PANCE Study Guide PDF

Welcome to the first five weeks of the comprehensive PANCE study guide offered by ThePAPapers! This study guide includes all of the topics listed on the 15-week PANCE study plan in order, which encompasses all of the topics listed on the NCCPA PANCE content blueprint + a few topics adde...

Welcome to the first five weeks of the comprehensive PANCE study guide offered by ThePAPapers! This study guide includes all of the topics listed on the 15-week PANCE study plan in order, which encompasses all of the topics listed on the NCCPA PANCE content blueprint + a few topics added for comprehension. The information in this guide was collected from multiple sources and is considered up to date as of March 2023. If you see anything that needs to be updated within this guide, please reach out to me on Etsy and I will update it and send you a new copy for free. In making this guide, I have tried to include the bare basics of what you need to know for the PANCE. I have also included some of my own commentary on topics that are difficult to understand. I’ve included a key below of some of my shorthand and format tools. As always, happy studying! One last push before you are a PA-C! – ThePAPapers If a word/phrase is bold and highlighted = NEED TO KNOW, HIGH YIELD TOPICS that are known for showing up on the PANCE If a word/phrase is bold OR highlighted = good to know, likely to be on the PANCE OR I’m making a discernment of a topic that is high yield Hx = history Tx = treatment Sx = symptoms MC = most common MCC = most common cause ASA = Aspirin UA = urinalysis ABX = antibiotics RF = risk factor HA = headache N/V = nausea/vomiting HEENT TOPICS GLAUCOMA Type Chronic Open Angle Acute Angle Closure Overview -Idiopathic etiology – thought to be due to decreased outflow of -Idiopathic etiology – thought to be due to obstruction of aqueous fluid outflow aqueous fluid through the trabecular meshwork through the trabecular meshwork due to the angle of the anterior chamber  -Most common type of glaucoma -Eventually causes blindness and vision loss without treatment OPHTHLAMOLOGIC EMERGENCY Risk Factors -Increased intraocular pressure (IOP) -Anatomically shallow anterior chamber (such as seen in individuals of Asian or -Older age Inuit descent) -African American & Hispanic descent -Small eye shape -Family hx of glaucoma -Pupillary dilation (due to dark environment, physical or emotional stress, -Hx of diabetes or other eye disease (i.e., thyroid eye disease) medications or mydriasis for eye exams) -Thin cornea -Large cataracts -Uveitis -Uveitis -Trauma -Hemodialysis -Medication (i.e., corticosteroids) -Trauma TEST TAKING TIP: look for vignettes describing a patient coming out of a DARK movie theater (pupil dilation) with sudden onset unilateral eye pain Presentation Often asymptomatic -Acute onset of unilateral, SEVERE eye pain -Vision changes: tunnel vision, blurry vision, letters appearing -Vision changes – specifically, blurred, cloudy or “steamy” and describing “halos” faded, increased glare, needing more light to see around lights -Headache -Nausea/vomiting -May report hx of trauma to the eye Exam Eye will likely appear normal without injection or pupil -Injected sclera Findings abnormalities -Cloudy cornea FUNDUSCOPIC EXAM: optic disc pallor and cupping -FIXED or MID-DILATED pupil *RED EYE IS NOT ASSOCIATED WITH CHRONIC GLAUCOMA* -Eye will be FIRM to the touch on palpation Diagnostics DIAGNOSTIC CRITERIA -Diagnosed through clinical evaluation + measurement of IOP with Tonopen (Must have 2 out of 3 criteria): -optic disc to cup ratio >0.5 -diminished visual fields -IOP >21mmHg Treatment Refer these patients to Ophthalmology Consult ophthalmology EMERGENTLY TREATMENT OPTIONS: TREATMENT OPTIONS: -Meds: Topical prostaglandins (Latanoprost, Bimatoprost, -Meds: Acetazolamide Tafluprost), Topical beta-blockers (Timolol, Betaxolol) -Laser intervention: iridotomy and/or iridoplasty -Laser intervention: utilized to create more options for aqueous -Surgical: iridectomy, cataract extraction, shunting fluid outflow -Surgical: trabeculectomy, shunting  Conjunctivitis Type Viral Bacterial Allergic Overview Most common cause (MCC): adenovirus MCC: Staph species, Strep species, Pseudomonas, MCC: seasonal allergies -Other causes: Herpes simplex virus Moraxella, Chlamydia, Gonorrhea GONOCOCCAL CONJUNCTIVITIS IS OPHTHALMOLOGIC EMERGENCY Risk factors -Exposure to sick individual -Contact lenses (HUGE RF FOR PSEUDOMONAS) -Hx of contact dermatitis -Exposure to sick individual -Exposure to allergens -Immunocompromise state -Sinusitis -Obstruction of puncta Presentation -Red eye with WATERY discharge -Red eye with THICK, YELLOW discharge -Red eyes with WATERY, STRINGY discharge -May be unilateral or bilateral -May be unilateral or bilateral -Usually bilateral -Pain -Eye pain -Rhinitis -Photophobia -Vision changes -Vision changes GONOCOCCAL INFECTION (also known as Ophthalmia neonatorum when diagnosed in the neonate): -COPIOUS, purulent eye drainage bilaterally Exam -Pre-auricular lymphadenopathy -Dried discharge on the eyelid and lashes -Chemosis Findings -HSV related will have vesicles -Cobblestoning of the pharynx -Allergic shiners Diagnostic Clinical diagnosis Clinical diagnosis Clinical diagnosis IF SEVERE: swab and culture GONOCOCCAL: -Microscopy smear with culture -STI testing Treatment Symptoms last 10-14 days Symptoms last 10-14 days Pharm therapy: Symptom management: Symptom management: -antihistamine eye drops (Pataday) -Cold compress -Cold compress -antihistamine oral -Artificial tears -nasal steroid spray IF HSV: Treatment: -AVOID TOPICAL STEROIDS -> will cause -Meds: topical antibiotics (Erythromycin ointment, Patient education: corneal ulcer Trimethoprim-polymyxin B drops) -avoid allergen triggers if possible -refer to ophthalmology --Want to start antibiotic tx prior to day 6 of -Anti-viral treatment symptoms for best results  --IN CONTACT LENS WEARERS: Fluoroquinolone + avoid wearing contact until asymptomatic for 24 hours GONOCOCCAL TX: -IM/IV Ceftriaxone with topical antibiotics PRN -Eye irrigation -Consider hospitalization due to risk of corneal perforation Patient -Wash hands to prevent the spread -Wear eye protection if working around Education -Avoid touching your face and eyes allergens -Avoid swimming pools -Frequent showers to wash away allergens -Sanitize surfaces -Avoid allergens -Discard and replace make-up Nystagmus Types Jerk Pendular Overview Can be in the following directions: Can be in the following directions: -downbeat -torsional -upbeat -horizontal -horizontal -vertical -torsional -combination of directions -mixed -Does not include a fast phase -Includes fast phase -Often gaze dependent and elicited at the extremes of visual fields Always due to pathology of the central nervous system -May be due to pathology of the central or peripheral nervous system Etiologies -Vertigo disorders and middle ear conditions -Multiple sclerosis and other demyelinating disorders -CVA -Congenital -Head trauma -Nystagmus of the blind -Brain tumors of the cerebellum or brain stem -Spasmus nutans Presentation -Vertigo -Blurred vision -Abnormal head position -Imbalance -Nausea/vomiting -Can be asymptomatic  Amaurosis fugax Overview Intermittent loss of vision in one or both eyes Diagnostics If concerned for ischemia -> CTA Head Coagulation studies Carotid duplex study ESR & CRP (to rule out giant cell) Echocardiogram Brain MRI (potentially performed – more commonly performed for bilateral vision loss) Etiology If unilateral: -carotid artery disease -giant cell arteritis -hypotension -> hypoperfusion -clotting disorder -embolism -optic neuropathy -retinal vein occlusion -increased IOP / acute glaucoma If bilateral: -migraine -seizure -vertebrobasilar ischemia Strabismus Overview Misalignment of the eyes -concerning finding after age 4-6 months Types -Horizontal (eso- & exo-) -Vertical (hyper- & hypo-) -Torsional/rotational Diagnostic Utilize 2 tests to identify: -Corneal light reflex: light reflection will not be in the same location on both eyes -Cover/uncover test: during covering of the strong eye, weak eye will drift from midline Treatment Treatment goal: strength muscles of the symptomatic eye -glasses -visual training -miotic drops *sometimes, but rarely, require surgery  Amblyopia Overview “Lazy eye” -unilateral eye that is not as strong as the other; unequal visual abilities out of both eyes MOST COMMONLY CAUSED BY UNCORRECTED STRABISMUS during infancy Presentation -Difficulty focusing -Double vision -Difficulty with depth perception Diagnostic Clinical diagnosis Treatment Glasses/corrective lenses May utilize eye patch over stronger eye Retinoblastoma Overview Childhood malignancy of the eye that initiates in the retina -MCC: genetic mutation Presentation Leukocoria is HALLMARK Vision changes Red eye Diagnostics Clinical exam finding Further testing performed by ophthalmology Treatment Ophthalmology referral for enucleation, chemotherapy and/or radiation Congenital Glaucoma Overview Increased IOP during infancy CONSEQUENCES: optic nerve damage and ultimately vision loss Presentation -Buphthalmos -Cloudy cornea on exam -Blepharospasm Diagnostic Clinical finding on funduscopic exam (will demonstrate optic nerve cupping abnormalities) Treatment Urgent ophthalmology referral for surgical intervention Diabetic Retinopathy Overview One of the leading causes of new blindness in adults Present in 40% of diabetic patients Categorized into 2 types:  -Non-proliferative -Proliferative (worse prognosis) Presentation Non-proliferative (on funduscopic exam): -Vein dilation -Microaneurysms -Retinal hemorrhages -Hard or Soft exudates (AKA – COTTON WOOL SPOTS) Proliferative: -Neovascularization (new development of vascular vessels) -Vitreous hemorrhage -Tractional retinal detachment Diagnostic HgA1C Fundoscopic exam findings Treatment Management of diabetes – reduce HgA1C Follow up with Ophthalmology annually Retinal Detachment Overview Separation of the neural retina from the underlying retinal epithelium Can be spontaneous (seen primarily in populations >50 y/o) or traumatic (seen s/p cataract surgery) OPHTHALMIC EMERGENCY Presentation -Curtain or “veil” coming down over the field of vision -Central vision intact (only if the macula is unaffected) -NO EYE PAIN OR REDNESS Diagnostic Based off clinical findings Test vision and visual fields Treatment Emergent ophthalmology referral If retina is torn: laser surgery If the retina is not torn: intravitreal surgery Macular Degeneration Overview Progressive deterioration of the macula (central portion of the retina) over time Usually impacts patients >60 yrs old May lead to legal blindness Maintain peripheral vision Classified into 2 categories: 1.Atropic: dry  2.Neovascular: wet Presentation -Painless and progressive loss of central visual acuity over time -Distortion/abnormal size of images -NO PAIN OR REDNESS OF THE EYES Exam Findings DRUSEN BODIES on funduscopic exam -will look like retinal pigment changes about the macula from the cell debri of retinal pigment epithelium Treatment Treatment for dry type: -Oral antioxidants Treatment for wet type: -Oral antioxidants -Laser therapy -Injections of vascular endothelial growth factor inhibitor Hypertensive Retinopathy Overview Stepwise retinal changes due to impacts of uncontrolled hypertension Potential complications: -Retinal detachment -Vision loss Presentation Vision changes over time --usually so subtle pt’s may not even notice Exam Findings Four grades of funduscopic findings: 1.Tortuousity of retinal arteries and silver and copper wiring occurs as the arteries thicken 2.AV Nicking as artery walls continue to thicken 3.Flame-shaped hemorrhages as arteries break down and cotton wool spots as hard exudates and ischemia occur 4.Papilledema as hypertension becomes severe enough to cause increased intracranial pressure and optic nerve changes Treatment Management of hypertension/blood pressure to prevent further progression of symptoms Corneal Abrasion & Metallic Foreign Body Overview Occurs secondary to trauma such as fingernails, contact lenses or foreign body (metallic or not) Presentation -Severe unilateral eye pain -Photophobia -Difficulty keeping eye open -Unilateral eye redness -Tearing of the affected eye -May observe “rust ring” if metallic foreign body has been present for >2 hours Diagnostics Fluorescein stain is HALLMARK of diagnostics --Area of abrasion will uptake the stain and be deep green in color compared to the surrounding cornea --Make sure to flip eyelid and check under the lid Visual acuity Treatment If foreign body is present: -apply topical anesthetic (if you haven’t already) then irrigate to remove foreign body -Educate pt that rust ring (if present) will resolve on its own Medications: -Topical antibiotics should be prescribed for patients to protect against potential infection -Typically ointment is preferred due to lubricating feel and protection of the repairing tissue -If pt wears contacts = protect against pseudomonas = Ciprofloxacin, Ofloxacin -If pt is not a contact lens wearer = Erythromycin Cycloplegic drops can be utilized for pain control in pts with large abrasions Blowout Fractures Overview Fractures of the floor of the orbit Commonly induced by strike to the eye with a small, round, hard object (baseball, golf ball, etc) Commonly causes entrapment of the inferior rectus muscle and/or orbital fat Presentation -Enophthalmos -Orbital dystopia -Proptosis -Extrusion of intraocular contents -Severe conjunctival hemorrhage -Afferent pupillary defect -Limited or painful extraocular motility -Vision changes/diplopia with movements Diagnostics CT Face Visual acuity Treatment Ophthalmology emergent consult -Depending on severity of fracture, these injuries sometimes require surgical intervention -If hospitalization not required, need outpatient follow up with ophthalmology within 24 hours Patient education for discharge: -sleep with head of the bed elevated -avoid nose blowing and sniffing -apply intermittent cold therapy over the injury for the first 48 hours  Globe Rupture Overview Full thickness break of the eye wall (includes the sclera and the cornea) Commonly the result of eye trauma through direct penetration (scissors, knifes, wooden sticks, etc) Presentation Hx of blunt trauma to the eye Unilateral severe eye pain Exam Findings AVOID ADDING ANY KIND OF PRESSURE TO THE EYE – including avoidance of use of tonometer, or retracting the eyelid -decreased visual acuity -afferent pupillary defect -eccentric / teardrop pupil -increased/decreased anterior chamber depth -extrusion of vitreous Diagnostics CT Face Visual acuity (if pt is stable) Treatment Emergent ophthalmology consult Place pt on NPO status Avoid placing any solutions in the eye Tetanus prophylaxis Empiric antibiotic treatment Scleritis Overview Inflammation and potentially blinding disorder of the sclera Thought to be caused by autoimmune processes, commonly vasculitis Scleritis sometimes, but not always, presents with systemic inflammation or occurrence of autoimmune disorder (rheumatoid arthritis, granulomatosis with polyangiitis) Can be divided into anterior scleritis or posterior scleritis Presentation -Severe, constant eye pain -Worsen in the morning or at night -Radiates to the face and periorbital region Diagnostic Anterior scleritis: -Eye pain -Tenderness to touch (tested by exerting pressure on the eyelid) -Injected sclera Posterior scleritis: -Eye will appear normal on exam Imaging: -Ultrasound  -CT -Biopsy Treatment Urgent referral to ophthalmology NSAIDs Glucocorticoids (if NSAIDs fail) Hyphema Overview Hemorrhage of the anterior chamber of the eye -usually a result of blunt force trauma to the eye -need to monitor these patients for acute glaucoma Presentation Pooling of blood in the inferior anterior chamber May also have evidence of trauma to the periorbita or face Diagnostics Clinical diagnosis Measure IOP Treatment Emergent referral to ophthalmology Cycloplegic eye drops for comfort (only if they don’t have glaucoma) Eye shield (to protect from further trauma) Topical glucocorticoids Congenital Neck Masses Overview Congenital masses of the neck that commonly become enlarged or infected Include thyroglossal duct cysts, branchial cleft cysts, dermoid cysts, lymphangiomas Types Thyroglossal duct cyst Branchial cleft cyst Presentation -midline cyst of the neck -cyst of the neck that is anterior to the sternocleidomastoid muscle -moves with swallowing and when the pt sticks their tongue out Diagnostic Neck CT Excisional biopsy Treatment If symptomatic, suspicious or prone to infection: -Excise the cyst (otherwise, leave it alone) Neoplastic Neck Masses Types -Salivary gland tumors -Thyroid tumors -HPV-related squamous cell carcinoma -Lymphoma metastasis  -Schwannoma -Lipoma Presentation Firm mass of the neck May/may not be tender Document growth rate, overlying skin changes and mobility Fever Other signs of infection Diagnostics Ultrasound CT neck Biopsy (fine needle or excisional) Treatment Excision +/- chemo or radiation Salivary Gland Tumors Types -Parotid -Submandibular/Sublingual Parotid -most common -mostly benign -TREATMENT: excisional biopsy Submandibular -Rare -Commonly malignant -TREATMENT: excision biopsy Overview Most common malignant tumor of the salivary gland = mucoepidermoid carcinoma Thyroid Carcinoma Types & Overview 1.Papillary -Most common -good prognosis -more common in females 2.Medullary -Associated with Multiple Endocrine Neoplasia (MEN) syndrome 3.Follicular 4.Anaplastic -highest death rate Risk Factors Exposure to radiation Family hx of thyroid cancer (especially medullary thyroid cancer) Male  45 yrs old Presentation Often asymptomatic -Hoarseness -Vocal cord paralysis Papillary type: -painless swelling near the thyroid -palpable nodule that is firm, non-tender to touch, fixed Medullary type specifically: -diarrhea -flushing -headache -tachycardia -HTN Diagnostics Fine needle biopsy Excisional biopsy (other diagnostics will be discussed further in the thyroid chart) Treatment Options: -surgical excision -Radio-ablation of thyroid tissue -radioactive iodine therapy (destroys gland) --remember: destruction or removal of thyroid gland will require lifelong thyroid replacement therapy with Levothyroxine Options for papillary & follicular type: -TSH suppression with thyroid replacement hormone Optic Neuritis Overview ASSOCIATED WITH MULTIPLE SCLEROSIS -NEED TO KNOW Inflammatory, demyelination of the optic nerve Risk Factors Twice more likely in women than men Age 20-40 y/o Presentation -Slow progression of unilateral eye pain/vision loss over hours-weeks -impaired color vision -photopsia (flashes of light in the vision field) Diagnostics Clinical diagnosis made on fundoscopy -Sluggish pupils -Papilledema Need to follow up with MRI Treatment IV Corticosteroids Ptosis Overview Drooping eyelid Correct tone relies on functional oculomotor nerve innervation and functional levator palpebrae superioris muscle of eyelid Etiology -disease/palsy of oculomotor n. -myasthenia gravis -Horner syndrome = ptosis + miosis + hemifacial anhidrosis --due to dysfunction of sympathetic nerves around the eye Presentation Drooping of unilateral eyelid Diagnostics Clinical diagnosis Treatment Treat underlying disorder Pinguecula Overview Callous-like lesion on the eye Consists of protein, fat or calcium Rarely grow in size Risk Factors >35 yrs of age Presentation Yellow, elevated conjunctival nodule, typically on the nasal aspect of the eye Diagnostics Clinical diagnosis Treatment -artificial tears -if inflamed: steroid eye drops -may not resolve; benign Pterygium Overview “Surfer’s eye” Caused by prolonged exposure to the elements (sun, sand, wind) Lesions grow slowly over time Presentation -Fleshy lesion on the medial aspect of the conjunctiva -Possibly painful -Vision changes (if lesion starts to cover the pupil) Diagnostics Clinical diagnosis Treatment -artificial tears -if inflamed: steroid eye drops POOR prognosis if the lesion extends over the pupil Cataracts Overview VERY COMMON in the US, especially in older populations Multiple etiologies, including: -age related -metabolic changes -systemic disease -medications -congenital -traumatic -uveitis Risk Factors >60 yrs of age Sun exposure to light colored eyes Cigarette smoking Having any of the above conditions Presentation First symptom usually night vision changes Gradual blurring of vision over time No eye redness Exam Findings Opaque lens visible on gross exam Absent red light reflex Diagnostics Clinical diagnosis Treatment Referral to ophthalmology Surgery: surgical removal of lens nucleus and implantation of a replacement lens -improvement in 95% of pts who undergo procedure Prevention: multivitamins and antioxidants Central Retinal Artery Occlusion Overview Typically, the result of vascular changes due to diabetes mellitus, hyperlipidemia and hypertension Keep CVA, giant cell arteritis and cardiac emboli on differential In younger patients, think etiology: OCPs, clotting disorders, migraine syndromes or trauma Presentation -unilateral, acute vision loss  -ABSENCE OF PAIN -Decreased visual acuity and visual fields on temporal side Exam Findings Fundoscopy: -veins appear segmented = “box car” appearance -fovea may show “cherry-red” spot, if hours have passed -pale optic disc -diffuse retinal pallor -no erythema of sclera Diagnostics Labs: -ESR/CRP -Blood glucose level -Cholesterol panel Imaging: -Duplex ultrasound of carotids -CT/MRI Other: -EKG Treatment OPHTHALMOLOGY EMERGENCY If thrombosis: increase O2 level to help with thrombolysis If embolus: find source and treat underlying cause (think anticoagulation) Blepharitis Overview Multiple etiologies: 1.clogged meibomian/oil gland at the base of the eyelashes 2.infectious: Staph (most common pathogen), virus, parasite 3.non-infectious: seborrheic Presentation Inflammation and redness of the lid margins with crusting Uncomfortable No vision changes Diagnostics Clinical diagnosis Treatment Self resolves within 2-4 weeks If unresolved: -topical antibiotic ointment If severe swelling: -topical steroid If refractory: -oral antibiotic and continue topical antibiotics  Prevention: Lid hygiene, proper make up removal *CHRONIC blepharitis can lead to ECTROPION (outward turn of the eyelid) or ENTROPION (inward turn of the eyelid) Dacryocystitis Overview Inflammation and infection of the lacrimal sac Presentation Swelling, red pustule with purulent drainage just inferior to the eye/tear duct Diagnostics Clinical diagnosis Treatment Systemic antibiotics Warm compresses, for symptom relief Chalazion Overview Inflamed meibomian gland Presentation Initially a painless and slow growing lesion Develops into inflammation and erythema localized to the body of the eyelid Diagnostics Clinical diagnosis Treatment Symptom management: -warm compress -massage If refractory: -consult specialty for corticosteroid or I&D Corneal Ulcer Overview Multiple etiologies: 1.direct injury to the cornea 2.bacterial/viral/fungal infection 3.ulcer 4.vitamin A deficiency Presentation Eye redness Eye pain Excessive tearing Sensation of foreign body Photophobia Blurry vision/ vision loss Diagnostics Slit lamp exam Fluorescein stain Treatment Ophthalmology referral Eye patch Antibiotic, antifungal or antiviral (depending on etiology) Corneal scrapings for culture and sensitivity may be recommended Periorbital Cellulitis Overview Acute bacterial infection of the orbit Sometimes secondary to sinusitis or bacteremia spread from pneumonia Presentation -eyelid edema -eyelid erythema -decreased vision -afferent pupillary defect --DETECTED BY shining light on unaffected pupil and seeing constriction of affected pupil, but when light is shined on affected pupil, it does not constrict -dysmotility -proptosis: protrusion of the eyeball Diagnostics Labs: -CBC -blood cultures Imaging: -CT with contrast of sinus and orbits Treatment EMERGENCY Hospitalization for immediate broad-spectrum IV antibiotics for 2-5 days May require I&D if underlying abscess seen on CT Hordeolum Overview Common acute bacterial infection of the sebaceous glands of the eye Multiple etiologies: 1.meibomian gland, Gland of Zeis, Moll gland infection 2.staph infection (MOST COMMON PATHOGEN) Presentation -red, PAINFUL, inflamed eyelid margin -if symptoms progress = pustule  -can be external or internal Diagnostics Clinical diagnosis Treatment Symptom management: -warm compresses If no resolution after 7-10 days = topical antibiotic for 7-10 days If cellulitis develops = oral antibiotics May need to encourage pt to discontinue use of contact lenses or wearing makeup until symptoms resolve Otitis Externa Type Bacterial Fungal Eczematous Overview Most common cause = Most common cause = Aspergillus sp., Candida Immune mediated Pseudomonas aeruginosa & Staph Caused by: Itch/scratch/itch cycle Aureus 1.recent antibiotic drops causing yeast infection of Caused by: the ear 1.wet ear: overgrowth of 2.diabetics pathogenic bacteria leads to 3.immunocompromised edema, erythema and purulent discharge 2.