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2060 Pharmacology > Module 14A CNS > Flashcards

Module 14A CNS Flashcards

(68 cards)

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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
Minimizing Wearing Off of L-Dopa
- Shortening dosing interval - Admin of inhibiting L-DOPA metabolism - Add dopamine agonist
26
Dopamine Agonist
- Activate dopamine receptors on post-synaptic membrane - Less effective as L-DOPA - First line treatment for mild symptoms
27
Adverse Effects of Dopamine Agonists
- Hallucinations - Daytime drowsiness - Orthostatic hypotension
28
Dopamine Releaser
- 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
Adverse Effects of Dopamine Releaser
- Dizziness - Nausea/vomit - Lethargy - Anticholinergic
30
Catecholamine-O-Methyltransferase Inhibitor (COMT)
- Adds methyl group to dopamine & L-DOPA - Greater fraction of L-DOPA for dopamine conversion - Combined with L-DOPA
31
Adverse Effects of Catecholamine-O-Methyltransferase Inhibitor
- Nausea - Orthostatic hypotension - Vivid dreams - Hallucinations
32
Monoamine Oxidase-B (MAO-B) Inhibitor
- MAO-B metabolizes dopamine/L-DOPA with oxidation - Inhibition allows more conversion to brain - Dopamine remains in nerve terminals - Combine with L-DOPA
33
Adverse Effects of Monoamine Oxidase-B (MAO-B) Inhibitor
- Insomnia - Orthostatic hypotension - Dizziness
34
MAO-B & MOA-A
- MAO-B inhibitors use to treat Parkinson's do not inhibit MAO-A - No hypertensive crisis when eating tyramine foods
35
Symptoms of Excess Acetylcholine
- Diaphoresis - Salivation - Urinary incontinence
36
Anticholinergic Drugs
- Block acetylcholine binding to receptor - Increase L-DOPA effectiveness - Cholinergic antagonists - Decrease diaphoresis, salivation, incontinence
37
Adverse Effects of Anticholinergic Drugs
- Dry mouth - Blurry vision - Urinary retention - Constipation - Tachycardia - CNS (elderly)
38
Alzheimer's Disease
- Progressive dementia - More common in women
39
Alzheimer's Symptoms
- Memory loss - Language issues - Judgement impairment - Intelligence decline - Confusion - Issues completing routine tasks
40
Alzheimer's Pathophysiology
- Degeneration of cholinergic neurons (hippocampus) - Degeneration of neurons (cerebral cortex) - Decreased cholinergic nerve function
41
Alzheimer's Diagnosis
- Brain sample analysis - After death - Neurofibrillary tangles & neuritic plaque hallmarks
42
Tau Protein
- Forming cross bridges between microtubules - Keeping their structure
43
Neuofibrillary Tangles
- Form inside neurons - Disruption of microtubule arrangement - Abnormal production of tau protein
44
Neuritic Plaques
- Found outside neurons - Beta amyloid core (protein fragments) - Kill hippocampal cells
45
Alzheimer's Etiology
- Genetically determined (20%) - DNA mutation (ApoE4) - Amyloid precursor protein gene mutation - Head injuries
46
Alzheimer's Drug Treatment
- Cholinesterase inhibitors - NMDA receptor antagonists
47
Cholinesterase Inhibitors
- Inhibit acetylcholine metabolism - More acetylcholine in synaptic cleft - Enhance cholinergic transmission of healthy neurons - Minimal effectiveness
48
Adverse Effects of Cholinesterase Inhibitors
- Nausea/vomit - Diarrhea - Insomnia
49
NMDA Receptor
- Ca++ channel - Blocked by magnesium at rest - Magnesium dissociates with glutamate binds to receptor - Magnesium returns to block with glutamate leaves
50
NMDA in Alzheimer's
- Excess glutamate release - NMDA receptor remains open - Excess Ca++ into cell
51
Consequences of Excess Calcium
- Detrimental to learning/memory - Degradation of neurons
52
NMDA Receptor Antagonists
- Block Ca++ influx into post-synaptic neuron - Well tolerated drug
53
Schizophrenia
- Difficulty identifying reality - Emotional response variation - Social behavior changes - Begins in adolescence/early adult
54
Positive Schizophrenia Symptoms
- Exaggerate/distort normal neurological function - Delusions/hallucinations - Agitation - Paranoia - Combativeness - Disorganized speech/thoughts
55
Negative Schizophrenia Symptoms
- Loss of normal neurological function - Social/emotional withdrawal - Poor insight/judgement - Speech poverty - Difficulty with self-care - Blunted affect - Lack of motivation
56
Schizophrenia Etiology
- Family history - Drug abuse (meth, angel dust, LSD) - Low birth weight (less than 5.5lbs) - Low IQ
57
Schizophrenia Pathophysiology
- Increased dopaminergic nerve transmission - 5-HT (serotonin) decreased - 2A receptors, increased 1A Glutamate, decreased NMDA receptors
58
Normal Dopamine Neurotransmission
- Some dopamine released - Bind to D2 receptors
59
Schizophrenia Dopamine Neurotransmission
- Increased dopaminergic neurotransmission - Increased dopamine binding to D2 receptors
60
Schizophrenia Diagnosis
- Changes in function - Developmental background - Family history - Medication response - Brain scan (enlarged ventricles, decreased frontal lobe activity)
61
Schizophrenia Drug Treatment
- Block dopamine/serotonin neurotransmission in brain - Conventional/atypical antipsychotics
62
Convention Antipsychotics
- 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
Adverse Effects of Conventional Antipsychotics
- Extrapyramidal symptoms - Sudden high fever - Anticholinergic effects - Orthostatic hypotension - Sedation - Skin reactions
64
Extrapyramidal Symptoms (EPS)
- Due to blockade of D2 receptors - Movement disorders - Resemble Parkinson's
65
EPS Types
- Acute dystonia (spasm of face, tongue, neck, back) - Parkinsonism (bradykinesia) - Akathesia (continuously in motion) - Tardive dyskinesia (face/tongue motion, switch to atypical)
66
Atypical Antipsychotics
- Block D2 receptors - Block 5-HT1A/2A - Low affinity
67
Conventional versus Atypical Antipsychotics
- Same efficacy versus positive symptoms - Atypical greater efficacy versus negative symptoms - Atypical lower risk from EPS symptom development
68
Adverse Effects of Atypical Antipsychotics
- Sedation - Orthostatic hypotension - Weight gain - Risk for type II diabetes development - Anticholinergic effects

2060 Pharmacology (18 decks)

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