Pathophysiology for Diagnosis (each diagnosis) with etiology 2. Pertinence of Research Article (for primary diagnosis) 3. Plan of Care: Testing/Studies:SAMPLE_CASESTUDY_

History Data:

Chief Concern: “I have been feeling generally unwell these last few months with increased fatigue and shortness of breath with barely doing anything.”

HPI: This 80-year-old Caucasian female who has a history of HTN and tobacco dependence. She stated she has been feeling generally unwell for the last couple months noting generalized weakness and becoming easily fatigued and short of breath with even minimal exertion. Over the last week she reports increased shortness of breath with minimal exertion, waking up in the middle the night short of breath, and difficulty breathing when lying flat or on her side propping herself up in bed with multiple pillows. She has also had swelling of her legs and feet, states her right foot has been swollen for a few months but left foot started within the last week. Patient has a pulse ox at home, noted that within the last few days her heart rate would increase up to 115, felt heart racing during this time, and her oxygen would drop to the low-mid80's with any activity or when awoken from sleep short of breath. She did have some dizziness with ambulation as well, denied any syncopal episodes. Patient reports single episode of chest pain after eating dinner 11/28/2023, described as sharp and over her left breast. There was no radiation no associated nausea, vomiting or diaphoresis, lasted 2-3 minutes, resolved after taking one of her husband’s nitroglycerin tablets. Denies any chest pain or chest discomfort at rest or with exertion since this episode.

Pertinent PMH: Patient is a 80-year-old female, who presented to the emergency room 11/28/2023, with complaints of increased fatigue and shortness of breath x1 month that has become much worse this past week. She denies any recent travel or any sick contacts at home or at work. Pt has a PMH of HTN and tobacco dependence. She is retired. Patient currently taking Buspar 15 mg BID for anxiety, metoprolol succinate 25 mg daily for HTN, and patient was started on Lasix IV 40 mg BID in the ER for bilateral pitting edema of BLE . Patient has NKDA, has seasonal allergies. Patient denies drug or alcohol use. Patient is currently a smoker, states she has been smoking since she was a teenager, and smokes a pack/pack and a half per day. Patient states she usually goes for walks a few times a week, but with her increased SOB and fatigue it has been difficult. Both parents have passed. Patient mother had no significant medical hx, passed from old age at 90 years old and father had a hx of CHF and passed away from “not controlling his CHF”. Patient has one sister who has a hx of atrial fibrillation, still living. She is not married and has no children. Her last BM was this morning. Patient states she is up to date on all his vaccines, including the flu shot, and has three Covid vaccines of Pfizer.

Differential Diagnosis: Differentials:

1. Exacerbation of Heart Failure: Congestive heart failure (CHF) is a complex clinical syndrome characterized by inefficient myocardial performance, resulting in compromised blood supply to the body (Malik&Brito, 2023). CHF results from any disorder that impairs ventricular filling or ejection of blood to the systemic circulation. Patients usually present with signs and symptoms of fatigue and dyspnea, reduced exercise tolerance, lower extremity swelling, and systemic or pulmonary congestion (Malik&Brito, 2023). This patient presented with increased fatigue and reduced exercise tolerance for about a month that significantly worsened over the last week. She also noted that, although her R foot and ankle have been “swollen for forever”, within the last week her L foot and ankle have become swollen as well. In the emergency room, patient’s CXR showed pulmonary congestion consistent with heart failure.

2. COPD Exacerbation: Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory lung disease that causes obstructed airflow from the lungs (Papadakis & McFee, 2018). Symptoms include breathing difficulty, cough, mucus production and wheezing. It's typically caused by long-term exposure to irritating gases or particulate matter, most often from cigarette smoke (Papadakis & McFee, 2018). People with COPD are at increased risk of developing heart disease, lung cancer and a variety of other conditions. Signs and symptoms of a COPD exacerbation include increased SOB with exertion, wheezing, chest tightness, a chronic cough that may produce sputum, swelling in ankles, feet or legs, and a lack of energy (Papadakis & McFee, 2018). This patient presented with increased SOB with exertion, +2 pitting edema in the lower extremities, and lack of energy that has been noted for the last month. Patient also has a significant hx of smoking one/one and a half packs of cigarettes per day for about 60 years. However, patient does not have a cough and denies every having a chronic cough. Patient had one episode of chest tightness, which was relieved with one nitro tab.

