Drugs Test 2 Flashcards
Ceftriaxone (3rd Generation)
MOA: Bind to penicillin binding proteins (transpeptidases) to inhibit cell-wall synthesis
Spectrum: Used for streptococci and more serious gram negative infection. CAN CROSS BLOOD BRAIN BARRIER
Resistance: inactivation of the drug by beta-lactamases
Side affects: allergies
Isoniazid
Inhibits mycolic acids (compnonent of mycobacterial cell wall).
Acetylation by liver varies genetically and fast acetylators may require higher dose.
Rifampin
Inhibits DNA-dependent RNA polymerase induces the formation of drug-metabolizing enzymes including cytochrome p450.
Ethambutol
Inhibits cell wall sythesis by binding arabinosyl
Pyrazinamide
unknown
Amphotericin B
Mechanism: Binds ergosterol creating holes in fungi membrane allowing leakage of electrolytes
Spectrum : Broad; invasive fungal infx in immunocompromised patients. Active against yeast and molds.
Distribution: Liposomal crosses blood brain barrier (large, lipophilic, and acted on by efflux)
Adverse effects: TOXIC because binds cholesterol. Decreases renal blood flow and can lead to permanent destruction of the basement membrane.
Resistance: rare
Flucytosine
Mechanism: Antimetabolite selectively taken up and converted to 5 - FU in fungi, interfering with DNA and RNA sythesis.
Spectrum: Narrow - yeast; Candida Albicans and Cryptococcus
Distribution: Oral, penetrates CNS
Toxicity: Bone marrow suppression - follow patient’s cell counts closely
Resistance: loss of converting enzyme or transporters, COTREAT with Amph B to minimize the develoment of resistance and to increase uptake.
Azoles - Fluconazole, Itraconazole, and Voriconazole
Mechanism - binds fungal p-450 enzyme (Erg 11) and blocks production of ergosterol
Spectrum - Systemic mycoses and yeast
Distribution - Orally available, substrate for efflux pumps in brain (Fluconazole and Voriconazole penetrate CNS)
Toxicity: Drug-Drug interactions, hepatotoxicity, neurotoxicity, alters hormone synthesis. Avoid during pregnancy
ResistanceL Altered cytochrome p-450, upregulation of efflux transporters.
Acyclovir
Antiviral prodrug which is acted on by cellular thymidine kinases to produce acyclovir triphosphate which blocks DNA and RNA chain elongation.
Used for alpha herpes viruses. (A in acylclovir = Alpha)
Gancylcovir
Antiviral prodrug which is acted on by cellular thymidine kinases to produce acyclovir triphosphate which blocks DNA and RNA chain elongation.
Used for beta and gamma herpes viruses. (G gancyclovir= gamma (beta too!)
Sumatriptan
MOA: 5-HT D and B receptor agonist. Causes Vasoconstriction and reduced release of pro-inflammatory neuropeptide (CPRG) release.
Uses: Migraine
Contraindications: Vascular diseases, basilar or hemiplegic migraine, with DHE
Fluoxetine (prozac)
MOA: Selective 5-HT Transport inhibitor (SSRI). Increases Serotonin in synaptic cleft
Uses: Depression, OCD, Panic, PTSD, Phobias
Amitryptaline
MOA: 5-HT transport inhibitor. Increasing serotonin in synaptic cleft. Works as migraine prophylaxis by increasing baseline 5-HT.
Uses: depression etc., MIGRAINE PROPHYLAXIS, and peripheral neuropathy
Side effects: Weight gain, constipation, dizziness, headache, blurred vision.
Drug-drug interactions: Slight interaction with warfarin possible increasing bleeding risk
Dihydroergotamine (DHE)
MOA: Fugal product that acts like triptans ( 5-HT D and B receptor agonist. Causes Vasoconstriction and reduced release of pro-inflammatory neuropeptide (CPRG) release.)
Uses: Migraine management
Side effects: Nausea and vomitting. CYP3A4 rxns.
Contraindicated in vascular, hepatic, or renal disease.
Benzodiazapines
Activate GABA receptors to cause sedation
Baclofen
GABA receptor agonist used as a muscle relaxant.
Strychnine
Antagonist of glycine receptors. Poison that causes intense muscle spasms.
Pregabalin
MOA: Blocks presynaptic VG Ca++ channels
Site of action: presynaptic nocioceptor
Side effects: weight gain, constipation, dizziness, headache, and blurred vision.
Caspacin
MOA: Depletes and prevents reaccumulation of substance P (found in slow-conducting, unmyelinated type C fibers) in PNS.
OR
Transient receptor potential vanilloid-1 (TRPV1) agonist; topical application causes initial TRPV1 stimulation that may cause pain, followed by pain relief by reduction in TRPV1-expressing nociceptive nerve endings
Side effects: Erythema, pain, and nausea.
Drug-drug interactions: Slight interaction with warfarin possible increasing bleeding risk
Opioids: (morphine, methadone, oxycodone, heroin)
MOA: Two main pathways:
Inhibit GABA inhibition of descending pain prevention pathways.
Bind to mu receptors which are GPCR’s which block presynaptic voltage gated calcium channels and increase permeabiltiy of postsynaptic potassium. This blocks ascending pain transmission pathway in peripheral tissues, spinal cord, and thalamus.
Pharmacokinetics: Many mechanisms of delivery. Significant first pass metabolism in oral form.
