Comprehensive Guide to Upper Respiratory Treatments for Rhinitis

School

CUNY Lehman College**We aren't endorsed by this school

Course

NUR 726

Subject

Nursing

Date

Dec 12, 2024

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Uploaded by MajorCrownReindeer41

MODULE 5: Lecture 1: Upper Respiratory DX & TX for Rhinitis, Cough, Cold (9Questions)Allergic Rhinitis •Overview of Pharmacotherapy Options•Glucocorticoids ~ nasal budesonide, prednisone•PX inflammatory response •ALL s/s, DOC (Drug Of Choice), best used prophylactically (before the ONSET of S/S)•Adverse Effects: Nasal irritation, effect on ped growth•Antihistamines ~ PO/nasal/ophthalmic•Blocks H-1 – Histamine Type 1•Best used PX- sneezing, itching, rhinorrhea (limited), conjunctivitis (ophthalmic form)•Adverse Effects: Sedation & anticholinergic effects, FG > SG•Main difference between first generation are highly sedative and second generation are considered to benon-drowsyIntranasal GlucocorticoidsHINT: Steroids end in -ide or -one•RX•Beclomethasone, flunisolide, Ciclesonide, Fluticasone furoate•MOA•Target MULTIPLE inflammatory mediators in addition to histamine(Others are leukotrienes, cytokienes, etc) - THAT IS WHY IT IS THE DOC•All of equal efficacy •Relieves all s/s •Use•DOC for TX & PX of both seasonal & perennial allergic rhinitis•Initial response may take about a few hours•Maximal benefits may be delayed ~7d seasonal ~2-3w perennial•Administration•QD > PRN•Prime device if not used >7d•Clear nasal passages prior to administration•Intranasal (aka topical) decongestant prior•Clean nasal sprayer q7d•ADE•⍉steroid abuse potential •Common•drying, irritation, burning & itching•Less common•sore throat, epistaxis, HA, GI upset•Systemic ADE possible, but rare •Least likely w/ ciclesonide, fluticasone, mometasone

•Still potential but usually occurs with PO steroids•Adrenal suppression •REMEMBER: adrenal medulla produces steroids (ie glucocorticoids) naturally on its own and that helps us survive periods of physiological stress•If patient is using steroids for a long time, it can suppress the body’s ability to produce its own•Slowing of linear pediatric growth•OsteoporosisHistamine•Physiological effects•H-1 activation – Concerns with respiratory•When H-1 is activated by histamine, it causes Vasodilation, ↑ capillary permeability leads to edema•Bronchoconstriction **limited role in asthma •Sensory nerves itching, pain, mucusAntihistamines•Terminology •Antagonists of H1 vs H2•MOA•⍉Blockade of release – They do NOT block the release; they simply sit on top of the receptor and prevent it from being activated•Selective H1 blockade•Peripheral•↓ flushing, edema, itching, pain •CNS•Drowsiness, 1st Gen > 2nd Gen (More common with 1stgeneration)•Paradox effect & OD ~ stimulation •For example, the young children or older population, will end up having energy and anxiety instead•Muscarinic blockade (minimal)•Slight anticholinergic benefits •Only has very minimal to modest benefits for Rhinorrhea•Use•Mild allergy•Seasonal rhinitis•Acute urticaria•Mild transfusion reactions•QD > PRN – Best taking daily prophylactically FG Antihistamines•All available PO

•OTC•Brompheniramine, chlorpheniramine,•Diphenhydramine, dimenhydrinate •RX•Diphenhydramine IV, IM *acute urticaria (- presentation of hives)•Promethazine IM, IV, SUPP•Hydroxyzine•Cyproheptadine•Cross BBB (Blood Brain Barrier) they will block the H1 receptor in CNS•It leads to Sedation, avoid •Diphenhydramine & promethazine >>>•Least w/ brompheniramine, chlorpheniramine•Anticholinergic effects•The most with Diphenhydramine & promethazine >>>SG agents•Largely devoid of sedation & anticholinergic effects•↓ synergy w/ EtOH, still avoid •If taken with alcohol, it can cause sedation•OTC•All PO•Loratadine, cetirizine, levocetirizine fexofenadine•ADE•Sedation•FG > SG•⍉concurrent CNS depressants, EtOH•Tolerance•If used as a sleep aid, something like Benadryl will not be helpful if used long term•Consider QHS OR SG (moving dose to bedtime or to a second generation)•Dizziness, incoordination, confusion•Geriatrics ~ reduced dosing, SG > FG (second generation is more preferred than first)•Paradox effects – CNS excitation or stimulation•GI upset, food permissible•Anticholinergic•FG > SG•Anti-SLUD (Dry mouth, dry eyes, urinary retention, constipation), ↑ BP & HR•Hydration •Caution w/ asthma, geriatrics, BPH, glaucoma & HTN•Intranasal forms•Epistaxis, HA, somnolence, unpleasant taste •Promethazine concerns•Severe local tissue injury

•IM>IV, SQ is CI•Subcutaneous routes are contraindicated – it can leak out to surrounding tissues (also known as EXTRAVASATION) and that can cause necrosis leadingto amputation•BBW: Severe respiratory depressionAntihistamine, NON-respiratory Applications•Motion sickness•Promethazine, dimenhydrinate•Insomnia•FG OTC sleep aids•Denoted w/ “PM”•Usually contain Diphenhydramine, doxylamine•Not always effective•Paradox effect Intranasal Cromolyn •MOA•Mast cell stabilizer•PX release of mediators•USE•QD PX > PRN, delayed response ~ 1-2w for medication to work•Administration•≥ 2yo: 1 spray EN TID-QID (MDD 6x/day)•If (+) congestion intranasal (topical) decongestantSympathomimetics•AKA decongestants•Available OTC •PO: PSE, phenylephrine•Intranasal: tetrahydrozoline, phenylephrine, oxymetazoline •Local ADE•Intranasal > PO•Nasal dryness, nasal irritation, sneezing•Rebound upon d/c •Limit use 3-5 days (Usually w/ nasal spray decongestant) ~avoid in chronic rhinitis •Topical > PO•Minimizing upon d/c•One nostril at a time•Intranasal GC 7d prior 2-6w•Systemic ADE•PO > intranasal •CNS stimulation•Restlessness, irritability, anxiety, insomnia•CV (cardiovascular conditions)•Vasoconstriction•Caution in CVD. HTN, CAD, arrhythmias

Intranasal Ipratropium (Atrovent)It is an internasal anticholinergic•MOA•Cholinergic blockade ↓ nasal secretions •Use•Rhinorrhea ≥ 12yo•⍉sneezing, nasal congestion, postnasal drip, ocular s/s•Available as inhaler for asthma & COPD Montelukast•MOA•LT receptor antagonist•These drugs block the binding of the receptor•NORMALLY: LT XX bind on receptor XX to promote vasodilation & ↑ capillary permeability•Use•Nasal congestion, rhinorrhea, ocular s/s•Limitations•Mono-TX < intranasal GC•Mild efficacy ~ sneezing, itching•Reserve•CI•TX failure w/ intranasal GC, antihistamines•ADE:•HA, dizziness, dyspepsia•Neuropsychiatric, rare•Agitation, aggression, hallucinations, depression, insomnia,restlessness, suicidal ideations•IMPORTANT: Caregiver education Cough•Agents used in cough•Antitussives (Cough suppressants)•Suppressants, CNS & peripheral actions•Opioid VS non-opioid•Expectorants•Mucolytics Opioid Antitussives•MOA•Act upon CNS, ↑ cough thresholdThins Mucus – drink fluids Guaifenesin – Guzzle Fluids IN (2L/day)•Formulations•Often in combo•Codeine CV (single entity CII)•Promethazine/codeine•Guaifenesin/codeine•Hydrocodone CII

•Hydrocodone/chlorpheniramine•Hydrocodone/homatropine•ADE•Abuse & dependence because they do derive from opioids•Hydrocodone > codeine •Respiratory depression ~ ⍉peds1. SLOW – can have orthostatic hypertension Slow position changesNOT for COPD Constipation •Interactions•CNS depressants•AVOID Use of AlcoholNon-opioid Antitussives•Dextromethorphan (Ie. Robitussin)•Opioid derivative, but NO potential for: •Dependence, analgesia•Risks•Abuse potential @HD•PCP-like euphoria, dissociation•Respiratory depression•Benzonatate•RX only•MOA•Structural analog of tetracaine & procaine ~ local anesthetics•↓ sensitivity of respiratory tract stretch receptors•ADE•⍉chew, sucking ~ laryngospasm, bronchospasm, circulatory collapse – circulatory collapse so must be swallowed whole b/w it is an anesthetic•Administration: as capsules•>10yo only•Swallow wholeExpectorants•MOA•Stimulate flow of respiratory tract secretions•↑ productive cough •Guaifenesin (Expectorant)•Available OTC (ie. Mucinex)•Efficacy requires high dosing ~ Mucinex •Combination w/ DXM Mucolytics•MOA•React directly with mucus•↑ productive cough•Agents

•Hypertonic Saline•Acetylcysteine•Administration via nebulizer•ADE•Smell ~ high sulfur content in acetylcysteine•Acetylcysteine formulations•Neb ~ Mucomist ~ mucolytic •Acetylcysteine – Serious Mucus – Cystic Fibrosis•IV ~ Acetadote, APAP OD (Antidote for Tylenol overdose) •IV ~ Acetadote, APAP OD (Antidote for Tylenol overdose) •Acetylcysteine - ACEtominophenCold•Clinical presentation •Rhinorrhea, nasal congestion, cough, sneezing, sore throat, hoarseness, HA, malaise, myalgia•Lack of evidence for PX supplements•Vitamin C•Zinc •Combo products•Reserved for multiple s/s•Agents contained target specific s/s at hand•Single symptom single-drug formulations•Disadvantageous dosing •Fixed dosing ~ subtherapeutic/excessive•Sometimes the medication will be too Low to treat infection or too high than it is needed•Unnecessary agents OTC Cold Remedies in Children•Minimizing risk•Avoid OTC products if <4-6y•Products labeled for pediatric use•Consult HCP prior & read all safety info to use•Use measuring device provided ~ NOT household •If s/s worsen d/c & contact HCP•Avoid antihistamine-containing products to sedateMODULE 5 LECTURE 2: Lower Respiratory DX & TX for Asthma/COPD– 13 QuestionsAsthma: Patho•Chronic immune mediated inflammation•Not cured, ability to control•Most live w/o limitations if using TX•Allergen IgE on mast cells inflammatory mediators (Which are theones responsible for the representation involved in asthma)•Bronchoconstriction•Histamine, LTs, ILs, PGs•Infiltration & activation of the immune system

•Eosinophils, leukocytes, macrophages•Airway inflammation•Edema, mucus production, smooth muscle hypertrophy•Bronchial hyperactivity•Mild triggers ~ cold air, exercise, tobacco smoke•Other contributing factors•Medications & drug ALL•Non-selective beta blockers•B1 receptors = heart (HAVE 1 HEART), B2 receptors = lungs (HAVE 2 LUNGS)•Patients who are placed on beta blockers need to know if it is selective. If the beta blocker, blocks B2 itcan lead to bronchoconstriction•ASA, NSAIDsTypes of Asthma•Extrinsic•Food, pollen, dust, meds •Intrinsic•URIs, air pollution, emotions, smoke, exercise, cold exposure•Onset >35yo•Nocturnal•Circadian rhythms•↓ cortisol & EPI, ↑ histamine•Epi is known to open airways and since it is decreasing levels it causes airways to close•Exercise-induced EIB (Exercise Induced Bronchospasms)•Loss of H2O & heat ~ compensatory mechanism •Refractory (symptom-free) period 30-90min BUT ANOTHER ATTACK CAN HAPPEN AFTER THAT SO THEY SHOULD GET MEDICAL ATTANTION ASAP•PX w/ SABA (Short Acting Beta Agonist) > or cromolyn prior to exercising•Drug induced•ASA & NSAIDs, non-selective BBlockers•Delayed onset ~ 12h•↓ PG ~ ↑ LT•Reduce the production of prostaglandins but at the same time increase the production of LT•Status asthmaticus•Life-threatening, prolonged attack•TX non-respondent•Airway maintenance, intubation, ventilation support •↑ CO2 expiration ~ respiratory alkalosis Diagnosis•DX pulmonary DX•FEV1

