PHARM GUIDE LAST QUIZ

***NSAID 2 Lecture***
**Rivaroxaban = PO
-MOA = factor 10a inhibitor
-indications = in place of warfarin or LMWH to prev venous thrombosis after hip or knee replacement
surgery
-ADR = bleeding
-no coagulation monitoring req, fast onset of action
-Drug interactions = CYP3A4 substrate
-Misc = avoid in impaired renal function
**Apixaban = out in 2012, factor 10a inhibitor too. More effective and less bleeding than warfarin?!
**Heparin = heterogenous mixture of mucopolysaccharides, very very huge
-traditional heparin therapy = UFH (beef and pork sources)
-drug but also a category; subcategory = LWMH
-prego cat C
-MOA = inhibits thrombin and 10a
-Dosing/PK = SC and IV (loading dose)
-heparin is parenteral only. Warfarin is PO
-t = 1-5 hrs (quick so overshooting not a big deal), aPTT monitoring (unfrac only)
-non-linear PK (little change is big difference in blood level)
-ADR = bleeding, allergic rxns, alopecia, osteoporosis w/ long-term therapy
-HIT = platelets not low but sticking together so N/A, hypercoagulable state in 1-4%, happens bc animal
origin
-rapid and consistent drop in pt is a red flag for HIT
-monitoring = platelets and aPTT
-info baseline, note specific and easy to follow protocols available
**LMWH = enoxaparin/Lovenox (1st out, most common, can get generically now), dalteparin, ardeparin,
tinzaparin
-can substitute for UFH, biggest issue is cost, dont haveta use aPTT
-MOA = inhibit 10a, insufficient length to inhibit thrombin
-Dosing/PK = SC only, daily (benefit)
-t 1/2 = longer than UFH
-predictable responses,
-ADR (sim UFH) = bleeding, thrombocytopenia (note not HIT not animal origin), hypersensitivity,
osteoporosis
**Misc Parenteral Anticoagulants = Fondaparinux
**Direct Thrombin Inhibitors = Desirudin, argatroban, bivalirudin, lepirudin
**Thrombolytic Agents = streptokinase, urokinase, anistreplase, tissue plasminogen activators,
reteplase, tenecteplase
-MOA = lyse clots, use in ischemic strokes

-Dosing/PK = time sensitive, > 3 hrs = contraindication

-Contraindications = worry pt will bleed out, specific protocols at all institutions
-only use thrombolytic in life/death
***URTI, LRTI Lecture***
**Therapeutic Mgmt mech = cough suppression is in part of brainstem that mediates cough reflex
1.) Codeine = opioid analgesic
-dose = prn
-schedule V (higher is less addictive)
-side fx = GI upset, CNS depression, drying fx on mucus
2.) Hydrocodone = opioid analgesic
-dose = prn
-schedule III
-side fx = CNS depression, GI upset (N/V, constipation). Stomach c/o most common, vomiting center
triggered. Pain meds shut down the gut.
-note side fx all different but not rly different
3.) dextromethorphan = d-isomer of opiod agonist levomethorphan, no pain control
-for sleep
-OTC, Rx
-robotripping abuse = 300-1800 mg lg dose, lasts 3-6 hrs, LSD-like fx
4.) Benzonatate
-work locally at lungs not centrally
-some ppl use this in pts allergic to opioids or abuse Hx
-take around the clock NOT prn
5.) local anesthetics = anesthetize stretch receptors in airways and pleura. Includes camphor and
menthol. Be careful in kids (def not in infants)
**Expectorants = red viscosity of tenacious secretions by inc res tract fluid (loosens/thins sputum and
bronchial secretions)
1.) guaifensin
-water is best
-many combo prods w/ cough suppressants, esp Robitussin counter intuitive
-immediate rel Robitussin, best are sustained release (only Mucinex imp in sinusitis, rest off market
now)
**Decongestants = sympathomimetics act on adrenergic receptors in the nasal mucosa, producing
vasoconstriction
A.) Topical (-zoline ending)
-intranasal = naphazoline, phenylephrine, oxymetazoline (Afrin - US most common), xylometazoline
-ophthalmic = naphazoline, oxymetazoline .. Same chemicals. <3 days. Overused > 3 days then rebound
congestion, can be worse off than started (rhinitis medicamentosa)
B.) Systemic
-phenylpropanolamine (PPA) and ephedrine off-market now
-pseudoephedrine (Sudafed) = OTC 30 mg, Rx 120 mg. Allegra D. BTC, more superior
-phenylephrine (Sudafed PE)
-Side FX::

