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100 Cards in this Set

  • Front
  • Back
Glaucoma drugs: classes and specific drugs
1. alpha agonists: epinephrine, brimonidine

2. beta blockers: timolol, betaxolol, careolol

3. diuretics: acetazolamide

4. cholinomimetics:
direct: carbachol, pilocarpine
indirect: physostigmine, echothiophate

5. prostaglandin: latanoprost
Glaucoma - Epinephrine

1. mechanism
2. side effects
3. c/i
1. decrease aq humour synthesis through vasoconstriction
2. mydriasis, stinging
3. DO NOT USE in closed angle glaucoma
Glaucoma - Brimonidine

1. mechanism
2. side effects
1. alpha-agonist, decreases aq humor synthesis
2. none
Glaucoma - Beta blockers

1. mechanism
2. side effects
1. decrease aq humour secretion
2. none

timilol, betaxolol, carteolol
Glaucoma - Acetazolamide

1. mechanism
2. side effects
1. decrease aq humour secretion by decreasing HCO3- via inhibition of carbonic anhydrase
2. none
Glaucoma - Cholinomimetics

1. mechanism
2. side effects
1. Increase outflow of aq humour, contract ciliary muscle (which produces aq humour) and opens trabecular network into canal of Schlemm
2. miosis, cyclospasm (accomodate)
Which glaucoma drug do you use in an emergency?
Pilocarpine
Glaucoma - Latanoprost

1. mechanism
2. side effects
1. Prostaglandin (PGFa2), increase outflow of aq humour
2. Darkens iris (browning)
Opioid analgesics - drugs
Morphine
Fentanyl
Codeine
Heroin
Methadone
Meperidine
Dextromethorphan
Opioid analgesics - mechanism
Agonist at opioid receptors, mu (morphine), delta (enkephalin), kappa (dynorphin)

K+ LEAVES THE CELL
Open K close Ca channels --> decrease synaptic transmission

Inhibit release of ACh, NE, 5HT, glutamate, substance P
Opioid analgesics - use
Pain
Cough suppression (dextromethorphan)
Diarrhea (loperamide and diphenoxylate)
Acute pulmonary edema
Maintenance program for addicts (methadone)
Which opioid is used for cough suppression?
Dextromethorphan
Which opioids are used for diarrhea?
Loperamide and diphenoxylate
Which opioids are used for maintenance in drug addicts?
Methadone
Toxicity of opioid analgesics
Tolerance
Respiratory depression
Constipation
Miosis
CNS depression with other drugs

can cause constriction of the smooth muscle of the sphincter of oddi leading to increase in pressures- use meperidine instead to avoid that
What do you treat opioid toxicity with?
Opioid receptor antagonists:
naltrexone
naloxone
What do you NOT develop tolerance to when using opioids?
Miosis
Constipation
Butorphanol/pentazocline

Mechanism
Use
Toxicity
1. Partial agonist at opioid mu receptors, agonist at kappa
2. Pain, causes less respiratory depression than full agonists
3. Causes withdrawal if on full agonists
Which opioid causes less respiratory depression in comparison to other opioids?
Butorphanol
Tramadol

1. Mechanism
2. Use
3. Toxicity
1. Weak opioid agonist, inhibits Serotonin and NE reuptake (works on multiple neurotransmitters)

2. chronic pain

3. decreases seizure threshold
Phenytoin

1. Tx's which seizures
2. Mechanism
3. Which drug can be used parenterally?
1. Simple Partial
Simple Complex
1st line for Generalized Tonic-Clonic
1st line for Status

2. Use dependent blockade of Na+ channels, decrease refractory period, inhibit glutamate release form excitatory presynaptic neurons

3. Fosphenytoin
Phenytoin toxicity
Gingival hyperplasia in kids
Hirsutism
Megaloblastic anemia (decreases folate absorption)
Teratogenesis (fetal hydantoin syndrome)
SLE-like syndrome
Cyt-P450 inducer
Carbamezapine

