Uploaded by Bansil, Kenneth Miguel

Parkin&MS

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3️⃣
Parkin & MS
Subject
106
Video
Axons = Myeline Sheets
Sclerosis - brain and spinal cord (disease in CNS), autoimmune disorder
results in sensory and motor problems
protected by blood brain barrier
Discussion:
Types of Multiple Sclerosis
1. Replasing - Remitting (RRMS) = common cause of inflamed t-cells
2. Secondary Progressive (SPMS)
3. Primary Progressive (PPMS)
4. Progressive - Relapsing (PRMS)
Symptoms:
20-40yrs
Charcotic Neurologic Triad = Dysarthria, Nystagmus, Intention Tremors
Have Plaques (in ANS)
Lhermiette’s Signs = electric signs
Diagnosis is MRI
Multiple Sclerosis - myeline sheet protects axons
chronic typically progressive disease involving damage to the sheaths of nerve cells in the brain and spinal cord
slow growing infection
attack myelin sheath
muscle weakness, spasticity, diplopia (two images)
elevated IgG in CSF, (MRI reveals lesions
Treatment Goal: = decrease inflammatory process
Symptoms: hearing, blurred vission, dysarthria, dysphagia, constipation
1. Acute Attack = (exacerbation (worsening), motor weakness, optic neuritis, spasticity
Medications: prednisone - glucocorticoids, ACTH (Adrenocorticotropic Hormone)
2. Remission = spasticity, clinical MS
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Medications: Betaseron, Imuran-suppress
3. Chronic Progressive (wheel chair-bond) - paraplysis -progress
Medications: Cytoxan, ACTH
1. Centrally Acting Muscle Relaxants
Baclofen - to treat muscle spasticity (drowsiness, headache, diarrhea, abdo disease)
2. Peripherally Acting Muscle
Dantrolene (Dantrium) - to treat spasticity
TEST:
1. Dystthira,
2. Nystagmus Diagnostic is = MRI,
3 .prednisone,
4.multiple sclerosis,
5.prenisone,
6.Betaseron,
7.Dysarthria,
8.Baclofen,
9.Dantrium,
10.Nystagmus
Lesson 5: Parkinson’s Disease (PD)
= Neurotransmitter: Dopamine
1st Video: PD
600k to 1M
60k per year has PD
happens when age increase
Test
Lab Test
Cholesterol
Medical History
Motor Movement Signs
Resting Tremors
Stiffness
Slow movement
Other SIgns
Consti, depression, cognitive, loss of smell
Dopamine stops in the brain
Factors affecting PD is unknown but it can be genetic or environmental
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To ease symptoms:
Have movement disorder specialist
Individualized
2nd Video: Dopamine
produces in 3 parts = substansia nigra, ventral tegmental area, and hypothalamus
made in tyrosine
purpose is to feel pleasure, shopping, smelling
4 Types:
Reward
Reinforcement
Movement
Prolactin = SE: low dopamine, postpartum depression
re-uptake of dopamine by postsynaptic vesicles
presynaptic
3rd Video: MAO Inhibitor
treats depression
synaptic cleft
Dopamine Synthesis:
Levodopa → dopamine
Monoamine Oxidase
MAO & COMT Inhibitor (enzymes)
degrade dopamine
Earliest develop anti-depressant
SE: Increase BP & blood sugar levels
SE of MOA:
Insomia, headache, dry mouth
Can be combine with MAOI
painkiller
cold & allergies
antidepressants
Discussion Parkinson’s Disease
neurologic disorder by muscle rigidity, tremor, bradykinesia, loss of postural
chronic progressive
involving substansia nigra & basal ganglia resulting in decease dopa and increase acetylcholine
Dopamine: Inhibitory neurotransmitter
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Acetylcholine: Excitatory “”
Signs & Symptoms
muscle rigidity/stiffness = passive movement
tremor = pill rolling
bradykinesia = arms, eyes decrease blink, loss smell
Tyrosine → Levodopa → Dopamine
Goal:
aimed at correcting the neurotransmitter imbalance
all forms of treatment for PD are palliative, not curaitve
DRUGS:
1. Anticholinergic (Symphathetic)
reduces excessive cholinergic activity
cliemts with minimal symptoms
decrease rigidity
