Health Variation 1- Perioperative

Running Head: HEALTH VARIATION 1- PERIOPERATIVE
Health Variation 1- Perioperative
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HEALTH VARIATION 1- PERIOPERATIVE 2
Question 1. Describe the structural and functional changes in the disease process that
led to Eleanor’s weight loss?
Structural, as well as functional changes in the weight loss of Eleanor, is due to
various reasons as it could be subsidised through the number of diverse processes. As
structural changes are concerned, increased in the amount of the colonic sulphate-decreasing
bacteria in ulcerative colitis, may result in a higher amount of the poisonous gas of hydrogen
sulphide. Compound N-butyrate which is the short-chain of fatty acid may get oxidised via
the beta-oxidation pathway into the gas carbon dioxide as well as ketone bodies (Bullock &
Manias, 2013). So it is observed that the N-butyrate aids supply of nutrients to this mucosal
epithelial barrier. Readings have anticipated that the hydrogen sulfide imparts a significant
role in damaging the beta-oxidation pathway by interfering this short chain acetyl-CoA
dehydrogenase, which is an enzyme inside this pathway. This process disrupts the eating
behaviour and hence results in weight loss (Craft et al. 2015).
Moreover, weight loss in Eleanor which are the consequences of the primary
physiological disruption which are functional changes, linked with this disease may perhaps
be considered as the marker of the disease action (Elsherif et al. 2014). Resting energy
spending has been demonstrated to be amplified during the acute flares of ulcerative colitis
because pro-inflammatory cytokines may exert the anorexic influence. The inflammatory
condition in the ulcerative colitis has been associated with the alterations in stages of the
number of the metabolic hormones comprising leptin, adiponectin, as well as ghrelin which
can upset satiety. Subsequently, in the main while, they might try to escape eating with the
intention to elude pain perceptions or the unpleasant abdominal symptoms (Nurgali, 2014).
Some medications as well as nutrient deficiencies may cause taste alterations and may lead to

HEALTH VARIATION 1- PERIOPERATIVE 3
loss of appetite (Nurgali, 2014). Moreover, these disease courses are related to the
malabsorption of equally macronutrients as well as micronutrients (Hwang et al. 2012).
Lastly, patient like Eleanor suffering from chronic ulcerative colitis may suffer from
an enhanced gastrocolic reflex in addition to a variety of the symptoms comprising pain
which is frequently associated with the ingestion of the food that may lead to escaping of the
meal (Nurgali, 2014). Alterations of digestive function across the life span. Chronic
malnourishment subsequently from the suboptimal enteral consumption because of the
condition anorexia in addition to abdominal discomfort, along with increased losses because
of the protein-losing enteropathy, so is deliberated to be the main etiologic reason of the
weight loss. Moreover, malabsorption of the food is infrequently seen if the patient with
ulcerative colitis has had a widespread intestinal resection (Bullock & Manias, 2013).
Question 2. Explain the pain pathway and how Morphine alters the conscious
perception of pain
In the pain pathway Nociceptive stimuli trigger the nerve endings; then first-order
neurons depolarise to fire action potentials. A (myelinated) delta fibres synapsis with release
glutamate onto second-order neurons, while C (unmyelinated) fibres release neuropeptide
neurotransmitters. These primary afferent nociceptors conduct nerve impulses to the spinal
cord (so if rise from the skull, then transmit directly to medulla oblongata of the brain stem).
So in the spinal cord, the primary afferent nociceptors lay off in the dorsal horn of the grey
matter. Then release chemical transmitter substances substance P and somatostatin, along
with glutamic acid or aspartic acid. Pain is then perceived by the somatosensory area of the
brain.
Morphine is an opiate drug, work together with the opioid receptors, in addition, alter
the conscious perception of pain as by the similar mechanisms as of the enkephalin, such that
hyperpolarisation of the interneurons as well as depressing the further discharge of the