OSCE prep

Anorexia Nervosa definition, highest what, clinical (general, 2 types, 3 signs/symp, 3 diagnostic criteria), diagnostics (2), tx (4)

General -failure to maintain normal body wt (15% below expected!) -highest mortality rate of all psychiatric conditions (due to arrhythmias) -Disturbance of body image and intense fear of becoming fat. -In females, absence of three consecutive menstrual cycles. Clinical -exhibits behaviors targeting at maintaining low wt, ego-syntonic (their behaviors are acceptable to them) -Types: 1) restrictive (strict reduced calorie), 2) binge eating/purging type (self-induced vomiting, diuretic, laxative, enema) -skin or hair changes (lanugo--fine/soft hair) -amenorrhea -BMI 17.5 kg/m^2 or less OR bodyweight <85% of ideal body wt -diagnostic criteria: 1) restriction of calorie intake --> signif low bw 2) intense morbid fear of fatness or gaining wt 3) distorted body image (self perception of being overwt when they're underwt) Diagnostics -hypokalemia -metabolic alkalosis Tx -medical stabilizations, nutritional rehabilitation, psychotherapy, pharmacotherapy if depressed (***SSRIs, which may also help with wt gain)

Epiglottitis

General: -***LIFE THREATENING EMERGENCY -Acute inflammation of supraglottic larynx, including the epiglottis -Can rapidly progress to airway obstruction -Children ages 2-7 (most common), can occur in adults -More common in those with DM -Symptoms can progress rapidly -Viral or bacterial -**H flu type B! is most common cause. Incidence is decreasing due to vaccinations Clinical: - Acute onset of high fever, sore throat, odynophagia - Irritability, hoarseness, restlessness - Rapid development - Symptom of odynophagia outweighs exam findings - Moderate-severe respiratory distress -***Drooling, inspiratory stridor -***Patient sitting forward, leaning with elbows on knees Diagnostics: -**Lateral Radiograph of the soft tissues of the neck - Epiglottis swelling "THUMB PRINT SIGN"! -Laryngoscopy Treatment: -Immediate ENT Consultation -Secure airway (often needs intubation, preferably nasotracheal intubation) -Hospitalization (ICU) -Oxygen -IV Antibiotics (Ceftizoxime, Cefuroxime) -IV Steroids (Dexamethasone) -All un-immunized contacts should be given prophylaxis with rifampin

Mononucleosis

General: -Epstein Barr Virus -Incubation period: 30-50 days -Transmitted via saliva Clinical: -Malaise, fatigue -Fever -Sore throat, +/- exudate -Palatal petechiae -Lymphadenopathy (posterior cervical chain) -Splenomegaly -Maculopapular rash (especially if PCN given) -Anorexia Diagnostics: -Monospot (Heterophile agglutination test) - may take 4 weeks to become positive -Lymphocytosis Treatment: -Symptomatic treatment -NSAIDS/APAP -Steroids (sometimes) -NO CONTACT SPORTS

Streptococcal Pharyngitis (bacterial pharyngitis/tonsillitis (streptococcal); "strep throat")

General: -Group A Beta-Hemolytic Streptoccous (GABHS) -Can lead to rheumatic fever and glomerulonephritis -***Bacterial pharyngitis can also be from diphtheria, mycoplasma, N gonorrhea, Chlamydia Clinical: -***CENTOR CRITERIA (4+ = treat, 3+ 2+ = test and treat if positive, 1+ = no treatment, no test) ●Fever > 38 C = 100.4 F ●Tender anterior cervical lymphadenopathy ●Absence of cough ●Tonsillar exudate -***Scarlatinaform rash - diffuse redness/papules, looks like a sunburn, feels like sandpaper -Look for trismus, look for voice changes -How does Strep Throat present in children? Abdominal pain? Abdominal pain! Diagnostics: -Rapid strep -Throat culture Treatment: - ***PO PCN VK = treatment of choice -Single IM Benzathine PCN 1.2 million units = treatment of choice of patients with poor compliance -PO Erythromycin = treatment of choice of PCN allergic patients

Rheumatic Fever what is it, age, pathophys, clinical, ***diagnosis, ***tx, complication

General -"Nonsuppurative" non-pus) consequence of infection with Group A ß-hemolytic Strep •****Strep throat!!! (first REQUIREMENT/criterion) •Scarlet fever -Occurs 2-3 weeks after acute pharyngitis -Can cause long-lasting effects in the skin, joints, heart, and brain Pathophys -Peak incidence ages 5-15 years -Group A strep antigens may resemble host tissues, so antibodies against Group A strep (GAS) may attack the host as well! Clinical -Fever, Arthralgias, Nausea/Vomiting, Stomach cramps -Arthritis, Carditis, Chorea, Subcutaneous nodules, Erythema marginatum Diagnosis -Jones criteria!***(other than strep throat which is requirement!!!! with history/centor criteria/strep test/culture): •2 major criteria or 1 major + 2 minor criteria PLUS •Evidence of GAS* infection Tx -***first-choice: penicillin! -Salicylates (symp relief; aspirin for adults only, not kids bc rye's syndrome) -corticosteroids: taper slowly -complication: •***mitral valve regurgitation in long-term!!** (MV>AV>TV>>PV)

Viral Conjunctivitis

General -***Adenovirus! -Can lead to keratoconjunctivitis (decreased vision, subepithelial infiltrates) -Enterovirus, Coxsackievirus -Can cause hemorrhagic conjunctivitis -Herpes virus -Unilateral, eyelid lesions too -Spreads easily -Usually lasts 10 days Clinical -Bilateral watery discharge -***Associated with pharyngitis, fever, malaise, pre-auricular lymphadenopathy! -Painless -1 eye involved initially, both eyes involved within a few days Diagnosis -Clinical Diagnosis Treatment -Symptomatic treatment with artificial tears, cool compresses -If HSV - topical antivirals -Wash hands, wash sheets/towels/pillows etc. Pt education -Do not wear contacts! wear your glasses -All contagious

Attention-deficit/hyperactivity disorder (ADD & ADHD) problems with what, usu comorbid with what, diagnostic criteria (3), tx (3, first line med tx)

General -***persistent patterns of inability to sustain attention, excessive motor activity/restlessness/impulsivity, or both -***symptoms interfere with daily functioning -***symptoms began prior to age 12 and in at least 2 settings (ie, schoolwork, home, with friends/family) -problems paying attention, impulsivity, & hyperactivity -67% comorbid with Conduct and Oppositional defiant disorders Clinical -diagnostic criteria: 1) symptom onset before 12 years of age and must be present for at least 6 mos 2) symptoms must occur in at least 2 settings 3) At least 6 inattentive symptoms (ex. distractions, hard to focus) AND/OR at least 6 hyperactivity/impulsivity symptoms (ex. fidgets and squirms in seat, impatient, blurts out inappropriate comments) Tx -multimodal approach: --stimulants = first-line med tx of choice (eg, Methylphenidate, Amphetamine/Dextroamphetamine) --nonstimulants = Atomoxetine --can add alpha agonists (eg, Guanfacine) -***CURRENT: stimulants such as Methylphenidate or Amphetamine + psychoeducation

Obsessive-compulsive disorders (OCD) what are obesessions and compulsions, pathophys, 4 clinical, first-line therapy (2)

General -***preoccupations or rituals (repetitive psychological triggered behaviors) that are distressing to the individual -***symptoms are excessive or persistent beyond potentially developmentally normal periods -obsessions: recurrent or persistent thoughts/images; usu ego-dystonic -compulsions: repetitive behaviors (rituals) the person feels driven to perform; can cause distress, impairment, or are time consuming Pathophys -theorized due to abnormal communication between the basal ganglia Clinical -4 major patterns: 1) Contamination (ex. cleaning/handwashing) 2) Pathologic doubt (ex. forgetting to unplug iron) 3) Symmetry/precision (ex. ordering or counting) 4) Intrusive obsessive thoughts (without compulsion) Tx -cognitive behavioral therapy = first-line therapy - exposure & response prevention -pharmacotherapy =SSRIs first line med therapy; tricyclic antidepressants (Clomipramine bc it is the most serotonin specific)

Schizophrenia disorders (schizophrenia spectrum disorders; mainly focused on schizophrenia here) what is it, better/worse prognosis, pathophys (risk factor and cause), dx criteria, dx (1 and its outcome, not part of criteria but sometimes on exam), first-line tx, other disorders on schizophrenia spectrum

General -***social withdrawal, usually slowly progressive, with decrease in emotional expression or motivation or both -***deterioration in personal care with disorganized behaviors or decreased reactivity to the environment or both -***disorganized thinking, often inferred from speech that switches topics oddly or is incoherent -***auditory hallucinations, often of a derogatory nature -***delusion, fixed false beliefs despite conflicting evidence, frequently of a persecutory nature - disorder of abnormal thinking, behavior, & emotion -better prognosis: later age at onset, acute onset, positive symptoms -worse prognosis: early age of onset, gradual onset, negative symptoms Pathophys -strong genetic predisposition -exact cause unknown but positive symptoms thought to be due to excess dopamine in the mesolimbic pathway Clinical -dx criteria: 1) 2 or more of the following symptoms - positive symptoms (eg, hallucination, delusion, disorganized speech), negative symptoms, grossly disorganized or catatonic behavior for at least 6 months 2) at least 1 must be hallucination, delusion, or disorganized speech & must manifest for a 1 month period 3) must impair function Diagnostics -Neuroimaging considered if first episode (ex. CT scan/MRI --> ventricular enlargement and decreased cortical volume) Tx -second-gen (atypical) antipsychotics first-line tx: ***Risperidone! (Clozapine is not used first-line but most effective med for tx-resistant psychosis) -first-gen (typical) antipsychotics: Haloperidol; increased risk of extrapyramidal symptoms, tardive dyskinesia, & neuroleptic malignant syndrome -hospitalize if behavior v disorganized, not needed as much if family/support sys -prevent harm to self/others! Other schizophrenia spectrum disorders: -delusion disorder: predominant symptom = persistent delusions with minimal impairment in daily functioning -schizoaffective: not fully fitting criteria of affective disorders (depress, mania, etc) or schizophrenia (psychotic symptoms); somewhere in between them -schizophreniform: similar to schizophrenia but symptom duration between 1-6 months -brief psychotic disorders: psychotic symptoms lasting less than 1 month, result of psychological stress, more acute onset Pt education -side effects of antipsychotics: --dry mouth --blurred vision --urinary retention --delayed gastric emptying --esophageal reflux --ileus --delirium --acute glaucoma --orthostatic hypotension --sexual dysfunction --ECG changes --diabetes --hyperlipidemia --weight gain --metabolic and endocrine effects --lactation and menstrual irregularities --inhibit sperm mobility --bone marrow depression --cholestatic jaundice --agranulocytosis --photosensitivity --retinopathy --hyperpigmentation --neuroleptic malignant syndrome --Akathisia MC EPS (inability to sit still, can cause pt to feel angry and suicidal) --Acute dystonias (spasms of head, neck, tongue; neck stuck in place) --Drug-induced parkinsonism (rigidity, loss of reflexes, pill-rolling) --tardive dyskinesia (abnormal involuntary movements of face, mouth, tongue, trunk, limbs after months of tx)

Tuberculosis origin/transmission, clinical (1), dx (3), Tx (KNOW 3 things!!!)

General -Airborne disease caused by Mycobacterium tuberculosis -Acid fast staining bacillus -if cant contain --> bacteria multiplies--> TB -Latent means doesn't spread, active is the one that spreads Clinical -***cough, night sweats, fever -fatigue, hemoptysis, chest pain, loss of appetite -majority is pulmonary, but can affect other systems (kidney, GI, GU, spine (back pain), meninges, larynx, lymph) Diagnosis -***PPD (skin test, aka TST) or IGRA (Interferon-gamma release assays; aka Quantiferon or T-spot) -CXR-abnormalities (usu in apical and posterior segment of the upper lobe or superior segments of the lower lobe ✦miliary TB (type that spreads throughout body) --> chest X ray shows tiny balls/dots that look like couscous/millet seeds -***AFB of sputum (stained in smear, will be red) -***Culture with drug sensitivities (gold standard) -Nucleic acid amplification (should be done on at least one sample) Tx -Tx if positive IGRA or PPD -***(KNOW!!!) Latent: Isonaizid/INH!!!! (duration varies from 6-9mos, just know it tends to be for long time) ✦missing doses is serious, if pt may be noncompliant can add RPT and shorter duration -(***KNOW!!!) Active TB: ✦First line: RIPE --> rifampin, Isonaizid, pyrazinamide, ethambutol; will be combo of RIPE drugs given;, 2 phases: initiation phase and continuation phase •(***KNOW!!!): combo (in both initiation and continuation phases) will always include Isonaizid/INH and rifampin/RIF!!! (KNOW!!!***) •(***KNOW!!!): Initiation phase its always 4 drugs; in continuation phase it's 2 drugs!!** ✦Second line: Fluoroquinolones, amikacin, kanamycin, capreomycin -follow-up: ✦during tx: every two weeks (depends on compliance, side effects of therapy) ✦After treatment: no need for follow-up if no problems ✦If resistant to INH/RIF, pts should be monitored for 2 yrs post-treatment

Measles aka, molecule, transmission, 1sign and triad KNOW!!, Dx (gold standard), tx (3)

General -Aka rubeola -RNA virus -2 dose school vax Pathophys -90% secondary infection rate! (wear all PPE!!!) -transmitted via respiratory droplets -vit A deficiency = risk factor (esp third world countries) Clinical -fever = first sign -Prodromal (intermed) phase: malaise, anorexia, and classic triad of conjunctivitis, cough, and coryza (3 Cs!!!*****KNOW 3 C's!!) -Koplik spots (white/blue dots on mucosa) -Complication: EENT keratitis Dx -***PCR is gold standard for all viral stuff!!! (Dipu said) -CBC: low neutrophil, high lymphocyte bc viral - IgG and IgM antibodies confirm Tx -Vaccinate! live virus (like Varicella); effective within 3 days of exposure -Human Ig sometimes given within 6 days -supportive: fever control, IV hydration, resp isolation)

Generalized anxiety disorder (GAD) general, clinical (7), DSM criteria (time, number of symptoms, nature of symptoms), tx (first-line, second-line, possible addition), pt ed (3)

General -Anxiety disorders are the most prevalent psychiatric disorders. Clinical -Apprehension, worry -Irritability, difficulty concentrating -Insomnia -Somatic complaints -Muscle tension -Tachycardia -Fatigue -***Symptoms present more days than not for at least 6 months -diagnosis criteria (DSM): 1) excessive anxiety or worry a majority of days for at least ***6 months! about ***various aspects! of life; the anxiety is usu out of proportion to event 2) at least 3 of these 6 symptoms: ***fatigue!, restlessness, difficulty concentrating, muscle tension, sleep disturbance, irritability, shakiness, & headaches Diagnosis -Rule out medical causes of symptoms (cardiac, neurological, endocrine, respiratory, substance abuse related) -Screening: GAD-7 Tx -First-Line: Anti-depressants (SSRI, SNRI) •SSRI: Escitalopram or Paroxetine (Selective serotonin reuptake inhibitors) •SNRI: Venlafaxine or Duloxetine (Serotonin and norepinephrine reuptake inhibitors) -2nd or 3rd Line: TCAs & MAOIs •Tricyclic antidepressants •Monoamine oxidase inhibitors •Why are these medications 2nd and 3rd line? bc can cause arrhythmias -Should we use benzodiazepines? Can use benzos short-term but pt can become dependent on them so tell them they can get addicted; also avoid in elderly population -Cognitive behavioral therapy -Note: Have to wean off meds, can't abruptly stop Pt education -first-line meds: •Takes 4-6 wks for SSRIs to work, so should tell them it won't work right away •Take every day whether feel good or not, and taking at same time each day -***Limit alcohol use! -Anxiety may worsen initially

