Term
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Definition
Glucocorticoid; Immunosuppressive agent
Prodrug that must be activated in the liver to prednisolone
4X stronger anti-inflammatory than cortisol and causes less Na+ retention in the kidneys
Intermediate duration of action
SE: glucose intolerance, immunosuppresion, osteoporosis, psychosis |
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Term
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Definition
Glucocorticoid
10X stronger anti-inflammatory than cortisol but causes 125X more Na+ retention in the kidneys
Short duration of action
Used in patients w/ hypoaldosteronism
SE: adrenal suppression, fluid/electrolyte abnormalities, metabolic changes, edema, HTN, osteoporosis, growth suppression in children, cataracts, behavioral changes |
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Term
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Definition
Mineralocorticoid
MOA: increases Na+ reabsorption in distal nephron/collecting ducts-> increased water reabsorption, K+ secretion, and HCO3- generation |
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Term
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Definition
Diuretic- steroid K+ sparing diuretic
MOA: mineralocorticoid receptor (MR) aka aldosterone receptor antagonist-> inhibits aldosterone induced expression of Na channels (ENaC) and Na/K ATPase=> reduced Na/water retention and decreased K, H+ excretion
Also inhibits androgen synthesis (use in prostate cancer)
Tx of hyperaldosteronism, HTN
Toxicity: cross rxn w/ androgen receptor (gynecomastia, impotence)-> less w/ eplerenone; hyperkalemia; metabolic acidosis
DI: ACE inhibitor/angiotensin receptor blocker-> hyperkalemia |
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Term
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Definition
IV- Ca chloride, Ca gluconate, Ca gluceptate
Oral- Ca carbonate, Ca citrate, Ca lactate |
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Term
Cholecalciferol
Ergocalciferol |
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Definition
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Term
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Definition
Vitamin D analog of 25-hydroxycholecalciferol
Treatment of osteoporosis, hypocalcemia, hypoparathyroidism, nutritional deficiency
Used in patients w/ hepatic disease (doesn't require hepatic 25-hydroxylation) |
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Term
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Definition
Vitamin D analog of 1,25-dihydroxycholecalciferol
Treatment of osteoporosis, hypocalcemia, hypoparathyroidism, nutritional deficiency
Used in patients w/ renal disease (doesn't require hepatic 25-hydroxylation or renal 1-hydroxylation) |
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Term
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Definition
Vitamin D synthetic derivative
Treatment of osteoporosis, hypocalcemia, hypoparathyroidism, nutritional deficiency
Does not require 1-OH for activation but does require 25-OH in liver
Able to use in patients w/ renal disease |
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Term
Doxercalciferol (1-hydroxyvitamin D2)
Alfacalcidol (1alpha-Hydroxycholecalciferol) |
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Definition
Vitamin D synthetic derivative
Treatment of osteoporosis, hypocalcemia, hypoparathyroidism, nutritional deficiency
Already contains the 1-OH but requires 25-OH in liver
Able to use in patients w/ renal disease |
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Term
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Definition
Calcitriol analog
Reduces PTH w/o hypercalcemia
Used in chronic renal failure
Little GI action |
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Term
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Definition
Calcitriol analog
MOA: suppressor of PTH gene expression
Limited action on intestine and bone; used in chronic renal failure w/secondary hyperparathyroidism or in primary hyperparathyroidism
Low affinity for serum binding protein leads to longer half-life than calcitriol |
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Term
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Definition
Phosphate binder
MOA: binds phosphate in the gut to prevent absorption |
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Term
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Definition
Calcimimetic
MOA: inhibits PTH secretion by lowering the concentration of Ca2+ at which PTH secretion is suppressed
Use: treatment of secondary hyperparathyroidism due to chronic renal failure |
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Term
| NSAIDs (e.g., indomethacin, naproxen, sulindac) |
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Definition
Tx of gout
MOA: decrease inflammation and pain
DO NOT use salicylates (aspirin)-> increase uric acid secretion=> increased risk of renal stones |
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Term
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Definition
NSAID- salicylic acid derivative
MOA: irreversibly acetylates and inactives COX-1 and COX-2
Use: anti-inflammatory, anti-pyretic, analgesic; prevention of cardiovascular disease; benefit in colon cancer
Toxicity: tinnitus; low dose cause decreased urate excretion and block probenecid, high dose uricosuric (blocks urate reabsorption)-> increased risk of renal urate stones; uncouples oxidative phosphorylation (overdose)-> acidosis
Toxicity tx: give HCO3- to alkalinize urine-> shifts HA to H+ and A-; A- cannot diffuse out of tubules-> ion trapping |
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Term
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Definition
Treatment of acute gout
MOA: binds tubulin and prevents polymerization of microtubules-> interferes with mitotic spindle function, inhibits migration and phagocytic actions of granulocytes, inhibits neutrophil secretion of chemotactic factors
SE: affects rapidly proliferating cells (i.e. GI)-> nausea, vomiting, diarrhea, abdominal pain |
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Term
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Definition
Treatment of chronic gout
MOA: allopurinol and it's metabolite alloxanthine inhibit xanthine oxidase-> decreased uric acid production
Can be used in patients w/ renal disease
Drug interactions: inhibits metabolism of azathioprine and 6-mercaptupurine (must lower chemo dose) |
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Term
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Definition
Treatment of chronic gout
MOA: nonpurine xanthine oxidase inhibitor
Can be used in patients w/ renal disease
Side effects: diarrhea, nausea, liver function abnormalities |
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Term
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Definition
Treatment of chronic gout
MOA: uricosuric agent-> inhibits uric acid renal tubular reabsorption; blocks organic acid transporter in PCT-> causes less organic acid secretion and balancing urate reabsorption
Cannot be used in renal failure or in pts w/ urate renal stones
Drug interactions: prevents renal secretion of penicillin and other drugs/organic acids |
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Term
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Definition
Treatment of chronic gout
MOA: uricosuric
Cannot be used in renal failure or in pts w/ urate renal stones
Lacks both anti-inflammatory and analgesic effects |
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Term
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Definition
Immunosuppressive
MOA: inhibits calcineurin phosphatase, which is needed to dephosphorylate and activate the transcription factor NFAT=> decreases IL-2 transcription-> suppression is somewhat selective for T cells
Toxicity: renal (less w/ tacrolimus); hyperglycemia w/ tacrolimus |
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Term
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Definition
Immunosuppressive, Chemo
MOA: blocks T cell response to IL-2 by binding FKBP-> complex binds and inhibits mTOR kinase (aka rapamycin)=> prevents Cdk2 activation of cell proliferation
T cell/tumor cell specific; cell cycle arrest at G1-S transition
Everolimus-> shorter 1/2-life and quicker time to steady-state concentration
SE: hyperlipidemia, myelosuppression, GI distress, mucocutaneous effects
D/I: some CytP450 inhibition, competes for efflux at efflux pump |
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Term
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Definition
Immunosuppressive
MOA: converted to 6-mercaptopurine-> acts as purine analog to inhibit purine synthesis, esp in B/T cells
Toxicity: inhibits proliferation of any rapidly dividing cell populations-> bone marrow suppressive
D/I: allopurinol inhibits aza. metabolism |
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Term
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Definition
Immunosuppressive
MOA: inhibition of inosine monophosphate dehydrogenase-> decreased de novo purine synthesis, esp in B/T cells (lack salvage pathway); anti-inflammatory via decreased leukocyte adhesion to endothelial cells by decreased E and P selectin synthesis
SE: bone marrow suppression |
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Term
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Definition
Immunosuppressive
MOA: alkylating agent-> inhibits B/Tcell proliferation
SE: acrolein made as a breakdown product, toxic to bladder-> neutralize w/ MESNA; immunosuppression; infertility; increased risk of infection and neoplasia |
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Term
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Definition
Immunosuppressive antibody-> tx of acute renal transplant rejection
MOA: mixture of cytotoxic Abs to various CD and HLA molecules on T cells-> block cell fxn and cytotoxic
SE: fever, chills, hypotension-> less if pretreated w/ corticosteroids, acetaminophen, or antihistamines |
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Term
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Definition
Immunosuppressive antibody-> tx of acute renal transplant rejection
MOA: Ab against CD3 prevents binding of APC to Tcell-> prevents antigen recognition and thus blocks Tcell function and decreases Tcell number
SE: initially induces cytokine release syndrome-> Ab binding causes initial Tcell activation=> increased serum levels of cytokines released by activated T cells and/or monocytes (fever, chills, nausea, vomiting, arthralgia > skin rxns, aseptic meningitis, pulmonary edema, cardiovascular collapse)-> decrease risk if pretreated w/ glucocorticoids |
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Term
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Definition
Immunosuppressive antibody-> tx of acute renal transplant rejection
MOA: monoclonal Ab against IL-2 receptor-> blocks Tcell activation
Daclizumab has a somewhat lower affinity but longer 1/2-life than basiliximab
SE: anaphylactic rxn |
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Term
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Definition
Only NT in parasympathetic, first NT in sympathetic
Muscarninc and nictonic receptors
acetyl CoA + choline via choline acetyltransferase -> acetylcholine
Hydrophilic-> poorly absorbed, poorly distributed to CNS; rapidly hydrolyzed
Effects: DUMBELSS *urination* |
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Term
Methacholine
Bethanechol
Carbachol
Pilocarpine |
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Definition
Muscarinic cholinergic receptor agonist
MOA: stimulates M3 receptors-> contracts detrusor, relaxes trigone and sphincter-> urination
Effects: DUMBBELLS *urination*
USE: post-op urinary retention (w/ no obstruction)
Meth- more resistant to hydrolysis than acetylcholine
Beth- nonselective, high resistance to hydrolysis
Pilo- partial agonist |
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Term
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Definition
AchE inhibitor; carbamate ester
MOA: forms covalent bond w/ AchE that is resistant to hydrolysis; excess activation of muscarinic and nicotinic Ach receptors by excess Ach in synapse-> parasympathetic affects predominate=> DUMBELSS
Hydrolysis can occur but at a slow rate (30min-6hr)
Does not enter CNS; poorly soluble
Use: postop paralytic ileus and urinary retention
Short acting requiring frequent dosing; oral or parenteral every 4 hours |
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Term
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Definition
AchE inhibitor; carbamate ester
MOA: forms covalent bond w/ AchE that is resistant to hydrolysis; excess activation of muscarinic and nicotinic Ach receptors by excess Ach in synapse-> parasympathetic affects predominate=> DUMBELSS
Hydrolysis can occur but at a slow rate (30min-6hr)
Well absorbed but in general carbamates are not
Use: glaucoma; antimuscarinic drug intoxication |
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Term
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Definition
AchE inhibitor; 4° alcohol
MOA: forms an electrostatic/H-bond with AchE that is reversible; excess activation of muscarinic and nicotinic Ach receptors by excess Ach in synapse-> parasympathetic affects predominate=> DUMBELSS
Short-lived inhibition (~2-10 min)
Poorly absorbed in brain due to its permanent charge
Use: diagnosis and treatment of myasthenia gravis; paralytic ileus; arrhythmias
Given parenterally |
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Term
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Definition
Muscarinic receptor antagonist- competitive antagonist
MOA: reversible blockade of Ach receptors; inverse agonist
Effects: eye dilation (mydriasis); cycloplegia (loss of accommodation); tachydcardia; bronchodilation; dry mouth; reduced GI motility; reduced urination; reduced sweating
Use: cholinergic poisoning; eye examination
Given IV, topically (drops)-> well absorbed from conjunctival and gut membranes
Toxicity: increased intraocular pressure in closed angle glaucoma; dry mouth, flushed skin; agitation; delirium; hyperthermia-> dry as a bone, blind as a bat, red as a beet, mad as a hatter |
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Term
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Definition
Muscarinic receptor antagonist
Effects: eye dilation (mydriasis); tachydcardia; bronchodilation; dry mouth; reduced GI motility
Use: vertigo; nausea
Given IM or transdermal
Faster onset of action than Atropine but shorter duration of effect and crosses CNS more readily -> well absorbed from gut and conjunctival membranes; can also cross skin
Toxicity: tachycardia, blurred vision, delirium, xerostomia (dry mouth), drowsiness, amnesia, hallucinations, coma |
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Term
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Definition
Antimuscarinic
MOA: competitive, nonselective antagonist for muscarinic receptors
Given via aerosol; poorly absorbed into circulation and does not enter CNS
Toxicity: xerostomia (dry mouth), cough |
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Term
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Definition
Anticholinergic
MOA: muscarinic antagonist, somewhat M3 selective-> reduces detrusor muscle tone
USE: relieve post surgical bladder spasms and reduce involuntary voiding in pts w/ neurologic disease=> improve bladder capacity and continence, reduce infection and renal damage
Oral, IV, intracatheter, transdermally
SE: tachycardia, constipation, increased intraocular pressure, xerostomia, pruritis (w/ trandermal administration) |
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Term
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Definition
Anticholinergic
MOA: M3-selective muscarinic antagonist
USE: adults w/ urinary incontinence |
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Term
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Definition
Tricyclic antidepressant w/ strong anticholinergic actions
USE: reduce incontinence in institutionalized elderly pts
CNS toxicity |
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Term
|
Definition
Anticholinergic
USE: reduce incontinence in institutionalized elderly pts |
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Term
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Definition
| Mixed α/β agonist; α1=α2; β1=β2 |
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Term
|
Definition
| Mixed α/β agonist; α1=α2; β1>>β2 |
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Term
|
Definition
Alpha agonist; α1 > α2
Not a catechol derivative so not inactivated by COMT-> longer duration of action
Use: treatment of urinary incontinence
Given oral, nasal, parenteral, and opthalmic |
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Term
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Definition
Alpha agonist; α1 > α2
Use: hypotensive states; treatment of urinary incontinence |
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Term
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Definition
Mixed-Acting Sympathomimetic
Excreted in urine-> a significant fraction remains unchanged
Use: decongestant; treatment of urinary incontinence |
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Term
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Definition
Beta agonist; β1=β2
Treatment: bradyarrhythmia; asthma
Given IV |
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Term
Terbutaline
Albuterol
Ritodrine |
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Definition
Beta agonist; β2>>β1
Treatment: asthma, suppression of premature labor (uterine relaxation) |
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Term
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Definition
Antihypertensive
MOA: centrally acting sympathoplegic-> partial α2 agonist (> α1)
Lipid soluble-> rapidly crosses BBB; half-life 8-12hrs
Reduction of dosage required in moderate renal insufficiency
Toxicity: dry mouth, sedation; withdrawal-> nervousness, tachycardia, sweating, headache, hypertensive crisis
Contraindications: depression; TCA-> block antiHTN effects |
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Term
Prazosin
Terazosin
Doxazosin |
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Definition
MOA: reversible α1 adrenergic receptor antagonist; allows NE to exert neg feedback on its own release (via α2)
Primarily used in men w/ HTN and prostatic hyperplasia (reduces bladder obstruction symptoms)
1/2-life: prazosin < terazosin < doxazosin
Toxicity: retention of salt and water; dizziness, palpitations, headache, lassitude, positive test for antinuclear factor (no rheumatic symptoms) |
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Term
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Definition
MOA: irreversible α-adrenoceptor antagonist (α1>α2)
Use: treatment of urinary obstruction (i.e. BPH)
Long duration (14-48hrs); given orally
Toxicity: orthostatic hypotension, tachycardia, MI; nasal stuffiness; inhibits ejaculation, fatigue, sedation, nausea |
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Term
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Definition
MOA: reversible α-adrenoceptor competitive antagonist (α1=α2)
Use: treatment of urinary obstruction (BPH)
Given IV and oral; half-life 45mins
Toxicity: severe tachycardia, arrhythmia, MI |
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Term
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Definition
Alpha adrengergic receptor antagonist alpha2>>alpha1
MOA: promotes NE release
Uses: orthostatic hypotension; erectile dysfunction; can reverse antihypertensive effects of alpha2 adrenergic agonists
Toxicity: anxiety |
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Term
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Definition
MOA: adrenergic antagonist (β≥α1>α2)
β antagonism-> decreased bladder relaxation, decreased renin release
α antagonism-> sphincter relaxation |
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Term
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Definition
MOA: nonselective β-adrenergic receptor antagonist; local anesthetic action
Inhibits renin production (β1)
Half-life 3-5hrs; given orally (sustained release prep available) or parenterally; highly lipid soluble
Toxicity: bradycardia; asthma; fatigue; vivid dreams; cold hands; withdrawal from β-receptor upregulation-> nervousness, tachycardia, angina, increase BP, MI
Contraindications: bradycardia, cardiac conduction disease, asthma, peripheral vascular insufficiency, diabetes |
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Term
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Definition
MOA: β-adrenergic receptor partial agonist
Half-life 3-4hrs; given orally
May potentiate actions of antidepressants
Toxicity: fatigue, cold hands, vivid dreams |
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Term
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Definition
β-adrenergic receptor antagonist (β1=β2)
Decreased bladder relaxation (β2) and decreased renin release (β1) |
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Term
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Definition
MOA: nonselective β-adrenergic receptor antagonist
