NR511 Midterm Study Guide Worksheet Study Guide, Exams of Nursing

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NR511 Midterm Study Guide Worksheet Study Guide

Disease Risk Subjective Finding Objective Findings Diagnostics Treatment Education

GI DISORDERS

Appendicitis - Most common between - Dx made clinically, - May have HTN\tachy - Labs are not - Surgical; preoperative - F\U with surgeon 10 - 30yrs; but can occur based primarily on H&P proportional to diagnostic and care, NPO, correction of - Ambulation after at any age; rare in exam pain\symptoms nonspecific fluid\electrolyte imbalances surgery infants and older adults - Classic presentation - When lying flat, may - Women should have - Avoid narcotics - Adv diet when

• men more at risk includes acute onset of flex R knee to relieve urine human chorionic - Atb with 3rd gen bowel sounds return
• Diets low in fiber, high mild to severe colicky, tension in abd muscle gonadotrophin to r\o cephalosporin; Ex: - Return to hosp with in fat, refined sugars, & other carbs at increased epigastric, or periumbilical pain - Pain with palpation in abd, diffuse in early ectopic pregnancy - +Rovsing’s Sign- ampicillin, gentamycin, flagyl s\s of infection - Avoid heavy lifting risk. - Pain is vague at first stages. Localized to deep palpation & for at least 2 wks
• Obstruction of appendix then localizes within RLQ later release in LLQ causes is cause of majority of 24hrs to RLQ - Positive for rebound rebound pain in RLQ appendicitis - Pain exacerbated by pain; ask pt to cough - +Psoas Sign - lift R
• contributing factors: walking\coughing to localize pain leg against gentle Intra-abdominal - Men may feel radiated location pressure causes pain tumors, positive family pain in testes - Sudden cessation of - +Obturator Sign- hx - Abd muscle rigidity, pain means perforation flex R hip & knee and
• Recent roundworm N\V, anorexia and is ER slowly rotate internally infection or viral GI infection
  • Mildly elevated temp 99 - 100F common causes pain
    • +McBurney’s Sign -
  • If RLQ accompanied pain with pressure by shaking chills, applied to point perforation should be between umbilicus & suspected ilium
  • Older adults may - x-ray\CT helpful present with weakness, when paired with anorexia, abd positive H&P findings distention, mild pain leading to delayed dx and increased morbidity. Celiac disease ** (autoimmune disorder caused by an immunologic response to gluten) Mostly diagnosed in adulthood. A family member with celiac disease or dermatitis herpetiformis Type 1 diabetes Down syndrome or Turner syndrome Autoimmune thyroid disease Microscopic colitis (lymphocytic or collagenous colitis) Addison's disease Many asymptomatic. May complain of diarrhea, gas, dyspepsia, wt. loss. Atypical symptoms: fatigue, bone or joint pain, arthritis, osteoporosis, or osteopenia (bone loss) liver and biliary tract disorders (transaminitis, fatty liver, primary sclerosing cholangitis, depression or anxiety peripheral neuropathy seizures or migraines missed menstrual periods infertility or recurrent miscarriage canker sores inside the mouth Muscle wasting (anemia), reduces subcutaneous fat, ataxia, & peripheral neuropathy (vitamin B12 deficiencies) osteoporosis or osteopenia (bone loss) hypothyroidism Pts with dermatitis herpetiformis found to have signs of celiac disease on intestinal biopsy. Serologic testing for anti-tTG IgA antibody Total IgA (2% of pts have IgA deficiency and will falsely test negative) duodenal biopsies Test for nutritional deficiencies associated with malabsorption of C.D. (hemoglobin, iron, folate, vit B12, Calcium, and Vitamin D.) lifelong adherence to a strict gluten-free diet. Referral to a dietician to help. Some pts may need treatment with immunomodulating agents. teaching related to gluten free diet. Some people with celiac disease have vitamin or nutrient deficiencies that do not cause them to feel ill, such as anemia due to iron deficiency or bone loss due to vitamin D deficiency. However, these deficiencies can cause problems over the long term. Untreated celiac/developing certain types of gastrointestinal cancer. This risk can be reduced by eating a gluten-free diet.

Immunosuppressive meds when unresponsive to other treatments. Diverticulitis ** - Uncommon under - 25% develop - LLQ abd tenderness - Abd x-ray can reveal - Asymptomatic cases - Increase fiber in diet 40yrs; risk rises after