“clean” ear: alkaline environment from too many Q-tips supports bacterial growth 3.trauma: route of infection into canal skin Can also include malignant otitis externa – commonly caused by pseudomonas Presentation -pain (can be severe) -Pruritus -Pruritus of the canal -swelling that can lead to occlusion -hearing loss (due to debris blocking canal), -mild erythema of the canal -drainage (otorrhea), often -recent hx of antibiotic ear drops -flaking of the canal skin purulent -eczematous findings of external ear structures -hearing loss -normal ear canal or too clean of an ear canal: -history of swimming, bathing, Q-tip denuded/weeping/ no cerumen use or trauma Exam Findings -visualization of a swollen, inflamed -less edema, erythema compared to bacterial -Flaking of the canal skin with erythema of the canal -“COTTAGE CHEESE”/ liquid discharge skin -otorrhea -Black or white spores -tenderness - +/-lymphadenopathy -fever Diagnostics Clinical diagnosis Clinical diagnosis Clinical diagnosis Can culture as needed KOH prep PRN Treatment IF UNCOMPLICATED: Debride ear Med options: -topical antibiotic or Med options: Vosol HC PRN antibiotic/steroid drops Lotrimin 1% solution OTC Dermotic oil IF COMPLICATED (with swollen Vosol HC prescription drops lymph nodes/fever): add oral Cipro PREVENTION: PREVENTION: Educate pt to discontinue Q-tips, pencils and *Can also place wick into ear: place DO NOT IRRIGATE paperclips wick into canal then insert topical -caution pt’s to keep ears dry ear drops so they absorb into the -avoid overuse of antibiotic drops wick and expand for full absorbency DO NOT IRRIGATE PREVENTION: Swimmer’s ear drops or hair drier on low settings Otitis Media Types Serous Purulent Caused by: eustachian tube dysfunction causing negative Middle ear infected with STREP PNEUMONIAE, H. INFLUENZAE, OR M. pressure in the middle ear and leading to clear fluid CATARRHALIS and can follow a cold or URI accumulation in the middle ear space Overview Inflammation/infection involving the middle ear space; known to be serous or purulent  More common in children than adults due to: --narrow/horizontal eustachian tubes --enlarged adenoids --bottle-feeding --preschool/daycare settings --tobacco smoke exposure Up to 84% of children will experience OM by age 3 Presentations YOUNG CHILDREN: undetected / incidental finding YOUNG CHILDREN: ADULTS: -fussy -hearing loss -tugging/playing with the ear -aural fullness - difficulty eating or sleeping -hearing loss -fever ADULTS: -ear pain -aural fullness -hearing loss -fever Exam Findings Otoscopic exam: Otoscopic exam: Clear fluid buildup with normal or retracted TM -Purulent fluid buildup -Inflamed and bulging TM -Tenderness of lymph nodes along mastoid bone Diagnostics Clinical diagnosis Can use tympanometry/pneumatic otoscopy to diagnose Treatment PEDIATRIC SEROUS OM: PEDIATRIC PURULENT OM: -RECOMMEND AGAINST SYSTEMIC ABX, ANTIHISTAMINES, Amoxicillin or Augmentin is first line choice DECONGESTANTS, NASAL STEROID SPRAYS -Monitor pt closely and use WATCHFUL WAITING ADULT PURULENT OM: -if effusion persists for >3 months, then refer to ENT for Augmentin is first line choice consult on surgical intervention (tympanostomy tubes/ Can use Cephalosporin for Penicillin allergy adenoidectomy) Need to refer to ENT for: ADULT SEROUS OM: -recurrent OM -Recurrent or persistent unilateral OM in an adult should -persistent hearing loss following OM infection be referred to ENT for eval of nasopharynx -chronic TM perforation Complications SURGICAL MANAGEMENT: Recurrent OM (3 episodes in 6 months or 4 in a year) needs to be referred to ENT for tympanostomy/ adenoidectomy Tympanostomy tubes: Tubes surgically inserted into the inferior aspect of the TM 1.Provide aeration and lead to fewer infections 2.Allow drainage and lead to less pain and discomfort 3.Allow for topical treatment -Ciprofloxacin-Dexamethasone otic drops -Ofloxacin otic drops -Ciprofloxacin-Fluocinolone Acetonide drops Prevention -Recommend against tobacco exposure -Recommend breastfeeding only for first six months of life -Encourage vaccination with Pneumococcal and annual influenza vaccines Tympanic Membrane Perforation Overview Can be a complication of OM or mastoiditis, penetrating foreign body or barotrauma Presentation -Asymptomatic - “pop” during infection -history of inciting event -hearing loss Exam Findings -perforation on exam with clear view of middle ear structures -findings consistent with OM, mastoiditis or barotrauma Diagnostics Typically clinical diagnosis -can be confirmed with tympanometry -document hearing loss with audiometry Treatment MEDS if inflammation or drainage is present: Ciprodex, Floxin Otic, or Otovel otic drops, Refer to ENT for further evaluation/management PROGNOSIS: should resolve within 6-8 weeks Bullous Myringitis Overview Infection leads to bullae and blebs (outpouching of the TM) -infection is typically acute OM  MOST COMMONLY CAUSED BY STREP PNEUMONIAE Presentation -Otic pain -Possible decreased hearing -Bullae (serous or sanguinous) seen on physical exam Diagnostics Clinical diagnosis Treatment Treat the acute otitis media with antibiotics Cholesteatoma Overview “Skin cyst” of the middle ear PATHOPHYS: can be congenital (uncommon) or acquired -ACQUIRED: usually due to retraction pocket in the pars flaccida (area of TM) which introduces squamous epithelium into the middle ear that proliferates and becomes osteoclastic --osteoclastic activity can destroy the ossicles, mastoid structures and bony plate protecting the brain -associated with effusions and infections Presentation -recurrent otorrhea -hearing loss/tinnitus -vertigo -facial palsy (CN VII) -meningitis OR, asymptomatic Exam Findings -retracted par flaccida -purulent otorrhea -granulation tissue -visualized pearly keratin debris superiorly behind the TM Diagnostics -Direct visualization -Audiogram: will show hearing loss -thin-slice CT Treatment -Treat infection if present -surgical resection and ossicular chain reconstruction PROGNOSIS: recurrence as high as 40%, must monitor Eustachian Tube Dysfunction Overview Issue with the eustachian tube ranging from the tube being obstructed/closed to refusing to open Prevents ventilation to the middle ear Children have shorter, more horizontal eustachian tubes, putting them at higher risk for dysfunction Presentation Asymptomatic History of recurrent otitis media Issues with barochallenge (popping your ears on an airplane) Loud perception of your own internal sounds Pulsatile tinnitus Diagnostics Clinical diagnosis If symptoms persist for >3 months – may need to order imaging – MRI/CT to check for neoplasms Treatment Dependent on etiology of symptoms -treat allergy symptoms -treatment of laryngeal reflux symptoms -excision of mass lesions Tinnitus Overview Perception of sound close to the head without anything physically making the sound Can be continuous or intermittent Usually a ringing, hissing or buzzing Multiple potential etiologies: -arterial bruits -AV shunts -vascular disease (atherosclerosis of vessels in the ear) -venous hums -spasm