Fa Neurology - Pharmacology

Front 1

What neurotransmitters are imbalanced in Parkinson's disease?

Back 1

loss of dopaminergic neurons and excess cholinergic activity.

Front 2

What are the 4 strategies used to treat PD?

Back 2

1) agonize the DA receptors
2) increase DA
3) prevent DA breakdown
4) curb excess cholinergic activity

Front 3

What agents are used to agonize DA receptors in PD pts? (3)

Back 3

-Bromocriptine (ergot alkaloid and partial
dopamine agonist)
-Pramipexole
-Ropinirole

Front 4

What agents are used to increase DA in PD pts? (2)

Back 4

-Amantadine (may ↑ dopamine release)
-L-dopa/carbidopa (converted to DA in CNS)

Front 5

What agents are used to prevent DA breakdown in PD pts? (3)

Back 5

-Selegiline (selective MAO type B inhibitor)
-Entacapone and Tolcapone (COMT inhibitors)

Front 6

What agent is used to curb excess cholinergic activity in PD pts? (1)

What symptoms does it affect and not affect?

Back 6

Benztropine (Antimuscarinic; improves tremor and rigidity but has little effect on
bradykinesia)

Front 7

Mneumonic to remeber PD drugs?

Back 7

BALSA:
-Bromocriptine
-Amantadine
-Levodopa (with carbidopa)
-Selegiline (and COMT inhibitors)
-Antimuscarinics

Front 8

MOA of L-dopa (levodopa)/carbidopa?

Back 8

↑ 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.

Front 9

Clinical use of L-dopa (levodopa)/carbidopa?

Back 9

Parkinsonism

Front 10

Toxicity of L-dopa (levodopa)/carbidopa?

Why is carbidopa used?

What are the long-term toxicities?

Back 10

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.

Front 11

MOA of Selegiline?

Back 11

Selectively inhibits MAO-B, thereby ↑ the availability of dopamine.

Front 12

Clinical use of Selegiline?

Back 12

Adjunctive agent to L-dopa in treatment of Parkinson’s disease.

Front 13

Toxicity of Selegiline?

Back 13

May enhance adverse effects of L-dopa.

Front 14

MOA of Sumatriptan?

Back 14

5-HT1D agonist. Causes vasoconstriction. Half-life < 2 hours.

Front 15

Clinical use of Sumatriptan? (2)

Back 15

-Acute migraine
-Cluster headache attacks

Front 16

Toxicity of Sumatriptan?

Who is it contraindicated in?

Back 16

Coronary vasospasm, mild tingling (contraindicated in patients with CAD or
Prinzmetal’s angina).

Front 17

See chart on p.369

Back 17

See chart on p.369

Front 18

What 2 drugs are 1st line for Generalized tonic-clonic seizures?

Back 18

Phenytoin
Carbamazepine

Front 19

What drug is 1st line prophylaxis for Status Epilepticus?

Back 19

Phenytoin

Front 20

MOA of Phenytoin and Carbamazepine?

Back 20

↑ Na+ channel inactivation

Front 21

What 2 things is Carbamazepine 1st line for?

Back 21

-tonic-clonic seizures
-trigeminal neuralgia

Front 22

MOA of Lamotrigine?

Back 22

Blocks voltage-gated Na+ channels

Front 23

MOA of Gabapentin?

Back 23

↑ GABA release

Front 24

What epilepsy drug can be used for peripheral neuropathy?

Back 24

Gabapentin

Front 25

MOA of Topiramate?

Back 25

Blocks Na+ channels, ↑ GABA action

Front 26

MOA of Phenobarbital?

Back 26

↑ GABA-A action

Front 27

What drug is 1st line for pregnant women and children with epilepsy?

Back 27

Phenobarbital

Front 28

What 3 drugs are considered 1st line for tonic-clonic seizures?

Back 28

-Phenytoin
-Carbamazepine
-Valproic acid

Front 29

MOA of Valproic acid?

Back 29

↑ Na+ channel inactivation, ↑ GABA concentration

Front 30

What 2 drugs can be used for absence seizures (which is 1st line)?

Back 30

-Valproic acid
-Ethosuxamide (1st line)

Front 31

What drug can be used for myoclonic seizures?

Back 31

Valproic acid

Front 32

MOA of Ethosuxamide?

Back 32

Blocks thalamic T-type Ca+ channels

Front 33

What class of drugs is 1st line for acute statis epilepticus?

Back 33

Benzodiazepines

Front 34

MOA of Benzos?

Back 34

↑ GABA-A action

Front 35

What 2 things can Benzos be used for as related to seizures?

Back 35

-1st line for acute status epilecticus
-Also used for seizures of eclampsia (1st line to prevent seizures of eclampsia is MgSO4)

Front 36

Toxicity of Benzodiazepines? (3)

Back 36

Sedation, tolerance, dependence.

Front 37

Tox of Carbamazepine? (7)

Back 37

Diplopia, ataxia, blood dyscrasias (agranulocytosis, aplastic anemia), liver toxicity, teratogenesis, induction of cytochrome P-450.

Front 38

Tox of Ethosuxamide? (5)

Back 38

GI distress, lethargy, headache, urticaria, Stevens-Johnson syndrome.

Front 39

Phenobarbital tox? (4)

Back 39

Sedation, tolerance, dependence, induction of cytochrome P-450.

Front 40

Phenytoin tox? (10)

Back 40

Nystagmus, diplopia, ataxia, sedation, gingival hyperplasia, hirsutism, megaloblastic anemia, teratogenesis, SLE-like syndrome, induction of cytochrome P-450.

Front 41

Valproic acid tox? (5)

Back 41

GI distress, rare but fatal hepatotoxicity (measure LFTs), neural tube defects
in fetus (spina bifida), tremor, weight gain.

