Pharmacology Flashcards
How do epinephrine and brimonidine treat glaucoma?
ALPHA-AGONISTS
decrease aqueous humor synthesis
What are side effects of epinephrine and brimonidine?
mydraisis BLURRY VISION ocular hyperemia foreign body sensation ocular allergic reactions ocular pruritis
How do beta-blockers (Timolol, Betaxolol, and Carteolol) treat glaucoma?
decrease aqueous humor synthesis
How does acetazomalide treat glaucoma?
decrease aqueous humor synthesis
How do pilocarpine and carbachol treat glaucoma?
DIRECT CHOLINOMIMETICS
increase outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork
How do physostigmine and echothiophate treat glaucoma?
INDIRECT CHOLINOMIMETICS
use of pilocarpine in emergencies - very effective at opening meshwork in canal of Schlemm
How does Latanoprost (PGF) treat glaucoma?
increase outflow of aqueous humor
What is a side effect of Latanoprost?
darkens color of iris (browning)
What is the MOA of opioid analgesics?
Act as agonists at opioid receptors (mu= morphine) to modulate synaptic transmission
Opens K+ channels, closes Ca2+ channels –> decrease synaptic transmission
Inhibit release of ACh, NE, 5HT, glutamate, and substance P
What are side effects of opioid analgesics?
addiction respiratory depression constipation miosis additive CNS depression with other drugs
**Tolerance does NOT develop to miosis and constipation
What is the antidote for opioid OD?
naloxone and naltrexone (opioid receptor antagonist)
What is the MOA of butorphanol?
mu-opioid receptor PARTIAL agonist and kappa-opioid receptor agonist –> produces analgesia
What is the MOA, TU, and TOX of tramadol?
MOA: very weak opioid agonist; also inhibits serotonin and NE repute (works on multiple neurotransmitters)
TU: chronic pain
TOX: similar to opioids, decreases seizure threshold, 5HT syndrome
What is the MOA, TU, and TOX of ethosuximide?
MOA: blocks thalamic T-type Ca2+ channels
TU: absence seizures
TOX: fatigue, GI distress, HA, itching, and Stevens-Johnson Syndrome
What is the MOA, TU, and TOX of benzodiazepines (when talking about seizures)?
MOA: increase GABA-A action
TU: status epilepticus
TOX: sedation, tolerance, dependence, respiratory depression
What is the MOA, TU, and TOX of phenytoin?
MOA: increase Na+ channel inactivation, zero-order kinetics
TU: simple, complex, tonic-clonic (1st line), and status epilepticus seizures
TOX: nystagmus, megaloblastic anemia, Stevens-Johnson syndrome, osteopenia, gingival hyperplasia, ataxia, hirsutism
What is the MOA, TU, and TOX of carbamazepine?
MOA: increase Na+ channel inactivation
TU: simple, complex, and tonic-clonic (all 1st line)
TOX: agranulocytosis, aplastic anemia, live toxicity, SIADH< Stevens-Johnson Syndrome, diplopia
**Also, 1st line treatment for trigeminal neuralgia
What is the MOA, TU, and TOX of valproic acid?
MOA: increase Na+ channel inactivation, increase GABA concentration by inhibiting GABA transaminase
TU: simple, complex, tonic-clonic (1st line), absence seizures
TOX: GI, fatal hepatotoxicity (measure LFTs), NEURAL TUBE DEFECTS (spina bifida), tremor, wt gain
**Also used for myoclonic seizures, bipolar disorder
What is the MOA, TU, and TOX of gabapentin?
MOA: primarily inhibits high-voltage-activated Ca2+ channels; designed as GABA analog
TU: simple, complex, tonic-clonic seizures
TOX: sedation, ataxia
**Also used for peripheral neuropathy, postherpetic neuralgia, migraine prophylaxis, bipolar disorder
What is the MOA, TU, and TOX of phenobarbital?
MOA: increase GABA-A action
TU: simple, complex, tonic-clonic seizures
TOX: sedation, tolerance, dependence induction of cyt P-450, cardiorespiratory depression
**1st line in neonates
What is the MOA, TU, and TOX of topiramate?
MOA: blocks Na+ channels, increase GABA action
TU: simple, complex, tonic-clonic seizures
TOX: sedation, mental dulling, kidney stones, wt loss
**Also used for migraine prevention
What is the MOA, TU, and TOX of lamotrigine?
MOA: blocks VG-Na+ channels
TU: simple, complex, tonic-clonic, and absence seizures
TOX: Stevens-Johnson Syndrome (MUST BE TITRATED SLOWLY)
What is the MOA, TU, and TOX of levetiracetam?
MOA: unknown
TU: simple, complex, tonic-clonic seizures
What is the MOA, TU, and TOX of tiagabine?
MOA: increase GABA by inhibiting repute
TU: simple and complex seizures
What is the MOA, TU, and TOX of vigabatrin?
