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Pharmacology Exam I

Classes 1-4

TermDefinition
Common Errors in Prescribing Medications for Children Fatigue, Hunger, Concentration, Stress, Distraction, Lack of Training, Lack of access to info
List the Steps you can take to prevent medication errors when prescribing I Can PresCribE A Drug indication, contraindication, precautions, cost/compliance, efficacy, adverse effects, dose/duration/direction
Describe what ENANTIONER DRUGS are drugs that exist in pairs usu one side is more effective the less active side is usu the cause of ADE
How do drug interactions affect ABSORPTION? absorbed best in neutral environment (unionized) Passive (high conc-> low conc) Facilitated (low conc-> high conc)*carrier Active (low conc-> high conc)*energy
How do drug interactions affect DISTRIBUTION? competition for plasma protein binding, displaces one drug from a binding site by another, increasing free concentration
How do drug interactions affect METABOLISM mainly involves CYP 450 system in the liver Phase 1 (small intestine major site of metabolism,contains enterocytes in bowel mucosa and CYP450 enzymes) phase2 (responsible for synthesis of water soluble compounds like morphine, propofol and caffeine)
How do drug interactions affect ELIMINATION? requires drug to be polarized, un-polarized drugs diffuse back into circulation *kidneys (major route)*liver (bile)
Explain principles of Therapeutic Monitoring use to monitor concentrations to adjust regimen to avoid ADR. to determine dosage, TR for patient and compliance
Why would you INCREASE/DECREASE a dose? changes the steady state peak concentration (inc the dose = inc SS = drug concentration)
Why would you INCREASE/DECREASE the dosing interval? Dosing interval influences peaks/troughs (inc interval = dec trough = allows time for M&E) ex if you check a trough and it is incr, then change the interval from Q12 to Q 24 = decrease trough
What is the difference between time vs. concentration-dependent killing of bacteria? time dependent (time the drug id above the MIC, so more freguent dosing or cont infusion)ex.PCN concentration dependent (increased effect (peak) when doses are above MIC, so larger less frequent doses)ex. aminoglycosides
What is the difference between ON vs. OFF label use of drugs OFF label (not illegal) NO peds dosing, NO warning of ADE, NO drug interaction info, NO liability sponsor, NO long term surveillance, NO peds formulations
What are LEGEND, OTC, and CONTROLLED drugs? Legend are prescription drugs Controlled drugs can be abused. NP can prescribe schedule II-V
Proprietary vs. Nonproprietary NON-Proprietary (generic/common name) ex. acetaminophen, ibuprofen, aspirin Proprietary (trade name by company) ex. Tylenol, Motrin, Vicodin
Pharmacokinetics and Pharmacodynamics Kinetics: what the body does to a drug Dynamics: what the drug does to the body
Hydrophilic vs. Lipophilic Drugs Hydrophilic (water soluble)drugs have a smaller Vd than lipophilic (lipid soluble)
P-glycoprotein reverse transporter protein is a membrane -bound transport sys responsible for drug transport across cell membranes
Bioavailability, including first pass hepatic metabolism the fraction of admin drug that reaches the circulation Affected by 1st pass (drug metabolized by gut wall or liver before entering into bloodstream) decrease concentration
CYP 450 enzyme system super family of over 100 different enzymes (phase 1 reaction)
Inducers vs. inhibitors Inducers (Increase rates of CYP enzymes & metabolism,decreases plasma conc, drug activity, and TE.Increases prodrug activity) Inhibitors (do the opposite)*grapefruit juice
Genetic variation in CYP metabolism can alter drugs efficacy and risk AE
Poor vs. Rapid Metabolizers Poor->Caucasians, Chinese/Japanese, Asians *cough syrup Rapid->Smoking can metabolize drugs faster Thyroid function, Age extremes, Pesticides
Vd distribution of drug in the body compared to unbound plasma conc *the more body the drug can be distributed to the more drug concentration is dec
