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CNS Flashcards

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1
Q

Neuropharmacology Definition

A

study of how drug affects function of CNS

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2
Q

5 mechanisms in which drugs act in CNS

A

Replacement (Drug replaces neurotransmitter) ,

Agonist/Antagonist (binds to receptor in the post-synaptic membrane)

Inhibit neurotransmitter breakdown

Blocking Reuptake (stops it from taking back into the pre-synaptic membrane, stay in synaptic cleft longer)

Nerve Stimulation (Stimulate nerve to release more neurotransmitters)

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3
Q

Symptoms, pathophysiology, and etiology of Parkinson

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4
Q

Symptoms, pathophysiology, and etiology of Alzheimer

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5
Q

Symptoms, pathophysiology, and etiology of Schizophrenia

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6
Q

MOA for Alzheimer’s drugs

A
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7
Q

MOA for Parkinson’s Drugs

A
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8
Q

What are Neurons?

A

Neurons are cells in the brain that act to process and transmit signals and information

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9
Q

How does a neuron transmit information?

A

By chemical or electrical signaling. It starts with the dendrite receiving a signal from another neuron. This causes AP to propagate along the axon and when AP reaches the synaptic nerve terminal, it causes the release of neurotransmitters which pass the signal along to the next neuron.

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10
Q

Resting potential of a cell

A

-70 mV

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11
Q

Threshold

A

If depolarizing stimulus is received, sodium gated channel opens and it allows sodium to enter cell. Na+ is positive so it begins to depolarize making membrane potential to get close to threshold.

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12
Q

Rising Phase

A

If threshold is achieved, other sodium channels open and sodium rush in. Membrane potential increases.

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13
Q

Falling Phase

A

Sodium channel closes and potassium channle open. K+ comes out of cell and membrane potential decrease back down, as membrane potential get close to resting potential more potassium channel open.

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14
Q

Hyperdepolarization

A

Membrane potential went under resting potential due to excess potassium leaving cells

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15
Q

Steady State

A

As it enter steady state, Potassium channels closed

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16
Q

How does a neuron transmit singals.

A

AP reach to presynatic terminal, causes influx of Ca+ which causes neurotransmitter containing vesicle to fuse with presynaptic membrane, vesicle releases neurotransmitter into the synaptic cleft. Neurotransmitters bind to receptors on the post-synaptic nerve membrane and signal continues.

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17
Q

Classes of neurotransmitter

A

Monoamines: Norepinephrine, Epinephrine, Dopamine, Serotonin
Amino acid - Excitatory, Inhabitory
Other - Acetylcholine

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18
Q

Neurotransmitters

A

chemical that transmits signals across the synapse.

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19
Q

Monoamines and related diseases

A

Norepinephrine- Depression and Anxiety
Epinephrine - Anxiety
Dopamine- Parkinson, Schizophrenia
Serotonin - Depression and Anxiety

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20
Q

Amino Acid and related diseases

A

Excitatory - glutamate (Alzheimer)
Aspartate - Alzheimer

Inhibitory - GABA (anxiety), Glycine (anxiety)

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21
Q

Other neurotransmitters and related disease

A

Acetylcholine - Alzheimer and Parkinson

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22
Q

Pathophysiology of Parkinson’s Disease

A
  • PD is a chronic movement disorder.
  • Caused by imbalances between acetylcholine and dopamine in the brain.
  • Symptoms arise because 1. dopamine release decreases, not enough dopamine to inhibit GABA release. 2. excess acetylcholine = increased GABA release 3. Excess GABA= movement disorder
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23
Q

Symptoms of Parkinson

A

chronic movement disorder
Tremor - in extremities hands, arm,legs, jaw, face
Ridigity - joint stiffness and increase muscle tone
Bradykinesia -slowness to initiate movement
Masklike face - can’t show facial expression, have difficulty blinking and swallowing
Postural Instability - balance is impaired, difficulty balancing with walking
Dementia - later stages

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24
Q

Etiology of Parkinson

A

Mostly unknown but some possible causes might be
- Drugs (MPTP, by-product of illicit street drugs, MPTP causes the irreversible death of dopaminergic neurons.)
- Genetics ( alpha synuclein, parkin, UCHL1, DJ-1 mutation)
- Environmental Toxin ( pesticide)
- Brain Trauma ( direct trauma - like boxing )
- Oxidative Stress ( Reactive oxygen species cause degeneration of dopaminergic neuron. eg, diabetes)

