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79 Cards in this Set

  • Front
  • Back
What neurotransmitters are imbalanced in Parkinson's disease?
loss of dopaminergic neurons and excess cholinergic activity.
What are the 4 strategies used to treat PD?
1) agonize the DA receptors
2) increase DA
3) prevent DA breakdown
4) curb excess cholinergic activity
What agents are used to agonize DA receptors in PD pts? (3)
-Bromocriptine (ergot alkaloid and partial
dopamine agonist)
What agents are used to increase DA in PD pts? (2)
-Amantadine (may ↑ dopamine release)
-L-dopa/carbidopa (converted to DA in CNS)
What agents are used to prevent DA breakdown in PD pts? (3)
-Selegiline (selective MAO type B inhibitor)
-Entacapone and Tolcapone (COMT inhibitors)
What agent is used to curb excess cholinergic activity in PD pts? (1)

What symptoms does it affect and not affect?
Benztropine (Antimuscarinic; improves tremor and rigidity but has little effect on
Mneumonic to remeber PD drugs?
-Levodopa (with carbidopa)
-Selegiline (and COMT inhibitors)
MOA of L-dopa (levodopa)/carbidopa?
↑ level of dopamine in brain. Unlike dopamine, L-dopa can cross blood-brain barrier and is converted by dopa decarboxylase in the CNS to dopamine.
Clinical use of L-dopa (levodopa)/carbidopa?
Toxicity of L-dopa (levodopa)/carbidopa?

Why is carbidopa used?

What are the long-term toxicities?
Arrhythmias from peripheral conversion to dopamine. Carbidopa, a peripheral
decarboxylase inhibitor, is given with L-dopa in order to ↑ the bioavailability of
L-dopa in the brain and to limit peripheral side effects. Long-term use can → dyskinesia following administration, akinesia between doses.
MOA of Selegiline?
Selectively inhibits MAO-B, thereby ↑ the availability of dopamine.
Clinical use of Selegiline?
Adjunctive agent to L-dopa in treatment of Parkinson’s disease.
Toxicity of Selegiline?
May enhance adverse effects of L-dopa.
MOA of Sumatriptan?
5-HT1D agonist. Causes vasoconstriction. Half-life < 2 hours.
Clinical use of Sumatriptan? (2)
-Acute migraine
-Cluster headache attacks
Toxicity of Sumatriptan?

Who is it contraindicated in?
Coronary vasospasm, mild tingling (contraindicated in patients with CAD or
Prinzmetal’s angina).
See chart on p.369
See chart on p.369
What 2 drugs are 1st line for Generalized tonic-clonic seizures?
What drug is 1st line prophylaxis for Status Epilepticus?
MOA of Phenytoin and Carbamazepine?
↑ Na+ channel inactivation
What 2 things is Carbamazepine 1st line for?
-tonic-clonic seizures
-trigeminal neuralgia
MOA of Lamotrigine?
Blocks voltage-gated Na+ channels
MOA of Gabapentin?
↑ GABA release
What epilepsy drug can be used for peripheral neuropathy?
MOA of Topiramate?
Blocks Na+ channels, ↑ GABA action
MOA of Phenobarbital?
↑ GABA-A action
What drug is 1st line for pregnant women and children with epilepsy?
What 3 drugs are considered 1st line for tonic-clonic seizures?
-Valproic acid
MOA of Valproic acid?
↑ Na+ channel inactivation, ↑ GABA concentration
What 2 drugs can be used for absence seizures (which is 1st line)?
-Valproic acid
-Ethosuxamide (1st line)
What drug can be used for myoclonic seizures?
Valproic acid
MOA of Ethosuxamide?
Blocks thalamic T-type Ca+ channels
What class of drugs is 1st line for acute statis epilepticus?
MOA of Benzos?
↑ GABA-A action
What 2 things can Benzos be used for as related to seizures?
-1st line for acute status epilecticus
-Also used for seizures of eclampsia (1st line to prevent seizures of eclampsia is MgSO4)
Toxicity of Benzodiazepines? (3)
Sedation, tolerance, dependence.
Tox of Carbamazepine? (7)
Diplopia, ataxia, blood dyscrasias (agranulocytosis, aplastic anemia), liver toxicity, teratogenesis, induction of cytochrome P-450.
Tox of Ethosuxamide? (5)
GI distress, lethargy, headache, urticaria, Stevens-Johnson syndrome.
Phenobarbital tox? (4)
Sedation, tolerance, dependence, induction of cytochrome P-450.
Phenytoin tox? (10)
Nystagmus, diplopia, ataxia, sedation, gingival hyperplasia, hirsutism, megaloblastic anemia, teratogenesis, SLE-like syndrome, induction of cytochrome P-450.
Valproic acid tox? (5)
GI distress, rare but fatal hepatotoxicity (measure LFTs), neural tube defects
in fetus (spina bifida), tremor, weight gain.
Lamotrigine tox? (1)
Stevens-Johnson syndrome.
Gabapentin tox? (2)
Topirimate tox?
Mental dulling
Kidney stones
Weight loss
MOA of Phenytoin?
Use-dependent blockade of Na+ channels

Inhibition of glutamate release from excitatory presynaptic neuron.
Clinical use of Phenytoin? (2)
Tonic-clonic seizures.

