Crohn’s Disease: Jordan’s Case History with Guided Questions
Question 1: Structural and Function Changes in the Diseases Process that led to Jordan’s Weight Loss
Structurally, mucosal and epithelial membranes act as physical-chemical barriers between the body and the intestinal environment (Hill, Hall,&Glew, 2017). Jordan has an impaired epithelial and mucosal barrier which has lead to interaction between the bacteria found in the intestine and the intestinal environment, which triggered an abnormal immune response. This abnormal immune response further leads to pro-inflammatory cytokine production that results in malnutrition and disease pathogenesis (Craft, Gordon, Heuther, McCance,& Brashers, 2018). Malnutrition is mainly as a result of alteration in the epithelial and mucosal inflammatory activities, which makes epithelial membrane-permeable antigens and energy intakes. The entire process leads to the high use of resting energy expenditure to fight the pathogens (Enck et al., 2016). Ultimately, this will require high energy intake that may not be attained by the patient and hence loss in weight.Also, nutrient malabsorption and loss could have resulted in Jordan’s weight loss. The alteration to the structure of the epithelial and mucosal membranecould result in the permeability of dietary antigens which in turn could affect negatively, the absorption of both macro and micronutrients required by the body hence resulting into rapid weight loss(Anbazhagan, Priyamvada, Alrefai, &Dudeja, 2018). Again, the alterations of the structure of epithelial and mucosal membrane could result in the alterations in the levels of metabolic hormones such as ghrelin, leptin, and adiponectin which could directly affect Jordan’s satiety levels (Anbazhagan, Priyamvada,Alrefai, &Dudeja,2018).
Functional changes and symptoms that could result in Jordan’s weight loss include abdominal pain, flatulence, luminal distension, motility changes, and induced bloating sensationthat are as a result of enhanced gastrocolic reflex in the bowel(Bullock & Mania, 2017-a). These functional changes are escalated in patients with CD by ingestion of food that is rich in fermentable oligosaccharides such as galactans and fructans, disaccharides such as lactose, monosaccharide such as fructose, and polyps collectively known as (FODMAP). The FODMAP are short-chain carbohydrates that are osmotically active, which means that they are poorly absorbed in the small intestine but rapidly fermented in the colon by bacteria(Bullock & Mania, 2017-a). It makes patient to have low FODMAP diet by avoiding a wide range of foods ignoring some critical nutrients required for a complete diet. Moreover, Jordan could have experienced pain when ingesting food which made him avoid eating or avoiding some food variety that could have contributed to balanced nutrient intake. All these factors could have significantly contributed to Jordan’s weight loss (Bullock & Mania, 2017-a).
Question 2.CD painpathwayandhowMorphinealterstheconsciousperceptionofpain
Pain is caused by specialized afferent neurons known as nociceptors whose membrane receptorsare responsive to thermal, chemical, and mechanical stimulus. Following stimulation, nociceptive transmission through ex-citatory glutamatergic synapses from primary afferents to second-order neurons located in the spinal cord is experienced (Sweeney et al., 2018). Transmission of the neural impulse to the brainstem, then thalamus, to high brain centres leads to a sense of pain when these neural signals reach cerebral cortex regions which include; somatosensory cortex, insula, and anterior cingulated cortex(Zielińska, Sałaga, Włodarczyk,&Fichna, 2019). As a result, multiple centres in the brain modulate the perception of nociceptive stimuli which makes an individual experience chronic abdominal pain. Chronic visceral pain and visceral hypersensitivity follow the recurrent inflammatory processes, mucosal signalling molecule release, and expression of changes in the ionic channel (Zielińska, Sałaga, Włodarczyk,&Fichna, 2019).
Morphinedrug binds to G receptor leading to activation of pre-synaptic and postsynaptic μ receptor. Pre-synaptic μ receptor inhibits calcium ion channel, consequently preventing the release of neurotransmitters (Bullock & Manias, 2017-b). Post-synaptic μ receptor inhibits potassium ion channel leading to hyper-polarization of projecting cell. All these blocks synaptic transmission (analgesia), thus limiting nociceptive stimuli reaching thalamus and cortex where the pain perception is experienced (Wang, 2017).
