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2060 Pharmacology > Module 14A CNS > Flashcards

Module 14A CNS Flashcards

1
Q

Neuropharmacology

A
  • Study of drug effects on CNS function
  • Treatment of biochemical imbalance
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2
Q

Neuron Function

A
  • Excitable cells
  • Transmit through electrical/chemical signals
  • Starting at dendrite
  • Cause action potentials
  • Pre-synaptic terminal release neurotransmitters
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3
Q

Action Potential

A
  • Neuron to neuron communication
  • Resting potential -70mV
  • Na+ enter cell during depolarization
  • K+ channels open after Na+ close
  • K+ leave cell during repolarization
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4
Q

Synapse

A
  • AP reaches pre-synaptic terminal
  • Influx of Ca++
  • Neurotransmitter vesicles fuse with membrane
  • Neurotransmitters release onto synaptic cleft
  • Bind to receptors on post-synaptic membrane
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5
Q

CNS Neurotransmitters

A
  • Chemicals transmit signals across synapse
  • Broken into classes
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6
Q

Monoamine Classes

A
  • Norepinephrine (depression/anxiety)
  • Epinephrine (anxiety)
  • Dopamine (parkinson/schizophrenia)
  • Serotonin (depression/anxiety)
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7
Q

Amino Acid Classes

A
  • Excitatory, glutamate/aspartate (alzheimers)
  • Inhibitory, GABA/glycine (anxiety)
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8
Q

Other Class

A
  • Acetylcholine (alzheimer/parkinson)
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9
Q

Replacement

A
  • Drug replaces neurotransmitters
  • Low in diseases
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10
Q

Agonist/Antagonist

A
  • Drug binds to receptors
  • Post-synaptic membrane
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11
Q

Neurotransmitter Breakdown Inhibition

A
  • Metabolism of neurotransmitters inhibited
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12
Q

Reuptake Blocking

A
  • Neurotransmitter reuptake blocked
  • Into pre-synaptic neuron
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13
Q

Nerve Stimulation

A
  • Drug directly stimulates nerve
  • Release of more neurotransmitter
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14
Q

Parkinson’s Disease

A
  • Progressive loss of dopaminergic neurons
  • Within substantia nigra of brain
  • 70-80% loss
  • 5-10 year progression
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15
Q

Parkinson’s Symptoms

A
  • Tremor (face, hands, arms, legs, jaw)
  • Rigidity (joint stiffness/increase muscle tone)
  • Bradykinesia (slow movement)
  • Masklike face (no expression/limited movement)
  • Postural instability (impaired balance)
  • Dementia (later stages)
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16
Q

Parkinson’s Pathophysiology

A
  • Decreased dopamine release
  • Inhibit GABA release
  • Excess of acetylcholine compared to dopamine
  • Increase GABA release
  • Excess GABA causes movement issues
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17
Q

Etiology Development

A
  • Drugs (street drugs produce MPTP compound)
  • Genetics (mutation in 4 genes)
  • Environmental toxins (pesticides)
  • Brain trauma
  • Oxidative stress (diabetes induced oxidative damage)
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18
Q

Parkinson’s Drug Treatment

A
  • Increasing dopamine
  • Decreasing acetylcholine
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19
Q

Dopamine Increasing Agents

A
  • Dopamine replacement
  • Dopamine agonist
  • Dopamine releaser
  • Catecholamine-O-methyltransferase inhibitor
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20
Q

Dopamine Replacement (Levodopa/L-DOPA)

A
  • Most effective drug treatment
  • Effects decrease as disease progresses
  • Cross BBB through transport protein
  • Converts to dopamine in dopaminergic nerve terminals
  • Conversion mediated by decarboxylase brain enzymes
  • Reaction sped up by vitamin B6 (pyridoxine)
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21
Q

Regular Dopamine

A
  • Dose not cross BBB
  • Short half-life in blood
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22
Q

Adverse Effects of L-Dopa

A
  • Nausea & vomiting
  • Dyskinesias (involuntary movement)
  • Cardiac dysrhythmias
  • Orthostatic hypotension
  • Psychosis (hallucinations)
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23
Q

Peripheral Metabolism of L-Dopa

A
  • Majority metabolized in intestine before reaching brain
  • Administered with carbidopa
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24
Q

