Structural and functional changes contributing the weight loss

Structural and functional changes contributing the weight loss

In three weeks Jordan lost 7 kilograms. Structural and functional changes contributing the weight loss include malnutrition, malabsorption, and diarrhea. Malnutrition is common with Crohn’s disease patients with nutritional deficiencies linked to the degree and activity of the condition. While several mechanisms may be involved in malnutrition, reduced food intake is due to anorexia, nausea, abdominal pain, and vomiting. The fear of diarrhea and that of colicky abdominal pain due to stricture act as a discourage Jordan from maintaining adequate nutrition. Jordan stated that he was reluctant to eating and drinking much during the previous five days. Inflammation related anorexia and poor appetite are the major causes of reduced food intake (Cronin & Shanahan, 2007). Anorexia is a symptom of Crohn’s disease as a result of inflammation and its presence even after continued weight loss suggests the failing of normal compensatory mechanisms that take effect following a period of reduced food intake. Concerning weight loss in Crohn’s disease, researchers propose that proinflammatory cytokines trigger the release of leptin from adipose tissue resulting in excessively high plasma concentration for the percentage of fat mass. Cytokine-mediated increased circulation of leptin during the first phase of inflammation plays a role in suppressing feeding.

Malabsorption occurs when mucosa inflammation involves a considerable length of the small bowel, and the effects of decreased transit time, lack of sufficient absorptive surface, and diminution of the bile salt pools. Although carbohydrates, proteins, and fats may be malabsorbed, clinical manifestations are mainly due to fat malabsorption (Cronin & Shanahan, 2007). Fat malabsorption occurs in about 30% of Crohn’s disease patients. The reduction of transit time in the small bowel may further reduce the time available for nutrient absorption.

Diarrhea is also a contributor to weight loss. Normal stool frequency varies in each individual but is somewhat consistent and a volume of about 100ml. Diarrhea is an increase in frequency, fluidity or volume of stool and is an increase to above 200g per day (Cronin & Shanahan, 2007). Diarrhea is related to the severity and degree of Crohn’s disease. Intestinal contents’ fluidity is vital for the digestion, distribution of digested nutrients along the absorptive epithelial surface, and the process of absorption. Diarrhea suggests lack of intestinal water regulation and may be due to reduced absorption or both or increased secretion. Inflammation in the intestinal tract may inhibit the absorption or increase section causing diarrhea. In Crohn’s disease, massive small bowel involvement and the presence of malabsorbed and maldigested nutrients may elevate the osmolarity of the intestinal fluid, increasing the severity of diarrhea.

Question 2: Pain Pathway and the Effect of Morphine

The general pain pathway consists of three orders of neurons. First-order (pseudounipolar) neurons contain nociceptors which are activated by various noxious stimuli. Nociceptors are present at the free nerve ending of the primary afferent neuron with the receptive field often overlapping with neighboring fields (Woller et al., 2017). Nociceptors are found in muscle, skin, bones, joints and organs and fire response to a number of stimuli. The second-order neurons receive signals from nociceptors, Aδ fibres, found in the rexed laminae of the spinal cord. The Aδ fibres transmit the first pain felt through the spinal cord. The third-order neurons lie in within the ventral posterolateral thalamus (VPL) of the thalamus. They terminate pain signals in the area of the cortex dedicated to specific organs.

Morphine alters the conscious perception of pain by exerting analgesic effects that suppress both affective and sensory dimensions of pain (Fornasari, 2014). Morphine significantly depresses neuronal activities in VPL, the somatosensory cortex (SI), anterior cingulate cortex (ACC), and medial dorsal thalamus (MD). The depressive effects include a decrease in the fraction of responsive neurons, a decrease in the neural response magnitude, and shortening of the neural duration (Fornasari, 2014). Morphine decreases the cortical and thalamic capability distinguishing pain from non-pain stimuli in both medial and lateral pathways. Additionally, morphine suppresses the pain-related changes in the flow of information from the cortex to the thalamus.

Question 3: Clinical Manifestations

Symptoms that may suggest the deterioration of Jordan’s Crohn’s condition include worsening pain and diarrhea. Diarrhea is related to the degree and severity of Crohn’s disease (as discussed in question 1 above). Most of Crohn’s disease patients experience relapses and remissions as in the case of Jordan (Cronin & Shanahan, 2007). He has had a number of exacerbations of Crohn’s disease since he was diagnoses eight years earlier. Jordan’s pain may arise from bowel distention due to obstruction, from inflammation going beyond the bowel wall, or perianal abscess. Generally, the degree of pain correlates to disease activity. The severity, distribution, and degree of the gastrointestinal inflammation determine the sign and symptoms of inflammatory bowel disease. Jordan’s clinical features related to the anatomical location of the disease. He has numerous large patches of inflamed mucosa and submucosa throughout his small bowel and colon. A stricture causes bowel obstruction in his terminal ileum, while intestinal inflammation causes his diarrhea (Cronin & Shanahan, 2007). Jordan’s weight loss, a feeling abdominal bloating, nausea and bilious vomiting and increased amount of abdominal gurgling and rumbling are mainly due to systematic consequences of intestinal inflammation. Additionally, Jordan developed a psychological response of decreased activity; he has not been able to keep up with his work demands and is not getting quality rest and sleep, contributing to his malaise.

Question 4: Hartmann’s Solution

Hartman’s solution (compound sodium lactate) is a sterile solution intended for intravenous. Its chemical composition is Sodium Lactate (3.17 g/L), Sodium Chloride (6.0 g/L), Potassium Chloride (400 mg/L) and Calcium Chloride Dihydrate (270 mg/L), with Sodium Hydroxide and Hydrochloric acid added for adjusting pH (McLoughlin & Bell, 2010). Hartmann’s solution is used for IVI and electrolyte replacement. In the case of Jordan, fluid loss through diarrhea resulted in an imbalance and loss of electrolytes. Bicarbonate in Hartmann’s solution is used in treating mild to moderate acidosis linked to dehydration. A combination of several electrolytes, sodium lactate, and an alkalinising agent provide electrolyte balance and normalize PH of the acid-base of the physiological system. Sodium is the major cation of extracellular fluid and primarily controls water distribution, fluid and electrolyte balance, and osmotic pressure of body fluids. Chloride is the major extracellular anion in the maintenance of the acid-base balance, isotonicity, and electrodynamic characteristics of the cells (McLoughlin & Bell, 2010). On the contrary, potassium is the major cation of the intracellular fluid and manly controls the composition of the body fluid and electrolyte balance. Calcium is critical in maintaining the functional integrity of the nervous, muscular, and skeletal systems and cell permeability. Sodium lactate is an alkalinising agent. The body slowly metabolizes lactate into bicarbonate and water.