Obesity definition/criteria, tx (2)

General -BMI 30 kg/m^2 or greater, or body wt 20% or greater over ideal wt Tx - anti-obesity meds: Orlistat, Lorcaserin

Erysipelas bacteria causing it/location, clinical (3), diagnosis, tx (initial tx and allergy)

General -Bacterial skin infection of the upper dermis which extends into the cutaneous lymphatics Pathophys (Etiology) -***on the face Grp A strep -***Lower extremity generally non-grp A strep Clinical ▪Erythematous; ***"fiery red and shiny"! ▪***Sharply raised demarcated border (which helps differentiate it from cellulitis) ▪***Burning sensation Diagnosis -just history and phys Tx -Rest and elevate -Cold compresses -Symptom relief of pain/fever -***first-line: Pen G IV or PenVK PO x 5 days; -***PCN allergic --> Erythromycin or Azithromycin

Bulimia Nervosa general def, unlike anorexia, MC in who, clinical (2), dx criteria (2, and types of second one), diagnostics (1), tx (2)

General -binge eating combined w compensatory behaviors -unlike anorexia, ***usu maintain normal wt (or may be overwt) and compensatory behaviors are ego-dystonic (troublesome to pt, they don't like it) -MC in females 10:1 Clinical -teeth pitting or enamel erosion (from vomiting) -Russell's sign: calluses on dorsum of hand from self-induced vomiting -Dx criteria: 1) recurrent episodes of binge eating occur at least weekly for 3 mos 2) compensatory behaviors --purging type: self-induced vomit, diuretic, laxative, enema abuse --non-purging: reduced calorie intake, dieting, fasting, excessive exercise, & diet pills Diagnostics -increased amylase Tx -psychotherapy -pharmacotherapy: Fluoxetine = only FDA approved med for it

DKA (Diabetic Ketoacidosis) what is it, MC where, causes (MC), clinical (3), diagnosis (2), Tx (acronym, tx goals, severe cases)

General -consequence of insulin deficiency & counterregulatory hormone excess -most common in TYPE 1 DM (insulin deficiency) -etiologies -- stressful triggers: ▪infection = MC cause! Clinical -abdominal pain -fruity (acetone) breath -Kussmaul respirations (deep, continuous respirations) Diagnosis -plasma glucose >250 -positive ketones in urine Tx -SIPS - Saline, Insulin (regular), Potassium repletion, Search for underlying cause ▪IV fluids: critical initial step! isotonic 0.9% (normal saline)! ▪potassium repletion: correction of DKA will invariably cause hypokalemia (recommended unless K+>5.3mEq/L) -Tx goals: closing anion gap; bicarbonate levels more import than glucose levels in determining severity of DKA! -bicarbonate administration only if severe bc complications

Vitamin K deficiency 3 causes, clinical signs (2), diagnostic results (2), 1 tx (route)

Pathophys -Causes 1)result of deficient dietary intake of vitamin K (from green leafy vegetables, soybeans, and other sources) 2) malabsorption 3)decreased production by intestinal bacteria (due to treatment with chemotherapy or antibiotics). Clinial -Petechiae, purpura Diagnostics -prolonged PT that corrects upon mixing -activity levels of individual clotting factors typically are low (except low Factor V indicates liver problem) Tx -vitamin K1 (phytonadione) IV/PO, not SQ! -should improve PT within day

Molluscum contagiosum - General - Pathophysiology - Clinical - Diagnosis - Treatment - Pt education

- General ● ***Benign infection with Molluscum contagiosum virus (***poxviridae! family), no systemic manifestations ●Transmission: highly contagious - direct contact (skin to skin) most common. Fomites ●Most common in children (if in genitalia area, usu NOT bc of abuse, just take careful history/physical as usual), sexually active adults (if in genitalia area, classified as STD), & patients with HIV (lesions will focus on face and genitalia) and other immunocompromised pts ●Children with atopy are less likely to clear on their own, and those with eczema or immunocompromised have it more widespread and prolonged ●Molluscum cause inflammation that can exacerbate atopic dermatitis; An eczematous reaction encircles lesions in approximately 10% of patients ●Scratching can spread the lesion in a linear mode (Koebner phenomenon) ●Adults with chronic MC outside the genital area should be evaluated for immunosuppression - Pathophysiology - Clinical ●***Single or multiple (2-20) firm dome-shaped, flesh-colored to pearly-white, waxy papules 2-5 mm in diameter some with central umbilication (like a belly button); commonly occur on the trunk, face, and extremities but are rarely generalized ●Curd-like material may be expressed from the center if lesion is squeezed ●Giant lesions can occur - Diagnosis ●Usually a clinical diagnosis ●Histology: Henderson-Paterson bodies (keratinocytes containing eosinophilic cytoplasmic inclusion bodies) - Treatment ●***No treatment needed in most cases (spontaneous resolution in 3-6 months usually) ●Cryotherapy, Podophyllotoxin, electrodesiccation. Imiquimod. ●HAART (highly active antiretroviral therapy) ●Topical retinoids may be needed in severe cases ●Therapy may be warranted to alleviate discomfort, (itch), Reduce autoinoculation, Limit transmission of the virus to close contacts, Reduce cosmetic concerns, Prevent scarring, Prevent secondary infection ●Genital lesions in sexually active patients should be treated to prevent spread to sexual contacts ●Cantharidin, Curettage, Cryotherapy ●When there is coexisting dermatitis: Apply mid-potency topical steroid (Triamcinalone 0.1% cream, Mometasone 0.1% cream) bid for 2 weeks, Treat Molluscum with Cantharidin or Liquid Nitrogen together with dermatitis treatment ●antibiotic treatment usu not necessary, but if one lesion has expanding erythema, consider a bacterial culture and treatment with antibiotics based on culture results. ●Development of tenderness, crusting, and erythema of Molluscum leads many physicians to suspect secondary bacterial infection, but these signs represent the host response that heralds resolution of the viral infection. (BOTE sign, for Beginning Of The End) ●In children, MC will spontaneously resolve but this may take months to years. - Pt education

Scabies - General - Pathophysiology - Clinical - Diagnosis - Treatment - Pt education

- General ●***highly contagious skin infection due to the mite ***Sarcoptes scabei! - Pathophysiology ●***Female mites ***burrow into the skin to lay eggs, feed, & defecate! (scybala are the fecal particles that precipitate a hypersensitivity reaction in the skin) - Clinical ●***Intense pruritis especially at night! ●Infected pts may remain without symptoms for up to 4-6 weeks ●***Multiple, ***small erythematous papules, excoriations! ●***Linear burrows (pathognomonic)! - commonly found in the ***intertriginous zones!, including the scalp and ***web spaces! between fingers & toes. Usu spares neck & face ●***Red itchy pruritic papules or nodules on the scrotum, glans or penile shaft, or body folds are pathognomonic! ●Immune suppressed (ex. HIV) or neurologically impaired individuals are at increased risk of developing crusted scabies - Diagnosis ●clinical. skin scapings (mineral oil prep): mites, eggs, and feces seen with magnification - Treatment ●***Permethrin (5%) topical drug of choice!. Applied topically from neck down for 8-14 hrs before showering. A repeat application after 1 week is recommended. safe in pregnancy and lactation ●***Lindane: cheaper. ***DO NOT use after bath/shower (causes seizures! due to increased absorption through open pores). Contraindications: ***Teratogenic, not usu used in breastfeeding women & children <2y ●6-10% sulfur in petroleum jelly for pregnant women/infants ●Ivermectin if extensive ●***All clothing, bedding, etc. should be placed in a plastic bag at least 72 hours then washed & dried using heat! ●All close contacts should be treated simultaneously as well - Pt education

E. coli mean girl, ***mc strain, vectors, what can it cause, tx

-Mean girl: Gretchen Weiners -***MC strain: Enterohemorrhagic (EHEC) -- E.coli 0157:H7 · Vectors include hamburgers, raw milk, or cider · can cause Hemolytic uremic syndrome. · Tx not recommended as may enhance toxin release and increase risk of HUS. · Begins 3-7 days after ingestion DO NOT WANT TO TREAT THIS!!!!!! THIS WILL MAKE IT WORSE!!!!! BLOODY - SEVERELY BLOODY!! - WANT TO WAIT WILL DO RAPID TEST IN LAB FIRST TO DETERMINE

Rosacea - General - Pathophysiology - Clinical - Diagnosis - Treatment - Pt education

- General ●Chronic acneiform skin condition ●Face most commonly involved. Most common in women age 30-50 yrs - Pathophysiology ●Etiology: unclear; persistent vasomotor instability, capillary vasodilation, and abnormal pilosebaceous activity ●***Triggers: If it makes you flush it can flare rosacea: ***alcohol, hot or cold weather, hot drinks, hot baths, spicy foods, sun exposure!, medication, emotional stress - Clinical ●***Acne-like rash (papulopustules) + centrofacial erythema, facial flushing, telangiectasias, skin coarsening with burning, & stinging!. Red eyes. ●***Absence of comedones (blackheads)! in Rosacea distinguishes it from acne ●***Rhinophyma! (red, enlarged nose). Cutaneous edema - Diagnosis ●Usu clinical ●Biopsy definitive (rarely needed) - Treatment ●Lifestyle modifications: sunscreen, avoid irritants (eg, toners, astringents, menthols, camphor) ●***Mild-moderate: ***topical Metronidazole first-line for papulopustules!, Azelaic acid, Ivermectin cream. Sulfacetamide, anti-acne topical antibiotics ●Moderate-severe: oral antibiotics (eg tetracyclines), Laser Therapy; could also use Metronidazole, amoxicillin, or rifaximin in refractory cases ●oral Isotretinoin may be used in refractory cases ●***Facial erythema: topical Brimonidine!, topical oxymetazoline, Laser or intense pulsed light ●drinking ice water may be effective in reducing facial erythema and flushing. - Pt education

Lice (Pediculosis): Head - General - Pathophysiology - Clinical - Diagnosis - Treatment - Pt education

- General ●Pediculus humanus capitis ●Transmission: person to person. Fomites (hats, headsets, clothing, bedding, etc.) ●***Head lice: girls! > boys. Less common in African-Americans ●Outbreaks commonly affect children 3-12 years old, warmer & humid weather - Pathophysiology - Clinical ●***intense itching! (esp in occipital area), ***papular urticaria near lice bites ●May also have posterior cervical lymphadenopathy ●Visualization of crawling nymphs or adult lice. The presence of nits alone does not confirm infestation. ●***Nits!: white, oval-shaped egg capsules at the base of the hair shafts •The most common sites to find nits are on the retroauricular and occipital scalp. •Nits within 1 cm of the scalp are typically viable (sometimes more in warm envir) - Diagnosis - Treatment ●***Permethrin (1%) topical drug of choice!. Capitis: Permethrin shampoo left on for 10 mins. ***A fine tooth comb should be used to remove nits!. Pubic/Corporis: Permethrin lotion for at least 8-10 hrs. Safe in children at least 2 months of age. Reapplication in 7-10 days recommended to destroy any newly hatched lice. Petroleum jelly can be used in addition to suffocate the lice; recommended repeat for a 2nd week and a 3rd week ●Malathion is a first-line alternative to Permethrin. causes paralysis in arthropods (organophosphate cholinesterase inhibitor). Requires 8-12 hr treatment period ●Benzyl alcohol, Spinosad and topical Ivermectin. Spinosad has ovicidal activity so combing to remove nits is not necessary ●***Lindane! adverse effect - **neurotoxin! (headaches, seizures - do not use after shower or a bath). Usu avoided in children ●Oral Ivermectin can be used in cases that are refractory to topical therapies ●***Aftercare: •***Contact items (eg, bedding & clothing) should be laundered in hot water with detergent & dried in hot drier for 20 mins.! Toys that cannot be washed are placed in air-right plastic bags for 14 days •Avoid sharing contact items. Prophylactic treatment for individuals who share bedding - Pt education ●Children should not be restricted from attending school because of lice.

Folliculitis - General - Pathophysiology - Clinical - Diagnosis - Treatment - Pt education

- General ●Skin infection/Acneiform Lesion ●***superficial hair follicle infection or inflammation ●Risk factors: more common in men, prolonged use of antibiotics, topical corticosteroids - Pathophysiology ●***Staphylococcus aureus most common ●Other gram positive & gram negatives and fungi ●Pseudomonas aeruginosa is the most common cause of hot tub-related Folliculitis - Clinical ●***Singular or clusters of ***perifollicular papules and/or pustules with surrounding erythema on hair bearing skin, raised, occasionally pruritic, <5mm diameter - Diagnosis - Treatment ●***Mild: ***Topical Mupirocin!, Clindamycin, Erythromycin, or Benzoyl peroxide ●Severe or refractory (stubborn): Oral antibiotics: Cephalexin or Dicloxacillin ●Gram-negative: Daily acetic acid or topical Benzoyl peroxide (usu resolves without treatment) - Pt education ●Genital folliculitis may be sexually transmitted ●Thoroughly cleanse the affected area with antibacterial soap and water 3x/day ●Superficial pustules will rupture and drain spontaneously ●Oral or topical (Mupirocin) anti-staphylococcal agents may be used ●Deep lesions of folliculitis represent small follicular abscesses and should be drained ***Infectious Disease**** General -Inflammation and infection of the hair follicle -Acne is a non-infectious form of folliculitis Pathophys/Etiologies -face: staph aureus -butt/legs: gram neg (***pseudomonas; from ***hot tubs!!!) Clinical -red papules and pustules Diagnostics -clinical diagnosis! -KOH if unsure if fungal Tx -good hygiene/soaps -usu no antibiotics needed (unless v deep and recurrent: Dicloxacillin or keflex) Pt educ -can be contagious through towels/hot tub if infectious

Contact Dermatitis - General - Pathophysiology - Clinical - Diagnosis - Treatment - Pt education

- General: ● Papulosquamous disease ● ***Inflammation of the dermis & epidermis from direct contact between a substance & the surface of the skin. Either irritant (most common; may develop superimposed Candida infection) or allergen (nickel most common worldwide, poison ivy) - Pathophysiology: ● ***Allergic: type IV hypersensitivity reaction (T cell lymphocyte-mediated - delayed by days), extends beyond area of contact with allergen;***itchiness is hallmark sign of this!!!; positive patch test; can also do patch test to exclude allergic contact dermatitis ● ***Irritant: non-immunologic reaction (immediate); occurs only in area of direct contact with irritant; ***the irritant type tends to burn and hurt more than itch but can still itch (severity of itching varies), while the allergic type's hallmark sign is itchiness; also irritant type resolves within few days rather than 1-3 wks like allergic - Clinical: ●erythema and edema, with pruritus, vesicles, bullae, weeping, or crusting ● ***Acute: erythematous papules or vesicles (linear or geometric). Localized pruritus/itch, stinging, or burning. May ooze, develop edema, & progress to blisters or bullae. ● Chronic: lichenification fissuring and scales - Diagnosis: ●***Patch testing! may identify potential allergens to prevent future exposures ●Histology not usually needed but will show spongiosis (intercellular edema in the epidermis) - Treatment: ● ***Identification & avoidance of irritants = most import. ● ***Topical corticosteroids first-line medical treatment (eg, ointments). Oral corticosteroids if severe or extensive reactions ● Topical calcineurin inhibitors (eg, Tacrolimus or Pimecrolimus) = alternatives ●***CURRENT: Local Measures:: Acute weeping: Gentle cleansing and drying compresses, Calamine lotion or zinc oxide paste between wet dressings esp for intertriginous areas or when oozing is not marked, Lesions on the extremities may be bandaged with wet dressings for 30-60 minutes several times a day, High-potency topical corticosteroids gel or cream (to help suppress acute contact dermatitis and relieve itching) followed by tapering of number of applications/day or switch to mid-potency corticosteroid to prevent rebound of the dermatitis; Subacute dermatitis (subsiding): med/high corticosteroid topical; Chronic dermatitis (dry and lichenified): high/super-high potency corticosteroid ointment, occlusion may be helpful on the hands. Systemic Measures:: acute severe cases: prednisone PO for 12-21 days, the key is use enough corticosteroid (and as early as possible) to achieve a clinical effect and to taper slowly over 2-3 weeks to avoid rebound. ●Refer patients when the allergen is unclear or the dermatitis is chronic - Pt education: ● Cool saline or astringent compresses, cool baths, skin emollients ● If oozing or weeping, drying agents (eg, aluminum acetate) can be used ● Burrow's solution. Itching can be relieved with antihistamines or calamine lotion - Examples ● diaper rash: irritant contact dermatitis, prolonged exposure to urine/feces, general skin care = first line (freq diaper changes, barrier of petroleum/zinc oxide, disposable diapers, periods of rest without diaper, keep affected area clean/dry) ● toxicodendron (rhus) dermatitis (poison ivy (east), poison oak (west of rocky mount.), poison sumac (southeast); localized pruritus, stinging, or burning; cool compress, oatmeal baths, high potency steroid may decrease itch, systemic glucocorticoids if extensive, wash exposed area with detergent soap ASAP

