Hospital Case Study: Eleanor Brown's Ulcerative Colitis Analysis
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Case Study
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This case study examines Eleanor Brown, a 48-year-old patient with a history of ulcerative colitis, focusing on her recent acute exacerbation. The study details her symptoms, including severe diarrhea, abdominal pain, weight loss, and fatigue. It explores the pathophysiology of ulcerative colitis, explaining the inflammatory processes and structural changes in the colon. The case study addresses the mechanisms of pain, the effects of morphine, and potential complications like pancolitis and colonic obstruction. It also discusses the rationale for administering Hartman's solution, considering Eleanor's dehydration and electrolyte imbalance. The assignment provides detailed answers to the questions posed in the case study, supported by current references, offering a comprehensive understanding of the condition and its management.
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Running head: HEALTH CASE STUDY
HEALTH CASE STUDY
Name of the Student:
Name of the University:
Author note:
HEALTH CASE STUDY
Name of the Student:
Name of the University:
Author note:
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1HEALTH CASE STUDY
Question 1
Ulcerative colitis is a chronic gastrointestinal condition which results in inflammation-
induced ulcer formation in the mucosal membrane of the colon – namely the sigmoid colon and
rectum. Such patients posses lesions in the colon, which may caused as a result of a number of
inflammatory, pathogenic and genetic mechanism (Hindryckx, Jairath & D'haens, 2016). These
include hunmoral immunity-induced macrophage activities of inflammation and cytotoxic
manifestations by T-lymphocytes as a part of pathogen-associated immune responses. Hence,
such inflammatory processes result in the structural and functional changes of the colon
characteristic of ulcerative colitis which comprises of inflammation in the large intestine,
namely, at the base of crypt of Lieberkuhn. This results in the formation of minor erosions in the
sigmoid colon, rectum or transverse colon which aggravate into ulcers and abscesses (Sroufe et
al., 2017). Such detrimental structural changes, if left unmanaged, result in the ragged ulceration,
cell atrophy and necrosis, bleeding, pus accumulation , edema, reddening and thickening of the
colonic mucosal layer (Nakagawa et al., 2015). Such processed result in functional changes such
as loss of the absorptive processes of the colon, gastrointestinal bleeding, severe spasms and
cramping, decreased transit time of the colon and hence, uncontrolled defecation. Defecation is
associated with the loss of necrotized absorption-associated colonic surfaces, blood and pus
formed from ulceration coupled with release of stools. Further, loss of functioning lumen of the
colonic mucosa hinders in the characteristic water absorption associated function of the colon
resulting in water loss and watery diarrhea (Craft & Gordon, 2011).
It can be observed that Eleanor is suffering from severe gastrointestinal pain, ulceration,
bleeding and diarrhea, whose underlying mechanism can be attributed to the above discussion.
Question 1
Ulcerative colitis is a chronic gastrointestinal condition which results in inflammation-
induced ulcer formation in the mucosal membrane of the colon – namely the sigmoid colon and
rectum. Such patients posses lesions in the colon, which may caused as a result of a number of
inflammatory, pathogenic and genetic mechanism (Hindryckx, Jairath & D'haens, 2016). These
include hunmoral immunity-induced macrophage activities of inflammation and cytotoxic
manifestations by T-lymphocytes as a part of pathogen-associated immune responses. Hence,
such inflammatory processes result in the structural and functional changes of the colon
characteristic of ulcerative colitis which comprises of inflammation in the large intestine,
namely, at the base of crypt of Lieberkuhn. This results in the formation of minor erosions in the
sigmoid colon, rectum or transverse colon which aggravate into ulcers and abscesses (Sroufe et
al., 2017). Such detrimental structural changes, if left unmanaged, result in the ragged ulceration,
cell atrophy and necrosis, bleeding, pus accumulation , edema, reddening and thickening of the
colonic mucosal layer (Nakagawa et al., 2015). Such processed result in functional changes such
as loss of the absorptive processes of the colon, gastrointestinal bleeding, severe spasms and
cramping, decreased transit time of the colon and hence, uncontrolled defecation. Defecation is
associated with the loss of necrotized absorption-associated colonic surfaces, blood and pus
formed from ulceration coupled with release of stools. Further, loss of functioning lumen of the
colonic mucosa hinders in the characteristic water absorption associated function of the colon
resulting in water loss and watery diarrhea (Craft & Gordon, 2011).
