28 April wk7-D

Question 1

MOA of Levodopa and what is it used for?

Answer 1

L-DOPA is a precursor to Dopamine–the NT that is deficient in the brain in Parkinson’s L-DOPA is used because it crosses the BBB where Dopamine does not, it is converted to Dopamine in the CNS by DOPA decarboxylase

Question 2

What is administered with Levodopa and why?

Answer 2

Carbidopa Inhibits peripheral conversion of L-DOPA to dopamine–preventing peripheral SE’s and making more available for the brain It is a peripheral DOPA decarboxylase inhibitor

Question 3

Selegiline

Answer 3

Inhibits MAO-B which preferentially metabolizes Dopa over NE Used to increase levels of dopamine in parkinson’s Often adjunct to L-Dopa for parkinson’s

Question 4

In one sentence, what is the cause of parkinson’s?

Answer 4

Too little Dopamine and too much Ach

Question 5

What are the major treatment strategies for Parkinson’s?

Answer 5

1) Dopamine agonists: Bromocriptine (Ergot), Pramipexole, Ropinirole (Non-ergot, preferred) 2) Inc Dopamine available: Amantadine–inc release and dec re-uptake of DA 3) Increase L-dopa: Levodopa=L-dopa, Carbidopa–inhibits DDC (conversion enzyme), Entacapone and Tolcapone (more centrally acting)–inhibit COMT that breaks down dopa to 3-OMD 4) Prevent dopa breakdown: Selegiline–selective MOA-B inhibition 5) Decrease Ach: Benztropine–antimuscarinic

Question 6

SE’s of Levodopa therapy

Answer 6

Peripheral conversion to Dopamine causes: N/V, arrhythmias from conversion to catecholamines, postural hypotension, hot flashes Central effects: agitation, anxiety

Question 7

What are the class Ia antiarrhythmic drugs and primary actions?

Answer 7

Quinidine, Procainamide, Disopyramide

Na channel blockers

Slow AP conduction velocity (Phase 0, depolarization of cardiac tissue)

Increase AP length and QT interval

Question 8

What are the class Ib antiarrhythmic drugs and main actions?

Answer 8

Lidocaine, Mexiletine, Tocainide

Na channel blockers

Decrease AP duration, no effect on AP conduction velocity

Best for after MI

Question 9

What are the class Ic antarrhythmic drugs and main actions?

Answer 9

Flecainide, Propafenone

Na channel blockers

Slows AP conduction velocity, little effect on duration

Question 10

What are the class II antiarrhytmic drugs and main actions?

Answer 10

Beta Blockers

Metoprolol, propranolol, esmolol, atenolol, timolol, carvedilol

Slows SA node and AV conduction

Increases PR interval

Primary effect on the phase 4 of nodes and the slope of depolarization

Question 11

What are the class III antiarrhythmic agents and main actions?

Answer 11

K channel blockers

Amiodarone, Ibutilide, Dofetilide, Sotalol

No effect on AP conduction velocity, Prolongs AP duration also causing prolonged QT potentially leading to torsades (Amiodarone least likely)

Question 12

What are the class IV antiarrhythmic drugs and main actions?

Answer 12

Ca channel blockers

Verapamil, Diltiazem

Decrease conduction velocity, increase PR interval

Prevent nodal arrythmias

Question 13

Which antiarrythmic classes are more nodal or myocyte oriented in their effects?

Answer 13

Nodal effects: Beta blockers (Class II), Ca channel blockers (Class IV), more likely to have prolonged PR

Myocyte: Na channel blockers (Class I), K channel blockers (Class III), more likely to have prolonged QT

Question 14

Of the antiarrhythmic drugs that cause prolonged QT, which has the smallest chance of causing Torsades?

Answer 14

Amiodarone

Question 15

What is the MOA for Adenosine on the heart?

Answer 15

Increases K conductance slowing AP cunduction through the AV node slowing the rate of the heart

Question 16

Drug of choice for diagnosing/treating SVTach

Answer 16

Adenosine

Question 17

What are the general drugs and actions to control cholesterol and lipids?

Answer 17

Question 18

Which cholesterol drugs are best for what effect?

Answer 18

Statins: lowering LDL

Niacin: increasing HDL

Fibrates: decreasing triglycerides

Question 19

Which cholesterol levels (LDL, HDL, Triglycerides) is most important to address to prevent CV events?

Answer 19

LDL is the most important and patients that have a normal LDL should still be placed on statins after a CV event to prevent secondary events

Question 20

Drugs and no drug approaches can raise HDL, what is the difference?

Answer 20

Drug raising of HDL does not improve CV outcomes whereas using exercise, stopping smoking, good diet does have significant CV benefits

Question 21

What prostaglandin causes elevated temperature set point in hypothalamus?

Answer 21

PGE2

Question 22

ACE inhibitor combined with a preceding administration of what kind of drug would cause significant first-dose hypotension?

Answer 22

Diuretics

They cause a volume depleted state that leads to high renin and high ANG II that maintains the BP

Rapid loss of ANG II causes hypotension

Hypotension can also occur in patients with heart failure

To prevent this, administer ACEI slowly

Question 23

What is a common cause of gingival hyperplasia among antiseizure drugs?

Answer 23

Phenytoin

Question 24

What are SE’s of phenytoin?

Answer 24

Gingival hyperplasia from increased PDGF

Cerebellar and Vestibular dysfunction leading to nystagmus

P450 induction

Question 25

DOC for status epilepticus

Answer 25

Benzos

Esp Lorazepam

Phenytoin is administered as well to prevent recurrence

Question 26

What can happen several days after a subarachnoid hemorrhage?

Answer 26

Blood breakdown products are believed to be the cause of vasospasm that occurs 3-8 days after the initial hemorrhage leading to focal neurological deficits

Prevented by Ca channel blockers that prevent the contraction of smooth muscle

Nimodipine specific drug

Question 27

What is a treatment for akathisia?

Answer 27

Beta blockers

Question 28

What is cataplexy and a potential treament?

Answer 28

Cardinal feature of narcolepsy

Sudden loss of muscle tone, happens with high emotion

Treated with muscarinic antagonists