NR 511 Midterm Exam Study Guide / NR511 Midterm Study Guide(Latest, 2024)(V1):Chamberlain, Study Guides, Projects, Research of Nursing

Download NR 511 Midterm Exam Study Guide / NR511 Midterm Study Guide(Latest, 2024)(V1):Chamberlain and more Study Guides, Projects, Research Nursing in PDF only on Docsity! 1 NR 511 Midterm Exam Study Guide Week 1 1. Define diagnostic reasoning: type of critical thinking  Critical thinking involves the process of questioning one’s thinking to determine if all possible avenues have been explored and if the conclusions that are being drawn are based on evidence  Diagnostic reasoning then includes a systematic way of thinking that evaluates each new piece of data as it either supports some diagnostic hypothesis or reduces the likelihood of others. 2. Discuss and identify subjective & objective data  Subjective: what the patient reports; complaints of; tells you  Example: fevers, chills, lethargy, headache, blurred vision, ST, etc.  Is the “S” part of the SOAP note which includes the CC, HPI, & ROS  Objective: what you can see, hear, or feel as part of your clinical exam; also includes laboratory data and tests results  Example: thin, obese, normocephalic, rapid stress test +, etc.  Is the “O” part of the SOAP note 3. Discuss and identify the components of the HPI  Should be focused on the complaint and relevant symptoms  Detailed breakdown of the CC, written out as the OLDCARTS acronym  Onset, Location, Duration, Characteristics, Aggravating Factors, Relieving Factors, Treatments, Severity.  Duration: not referring to the onset of the symptom. Rather, it is an assessment of whether the symptom is constant or if it comes and goes.  Severity: level of pain, impact on work/school or ADLs. 4. Describe the differences between medical billing and medical coding  Medical coding is the use of codes to communicate with payers about which procedures were performed and why  Medical billing, on the other hand, is the process of submitting and following up on claims made to a payer in order to receive payment for medical services rendered by a healthcare provider. 5. Compare and contrast the 2 coding classification systems that are currently used in the US healthcare system  Common Procedural Terminology (CPT) system: offers the official procedural coding rules and guidelines required when reporting medical services and procedures performed by physician and nonphysician providers  Recognized universally and also provide a logical means to be able to track healthcare data, trends, and outcomes. Each service or procedure is represented by a five-digit code that is presented in six sections, including 2 1. Evaluation & Management 2. Anesthesiology 3. Surgery 4. Radiology 5. Pathology 6. Medicine  International Classification of Diseases (ICD) system: we are in the tenth revision of the system, and, therefore, the classification system is known as ICD-10  ICD-10 codes are shorthand for the patient’s diagnoses, which are used to provide the payer information on the necessity of the visit or procedure performed. This means that every CPT code must have a diagnosis code that corresponds. 6. Discuss how specificity, sensitivity & predictive value contribute to the usefulness of the diagnostic data  When we describe the specificity of a test, we are referring to the ability of the test to correctly detect a specific condition. If the patient has the condition but testing is negative, we describe this as a false negative. If the patient does not have the condition but the test result is positive, this is considered to be a false positive test.  When a test is very sensitive, we mean it has few false negatives. The higher the sensitivity, the lesser the likelihood of a false negative. A sensitivity of 99% means that it is very unlikely for a false negative result.  Predictive value is the likelihood that the patient actually has the condition and is, in part, dependent upon the prevalence of the condition in the population. If a condition is highly likely, a positive test result is more likely to be accurate. If a condition is very unlikely, a positive test needs to be questioned and perhaps additional testing would need to be done.  5 things to consider before ordering a test: cost, convenience, sensitivity, specificity, risk of missing a condition (predictive value) 7. Discuss the elements that need to be considered when developing a plan  Evidence based care: providing care and making treatment and screening choices based on current research findings. Generally, EBP refers to using research findings from multiple studies that are convincing enough that a consensus is formed recommending the findings be used for clinical decision-making or practice guidelines.  EBP also involves inclusion of patient and provider preferences, patient values, and cultural considerations in the clinical decision-making process. Guidelines should be followed in the majority of cases unless there is a clear rationale for deviating from them to serve the particular needs of the patient.  Elements include clinical state and circumstances, patient’s preferences and actions, research evidence, and clinical expertise 8. Discuss a minimum of three purposes of the written history and physical in relation to the importance of documentation  It is an important reference document that gives concise information about a patient's history and exam findings. 5 1. Identify the most common type of pathogen responsible for acute gastroenteritis  Acute Gastroenteritis (AGE) is essentially an inflammation of the stomach and intestine. When inflammation of the stomach is predominant, nausea and vomiting are prominent symptoms. When the intestines are most affected, abdominal cramps and diarrhea dominate the picture.  Pathophysiological causes of AGE are numerous, however viral, bacterial, and parasitic are the most common with viral being the most likely.  Viral gastroenteritis can be caused by several viruses. Norovirus is the leading cause of acute diarrhea for adults, whereas rotovirus is the leading cause of gastroenteritis for the pediatric population, especially for children up to 2 years of age.  Bacteria: Staphylococcus  Viral: Norovirus (Norwalk virus) in adults and Rotavirus in Peds up to 2 yrs old.  Symptoms: n/v, diarrhea, fever, abd pain/cramping, fatigue, malaise, anorexia, tenesmus, rectal burning d/t frequent diarrhea, rectal abrasion, rectal bleeding, passing stool w/blood and mucus, severe dehydration, increased HR, & dizziness  Treatment: fluid and diet  PO pts: pedialyte, gatorade, oral rehydration salts, sports drinks, diluted fruit juices, broths, soups.  Boiled starches/cereals to facilitate enterocyte renewal  Hospitalized patients: IV fluid  Diarrhea: Pepto (can be used to treat acute diarrhea, but not as effective as loperamide; don't use w/abx in pts with HIV)  Loperamide (Imodium): drug of choice for afebrile, nondysenteric cases of acute diarrhea  Lomotil: Rx only, used in afebrile, nondysentery of acute diarrhea, has central opiate effects.  Antibiotic treatments: Bacterial: o C-diff (metronidazole/Flagyl 250mg x4 daily x10 days; vanc 125mg x4 daily x10 days). o Vibrio cholerae (tetracycline 500mg PO q5hr x2 days; bactrim DS q12hr x2 days). o Yersinia enterocolitica (tetracyclines 250-500mg q6hr x7-10days; cipro 500mg BID; tobramycin 3-5mg/kg q8h). o Salmonella (Bactrim DS or quinoline, norfloxin 400mg or ofloxin 400mg x2 daily x7-10 days). Shigella (Bactrim DS BID x3 days)  Viral: Rotavirus/norwalk virus: no treatment, treat symptoms 2. Recognize that assessing for prior antibiotic use is a critical part of the history in patients presenting with diarrhea  Any patient who develops diarrhea after initiation or completion of antibiotic therapy should have tissue culture assay or ELISA test for C. difficile toxin. 3. Describe the difference between Irritable Bowel Syndrome (IBS) and Inflammatory Bowel Disorder (IBD)  Irritable Bowel Syndrome (IBS): a disorder of bowel function (as opposed to being due to an anatomic abnormality) 6  Associated with changes in bowel habits, such as constipation or diarrhea, and abdominal pain along with other symptoms including abdominal bloating and rectal urgency with diarrhea.  May be associated with a number of nonintestinal (or extra-intestinal symptoms), such as difficulty with sexual function (pain on intercourse or lack of libido), muscle aches and pains, fatigue, fibromyalgia syndrome, headaches, back pain, and sometimes urinary symptoms including urinary urgency, urinary hesitation, or a feeling of spasm in the bladder.  