Decreased bladder relaxation (β2) and decreased renin release (β1)
Little metabolism, excreted in urine
Reduction of dosage required in moderate renal insufficiency |
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Term
Metoprolol
Acebutolol
Atenolol |
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Definition
MOA: β-adrenergic receptor antagonist (β1>>>β2)
Reduce renin secretion
Toxicity: bradycardia, fatigue, vivid dreams, cold hands |
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Term
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Definition
MOA: selective β1 adrenergic receptor antagonist (β1>>>β2)
Rapidly metabolized via hydrolysis by RBC esterases; half-life 9-10mins
Given constant IV infusion for intra and postop HTN, hypertensive emergencies
Toxicity: bradycardia, hypotension |
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Term
Acetazolamide
Methazolamide
Dichlorphenamide |
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Definition
Diuretic
MOA: carbonic anhydrase inhibitor-> luminal inhibition prevents H2CO3-> H20+CO2 so less entry into cell and intracellular inhibition prevents HCO3- formation=> decrease basolateral Na+ reabsorption via Na/HCO3- (1:3) symport
Acts at PCT-> Low diuretic b/c of TGF activation in macula densa (decrease RBF/GFR)-> self-limited diuresis
Potency: acetazolamide < methazolamide < dichlorphenamide (30X more potent that acetazolamide)
USE: glaucoma, urinary alkalinization; metabolic alkalosis
SE: metabolic acidosis; Ca-Ph stone formation; hypokalemia; allergic sulfur rxn |
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Term
Mannitol
Urea
Isosorbide
Glycerin |
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Definition
Diuretic
MOA: osmotic diuretic-> increases oncotic P and pulls water from ICF to expand extracellular V=> causes decreased renin release and increased RBF which causes medullary washout and thus diuresis (decreased concentrating ability)
Isosorbide/Glycerin-> oral
Mannitol/Urea-> IV-> more for increased intracranial P
USE: tx of acute renal failure, reduction of intracranial/intraocular P; tx of dialysis disequilibrium (loss of solutes causes shift from ECF->ICF)
SE: pulmonary edema, exacerbating symptoms of CHF; electrolyte loss; hyperglycemia w/ Glycerin
Contraindications: Mannitol/Urea w/ inctracranial bleeding; Urea w/ liver dysfunction |
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Term
Furosemide (Lasix)
Bumetanide
Ethacrynic acid
Torsemide |
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Definition
Diuretic
MOA: loop diuretic (3 part MOA) in TAL
1. inhibits Na-K-2Cl symport-> increased luminal [salt] = decreased water reabsorption
2. inhibits macula densa sensing mechanism-> interprets this as low luminal [NaCl]-> afferent dilation and increase GFR
3. loss of interstitial gradient from medullary washout-> decreased urine concentrating abilities-> diuresis
Increased urinary excretion of Na, Cl, K, and Ca/Mg (less positive lumen so decrease electrical gradient)
Potency: ethacrynic acid < furosemide < torsemide < bumetanide
Dose-response curve shift to R w/ chronic renal failure (impaired drug secretion into PCT)
USE: edematous states, CHF, HTN, acute renal failure
SE: ototoxicity (esp. Ethacrynic acid); electrolyte loss; metabolic alkalosis; allergic sulfur reaction (not w/ Ethacrynic acid); hyperglycemia, hyperuricemia
D/I: compounded ototoxcitiy w/ aminoglycosides, cisplatin/carboplatin, paclitaxel |
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Term
| Hydrochlorothiazide Chlorothiazide Methyclothiazide Bendroflumethiazide Hydroflumethiazide Polythiazide Trichlormethiazide Indapamide Chlorthalidone Quinethazone Metolazone |
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Definition
Diuretic
MOA: thiazide diuretics-> inhibit Na/Cl symport in DCT=> decreased water reabsorption = diuresis
Increased excretion of Na, Cl, and K and decreased excretion of Ca2+ (stimulated reabsorption)
No tubuloglomerular feedback (after macula densa)
Chlortiazide-> lowest potency
Polythiazide/Trichlormethazide-> highest potency
Chlorthalidone-> longest 1/2-life (47hrs)
USE: HTN, mild edema, calcium nephrolithiasis, diabetes insipidus (reduces free water excretion)
SE: hyponatremia, hypokalemia, hypercalcemia, metabolic alkalosis, allergic sulfur rxn, hyperglycemia (diabetes mellitus)
D/I: Quinidine-> hypokalemia increases risk of torsades de pointes (ventricular tachycardia) |
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Term
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Definition
Diuretic
MOA: K+ sparing diuretic-> inhibition of ENaC Na channels in late distal tubule/collecting ducts=> decreased Na reabsorption = decreased water reabsorption and decreased K loss
Amiloride-> longer 1/2-life, more potent, renal excretion
Triamterene-> metabolized for excretion
USE: HTN, mild edema
SE: hyperkalemia; metabolic acidosis
D/I: pentamide/trimethoprim (used to treat Pneumocystis infxn in AIDS pts)-> also ENaC inhibitors |
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Term
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Definition
Chemo- prostate cancer
MOA: GnRH agonist-> 1st 2-4 wks causes agonism at receptor to exacerbate symptoms via promotion of testosterone production=> eventually downregulate GnRH receptors to decrease LH production and thus androgen production => pharmacological castration