•Forced expiratory volume in 1 second •<75% of predicted normal value if patients have pulmonary disease•↓ 10% post exercise•Forced vital capacity FVC•Total volume exhaled after full inhalation•FEV1/FVC ratio•% of vital capacity exhaled during the 1st second of forced expiration•Normal ranges from 70% -85% •Peak flow meters•Variable ~ height, age gender•Home monitoring•Personal best, QAM•Before bronchodilators •Record highest number (not avg) •3 close readings•Peak expiratory flow PEF•<80% = more frequent monitoring •Stepwise approach•Initiation ~ asthma severity classification•Stepping-up/down ~ control•Sustained control attempt step-downHighlights of GINA Recommendations for ≥ 12yo •SABA PRN for all steps, max q20min x 3Pharmacotherapy via Inhalation•Formulations for inhalation products•Metered-dose inhalers MDIs•Dry-powder inhalers DPIs•NebulizedMetered-Dosed Inhalers MDIs•Proper administration•Requirement: patients must have good Hand-breath coordination•Priming prior to using inhaler•>1 inhalation, separate by at least 1 minute•Inhale before activating device (press button) inhale SLOWLY •Devices used to increase drug delivery •Chamber & spacers•MasksDry-Powder Inhalers DPIs•Breath activated•No coordination needed•↑ lung delivery 20% DPI > 10% MDI•Limitations•Irritation •Deep/fast inhalations peds & elderly 

•⍉use w/ spacersNebulizers•Small machines that convert drug solution into mist•Benefits•Finer droplets > inhalers•Option for non-responsive patients•No coordination ~ mask/mouthpiece•Delivery of large doses•Disadvantage•Time•Size•CostPharmacotherapy Overview•2 main MOA: agents will target inflammation and bronchodilation•Anti-inflammatory agents•1stline: ICS•LTM, cromolyn, omalizumab •Bronchodilators•1stline: Beta-2 agonists B2A ~ SABA, LABA•Methylxanthines •Anticholinergic agents, as adjunct•Mainly for COPD•Combo products•ICS+ LABA•Anticholinergic + B2A (COPD only)•Foundation TX •B2A “terol” albuterol •PRN, acute attack ~ SABA albuterol QD, long-term maintenance therapy ~ LABA ~ Formoterol, SalmeterolAIM for Acute Asthma Attack-sequence is KEYALBUTEROL-1stfor BRUTAL ASTHMAIprotropirum – 2ndMethypredinosolone – STEROID (used last because steroids work SLOW)Anti-inflammatory Agents – SLAM – ANTIINFLAMMATORY AGENTS THAT SOOTHE THE INFLAMMATIONoSteroids – BACLOMETHASONE – “-SONE”oLeukotriene Inhibitor – MONTELUKAST oM – Mast Cell Stabilizers - CROMOLYNGlucocorticoids - -“one”, “-ide” KEY POINTS:oSwelling and Inflammation

oSlow Onset oSugar IncreaseoSores on the mouth•Inhalers•Beclomethasone, ciclesonide, flunisolide, fluticasone, mometasone•Nebulizer•Budesonide ~ persistent asthma 1-8yo•PO•Methylprednisolone, prednisone, prednisolone•Standard dosing same, regardless of agent•MOA•Suppress inflammation ↓ bronchial hyperactivity & mucus•↓ inflammatory mediators ~ LT, PGs, histamine•↓ infiltration ~ eosinophils, leukocytes•↓ permeability •Beclomethasone – decreases Bronchi•Inhalation•1stline long-term control, SABA prior •Chronic asthma•PX as QD, ⍉PRN•⍉ongoing attack, natural course •Slow Onset•Systemic PO•Acute exacerbations•Moderate to severe persistent asthma•↑ ADEs > inhalation•Since it has more adverse effects, we try to use the lowest dose for the shortest period of time •Short-term use >>•Long-term use•QOD (every other day) •Taper once controlled x3m (At least 3 months) •Because of adrenal suppression – it will inhibit the body from creating its own glucocorticoids which is adrenal suppresion•↑ doses w/ physiological stressGCs &Adrenal Insufficiency •Adrenal cortex endogenous GCs (naturally) PX vs physiological stress•Adrenal suppression occurs with Long term use of GCs ~ More so PO than inhaled•Supplement w/ physiological stress•SX (surgery) , trauma, infection

•Minimize with QOD dosing•Switching from PO inhaled•D/C via gradual slow taper•Medical alert bracelet ADEs of Inhaled forms•Candidiasis & dysphonia•Avoid by Gargling after use of each steroid & spacers – Don’t SWALLOW water•WASH DAILY – STEROIDS GO IN SINK•AF upon DX ~ NystatinADEs of PO forms•Long-term use•Adrenal suppression•Osteoporosis•Growth suppression in peds•Hyperglycemia – Normal – No need to notify HCP•Hypokalemia •PUD (Peptic Ulcer Dx)•Minimize w/ acute use <10d QODLeukotriene LT Modifiers LTM “- LUKAST”3 LsoLuke Likes to SING (Airway opens) oLong term management – combo with albuterol and steroidsoLong Onseta: (1-2 weeks to reach therapeutic range)GIVEN FOR PREVENTION NOT A RESCUE DRUG•LTMs•Zileuton, zarfirlukast, montelukast •LTs ~ potent inflammatory mediators•When they bind to receptor, SM constriction, ↑ permeability, inflammatory recruitment•MOA•Zarfirlukast & montelukast•LT receptor antagonist LTRA•They bind to the LT so that LT cannot bind to its receptor•↓ bronchoconstriction•↓ inflammatory response ~ ↓ edema, mucus•Neuropsychiatric effects (predominant in peds and adolescents)•Depression, suicidal ideations behavior △, insomnia, abnormal dreams, anxiety, hallucinations•Caregiver education•D/C consider alternativeCromolyn

•MOA•Mast cell stabilizer•PX (prevents) mediator release•Prevents activity induced asthma – 10 -15 minutes before physical activity •Inhibits inflammatory cells•Eosinophils, macrophages•↓ bronchial inflammation•⍉bronchodilation Bronchodilator AgentsBronchodilators: BAM - DILATE BRONCHI IN LUNGSoBeta 2 Agonist – ALBUTEROLoAnticholinergics – IPRATROPIUM oMethylxanthines - THEOPHYLLINEBeta-2 Adrenergic Agonists B2A– “-BUTEROL” Used for BRUTAL asthma attacks and fastest acting dilator RESCUE INHALER – BEFORE STEROID INHALER•MOA•Sympathomimetics•Activate beta-2 in lungs Dilate the bronchiopen up the airways•Limited role ~ histamine release•Use•1stline symptomatic relief ~ SABA•Mono-TX for mild & infrequent attacks•Classification •Inhaled SABA•Albuterol, levalbuterol•1st line•Ongoing attack•PX EIB (Prevent exercise induced bronchospasms) if used immediately prior•Dosing: 1-2 puffs TID-QID PRN•Limit use to BIW (two times a week), notify if s/s worsen •Inhaled LABA•Salmeterol, formoterol •S in Salmeterol means SLOWER ACTING-not a rescue inhaler•Long term control•Dosing: fixed QD•Combine w/ GC , BBW for increased mortality If used on their own•PO LABA