Non-genetic vs. Non-drug considerations for metabolism Can inhibit (grapefruit juice, charbroiled food, cruciferous veggies (broccoli, cauliflower,cabbage) Smoking can metabolize drugs faster Thyroid function, Age extremes, Pesticides
Slow vs. Fast acetylators (How fast does this affect drug availability) Slow->more drug in plasma, risk of toxicity * children= increase with age Fast-> too little drug in plasma, decreased Therapeutic effect
Properties of drugs that increase their renal clearance Incr renal flow=incr excretion incr protein binding=decr excretion mainly by acid/base transport (pcn, histamine) incr secretion in drug poisoning alkaline urine= prevent reabsorption of acid acidic urine=prevents reabsorption of bases
T 1/2 Time to 50% reduction of drug in the body *time required to meet steady state *it takes 3-5 1/2 lives to get up to the steady state, reached faster with loading dose
steady state steady state achieved when rate of elimination=rate of administration(amt taken) *represewnts equilibrium in drug concentration
Drug-receptor binding Most drugs exert their effect by binding to a receptor a protein on or w/I a cell
Agonists vs. Antagonist Agonist->drug that binds to a receptor to stimulate the target organ Antagonist-> drug that decreases or opposes responses caused by drug agonists *if stopped can have rebound effect
Tachyphylaxis Repeated/continuous stimulation of a receptor by a drug can desensitize the drug *protects the cell from excessive stimulation, lowers the response of the drug
Therapeutic index (TI) and drug safety measure of safety of drugs large value indicates wide margin b/t effective and toxic bioavailability is critical in drugs with narrow TI
Difference in pharmacokinetics in adults vs. infants/children
Prodrug and how metabolism effects drug effectiveness
Factors contributing to ABX resistance and measures to minimize inapprop use, inadequate coverage, excessive broad spectrum use, poor adherence, retained abx for later use, prolonged hosp saty immunosuppressed population, invasive device reducing resistance->education, abx stewardship, infection control, vaccinations
STAPH gram + cocci aerobic catalase + aureus(coagulase +) epidermis (coagulase -)
STREP gram + cocci aerobic catalase - pneumoniae (a-hemolysis) GAS (B-hemolysis)
Pseudomonas gram - rods aerobic (e.coli, salmonella, shigella) cocci->nisseria
Distinguish normal flora vs. disease causing see chart
Drug Classes Beta lactams(pcn, cephalosporins,carbapenems) fluoroquinolones aminoglycosides macrolides
Bactericidal vs. Bacteriostatic Bactericidal-> kills bacteria Bacteriostatic-> suppress growth allowing the immune sys to fight infection
Different approaches to antimicrobial therapy (prophylaxis, empirical tx, definitive) P=prevent infection E=treatment of infection prior to knowing known organisms D=culture & sensitivities narrow the treatment specturm
beta lactamase- producing microbes (their consequences and treatment) M.catarrhalis, H. influenzae
Common bacterial organisms for HEENT infections RSV, Parainfluenza, FLU, Coronavirus, M.catarrhalis,Recurrent OM: Parechovirus Chlamydia, Mycoplasma
Drugs used to treat HEENT infections (indication, primary and alternate, instru) Amoxicillin, Azithromycin, Ceftriaxone, Augmentin, Levofloxacin
Amoxicillin 25-45mg/kg/dose BID 80-90mg/kg/dose BID
Amoxicillin-clavulante <3mo (20-40mg/kg/d)BID 4:1ratio 3mo and older (25-45mg/kg/dose)BID 7:1ratio 3mo to <40kg (90mg/kg/d)BID 14:1ratio >16 yo (1000mgamox/62.5mgclav) 16:1ratio
Azithromycin 10mg/kg/24hr QDx3days
Guideline for non-treatment of AOM Observation is approp, if follow-up can be ensured nonsevere illness in mild otalgia and temp<39. severe illness w/ otalgia temp>39.0 A cetain dx meets 3 criteria 1. rapid onset 2. signs of middle ear effusion 3. s/s of middle ear inflammation
3 first-line ophthalmic abx pathogens treated and age guidelines Ciprofloxacin, polymyxin B-bacitracin, Polymyxin B-trimethoprim