It can be observed that Eleanor is suffering from severe gastrointestinal pain, ulceration,
bleeding and diarrhea, whose underlying mechanism can be attributed to the above discussion.

2HEALTH CASE STUDY
Eleanor’s weight loss can be attributed to the structural and physiological effects of ulcerative
colitis such as bleeding, inflammation and watery diarrhea. Bleeding results in loss of essential
nutrients and tissue components from the body which results in long term weight loss and
hemoglobin induced nutrient transportation (Schniers et al., 2019). The loss of colonic lumen in
ulcerative colitis further hinders its micronutrient absorptive processes hence preventing essential
nutrient uptake by tissues, poor nutritional status and weight loss. The high rates of inflammation
in ulcerative colitis results in tissue catabolism – another causative mechanism of weight loss.
The associated watery diarrhea results in loss of water and electrolytes, loss of muscle tone and
hence the resultant weight loss (Craft & Gordon, 2011).
Question 2
The general pathway of pain is caused due to a complex interplay of nervous system
functioning which is hindered by morphine. Ulcerative colitis in Eleanor, will result in
inflammation which results in activation of nociceptors or microscopic receptors of pain in the
skin. Each of these are interlinked to the spinal cord via nervous fibers. Upon activation of the
nociceptors in the gastrointestinal regions, the electrical signals of pain are transmitted to the
concerned nerve fibers (Chen et al., 2015). Such transmissions travel across the nerve fiber
bundles to the peripheral nerve and to the spinal cord. Neurotransmitters in the dorsal horn of the
spinal cord the relay the impulse to the thalamus of the brain which further transmits the same to
the frontal cortex (associated with Eleanor’s thinking and preoccupation concerning her pain),
limbic system (associated with emotions, hence making Eleanor feel distressed, discomfort and
agitatin due to pain) and somatosensory cortex (results in physiological sensations hence,
compelling Eleanor to perceive her abdominal pain) (Yam et al., 2018). Morphine hinders this
Eleanor’s weight loss can be attributed to the structural and physiological effects of ulcerative
colitis such as bleeding, inflammation and watery diarrhea. Bleeding results in loss of essential
nutrients and tissue components from the body which results in long term weight loss and
hemoglobin induced nutrient transportation (Schniers et al., 2019). The loss of colonic lumen in
ulcerative colitis further hinders its micronutrient absorptive processes hence preventing essential
nutrient uptake by tissues, poor nutritional status and weight loss. The high rates of inflammation
in ulcerative colitis results in tissue catabolism – another causative mechanism of weight loss.
The associated watery diarrhea results in loss of water and electrolytes, loss of muscle tone and
hence the resultant weight loss (Craft & Gordon, 2011).
Question 2
The general pathway of pain is caused due to a complex interplay of nervous system
functioning which is hindered by morphine. Ulcerative colitis in Eleanor, will result in
inflammation which results in activation of nociceptors or microscopic receptors of pain in the
skin. Each of these are interlinked to the spinal cord via nervous fibers. Upon activation of the
nociceptors in the gastrointestinal regions, the electrical signals of pain are transmitted to the
concerned nerve fibers (Chen et al., 2015). Such transmissions travel across the nerve fiber
bundles to the peripheral nerve and to the spinal cord. Neurotransmitters in the dorsal horn of the
spinal cord the relay the impulse to the thalamus of the brain which further transmits the same to
the frontal cortex (associated with Eleanor’s thinking and preoccupation concerning her pain),
limbic system (associated with emotions, hence making Eleanor feel distressed, discomfort and
agitatin due to pain) and somatosensory cortex (results in physiological sensations hence,
compelling Eleanor to perceive her abdominal pain) (Yam et al., 2018). Morphine hinders this

3HEALTH CASE STUDY
pathway by binding to opioid receptorsm which further prevent the transmission of nerve
impulses from the primary afferent nociceptors to the spinal chord’s dorsal horn cells of sensory
projection (Yadlapalli et al., 2017).
Question 3
If left inadequately treated, Eleanor’s ulcerative colitis can exacerbate into severely
detrimental clinical manifestations. One of the key clinical manifestations which has already
occurred in Eleanor is pancolitis, which is characterized by absolute inflammation of the colon.
This occurs due to exacerbations and proliferation of the ulceration of the colon from a single
section to multiple lumen areas (Stenson, Tremaine & Cohen, 2016). Perforations in the colon is
another clinical manifestation which may occur as an exacerbated symptom in the colon.