• Rare in pediatric; equal symptoms
  • LLQ abd pain, worsens with possible Firm, fixed mass may be free air, ileus, obstruction managed with high fiber diet or fiber supplement to avoid constipation and straining in men\women after eating identified in area of - Barium studies show with psyllium - H2O intake of at
• More common in - Pain sometimes diverticula sinus tracts, fistulas, - Mild symptoms managed least 8 \8oz glasses developed countries relieved with BM or - May have rebound obstruction outpatient with clear liquid to promote bowel
• High in low fiber, high fat\red meat diets flatus
  • BM may alternate tenderness with guarding\rigidity - Colonoscopy to r\o Ca, but less sensitive diet and rest - Atb should not be routinely regularity - Bulk-forming
• Obesity, chronic between diarrhea\ - Tender rectal exam; than barium for used but can be with laxative may be constipation, h\o constipation stool usually + for diverticula diverticula abscess culture needed Ex: psyllium, diverticulitis, & number of - May present with occult blood - CT with contrast - Amoxicillin\clavulanate K FiberCon, Metamucil diverticula which occur in sigmoid colon. bleeding w\o pain or discomfort (or) flagyl with bactrim - Symptoms usually subside
  • Fever, chills, tachy; quickly and diet can be LLQ with anorexia, N\V advanced slowly
  • Fistula may form - Pain managed with causing dysuria, pneumaturia, fecaluria antispasmotics Ex; Levsin, Bentyl, BuSpar
    • Avoid morphine
    • NG for ileus or intractable N\V
    • Pt can be D\C’d from hosp once able to maintain adequate nutrition
      hydration if acute phase resolved
    • Colon resection may be necessary if no improvement or deterioration after 72hrs of treatment GERD ** - Can occur at any age - Heartburn; mild to - H&P usually normal - Usually Hx alone - 8wk trial of PPI; weight - Weight loss, med
• Risk increases with age, severe - May be + for occult diagnoses loss, avoiding triggers compliance and then decreases after - Regurgitation, water blood in stool - May manifest with - If unresponsive to once avoidance of triggers 69yrs brash, dysphagia, sour atypical symptoms daily dosing; can increase - Small frequent
• Prevalence equal taste in AM, belching, such as adult-onset to twice daily; if no relief meals; main meal across gender, ethnic, coughing, odynophagia asthma, chronic EGD needed mid-day, avoid cultural (painful swallow), cough, chronic - PPI and H2-RA should not eating 4hrs before
• Obesity, alcohol, caffeinated beverages, chocolate, fruit, decaf hoarseness or wheezing at night
• Substernal
  laryngitis, sore throat, noncardiac chest pain
• If pt fails to respond to be taken together
• Pt’s on long term therapy should be re-eval’d q6mos bed, avoid straining, sleep with HOB elevated, smoking coffee, fatty foods, retrosternal pain 4 - 8wks PPI, EGD is cessation, stress onions, peppermint\ - Worsens if reclined ordered mgmt spearmint, tomato after eating, eating - EGD warranted over products large meals, empiric treatment Anticholinergics, beta- constrictive clothing when heartburn & adrenergics, CaChannel - May present with dysphagia, bleeding, blockers, diazepam, dysphagia; dysphagia anemia, weight loss, Estrogen\ progesterone, Nicotine, Theophylline should only occur with first bite or recurrent vomiting
• EGD with Barrett’s esophagus q3-5yrs

Peptic ulcer disease ** 3 major causes: (1) Hallmark: c/o burning or Pts w/ duodenal ulcers Routine lab tests: Aim to relieve pain, heal Smoking cessation; (includes gastric ulcers Infection w/ H.Pylori, (2) gnawing (hunger) often demonstrate normal unless ulcer, & prevent avoid foods that and duodenal ulcers) chronic ingestion of ASA sensation or pain epigastric tenderness significant bleeding or complication and precipitate and other NSAIDs, (3) (dyspepsia) in 2.5cm to right of vomiting. Pt actively recurrences. dyspepsia. acid hypersecretion such epigastrium, often midline, but this may bleeding à CBC w/ diff. as in Zollinger-Ellison relieved by food or also be present in to eval HGB levels is - PPIs: drugs of choice & MUST follow syndrome. Genetics, antacids. Pts describe cholecystitis, paramount. Most pts includes omeprazole, treatment regimen. blood type, personality pain episodic pattern of pancreatitis, non-ulcer w/ upper GI bleeding raveprazole, lansoprazole, Educate about side type, and cigarette c/o in which the pain dyspepsia, and other should have restrictive esomeprazole, effects such as smoking may also play a tends to cluster and last GI disorders. Reports strategy, defined as dexlansoprazole, change in stool color role in the development for minutes, w/ of melena or coffee- transfusing when HGB pantoprazole. PPIs heal to black with bismuth of PUD. Pts w/ COPD, episodes separated by ground-like emesis levels fall below 7 duodenal ulcers in 4 wks preparations. If cirrhosis, renal failure, periods of no sx. usually indicate g/dL. Diagnostic therapy and gastric ulcers sucralfate with and renal transplant Almost half w/ NSAID- bleeding ulcer, and standard à upper GI after 8 wks. antacid, PPI, H2RA have higher incidence. induced ulcers are perforated ulcer may endoscopy. Serology being taken, stress asymptomatic. present w/ abdominal test or direct - H2-R that sucralfate rigidity. bacteriological eceptor Antagonists: Used cannot be taken with Nocturnal pain: in 2/3 of analysis via an for mild symptoms with no other meds or with pts w/ duodenal ulcers esophagogastroduode complication or serious digoxin, and 1/3 of those w/ noscopy (EGD) Bx à disease; treatment for 2 ciprofloxacin, gastric ulcers. to check for H. Pylori. wks. If symptoms persist phenytoin due to it EGD is ordered for pts past 2 weeks, EGD binding with these

• Nausea & anorexia who have failed the considered. If used for meds. sometimes occur in pts standard triple-drug peptic ulcer tx, standard w/ gastric ulcers. therapy for H. Pylori. A therapy is daily x 6 wks or Vomiting and weight serological antibody half the dose bid x 8 weeks loss indicate more (enzyme-linked (cimetidine, ranitidine, serious complications immunosorbent assay) nizatidine, famotidine) like gastric malignancy test can be used or pyloric obstruction. Pts w/ duodenal ulcers detect infection w/ H. Pylori, doesn’t - Other agents: antacids were mainstay of ulcer may report a reduction distinguish between treatment. Do not use in pain after eating; pts active or past (treated) antacids with calcium in w/ gastric ulcers tend to infection and is PUD because calcium experience more expensive. Urease is causes rebound acid intense pain after plentiful in pts w/ secretion. eating. H.Pylori infection. Sucralfate 1g QID heals Breath tests for H. duodenal ulcers, bismuth Pylori are based on (also has antimicrobial the production of action against H. Pylori), ammonia from the misoprostol (Cytotec) used metabolism of urea by for prophylactic measure to urease à indicate prevent gastric ulcer active infection and formation in pts who use are noninvasive way of NSAIDs. dx H. Pylori. In pts w/ Triple therapy for H. Pylori increase in gastric acid is a combination of 2 secretion is suspected, antibiotics (clarithromycin a fasting serum gastrin and either amoxicillin or level should be drawn. metronidazole) w/ a PPI Levels higher than 200 BID x 14 days. Amoxicillin pg/mL should be preferred over confirmed on repeat metronidazole due to testing and followed by resistant h. pylori strains. basal and peak acid- Bismuth subsalicylate & 2 output measurements. antibiotics is also effective Zollinger-Ellison but dosing is QID.

syndrome should be suspected in pts whose fasting serum gastrin level is > 600 pg/mL and who have a basal acid output > 15 mmol/hr. Pancreatitis ACUTE \ CHRONIC ACUTE : About 80% of hospital admissions are a result of biliary tract disease (passing gallstones) or alcoholism. --Risk: Infection (mumps), Hyperlipidemia, Metabolic disorders (hyperparathyroidism, hypercalcemia), Drugs (furosemide, valproic acid, sulfonamides, thiazides), Endoscopic retrograde cholangiopancreatograp hy (ERCP), Abn pancreatic duct (stricture, carcinoma, pancreas divisum), Abn Common bile duct and ampullary region, Surgery of stomach and biliary tract, vascular disease (artherosclerosis, severe hypotension), trauma. CHRONIC: Slow progressive process --Risk: alcoholism, diets high in protein combined with high/low fat can further predispose to pancreatic injury from alcohol, autoimmune disease, genetic mutations, hereditary predisposition, high triglycerides, severe malnutrition, tropical pancreatitis, obstruction caused by stenosis, stones, tumor, cystic fibrosis. ACUTE: Pain that is intense, abrupt onset deep epigastric pain that last for hours to days. Radiates straight through the back. Pain is often refractory to narcotics. Aggravated by vigorous activity (coughing) and lying supine. Alleviated when seated and leaning forward. Intractable nausea/vomiting. Depending on severity may present with seating, weakness and anxiety. May report ingestion of alcohol or big meal before onset of symptoms. CHRONIC: Patient presents with intractable abdominal pain, weight loss, diarrhea but can be mild (dyspepsia, nausea, vomiting). Abdominal pain normally epigastric/LUQ that may radiate to back or left lumbar region that is described as dull and constant. Pain is aggravated by food or alcohol. ACUTE: Severe abdominal tenderness over epigastric area accompanied by guarding. Abdominal distension presents in about 20% of patients. Bowel sounds hypoactive or absent if paralytic ileus present. Tachycardia (100- 140 b/min) with rapid, shallow respirations. Increased blood pressure due to pain. Temp initially normal but increases to 100.4- 102.2. CHRONIC: Mild to Moderate epigastric tenderness without rebound tenderness or guarding. ACUTE: Abdominal Pain Elevated Serum Amylase/Lipase that return to normal after 3 - 7 days WBC between 12 - 20, 000 CT of abdomen: provides fast and accurate for definitive diagnosis CHRONIC: CT and /or US of the abdomen to show abnormal size or consistency of pancreas. Evaluation of pancreatic function: Bentiromide Test-- collections of normal volume and low in bicarbonate suggest chronic pancreatitis. ACUTE: Management is aimed at limiting severity of pancreatic inflammation, preventing further complications and managing symptoms. Mild symptoms can resolve on its own and managed outpatient conservatively. Fasting is necessary until symptoms have subsided. Maintain fluid status with parenteral fluids Pain medication other than opiates (to prevent pressure within sphincter of Oddi). Introduction of clear fluids implemented once pain free, amylase/lipase levels returned to normal, bowel sounds have returned, Low fat diet as patient tolerates. CHRONIC: Aimed at preventing further pancreatic damage, managing pain and supplementing exocrine and endocrine function. Sustaining from alcohol use. Relief of pain by pancreatic enzymes in some patients and others may need narcotic pain management. Operative treatment considered in patients that fail pain management with pancreatic enzymes or analgesics. Malabsorption managed with low-fat diet and oral pancreatic enzymes (Viokase/Cotazym/Pancrea se/Creon/Donnazyme). ACUTE: Informed the cause of pancreatitis Reduction of dietary intake of fat Abstain from alcohol abuse Drug induced--avoid causing agent Hyperlipidemia--diet instruction and information on avoidance of factors such as alcohol, estrogens. CHRONIC: Patho of disease and long- term outlook Decrease in frequency in attacks after 5-10 years Medication regimen/Rational for medications (control diarrhea and gain body weight) Pain management if long term narcotic is needed. Salmonella ** (^) One of the major causes of diarrhea worldwide. Three species: S. typhi, S. choleraesuis, and S. Present with varying degrees of nausea, vomiting, diarrhea, fever, and abdominal Present with varying degrees of nausea, vomiting, diarrhea, fever, and abdominal The physical exam is usually normal except for the aforementioned GI problems. Treatment includes trimethoprim- sulfamethoxazole (Bactrim DS) or a quinoline, Stress proper handling of food, thorough cooking,

