Drugs Exam 5 Flashcards
(36 cards)
Diphenhydramine (Benadryl) OTC
Class: first generation antihistamine
MOA: Blockade H1, muscarinic, alpha adrenergic, and 5HT receptors.
PK: well absorbed orally. Widely distributed including CNS.
Can be used as opthalmic solutions.
Side effects:
- Sedation (can potentiate other CNS depressants)
- Drying of secretions
- GI disturbances (N/V, diarrhea, constipation –> give w/ meals)
Acute poisoning treatment is symptomatic and supportive (dilated pupils, flushed face, fever, dry mouth, excitation, hallucinations, in-coordination, coma, CV collapse.)
Diphenydramine is specific for low incidence of GI side effects and causing sedation.
Uses: Allergy (rhinitis, urticaria, and atopic dermatitis),motion sickness, and sleep aid
Chlorpheniramine (OTC)
Most suitable first generation anithistamine for day time use
Cetrizine OTC
(Zyrtec)
Class: Second generation (non-sedating)
Only a small amount cross BBB. They are also actively effluxed by P-glycoprotein from the CNS.
MOA: inverse agonists and act as competitive inhibitors of histamine. No anticholinergic properties.
Therapeutic uses:
Allergy (rhinitis, urticaria, and atopic dermatitis),
Ibuprofen
Fewer GI side effects than aspirin.
Reversible COX inhibitor
Naproxen
Longer half life
Ketorolac
Given IV
Analgesia and anti-inflammatory
Ketopfofen
Related to Ibuprofen
Indomethacin
Most potent NSAID
Uses: Severe frontal headache and blood disorders. Also PDA
Piroxicam
Once a day administration, but can cause dose related serious GI bleeding.
Celecoxib
10-20x more selective for COX-2.
200mg/day
Acetaminophen
not an NSAID
Analgesic, antipyretic, but NOT antiinflammatory. Effectively inhibits COX in brain, but not in periphery.
OD can cause hepatic injury. Lower TI.
NSAIDs
Block COX 1 & COX 2 causing a decrease in prostaglandins, thromboxanes, and prostacyclins. Analgesic, antiinflammatory, antipyretic.
Platelets don’t have COX 2
Adverse effects: GI ulceration, prolongation of gestation, decreased renal function, increased bleeding time. hypersensitivity (Aspirin = 3-10% of asthmatics.
Acetylsalicylate (aspirin)
Irreversibly inhibits COX (8-10 days). Used in 81mg doses for heart patients.
Adverse effects: Reye’s syndorme (encpephalopathy, and fatty liver), hypersensitivity in 3-10% of asthmatics.
Zileuton
MOA: Inhibits the enzyme 5-lipoxygenase and thus prevents the synthesis of LTB4 as well as the peptide leukotrienes.
Decreases the use of beta-agonists.
Moderately effective in maintenance treatment of chronic asthma.
PK: metabolized by cyp 450
Toxicities: monitor for hepatic toxicity.
Zafirlukast
MOA: luekotriene receptor antagonoist (LTD4 receptor, Cys LTR1)
PK: inhibits CYP450.
Montelukast
MOA: luekotriene receptor antagonoist (LTD4 receptor, Cys LTR1)
Perscribed more because once daily administration w/o meal restrictions.
Hydrocortisone
MOA: Corticosteroid–> blocks phospholipase A-2 inhibiting the creation of leukotrienes, prostaglandins, prostacyclins, thromboxanes, etc. Used mainly for for anti-inflammatory and immunosuppressive purposes.
Antinflammtory (compared to cortisol) - 1 Sodium retention (compared to cortisol) - 1
Duration: Short (8-12 hours)
PK; administered orally, parenterally, and topically. Some systemic absorbtion occurs with all forms. Metabolized in liver and excreted by kidney.
Betamethasone
MOA: Corticosteroid–> blocks phospholipase A-2 inhibiting the creation of leukotrienes, prostaglandins, prostacyclins, thromboxanes, etc. Used mainly for for anti-inflammatory and immunosuppressive purposes.
Antinflammtory (compared to cortisol) - 25 Sodium retention (compared to cortisol) - 0
Duration: long (36-72 hours)
PK; administered orally, parenterally, and topically. Some systemic absorbtion occurs with all forms. Metabolized in liver and excreted by kidney.
Dexamethasone
MOA: Corticosteroid–> blocks phospholipase A-2 inhibiting the creation of leukotrienes, prostaglandins, prostacyclins, thromboxanes, etc. Used mainly for for anti-inflammatory and immunosuppressive purposes.
Antinflammtory (compared to cortisol) - 25 Sodium retention (compared to cortisol) - 0
Duration: Long (36-72 hours)
PK; administered orally, parenterally, and topically. Some systemic absorbtion occurs with all forms. Metabolized in liver and excreted by kidney.
Methylprednisolone
MOA: Corticosteroid–> blocks phospholipase A-2 inhibiting the creation of leukotrienes, prostaglandins, prostacyclins, thromboxanes, etc. Used mainly for for anti-inflammatory and immunosuppressive purposes.
Antinflammtory (compared to cortisol) - 5 Sodium retention (compared to cortisol) - 0.5
Duration: Intermediate (12-26 hours)
PK; administered orally, parenterally, and topically. Some systemic absorbtion occurs with all forms. Metabolized in liver and excreted by kidney.
Prednisone
MOA: Corticosteroid–> blocks phospholipase A-2 inhibiting the creation of leukotrienes, prostaglandins, prostacyclins, thromboxanes, etc. Used mainly for for anti-inflammatory and immunosuppressive purposes.
Antinflammtory (compared to cortisol) - 4 Sodium retention (compared to cortisol) - 0.8
Duration: Intermediate (12-36 hours)
PK; administered orally, parenterally, and topically. Some systemic absorbtion occurs with all forms. Metabolized in liver and excreted by kidney.
Corticosteroids General
MOA: Corticosteroid–> blocks phospholipase A-2 inhibiting the creation of leukotrienes, prostaglandins, prostacyclins, thromboxanes, etc. Used mainly for for anti-inflammatory and immunosuppressive purposes.
Bind glucocorticoid receptors which are located intracellularly changing DNA transcription of glucocorticoid response elements (GREs).
Also interact with NF-kB and AP-1.
Time lag in steroid action.
Cell movement: More neutrophils (demarginalization and increased produciton). Lymphopenia, decreased monocytes and eosinophils.
Effects on inflammatory mediators:
-reduced COX 2 espression, decreased arachadonic release from phospholipids, inhibits degranulaiton, inhibits synthesis and release of TNF, IL-1, IL-2, and IFN.
Side effects: immunosuppression (microbial and fungal infxs.), ulcers, behavioral disurbances, cataracts, osteoporosis, inhibition of growth.
From withdrawal w/o taper: acute adrenal insufficiency –> fever, myalgia, arthralgia, malaise, death from hypotension and shock
Therapeutic principles:
- trial and error for proper dose
- singe dose = no harmful effects
- prolonged therapy increases incidence of lethal effects
- risk of adrenal insufficiency with abrupt cessation of prolonged, high-dose therapy.
- dosage varies greatly with condition.
PK; administered orally, parenterally, and topically. Some systemic absorbtion occurs with all forms. Metabolized in liver and excreted by kidney.
Autograft
Self to self.
i.e. skin graft
Isograft
Syngeneic. Between two identical twins