Atopic Dermatitis (Eczema) - General - Pathophysiology - Clinical - Diagnosis - Treatment - Pt education

- General: ● Papulosquamous disease ● ***rash due to defective skin susceptible to drying, leading to itch/inflamm ●chronic, pruritic, inflammatory skin disease with a wide range of severity ● ***atopic triad: eczema/atopic dermatitis + allergic rhinitis + asthma (50-80% of children with Atopic Dermatitis will have one of those other 2 atopic diseases) ● Triggers: heat, sweat, allergen, contact irritant (food, wool, nickel, synthetic fabrics) ●called "the itch that rashes"; scratching exacerbates it ●multi-factorial: Genetics, Skin Barrier Dysfunction, Impaired Immune Response, Environment - Pathophysiology: ● disruption of skin barrier (filaggrin gene mutation; Filaggrin is needed to produce normal corneocytes and produce the natural moisturizing substance of the skin to assist in water retention) and disordered immune response. Most manifest in infancy and always by age 5 - Clinical: ● ***pruritus (severe itching of the skin) = required for diagnosis ● ***ill-defined erythematous blisters/plaques/papules; most common in flexor creases (antecubital & popliteal folds) in older children, adolescents, and adults; but on extensors/forehead/cheeks/scalp in infants/toddlers ● erythematous papules --> coalesce to form erythematous plaques that may display weeping, crusting, or scale ●Xerosis (rough and dry) common bc of trans-dermal water loss due to impaired production of filaggrin and impaired lipids ●food only associated if GI symptoms accompany exacerbation of symptoms right after exposure to the food - Diagnosis: ●clinical, increased IgE supports diagnosis - Treatment: ●4 major components of treatment: 1) antibacterial, 2) anti-inflammatory (topical steroids), 3) antipruritic/itch (antihistamine), 4) moisturizer ●moisturizer: ceramide based moisturizers are important; Greasier ointments are better (less preservatives than creams, occlusive agents (can be applied after ceramide cream), don't sting or burn), but grease may be unpleasant for some pts so adherence may suffer; in this case, heavier creams are superior to lotions) (acute management): ●***topical corticoids first-line; antihistamines for itching, wet dressings (Burrow's solution), antibiotics if secondary staph infection (Yellow honeycomb, impetiginized); topical calcineurin inhibitors and phosphodiesterase 4 inhibitor = alternatives to steroids (don't cause skin atrophy; antiinflamm; may sting/burn), systemic: phototherapy, other drugs ●Avoid high potency steroids on face and body folds. ●Rule of thumb: Use topical steroids twice daily for 2 weeks then stop for 2 weeks. (chronic management): ●***maintain skin hydration (emollients twice daily and within 3 mins of exiting a lukewarm shower/tepid bath), oral antihistamines for itch and other drugs, ***trigger avoidance (heat, low humidity) or irritants (soap, detergent, frequent bath, washcloth) - Pt education: see above Pt education: ●Pityriasis alba (post inflammatory hypopigmentation): Poorly defined hypopigmented, scaly patches on the face; Treat with emollients and sunscreen; Not permanent

Tinea pedis - General - Pathophysiology - Clinical - Diagnosis - Treatment - Pt education

- General: ● Papulosquamous disease / infectious disease ●***Athlete's foot - most common dermatophyte infection; ***Trichophyton rubrum (most commonly caused by this), interdigitale, floccosum ●transmission: direct contact (barefoot in pools/gyms) ●most common in adolescents and young men - Pathophysiology: - Clinical: ●***interdigital: most common - pruritic, erythematous erosions or scales between toes, most common in 3rd and 4th, or 4th and 5th, digital interspaces ●hyperkeratotic on soles, lateral/med surfaces of feet with moccasin distribution, onychomycosis (fungal infection of the nails), may have associated maceration (breaking down of skin from prolonged moisture) ●vesiculobullous: pruritic vesicular or bullous eruption with underlying erythema, esp medial surfaces of foot (may be painful) - Diagnosis: ●KOH prep: scrape, segmented hyphae ●Wood's lamp: no fluorescence with tricohyt; fluorescence with microsporum ●Culture: definitive - Treatment: ●***Topical antifungals first line (Butenafine, Tolnaftate, Ciclopirox, azoles) - 4 week duration, Terbinafine 1% cream x 1 week. Burrows solution for hyperkeratotic ●PO Terbinafine, fluconazole or Itraconazole if topical are ineffective. Griseofulvin. ●Clean shoes with antifungal spray, keep cool/dry - Pt education:

Tinea corporis - General - Pathophysiology - Clinical - Diagnosis - Treatment - Pt education

- General: ● Papulosquamous disease / infectious disease ●***superficial fungal infection of the body (trunk, legs, arms, or neck). Does not include the feet, hands, groin, or scalp - Pathophysiology: ●***Fungi of the trichophyton and microsporum genera. Trichophyton most common in US, microsporum most common worldwide; T. rubrum most common cause of tinea (except captitis), Microsporum canis is zoophilic (cats & dogs)that can also cause human infections. ●***transmission: ***direct contact (common in preadolescents eg wrestlers), infection from animals (dog/cat), infec from other body part - Clinical: ●***single or multiple pruritic, erythematous, scaly, circular or oval plaques or patches with central clearing and well-defined raised borders tat spread outwardly. May have pustules - Diagnosis: ●***KOH prep: best initial test - scrapings from lesions reveals segmented hyphae; Scrape in scaly border! ●culture: definitive diagnosis (slower method) - Treatment: ●***topical antifungals first line: "azoles" (eg, Clotrimazole, Ketoconazole), Butenafine, Terbinafine, Naftifine, Ciclopirox, and Tolnaftate. Duration is usually 1-3 wks ●oral antifungals: if topical ineffective or extensive --Itraconazole or Terbinafine. Griseofulvin or Fluconazole second-line systemic therapies ●Don't put steroids! and don't cover/occlude! - Pt education:

Pityriasis rosea - General - Pathophysiology - Clinical - Diagnosis - Treatment - Pt education

- General: ● papulosquamous disease ●acute exanthematous eruption that mainly occurs in young people ● etiology: uncertain; maybe viral infections (human herpes virus (HHV) 6/7 (roseola)) ● mostly in children/young adults (; usu 10-35; rare in >35yo), spring&fall - Pathophysiology: - Clinical: ● ***Herald patch (solitary salmon-colored macule) on trunk, 2-10 cm diameter then general exanthem 1-2 wks; ***smaller, v pruritic 1 cm round or oval salmon-colored papules with white circular ***(collarette) scaling in ***Christmas tree pattern (oriented along skin cleavage liens), peripheral scaling, central clearing; in darker skin types, it will be shades of purple, brown, or gray, some call it lilac or violaceous; pts usu don't remember or never had a herald patch ● ***Confined to trunk & proximal extremities (usu spares face, palms, & soles, but possible) ● follows skin lines - Diagnosis: ●***in young adults, ***RPR (Rapid plasma reagin) should be ordered to rule out secondary Syphilis; when soles and palms affected, probably syphillis ●Usually asymptomatic, may have associated flu-like symptoms (Malaise, nausea, loss of appetite, gastrointestinal upset, upper respiratory symptoms; Less common: fever, swollen lymph nodes, pain, sore throat) - Treatment: ● ***no management needed for most (self-limiting; >80% resolves by 8 wks without treatment) - educ, reassurance, treatment of pruritis (if present; PO antihistamines, topical corticosteroids, oatmeal baths); resolves spontaneously in 6-12 wks (mean: 5wks) ●OTC lotions or emollients for scaling and itching ●UVB phototherapy help if severe and within 1st week of eruption ● Oral Acyclovir or Erythromycin may speed up healing not not usu used - Pt education:

Cellulitis - General - Pathophysiology - Clinical - Diagnosis - Treatment - Pt education

- General: ●Infectious disease ●acute spreading infection of the deeper dermis & subcutaneous tissues ●bacterial entry usu occurs after a break in skin, such as underlying skin problems (eg, Impetigo, Tinea), trauma (eg, bites, wounds, pressure ulcers), and surgical wounds, previous or secondary skin infection, edema or lymphatics problems - Pathophysiology: ●***most commonly caused by Group A Streptococci ●***Staphylococcus aureus is an import but less common cause - Clinical: ●***Localized macular erythema (flat margins ***not sharply demarcated), swelling, warmth, and tenderness, non-fluctuant (non-movable) edematous plaque surrounding central bulla ●***Systemic symptoms not common - fever, chills, regional lymphadenopathy, myalgias, vesicles, bullae, hemorrhage. May develop ***lymphangitis (streaking; inflammation or an infection of the lymphatic channels that occurs as a result of infection at a site distal to the channel) ●More commonly found on the lower leg - Diagnosis: ●primarily clinical - Treatment: ●***It is important to recognize and treat cellulitis early as untreated cellulitis may lead to sepsis and death ●***oral antibiotics: Cephalexin!, Dicloxacillin!, Clindamycin or Erythromycin if penicillin-allergic ●***IV antibiotics: ***Cefazolin!, Ampicillin-sulbactam, Ceftriaxone, & Clindamycin ●***Cat bite (Pasteurella multocida): Amoxicillin-clavulanate!; Doxycycline if PCN allergic ●Dog or human bite: Amoxicillin-clavulanate. Clindamycin + either Ciprofloxacin or Trimethoprim-sulfamethoxazole ●elevate affected area ●Cultures from abscesses and other purulent skin and soft tissue infections (SSTIs) are recommended in patients treated with antibiotic therapy ●MRSA treatment (for purulent cellulitis/hospitalized pts): •***Oral: Clindamycin!, Doxycycline!. Trimethoprim-sulfamethoxazole! (good for Staph but doesn't cover Streptococcus) •***IV: Vancomycin! or Linezolid - Pt education: ●Treat tinea pedis if present - ***Example pt: ●Vital signs: ***T 100.4!, HR 90, BP 120/70, RR 14, O2 sat 97% on RA ●Skin: erythematous plaque with ill-defined borders. Lesion is ***tender! to palpation. ●Tender, slightly enlarged right inguinal lymph nodes (not shown) ●Laboratory data: ***Wbc 12,000 (75% neutrophils, 10% bands)!, Hct 44, Plts 335 *****Infectious Disease***** General -Inflammation of the skin and subcutaneous tissues, usually due to infection -Non-necrotizing Pathophys -Etiology ▪Usually occurs after skin is compromised, i.e. scratching, shaving, laceration, IV ▪Risk fx: DM, immunocompromised, certain medications, IV drug users ▪***Most commonly caused by Streptococcus pyogenes, Staphlyococcus aureus comes in second Diagnosis -Usually made by history and physical exam -if infection: ▪CBC/metabolic panel ▪Creatinine ▪Gram stain ▪Blood cx ▪Hospitalization for IV meds Clinical -Erythema -Edema -Warmth -Pain -maybe fever, chills, lymphadenopathy, circumferential rash Tx ▪***Keflex (Cephalexin), Bactrim (TMP-SMZ) (PO most common) ▪***if suspect MRSA (rx actors: Healthcare workers, prisonisers, wrestling teams, nursing homes, any hosptialzied): Clindamycin or Bactrim* ▪TDap ▪Drain abscess if present (I&D) ▪***If PCN allergy: clindamycin! or a macrolide (clinda or vanco if severe) ▪Severe: IV cefazolin (first gen), cefuroxime (second gen), ceftriaxone (third gen) Pt education ▪Wound re-check in 48 hours ▪Mark the area ▪Elevation (not of the face!:)) ▪Pain control ▪Can shower but pat dry area ▪Not contagious

Tinea Versicolor - General - Pathophysiology - Clinical - Diagnosis - Treatment - Pt education

- General: ●aka Pityriasis versicolor; is not caused by a dermatophyte ●colonization caused by species of Malassezia ●Cause spots/discoloration (hypo- or hyper- pigmentation, light/dark, pink/tan) ●Yeast like fungus infection of the skin. Caused by a type of yeast that naturally lives on your skin. When the yeast grows out of control, the skin disease, which appears as a rash, is the result. ●The infection can happen if: oily skin, live in hot climate, sweat a lot, weak immune system ●called "versicolor" because it can be light, dark, or pink to tan - Pathophysiology: - Clinical: ●well-demarcated, tan, salmon, or hypopigmented or hyperpigmented patches, most commonly on trunk and arms ●Macules will grow, coalesce and various shapes and sizes are attained in an asymmetric distribution ●Visible scale is not often present, but when rubbed with a finger or scalpel blade, scale is readily seen ●not contagious - Diagnosis: ●Test will always say short hyphae and small round spores - Treatment: ●Shampoos: selenium sulfide 2% shampoo, ketoconazole shampoo, zinc pyrithione shampoo: Apply daily to affected areas, wait 10 minutes, then rinse, Repeat daily for 1-4 weeks, As effective as oral therapy ●Imidazole creams: ketoconazole, clotrimazole: Apply daily or bid for 1-4 weeks, very effective for limited areas, Usually more expensive than shampoos due to surface area ●Oral medication may be used when topical therapy fails, if the benefits outweigh the risks or the patient has a strong preference for oral therapy •Fluconazole 100- 200 mg / week for 2-4 weeks Itraconazole 200 mg / day for 7 days or 100 mg/day for 14 days; Monitor liver function if giving more than 30 days If relapse, maintenance therapy: topicals are used 1-2x/week; Ketoconazole shampoo, Selenium sulfide (2.5%) lotion or shampoo, Zinc pyrithione (bar or shampoo), Leave on for 10 minutes before rinsing off - Pt education:

Psoriasis (all types) - General - Pathophysiology - Clinical - Diagnosis - Treatment - Pt education

- General: ●immune-mediated multi-systemic disease with a genetic predisposition; chronic, inflammatory, mostly involves skin & joints - Pathophysiology: ●***keratin hyperplasia & proliferating cells in the ***stratum basale + stratum spinosum due to ***T cell activation & cytokine release ●***causes greater epidermal thickness & ***accelerated epidermis turnover - Clinical: ●Plaque: most common type. Raised, well-demarcated, pink-red plaques or papules with thick silvery white scales. Most common on the extensor surfaces of elbows & knees, scalp (most common initial spot), & nape of the neck, and umbilicus. Usu pruritic ●***Auspitz sign: punctuate bleeding with removal of plaque or scale. not specif to Psoriasis (may be seen in Actinic keratosis as well) ●***Koebner's phenomenon: new isomorphic (similar) lesions at the sites of trauma (also seen in Eczema and Vitiligo) ●***Nail involvement: ***pitting! (25%). yellow-brown discoloration under the nail (oil spot) pathognomonic (specific characteristic of this disease). Separation of nail from nail bed (onycholysis); esp in pts with psoriatic arthritis; 50% have fingernail involvement, 35% have toenail involvement; could also have Trachyonychia (rough nails as if scraped with sandpaper longitudinally), Onycholysis (separation of the nail plate from the nail bed. +/- "oil drop sign"), or Subungual hyperkeratosis (abnormal keratinization of the distal nail bed) ●***Other variants: 1)***Guttate: small, erythematous "tear drop" papules with fine scales, discrete lesions & confluent plaques. Spares palms & soles. ***Often appears after group A beta-hemolytic Streptococcal pharyngitis/infections 2) Inverse (Flexural): erythematous (lacks scale). Most commonly in skin folds (groin, gluteal fold, axilla, umbilicus) 3) Pustular: deep, yellow pustules that coalesce to form large areas of pus. fever, leukocytosis may be seen; includes "von Zumbusch variant" & Palmoplantar type 4) Erythroderma: generalized erythematous rash involving most of the skin (worst type) - Diagnosis: ●usu clinical - Treatment: ●Treatment depends on age, type of psoriasis, site & extent, previous treatment, and other medical conditions ●***Mild = <3% of the body, moderate = 3-10%, severe = <10% ●Extent: localized = <5% of BSA, generalized = diffuse or >30% involvement ●***Mild-moderate: ***topical corticosteroids first line (high potency), vitamin D analogs (***Calcipotriene), topical coal tar, topical Retinoids/Vitamin A analogs (eg, Tazarotene); Calcineurin inhibitors (eg Pimecrolimus & Tacrolimus can be used on delicate areas, such as face penis) ●***Moderate-severe: ***Phototherapy: UVB, PUVA (oral Psoralen followed by ultraviolet A) ●Severe: Systemic treatment eg, Cyclosporine, Retinoids (Acitretin), biologic agents (eg, TNF inhibitors Etanercept, Adalimumab, & Infliximab) ●Methotrexate is usu the last resort (due to liver lung and marrow effects) except in Psoriatic arthritis, where it is the first management of severe disease ●Systemic treatment of severe psoriasis depends on convenience, side effect risk profile, presence or absence of psoriatic arthritis, and co-morbidities; 3 choices: 1.Phototherapy, 2.Oral medications: methotrexate, acitretin, cyclosporine, apremilast, etc., 3.Biologic Agents: TNF-α inhibitors (infliximab, etanercept, adalumimab), IL 12/23 blocker (ustekinumab), IL 17A blocker (secukinumab, ixekizumab, brodalumab - IL 17aR), IL 23 blocker (guselkumab, tildrakizumab, risankinumab). ●don't use oral prednisone which can cause pustular psoriasis ●***Oral/Systemic steroids/corticosteroids should NEVER be used in psoriasis as they can severely flare psoriasis upon discontinuation!!! - Pt education: ●In this condition, immune system sends out abnormal signals to speed up the cycle of skin cell production ●occurs when skin cells quickly rise from their origin below the surface of the skin and pile up in raised, red patches covered with silvery scales on the surface before they have a chance to mature ●Usually, normal skin turnover takes about a month, but in psoriasis it occurs in only a few days ●***ask about fam history; 1/3 of psoriasis patients have a positive family history ●***Triggers --Psoriasis can be triggered or exacerbated by a number of medications including: •Systemic corticosteroid withdrawal •Beta blockers •Lithium •Antimalarials •Interferons ●Possible health-related behaviors associated with psoriasis: smoking, alcohol, higher BMI

Salmonella mean girl, cause, clinical, diagnosis, tx

- Mean girl: Karen Smith -Frequently acquired from poultry and their eggs -Enteric fever -Signs/Symptoms: 6 - 72 hours after ingestion •Gastroenteritis: N/V DIARRHEA •Extraintestinal: reactive arthritis, osteomyelitis -Diagnosed by culture (stool, blood) -Tx with ***ciprofloxacin or ampicillin!, TMP-SMZ (Increasing resistance a treatment issue)

Impetigo what is it, contagious, types & causative agents, tx (general and 3 meds)

-Bacterial infection of the superficial layers of the epidermis -highly contagious -nonbullous (MC; Honey colored crusty lesions; strep & staph or combo) or bullous (only staph, can see on butt while nonbullous dont see on butt) -clinical diagnosis -Tx ▪Don't touch lesions, clean them, stay home for 24 hrs after starting abx, abx: Topical: ***mupirocin (Bactroban) 2-3 times a day x 7 days; PO: ***cephalexin (Keflex) or ***augmentin x 10 days

Acute sinusitis

-General ●Inflammation of nasal cavity, obstruction of ostiomeatal complex, accumulation of mucous ●S. pneumonia, Streptococcus species, H. influenza, S. aureus, M. catarrhalis ●Acute <4 weeks, Subacute 4-12 weeks, Chronic >12 weeks -Clinical ●Purulent yellow-green discharge ●Facial pain/pressure over sinuses ●Acute symptoms, 1-4 weeks ●Cough, malaise, headache ●Fever ●***Do a neurological examination -Diagnosis ●Clinical diagnosis ●***"Waters View"! Skull X-Ray ●***CT Scan or MRI! -Treatment ●Antibiotics ●***Augmentin! ●Doxycycline or Clindamycin if PCN allergic ●Symptom control ●NSAIDS ●Decongestants

Acute Viral Rhinosinusitis (Common Cold)

-General ●Self-limited, 10-14 days ●***Rhinovirus, adenovirus! -Signs/symptoms ●Nasal congestion, ***clear rhinorrhea! (no purulent discharge) ●Hyposomia ●Malaise, cough, headache ●***Erythematous!, engorged nasal mucosa -Diagnosis ●Clinical Diagnosis -Treatment ●Oral decongestants ●NSAIDS ●Nasal saline sprays

Allergic Rhinitis

-General ●Very common ●Environmental ***allergen exposure in the presence of IgE ●Flowering plants, pollen, ragweed, mold (seasonal) ●Dust, household mites, pet dander (perennial) -Clinical ●***Clear rhinorrhea!, tearing ●Sneezing, eye irritation, pruritus ●***May be associated with cough, bronchospasm, eczema! ●Pale turbinates ●Nasal polyps with chronic symptoms -Diagnosis ●Clinical diagnosis -Treatment ●Intranasal corticosteroids (Flonase) ●Antihistamines (Loratadine) ●Antileukotriene medications (Montelukast)

Herpes simplex - General - Pathophysiology - Clinical - Diagnosis - Treatment - Pt education

-Herpes simplex viruses 1 and 2 cause painful, grouped vesicles on an erythematous base ●Vesicles may appear pustular (white to yellow) ●Tends to recur in the same place ●HSV 1 favors the mouth and nose ●HSV 2 favors the genitalia, buttocks, thighs ●Perianal erosions or ulcerations in immunosuppressed patients are usually HSV -Often don't see vesicles, just the erosions ●Look for bright red rim on erosion ●Pain and recurrence suggests HSV -Recurrent vesicles on genitalia, buttocks, or thighs, are HSV until proven otherwise -HSV usually has ***bright red borders and may present as ***pustules, or erosions; when drying up, crusts or ulcerations -Severe perianal HSV may occur in HIV or other immunosuppression -Single genital ulcers could be syphilis or chancroid as well -Tests/Diagnosis: ●Tzanck prep can be used to confirm herpes family viruses, but it does not differentiate them from one another. It requires scraping the base of an active vesicle or erosion. Results are immediate. ●Viral culture can be performed when there is fluid present, but it is less helpful once crusts have formed. Results in 1-3 weeks. Not as helpful for VZV. The gold standard for HSV. ●Direct fluorescent antibody (DFA) test can differentiate HSV 1 and 2, as well as VZV. Like Tzanck prep, scrape the base of a vesicle or erosion. Results in 48 hours. ●The HerpSelect test is a blood test, which uses IgG antibodies to differentiate past exposures to HSV 1 and 2 but not VZV. Results in days to weeks. ●Acyclovir is a safe, cheap, and reliable treatment for HSV •Should be started immediately at first sign of recurrence •Acyclovir can be used in pregnancy •Intravenous acyclovir is available for generalized HSV or VZV in the immunocompromised ●Famciclovir and valacyclovir are more expensive but have easier dosing - Treatments ●Patients start taking at earliest sign of outbreak (burning, pain, itching, etc.) ●Short therapies work as well as longer ones for Herpes Simplex Type 1 •Acyclovir 800 mg TID x 2 days •Famciclovir 1 gram BID x 1 day •Valacyclovir 2 grams BID x 1 day ●Genital Herpes Type 2 •1st episodes treat for 7-10 days •Recurrent episodes - see next slide •Suppressive treatment: Valacyclovir 500-1000 mg daily, Famciclovir 250 mg 2x day, or Acyclovir 400 mg 2x day *****Infectious Disease**** General -oral herpes -contagious from skin to skin/sore/saliva contact Clinical -***oral mucosa/lips (may have difficulty eating and drinking), vesicles on fingers (herpetic whitlow, DO NOT I&D), keratitis (cornea dendritic lesion can see with UV light; DO NOT give steroids, just cyclovirs/give to ophthalmologist)! -may have Prodrome of fever, submandibular and cervical lymphadenopathy -Heal in 10-14 days Dx -usu clinical diagnosis -Tzanck smear will show giant multi-nucleated cells! -PCR is most sensitive and most specific! (Dipu said trend: PCR is the way to go for all these viruses) Tx -oral analgesics, supportive measures (ice pops, ice cream, miracle mouthwash) -***antiviral •primary outbreak: Valacyclovir 1g BID x 7-10 days •secondary outbreak: Valacyclovir 500mg BID x 3 days (half the dose/duration as primary) •prophylaxis: Valacyclovir 500mg-1g QD (once a day)

ROS

1) Constitutional: -weight loss, weight gain, fatigue, weakness, fever, chills, and night sweats. 2) Eyes: -change in vision, date of last visual examination, glasses or contact lenses, history of eye surgery, eye pain, photophobia, diplopia, spots or floaters, discharge, excessive tearing, itching, cataracts, or glaucoma. 3) Ears, nose, and mouth/throat (ENT): • Ears: change in or loss of hearing, date of last auditory evaluation, hearing aids, history of ear surgery, ear pain, tinnitus, drainage from the ear, history of ear infections. • Nose: changes in or loss of sense of smell, epistaxis, obstruction, polyps, rhinorrhea, itching, sneezing, sinus problems. • Mouth/throat: date of last dental examination, ulcerations or other lesions of tongue or mucosa, bleeding gums, gingivitis, dentures or any dental appliances. 4) Cardiovascular (CV): -chest pain, orthopnea, murmurs, palpitations, arrhythmias, dyspnea on exertion, paroxysmal nocturnal dyspnea, peripheral edema, claudication, date of last electrocardiogram or other cardiovascular studies 5) Respiratory: -dyspnea, cough, amount and color of sputum, hemoptysis, history of pneumonia, date of last chest radiograph, date and result of last tuberculosis testing. 6) Gastrointestinal (GI): -abdominal pain; dysphagia; heartburn; nausea; vomiting; usual bowel habits and any change in bowel habits; use of aids such as fiber, laxatives, or stool softeners; melena; hematochezia; hematemesis; hemorrhoids; jaundice. 7) Genitourinary (GU): -frequency, urgency, dysuria, hematuria, polyuria, incontinence, sexual orientation, number of partners, history of sexually transmitted infections, infertility. • Males: hesitancy, change in urine stream, nocturia, penile discharge, erectile dysfunction, date of last testicular examination, date of last prostate examination, date and result of last prostate-specific antigen (PSA) test. • Females: GU symptoms as above and gynecologic symptoms; age at menarche; gravida, para, abortions; frequency, duration, and flow of menstrual periods; date of last menstrual period; dysmenorrhea; type of contraception used; ability to achieve orgasm; dyspareunia; vaginal dryness, menopause; breast lesions, date of last breast examination; breast self-examination; date and result of last Papanicolaou smear, date of last pelvic examination. 8) Musculoskeletal (MSK): -arthralgias, arthritis, gout, joint swelling, trauma, limitations in range of motion, back pain. (Note that numbness, tingling, and weakness are typically not included in musculoskeletal but in neurological system.) 9) Integumentary: -rashes, pruritus, bruising, dryness, skin cancer or other lesions. 10) Neurological: -syncope, seizures, numbness, tingling, weakness, gait disturbances, coordination problems, altered sensation, alteration in memory, difficulty concentrating, headaches, head trauma, or brain injury. (Headache, head trauma, or brain injury may also be listed under head, as part of Head, Eyes, Ears, Nose, Mouth/Throat, or HEENT.) 11) Psychiatric: -emotional disturbances, sleep disturbances, substance abuse disorders, hallucinations, illusions, delusions, affective or personality disorders, nervousness or irritability, suicidal ideation or past suicide attempts. 12) Endocrine: -polyuria, polydipsia, polyphagia, temperature intolerance, hormone therapy, changes in hair or skin texture. 13) Hematologic/lymphatic: -easy bruising, bleeding tendency, anemia, blood transfusions, thromboembolic disorders, lymphadenopathy. 14) Allergic/immunologic: -allergic rhinitis, asthma, atopy, food allergies, immunotherapy, frequent or chronic infections, HIV status; if HIV positive, date and result of last CD4 count.

Patient Education

1) General: What is it? 2) Etiology: How did they get it? 3) Clinical: Classic symptoms? Contagious? 4) Diagnosis: How did I diagnose? 5) Treatment: How will I treat? -- what, how to take, side effects, follow-up 6) !!!***Any questions for me???

History Taking

1) HPI -OPQRST •Onset (when/where) •Provocation •Quality •Radiation •Severity •Timing -PRACTL •Previously had this before •Recent travel •Associated symptoms •Contacts (sick ppl, pets) •Treatments tried and have they helped •Last oral intake 2) ROS -Constitutional -Eyes -ENT (Ears, Nose, Mouth/Throat) -CV -Resp -GI -GU -MSK -Integumentary -Neurological -Psychiatric -Endocrine -Hematologic/lymphatic -Allergic/immunologic -a way to remember: "Conner Skateboards Everywhere Rapidly Entering CVS Getting New Mint Gum Pieces Always Endlessly Humorous" 3) PMH -Medical problems -Medications -Allergies -Immunizations -Sexual History 4) Surgical History/Hospitalizations -what, when, complications 5) Social History -living situation -job -education -ETOH -smoke (cigarettes, marijuana, vape)--pt or anyone in house -recreational drugs -sports -hobbies -sexual activity 6) Family History -parents/siblings (alive/dead, age, PMH)

Sickle cell disease main symptom (and 3 other ones that may appear), dx (3, initial, definitive), dx findings (4), tx (mainstay, severe, prophylaxis)

Clinical: -***begin as early as 6 mos -***Dactylitis (inflamed digits) most common initial presentation; delayed growth, fever, infections -infections: ●asplenia (increased risk of infection with encapsulated organisms) ●osteomyelitis: Salmonella spp. ●Aplastic crisis: Parvovirus B19 infections -splenomegaly and rapid decrease in Hb -hemolytic anemia (jaundice, gallstones) -painful vaso-occlusive "crisis": ***acute chest syndrome, back abdomen, bone pain. Priapism common! -bony vaso-occlusion: ***ischemic necrosis of bones (eg, femoral or humeral head), "H" shaped vertebrae! -skin ulcers -chronic hypoxia -***stroke! Diagnosis: -***smear: best initial test! ●***sickled erythrocytes ●***Howell-jolly bodies! indicated asplenia ●normochromic-normocytic -Hb electrophoresis ●***sickle disease: HbS, little to no HbA, increased HbF! -DNA analysis definitive! Treatment: -Supportive care is the mainstay of treatment for sickle cell anemia ●***Pain control: IV hydration & o2 first step in management of pain crisis ●folic acid supplementation ●RBC transfusions in crises ●Exchange transfusion if severe ●Allogenic stem cell transplant may be curative but lots of side effects Reduction of episodes: Hydroxyurea (chemotherapy) -Mechanism of Action: increases HbF (which doesn't sickle and has higher affinity of O2), reduces RBC sickling -Indications: ●mainstay of treatment - reduces frequency and severity of pain episodes, decreases hospitalization rates, and prolongs survival ●not used for acute bc it takes wks-mos -Infection prevention in children ●prophylactic penicillin given as early as 2-3 mos of age until at least 5 yrs of age to prevent infectious complications

Otitis externa

General - Inflammation of external auditory canal -Etiology: Compromise of skin of canal (Moisture, trauma, immunocompromised, DM, Furuncles) and this then puts at risk for infection Pathophysiology -***Water immersion! aka "swimmer's ear" - excess moisture raises pH from normal acidic pH of ear, facilitating bacterial overgrowth -***Local mechanical trauma! (eg, use of Q-tips, age 7-12 yrs, aberrant ear wax (too much or too little) -Etiologies: ●***Pseudomonas aeruginosa most common! (50%) ●Staphylococcus (eg, aureus & epidermis), GABHS, Proteus, anaerobes; Aspergillus. Fungi (usu have black dots/spores). Clinical -***Ear pain, pruritis! in the ear canal (may have recent activity of swimming) -Auricular discharge (can cause conductive hearing loss), ear pressure or fullness, hearing loss, decreased/muffled hearing -Physical exam: ***pain on traction of ear canal or tragus, purulent auricular discharge! Diagnosis -clinical + otoscopy: ***edema of the external auditory canal! with erythema, debris, or discharge -culture for refractory cases -Imaging - possibly CT if concerned for malignant Otitis externa Treatment -Protect ear against moisture (drying agents/acidification include isopropyl alcohol & acetic acid) + removal of debris & cerumen + topical antibiotics with coverage against Pseudomonas & Staphylococcus (with or without glucocorticoids for inflammation) -Topical antibiotics: ●Ciprofloxacin-dexamethasone, Ofloxacin (fluoroquinolones) ●Aminoglycoside combination: Neomycin/Polymyxin-B/Hydrocortisone otic. ***Not used it tympanic perforation suspected or if TM cannot be visualized - aminoglycosides are ototoxic! -Treatment should last three days beyond the cessation of symptoms ●Typically five to seven days ●More severe infections, 10 to 14 days -Ear Wick - gauze soaked in drops (gtts should be applied every three to four hours while the patient is awake), decreases swollenness of ear canal; if give them ear wick in ear should see them for follow-up 48-72 hrs to make sure it's good then when see it's good and working dont need to see them again just tell them will fall out on own may gind on pillow one day; wick is only ued if severe; if used wick, usu need oral medication/antibiotic ●If fever, persistent, spread, severe, lymphadenopathy, or wick, then use oral agents/fluoroquinolones ●***order of what Theresa recommends for treatment: acetic acid solution, then aminoglycoside then fluoroquinolone ● When simple: avoid water/moisture/trauma + drying agent (acetic acid) ●when ear canal gets narrow and cant get drops in: ear wick (with aminoglycocide or cephalosporin, NOT acetic acid/drying agents) and oral antibiotic/fluoroquinolone like cipro -Pain relief ●Acetaminophen (Tylenol) ●Naproxen (Alleve) ●Ibuprofen (Motrin) -Ok to consider small amount of narcotics - can be very painful Pt education -Treatment Pearls ●Warming the bottle of drops in the hands before instillation minimizes dizziness ●A small cotton plug moistened with the drops can be used to help retain the drops in the ear if the patient cannot lie still long enough to allow absorption. ●Absorption may also be facilitated by manipulating the tragus to help distribute the drops throughout the external auditory canal. ●put some vaseline on cotton ball and put in ear, that can stop water from coming in ear -Complications: Malignant Otitis Externa, Chronic Otitis Externa)

Major depressive disorder (aka MDD; unipolar depression) risk factor, subtypes (5), more general, pathophys, clinical, diagnostic criteria (2), diagnosis (2, including screening), tx (2)

General -Can occur at any time of life -risk factors: female (2 times more likely) -subtypes: 1) Psychotic major depression 2) Major depression with atypical features 3) Major depression with peripartum onset 4) Melancholic major depression 5) Major depression with seasonal onset -Not due to substance use, bereavement or underlying medical condition -Symptoms cause clinical distress or impairment in social, occupational or other important areas of functioning -Multi-factorial -Genetic factors -Alteration in neurotransmitters: serotonin, epinephrine, norepinephrine, dopamine, acetylcholine -Adrenal, thyroid or growth hormone dysregulation -Associated with unemployment -Symptoms may improve as the day goes on -***Psychotic depression can occur -15% of patients commit suicide (men > women) •More common in those with substance abuse hx •White males >45 at greatest risk Pathophys -alteration in neurotransmitters Clinical -Depressed mood -Anhedonia (loss of pleasure) -Loss of interest in activities ->5 associated symptoms: Fatigue, insomnia or hypersomnia, feelings of guilt or worthlessness, recurring thoughts of death or suicide, psychomotor agitation, significant wt changes (gain/loss), decreased appetite, decreased concentration -diagnostic criteria: 1) @ least 5 associated symptoms (must include either depressive mood or anhedonia--inability to feel pleasure) almost every day for at least 2 weeks 2) symptoms must cause significant distress or impairment (social or occupational) Diagnosis -Evaluate for underlying causes -PHQ-9 Questionnaire Tx -Psychotherapy -Medications •1st line: SSRI •2nd line: SNRI •3rd line: TCA, MAOI -Electroconvulsive Therapy (ECT) •Used for patients who do not respond to medical mgmt -more specific examples: 1) seasonal (ex. winter blues): SSRIs, light therapy, Bupropion 2) atypical (mood reactivity--improved mood in response to positive events): MAO inhibitors 3) melancholia (anhedonia, lack of mood reactivity, increased REM time and reduced sleep, mood worse in morning) 4) Catatonic depression (motor immobility, stupor & extreme withdrawal)

Iodine deficiency mc cause of what, pathophys (high rate of what, min iodine dietary requirement), clinical (7), diagnosis (5), tx (2), pt educ (prevention)

General -Common in regions with low-iodine diets. -Most adults with endemic goiter are euthyroid -MC cause of endemic goiter Pathophys -High rate of congenital hypothyroidism and cretinism. -daily minimum dietary requirement for iodine is 150 mcg/day in nonpregnant adults and 250 mcg/day for pregnant or lactating women. Clinical -Goiters may become multinodular and enlarge. -resp distress, dysphagia, cardiac issues, bleeding from esophagus, palsies of phrenic/laryngeal nerves, or Horner syndrome (small pupil, drooping eyelid, and decreased sweating on one side of face) Diagnosis -serum T4 and TSH = normal. -Thyroid RAI uptake is usually elevated -Serum levels of antithyroid antibodies low/absent -Serum thyroglobulin elevated above 13 mcg/L. -Urine iodine concentrations are low. Tx -iodine supplementation (not effective in adults with large multinodular goiter) -Thyroidectomy Pt education -Prevention: sources of iodine --> iodized salt, commercial bread, milk, and seafood

Candidiasis - General - Pathophysiology - Clinical - Diagnosis - Treatment - Pt education

General -Common normal flora but opportunistic pathogen. -Typically mucosal disease, particularly vaginitis and oral thrush/esophagitis. -Persistent, unexplained oral or vaginal candidiasis: check for HIV or diabetes mellitus. -(1,3)-beta-D-glucan results may be positive in candidemia even when blood cultures are negative. -Candida albicans can be cultured from the mouth, vagina, and feces of most people. - Cellular immunodeficiency predisposes to mucocutaneous disease. -When no other underlying cause is found, persistent oral or vaginal candidiasis should arouse a suspicion for HIV infection or diabetes. -The risk factors for invasive candidiasis include prolonged neutropenia, recent abdominal surgery, broad-spectrum antibiotic therapy, kidney disease, and the presence of intravascular catheters (especially when providing total parenteral nutrition). -For Candida glabrata resistant to azoles and echinocandins, lipid formulation amphotericin B (3-5 mg/kg intravenously daily) may be used. Clinical: A. Mucosal Candidiasis -Vulvovaginal candidiasis occurs in an estimated 75% of women during their lifetime. -Risk factors include pregnancy, uncontrolled diabetes mellitus, broad-spectrum antimicrobial treatment, corticosteroid use, and HIV infection. Symptoms include acute vulvar pruritus, burning vaginal discharge, and dyspareunia. -Esophageal involvement is the most frequent type of significant mucosal disease. -Presenting symptoms include substernal odynophagia, gastroesophageal reflux, or nausea without substernal pain. Oral candidiasis, though often associated, is not invariably present. Diagnosis is best confirmed by endoscopy with biopsy and culture. B. Candidal Funguria Most asymptomatic and represent specimen contamination or bladder colonization. However, symptoms and signs of true Candida urinary tract infections are indistinguishable from bacterial urinary tract infections and can include urgency, hesitancy, fever, chills, or flank pain. C. Invasive Candidiasis -Invasive candidiasis can be (1) candidemia (bloodstream infection) without deep-seated infection; (2) candidemia with deep-seated infection (typically eyes, kidney, or abdomen); and (3) deep-seated candidiasis in the absence of bloodstream infection (ie, hepatosplenic candidiasis). - risk factors (ie, neutropenia, indwelling vascular catheters, postsurgical). -The clinical presentation of candidemia varies from minimal fever to septic shock that can resemble a severe bacterial infection. - Consecutively positive (1,3)-beta-D-glucan results may be used to guide empiric therapy in high-risk patients even in the absence of positive blood cultures. -Hepatosplenic candidiasis can occur following prolonged neutropenia in patients with underlying hematologic cancers, but this entity is less common in the era of widespread antifungal prophylaxis. Typically, fever and variable abdominal pain present weeks after chemotherapy, when neutrophil counts have recovered. Blood cultures are generally negative. D. Candidal Endocarditis -Candidal endocarditis is a rare infection affecting patients with prosthetic heart valves or prolonged candidemia, such as with indwelling catheters. The diagnosis is established definitively by culturing Candida from vegetations at the time of valve replacement. Treatment: A. Mucosal Candidiasis Vulvovaginal candidiasis can be treated with topical or oral azoles. (fluconazole, clotrimazole, or miconazole. Options for patients with fluconazole-refractory disease include oral itraconazole solution, oral or intravenous voriconazole, or an intravenous echinocandin; Posaconazole tablets, 300 mg/day, may also be considered for fluconazole-refractory disease. Relapse is common with all agents when there is underlying HIV infection without adequate immune reconstitution. B. Candidal Funguria Candidal funguria frequently resolves with discontinuance of antibiotics or removal of bladder catheters. When symptomatic funguria persists, oral fluconazole. Newer generation azoles (eg, voriconazole) and echinocandins are NOT considered standard therapy for candidal urinary tract infections due to low levels of active drug in the urine. C. Invasive Candidiasis intravenous echinocandin as first-line therapy ie, caspofungin , micafungin, or anidulafungin Intravenous or oral fluconazole is an acceptable alternative for less critically ill patients without recent azole exposure. Voriconazole is also effective for candidemia but offers little advantage over fluconazole unless infection is due to fluconazole-resistant isolates. Therapy for candidemia should be continued for 2 weeks after the last positive blood culture and resolution of symptoms and signs of infection. D. Candidal Endocarditis Best results are achieved with a combination of medical and surgical therapy (valve replacement). Lipid formulation amphotericin B or high-dose echinocandin (caspofungin 150 mg/day, micafungin 150 mg/day, or anidulafungin 200 mg/day) is recommended as initial therapy. Step-down or long-term suppressive therapy for nonsurgical candidates may be done with fluconazole at 6-12 mg/kg/day for susceptible organisms. E. Prevention of Invasive Candidiasis In high-risk patients undergoing induction chemotherapy, bone marrow transplantation, or liver transplantation, prophylaxis with antifungal agents has been shown to prevent invasive fungal infections, although the effect on mortality and the preferred agent remain debated. Although the isolation of Candida species from mucosal sites raises the possibility of invasive candidiasis among critically ill patients, trials of empiric antifungal agents in such situations have not shown clear clinical benefit.

Infective Endocarditis (IE) what is it, cause, categories, pathophys, risk factors, what valves affected, MC/2nd MC bacteria (in all, in IVDU, community-acquired), community-acquired triad, top 3 MC findings, 3 other import findings, dx (MC, gold standard, practical and how, criteria, ***tx, ***prophylaxis (who and what)

General -Infection of endocardium; Primarily affects the valves -Usually bacterial (may be viral or fungal) -categorized: native valve vs prosthetic valve Pathophys -Endocardial damage --> Platelet & fibrin aggregation (sterile vegetation) --> bacteria lands on aggregation (called vegetation seeding) --> bacteria proliferates --> spreads/Metastatic infection to organs and brain -Risk factor: underlying conditions (**IVDU, **prosthetic valve, shunt, *prev IE, heart surgery, congenital, HIV, pacemaker, IV catheter/nutrition) -***mitral valve MC affected (like in rheumatic fever), but in IVDU tricuspid valve is MC affected!!! -***Staph. aureus (MC in all except community-acquired), then in IVDU gram neg HACEK is 2nd (***KNOW IVDU are more prone to HACEK infec!!! which is gram neg so hard to grow in culture) -***In community acquired/splenectomy: MC = strep!!! and usu have "Osler's triad" ("Austrian syndrome": Endocarditis, Meningitis, Pneumonia) Clinical -can be acute (sudden sx over several days) or subacute (progressing wks/months) -***Fever (MC finding!!!), ***new murmur (3rd MC finding!), ***wide pulse pressure (systol BP-diastol BP), Malaise, Anorexia, Arthralgias/Mylagias/Arthritis -***examine skin and nails!!!: •Petechiae (conjunctiva, palate, and extremities) •Osler's nodes (painful nodules on palmar surfaces (pads) of fingers and toes) •Janeway lesions (hemorrhagic, nonpainful macules on palms and soles) •Splinter hemorrhages (nonblanching, linear, brownish/red lesions in nail beds) -***Fundoscopic exam: Roth's spots! (Areas of hemorrhage with white central dots) -4 complications: valve/local damage, emboli (can see in R lung on chest x-ray if aspirated), spread to diff organs, circulating immune complexes to other organs) Dx -***elevated ESR (2nd MC finding!!) -***gold standard = culture of tissue (but not practical unless in valve replacement) -***blood cultures and echocardiogram (clinical criteria) more practical!! •***(KNOW; ON EXAM): suspect endocarditis --> order echo!!!! •***cultures: 3! sets from diff sites over @ least an hour! •HACEK hard to grow! -***DUKE criteria: ****2 majors, or one major and one minor, or 3 minor!!!; v diff than rheumatic fever) -CBC w differential (leukocytosis, bandemia, anemia of chronic disease) -renal assessment (UA, Cr/BUN) -rheumatoid factor -chest x-ray -ECG: prolonged PR interval Tx -****Broad spectrum antbitocs for up to 4-6 weeks!!** (***Combo that always includes Gentamicin!!!! (KNOW!!))!!! -surgery if (Symptomatic CHF, Fungal or pseudomonal IE, Myocardial abscesses) -antibiotic prophylaxis only in ***high-risk pts!!! doing I&D, or GI/GU procedures w infec •high-risk pts: prosthetic valve, prev IE, congenital heart disease, cardiac transplant w valve issues •***prophylaxis: 2mg Amox 1 hr before procedure!!; if pen allergy, Clinda 600mg 1hr before procedure!!

Acute otitis media (AOM)

General -Infection of middle ear, temporal bone, & mastoid air cells (the classic ear infection) -Bacterial infection of the mucosally lined air-containing spaces of the temporal bone; Often preceded by URI, eustachian tube dysfunction -Acute otitis media: rapid onset + signs of symptoms of inflamm -Risk factors: peak age 6-18 months (Eustachian tube in children is shorter, narrower, & more horizontal), day care, pacifier or bottle use, second-hand smoke, not being breastfed -4 most common organisms: ***Strep neumo most common!, H. influenzae, Moraxella catahhralis, Group A Strep (same organisms as in Acute sinusitis) Pathophysiology -***Most commonly preceded by viral URI!, leading to blockage of Eustachian tube Clinical -Fever, ***otalgia! (ear pain), ***ear tugging in infants!, stuffiness, conductive hearing loss, aural pressure -Tympanic membrane rupture: rapid relief of pain + otorrhea (usu heals in 1-2 days) -***Bulging & erythematous tympanic membrane (TM) with effusion!, loss of landmarks -Pneumatic otoscopy: ***decreased TM mobility (most sensitive)! Diagnosis -Clinical -Tympanocentesis for a sample of fluid for culture definitive (eg, in recurrent cases) Treatment -Observation can be done depending on age and severity. Children over age of 2 should receive antibiotics if the diagnosis is certain and the infection is severe -Symptomatic -->Analgesics -***Amoxicillin initial antibiotic of choice -second-line: amoxicillin-clavulanic acid, Cefuroxime, Cefdinir, Cefpodoxime -penicillin allergy: azithromycin, clarithromycin, erythromycin-sulfisoxazole, trimethoprim-sulfamathoxazole -severe or recurrent cases: myringotomy (surgical drainage) with tympanostomy tube insertion -in children with recurrent otitis media, may need an iron deficiency anemia workup & CT scan -Antibiotic treatment after 48-72 h of failure of initial antibiotic treatment -No follow-up needed -Complications: perforation or spread to temporal bone/mastoid, but these are not likely

Encephalitis general, pathophys (usu origin, 2 endemic causes), diagnostic test and findings and gold standard, tx

General -Inflammation of the brain parenchyma Pathophys -usu viral -2 endemic causes in US: HSV, Rabies Clinical -Fever, headache, altered level of consciousness, seizures Diagnosis -***CSF: looking for elevate proteins and wbcs but normal glucose! -later on can do EEG (should be abnormal) -head CT/MRI = Bilateral asymmetrical hypodense (swelled/edema) area in the temporal region with hyperdense focus -Gold standard is brain biopsy (but v rare, don't do) Tx -Acyclovir or any of the cyclovirs; IV 2-3 wks

Type I diabetes mellitus general (what is it), age onset, etiologies of types, clinical (4), tests for ketone bodies

General -Insulin deficiency due to pancreatic beta cell destruction -onset usu <30 yrs of age (3/4 diagnosed in childhood) Pathophys -Etiologies: Type 1A is autoimmune (MC) and Type 1B is non-autoimmune Clinical -Hyperglycemia without acidosis: MC initial presentation--polyuria, polydipsia, polyphagia -wt loss, lethargy -diabetic ketoacidosis: second MC initial presentation (MC in type 1) Diagnostics: - ketone bodies detected by nitroprusside tests (Acetest or Ketostix)

Pneumonia leading cause of what, ***(KNOW): MC cause, clinical (4), dx (5), tx!!

General -Leading infectious cause of death (US) (not of death overall) Pathophys -(KNOW!!!) MC cause: strep pneumoniae!!! (gram positive purple rods and chains!!!); also the MC cause of CAP requiring hospitalization!!! Clinical -***Fever, cough with sputum production (sputum color doesn't matter!), dyspnea with or without pleurisy -***probably NOT pneumonia if have rhinorrhea or sore throat, more of viral upper resp infec -***Elderly patients: may have few or no respiratory symptoms (e.g. ***confusion or abdominal pain) -**abdominal pain in kids and elderly!! Diagnostics -***mainly clinical diagnosis, but like to do tests (but don't delay tx waiting for results!) -Sputum for Gram stain and Culture (2 samples at diff times to ensure no contamination) -Blood cultures (used to be required but not anymore; Positive in only about 12% of pneumonia patients) - Urine antigen tests -***nasopharyng swab to r/o viral to use abx -***AFB staining from sputum! (2 samples usu separated 24-72 hrs) -***chest x-ray: location/pattern of infiltrate can help us identify organism but not definite!! (btw can take time before showing up so don't exclude quickly, and also takes very long to disappear/clear) -***CBC: LEFT SHIFT (increased leukocytes w increased bands)!!!!! ***Tx -Antibiotic Rx within ***4 hours of hospitalization (not like 30 mins like in meningitis though, but still fast) -***Cover atypical pathogens in ALL CAP ***Summary of abx tx: -OP (outpatient) without complications, low risk: •Doxycycline, macrolide -OP (outpatient) with comorbidities/IP CAP: •Macrolide and Beta-lactam, or •FQ -IP (inpatient) severe CAP: •FQ and Beta-lactam •Add Vancomycin or Linezolid if risk of MRSA ***Import details: -Duration: once fever goes away, wait 5 more days after that then stop the med -IP: IV then PO when pt can tolerate -OP: PO Btw/side note/key: -OP = outpatient -IP = inpatient -FQ = fluoroquinolone -FQ (end in "oxacine"), macrolide (ex. azithromycin), beta-lactam (amoxicillin, augmentin, etc.)

Graves Disease mc cause of what, mc in who, pathophys, clinical (6), diagnostics (2), tx (4)

General -MC cause of hyperthyroidism in the US -usu in women 20-40y Pathophys -Autoimmune disease - TSH-receptor autoantibodies target & stimulate the TSH receptor Clinical -symptoms of hyperthyroidism (eg, atrial fibrillation) -Ophthalmopathy: proptosis, exophthalmos, lid lag -Pretibial myxedema: (swollen red or brown patches) -enlarged nontender goiter -thyroid bruits -Onycholysis (separation of the nail from its bed) Diagnostics -Primary hyperthyroidism profile: decreased TSH + increased free T4 (or T3) - (+) Thyroid-stimulating immunoglobulins (TSH-receptor antibodies) Tx -***Radioactive iodines = MC therapy -***Thioamides/Thiourea drugs: Methimazole (usu preferred) or Propylthiouracil (preferred in first trimester & for thyroid storm) -***beta-blockers (eg, propranolol): rapidly ameliorate symptoms -Opthalmopathy: glucocorticoids best initial tx -other: iodinated contrast agents, lithium carbonate, thyroid surgery

Cushing's syndrome aka, 4 main causes, clinical, diagnostic tests (results for cushings disease and adrenal tumors/steroids), tx (general and for Cushing's disease)

General -aka Hypercortisolism -Cushing's syndrome: symptoms and signs related to cortisol excess -4 main causes: 1) long-term high-dose glucocorticoid therapy most common cause overall (exogenous) 2) Cushing's disease: pituitary gland ACTH overproduction (MC endogenous cause) 3) Ectopic ACTH-producing tumor (ex. small cell lung cancer) (endogenous) 4) Adrenal tumor (adenoma) Clinical -weight gain -central obesity, ***"moon face" (round puffy red face) -***striae (red/purple, 1cm wide) -***buffalo hump (between shoulders) -Acanthosis nigricans -HTN -muscle wasting -hirsutism (abnormal hair growth on face/body) -Psychological changes. -Osteoporosis -poor wound healing. Diagnostics -Baseline ACTH + High-dose Dexamethasone suppression test (result: Lack of normal suppression by dexamethasone) ▪Cushing's disease --> increased ACTH + suppression of cortisol on high dose ▪Adrenal tumor/steroids --> decreased ACTH -Labs: hyperglycemia, leukocytosis, lymphocytopenia, hypokalemia -salivary cortisol: Elevated serum cortisol and urinary free cortisol. Tx -corticosteroid use: gradual taper -Cushing disease: Transsphenoidal resection

Social anxiety disorder (formerly called Social Phobia) MC what, clinical (2), diagnostic criteria (2), DSM criteria, diagnosis (1), tx (2)

General -MC type of phobia (public speaking) -Fear of specific object or situation that are out of proportion to danger posed -Social phobias (social anxiety disorder) ´Global - all social situations are poorly tolerated ´Specific - fear of public speaking -Agoraphobia ´Fear of common places (grocery store, movies, being outside) ´*common in panic disorder ´*can be debilitating -Specific (simple) phobia ´Fear of a specific situation, object or place (heights, flying, snakes, blood, hospitals etc.) Clinical -Phobic object/situation/place is actively avoided due to intense fear or anxiety -Disabling fear out of proportion -diagnostic criteria: 1) persistent (at least 6 mos) intense fear of social or performance situation in which person is exposed to scrutiny of others 2) causes EXPECTED panic attacks -DSM criteria: `specific object or situation ` Diagnosis -Rule out medical causes of symptoms (cardiac, neurological, endocrine, respiratory, substance abuse related) `actively avoided `fear or anxiety is out of proportion `6 months or more `The fear, anxiety, or avoidance causes clinically significant distress or impairment in social, occupational, or other important areas of functioning. Tx -Pharmacologic therapy ´SSRIs (Paroxetine, Sertraline) ´SNRIs (Venlafaxine) ´Gabapentin is an alternative tx ´Beta blockers (Propranolol)--situational for performance anxiety & public speaking they can take when they know they will be doing those things -***Behavioral therapy! ´Relaxation techniques ´***Desensitization therapy/exposure therapy! ´Group therapy for social phobias

Acute Angle-Closure Glaucoma (Acute Narrow Angle-Closure Glaucoma)

General -Older population (farsighted individuals) -Increased incidence as individuals age, lens becomes thicker, cataracts develop -Farsighted individuals have a flatter cornea, narrower angle increasing incidence -Pre-existing narrow anterior angle ●Individuals who already have a shallow anterior chamber -Closure of angle is precipitated by pupillary dilation: ●Pt leaves dark movie theater, times of stress, medications that dilate pupils ●Medications: mydriatics, antihistamines, epinephrine, emotionally upsetting events, leaving a dim room (PPP: dim lights, anticholinergics, sympathomimetics) Clinical -***OCULAR EMERGENCY! -Rapid onset of ***severe eye pain! -***Vision loss!, or blurred vision -"Halos around lights" -Red eye -***Hazy, cloudy/steamy cornea! -***Dilated pupil (mydriasis), non-reactive to light! -***Eye is hard/firm on palpation! -Intraocular pressure is >50 (normal pressure 10-20mmHg) -Nausea/abdominal pain may occur -Frontal/orbital headache -PPP: ***loss of peripheral vision (aka tunnel vision) and mid dilated pupil Diagnosis -Measure the IOP (Tonometry) Treatment -Reduce the IOP ●IV Acetazolamide immediately, then PO acetazolamide (blocks production of aqueous humor) ●Timolol drops (blocks production of aqueous humor) ●Pilocarpine (facilitates outflow of aqueous humor) ●Reduce volume of aqueous humor (Mannitol) -Definitive treatment ●Laser peripheral iridotomy ●Surgical peripheral iridectomy

Panic disorder general, clinical (8) dx criteria (3), DSM criteria (2), diagnosis (2 including screening), tx (first-line)

General -Panic attacks: recurrent, unpredictable episodes of intense surges of anxiety accompanied by marked physiologic manifestations -Agoraphobia may be present -Commonly develops in those <25 -Females > males -Premenstrual period may be more common for symptoms -*Look for underlying medical condition -*Patients are at increased risk for depression and suicide -Alcohol and sedative abuse often result from self-treatment -*OCD is common in these patients -Acute and chronic emotional distress - physical, occupational, social dysfunction -Assess patients impression of the event Clinical -Dyspnea, tachycardia, palpitations -Dizziness, paresthesias, choking, smothering feeling, nausea -Seizure-like activity can occur -Feelings of impending doom -Chills/hot flashes, nausea, abdominal discomfort -Accompanied by chronic fear of recurrence of attack or a maladaptive change in behavior to try to avoid potential triggers -Recurrent sleep panic attacks can occur -Anticipatory anxiety develops and constricts daily activities -Dx criteria: 1) recurrent, unexpected panic attacks 2) at least 1 of the following must occur for at least 1 month: 1) ***panic attacks often followed by persistent concern about future attacks!, 2) persistent worry about implication of attacks, 3) signif maladaptive behavior related to attacks 3) Agoraphobia: anxiety about being in places or situations from which escape may be difficult -DSM criteria: 1) abrupt surge of intense fear or intense discomfort 2) 4 (or more) of the symptoms occur 3) At least 1 of the attacks has been followed by 1 month (or more) of 1 or both of the following: ´Persistent concern or worry about additional panic attacks or their consequences (eg, losing control, having a heart attack, or "going crazy") ´A significant maladaptive change in behavior related to the attacks (eg, behaviors designed to avoid having panic attacks, such as avoidance of exercise or unfamiliar situations) Diagnosis -Rule out medical causes of symptoms (cardiac, neurological, endocrine, respiratory, substance abuse related) -PADIS (Panic Disorder Screener) Tx -***pharmacotherapy + CBT most effective! -SSRI (Fluoxetine, Paroxetine, Sertraline) -SNRI (Venlafaxine) -consider Benzos for acute panic attacks -Beta blockers (propranolol) -Cognitive behavioral therapy

HIV what is it/what does it attack and how, infectiousness, clinical, Diagnosis (4), Tx (1)

General -RNA virus -Lipid/fatty membrane bilayer -attaches to cd4 Pathophys (import for understanding tx) -HIV virus finds cd4 cell in host, its proteins attach to outer layer of cd4 cell, and docks/sits like spaceship and expels rna inside cd4 by uncoating - rna is then converted to dna now floating around and integrated into host dna, so when host copies its dna it copies the hiv dna along with it -Hiv dna has several copies, can then be recoated, merge with membrane, then bud off as new virus, that's how it reproduces -Always infectious if you have it, does not become dormant -don't have to have the symptoms to spread it to people (Clinically latency does not equal viral latency) Clinical -acute retroviral syndrome: symptoms look like mono (flu-like) Diagnosis -***On average, HIV infection leads to loss of 50-100 cd4 cells/yr if untreated -Rises routinely seen with effective antiviral therapy, rarely to normal -***initial large rise in virus and drop in cd4, then evens out and feel better for while; then months and yr s later they do the same thing about the same number and then immunocompromised; (***KNOW): when drop below 200!!!!!! cd4 count, now it's AIDS) -HIV antibody (confirm with ELISA screening followed by Western Blot for confirmation; shows if been exposed, doesn't give you immunity to it though, and doesn't say whether have it now or no) -HIV rapid testing (used for screening; confirm with EIA and Western blot; says you've been exposed, not whether have it or not) -***CD4 cell count (but can be undetectable w therapy or can be artificially high temporarily with concurrent illness) -HIV Viral Load (VL; how much virus there is) and typing (to tell if type 1/2) •***gold standard = viral load!!! (PCR) (higher viral load indicates more likely to have more difficult clinical course) -***4th generation rna test!!! -LFTs -Genotypic resistance test -STI screen -Lipid panel Tx -***ART/HAART (highly active antiretroviral therapy): Initial 2 nrti's + 1 nnrti OR boosted PI OR raltegravir/INSTI (***so will always bs 2 NRTI's!!!) •Initiate when CD4 count <500 cells/mm3 or w/ anyone willing to start sooner at higher CD4 count

Influenza general (molecule), ***types (based on what?) and ***features, ***pathophys (transmission KNOW), diagnosis (2), ***tx (what you will use/dose KNOW, categories of antivirals KNOW)

General -RNA, single-stranded -Three basic types of influenza virus: A, B, C (don't worry about C!) •A is more pathogenic than B and is found most commonly in humans and avian species -Typing of influenza is based on identification of hemagglutinin (H) and neuraminidase (N); need both to be infected -human pandemics (A), human epidemics (A & B), antigenic changes (A shift and drift, B and C only drift) -The 1918 influenza pandemic killed more people than died in WWI (mostly killed young adults) Pathophys -***(KNOW): Transmitted via large particle respiratory droplets!! -Incubation period is 1-4 days Clinical -severe cold symptoms Diagnosis -Rapid flu test done on throat or nasal swabs -if cough for long time do chest x ray to rule out secondary pneumonia Tx -Prevention is key! Vaccinate -supportive -antiviral (Oseltamivir and zanamivir; keep in mind local antiviral resistance patterns) •***(KNOW) Oseltamivir (Tamiflu) 75mg BID (twice a day) for 5 days!!! •***(KNOW) there are 2 categories (neuroaminidase inhibitors and Adamantanes); neuroaminidase inhib is what you'll use!! they work on types a and b (while adamantanes only work on type A) and includes tamiflu (Oseltamivir; cheapest, most readily avail)

Hyperthyroidism aka, what does it entail, MC cause, clinical (13, focus 5), diagnosis (2), tx (2)

General -aka thyrotoxicosis -The term "thyrotoxicosis" refers to the clinical manifestations associated with elevated serum levels of T4 or T3 that are excessive for the individual (hyperthyroidism). Pathophys -Graves disease is most common cause of hyperthyroidism Clinical -Sweating, weight loss or gain, anxiety, palpitations, loose stools, heat intolerance, menstrual irregularity. -Tachycardia -***warm, moist skin -***stare -tremor. - ***palpable goiter (sometimes with bruit) -***Cardiopulmonary manifestations -***ophthalmopathy (Eye manifestations) Diagnosis -Suppressed TSH in primary hyperthyroidism; usually increased T4, FT4, T3, FT3. Tx -Propranolol for cardiac symptoms -Thiourea drugs (Methimazole or propylthiouracil) for young adults or mild cases

Rabies reservoir and not reservoir, transmission depends on, clinical (3 phases)

General -Reservoir: Bats, skunks, raccoons, wolves: highest risk; Cat > dogs (b/c of raccoons); Rodents, rabbits, farm animals can harbor the virus but no reports of human transmission -Birds and reptiles do not carry virus Pathophys -Transmission depends on: •Number of bites •Distance from CNS •Presence of virus in animal's saliva -Entry via peripheral nerve; Amplified in skeletal muscle Clinical -3 Phases: 1) Prodrome: (2-14 days) •Irritation/paraesthesia at original bite •Flu-like symptoms 2) Acute neurologic phase: Classic "furious" •Encephalitis: Fever, altered personality, agitation, hallucinations 3) Acute neurologic phase: Paralytic "dumb" •Ascending paralysis ***Infectious Disease**** General -RNA virus, Lyssavirus genus -Mortality rate is 100% after the virus enters motor and sensory axons Pathophys -Transmitted via saliva or aerosolized secretions (not necessarily by bite from rabid animal) Clinical -neuro and muscular, fever and chills, GI, pain/itching at bite, resp symp in late stage -2 stages: 1) neurological (hydrophobia: can't drink water) and 2) coma Dx -involves public authorities -WBC elevated, increased/atypical monocytes, albuminuria, pyuria, viral cx, PCR saliva, CSF, imaging if indicated -***on autopsy: Brain tissue will show Negri bodies!! Tx -wound: clean, debride, explore, keep open -consider abx -administer human rabies immunoglobulin (half in wound, half in gluteal area IM) -rabies vaccine series IM in deltoid (day 0, 3, 7, and 14; if immunocompromised add day 28 dose; just 0 and 3 if had vaccine before); safe in preg -pre-exposure prophylaxis

Syphilis what is it, transmission, rx factors, categories and symp, dx (4), ***tx (KNOW THIS!)

General -STI -transmitted in utero (and early on, can infect through intact skin) -TORCH disease (Toxoplasmosis, Other (syphilis, chickenpox, HIV), Rubella, CMV, Herpes 2) -Categories: •Early: primary (within 3 wks), secondary (within 10 wks), latent (about 1 yr) •Late: latent (>1yr, can last 25 yrs)), tertiary •Neurosyphilis: early, late Pathophys -Risk fx: unprotected intercourse, promiscuous intercourse, IVDU, HCW, MSM -spirochete: Penetrates intact or microscopic abrasions on the skin→lymphatics→blood stream (a few hours), spirochete binds to endothelial cells Clinical -Early primary: painless chancer that can get infected, infectious! -Early secondary: rash on palms and soles!, infectious! (do not shake hands, wear gloves, as this stage can still infect through intact skin!) -Early latent: serologic testing shows you have it, but no symptoms (after resolution of previous symptoms) -Late latent: asymptomatic, not infectious except in utero, if not told assume in this phase! -Tertiary: jaundice, anemia, CNS symptoms, gummas (within 3-10 yrs of infec, MC on leg below the knee), noninfectious -Neurosyphilis: Argyll Robertson pupil (small irregular pupil that reacts normally to accommodation but not to light; widens instead of constricts to light; way to remember: syphilis common in prostitutes, prostitutes accommodate don't react) Dx: -Non-treponemal tests (screening, so done first, then if positive go to next one) •***RPR •***VDRL -Treponemal tests (look for spirochete itself) •***FTA-ABS •MHA-TP -***ALL stages are highly sensitive to all these test! -***Darkfield microscopy -***must do LP! Tx -***(KNOW THIS!!!): Penicillin G 2.4 million units and single dose!!!!!!! (IM 1.2mU in each cheek total 2.4); late latent same but weekly for 3 wks rather than single dose

Bacterial conjunctivitis

General -Staph, Strep, Haemophilus, Pseudomonas, Moraxella Clinical -***Purulent drainage! -Eye crusted shut in AM -Mild discomfort -10-14 days if untreated, treatment shortens course -Painless -Unilateral or bilateral -Chemosis (edema or conjunctiva) Diagnosis -Clinical -Swab of drainage if suspected gonococcal or chlamydial or severe or recurrent infection Treatment -**Topical abx! ●Polymyxin b and trimethoprim ●Erythromycin ointment -If no improvement in 48-72 hrs needs referral to ophthalmologist -Contact lens wearers - no contacts until resolution of infection/abx course completed, dispose of current contacts, disinfected contact lens case ●***Must be given a fluoroquinolone! to cover for pseudomonas, so would be given a topical fluoroquinolone

Tetanus what is it, what causes it and how, wounds of concern, ***clinical (KNOW), dx, ***tx

General -a bacterial disease marked by rigidity and spasms of the voluntary muscles -"Lockjaw"; trismus -bug causing it: C. tetani; releases toxins that act on CNS, anaerobic -causes opisthotonos (arching of back due to involuntary spasm of muscles, can lead to spine fracture) Pathophys -C. tetani: •Spores are found in soil, animal feces •Enters through wounds -tetanus-prone wounds: •Wounds over 6 hours •Greater than 1 cm deep •Stellate lacerations •Medical conditions that impair wound healing •Soiled with feces, saliva, gunshot, puncture, burn, frostbite Clinical -***Generalized (KNOW that generalized is the most common!!!): follows a descending pattern, trismus→neck stiffness→dysphagia→abd muscle rigidity •Fever, diaphoresis, hypertension, tachycardia Dx -clinical! culture not needed/hard to show bc anaerobe Tx -***Wound care: remove necrotic tissue and FB -***Manage airway; treat HTN; supportive measures -***TIG (tetanus immunoglobulin) -***Tetanus toxoid (in ***TDap vaccine; Give boosters every 10 years; nearly 100% efficacy!!!; DTap at 2,4,6,15-18mos, then 11-12yo, then every 10 yrs) •clean and had within 10 yrs --> no need •dirty --> stay on safe side and give UptoDate says: •clean/minor: give vaccine if previously had less than 3 doses or unknown, or if last dose was given >10yrs ago; no need for immunoglobulins •other wounds: give vaccine and immunoglobulins if previously had less than 3 doses or unknown, or give only vaccine if 3 or more doses previously but last dose was more than 5 years ago

Parasomnias what is it more common in who, 4 examples, tx of each

General -abnormal behaviors during sleep - fairly common in children but less so in adults. -examples: 1) sleep terror (pavor nocturnus): abrupt, terrifying arousal from sleep 2) nightmares: occur during REM sleep, so sleep terrors in stage 3 or 4 sleep 3) sleepwalking (aka Somnambulism): ambulation or other intricate behaviors while still asleep, with amnesia for the event 4) enuresis: involuntary micturition during sleep in a person who usually has voluntary control Tx -sleep terrors and sleep walking/Somnambulism --> benzodiazepines (eg, diazepam at bedtime) -Enuresis --> 1) desmopressin nasal spray (an ADH preparation) is tx of choice 2) may also respond to imipramine at bedtime 3) Behavioral approaches (eg, bells that ring when the pad gets wet) have also been successful.

Adrenal (Addisonian) Crisis aka, general, MC cause, clinical (main), diagnostic findings (3), tx

General -aka Acute Adrenocortical Insufficiency -sudden worsening of symptoms of someone with chronic adrenal insufficiency, ***precipitated by "stressful" event! Pathophys -MC cause: abrupt withdrawal of glucocorticoids (esp without tapering) Clinical -Shock primary manifestation - hypotension, hypovolemia Diagnosis: -Labs: hyponatremia, hyperkalemia, hypoglycemia Tx -Isotonic fluids (normal saline or D5NS) + IV hydrocortisone (if known Addison) OR Dexamethasone (if undiagnosed)

Diabetes insipidus general (what is going on), 2 types (MC) and their cause, clinical (4), diagnosis (3, 6 findings), tx for 2 types (2 each)

General -inability of kidney to concentrate urine --> production of large amts of dilute urine -2 types: 1) central: no production of ADH (MC type) 2) Nephrogenic: partial or complete renal insensitivity to ADH. Medications (Lithium). Hypokalemia. Clinical -Polyuria (up to 20 L daily) + polydipsia -Neurologic symptoms of hypernatremia -hypotension Diagnosis -labs: increased serum osmolarity, decreased urine osmolality & specific gravity, increased urine volume, hypernatremia if severe -***Fluid deprivation test: establishes diagnosis if DI! (DI = continued production of large amts of dilute urine--low urine osmolality) -Desmopressin (ADH) stimulation test: distinguishes central from nephrogenic ▪Central = reduction in urine output + increase in urine osmolality ▪Nephrogenic = continued production of large amts of dilute urine Tx -Central: ▪Mild --> no treatment other than adequate fluid intake and reduction of aggravating factors (eg, corticosteroids) ▪Desmopressin (DDAVP) first-line: intranasal injection or oral -Nephrogenic: ▪correct underlying cause (sodium and protein restriction) ▪Hydrochlorothiazide, Indomethacin, or Amiloride if symptoms persist

Meningitis what is it, acute v chronic time, MC and 2nd MC bacterial agents, risk factor, clinical (triad and tests), diagnosis (4), tx (bacteria, viral, parasitic, fungal)

General -inflammation of meninges -chronic = >4 wks; less than that is acute Pathophys -MC bacterial agents: #1) ***Strep pneumo!, #2) N. meningitidis -MC viral agent: Enteroviruses!; herpes simplex is 2nd -ex. of parasitic agent: Naegleria fowleri (in lakes in the south, go into nose then brain then death) -Risk factor: lack of splenic function (***Howell Jolly bodies on peripheral smear!!) Clinical -***triad: fever, headache, neck stiffness (99% of the time have at least 1 of these!) -positive Brudzinski or Kernig's signs (pain should be in center of neck not on sides!) -Jolt Accentuation Test positive (increase headache when shake head) Diagnosis -CBC with diff (elevated white count w left shift) -Blood cultures (do this before treating with antibiotic for bacterial!!) -CSF studies •i.e. Lumbar puncture (LP) -Radiology •CT Head (do before LP in pts that are not very alert/oriented, mass lesion, or v high ICP!) •MRI Tx -bacterial: antibiotic (*****Vanco plus a cephalosporin like Ceftriaxone for 10 days; start IV then oral when pt can tolerate it/stabilizes!!!!) ***plus a corticosteroid CONCURRENTLY (Dexamethasone in adults, Decadron in kids)!!! •can add ampicillin in complicated pts (preg, HIV, alcohol, elderly, transplant), and can change Ceftriaxone to Ceftazidime for pseudomonal coverage •give antibiotics within 2 hrs of arrival (optimal = 30 mins) -viral: supportive tx -fungal: anti-fungal -parasitic: anti-parasitic

Type II diabetes mellitus general (what is it), risk factors (2), clinical (6), tx (2)

General -insulin insensitivity (resistance) & relative impairment of insulin secretion Pathophys -risk factors: genetic & envir factors (esp obesity greatest risk factor & decrease phys activity), family history (of diabetes or CHAOS: chronic HTN, atherosclerosis, obesity (central), stroke) Clinical -classic symptoms: polyuria, polydipsia, polyphagia -poor wound healing, increased infections -obese, Acanthosis nigricans -hyperglycemic hyperosmolar syndrome Tx -Diet, exercise, and lifestyle changes initial management -oral antihyperglycemic medications if lifestyle changes aren't enough (eg, ***Metformin!!! initial/first-line therapy in most; sulfonureas like Tolbutamide)

Narcolepsy what is it, clinical (4), dx (2), tx

General -long-term neurological disorder characterized by decreased ability to regulate sleep-wake cycles Clinical -chronic daytime sleepiness -cataplexy -hypnagogic hallucinations -sleep paralysis Diagnostics -polysomnography -multiple sleep latency (the naps usu include sleep onset rapid eye movements) tx -stimulant: dextroamphetamine sulfate, Modafinil, or armodafinil (keep in mind that modafinil can reduce efficacy of other drugs like contraceptives)

Thyroid crisis / storm (Thyrotoxic crisis/thyroid storm) general (cause), symptoms (3), diagnosis (1 test, 2 findings), tx (6, what to avoid)

General -potentially fatal complication of untreated thyrotoxicosis usu after a precipitating event (ex. surgery, trauma, infec, pregnancy) Clinical -Hyperthyroid symptoms ▪Cardiovascular dysfunction: palpitations, tachycardia, atrial fibrillation, CHF ▪high fever, tremors ▪CNS dysfunction Diagnosis -Primary hyperthyroid profile: increased free T4 or T3 + decreased TSH (may be so low it's undetectable) Tx -IV fluids + propanolol + antithyroid medication (eg, Propylthiouracil preferred, methimazole) + IV Glucocorticoids (hydrocortisone) -followed by oral or IV sodium iodide -Antipyretics (but AVOID ASPIRIN) -Cooling blankets

Bipolar II disorder diagnostic criteria, first line tx

General -recurrent major depressive episodes with hypomania Clinical -diagnostic criteria: 1) history of ***at least 1 major depressive episode! + at least 1 ***hypomanic! episode (any current or prior manic episode makes the diagnosis bipolar I) 2) Hypomania < 1 week, does not require hospitalization, not associated with marked impairment of social/occupational function Tx -Mood stabilizers: Lithium first line (also decreases suicide risk) or second generation (atypical) antipsychotics (Risperidone, Olanzapine)

Bipolar I disorder strongest risk factor, diagnostic criteria (2), first-line therapy

General -risk factors: family history (1st degree relatives) strongest risk factor (10 times more likely), men = women Clinical -diagnostic criteria: 1) at least 1 Manic or mixed episode (only requirement) 2) mania = abnormal & persistently ***elevated, expansive or irritable mood at least 1 week! (or less if hospitalized) with ***marked impairment of social/occupational function! -- at least 3: ***mood! (euphoria, irritable, labile, dysphoric), ***thinking! (racing, flight of ideas, disorganized, easily distracted, expansive or grandiose thoughts--highly inflated self-esteem--, impaired judgment--spending sprees--), ***behavior! (physical hyperactivity, pressured speech, decreased need for sleep--may go days without sleep--, increased impulsivity, excessive involvement in pleasurable activities including risk-taking, hypersexuality, disinhibition. & increased goal directed activity) Tx -mood stabilizers: ***Lithium first-line (acute or long-term; also decreases suicide risk)! -2nd gen (atypical) antipsychotics: Risperidone or Olanzapine > Haloperidol) can be used for acute too -Psychotherapy -antidepressant therapy can be used with mood stabilizers but may precipitate mania or hypomania

Hypothyroidism general, MC cause, clinical, dagnosis (2), Tx (1)

General -underactive thyroid Pathophys -Hashimoto thyroiditis = MC cause Clinical -Fatigue, cold intolerance, constipation, weight change, depression, menorrhagia, hoarseness. -Dry skin, bradycardia, delayed return of deep tendon reflexes. Diagnosis -FT4 level is usually low. -***TSH elevated in primary hypothyroidism (disease in thyroid) and decreased in secondary hypothyroidism (disease in pituitary or hypothalamus) Tx -***Synthetic levothyroxine!