3. Pneumonia: Pneumonia is an infection that inflames the air sacs in one or both lungs (Papadakis & McFee, 2018). The air sacs may fill with fluid or pus, causing cough with phlegm or pus, fever, chills, and difficulty breathing (Papadakis & McFee, 2018). A variety of organisms, including bacteria, viruses and fungi, can cause pneumonia. Pneumonia can range in seriousness from mild to life-threatening. It is most serious for infants and young children, people older than age 65, and people with health problems or weakened immune systems (Papadakis & McFee, 2018). Signs and symptoms of pneumonia include chest pain when breathing or coughing, confusion or decreased mental awareness, fatigue, fever, sweating, chills, shortness or breath (Papadakis & McFee, 2018). This patient presented with shortness of breath, fatigue, and one episode of chest pain that was relieved with one tablet of Nitroglycerin. Patient does not have a cough presently and denies ever having a cough. Patient also denies being around any sick contacts recently. Blood work did not show an increase in WBC, patient also has not had a fever documented while in the hospital.

Pathophysiology for Diagnosis:

1 . Exacerbation of Heart Failure: There are many causes of CHF, and coronary artery disease (CAD) causing ischemic heart disease is the most common cause (Malik & Brito, 2023). The 4 most common etiologies responsible for about two-thirds of CHF cases are ischemic heart disease, COPD, hypertensive heart disease, and rheumatic heart disease (Malik & Brito, 2023). Ischemic heart disease is by far the most common cause of CHF, leading to a lack of blood flow to heart muscles, reducing the EF. Heart failure is a clinical syndrome characterized by typical symptoms (e.g., dyspnea, ankle swelling, fatigue) that may be accompanied by signs (e.g., elevated jugular venous pressure, pulmonary crackles, peripheral oedema) caused by a structural and/or functional cardiac abnormality, leading to a reduced cardiac output and/or elevated intracardiac pressures at rest or during stress (Malik & Brito, 2023). In the initial stages of CHF, several compensatory mechanisms attempt to maintain cardiac output and meet the systemic demands (Schwinger, 2021). The chronic activation of the sympathetic nervous system results in reduced beta-receptor responsiveness and adrenaline stores (Schwinger, 2021). This results in changes in myocyte regeneration, myocardial hypertrophy, and myocardial hypercontractility. Patients with heart failure may present with low or reduced ejection fraction (HFrEF: EF <40%; also systolic heart failure), preserved ejection fraction (HFpEF: EF >50%; also diastolic heart failure) (Schwinger, 2021). Depending on the type of heart failure, there are certain guideline directed medical therapies that should be initiated to decrease symptoms, improve quality of life as well as improve cardiac mortality (Schwinger, 2021).

2. COPD Exacerbation: COPD is an umbrella term for a range of progressive lung diseases consisting of chronic bronchitis and/or emphysema (Norris, 2019). COPD can progress gradually, making it harder to breathe over time. Chronic bronchitis irritates your bronchial tubes, which carry air to and from your lungs (Norris, 2019). In response, the bronchi become inflamed and mucus builds up along the lining. The buildup narrows the tube’s opening, making it hard to get air into and out of your lungs (Norris, 2019). Cilia on the inside of your bronchial tubes normally move mucus out of your airways, but irritation from chronic bronchitis and/or smoking damages them (Norris, 2019). Emphysema is the breakdown of the walls of the alveoli. Alveoli play a crucial role in transferring oxygen into your blood and carbon dioxide out (Norris, 2019). The damage caused by emphysema destroys the walls of the alveoli, making it hard to get a full breath (Norris, 2019).

3. Pneumonia: Pneumonia is an infection in your lungs caused by bacteria, viruses or fungi (Norris, 2019). Pneumonia causes your lung tissue to become inflamed and can cause fluid or pus to accumulate in the lungs (Norris, 2019). Many pathogens can cause pneumonia, but the most common are bacteria and viruses in the air we breathe (Norris, 2019). Your body usually prevents the bacteria or virus from infecting your lungs, however, sometimes they can overpower your immune system, even if your health is generally good (Norris, 2019). Bacterial pneumonia is usually more severe than viral pneumonia, which often resolves on its own (Norris, 2019). Pneumonia can affect one or both lungs, and infection with Streptococcus pneumoniae bacteria, also called pneumococcal disease, is the most common cause of community acquired pneumonia (Norris, 2019). Viruses that cause the common cold, the flu (influenza), COVID-19 and respiratory syncytial virus (RSV) can sometimes lead to pneumonia (Norris, 2019).