Uses: Analgesia (severe acute pain and cancer/chronic illness), Obstetric labor, anesthesia, cough, diarrhea
Side effects: Euphoria, respiratory depression, antitussive (cough), nausea, vomiting, Miosis (good indicator of use), increased GI tone/ constipation, and itching/flushing.
Tolerance, Dependence, and Addiction all problems
Codeine
Partial opiate agonist. Less efficacious and addictive than opiods.
Uses: analgesia and cough suppression.
Pentazocine
Mixed agonist-antagonist. Agonist of kappa and antagonist of Mu. Used to help with opioid withdrawal
Buprenorphine
Mixed agonist-antagonist. Partial Mu agonist, antagonist at others. Often used with naloxone (Suboxone) for opioid addiction treatment.
Loperamide (Immodium)
Opioid that acts solely on GI causing constipation.
Naloxone (Narcan)
Short acting opioid antagoinist used in acute OD. Can wear off in 1-2 hrs causing relapse.
Injection used to avoid first pass effect.
Naltrexone
Orally effective opiod antagonist used to prevent relapse in opioid addiction and alcohol addiction.
Suboxone
Mix of Buprenorphine (mixed agonist/antagoinist) and Naloxone (antagonist) used in opioid addiction treatment to help with withdrawal.
Low abuse potential due to naloxone.
Methadone
Treatment for opioid addiction that is orally effective, long half life, low cost.
High risk for respiratory depression and death. <10% of perscriptions.
Aspirin (Acetylsalicylic Acid)
Irreversibly inhibits both COX1 and COX2. Lasts life of platelet (7 days).
Uses: Analgesic (reversal of peripheral nocioceptor sensitization), Antipyretic (Blocks PGE2 from acting on hypothalamus) , Anti-inflammatory (Blocks vasodialation of PGE2), prevention of clotting (blocking of thrombaxanes).
Adverse effects: GI distress, GI bleeding, decreased clotting, respiratory and electrolyte disturbances, tinnitus,
Special notes: Use 81mg aspirin for heart patients to prevent clotting while minimizing other effects. Contraindicated in children due to Reye’s Syndrome. Hypersensitivity possible due to shifting of Arach Acid to Leukotrienes –> respiratory issues (treat with epi)
Overdose treatment: induce vomiting/ gastric lavage, correct acid-base imbalance, transfusion, and dialysis.
N-Acetylcysteine
Free radical scavenger used in Acetaminophen OD. Exogenous version of glutathione.
Acetaminophen
Not an NSAID but similar unknown mechanism. Not antiinflammatory. Antipyretic and analgesic. Works more centrally.
Minimal GI irritatation, bleeding effects, and respiratory effects.
Lower therapeutic index. Toxic, free radical metabolite in liver exacerbated by EtOH. Treat with N-acetylcysteine as scavanger drug (exogenous glutathione).
Celecoxib
A selective COX-2 inhibitor. Reduces inflammation without affecting normal physiology (GI etc.)
Other COX-2’s increased risk of heart attack and stroke.
Ketorolac
Injectible NSAID (IM, IV) Can replace morphine if opioid addiction is an issue. When combined with opioid it can decrease opioid requirement by 25-50%.
Indomethacin
Most potent COX inhibitor primarily used when other NSAIDs have failed.
Adverse effects: Significant toxicity –> GI distress, abdominal pains, ulcers, blood loss, headaches.
Used to treat PDA
Naproxen
Longer acting ibuprofen
Ibuprofen
Reversible NSAID with analgesic, antipyretic, and anti-inflammatory actions. Fewer GI side effects than aspirin and clotting effects are reversible.
Lidocaine
MOA: Amide local anesthetic. Works via blocking Na channels in their inactivation state (preferentially affects active, small, and myelinated fibers).
Pharmacokinetics: injected into target region (topical applications possible as well EMLA) –> systemic distribution NOT desired (decreased effectiveness and toxicity). Distribution can be affected by tissue pH (lower in infx = less distribution) Distribute widely after absorption. Metabolized in the liver.
Vasoconstrictors often coadministered to decrease absorbtion and bleeding.
Adverse effects: Allergic rxn (less than esters) Tongue numbness, dizziness, cns complications, hemodynamic instability, decreased myocardial excitabiltiy (ASPIRATE!)
*Also used as antiarrhythmic agent
EMLA
Eutectic Mixture of Local Anesthetics (Lidocaine and Prilocaine)
Mixture’s melting point less than either compound alone. Oil at room temp that can enter skin. Effective for procedures such as LP, venipuncture, skin graft harvesting etc.
Mepivicaine
Amide-type that is similar to lidocaine. Not effective topically, and a little longer lasting than lido.
Bupivicaine
Amide-type that is long-acting and potent local anesthetic.
Most commonly used for regional and epidural blocks. Prolonged surgery.
Ropivacaine
Amide-type long lasting local anesthetic.
Less CV and CNS toxicity than Bupivicaine.
Tetracaine
Ester type used primarily for topical anesthesia of the eye, nose, throat and for spinal anesthesia.
Cocaine
Ester type that penetrates tissues well and has vasoconstrictor action.
Primarily used on upper respiratory tract, mucosal membranes.
Abuse potential, controlled substance, inconvenient.
Procaine
Ester type short acting local anesthetic that is commonly given with vasoconstrictor. Rapid metabolism in plasma with higher risk of allergic reaction. Higher pK so onset of action is slower.
Mannitol
Osmotic diuretic used to treat vasogenic cerebral edema.
Typically lasts 4-6hrs.
MOA: Small sugar that doesn’t cross BBB –> osmotic force pulls water across membranes out of brain.
