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neuro 2019 Exam 3 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

10 major sites of drug action in the CNS

A 
action potential propogation
synthesis
storage
metabolism
release
uptake
degradation
receptor
ion conductance
retrograde signaling (like glutamine to glutamate by glia)
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2
Q

monoamine transporters

A

VMAT- vesicle for monoamines

MAO- on mitochondria of nerves
COMT- in cytoplasm in liver. functions: breakdown dopamine/ Norepi/ Epi, etc.

Therapeutic applications of monoamine transporters as sites of drug action: ADHD: methylphenidate, amphetamine
Depression: SSRIs, SNRIs, TCAs

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3
Q

Glutamate: The Primary Excitatory NT

A 
Localized throughout the CNS
Glutamate accounts for most fast synaptic transmission in the CNS and spinal cord
Pathophysiology
Ischemic injury, stroke
Migraine
Alzheimer’s disease
Lou Gehrig’s disease
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4
Q

GABA: The Primary Inhibitory NT

A

Localized throughout the CNS
Principal NT of interneurons
Neurons in striatum, globus pallidus, and Purkinje cells of cerebellum
Roles
Balances excitatory activity of glutamate
GABA dysfunction leads to hyperexcited states
GABA-mimetic drugs are used to induce sleep and control anxiety and seizures

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5
Q

Acetylcholine in the CNS

A

Functions
Wakefulness
Motor control
Memory
Drowsiness, sedation, and memory loss can occur when central ACh receptors are blocked
Many CNS drugs have significant affinity for muscarinic ACh receptors

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6
Q

Monoamine Regulation of Major Depressive Disorder Symptoms

A

Dopamine: Attention, motivation, pleasure, reward

norepinephrine: alertness, energy
Serotonin: obsessions and compulsions

Serotonin & norepinephrine together: anxiety

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7
Q

Dopamine Pathophysiology

A

SN → striatum regulates voluntary movement
- Striatal DA neurons degenerate in Parkinson’s disease

VTA “reward pathway” mediates
Drug addiction
- Cocaine blocks DA uptake
- Amphetamines increase DA release

Psychiatric disorders

  • Schizophrenia involves increased DA activity
  • Classical antipsychotics work (in part) by blocking dopamine D2 receptors
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8
Q

Serotonin (5-Hydroxytryptamine, 5-HT)

A

Mediates affective processes such as aggressive behavior and arousal
Descending pain pathways
Sensory enhancement
Depression is associated with decreased 5-HT function
Treated with SSRIs
Ectasy (MDMA), LSD and other hallucinogens probably act in part by interacting with 5-HT receptors

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9
Q

Norepinephrine

A

Modulates sleep, wakefulness, attention, and feeding behaviors

Roles in learning and memory, anxiety and pain, and mood

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10
Q

general wiring of the ANS (transmitters, receptors)

A

Parasympathetic
Neurotransmitter: ACh
Receptors: nAChR, mAChR

Sympathetic
Neurotransmitters: NE > Epi (DA); ACh
Receptors: α, β, (D), nAChR, mAChR

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11
Q

ionotropic vs metabotropic Ach receptors

A

Nicotinic is ionotropic, muscarinic is metabotropic

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12
Q

Rules of Thumb for Smooth Muscle and Autonomic Receptors

A

Alpha1 (α1) receptors
Stimulate contraction of all smooth muscle
Vascular smooth muscle – vasoconstriction

Beta2 (β2) receptors
Relax smooth muscle – vasodilation

Muscarinic receptors
Contract smooth muscle (different intracellular signal than α1 receptors)
Apparent discrepancy – ACh & muscarinic agonists given IV cause vasodilation due to release of nitric oxide (NO)

Norepinephrine happens with normal nerve stimulation ; does not have high affinity for B2 receptors. Most of the B2 relaxation will happen with epinephrine (stimulation of adrenal medulla)

Epinephrine is potent at all adrenergic receptors

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13
Q

Sympathetic vs. Parasympathetic Tone

A 
Sympathetic
Adrenergic (anticholinergic)
Cutaneous vasodilation
Pupil constriction (myosis)
Increase in HR
Reduction/elimination of the desire to urinate
Decreased secretion and motility

Fight or flight
Smooth muscle relaxation

Parasympathetic
Cholinergic
Salivation, lacrimation
Pupil constriction (myosis)
Decrease in HR
Urination, defecation
Increased secretion and motility

Rest and digest
Smooth muscle contraction

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14
Q

High heart rate, pupillary dilation (not constricting the pupil anymore) comes from blocking

A

muscarinic receptors– inhibition of the parasympathetic system

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15
Q

AChE inhibitor acute intoxication

A

Parasympathetic effects

SLUDGE acronym – Salivation, Lacrimation, Urination, Defecation, GI distress, Emesis

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16
Q

Example of an antidiarrheal:

A

diphenoxylate and atropine (Lomotil)
Diphenoxylate – opioid receptor agonist (schedule V narcotic); inhibits excessive GI motility
Atropine – added to discourage abuse

17
Q

Pheochromocytoma Treatment

A

Surgical resection of the pheochromocytoma following medical preparation to control hypertension and volume expansion
The use of a selective beta-blocker in a patient with a pheochromocytoma will result in symptoms of ‘unopposed alpha’ stimulation (i.e., vasoconstriction)
Although nonselective beta-blockers (e.g., labetalol) can be used to block both alpha- and beta-receptors, use as the initial antihypertensive agent may cause paradoxical hypertension
The preferred agent for controlling blood pressure is an irreversible, long-acting, nonspecific alpha adrenergic antagonist (phenoxybenzamine)

18
Q

Clonidine suppression test

A

Clonidine activates central pre-synaptic alpha-2 receptors and suppresses the release of catecholamines from neurons
Clonidine has no effect on catecholamine secretion from a pheochromocytoma

19
Q

Adrenergic transmission

A

Tyrosine–> Dopa–> dopamine–> NE

VMAT involved in storage

cocaine interferes with reuptake

20
Q

AChE (organophosphate) Inhibitor Toxicity

A

SLUDGE– Salivation, Lacrimation, Urination, Defecation, Gastrointestinal pain & gas, Emesis

DUMBELS – Defecation, Urination, Miosis, Bronchorrhea/Bronchospasm/ Bradycardia, Emesis, Lacrimation, Salivation

Ingestion: GI symptoms occur first

Percutaneous absorption: localized sweating and muscle fasciculations

Lipid-soluble agents: CNS involvement follows rapidly

21
Q

what do alpha 1 and 2 do?

A

vasoconstrict

22
Q

What does beta 1 do?

A

increase heart rate and contractility

23
Q

what does beta 2 do?

A

bronchial dilation

24
Q

autoreceptors are typically

A

inhibitory

25
Q

characterize nicotinic receptors

A

ionotropic
ligand gated
IPSP or EPSP– on and off switches

26
Q

characterize muscarinic receptors

A

GPCR
metabotropic
change the quality of something rather than on vs off

neuro 2019 Exam 3 (17 decks)

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