1. Tx's which seizures
2. Mechanism
1st line for all Simple Partial, Simple Complex, Generalized Tonic-Clonic

2. Increases Na channel inactivation
Which drug is 1st line for trigeminal neuralgia?
Carbamezapine
Lamotrigine

1. Tx's which seizures
2. Mechanism
1. PS, PC, GTC can do absence too

2. Blocks voltage-gated Na channels
Gabapentin

1. Tx's which seizures
2. Mechanism
1. PS, PC, GTC

2. GABA analogue, blocks high voltage activated Ca channels
Topiramate

1. Tx's which seizures
2. Mechanism
1. PS, PC, GTC

2. Blocks Na channels, increases GABA action
Phenobarbital

1. Tx's which seizures
2. Mechanism
1. PS, PC, GTC

2. Increases duration of Cl- channel opening, increases GABA action
Which AED is the first line for kids and pregnant women?
Phenobarbital
Which drugs are first line for GTC seizures?
Phenytoin
Carbamezapine
Valproic acid
Valproic acid

1. Tx's which seizures
2. Mechanism
1. PS, PC, 1st line for GTC

2. Increase Na inactivation, increase GABA action
Which AED is also used for myoclonic seizures?
Valproic acid
Ethosuximide

1. Tx's which seizures
2. Mechanism
1. 1st line for absence seizures

2. Block Ca channels in thalamus
Benzo's

1. Tx's which seizures
2. Mechanism
1. first line for acute status epilepticus

2. increase frequency of Cl- channel opening
Tiagabine

1. Tx's which seizures
2. Mechanism
1. PS, PC

2. inhibit GABA reuptake
Vigabatrin

1. Tx's which seizures
2. Mechanism
1. PS, PC

2. inhibits GABA transaminase, increasing GABA
Levetiracetam

1. Tx's which seizures
2. Mechanism
1. PS, PC, GTC

2. Unknown
Which AEDs are first line for status epilepticus?
Prophylaxis: Phenytoin

Acute: Benzo
Which AED is used for seizures in eclampsia?
Benzo

MgSO4 is first line
What are the only drugs for absence seizures?
ethosuximide is first line for absence and is only used for that
valproic acid and lamotrigine can be used
Most of the seizure drugs are associated with what classes?
simple, complex, tonic-clonic
Benzodiazepine toxicities
Sedation
Tolerance
Dependance
Carbamezapine toxicity
Blood dyscrasias (aplastic anemia and agranulocytosis)

Liver toxicity

Teratogenesis

CHECK LFTS!
Cyt-P450 inducer

SIADH

Stevens-Johnsons syndrome
Ethosuximide toxicity
"EFGH"

Ethosuximide:
Fatigue
GI Distress
Headaches

Stevens-Johnsons syndrome
Stevens-Johnsons syndrome

Sx's
3 AEDs that have this SE
1. Prodrome of malaise and fever

Rapid onset erythematous/purpuric macules (oral, ocular, genital)

Epidermal necrosis and sloughing

2. Ethosuximide
Carbamezapine
Lamotrigine
Phenobarbital toxicity
Sedation
Tolerance/Dependance
Cyt-P450 inducer
Valproic acid toxicity
Fatal hepatotoxicty
NTDs/spina bifida in fetus
Weight gain

C/i in pregnancy
Lamotrigine toxicity
Stevens-Johnsons syndrome
Gabapentin toxicity
Sedation
Ataxia
Topiramate toxicity
Sedation
Kidney stone
Weight loss
Phenytoin is also what type of drug in addition to being an AED?
Class I antiarrhythmic
Barbiturates:

1. Examples of drugs
2. Use
3. Toxicites
4. Tx overdose?
1. Phenobarbital, Thiopental
2. Anxiety, seizures, induction for anesthesia
3. additive CNS depression
respiratory/CV depression
induction of Cyt-P450
4. symptom management -- assist respiration and increase BP
Which AED is c/i in porphyria?
Barbiturates
Benzodiazepines

