Pharmacology - Neurology

Front 1

Parkinsonism -
mechanism of dz
-loss of _ neurons
-excess _ activity

Back 1

loss of dopaminergic neurons
excess cholinergic activity

Front 2

Parkinsonism -
name the drugs:

"BALSA"

Back 2

Bromocriptine
Amantadine
Levodopa (with carbidopa)
Selegiline (and COMT inhib)
Antimuscarinics

Front 3

Which drugs...
Agonize dopamine receptors

Back 3

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

Front 4

Which drugs...
increase dopamine

Back 4

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

Front 5

Which drugs...
prevent dopamine breakdown

Back 5

Selegiline (selective MAO type B inhibitor)
Entacapone (COMT inhibitor)
Tolcapone (COMT inhibitor)

Front 6

Which drugs...
curb excess cholinergic activity

Back 6

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

Front 7

L-dopa's other daym

Back 7

levodopa

Front 8

l-dopa/carbidopa:
-mechanism

Back 8

-increases level of DA in brain.
-unlike DA, L-dopa can cross BBB and is converted by DOPA DECARBOXYLASE in the CNS to DA

Front 9

L-dopa/carbidopa:
-toxicity

-longterm toxicity

Back 9

-Arrhythmias (peripheral conversion to DA -> decreased by Carbidopa)

-Longterm -> dyskinesia following administration, akinesia between doses

Front 10

Carbidopa
-mechanism

Back 10

A peripheral dopa decarboxylase inhibitor
-given with L-dop to increase bioavailability of L-dopa in brain, and to limit peripheral side effects (i.e. arrhythmias)

Front 11

Selegiline
-mech
-clin use
-toxicity

Back 11

-Selective MAO-B inhibitor, thereby increased availability of dopamine
-adjunct to L-dopa in tx of Parkinson's dz
-may enhance adverse effects of L-dopa

Front 12

Sumatriptan
-mech, t 1/2
-clin use
-tox & CONTRAINDICATOINS

Back 12

-5-HT(1D) Agonist -> Vasoconstriction (t 1/2 = 2hrs)
-for acute migraine, cluster HA attacks
-Tox: coronary vasospasm, mild tingling
CONTRAINDICATED in CAD or PRINZMETAL's ANGINA

Front 13

1st Line Epilepsy drugs for
- tonic-clonic sz (3)
- absence sz (1)
- acute status sz (1)

Back 13

-phenytoin, carbamazepine, valproic acid
-ethosuximide
-diazepam, lorazepam

Front 14

1st line drug for trigeminal neuralgia

Back 14

carbamazepine

Front 15

epilepsy drug also a class Ib antiarrhythmic

Back 15

phenytoin

Front 16

epilepsy drug also used for peripheral neuropathy

Back 16

Gabapentin

Front 17

1st epilepsy drug in pregnant women, children

Back 17

phenobarbital

Front 18

Epilepsy drug also used for MYOCLONIC SZs

Back 18

valproic acid

Front 19

1st line for acute Status/generalized sz, also used for seizures of eclamspia

Back 19

benzodiazepines (diazepam, lorazepam)

Front 20

1st line to prevent seizures of eclampsia

Back 20

MgSO4

Front 21

1st line for PROPHYLAXIS of status/generalized szs

Back 21

phenytoin

Front 22

phenytoin
-mechansim

-1st line for...(2)

Back 22

increases Na+ channel inactivation (use-dependent blockage)
-inhibition of glutamate release for excitatory presynamptic neuron

-tonic-clinic sz, prophy for status/gen sz

Front 23

carbamazepine
-mech

-1st line for (1)
-special use (1st line)

Back 23

increases Na+ channel inactivation

-tonic-clonic sz
-trigeminal neuralgia

Front 24

Lamotrigine
-mech

-used for... (3)

Back 24

-blocks VOLTAGE-gated Na+ channels

-for partial (simple, complex) and tonic clonic szs

Front 25

Gabapentin
-mech

-used for...
-special use

Back 25

increases GABA release

-for partial (simple, complex) and tonic clonic szs, and PERIPHERAL NEUROPATHY

Front 26

Topiramate
-mech

-used for...

Back 26

-blocks Na+ channels AND increases GABA action

-for partial (simple, complex) and tonic clonic szs

Front 27

Phenobarbital
-mech

-used for... (3)
-special use

Back 27

-increases GABA-A action (by increases DURATION of Cl-channel opening)

-for partial (simple, complex) and tonic clonic szs
-1st line in pregnant women and children

Front 28

Valproic acid
-mech

-1st line for
-also used for
-another use

Back 28

-increases Na_channel inactivation AND increases GABA concentration

-1st line for tonic-clonic
-for partial (simple, complex) and tonic clonic szs
-also for ABSENCE szz
-also for myoclonic szs

Front 29

ethosuximide
-mech
-1st line for

Back 29

-blocks thalamic T-type Ca2+ channels
-absence szs

Front 30

benzodiazepines (diazepam, lorazepam)
-mech
-1st line for ... (1)
-also used for... (1)