Not associated with serious medical consequences. People with IBS tend to live long. IBS is not a risk factor for other serious GI diseases such as inflammatory bowel disease (Crohn’s disease or ulcerative colitis) or colon cancer  Major problem is that it changes the quality of life for people who suffer from it  Symptoms: result from disordered sensation or abnormal function of the small and large bowel. o Fall into 2 broad categories: 1) those with abdominal pain and altered bowel habits, consisting of diarrhea and/or constipation, and 2) painless diarrhea o Pain as originating over some area of the colon with LLQ pain o Pain can wax and wane in intensity and may occur more often following a meal or in stressful situations o Most consistent characteristic symptom is alteration in bowel habits  Physical exam: normal except some tenderness in some area of the colon, most often LLQ, umbilicus, or epigastric area. Digital rectal exam is normal  Lab testing: CBC and ESR; Elevated ESR and leukocytosis typically seen with IBD, not IBS. o Thyroid function studies, stool for ova and parasites, and abdominal imaging is not performed for typical IBS symptoms  Diagnosis: based on careful history and physical exam that reveals an increase in bowel symptoms with the onset of pain, relief of pain with defecation, heightened sensation in bowel activity, or sense of incomplete defecation. Symptoms are not accompanied by fever or bleeding.  Treatment: make the diagnosis and then identify the symptom pattern for each individual patient (in other words, is it IBS-C, IBS-D, or IBS-C&D). o Therapy may include diet, education, pharmacological and supportive interventions such as a focus on lifestyle, diet, and reduction of stress. o Pharmacological treatment is reserved for patients with moderate to severe symptoms and is directed at specific symptoms. o Anti-diarrheals should be used as a temporary measure and reserved for severe cases. Loperamide (Imodium) 2 mg or Diphenoxylate (Lomotil) 2.5– 5.0 mg every 6 hours are generally effective. The use of codeine, tincture of opium, and paregoric should be avoided because of the potential for addiction and misuse. o Constipation: 1st line treatment is high fiber diet/hydration, exercise, and bulking agents  If not effective, may consider intermittent use of stimulant laxatives such as lactulose or magnesium hydroxide; long-term use of laxatives is discouraged 7  If these fail, consider Linzess (linaclotide), Trulance (plecanatide), and Amitiza (lubiprostone). These drugs work by acting locally on the apical membrane of the GI tract to increase intestinal fluid secretion and improve fecal transit. o Abdominal pain: caused by intestinal spasm can be controlled with antispasmodic agents. Post-prandial pain can be treated with Bentyl (dicloclymine) 10 to 20 mg TID-QID prn or Levisn (hyoscyamine) 0.125–0.75 mg BID.  Avoid anticholinergics in those with BPH and glaucoma b/c of adverse effects, especially in the elderly.  Tricyclic antidepressants and SSRIs have been shown to relieve symptoms in some individuals.  Patients who are not responding to treatment should be referred to a gastroenterologist.  Inflammatory Bowel Disorder (IBD): a chronic immunological disease that manifests in intestinal inflammation  There is no single explanation for the development of IBD. A prevailing theory holds that a process, possibly viral, bacterial, or allergic, initially inflames the small or large intestine and, depending on genetic disposition, results in the development of antibodies that chronically attack the intestine, leading to inflammation.  Ulcerative colitis and Crohn's disease are the two most common types of Inflammatory Bowel Disorders (IBD). UC and CD are both IBDs that share similar characteristics and causes but are considered two separate diseases.  Patho: o Crohn’s Disease (CD): there are abnormalities in the intestinal immune response that produce areas of tissue damage. With progression of the disease, fibrosis thickens the bowel wall, narrowing the lumen, which, in turn, can lead to obstructions, fistulas, and ulcerations. Individuals with CD are at greater risk for developing colorectal cancer than the general population. o Ulcerative Colitis (UC): the inflammatory response that occurs in the thinner mucosa of the rectum and sigmoid colon is responsible for tissue damage. Ulcers form in the eroded tissue, and abscesses form in the crypts, which become necrotic and ulcerate. The mucosa becomes edematous and thickened, narrowing the lumen of the colon. Patients with UC are at risk for perforated colon and require close observation with a gastroenterologist and possibly a surgeon.  Symptoms: develop from inflammation of the intestine such as bleeding, fever, elevation of the white blood cell count (leukocytosis), as well as diarrhea and cramping abdominal pain in both UC and CD o The abnormalities in IBD can usually be visualized by cross-sectional imaging or colonoscopy. o Crohn’s disease (CD): periods of exacerbation alternating with remission Most common presenting symptoms of CD are abdominal cramping, fever, anorexia, weight loss, spasm, flatulence, and RLQ pain or mass.  Stools may contain blood, mucus, and/or pus. 10  On rectal examination, the stool is usually positive for occult blood.  Testing: CBC can show mild to moderate leukocytosis  H&H may be low if there is associated rectal bleeding.  Abdominal X-ray films should be obtained on all patients with suspected diverticulitis to look for free air (indicating perforation), ileus, or obstruction.  Diverticulitis can often be diagnosed clinically, but a CT scan with oral and IV contrast is very sensitive and accurate for a definitive diagnosis.  In other words, if the patient presents with a clinical picture of diverticulitis, get an abdominal X-ray to R/O perforation or obstruction and treat empirically. Do not delay treatment to wait for CT confirmation. Some patients will need to be hospitalized due to intractable abdominal pain or vomiting.  Treatment:  10-14 days of Metronidazole 500 mg TID along with Ciprofloxacin 500 mg BID or Trimethoprim/Sulfamethoxazole DS 160/800 mg BID  Close office follow-up should occur upon completion of antibiotic therapy to ensure that the patient has had resolution of symptoms as complications such as abscess and perforation can occur with diverticulitis. 6. Identify the significance of Barrett’s esophagus  Barrett's esophagus is associated with an increased risk of developing esophageal cancer. Although the risk is small, it's important to have regular checkups for precancerous cells (dysplasia). If precancerous cells are discovered, they can be treated to prevent esophageal cancer.  In GERD, stomach contents wash back into the esophagus, damaging esophagus tissue. As the esophagus tries to heal itself, the cells can change to the type of cells found in Barrett's esophagus.  Thought to be caused by chronic GERD. Gastric contents are so irritating, an inflammatory response is established in the esophagus. Erosion occurs due to increased blood flow due to inflammation. As the erosion heals, the body replaces the normal squamous epithelium with metaplastic columnar epithelium (Barrett’s epithelium) containing goblet and columnar cells. These are more resistant to acid and support esophageal healing. Barrett’s epithelium is a premalignant tissue and presents a 40 fold increased risk for esophageal adenocarcinoma. Fibrosis and scarring occur, leading to esophageal strictures.  Upper endoscopy with a biopsy is the test of choice to document the type and extent of tissue damage (e.g., Barrett’s esophagus) in the esophagus.  It is also recommended for surveillance evaluation in anyone with Barrett’s esophagus every 3 to 5 years and more frequently if there is Barrett’s esophagus with dysplasia. 7. Discuss the diagnosis of GERD, risk factors, and treatments  The primary cause of GERD is the inappropriate, spontaneous, transient relaxation of the lower esophageal sphincter (LES) to an unknown stimulus.  The incompetent LES results in free reflux during abdominal straining, lifting, bending, and recumbency.  Gastric contents are acidic, and it is this low pH (less than 3.9) that causes injury to the esophageal mucosa in the majority of patients with GERD. 11  Delayed gastric emptying, which often worsens as people age, causes increased intra-abdominal pressure and may contribute to reflux.  Obesity is also a risk factor for GERD. A number of foods and pharmacological agents are known to lower LES pressure.  