1. use
2. list short-acting drugs
3. toxicity
1. anxiety, spasticity, epilepticus, detox from EtOH, night terrors, sleep walking, general anesthetic, hypnotic

2. TOM thumb is short
Triazolam
Oxazepam
Midazolam

3. dependance
additive CNS depression with EtOH
less risk of respiratory depression and coma
How do you Tx benzo overdose?
Flumazenil

GABA receptor antagonist
Which benzo's have the highest addictive potential?
Short acting

Triazolam
Oxazepam
Midazolam
Which 2 AEDs are used for acute status epileptices?
Diazepam
Lorazepam

(Benzo's)
How do CNS drugs cross BBB?
1. soluble in lipid

OR

2. transporter
Drugs with decreased solubility in the blood have:
rapid induction and recovery times
Drugs with increased solubility in lipids have:
Increased potency
Potency of anesthetic drug =
1/MAC

MAC = minimal alveolar concentration
What does a large MAC mean in terms of potency?
low potency
MAC
minimal alveolar concentration at which 50% of population is anesthetized
Halothane has increased blood and lipid solubility, what does this mean in terms of potency and induction?
increased blood solubility: slow induction

increased lipid solubility: high potency
Mechanism of anesthetic action in lungs
increases rate and depth of ventilation
Mechanism of anesthetic action in blood
increased blood solubility: increase gas required to saturate blood --> slow induction time
Mechanism of anesthetic action in tissue (i.e. brain)
increased solubility: increased gas required to saturate tissue --> slower onset of action
Inhaled anesthetics

1. Drug examples
2. Mechanism
3. Effects
4. Toxicity
1. Halothane, isoflurane, nitrous oxide

2. unknown

3. myocardial and respiratory depression
nausea/emesis
increased cerebral blood flow (decreased cerebral metabolic demand)

4. Hepatotoxicity - halothane
Nephrotoxicity - methoxyflurane
Proconvulsant - enflurane
Malignant hyperthermia
IV anesthetics (5)
BBKing on OPIATES PROPoses FOOLishly

Barbiturates
Benzodiazepine
Ketamine
Opiates
Propofol
Thiopental

1. Potency, lipid solubility, entry time into brain
2. use
3. effect terminated by
4. effect on cerebral blood flow
IV anesthetic, barbiturate

1. high potency, high lipid solubility, rapid entry

2. induction anesthesia, short surgical procedures

3. redistribution into fat and tissues

4. decreases cerebral blood flow
Benzo's

1. use in anesthesia
2. used in conjuction with
3. toxicity
1. IV anesthetic, midazolam most commonly used for endoscopy
2. gas anesthetics and narcotics
3. severe post-op respiratory depression, amnesia
Ketamine

1. analog of
2. blocks which receptors
3. simulates
4. side effects
1. PCP, dissociative anesthesia
2. NMDA
3. CV system
4. disorientation, hallucination, bad dreams, increases cerebral blood flow
Opiates used as IV anesthetics
Morphine, fentanyl
Propofol

1. use
2. mechanism
1. IV rapid induction of anesthesia, short procedures

2. potentiates GABA

Less post-op nausea than thiopental
Ester local anesthetics
Procaine, cocaine, tetracaine

only 1 "i"
Amide local anesthetics
lidocaine, mepivacaine, bupivacaine

(amides have 2 i's each)
Local anesthetics: mechanism
block Na channels

binds better to activated Na channels, so most effective in rapidly firing neurons
Tertiary local amides penetrate membrane in what form and bind to ion channels in what form?
penetrate in uncharged
bind in charged form
In infected (acidic) tissue, how must local anesthetics be administered differently?
Alkaline anesthetics are charged and can't penetrate acidic membrane effectively, so must administer more
Order of nerve blockade in local anesthetics
small fibers > large fibers

myelinated fibers > unmyelinated

Size factor predominates over myelination.
Order of sensory loss in local anesthetics
Pain>temperature>touch>pressure
Local anesthetics are usually given with what drug and why?
Vasoconstrictors (epi), they enhance local action