Altered amino acid sequence-> less degradation and greater affinity for GnRH receptor compared to GnRH
SE: headache, light-headedness, nausea, injection site reactions; hypogonadism |
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Term
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Definition
Chemo- prostate cancer
MOA: decreases CytP450 production and inhibits sex steroid synthesis |
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Term
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Definition
Chemo Hormonal tx- benign prostatic hypertrophy
MOA: inhibits 5α-reductase-> prevents conversion of testosterone to dihydrotestosterone
SE: impotence, gynecomastia |
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Term
Flutamide
Bicalutamide
Nilutamide |
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Definition
Chemo- prostate cancer
MOA: nonsteroidal androgen receptor antagonist-> inhibit ligand binding of receptor and translocation of the androgen receptor-ligand complex to the nucleus
Rarely used alone; used in combo w/ GnRH agonist during first few weeks of treatment to prevent excess androgen production
Bicalutamide/Nilutamide-> orally active, more potent w/ fewer side effects compared to Flutamide
SE: gynecomastia, mild hepatic toxicity |
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Term
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Definition
Chemo- prostate cancer
MOA: steroidal androgen receptor antagonist/partial agonist
Rarely used alone; used in combo w/ GnRH agonist during first few weeks of treatment to prevent excess androgen production |
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Term
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Definition
Chemo- hormone refractory/metastatic prostate cancer
MOA: intercalates DNA
SE: myelosuppression, cardiac toxicity (less than doxorubicin), mucositis
Contraindications: cardiac disease |
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Term
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Definition
Chemo- prostate cancer
MOA: inhibit mitosis by binding to beta-tubulin-> blocks disassembly of microtubule strands
Used in combo w/ estramustine
MOR: multidrug resistance pumps, beta-tubulin mutations
Tox: neutropenia, peripheral neuropathy, hypersensitivity (can use w/ dexamethasone) |
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Term
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Definition
Chemo- advanced hormone refractory prostate cancer
MOA: combo of estradiol and normustine-> estradiol directs drug to prostate gland and normustine promotes microtubule disassembly=> inhibits mitosis
Oral administration
Synergistic w/ Docetaxel
SE: hypercalcemia, acute attacks of porphyria, impaired glucose tolerance, hypersensitivity, angioedema; estradiol-> impotence, gynecomastia, thrombosis |
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Term
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Definition
Chemo- prostate cancer
MOA: decrease testosterone production via negative feedback of the hypothalamic-pituitary axis; may also compete at androgen receptors for binding and induce cytotoxic cell damage
SE: increased myocardial infarctions, strokes, and pulmonary emboli; increased mortality; impotence, loss of libido, and lethargy
Benefit: estrogens prevent bone loss |
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Term
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Definition
Chemo- bladder cancer
MOA: live, attenuated Mycobacterium bovis-> induces granulomatous rxn in bladder wall
Given intravesicularly
SE: hypersensitivity, shock, chills, fever, malaise, immune complex disease |
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Term
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Definition
Chemo- bladder cancer
MOA: activated by CytP450 to an alkylator-> crosslinks DNA
Intravesicular agent
SE: mild myelosuppression due to some systemic absorption |
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Term
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Definition
Chemo- bladder cancer
MOA: dual alkylator-> crosslinks DNA @ G and A=> prevents DNA synthesis and repair attempts lead to strand breaks
Req activation for alkylation
Intravesicular agent
MOR: decreased activation, efflux pump
SE: myelosuppression, nephrotoxicity |
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Term
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Definition
Chemo- advanced metastatic bladder cancer
MOA: displacement of Cl by water activates-> crosslinks DNA by binding guanines to prevent replication; drug-DNA complex attracts HMG-1 (high mobility group-1) repair proteins which become irreversibly bound-> prevents effective repair and leads to apoptosis
Activation occurs more slowly in Carboplatin
MOR: increased nucleotide excision repair protein; loss of function of mismatch repair (HMG-1)
Tox: nephrotoxicity (minimized w/ hydration/saline diuresis), ototoxicity, marked nausea/vomiting (given w/ anti-emetic); myelosuppression (Carboplatin)
MVAC combination-> methotrexate, vinblastine, doxorubicin, cisplatin
Carboplatin is generally less toxic-> used for pts w/ renal dysfunction in combo w/ paclitaxel
Cisplatin/Carboplatin also used in combo w/ gemicitabine |
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Term