decrease some tremors but minimal effect on bradykinesia
Drug of Choice = Cogentin (Benztropine Mesylate)
SE: nausea, dry mouth, nervousness, blurred vision, constipation, urinary retention
Caution: narrow-angle glaucome, GI obstruction, ulcerative colitis, benign prostoratic, hyperplasia(BPH)
NR: monitor vs, urine output, bowel sounds, increase fiber/fluid in diet
provide candies, gum, eye examination
2. Dopaminergics (Dopamine Agonist)) - stimulate dopamine receptor
a. Levodopa - amino acid like tyrosine
most effective drug
dopamine replacement agent
precursor of dopamine
given in increase dosage (DOPA DECARBOXYLASE)
short half life (3-4x day)
initially low does then gradually increase weekly
maximum effect after 2-4mos
b. Carbidopa
alternative to levodopa
inhibits the enzymes DOPA DECARBOXYLASE periphery → periphery →more→ levodopa reaches the blood brain
barrier
combined with levodopa in a ratio of 1:10
sinemet 10-100 )brand name)
Advantage: more dopa reaches the basal ganglia, single dose/day of levodopa to achieved desired effect
SE: n/v, dystonic movement, psychotic, behavior, cardiac, dysrhythmia, palpitation & orthostatic hypertension
3. Dopamine Agonists - stimulate the dopamine receptors
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a. Amantadine HCI
symmetrical (brand name) (anti-parkinsons)
believe to release dopa & noreph
SE: GI Distress, nervoucness, anxiety, Livdeo Reticularis
b. Parlodel (Bromocriptine Mesylate)
Ergot derivative with potent dopa recpetor agonist activity in CNS, CV, & GI systems
activity postsynaptic dopa receptors in the corpus stratum
substitute for levodopa
4. Monoamine Oxidase - B (MAO-B) Inhibitors
Enzyme causes the catabolism of dopa
increase the activity of dopa
a.Selegine HCI (Eldepyl, Carbex)
inhibits MAO-B thus prolong effect of Levodopa
Drug Interactions:
VIT-B increase DOPA DECARBOXYLASE action
Anti-psychotic drugs - block dopamine receptors
Large dose of Selegiline = Hypertensive Crisis
5. Cathecol-o-methyl Trasferase (COMT) Inhibitors
enzyme that inactie dopamine
Increase amount of levodopa concentration in brain
Tolcapone, Entacapone
SE: dyskinesia, urine discoloration, anxiety, abdo pain, consti, dyspeia, dizzness
NR: obtain baseline data, taking levodopa should be monitored for orthosatic hypertension, cardiac dysrhythmia, psychotic
disturbance.
receiving dopaminergic = closely monitor for dizziness and risk for fall
agents should not be stooped abruptly
urine maybe disclosed & wlll obtain darken with air exposure, perspiration may be dark = harmless
Decrease intake of protein rich foods interfering drug transport
COMT inhibitor should not be take with MAOB Inhibitor
SGOT & SGPT
Test:
Major Signs of Parkinson’s Disease
tremors
muscle stiffness
impaired balance & coordination
Face of pt. with PD = expressionless
tremors description = pill rolling
Drug of choice for anti-cholinergic drug = congentin
2 symptoms can be treated for= tremors, muscle stiffness & rigidity
Most effective dopaminergic drug = levodopa
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levodopa is the best drug choice instead of dopamine where = blood brain barrier
enzyme that converts levodopa to dopamine = DOPA DECARBOXYLASE
drugs given in combine with levodopa = caridopa
substitute for levodopa = parlodel
2 enzymes that catabolyized dopamine = MAO & COMT
increase BP
selegilin cant be take bcoz of = anti-psychotic drug
has a label warning of what = hepato - toxicity
Causes of Parkinson = Genetic & Enviromental
Precursor of levodopa = tyrosine
funcitons of dopamine = reward, reinforcement, movement, prolactin
3 peripheral symptoms of PD = pain, numbness, tingling or muscle weakness,
enzyme = SGOT & SGPT
neurotransmitter = dopamin
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