*except cocaine
NMJ blockers

1. use
2. selective for which receptor
3. types
1. muscle paralysis in surgery or mechanical ventilation
3. Motor nicotinic
3. Depol and Non-depol
Local anesthesia toxicity
CNS excitation
Severe CV toxicity (bupivacaine)
HTN
Hypotension
Arrhythmias (cocaine)
Succinylcholine

1. class
2. reversal of blockade
3. complications
1. cholinomimetic, NMJ depolarizing blocker

2. Phase 1: prolonged depol, no antidote
Phase 2: repolarized but blocked, can reverse with AChE inhibitor (neostigmine)
3. Hypercalemia, Hypercalcemia
Non-depolarizing NMJ blockers

1. examples
2. mechanism
3. reversal of blockade
1. tubocurarine, atracurium, pancuronium, etc.

2. competitive antagonists for ACh

3. AChE inhibitors (neostigime, edrophonium, etc.)
Dantrolene: use and mechanism
tx for malignant hyperthermia and neuroleptic malignant syndrome

prevents release of Ca from sarcoplasmic reticulum of skeletal muscle
Malignant hyperthermia is caused by
concomitant use of inhalational anesthetics (except N2O) and succinylcholine
Parkinson's has excess____ activity
cholinergic due to loss of dopaminergic neurons
PD drug classes
1. dopamine agonists - Bromocriptine

2. drugs that increase dopamine - Amantadine, L-dopa/carbidopa

3. prevent dopamine breakdown - Selegiline

4. decrease cholinergic activity - Benztropine
PD drugs mnemonic
"BALSA"

Bromocriptine
Amantagine
Levodopa/Carbidoma
Selegiline
Anti-muscarinics
Dopamine agonists in PD:

examples
side effects
1. Bromocriptine (ergot), pramipexole, ropinorole (non-ergot, preferred)

2. gambling
Amantadine in PD
Increases dopamine release

also used as antiviral against influenza A

toxicity: ataxia
Selegiline

1. MOA
2. examples
3. adjunctive to what PD drug
4. toxicity
1. selective MAO-B inhibitor, which prefers metabolism of dopamine instead of NE or 5-HT

2. Entacapone, tocapone (COMT inhibitors)

3. L-dopa

4. enhance adverse effects of L-dopa
Benztropine in PD: MOA
anti-muscarinic (decreased cholinergic activity), improves tremor and rigidity, but little effect on bradykinesia

"Park your Benz"
L-Dopa/carbidopa toxicity
arrhythmias from peripheral conversion of L-dopa

Long-term: dyskinesia after administration
Short-term: akinesia b/w doeses
Why is carbidopa given in PD?
peripheral decarboxylase inhibitor

decreases peripheral side effects of L-dopa and increases bioavailability in brain
AD Drugs (2)

1. MOA
2. toxicity
Memantine
1. NMDA receptor antagonist, helps prevent excitotoxicity mediated by Ca
2. dizziness, confusion, hallucinations

Donezapil, galantamine, rivastigmine
1. AChE inihibitor
2. Nausea, dizziness insomnia
Huntington's Drugs

1. alterations in NTs
2. drug classes and examples
1. Increased dopamine, decreased GABA and ACh

2. Reserpine + tetrabenzine - amine depleting
Haloperidol - dopamine receptor antagonist
Sumatriptan

1. MOA
2. Half-life
3. Use
4. Toxicity
5. c/i in
1. 5-HT agonist. Causes vasoconstriction, inhibits trigeminal activation and vasoactive peptide release.

2. <2hrs

3. Migraine and cluster HAs

4. Coronary vasospasm, mild tingling

5. CAD, Prinzmetal's angina