Soap note about chronic Disease in these case I selected: Gastroesophageal Reflux Disease.
EXAMPLE:
PATIENT INFORMATION
Name: Mr. W.S.
Age: 65-year-old
Sex: Male
Source: Patient
Allergies: None
Current Medications: Atorvastatin tab 20 mg, 1-tab PO at bedtime
PMH: Hypercholesterolemia
Immunizations: Influenza last 2018-year, tetanus, and hepatitis A and B 4 years ago.
Surgical History: Appendectomy 47 years ago.
Family History: Father- died 81 does not report information
Mother-alive, 88 years old, Diabetes Mellitus, HTN
Daughter-alive, 34 years old, healthy
Social Hx: No smoking history or illicit drug use, occasional alcoholic beverage consumption on social celebrations. Retired, widow, he lives alone.
SUBJECTIVE:
Chief complain: “headaches” that started two weeks ago
Symptom analysis/HPI:
The patient is 65 years old male who complaining of episodes of headaches and on 3 different occasions blood pressure was measured, which was high (159/100, 158/98 and 160/100 respectively). Patient noticed the problem started two weeks ago and sometimes it is accompanied by dizziness. He states that he has been under stress in his workplace for the last month.
Patient denies chest pain, palpitation, shortness of breath, nausea or vomiting.
ROS:
CONSTITUTIONAL: Denies fever or chills. Denies weakness or weight loss. NEUROLOGIC: Headache and dizzeness as describe above. Denies changes in LOC. Denies history of tremors or seizures.
HEENT: HEAD: Denies any head injury, or change in LOC. Eyes: Denies any changes in vision, diplopia or blurred vision. Ear: Denies pain in the ears. Denies loss of hearing or drainage. Nose: Denies nasal drainage, congestion. THROAT: Denies throat or neck pain, hoarseness, difficulty swallowing.
Respiratory: Patient denies shortness of breath, cough or hemoptysis.
Cardiovascular: No chest pain, tachycardia. No orthopnea or paroxysmal nocturnal
dyspnea.
Gastrointestinal: Denies abdominal pain or discomfort. Denies flatulence, nausea, vomiting or
diarrhea.
Genitourinary: Denies hematuria, dysuria or change in urinary frequency. Denies difficulty starting/stopping stream of urine or incontinence.
MUSCULOSKELETAL: Denies falls or pain. Denies hearing a clicking or snapping sound.
Skin: No change of coloration such as cyanosis or jaundice, no rashes or pruritus.
Objective Data
CONSTITUTIONAL: Vital signs: Temperature: 98.5 °F, Pulse: 87, BP: 159/92 mmhg, RR 20, PO2-98% on room air, Ht- 6’4”, Wt 200 lb, BMI 25. Report pain 0/10.
General appearance: The patient is alert and oriented x 3. No acute distress noted. NEUROLOGIC: Alert, CNII-XII grossly intact, oriented to person, place, and time. Sensation intact to bilateral upper and lower extremities. Bilateral UE/LE strength 5/5.
HEENT: Head: Normocephalic, atraumatic, symmetric, non-tender. Maxillary sinuses no tenderness. Eyes: No conjunctival injection, no icterus, visual acuity and extraocular eye movements intact. No nystagmus noted. Ears: Bilateral canals patent without erythema, edema, or exudate. Bilateral tympanic membranes intact, pearly gray with sharp cone of light. Maxillary sinuses no tenderness. Nasal mucosa moist without bleeding. Oral mucosa moist without lesions,.Lids non-remarkable and appropriate for race.
Neck: supple without cervical lymphadenopathy, no jugular vein distention, no thyroid swelling or masses.