Ulceration is one of the characteristic features of ulcerative colitis and hence, if left untreated,
such ulceration, can aggravate and damage the colon tissues resulting in perfusions and
perforations. Hemorrhages can occur as a clinical manifestation if the symptoms of bleeding are
aggravated in Eleanor’s condition of ulcerative colitis (Yangyang & Rodriguez, 2017). An
additional key clinical manifestation which may indicate Eleanor’s deterioration is colonic
obstruction. This can occur due to increased necrosis of the colonic lumen which may
accumulate and block the colon. Additionally, obstruction may also occur due to narrowing of
the colonic lumen, which is caused due to aggravation of the previous ulcerative colitis
symptoms of wall thickening and edema which cause strictures and narrowing of the colon wall
(Craft & Gordon, 2011).
pathway by binding to opioid receptorsm which further prevent the transmission of nerve
impulses from the primary afferent nociceptors to the spinal chord’s dorsal horn cells of sensory
projection (Yadlapalli et al., 2017).
Question 3
If left inadequately treated, Eleanor’s ulcerative colitis can exacerbate into severely
detrimental clinical manifestations. One of the key clinical manifestations which has already
occurred in Eleanor is pancolitis, which is characterized by absolute inflammation of the colon.
This occurs due to exacerbations and proliferation of the ulceration of the colon from a single
section to multiple lumen areas (Stenson, Tremaine & Cohen, 2016). Perforations in the colon is
another clinical manifestation which may occur as an exacerbated symptom in the colon.
Ulceration is one of the characteristic features of ulcerative colitis and hence, if left untreated,
such ulceration, can aggravate and damage the colon tissues resulting in perfusions and
perforations. Hemorrhages can occur as a clinical manifestation if the symptoms of bleeding are
aggravated in Eleanor’s condition of ulcerative colitis (Yangyang & Rodriguez, 2017). An
additional key clinical manifestation which may indicate Eleanor’s deterioration is colonic
obstruction. This can occur due to increased necrosis of the colonic lumen which may
accumulate and block the colon. Additionally, obstruction may also occur due to narrowing of
the colonic lumen, which is caused due to aggravation of the previous ulcerative colitis
symptoms of wall thickening and edema which cause strictures and narrowing of the colon wall
(Craft & Gordon, 2011).
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4HEALTH CASE STUDY
Question 4
Eleanor has been administered of the intravenous fluid of Hartman’s solution. Hartman’s
solution is also known as sodium lactate solution or ringer’s lactate solution, and is comprised of
sodium lactate, sodium chloride, calcium chloride and potassium chloride in water. It is
commonly used for the treatment of conditions such as decreased blood volume, dehydration or
dyselectrolytemia (Kim et al., 2015). It can be observed that she has slow capillary refill,
decreases urinary output, darkening of urine and a higher than normal specific gravity in her
urine. Such conditions are indicative of a status of dehydration and shock (Keller et al., 2016).
Eleanor’s condition of dehydration and loss of electrolytes may be caused due to her ulcerative
colitis symptoms of extreme internal bleeding and watery diarrhea. Lactate metabolism-induced
hepatic by-products are the chemical components present in Hartman’s solution, and mitigate
acidosis in the body (Weinberg et al., 2018). Extreme fluid and electrolyte loss due to ulcerative
colitis may result in acidosis in Eleanor and further lead to life threatening convulsions. The
prevention of dyslelectrolytemia, dehydration and associated acidosis are underlying rationales
for prescribing Hartman’s solution to Eleanor. Considering her disrupted abilities to ingest and
digest food, intravenous administration will allow easy and quick reuptake of essential
micronutrients (Yung, Letton & Keeley, 2017).
Question 4
Eleanor has been administered of the intravenous fluid of Hartman’s solution. Hartman’s
solution is also known as sodium lactate solution or ringer’s lactate solution, and is comprised of
sodium lactate, sodium chloride, calcium chloride and potassium chloride in water. It is
commonly used for the treatment of conditions such as decreased blood volume, dehydration or
dyselectrolytemia (Kim et al., 2015). It can be observed that she has slow capillary refill,
decreases urinary output, darkening of urine and a higher than normal specific gravity in her
urine. Such conditions are indicative of a status of dehydration and shock (Keller et al., 2016).