•Albuterol•Last line ~ long term control•⍉ongoing attack – DOES NOT ABORT AN ONGOING ATTACK LIKE THE INHALE FORMEDBeta-receptor selectivity•B2 selectivity not absolute•Drugs have potential to activate B1 in the heart•Report tachycardia, angina, tremor, dysrhythmia•ALBUTEROL AMMMps up the body•EXPECTED SE: AlbuTerol •T – Tachycardia •T – Tremor •T – Toss and Turning at Night “insomnia”do not taje at night•CI for PO & IV•Digoxin-induced tachdysthymia & tachycardia•Caution•DM, hyperthyroidism, HTN, angina•Avoid Beta Blockers (Atenolol), NSAIDS (naproxen)•BBW for all inhaled LABA•⍉monotherapy •Combo w/ ICS TheophyllineMETHYLXANTHINES•Metabolism & interactions•Substrate of CYP-1A2, 2E1, 3A4•As a consequence, it can lead to many drug interactions•Inhibitors•FQs ABX – Floxacin (Question order for antibiotic if they arecontaining theophylline) – INCREASE TOXICITY RISK•Cimetidine (H2 Blocker )- INCREASES RISK OF TOXICITY•Take in AM and avoid Caffeine•Caffeine & beverages containing can augment effects of theophylline•Monitoring•Periodic blood testing•Narrow TI•Traditional: 10-20mcg/mL•5-15mcg/mL for most•- Phylline -has youfeeling caffeinated and toxic•3 Ts: •TOXIC: OVER 20 – FREQUENT BLOOD DRAWS•Tonic Clonic Seizures – sever toxicity – 1st Priority•Tachycardia and Dysrhytthmias •Toxicity s/s D/C•Antidote: Activated charcoal which accelerates excretion of theophylline cathartic

•Lidocaine – anti-arrhythmic•IV BDZ – helps with restlessnessAnticholinergic Agents•MOA•Muscarinic antagonists -> they sit on top of muscarinic receptor and block that receptor from becoming activated and in doing so prevent bronchoconstriction•↓ bronchoconstriction •Ipratropium, tiotropium •COPD approval•ADE•Systemic effects, minimal•↑ IOP (IntraOcular pressure), caution glaucoma•CVE rare•Constipation, blurred vision, urinary retention, dry mouth•CANT PEE with them without your “–pium”•Cant SEE, PEE, SPIT or SHIT•Common•dry mouth, pharyngitis -•use gum and candy •drink fluidsAnticholinergic Agents (for COPD ONLY)•Tiotropium•Longer DOA (Duration of Action) ~ QD•Plateau effect ~ 8thdose •⍉rapid relief •Transient xerostomia (dry mouth)•Handihaler VS respimat•Handihaler approved, 1 puff QD•Respimat for asthma, 2 puff QD•NEVER SWALLOW PILL, PUT PILL INSIDE DEVICECombination ProductsA.Combos Products: GC/LABA •BBW as per LABAManagement of Acute Severe Asthma Exacerbation•Ellicit SABA use prior – how much of SABA did you use? •Initial TX•Systemic GC ~ prednisone •Nebulized high-dose SABA ~ albuterol•Nebulized ipratropium•Upon D/C•Start PO GC x 5-10d•Inhaled medium-dose GCChronic Obstructive Pulmonary Disease COPDPatho:

•Chronic, irreversible tissue damage & airway obstruction•Irritants inflammatory response •Frequent, recurrent irritation & pathologic changes•Bronchial edema, mucus secretion ~ bronchitis •Inhibition of protease inhibitors (anti-proteases)•Elastin breakdown•Destruction of alveolar walls, ↓ in elastic recoil ~ Emphysema•Causes•Cigarette smoking *most•Genetics ~ alpha-1 antitrypsin deficiency•Pollution, chemicals •Chronic bronchitis•Inflammation of the bronchi•Hypertrophy of mucus-secreting glands •Chronic cough, excessive sputum production•Different from acute form (due to infection)•Emphysema•Airway wall deterioration air space in bronchioles & alveoli•Permanently inflated alveoli•Remodeling of lung tissue ~ enzyme deficiency •Elastic fibers & surfactant destroyed•Narrow terminal bronchioles, inspiration not affected•Limits O2 entering bloodstreamDX based on Lung Function•Measuring lung function•FEV1/FVC < 0.70•Post-bronchodilator resultsModule 6: Lecture 1: Muscle Spasms & Muscle Relaxers– 4 questionsMuscle Spasticity •Group of movement disorders of CNS origin•Heightened muscle tone•Loss of dexterity•Common causes•Multiple sclerosis•Cerebral palsy•Traumatic spinal cord lesions•Stroke•Physical therapy•Drug TX •Centrally acting •Baclofen, diazepam, tizanidine•Direct actions on skeletal muscle•DantroleneMuscle Spasm

•Involuntary contraction of a muscle or muscle group•Drug TX•Analgesics•APAP (Tylenol), NSAIDs•Centrally acting•Cyclobenzaprine•Carisoprodol•Chlorzoxazone•Cyclobenzaprine•Diazepam•Metaxalone•Methocarbamol PO Hormonal TX•COCs•Spironolactone••OrphenadrineNotable Points for PharmacotherapyMuscle Relaxers cause dizziness and drowsiness it is expected DO NOT ABRUPTLY STOP – REBOUND EFFECT•Dantrolene•Only agent acting directly on skeletal muscle •Calcium COtracts the muscle•Liver Toxicity•Centrally acting agents•CNS depression•Potential dependence•⍉abrupt d/c ~ abstinence syndrome therefore they should be taper slowly •⍉concurrent EtOH, opioids, antihistamines•Baclofen•DOES NOT REDUCE MUSCLE STRENGTH•Abrupt d/c of PO•Visual hallucinations, paranoid ideation, and seizures•Avoid abrupt d/c of intrathecal form•Rhabdomyolysis, multiple organ system failure, death•Metaxalone•Baseline LFTs•Avoid in active or PMH liver DX•Caution w/ metaxalone & SSRIs ~ serotonin syndrome•Tizanidine•Baseline LFTs•Avoid in active or PMH liver DX•More sedation > other agents.•Chlorzoxazone•PO

•Paradoxical CNS stimulation•Diazepam•Benzodiazepine ~ CIV (NYS CII - NARCOTIC) – anxiolytic but also FDA approved to be used for muscle spasm•PO & IM•Cyclobenzaprine•PO +/- food•Anticholinergic ADEs ~ ↑ fiber & fluid due to side effect of constipation•CI w/ MAO-Is•Caution w/ SSRIs ~ serotonin syndrome•Methocarbamol•PO & IM•Harmless urine discoloration ~ green/brown black •Less sedation < other agents]Module 6 - Lecture 2: Rheumatoid Arthritis & Antirheumatics– 4 QuestionsPatho•Autoimmune condition•Systemic, multiple joints involved•Remissions & exacerbations•Potential effects on other organs•Heart, skin, eyes•Initial acute episode recovery•Acute episode begins with the inflammation of synovial membrane Synovitis•Cumulative effect of recurrence •Synovium thickening•Bone & cartilage destruction•Weakening & stretching of muscles, tendons, ligaments •Risk factors•FH•Advancing age•Juvenile form exists tooClinical Manifestations•Morning subsiding throughout the day but worse in the morningRA vs OA – KNOW THE DIFFERENCEPharmacotherapy: NSAIDs •Use•Initial management•Rapid relief of pain & inflammation•⍉slow disease progression•Safer than other agents•Role of cyclooxygenase•COX-1

•GI mucosal integrity•Platelet homeostasis•Renal function•COX-2•Inflammation, fever, and pain•Effects on blood flow, mucus & bicarbonate, gastric acid secretion•COX-1 vs COX-2 •BBW•Thrombotic events•GI ulceration, bleeding•FG – non-selective•Salicylates - irreversible•ASA•Non-salicylates- reversible•Diclofenac, etodolac, ibuprofen, indomethacin, ketoprofen, meloxicam, nabumetone, naproxen, piroxicam, sulindac•SG- selective to COX2•Celecoxib •↓ risk for GI ADEs•↑ risk for thrombotic eventsPharmacotherapy: GCs (Glucocorticoids)•Agents•Prednisone•Prednisolone •Actions•Rapid relief of pain & inflammation•UNLIKE NSAIDS, Slow disease progression•Risks w/ prolonged use •Osteoporosis, gastric ulceration, adrenal suppression •Short-term only•Long-term only if ALT options failedPharmacotherapy: NON-biologic DMARDs•Methotrexate•Major toxicities, many BBW•Hepatic fibrosis•Bone marrow suppression•GI ulceration•Pneumonitis•Fetal death and congenital abnormalities ~ CI in pregnancy•Malignancy ~ melanoma, lung cancer, non-Hodgkin's lymphoma•Monitoring•LFTs; jaundice, dark, colored urine•Kidney function; creatinine

•CBC: fever•Platelet counts: thrombocytopenia•Concurrent folic acid•5mg/week•Folic acid helps ↓ GI & hepatic toxicityModule 6: Lecture 3: Gout & Anti-Gout Agents= 4 questionsPatho•Normal A&P•Purines•Endogenous •Dietary Intake: Organ meats, shellfish, anchovies, herring, asparagus, mushrooms•Purines UA dissolution in blood renal elimination•Inflammatory DX•Deposits of UA crystals•Tissues, joints, fluids •Overproduction of uric acid•Hyperuricemia ⍯gout for all•Underexcretion, most common•More common in males & African Americans•Causes•Primary inborn error in metabolism•Secondary contributing factors•Obesity•HTN•DM•Renal DX•Sickle cell anemia•EtOH ~ beer & spirits > wine•Meds: diuretics•Diet ~ rich in meat & seafood•4 phases•Initially asymptomatic, despite ↑ UA•Crystal accumulation & tissue damage•Typically affecting lower extremities•Acute inflammation•Leukocyte infiltration •Phagocytize UA crystals •Release of destructive lysosomal enzymes•Flares/attacks ~ days to weeks•Varying pain, burning, redness, swelling•Warmth @ affected joint ~ metatarsophalangeal of big toe•Inter-critical periods•Clinically inactivesubsequent recurring flares

•Periods become shorter w/ DX progression•Can Lead to Chronic arthritis•Soreness & aching of joints•Development of tophi•Large, hard nodules of UA crystals in soft tissue•Cooler areas of the body ~ toes, elbows, ears, finger •Renal calculi & damageClinical Manifestations•Vary depending on phase•Manifestations of acute attacks•Intense pain @ affected joint•Big toe•Occurring @ night•Joint warmth, redness, swelling•Tenderness (even to light touch)•Fever•Proceeding 1stattack•⍉symptoms•Varying length of time ~ months-years•Some have no further attacks•Chronic gout•Arthritis, joint deformities•Limited mobility•S/S present most of the time•Tophi local inflammatory responseManagement Overview•Diagnostics•PMH•PE•Serum UA, hyperuricemia•M: > 7 mg/dL •F: > 6 mg/dL •Urine UA ~ low if due to underexcretion•Synovial fluid analysis•Joint X-rays•Treatment strategies ~ aim at lowering ↓ UA•△diet ~ ⍉high protein & purines, EtOH•Avoid triggers, stress•Medications•TX for acute gout attacks•NSAIDs: indomethacin, naproxen, diclofenac•First-line•Control inflammation & pain•Higher doses to stop acute attacks•Corticosteroids: prednisone, triamcinolone

•ALT to NSAIDs•Relieve inflammation & pain•Anti-gout anti-inflammatory: colchicine•Reserve if unresponsive•Add-on TX for frequent attacks•≥ 3 episodes/year ~ ADD urate lowering drugs•⍉anti-inflammatory actions•⍉analgesic actions•⍉efficacy in active acute attack•They are an add on treatment to prevent an attack in the future•XO inhibitors: allopurinol, febuxostat•Block UA production•Uricosuric drugs: probenecid •↑ renal excretion of UA•Urate-oxidase enzyme: pegloticase•UA allantoin (more readily excreted)Pharmacotherapy for Acute Attacks•NSAIDs•Indomethacin, naproxen, diclofenac •GI precautions•Bleeding, ulceration, and perforation•Administer w/ food ~ ↓ GI upset•CV precautions•MI, stroke, thromboembolic events•GC (Glucorticoids)•Hyperglycemia ~ avoid in DM•ColchicineColchicine – aCute gout attacks•Second line•Metabolism via CYP3A4 & PGP•⍉PGP inhibitors: cyclosporine, ranolazine•⍉3A4 inhibitors: ketoconazole, clarithromycin, nelfinavir, ritonavir•⍉GFJ•CI in hepatic/renal impairment•Severe GI ADE ~ n/v/d, abdominal pain•D/C regardless of pain•Rhabdomyolysis•↑ risk w/ hepatic/renal impairment•Caution w/ concurrent statinsUrate-lowering Pharmacotherapy: AllopurinolAlloPurinol – Prevents gout•Use•1stline DOC for chronic gout•Renal elimination

•↓ dose for impairment •Paradox acute attack w/ initiation•PX, concurrent NSAID/colchicine first before starting therapy•Interactions•Warfarin, ↓ dose warranted•Probenecid•MOA ~ uricosuric agent•Inhibition of UA tubular reabsorption•Paradox exacerbation of gout•⍉Never used during attack•Hold until controlledModule 6: Lecture 4: Osteoporosis & Agents for TreatmentNormal A&P•Bone Mass △across life span•Continuous remodeling ~ marrow•Osteoclasts•Bone resorption (breakdown)•Osteoblasts•Bone deposition•Osteoid deposits ~ matrix of collagen & proteins calcificationNormal A&P: Calcium•Majority stored in bone ~ 98%•Calcium absorption•Small intestines ~ 1/3 of ingested calcium •Increased by PTH (ParaThyroid Hormone) & vitamin DCalcium excretion•Primarily through kidney•Loss determined by GFR & tubular reabsorption•Reduced by PTH & vitamin D•Factors affecting regulation•PTH•Vitamin D•Calcitonin•↓ serum Ca•Ca moved towards blood •PTH secretion, promotes•Resorption in bone•Tubular reabsorption•Activation of vitamin D•Vitamin D, promotes •Same effects on resorption & tubular reabsorption•Intestinal absorption of calcium•↑ serum Ca•Ca leaves blood

•Suppression of PTH release•⍉vitamin D activation •Calcitonin, released by thyroid•Works in opposition to PTH & vitamin D•Inhibits calcium resorption in bone•↑ renal excretionVitamin D•Forms•Ergocalciferol (D2)•Physiologic actions•Regulates Ca•↑ intestinal absorption •↑ resorption in bone •↓ renal excretionPatho of Osteoporosis•Pathogenetic mechanisms•↓ osteoblast activity•↑ osteoclast activityFracture riskPrimary Prevention of Osteoporosis•Calcium •Older adults ~ 1200mg/d – Can only absorb max of 600 mgat a time•Vitamin D•Ensures Ca absorption•Lifestyle•Regular weight-bearing exerciseAgents for Primary Prevention•Calcium salts•Carbonate requires acidic pH•Use citrate for geriatrics•PPI/H2RA use; if patient is on PPI, then you want them to beon citrate > carbonate•Max 600mg per dose, limited absorptionVitamin D supplementation•Adults 19yo+ : 10,000 IU/dPharmacotherapy for OsteoporosisMale osteoporosis•5 agents approved **•Testosterone replacement if secondary•CI: testicular cancerAgents most likely to reduce fracturesoZoledronateoDenosumaboTeriparatide

oBisphosphonatesAlendronate, risedronate, zoledronate **oMonoclonal antibody: Denosumab **Agents that promote bone formationoPTH analogue: Teriparatide **Bisphosphonates – “-dronate”Administration•Typically QWK (some given 1x/month **)•QAM (every morning) , empty stomach•⍉food ≥ 30min•Full glass of water•Upright position ≥ 30min to prevent esophagitis•ADEs•Esophagitis, report dysphagia – SIT UP 30 MINUTES•Oseteonecrosis of the jaw ONJ, rare (mostly w/ IV forms)•Interactions•Ca products, mineral supplements, antacids•Separate ≥ 60minSERM: Raloxifene•MOA•Selective estrogen receptor modulator•Binds to estrogen receptor•Agonist•Estrogenic effects in bone•PX postmenopausal osteoporosis•Antagonist•Antiestrogenic effects in breast•PX breast cancer•Use•PX & TX of postmenopausal osteoporosis•Only reduces risks of spinal fractures, no other sites•ADEs•Thromboembolic DX (DVT, PE)•Listed as BBW•D/C 74h before planned immobilization or surgery•Teratogenic Risk > BenefitModule 7 – Lecture 1: Ophthalmic Conditions & Agents. 3 questionsGlaucoma: Patho•Normal conditions•Aqueous humor ~ role in maintaining IOP•Normal IOP < 20mmHg•Produced by ciliary body posterior chamber of eye•Circulates around iris anterior chamber exits•Common forms•Primary open-angle POAG, more common

•Acute angle-closure (narrow-angle)•Impeded outflow from anterior chamber ~ ↑ IOP•POAG ~ clogged•Acute-angle ~ displaced iris, blockedClinical Manifestations & DX•POAG•Progressive & insidious onset•Bilateral vision impairment•Acute-angle•Rapid onset•Painful•Typically unilateralPharmacotherapy•Beta-adrenergic blocking agents, end in “-lol_•Agents•NON-selective: timolol, carteolol (block B1 and B2) ~ avoid in asthma and COPD•Selective: betaxolol (preferred for pt w/ asthma, COPD•MOA•↓ aqueous humor production•Prostaglandin analogs, end in “-prost”•Agents•Latanoprost, travoprost, bimatoprost•MOA•↑ aqueous humor outflow•Harmless brown pigmentation of iris: light colored eyes will turn to brownManagement of POAG•Goal: ↓ IOP•⍉cure, chronic use req.•Drug actions•Facilitate aqueous humor outflow•↓ aqueous humor production•Treatment model•Ophthalmic route preferred•Systemic ADEs uncommon •Different MOAs•Combo TX may be more effective > mono-TX•PO meds•⍉effective as mono-TX ~ add on to ophthalmic drug•Carbonic anhydrase inhibitors•1stline agents ~ opthalmic•Beta-adrenergic blocking agents•Alpha2-adrenergic agonists•Prostaglandin analogs

•2ndline options ~ PO•Carbonic anhydrase inhibitors•Procedures last line•Laser SX•Filtering SX •Drainage implantsManagement of Acute-Angle Glaucoma•Drug therapy•Control acute attack•Cholinergics ~ muscarinic agonists•Carbonic anhydrase inhibitors ~ PO•Beta-adrenergic blockers ~ opthalmic•Emergency managementConjunctivitis Patho•Infection or inflammation of conjunctiva•Types•Infectious•Highly contagious via direct contact•Viral, most common•Bacterial ~ Staphylococcus, Chlamydia, gonorrheaAllergic ~ IgE-mediatedConjunctivitis Clinical Manifestations•General•Blurry vision or photophobia•Viral•Watery or mucus-like exudate from the eye•Bacterial•Yellow-green exudate•Allergic•Redness, itching•Excessive tearingPharmacotherapy for Conjunctivitis •Ophthalmic ABX•For bacterial only, ⍉viral•Fluroquinolones•Ciprofloxacin, levofloxacin , moxifloxacin, gatifloxacin, Ofloxacin•Polymixin B + TMP•Sulfacetamide•Aminoglycosides, reserved for severe cases•Gentamicin, Tobramycin•Ophthalmic mast-cell stabilizers•Ophthalmic antihistamines•H1-receptor antagonists•Immediate symptomatic relief•Agents ~ azelastine, olopatadine

•Additional actions, stabilize mast cells•Ophthalmic NSAIDs•Ketorolac•Inhibits COX to prevent formation PGs•Ophthalmic GCs•Loteprednol•Inhibit production of PGs, LTs, thromboxane•2ndline•⍉prolonged use ~ ADEs•Cataracts•Eye infection•↑ IOP ** caution if glaucoma* •Ophthalmic decongestants •Alpha-1 activation•Vasoconstriction•↓ erythema & edema •Naphazoline, phenylephrine•Symptomatic benefits only•⍉interrupt immune response•Regular use ~ rebound upon d/c•Max 2 weeksModule 7: Lecture 2: Otic Conditions & AgentsAOM (Acute Otitis Media) Patho•Infection, inflammation,&fluid in middle ear•Bacterial vs Viral•More common Children•AOM (Acute Otitis Media) •Criteria•Acute onset s/s•Middle-ear effusion MEE•More common > AOM•Upper respiratory tract infections•May precede OR proceed AOM•Criteria•(+) middle-ear fluid AOM DX & ManagementAOM non-drug measures•Tympanostomy tubes ~ replacement if recurrent AOM•Adenoidectomy•AOM drug TX•ABX PO & gtts**•Analgesics PO & gtts**•Benefits of using Otic formulations** over PO•↓ ADE (local) •↓ resistance (Local vs systemic)

Pharmacotherapy for AOM•Analgesics for all•⍉ASA (aspirin) in peds – Reyes Syndrome•Mild-mod: APAP, ibuprofen•Initial PO ABX, only for some•<6m•Yes always, even if uncertain•6m-2yo•Yes, if certain about dx•Yes, if uncertain & severe s/s like fever, very painful, sleep disturbed•≥ 2yo•Only if certain, but only severe cases•Agents•Non-severe: amoxicillin BID•Severe: amoxicillin + CVA (Augmentin) BIDIf observation ~ 48-72h•TX-failure, 48-72h post initiation•Non-severe•Amoxicillin + CVA (Augmentin) BID PORecurrent AOM (Acute Otitis Media) & Management•Recurrent AOM •≥ 3x/6m or ≥ 4x/12m•Short-Term ABX PO•High-dosed amoxicillin•Amoxicillin + CVA (Augmentin)PX treatment•⍉recommended Influenza vaccine•PX during flu season onlyTympanostomy Tubes•Placed into incision in TM•Allows drainage of middle ear•Many otic agents contraindicated if ear tubes are placedOtitis Externa OE Patho•AKA “swimmer's ear”•Infection of EAC•3-10d course•Common pathogens, bacterial•P. aeruginosa•S. aureus•Less common•Bacterial ~ S. epidermidis, M. otitidis•FungalOE Clinical Presentation & Management•Rapid-onset ear pain associated w/

•Pruritus ~ fungal•Sensation of ear fullness•Tenderness on manipulation•Edema/erythema of EAC•Impaired hearing•Purulent discharge ~ fungalPharmacotherapy for OE•Otic ABX > PO (Ear is better than PO) •First line•Acetic acid 2% (otic gtts) +/- EtOHModule 7: Lecture 3: Dermatological Conditions & Agents.= 4 questions Skin A&P RecapTopical Formulations•Ointments•Thick, greasy •Use•Dry skin conditions •⍉weeping or oozing skin•⍉areas prone to heavy perspiration•⍉oily skin•Creams•Oil & H2O emulsion•Inflamed skin & dry sensitive skin •Use•Inflamed skin & dry sensitive skin •⍉oily skin•⍉oozing lesions•Lotions•H2O based (little, if any, oil)•Intertriginous areas - skin flaps•Oily skin •May contain EtOH or acids ~ burning•Non-greasy ~ patient satisfaction•Easily spread ~ large or hairy areas•Gels•Transparent preparations•Non-greasy, drying ~ oily skin •Easily spread ~ large or hairy areas •Dry as clear & invisible ~ facial regions •Burning typically due to inactive ingredients•Foams•Aerated solutions•Easily spread ~ large or hairy areas •Little residue ~ oily skin Powders

•Talc or cornstarch base•↓ friction b/w surfaces ~ skin folds•Useful for regions that tend to perspire ~ feet or axillae•Pastes•Mixtures of ointment & powder•↑ adherence to the skin•Can be used safely in areas that are occluded ~ diaper rash ~ can cover the areaAcne: Patho•Onset @ puberty•Can occur @ any age•Male > Female•↑ androgen production•↑ sebum production•↑ follicular epithelial cell turnover•Clogging•Clogged pores •Oil, debris, bacteria•Sebum + keratin comedone (surface)•Rupture•Spread to surrounding area Presentation & DX•Whitehead•Open comedones•More common•Blackhead•Closed comedones•Oxidation of sebum @ surfaceNon-Drug Management: Acne•Cleansing•Mild, nondrying soap•QD-BID•Post exercising•⍉excessive washing•Dietary △⍯beneficial Pharmacotherapy•Topical ABX•Benzoyl peroxide BP•Clindamycin•Erythromycin•BP + Clindamycin (Benzaclin)•BP + Erythromycin (Benzamycin)•Dapsone•Topical retinoids – vit A derivatives (Produces new skin) •Tretinoin

•Adapalene•Tazoretene•Keratolytics•Azelaic acid•Salicylic AcidPO ABX•Doxycycline•Minocycline•Tetracycline•Erythromycin•PO Hormonal TX•COCs - oral BC•Spironolactone – aldosterone antagonist•PO retinoids•Isotretinoin – last line option for severe cystic acne. Brand name = “acutane’Topical ABX•Dapsone•Reserved for intolerance•MOA not established•5% gel•⍉combo w/ BP – SHOULD NOT BE COMBINED WITH BENZOYL PEROXIDE•yellow/orange skin discolorationTopical Retinoids•Vitamin A derivatives •Normalize hyperproliferation of epithelial cells•Unplug existing comedones•PX (Prevent) new formation•↓ inflammation•Photosensitivity ~ QHS•Tazarotene•Gel & cream•See psoriasis agentsAdapalene•OTC gel•8-12w for full benefit•Exacerbation of acne in early TX•ADEs•Early localized reactions, subside•Photosensitivity ~ QHS (apply at bedtime)•Also available w/ BP•Tretinoin•Gel & cream•Mild to moderate acne•Also approved for fine wrinkles

•ADEs•Localized reactions•⍉systemic toxicity Oral ABX•Use•For moderate-severe acne•May be combined w/ topical retinoid•MOA•Suppresses P. acne growth•Directly suppresses inflammation•Tetracyclines (avoid w/ pregnancy and lactation b/c of teeth deformities)•Doxycycline•Minocycline•TetracyclineOral Retinoids: Isotretinoin•Use•Severe nodulocystic acne•Last-line•Common ADEs•Nosebleeds•Inflammation of lips & eyes•Dryness or itching of the skin, nose, mouth •Pain, tenderness, stiffness in muscles, bones, joints•Back pain ~ peds•Photosensitivity •Less common ADEs•Rash, HA, hair loss (less common but expected) •Peeling from palms & soles•↓ night vision, onset may be sudden – important to report•Rare ~ cataracts, optic neuritis, papilledema •Pseudotumor cerebri (benign ↑ ICP)•ED (erectile dysfunction_•Metabolic effects•↑ TG (tryglycerides)•Baseline & periodic monitoring•⍉EtOH (b/c it will further dry skin & elevated TGD) •Reversible upon d/c•Depression & suicidal ideations•Report•CI for pregnancy•iPledge ~ REMs•Patients, HCPs, Pharmacy•30-day supply max•R/O pregnancy prior & upon refill

•2 methods of contraception•30d prior to initiation 30d post d/c•Even if tubal ligation or vasectomy•7-day window to pick up drug or else they will have to do pregnancy test againOral Hormonal TX•For acne in younger females•MOA•↓ androgens•↓ sebum production•COC•Effects•↓ ovarian androgen production•↑ production ofsex hormone–binding globulin (renders androgens inactive)•Approved in ≥ 15y•Must have reached menarche•Spironolactone•Effects•Blockade of aldosterone & sex hormone receptors•Used if COC failed•Teratogenic•Contraception required•ADEs•Menstrual irregularities•Breast tenderness•HyperkalemiaContact Dermatitis: Patho•Acute inflammatory reaction •⍉contagious•⍉life threatening•Triggered by direct exposure •Irritant•Allergen-producing substance Types•Irritant contact dermatitis•Causes•Chemicals, acids, soaps•Allergic contact dermatitis •Causes•Metals, chemicals, cosmetics, plants•Sensitization on 1stexposure•Subsequent exposure•Type IV cell-mediated hypersensitivity•Manifestations

•24-48h post-exposure.Both forms typically Resolution in 2-4 weeksTopical GCs: Know some drugs are more potent than others•Higher absorption•Axilla, face, eyelids, neck, perineum, genitalia•Inflamed skin•Application of occlusive dressings ⍉- covering wll increase absorption so it will yield more ADE•Lower absorption•Palms, soles•Intact skin•Application•Thin film•Gentle rubbing•⍉occlusive dressings, unless directed •Local Reactions•Long-term use•Skin atrophy •Striae ~ stretch marks•Purpura•Local hemorrhage red spots•Telangiectasis•Capillary dilation red, wart-like lesions, •Acne•Hypertrichosis (excessive hair growth) ~ face•Systemic absorption possible•Children ~ delayed growth•Adrenal suppression•↑ risk w/ occlusive dressingsPsoriasis : Patho•Common chronic inflammatory DX•Affects skin cell life cycle•↑↑ cellular proliferation•Rapid cell build up on skin’s surface•Buildup thickening of dermis & epidermis•Dead cells cannot shed fast enough•Onset•Sudden or gradual•@ 15-35yo•Remissions & exacerbations•Familial tendency•Triggers •Meds•Antimalarials (hydroxychloroquine), •Beta-blockers

•LithiumClinical Manifestations•Plaque lesions•Red patched covered w/ silvery scales•Most common typeDX And Management: •⍉cure •Multipronged approach•Stress management•Trigger avoidancePharmacotherapy•Topical TX•GCs•See contact dermatitis Systemic TX•Methotrexate•Immunosuppressant•Reserved for severe TX-resistant•PO, IM, IV, SQ•Risk of toxicity & death•ADEs•GI•Bone marrow suppression•Liver DX ~ monitor LFTs•CI in pregnancyImpetigo•Superficial infection•Staphylococcus aureus•Toxins attack collagen & spread•Most common & highly contagious•Peds 2-5yo•Bullous form•S. aureus•Nonbullous•Most forms•AKA crusted impetigo•S. aureusand/orStreptococcus pyogenes.•TX for mild-moderate ~ topical•Mupirocin•Ointment or cream•TID x 3-5d•Retapamulin •Ointment•BID x 5d•TX for severe ~ PO

•Cephalexin•Dicloxacillin•ClindamycinTopical Sulfonamides •Suppress bacterial colonization in 2nd& 3rddegree•Proper Application: thin layer AAA QD-BID•Silver Sulfadiazine aka SSD •MOA: release of free silver•ADE: skin discoloration ~ ⍉face•Mafenide •MOA: sulfonamide•Keep•If dressings used, only thin non-occlusive•ADE: stinging, potential acidosisSeborrheic Dermatitis & Dandruff•Chronic, relapsing condition •Inflammatory reaction to infection w/ Malassezia (yeast)•Inflammation & scaling of scalp & face•Underarms, chest, anogenital region may also be affected•Topical ketoconazole•Cream, shampoo, gel•Concurrent GC ↑ response•Maintain remission w/ periodic useIssues w/ Hair Growth•Hair loss•Topical minoxidil•5% males only, 2% for females•Applied to scalp BID•Delayed benefits ~ months•Hair loss @ 3-4m post d/c•Few local reactions•Systemic ADEs rare•Finasteride PO•1mg vs 5mg for BPH•For androgenic alopecia•Male-pattern baldness