MOA: increase GABA by irreversibly inhibiting GABA transaminase
TU: simple and complex seizures
What is the MOA, TU, and TOX of barbiturates?
phenobarbital, pentobarbital, thiopental, secobarbital
MOA: facilitate GABA-A action by increasing DURATION of Cl- channel opening –> decreases neuronal firing
TU: sedative for anxiety, seizures, insomnia, induction of anesthesia (thiopental)
TOX: respiratory and CV depression, dependence, drug interactions (induces P-450)
OD Tx: supportive (assist respiration and maintain BP)
*Contraindicated in porphyria
What is the MOA, TU, and TOX of benzodiazepines?
MOA: facilitated GABA-A action by increasing FREQUENCY of Cl- channel opening
TU: anxiety, spasticity, status epilepticus (lorazepam and diazepam), detoxification (esp. EtOH withdrawal - DTs), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia)
TOX: dependence, additive CNS depression effects with EtOH (less risk than barbiturates)
OD Tx: flumazenil (competitive antagonist of GABA benzodiazepine receptor)
What is the MOA, TU, and TOX of nonbenzodiazepine hypnotics?
zolpidem (ambien), zaleplon, eszopiclone
MOA: act via the BZ1 subtype of the GABA receptor
TU: insomnia
TOX: ataxia, HAs, confusion
OD Tx: flumazenil
How does lipid solubility affect the potency and induction time of anesthetics?
LOW blood and lipid solubility –> fast induction and low potency
HIGH lipid and blood solubility –> high potency and slow induction
What is the MOA, TU, and TOX of inhaled anesthetics?
halothane, enflurance, isoflurance, sevoflurane, methoxyflurane, nitrous oxide
MOA: unknown
Effects: myocardial depression, respiratory depression, N/V, increase cerebral blood flow (decreases cerebral metabolic demand)
TOX: halothane - hepatotoxicity, malignant hyperthermia
desflurane - airway irritability
methoxyflurane - nephrotoxicity
enflurane - pro-convulsant
OD Tx: dantrolene
Which IV anesthetic has high potency, high lipid solubility, rapid entry into the brain and whose effect is terminated by rapid redistribution into tissue?
thiopental (barbiturate)
Which IV anesthetic is MC used for endoscopy?
midazolam (benzodiazepine)
Which PCP analog can be used as an IV anesthetic?
ketamine
What is the MOA of ketamine?
blocks NMDA receptors –> CV stimulant –> disorientation, hallucination, bad dreams, and increase cerebral blood flow
What are the uses of propofol as an IV anesthetic?
sedation in ICU
rapid anesthesia induction
short procedures
What is the MOA, TU, and TOX of local anesthetics?
Esters - procaine, cocaine, tetracaine
Amides - lidocaine, mepivacaine, bupivacaine, (amides have 2 I’s in name)
MOA: block Na+ channels by binding to specific receptors on inner portion of channel
What drug can be given with local anesthetics to enhance local action?
vasoconstrictors
What is the order of nerve blockade of local anesthetics?
small myelinated fibers > small unmyelinated fibers > large myelinated fibers > large unmyelinated fibers
What is the order of loss of sensation?
- pain
- temperature
- touch
- pressure
What should you remember about allergies and local anesthetics?
If allergic to esthers, give amides!
What is the mechanism of succinylcholine in neuromuscular blockade?
DEPOLARIZING
strong ACh receptor agonist –> produces sustained depolarization and prevents muscle contraction
What is the mechanism of non depolarizing neuromuscular blocking drugs?
tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium
MOA: competitive antagonists
What is the reversal treatment for non depolarizing neuromuscular blocking drugs?
neostigmine and edrophonium
What is the MOA, TU, and TOX of dantrolene?
MOA: prevents the release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle
TU: used to treat malignant hyperthermia and neuroleptic malignant syndrome
What are the drugs used to treat Parkinson disease?
Bromocriptine - DA agonist Amantadine - increase DA L-dopa/carbidopa - increase DA Selegiline - MOA -B inhibitor Benztropine - antimuscarinic
What is the MOA, TU, and TOX of L-dopa (levodopa)/carbidopa?
MOA: increase level of DA in brain b/c L-dopa can cross BBB and is converted by dopa decarboxylase in the CNS to DA
*Carbidopa inhibits peripheral decarboxylase to increase the bioavailability of L-dopa and to limit peripheral SEs
TOX: dyskinesia (“on-off” phenomenon)
What is the MOA, TU, and TOX of selegiline?
MOA: selectively inhibits MOA-B
What are the MOA, TU, and TOX of the following Alzheimer drugs?
Memantine
Donepezil, galantamine, rivastigmine
Memantine
MOA: NMDA receptor antagonist; helps prevent excitotoxicity
TOX: dizziness, confusion, hallucinations
Donepezil, galantamine, rivastigmine
MOA: AChE inhibitors
TOX: nausea, dizziness, insomnia
What is the MOA of treatment of Huntington Disease?
Tetrabenzine and reserpine - inhibit vesicular monoamine transporter (VMAT); limit dopamine vesicle packaging and release
Haloperidol - DA receptor antagonist
What is the MOA, TU, and TOX of sumatriptan?
MOA: 5-HT agonist; inhibits trigeminal nerve activation; prevents vasoactive peptide release; induces vasoconstriction
TU: acute migraine, cluster HA
TOX: coronary vasospasm
*contraindicated in CAD or Prinzmetal angina
