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Pharm blk4- PD

Parkinson's Dz

What are the 4 cardinal signs of parkinson’s 1.resting tremors, 2.bradykinesia, 3.lead-pipe rigidity, 4.poor balance (you need 2 to be dxed)
What happens to what part of the brain in parkinson’s (how much, + compared to normal) 80% Loss of DA neurons in substantia nigra (normal is 5% loss per decade)
What are 3 hypothesis on how DA neurons are destroyed 1.mitochondia dysfunction, 2.glutamate toxicity, 3.oxidative stress
What is the life expectancy once dxed with parkinson’s 3-5 yrs
What is one neuro-muscular feature which is intact in parkinson’s (think) Reflexes
What drugs often lead to PD-like Sxs Antipsychotics (anti-DA)
What drug have we learn can lead to PD Sxs (1~2) Meperidine (MPPP) contaminated with MPTP
How does MPTP lead to PD-like Sxs MPTP is taken by DA neurons, and it is converted to MAOB, which causes free radical stress on the mitochondrial (and neuron death)
Describe the basal ganglia system: (precise) (start with SN) Substansia Nigra has DA neuron that project on the Striatum, when activated those prevent the Globus Pallidus from inhibiting the thalamus (thus preventing motion, and resting inhibition)
Where in the basal ganglia system is DA missing STRIATUM not substansia nigra (SN is missing neurons)
Describe the dopamine receptors 1.D1 is excitatory (increase cAMP, and Ca), 2.D2 is inhibitory (decrease cAMP, and increase K)
What enzyme is central to the oxidative stress theory of PD MAO (monoamine oxidase)
what is the gold standard drug for PD (describe it quickly) L-Dopa, precursor for DA
what is the main difference btw L-Dopa and DA: L-Dopa crosses the BBB
How come L-Dopa is so selective It is only decarboxlated to DA in the nigrostriatal neurons
Describe the efficacy of L-Dopa on patients: 1/3 well, 1/3 moderate, 1/3 poor (75% works)
what are the 3 MOA, disadvantages of L-Dopa 1.decrease efficacy over time (only works for few years), 2.doesn’t stop progression of disease, 3.doesn’t work on very advanced cases (can’t be decarboxylated if no neurons are left)
Mention the pharmaco of L-Dopa: (4: absorption, peak , T1/2, brain penetrance) 1.amino acids in diet decrease gut and BBB absorption, 2.peak: 1-2 hrs, 3. Short T1/2 (2hrs), thus must be given multiple times a day, 4.only 2% enters brain
What are the sides effect of L-Dopa: Peripheral DA:1.GI, 2. tachycardia, 3.hypotension, Central DA:4.AIMs (jerky movements), 5.Psychotomimetic (txed w/ antipsychotics)
Discuss wearing off and on/off problems with L-Dopa: As tolerance progresses: you get wearing off (drug stops working before next drug schedule), or on/off (drug stops working in middle of tx)
What is often given with L-Dopa to improve brain penetrance (what is it) Carbidopa (DOPA decarboxylase inhib, prevents the decarboxylation outside nigrostriatal neurons – it does not cross the BBB)
Carbidopa reduces which AE (3) 1.GI (nausea/vomiting), 2.tachycardia, 3.hypotension
What is carbidopa + L-dopa called: Sinemet
what awkward regimen used to be recommend to PD patients (why And why not anymore(2) Drug holiday to improve response. It causes more problem: depression, immobility Cx
Discuss drug interaction of L-Dopa: (2) Vit B6 (increase peripheral metabolism), MAOA inhib (can lead to hypertensive crisis)
Who should not get L-Dopa: (5) 1.psychosis, 2.glaucoma, 3.cardiac disease (ok if carbidopa), 4.peptic ulcers, 5.skin tumors Hx (melanoma)
what is often added to sinemet (why, what is the new mix called) Entacapone (COMT inhib). COMT transforms L-Dopa in 3OMD, which competes with L-Dopa for BBB penetration. The new mix is Stalevo.
what are the AE of stalevo (5) Mostly due to increase L-Dopa: 1.orange urine, 2.nausea, hypotension, 3.dyskinesia, 4.hallucinations, 5.sleep problems
what is the monotherapy agent of choice for PD DA agonists
List the DA agonist (5 in 3 categories) (include receptors targeted) Ergot: 1.bromocriptine (D2), 2.pergolide (D1-D2), Non-ergo: 3.pramipexole (D3), 4.ropinarole (D2), Rescue :Apomorphine
What are 2 MOA advantages of DA agonist over L-Dopa  1.doesn’t require conversion (which can lead to free radicals), 2.doesn’t need working neurons
What are the 2 ways DA agonist are introduced: 1.bythemselves, 2.with Sinemet as it starts losing its effect
Which DA family are preferred Non-ergot
What is 1 pro and 1 con of pergolide: Pro: increase time on (in on/off problem), Con: valvular disease
what is 2 pro and 1 con of pramipexole: Pro: increase time on (in on/off problem) & antioxidant, Con: kidney problems
What is 1 pro and 1 con of ropinirole Pro: increase time on (in on/off problem), Con: CYP1A2
what was apomorphine 1st used for Induce vomiting
What is apomorphine used for Someone stuck in off state
How is apomorphine given: Subcu
Main AE of apomorphine: Vomiting (trimethobenzamide must be given 3 days before, and till one month after)
AE of DA agonist: Same as L-dopa go look + perivascular disease if from ergot family
Other than DA agonist and L-dopa, what else is commonly used in PD: 1.MAO inhib (selegiline), 2.amantadine, 3.muscarinic receptor antagonist (benztropine mesylate)
What are the 2 MOA of MAO inhib 1.blocking MAO-B increase DA (MAO-A is for NE), 2.blocking MAO decrease oxidative stress)
Selegiline is what type of MAO inhib: Irreversible (thus long T1/2)
Selegiline can also be used to prevent: MPTP toxicity
What should not be used with Selegiline: MAO, SSRIs
How does amantadine work: unknown
what is the main advantage of amantadine: Decrease dyskinesia
AE of amantadine: Like L-Dopa + livedo reticularis, peripheral edema
Who should not get amantadine: (2) Hx of seizure, Hx of heart failure
How is amantadine given: With sinemet
MOA of benztropine: Reduce ACh to balance ACh:DA ratio
AE of benztropine: 1.abuse, 2.hallucination, anti-cholinergic: 3.tachycardia, tachypnea
Name 4 meds and 4 procedure that can/could be use for PD: Meds: 1.beta-block, 2.NE, 3.benzos, 4.antihistamines, Procedures: 1.thalamomotomy, 2pallidotomy, 3.thalamic or palladic deep brain stimulation, 4.fetal allograft
Created by: mcafej02