Carbidopa with L-Dopa

A
  • Decarboxylase inhibitor of peripheral metabolism
  • More levodopa reaches brain
  • Allows for lower dose of levodopa
  • Decreases nausea/vomiting, cardiac dysrhythmias
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25
Q

Minimizing Wearing Off of L-Dopa

A
  • Shortening dosing interval
  • Admin of inhibiting L-DOPA metabolism
  • Add dopamine agonist
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26
Q

Dopamine Agonist

A
  • Activate dopamine receptors on post-synaptic membrane
  • Less effective as L-DOPA
  • First line treatment for mild symptoms
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27
Q

Adverse Effects of Dopamine Agonists

A
  • Hallucinations
  • Daytime drowsiness
  • Orthostatic hypotension
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28
Q

Dopamine Releaser

A
  • Stimulate release for dopaminergic neurons
  • Blocks reuptake into pre-synaptic terminals
  • Blocks NMDA receptors (decrease dyskinesia)
  • 2-3 day response
  • Combined with L-DOPA
29
Q

Adverse Effects of Dopamine Releaser

A
  • Dizziness
  • Nausea/vomit
  • Lethargy
  • Anticholinergic
30
Q

Catecholamine-O-Methyltransferase Inhibitor (COMT)

A
  • Adds methyl group to dopamine & L-DOPA
  • Greater fraction of L-DOPA for dopamine conversion
  • Combined with L-DOPA
31
Q

Adverse Effects of Catecholamine-O-Methyltransferase Inhibitor

A
  • Nausea
  • Orthostatic hypotension
  • Vivid dreams
  • Hallucinations
32
Q

Monoamine Oxidase-B (MAO-B) Inhibitor

A
  • MAO-B metabolizes dopamine/L-DOPA with oxidation
  • Inhibition allows more conversion to brain
  • Dopamine remains in nerve terminals
  • Combine with L-DOPA
33
Q

Adverse Effects of Monoamine Oxidase-B (MAO-B) Inhibitor

A
  • Insomnia
  • Orthostatic hypotension
  • Dizziness
34
Q

MAO-B & MOA-A

A
  • MAO-B inhibitors use to treat Parkinson’s do not inhibit MAO-A
  • No hypertensive crisis when eating tyramine foods
35
Q

Symptoms of Excess Acetylcholine

A
  • Diaphoresis
  • Salivation
  • Urinary incontinence
36
Q

Anticholinergic Drugs

A
  • Block acetylcholine binding to receptor
  • Increase L-DOPA effectiveness
  • Cholinergic antagonists
  • Decrease diaphoresis, salivation, incontinence
37
Q

Adverse Effects of Anticholinergic Drugs

A
  • Dry mouth
  • Blurry vision
  • Urinary retention
  • Constipation
  • Tachycardia
  • CNS (elderly)
38
Q

Alzheimer’s Disease

A
  • Progressive dementia
  • More common in women
39
Q

Alzheimer’s Symptoms

A
  • Memory loss
  • Language issues
  • Judgement impairment
  • Intelligence decline
  • Confusion
  • Issues completing routine tasks
40
Q

Alzheimer’s Pathophysiology

A
  • Degeneration of cholinergic neurons (hippocampus)
  • Degeneration of neurons (cerebral cortex)
  • Decreased cholinergic nerve function
41
Q

Alzheimer’s Diagnosis

A
  • Brain sample analysis
  • After death
  • Neurofibrillary tangles & neuritic plaque hallmarks
42
Q

Tau Protein

A
  • Forming cross bridges between microtubules
  • Keeping their structure
43
Q

Neuofibrillary Tangles

A
  • Form inside neurons
  • Disruption of microtubule arrangement
  • Abnormal production of tau protein
44
Q

Neuritic Plaques

A
  • Found outside neurons
  • Beta amyloid core (protein fragments)
  • Kill hippocampal cells
45
Q

Alzheimer’s Etiology

A
  • Genetically determined (20%)
  • DNA mutation (ApoE4)
  • Amyloid precursor protein gene mutation
  • Head injuries
46
Q

