOA?

A

Atropine is an antimuscarinic and competitively inhibits muscaniric receptors to aceytlcholine.

71
Q

How can atropine be used preoperatively?

A
  • Help prevent vagal stimulation and potential bradycardia
  • Reduce respiratory secretions
  • Block unwanted GI activity
  • Postoperative nausea (scopalamine patch)
72
Q

What are indications for atropine in the respiratory system?

A

To treat bronchospasm in COPD to bronchodilate

Atrovent

73
Q

What are atropine’s effects on the eye?

A
  • Dilation - used in cycloplegia (tropicamide)
  • Decreased watering
74
Q

What are atropine’s effect on the heart?

A

Increase in HR, treatment for bradycardia

75
Q

What are the clinical indications for atropine?

A

Parkinson’s - adjunctive
Motion sickness - scopalamine
Opthalmic - dilation of the eye (tropicamide)
Asthma- ipratropium bromide
Bradycardia - Atropine IV

76
Q

What are the clinical contraindications for atropine?

A
  • Glaucoma patients
  • Elderly men with known BPH (atropine causes swelling of the prostate gland)
77
Q

What are the symptoms of atropine overdose?

A

Hot as a hare
Blind as a bat
Dry as a bone
Red as a beet
Mad as a hatter

78
Q

What is te treatment for atropine overdose?

A

Pyridostigmine or other parasympathomimetic

79
Q

What are the two categories of muscle relaxants?

A

Depolarizing and non-depolarizing

80
Q

What is a depolarizing muscle relaxant? How does it work? What are its effects?

A
  • Succinylcholine
  • Strucurally resembles ACh and acts as ACh receptor agonist.
  • This causes continuous end plate depolarization (cell cannot repolarize) resulting in relaxation/paralysis
81
Q

What are the non-depolarizing muscle relaxants? How do they work?

A
  • Pancuronium, Atrocurium, Mivacurium
  • They are competitive antagonists of ACh. They do not depolarize the motor end plate.
82
Q

How can you reverse the effects of NMB?

A

Neostigmine and suggamadex

83
Q

What are the two types of nicotinic antagonists?

A

Ganglion blockers (Nn) and neuromuscular blockers (Nm)

84
Q

What is the MOA of direct and indirect adregenergic agonists?

A
  • Direct - bind dierectly to and activate adrenergic receptors
  • Indirect - cause an increase in the amount of norepinephrine in the synapse
85
Q

What is the basic structure of a catecholamine?

A
  • Benzene ring with OH group at 3 and 4 carbons.
86
Q

How do substitutions on the benzene ring of catecholamines effect their degredation?

A
  • Greatly reduces their potency
87
Q

How do substitutions at the alpha carbon effect catecholamine degredation?

A

They have a prolonged action because oxidation by MAO is blocked

Phenylephrine, ephedrine, amphetamine

88
Q

What are the major adrenergic receptor types and subtypes?

A
  • Alpha- alpha 1 and alpha 2
  • Beta - Beta 1, 2, and 3
  • Dopamine - dopamine 1-5
89
Q

What are the effects in the CV system after administering an alpha agonsit?

A
  • Strong increase in vascular tone
  • Strong increase in BP
  • No real effect on contraction
90
Q

What are the effects on the CV system by a beta agonist?

A
  • Decreased vasular tone
  • Strongly increases contractility and HR
  • Decreases blood pressure
91
Q

What are the effects on the CV system by a mixed alpha and beta agonist?

A
  • Mixed increase/decrease vascular tone
  • Strong increase in contractility
  • Increase HR
  • Increase in BP

Ex: Epinephrine and norepinephrine

92
Q

Name a nonselective alpha agonist?

A

Phenylephrine

93
Q

Name a selective alpha 2 agonist?

A

Clonidine and dexmedetomidine

94
Q

Name a non-selective beta agonist?

A

Isoproterenol

95
Q

What is a selective beta 1 agonist?

A

Dobutamine

96
Q

What is a selective beta 2 agonist?

A

Albuterol

97
Q

What tissues contain significant numbers of alpha 1 and alpha 2 receptors?

A

Alpha 1- Most vascular smooth muscle, prostate, heart
Alpha 2 - Adrenergic and cholinergic nerve terminals

98
Q

What tissues contain significant numbers of beta 1 or beta 2 agonists?

A

Beta 1 - Heart
Beta 2 - Respiratory, uterine, and vascular skeletal muscle

99
Q

What are the major clinical effects of adrenoreceptor agonist in different organs?

A
  • Eye - Alpha agonist = dilation
  • Lungs - Beta 2 = bronchodilation
  • GI - alpha and beta = relaxation
  • CNS - catecholamines don’t cross BBB unless very large doses
100
Q

What are the trophasic effects of dopamine?

A
  • Low dose - DA1 in kidney = diuresis
  • Moderate dose - B1 = increase in contraction
  • High dose - alpha = increase in PVR/BP

Advanced Pharmacology (2 decks)

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