The Crohn Disease Case Study Discussion
The Crohn Disease Case Study Discussion
Patient Case Question 1
Well, the adrenal insufficiency in this patient is most probably caused by the long-term use of steroids. Corticosteroids, for example Prednisone, if used over a long period of time, will interfere with the normal functioning of the Hypothalamic-Pituitary-Adrenal (HPA) axis. Exogenous corticosteroids suppress discharge of corticotropin-releasing hormone and adrenocorticotropic hormone from hypothalamus and pituitary respectively, and thus cause adrenal atrophy and reduced levels of endogenous cortisol. The Crohn Disease Case Study Discussion
There are also side effects that occur when steroids are tapered or stopped, the body cannot produce enough cortisol and this leads to adrenal Insufficiency (Hindmarsh & Geertsma, 2024)The Crohn Disease Case Study Discussion. Although some patient may be asymptomatic, the following signs and symptoms may be exhibited: fatigue, abdominal pain, and electrolyte derangement due to the inability of the body to produce stress hormones.
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Patient Case Question 2
Prednisone (40 mg po QD)
Mechanism: Anti-inflammatory drug that works by modulating immunosuppressive functions; which is useful in managing episodes of Crohn’s disease. Reason for use: For the management of inflammation as well as to reduce the chances of recurrence in Crohn disease (Lawrence & Marcus, 2018). Some of the challenges have been as a result of long-term use such as adrenal insufficiency.
Trazodone (100 mg po BID)
Mechanism: A pharmaceutical product that is utilized mainly for treating instances of depression and insomnia due to the fact that it belongs to a class of drugs referred to as serotonin antagonist and reuptake inhibitor (SARI). Reason for use: For treatment of major depression and possibly for amelioration of sleep disturbances as part of chronic illness.
Cyanocobalamin (250 μg IM Q month)
Mechanism: A man made form of vitamin that is important in the formation of red blood cells and DNA synthesis as well as the normal functioning of the nervous system. Reason for use: For the management and also as prophylaxis for B12 deficiency that is often observed in Crohn’s disease attributed to malabsorption issues including after bowel surgery (Lawrence & Marcus, 2018)The Crohn Disease Case Study Discussion.
Patient Case Question 3a
Fasting glucose (120 mg/dL)
Raised courtesy of chronic steroid use (exogenous steroids cause a rise in insulin resistance hence hyperglycemia).
White blood cells (11,700/mm3):
Slightly raised owing to the inflammation that is characteristic of the Crohn’s disease.
C-reactive protein (1. 6 mg/dL)
It is up regulated as a biomarker of systemic inflammation. In Crohn’s disease, as is the case with other diseases, CRP rises during periods of inflammation activity.
Erythrocyte sedimentation rate (24 mm/hr)
They are also raised in Crohn’s disease because of inflammation, more so during the flare of the disease.
Patient Case Question 3b
Potassium (3. 0 mEq/L)
The most probable cause of hypokalemia is diarrhoel which makes the patient lose K and the use of steroids.
Albumin (2. 4 g/dL)
Moderate to low as a result of malnutrition which is frequently seen in CD due to malabsorption resulting from inflammation, reduced nutrient intake following resection of bowel and chronic diarrhea. The Crohn Disease Case Study Discussion
Total protein (3. 9 g/dL):
As the result, the level of albumin reduced due to observed chronic protein loss from malabsorption, inflammation and possible protein-losing enteropathy.
Adrenocorticotropic hormone (2 pg/mL)
Low because of suppression of the adrenal glands when one is taking steroids from outside, thus the adrenal glands produce little or no ACTH at all.
References
Hindmarsh, P. C., & Geertsma, K. (2024). Adrenal insufficiency. Replacement Therapies in Adrenal Insufficiency, 3-22. https://doi.org/10.1016/b978-0-12-824548-4.00007-3
Lawrence, L., & Marcus, k. (2018). Crohn disease in patients with VW disease. Journal of Gastroenterology & Digestive Systems, 2(2). https://doi.org/10.33140/jgds.02.02.11 The Crohn Disease Case Study Discussion
Crohn Disease Case Study
History of Present Illness:
C.D. is a 32-year-old woman with a 14-year history of Crohn disease who presents with a three-day history of diarrhea and steady abdominal pain. She has been referred by her PCP to the GI clinic. The clinical course of her disease has included obstruction due to small intestine stricture and chronic steroid dependency with disease relapse when attempting to taper steroids. Endocrine tests reveal that she has developed adrenal insufficiency as a result of steroid use and a DEXA scan has demonstrated significant demineralization of bone.
Patient Case Question 1. What is the pathophysiologic mechanism for adrenal insufficiency in this patient?
Past Surgical History:
• Portion of small bowel resected 5 years ago (obstruction from scarring and stricture)
• Ovarian cyst drained, age 18
• Appendectomy, age 13
Past Medical History:
• Crohn Disease diagnosed 14 years ago (weight loss and severe diarrhea with multiple bowel movements, abdominal pain, dehydration)
• Major Depression
Family History:
• No family Hx of IBD
Social History:
• Married for 11 years and has two daughters who are healthy
• Works as a nurse with a local home healthcare agency
• Never-smoker and non-drinker
Review of Systems:
• Up to 10 loose to semi-solid stools/day, non-bloody
• Denies chills and canker sores
• Stable weight with good appetite
• Denies joint pain, skin lesions, blurred vision, and eye pain • Some mild fatigue
Medications:
• Prednisone, 40 mg po QD
• Trazodone, 100 mg po BID
• Cyanocobalamin, 250 μg IM Q month
Patient Case Question 2. Briefly explain the mechanism and reason for use of each of the listed medications.
Allergies:
Codeine → nausea and vomiting • IV dye → acute renal failure
Physical Exam:
Overweight white female, somewhat anxious, moderate acute distress from chronic pain Cushingoid facial appearance
BP 165/95, P 69, RR 15, afebrile, Ht. 61 in, Wt. 154 lbs.
Skin
• Warm and dry with flakiness • Poor turgor
Abdomen
• Truncal obesity with abdominal striae
• Soft abdomen, no distention, no bruits
• Guarding with pressure to RLQ
• Hyperactive bowel sounds
Laboratory Blood Test Results
Sodium 141 mEq/L Aspartate aminotransferase 22 IU/L
Potassium 3.0 mEq/L Alanine aminotransferase 54 IU/L
Chloride 106 mEq/L Total bilirubin 0.8 mg/dL
Bicarbonate 23 mEq/L Total protein 3.9 g/dL
Blood urea nitrogen 19 mg/dL Albumin 2.4 g/dL
Creatinine 1.0 mg/dL Calcium 8.7 mg/dL
Glucose, fasting 120 mg/dL Magnesium 2.9 mg/dL
Hemoglobin 13.8 g/dL Phosphorus 3.3 mg/dL
Hematocrit 39% Adrenocorticotropic hormone 2 pg/mL
Platelets 180,000/mm3 Erythrocyte sedimentation rate 24 mm/hr
White blood cells 11,700/mm3 C-reactive protein 1.6 mg/dL
Patient Case Question 3a. Identify the four abnormally elevated laboratory findings above and provide a brief and reasonable pathophysiologic explanation for each of them.
Patient Case Question 3b. Identify the four abnormally low laboratory findings above and provide a brief and reasonable pathophysiologic explanation for each of them.