Alzheimer’s Drug Treatment

A
  • Cholinesterase inhibitors
  • NMDA receptor antagonists
47
Q

Cholinesterase Inhibitors

A
  • Inhibit acetylcholine metabolism
  • More acetylcholine in synaptic cleft
  • Enhance cholinergic transmission of healthy neurons
  • Minimal effectiveness
48
Q

Adverse Effects of Cholinesterase Inhibitors

A
  • Nausea/vomit
  • Diarrhea
  • Insomnia
49
Q

NMDA Receptor

A
  • Ca++ channel
    • Blocked by magnesium at rest
  • Magnesium dissociates with glutamate binds to receptor
  • Magnesium returns to block with glutamate leaves
50
Q

NMDA in Alzheimer’s

A
  • Excess glutamate release
  • NMDA receptor remains open
  • Excess Ca++ into cell
51
Q

Consequences of Excess Calcium

A
  • Detrimental to learning/memory
  • Degradation of neurons
52
Q

NMDA Receptor Antagonists

A
  • Block Ca++ influx into post-synaptic neuron
  • Well tolerated drug
53
Q

Schizophrenia

A
  • Difficulty identifying reality
  • Emotional response variation
  • Social behavior changes
  • Begins in adolescence/early adult
54
Q

Positive Schizophrenia Symptoms

A
  • Exaggerate/distort normal neurological function
  • Delusions/hallucinations
  • Agitation
  • Paranoia
  • Combativeness
  • Disorganized speech/thoughts
55
Q

Negative Schizophrenia Symptoms

A
  • Loss of normal neurological function
  • Social/emotional withdrawal
  • Poor insight/judgement
  • Speech poverty
  • Difficulty with self-care
  • Blunted affect
  • Lack of motivation
56
Q

Schizophrenia Etiology

A
  • Family history
  • Drug abuse (meth, angel dust, LSD)
  • Low birth weight (less than 5.5lbs)
  • Low IQ
57
Q

Schizophrenia Pathophysiology

A
  • Increased dopaminergic nerve transmission
  • 5-HT (serotonin) decreased - 2A receptors, increased 1A
    Glutamate, decreased NMDA receptors
58
Q

Normal Dopamine Neurotransmission

A
  • Some dopamine released
  • Bind to D2 receptors
59
Q

Schizophrenia Dopamine Neurotransmission

A
  • Increased dopaminergic neurotransmission
  • Increased dopamine binding to D2 receptors
60
Q

Schizophrenia Diagnosis

A
  • Changes in function
  • Developmental background
  • Family history
  • Medication response
  • Brain scan (enlarged ventricles, decreased frontal lobe activity)
61
Q

Schizophrenia Drug Treatment

A
  • Block dopamine/serotonin neurotransmission in brain
  • Conventional/atypical antipsychotics
62
Q

Convention Antipsychotics

A
  • Block D2 receptors
  • Mesolimbic brain area
  • Potency proportional to ability to inhibit receptor
  • Block acetylcholine, histamine, norepinephrine receptors
  • Treatment of positive symptoms
  • 2-4 weeks for symptoms improvement (1-2 days minimum)
63
Q

Adverse Effects of Conventional Antipsychotics

A
  • Extrapyramidal symptoms
  • Sudden high fever
  • Anticholinergic effects
  • Orthostatic hypotension
  • Sedation
  • Skin reactions
64
Q

Extrapyramidal Symptoms (EPS)

A
  • Due to blockade of D2 receptors
  • Movement disorders
  • Resemble Parkinson’s
65
Q

EPS Types

A
  • Acute dystonia (spasm of face, tongue, neck, back)
  • Parkinsonism (bradykinesia)
  • Akathesia (continuously in motion)
  • Tardive dyskinesia (face/tongue motion, switch to atypical)
66
Q

Atypical Antipsychotics

A
  • Block D2 receptors
  • Block 5-HT1A/2A
  • Low affinity
67
Q

Conventional versus Atypical Antipsychotics

A
  • Same efficacy versus positive symptoms
  • Atypical greater efficacy versus negative symptoms
  • Atypical lower risk from EPS symptom development
68
Q

Adverse Effects of Atypical Antipsychotics

A
  • Sedation
  • Orthostatic hypotension
  • Weight gain
  • Risk for type II diabetes development
  • Anticholinergic effects

2060 Pharmacology (18 decks)

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