Back 30

-increases GABA-A action

-ACUTE status/generalized szs
-for seizures of eclampsia (MgSO4 is 1st line to prevent)

Front 31

Benzo toxicities

Back 31

-Sedation
-Tolerance
-Dependence

Front 32

Carbamazepine toxicity

Back 32

-Diplopia
-Ataxia
-AGRANULOCYTOSIS, APLASTIC ANEMIA
-LIVER toxicity
-teratogenesis
-induction for cytochrome P-450

Front 33

Ethosuximide toxicity

Back 33

-GI distress
-Lethargy
-HA
-Urticaria
-Stevens-Johnson syndrome

Front 34

Phenobarbital toxicity

Back 34

Sedation
Tolerance/dependence
Induction of cytochrome P-450

Front 35

Phenytoin toxicity

Back 35

-Nystagmus
-Diplopia
-Ataxia
-Sedation
-GINGIVAL HYPERPLASIA (kids)
-HIRSUTISM
-megaloblastic anemia (decrease folate absorption)
-teratogenic (fetal hydantoin syndrome)
-SLE-like syndrome
-induction of cyt P-450
-malignant hyperthermia (rare)

Front 36

Valproic acid toxicity

Back 36

-GI distress
- HEPATOXICITY (rare but fatal -must MEASURE LFTs)
-NTD (spina bifida)
-tremor
-weight gain

Front 37

Lamotrigine toxicity
(1)

Back 37

Stevens Johnson syndrome
-(hypersensitivity complex affecting the skin and the mucous membranes ~ toxic epidermal necrolysis)

Front 38

Gabapentin

Back 38

Sedation
Ataxia

Front 39

Topiramate

Back 39

Sedation
Mental dulling
KIDNEY STONES
Weight loss

Front 40

Barbiturates
- name 4

Back 40

Phenobarbital
Pentobarbital
Thiopental
SECObarbital

Front 41

Barbiturates
-mechanism

Back 41

factilitate GABA-A action by increasing DURATION of Cl- channel opening (thus decreasing neuron firing)

Front 42

Barbiturates
-clin use
-contraindicated in... (1)

Back 42

-sedative for anxiety
-sezures
-insomnia
-induction of anesthesia (thiopental)
*Contraindicated in porphyria

Front 43

Barbiturate toxicity
-important:
-additive effect with (1)
-_ or _ depression (can lead to death)
-drug interactsion d/t )

Back 43

-Dependence
-ADDITIVE CNS depression with Alcohol
-resp or CV depression can lead to death
-drug interaction d/t induction of liver microsomal enzymes (cyt P-450)

Front 44

Treatment for Barbiturate overdose

Back 44

Symptom mgmt (assist respiration, increase BP)

Front 45

Benzodiazepines
name them (8)

Back 45

diazepam, loarzepam, triazolam, temazepam, oxazepam, midazolam, chlordiazepoxide, alprazolam

Front 46

Benzos
-mechanism: facilitate GABA-A action by...

hint: "FREnzodiazepines"

Back 46

increasing FREQUENCY of Cl-channel opening

-most have long half-lives and active metabolites

Front 47

Short-acting benzos
"TOM thumb"

Back 47

Triazolam
Oxazepam
Midazolam

Front 48

Benzos - clinical use

Back 48

-anxiety, spasticity
-acute STATUS EPILEPTICUS (lorazepam and idazepam)
-detoxification (esp alcohol withdrawal - DTs)
-night terrors
-sleep walking

Front 49

Benzo toxicity

Back 49

dependence
ADDItive effect with EtOH
*less risk of resp depression ad coma with barbiturates

Front 50

Benzo overdose treatment

Back 50

FLUMAZENIL

Front 51

Flumazenil
-mech

Back 51

competitive antagonist at GABA receptor

-treat benzo overdose

Front 52

Anesthetics Principles
-to reach CNS, drugs must be ___-soluble (cros BBB) or be actively transported

Back 52

lipid-soluble

Front 53

Anesthetic drugs with decreased solubility in BLOOD have ___ induction and recovery times (slow or rapid?)

Back 53

rapid

Front 54

Anesthetic drugs with increased solubility in LIPIDS have ___ potency = 1/MAC

MAC = ?

Back 54

increased potency

MAC = minimal anesthetic concentration

Front 55

N2O has low blood and lipid solubility.
Is induction fast or slow?
Is potency high or low?

Back 55

Induction fast

Potency low

Front 56

Halothane has high blood and lipid solubility.
Is induction fast or slow?
Is potency high or low?

Back 56

Induction is slow

Potencty is high

Front 57

Inhaled Anesthetics
-name them

-mechanism? unknown!

Back 57

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

Front 58

Inhaled anesthetics
effects

what happens to cerebral blood flow?