Front 42

Lamotrigine tox? (1)

Back 42

Stevens-Johnson syndrome.

Front 43

Gabapentin tox? (2)

Back 43

-sedation
-ataxia

Front 44

Topirimate tox?

Back 44

Sedation
Mental dulling
Kidney stones
Weight loss

Front 45

MOA of Phenytoin?

Back 45

Use-dependent blockade of Na+ channels

Inhibition of glutamate release from excitatory presynaptic neuron.

Front 46

Clinical use of Phenytoin? (2)

Back 46

Tonic-clonic seizures.

Also a class IB antiarrhythmic.

Front 47

Toxicity of Phenytoin? (many!)

Back 47

Nystagmus
Ataxia
Diplopia
Sedation
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).

Front 48

What drugs are Barbituates? (4)

Back 48

Phenobarbital
Pentobarbital
Thiopental
Secobarbital

Front 49

MOA of Barbituates?

Back 49

Facilitate GABA-A action by ↑ duration of Cl− channel opening, thus ↓ neuron firing.

Front 50

Clinical use of Barbituates? (4)

Back 50

Sedative for anxiety, seizures, insomnia, induction of anesthesia (thiopental).

Front 51

C/I of Barbituates?

Back 51

porphyria

Front 52

Toxicity of Barbituates?

How do you treat overdose?

Back 52

-Dependence
-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).

Front 53

What drugs are Benzodiazepines?

Back 53

Diazepam, lorazepam, triazolam, temazepam, oxazepam, midazolam, chlordiazepoxide,
alprazolam.

Front 54

MOA of Benzos?

Back 54

Facilitate GABAA action by ↑ frequency of Cl− channel opening. Most have long half-lives and active metabolites.

Front 55

Clinical use of Benzos?

Back 55

-Anxiety
-Spasticity
-Status epilepticus (lorazepam and diazepam)
-Detoxification (especially alcohol withdrawal–DTs)
-Night terrors
-Sleepwalking.

Front 56

Toxicity of Benzos?

Why better than Barbituates?

How do you treat Benzo toxicity?

Back 56

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).

Front 57

What Benzos are short-acting?

Back 57

Short acting = TOM Thumb = Triazolam, Oxazepam, Midazolam

Front 58

start with anesthetics on p.372

Back 58

start with anesthetics on p.372

Front 59

CNS drugs must be ---- so they can cross the ---- or be actively transported

Back 59

CNS drugs must be lipid soluble so they can cross the BBB or be actively transported

Front 60

Drugs with ↓ solubility in blood have --- induction and recovery times.

Back 60

rapid

Front 61

Drugs with ↑ solubility in lipids have ---potency = 1/MAC.

Back 61

increased potency

Front 62

What is MAC?

Back 62

minimal anesthetic concentration.

Front 63

What drugs are inhaled anesthetics? (6)

Back 63

Halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, nitrous oxide.

Front 64

MOA of inhaled anesthetics?

Back 64

Mechanism unknown. The lower the solubility in blood, the quicker the anesthetic induction and the quicker the recovery.

Front 65

Effects of inhaled anesthetics? (4)

Back 65

Myocardial depression
Respiratory depression
Nausea/emesis
↑ cerebral blood flow (↓ cerebral metabolic demand).

Front 66

Toxicity of inhaled anesthetics? (4)

Back 66

Hepatotoxicity (halothane)
nephrotoxicity (methoxyflurane)
proconvulsant (enflurane)
malignant hyperthermia (rare).

Front 67

5 types of drugs used as IV anesthetics?

Back 67

"BB King on OPIATES PROPOses FOOLishly"

Barbituates
Benzos
Arylcyclohexamines (Ketamine)
Opiates
Propofol

Front 68

What is Thiopental?

MOA?

Clinical uses?

Back 68

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.

Front 69

What is Midazolam?

Used for what?

Bad S/Es?

Back 69

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.

Front 70

What are Arylcyclohemaxines (Ketamine)?

S/Es? (3)

Back 70

PCP analogs that act as dissociative anesthetics. Cardiovascular stimulants. Cause disorientation, hallucination, and bad dreams. ↑ cerebral blood flow.

Front 71

What 2 opiates are used for IV anesthesia?

What are they used with?

Back 71

Morphine, fentanyl used with other CNS depressants during general anesthesia.

Front 72

What is Propofol used for?

Why is it better than thiopental?

Back 72

Used for rapid anesthesia induction and short procedures. Less postoperative nausea than thiopental.

Front 73

What are neuromusclular blocking drugs used for?

What receptor are they selective for?

Back 73

Used for muscle paralysis in surgery or mechanical ventilation. Selective for motor (vs. autonomic) nicotinic receptor.

Front 74

What drug is a depolarizing neuromuscular blocking drug?

Back 74

Succinylcholine.

Front 75

How do you reverse the blockade of depolarizing neuromuscular blockers?

Back 75

Phase I (prolonged depolarization)––no antidote. Block potentiated by cholinesterase inhibitors.

Phase II (repolarized but blocked)––antidote consists of cholinesterase inhibitors (e.g., neostigmine).

Front 76

What drugs are nondepolarizing neuromuscular blockers?

What are they competitive with?

Back 76

Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rapacuronium.

compete with ACh for receptors.

Front 77

What drugs can be used to reverse the blockade of nondepolarizing neuromuscular blockers? (3)

Back 77

Reversal of blockade––neostigmine, edrophonium, and other cholinesterase inhibitors.

Front 78

What is Dantrolene used for?

Back 78

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).

Front 79

MOA of Dantrolene?

Back 79

Mechanism: prevents the release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle.