Steve Stielberg's Pharmacology Phrenzy Flashcards
Km means what
Is the concentration of Substrate at 1/2Vmax;
it is inversely related to the affinity of the enzyme for it substrate
Pharmacokinetics
the effects of the body on the drug;
ADME: Absoprtion, Distribution, Metabolism, Excretion
Pharmacodynamics
The effects of the drug on the body; Includes concepts of receptor binding, drug efficacy, drug potency, toxicity
Pharmacokinetics: Bioavailability (F)
Fraction of administered drug that reaches systemic circulation unchanged. IV dose is F=100%, oral is usually lower
Pharmacokinetics: Volume of Distribution (Vd)
Theoretical volume occupied by the total absorbed drug amount at the plasma concentration. Apparent Vd of plasma protein-bound drugs can be altered by liver and kidney disease (decreased protein binding, increased Vd). Drugs may distribute in more than one compartment. Vd= (amount of drug in the body)/ (plasma drug concentration)
Pharmacokinetics: half life (t1/2)
The time required to change to amount of drug in the body by 1/2 during elimination (or constant infusion). Porperty of first-order elimination A drug infused at a constant rate takes (4-5) half lives to reach steady state. It takes 3.3 half lives to reach 90% of steady state level:
T1/2=(.693 X Vd)/CL
Pharmacokinetics: Clearance (CL)
The volume of plasma cleared of drug per unit time. Clearance may be impaired with defects in cardiac, hepatic, or renal function:
CL=(rate of elimination of the drug)/(Plasma drug concentration) = Vd x Ke (elimination constant)
Pharmacokinetics: Loading dose calculations
Loading dose= (Cp x Vd)/F;
Cp= target plasma concentration;
Note- in renal disease you do not change loading dose
Pharmacokinetics: Maintenance dose calculations
Maintenance dose= (Cp x CL x τ)/ (F);
τ= dosage interval, if not administered continuously;
Cp= target plasma concentration at steady state;
Note= in renal disease you adjust the maintenance dose
Zero order elimination
rate of elimination is constant regardless of Cp (i.e. constant amount of drug eliminated per unit time). Cp decreases linearly with time. Examples are Phenytoin, Ethanol, Aspirin (at high or toxic levels);
Capacity limited elimination
First order elimination
rate of elimination is directly proportional to the drug concentration (i.e. constant fraction of drug eliminated per unit time). Cp decreases exponentially over time.
Urine pH and drug elimination: Weak acids
Examples would be phenobarbital, methotrexate, aspirin. Trapped in basic environments. Treat overdose with bicarbonate. Remember that ionized species are trapped in urine and cleared quickly, neutral forms can be reabsorbed.
Urine pH and drug elimination: Weak bases
Examples: amphetamines, trapped in acidic enivronments. Treat overdose with ammonium chloride. Remember that ionized species are trapped in urine and cleared quickly, neutral forms can be reabsorbed.
Phase 1 drug metabolism
Reduction, oxidation, hydrolysis with cytochrome P-450 usually yield a slightly polar, water-soluble metabolite (often still active).
Geriatric patients often lose phase 1 first
Phase 2 drug metabolism
Conjugation (Glucuronidation, Acetylation, Sulfation) usually yields a very polar, inactive metabolite (Renally excreted). Patients who are slow acetylators have greater side effects from certain drugs because of decreased rate of metabolism
Define efficacy of a drug
Maximal effect a drug can produce. High efficacy drug classes are analgesic, antibiotics, antihistamines, and decongestants. Partial agonists have less efficacy than full agonists.
Define potency of a drug
Amount of drug needed for a given effect. Increased potency, increased affinity for receptor. Highly potent drug classes include chemotherapeutic drugs, antihypertensive drugs, and lipid lowering drugs.
Competitive Antagonist
Effect: shifts curve to right (decrease potency), no change in efficacy. Can be overcome by increase in the concentration of agonist substrate
Noncompetitive antagonist
shifts curve down (decrease efficacy). Cannot be overcome by increase agonist substrate.
Irreversible antagonist is the same idea, it just never lets go.
Partial agonist
Acts at the same site as full agonist but with lower maximal effect (decrease efficacy). Potency is an independent variable.
Therapeutic index
Measurement of drug safety:
TD50/ED50=(median toxic dose)/(median effective dose)
Safer drugs have higher TI values. LD50 (lethal dose) is used in animal studies
Nicotinic ACh receptors
ligand-gated Na/K channels; Nn (found in autonomic ganglia) and Nm (found in neuromuscular junction) subtypes.
Muscarinic ACh receptors
Are G-protein-coupled receptors that usually act through 2nd messengers, 5 subtypes: M1, M2, M3, M4, M5
What G protein does this receptor work through and what is its functions: alpha 1
q class; increases vascular smooth muscle contraction, increases pupillary dilator muscle contraction (mydriasis), increases intestinal and bladder sphincter muscle contraction. Phenylephrine and midodrine are alpha 1 agonists
What G protein does this receptor work through and what is its functions: alpha 2
i class; decreases sympathetic outflow, decreases insulin release, decreases lipolysis, increases platelet aggregation
What G protein does this receptor work through and what is its functions: beta 1
s class; increases hear rate, increases contractility, increases renin release, increases lipolysis
What G protein does this receptor work through and what is its functions: beta 2
s class; Vasodilation, bronchodilation, increases hear rate, increases contractility, increases lipolysis, increase insulin release, decrease uterine tone (tocolysis), ciliary muscle relaxation, increase aqueous humor production.
M1 receptor: what does it work through, major functions
q subtype of g protein class; CNS, enteric nervous system
M2 receptor: what does it work through, major functions
i subtype of the g protein class; decreases heart rate and contractility of atria
M3 receptor: what does it work through, major functions
q subtype of g protein; Increases exocrine gland secretions (lacrimal, salivary, gastric), increases gut peristalsis, increases bladder contraction, bronchoconstriction, increases pupillary sphincter muscle contraction (miosis), ciliary muscle contraction (accommodation)
D1 dopamine receptor: what does it work through, what does it do
s subtype of g protein; relaxes renal vascular smooth muscle
D2 dopamine receptor: what does it work through, what does it do
i subtype of g protein; modulates transmitter release, especially in the brain
Histamine H1 receptor: what does it work through, what does it do
q subtype of g protein; increase nasal and bronchial mucus production, increases vascular permeability, contraction of bronchioles, pruritus, and pain
Histamine H2 receptor: what does it work through, what does it do
S subtype of g protein: increased gastric acid secretion
Vasopressin V1 receptor: what does it work through, what does it do
q subtype of g protein; increases vascular muscle contraction
Vasopressin V2 receptor; what does it work through, what does it do
S subtype of g protein; increases H2O permeability and reabsorption in the collecting tubules of the kidney (V2 is found in the 2 kidneys)
What is the downstream effect of a Gq receptor being stimulated (and what are the types of Gq receptors)
(h1, alpha1, V1, M1, M3); Gq activates Phospholipase C which cleaves PIP2 into DAG and IP3. DAG activates protein kinase C while IP3 increases Ca in the cell and you get smooth muscle contraction
What is the downstream effect of a Gs receptor being stimulated (what are the types of Gs receptors)
Beta1, Beta2, D1, H2, V2; Activates Adenylyl cyclase which turns ATP into cAMP. cAMP goes into protein kinase A which increase Ca inside heart cells and inactivates myosin light chain kinase in smooth muscle
What is the downstream effect of a Gi receptor being stimulated (and what are the types of Gi receptors)
M2, alpha 2, D2; Gi blocks the activation of Adenylyl cyclase (the same molecule that Gs stimulates)
Betanechol
Cholinomimetic agent; direct agonist; Activates bowel and bladder smooth muscle; resistant to AChE. Postoperative ileus, neurogenic ileus, and urinary retention
Carbachol
Cholinomimetic agent; direct agonist; Glaucoma, pupillary constriction, and relief of intraocular; Carbon copy of acetylcholine
Pilocarpine
Cholinomimetic agent; direct agonist; Contracts ciliary muscle of eye (open-angle glaucoma), pupillary sphincter (closed-angle); resistant to AChE. “you cry, drool and sweat on your PILOw.
Methacholine
Cholinomimetic agent; direct agonist; Stimulates muscarinic receptors in airway when inhaled. Challenge test for diagnosis of asthma
Neostigmine
Indirect agonist (anticholinesterase); Increases endogenous ACh Neo CNS= No CNS penetration; Postoperative and neurogenic ileus and urinary retention, myasthenia gravis, reversal of neuromuscular junction blockade (postoperative)
Pyridostigmine
Indirect agonist (anticholinesterase); Increases endogenous ACh; increases endogenous ACh; increases strength. long acting myasthenia gravis treatment, does not penetrate CNS
Physostigmine
Indirect agonist (anticholinesterase); Anticholinergic toxicity (crosses BBB); increases endogenous ACh; fixes atropine overdose
Donepezil
Indirect agonist (anticholinesterase); Used in alzheimer dieases; Increase endogenous ACh
Rivastigmine
Indirect agonist (anticholinesterase); Used in alzheimer dieases; Increase endogenous ACh
Galantamine
Indirect agonist (anticholinesterase); Used in alzheimer dieases; Increase endogenous ACh
Edrophonium
Indirect agonist (anticholinesterase); old way of diagnosing myasthenia gravis (extremely short acting); now we look for anti-AChR Ab
With all cholinomimetic agents the side effects are
Exacerbation of COPD, asthma, and peptic ulcers in susceptible patients
Cholinesterease inhibitor poisoning
often due to organophosphate, such as parathion, that irreversibly inhibit AChE. Causes DUMBBELSS: Diarrhea, Miosis, Bronchospasm, Bradycardia, Excitation of skeletal muscle and cns. Lacrimation, Sweating, and Salivation.
Antidote is atropine (competitive inhibitor) with prazlidoxime (regenerates AChE if given early)
what organ does it work in and its application: Atropine, homatropine, tropicamide
eye, produce mydriasis and cycloplegia (paralysis of ciliary muscle); muscarinic antagonist
what organ does it work in and its application: Benztropine
CNS; Parkinson (PARK my BENZ); muscarinic antagonist
what organ does it work in and its application: Scopolamine
CNS; Motion sickness; muscarinic antagonist
what organ does it work in and its application: Ipratropium, tiotropium
Respiratory; COPD, asthma; muscarinic antagonist
what organ does it work in and its application: Oxybutynin, darifenacin, solifenacin
Genitourinary; reduce urgency in mild cystitis and reduced bladder spasms. Other agents are tolterodine, fesoterodine, trospium (used for urinary incontinence); contraindicated in closed angel glaucoma and elderly; muscarinic antagonist
what organ does it work in and its application: Glycopyrrolate
muscarinic antagonist; gastrointestinal and respiratory; Parenteral: preoperative use to reduce airway secretions; Oral: drooling, peptic ulcer
Atropines effect on the: eyes
increase pupal dilation, cycloplegia
Atropines effect on the: airway
Decreases secretions
Atropines effect on the: Stomach
decreases stomach acid
Atropines effect on the: Gut
decreases motility
Atropines effect on the: Bladder
decreased urgency in cystitis
Atropines side effects
Increased body temperature (can’t sweat); rapid pulse, dry mouth, flushed skin; cycloplegia; constipated; disorientation; blind as a bat, mad as a hatter, red a beet, hot as a stone, dry as a bone
Can cause acute angle glaucoma in elderly due to mydriasis, urinary retention in men with prostatic hyperplasia, and hyperthermia in infants
What is this drugs effect on alpha, beta receptors and what is it used for: Epinephrine
beta > alpha; anaphylaxis, open angle glaucoma, asthma, hypotension; alpha effects predominate at high doses
What is this drugs effect on alpha, beta receptors and what is it used for: norepinephrine
alpha 1> alpha 2> Beta 1; Hypotension (but decreased renal perfusion)
What is this drugs effect on alpha, beta, and dopamine receptors and what is it used for: Dopamine
D1=D2 > Beta > alpha; Unstable bradycardia, heart failure, shock; inotropic and chronotropic alpha effects predominate at high doses.
What is this drugs effect on alpha, beta receptors and what is it used for: Dobutamine
Beta1 > Beta2, alpha; heart failure (inotropic > chronotropic), cardiac stress test
What is this drugs effect on alpha, beta receptors and what is it used for: Isoproterenol
Beta1=Beta2; Electrophysiologic evaluation of tachyarrhythmias. Can worsen ischemia
What is this drugs effect on alpha, beta receptors and what is it used for: Phenylephrine
alpha 1 > alpha 2; Hypotension (vasoconstrictor), ocular procedures (mydriatic), rhinitis (decongestant)
What is this drugs effect on alpha, beta receptors and what is it used for: Albuterol, salmeterol, terbutaline
Beta 2> Beta 1; Albuterol for acute asthma; salmeterol for long-term asthma or COPD control; terbutaline to reduce premature uterine contractions
What is this drugs effect on alpha, beta receptors and what is it used for: Amphetamine
indirect sympathomimetics; indirect general agonist, reuptake inhibitor, also releases stored catecholamines; Used for Narcolepsy, obesity, attention deficit disorder
What is this drugs effect on alpha, beta receptors and what is it used for: Ephedrine
Indirect general agonist, releases stored catecholamines; Nasal decongestion, urinary incontinence, hypotension
What is this drugs effect on alpha, beta receptors and what is it used for: Cocaine
Indirect general agonist, reuptake inhibitor; Causes vasoconstriction and local anesthesia; never give beta blockers if cocaineintoxication is suspected (can lead to unopposed alpha 1 activation and extreme hypertension)
Norepinephrine vs isoproterenol
NE causes increase in systolic and diastolic pressures as a result of alpha1 mediated vasoconstriction leading to an increase in mean arterial pressure causing bradycardia. However, isoproterenol (no longer commonly used) has little alpha effect but causes beta 2 mediated vasodilation, resulting in decrease mean arterial pressure and increase heart rate through beta 1 and reflex activity.
Clonidine
alpha 2 agonist so it decreases sympathetic output; used for HTN urgency; does not decrease renal blood flow; ADHD, severe pain, and off label ethanol and opioid withdrawl;
Toxicity: CNS depression, bradycardia, hypotension, respiratory depression, and small pupil size
alpha methyldopa
alpha 2 agonist so it decreases sympathetic output; used for pregnancy HTN; toxicity direct coombs test will be positive for hemolytic anemia; SLE like syndrome
Pheoxybenzamine
irreversible non selective alpha blocker; used for pheochromocytoma (used preoperatively) to prevent catecholamine (HTN) crisis;
Toxicity are orthostatic hypotenstion; reflex tachycardia
Phentolamine
Reversible non selective alpha blocker; Give to patients on MAO inhibitors who eat tyramine-containing foods;
What are the alpha 1 selective alpha blockers
Prazosin, terazosin, doxazosin, tamsulosin (-osin); used to treat urinary symptoms of BPH; PTSD (prazosin); hypertension (except tamsulosin); Toxicity is 1st dose orthostatic hypotension, dizziness, and headache
what is the Alpha 2 selective alpha blocker
Mirtazapine; used to treat depression; side effects are sedation increased serum cholesterol; increased appetite
Beta blockers: name them
Metoprolol, acebutolol, betaxolol, carvedilol, esmolol, nadolol, timolol, pindolol, labetalol
Beta blockers use in angina pectoris
decreases HR and contactility resulting in decreased O2 consumption
Beta blockers use in MI
Beta-blockers (metoprolol, carvedilol, and bisoprolol) decrease mortality
Beta blockers use in SVT
(metoprolol, esmolol); decrease AV conduction velocity (class II antiarrhythmic)
Beta blockers in HTN
Decrease cardiac output, decrease renin secretion (due to beta 1 receptor blockade on JGA cells)
Beta blockers in CHF
slows progression of chronic failure
Beta blockers in Claucoma
timolol; decreases secretion of aqueous humor
Toxicity of beta blockers
Impotence; cardio vascular adverse effects (bradycardia, AV block, CHF), CNS adverse effects (seizures, sedation, sleep alterations), dyslipidemia (metoprolol), and asthamatics/COPD patients it causes exacerbations;
Don’t give to cocaine users (unopposed alpha adrenergic receptor agonist
Selectivity of beta blockers
Beta1 selective start with letters A to M (first half of alphabet); beta 2 selective start with letters N to Z (second half of alphabet; Nonselective alpha beta antagonists have ending other than olol
Nebivolol what receptors does it block
combines cardiac selective Beta1 adrenergic blockade with stimulation of Beta3 receptors, which activate nitric oxide synthase in the vasculature
what is the antidotes for toxic levels of: acetaminophen
N-acetylecystine (replenishes glutathione)
what is the antidotes for toxic levels of: AChE inhibitors, orgaophosphates
Atropine followed by pralidoxime
what is the antidotes for toxic levels of: Amphetamines
NH4Cl to acidify the urine
what is the antidotes for toxic levels of: Antimuscarinics, anticholinergic agents
Physostigmine salicylate, control hyperthermia
what is the antidotes for toxic levels of: Benzodiazepines
Flumazenil
what is the antidotes for toxic levels of: Beta blockers
glucagon
what is the antidotes for toxic levels of: Carbon mooxide
100% O2 or hyperbaric O2
what is the antidotes for toxic levels of: copper, arsenic, gold
Penicillamine
what is the antidotes for toxic levels of: Cyanide
nitrite + thiosulfate, hydroxocobalamin
what is the antidotes for toxic levels of: Digitalis
Anti-dig Fab fragments
what is the antidotes for toxic levels of: Heparin
Protamine sulfate
what is the antidotes for toxic levels of: Iron
DeFEroxamine, deFErasirox (de FE)
what is the antidotes for toxic levels of: lead
EDTA, dimercaprol, succimer, penicillamine
what is the antidotes for toxic levels of: Mercury, arsenic, gold
Dimercaprol (BAL), Succimer
what is the antidotes for toxic levels of: Methanol, ethylene glycol
Fomepizole > ethanol, dialysis
what is the antidotes for toxic levels of: Methemoglobin
Methylene blue, Vitamin C
what is the antidotes for toxic levels of: opioids
Naloxone
what is the antidotes for toxic levels of: Salicylates
NaHCO3 (alkalinize the urine), dialysis
what is the antidotes for toxic levels of: TCAs
NaHCO3 (alkalinize the plasma)
what is the antidotes for toxic levels of: tPA, streptokinase, urokinase
Aminocaproic acid
what is the antidotes for toxic levels of: Warfarin
Vitamin K, plasma if active bleed
What is the likely drugs to cause: Coronary vasospasm
Cocaine, sumatriptn, ergot alkaloids
What is the likely drugs to cause: cutaneous flushing
Vancomycin, Adenosine, Niacin, Ca2+ channel blockers
What is the likely drugs to cause: dilated cardiomyopathy
Doxorubicin, daunorubicin
What is the likely drugs to cause: Torsades de pointes
Class III (e.g. sotalol) and class IA (e.g. quinidine) antiarrhythmics, macrolide antibiotics, antipsychotics, TCAs
What is the likely drugs to cause: Adrenocortical insufficiency
HPA suppression secondary to glucocorticoid withdrawal
What is the likely drugs to cause: Hot flashes
Tamoxifen, clomiphene
What is the likely drugs to cause: Hyperglcemia
Tacrolimus, Protease inhibitors, Niacin, HCTX, Beta blockers, corticosteroids
What is the likely drugs to cause: Hypothyrodism
lithium, amiodarone, sulfonamides
What is the likely drugs to cause: Acute cholestatic hepatitis, jaundice
Erythromycin
What is the likely drugs to cause: Diarrhea
Metformin, Erythromycin, Colchicine, Orlistat, Acarbose
What is the likely drugs to cause: Focal to massive hepatic necrosis
Halothane, Amanita phalloides (death cap mushrooms), Valproic Acid, Acetaminophen
What is the likely drugs to cause: Hepatitis
INH (Isoniazid)
What is the likely drugs to cause: Pancreatitis
Didanosine, Corticosteroids, Alcohol, Valproic acid, Axathioprine, Diuretics (furosemide, HCTZ)
What is the likely drugs to cause: Pseudomembranous Colitis
Clindamycin, ampicillin, cephalosporins; antibiotics predispose to superinfection by resistant C difficile
What is the likely drugs to cause: Agranulocytosis
Dapsone, Clozapine, Carbamazepine, Colchicine, Methimazole, Propylthiouracil,
What is the likely drugs to cause: Aplastic anemia
Carbamazepine, Methimazole, NSAIDs, Benzene, Chloramphenicol, Propythiouracil
What is the likely drugs to cause: Direct coombs- positive hemolytic anemia
Methyldopa, penicillin
What is the likely drugs to cause: Gray baby syndrome
Chloramphenicol
What is the likely drugs to cause: Hemolysis in G6PD deficiency
INH (isoniazid), Sulfonamides, Dapsone, Primaquine, Aspirin, ibuprofen, Nitrofurantion; hemolysis IS D PAIN
What is the likely drugs to cause: Megaloblastic anemia
Phenytoin, Methotrexate, sulfa drugs; having a blast with PMS
What is the likely drugs to cause: Thrombocytopenia
Heparin, Cimetidine
What is the likely drugs to cause: Thrombotic complications
OCPs (e.g. estrogens)
What drugs cause the side effect of: Fat redistribution
Protease inhibitors, Glucocorticoids
What drugs cause the side effect of: Gingival hyperplasia
Phenytoin, verapamil, cyclosporine, nifedipine
What drugs cause the side effect of: Hyperuricemia (gout)
Pyrazinamide, Thiazides, Furosemide, Niacin, Cyclosporine
What drugs cause the side effect of: Myopathy
Fibrates, niacin, colchicine, hydroxychloroquine, interferon alpha, penicillamine, statins, glucocorticoids
What drugs cause the side effect of: Osteoporosis
Corticosteroids, heparin
What drugs cause the side effect of: Photosensitivity
Sulfonamides, Amiodarone, Tetracyclines, 5-FU
What drugs cause the side effect of: Rash (steven-johnson syndrome)
Anti-epileptic drugs (ethosuximide, carbamazepine, lamotrigine, phenytoin, phenobarbital), Allopurinol, Sulfa drugs, Penicillin
What drugs cause the side effect of: SLE-like syndrome
Sulfa drugs, hydralazine, INH, Procainamide, Phenytoin, Etanercept
What drugs cause the side effect of: Teeth discoloration
tetracyclines
What drugs cause the side effect of: Tendonitis/tendon rupture/ cartilage damage
Fluoroquinolones
What drugs cause the side effect of: Cinchonism
Quinidine, quinine
What drugs cause the side effect of: Parkinson like syndrome
antipsychotics, Reserpine, Metoclopramide
What drugs cause the side effect of: Seizures
INH (vitamin B6 deficieny), Bupropion, Imipenem/cilastatin, Tramadol, Enflurane, Metoclopramide
What drugs cause the side effect of: Tardive dyskinesia
Antipsychotics, metoclopramide
What drugs cause the side effect of: Diabetes insipidus
Luthium, demeclocycline
What drugs cause the side effect of: Fanconi syndrome
expired tetracycline
What drugs cause the side effect of: Hemorrhagic cystitis
Cyclophosphamide, ifosfamide (give with mesna to prevent
What drugs cause the side effect of: interstitial nephritis
Methicillin, NSAIDs, Furosemide
What drugs cause the side effect of: SIADH
Carbamazepine, Cyclophosphamide, SSRIs
What drugs cause the side effect of: dry cough
ACE inhibitors
What drugs cause the side effect of: pulmonary fibrosis
Bleomycin, amiodarone, busulfan, Methotrexate
What drugs cause the side effect of: Antimuscarinic
atropine, TCAs, H1 blockers, antipsychotics
What drugs cause the side effect of: Disulfiram-like reaction
Metronidazole, certain cephalosporins, griseofulvin, procarbazine, 1 st generation sulfonylureas
What drugs cause the side effect of: Nephrotoxicity/ ototoxicity
Aminoglycosides, vancomycin, loop diuretics, cisplatine
Positive inducers of Cytochrome P-450
Chronic alcohol use, modafinil, st john’s wort, Phenytoin, Phenobarbital, Nevirapine, Rifampin, Griseofulvin, Carbamazepine: Chronic alcoholic Mona Steals Phen-Phen and Never Refuses Greasy Carbs
Substrates for Cytochrome P-450
Anti-epileptics, Antidepressants, Antipsychotics, anesthetics, Theophylline, Warfarin, statins, OCPs
Negative inhibitors of Cytochrome p-450
Acute alcohol use, Gemifibrozil, Ciprofloxacin, Isoniazid, Grapefruit juice, Quinidine, Amiodarone, Ketoconazole, Macrolides, Sulfonamides, Cimetidine, Ritonavir, Acute Gentleman “Cipped” Iced grapefruit juice quickly and kept munching on soft cinammon rolls
Name all the sulfa drugs, what are the side effects
Probenecid, Furosemide, Acetazolamide, Celecoxib, Thiazides, Sulfonamide antibiotics, Sulfasalazine, Sulfonylureas;
Patients with sulfa allergies may develop fever, urinary tract infeciton, steven johnson, hemolytic anemia, thrombocytopenia, agranulocytosis, and urticaria, symptoms can be mild to life threatening
Drugs ending in: -azole
Ergosterol synthesis inhibitors
Drugs ending in: -bendazole
antiparasitic/antihelmintic
Drugs ending in: -cillin
peptidoglycan synthesis inhibitors
Drugs ending in: -cycline
protein synthesis inhibitors
Drugs ending in: -ivir
Neuraminidase inhibitor
Drugs ending in: -navir
protease inhibitor
Drugs ending in: -ovir
DA polymerase inhibitor
Drugs ending in: -thromycin
Macrolide antibiotic
Drugs ending in: -ane
inhalation general anesthetic (halothane)
Drugs ending in: -azine
Typical antipsychotic (thioridazine)
Drugs ending in: -barbital
Barbiturate (phenobarbital)
Drugs ending in: -caine
local anesthetic (lidocaine)
Drugs ending in: -etine
SSRI (fluoxetine)
Drugs ending in: -ipramine
TCAs (imipramine)
Drugs ending in: -triptan
5HT 1B/1D agonist (sumatriptan)
Drugs ending in: -Triptyline
TCA (amitriptyline)
Drugs ending in: -zepam
Benzodiazepine (diazepam)
Drugs ending in: -zolan
Benzodiazepine (alprazolam)
Drugs ending in: -chol
cholinergic agonist (betanechol/carbachol)
Drugs ending in: -curium or -curonium
non-depolarizing paralytic (atracurium or vecuronium )
Drugs ending in: -olol
beta blocker
Drugs ending in: -stigmine
AChE inhibitor (neostigmine)
Drugs ending in: -terol
beta2-agonist albuterol
Drugs ending in: -zosin
Alpha 1-antagonist (Prazosin)
Drugs ending in: -afil
PDE-5 inhibitor (sildenafil)
Drugs ending in: -dipine
Dihydropyridine CCB (amlodipine)
Drugs ending in: -pril
ACE inhibitor (captopril)
Drugs ending in: -Sartan
Angiotensin-II receptor blocker (Losartan)
Drugs ending in: -statin
HMG-CoA reductase inhibitor (Atorvastatin)
Drugs ending in: -dronate
Bisphosphonate (Alendronate)
Drugs ending in: -glitazone
PPAR-gamma activator (Rosiglitazone)
Drugs ending in: -prazole
PPI
Drugs ending in: -prazole
prostaglandin analog (latanoprost)
Drugs ending in: -tidine
H2 antagonist (cimetidine)
Drugs ending in: -tropin
Pituitary hormone (somatotropin)
Drugs ending in: -ximab
chimeric monoclonal Ab (Basiliximab)
Drugs ending in: -zumab
Humanized monoclonal Ab (Daclizumab)
Calculation for steady state when drug is given continuously IV
Css=Dosing rate/Clearance