Posted: July 2nd, 2024

Crohn’s Disease: Pathophysiological Insights and Complications

Based on the patient case study provided, I will compose a scholarly analysis focusing on the pathophysiological aspects of Crohn’s disease and its complications, as observed in the presented case. This analysis will address key aspects of the patient’s condition, treatment, and associated complications.

Crohn’s Disease: Pathophysiological Insights and Complications

Crohn’s disease is a chronic inflammatory bowel disease characterised by transmural inflammation that can affect any part of the gastrointestinal tract. The case of C.D., a 32-year-old woman with a 14-year history of Crohn’s disease, illustrates several important pathophysiological aspects and complications associated with this condition and its treatment.

Adrenal Insufficiency and Steroid Dependency

One of the significant complications observed in this patient is adrenal insufficiency, which has developed as a result of chronic steroid use. The pathophysiological mechanism underlying this complication involves the suppression of the hypothalamic-pituitary-adrenal (HPA) axis due to prolonged exogenous glucocorticoid administration (Prete et al., 2020). Chronic exposure to high doses of steroids, such as prednisone, leads to negative feedback on the hypothalamus and pituitary gland, reducing the production of corticotropin-releasing hormone (CRH) and adrenocorticotropic hormone (ACTH), respectively. This, in turn, results in atrophy of the adrenal glands and diminished endogenous cortisol production.

The patient’s laboratory results confirm this condition, with an ACTH level of 2 pg/mL, which is significantly below the normal range. This low ACTH level indicates suppression of the HPA axis and consequently, inadequate stimulation of the adrenal glands to produce cortisol.

Bone Demineralisation and DEXA Scan Abnormalities

The abnormal DEXA scan demonstrating significant bone demineralisation in this patient can be attributed to multiple factors. Primarily, the chronic use of glucocorticoids is a significant contributor to bone loss. Glucocorticoids impair bone formation by inhibiting osteoblast function and promoting osteoblast and osteocyte apoptosis (Compston, 2018). Additionally, they enhance bone resorption by increasing osteoclast activity and lifespan.

Furthermore, Crohn’s disease itself can contribute to bone loss through various mechanisms. These include malabsorption of calcium and vitamin D due to intestinal inflammation and resection, chronic inflammation leading to increased cytokine production that promotes bone resorption, and reduced physical activity during disease flares (Szafors et al., 2020).

Nutritional Deficiencies and Malabsorption

The patient’s medication regimen includes intramuscular cyanocobalamin (vitamin B12) supplementation, indicating the presence of vitamin B12 deficiency. This deficiency is common in Crohn’s disease patients, particularly those with ileal involvement or resection, as the terminal ileum is the primary site of vitamin B12 absorption. The pathophysiology involves either direct inflammatory damage to the ileal mucosa or surgical removal of the absorption site, leading to impaired vitamin B12 uptake (Weisshof and Chermesh, 2015).

Cushingoid Appearance and Metabolic Alterations

The patient’s cushingoid facial appearance and truncal obesity with abdominal striae are likely consequences of chronic glucocorticoid therapy. These features result from the metabolic effects of excess glucocorticoids, including increased fat deposition in characteristic areas (face, trunk, and dorsocervical region) and protein catabolism leading to skin thinning and striae formation (Prete et al., 2020).

The patient’s laboratory results also reveal metabolic alterations consistent with chronic glucocorticoid use, including hypokalemia (3.0 meq/L) and hyperglycemia (fasting glucose 120 mg/dL). These findings reflect the mineralocorticoid effects of prednisone and its impact on glucose metabolism, respectively.

In conclusion, this case illustrates the complex interplay between Crohn’s disease pathophysiology and the side effects of long-term glucocorticoid therapy. It underscores the importance of careful monitoring and management of patients with chronic inflammatory bowel diseases to prevent and address complications associated with both the disease and its treatment.

References

Compston, J., 2018. Glucocorticoid-induced osteoporosis: an update. Endocrine, 61(1), pp.7-16.

Prete, A., Yan, Q., Al-Tarrah, K., Akturk, H.K., Prokop, L.J., Alahdab, F., Foster, M.A., Lord, J.M., Karavitaki, N., Wass, J.A. and Murad, M.H., 2020. The cortisol stress response induced by surgery: A systematic review and meta-analysis. Clinical Endocrinology, 93(6), pp.728-743.