Pertinence of Research Article

The research article that I used was “Congestive Heart Failure” by Ahmad Malik and Daniel Brito, 2023. This article discusses etiology, pathophysiology, history and physical, as well as the treatment and management of congestive heart failure. Congestive heart failure (CHF), as defined by the American College of Cardiology (ACC) and the American Heart Association (AHA), is "a complex clinical syndrome that results from any structural or functional impairment of ventricular filling or ejection of blood” (Malik &Brito, 2023). Ischemic heart disease is the leading cause of death worldwide and also the leading cause of CHF. CHF is a common disorder worldwide with a high morbidity and mortality rate, and contributes to increased healthcare costs, reduces functional capacity, and significantly affects quality of life (Malik &Brito, 2023). It is imperative to diagnose and effectively treat the disease to prevent recurrent hospitalizations, decrease morbidity and mortality, and enhance patient outcomes (Malik &Brito, 2023). There are many etiologies of CHF, and coronary artery disease (CAD) causing ischemic heart disease is the most common cause (Malik &Brito, 2023). Every attempt should be made to identify causative factors to help guide treatment strategies. The etiologies can be broadly classified as intrinsic heart disease and pathologies that are infiltrative, congenital, valvular, myocarditis-related, high-output failure, and secondary to systemic disease (Malik &Brito, 2023). The 4 most common etiologies responsible for most CHF cases are ischemic heart disease, chronic obstructive pulmonary disease (COPD), hypertensive heart disease, and rheumatic heart disease (Malik &Brito, 2023). Ischemic heart disease is by far the most common cause of CHF worldwide. Ischemia leads to a lack of blood flow to heart muscles, reducing the EF (Malik & Brito, 2023). Hypertension causes CHF even in the absence of CAD or ischemic heart disease. High blood pressure causes stress by increased afterload and neurohormonal changes that increase ventricular mass (Malik & Brito, 2023). HTN is also strongly associated with other comorbidities for CHF development, and aggressively treating hypertension is shown to lower the incidence of CHF (Malik & Brito, 2023). HF is a progressive disease, and any acute insult to cardiac structure or acute alteration secondary to genetic mutation, cardiac tissue infiltration, ischemia, valvular heart disease, myocarditis, or acute myocardial injury may initiate the compensatory mechanism, which, once exhausted, results in maladaptation (Malik & Brito, 2023). In the initial stages of CHF, several compensatory mechanisms attempt to maintain cardiac output and meet the systemic demands. The chronic activation of the sympathetic nervous system results in reduced beta-receptor responsiveness and adrenaline stores (Malik & Brito, 2023). This results in changes in cardiac muscle regeneration, myocardial hypertrophy, and myocardial hypercontractility. The increased sympathetic drive also results in the activation of the renin-angiotensin-aldosterone system (RAAS) system, systemic vasoconstriction, and sodium retention (Norris, 2019). A decrease in cardiac output and increased sympathetic drive stimulate the RAAS, leading to increased salt and water retention, along with increased vasoconstriction. This further fuels the maladaptive mechanisms in the heart and causes progressive HF (Norris, 2019). The diagnosis and classification of HF are primarily based on the presence and severity of symptoms and physical exam findings (Malik &Brito, 2023). It is imperative to obtain a detailed history of symptoms, underlying medical conditions, and functional capacity to treat the patient adequately. Acute CHF presents primarily with signs of congestion with the most reported symptom is shortness of breath (Malik &Brito, 2023). This must be further classified as exertional, positional (orthopnea), and whether acute or chronic.

Other commonly reported symptoms of CHF include chest pain and exertional fatigue (Norris, 2019). Another symptom that increases morbidity is edema, especially of the lower extremities, and weight increases of > 20 lbs are not uncommon (Norris, 2019). While patients with acute HF present with overt respiratory distress, orthopnea, and paroxysmal nocturnal dyspnea, patients with chronic heart failure tend to curtail their physical activity; hence, symptoms may be obscured (Malik &Brito, 2023). It is essential to identify triggers of acute decompensation such as recent infection, noncompliance with cardiac medications, use of NSAIDs, or increased salt intake (Malik &Brito, 2023). The general appearance of patients with severe CHF or those with acutely decompensated heart failure include anxiety, diaphoresis, tachycardia, and tachypnea (Malik &Brito, 2023). On chest examination, the classical finding of pulmonary rales translates to heart failure of moderate-to-severe intensity (Norris, 2019). Wheezing may be present in acute decompensated heart failure. As the severity of pulmonary congestion increases, frothy and blood-tinged sputum may be seen (Norris, 2019). Jugular venous distention is another classical finding that must be assessed in all patients with heart failure (Norris, 2019).

