It’s 3 case studies. Please read and answer questions. Citations and references must be in APA format. See attached.
endocrine_case_studies_pathophysiology_1.docx
endocrine_case_studies.docx
endocrine_case_study_1.docx
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Endocrine Case Study: Pathophysiology
A 25-year-old woman presents with a complaint of rapid weight loss despite a voracious
appetite. Physical examination reveals tachycardia (pulse rate 110 bpm at rest), fine moist skin, a
symmetrically enlarged thyroid, mild bilateral quadriceps muscle weakness, and fine tremor.
These findings strongly suggest hyperthyroidism.
A. What other features of the history should be elicited?
B. What other physical findings should be sought?
C. Serum TSH and free thyroxine level are ordered. What results should be anticipated?
D. What are the possible causes of this patient’s condition?
E. What is the most common cause of this patient’s condition, and what is the pathogenesis of
this disorder?
F. What is the pathogenesis of this patient’s tachycardia, weight loss, skin changes, goiter, and
muscle weakness?
Case Presentation One
A 54-year-old female presented with proximal muscle weakness, easy bruising, weight gain, and
worsening of hypertension. She had also noticed increasing facial hair for six months and fat
deposition in the back of her neck. A recent laboratory test had shown high fasting blood
glucose. She had history of hypertension, hyperlipidemia, and osteoporosis for the past five
years. She was on a bisphosphonate therapy. There was a family history of hypertension,
diabetes mellitus type 2, and coronary artery disease. She never smoked and did not drink
alcohol.
On examination her blood pressure was 140/90 mm/Hg. She was obese but she felt that her face
was fuller than before. Examination revealed dorsocervical fat pad, ecchymosis on skin, and a
few coarse plucked hairs on her chin. She had thin legs with mild edema and was unable to stand
without taking support of the chair.
1. What is your primary diagnosis, and why?
2. What is the pathophysiology of the diagnosis?
3. One differential diagnosis for the case.
Case Presentation Two
A 16 year old boy was brought to the ED with rapid breathing of 8 hours duration. He had been
symptomatic for the last 10 days in the form of polyuria, polydipsia, tiredness, and weight loss.
Since the previous 24 hours, he was complaining of abdominal pain and had two episodes of
vomiting. Parents did not give any history of fever, cough, altered sensorium, or any similar
episode in the past. The child was passing urine at regular intervals. He has no known past
medical history.
1. At this point, what are you thinking could be the possible diagnosis?
At the time of presentation, he was very dehydrated.
HR: 120 beats/min
B/P: 100/70
RR: 44 breath/minute, deep and rapid
Temp: 98.1 F
Chest: Clear to auscultation (CTA) bilaterally
Neuro: intact
2. What would you expect to find on examining his lab values?
3. What is your primary diagnosis, and why?
2. What is the pathophysiology of the diagnosis?
3. One differential diagnosis for the case.
Endocrine Case Study: Pharmacology
A 55-year-old African American female presents to clinic as a new patient. She has not seen a
physician in many years and would like a general health checkup. The patient is not treated for
any chronic health problems. However, her mother had type 2 diabetes, and she would like to be
screened.
Physical examination is unremarkable except for weight of 180 lb (81.8 kg; height 165 cm, BMI
30.3 kg/m2). The patient has multiple risk factors for type 2 diabetes including age, ethnicity,
and family history that justify screening. Since the patient is not fasting, hemoglobin A1c
(HbA1c) is measured and found to be elevated at 6.8%. Morning fasting plasma glucose is 145
mg/dL.
The patient returns to the office to discuss management of her newly diagnosed type 2 diabetes.
She is started on metformin and titrated to 1000 mg twice daily without side effects. She also
modifies her diet and starts an exercise program. Three months later, capillary blood glucose
measurements are consistently below 130 mg/dL, and HbA1c improves to 6.0%. Four years
later, HbA1c increases steadily to 7.5% despite compliance with diet, exercise, and metformin.
Dilated fundoscopy and foot examination are unremarkable, and urine albumin/Cr ratio remains
below 30 mg/g.
Initially, HbA1c improves with the addition of glimepiride to metformin. Exenatide is then
started 18 months later due to worsening glycemic control. Two years later, the patient returns to
discuss treatment options. Despite taking maximal effective doses of metformin (1000 mg BID),
glimepiride (8 mg QD), and exenatide (10 μg BID), HbA1c is 8.5%. Fasting glucose
measurements fall mostly in the range of 140 to 180 mg/dL, and glucose measurements during
the day increase steadily and are often more than 200 mg/dL.
1. Who should be screened for type 2 diabetes mellitus?
2. How is type 2 diabetes initially managed?
3. What regular screening is necessary for type 2 diabetes patients?
4. What additional therapies can be added if metformin monotherapy is ineffective?
5. What is the next step in management for patients with progressively worsening glycemic
control despite multiple oral medications or glucagon-like peptide-1 (GLP-1) analog therapy?

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