Parkinson's Dz
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| 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)
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| 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)
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| What are 3 hypothesis on how DA neurons are destroyed | 1.mitochondia dysfunction, 2.glutamate toxicity, 3.oxidative stress
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| What is the life expectancy once dxed with parkinson’s | 3-5 yrs
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| What is one neuro-muscular feature which is intact in parkinson’s (think) | Reflexes
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| What drugs often lead to PD-like Sxs | Antipsychotics (anti-DA)
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| What drug have we learn can lead to PD Sxs (1~2) | Meperidine (MPPP) contaminated with MPTP
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| 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)
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| 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)
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| Where in the basal ganglia system is DA missing | STRIATUM not substansia nigra (SN is missing neurons)
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| Describe the dopamine receptors | 1.D1 is excitatory (increase cAMP, and Ca), 2.D2 is inhibitory (decrease cAMP, and increase K)
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| What enzyme is central to the oxidative stress theory of PD | MAO (monoamine oxidase)
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| what is the gold standard drug for PD (describe it quickly) | L-Dopa, precursor for DA
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| what is the main difference btw L-Dopa and DA: | L-Dopa crosses the BBB
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| How come L-Dopa is so selective | It is only decarboxlated to DA in the nigrostriatal neurons
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| Describe the efficacy of L-Dopa on patients: | 1/3 well, 1/3 moderate, 1/3 poor (75% works)
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| 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)
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| 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
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| 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)
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| 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)
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| 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)
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| Carbidopa reduces which AE (3) | 1.GI (nausea/vomiting), 2.tachycardia, 3.hypotension
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| What is carbidopa + L-dopa called: | Sinemet
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| 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
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| Discuss drug interaction of L-Dopa: (2) | Vit B6 (increase peripheral metabolism), MAOA inhib (can lead to hypertensive crisis)
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| 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)
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| 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.
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| 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
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| what is the monotherapy agent of choice for PD | DA agonists
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| 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
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| 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
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| What are the 2 ways DA agonist are introduced: | 1.bythemselves, 2.with Sinemet as it starts losing its effect
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| Which DA family are preferred | Non-ergot
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| What is 1 pro and 1 con of pergolide: | Pro: increase time on (in on/off problem), Con: valvular disease
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| what is 2 pro and 1 con of pramipexole: | Pro: increase time on (in on/off problem) & antioxidant, Con: kidney problems
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| What is 1 pro and 1 con of ropinirole | Pro: increase time on (in on/off problem), Con: CYP1A2
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| what was apomorphine 1st used for | Induce vomiting
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| What is apomorphine used for | Someone stuck in off state
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| How is apomorphine given: | Subcu
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| Main AE of apomorphine: | Vomiting (trimethobenzamide must be given 3 days before, and till one month after)
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| AE of DA agonist: | Same as L-dopa go look + perivascular disease if from ergot family
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| 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)
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| 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)
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| Selegiline is what type of MAO inhib: | Irreversible (thus long T1/2)
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| Selegiline can also be used to prevent: | MPTP toxicity
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| What should not be used with Selegiline: | MAO, SSRIs
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| How does amantadine work: | unknown
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| what is the main advantage of amantadine: | Decrease dyskinesia
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| AE of amantadine: | Like L-Dopa + livedo reticularis, peripheral edema
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| Who should not get amantadine: (2) | Hx of seizure, Hx of heart failure
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| How is amantadine given: | With sinemet
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| MOA of benztropine: | Reduce ACh to balance ACh:DA ratio
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| AE of benztropine: | 1.abuse, 2.hallucination, anti-cholinergic: 3.tachycardia, tachypnea
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| 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
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