Duration usually 4– 7 days and is self-limiting. Incubation period of 1 – 2 days after exposure or ingestion of pathogen. persist for 2 – 20 days. Complications can include hemolytic- uremic syndrome and colitis. Ulcerative Colitis ** (^) Peak age of onset: 15 to 30 y/o, but may occur at any age. More common in males. Familial tendency. Mild: 4 or fewer loose BMs per day associated w/ abdominal cramps relieved w/ defecation, small amounts of blood and mucus in the stool, and sometimes tenesmus Moderate: 4-6 loose BMs per day w/ more blood and mucus. Systemic Sx: tachycardia, mild fever, weight loss and mild edema depending on serum albumin levels Severe: more frequent blood BMs (6-10 per day, abdominal pain and tenderness, Sx of anemia, hypovolemia, and impaired nutrition If Ulcerative Colitis (UC) confined to rectal or sigmoid area, stools can be normal or hard and dry; however, the rectum will continue to dispel mucus containing both RBCs and WBCs. As disease process moves proximally, the stools become looser. Pts may report eating less to decrease BM frequency, which leads to further nutritional deficiencies. Tenderness in LLQ or across the entire abdomen, often accompanied by guarding and abdominal distention. Depending on severity: S/S of ileus and peritonitis may be found. Serological: + for antineutrophil cytoplasmic antibodies (pANCA). Fever & malaise w/ severe disease. Early disease: mucous membrane is granular, friable, and edematous w/ loss of normal vascular pattern. May be scattered areas of hemorrhage that bleed w/ minor trauma. Resulting ulcerations develop after mucosa breaks down, leaving the mucous membranes dotted w/ numerous bleeding and pus-oozing ulcers. Severe disease: Copious amounts of purulent exudate. Periods of remission, sigmoidoscopy always shows some friability and granulation present Digital Rectal Exam: to assess for anal and perianal inflammation, rectal tenderness, and blood in the stool. Dx made by correlating sx w/ hx and physical exam. Stool analysis and Cx are obtained to r/o bacterial, fungal, or parasitic infection (ova & parasites) as cause for diarrhea. Stool is examined for mucus and blood. Contrast radiography and endoscopy primary diagnositic tool to confirm IBD (Irritable Bowel Disease). Sigmoidoscopy, defines the actual extent of the mucosal inflammation. Bx results à chronic inflammation. Colonoscopy to determine the extent of the disease, to avoid perforation, usually reserved for pts who have started tx. Initial: nutrition counseling. Parenteral nutrition may be necessary w/ severe anorexia or uncontrollable diarrhea. Pts w/ mild-mod diarrhea may benefit from diphenoxylate w/ atropine (Lomotil) 2.5 to 5.0 mg PO BID up to 4x daily, loperamide (Imodium) 2 mg after each BM, or codeine 15 to 30 mg PO Q4-6H. Disease limited to rectosigmoid area: topical steroids or mesalamine. Steroid enemas and foams (hydrocortisone [Cortifoam] 100 mg) nightly x 2 wks. PO formulation of Asacol (5-ASA) med help maintain remission after enemas have been d/c’d More advanced disease: Systemic glucocorticoid in combo w/ sulfasalazine or 5 - ASA therapy. Glucocorticoids esp. helpful in controlling extracolonic manifestations à peripheral arthritis, ankylosing spondylitis, erythema nodosum, anterior uveitis, and pyoderma gangrenosum: Oral prednisone (Prelone), up to 40 to 60 mg in single or divided doses, tapered and not d/c’d abruptly. Severe or fulminant: (10 or

bloody stools per day): abdominal tenderness, fever, colon dilation and tachycardia à require hospitalization, monitor closely for development of toxic megacolon and Colonoscopy should be avoided w/ severe colitis or deep ulcerations because of risk of perforation or development of toxic megacolon. Pts should avoid caffeine, raw fruits, vegetables, and other foods high in fiber à can cause trauma to the already inflamed mucosal surface. Some pts may benefit from lactose- free diet, but not recommended unless a trial produces symptomatic relief. Bland diet high in calories and protein yet low in fat can help to control diarrhea and flatulence and maintain nutrition and weight. Antidiarrheal meds should be avoided in acute phase but can be helpful for pts w/ mild sx. All pts should be informed of disease process, tx options, and expected outcomes. Education about diet and lifestyle changes. Importance of adequate rest and stress reduction to decrease bowel

colonic perforation. If no improvement after 7- 10 days; consider surgical intervention. Surgery: Subtotal or total colectomy à prevent perforation of bowel and its complications. Some pts may need fluid/electrolyte management and/or blood transfusions. Most common procedure protocolectomy: Brooke ileostomy, curative and functional procedure. Immunosuppressive agents: azathioprine (Imuran), cyclosporine, and metabolit 6 - mercaptopurine (6MP) à used in cases unresponsive to other medical management and in pts who are not surgical candidates. For disease unresponsive to other therapies: anti- tumor necrosis factor (anti- TNF) agents can be used à infliximab (Remicade) 5 mg/kg and adalimumab (Humira) administered SubQ 160 mg @ wk 1, 80 mg @ wk 2, then maintenance of 40 mg Q other Wk beginning @ wk

Pts w/ toxic megacolon: NG tube placement for intermittent suction, NPO, antidiarrheal meds should be d/c’d. F/E imbalances need corrected: hypokalemia. Total parenteral nutrition may be necessary short term. Daily abdominal x-rays. motility and promote healing. Stress management techniques: guided imagery, referred for counseling if necessary. Provided information and addresses for national organizations à Crohn’s and Colitis Foundation of America: up-to-date info and local support groups. If no S/S of acute attack, they can eat whatever they want or can tolerate. About possibility of parenteral nutrition or oral supplementation during acute attacks. Foods that can cause diarrhea and gas-producing foods should be avoided during acute attacks. Female pts require special guidance and counseling before attempting pregnancy. If pregnancy occurs, pt must be followed closely by gastroenterologist Viral gastroenteritis ** (^) Causes of gastroenteritis are numerous; however, bacterial, viral, and parasitic infections are among the most common. Almost all forms of enteric infection manifest with diarrhea. Several different viruses including rotavirus, norovirus, adenovirus, See Salmonella See Salmonella (^) Viral gastroenteritis is a known cause of nausea, vomiting, diarrhea, anorexia, weight loss, and dehydration. Clinical manifestations for viral gastroenteritis are due to the effects that the viruses, along with specific cytotoxins, Most important goal of treatment is to maintain hydration status and effectively counter fluid and electrolyte losses. Antimotility drugs are the most frequently prescribed and most effective drugs for the treatment of symptomatic gastroenteritis. These Prevention of the spread of disease from patients with infectious diarrhea to other individuals. Teaching includes good hand washing and safe disposal of waste products. Any infant or child with infectious diarrhea