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Definition
Chemo- renal cell carcinoma and melenoma
MOA: stimulate proliferation and activation of lymphokine-activated killer cells and CTLs
Used in cancers that are refractory to conventional treatment
SE: hypotension, arrhythmia, peripheral edema, azotemia, increased liver enzymes, anemia, thrombocytopenia, nausea, vomiting, diarrhea, confusion, fever |
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Term
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Definition
Chemo- renal cell carcinoma
MOA: inhibitor of receptor tyrosine kinases (including PDGF-R, VEGF-R)-> decreased angiogenesis and proliferation
SE: bleeding, HTN, proteinuria, thromboembous, intestinal perforation, myelosuppression |
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Term
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Definition
Chemo- renal cancer
MOA: humanized monoclonal Ab against VEGF-> inhibits interaction with VEGF receptors (VEGF-Trap)=> inhibits angiogenesis in tumors
Tox: severe HTN, proteinurea, congestive HF, hemorrhage, stroke, MI, gastric perforation |
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Term
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Definition
Antimicrobial- good for gram (-) organisms
MOA: inhibits transpeptidase-> blocks cell wall synthesis
MOR: penicillinase, beta-lactamase
High dose given IV |
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Term
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Definition
Antimicrobial
MOA: inhibition of cell wall synthesis by binding penicllin binding protein, preventing peptidoglycan crosslinking
MOR: beta-lactamase
Amoxicillin-Clavulanate (oral)-> uncomplicated cystitis, uncomplicated pyelonephritis
Ampicillin + Gentamicin (IV)-> uncomplicated and complicated pyelonephritis=> esp by Enterococcus |
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Term
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Definition
Antimicrobial
MOA: inhibit cell wall synthesis by binding penicllin binding protein, preventing peptidoglycan crosslinking-> activity against gram +/- aerobic/anaerobic bacteria; used together with a beta-lactamase inhibitor tazobactam/clavulanate
Effective against Pseudomonas aeruginosa
USE: complicated pyelonephritis (IV)
Tox: defect of hemostasis |
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Term
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Definition
Antimicrobial
MOA: Imipenem inhibits cell wall synthesis by binding penicllin binding protein, preventing peptidoglycan crosslinking; paired w/ Cilastatin-> inhibits dehydropeptidase in PCT brush border=> prevents Imipenem break down
Very resistant to beta-lactamases, including chromosomal
Broad spectrum
Treatment of complicated pyelonephritis (IV) |
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Term
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Definition
Antimicrobial
MOA: prevents cell wall synthesis by binding penicllin binding protein, preventing peptidoglycan crosslinking; activity only against gram-negative bacteria
Resistant to beta-lactamases (but not chromosomal)
Effective against Enterobacteriaceae and P. aeruginosa
Treatment of uncomplicated pyelonephritis or septicemia in extremely ill pts |
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Term
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Definition
Antimicrobial-> 3rd generation cephalosporin
MOA: interferes w/ cell wall synthesis by binding penicllin binding protein, preventing peptidoglycan crosslinking
MOR: beta-lactamase
Given IV every 12-24 hours; half-life = 8hrs
Effective against S. aureus, Streptococcus pneumoniae, Pseudomonas aeruginosa
Treatment of suspected septicemia and uncomplicated pyelonephritis (oral) |
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Definition
Antimicrobial-> 4th generation cephalosporin
MOA: interferes w/ cell wall synthesis by binding penicllin binding protein, preventing peptidoglycan crosslinking; even more resistant to beta-lactamases than 3rd generations
MOR: beta-lactamase
Treatment of extremely ill pts and those w/ complicated pyelonephritis (IV) |
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Term
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Definition
Beta-lactamase Inhibitor
MOA: suicide inhibitor that irreversibly binds and inhibits beta-lactamase |
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Definition
Beta-lactamase Inhibitor
MOA: beta-lactamase inhibitor
Poor activity against the inducible chromosomal beta-lactamases; good activity against the plasmid beta-lactamases |
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Term
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Definition
Antimicrobial
MOA: binds 30S subunit and interferes w/ protein synthesis by fixing the 30S-50S ribosomal complex at the start of mRNA-> causes misreading leading to premature termination of translation and incorporation of incorrect amino acids=> abnormal proteins
Bacteriacidal
Use in complicated pyelonephritis and catheter associated UTI (given IV) in combo w/ a fluoroquinolone, 3rd gen cephalosporin, or pipercillin-tazobactam
MOR: resistance via plasmid mediated enzymes that inactivate the drug-> acetylase, adenylase, phosphorylase