Symptoms: heartburn, regurgitation, water brash (reflex salivation), dysphagia, sour taste in the mouth in the morning, odynophagia, belching, coughing, hoarseness, or wheezing at night, substernal or retrosternal chest pain. Only physical exam sign may be a stool positive for occult blood on rectal exam resulting from microhemorrhages in the irritated esophageal epithelium  Diagnostic tests: made by history alone & has a sensitivity of 80%  When patient fails to respond to 4 weeks of empiric therapy, most accurate method of diagnosing the disease is by ambulatory esophageal pH monitoring, which involves placing pH probes 5 cm above the LES. If the pH is < 4 above the LES and correlates with the occurrence of symptoms, the test is definitive for GERD  Treatment: the goal of the management of GERD is to rapidly eliminate or reduce symptoms; to prevent meal- or exercise-related symptoms; and to prevent the complications of esophageal stricture, esophageal ulcer, Barrett’s esophagus, pulmonary aspiration, and esophageal hemorrhage all in the most cost-effective way.  Focus is patient education with pharmacological intervention  Lifestyle modifications include elevating the HOB 6-8 inches, smoking cessation, and avoiding high-fat meals, large meals, and certain foods such as chocolate, alcohol, peppermint, caffeine, onions, garlic, citrus, and tomatoes  Avoid recumbency or sleeping for 3-4 hours after a meal and avoid bedtime snacks  Medications such as CCB, BB, alpha-adrenergic agonists, theophylline, nitrates, and some sedatives should be avoided b/c they affect the LES pressure  Weight loss encouragement in those overweight or obese  If diet and lifestyle modification are ineffective for 4 wks, treatment is stepped up to medications  For patients with mild-moderate symptoms, first step-up is H2-RAs such as cimetidine (Tagamet), ranitidine (Zantac), famotidine (Pepcid), and nizatidine (Axid) – available OTC as well as in prescription dosages for 6 wks.  If symptoms persist after 6 weeks, step up + referral to GI, diet/lifestyle modification, & H2-RAs or PPIs for 8 weeks.  If no improvement after 8 wks, surgical intervention may be needed.  Another alternative is to begin with PPIs at higher doses and “step down” treatment to the lowest dose that effectively suppresses acid secretion.  Those who have erosive esophagitis or Barrett’s esophagus are treated with PPIs once a day 30 minutes before breakfast.  Evidence suggests that PPIs are more effective than H2-RAs in all cases of GERD 8. Discuss the differential diagnosis of acute abdominal pain, work-up and testing, treatments  Acute Appendicitis: 12  Function of appendix is unknown; theories include bacteria “safe-house,” immune system, or just a vestigial organ  Appendicitis: inflammation of appendix  Most common cause is obstruction such as fecalith “pop rock,” undigested seeds, pinworm infection, or lymphoid hyperplasia (common cause in adolescents).  Appendix keeps secreting mucus even when it’s plugged; this causes fluid and mucus to build up and increases pressure in the appendix. This pushes on afferent visceral nerve fibers causing abdominal pain. Flora and bacteria are now trapped. Gut flora is now free to multiply which causes activates immune system causing elevated WBCs, fever, RLQ pain (McBurney’s point), nausea/vomiting.  If obstruction persists, pressure increases and pushes and compresses blood vessels that supply the appendix with blood and oxygen. Without oxygen, cells in the walls of appendix become ischemic and eventually die. Growing colony of bacteria can invade wall of appendix. Wall becomes weaker and can cause rupture. This causes bacteria to escape the appendix and get into the peritoneum which causes peritonitis & rebound tenderness. Patient may also have abdominal guarding.  Common complications of rupture is pus and fluid getting out and forming abscess around the appendix called a periappendiceal abscess  Standard tx includes appendectomy along with antibiotics  Acute pancreatitis:  Sudden inflammation and hemorrhaging of the pancreas due to the destruction of its own digestive enzymes known as autodigestion  Critical to diagnosed and treat quickly  It plays endocrine (alpha & beta cells make insulin & glucagon) & exocrine role (acinar cells make digestive enzymes to help digest food)  Acinar cells produce enzymes that are inactivated to protect itself  They are activated in the small intestine  If they become activated too early, it can cause acute pancreatitis. This can happen as a result of injury to acinar cells or impaired secretion of proenzymes  2 leading cause are alcohol abuse and gallstones  Other causes of acute pancreatitis: I GET SMASHED o Idiopathic, Gallstones, Ethanol abuse, Trauma, Steroids, Mumps virus, Autoimmune diseases, Scorpion stings, Hypertriglyceridemia/Hypercalcemia, Endoscopic retrograde cholangiopancreatography ERCP, & Drugs  Complications include formation of a pancreatic pseudocyst (fibrous tissue surrounds the liquefactive necrotic tissue which fills up with pancreatic juice) – may cause abdominal pain, loss of appetite, palpable mass, elevated amylase, lipase, and bilirubin. Abdominal CT scan is gold standard to dx pseudocyst.  Other complications include hemorrhage from damaged blood vessels (hypovolemic shock), systemic activation of coagulation factors (DIC), ARDS (#1 cause of death of pancreatitis)  Other symptoms include N/V, hypocalcemia (d/t fat necrosis b/c that process uses up calcium), bruising around abdominal area (cullen’s sign), flank of the body (Grey turner’s sign) 15  Sudden hearing loss may respond to corticosteroids if delivered within several weeks of onset.  Identification of sensorineural hearing loss is usually made by performing audiometry (an audiogram) in which bone conduction thresholds are measured.  Tympanometry and speech audiometry may be helpful. Testing is performed by an audiologist.  There is no proven or recommended treatment or cure for SNHL; management of hearing loss is usually by hearing strategies and hearing aid.  In cases of profound or total deafness, a cochlear implant is a specialized hearing aid which may restore a functional level of hearing.  Tinnitus is defined as the sensation of sound in the absence of an exogenous sound source. It may be intermittent, continuous, or pulsatile (synchronous with the heartbeat). o The causative mechanism is poorly understood. A few theories include chronic exposure to noise, especially high pitched sounds, that may damage the cilia and auditory hair cells or spontaneous activity in individual auditory nerve fibers. o Tinnitus is strongly associated with age and hearing loss, but it can also be the result of many underlying conditions that include but are not limited to an infectious origin (as in the case of AOM or chronic OME), metabolic disorders (such as anemia, thyroid disease, hyperlipidemia, or B12 deficiency), autoimmune disorders, head or ear trauma, ototoxic medications, vascular, or neurogenic causes. o The sound is often described differently by patients. It may be described as the sound of escaping air or running water or the sound heard inside a large seashell. It may be described as a buzzing ringing, humming, hissing, popping, roaring, or pulsatile to name a few. o The sound can be loud or soft, low pitched or high pitched, coming from one or both ears. Tinnitus may cause emotional distress and anxiety. o Gradual loss may lead to complete deafness. o The DDx for tinnitus should include the following: meniere’s disease, acoustic neuroma, otitis media, otosclerosis, cerebral vascular disease, & salicylate overdose o Physical exam for a patient with complaints of tinnitus should include orthostatic blood-pressure readings, gross hearing test (whisper test), as well as Weber and Rinne tests to detect conductive versus sensorineural hearing loss. A thorough otologic exam with pneumatic otoscopy (if possible) should be performed.  Diagnosis can be difficult and involves determining the etiology. The workup involves that very important history as well as physical exam.  Basic laboratory tests to evaluate for metabolic abnormalities include TSH, CBC, B12, and lipid panel and should be performed by the primary care provider.  If a metabolic cause cannot be identified, a referral to ENT is appropriate for further work-up and specialized testing needed to establish the etiology. 16  Additional workup may include audiometry and tympanometry. Imaging studies such as CT, MRI or MRA, and venography may also be needed to make a diagnosis. o Tinnitus is difficult to treat successfully. However, management of symptoms and treatment of the underlying disorder (if one can be identified) may help.  Elimination of possible offending medications (such as aspirin containing products and NSAIDS) is a priority.  Patients with tinnitus due to otitis media or infections should be treated with antibiotics for an adequate duration.  Although there has been not medication to help tinnitus, oral antidepressants may be effective in reducing symptoms.  Nortriptyline (Elavil) 50 mg at bedtime is often used. Meclizine (Antivert) is a commonly used vestibular suppressant. It is important to note, however, that there is no evidence to support the use of any medication, vitamin, or nutritional supplement in the treatment of tinnitus.  If the patient is severely emotionally disturbed by the sound, a referral to a psychiatrist or otolaryngologist is recommended.  Meniere’s disease is a condition that you need to be able to recognize in primary care. Meniere’s disease is a sensory disorder of both the labyrinth (semicircular canal system) and cochlea of the inner ear. o The precise cause of Meniere’s disease is not fully established, but theories have implicated the inflammatory response of the inner ear due to a variety of insults, including blunt trauma, viral infection, allergies, reduced or negative middle ear pressure, and various vascular, endocrine, and lipid disorders. o A genetic predisposition has also been suggested. o Migraine headaches, autoimmune conditions, and certain thyroid disorders may predispose patients to Meniere’s disease. o Acute episodes of Meniere’s disease are associated with a characteristic triad of symptoms: vertigo, hearing loss, and tinnitus. o Acute attacks can last from 20 minutes to 3 hours, and the frequency and severity of the attacks may decrease over time. o Hearing loss is typically low-frequency loss and may improve immediately after an acute attack. o Differential for Meniere’s should include the following: OM, vestibular neuritis, benign paroxysmal positional vertigo (BPPV), acoustic neuroma, CNS lesions, & acute vestibular labyrinthitis o Diagnosis of Meniere’s disease is based on history and is a diagnosis of exclusion.  Otoscopic exam is generally normal unless underlying otitis media is present.  A Weber and Rinne hearing test will reveal sensorineural hearing loss on the affected side.  Diagnosis can be difficult and involves determining the etiology. The workup involves that very important history as well as physical exam. Basic laboratory tests to evaluate for metabolic abnormalities include 17 TSH, CBC, B12, and lipid panel and should be performed by the primary care provider.  If a metabolic cause cannot be identified, a referral to ENT is appropriate for further work-up and specialized testing needed to establish the etiology.  Additional workup may include the following: audiogram, electronystagmography, ectrocochleography, vestibular evoked myogenic potential, & MRI to rule out acoustic neuroma o Acute attacks are best treated by bedrest with the eyes closed and protection from falling. Attacks rarely last more than 4 hours.  Pharmacological therapy, if necessary, is directed at symptomatic relief.  Maintenance therapy with a mild diuretic such as chlorothiazide (Diurel) 500 mg/day is often used. The theory is that a reduction in lymphatic pressure and volume may improve symptoms.  Meclizine, Promethazine, Dimenhydrinate, Diphenhydramine, or Metoclopramide are also advocated.  Of note, these treatments are most effective for vertigo symptoms, whereas tinnitus and hearing loss are less effective.  Conductive hearing loss is a result of obstruction between the middle ear and outer ear. Often reversible.  This can occur with cerumen accumulation or impaction, a foreign body in the ear canal, otitis externa, chronic otitis media, middle ear effusion, otosclerosis (scarring of the TM), a vascular anomaly or a cholesteatoma.  To treat conductive hearing loss appropriately, an etiology must be accurately identified. Most types of conductive hearing loss are reversible.  Cerumen impaction is a very common occurrence in primary care. Cerumen is the protective secretion produced by the outer portion of the ear canal. Most impactions occur from person’s who try to clean the canal improperly with Q-tips. Therefore, recommended hygiene instructions should consist of cleaning the external opening with a cloth over the index finger. o Impactions can be removed by detergent ear drops (otc debrox or cerumenex), and mechanical removal, including OTC kits that have a bulb syringes or syringes. o Many PCP offices provide irrigation and manual removal under otoscopic examination. Water should be body temperature water in order to avoid dizziness. Irrigation should only be done if the provider is sure the tympanic membrane is intact and the external canal is not infected. o Having the patient pre-treat with detergent ear drops for 3–5 days prior to irrigation is particularly helpful when the cerumen is hard.  Foreign bodies in the ear canal are more common in children than adults. o Small pieces of toys, crayons, beads, and erasure tips are commonly seen. o In adults, cotton pieces from a Qtip may be found lodged up against the TM. o Material that is firm may be removed with a hook or loop being careful not to push it back to the TM. o If manual removal is unsuccessful in your office, a referral to an ENT for suction removal is warranted. 20 appears retracted or “sucked back.” Notice the prominent malleus in this picture. Effusion may or may not be present with ETD. o 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.  The key to successful treatment of ETD is to treat the underlying problem.  If the problem is 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 and used in caution in people with HTN or cardiovascular disease o Comfort measures can include acetaminophen or ibuprofen. o Patients can be instructed to attempt to relieve pressure by yawning, chewing, or sucking. o Holding the nose and blowing out is not recommended due to risk of TM performation. o For chronic ETD that is unresponsive to treatment, an ENT referral is warranted. o In some cases, tympanostomy tubes may be placed to equalize pressure.  A quick bedside test that can be done to differentiate sensorineural versus conductive hearing loss is the Weber and Rinne test. This is a valuable screening tool that primary care providers tend to underutilize.  The Weber hearing test evaluates lateralization (if hearing is better on one side) and involves placing a vibrating tuning fork midline on the top of the head and equidistant between the ears. The patient is asked to report in which ear the sound is heard louder.  A normal Weber test will result in the patient hearing the sound equally on both sides.  In Sensorineural Loss: The patient reports that the normal ear hears the sound better, so sensorineural hearing loss is on the defective ear.  In Conductive Loss: The patient reports that the defective ear hears the tuning fork louder.  The Rinne test evaluates air and bone conduction hearing loss and involves placing a vibrating tuning fork initially on the mastoid process behind each ear until sound is no longer heard. The fork is then immediately placed just outside the ear and the patient is asked to report when the sound caused by the vibration is no longer heard.  A normal test is when the sound heard outside the ear is audible when the sound from over the mastoid bone can no longer be detected. In other words, air conduction is louder than the bone conduction.  In conductive hearing loss, BC is greater than AC, so the patient will report the bone conduction sound longer than the AC sound. 10. Identify the triad of symptoms associated with Meniere's disease  Acute episodes of Meniere’s disease are associated with a characteristic triad of symptoms: vertigo, hearing loss, and tinnitus. 21  Pharyngitis & Tonsillitis: 2 common inflammatory disorders involving the posterior pharynx.  Bacterial and viral etiologies  May co-exist or exist independently of one another  Share common etiology, clinical course, and treatment requirements  Viral pharyngitis: most viral related cases are self-limiting.  Causes of viral pharyngitis include adenovirus, RSV, Influenza A&B, Epstein- Barr, coxsackie, enteroviruses and herpes simplex are common viral origins  Symptom: mild to severe sore throat, tickle or pruritis in throat, rhinorrhea, conjunctivitis, and cough.  Symptoms are rapid in onset but systemic symptoms are few  Mononucleosis: Epstein-Barr Virus; most common in adolescents & young adults  Transmission requires person-to-person contact between susceptible persons and symptomatic viral shredders.  Mono is often referred to as the “kissing disease” for this reason.  Mononucleosis is infamous for a gradual onset of fever and marked malaise with severe sore throat.  