HEENT DISORDERS

Bacterial conjunctivitis (viral is most contagious) Occurs in fall and winter. More common in children than adults. Direct contact with secretions or with contaminated objects and surface. Discharge is purulent, thick with crusted eyelids shut in the morning. Sandy, gritty feeling in eye. Unilateral but usually becomes bilateral due to contamination. Normal visual acuity. No pupillary abnormalities. No photophobia. Lymph nodes NOT palpable. Reddened conjunctiva (both over the eyeball and inside lid) and eyelid swelling. Hallmark symptom of bacterial conjunctivitis is purulent discharge. Usually none. Consider culture of exudates for recurrent conjunctivitis but rarely indicated. Consider fluorescein staining is corneal abrasion suspected. Bacterial form is also self- limited. Treatment shortness course if initiated early. Self-limiting in 5-7 days; can delay treatment until third day

• Eyedrops or ointment: trimethoprim/polymyxin B (Polytrim), erythromycin, tobramycin, gentamicin, sodium sulfacetamide, or ciprofloxacin, levofloxacin
• Contact lens wearers: fluoroquinolones are first line Tobramycin (These medicines include ciprofloxacin (Cipro), gemifloxacin (Factive), levofloxacin (Levaquin), moxifloxacin (Avelox), norfloxacin (Noroxin), and ofloxacin (Floxin) Children: ointment preferred over drops One exception to the rule in regards to the effectiveness of antibiotic drops for all bacterial conjunctivitis cases is gonococcal infections. Gonococcal conjunctivitis is sight threatening because it can affect the cornea , so patients should be sent to the ER immediately. Gonococcal conjunctivitis is associated with hyper- purulent discharge
  • Good hand hygiene and eye hygiene.
  • Use clean washcloth each time face is washed.
  • Change pillowcases daily.
  • Warm compresses for infectious origin.
  • do not wear contact lenses until inflammation resolved (1 week); discard current contact lenses.
  • Discard makeup used.
  • Symptoms should improve in 2 - 4 days
  • Instruct patients to treat the eye that is affected but to start treatment in the other eye if symptoms develop
  • Bacterial conjunctivitis very contagious; stay home from work or school until 24 hours of antibiotic treatment or as soon as clinical improvement (decreased redness and discharge) Corneal abrasion (^) Mechanical or chemical means; Trauma induced by contact lenses, damaged contact lenses, or foreign body. Spontaneous induced and often known as recurrent erosions that stems from a previous Excessive tearing , severe eye pain and inability to open eye due to foreign body sensation, photophobia, conjunctival hyperemia. Hx of scratching the eye, contact lens
• Constricted pupil, foreign body, lacrimation. Profuse tearing.
• Invert eyelid to r/o foreign body underneath. Stain the eye with fluorescein and use a cobalt blue filter light or slit lamp to inspect the eye for foreign objects or scratches. Areas of epithelial disruption fluoresce Treatment includes antibiotic eye drops or ointment for 5 – 7 days to prevent bacterial infection. Traumatic/foreign body/recurrent abrasions : Erythromycin ointment OR sulfacetamide Patching is not usually necessary. The patient should avoid wearing contact lenses until the abrasion heals. f/u in 24 - 48 hours if no improvement

injury. More common in young, active patient. Uncommon in older adults. irritation, or actual trauma. Patients with recurrent corneal erosion syndrome experience searing pain in the middle of the night. It awakens them, or they feel pain on awakening green when exposed to a Wood’s lamp. Access visual acuity: should be normal unless abrasion is large. Contact lens abrasion: ofloxacin, ciprofloxacin OR tobramycin drops/ointment Oral analgesics for pain Only ophthalmologists should prescribe topical anesthetics due to delayed wound healing and risk of ulceration, scarring, perforation and blindness Tetanus prophylaxis Normal saline to irrigate eye. f/u in 24 hours to assess healing f/u by eye doctor Epiglotittis Common in young children 2 - 4 years; most common >7 years; may occur in older children and adults. Men > women. Infection with Haemophilus influenzae B (Hib) (most common); streptococci now major pathogen of cause. Odynophagia (pain on swallowing), dyspnea, drooling, stridor. Never use tongue blade or light due to laryngospasm and airway obstruction may occur. Transport to OR for fiberoptic laryngoscope visualization showing that epiglottis is swollen and erythematous (cherry red). Endotracheal tube should be inserted. ER care for adequate airway control. Needs hospitalization for IV antibiotics such cefuroxime (Ceftin), ceftriaxone (Rocephin), or ampicillin/sulbactam (Unasyn). Dexamethasone (Decadron) should also be administered IV and tapered as signs and symptoms resolve. Continuous pulse oximetry and careful monitoring of the patient’s airway are critical. Patients who develop hypoxemia and respiratory distress will require intubation. Eustachian tube disorder Some of the most common causes include conditions causing nasal congestion as is seen with allergic rhinitis, sinusitis, URIs, enlarged adenoids, and pregnancy. Additionally, those who have recently traveled in an airplane or who have been scuba- diving are at risk for ETD. Often people complain of decreased hearing or a fullness in the ears. Hearing may be muffled or diminished. May report an inability to “pop” or “clear” their ears, which normally occurs with changes of barometric pressure. They may have accompanying tinnitus or disequilibrium. Patients may come to you thinking that they have an ear infection due to pain or pressure. They may also be concerned of cerumen impaction if they are Physical exam findings with ETD depend on precipitating event. Nasopharyngeal examination may reveal findings consistent with allergic rhinitis, sinusitis, or URI. On the affected side, typically you will see a TM that appears retracted or “sucked back.” Diagnosis of ETD is based on the history and physical exam. If pneumatic otoscopy is performed, the affected TM will be immobile. A Weber and Rinne hearing test will reveal conductive hearing loss on the affected side. Key it to treat underlying problem.