Toxicity: ototoxicity (irreversible damage to vestibular and cochlear sensory cells), neuomuscular blockade (inhibits ACh release from preganglionic terminal via competition w/ Ca2+-> antagonized by Ca2+ salts and anti-AChE), nephrotoxicity (mild reversible impairment (decreased concentrating, mild proteinuria, casts) > acute tubular necrosis-> due to accumulation of and retention of drug in PCT cells)=> may prevent drug excretion and increase ototoxicity; teratogenic |
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Term
Gentamicin
Tobramycin
Amikacin
Netilmicin
Streptomycin
Neomycin |
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Definition
Aminoglycosides
Gentamicin- IV or IM; use in combo in lower concentrations of high renal toxicity
Tobramycin- IV, IM, or inhalation; superior activity against P. aeruginosa in combo w/ pseudomonal beta-lactamase inhibitor
Amikacin- IV or IM; broad spectrum against gram -; lowest resistance rates
Netilmicin- broad spectrum against gram -
Streptomycin- higher ototoxicity
Neomycin- oral, topical, and bladder irrigation; hypersensitivity toxicity |
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Term
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Definition
Antimicrobial
MOA: prevent tRNA binding to 30S
MOR: influx/efflux, binding site mutation, inactivation
SE: GI, photosenitivity, brown teeth for fetus/young children, neuromuscular blockade (Ca2+ chelation); nephrotoxicity (renal tubular acidosis, azotemia, Fanconi's syndrome)-> not in doxycycline b/c not secreted by kidney
Doxycycline used in women w/ UTIs and risk factors for STDs; E. coli is resistant to doxy |
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Term
Azithromycin
Clarithromycin
Erythromycin |
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Definition
Antimicrobials- macrolides
Use in women w/ UTIs and risk factors for STDs (especially Chlamydia)
MOA: binds 50S peptidyltransferase to block translocation
Large tissue distribution, high cellular concentration (not erythromycin)
MOR: efflux pumps; these drugs induce methylation of 50S and cannot bind-> cause resistance to self
Tox: hypersensitivity; GI problems; arrhythmia (QT prolongation); hepatitis (erythromycin)
Drug interactions: decrease cytP450s (except azithromycin) |
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Term
| Trimethoprim-Sulfamethoxazole |
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Definition
Antimicrobial
Tx and prophylactic use in women w/ frequent UTIs; also for cystitis, pyelonephritis, prostatitis
MOA: inhibits 2 steps of the THF synthesis pathway; sulfamethoxazole inhibits incorporation of PABA into folic acid; trimethoprim inhibits DHFR
20:1 sulfamethoxazole:trimethoprim concentration; oral
MOR: altered DHFR
Tox: myelosuppression, Stevens-Johnson syndrome, nausea/vomiting |
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Term
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Definition
Quinolones
MOA: inhibits DNA gyrase > topoisomerase IV (at higher concentrations)
Given orally
MOR: DNA gyrase mutation
Compared to fluoroquinolones-> narrow spectrum (gram - only), requires high doses, widespread resistance |
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Term
Ciprofloxacin
Ofloxacin
Levofloxacin
Norfloxacin |
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Definition
Fluoroquinolones
MOA: inhibits DNA gyrase and topoisomerase IV
Given orally
Use in complicated and uncomplicated cystitis, pyelonephritis, prostatitis
MOR: DNA gyrase mutation
SE: GI distress, arthritis in children
C/I: children |
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Term
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Definition
Urinary antiseptic
MOA: unchanged drug (~40%) is excreted into urine; bacteria in urinary tract reduce drug to reactive intermediate that damages DNA
Active against gram + enterococci and gram - E. coli
Proteus, Pseudomonas, Enterobacter, and Klebsiella are resistant
More active at low pH (do not use w/ urease forming bacteria Proteus) |
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Term
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Definition
Urinary antiseptic
MOA: metabolized to toxic formaldehyde spontaneously in low urine pH, but not in plasma
Prophylaxis of chronic UTI
Do not use w/ urease forming Proteus-> alkalinizes pH and prevents drug activation |
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Term
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Definition
Antischistosomal- 1st choice agent effective against all 3 forms: S. mansoni, S. haematobium, and S. japonicum
MOA: causes influx of Ca to produce contraction and paralysis of worm musculature; helminth tegumental damage at higher drug levels from Ca influx
SE: dose related transient abdominal distress |
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Term
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Definition
Antischistosomal- effective against and used as secondary treatment of S. mansoni only
MOA: forms an ester that binds and alkylates DNA, resulting in contraction and paralysis of the worms
Acts mainly on male worms
No longer used in US |
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Term
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Definition
Antischistosomal- effective against S. haematobium only
MOA: organophosphate converted to dichlorvos w/in worm-> AChE inhibitor |
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