Mononucleosis may present with exudative tonsillitis (50% of cases) in addition to palatal petechiae and rash. Anterior and posterior cervical lymphadenopathy are common. Splenic enlargement can occur.  Diagnosis is made usually by a + Point Of Care (POC) monospot test but in the absence of the availability of this test, a CBC will show atypical lymphocytes. It is important to note that this may not be observed though until the patient has had a few weeks of symptoms.  Treatment is symptomatic & may take weeks to resolve; no contact sports to prevent splenic rupture  Antibiotics are usually not given for treatment of viral pharyngitis due to mono  However, there are times when mono may not be suspected as in the case of a + RSA or a GAS+ throat culture. When amoxicillin or ampicillin is given to a person infected with mono, roughly 90% of patients will develop an erythematous, macular rash. The rash coincides with antibiotic use and is often the first indication that the patient also has mono. It is important to note that this reaction is not an allergic reaction; therefore, the patient should not be identified as having an amoxicillin allergy.  Bacterial pharyngitis: Group A Beta Hemolytic Streptococcus (GABHS) common  Identification of GABHS is essential as this can cause complications such as rheumatic fever, peritonsillar abscess, scarlet fever or glomerulonephritis.  GAS infections are most commonly observed in children 5-15 years of age in the winter and early spring.  Strep typically present with an acute onset of fever and moderate to severe sore throat. Systemic symptoms may include headache, malaise, neck pain, odynophagia, and otalgia.  The Differential Diagnosis for pharyz-ngitis and tonsillitis should include: GABHS, epiglottitis, pharyngitis secondary to post nasal drip from rhinitis or sinusitis, hand, foot and mouth disease (Coxsackie virus), HSV-1, mononucleosis, & stomatitis 22  Physical exam: the inflamed throat typically appears reddened with both viral and bacterial causes; exudates and enlarged tonsils (more likely bacteria) o GABHS pharyngitis (streptococcal infections) or tonsillitis may produce while to yellow exudate on the tonsils, a red tongue with enlarged papillae (AKA strawberry tongue), and a red, swollen uvula. A sandpaper-like scarletiniform rash may be present with a streptococcal infection. o HSV-1: 1-2 mm vesicular lesions which can extend from the pharynx to gingiva, buccal mucosa, tongue, and lips. o Hand, foot and mouth disease present with oral lesions co-occurring with xantham on the hands and feet.  Testing: there is broad overlap of streptococcal and nonstreptococcal (usually viral) pharyngitis, and the ability to diagnose GAS pharyngitis based on clinical presentation alone is poor. o As a result, testing for GAS is unnecessary if the patient’s clinical picture and epidemiological features are consistent with a viral etiology (i.e., presence of conjunctivitis, cough, oral ulcers, etc). o Bloodwork is rarely needed, but a CBC and monospot is recommended if diagnosis is unclear or if patient reports close contact with a person infected with mononucleosis. o Rapid strep antigen (RSA) testing and throat culture should be performed on patients with pharyngitis who do not meet history and physical findings that are most likely associated with a viral etiology.  Throat culture is GOLD STANDARD in identifying the causative organism of pharyngitis and tonsillitis but takes 24 hrs+  POC RSA test (specificity 90-99%; sensitivity 90-95%)  Negative RSA test should have throat culture sent of the posterior pharynx for maximal sensitivity  Empiric treatment for GABHS o Centor Criteria (strongly suggest GABHS): fever (>100.5 F or >38 C), tender anterior cervical adenopathy, lack of cough, and a pharyngotonsillar exudate. Presence of these clinical features suggest bacterial pharyngitis. o Patients with ≥ 3 of Centor criteria may be empirically diagnosed with GAS and treated without further testing. o However, empiric treatment of asymptomatic household contacts of patients with acute streptococcal pharyngitis is not routinely recommended.  Treatment: o PCN remains the treatment of choice because of its proven efficacy and safety, its narrow spectrum, and its low cost.  PCN VK 250 mg TID or 500 mg BID x 10 days o Amoxicillin equally effective (kids like taste)  50 mg/kg up to 1000 mg maximum once daily effective o Macrolide if PCN allergy (e.g. erythromycin or azithromycin) – 10 days of all macrolides except for azithromycin which is for 5 days  Azithromycin 12 mg/kg/day, max of 500 mg daily x 5 days  Supportive Treatment 25  Abdominal X-ray films should be obtained on all patients with suspected diverticulitis to look for free air (indicating perforation), ileus, or obstruction.  Diverticulitis can often be diagnosed clinically, but a CT scan with oral and IV contrast is very sensitive and accurate for a definitive diagnosis.  In other words, if the patient presents with a clinical picture of diverticulitis, get an abdominal X-ray to R/O perforation or obstruction and treat empirically. Do not delay treatment to wait for CT confirmation.  Some patients will need to be hospitalized due to intractable abdominal pain or vomiting. 15. Discuss colon cancer screening recommendations relative to certain populations  If you are at an increased or high risk of colorectal cancer, you might need to start colorectal cancer screening before age 50 and/or be screened more often.  Following conditions make your risk higher than average:  A personal history of colorectal cancer or adenomatous polyps  A personal history of inflammatory bowel disease (ulcerative colitis or Crohn’s disease)  A strong family history of colorectal cancer or polyps  A known family history of a hereditary colorectal cancer syndrome such as familial adenomatous polyposis (FAP) or Lynch syndrome (hereditary nonpolyposis colon cancer)  Anyone age 50 or older should have a colonoscopy as part of a routine screening examination to rule out colon cancer.  African Americans are more likely to develop colon cancer at an earlier age and should also consider colonoscopy screening at age 40.  Individuals with a single first-degree relative with colorectal cancer (CRC) or advanced adenomas diagnosed at age ≥60 years can be screened like average-risk persons.  Screening is recommended in African Americans beginning at age 45 years.  In the office setting, though, if you have a patient that has alarm symptoms such as unintentional weight loss, rectal bleeding, diffuse lower abdominal pain, new onset of severe diarrhea or constipation, early satiety, or loss of appetite should be referred to a gastroenterologist for consideration of a colonoscopy and/or upper endoscopy. Risk Screening Recommendations Average risk Annual fecal occult blood (FOB) test Flexible sigmoidoscopy every 5 years beginning at age 50 or colonoscopy every 10 years High risk (general) Annual FOB testing 26 Double-contrast barium enema OR Colonoscopy every 3–5 years starting at age 40 Specific High-Risk Groups Prior colorectal cancer Colonoscopy 1 year postfinding, then every 3 years Hereditary nonpolyposis colorectal cancers Colonoscopy screening must begin 10 years before the age at onset of the earliest affected family member OR Colonoscopy every 1–2 years beginning at age 20–25 and continuing until age 35 and then yearly Inflammatory bowel disease Annual colonoscopy beginning 8 years after onset of disease First-degree family history Colonoscopy every 3–5 years beginning 5 years before the age at onset of the youngest affected relative 16. Identify at least two disorders that are considered to be disorders related to conductive hearing loss  Conductive hearing loss is a result of obstruction between the middle ear and outer ear. This can occur with cerumen accumulation or impaction, a foreign body in the ear canal, otitis externa, chronic otitis media, middle ear effusion, otosclerosis (scarring of the TM), a vascular anomaly or a cholesteatoma. 27 17. Identify the most common bacterial cause of pharyngitis  Most common bacterial cause is from Group A Beta Hemolytic Streptococcus (GABHS)  Treatment: PCN is treatment of choice for GAS pharyngitis b/c of its efficacy, safety, narrow spectrum, and low cost.  PCN is the only antibiotic that has been studied and shown to reduce rates of acute rheumatic fever.  For most adult patients: Penicillin V 500mg BID-TID x10 days.  For most kids: Penicillin V or amoxicillin  Alternatives for those with PCN allergies: 1st gen cephs, erythromycin, clinda, clarithromycin, azithromycin. 