Also a class IB antiarrhythmic.
Toxicity of Phenytoin? (many!)
SLE-like syndrome
Induction of cytochrome P-450

Chronic use produces gingival hyperplasia in children, peripheral neuropathy, hirsutism, megaloblastic anemia (↓ vitamin B12), and malignant hyperthermia (rare); teratogenic (fetal hydantoin syndrome).
What drugs are Barbituates? (4)
MOA of Barbituates?
Facilitate GABA-A action by ↑ duration of Cl− channel opening, thus ↓ neuron firing.
Clinical use of Barbituates? (4)
Sedative for anxiety, seizures, insomnia, induction of anesthesia (thiopental).
C/I of Barbituates?
Toxicity of Barbituates?

How do you treat overdose?
-Additive CNS depression effects with alcohol, respiratory or cardiovascular depression (can lead to death), drug interactions owing to induction of liver microsomal enzymes (cytochrome P-450).

Treat overdose with symptom management (assist respiration, ↑ BP).
What drugs are Benzodiazepines?
Diazepam, lorazepam, triazolam, temazepam, oxazepam, midazolam, chlordiazepoxide,
MOA of Benzos?
Facilitate GABAA action by ↑ frequency of Cl− channel opening. Most have long half-lives and active metabolites.
Clinical use of Benzos?
-Status epilepticus (lorazepam and diazepam)
-Detoxification (especially alcohol withdrawal–DTs)
-Night terrors
Toxicity of Benzos?

Why better than Barbituates?

How do you treat Benzo toxicity?
Dependence, additive CNS depression effects with alcohol. Less risk of respiratory depression and coma than with barbiturates.
Treat overdose with flumazenil (competitive antagonist at GABA receptor).
What Benzos are short-acting?
Short acting = TOM Thumb = Triazolam, Oxazepam, Midazolam
start with anesthetics on p.372
start with anesthetics on p.372
CNS drugs must be ---- so they can cross the ---- or be actively transported
CNS drugs must be lipid soluble so they can cross the BBB or be actively transported
Drugs with ↓ solubility in blood have --- induction and recovery times.
Drugs with ↑ solubility in lipids have ---potency = 1/MAC.
increased potency
What is MAC?
minimal anesthetic concentration.
What drugs are inhaled anesthetics? (6)
Halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, nitrous oxide.
MOA of inhaled anesthetics?
Mechanism unknown. The lower the solubility in blood, the quicker the anesthetic induction and the quicker the recovery.
Effects of inhaled anesthetics? (4)
Myocardial depression
Respiratory depression
↑ cerebral blood flow (↓ cerebral metabolic demand).
Toxicity of inhaled anesthetics? (4)
Hepatotoxicity (halothane)
nephrotoxicity (methoxyflurane)
proconvulsant (enflurane)
malignant hyperthermia (rare).
5 types of drugs used as IV anesthetics?
"BB King on OPIATES PROPOses FOOLishly"

Arylcyclohexamines (Ketamine)
What is Thiopental?


Clinical uses?
Thiopental––high potency, high lipid solubility, rapid entry into brain. Used for induction of anesthesia and short surgical procedures. Effect terminated by redistribution from brain. ↓ cerebral blood flow.
What is Midazolam?

Used for what?

Bad S/Es?
Midazolam (a Benzo) most common drug used for endoscopy; used adjunctively with gaseous anesthetics and narcotics. May cause severe postoperative respiratory depression, ↓ BP (treat with flumazenil), and amnesia.
What are Arylcyclohemaxines (Ketamine)?

S/Es? (3)
PCP analogs that act as dissociative anesthetics. Cardiovascular stimulants. Cause disorientation, hallucination, and bad dreams. ↑ cerebral blood flow.
What 2 opiates are used for IV anesthesia?

What are they used with?
Morphine, fentanyl used with other CNS depressants during general anesthesia.
What is Propofol used for?

Why is it better than thiopental?
Used for rapid anesthesia induction and short procedures. Less postoperative nausea than thiopental.
What are neuromusclular blocking drugs used for?

What receptor are they selective for?
Used for muscle paralysis in surgery or mechanical ventilation. Selective for motor (vs. autonomic) nicotinic receptor.
What drug is a depolarizing neuromuscular blocking drug?
How do you reverse the blockade of depolarizing neuromuscular blockers?
Phase I (prolonged depolarization)––no antidote. Block potentiated by cholinesterase inhibitors.

Phase II (repolarized but blocked)––antidote consists of cholinesterase inhibitors (e.g., neostigmine).
What drugs are nondepolarizing neuromuscular blockers?

What are they competitive with?
Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rapacuronium.

compete with ACh for receptors.
What drugs can be used to reverse the blockade of nondepolarizing neuromuscular blockers? (3)
Reversal of blockade––neostigmine, edrophonium, and other cholinesterase inhibitors.
What is Dantrolene used for?
Used in the treatment of malignant hyperthermia, which is caused by the concomitant use of inhalation anesthetics (except N2O) and succinylcholine.

Also used to treat
neuroleptic malignant syndrome (a toxicity of antipsychotic drugs).
MOA of Dantrolene?
Mechanism: prevents the release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle.