NR 667 VISE STUDY GUIDE REVIEW- BEST REVISION MATERIAL FOR FINAL EXAM

1 / 41 NR 667 VISE STUDY GUIDE REVIEW BEST REVISION MATERIAL FOR FINAL 1. Etiology: Hypertension: -No known cause in 90% of cases of primary HTN -Secondary causes: renal failure, kidney disease, renal artery stenosis, Cushing syndrome, hyper/hypo thyroidism, increased ICP, sleep apnea, oral contraceptives, steroids, cocaine, NSAIDs, decongestants, sympathomimetics, alcohol, antidepres- sants, caffeine 2. Risk Factors: Hypertension: -Modifiable: smoking, DM, high cholesterol, obesity (single most important factor in children), physical inactivity, poor diet, excessive sodium intake, excessive alcohol consumption -Non-modifiable: CKD, family hx, increased age (55 men, 65 women), low socioeconomic status, low educational status, male sex, OSA, stress, pregnancy 3. Assessment: Hypertension: -Most are asymptomatic; occipital headache, headache upon waking, blurry vision, fundoscopic exam (AV nicking, exudates, papilledema), left vent. hypertrophy, pregnancy w/HTN and proteinuria, edema, and excessive weight gain 4. Differential Diagnosis: Hypertension: -Secondary HTN, white coat HTN (artifi- cial elevation d/t medical environment anxiety) 5. Final Diagnosis: Hypertension: -Urinalysis = proteinuria -Electrolytes, creatinine, calcium -Fasting lipid profile and BS -ECG -Measure BP twice, 5 mins apart -Patient should be seated; use proper cuff size and application 6. Prevention: Hypertension: -Maintaining healthy weight and BMI -Smoking cessation -Regular aerobic exercise -Alcohol in moderation ( 1 oz/day) -Stress management -Medication compliance -Assess for and treat OSA 7. Non-pharm management: Hypertension: -Stage 1: Risk score 10% =lifestyle modification -Stage 2: lifestyle + medication -DASH eating plan: high fruit, veggies, grains; low fat dairy, fish, poultry, beans, nuts -Reduce dietary sodium to 2,300mg/day, increase K+ -Reduce sat. fat intake -Body weight reduction; 1kg of weight reduction = 1 mm/hg bp reduction -150 mins of aerobic exercise and/or 3 sessions of isometric resistance per week -Treat other underlying diseases -Check bp 2x/week during pregnancy2 / 41 8. Pharmacological management: Hypertension: -Start medication for primary prevention of CVD if pt. has ASCVD risk e 10% and stage 1 HTN or if ASCVD is 10% with bp 140/90 -Stage 2: start 2 bp-lowering medications -African Americans: 2+ medications recommended; thiazide and CCBs are the most effective *DO NOT use ACE and ARB concurrently -Beta blockers are NOT first line -Thiazides, CCBs, ACEIs, and ARBs can be used alone or in combo 9. Pregnancy considerations: Hypertension: -Can use beta blockers (labetalol), methyldopa, CCBs (nifedipine) -AVOID ARBs and ACEIs 10. Follow-up: Hypertension: -Inquire about adherence and any side effects -Reassess monthly until patient reaches goal, then every 3-6 months as needed 11. Expected course: Hypertension: -Only 54% of treated patients are at goal treatment; expect complications if under treated -Most patients require more than one medication to reach goal bp 12. Possible Complications: Hypertension: -Stroke, CAD, MI, renal failure, heart failure, eclampsia (seizures), pulmonary edema, hypertensive crisis, hypertensive retinopathy, ED 13. Etiology: Hyperlipidemia: -Inherited disorder, high dietary intake, obesity, sedentary lifestyle, DM, hypothyroidism, anabolic steroid use, hepatitis, cirrhosis, uremia, nephrotic syndrome, stress, druginduced (thiazide diuretics, beta blockers, cyclosporine), alcohol, caffeine, metabolic syndrome 14. Risk factors: Hyperlipidemia: -Family history, physical inactivity, smoking, age (men 45, women 55 or premature menopause without estrogen replacement), obesity, diet high in sat. fat, DM 15. Assessment findings: Hyperlipidemia: -Few physical findings; xanthomata (fat deposits in the skin), xanthelasma (yellow plaques on the eyelid), corneal arcus prior to age 50 (arc of cholesterol around the iris), bruits, angina pectoris, MI, stroke 16. Differential diagnosis: Hyperlipidemia: -Secondary causes: hypothyroidism, pregnancy, DM, nonfasting state 17. Final diagnosis: Hyperlipidemia: -Fasting lipid profile: 9-12 hours -Glucose level -Urinalysis, creatinine (for detection of nephrotic syndrome which can induce dys- lipidemia) -Baseline transaminases -TSH for detection of hypothyroidism (which can cause secondary dyslipidemia) -Calculate ASCVD 10-year risk3 / 41 18. Prevention: Hyperlipidemia: -Healthy lifestyle reduces ASCVD in all age groups -Dietary interventions: encourage mediterranean and DASH diet; limit saturated and trans fats; limit sodium intake; increase fiber, vegetables, fruits, and other whole grains; eat lean meats (poultry, fish); eggs, beans, nuts, low-fat dairy, avoid red meat, limit sugary drinks and sweets -Mod to vigorous exercise of at least 40 mins 3-4x/week (sustained aerobic activity increases HDL, decreases total cholesterol) -Avoid tobacco -Appropriately manage systemic diseases (DM, hypothyroidism, HTN) 19. Non-pharm management: Hyperlipidemia: -Nutrition, weight reduction, in- creased physical activity, patient education about risk factors 20. Pharmacological management: Hyperlipidemia: -Assign to a statin treatment group using ASCVD 10-year risk calculator -Primary lipid target it LDL -Statins are 1st-line therapy -Combo of statin and non-statin in some patients -Consider adding non-statin if unable to achieve LDL 70mg/dl, but VERIFY adher- ence to statins and lifestyle changes -Non-statins: ezetimibe (1st), bile acid sequestrant, vibrate, PCSK9 inhibitor 21. Pregnancy/lactation consideration: Hyperlipidemia: -Cholesterol is usually elevated during pregnancy; measurement is not recommended and treatment is contraindicated 22. Follow-up: Hyperlipidemia: -Check fasting lipid panel 4-12 weeks after starting or adjusting a statin or non-statin -Monitor for medication compliance and lifestyle modification, especially if LDL drop is less than expected 23. Expected course: Hyperlipidemia: -Depends on etiology and severity of dis- ease -1% decrease in LDL value decreases CHD risk by 2% 24. Possible complications: Hyperlipidemia: -CAD, cerebrovascular disease, PVD, arteriosclerosis 25. Etiology: DM II: -Influences by genetics and environmental factors -High body mass and central obesity -Drug or chemical-induced: glucocorticoids, highly active antiretroviral therapy 26. Risk factors: DM II: -BMI 25 -History of gestational DM and/or macrocosmic infant -Family history of T2DM -Conditions associated with insulin resistance: PCOS, acanthosis nigricans)4 / 41 -HDL-C 35 and/or TG 250 -HTN -History of CVD -Hemochromatosis -Impaired fasting glucose -Physically active 3 days/week 27. Assessment findings: DM II: -Usually discovered on routine exam -CMP and urinalysis: glycosuria, proteinuria, hyperglycemia -Obesity -Acanthosis nigricans -Polydipsia, polyuria, polyphagia -Fatigue -Blurred vision -Chronic skin infections -Balanitis in men 65 years -Chronic candidiasis vulvovaginitis -Hyperosmolar state or coma 28. Differential diagnosis: DM II: -TIDM -Prediabetes -Gestational diabetes -Cushing's syndrome -Pheochromocytoma -Acromegaly -Corticosteroid use -Pancreatic insufficiency 29. Final diagnosis: DM II: -Fasting plasma glucose: 126 -HgA1c: e 6.5% -Random plasma glucose + oral glucose tolerance test: e200 with symptoms OR 2-hour plasma glucose e 200 on OGTT with 75g glucose load -Prediabetes: fasting glucose 100-125 OR A1C 5.7-6.4% OR OGTT 140-199 -A1C every 3 months until goal is met or therapy is changed, then twice yearly with stable glycemic control 30. Prevention: DM II: -Weight loss of 7-10%; reach and maintain normal BMI -Exercise 150 mins or more per week; no more than 2 consecutive days without activity -Resistance training 2-3x/week -Reduce length of sedentary intervals by interrupting prolonged sitting every 30 mins -Screen for tobacco use; provide smoking cessation counseling and referral -Screen for depression, distress, anxiety, eating disorders, cognitive impairment5 / 41 -Screen for ability to afford meds, access to healthy food, food insecurity, and community support 31. Non-pharm management: DM II: -Weight loss is primary goal for all obese patients; modest weight loss of 5-10 lb can increase insulin sensitivity -Refer to diabetes educator for management education and support -Nutrition plan: 3 visits with dietician at diagnosis + f/u visits -Avoid alcohol and smoking -Assess medication compliance -Assess technology use to assist in reaching goals -Routine dental visits, thyroid palpation, skin exam, neuro exam, abdominal exam, cardiac exam, foot exam 32. Pharmacological management: DM II: -Consider effects of weight and comor- bid conditions when selecting medications -First line: biguanides (metformin) at dx unless contraindicated; consider XR to reduce GI side effects -2nd/3rd line is based on established ASCVD or CKD and patient characteristics, preferences, potential adverse effects, expected A1c reduction, and cost -Start dual therapy if A1c e 1.5% above glycemic target -Early insulin introduction: A1c 8-10%, BS 300, catabolism (weight loss) -Consider GLP-1 as first injectable before insulin -ASCVD history: GLP-1 or SGLT2 inhibitor (if adequate eGFR) -HF or CKD: SGLT2 inhibitor -Insulin: when oral medications have been exhausted; 0.1-0.2 units/kg/day or 10 u daily of peakless basal insulin -If unable to reach goal, administer meal-time insulin 33. Pregnancy/lactation considerations: DM II: -7% of pregnancies are compli- cated by diabetes; 90% of these are gestational diabetes -Screen for undiagnosed DM II at first prenatal visit -Universal screening for GDM at 24-28 weeks gestation -Pre-existing DM should be managed by endocrinologist, MFM, dietician, and dia- betes educator -Ideal A1c during pregnancy is 6.0% to reduce the risk of maternal and fetal complications *Increased risk of spontaneous abortion, stillbirth, congenital anomalies -Insulin is the preferred treatment in GDM, T1DM and T2DM in pregnancy because it doesn't cross the placenta 34. Follow-up: DM II: -Individualized based on findings of initial evaluation, attain- ment of metabolic targets, and risk for complications -Follow ADA standards of care for f/u recommendations6 / 41 35. Expected course: DM II: -Dependent on glucose control; poor control results in increased risk for vascular complications -Complications typically develop 10-15 years after onset but can present earlier if DM is undetected for years before diagnosis 36. Possible complications: DM II: -Diabetic kidney disease, renal failure -Peripheral neuropathy -Retinopathy -Cardiovascular and peripheral vascular disease -Glaucoma, cataracts, blindness -Skin ulcerations, gangrene of lower extremities, limb amputations -Charcot foot -DKA -Hyperosmolar hyperglycemic state -Gastroparesis 37. Etiology: Back pain: -Often unclear -Can be caused by tearing or stretching of nerves, muscles, tendons, ligaments, discs, or fascia secondary to trauma or chronic mechanical stress -Can occur as a symptom of a degenerative disorder (spinal stenosis, DDD, disc herniation) -Compression or irritation of a nerve root can occur along with back pain, causing radiculopathy -Most commonly affected discs are L4-L5, and L5-S1 38. Risk factors: Back pain: -Obesity -Sedentary lifestyle inadequate conditioning -Smoking -Preexisting psychological conditions -Chronic occupational strain with improper lifting techniques -Exaggerated lumbar lordosis, chronic poor posture -Leg length discrepancy -Age 65 -Job dissatisfaction 39. Assessment findings: Back pain: -Cauda equina is a surgical emergency that presents with back pain + 1. perineal anesthesia, 2. loss of bladder/bowel control, 3. loss of rectal sphincter tones with digital exam, 4. bilateral radicular pain, numbness and weakness -Back, but, and thighs may be aggravated by movement, rising from seated position, standing, and flexion; may be relieved by rest, repositioning, or reclining -Muscle spasm may be present over lumbosacral area due to ligament or muscle involvement7 / 41 -Pain may radiate down leg below knee with with spinal nerve irritation and radicu- lopathy -Motor, sensory, and reflex exams are essential; note asymmetry of findings -Observe gait, lower extremity strength, and muscle bulk 40. Differential Diagnosis: Back pain: *New onset radicular pain in older patients is often a sign of spinal stenosis -Low back strain -Herniated disc -Multiple myeloma -Osteomyelitis -Prostatitis, pyelonephritis -Vascular occlusion at level of bifurcation; AAA -Carcinoma if bony metastasis occurs -Endometriosis, fibromyalgia -Depression, hysteria -Malingering (get out of work card) -Compression fracture, osteoporosis -Osteoarthritis -Ankylosing spondylitis -Cauda equina -Hip/pelvic pathology -Drug-seeking 41. Final diagnosis: Back pain: -Routine imaging is nor recommended with new onset mechanical back pain and no red flags -Red flags: cauda equina, fracture, malignancy, infection -Lack of improvement over 6-8 weeks warrants AP and lateral x-rays of the spine -Red flags or severe/progressive neuro deficits, consider MRI, CT, bone scan, CBC, ESR, UA 42. Prevention: Back pain: -Proper lifting technique, body mechanics, and posture -Conditioning exercises -Maintenance of appropriate weight for height -Avoid smoking 43. Non-pharm management: Back pain: -Patient education and reassurance that recovery occurs in 6- 8 weeks in 80-90% of patients -Avoid bed rest; no more than 1-2 days -PT: for subacute or chronic back pain -Chiropractics: limited evidence of improvement -Acupuncture: short-term pain relief -Hot/cold application for 20-30 mins several times per day8 / 41 -Gradually resume activities as tolerated -Shoe insoles recommended for leg length discrepancies -CBT to reduce disability related to subacute and chronic pain 44. Pharmacological management: Back pain: -Tylenol: common first-line agent -NSAIDs: effective first-line agent for short-term relief of acute and subacute low back pain; all are though to have equal efficacy -Muscle relaxers: to reduce/eliminate muscle spasm -Opioids: effective but significant concern for abuse, misuse, and addiction -Tramadol: for acute or chronic back pain; short-term use -Antidepressants: TCAs can be used for chronic back pain -Topical agents: little evidence -Steroid: No evidence supports use in acute non-specific low back pain 45. Follow-up: Back pain: -Return for evaluation in 24-48 hours if pain is severe, or in 7-10 days if pain is moderate -F/u ever 2 weeks until able to resume lifestyle -If unable to tolerate activities despite no serious underlying pathology, consider psychosocial factors 46. Expected course: Back pain: -In 80-90% of cases, symptoms resolve in 4-6 weeks 47. Possible complications: Back pain: -Prolonged disability -Chronic pain -Renal, hepatic, cardiac, or gastric complications with NSAID therapy 48. Etiology: Anxiety: -Behavioral theory: a conditioned response to specific envi- ronmental stimuli -Genetic component: 1st degree relatives increases the likelihood 8-fold -Biologic theories: Norepi, serotonin, and GABA are poorly regulated; the ANS inappropriately responds to stimuli; cerebral pathology causes anxiety; HPA axis highly implicated 49. Risk factors: Anxiety: -Organic causes: endocrinopathies, cardiorespiratory disorders, anemia -Use or withdrawal from medications/substances: alcohol, caffeine, cocaine, steroids, lidocaine, oral contraceptives, NSAIDs, SSRIs, -Family history -Psychiatric disorders: MDD, PTSD, personality disorders, schizophrenia 50. Assessment findings: Anxiety: -Children: separation anxiety after age 3-4 years (can be present in adulthood); unrealistic worry about harm to self or family; persistent worry about past behavior, competence, or future events -Adults: apprehension, restlessness, edginess, distractibility, insomnia -Somatic complaints: fatigue, headaches, paresthesia, near syncope, derealization,9 / 41 dizziness, diaphoresis, palpitations, tachycardia, chest pain/tightness, dyspnea, hyperventilation, N/V/D, excessive rumination 51. Differential diagnosis: Anxiety: -OCD -Oppositional defiant disorder -Personality disorder -Depression -Bipolar disorder -ADD -Cognitive disorder (i.e. delirium) -Substance intoxication or withdrawal -PTSD -Any medical condition that involves stimulation of the sympathetic nervous system 52. Final diagnosis: Anxiety: -TSH, CBC, UA, urine drug screen, arrhythmias, hyperthyroidism, drugs -Psychologic testing: PROMIS, Hamilton anxiety scale, Zung anxiety self-assess- ment, GAD-7 53. Non-pharm treatment: Anxiety: -Psychotherapy: education about dx, treat- ment plan, and prognosis; support and empathetic listening; 1st-line treatment for children and adolescents; relaxation techniques; CBT; reconditioning (exposure to feared stimuli in a controlled setting to develop tolerance and eventually eradicate the anxiety response) -General measures: regular exercise, healthy diet, adequate sleep, limit caffeine, serial office visits 54. Pharmacological management: Anxiety: -Benzodiazepines should be of lim- ited duration with the intent of allowing the patient to benefit from behavioral treat- ments -Drugs should play an adjunctive role, except in panic disorder -Drugs reduce, not eradicate, symptoms -Long-term use of SSRIs may be required 55. Pregnancy/lactation considerations: Anxiety: -Sertraline may be used 56. Follow-up: Anxiety: -Regular f/u visits are importance to reinforce education about non-pharm management and proper medication use -Avoid prescribing anxiolytics by phone -Watch for signs of medication misuse -TCAs require periodic serum levels + baseline and f/u EKGs 57. Expected course: Anxiety: -Anxiety in children can be a precursor to agora- phobia (severe social anxiety) or panic disorder in adulthood -Treatment of medical cause usually initiates improvement10 / 41 -Short-term anxiety disorders usually respond well to treatment -OCD requires long-term pharmacologic therapy and psychotherapy 58. Possible complications: Anxiety: -Work/school related difficulties -Self-medication leading to alcohol abuse, benzodiazepine dependence -Social impairment -Cardiac arrythmias d/t TCA use -Falls d/t sedating effects of medications esp. in older adults -Suicide 59. Etiology: Obesity: -Multifactorial: physiologic, genetic, environmental, psycho- logical, cultural -physiologic: imbalance between food intake and energy expenditure; dysregulation between hunger and satiety hormones -Genetic: several single genes cause rare forms of obesity; dozens of genes influ- ence common forms -Environmental: decreased activity, energy-dense foods -Obesogenic medications: antihistamines, steroids, beta blockers, SSRIs) can cause or contribute to weight gain 60. Risk factors: Obesity: -Parental obesity -Decreased socioeconomic status -Intake of calorically dense, nutrient-deficient, highly palatable foods -Sedentary lifestyle/inactivity -Increased screen use, esp. among children 61. Assessment findings: Obesity: -Staging is based on complication-specific criteria -Waist circumference: Women 35 inches; men 40 inches 62. Differential diagnosis: Obesity: -Acromegaly -Ascites -Iatrogenic Cushing syndrome -Mesomorphic body states: elevated BMI due to muscle mass rather than adiposity 63. Final diagnosis: Obesity: -Perform focused history and physical exam to eval- uate for obesity complications and comorbidities -None needed for dx, but can assist with identifying obesity-related comorbidities: thyroid function, lipid panel, fasting glucose, A1C, fasting insulin, LFTs, CBC, CMP, lipase, amylase, ECG, screening for anxiety/depression and OSA 64. Prevention: Obesity: -Well-balanced diet -Reduce sedentary behavior, increase regular physical activity; goal 150 mins/week, including resistance exercise -Sufficient sleep: inadequate sleep causes gherkin to increase and leptin to de- crease, producing greater hunger than when rested11 / 41 65. Non-pharm management: Obesity: -Counseling about lifelong strategies with use of 5As of obesity: ask, assess, advise, aggress, assist -Behavioral interventions: realistic goal setting, education, health outcomes, focus on progress -Determine caloric requirement for body weight, then institute a 500 cal/day deficit during weight loss -Track food and activity -Regular f/u for health outcomes, weight loss tracking, motivation, and improvement of obesity-related complications 66. Pharmacological management: Obesity: -May be helpful as adjuvant therapy with lifestyle interventions for patients with BMI 30 or 27 with comorbidities -If one option doesn't work, consider others -D/c medications in patients who do not respond with weight loss of at least 5% in 12 weeks -Avoid in pregnancy 67. Follow-up: Obesity: -Long-term, frequent f/u as for most chronic conditions; this disease has a relapsing nature based on physiology, so patients require close monitoring -Surgical patients need long-term f/u with surgeon and primary care to monitor weight loss and nutrition -Annual labs as indicated by medication administration, comorbidities, and annual needs 68. Expected course: Obesity: -Chronic condition: rarely cured but can be con- trolled -Long-term maintenance of weight loss difficult due to metabolic adaptation -Dependent on sustained patient motivation and circumstances 69. Possible complications: Obesity: -Prediabetes -Metabolic syndrome -DM II -Dyslipidemia -Cancer -Hypertension -CVD -Non-alcoholic fatty liver disease and steatohepatitis -PCOS, infertility -Male hypogonadism -Respiratory disease, including asthma -Osteoarthritis -Urinary stress incontinence12 / 41 -GERD -Psychiatric disorders -Increased mortality -Cholelithiasis, esp. with rapid weight loss -Thromboembolism -Decreased mobility -Decreased exercise tolerance -OSA 70. Etiology: Allergic rhinitis: -Any substance or condition that causes an IgE-me- diated response characterized by rupture of mast cells and release of histamines, leukotrienes, prostaglandins, and other compounds -Seasonal allergens: pollens from grass, trees, weeds -Perennial allergens: mold, animal dander, dust mites, smoke 71. Risk factors: Allergic rhinitis: -Family history -Other topics diseases (asthma, atopic dermatitis, allergic conjunctivitis, food aller- gy) -Repeated exposure to the allergen -Non-adherence to treatment 72. Assessment findings: Allergic rhinitis: -DX is based on h+p findings consis- tent with allergy-related cause; presence of one or more of these symptoms: nasal congestion, rhinorrhea, itchy nose, sneezing -Conjunctival injection, watery eyes -Pale, boggy nasal mucosa with congestion and clear rhinorrhea -Transverse crease on tip of nose due to allergic salute-repeated wiping of nose in an upward direction -Mouth breathing, dry lips -Sore throat, dry mouth upon waking -Palpable lymph nodes -Enlarged tonsils and adenoids -Presence of associated conditions: sleep-disordered breathing, otitis media, rhinos- inusitis, conjunctivitis, asthma, atopic dermatitis 73. Differential diagnosis: Allergic rhinitis: -Vasomotor rhinitis -Rhinitis medicamentosa -Infection -Tumors -Nasal foreign body -Common cold -Granulomatous diseases -CSF rhinorrhea13 / 41 74. Final Diagnosis: Allergic rhinitis: -Usually none -CBC: eosinophilia if acute reaction -CT scan is primary imaging study -Allergy testing for those that don't respond to empiric treatment (stop antihistamines 1 week before testing) -RAST: specific IgE test for patients in whom severe reaction is possible 75. Prevention: Allergic rhinitis: -Minimize continuous exposure to commonly known allergens -Remove offending allergens from environment -Adherence to pham regimen -Avoidance of allergen is first-line treatment 76. Non-pharm management: Allergic rhinitis: -Avoid/eliminate allergens -Immunotherapy -Nasal airway obstruction and enlarged inferior turbinates, refer to ENT -Acupuncture 77. Pharmacological management: Allergic rhinitis: -Saline nasal spray to rinse nasal passages of pathogens -Antihistamine -Inhaled nasal steroid; preferred for most cases -Nasal antihistamine: for seasonal, perennial, or episodic cases -Combo therapy when mono therapy fails -Systemic steroid short term -Topical cromolyn -Leukotriene modifier for patients with other allergies; not recommended as primary therapy -Decongestants, topical or oral 78. Pregnancy/lactation considerations: Allergic rhinitis: -If pregnant with histo- ry of AR, may continue previous INS if symptoms are controlled -May use loratidine or cetirizine -If pregnant with new diagnosis, use budesonide 79. Follow-up: Allergic rhinitis: -2-4 weeks after initial evaluation and then every 3-6 months, depending on the patient and symptom severity 80. Expected course: Allergic rhinitis: -Allergies tend to diminish in severity as people age -Allergic response usually not seen at first exposure; response is heightened each time allergen is contacted -Risk for developing asthma or atopic dermatitis 81. Possible complications: Allergic rhinitis: -Otitis media -Secondary infections: sinusitis, tonsilitis, pharyngitis14 / 41 -Epistaxis -Facial changes: allergic shiners, allergic salute, chronic dry lips, chronic nasal flaring -Snoring 82. Etiology: GERD: -Facilitated by decreased lower esophageal sphincter (LES) tone -Some cases are physiologic -GERD is present when gastric contents flow upward into the esophagus or orophar- ynx, producing symptoms 83. Risk factors: GERD: -Factors that reduce LES tone: alcohol, anticholinergics, CCBs, caffeine, chocolate, peppermint, fatty/spicy/citrus foods, hormones, meperi- dine, nicotine, overweight, pregnancy -Aging -DM, gastroparesis -Delayed gastric emptying -Increased gastric acid secretion -Irritation of esophageal mucosa: NSAIDs, tetracycline, quinidine, caffeine, SSRIs, hydrocodone -Zollinger-Ellison syndrome (too much acid) -Childhood GERD 84. Assessment findings: GERD: -Chest pain (requires cardiac workup) -Chronic sore throat/hoarseness -Dysphagia -Erosion of tooth enamel -Esophageal pain referred to neck, midback, upper abdomen -Extra-esophageal presentation: asthma, chronic cough, laryngitis -Post-nasal drip, throat clearing -Pyrosis (heartburn) -Regurgitation -Sensation of lump in throat -Ulceration: hematemesis, fatigue, anemia 85. Differential diagnosis: GERD: -Asthma -Cardiac disease -Cholelithiasis -Esophageal spasm, infection, cancer -H. pylori -Hiatal hernia -IBS -Intestinal motility disorders15 / 41 -Lower resp. infection: bronchitis, pneumonia -PUD (often coexists) 86. Final diagnosis: GERD: -Presumptive DX can be made based on sx of heart- burn and regurgitation -Empiric PPI therapy for 8 weeks should be initiated -Endoscopy is recommended for patients with GERD that do not respond to empiric PPI treatment 87. Prevention: GERD: -Lifestyle modification -Maintain a healthy weight (BMI 25) -Eat smaller meals -Avoid trigger foods (fatty, spicy, acidic, mint, chocolate, garlic/onion, caffeine, car- bonation) -Don't lie down for 2-3 hours after eating -Elevate head 6-8 inches -Quit smoking -Limit alcohol consumption 88. Non-pharm treatment: GERD: -Education of physical causes, aggravating fac- tors, and lifestyle changes to control it 89. Pharmacological management: GERD: -8 week course of PPI therapy -PPIs should be dosed once daily and before the first meal of the day -If partial response to PPI, increase to BID dosing -If symptoms persist after 8 weeks, refer to gastro 90. Follow-up: GERD: -Consider maintenance therapy to manage symptoms and prevent long-term complications -CBC -Screen for B12 deficiency and increased risk of osteopenia after long-term PPI use 91. Expected course: GERD: -Most patients respond well to combined therapies -Symptoms may return once mediation is withdrawn 92. Possible complications: GERD: -Erosion/ulceration -Stricture -Barrett's esophagitis -High-grade dysplasia -Esophageal adenocarcinoma -Aspiration pneumonia 93. Etiology: URI: -Rhinoviruses are the most common cause (30-50%) -Parainfluenza and influenza virus -Adenovirus -Coronaviruses (20%) -Enteroviruses, including coxsackievirus16 / 41 -Moraxella catarrhalis (children more than adults) -RSV -Human metapneumovirus 94. Risk factors: URI: -Exposure to infected people via inhaled droplets when coughing/sneezing -Psychological stress -Touching contaminated surfaces then touching nose or conjunctiva -Infants and children are the most susceptible d/t lack of immunity -Inflammation and obstruction due to allergic rhinitis and asthma -Smoking/secondhand smoke exposure -Expose to large numbers of people in close proximity 95. Assessment findings: URI: -Obtain thorough history to aid dx -Most common symptoms: nasal stuffiness, sneezing, scratchy/irritated throat, hoarseness, runny nose, red/irritated nasal mucosa -Nasal secretions: initially clear, progress to cloudy, yellow, or green -Malaise, headache -Halitosis -Cough -Occasional low-grade fever 96. Differential diagnosis: URI: -Allergic or vasomotor rhinitis -Pharyngitis (viral vs bacterial) -Acute bronchitis -Influenza -Sinusitis -Pertussis -Mono -Epiglottitis -Mumps -Rubeola -Varicella 97. Final diagnosis: URI: -Usually none indicated -Tests may be helpful to r/o other diseases: strep, flu, mono, pertussis -CBC if symptoms persist; elevated WBC indicates bacterial infection 98. Prevention: URI: -Good hand washing! -Alcohol-based hand sanitizers -Avoid exposure to infected people -Adequate rest -Stress management -Flu vaccine can prevent colds caused by influenza pathogens17 / 41 99. Non-pharm management: URI: -Increase rest, fluids -Humidified air -Hard candy/lozenges for scratchy throat -Saline nose drops and bulb syringe for infants -Avoid secondhand smoke; d/c tobacco -Avoid alcohol *Teach patients that hand washing is the single most effective preventive measure 100. Pharmacological management: URI: -Don't use OTC cold medications in patients 4 -Children: time, nasal saline, analgesics -Pregnancy: avoid systemic therapy -Topical decongestants: reduce edema in nasal passages, promote drainage, are OTC 101. Follow-up: URI: -None usually needed unless symptoms persist past 2 weeks or worsen 102. Expected course: URI: -Complete resolution within 10-14 days -Fever, sneezing, pharyngitis usually resolve first -Cough and nasal discharge usually last longer 103. Possible complications: URI: -Sinusitis -Bronchitis, bronchiolitis -Pneumonia -Otitis media -Asthma in patients who's asthma is triggered by viral infections 104. Etiology: Hypothyroidism: -Majority of cases are due to primary thyroid gland failure resulting from autoimmune destruction (Hashimoto's thyroiditis) -Iatrogenic -Iodine deficiency or excess -Lithium -Amyloidosis -Sarcoidosis -Scleroderma -Ablative therapy for hyperthyroidism -Other causes are congenital, secondary or tertiary due to pituitary or hypothalamic disease 105. Risk factors: Hypothyroidism: -Increasing age -Family history -Postpartum -Pituitary disease -Hypothalamic disease18 / 41 -Autoimmune diseases -History of head or neck irradiation -Treatment of hyperthyroidism -Treatment with lithium or iodine-containing amiodarone 106. Assessment findings: Hypothyroidism: -Clinical symptoms range from asymptomatic to myxedema coma -Lethargy, delayed DTRs -Mild weight gain, swelling of hands/feet, macroglossia (large tongue), periorbital edema -Cold intolerance -Constipation -Menstrual irregularities, decreased libido, infertility -Memory loss, depression -Course dry skin; body and scalp hair loss, brittle nails -Bradycardia, enlarged heart -Anemia *Expect lipid levels to be elevated 107. Differential diagnosis: Hypothyroidism: -Depression -Dementia -Heart failure -Kidney failure 108. Final diagnosis: Hypothyroidism: -Serum TSH is increased in thymoprivic (rare) and goitrous hypothyroidism (20) -TSH is normal or undetectable in pituitary or hypothalamic hypothyroidism -T43 decreased most commonly; occasionally t3 109. Prevention: Hypothyroidism: -Periodic monitoring of thyroid hormone levels for patients treated for hyperthyroidism -Identification of risk factors -Newborn thyroid screening at 2-6 days of age 110. Non-pharm management: Hypothyroidism: -Educate patients that children may have behavioral problems at the start of treatment -High-fiber diet to prevent constipation -If obese, diet for weight loss/body fat reduction -Educate about the need for life-long adherence to thyroid replacement and to report signs of toxicity, infection, or cardiac symptoms -Annual lipid level assessment 111. Pharmacological management: Hypothyroidism: -L-thyroxine daily; begin at lower dose in older adults or in the presence of cardiac disease (25 mcg/daily) -In young healthy patients: 1.6mcg/kg/day19 / 41 -Older patients: start at 12.5-50mcg/day -Adult maintenance: 50-200mcg/day -Infants: 6-15 mcg/kg/day based on age -Children: 4-6 mcg/kg/day based on age *Rapid replacement in infants and children results in attainment of normal IQ 112. Pregnancy/lactation considerations: Hypothyroidism: -At 8 weeks gesta- tion, levothyroxine dose requirements rise by 25-50% -TSH should be assessed every 4 weeks during the first half of pregnancy, then less frequent (once every trimester) -Reduce levothyroxine dose to pre-pregnancy dose immediately after delivery -Breastfeeding is not a contraindication to levothyroxine therapy 113. Follow-up: Hypothyroidism: -Measure TSH after 6 weeks of therapy and every 6-8 weeks until goal is met; then annually UNLESS symptomatic -Examine periodically for signs of thyrotoxicity (i.e. tremor or tachycardia) -Congenital hypothyroidism: periodically monitor t4 and TSH 114. Expected course: Hypothyroidism: -Improvement is expected 2 weeks after medication initiation -Signs and symptoms shoulder resolve in 3-6 months -Lifelong therapy is needed 115. Possible complications: Hypothyroidism: -Myxedema coma: life-threaten- ing, severe hypothyroidism; may require IV levothyroxine and cardiorespiratory assistance -Thyrotoxicity -Treatment-induced heart failure in older adults or patients with CAD -Bone demineralization due to over treatment for a long period -Without treatment, congenital hypothyroidism may lead to mental retardation -Growth and development delays -Increased risk of infection -Sexual dysfunction -Infertility -Miscarriage -Megacolon -Adrenal crisis 116. Etiology: Osteoarthritis: -Primary OA can be a localized or generalized dis- ease with no known cause -Secondary OA is associated with trauma, infection, genetic, or metabolic disorders 117. Risk factors: Osteoarthritis: -Obesity -Age -Trauma20 / 41 -Prolonged use or overuse of joints related to occupation or activity -Family history -History of developmental dysplasia of the hip or slipped femoral epiphysis -Hemophilia -Paget's disease 118. Assessment findings: Osteoarthritis: -Joint pain, usually asymmetrical, de- velops insidiously and accompanies or follow physical activity -Morning stiffness lasting 1 hour; stiffness resumes toward the end of the day after periods of activity -Joints are cool with possible crepitus and limited ROM -Overgrowth of osteophytes results in bony enlargement, especially bunions (MTP joint), Heberden's nodes (DIP), and Bouchard's nodes (PIP) -Joint instability, particularly the knees 119. Differential diagnosis: Osteoarthritis: -Gout, pseudogout -Infective arthritis -Inflammatory arthritis -Joint injury -Soft tissue injury -PVD -Giant cell arteritis -Bursitis -Tendinitis -Osteopenia -Neuropathy -Hemochromatosis 120. Final diagnosis: Osteoarthritis: -No diagnostic lab tests are available; dx is based on h+p, and xray findings -X-rays: osteophytes, joint space narrowing, and subchondral sclerosis -Inflammation markers: negative -Iron sat or ferritin to r/o hemochromatosis -US can identify OA changes and can help detect synovial inflammation 121. Prevention: Osteoarthritis: -Weight control -Management of underlying causes of secondary disease 122. Non-pharm management: Osteoarthritis: -Weight loss if indicated; loss of 10% body weight can lead to improvement in reported symptoms -OA is a chronic disorder that requires muscle strengthening to provide joint support -Knee/elbow braces to stabilize joints during exercise -Heat/cold application to affected joints21 / 41 123. Pharmacological management: Osteoarthritis: -Use only when symptoms are present; routine use won't modify disease -Usually needed long-term -Short-acting NSAIDs are associated with fewer side effects than long-acting forms -Consider COX-2 inhibitors for GI protection -Topical NSAIDs are good alternative -Tramadol can be used as add-on therapy -Intra-articular steroid injections limited to 4x/year 124. Follow-up: Osteoarthritis: -Regularly scheduled return visits for evaluation, support, and education -NSAID therapy requirements: periodic CBC, renal function, stool for occult blood -Periodic clinical assessment to evaluate symptom management and functionality status 125. Expected course: Osteoarthritis: -Usually progressive with more pain at rest, joint effusions, and bony enlargement -Goals of therapy are to minimize pain and optimize functioning while targeting modifiable risk factors 126. Possible complications: Osteoarthritis: -Adverse reactions from NSAIDs, corticosteroids -depression associated with chronic illness -Disability due to disease progression 127. Etiology: Fibromyalgia: -Unknown, but likely involves nervous system -Possible disorder of pain regulation 128. Risk factors: Fibromyalgia: -Age 30-50 years -Genetics -Infections -Physical or emotional trauma -Rheumatic disease (OA, lupus, rheumatoid, arthritis, ankylosing spondylitis) 129. Assessment findings: Fibromyalgia: -Multisite pain defines as 6 or more pain sites from 9 possible sites -Moderate to severe sleep problems or fatigue -Both for at least 3 months -Tenderness of soft tissue and muscles -Musculoskeletal stiffness -Headache, TMJ pain, GI symptoms, back/neck pain 130. Differential diagnosis: Fibromyalgia: -Chronic pain disorder -Hypothyroidism -Metabolic and inflammatory myopathies -Polymyalgia rheumatica22 / 41 -Mood/anxiety disorder -Myofascial pain syndrome -OA -Rheumatoid arthritis -SLE 131. Final diagnosis: Fibromyalgia: -Structured questionnaire: 3-month history of pain and symptoms of fatigue, awakening with feelings of fatigue, cognitive problems, and no other health/mental problem explains pain/symptoms -Labs: CBC, CMP, UA, ESR, RF, ANA, cascading reflex, TSH, T3, T4, Creatinine, Vit. D, Vit. B12, Iron panel, Mag, CRP -X-rays, scans, and muscle biopsy are normal *Labs are not diagnostic but are necessary to r/o other disorders 132. Prevention: Fibromyalgia: -None known 133. Non-pharm management: Fibromyalgia: -Goal of treatment is to improve function, quality of life, and to reduce pain -Stress management -Exercise -Alternative therapies -Patient education: avoid diet changes, highly processed foods, tobacco smoke exposure -Pace activities, reduce stress -Relaxation -Improve nutrition 134. Pharmacological management: Fibromyalgia: -3 medications have FDA in- dications: duloxetine (Cymbalta), milnacipran (Savella), and pregabalin (Lyrica) -Avoid opioids which can worsen pain; if already on them, recommend gradual withdrawal over 2-3 weeks -Tramadol may be used short-term and intermittently as needed -Tylenol and NSAIDs are not effective -Benzos and other hypnotics are not recommended for sleep 135. Follow-up: Fibromyalgia: -Refer non-responders to a pain specialist or rheumatology -Variable and depots on symptom severity, coping abilities, and patient resources -Within 2 weeks after initiating mediations 136. Expected course: Fibromyalgia: -Fluctuating, chronic course -Consider dual diagnosis of autoimmune disease 137. Possible complications: Fibromyalgia: -Chronic pain -Chronic work loss23 / 41 -Marked functional impairment -Severe depression/anxiety 138. Etiology: BPH: -Exact cause unknown -Age-related hormone changes, androgen/estrogen imbalance, increased growth-factor signaling -Age-related epithelial ratio changes increase the number of prostatic stem cells and decrease cell death -The presence of testosterone and DHT is necessary for the development of BPH 139. Risk factors: BPH: -Elevated PSA -Increasing age -Family genetics -Black men more likely to be affected -Asian men less likely to be affected -Cigarette smoking, male-pattern baldness, and metabolic syndrome -DM II -Obesity -Increased alcohol consumption -Physical inactivity 140. Assessment findings: BPH: -Obstructive: incomplete bladder emptying, hes- itancy and post-void dribbling, straining to void, weak urine stream -Irritative: nocturia, frequency, urgency, dysuria -Urinary incontinence -Urinary retention -Hematuria: gross or microscopic -Firm, smooth, symmetrically enlarged prostate 141. Differential diagnosis: BPH: -Prostatitis -Prostate cancer -Urethral stricture -Neurogenic bladder -Side effect of meds (sympathomimetic, opiates, antihistamines, anticholinergics) -UTI -Malignancy (bladder or prostate) 142. Final diagnosis: BPH: -Initial evaluation: urological association symptom in- dex; selfadministered tool that asks about BPH symptoms (incomplete emptying, frequency, intermittency, urgency, weak stream, hesitancy, and nocturia) -Mild: 0-7; mod: 8-19; severe: 20-35 -UA: pyuria if residual urine present -Renal panel to assess function -PSA: may be elevated, but 1024 / 41 -Obstruction: ultrasound and assess renal function -Needle biopsy -US, CT, MRI 143. Non-pharm management: BPH: -Lifestyle modification: limit fluids 1-2 hours before bed; frequent voiding; avoid sympathomimetic (decongestants) or anticholin- ergic medications d/t increased risk of urinary retention -Avoid caffeine, alcohol -Sitting vs standing may reduce symptoms -Limit salt intake (water retention) 144. Pharmacological management: BPH: -Assess for infection, prostate cancer, stricture disease, hypotonic bladder, or other neurogenic disorders that could mimic BPH -Indicated in mild-mod disease -Mild-mod warrant tx with an alpha-1 as monotherapy; provides immediate thera- peutic benefits -5-alpha-reductase inhibitors should be used long-term for maximum efficacy: 6-12 months of treatment may be required for symptom improvement -Severe disease: initiate treatment with both alpha-1 and 5-alpha-reductase 145. Follow-up: BPH: -Annual digital rectal exam -PSA annually -Review possible side effects of medications -Screen for ED -Encourage patient to keep log of symptoms and voiding patterns, including volume of urination 146. Expected course: BPH: -Symptoms improve or stabilize in 70-80% of patients -20-30% of patients require treatment due to worsening symptoms 147. Possible complications: BPH: -Acute urinary retention -Urinary incontinence (nocturnal is common) -Nocturia -UTI -Prostatitis -Hydronephrosis 148. Etiology: ACL Injury: -Usually injured during non-contact maneuvers which the foot is planted firmly on the ground and the knee and leg are twisted while the body is stationary -Often a low-velocity injury -Often involves hyperextension with internal rotation of the tibia, or external rotation of the tibia with the knee flexed and valgus force to the knee -Often accompanies meniscus or associated collateral/PCL ligament injury25 / 41 149. Risk factors: ACL Injury: -Athletic activities including running, cutting, jumping -Deceleration accounts for 40% of ACL injuries -Improper training surfaces footwear -Hamstring weakness 150. Assessment findings: ACL Injury: -Timing -Mechanism -Popping sound at the time of injury -Acute pain -Inability to weight bear after injury -Acute swelling/hemarthrosis with rapid onset -Joint instability, "giving out" -Positive lachman test -Positive pivot shift "clunk" -Positiv anterior drawer test -Medial/lateral laxity 151. Differential diagnosis: ACL Injury: Children: Avulsion of bone at tibial spine, physical injury Adults: Avulsion fracture of proximal tibia, PCL injury, patellar subluxation/disloca- tion, meniscus tear, MCL/LCL injury, patellar tenon/quadriceps tendon tear 152. Final diagnosis: ACL Injury: -Plain x-ray to r/o fracture; lateral proximal tibial fracture is highly correlated MRI: primary diagnostic test; highly specific and sensitive for meniscus, cartilage, and ligament injury 153. Prevention: ACL Injury: -Physical training including neuromuscular training and extrinsic supports (braces/taping) -Increase hamstring strength 154. Non-pharm management: ACL Injury: -Acute: RICE; if unstable, use crutch- es -Knee immobilizer -PT -Functional bracing -Arthroscopy for ruptured ACL -ACL reconstruction 155. Pharmacological management: ACL Injury: -Tylenol, NSAIDs -Opioids during acute phase if necessary 156. Follow-up: ACL Injury: -Within 1 week after acute injury and treatment initia- tion -Subsequent f/u depends on degree of pain, instability, referral to a surgeon, and rehabilitation26 / 41 157. Expected course: ACL Injury: -Varies with severity of injury and treatment plan -Many patients treated 2-3 weeks with knee immobilizer followed by 2-4 weeks of hinged knee brace -Younger active patients benefit to a greater extent from ACL reconstruction 158. Possible complications: ACL Injury: -Recurrent knee injury -Injuries to other ligaments -Meniscal injury -Articular cartilage injury -Chronic joint instability -Deconditioning -Disability -Arthritis -Post-op infection or DVT 159. Etiology: Rotator cuff syndrome: -May occur as a result of acute injury or due to degeneration, chronic muscle impingement, or inadequate blood supply to the tendons -Most involves the supraspinatus muscle and tendon 160. Risk factors: Rotator cuff syndrome: -Advancing age -Repetitive use of upper extremities/shoulders -Overhead activity in work/sports -Shoulder instability 161. Assessment findings: Rotator cuff syndrome: -Pain, often at night; may be referred to deltoid; may increase with overhead movement -Tenderness over rotator cuff area -Weakness with abduction or forward flexion -Pain during abduction motion -positive impingement signs: Hawkins, neer, empty can, lift off tests -Atrophy of supra and infraspinatus muscles resulting in shrunken area in back of shoulder -Limited AROM -Grating sensation at tip of shoulder when lifting arm -Positive drop-arm test: loss of strength with abduction against downward pressure @ 90° -Pain with internal rotation at the shoudler 162. Differential diagnosis: Rotator cuff syndrome: -Shoulder instability, frozen shoulder -AC joint injury -Degenerative glenohumeral arthritis27 / 41 -Cervical radiculopathy -Cervical strain -Avascular necrosis -Contusion -Biceps tendinitis -Suprascapular nerve entrapment -Thoracic outlet syndrome -Subacromial bursitis -Superior labrum injury -Pancoast tumor 163. Final diagnosis: Rotator cuff syndrome: -X-rays are typically normal -MRI to diagnose partial or full-thickness tears or labral tear -Subacromial lidocaine injection can clarify clinical picture and assist the examiner in proper diagnosis -Patients with tendinitis or bursitis will generally have normal strength 164. Prevention: Rotator cuff syndrome: -Maintain adequate flexibility and strength of the shoulder girdle, including the rotator cuff -Limit over-head activities 165. Non-pharm management: Rotator cuff syndrome: -Rest to avoid overhead activity during acute phase -Ice/head for comfort -PT or home exercises for strengthening and stretching -Work activity modification as indicated 166. Pharmacological management: Rotator cuff syndrome: -Oral/topical NSAIDs -Subacromial steroid injection -Avoid shoulder injections in the presence of infection -Repeated injections may accelerate rotator cuff tear 167. Follow-up: Rotator cuff syndrome: -With conservative treatment, follow up in 2-4 weeks to evaluate effectiveness 168. Expected course: Rotator cuff syndrome: -Highly dependent on then degree of pathology or injury present 169. Possible complications: Rotator cuff syndrome: -Loss of shoulder function -Chronic pain -Joint degradation with long-standing tears -Progression to full-thickness tear 170. Etiology: Transient Synovitis of the Hip: -Uncertain -Possibly related to a recent virus, trauma, or hypersensitivity (allergic) reaction28 / 41 171. -Risk factors: Transient Synovitis of the Hip: -History of URI 7-14 days before symptom onset in 70% of affected children -History of trauma 172. Assessment findings: Transient Synovitis of the Hip: -Acute onset of groin, anterior thigh, or knee pain -Child remains ambulatory but walks with a limp to avoid pain (antalgic gait) -May have low-grade temp -Does not hold hip flexed or abducted; abduction and internal rotation are restricted -Hip may be tender to palpation -Most sensitive test is log roll: roll affected hip from side to side-may see guarding or decreased ROM -May have decreased ROM in knee on affected side -Usually unilateral, but may affect both hips 173. Differential diagnosis: Transient Synovitis of the Hip: -Legg-calve-perthes disease -Septic arthritis: MUST NOT MISS -Osteomyelitis -Slipped capital femoral epiphysis -Femoral neck stress fracture -Lyme arthritis -Juvenile idiopathic arthritis 174. Diagnostic studies: Transient Synovitis of the Hip: -ESR -CRP -A/P and lauenstein x-rays of the pelvis-normal -US: effusion detected in 25% of cases -bone scan or MRI to r/o infection or LCP disease 175. Prevention: Transient Synovitis of the Hip: -Unable to prevent due to un- known cause 176. Non-pharmacological management: Transient Synovitis of the Hip: -Mini- mize walking for 24 hours -Close observation -Limited activities as tolerated for 2 weeks until pain resolves -Monitor temp to exclude possibility of septic arthritis -US guided hip aspiration may speed recovery 177. Pharmacological management: Transient Synovitis of the Hip: -NSAIDs -Avoid aspirin d/t risk of Reye syndrome 178. Follow-up: Transient Synovitis of the Hip: -PCP or orthopedics in 24-48 hours, then in 1 week as recommended to confirm symptom resolution -Consider repeat x-ray in 6 months to r/o LCP disease29 / 41 179. Expected course: Transient Synovitis of the Hip: -Symptoms begin to re- solve in 24-48 hours -Complete resolution of joint irritability in 1-2 weeks -Delay in resolution may occur if child becomes active too soon 180. Possible complications: Transient Synovitis of the Hip: -Recurrence if ac- tivity isn't sufficiently limited -Recurrence rate is 20% -Coxa magna: enlargement and deformity of the femoral head and neck -LCP disease 181. Etiology: Pharyngitis/tonsilitis: -Viral: (most common etiology)l; rhinovirus, adenovirus, parainfluenza, EBV, RSV, HIV, HSV -Bacterial: GAS, h. influenzae, m. pneumoniae, c. pneumoniae, n. gonorrhoeae -In many cases, no pathogen can be isolated 182. Risk factors: Pharyngitis/tonsilitis: -Exposure during GAS outbreaks -Family history of rheumatic fever increases risk if GAS is untreated -Crowded conditions -Daycare/school attendance -Chronic illness -Oral sex 183. Assessment findings: Pharyngitis/tonsilitis: -Sore throat, pharyngeal ede- ma -Tonsillar exudate and/or enlarged tonsils -Malaise -Suggestive of strep: cervical adenopathy, fever 102, absence of other upper resp. findings, petechiae on soft palate, "beefy" red tonsils, "sandpaper" rash, abd. pain, headache, distinct odor Suggestive of viral infection: concurrent conjunctivitis, nasal congestion, hoarse- ness, cough, diarrhea, viral rash 184. Differential Diagnosis: Pharyngitis/tonsilitis: -URI -Tonsilitis -Mono -Peritonsilar abscess -Epiglottitis 185. Diagnostic studies: Pharyngitis/tonsilitis: -Rapid antigen strep test -Throat swab for culture -In children, culture throat swab to confirm strep results; not necessary in adults as acute rheumatic fever is less likely -Strep is uncommon in children 3 *10% of patient with mono have concomitant strep30 / 41 186. Prevention: Pharyngitis/tonsilitis: -Avoid contact with infected people during outbreaks -Thorough hand washing, especially during cold weather months -Prompt treatment of patients with family history of rheumatic fever 187. Non-pharmacological management: Pharyngitis/tonsilitis: -Gargling with warm salt water -Increased fluid intake -Change toothbrush after treatment 188. Pharmacological management: Pharyngitis/tonsilitis: -Antipyretics/anal- gesics are adjunct treatment for for fever and throat pain -For GAS, a 10-day regimen for amoxicillin or PCN V is first-line; if PCN allergic, may use cephalexin or clindamycin (10 days), or macrolides (5 days) 189. Follow up: Pharyngitis/tonsillitis: -None usually needed -No longer contagious after 24 hours on abx 190. Expected course: Pharyngitis/tonsilitis: -Peak fever and pain on days 2 and 3 -Lasts 4-10 days 191. Possible complications: Pharyngitis/tonsilitis: -Upper airway obstruction -Acute post-strep glomerulonephritis -May develop sloughing of skin on fingertips and toes in weeks following strep infection 192. Etiology: Sinusitis/rhinosinusitis: -Bacterial: s. pneumoniae (most com- mon), h. influenzae (common in smokers), moraxella catarrhalis -Viral: Rhinovirus, coronavirus, influenza A and B, parainfluenza, RSV -Chronic: gram-negative more likely; s. aureus, p. aeruginosa, anaerobic organisms *The vast majority of cases are due to viruses 193. Risk factors: Sinusitis/rhinosinusitis: -Allergies, asthma -Tooth abscess (25% of chronic sinusitis) -Smoking -URI -Swimming in contaminated water -Anatomical abnormalities -Any condition causing swollen nasal mucous membranes i.e. allergic rhinitis, com- mon cold 194. Assessment findings: Sinusitis/rhinosinusitis: -Fever (may or may not be present) -Persistent URI symptoms ( 10-14 days) -Nasal congestion and/or discharge; may be bloody or purulent -Headache31 / 41 -Sore throat from persistent post-nasal drip -Pain/pressure over cheeks, upper teeth, eyebrows, behind/between eyes -Cough -Anosmia -Halitosis -Periorbital edema 195. Differential diagnosis: Sinusitis/rhinosinusitis: -Viral URI -Allergic rhinitis -Nonallergic rhinitis -Dental abscess -Headaches -Nasal foreign body -Wegener's granulomatosis 196. Final diagnosis: Sinusitis/rhinosinusitis: -No imaging for patients who meet dx criteria -CBC: elevated WBC if bacterial infection -CT scan: most useful to differentiate between viral and bacterial -Imaging recommended for unilateral CRS to exclude tumor, anatomical defect, or foreign body; MRI is superior to CT for soft tissue imaging 197. Prevention: Sinusitis/rhinosinusitis: -Promote drainage by avoiding irritants that increase swelling in the mucous membranes and cause retention of sinus exudate -Blow rather than "sniff" nose -Good hand washing to prevent URI -Management of allergic rhinitis 198. Non-pharm management: Sinusitis/rhinosinusitis: -Humidified air -Increase fluid intake -Sleep with head of the bed elevated to promote drainage 199. Pharmacological management: Sinusitis/rhinosinusitis: -Current data supports watchful waiting for 10 days; start abx if symptoms persist past 10 days -First-line treatment: amoxicillin, augmentin -PCN allergy: Doxycycline, levofloxacin, moxifloxacin -Macrolides are not recommended d/t high resistance -Oral/topical decongestants and/or antihistamines are not beneficial -Use topical intranasal steroids as monotherapy or in conjunction with abx -Saline irrigation 200. Follow-up: Sinusitis/rhinosinusitis: -Indicated until clinically free of infection -If symptoms worsen or are unresolved after 3-5 days of abx therapy32 / 41 201. Expected course: Sinusitis/rhinosinusitis: -Acute sinusitis: good prognosis -Chronic sinusitis often recurs unless causative factor is treated or eliminated 202. Possible complications: Sinusitis/rhinosinusitis: -Abscess -Meningitis -Periorbital cellulitis 203. Etiology: Bronchitis: -Viral: adenovirus, rhinovirus, flu A and B, parainfluenza, RSV, Coxsackievirus, Metapneumovirus -Secondary bacterial infection: s. pneumoniae, h. influenzae, m. catarrhalis, c. pneu- moniae, bordetella pertussis -Inhaled chemical irritant -Fungal infection 204. Risk factors: Bronchitis: -URI -Air pollutants -Smoking or secondary exposure -GERD -Allergy -COPD -Acute/chronic sinusitis -Infants -Older adults -Immunosuppression -Environmental changes 205. Assessment findings: Bronchitis: -Cough: dry and non-productive, then pro- ductive, may be purulent -URI symptoms -Fatigue -Fever due to bacterial infection; more common in smokers and those with COPD -Fever due to virus; unusual after the first few days -Burning sensation in chest -Crackles, wheezes -Chest wall pain 206. Differential diagnosis: Bronchitis: -Common cold -Acute rhinosinusitis -Pneumonia -Influenza -Rhinosinusitis -Bronchiectasis -Chronic cough -Heart failure33 / 41 207. Final diagnosis: Bronchitis: -No routine chest x-ray unless cough per- sists/worsens -Criteria for CXR: tachypnea, hypoxia, fever, abnormal lung exam -Only consider CXR if high index of suspicion for pneumonia or heart failure -Consider PPD: expect negative result 208. Prevention: Bronchitis: -Smoking cessation -Avoid known respiratory irritants -Treat underlying conditions that contribute to risk i.e. asthma, GERD -Flu/pneumococcal immunization for high-risk patients 209. Non-pharm management: Bronchitis: -Increase fluid intake -Use humidifier -Rest -Smoking cessation -Honey in children older than 1 210. Pharmacological management: Bronchitis: -2020 guidance suggests NO routine abx, antivirals, antitussives, inhaled beta agonists/anticholinergics/ steroids, NSAIDs 211. Follow-up: Bronchitis: -7 days if not improved or condition worsens -High-risk groups 212. Expected course: Bronchitis: -Shorter symptom duration if causative agent is rhinovirus or coronavirus -Symptoms may persist for 3-4 weeks 213. Possible complications: Bronchitis: -Pneumonia -Chronic cough -Chronic bronchitis -Secondary bacterial infection -Bronchiectasis 214. Etiology: Asthma: -Inflammation of the bronchial mucosa and spasm of the bronchial smooth muscle lead to narrowing of the small and large airways -Produces characteristic cough and wheezing 215. Risk factors: Asthma: -Comorbid conditions: URI, COPD, GERD, obesity, OSA, chronic sinusitis, cystic fibrosis -Irritant triggers: tobacco smoke, wood smoke, perfume, pollution, cockroaches, dust mites -Exercise -Urban areas -Family history -Female sex; women = 65% of all asthma deaths -Black race: 3x more likely to die from asthma34 / 41 216. Assessment findings: Asthma: -Free of symptoms between attacks -Airway constriction causing expiratory wheezing -SOB -Tachypnea, tachycardia -Nonproductive cough -Chest tightness -Hyper-resonance -Prolonged expiration -Accessory muscle use in severe attack -Sudden nocturnal dyspnea -Decreased exercise tolerance 217. Differential diagnosis: Asthma: -URI, sinusitis, vocal cord dysfunction -Heart failure -GERD -Habitual cough -COPD -Cystic fibrosis -Medications (ACEIs) -TB -Tumors -PE -Foreign body aspiration, esp. in children 218. Final diagnosis: Asthma: -Requires presence of intermittent dyspnea, cough, wheezing, chest tightness, and variable expiratory airflow obstruction -Spirometry, PFTs -Allergy testing -Peak-flow monitoring 219. Prevention: Asthma: -Symptom prevention -Identify and minimize known triggers -Take prescribed medications consistently -Implement asthma action plan -Monitor peak-flow values -Correct use of inhalers 220. Non-pharm management: Asthma: -Peak flow monitoring -Avoid triggers -Keep windows closed during pollen season -Control heartburn -Healthy weight and exercise regimen to maintain lung health -Smoking cessation35 / 41 221. Pharmacological management: Asthma: -Inhaled steroids: beta-agonists, short and long acting -Inhaled corticosteroids: mainstay of treatment for all categories of persistent asthma -Fluticasone has greater systemic side effects than other steroids; budesonide has a greater systemic adverse effect profile 222. Follow-up: Asthma: -Establish asthma action plan -F/u every 3-6 months for stable disease 223. Expected course: Asthma: -Excellent with adherence to asthma action plan -Small % of patients have poor control, even with proper medication use -Risk of mortality is increased by nocturnal symptoms, history of intubation, hospi- talization, or more than 3 annual ED visits for asthma 224. Possible complications: Asthma: -Respiratory failure/death from unrelieved bronchospasm -Steroid dependence 225. Etiology: Depressive disorder: -Still no well understood -Impaired synthesis/metabolism of norepinephrine, serotonin, dopamine, other neu- rotransmitters -Genetic predisposition in 30-40% -60-70% related to specific environmental factors: adverse childhood events, ongo- ing/recent stress, childhood sexual abuse, other lifetime trauma, decreased/absent social support, marital discord 226. Risk factors: Depressive disorder: -Psychosocial stressors -Postpartum period -Physical or chronic illness, esp. migraines and back pain -Prior history of depression and suicide attempts -Family history of suicide -Alcohol or substance abuse -Abuse or bullied as a child -Retirement, aging -Significant loss of loved one -Isolation -Comorbidities 227. Assessment findings: Depressive disorder: -Depressed mood for 2 weeks or longer and/or anhedonia (inability to feel pleasure) -Increased/decreased appetite -Weight loss or gain -Sleep disorder -Psychomotor agitation or retardation -Fatigue, loss of energy36 / 41 -Feelings of worthlessness, inappropriate guilt -Recurrent thoughts of death -Difficulty thinking/concentrating, indecisiveness 228. -Differential diagnosis: Depressive disorder: -Bipolar disorder -ADD -Chronic physical illness -Physical/sexual abuse -PTSD -Substance abuse -Grief reaction -Hypothyroidism/B12 deficiency -Dementia 229. -Diagnostic studies: Depressive disorder: -Structured interviews/question- naire -DSM-5 -PROMIS (ages 6-17) -PHQ-9 -Zung- self-rating depression scale -Laboratory studies to rule out other conditions: TSH, urine drug screen, ECG, Vit D, genetic testing to help with medication selection 230. Prevention: Depressive disorder: -Maintain high index of suspicion in ado- lescents with family/personal history, suicide attempts, chronic illness, recent loss -Ask about plans for suicide -Routine questioning about then use of alcohol/drugs 231. Non-pharm management: Depressive disorder: -Establish safe environ- ment -Community resources, suicide hotline -Suicide threats = communication of desperation -Psychoeducation -Psychotherapy 232. Pharmacological treatment: -Determine current substance use disorders and medical conditions -SSRIs -SNRIs -TCAs 233. Follow-up: Depressive disorder: -Within 2 weeks of initiating medication or sooner if needed -For 1st episode, continue antidepressants for 4-6 months after complete remission of symptoms; for 2nd episode, continue for 2 years; 3 or more episodes may warrant37 / 41 lifetime treatment -Antidepressants should be tapered rather than abruptly discontinued 234. Expected course: Depressive disorder: -The most common reason for treat- ment failure is inadequate dosage, trial, or length of treatment on medication. -60-70% response rates to all classes of antidepressants -4-6 weeks is required to fully respond to medication -Depression should be treated to remission, not some degree of symptom relief -High relapse rate during the first 8 weeks after resolution of symptoms 235. Possible complications: Depressive disorder: -Suicide; overdose of TCAs is potentially lethal -Bizarre behavior may endanger social relationship and reputation -Increased risk of suicide at the start of antidepressant therapy -Serotonin syndrome from combining several meds -Substance abuse from attempts to self-medicate *Most patients with bipolar disorder present with symptoms of depression, not mania. Careful screening is critical because antidepressants can cause mania 236. Etiology: Tinea unguium/corporis: -Different types of fungus 237. -Risk factors: Tinea unguium: -Excessive exposure to water, soap, detergent -Distor