Cardiovascular: S1S2, regular rate and rhythm, no murmur or gallop noted. Capillary refill < 2 sec. Respiratory: No dyspnea or use of accessory muscles observed. No egophony, whispered pectoriloquy or tactile fremitus on palpation. Breath sounds presents and clear bilaterally on auscultation. Gastrointestinal: No mass or hernia observed. Upon auscultation, bowel sounds present in all four quadrants, no bruits over renal and aorta arteries. Abdomen soft non-tender, no guarding, no rebound no distention or organomegaly noted on palpation Musculoskeletal: No pain to palpation. Active and passive ROM within normal limits, no stiffness. Integumentary: intact, no lesions or rashes, no cyanosis or jaundice. Assessment Essential (Primary) Hypertension (ICD10 I10): Given the symptoms and high blood pressure (156/92 mmhg), classified as stage 2. Once the organic cause of hypertension has been ruled out, such as renal, adrenal or thyroid, this diagnosis is confirmed. Differential diagnosis: Ø Renal artery stenosis (ICD10 I70.1) Ø Chronic kidney disease (ICD10 I12.9) Ø Hyperthyroidism (ICD10 E05.90) Plan Diagnosis is based on the clinical evaluation through history, physical examination, and routine laboratory tests to assess risk factors, reveal identifiable causes and detect target-organ damage, including evidence of cardiovascular disease. These basic laboratory tests are: · CMP · Complete blood count · Lipid profile · Thyroid-stimulating hormone · Urinalysis · Electrocardiogram Ø Pharmacological treatment: The treatment of choice in this case would be: Thiazide-like diuretic and/or a CCB · Hydrochlorothiazide tab 25 mg, Initial dose: 25 mg orally once daily. Ø Non-Pharmacologic treatment: · Weight loss · Healthy diet (DASH dietary pattern): Diet rich in fruits, vegetables, whole grains, and low-fat dairy products with reduced content of saturated and trans l fat · Reduced intake of dietary sodium: <1,500 mg/d is optimal goal but at least 1,000 mg/d reduction in most adults · Enhanced intake of dietary potassium · Regular physical activity (Aerobic): 90–150 min/wk · Tobacco cessation · Measures to release stress and effective coping mechanisms. Education · Provide with nutrition/dietary information. · Daily blood pressure monitoring at home twice a day for 7 days, keep a record, bring the record on the next visit with her PCP · Instruction about medication intake compliance. · Education of possible complications such as stroke, heart attack, and other problems. · Patient was educated on course of hypertension, as well as warning signs and symptoms, which could indicate the need to attend the E.R/U.C. Answered all pt. questions/concerns. Pt verbalizes understanding to all Follow-ups/Referrals · Evaluation with PCP in 1 weeks for managing blood pressure and to evaluate current hypotensive therapy. Urgent Care visit prn. · No referrals needed at this time. References Domino, F., Baldor, R., Golding, J., Stephens, M. (2017). The 5-Minute Clinical Consult 2017 (25th ed.). Print (The 5-Minute Consult Series). Codina Leik, M. T. (2014). Family Nurse Practitioner Certification Intensive Review (2nd ed.). ISBN 978-0-8261-3424-0 ____________________________ Gastroesophageal Reflux Disease: Pathophysiology, Diagnosis, and Management Introduction Gastroesophageal reflux disease (GERD) is a common condition that affects approximately 20% of the adult population in Western countries (El-Serag et al., 2014). It occurs when stomach contents, including acid and digestive enzymes, back up from the stomach into the esophagus. Left untreated, GERD can lead to complications such as esophagitis, strictures, and Barrett's esophagus, which increases the risk of esophageal adenocarcinoma (Shaheen & Richter, 2009). This article will discuss the pathophysiology, diagnosis, and management of GERD. Pathophysiology The lower esophageal sphincter (LES) acts as a valve between the esophagus and stomach. Under normal circumstances, it remains closed to prevent reflux of stomach contents into the esophagus. However, in individuals with GERD, the LES does not function properly. There are several factors that can contribute to impaired LES function (Sifrim & Castell, 2001): Transient LES relaxations (TLESRs): The LES relaxes involuntarily in response to factors like eating or abdominal pressure. Increased frequency of TLESRs allows reflux to occur more easily. Hiatal hernia: Part of the stomach protrudes through the diaphragmatic hiatus into the chest, bringing the stomach closer to the esophagus. This weakens the LES barrier. Delayed gastric emptying: Slow stomach emptying causes increased pressure in the stomach, making reflux more likely. Low LES pressure: The LES does not close tightly enough to prevent backflow of stomach contents. Excessive acid production: Increased