How do Drug transfer increase throughout pregnancy Placental Anatomy, Placental and Maternal Factors
What influences Placenta development and gestational changes in fetal drug delivery Surface Area (stretches and accommodates the fetus) Membrane thickness decreases overtime->term Increased bd flow to membrane (500ml to 600ml/min) pH differences b/w mom and fetus
What are the contributing factors to drug trapping in the fetus Ion trapping occurs when ionized drugs are trapped in the fetal circulation fetus(7.3) mom(7.4) so when weak bases are more ionized, they will also be more ionized in the fetal circulation->net circulation
Describe the mechanism of drug transfer across the placenta Simple diffusion(passive), facilitated(carrier mediated), active transport(carrier medicated/ATP)P-glycoprotein(pumps drugs back into the maternal circulation=decr fetal transfer)
Which drugs have rapid placental transfer ABX, Benzo, Phenytoins, Barbi, etoh, meperidine, salic, lido, propranolol, cocaine, heroin
Which drugs/chemicals can pass into the breast milk Diffusion is most common mechanism *milk is very acidic and can also cause ion trapping radio active chemicals cross over easily *DDT
What are the FDA teratogenic risk categories Category A(no risk to fetus) Category B(animal studies have not shown risk) Category C(animal studies have shown risk, but benefit to mom may out way harm to fetus) Category D(studies show harm, but may warrant use anyway) Category X(risk outweigh ben
What are the significant developmental changes of the skin 13% of infant total body is skin vs. 3% adult infants have greater total surface area preemie have thinner epidermis and dcer fat, which icre perfusion/hydration of the skin infants have incre risk of toxicity from topical drugs
Identify common age related areas of atopic dermatitis less than 2->face, scalp, hands, feet older ->adolescent->inside knees/elbows, neck, hands, feet
What is the stepwise treatment of atopic dermatitis 1st line tx->topical corticosteroids (non-specific anti-inflam)immunosupre, vasoconstr Oint->Gels->Creams->Lotion
How do you treat itching and super infections in AD itching->Benadryl, hydroxyzine, cetirizine, montelukast, emollients Super infections-> topical (mupirocin) po-cepalexin(keflex), augmentin, cefprozil
What important educational points to remember with AD apply thinly BID, start at 1st sign of flair, then taper to moisturizer don't use steroids in infected areas don't apply to wet skin and wash hands after application chill before use to decr sting apply moisturizer on top after
Contact dermatitis and treatment irritant, rash usu at the point of contact Tx: low->interm steroids (1%, 2.5%) high potency if plant dermatitis oral steroid if sever x2-3wks to prevent rebound prednisone1mk/kg/d, max40mg/d methylprednisone(Medrol pack)6day, 24mg d1 taper to 4mg->d
Diaper rash and treatment irritant due to urine, feces under occlusion infectious: candida Tx:frequent diaper changes, open to air, keep dry,no chemicals/powder OTC barrier: A&D, zinc ox (desitin)balsam of peru(balmex)
Tinea Corporis 1st line tx:(allyamines,fungicidal):terbinafine(lamisil), naftifiine 1%(naftin)
What are the causes of acne and common bacterial flora incr sebum production, occlusion of hair follicle colonization by propionibacterium acnes control inflammation by altering bacterial flora
What is the algorithm for treatment of each level of acne see chart
Topical retinoid and retinoid like compounds 1st line Tretinoin (Retin-A)(0.025%, 0.1%) start w/lowest concentration then incr ifneed Adapalene (Differin)a retinoid like comp gel(0.1%) >than 12 y.o *increase photosensitivity
Topical abx Clinda (Clinda-Derm)use in >12yrs Erythro (Akne-Mycin)solu->1,2% oint/gel 2%
Tetracycline inhibits growth of P acnes use for 4-6 months, then go back to topical 1st line po take on empty stomach photsensivity, staining teeth<12yrs
Isotretinoin Accutane *most potent agent for acne tx decr sebum production tx for 20weeks ADE: IBS and teratogenicity iPledge
What are the common causative organisms for bacterial skin infections s. arues, s.pyogenes, GAS
Impetigo Extensive lesions Cephalexin (50-75mg/kg/d TID) Amoxicllin-calvulante (45mg/kg/d) if CA-MRSA Clinda(30mg/kg/d TID) Bactrim (8mgTMP/kg/d BID)
Cellulitis s. aureus, s.pyogenes human bite(bacteroides)anmi bite(pasteurella)
What organisms causes lice and scabies Pediculus humanus and Sacroptes scabiei
Scabies treatment 5% cream (Elimite Rx)>2yr
Lice treatment 1% cream rinse >2mos (NIX, OTC)
What are the 3 factors affected by absorption 1. Blood flow at the site (poor blood flow delays absorption) 2.GI function (varies until 20-30 mths) 3.Thin stratum corneum
Beta Lactams 1/2 abx can have hypersensitivity reactions (rash, interstitial nephritis, anaphylaxis) adjust for renal function *seizures safe to give in pregnancy *decr contraception
Bactericidal Agents PCN, Cephalosporins, Carbapenems, Fluoroquinolones (Quinolones),Aminoglycosides*,Glycopeptides, Folate Antagonist, Nitroimidazoles
Natural Penicillin PCN G*does not survive in stomach (parental) PCN V (oral) *gram + use:syphilis, step pharynx, endocarditis
Anti-staphylococcal PCN nafcillin, oxacillin, dicloxacillin *gram + metabolized by the liver crosses blood-brain barrier AE: acute interstitial nephritis Use:MSSA (endocarditis, skin/soft tissue inf)
Aminopenicllins amoxicillin (oral), ampicillin (IV) *gram + good gram - cocci coverage use: URI (pharyngitis, otits media)
Beta-lactam/beta-lactamase inhibitor combinations amoxicillin/clavulante,ampicillin/sulbactam piperacillin/tazobactam,ticarcillin/clavulana *use:empiric tx for nosocomial inf, per appy, diabetic ulcers, aspir pna
Anti-pseudomonal PCN extended spectrum PCN piperacillin, ticarcillin *gram +/incr gram- use:infections caused by pseudomonas or GNR *often use with beta-lactamase inhibitor interacts with Warfarin
Cephalosporins grouped by generations cross allergenicity with pcn (mostly 1st gen) most excreted by kidneys in general are safe *phlebitis at IV site, false + glucose test
1st generation Cephalosporins cefazolin, cephalexin (Kelfex) less frequent dosing use: Skin/soft tissue (s.aurues, strep), surgical prophylaxis, MSSA endocarditis
2nd generation Cephalosporins cefotetan (po) cefuroxime (po,IV) cefoxitin cefprozil *gram - AE: inhibit Vit K production and prolong bleeding, disulfiram-like rx w/ etoh (cefotetan) use:URI & community acquired pna
3rd generation Cephalosporins ceftriaxone, cefotaxime, cefdinir, ceftazidime *Broad Spectrum Agents* AE:C-diff assoc, vit k inhibition, iron antacids, H2 blockers reduce absorption ceftriaxone-> calcium forming crystals *Avoid use in neonates with hyperbili use:lowerURI,pyelo,men
4th generation Cephalosporins cefipime (IV only) *Broadest Spectrum gram+ and - (pseudomonas) use:febrile neutropenia, nosocomial pna, UTI
5th generation Cephalosporins ceftaroline *newly approve, not for kids use: MRSA, community acquired pna
Carbapenems (IV or IM) imipenem/cilastatin, meropenem, ertapenem *Broadest spectrum agents gram+ and - use: MSSA, Pseudomonas, Superbugs(complicated peds UTIs) AE:sz, avoid in meningitis and PCN allergy
Fluoroquinolones (Quinolones) ciprofloxacin, levofloxacin, moxfloxacin, gemifloxacin Broad spectrum AE: photosensitivity, nephritis, prolong QT Black box->worsening MG and Achilles tendon bioavil->decr w/Ca, Fe, antacids, milk, mvit use:pna, sinusitis, gonorrhea, pseudo(cipro)
(Quinolones) increase levels of theophylline, phenytoin, warfarin concurrent use of Nsaids incr risk of sz
Aminoglycosides gentamycin, tobramycin, amikacin gram- bacilli AE:ototoxicity, nephrotoxicity, renal failure avoid in preg(8th cranial nerve fetal toxic) narrow TI *dose based on ideal body wt use:febrile neutropenia, sepsis, VApna endocarditis, osteomyelitis
Macrolides clarithromycin, azithromycin *not used for serious infections AE:sign GI, prolong QT interval, extensive drug interaction (CYP450)*azithro use:travelers diarrhea(azithro)h.pylori(clar)