• If a cold, then nasal saline drops or a neti pot may help.
• AOM and sinus infections are treated with antibiotics.
• Allergic rhinitis should be treated with nasal steroids and decongestants; however, decongestants are contraindicated in children under 6 years of age. Comfort measures can include acetaminophen or ibuprofen. Patients can be instructed to attempt to relieve

autoimmune conditions (systemic lupus erythematosus), RA, certain thyroid disorders. Frequency and severity may decrease over time with hearing improvement post attack, but some episodes may last 24 hours. reduced in the affected ear, as demonstrated by electronystagmograph y or direct patient observation (while wearing 40-diopter Frenzel lenses); the direction of the fast phase of nystagmus is variable. These findings are not diagnostic for Ménière’s disease. Last resort: Aminoglycosides like streptomycin or gentamicin ablation therapy to reduce unbearable vestibular symptoms. Reduce food intake during episodes to avoid n/v. Mononucleosis: primarily caused by EBV Angie

RISK

• Common: Adolescents, young adults (especially college students)
• Rarely: Elderly
• Immunocompromised persons.

SUBJECTIVE

• Gradual onset
• Mild to Severe throat pain, but mono tends to be the most painful.
• low grade fever
• Marked fatigue
• Tickle sensation
• Head and body aches
• swollen lymph nodes in the neck and armpits
• swollen liver/spleen or both (less common).
• rash
• spread through saliva (kissing, sharing drinks/cups.

OBJECTIVE

• Exudative tonsillitis (50% of cases).
• Palatal petechiae
• exanthem (rash) maculopapular rash
• Posterior cervical lymphadenopathy (90%) *OCC. OCCURS - significant tender lymphadenopathy of the draining anterior cervical lymph nodes.

DIAGNOSTIC

• VCA (viral capsid antigen Anti-VCA IgM appears early in EBV)
• VCA Anti-VCA IgG appears in the acute phase of EBV
• Monospot test positive by wk 2- 3 (nonspecific heterophile antibody test) and decreases in sensitivity when used at the extremes of age (not recommended for general use).
• CBC if viral will show 60% lymphocytes, of which at least 10% show atypical morphology.
• fewer normal neutrophils or platelets
• Liver enzymes: abnormal liver function
• US-dx splenomegaly
• consider rapid strep/throat culture: pharyngitis is similar to presentation of strep.

TREATMENT

• No specific treatment for EBV
• Relief of symptoms
• drink fluids to stay hydrated
• get plenty of rest
• take OTC medication for pain/fever relief.
• No vigorous exercise, sport or heavy lifting
• warm salt-water gargle
• avoid stress
• eat a balanced diet PHARMACOLOGIC:
• Acetaminophen for fever, aches, pain--Avoid if elevated liver function.
• Ibuprofen: AVOID:
• ampicillin or amoxicillin due to increased susceptibility to reaction (rash).
• Steroids unless severe pharyngeal erythema or tonsillar hypertrophy develops, resulting in obstruction (may prolong illness)
• Aspirin (risk of Reye’s syndrome)

EDUCATION

Instruct patient:

• drink plenty of fluids and get plenty of rest.
• No vigorous exercise, sports or heavy lifting for 6 wks to avoid rupture spleen.
• symptoms may subside in 1 - 3 wks, but fatigue may last for several more weeks.
• perform good hand washing
• avoid stress
• eat a balanced diet
• Contagious for 3 months after symptoms subside and could last as long as 18 mo.
• Can be spread through saliva, bodily fluids such as blood, sexual contact, organ transplant, cough, sneeze, kissing, sharing food/drinks. Nasal polyps Caused by poorly controlled rhinitis. increases with age, female>male. Associated with cystic fibrosis, Asthma, bronchiectasis, ASA Rhinorrhea, nasal congestion, postnasal drainage, hyposmia (inability to smell), inability to breath through nose, dull headache, facial Gray-blue to yellow-tan nasal polyps may present with chronic perennial rhinitis If large posterior nasal polyps, examine Flexible/rigid endoscopy (gold standard of diagnosis) Pale-translucent mass on anterior rhinoscopy. Goal – reduce size or eliminate polyp. Daily intranasal corticosteroid use with saline irrigation 1st-line therapy. Treat for minimal