A comprehensive assessment is required when evaluating a patient with heart failure. This includes a CBC, iron profile, renal profile, and liver profile (Malik &Brito, 2023). After the basic metabolic and blood panel, patients require further investigations, depending on the etiology and clinical stage. The most important test to classify heart failure to allow the primary doctor to begin to treat the CHF is an echocardiogram (Malik &Brito, 2023). Left ventricle ejection fraction (LV EF) is used to classify CHF (Malik &Brito, 2023):

 HF with reduced ejection fraction: LV EF ≤ 40%

 HF with mildly reduced ejection fraction: EF 41% – 49% and evidence of HF (elevated cardiac biomarkers or elevated filling pressures)

 HF with preserved ejection fraction: LV EF ≥ 50% and evidence of HF (elevated cardiac biomarkers or elevated filling pressures)

 HF with improved ejection fraction:EF >40%, with previously documented LV EF ≤ 40%

Guideline-directed medical therapy (GDMT) for heart failure with reduced ejection fraction now includes 4 medication classes which now includes sodium-glucose cotransporter-2 inhibitors (Malik &Brito, 2023). The first class of medications that is recommended for CHF is ACE-inhibitors, which act to alter the RAAS, ultimately decreasing the amount of fluid the body retains (Malik &Brito, 2023). The second class of medications are beta-blockers, which lower the heart rate and begin to work on repairing any possible heart damage (Malik &Brito, 2023). The third class of medications is sodium-glucose cotransporter-2 inhibitors (SGLT2i), which are also used to treat diabetes. This class of medications reduce interstitial fluid, reduce blood pressure, decrease oxidative stress and improve vascular health (Malik &Brito, 2023). The last class of medication are mineralocorticoid-receptor-antagonists, which act as a diuretic to rid the body of any extra fluid that may increase the workload on the heart (Malik &Brito, 2023). The four medications included with GDMT do the following: help the heart pump better, regulate blood pressure, reduce heart rhythm problems, slow the progression of heart failure, and reduce heart failure symptoms such as shortness of breath, chest pain, and fatigue (Malik &Brito, 2023).

Plan of Care: Testing/Studies:- Patient had a CBC and BMP in order to monitor renal function and electrolytes closely while on IV Lasix while in hospital. – Troponins were ordered as patient had a single episode of chest pain prior to admission, not altogether typical for angina, however relieved with nitroglycerin. As she has never had an ischemic workup in the past but has multiple risk factors for coronary artery disease including age, gender, tobacco abuse, and hypertension.

– Upon admission to the emergency room, the patient had a CXR done, which did show pulmonary edema consistent with heart failure.- Cardiology ordered an echocardiogram to be done for patient, which would measure the left ventricular ejection fraction in order to classify the heart failure, and allow cardiology to start treating the heart failure with specific medications.- Since admission to the medical surgical floor, patient has been placed on telemetry to allow for continuous cardiac monitoring.

Pharmacological: – Patient was started on Lasix IV 40 mg BID by the primary team in the emergency room, which will help with pulmonary congestion and symptomatic improvement and improvement in her volume status. – Patient blood pressure is presently controlled on metoprolol 25 mg daily and the IV Lasix 40 mg BID. Patient was on amlodipine 5 mg and irbesartan 150 mg prior to admission, however both of these medications were placed on hold due to AKI and need for diuresis.

o Will continue to monitor blood pressure closely and can restart amlodipine at 5 mg daily if needed for high blood pressure.- Patient to start Jardiance 10 mg PO daily per GDMT for heart failure. Continue metoprolol 25 milligrams PO daily.

o Still pending echocardiogram results, however if echocardiogram results show systolic heart failure further GDMT will be recommended for optimal heart failure treatment.

o The two medications that are missing per GDMT is Aldactone and an ACEI/ARB. As stated before, patient was on irbesartan 150 mg PO daily, an ARB, but is being held due to acute kidney injury and need for diuresis.- Primary medical team to prescribe nitroglycerin sublingual PRN tablets for patient on discharge.

NONPHARMACOLOGIC METHODS SHOULD BE DISCUSSED ALSO

Patient Education:

– As patient admitted to a history of smoking 1 to 1 1/2 packs of cigarettes per day since she was a teenager, she was educated on and strongly advised on smoking cessation and benefits to health of quitting.

– Patient was educated on heart failure, including the risks, management, the new medications she was placed on, and the purpose of each medication with the treatment of heart failure. – As patient admitted to taking a nitroglycerin tablet that was not hers, but her husbands, patient was educated on only taking prescribed medication for oneself. Patient was educated on when to take Nitro tablets, how to take the tablets, and to call 911 if she has taken three tablets with no resolving chest pain

.- Patient was educated on the importance of daily weights, and was told to call her primary doctor if she gains 3 lbs overnight or 5 lbs within one week.- Patient was also educated on fluid and sodium restriction, and the importance of this restriction in regard to fluid management and decreasing the workload on the heart.