Glycopeptides vancomycin *broad gram + AE:red man syn,ototoxicity, nephrotoxicity use:drug of choice MRSA, po tx for Cdiff *troughs are important->gives an idea if drug is being excreted properly. incr torugh=incr nephrotoxicity
Tetracyclines doxycycline,tigecycline (most used) minocycline, tetracycline, gram - bacilli AE: discoloration of teeth child<8yo, affect bone deve in fetus use:URI, CAP, malaria prophylaxis, complicated skin/soft tissue inf
Folate Antagonist trimethoprim/sulfamethoxazole (TMP/SMX) *dose based on TMP* (ex)broad spectrum *bacterial resistance common AE: photosensitivity, multi drug interactions (warfarin, phenytoin)*avoid w/ sulfa allergy *avoid in term infants/pregn (neonatal kernicterus)
Lincosamides clindamycin *gram + AE: high risk Cdiff use:skin/soft tissue (oral cavity)
Nitroimidazoles metronidazole *gram+and-(wipes out anaerobes) AE: metallic taste, reversible peripheral neuropathy, disufiram-like rx use:vaginal tric h.pylori gi ulcers, drug of cjoice for cdiff
Ciprofloxacin 3.3mg/g Staph, s.pneum, s.pyogens drops >1yr (1-2 Q2hx 2d, then Q4hx 5d) oint >2yr (1/2in TIDx2d, then BIDx 5d)
Polymyxin B-bacitracin 10000U:500U staph, strep, clostridia, gm- gonococci, meningococci, p.aeruginosa, H.influ all ages oint: 1/2in BID Q3hx7-10d
Polymyxin B-trimethoprim 10000U: 1mg/ml s.aureus, s. pneumon, s. pyogen, p. aerugin. H.influ drops >2mo-> 1 drop Q3h (max 6dr/day)x7-10d
Acute Otits Media middle ear infection ear pain, fever, otorrhea, bulging TM causes: gm+ strep, gm- h.influ & m.cata 1st line tx: high dose amox 80-90mg/kg 5-7d if>6yo,intact TM, no AOM w/i 1mo 10d if<6yo,severe ds, recent AOM pcn allergic:azithro 10/kg, 5mg/kg 2-5d
Otitis media with Effusion (OME) presence o fluid in middle ear w/o ss in infec tx: observation for 3mo w/observation chronic OME ->persisent for >3mo cause:s.pneum, h.influ,m.catarr 1st line treatment tympanostomy tubes
Chronic Suppurative Otitis Media (CSOM) Purulent otorrhea associated w/ chronic TM perforation >6mo causes: p. aeroginosa, CA-MRSA, s aureus tx: topical fluroquinolones w/ or w/o steriod ciprofloxacin drops BIDx7d or Ofloxacin
Pharyngitis viral:sugessted by rhinorrhea, pink eye, cough bacterial:GAS, if untx causes rheumatic fever endocarditis or poststrep glomer 1st line:amox 50-75mg/kg, pcn 50-75, azith 12mg/kg 2nd line: Augmentin or clinda
Acute Bacterial Sinusitis paranasal sinuses lasting<30d symp:nasal/postnasal discharge, cough, fevers tx:high dose amox for 14d or until symp free
Conjunctivitis "pink eye" infectious often bilateral common in winter rx:polmyxin Bsulfate and trimethoprin sulfate (Polytrim) or ciproflozacin if no improvement in48-72hrs, send cx pink eye & OM-> Augmentin x10days
Chronic conjunctivitis R/O tear duct obstruction (dacryocystitis) -no abx needed, only if infected Treatment should be based in cx -Gent drops (staph, pseudo) -erythro oint 0.5% (staph, strep) if no improvement in 3 days, refer to ophal
Common causes of ophthalmia neonatorum (neonatal conjunctivitis) any infant<1mo *send cx to r/o gonococcal, chlamydial or hsv gonococcal prophylaxis->erthro oint w/i 1hr
Blepharitis acute/chronhic inflam of eyelash follicules cause:s.aureus,poor hygiene,eczema,lice,makeu cleanse w/no tear shampoo, erythro oint BID tx for extra week after symptoms resolve
Hordeolum (stye) infection of the sebaceous gland of eyelash/lid not usu tx w/ abx if needed eryth oint
Periorbital cellulitis infection/inflammation of tissue surrounding eye-> orbit not involved acute onset, pain, swelling/redness, fever kids<2 unilateral infection cases:bacteremia,sinusitis,trauma,insect bite makeup-> adolescent females Ceftriaxone50-75mg/kg(IV) Augmentin
What is significant about Placental Anatomy Uteroplacental circulation is established in the 2nd week after fertilization, but not well established until 4th week ->fetus is somewhat protected for a short time
What is the function of the placenta delivers o2, water & electrolytes also filters waste
When is fetus most at risk Fetus is at risk early on during pregnancy