acid in the stomach overcomes the LES barrier more readily. Genetic factors also play a role in GERD susceptibility. For example, single nucleotide polymorphisms in genes encoding LES structure and function have been linked to GERD (El-Serag et al., 2014). Obesity is another important risk factor, as it increases abdominal pressure on the LES (Nilsson et al., 2004). Diagnosis The diagnosis of GERD is usually made based on clinical symptoms, though testing may be used to confirm the diagnosis or assess for complications. Heartburn and regurgitation are the classic symptoms of GERD. However, not all patients experience heartburn, and atypical symptoms like cough, asthma, or laryngitis can also indicate GERD (Fass & Dickman, 2006). If symptoms are suggestive of GERD but testing is needed, initial options include (Gyawali et al., 2018): Upper endoscopy: Visualizes the esophagus, stomach, and duodenum. Allows biopsy if Barrett's esophagus or esophagitis are seen. Ambulatory pH monitoring: Measures acid exposure in the esophagus over 24-48 hours using a catheter-based pH probe. Esophageal manometry: Assesses LES pressure and coordination of esophageal contractions. For patients with uncomplicated GERD who respond well to proton pump inhibitors (PPIs), testing may not be necessary. However, those with alarm symptoms, refractory symptoms, or suspected complications usually require endoscopy and/or pH testing to establish the diagnosis and guide management (Gyawali et al., 2018). Management The goals of GERD treatment are symptom relief, healing of esophagitis if present, and prevention of complications. Lifestyle modifications and medications are the mainstays of management. Lifestyle changes with proven benefit include weight loss, head-of-bed elevation while sleeping, limiting foods that trigger symptoms, and cessation of smoking (Vakil et al., 2006). Medications: PPIs are the most effective pharmacologic treatment for GERD. Examples include omeprazole, esomeprazole, lansoprazole. PPIs heal esophagitis in 80-90% of patients (Fass & Dickman, 2006). H2 receptor antagonists (H2RAs) such as ranitidine are less potent acid suppressors and less effective than PPIs for GERD (Vakil et al., 2006). Antacids provide rapid, short-term relief but do not heal esophagitis. Prokinetic agents like metoclopramide may help if delayed gastric emptying contributes to symptoms. However, these drugs have more side effects than acid suppressors (Fass & Dickman, 2006). For patients with Barrett's esophagus, long-term high-dose PPI therapy aims to prevent progression to cancer. In some cases of large hiatal hernia or failed medical management, surgical intervention such as fundoplication may be considered (Gyawali et al., 2018). Close monitoring is also needed for patients at high risk of complications. Conclusion GERD is a prevalent condition resulting from impaired LES function and abnormal reflux of gastric contents into the esophagus. A thorough history and physical exam usually establish the diagnosis, though testing may be needed in some cases. Lifestyle modifications and acid-suppressing medications effectively manage symptoms and prevent complications in most patients. With proper long-term treatment, individuals with GERD can maintain remission and reduce cancer risk. References El-Serag, H. B., Sweet, S., Winchester, C. C., & Dent, J. (2014). Update on the epidemiology of gastro-oesophageal reflux disease: a systematic review. Gut, 63(6), 871–880. https://doi.org/10.1136/gutjnl-2012-304269 Fass, R., & Dickman, R. (2006). Clinical consequences of failure to recognize nocturnal gastroesophageal reflux disease. The American journal of medicine, 119(10), S21–S29. https://doi.org/10.1016/j.amjmed.2006.07.017 Gyawali, C. P., Kahrilas, P. J., Savarino, E., Zerbib, F., Masaoka, T., Sifrim, D., ... Roman, S. (2018). Modern diagnosis of GERD: the Lyon consensus. Gut, 67(7), 1351–1362. https://doi.org/10.1136/gutjnl-2018-316547 Nilsson, M., Johnsen, R., Ye, W., Hveem, K., & Lagergren, J. (2004). Obesity and estrogen as risk factors for gastroesophageal reflux symptoms. JAMA, 291(1), 72–78. https://doi.org/10.1001/jama.291.1.72 Shaheen, N. J., & Richter, J. E. (2009). Barrett's oesophagus. Lancet (London, England), 373(9666), 830–841. https://doi.org/10.1016/S0140-6736(09)60016-1 Sifrim, D., & Castell, D. (2001). Diagnosis and management of gastroesophageal reflux disease. Journal of the American Medical Association, 286(8), 936–945. https://doi.org/10.1001/jama.286.8.936 Vakil, N., van Zanten, S. V., Kahrilas, P., Dent, J., & Jones, R. (2006). The Montreal definition and classification of gastroesophageal reflux disease: a global evidence-based consensus. The American journal of gastroenterology, 101(8), 1900–1920. https://doi.org/10.1111/j.1572-0241.2006.00630.x
