Celiac Disease and Diabetes Insipidus

Hello Kathryn

Thanks for discussing the patient’s case with a history of celiac disease. The discussion is good, and the case presented enhances understanding of celiac disease. Other than understanding that a gluten-free lifestyle is essential for managing celiac disease, it explains the physiology of the condition. I would, however, like to highlight that the case presented was a reoccurring occurrence of celiac disease; therefore, it would be essential to consider the possible triggers that could have made the disease active again. For instance, it’s known that severe emotional stress, surgery, pregnancy, infection, or childbirth can cause celiac disease even after a patient has successfully managed the condition before.

Recommending supplements that reduce gluten senility or intolerance, like vitamin D, magnesium, and calcium, should reduce the severity of celiac symptoms (Naik et al., 2018). To minimize the occurrence, I would also recommend that the patient take digestive enzymes before meals to help digestion, facilitating healing and reversing the celiac symptoms.

References

Naik, R. D., Seidner, D. L., & Adams, D. W. (2018). Nutritional consideration in celiac disease and non-celiac gluten sensitivity. Gastroenterology Clinics, 47(1), 139-

 Hello Amber

Great response!! I agree with you that the sodium levels for the case patient diagnosed with diabetes Ininsipidus should be high; given her case, she presents symptoms of urinary tract infection, but no disease was found following the diagnosis and treatment for management. Sodium levels are high because of increased urine frequency, leading to water loss in the body, resulting in polydipsia. The rationale for elevated osmolality is embedded in the increased frequency of water loss during urine excretion, resulting in a higher concentration of particles in the serum since the blood contains insufficient water.

The comparison is simple; while central diabetes Ininsipiduss is associated with insufficient ADH, nephrogenic Diabetes Insipidus is related to the failure of kidneys to concentrate the urine caused by impaired renal tubule (Bichet, 2020). For nephrogenic Diabetes Insipidus, the DH is available and sufficient, but the failure of the kidneys leads to the excretion of vast amounts of dilute urine. dDAVP works by increasing the concretion of VWF, FVIII, and t-PA in plasma.

References

Bichet, D. G. (2020). GENETICS IN ENDOCRINOLOGY Pathophysiology, diagnosis, and treatment of familial nephrogenic diabetes insipidus. European Journal of Endocrinology, 183(2), R29-R40.

ORDER A PLAGIARISM-FREE PAPER HERE

We’ll write everything from scratch

1. Kathryn
A 19-year-old co-ed presents with increasing diarrhea and constipation over the last two weeks. She has a history of celiac disease.

Celiac Disease and Diabetes Insipidus

Gluten-related diseases such as celiac disease and gluten ataxia are rare conditions, affecting roughly less than 1% of the population in the United States. Despite the rarity of these diseases, there have been significant increases in the adoption of a gluten-free lifestyle and the consumption of gluten-free foods in the United States over the last three decades (Niland & Cash, 2018). Celiac disease (CD) is a T-cell-mediated enteropathy with an autoimmune component that occurs in the small intestine of genetically predisposed individuals in response to the gluten protein found in wheat, barley, and rye (Dlugasch & Story, 2021). Diagnosis is based on abnormalities of a small intestinal biopsy. However, screening for celiac disease can be initially performed using serologic markers with high sensitivity and specificity for diseases such as IgA antibodies to tissue transglutaminase (TG) (Barker & Liu).

What is the role of immunity and celiac disease?

Celiac disease is a T-cell-mediated immune disorder characterized by losing oral tolerance to dietary gluten and licensing intraepithelial lymphocytes to kill intestinal epithelial cells, leading to villous atrophy (Kim & Mayassi, 2018).

What is the effect of gluten on celiac disease?

Gluten includes a family of proteins known as prolamins (mainly glutenin and gliadin) found in cereal grains such as wheat, barley, and rye. Each type of cereal grain contains differing amounts of gluten and other proteins. Gluten proteins’ permeability is one beneficial characteristic that produces palatable dough and bread products. Gluten-containing grains such as wheat comprise much of the modern Western diet. This is partly due to their pala’s ease of cultivation and procession into various foods, large-scale production ability, and high nutritional content by weight (Niland & Cash, 2018). Gluten irritates the small intestine, which produces an inflammatory response. Some symptoms include bloating, diarrhea, constipation, stomach cramping, and vomiting. Others may even experience a skin rash.