Oral candidiasis (oropharyngeal candidiasis - thrush)

General: -Opportunistic infection (infants, denture wearers, chronic corticosteroid users, pt's on antibiotics, immunocompromised host (AIDS, chemo, DM) -Inflammation and edema of underlying epithelium Clinical: -Difficult to tolerate hot/cold beverages and solid food -Tongue may be de-papillated, shiny and smooth -Can occur on any mucosal surface -***White patches that leave a raw, inflamed area when rubbed off! -Painful -Mucosa may be normal or erythematous Diagnostics: -KOH Prep if unsure (spores) -Usually a clinical diagnosis -If recurrent, see if they have HIV, check blood sugar (to check for diabetes), and can also do CBC to check WBC count to see if neutropenic Treatment: -Topical Clotrimazole or PO Anti-fungal therapy (Fluconazole) -If severe or if tx fails = IV amphotericin B Patient Education: - For recurrent oral thrush: 1) Oral hygiene, 2) make sure to use inhaler/spacer to ensure med is going all the way in their throat, and 3) antibiotics ***Infectious Disease*** General -Fungal infection caused by overgrowth of yeast (candida albicans) -CD4 200-500 Clinical -***beefy red tongue, angular cheilitis (fissuring of corners of mouth), thick white patches on oral mucosa and sometimes extend to esophagus, painful swallowing! -can cause sore throat -can mimic MI (chest pain and SOB) Diagnostics -clinical diagnosis, but ***ALWAYS do cd4 count no matter what!!!!*** but don't need to wait to treat after results come back, can treat right away -can do KOH -if esophageal involvement is suspected, endoscopy is helpful Tx -***Fluconazole 100mg PO QD x 1-2 weeks; 2-3 weeks if esophageal involvement!!! -no prophylaxis -Symptom management with miracle mouthwash to protect gag reflex! (before/after eating)

Iron deficient anemia general (MC what), 2 causes, who's at risk, symptoms (3 unique), CBC & iron, 3 treatments

General: -***most common cause of anemia worldwide! -microcytic -lack of iron/ferritin --> low RBC production (as bone marrow needs iron to make hemoglobin) -Iron deficiency: serum ferritin is less than 12 ng/mL (27 pmol/L) or less than 30 ng/mL (67 pmol/L) if also anemic. -Caused by bleeding unless proved otherwise. Pathophysiology: -Etiologies: ●***Chronic blood loss: most common cause in US (ex. colon cancer) ●Decreased absorption: ***diet (most common cause in world!) -Risk factors: ●ppl with increased metabolic needs (kids, pregnant, lactating women) ●Cowmilk ingestion in toddlers/infants Clinical: -classic anemia symptoms: fatigue, weakness, exercise intolerance, dyspnea -CNS: ex. poor concentration -***Pagophagia!: craving for ice -***Pica: appetite for non-food (ex. clay, starch) -***Koilonychia: spooning of nails -smooth tongue, brittle nails, and cheilitis Diagnosis: -CBC: ***microcytic hypochromic anemia classic, increased RDW! -Iron studies: ***decreased ferritin, increased TIBC, decreased transferrin saturation! -Bone marrow for definitive diagnosis (rare) Treatment: -***Iron replacement! -***vitamin C (ascorbic acid)! -- with water or orange juice & on empty stomach! -life-threatening --> red blood cell transfusion Pt education: -Adverse effects: GI effects

Folate deficient anemia cause (2, 1 is MC), clinical (how to distinguish from B12), diagnostic test (4 findings), tx

General: -causes ***abnormal DNA synthesis Pathophysiology: -Etiologies: ●***inadequate intake: most common cause (eg, alcoholics, unbalanced diet) ●***impaired metabolism: methotrexate, trimethoprim Clinical: -***similar to B12 deficiency but without neurologic abnormalities Diagnosis: -***CBC with peripheral smear: increased MCV (macrocytic anemia) + megaloblastic anemia (***hypersegmented neutrophils, macro-ovalocytes) -***increased homocysteine, normal methylmalonic acid Treatment: -oral folic acid, parenteral if severe deficiency -in B12 def., folate may help anemia but neuro symptoms may worsen Pt education:

B12 (cobalamin) deficient anemia cause, type of anemia, smear, causes, symptoms, 3 diagnostics, tx

General: -sources of B12: ***mainly animal in origin -absorption: ***combines with intrinsic factor, where it's absorbed mainly in distal ileum -***macrocytic anemia! Pathophysiology: -Etiologies: ●decreased absorption: pernicious anemia most common cause, Crohn disease, chronic alcohol use, H2 blockers & PPIs, Metformin ●decreased intake: ***vegans! Clinical: -anemia symptoms ***similar to folate but associated with neurologic abnormalities! -hematologic: fatigue, exercise intolerance, pallor -epithelial: glossitis, diarrhea, malabsorption -***Neurologic symptoms: symmetric paresthesias (burning/pricking feeling) most common initial symptom, spinal cord demyelination, & degeneration: vibratory, sensory, & proprioception deficits, decreased reflexes! Diagnosis: -CBC: ***increased MCV (macrocytic anemia), hypersegmented neutrophils, macro-ovalocytes!, usu normochromic or with hypochromic RBCs if associated with iron deficiency -***increased homocysteine -***increased methylmalonic acid (distinguishes B12 from folate deficiency) Treatment: -B12 replacement: oral, sublingual, nasal, IM/SQ -***start with IM B12 for anemia and neurological symptoms! (***pernicious anemia: lifelong IM therapy or high-dose oral therapy)! -dietary deficient: oral B12 replacement (after IM/SQ and deficiency initially fixed) Pt education:

Varicella-zoster virus infections

Varicella (Chicken Pox) -Varicella zoster virus (VZV) infection lasts about 7-10 days -***Diffusely scattered vesicles on an erythematous base (***dew drop on rose petal) -***Can be extensive and severe, especially in adult/neonatal causing ***pneumonia or encephalitis -Confirm diagnosis with Tzanck prep, or direct fluorescent antibody (DFA) test -Vaccination (Varivax) available, live vaccine. Treat with Acyclovir Herpes zoster (shingles) -Herpes zoster (shingles) is caused by an eruption of latent varicella zoster virus (VZV) -The clues to the diagnosis of shingles are: ●***Dermatomal (zosteriform) eruption on one side of the body; multiple dermatomes can be involved ●***Grouped vesicles on an erythematous base are typical of the herpes family of viruses, including VZV ●Shingles appears most often on face or trunk but can be anywhere ●***Usually preceded by ***pain or burning! ●***Generally shingles occurs only once in the immunocompetent, in contrast to ***herpes simplex virus (HSV), which frequently recurs! ●***Ophthalmic zoster: Vesicles on the tip of the nose or on the side of the nose (called ***Hutchinson's sign!), precedes the development of ophthalmic herpes zoster bc ophthalmic branch of the trigeminal nerve innervates both the cornea and the lateral dorsum of the nose as well as the tip of the nose.; Ocular complications occur in approximately one half of patients with involvement of the ophthalmic division of the trigeminal nerve, such as mucopurulent conjunctivitis, episcleritis, keratitis and anterior uveitis. ●Shingles cannot be passed from one person to another. However, the virus that causes shingles, the varicella zoster virus, can be spread from a person with active shingles to another person who has never had chickenpox. In such cases, the person exposed to the virus might develop chickenpox, but they would not develop shingles. ●Most common problem: Post-Herpetic Neuralgia; can cause pain, numbness, itching, and tingling; can last for months — or even years; may have fatigue, little appetite, and trouble sleeping; Sometimes experience intense pain from something as harmless as a light touch; most likely in People over age 60; Antiviral treatment within 72 hours, lessens the duration and severity of PHN; Gabapentin (Neurontin) is FDA approved to control neuropathic pain; Tricyclic antidepressants can be helpful in the treatment of postherpetic neuralgia. (e.g.amitriptyline/Elavil, or nortriptyline/ Pamelor); These drugs are best tolerated when they are started in a low dosage and given at bedtime. ●Treatment •Acyclovir 800 mg 5x/day for 7-10 days •Valacyclovir 1000 mg 3x/day for 7 days •Famciclovir 500 mg 3x/day for 7 days •Prednisone can be used to help with inflammation and pain •Consider antibiotics if you suspect secondary bacterial infection •Refer patient if immunosuppressed and/or more than two dermatomes are involved •Zoster vaccine recommended for individuals > 50 years old. ***Infectious Disease**** ***Chickenpox: General -DNA, double stranded, member of herpes virus group (HHV 3) -primary infec = chickenpox (varicella), and recurrent infec = herpes zoster aka shingles -falls under TORCH infections (Toxoplasmosis, Other (syphilis, VZV, parvovirus B19, zeka), Rubella, CMV, and Herpes) which lead to fetal malformations if momgets infected with them in first 20 wks of gestation Pathophys -Enters via the respiratory tract and conjunctiva (airborne and direct contact) -contagious 1-2 days prior to rash onset -Viremia occurs 4-6 days after infection and then spreads to other organs -Incubation period is 14-16 days (can take that long before manifest symptoms) Clinical -red macules/papules/***vesicles (classically described as dewdrop on a rose petal!!!!) always in order of head, then trunk then extremities!! could look like back acne Diagnosis -clinical diagnosis -ELISA to determine if a person has antibodies to VZV from past varicella disease -PCR is gold standard! Tx -vaccinate (Two doses: 12-15 months, then 4-6 yrs) and educate •Varicella vaccine and Combo MMR-VZV = live! (do not give live vaccine to 1) immunocompromised, 2) young age, 3) pregnancy, 4) fever) •VariZIG can be given to immunocompromised -supportive care, analgesics (not aspirin in kids bc rye!), cut fingernails. isolate from preg women/immunocompromised/unvaccinated kids, calamine lotion, oatmeal baths, acyclovir only if high risk ***Herpes Zoster General -secondary varicella zoster virus (HHV 3) Pathophys -Risk factors: stress, aging, immunosuppression, fetal exposure to VZV -occurs in people who had primary chicken pox, virus becomes dormant in spinal root ganglia, then reactivated in times of stress Clinical -Unilateral distribution of vesicular lesions along a sensory nerve; commonly involved 5th cranial nerve; start as maculopapular then turn into vesicles with crust; May last anywhere from 2-4 weeks -Complications: Post herpetic neuralgia (Persistent pain in the area where the rash once was), eye involvement (emergency!) Dx -***Tzanck smear and will see Giant multinucleated cell = textbook answer! -can do PCR but not v available -clinical diagnosis, viral culture if anything Tx -Burow's solution, calamine lotion, analgesics, antiviral like acyclovir within 72 hrs for 7-10 days -Prevention = vaccines: Zostavax and Shingrix for ages 50-59; don't give to pts with prolonged steroids, chemo, radiation, pts getting biologics, HIV/AIDS

Low reticulocyte anemia overview: Microcytic (4) Normocytic (6) Macrocytic (6)

microcytic (MCV<80): -iron def -Lead -Thalessemia -Early Anemia of Chronic Dz normocytic (MCV 80-100): -Anemia of Chronic Dz ●Renal ●Mixed Anemia ●Endocrine ●Dilutional ●Early Fe Def macrocytic (MCV>100): -folic acid(b9) def -b12 def -Liver disease -ETOH -Hypothyroidism -drug toxicity (from quizlet)

Lyme Disease

•most common vector-borne illness in the U.S. •caused by the bacterium Borrelia burgdorferi and is transmitted to humans through the bite of infected blacklegged ticks (deer tick) Ixodes scapularis or Ixodes pacificus •***Typical symptoms include fever, headache, fatigue, and a characteristic skin rash called ***erythema migrans! may appear 3-30 days after tick bite, looks like ***bull's eye!, starts off localized then can disseminate •Not all ticks carry borellia, and diff ticks need diff times to transmit disease to host •Lyme disease is diagnoses based on symptoms, physical findings (e.g., rash), and the possibility of exposure to infected ticks •If left untreated, infection can spread to joints, the heart, and the nervous system. •***Treatment: ***Doxycycline! 100 mg twice per day for 14 days (range 10 - 21 days). If allergy to Tetracycline: Amoxicillin 500 mg 3 times per day, or cefuroxime axetil 500 mg twice per day for 14 days (range 10 - 21 days). Prophylaxis - Doxy 200 mg one dose •***Lyme disease is a ***clinical diagnosis!—based on your medical history, symptoms and exposure to ticks. •sometimes use antibody tests like the enzyme-linked immunosorbent assay (ELISA) and the Western blot. The CDC recommends that doctors first order an ELISA to screen for the disease and then confirm the disease with a Western blot. but these tests are highly insensitive, so a negative test result does not mean you don't have Lyme. ***Infectious Disease*** Pathophys -Caused by the bite of a deer tick (Ixodes scapularis) which contains spirochete Borrelia burgdorferi and Borrelia mayonii -***Deer tick/ borrelia burgdoferi -Must be attached for 36-48 hrs Clinical -Incubation period 3-30 days (can go a month without presenting!) -early = ***erythema migrans bull's eye rash!! (Doesn't necessarily have to present where tick bit) and flu-like symptoms, late = joint pain, chest pain, SOB Dx -***Two tier testing-EIA/ELISA or IFA first then Western blot to confirm! -IgM spikes up upon exposure and then decreases by 2-3 weeks; IgG increases gradually upon exposure; so early will find IgM high and later will find IgG high Tx -***(KNOW THIS!!!): Doxycycline 100 BID PO x14-21 days -amoxicillin for kids -ceftriaxone in late stage -Analgesics and fever control -***(KNOW THIS): Give single dose of doxy 200mg!!!! IF all of these are true: •adult/nymph deer tick •Tick attached >36 hours (by degree of engorgement or time of exposure) •it is within 72 hours of tick removal •Local rate of infection of ticks with B. burgdoferi is >20% Pt educ -light colored long sleves -Check for ticks after being outdoors, including gear -DEET repellents