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25
Drug treatment of PD
- only treat symptoms - improves balance of dopamine or acetylcholine - increase dopamine or decrease acetylcholine
26
5 major classes of drugs that treat PD
- Dopamine replacement - Dopamine Agnoist - Dopamine Release - Catecholamine-O-Methyltransferase inhibitor - Monoamine Oxidase- B inhibitor (MAO-B inhibitor)
27
Dopamine replacement drugs- L-Dopa
Levodopa (L-DOPA) most effective . -L-dopa cross the blood-brain barrier via active transport protein -inactive on its own but once in the dopaminergic nerve terminal turn into dopamine - Conversion from l-dopa to dopamine, mediated by decarboxylase enzymes -cofactor pyridoxine (B6) speed this up
28
L-DOPA MOA
- transported into the brain via active transporter - decarboxylase enzymes convert to dopamine - packaged into vesicles - increase the amount of dopamine in dopaminergic neurons when AP comes Why not give Dopamine directly - Because dopamine does not cross blood-brain barrier and has a short half-life in blood
29
L-Dopa adverse effect
- nausea and vomiting (dopamine mediate activation of chemoreceptors trigger zone in the medulla of the brain) Dyskinesia - abnormal involuntary movements Cardiac dysrhythmias - conversion of L-dopa in the periphery result in cardiac beta 1 receptor Orthostatic hypertension Psychosis - 20% of patients
30
Peripheral L-Dopa Metabolism
-only 1% of L-dopa reaches the brain - the rest in peripheral tissues (mostly in the intestine) before reaching the brain - always given with carbidopa, decarboxylase inhibitor (stops from peripheral metabolism of L-dopa) - with carbidopa about 10% reaches the brain - carbidopa allows a lower dose of Ldopa and increases cardiac dysrhythmia and nausea and vomiting
31
2 types of Loss of effect L-Dopa
- wearing off (gradual loss) : occurs at ends of dosing interval , drug lvl might be low, Can be minimized by shortening dosing interval, another drug COMT inhibitor that inhibits L-Dopa metabolism) , add dopamine agonist to therapy - On-off (abrupt): occurs even when drugs lvl are high minimized by dividing meds into 3-6 doses per day, controlled release formulation, and more protein-containing meals in the evening.
32
Dopamine Agonist how does it work?
It crosses blood brain barrier, and then directly binds to dopamine receptors in the post-synaptic cell membrane. Not as good as L-dopa but used in mild cases
33
Adverse effect of dopamine agonist
Hallucination, daytime drowsiness, orthostatic hypotension
34
How does Dopamine releaser work?
1. Stimulate the release of dopamine from dopaminergic neuron 2. Block the reuptake of dopamine in the presynaptic nerve terminal (make dopamine stay in postsynaptic terminal 3. Block NMDA receptor
35
How is Dopamine release different from L-Dopa
Works rapidly. Not as effective as L-Dopa but usually use in combination or only in mild PD cases.
36
Why is blocking NMDA receptor important?
Decrease dyskinesia
37
What are the adverse effects of Dopamine releaser ?
- dizziness, nausea, vomiting, lethargy, anticholinergic drug adverse effects
38
What is Catechol-O-Methyltransferase (COMT)
An enzyme that add methyl group to Dopamine and L-Dopa and makes them inactive
39
What does COMT inhibitor do
By stopping COMT, it stops from L-dopa and dopamine getting inactivated so greater fraction of L-Dopa is available to be turn into dopamine
40
COMT Inhibitor VS L-Dopa, how does it work
Only treat moderately, need to use in combination with L-Dopa
41
Adverse Effect of COMT Inhibitor
Dizziness, nausea, vivid dream, hallucination, orthostatic hypertension.
42
MAO-B
Enzyme that metabolize dopamine and L-dopa by oxidating, thus making it inactive
43
Where can MAO-B found
Found in periphery and brain
44
How does MAO-B inhibitor work?
By stopping MAO-B to metabolize L-Dopa. So allow more conversion of dopamine in brain. And inhibit dopamine metabolism which means more dopamine left in nerve terminal for action potential
45
MAO-B VS L-Dopa
Only moderately effective. Often combine with L-Dopa
46
Adverse Effect of MAO-B
Insomnia, Dizziness, Orthostatic Hypotension.
47
MAO-B and hypertension
MAO-B inhibitor does not inhibit MAO-A in the liver at the therapeutic dose of PD tx, so no hypertension crisis when acting with tyramine-containing food.