Describe the pathophysiology of diarrhea and constipation.

Diarrhea is the most common symptom of untreated celiac disease and is present in 45-85% of all patients (Barker & Liu, 2008). Diarrhea caused by celiac disease is due to the maldigestion and malabsorption of nutrients. The stool might be watery or semi-formed, light tan or gray, and oily or frothy. On the other hand, Celiac disease may cause your small intestine to absorb moisture from the stool. This would lead to constipation. Also, a gluten-free diet may decrease fiber intake and cause constipation.
2. Amber
A 23-year-old female presents with urinary frequency absent of infection. The final diagnosis is Diabetes Insipidus. She is treated with dDAVP.

What would you expect her sodium level to be, high or low? Defend your answer.

Clinical manifestations of Diabetes Insipidus (DI) include polyuria, nocturia, and polydipsia (Dlugasch & Story, 2019). Because of this water loss with frequent urination, the sodium levels would be high, ultimately leading to polydipsia, which is suitable for the patient to help balance or lower their sodium levels with the fluid intake. However, this does not work if the patient has impaired thirst or inability to drink, ultimately causing the sodium levels to increase further (Dlugasch & Story, 2019).

Her osmolarity is elevated. Why?

Serum osmolarity will typically be more significant than 295mOsm/kg for the same reasons discussed in the previous question. If there is an increased amount of urine output, but you are not replacing what you are putting out, this will cause levels to rise. DI occurs due to insufficient ADH production, causing polyuria and polydipsia (Dlugasch & Story, 2019). Causes of inadequate ADH production may be poor excretion due to hypothalamus or pituitary disorders or inadequate renal tubule response to ADH (Dlugasch & Story, 2019). The inadequate renal tubule response leads to the next question because it is called nephrogenic diabetes insipidus.

Compare and contrast central vs. nephrogenic Diabetes Insipidus.

Diabetes Insipidus (DI) is a disease process that results in either decreased release or a decreased response of antidiuretic hormone (ADH), which is also known as vasopressin c, causing electrolyte imbalances as discussed above (Kui et al., 2021). DI is broken down into two types: central and nephrogenic. Both of these conditions have congenital and acquired causes. Central DI is the case where your body does not make enough vasopressin. When the amount of fluid in your body decreases, the pituitary gland releases vasopressin into the bloodstream, signaling the kidneys to conserve fluid from urine into the bloodstream (Kui et al., 2021). So, without adequate vasopressin production, the liquid is not retained and is flushed out of your body by voiding. Nephrogenic DI is the other case where there is a decreased response to vasopressin use. Your body may make enough. However, the kidneys don’t respond to this hormone as they should, again triggering more fluid to be lost in voiding (Kui et al., 2021). An inherited gene mutation cloth of these coconditionsentral DI and magAutoimmune disorders can cause central DIe to the hypothalamus or pituitary gland from surgery, infection, a tumor, or even head injury (Kui et al., 2021). Nephrogenic DI can be caused by medications, hypokalemia, hypercalcemia, a blocked urinary tract, or chronic kidney disease (CKD) (Kui et al., 2021).

Explain the mechanism of dDAVP.

dDAVP is also known as desmopressin, which is a medication made to mimic vasopressin and is typically used in individuals with DI to help control polydipsia and polyuria. dDAVP is a selective vasopressin V2 receptor agonist that is present through collecting ducts and tubules of the kidneys (McCarty & Shah, 2020); when this receptor is activated, a signaling cascade of adenyl-cyclase starts and ultimately results in increased water permeability or a decrease in urine volume with an increase in urine osmolality (McCarty & Shah, 2020).

dDAVP is primarily used in central DM and is often given to distinguish between primary and nephrogenic DI (McCarty & Shah, 2020). If there is a positive response to this medication, it means the kidneys are responding appropriately. The minimum dose should be administered to control polyuria adequately, and it is essential to monitor for hyponatremia during this course of treatment due to excess water retention potentially leading to increased levels of sodium in the brain causing brain injury (McCarty & Shah, 2020).