Szafors, P., Che, H., Barnetche, T., Morel, J., Gaujoux-Viala, C., Combe, B. and Lukas, C., 2020. Risk of fracture and low bone mineral density in adults with inflammatory bowel diseases. A systematic literature review with meta-analysis. Osteoporosis International, 31(8), pp.1479-1490.

Weisshof, R. and Chermesh, I., 2015. Micronutrient deficiencies in inflammatory bowel disease. Current Opinion in Clinical Nutrition & Metabolic Care, 18(6), pp.576-581.

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PATIENT CASE
HPI
C.D. is a 32 yo woman with a 14-year Hx of Crohn disease who presents with a three-day Hx 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?
Patient Case Question 2. What is a potential cause of the abnormal DEXA scan in this patient?
PSH
• Portion of small bowel resected 5 years ago (obstruction from scarring and stricture)
• Ovarian cyst drained, age 18
• Appendectomy, age 13
PMH
• Crohn disease diagnosed 14 years ago (weight loss, severe diarrhea with multiple bowel movements, abdominal pain, dehydration)
• Major depression
CASE STUDY
CROHN DISEASE 21
For the Disease Summary for this case study,

FH
No family Hx of IBD
SH
• Has been married for 11 years and has two daughters who are healthy
• Works as a nurse with a local home healthcare agency
• Non-smoker and non-drinker
ROS
• 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
Meds
• Prednisone, 40 mg po QD
• Trazodone, 100 mg po BID
• Cyanocobalamin, 250 µg IM Q month
Patient Case Question 3. For which condition has trazodone been prescribed for this
patient?
Patient Case Question 4. Why is this patient taking cyanocobalamin IM?
Patient Case Question 5. Based on your analysis of this patient’s medication profile
alone, what can you deduce about the degree of severity (mild to moderate or severe) of
Crohn disease in this patient?
All
• Codeine → nausea and vomiting
• IV dye → acute renal failure
PE and Lab Tests
Gen
• Overweight white female, somewhat anxious, moderate acute distress from chronic pain
• Cushingoid facial appearance
Patient Case Question 6. What is likely the cause of this patient’s cushingoid facial appearance?
Patient Case Question 7. Briefly describe a cushingoid facial appearance.
VS
BP 165/95, P 69, RR 15, afebrile, Ht 61 in, Wt 154 lbs
Patient Case Question 8. What is the most likely cause of the abnormal vital sign of most concern above?
Skin
• Warm and dry with flakiness
• Poor turgor
Patient Case Question 9. What do the examination findings in the skin suggest?
HEENT
• PERRLA
• EOMI
• Mild arteriolar narrowing on funduscopic exam without hemorrhages, exudates, or
papilledema
• Sclera without icterus
• TMs intact and clear throughout with no drainage
• Dry mucous membranes
Patient Case Question 10. What does the phrase “sclera without icterus” suggest?
Patient Case Question 11. Identify the two abnormal HEENT findings above and provide a pathophysiologic explanation for each of them.
Neck
• Supple
• No masses, JVD, lymphadenopathy, or thyromegaly
Lungs
CTA, no crackles or rales noted
Heart
RRR with no murmurs, rubs, or gallops
Abdomen
• Truncal obesity with abdominal striae
• Soft abdomen, not distended, and without bruits
• Guarding with pressure to right lower quadrant
• BS hyperactive

CASE STUDY 21 ■ CROHN DISEASE 101
Patient Case Question 12. What is a likely cause of “truncal obesity with striae”?
Patient Case Question 13. What are striae?
Patient Case Question 14. What is meant by guarding?
Rectal
• No perianal lesions or internal masses
• Stool is heme-negative
MS/Ext
• No clubbing, cyanosis, or edema
• Appropriate strength and ROM
• Pulses 2
throughout
• No femoral bruits
Neuro
• A & O 3
• No gross motor or sensory deficits noted
• CNs II–XII intact
• DTRs 2

Laboratory Blood Test Results
See Patient Case Table 21.1
Patient Case Table 21.1 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 15. Identify the four abnormally elevated laboratory findings above and provide a brief and reasonable pathophysiologic explanation for each of them.
Patient Case Question 16. Identify the four abnormally low laboratory findings above and provide a brief and reasonable pathophysiologic explanation for each of them.

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Tags: C.D. is a 32 yo woman with a 14-year Hx of Crohn disease, Crohn's Disease: Pathophysiological Insights and Complications