of the muscles in the ear -eustachian tube dysfunction -TMJ dysfunction -ototoxic medications -presbycusis -vestibular schwannoma Presentation -hearing loss -hx of ear disease -loud noise exposure -ear drainage -ear pain -vertigo symptoms Diagnostics Try to identify etiology May need imaging of head and neck (CT) Treatment Dependent on etiology  Acoustic Neuroma Overview Benign growth of CN VIII leads to disrupted transmission of sound information to the brain and diminished speech discrimination -potential for mass effect with growth LOCATION: internal auditory canal or cerebellopontine angle Presentation -hearing loss or distortion -tinnitus -vertigo -facial N or trigeminal N dysfunction Diagnostics -Audiogram: reduced speech discrimination, normal or reduced hearing unilaterally -MRI -Auditory brainstem response testing Treatment Tx is dependent on severity -observation -surgical removal Cerumen Impaction Overview Research has not yet indicated why some patients secrete more ear wax than others -typically due to interference in the self-cleaning process (cotton swabs, hearing aids) Presentation -hearing loss (worsening with time and exposure to water) -ear discomfort -dizziness/tinnitus if against TM -can also be asymptomatic Diagnostics Clinical diagnosis on otoscopic exam Treatment -hydrogen peroxide or OTC wax-dissolving drops -irrigation (if TM is intact! Otherwise, do not irrigate!) --loop curette, suction or forceps -refer to ENT if unable to remove cerumen atraumatically Vertigo Disorders Types Meniere’s Disease Benign Paroxysmal Positional Vertigo Labyrinthitis Vestibular Neuritis Overview -40-60 yr old -occurs equally in males and females Inflammation of the labyrinth Inflammation of the vestibular -unknown cause, but has -typically during 5th decade of life nerve genetic link -idiopathic etiology, but potentially due Commonly associated with recent Commonly associated with to trauma or vestibular neuronitis viral URI recent viral URI PATHOPHYS:  TRIGGERS: allergies, -Otoconia become dislodged from their BACTERIAL LABRINTHITIS: OM menstruation, diet, stress, positions in the utricle and move into extension into the labyrinth comorbid illness the semicircular canals. Indecipherable PATHOPHYS: signals from the balance system are -Increased endolymphatic sent to the brain. fluid pressure in the inner ear causes distortion of information from the organs of balance and hearing Presentation Distinct episodic attacks of: -Episodic room-spinning vertigo -Acute vertigo for hours to days, -Acute vertigo for hours to days -prolonged vertigo --seconds to minutes in duration nausea, vomiting, nystagmus -nausea/vomiting -fluctuating hearing loss --preceded by change in head position -tinnitus -nystagmus -tinnitus (turning over in bed, looking up, sitting - +/- hearing loss -aural fullness up from laying down) -can have associated nausea Episodes are brief lasting -HEARING NOT AFFECTED minutes to an hour No specific exam findings Will usually have hx of similar episodes No specific exam findings Diagnostics Audiometry: low-frequency Audiogram: no specific findings Audiogram: may show hearing Audiogram: may show hearing hearing loss Dix-Hallpike maneuver: nystagmus to loss loss Electrocochleography: affected side -rule out other etiologies -rule out other etiologies increased endolymphatic fluid pressure Treatment DIETARY RESTRICTIONS: Epley maneuver: repositions otoconia MEDICATIONS: MEDICATIONS: decreased sodium intake, into the utricle where they are no -Antivert (Meclizine) -Antivert (Meclizine) avoidance of EtOH and longer affecting balance system -Valium -Valium caffeine -Possibly oral steroids, but no -Possibly oral steroids, but no DIURETIC: Dyazide/Maxzide PROGNOSIS: up to 10-15% recurrence antivirals antivirals For management of acute rate per year phase: oral or intratympanic Complications: If symptoms persist, refer to ENT steroids, Valium -recurrent episodes for vestibular rehab  -persistent hearing loss Presbycusis Overview Sensorineural hearing loss associated with advanced age -symmetrical, high-frequency hearing loss ETIOLOGY: -loss of functional sensory hair cells -neural pathway degeneration Risk Factors -age -genetic predisposition -noise exposure -diabetes/atherosclerosis Presentation -Long-term worsening bilaterally -difficulty in social situations -difficulty localizing sounds -tinnitus -isolation -patient’s spouse/adult children may “make” them come in No specific exam findings Diagnostics AUDIOGRAM: high-frequency symmetrical sensorineural hearing loss Treatment Hearing aids Avoid excessive noise exposure Hearing amplification tools Mastoiditis Overview Most common complication of purulent acute otitis media Suppurative infection of mastoid air cells Can be acute or chronic in nature Most common causative pathogen: Strep pneumo and Strep pyogenes Presentation Postauricular tenderness, pain, redness or swelling Protrusion of the auricle Non-specific ear pain  Fever Exam Findings TM bulging, perforation or effusion Swelling of the external auditory canal Otorrhea Postauricular erythema and tenderness Diagnostics Usually clinical diagnosis Imaging options: CT with contrast Labs: CBC with left shift Elevated ESR and CRP Treatment Referral to ENT Meds: IV antibiotics -with history of acute otitis media: Zosyn -without history of acute otitis media: Unasyn Interventions: Myringotomy tube placement Severe disease may require mastoidectomy emergently Rhinitis Types Viral Allergic Vasomotor Overview “Common cold” -20-30% of US adults are affected every year Etiology: suggestive of hyperactivity of Most common cause: Rhinoviruses -40% of US children affected parasympathetic tone, not the Other viruses include: adenovirus, histamine/IgE pathway respiratory syncytial virus, influenza PATHOPHYS: Triggers: perfume, smoke, change in viruses, parainfluenza virus and -IgE mediated cascade: triggers release of histamines temperature, stress, hormonal coronaviruses and cytokines fluctuations -Genetic predisposition can lead to atopic triad (allergic PATHOPHYS: Neutrophilic response leads rhinitis, asthma, atopic dermatitis) to vascular permeability, edema and increased mucous secretion Seasonal allergies are typical cause: Spring: tree pollen Complications: Summer: grass pollen -Acute rhinosinusitis Fall: weed pollen -acute OM Winter: mold  -asthma flare -bronchitis/pneumonia Presentation -fatigue -hx of seasonal/perennial symptoms Similar presentation to allergic rhinitis -headache -nasal congestion, sneezing, itchy/runny nose, allergic (See left) -nasal congestion conjunctivitis, itchy irritated throat, hyposmia, sleep -rhinorrhea disturbance and cough -sneezing -hyposmia (reduced sense of smell) - throat pain Exam Findings NOSE: swollen, erythematous nasal -pale, blue-tinged nasal mucosa -Clear rhinorrhea turbinates, clear rhinorrhea -boggy, congested turbinates -postnasal drip THROAT: mildly erythematous pharynx -occluded nasal airway -clear rhinorrhea/Postnasal drip MAY ALSO FIND: -dennie lines: lines under eyes bilaterally that develop due to genetic predisposition to allergies/eczema -allergic shiners: resembles a black eye -allergic salute: vertical line across nasal bridge from constantly Diagnostics Clinical diagnosis 1.Skin pricking test: measures wheal and flare of Clinical diagnosis histamine response to allergens in vivo 2.RAST (radioallergosorbent test) blood testing: measures amount of IgE tagged to each allergen in vitro Treatment Treat symptoms Non-pharm options: Difficult to treat Self-limiting 1.avoidance of allergens -can use corticosteroid sprays (Flonase) -wear a mask when cutting grass -can use intranasal anticholinergic PREVENTION: -keep pets off the bed sprays -cover mouth when sneezing or coughing 2. removal (rinse nose with saline, bath regularly to -frequent handwashing remove spores from body) -avoid sick contacts Pharm therapy: -Nasal steroid sprays -Antihistamines -Leukotriene antagonists, decongestants, oral steroids  Immunotherapy: -allergy injections: help with immunity, typically given over 3-5 years -sublingual immunotherapy Nasal Polyps Overview Immune mediated (atopic) development of edematous tissue Samter’s Triad: Nasal polyps + ASA allergy + asthma (improves with desensitization to ASA) Presentation -nasal obstruction -hyposmia Exam findings -polyps visible within the nose (will look like peeled grapes) Diagnostics Clinical diagnosis Can utilize CT imaging if needed Treatment Pharm therapy -oral steroid taper Intervention: -surgical resection Prevention: -allergy management -leukotriene inhibitors Nasal Foreign Body Overview Common items: Food, beads, small toys, pen caps, button batteries (BUTTON BATTERIES NEED TO BE REMOVED IMMEDIATELY AS THEY CAN BE NECROTIZING WITHIN FOUR HOURS) Presentation -May have been witnessed -foul smelling purulence from one nostril -unilateral nasal obstruction Diagnostics Clinical diagnosis Can utilize x-ray imaging as needed Inspect the nose bilaterally and posteriorly if possible Treatment MANAGEMENT: -attempt removal in a cooperative child -REFER uncooperative child to ENT --place them on antibiotic therapy until consult  -removal under brief anesthesia Sinusitis Overview Acute: 12 weeks Viral rhinosinusitis: common cold symptoms + sinus symptoms 10 days, severe or worsening -typically caused by strep pneumoniae, H.influenzae, M. Catarrhalis -also can be caused by allergic rhinitis or fungal sinusitis (VERY RARE) PATHOPHYS: Osteaomeatal complexes (OMCs) become compromised and cause sinuses to have reduced airflow and reduced drainage outflow, leading to multiplication of infection and inflammation increase, causing pressure and pain MOST COMMON IN THE MAXILLARY SINUS, causing pain in the cheeks, upper teeth and upper jaw Presentation -sinus pain or pressure -thick, discolored nasal and postnasal secretions -nasal congestion/obstruction -headache -tooth/jaw pain (upper) -anosmia (loss of smell) -foul breath -throat discomfort -cough -fever -fatigue Exam findings -erythematous nasal mucosa -narrowed nasal airway -thick, discolored nasal/ postnasal drainage -tenderness to palpation over sinuses -pharyngeal erythema Diagnostics Clinical diagnosis  If complicated or refractory: -nasal endoscopy -Imaging: CT scan -Culture & sensitivity of discharge Treatment ACUTE: Non-pharm: -NetiPot -Nasal saline rinse Pharm therapy: -Symptomatic relief (OTC): --steroid nasal sprays --analgesics -Prescription: --watchful waiting vs antibiotics: studies have shown no decrease in # of days of infection when antibiotics are administered -pt’s will typically resolve on their own CHRONIC: -Acute sinusitis treatment + Identification and treatment of nasal polyposis + identification and treatment of allergic rhinitis -referral to ENT for surgical management Epistaxis Overview Etiology: -Nasal trauma: blunt trauma, nose picking, blowing nose too hard -rhinitis -exposed nasal vasculature: deviated nasal septum, dry mucosa -inhaled drugs -alcohol use -anticoagulants -Osler-Weber-Rendy syndrome (Hereditary Hemorrhagic Telengectasia) -Typically stems from Kiesselbach’s venous plexus located on the anterior septum bilaterally Presentation -nasal bleeding -unilateral or bilateral -NEED TO KNOW: length of time, measures to stop bleeding, inciting event/etiology, comorbid illnesses, medications Exam Findings -visualization of the origin of the bleed -visualization of bright red blood and/or clots in the nasal cavity or oropharynx  -May need to suction for better visualization Diagnostics Clinical diagnosis Labs: PTT, PT/INR, LFTs Treatment Initial treatment of anterior epistaxis: -pinch the nose closed anteriorly for 15 minutes and lean head forward DO NOT LEAN HEAD BACK, WILL CAUSE BLOOD TO RUN DOWN THE BACK OF THE THROAT AND CAUSE NAUSEA, VOMITING, DIARRHEA Further treatment of anterior epistaxis: -suction of nasal passages clear of blood and clots -topical intranasal decongestant -cauterize with silver nitrate -anterior packing or pneumatic tamponade as needed (plus oral antibiotic) -remove packing within 2-5 days In the days following epistaxis, you should avoid: -activities that would increase blood flow to the area (straining, exercise) -leaning forward -hot food or drinks -nose picking (digital manipulation) -NSAID/EtOH use -nasal saline gel -humidification When to refer to ENT: -Anterior recurrent or refractory nosebleeds -Posterior epistaxis (rarer, more severe, more difficult to control) ENT management: -anterior or posterior nasal packing -surgical electrocautery -surgical vessel ligation ED management: send to ED for: -packing -IV access and blood products -control of hypertension -lab analysis: CBC, analysis of bleeding state -Possible surgical electrocautery or ligation  Acute Pharyngitis & Tonsillitis Types Group A Beta Hemolytic Strep Epstein Barr Virus Other Overview Group A Strep infection of the HERPES VIRUS that can have symptoms ranging from mild to Other MCC: oropharynx severe -viruses (adenoviruses, rhinoviruses) -also called “kissing disease” -gonorrhea COMPLICATIONS: PATHOPHYS: lymphoproliferative response resulting in -trachomatic -local abscesses significant enlargement of affected lymph tissues -mycoplasma -rheumatic (scarlet) fever -Immunocompromised patients can develop lymphoma and -Coxsackie virus (herpangina: vesicular -rheumatic heart disease nasopharyngeal carcinoma lesions and inflammation of the pharynx) -glomerulonephritis -Corynebacterium diphtheria: rare, gray pseudomembrane adherent to tonsils/pharynx -candida (oral thrush) Presentation -fever > 38 degrees C -pharyngitis Sore throat -swollen glands -tonsillar enlargement with gray-white exudate Fever -swollen tonsils +/- -throat pain Exudates at the posterior oropharynx drainage/exudate -fever, fatigue -lack of cough -lymphadenopathy -throat pain or soreness -hepatosplenomegaly, abdominal pain -odynophagia (pain with swallowing) -rash (scarlatiniform) Diagnostics -rapid antigen detection test (99% -Lymphocyte/WBC ratio >35% (90% sensitive) May need to swab for culture sensitive) -atypical lymphocyte on peripheral smear Otherwise, usually clinical diagnosis -throat culture (95% sensitive AND -elevated anti-EBV titer can detect for other bacteria) -heterophil agglutination (Monospot) test CENTOR CRITERIA: strong indication of GABHS if first four features are present -Criteria: absence of cough, tonsillar exudate, cervical lymphadenopathy, fever Treatment General recommendations: -hydration, rest and OTC analgesics Dependent upon etiology -Centor 0-1 score (low risk) for -oral steroids GABHS: NO LABS, NO ABX -hospitalization if there is airway compromise Pharm therapy:  -Centor 2-4 score (medium to high -Abdominal precautions if hepatosplenomegaly -antivirals risk) for GABHS: labs, then ABX if -antifungals positive EBV AND STREP CAN COEXIST ABX: refer to pharm Symptomatic care: SX treatment: OTC analgesics, -antipyretics saltwater gargle -analgesics -fluid hydration RECURRENT GABHS: -chronic tonsillitis should be referred to ENT Acute Laryngitis Overview -most common cause of hoarseness/loss of voice -historically thought of as viral etiology, but recent evidence shows that H.flu and M. catarrhalis may also contribute Presentation Hoarse voice Loss of voice entirely Diagnostics Clinical diagnosis Treatment -conservative treatment of symptoms -typically self-limited -Antibiotics rarely shorten course -vocal rest: avoid loud use of voice, avoid whispering Refractory: -refer to ENT Aphthous Ulcers Overview “canker sores” -common and typically related to stress or URI Presentation Painful, white-grey ulcers on erythematous base within the mouth Diagnostics Clinical diagnosis Treatment Pharm therapy: -steroid impregnated oral gel or Alum If refractory: biopsy Peritonsillar Abscess Overview Bacterial infection of the potential space alongside the tonsil -usually caused by GABHS, but has many causes -can become recurrent due to compromise of the space Presentation -sore throat (severe) -trismus -“hot potato” voice -fever Exam Findings uvular deviation away from involved tonsil -erythema - +/- exudate -can cross midline of the oral airway -SPACE AROUND THE TONSIL (not the actual tonsil) IS INFLAMED AND PUSHING TONSIL INTO AIRWAY Diagnostics CT imaging Strep swab Treatment Interventions: -Needle aspiration -Incision and drainage -Tonsillectomy Other options: -Antibiotic treatment and referral if less severe -needle aspiration and I&D are first line treatments, tonsillectomy is further down the line Epiglottitis Overview Inflammation/infection of the epiglottitis ETIOLOGY: H. Flu B -rarer now due to HiB vaccine Presentation Bright red epiglottis on exam THE FOUR D’s symptoms: -dysphagia -drooling -dysphonia (muffled voice) -distress (tripod position/sniffing dog posture) -stridor present but not as severe as croup CHILDREN: avoid visualizing epiglottis if not intubating -> can cause respiratory failure requiring intubation!!! Diagnostics Clinical diagnosis (but not necessarily through visualization, more so through hx)  Imaging may demonstrate “thumb print sign” on lateral x-ray Treatment CHILDREN: -immediate intubation -IV antibiotics ADULTS: -IV antibiotics -IV steroids Sialadenitis Overview Infection/inflammation of the salivary glands PATHOPHYS: MC INFECTING PATHOGEN = Staph aureus -Stasis and infection due to: 1.thickened secretions (dehydration, lack of oral intake) 2.physical obstruction (calculi, tumors) Presentation -typically unilateral -swollen, tender salivary gland -INTRAORALLY: purulent drainage from duct -+/- fever Diagnostics Clinical diagnosis Treatment Non-pharm: -Hydration (thins salivary secretions) -lemon drops/sour candy (to promote secretion) -warm compresses, massage Med options: -antibiotic with staph coverage Retropharyngeal Abscess Overview Suppurative infection of the retropharyngeal space Commonly a polymicrobial infection Most common pathogens: group A strep, staph aureus (including MRSA) and respiratory anaerobes Presentation Difficulty swallowing Pain with swallowing Fever Cervical lymphadenopathy Drooling / difficulty swallowing secretions “Hot potato” voice / change in voice Trismus Neck swelling Neck stiffness Diagnostics Labs: -CBC: elevated WBC count with left shift -Blood culture Imaging: -CT neck with contrast Treatment Make sure airway is secured Hospitalization necessary for observation Meds: IV antibiotics IV hydration Intervention: -dependent on abscess size, may require surgical drainage Suppurative Parotitis Overview Acute bacterial infection of the parotid gland Most commonly caused by staph aureus Presentation Sudden onset, unilateral, firm pre-auricular area over the parotid gland Erythema over the parotid Swelling over the parotid Fever Drainage from Stensen’s duct Diagnostics Clinical diagnosis CT face if etiology of symptoms is unclear Treatment Requires hospitalization Pharm therapy: IV hydration IV antibiotics If no improvement after 48 hours:  Swab and culture drainage Re-image the area with CT Empiric therapy started Leukoplakia Overview White patches on the oral mucosa Benign, but may demonstrate malignancy Presentation White, thin plaque with well-defined margins found on the oral mucosa surface Diagnostics Biopsy should be taken Treatment Dependent on etiology Interventions: -surgical removal -ablation -cryotherapy Meds: -retinoids -NSAIDs -vitamin A Dental Trauma Overview Injuries to the teeth that may result in cracked, avulsed or broken teeth Presentation History of injury to the mouth Need to know what time the injury took place Diagnostics Clinical diagnosis Treatment PRIMARY TEETH: -Avulsed teeth should not be replanted -extrusion injuries should be referred to a dentist immediately -lateral luxation: observe, as long as bite is not affected PERMANENT TEETH: -avulsed teeth: if the tooth has only been out of the mouth for less than one hour, it can be replanted (or longer if stored in milk) -other injuries should be sent to dentist asap  PULMONOLOGY Acute Bronchiolitis Overview Inflammation of the airway 7) Bactrim can also be given 3.RR >30 prophylactically to HIV 4.Systolic BP < 90, Diastolic BP < 60 patients if their CD4 count 5. Age >65 falls below 200 Meds: Community acquired requiring hospitalization: IV beta-lactam + Doxycycline Community acquired outpatient treatment: oral Azithromycin or Doxycycline or Levofloxacin Mycoplasma pneumonia: Macrolides (Azithromycin) or Doxycycline Legionella pneumonia: Macrolides (Azithromycin) or Fluoroquinolones (Levofloxacin) Hospital acquired: anti-pseudomonal beta lactam + fluoroquinolone SUPPORTIVE CARE: -fluids -cough suppressants: Codeine, Dextromethorphan -Expectorants: Guaifenesin  Acute Bronchitis Overview Ranks within the top 10 most common outpatient diagnoses in the world ETIOLOGY: often undetermined -most common cause is viral --more commonly viral than bacterial -Flu A & B (most common), rhinovirus, adenovirus -Strep pneumo, H. flu role is unclear, as they are found in the respiratory flora normally -Mycoplasma, C. pneumoniae, Bordetella pertussis PATHOPHYS: Phase 1: tracheobronchial epithelium becomes infected, leading to fever, malaise and myalgias Phase 2: tracheobronchial lining becomes hypersensitized, leading to cough, with increased sputum production and inflammation of the airways Presentation -cough (+/- productive) for longer than 5 days, up to 3-4 weeks -wheeze, dyspnea -fever, malaise, sore throat, myalgias Exam Findings -could be normal OR -increased HR, RR, temperature -rhonchi, rales or wheezes on pulmonary exam -inspiratory whoop suggestive of pertussis Diagnostics -Clinical diagnosis that correlates with acute bronchitis, not PNA -Questionable? Chest Xray -Pertussis testing Treatment If wheezing = bronchodilators rarely indicated: antibiotics, antihistamines, antitussives Croup Overview Caused by: Parainfluenza RNA virus Transmission: droplet Presentation Adults: URI, bronchitis, prolonged cough Children 6 months --trivalent vs quadrivalent vaccines: 2 flu A and 1-2 flu B strains --high dose if >65 y/o --takes about 2 wks to develop antibodies Asthma Overview EPIDEMIOLOGY: -can impact any age group -genetic predisposition (think atopic triad) -male predominance in childhood, female in adulthood -bimodal severity over a lifetime -highest death rate in young African Americans PATHOPHYS: 1.Bronchial hyper-responsiveness to triggers causes bronchial muscle spasm (bronchoconstriction) 2.airway narrowing due to inflammation/edema of mucosa 3.airway obstruction (can be exacerbated by mucous plugging in the lumen of the airway) ENDOGENOUS/ENVIRONMENTAL FACTORS CONTRIBUTE: -atophy, genetics, ethnicity, obesity, viruses, sinusitis, GERD, stress, emotions, exercise -allergens, passive smoking, occupational (if pt improves on holiday and weekends), cold air temp, meds (Aspirin & beta blockers), pollution Presentation HISTORY: -wheezing, dyspnea -chest tightness -cough – chronic, dry or productive -+/- prodromal symptoms before acute asthma attack (itching under chin, discomfort between scapulae, sense of doom) -symptoms frequently worse at night (nighttime cough) MAKE SURE TO ASK (factors that are incorporated into developing treatment plan): -Frequency of symptoms? -exacerbating/alleviating factors? -night symptoms? Seasonal? With exercise? -hx of atophy? Rhinosinusitis? GERD? Exam Findings VS: increased RR, HR, BP GA: distressed, hunched over posture, +/- audible, non-productive cough Chest: accessory muscle use, retractions, hyperinflation, wheeze, prolonged expiratory phase Diagnostics KNOW HOW TO CLASSIFY ASTHMA BASED ON SEVERITY & FREQUENCY OF SYMPTOMS Spirometry should be used in pt’s: -over 5 yrs of age -at time of diagnosis, after treatment initiation, and every 1-2 years -if loss of control of symptoms -document presence, extent and reversibility of obstruction Methacholine or Mannitol challenge (aka: Bronchoprovocation test): -if unclear -may be useful when chronic cough + normal PFTs Exercise challenge: To support dx of exercise-induced asthma Allergen testing: provides target for avoidance, immunotherapy Arterial blood gas (if in acute distress): -may be normal in mild attack -severe attack can lead to respiratory acidosis then to intubation CXR: shows hyperinflation -not routinely done unless other pathology is suspected Treatment Meds: Dependent on severity of disease Intermittent: SABA therapy PRN Mild persistent: SABA + low dose ICS (inhaled corticosteroid) PRN Moderate persistent: SABA (PRN) + moderate dose ICS maintenance + /- LABA  Severe persistent: SABA (PRN) + high dose ICS + LAMA Non-pharm: -avoid triggers Pulmonary Embolism Overview ETIOLOGY: PE is a complication, not a primary condition -Proximal DVT is most common cause (popliteal and iliofemoral vein thrombi growing upward from calf thrombi) --symptoms of DVT: swelling in affected limb, warmth, pain or tenderness, redness/pallor/other changes in skin -Cardiac emboli: AFib, endocarditis -Other emboli: air, fat, foreign bodies, tumors Saddle PE: lodges at bifurcation of the pulmonary artery and inhibits blood flow bilaterally PATHOPHYS: -embolus enters the pulmonary vasculature, preventing blood flow and resulting in hypoxemia -obstruction can cause increased pulmonary vascular resistance and potentially right heart failure -effects to the lung tissue can include atelectasis and bronchoconstriction Risk Factors RISK FACTORS: Virchow’s Triad of thrombus formation 1.Venous stasis: immobility (bed rest, air travel, obesity), increased viscosity of blood, pregnancy 2.Venous injury: thrombosis, surgery, trauma 3.Hypercoagulable state: medications (OCP,HRT), malignancy, genetic disease (MCC Factor V Leiden associated) -OTHER RISKS: smoking, HTN Presentation CLASSIC TRIAD: dyspnea, pleuritic/substernal chest pain, hemoptysis (uncommon) -syncope -anxiety Exam Findings -tachypnea -hypotension -increased work of breathing, wheeze -cyanosis, diaphoresis -evidence of DVT (swelling, tenderness, erythema over calf/thigh) Diagnostics -Wells criteria and Pulmonary embolism rule-out criteria (PERC) are helpful clinical tools → BE FAMILIAR WITH SCALING DIAGNOSTIC TESTING: -ABG: respiratory alkalosis (hyperventilation)  -abnormal arterial PO2 in most patients -D-dimer: 500 ng/mL will require further investigation -EKG: abnormal in most patients but non-specific --S1Q3T3 evidence of RV strain/ischemia (T-wave inversions V1-V4) -CXR: if normal in a setting of significant hypoxia, then SUSPECT PE --Other possible findings: --Atelectasis, effusions, infiltrates --Westermark’s sign (decreased vasculature) --Hampton’s hump (wedge shaped density above the diaphragm) --Palla’s sign (enlarged R pulmonary artery) -Helical CT PA (pulmonary angiogram): initial study/first line choice for diagnosing PE -V/Q Scan (Ventilation/perfusion scan): most helpful if normal or if very significant defects ---useful in patient that cannot undergo helical CT PA – typically due to contrast allergy IDENTIFYING DVT: -Venous US: initial test of choice --Wink sign: Demonstrates easy collapsibility (absence of clot) of vein or may show thrombus (vein with clot will not be collapsible) -Contrast Venography: gold standard for DVT dx (but not as commonly used) -shows filling defect in lower extremity vein Treatment MANAGEMENT: -supplemental O2 -watch for signs of right heart strain Thrombolytic therapy used for massive PE characterized by hemodynamic instability: --recombinant tissue plasminogen activator (rt-PA, alteplase), streptokinase, urokinase --more effective the sooner it is given after the PE event, can be catheter-directed Anticoagulation is recommended for any PE presentation UNLESS THE PATIENT IS CONTRAINDICATED -Heparin in hospital -Warfarin or other oral anticoagulant after discharge Pulmonary embolectomy – Dependent on size and severity of clot PREVENTION: -Manage the DVT -inferior vena cava filters PROGNOSIS: -good if diagnosed and treated quickly  Pulmonary Hypertension Overview Sustained elevation in pulmonary blood pressure as follows: Systolic pulmonary BP: >30mmHg (normal 15-30 mmHg) Mean pulmonary BP: >20 mmHg (normal 10-18mmHg) ETIOLOGY/PATHOPHYS: -Sustained increase in pulmonary vascular resistance or in the amount of blood backed up from the L heart leads to sustained increased pressure in the pulmonary vascular system -local changes of inflammation, smooth muscle, hypertrophy, fibrosis and thrombosis characterize the disease Presentation -Dyspnea at rest or with exertion -varied levels of physical limitation -chest discomfort/pain -nonproductive cough -fatigue -potential syncope when patient is active (because cardiac output is not sufficient to maintain circulation/oxygenation) -hemoptysis due to ruptured pulmonary artery Diagnostics LABS: -routine bloodwork: results typically normal -HIV testing -collagen vascular disease testing IMAGING: -ECHO with doppler: screens for dx (increased RV systolic pressure, RV side, function) -cardiac catheterization: gold standard for dx -CXR/CT: enlarged pulmonary arteries (centrally) -EKG: normal early; late disease -> Right atrial enlargement, RVH/strain -PFTs: to detect severity -Pulmonary angiogram: to detect severity P/A CXR: demonstrates widened pulmonary hila (main pulmonary arteries) Treatment MANAGEMENT: -complicated and class dependent so refer to pulmonary/cardiology specialists - (don’t have to memorize this list-just know they’re very wide and varied): various treatments of calcium channel blockers, endothelin receptor antagonists, phosphodiesterase inhibitors, prostaglandins, O2, anticoagulation, lung transplant -if underlying condition is identified, then treat that COMPLICATIONS:  -pulmonary edema -Right ventricular hypertrophy -R-sided heart failure -> death PROGNOSIS: -idiopathic etiology or cor pulmonale: poor -underlying condition: dependent on that condition -RVF is most applicable factor when determining prognosis Cor Pulmonale Overview Right sided heart failure due to strain within the pulmonary system, often pulmonary hypertension, pulmonary embolism, or ARDS Presents as acute onset right heart failure Presentation Symptoms of right sided heart failure: -peripheral edema -JVD -shortness of breath -cough Diagnostics Assess for underlying etiology -CTA chest -echocardiogram Labs: -BNP -CBC -CMP -Troponin Treatment Treat the underlying etiology -supplemental O2 & ventilatory support -monitoring fluid status and sodium values Pertussis Overview “whooping cough” -50% of cases occur before age 2 -neither illness nor vaccine confer immunity Presentation Catarrhal stage: 2 wk prodrome, malaise, cough, coryza, anorexia Paroxysmal stage: lasts about 2 wks, rapid consecutive cough with deep high-pitched inspiration / “whoop” – KNOW THAT THE RAPID, CONSECUTIVE COUGH IS ESPECIALLY CHARACTERISTIC OF WHOOPING COUGH  Convalescent stage: 4 wks after onset, slow resolution -may last for 2 months, just don’t want it to get worse during this period Diagnostics Clinical diagnosis Treatment Treatment shortens duration and reduces severity Pharm therapy: -Azithromycin or other macrolide -Bactrim Complications Incontinence, rib fractures, weight loss due to severe coughing Prevention: -Tdap -children >7 yrs, adult boosters every 10 yrs, booster with every pregnancy Respiratory Syncytial Virus Overview Leading cause of bronchiolitis in children 0.5 -fluid LD/serum LD >0.6 -fluid LD >2/3rds normal serum LD Other helpful labs: -amylase: elevated in pancreatic disease, lung cancer and rupture of esophagus -culture and sensitivity: pathogen ID and treatment options -cytologic evaluation: identification of malignant cells Treatment 1.Thoracentesis: for removal of pleural fluid or air  -diagnostic as effusion fluid can be analyzed to help identify etiology -may be therapeutic Empyema must be drained -infectious effusions with pH < 7.3 or LD >1000 units/L should be drained -Hemothorax MUST be drained -Transudative effusion: treat the underlying disease (these effusions typically recur so drainage is not as helpful) Pneumothorax Overview Accumulation of air in the pleural space ETIOLOGIES: Spontaneous: -Primary: occurs without pulmonary disease; tall, thin, young males -Secondary: occurs with pulmonary disease Traumatic: -Trauma: acc