How does GI and Cardio changes in pregnancy effect drug delivery to the fetus Gi-> gastric emptying time is incr and intestinal motility is decr =incr extracelluar fluid/plasma vol= incr free drug Cardio->bd vol incre, CO incr 40-50%
What are the characteristics of Atopic Dermatitis (Eczema) chronic skin disorder, hypersensitivity rx(incr IgE) asso w/ asthma, allergies (triad) itchy,dry,raw red, inflam, oozing, crusted lichenification->thickening of skin
Tinea Vesicolor organism:pityrosporum orbiculare tx: selenium sulfaide or ketoconazole shampoo
Where is the major site of drug metabolism and why? small intestine, b/c it contains enterocytes in the bowel mucosa (CYP contining enzymes)
Large therapeutic window allows for? less frequent dosing
Narrow therapeutic window requires? more frequent dosing to avoid toxicity
Which Enantiomer is usu responsible for ADEs? the less active enantiomer is often responsible (eg. tachcardia with albuterol)
What is Passive Diffusion diffusion from low concentration->high concen vast majority of drugs use this process hydrophilic drugs->aqueous pores lipophylic->dissolve through lipid layer
What is Facilitated Diffusion low concentration->high concentration carrier proteins factiliate diffusion of drugs acros membrane
What is Active Transport Diffusion low concentration->high concentration carrier proteins actively carry drugs acros membrane
How are drugs affected by pH most drugs are weak acids or bases drugs pass through membranes more easily if UNIONIZED
Which drugs have a greater 1st pass effect Lidocain, Morphine, Nitroglycerine, Warfarin
What happens to a drug with a greater 1st pass effect? Drug concentration is decreased in the blood stream
What factors influence Bioavailability Enterohepatic recycling, drug solubility, and chemical insability
Why do hydrophilic drugs have higher Vd in newborns because the water content is higher than adults
Why do lipophilic drugs have reduced Vd in preterm newborns because pretern newborns have reduced percent of body fat
What happens during Biotransformation it is the process of chemically changing drugs mainly occurs in the liver
What is the result of biotransformation Increases water solubility, decreases lipid sol increase polarity resulting compounds readily excreted in urine can result in metabolites with potent toxicity (prodrugs)
Describe Phase I of biotransformation Most common drugs are oxidized and reduced to a more polar form Most frequently catalyzed by CYP450
What is the mechanism of CYP inducers Increases rate of CYP enzyme synthesis Decreases rates of enzyme degradation Increases drug meatbolism
What is the consequence of CYP inducers Decreases plasma concent, drug activity, and Thera effect Increases prodrug activity
What is the mechanism of CYP inhibitors decreases drug metabolism increases plasma concent, and thera effect decreases prodrug effect increases toxic effects
What happens in Phase II Biotransformation Conjugation or linking drugs with a polar chemical Increase water solubility and renal excretion by further increasing polarity
What is Acetylation Detoxification pathway in the liver
Why does acetyl radical congugation to a drug do? increases excretion
What happens with slow acetylators risk of toxiciity more drug in the plasma
What happens with fast acetylators Decreased therapeutic effect too little drug in plasma
Name types of clearance First order Zero Order
What is First Order flow limited clearance amt eliminated (per time)portional to amy in body t1/2 constant, not dependent on concentraton
What is Zero Order capacity limited clearance amt eliminated (per time)is constant t1/2 increases as concentration increases
What is EC50 concentration of drug producing more potent drug
What does a low EC50 indicate it diciates a more potent drug, where less of the drug is needed to produce the same effect
Name the antibacterial drug classes Beta lactams, Fluoroquinolones, Aminoglycosides, Macrolides, Tetracyclines, Gycopeptides, Nitroimidazoles, Folate antagonists, Lincosamides
Created by: barber5481