Question3. Clinical manifestations that may indicate the deterioration of Jordan’s Crohn’s condition and why they occur
Jordan’s clinical manifestation is recorded in his vital signs and initial pathology results (LeMone et al., 2017). Jordan has a fever due to his abnormal temperature of 38.30C. The average temperature is between 36.5-37.5°C. The high temperature may have been caused by elevated resting energy expenditure by the body is trying to fight pathogens. Secondly, Jordan has a lowerhaemoglobin at 7.9mmol/L (8.1 -11.2mmol/L). Normal haemoglobin is at 12.6-17.5 mmol/L. It shows anemia as a result of reduced intake of food rich in iron and malabsorption syndromes where there is defective absorption of iron from food. Thirdly, Haematocrit level of 51% (35 – 47%) is higher than average, which should be between 38%-47.7%.A higher than average hematocrit can be caused by dehydration due to diarrhea.
The most important clinical manifestation that Jordan’s condition has deteriorated includes bowel obstruction and abscess formation. Bowel obstruction was caused by a stricture that results from scarring and narrowing of the intestinal tract due to multiple chronic inflammations of the intestines(LeMone et al., 2017). Abscess formation is as a result of continued perforation of intestines due to continued inflammation leading to the collection of pus and formation of cavities in mucosa and submucosa, which when ruptured lead to severe bleeding.
Question 4. Characteristics of the intravenous fluid that was ordered for Jordan and explain the rationale for the administration of the IV fluid relating to Jordan’s specific fluid balance.
Hartman’s solution is a maintenance fluid that is made up of 130 mmol/L Sodium (Na+), 5.4 mmol/L potassium (K+), 112 mmol/L of chloride ion (Cl–), 1.8 mmol/L Calcium (Ca+), and 27 mmol/L of Lactate. The characteristic of this fluid is that itmaintains normal fluid balance which ensures optimal water and electrolyte transport to reduce diarrhea and other solute-related complications(Enck et al., 2016). Water and electrolytes are transported in the intestine through osmosis via selective permeability through the epithelial membranes. This process is important for the bidirectional transport of nutrients, fluids and electrolytes from the intestinal lumen to the tissues. CD impairs this function; therefore, the present solution composition is meant to pay for the poor Na+ and K+ absorption due to the impaired functions of epithelial and mucosal membranes in the intestines(Enck et al., 2016). The impairment of these membranes is the major cause of diarrhea. Jordan was administered this IV fluid to ensure that there is the maintenance of normal fluid homeostasis to ensure a reduction in diarrhea and related conditions. The fluid was administered using intravenous means because of the existence of malabsorption so as to ensure that there is maximum absorption and assimilation of electrolytes for the reduction of CD symptoms (Enck et al., 2016).
Anbazhagan, A. N., Priyamvada, S., Alrefai, W. A., &Dudeja, P. K. (2018). Pathophysiology of IBDassociated diarrhea. Tissue Barriers, 6(2), e1463897.doi:10.1080/21688370.2018.1463897
Bullock, S., & Manias, M. (2017-a). Understanding pathophysiology. Melbourne: P. Ed Australia.
Bullock, S., & Manias, M. (2017-b). Fundamental of pharmacology. Melbourne: P. Ed Australia.
Craft,J., Gordon, C., Heuther, S., McCance, K., & Brashers, V. (2018). UnderstandingPathophysiology.Milton, Ontario: Elsevier.
Enck, P., Aziz, Q., Barbara, G., Farmer, A. D., Fukudo, S., Mayer, E. A., …& Spiller, R. C.(2016). Irritable bowel syndrome. Nature Reviews Disease Primers, 2(1),doi:10.1038/nrdp.2016.14
Hill, R., Hall, H., &Glew, P. (2017). Fundamentals of nursing and midwifery: A person-centredapproach to care. North Ryde, N.S.W.: Lippincott Williams and Wilkins.
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Sweeney, L., Moss-Morris, R., Czuber-Dochan, W., Meade, L., Chumbley, G.,& Norton, C.(2018). Systematic review: Psychosocial factors associated with pain in inflammatory bowel disease. Alimentary Pharmacology Therapeutics, 47(6), 715–729. doi:10.1111/apt.14493
Wang, D. (2017). Opioid medications in the management of chronic abdominal pain. Curr PainHeadache Rep, 21(9). doi:10.1007/s11916-017-0640-x
Zielińska, A., Sałaga, M., Włodarczyk, M.,&Fichna, J. (2019). Focus on current and futuremanagement possibilities in inflammatory bowel disease-related chronic pain. International Journal of Colorectal Disease, 34(2), 217–227. https://doi.org/10.1007/s00384-018-3218-0
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