18. Identify the clinical findings associated with mononucleosis  Gradual onset of fever, malaise, severe sore throat, exudative tonsillitis (50% of cases), palatal petechiae, rash, anterior and posterior cervical lymphadenopathy, and splenic enlargement (NO CONTACT SPORTS)  (FOR OUR BOARD EXAM REMEMBER THAT POSTERIOR CERVICAL NODE ENLARGEMENT IS CLASSIC).  Diagnosis: CBC atypical lymphocytes, POC Monospot + 19. Identify common characteristics in a rash caused be Group A Strep  A sandpaper-like scarletiniform rash may be present with a streptococcal infection.  These turn into a fine pink-red rash that looks like sunburn. The skin feels rough when touched, like sandpaper. The rash spreads to the ears, neck, elbows, inner thighs and groin, chest, and other parts of the body. 20. Discuss that the diagnosis of streptococcal pharyngitis can be made clinically based on the Centor criteria  Centor Criteria (strongly suggest GABHS): fever (>100.5 F or >38 C), tender anterior cervical adenopathy, lack of cough, and a pharyngotonsillar exudate. Presence of these clinical features suggest bacterial pharyngitis.  Patients with ≥ 3 of Centor criteria may be empirically diagnosed with GAS and treated without further testing. 21. Describe an intervention for a patient with gastroenteritis  AGE is usually self-limiting and resolves within a week after onset of symptoms  Tx should consist of supportive measures including fluid repletion and nutrition  Avoid dehydration with fluid and electrolyte management (particularly with children, older adults, and immunocompromised patients)  Oral rehydration: fluids with sodium content of 45-75 mEq/L (Pedialyte or Gatorade), broths, soups, fruit juices. IV rehydration: severe dehydration or patients with chronic diseases and are hypotensive  Stool samples for prolonged diarrhea, fever >= 38.5C, bloody stools, or +leucocytes. 22. Discuss an appropriate treatment for prophylaxis or treatment of traveler's diarrhea 30 1. Discuss that the majority of dyspnea complaints are due to cardiac or pulmonary decompensation  Dyspnea descriptions include shortness of breath, difficulty breathing, can’t get enough air, breathlessness, suffocation or smothering, air hunger and winded.  In the majority of cases, dyspnea is a result of cardiac or pulmonary decompensation. However other etiologies can include metastasis, neuromuscular disease, spinal cord lesions that affect the innervation to the diaphragm, pain and panic disorders.  Common cardiopulmonary conditions include asthma, chronic obstructive lung disease, malignancy, heart failure, interstitial lung disease, pneumonia, valvular heart disease, intracardiac shunt, arrhythmias, cardiomyopathies, & myocardial ischemia. 2. Explain the differences between intra-thorax and extra-thorax flow disorders  Intra-thorax: Obstruction of distal/smaller airway  Extra-thorax: Obstruction of proximal/larger airway 3. Identify at least three examples of flow and volume disorders (intra and/or extra thorax)  Flow intra-thorax: Obstruction of distal/smaller airway  Ex: asthma, bronchiolitis, vascular ring, solid foreign body aspiration, & lymph node enlargement pressure  These types of disorders cause expiratory effort in infants and also in children less than 5 years of age (bronchiolitis).  Flow extra-thorax: Obstruction of proximal/larger airway  Ex: rhinitis with nasal obstruction, nasal polyp, cranio-facial malformation, OSA, tonsil-adenoid hypertrophy, laryngo-tracheo-malacia, larynx papilloma, diptheria, croup, epiglottis, & thymus hypertrophy  Infants or children ages 5 and younger are affected, and they have clinical findings of inspiratory stridor  Volume intra-thorax: lung parenchyma disorders & extrapulmonary disorders  Ex: pneumonia (infection, aspiration), atelectasis, pulmonary edema, near drowning, and sepsis  These disorders affect inspiratory effort  Volume extra-thorax: lung compliance disorders & respiratory center disorders  Ex: pneumothorax, pneumomediastinum, cardiomegaly, heart failure (perfusion), pleural effusion (including empyema, hemothorax), hernia diaphragmatica, diaphragmatica eventration, intra-thorax mass (nonpulmonary), chest trauma (rib fx, lung contusion), & thorax deformity (pectus excavatum, scoliosis) o These disorders also affect inspiratory effort  Extra-thorax volume disorders due to lung compliance issues include neuromuscular disorders (CP, GBS, MG), gastritis, peptic ulcer, extreme obesity, peritonitis, appendicitis, acute abdomen, aerophagia, meteorismus, ascites, hepato-splenomegaly, & abdominal solid tumor. o These disorders cause inspiratory constraint  Extra-thorax volume disorders due to respiratory center disorders include anemia, metabolic acidosis, CNS infections: meningitis, encephalitis, encephalopathy (typhoid, DHF, metabolic), psychologic (anxiety, usually adolescent), poisoning (salycylate, alcohol), trauma capitis, and CNS disease sequelae. o These disorders cause deep rapid breathing 31 4. Discuss diagnosis, risk factors and treatments for asthma  Diagnosis: expiratory airflow measurements are essential to the differential diagnosis of asthma.  PFTs, complete history, lab tests can differentiate asthma from other disease  Common feature is nocturnal awakening with one or more of the symptoms: dyspnea, cough, and wheezing.  History of cough (especially nocturnal), recurrent wheeze, recurrent episodic dyspnea, recurrent chest tightness  Symptoms worsen in relation to specific factions: airborne chemicals or dust, animals with fur or feathers, change in weather, exercise, GERD, sensitivity to aspirin, other NSAIDs, & sulfites, dust mites in house, menses, mold/pollen, nighttime (patient awakens), nonselective BB, pollen, smoke, strong emotional expression, viral infection/rhinitis/sinusitis  To establish the diagnosis of asthma, episodic symptoms of airflow obstruction must be present, airflow obstruction must be at least partially reversible, and the provider must have ruled out any alternative diagnoses  Spirometry is recommended for the diagnosis of asthma  Forced vital capacity (FVC) and forced expiratory volume in 1 second (FEV1) are helpful measurements.  The diagnosis is made by demonstrating the reversibility of the airway obstruction from the prebronchodilator and postbronchodilator PFTs.  Reversibility is defined as a 15% or greater increase in the FEV1 after two puffs of a beta-adrenergic agonist have been inhaled.  When spirometry is nondiagnostic, bronchial provocation testing may be useful with histamine, methacholine, or exercise.  Risk factors: family or personal history- allergic rhinitis, eczema/atopic diseases, residing in urban area, exposure to smoke or air pollution, cockroaches and dust, viral respiratory infections, cold air intolerance, & obesity  Treatment: short acting bronchodilator (albuterol) is a mainstay of treatment for ALL asthma patients Classification of Asthma Severity Mild Intermittent Symptoms < once per week OR < 2 nights per month. Exacerbations brief; PEFR or FEV1: >80% predicted; PFT variability > 20% Mild Persistent Symptoms > 2 times per week, but <1x per day; OR 3-4 times per month at nighttime. Exacerbations affect activity/sleep; PEFR or FEV1: >80% predicted; PFT variability 20% - 30% Moderate Persistent Daily symptoms OR >1 night per week but not nightly. Exacerbations affect activity/sleep. Daily use of inhaled short- acting beta-2 agonist. PEFR or FEV1: 60-80% predicted; PFT variability > 30% Severe persistent Symptoms throughout the day; often 7 nights per week. 32 Frequent exacerbations; limited physical activity. PEFR or FEV1 ≤ 60% predicted; PFT variability > 30% Pharmacologic Management Intermittent Short-acting bronchodilator (albuterol): for exacerbations (inhaled or nebulized) Mild Persistent Short acting bronchodilator + Preferred tx- Low-dose inhaled corticosteroids (fluticasone/Flovent, budesonide/Pulmicort, mometasone/Asmanex) Moderate Persistent Short acting bronchodilator + Preferred tx- low to medium dose inhaled corticosteroid AND Long acting inhaled bronchodilator (salmeterol/serevent, formoterol/Foradil) Alternative tx-low to med dose inh. Corticosteroid AND Either leukotriene blocker (Montelukast/singulair) OR theophylline Severe Persistent Short acting bronchodilator + Medium dose inhaled corticosteroids AND Long acting inhaled bronchodilator AND If needed, oral corticosteroids (2mg/kg/day, 60mg/day max) 5. Describe appropriate tests in the work up for dyspnea  CXR to rule out tumors, TB, pneumonia, and other major pulmonary disorders  CBC with differential to rule out anemia and infection  Peak expiratory flow test (in office) to determine the degree of expiratory airflow obstruction in patients with asthma and COPD  Electrocardiography & echocardiography to test function and activity of the heart  Spirometry to determine obstructive, restrictive, and mixed lung disease 6. Discuss clinical findings and PFTs for asthma, chronic bronchitis, emphysema, and COPD  Asthma: chronic, inflammatory, obstructive disease in airways.  May occur at any age and presents with wheezing (airway spasms), chest tightness, dyspnea, cough.  Reversible hyperreactivity of bronchi and bronchioles to a variety of stimuli.  Forced Vital Capacity (FVC): normal, Residual Volume (RV): normal, increased during attacks, Total Lung Capacity (TLC): normal to increased, RV/TLC: normal to increased, Expiratory Flow Rates (EFR): normal to decreased, FEV1/FVC: normal to decreased 35 o The skin rash presents with light pink, erythematous macules and papules on the face, neck, and extremities. The rash usually resolves in 1–3 days.  Differential diagnosis: Measles, drug eruption, rubella, or other viral rashes.  Testing & Treatment: o Clinical diagnosis based on clinical presentation and history o Management of the virus is to treat the patient symptomatically o These patients are contagious 1–2 days before the fever starts and are able to return to activities once fever, fatigue, cough, or diarrhea have subsided.  5ths disease: AKA erythema infectiosum or human parvovirus  This is spread through respiratory droplets and blood products.  Patient starts with headache, fever and chills, and possible cough  There are three stages to this virus: o Stage 1: Classic “slapped cheek” rash, bright red bilateral cheeks which spare the forehead, nasal bridge, and perioral area. o Stage 2: Pink lacy (or reticulated) erythematous macules on all extremities and trunk spare the palms and sole surfaces. The rash may be itchy at this stage. o Stage 3: 2–3 weeks of the body rash. This rash may come and can last for up to 3 weeks.  Differential Diagnosis: Phototoxic reaction, Systemic lupus, Drug eruption, and other virural xanthams.  Testing & Treatment: o Diagnosis may be done by blood test, but results will not be detected for 3 weeks after rash, so it’s not valuable because the patient should be symptom free by then. o The lab test is IgG antibodies to parvovirus. o Management for patients is symptomatic care o They should be advised to avoid heat as this will exacerbate the rash. o Patients with fifth disease are contagious days before they develop the rash and can return to activities after the initial signs and symptoms of headache, fever, and chills have subsided even if there is still a rash.  Pityriasis rosea:  Has a viral etiology but it is difficult to confirm.  Common in ages 10–35, and there is a greater ratio of females to males.  It is more common for breakouts of this virus in the springtime.  Symptoms: a solitary 2–4 patch or plaque on the trunk that starts 2–3 weeks prior to the general rash. This patch is known as the herald patch. o The rash is pink to erythematous, round to oval plaques and papules with possible scaly borders. o PR rash resembles the shape of a Christmas tree on the trunk. The face, palmar, and sole surfaces are usually spared. o The rash can be itchy, and the patient may have a low-grade fever, headache, and fatigue. o The rash can possibly last 1–2 months or even longer.  Differential diagnosis is tinea versicolor, drug eruption, or psoriasis  Testing & Treatment: o Clinical diagnosis made by history and physical o Management includes antihistamines, and unlike Fifth’s disease the sun could help the rash instead of exacerbate the rash. 36 o Acyclovir for 1 week may decrease severity. o Patients may be contagious 7-14 days prior to rash eruption. o Returning to activities will depend on the patient’s symptoms, by the time the rash has appeared though, the patient is not contagious anymore.  Hand, foot and mouth disease: contagious virus mostly occurring in young children  Caused by the HFMD or coxsackievirus A16 and enterovirus 71.  Symptoms: low-grade fever, fatigue, or sore throat 1–2 days prior to rash. o The virus skin presentation is vesicles on the hands and feet with mouth sores. o Mouth sores are in almost 90% of the cases and are usually the first sign. There can be more than 10 mouth apthae (sores) anywhere in the oral cavity and frequently are asymptomatic. o The hand vesicles appear with erythematous halos and appear mostly on the soles and palms. o Vesicles might appear on the legs, buttocks, and face. o The lesions usually resolve around 7 days.  Differential diagnosis is varicella and herpes.  Testing & Treatment: o Clinical diagnosis o The management is symptomatic care for the patient. o The patient or the patient’s parents need reassurance that there won’t be scarring and/or that it is not some other rare skin disorder. o The patient is considered contagious 4–6 days prior to outbreak and should not return to school or activities until the lesions are scabbed.  Molluscum contagiosum: from the family of Poxviridae – can affect kids & adults  This virus is encased in a protective sac that prevents the immune system from being triggered.  Symptoms: o The skin presentation is tiny pustules which are 2–5 mm, and some even have a slight depression in the center of the flesh-colored dome. o A single lesion or multiple lesions may occur. o They are spread by contact, scratching, autoinoculation, or shaving. o The most common places on children are thighs and arms, but the adult presentation is primarily the genital region spread from sexual contact. o Soles and palms are always spared. o Some patients present with erythematous papules and scaling from the itching. o Papule can last up to 8 weeks; due to the autoinoculation the virus can last up to 8 months or longer.  Differential diagnosis includes genital warts, hypersensitivity reaction, folliculitis in the genital region.  Testing & Treatment: o Clinical diagnosis o Often misdiagnosed as genital warts. o Management: Non-prescription over the counter medications for molluscum such as Zymaderm can be used. o Personally, I have found this to be beneficial only in approximately 50% of the patients have that have tried it. o Prescription topical retinoids may be helpful. 37 o Oral Cimetidine (Tagamet) 40mg/kg/day for 2 months can also be tried and cryosurgery with liquid nitrogen can be performed, however there may be scaring or hypopigmentation of the skin so educating the parent or patient before this therapy is important. o Anticipatory guidance should be provided to the patient and/or parents regarding potential for scarring and contagiousness. o Should be excluded from activities or sports until symptom-free 8. Differentiate between the following tineas: pedis, cruris, corporis and unguium and describe an appropriate treatment  Pedis: occurs on the feet  Symptoms: erythematous, scaly, with possible inflammation or itching/burning on the feet  Treatment: antifungal cream and use a vinegar soak or Burrow solution to decrease the itch. o Ketaconozole is the topical treatment of choice and is used for at least 4 weeks if not longer to resolve symptoms. o I always have my patients use an over the counter anti-fungal spray for all of their shoes during and after treatment. o Sometimes systemic antifungals like Terbanifine are needed for prolonged or severe cases.  Cruris: jock itch that can present on the inner thigs, buttocks, or groin area  Symptoms: well-demarcated erythematous or tan plaques with raised scaly borders.  Treatment: topical antifungal x4 weeks and if patients have repetitive infections, the use of over the counter zeabsorb powder is an antifungal powder which I advise patients to use routinely which can help prevent fungal breakouts on the skin  Corporis: AKA ringworm, fungal infection on the extremities or trunk  Symptoms: erythematous annular lesion with scaly macules and papules, a well-defined edge (well-demacrated). o The lesion may be itchy. The edge of the lesion is raised and the center of the lesion is flattened. o This lesion can be small or cover a large body surface area  Treatment: antifungal topical cream x4 weeks or an oral antifungal agent like Terbanafine if the lesion is widespread. o Follow-up for these patients with any fungal infection is 3–4 weeks to make sure that they are improving.  Unguium: AKA onychomycosis, fungal infection of the fingernail or toenails  Symptoms: nails may vary and might be yellowish, greenish, sometimes black or white ridging with possible cracking of the nails.  