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Acetaminophen
MOA
Use
Toxicity
- MECHANISM: Reversibly inhibits cyclooxygenase, mostly in CNS. Inactivated peripherally.
- CLINICAL USE: Antipyretic, analgesic, but not anti-inflammatory. Used instead of aspirin to avoid Reye syndromein children with viral infection.
- TOXICITY: Overdose produces hepatic necrosis; acetaminophen metabolite (NAPQI) depletes glutathione and forms toxic tissue byproducts in liver. N-acetylcysteine is antidote—regenerates glutathione
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montelukast and zafrilukast MOA
- inhibits LTC4, LTD4, LTE4
- inc bronchial tone
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Zileuton MOA
- inhibits Lipoxygenase
- dec Leukotrienes
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what is Epoprostenol
- PGI2
- dec Plateletaggregation
- dec Vascular tone
-
-
-
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TXA2 action
- inc Platelet aggregation
- inc Vascular tone
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LTB4 action
LTB4 is a neutrophil chemotactic agent
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PGI2 action
PGI2 inhibits platelet aggregation and promotesvasodilation
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Aspirin MOA
Irreversibly inhibits cyclooxygenase (both COX-1 and COX-2) via acetylation, which dic synthesis of TXA2 and prostaglandins. inc bleeding time. No effect on PT, PTT. A type of NSAID.
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Celecoxib MOA
Reversibly inhibits specifically the cyclooxygenase (COX) isoform 2, which is found in inflammatory cells and vascular endothelium and mediates inflammation and pain; spares COX-1, which helps maintain gastric mucosa. Thus, does not have the corrosive effects of otherNSAIDs on the GI lining. Spares platelet function as TXA2 production is dependent on COX-1.
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Celecoxib toxicity
inc risk of thrombosis. Sulfa allergy.
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NSAIDs
Ibuprofen, naproxen, indomethacin, ketorolac, diclofenac
MOA
Reversibly inhibit cyclooxygenase (both COX-1 and COX-2). Block prostaglandin synthesis.
-
NSAID toxicity
Interstitial nephritis, gastric ulcer (prostaglandins protect gastric mucosa), renal ischemia(prostaglandins vasodilate afferent arteriole).
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Bisphosphonates
Alendronate, other -dronates.
MOA
Pyrophosphate analogs; bind hydroxyapatite in bone, inhibiting osteoclast activity
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Teriparatide MOA ans Use
- Recombinant PTH analog given subcutaneously daily. inc osteoblastic activity.
- use: Osteoporosis. Causes bone growth compared to antiresorptive therapies (e.g., bisphosphonates).
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Chronic gout drugs (preventive)
- Allopurinol
- Febuxostat
- pegloticase
- probencid
-
Acute gout drugs
- NSAID
- Glucocorticoids
- Colchicine
-
about TNF-α inhibitors
All TNF-α inhibitors predispose to infection, including reactivation of latent TB, since TNF is important in granuloma formation and stabilization.
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Etanercept
MOA
USe
- Fusion protein (receptor for TNF-α + IgG1 Fc),produced by recombinant DNA. Etanercept is a TNF decoy receptor.
- use: Rheumatoid arthritis, psoriasis, ankylosingspondylitis
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Infliximab,adalimumab
MOA
Use
- Anti-TNF-α monoclonal antibody.
- use: Inflammatory bowel disease, rheumatoid arthritis,ankylosing spondylitis, psoriasis
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Glaucoma drugs goal
dec IOP via dec amount of aqueous humor (inhibit synthesis/secretion or inc drainage).
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Glaucoma drugs
- 1-α-agonists: Epinephrine (α1), Brimonidine (α2)
- 2-β-blockers:Timolol, betaxolol,carteolol
- 3-Diuretics: Acetazolamide
- 4-Cholinomimetics: Direct(pilocarpine,carbachol) Indirect(physostigmine,echothiophate)
- 5-Prostaglandin: Latanoprost (PGF2α)
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Epinephrine (α1)
Brimonidine (α2)
Mydriasis (α1); do not use in closed-angle glaucoma Blurry vision, ocular hyperemia, foreign bodysensation, ocular allergic reactions, ocularpruritus
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Cholinomimetics
SE
Miosis and cyclospasm (contraction of ciliary muscle)
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Prostaglandin
SE
Darkens color of iris (browning)
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Opioid analgesics
Morphine, fentanyl, codeine, loperamide, methadone, meperidine, dextromethorphan, diphenoxylate, pentazocine.