48
Acetylcholine role in PD
excess of acetylcholine in PD in part causes diaphoresis (excessive sweating), salivation, and urinary incontinence.
49
Anticholinergic drug how does it work?
Block acetylcholine from binding to receptor.
50
How does anticholinergic work with L-dopa
It helps by increasing the effectiveness of Ldopa, and decrease the incidence of excess acetylcholine - diaphoresis, salivation, urinary incontinence
51
Adverse effect of anticholinergic
Dry mouth, blurred vision, urinary retention, constipation, tachycardia Adverse Effects of Anticholinergic Drugs 💡 Mnemonic: "Can't See, Can't Pee, Can't Spit, Can't Sh*t" 🚫👀🚽💦💩 Can't See → Blurred vision (due to pupil dilation) Can't Pee → Urinary retention (difficulty urinating) Can't Spit → Dry mouth (lack of saliva) Can't Sh*t → Constipation (slowed digestion) Increased heart rate (tachycardia) Confusion, memory problems (especially in elderly) Flushed skin & overheating (due to decreased sweating)
52
Which population should not be treated with anticholinergic
Elderly because of the CNS side effects like confusion, hallucination, and delirium.
53
What is Alzheimer
Irreversible form of progressive form of dementia
54
Symptoms of Alzheimer
Early symptoms : confusion, memory loss, problem with conducting routine task General Symptoms: memory loss, problem with language, judgement and behavior and intelligence As disease progress, have issues with ADL
55
Pathophysiology of Alzheimer
Degeneration of cholinergic neurons in the hippocampus and followed by the degeneration of cholinergic neurons in the cerebral cortex. Linked with decreased cholinergic nerve function
56
Hallmarks of Alzheimer Disease
Neurofibrillary tangles and neuritic plaques.
57
Neurofibrillary tangels
These form inside neurons. This is the result of when microtubule arrangement is disrupted. This happened due to the abnormal production of a protein called tau. Tau is responsible for forming cross-bridges between microtubules keeping their structure.
58
Neuritic Plaques
Found outside of the neuron. Composed of a core that has a protein fragment called beta-amyloid. This beta-amyloid is shown to kill hippocampal cells
59
Etiology of Alzheimer
- Unknown. - Familiar linkage, 20% of cases run in the family. - Mutation in Apolipoprotein ApoE4, in pt has two copies of ApoE4 - increased risk of Alzheimer disease. ApoE4 promotes neuritic plaque, by binding to beta-amyloid and promoting it deposition. -Gene mutation in amyloid precursor protein gene. Also involved in the production of beta-amyloid. -head injury
60
Drug treatment for Alzheimer
1. Cholinesterase inhibitor- stop breakdown of acetylcholine 2. NMDA receptor antagonist - block NMDA mediated increase in calcium inside the neuron
61
Cholinesterase inhibitor
- inhibit the metabolism of acetylcholine by the enzyme acetylcholinesterase - so more acetylcholine remains in the synaptic cleft -only able to enhance in healthy neuron - only effective in 25% of patient
62
Adverse effect of cholinesterase
Nausea and vomiting, diarrhea, Insomnia
63
NMDA receptor what does it do?
NMDA is a Calcium channel, blocked by magnesium at rest. When glutamate release from the presynaptic neuron, binds to NMDA receptor, dissociates magnesium, this allow calcium to enter post synaptic neuron. Glutamate leaves the receptor, magnesium return and block entry of calcium. Normal calcium influx is important for learning and memory. In Alzheimer, there is excessive glutamate release so NMDA receptor stays open so excess calcium to enter the cell It's bad because 1. affect learning and memory (overpower normal calcium signal) 2. cause degradation of neuron (too much ca is toxic )
64
NMDA antagonist how it works?
NMDA antagonist binds to glutamate receptors before excess calcium goes into the cell. Prevents degradation of cholinergic neurons.
65
NMDA antagonist adverse effect
Nothing to report very well, tolerated.
66
Schizophrenia Positive Symptoms
exaggerate or distort normal neurological function Delusion Hallucination Agitation Combativeness Disorganized Speeach
67
Schizophrenia Negative Symptoms
Loss of Normal neurological function Poor Self Care Poverty of Speech Social Withdrawal Emotional Withdrawal Poor Insight Poor Judgement