Treatment: determined by the severity and patient’s age. o Topical agent such as Ciclopirox nail laquer 8% applied daily for 3 months at the base of the nail is a good choice. o An oral antifungal like Terbanafine 250mg daily for 2 weeks has a high cure rate but the patient has to have a healthy liver in order to use oral antifungals, so a CMP should be done prior to initiation of the medication. o Provider education is key since the process to cure a fungal infection of the nails is very slow. 40  Chalzion: chronic internal granulomatous reaction of the Meibomian gland that produces a mass in the lid.  Its onset is acute and is usually found in the mid-portion of the upper lid away from the margin.  Symptoms: not painful or tender and looks slightly red but swollen.  Treatment: conservative to start, using warm compresses, time, and patience. o Chalazions usually resolve in a few weeks to months, and antibiotic drops do not help. o If there is no resolution within a few months, referral to optho is appropriate for incision and drainage or steroid injection. o One side note: squamous cell carcinoma looks similar, so again, if not improving, refer to optho.  Hordeolum: AKA stye.  A stye is an abcess of the lid margin caused from a staph infection.  Styes have a very acute and painful onset associated with redness and swelling and are usually on the outside of the lid.  Treatment: with warm compresses and topical antibiotics. One way to remember the difference between chalazion and hordeolum is with the mnemonic device: “Hoarders” typically live in a pig “stye.” 12. Differentiate between viral, allergic, bacterial, toxic and HSV conjunctivitis  Bacterial: AKA pink eye  Cause includes direct hand-to-eye contact with an infected individual or spread of one’s own nasal and sinus bacteria during an illness  Hallmark symptom is purulent discharge  Other symptoms include reddened conjunctiva & lid swelling, unilateral to start but typically spreads to other side  Treatment: may resolve without treatment o Antibiotics can shorten duration. Nearly every antibiotic is effective and should be used 4x per day for 5-7 days. o The choice should be based on the patient’s allergies, preference, formulary coverage (i.e., cost), and availability. o Instruct patients to treat the eye that is affected but to start treatment in the other eye if symptoms develop. o It is important to teach the patient how to put drops in and advise to avoid touching the tip of the bottle to any conjunctival or skin surface. o Women should be instructed to throw away all eye makeup products due to contamination and to start with new products when the infection clears. o Likewise, disposable contact lens wearers will need to discard the contacts, refrain from wearing any during treatment, and start with a new pair when clinical symptoms resolve. o Very contagious so patients should stay home from work or school until 24 hours of antibiotic treatment or as soon as clinical improvement (decreased redness and discharge) o There is one exception to the rule in regards to the effectiveness of antibiotic drops for all bacterial conjunctivitis cases, and the exception is gonococcal infections. o GONOCOCCAL CONJUNCTIVITIS IS SIGHT THREATENING BECAUSE IT CAN AFFECT THE CORNEA, SO PATIENTS SHOULD BE SENT TO THE 41 ER IMMEDIATELY. Gonococcal conjunctivitis is associated with hyperpurulent discharge.  Viral: most caused by adenovirus, commonly associated with URIs or common cold  Other viruses include HSV, HZV (zoster), and Molluscum contagiosum.  Symptoms: irritation, mild light sensitivity, and swollen lids, and the patient may complain of a mild foreign body sensation. o On physical exam, mild conjunctival hyperemia to intense hyperemia and watery or mucousy drainage can be seen. However, the drainage is not purulent, which is the distinguishing characteristic between bacterial and viral conjunctivitis. o There are often enlarged tender preauricular lymph nodes on the affected side and patients will have other nonspecific physical exam findings associated with URIs such as red throat, nasal drainage, ear infection. o Adenoviral conjunctivitis: clinical diagnosis unless point-of-care (POC) rapid adenovirus testing is available  Treatment: abx drops are not effective, usually self-limiting o Resolve on its own from a few days to few weeks o Highly contagious o No firm guidelines on return to school or work but AAO textbook recommends absence from work or school until redness or tearing has resolved.  HSV: Two types: HSV 1 (above the waist) & HSV 2 (below the waist)  Spread by contact with persons who have visible, infection lesions and with persons symptomatically shedding the virus (before lesions appear – prodrome of ill-related symptoms such as malaise, low-grade fever, pain or tingling near site of lesions)  Symptoms: skin vesicles (if these are present, they often help with the diagnosis), conjunctivitis (same as viral conjunctivitis, so it alone is not helpful in making the determination), & corneal infection with the hallmark “dendrite” appearance  SAME DAY OPHTHALMOLOGY REFERRAL OR NEEDS TO GO TO ER  Allergic: usually caused by an environmental allergen such as pollen, grass, trees, and so on.  Occurrence can be seasonal and can be isolated to the eyes or include upper respiratory allergy symptoms such as rhinitis.  The hallmark characteristic symptom is itching.  Other symptoms can include a diffuse, milky, conjunctival hyperemia; swollen conjunctiva; tearing; and symptoms are almost always bilateral.  There may also be uniquely identifying “bumps” on the conjunctiva which are called follicles and when present are a hallmark symptom of allergy.  Treatment: symptomatic, but it is important to advise the patient not to scratch as this can result in a corneal abrasion and induces more itching by the inflammatory response. o Cool artificial tears, anti-allergy eye drops (either OTC or RX) can be helpful, but prescription drops are very expensive, so start with OTC first. o Systemic antihistamines are not very helpful for symptoms.  Toxic: due to overuse of topical ocular medications such as Visine, but antibiotic drops are most common.  The classic scenario is the patient who continues to use the antibiotic drops prescribed for longer than necessary or for viral infections. 42  Symptoms: clear, watery discharge and red conjunctiva, so the diagnosis is mainly established from the history.  Treatment obviously is to stop the drops. 13. Discuss which chemical injury is associated with the most damage and highest risk to vision loss  The severity of a chemical eye injury depends on three things: pH, volume, & duration  Alkaline agents are much more damaging to the eye than acids, and either can come in the form of liquid, solid, powder, mist, or vapor.  Common acids include battery acid, bleach, and vinegar, which are sulfuric, sulfurous, and acetic acid, respectively.  Common alkaline agents include ammonia, drain cleaners, cement, plaster or mortar, airbag rupture, and fireworks. These agents contain ammonia, lye, lime, sodium, and magnesium hydroxide.  Treatment: immediately irrigate with water or normal saline, using copious amounts of water (i.e., shower or hose if needed).  Do not use artificial tears or eye wash.  The American Academy of Pediatric Ophthalmologists advocate that you send the patient in an ambulance to the ER.  Acidic burns will produce large conjunctival and corneal abrasion and a mild corneal haze. Prognosis is good for a full recovery. Heal with little to no corneal scar  Alkali burns cause damage to the epithelium and deep corneal layer, which has a poor prognosis. In these pictures, you can see corneal scarring and vascular growth. Minor will heal without a corneal scar. Mod-severe can cause permanent scarring & vision loss 14. Recognize common eye emergency conditions that require emergency room evaluation  Gonococcal infections  Eyelid lacerations: often require repair in OR. Put gauze over eye & send to ER  Subconjunctival hemorrhage (blood trapped under the conjunctiva): occurs from direct trauma or sudden increase in pressure of the chest from sneeze, cough, straining with a BM, vomiting, and strangulation.  With mild cases w/o any signs of ocular injury, condition is benign and will disappear within a weak. No need for tx or referral  If hemorrhage is mod-severe or there are other signs of trauma, or there is concern for more extensive eye injury based on history, a referral to ophthalmology or ER is appropriate. Make sure to do a vision test for all eye complaints  Foreign bodies  Hyphema: blood trapped between iris and cornea. Can be caused by blunt or penetrating trauma or can be associated with other eye injuries. Tx is to protect eye with patch or shield & refer to ER/Optho  Ruptured globe: blunt or penetrating trauma, vision threatening, requires surgery 15. Discuss glaucoma, diagnosis and treatment