Back 58

myocardial depression
respiratory depression
nausea/emesis
INCREASED CEREBRAL BLOOD FLOW (decreased cerebral metabolic demand)

Front 59

Inhaled anesthetics: Toxicity
-Halothane
-Methoxyflurane
-Enflurane

Back 59

Halothane - Hepatotoxicity
Methoxyflurane - Nephrotoxicity
Enflurane - Proconvulsant

*malignant hyperthermia (rare)

Front 60

Intravenous anesthetics:
name the types (5)

Hint: B.B. King on OPIATES PROPOses FOOLishly

Back 60

Barbiturates (thiopental)
Benzodiazepine (Midazolam)
arylcyclohexamines (Ketamine)
Opiates (morphine/fentanyl)
Propofol

Front 61

Barbiturates (IV anesthetic)
-Thiopental features
-Anesthesia use
-Termination of effect
-effect on cerebral blood flow?

Back 61

high potency, high lipid solubility, rapid entry into brain
-for induction of anesthesia and SHORT surgical procedures
-DECREASES cerebral blood flow

Front 62

Benzos (IV anesthetic)
-Midazolam
-Anesthesia use
-toxicity/antidote

Back 62

-most common drug for ENDOSCOPY
-adjunctive to inhaled anesthetics and narcotics
-tox - resp depression, decreased bp (tx: flumazenil), AMNESIA

Front 63

Ketamine (IV anesthetic)
-mech
-tox
-effect on blood flow?

Back 63

-PCP analog - act as DISSOCIATIVE ANESTHETICS
-CV stimulants

tox - disorientation, hallucination, bad dreams
*INCREASES cerebral blood flow

Front 64

Opiates (IV anesthetic)
-morphine, fentanyl

Back 64

used with other CNS depressants during general anesthesia

Front 65

Propofol (IV anesthetic)
-use
-less __than thiopental

Back 65

-for rapid anesthesia induction and SHORT procedures
-less post-op nausea than thiopental

Front 66

LOCAL anesthetics
-type of compounds (2)
-name them

Back 66

ESTERS: procaine, cocaine, tetracaine

AMIDES: lidocaine, mepivicaine, bupivacaine (2 i's in name)

Front 67

LOCAL anesthics
-mechanism
*how do tertiary amines bind?

Back 67

block Na+ channels by binding to specific receptors on inner portion of channel
*tertiary amine local anesthetics penetrate mb in uncarged form, then bind to ion channels as charged form

Front 68

LOCAL Anesthetic principles
1 of 3: how much anesthetic needed in infected tissue?

Back 68

Infected tissue is acidic -> anesthetics are charged and cannot penetrate membrane effectively.
*More anesthetics needed in this case

Front 69

LOCAL Anesthetic principles
2 of 3: order or nerve blockade; order of sensation loss

Back 69

Nn blockade:
Diameter: small > large
Myelin: myelinated > unmyelinated
*Size factor predominates over myelination: v.small unmyelinated pain fibers > small myelinated autonomic fibers > large myelinated autonomic fibers
Order of sensation loss: Pain (first) > temp > touch > pressure (last)

Front 70

LOCAL Anesthetic principles
3 of 3: why given with vasoconstrictors (epi)?

Back 70

to enhance local action
-decreases bleeding
-increases anesthesia by decreases systemic concentration

Front 71

LOCAL Anesthetic
-clinical use
-if allergic to esters? give what?

Back 71

minor surgical procedures
spinal anesthesia

-if allergic to esters, give amide

Front 72

LOCAL anesthetic toxicities

Back 72

CNS excitation
severe CV toxicity (BUPIVICAINE)
HTN
hypotension
Arrhythmias (COCAINE)

Front 73

Neuromuscular blocking agents
-use

Back 73

for mm. paralysis in surgery or mechanical ventilation
*selective for motor (vs. autonomic) NICOTINE receptor

Front 74

Name the
-Depolarizing neuromusc blocker (1)
-Nondepolarizing (6)

Back 74

-Succinylcholine

-Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rapacuronium

Front 75

Depolarizing nueromuscular blocker = Succinylcholine
*Reversal of blockade with ?:
PHASE 1
PHASE 2

Back 75

PHASE 1 (prolonged depolarization) - NO ANTIDOTE (block potentiated by cholinesterase inhibitors)

PHASE 2 (repolarized but blocked) - ANTIDOTE = CHOLINesteraSE INHIBITOR (eg, NEOSTIGMINE)

Front 76

Nondepolarizing neuromuscular blocking agents - mechanism

-reversal of blockade with... (3)

Back 76

-competitive with ACh for nicotinic receptors

*reversal of blockade with NEOSTIGMINE, EDROPHONIUM, and other cholinesterase inhibitors

Front 77

Dantrolene
-clinical use (2)

Back 77

-for MALIGNANT HYPERTHERMIA (caused by concomitatn use of inhalation anesthetics except N2O and succinylcholine)
-also to treat NEUROLEPTIC MALIGNANT SYNDROME (toxicity of antipsychotic drugs)

Front 78

Dantrolene
-mechanism

Back 78

prevents release of Ca2+ from sarcoplasmic reticulum of skeletal muscle