68
Schizophrenia Etiology
Largely Unknown increase risk if you have Family Hx Drug Abuse: Meth, LSD, PCP Low Birth Weight: <5.5 lbs Low IQ
69
Brain Region Affected by Schizophrenia
Funny → Frontal Lobe → Problem-solving, planning, insight issues. Hippos → Hippocampus → Memory and learning impairments. Audition → Auditory System → Overactivity causes hallucinations. Before → Basal Ganglia → Movement, emotions, paranoia, hallucinations. Olympic → Occipital Lobe → Visual processing, recognizing emotions. Long Jump → Limbic System → Emotional regulation, agitation.
70
Pathophysiology of Schizophrenia
Increase Dopaminergic nerve transmission, opposite to PD Neurotransmitters like 5HT (2A) (serotonin) decrease in number but increase in the number of 5HT1A receptors in the frontal cortex Glutamate binds to and activates the NMDA receptor, PCP is a strong antagonist for the NMDA receptor and causes schizophrenia symptoms. Decrease number of NDMA receptor in some region of the brain.
71
Which drug helps the positive symptoms of schizophrenia
Drugs that block dopaminergic nerve function
72
Diagnosis of Schizophrenia
No definitive test. A psychiatrist may interview friends and family and evaluate - changes in function from before illness, family hx, developmental background, and responses to meds, brain scan : enlarge ventricle and decrease frontal lobe activity.
73
Drug treatment of schizophrenia
conventional and atypical antipsychotic, treat symptoms by blocking dopamine, serotonin and or glutamate
74
How does conventional antipsychotics work?
By Blocking the binding of the dopamine 2 receptor in the mesolimbic system of the brain, can mildly block acetylcholine, histamine, and norepinephrine. The initial effect may be seen in 1-2 days, substantial improvement in 2-4 wks
75
Adverse Effect of conventional antipsychotic
Extrapyramidal symptoms ( relating to or denoting nerves concerned with a motor activity that descends from the cortex to the spine and is not part of the pyramidal system.) Sudden High Fever Anticholinergic effects Orthostatic Hypotension Sedation Skin Reaction
76
Extrapyramidal symptoms
- Movement disorders that resembles to PD Acute dystonia, Parkinsonism, Akathesia, Tardive Dyskinesia.
77
Acute Dystonia
Acute Dystonia - involuntary spasm of face, tongue, neck or back. Occurs Early in therapy
78
Parkinsonism
Parkinsonism - mask like face, bradykinesia (slow movement), stoop posture, rigidity. Occurs early in therapy. Avoid L-Dopa
79
Akathesia
pacing, squirming, desire to continue in motion
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Tardive Dyskinesia
Occurs in 20% of pt in therapy, irreversible. 💡 "TARDIVE" → T → Tongue movements (protruding, twisting) A → Abnormal facial expressions (grimacing, lip-smacking) R → Repetitive movements (uncontrollable) D → Dopamine receptor hypersensitivity (cause of TD) I → Irreversible in severe cases V → Vacant chewing motion (as if chewing gum) E → Excessive blinking & jerky limb movements Should be switched to Atypical Antipsychotic
81
How does Atypical Antipsychotics work?
Block both Dopamine and Serotonin receptors ( 5HT1A and 5HT2A)
82
Atypical Antipsychotic VS Conventional Antipsychotic
Atypical block dopamine (D2) receptors, but not as strongly as older antipsychotics. They also block serotonin (5-HT1A & 5-HT2A) receptors, which helps improve symptoms. Why Are They Better Than Older Antipsychotics? ✅ Equally effective at treating positive symptoms (hallucinations, delusions). ✅ Much better at treating negative symptoms (social withdrawal, lack of motivation). ✅ Lower risk of movement disorders (like tardive dyskinesia) because they don’t block dopamine as strongly.
83
Adverse Effects of Atypical Antipsychotic
-Sedation -Orthostatic Hypotension -Weight Gain (up to 75lbs) -Risk to developing type 2 diabetes -Anticholinergic effects Use "SOW RA" 🐷 (Imagine a lazy pig "sowing" seeds but feeling sleepy and heavy.) S → Sedation (makes you feel drowsy) O → Orthostatic hypotension (dizzy when standing up) W → Weight gain (can be severe) R → Risk of type II diabetes (due to weight gain & metabolism changes) A → Anticholinergic effects (dry mouth, constipation, blurry vision)
84

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