hypersensitivity, chronic sinusitis, primary ciliary dyskinesia (Kartagener syndrome), and laryngopharyngeal reflux. pain/pressure over middle 3 rd^ of face or No symptoms in some cases. Usually bilateral; if unilateral is reported; check for malignancy tympanic membrane for ETD. If unilateral, check for malignancy. CT scan may help reveal extent of disease and differentiate a polyp from another mass. MRI if neoplasia, mycetoma, or encephalocele suspected. of 12 weeks. Use budesonide, beclomethasone dipropionate, fluticasone, mometasone furoate. Mometasone furoate preferred for children. Short course of oral corticosteroids (14- 21 days) and/or doxycycline ( days) in symptomatic patients despite initial tx. (prednisone, prednisolone, doxycycline) Otitis Externa (AKA swimmer’s ear) ** Common in warmer months. No ethnic predisposition. Men/women equally affected. Those at risk: Immunocompromised pts on corticosteroid therapy or with chronic conditions such as DM. Pseudomonas infection common from excess swimming in hot, humid weather, especially in polluted water. Highly chlorinated pool water leads to drying out of ear canal creating potential entry of bacteria and fungi. Inadequate cerumen (a protective barrier). Patients with seborrhea due to excess sebum production. Manual ear picking; forging bodies in auditory canal(like leaving cotton in ear); long use of ear plugs, hearing aids, cotton swabs may lead to local irritation and predispose to infection. Previous ear infections and hx of skin allergies. Acute, often severe otalgia of sudden or gradual onset; may be bilaterally. Pain may be worse at night, more severe when pulling on pinna or earlobes or applying pressure to tragus. Chewing may elicit pain. Initially, ear may feel full or obstructed with temporary conductive hearing loss if edema present. May be pruritic. Purulent drainage. Fever/chills. chronic otitis externa may have dryness and pruritus of ear canal. Ear canal may be erythematous and edematous; absence or presence of cerumen or accumulation of purulent drainage. Tenderness on traction of pinna and/or pain with pressure over tragus. May be diffused with complete involvement of auditory canal or localized with focal lesions (pustules or furuncles) along auditory or external ear structures. Sebaceous secretions in those with seborrhea. Fluid may be apparent: Pseudomonas - copious green exudate Staphylococcus infection - yellow crusting with purulent exudate. Fungal infections - fluffy white or black malodorous carpet of growth. Rarely needed if symptoms fits classic pic or otitis externa. Fluid from ear may be cultured and antibiotic sensitivity tested if organisms found. Done for those who do not respond to treatment or those with chronic otitis externa, especially those with purulent exudates indicating bacterial infection. Culture also done for immunocompromised pts. Rule our fungi and mycobacteria in these pts. ESR level may be elevated. CT and MRI used to determine soft tissue or bony involvement in malignant disease. Temporal bone 1st bone affected. Treat pain: local application of heat or ice-pack to outer ear. Nonprescription pain relievers: aspirin or acetaminophen or NSAIDS

• 1st line agents. Extreme pain: Acetaminophen/codeine 325mg/5mg 1-2 tabs po q6h OR Acetaminophen/hydrocodo ne (Vicodin) 325mg/5mg po q8h for 1st 24-48 hours (risk for abuse). To facilitate healing: Clean ear canal to remove Cerumen, exudate, debris with cotton pledget or gentle irrigation using warm water. 1 st^ line agents: Acetic acid/aluminum acetate, acetic acid/hydrocortisone, ciprofloxacin/hydrocortison e, ciprofloxacin/dexamethas one , neomycin/polymyxin B/hydrocortisone , and ofloxacin. Liquid ophthalmic preparations of gentamicin and tobramycin may be used otically to cover both P. aeruginosa and S. aureus. Bacterial otitis externa Safe with perforated tympanic membrane Keep ear dry, avoid swimming or submersion of ear during and after acute episodes for 4 - 6 wks. Use shower caps and ear plugs to shower. Those susceptible to repeated infections, a 2% acetic acid solution may be used prophylactically to acidify ear canal whenever ears get wet. Teach proper method to clean ears using soft cotton pledget NOT swabs, sticks, or agents. Excessive cleaning harmful; small earwax necessary to prevent infection. Cured 7-10 days of treatment. F/U 1 week for uncomplicated pts. If ear wick placed, F/U 2 days for removal and canal cleaning and symptoms should begin to subside in 48h - pt to call if unresolving. F/U daily in hospitalized patients immunocompromise

monitoring serum levels and renal function) and ticarcillin (3 g IV Q4H). These regimens carry significant risk of nephrotoxicity, ototoxicity, and bleeding diatheses. Otitis Media (^) More common in infants/young children. Increases in winter months. Native Americans (Navajos and native Alaskans) higher prevalence rate. Americans of European descent. Equal in men/women. Dysfunction in eustachian tube. Genetic conditions such as Down syndrome at risk. Active/passive smoking, crowded or unsanitary living conditions, exposure to wood- burning stoves, family history of OM. AOM risk factors: child in daycare, presence of tobacco smoke in home, and residing in communities where antibiotic-resistance forms of S. pneumoniae are endemic. Acute OM: Otalgia, Otorrhea, and fever. Unilateral hearing loss, recent hx of URI. Dizziness, vertigo, tinnitus, vomiting, or nausea possible. Pain subsides with TM rupture and then complain of optic drainage. Recurrent OM: clearance of middle ear effusions between acute episodes of inflammation. Chronic OM: Presents with history of repeated bouts of AOM followed by a period of continuous or intermittent otorrhea lasting for more than 3 months. Pain is rare: hearing loss primary concern. OM w/ effusion: absence of s/s of infection. Typically complain of stuffiness, fullness, and loss of auditory acuity in affected ear. May hv pooping, crackling, gurgling sounds when chewing, yawning, blowing the nose. Pain rare. Vertigo rare. Usually afebrile and may have hs of recent viral URI or either allergic or vasomotor rhinitis. AOM: Auralgan otic solution (combination analgesic and anesthetic agent; contra in ruptured TM) may be needed to assess ear. TM may be amber or yellow- orange, or may be infected and pinkish gray to fiery red. T M usually full or bulging in acute cases; absent/ obscured bony landmarks and cone light reflex. Chronic OM: perforated, draining tympanic membrane and possibly granulation tissue. Chronic, foul-smellling otorrhea typical of anaeroobic bacterial infection; a chronic grayish-yellow suppuration may be a cholesteotoma at site of infection. Bullae in rare cased forms between tympanic membrane from M. Pneumoniae or certain viruses. Acute infection: lymphadenopathy of preauricular and posterior cervical nodes common. OME: examination of external ear unremarkable; mucous membranes of nasal and oral cavities may be infected or edematous from recent URI. Decrease Rarely needs if symptoms fit picture of OM. If confirmation is desired, pneumatic otoscopy will demonstrate decreased or absent tympanic membrane mobility in serous, acute, or chronic OME. Tympanometry may be useful if fluid buildup behind middle ear suspected in absence of other clinical signs; a flat tympanogram is consistent with restrictive disease of the middle ear cavity In subacute, recurrent, or chronic cases of OM, cultures and antibiotic sensitivity testing helpful in guiding alternative treatment. If cultures are obtained, fungi and mycobacteria should be specifically ruled out. sinus x-rays and CT scan to reveal mucosal thickening in middle ear in those with recurrent infection. Weber (sound lateralizes to affected ear) and negative Rinne test (bone conduction superior in duration and volume to air conduction). Uncomplicated OM may not require specific intervention other than pain and symptomatic relief: Acetaminophen, Ibuprofen. If signs and symptoms of AOM persist for 48 to 72 hours in spite of using systemic analgesics, the child should be reassessed, and antibiotic treatment should be considered. No-day care; no ABX in past 90 days: amoxicillin standard dose Day-care or ABX in past 90 days: amoxicillin high dose. mild PCN allergy : use 2nd generation cephalosporin: cefuroxime axetil (Ceftin), or cefprozil (Cefzil). Severe PCN allergy or cephalosporin allergy : extended spectrum ABX: Clarithromycin (Biaxin) or a sulfonomide like TMP/SMX; Bactrim Failure of initial AOM tx in Pedi pts with amoxicillin: give Amoxicillin- Clavulanate (Augmentin) Complicated and recurrent OM require tx Teach preventive measures: avoid tobacco exposure, exclusive breastfeeding for 1st 6 mths of life or longer, annual influenza 6 months and older, pneumococcal 13 6 weeks of age and older, pneumococcal 23 for high risk children 2 years and older. Demonstrate proper cleaning technique. Bedrest or reduced activity may be suggested in severe cases until fever and pain subside, and the importance of completing the full regimen of all antibiotic therapies should be emphasized. Avoid swimming until OM clears; immersion in water may lead to otitis externa, complicating the middle ear infection. Keep ear canal dry. T M perforation can be avoided by not using cotton swabs or sharp objects to clean ears. Traumatic injuries to the middle ear should be avoided as well to prevent perforation.