Sympathetic
Topical = local irritation, prolonged vasoconstriction, rebound congestion
Systemic = CV (inc BP and HR, palpitations), CNS (nervousness, irritability, restlessness,
insomnia)
-2 yo cutoff
-co-morbid dis states contraindications: glaucoma (specific type), thyroid dis, cardiac dis (HTN
controlled HTN is ok tho, angina, post-MI)
C.) Analgesics/antipyretics = aspirin, acetaminophen, ibuprofen, naproxen
**URTI
A.) Pharyngitis
-Viral (lgst portion) 85% in kids, 90% adults. Bacteria (GABHS) 15% kids, 10% adults
-Clinical presentation::
fever, H/A, chills, sore throat, cough, PND = mult symptoms in multiple places and diverse so
usually means viral inf
fiery red mem, tonsillar exudate; edematous uvula, tender and enlgd l nodes; scarlitiniform rash
(sandpaper feeling) = usually means bac inf
-Treatment
lim ab for ppl likely w/ GABHS
clinically screen all adults for 4 criteria: Hx fever, tonsillar exudates, no cough, and tender
anterior cervical lymphadenopathy (lymphadenitis)
dont test and dont treat pts w/ none or bc GABHS is unlikely
RAT (rapid ag test) valuable, 95% accuracy
DOC = penicillin, amoxicillin (BID, traditional 30-40 mg/kg or high dose 80-90 mg/kg for decent
strep pneumo coverage). Dont use NVK bc QID is annoying and compliance issues
use macrolide if PCN allergy for 10 days to treat symptoms
B.) Sinusitis can be nebulous
-Haemophilus influenza, Streptococcus pneumonia
-Clinical presentation::
Rhinorrhea, persistent daytime cough > 10-14 days bacterial
Severe symptoms = fever > 39C/102.1F w/ purulent nasal discharge, facial pain or tenderness w/
periorbital swelling
-Treatment::
Acute bac rhinosinusitis resolves w/o ab treatment usually
Symptomatic treatment and reassurance is pref intial mgmt strategy for mild symptoms
Ab reserved for ppl with all 4 criteria
Use most narrow-spectrum agent for initial treatment
-DOC = high dose amoxicillin, amoxicillin/calvulanate (bad bc B-lactamase resistance)
-PCN allergic = use azithromycin (length of time downside), clarithromycin, FQ. See improvement in 2-3
days, cont treatment for 7 days after symptoms improve (us 10-14 days)
-Drug interactions:: ETOH/CNS depressants esp w/ 1st gen
**LRTI
A.) Acute Otitis Media (AOM)
-most common inf in kids for ab

-controversy: treat (US) or not (Euro)

Does the pt have effusion? Look for bulging and swollen eardrum
Signs or symptoms of AOM? Ear pain, fever, and bulging yellow or red TM
NO:: OME (otitis media w/ effusion) = effusion w/o signs/symptoms acute inf. Nonspecific signs
and symp (rhinitis, cough, diarrhea nonspecific so viral) us present.
YES:: AOM = Hx acute onset of signs and symptoms w/ middle ear effusion and signs/symp of
middle-ear inflame. Go to Tx table. <6 mos all get ab therapy; 6 mo 2 yrs (certain dx then ab tx,
if uncertain dx then ab if severe or observation 2- 3 days if nonsevere); >2 yo (certain dx then ab
if severe or observe in nonsevere, uncertain than observe)
mgt should include assessment of pain. If present, recommend ibuprofen or acetaminophen (< 6
mos use only this). Can give steroids and/or numbing eardrops ok but fewer is better so consider
-See drug chart in PPT slide
B.) CAP
-common inf dis, acquire thru inhalation or aspiration
-IDSA = inf dis society of america, give guidelines
-etiology (5) = strep pneumo, H flu; DIFF is location (not all ab can get in high enough conc in lungs).
Atypical mycoplasma* pneumoniae, chlamydophila pneumoniae. Also res viruses
-minor and major criteria, observe for a few days
-outpt tx = prev healthy and no use of antimicrobials within prev 3 mos beware of resistance. Macrolide
(azithro, clarithro), doxycycline (choose if smoker)
-usually from atypical orgs, strep pneumo us sicker
-otherwise, if presence of comorbidities like chronic heart, lung, liver, or renal dis, DM, alcoholism,
malignancies, asplenia, immunosuppresing cond/drugs, or use of antimicrobials last 3 mos = at risk for
drug-res strep pneumo (DRSP).
use respiratory FQ (moxiflox, gemi, levo)
b-lactam + macrolide (high dose amoxicillin; amox/clav preferred, alts ceftriaxone, fepodoxime,
cefuroxime)
-duration of therapy = tx min 5 days (from zpac), should be afebrile 2-3 days and no more than 1 CAPassoc sign of clinical instability before discont therapy, longer therapy if initial therapy unactive. 10 days
is typical duration (same w/ sinusitis and AOM)
C.) HAP aka Nosocomial = 48+ hrs after adm. (How to distinguish btwn CAP and HAP)
-early onset = w/in 4 days
-late onset = 5th day or after
-Etiologies: very broad g (-), g (+), atypical Pseudomonas aeruginosa, Klebsiells, E. coli, Acinetobacter,
MRSA, S. pneumo, H. flu
-Tx duration = 14 days
ALLERGIES LECTURE
**Antihistamines
-reacts w/ H1-3
-H1 receptors = inc bv dilation, contraction bronchi and intestines, inc itch and pain perception, dec
autonomic muscarinic and vestibular activity
-H2 receptors = inc secretion gastric HCl and pepsin

-H3 receptors = inhibit rel histamine

-excessive exposure to H1= Type 1 Hypersensitivity (Allergy)
triple histamine response = simultaneous redness (vessel dilation) + flare (vessel dilation due to
nerve stim) + wheal (inc vessel perm/edema)
drugs bind to H1 receptors in Type 1 Hypersensitivity
-pathogens have high affinity for IgE receptors
-drugs target H1-H3, IgE receptors, mast cells and basophils
-H1 receptor agonists = 1st gen penetrates CNS, 2nd does not
**1st gen:: (-amine, -zine)
-diphenhydramine (Benadryl), dimenhydramine (motion sickness too), brompheniramine,
chlorpheniramine, doxylamine, meclizine (#1 for motion sickness), cyclizine, promethazine, hydroxyzine
-drowsiness bc cross CNS why can treat anaphylactic rxns and has many ADRs
-inhibit histamine from binding in sm mus of sm veins, bronchi, and intestines
-Blocking at muscarinic/cholinergic/parasympathetic
-used in Type 1 hypersensitivity rxns (rhinitis, urticaria, conjunctivitis, and anaphylaxis), prophylaxis for
motion sickness and vestibular disease (Menieres Disease)
-Bromopheniramine and Chlorpheniramine = least sedating, Children 2-5 yrs (lowest age 2 bc higher
likelihood of morbidity and mortality)
-Clemastine mod sedation
-Diphenhydramine most sedating
**2nd Gen
-systemic:: cetririzine (Zyrtec) most sedating can penetrate CNS a lil and cause drowsiness and struc
related to Hydroxyzine, levocetirizine, desloratadine (Clarinex), Loratidine (Claritin), Fexofenadine
(allegra)
-Nasal Sprays:: Azelastine just as well as Zyrtec
-Opthalmic antihistamines:: Azelastine, emedastine. Most expensive in pharmacies
-Opthalmic Antihistamines/Decongestant combos:: Antazoline + Naphazoline, Pheniramine +
Naphazoline
-Prevent histamine from binding in smooth muscle of: small veins, bronchi, and intestines, Inhibit IgEinduced mediator release from mast cells and basophils
-Used in Type 1 hypersensitivity rxns (rhinitis, urticaria, conjunctivitis, NOT anaphylaxis)
-Side Fx: anticholinergic (1st gen only dry eyes/mouth/nose, blurred vision, urinary retention, mental
status change in older pts) and CNS (mostly 1st gen sedation, impaired motor/mental performance)
DERM LECTURE
-Consider::
Duration
freq (some topical agents use skin as reservoir, need only 1x/day despite short t1/2)
sparingly vs liberally sparingly most of the time. More is not better!
Absorption
o occlusive dressing not breathable/permeable, dangerous bc inc absorption by 5070
fold. can be put over a numbing cream. Ex: disposable diapers (diaper rash)
o Humidity higher then more absorbed
o Temperature higher then more absorbed

o Thickness of skin thicker then less. Ex: More easily at head than palms
-At a glance::
topical most freq prescribed
Effective to reduce inflam sx, doesnt address underlying cause of dis
Topical glucocortoid research aim to optimize potency while min side fx; class # differs (1 is
worst)
New molecules w/ higher anti-inflam, good compliance (1x/day ok), rare cross-sensitivity rxns,
less skin-atrophy (more w/ injected)
**Topical corticosteroids
-indications = Dermatitis, eczema, psoriasis, diaper rash, etc.
-MOA = Vasoconstriction and dec inflammation - local
-Guidelines:
Potency low-medium on thin skin vs med-high on thick skin
Vehicle lotions < cream < ointment < gels; Ex: B-methazone
-ADR = 3 mos high risk for ADRs.
Hypopigmentation bleached skin
Typically no real HPA-axis suppression - aka no real steroid crisis if used appropriately
High potency for prolonged time inc systemic ADRs esp in PEDs
Acne
Atrophy
Tachyphylaxis tolerance to vasoconstriction of topical steroids
Telangiectasia
Delayed wound healing used as immunosuppressants
**Classes::
1) Class 1 super potent
Strongest anti-inflam fx
Alternative to systemic steroids
For short duration and small surfaces
Avoid occlusive dressings
Uses thick chronic lesions
Optimized vehicle aka augmented inc solubility and absorption w/ fewer side fx. ONLY CLASS 1
Inc risk side fx skin atrophy
2) Class 2 potent
Strong
Intermediate duration, or longer periods w/ thickened skin sec to chronic cond
Ok on face and intertriginous areas for short duration
3) Classes 3 (potent, upper mid-strength), 4 (mid), 5 (lower-mid)
Moderate
Face and intertriginous for lim duration
Uses chronic eczematous dermatoses
4) Class 6 (mild) and 7 (least)
Lowest
Safest long term
Safe on face, intertiginous, w/ occlusion on infants and children

**Potency of Selected Topical Gluocorticoids

-1::
Betamethasone dipropionate cream and ointment (both diff, optimized vehicle for better
efficacy)
Clobetasol propionate cream and ointment (Class 1 only)
Diflorasone diacetate - Formulated slighly diff in diff classes
Halobetasol propionate
-2:: lost optimized vehicle
-3:: lost ointment and optimized vehicle
-5:: lotion
-7:: Hydrocortisone O.5 and 1% OTC, higher (2.5%) is prescription only
**Definitions
SSTI skin and soft tissue inf; inf inv any or all layers of skin, SC fat, fascia, and muscle
Cellulitis inflam skin and SC fat, acute
Diabetic foot ulcer open wound on foot of DM pt, may not necessarily be infectious
Osteomyelitis may result from SSTI, inflam of bone marrow and surr bone
Why tx? Bc if untreated septic arthritis, osteomyelitis, or bacteremia
**Most likely orgs:
1.) Non-DB = typically 1 organism
G (+) aerobes = S. Aureus resistant? (MSSA, MRSA, 90% of skin inf and 10-15% of these are
MRSA) and Strep pyogenes
G (-) aerobes = E. coli, Pseudomonas aeruginosa, Klebsiella pneumoniae;
-Most skin inf :: non-resistant g (+) organism
2.) DB = may be polymicrobial
G (+) aerobes = S. aureus (MSSA, MRSA), Strep pyogenes, S. epidermis, Enterococcus faecalis
G (-) aerobes = E. coli, Pseudomonas aeruginosa, Klebsiella pneumonia, Proteus spp
Anaerobes
-Best tx complicated cellulitis? Find something w/ g (+), g (-), and anaerobes
**Cellulitis - Correct tx can fix in 1 dose
lesions typ hot, painful, eythematous w/ poor margins, may or may not see entry pt
Us sec to trauma/lesion
Mild no evidence of systemic inf (no fever, no toxic) can respond to local tx (cleaning and
irrigation w/ soap and water)
**Tx:: Empiric therapy in healthy, non-DB pt is typically mono-microbial and strep before staph (unless
abscess or penetrating trauma MRSA worry)
10 days
Use anti staph PCN (PO dicloxacillin in mild ambulatory and IV nafcillin in mod-severe
hospitalized) in healthy pts
o good vs MSSA and strep, well tolerated
Cephalosporin (1st gen PO Cephalexin, IV Cephazolin)
o more broad than what you need
o Some give 1 parental dose of ceph (more $$) then switch to PO
Macrolides, Quinolones

PCN allergic:: use erythromycin and clindamycin (also good in CA-MRSA)

**Resistant Staph Infections

-CA-MRSA (10-15% endemic res), often causes SSTI (>90%) from close contact
-AB Tx?
Bactrim (TMP-SMX)
Doxycycline
Clindamycin (some abcess penetrating ability)
Rifampin NEVER by itself bc can develop resistance
-AB Tx in Serious CA-MRSA in Hospitalized AND Tx HA-MRSA except Clindamycin?
Vancomycin and telavancin
Linezolid
Daptomycin
clindamycin
-Definitive therapy in healthy, non-DB
Strep spp: switch to PCN VK or G
Staph spp: MSSA leave on diclox, MRSA swith to vanco or linezolid
-Empiric Therapy in DB
Typically polymicrobial: g (+), g (-), anaerobes. Tx for 3-4 days after ALL signs of inf are gone
Mild same as non-DB. If anaerobes add clindamycin or metronidazole
mod-severe expand ab coverage. also culture, drainage, and surgical debridement. Ex:
clindamycin IV (G+ and anaerobes) + ciprofloxacin IV (g- aerobes, some g- anaerobes, some g+
aerobes), clindamycin + 3rd gen Ceph (g+ and g-), Beta-lactam/Beta-lactamase inhibitor combo
(extend g+ and g- to include B-lactamase prod organisms), Carbapenem (very broad), Cefoxitin
(treats g+, g-, and anaerobes)
-Definitive therapy in Diabetics
Based on C & S results