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Opioid analgesics
MOA
Act as agonists at opioid receptors (μ = morphine, δ = enkephalin, κ = dynorphin) to modulate synaptic transmission—open K+ channels, close Ca2+ channels --> dec synaptic transmission. Inhibit release of ACh, norepinephrine, 5-HT, glutamate, substance P.
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dextromethorphan use
cough suppression
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loperamide, diphenoxylate
use
diarrhea
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maintenance programs for heroin addicts what do u do?
methadone, buprenorphine +naloxone
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in opioid tx Tolerance does not develop to
miosis and constipation
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Butorphanol moa
κ-opioid receptor agonist and μ-opioid receptor partial agonist; produces analgesia
-
Butorphanol Use
Severe pain (e.g., migraine, labor). Causes less respiratory depression than full opioid agonists.
-
Butorphanol toxicity
Can cause opioid withdrawal symptoms if patient is also taking full opioid agonist (competition for opioid receptors). Overdose not easily reversed with naloxone.
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Tramadol
Very weak opioid agonist; also inhibits 5-HT and NE reuptake (works on multiple neurotransmitters—“tram it all” in with tramadol).
-
Tramadol toxicity
Similar to opioids. Decreases seizure threshold. Serotonin syndrome.
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tx for ABSENCE seizure
- fist line tx Ethosuximide
- Valporic acid
- Lamotrigine
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tx for simple and complex partial (focal) seizure
- All drugs including Tiagabine and Vigabatrin except Ethosuximide.
- Carbamazepine fist line tx
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tx for status epilepticus
- Benzodiazepines (diazepam,lorazepam)1st line for acute
- Phenytoin 1st line for prophylaxis.
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first line tx for tonic clonic seizure
- Phenytoin
- Carbamazepine
- Valproic acid
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Ethosuximide
moa
Blocks thalamic T-type Ca2+ channels
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Benzodiazepines(diazepam,lorazepam)
MOA
INC GABAA action
Also for eclampsia seizures (1st line is MgSO4)
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Phenytoin MOA
INC Na+ channel inactivation;zero-order kinetics
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Carbamazepine MOA AND NOTE
Na+ channel inactivation
- 1st line for trigeminalneuralgia
-
Valproic acid MOA AND NOTE
INC Na+ channel inactivation, INC GABA concentrationby inhibiting GABA transaminase
- Also used for myoclonicseizures, bipolardisorder
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Gabapentin MOA AND NOTE
Primarily inhibits high voltage-activated Ca2+channels; designed as GABA analog
Also used for peripheral neuropathy, postherpetic neuralgia
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Phenobarbital MOA
INC GABAA action
1st line in neonates
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Topiramate MOA AND NOTE
Blocks Na+ channels, INC GABA action
Also used for migraine prevention
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Lamotrigine MOA
Blocks voltage-gated Na+channels
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Levetiracetam MOA
Unknown; may modulateGABA and glutamaterelease
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Tiagabine MOA
INC GABA by inhibitingreuptake
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Vigabatrin MOA
INC GABA by irreversibly inhibiting GABA transaminase
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Ethosuximide SE
GI, fatigue, headache, urticaria,Stevens-Johnson syndrome.
EFGHIJ—Ethosuximide causesFatigue, GI distress, Headache,Itching, and Stevens-Johnsonsyndrome
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Benzodiazepines(diazepam,lorazepam)
SE
Sedation, tolerance, dependence,respiratory depression
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Phenytoin
SE
Nystagmus, diplopia, ataxia,sedation, gingival hyperplasia,hirsutism, peripheral neuropathy,megaloblastic anemia,teratogenesis (fetal hydantoinsyndrome), SLE-like syndrome,induction of cytochrome P-450,lymphadenopathy, Stevens-Johnson syndrome, osteopenia
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Carbamazepine
SE
Diplopia, ataxia, blood dyscrasias(agranulocytosis, aplastic anemia),liver toxicity, teratogenesis,induction of cytochrome P-450,SIADH, Stevens-Johnsonsyndrome
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Valproic acid SE
GI, distress, rare but fatal hepatotoxicity (measure LFTs),neural tube defects (e.g., spinabifida), tremor, weight gain,contraindicated in pregnancy
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Gabapentin
SE
Sedation, ataxia
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Phenobarbital SE
Sedation, tolerance, dependence,induction of cytochrome P-450,cardiorespiratory depression
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Topiramate SE
Sedation, mental dulling, kidneystones, weight loss
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Lamotrigine SE
Stevens-Johnson syndrome (must be titrated slowly)
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