tympanic mobility of pneumatic otoscopy. All cases, especially with ruptured T M blowing of the nose should be avoided ; do gently as possible if needed. Nasal saline used to liquefy nasal secretions and facilitate drainage. Presbycusis ( sensorineural hearing loss; not reversible ) Affects older adults 50 and >; tinnitus may be associated with presbycusis. Some contributing factors include environmental noise, loss of hair cells, hereditary factors, aging, health, and side effects of medication “difficulty hearing,” hears mumbled or slurred speech, difficult hearing made worse with background noise, men’s voices easier to hear, some sounds seem overly loud, possible tinnitis in one or both ears Bilateral hearing loss to high frequencies. Patient unable to hear you clearly at high frequencies. Perform Weber, RInne, and Schwabach tests. For sensorineural hearing loss: Weber ( sound in less affected/unaffected ear is louder ). Rinne (air should be 2 as long as bone conduction; but in sensorineural loss, the ratio is equal ). Revealed by audiometric testing including pure tone and speech testing. Hearing loss irreversible. Education should be provided to avoid further damage such as avoiding loud noises, wearing ear plugs, and hearing aids for hearing. In cases of presbycusis it is important to educate and support the pt so that no further damage will occur; for example, exposure to excessive noise and ototoxic drugs should be avoided. Rhinosinusitis - viral URI, airplane travel, smoking, air pollution, sneezing with mouth closed, chronic use of decongestants, cold damp weather, dry indoor heat, dental abscesses, swimming in contaminated water, nasal trauma URI, airplane travel, smoking, air pollution, sneezing with mouth closed, chronic use of decongestants, cold damp weather, dry indoor heat, dental abscesses, swimming, nasal trauma. All sinusitis – present with nasal congestion, mucopurulent rhinorrhea, head pressure, maybe cough, maybe sore throat, eye pain, malaise, fatigue. Pain exacerbated by sudden head movements. Frontal sinus pain worsens when lying down; maxillary sinus pain worsens when erect; ethmoid sinusitis associated with retro- orbital pain. Tender sinuses on palpation, nasal congestion, opacification of sinuses on transillumination, red/swollen nasal turbinates Acute sinusitis: total opacification on transillumination On palpation, the affected sinuses may be tender to palpation. Sphenoid sinusitis presents as tenderness over the vertex or mastoids, ethmoid sinusitis as retro-orbital or nasal bridge tenderness, maxillary sinusitis as cheek or dental tenderness, and frontal sinusitis as tenderness of the forehead. In the event of maxillary sinusitis related to a Noncontrast head CT recommended in more complicated cases, will show sinus opacification, air-fluid level or mucosal thickening Saline nasal flushes, cool- mist humidifier, increase fluid intake, hot shower or compress for facial pain; ibuprofen, tylenol for pain, OTC decongestant (not longer than 4 days r/t rebound congestion); expectorants such as guaifenesin. Prescription drugs: fluticasone (Flonase), mometesone (Nasonex), triamcinocole (Nasocort). Oral antihistamines not indicated unless allergic component is evident. They dry the mucosa, thicken purulent sinus fluid, & slow mucosal drainage. Majority of acute rhinosinusitis cases are caused by viruses rather than bacteria, antibiotics are largely unhelpful Increase fluids to thin nasal secretions, avoid aggravating factors such as smoke, air pollution. Report complications such as peri-orbital swelling, visual impairments, AMS, visual impairments, facial palsy. Avoid OTC decongestants with antihistamine.