– Patient was educated on signs and symptoms of an exacerbation of heart failure, including increased exertional dyspnea, orthopnea, proximal nocturnal dyspnea, lower extremity edema, and increased fatigue.- Patient was educated on a heart healthy diet, and how this can help manage her heart failure. She was also educated on avoiding extra sources of sodium in canned foods, prepared foods, and to avoid adding salt to meals.

Follow up:

– As the patient does not have an outpatient cardiologist to follow up with, the cardiology team took the liberty of setting up a follow up appointment for patient with the outpatient cardiology clinic at Sister's Hospital.

– Patient was told to follow up with PCP within one to two weeks of discharge for a hospital follow up appointment period.

– The cardiology team will continue to follow with patient throughout entire hospital admission, and continue to make recommendations based off of pending echocardiogram results, lab results, and patient assessment.

References

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History Data:

Chief concern: “I have been having nasal congestion and Right ear itchy with tenderness for the past two weeks”

HPI: This is 64 years old African American male who has history of HLD, severe rheumatoid arthritis s/p multiple surgeries and s/p right knee replacement in October 2023, Pseudo-GOUT and Anemia secondary to chronic disease. He stated that he has nasal congestion and right ear itchy with tenderness for the past two weeks. he has also had swelling of his both knees and feet for the past two weeks, states that his right knee is more swollen than the left. He stated that he visited surgeon and was diagnosed to be pseudo-gout and prescribed Colchicine 1.2 mg per day and also had arthrocentesis. He denies feeling tired , fever, cough, SOB, night sweats, pain, denies dizziness

Pertinent PMH: This is 64 years old African American male who present to the office on 06/05/2024, with complaint of increased nasal congestion and Right ear itchy with tenderness for the past two weeks. he denies any recent travel or any sick contact at home or at work. Pt has a PMH of pseudo-gout currently taking Colchicine 1.2 mg per day, HLD on Crestor 5 mg tablet , RA, Rt knee replacement, left wrist fusion, right open reduction fixation of the right thumb, s/p colostomy and abdominal surgery post gun shot. Anemia secondary to chronic disease on Cyanocobalamin injections, endorses that he drinks alcohol occasionally, denies tobacco use or recreational drugs. Patient has NKDA, has seasonal allergies. no significant family medical hx, both parents passed from old age. Patient is not married but has one daughter who lives in Atlanta Geogia no health problems were reported His last BM was this morning. Patient is not up to date on his vaccines, refused yearly flu shot, received two Covid vaccines of Pfizer, refused the booster

Currently medications

· vit d2 1.25 mg (50,000 unit), take 1 capsule (50,000 unit) by oral route once weekly 

· cyanocobalamin 1,000 mcg/ml, inject 1 milliliter (1,000 mcg) by intramuscular monthly

· folic acid 1 mg tablet, take 1 tablet (1 mg) by oral route once daily 

· protonix dr 40 mg tablet, take 1 tablet (40 mg) by oral route once

· Crestor 5 mg tablet, take 1 tablet (5 mg)

· multi-day plus minerals tablet, one once a day

· azelastine 0.1% (137 mcg) spry, spray 2 sprays in each nostril by intranasal route 2 times per day 

· singulair 10 mg tablet, take 1 tablet (10 mg) by oral route once daily in the evening 

· neomycin-polymyxin-hc ear susp, instill 2 drops into affected ear(s) by otic route 3 times per day left ear and right ear 3 days;

· Claritin 10 mg liquid-gel cap, Flonase allergy rlf 50 mcg spry, inhale 2 sprays (100 mcg)

INSTRUCTIONS

1. Three Differential Diagnosis: ( first one must be the primary diagnosis)

2. Pathophysiology for Diagnosis (each diagnosis) with etiology

3. Pertinence of Research Article (for primary diagnosis)

4. Plan of Care: Testing/Studies:

5. Pharmacological:

6. NONPHARMACOLOGIC METHODS SHOULD BE DISCUSSED ALSO

7. Patient Education:

8. Follow up:

This is just a sample, don’t use these medications NOTE: Pharmacology interventions: MUST BE IN THIS FORMAT

APA FORMAT, AND REFERENCES, peer review scholarly resource cited in APA format from 2019-2024 only. (Within the last 5 years)

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