Eleanor’s condition of dehydration and loss of electrolytes may be caused due to her ulcerative
colitis symptoms of extreme internal bleeding and watery diarrhea. Lactate metabolism-induced
hepatic by-products are the chemical components present in Hartman’s solution, and mitigate
acidosis in the body (Weinberg et al., 2018). Extreme fluid and electrolyte loss due to ulcerative
colitis may result in acidosis in Eleanor and further lead to life threatening convulsions. The
prevention of dyslelectrolytemia, dehydration and associated acidosis are underlying rationales
for prescribing Hartman’s solution to Eleanor. Considering her disrupted abilities to ingest and
digest food, intravenous administration will allow easy and quick reuptake of essential
micronutrients (Yung, Letton & Keeley, 2017).

5HEALTH CASE STUDY
References
Chen, N., Zhang, J., Wang, P., Guo, J., Zhou, M., & He, L. (2015). Functional alterations of pain
processing pathway in migraine patients with cutaneous allodynia. Pain Medicine, 16(6),
1211-1220. doi: https://doi.org/10.1111/pme.12690.
Craft, J., & Gordon, C. (2011). Alterations of digestive function across the life span.
In Understanding Pathophysiology (pp. 806-863). Elsevier. Retrieved from:
https://books.google.co.in/books?
id=Re2DDwAAQBAJ&pg=PR11&lpg=PR11&dq=Alterations+of+digestive+function+a
cross+the+life+span+Kulmira+Nurgali+and+Carolyn+Wildbore&source=bl&ots=rJOQo
R5sWx&sig=ACfU3U012JPkOh7Cu2AknuotWCV3cUmr3w&hl=en&sa=X&ved=2ahU
KEwjU2KGl-pzhAhWbXCsKHRW-
BEYQ6AEwAHoECAgQAQ#v=onepage&q=Alterations%20of%20digestive
%20function%20across%20the%20life%20span%20Kulmira%20Nurgali%20and
%20Carolyn%20Wildbore&f=false.
Hindryckx, P., Jairath, V., & D'haens, G. (2016). Acute severe ulcerative colitis: from
pathophysiology to clinical management. Nature Reviews Gastroenterology &
Hepatology, 13(11), 654. doi: https://doi.org/10.1038/nrgastro.2016.116.
Keller, D. S., Cologne, K. G., Senagore, A. J., & Haas, E. M. (2016). Does one score fit all?
Measuring risk in ulcerative colitis. The American Journal of Surgery, 212(3), 433-439.
doi: https://doi.org/10.1016/j.amjsurg.2015.10.033.
References
Chen, N., Zhang, J., Wang, P., Guo, J., Zhou, M., & He, L. (2015). Functional alterations of pain
processing pathway in migraine patients with cutaneous allodynia. Pain Medicine, 16(6),
1211-1220. doi: https://doi.org/10.1111/pme.12690.
Craft, J., & Gordon, C. (2011). Alterations of digestive function across the life span.
In Understanding Pathophysiology (pp. 806-863). Elsevier. Retrieved from:
https://books.google.co.in/books?
id=Re2DDwAAQBAJ&pg=PR11&lpg=PR11&dq=Alterations+of+digestive+function+a
cross+the+life+span+Kulmira+Nurgali+and+Carolyn+Wildbore&source=bl&ots=rJOQo
R5sWx&sig=ACfU3U012JPkOh7Cu2AknuotWCV3cUmr3w&hl=en&sa=X&ved=2ahU
KEwjU2KGl-pzhAhWbXCsKHRW-
BEYQ6AEwAHoECAgQAQ#v=onepage&q=Alterations%20of%20digestive
%20function%20across%20the%20life%20span%20Kulmira%20Nurgali%20and
%20Carolyn%20Wildbore&f=false.
Hindryckx, P., Jairath, V., & D'haens, G. (2016). Acute severe ulcerative colitis: from
pathophysiology to clinical management. Nature Reviews Gastroenterology &
Hepatology, 13(11), 654. doi: https://doi.org/10.1038/nrgastro.2016.116.
Keller, D. S., Cologne, K. G., Senagore, A. J., & Haas, E. M. (2016). Does one score fit all?
Measuring risk in ulcerative colitis. The American Journal of Surgery, 212(3), 433-439.
doi: https://doi.org/10.1016/j.amjsurg.2015.10.033.

6HEALTH CASE STUDY
Kim, M. Y., Jeon, N. Y., Hyun, S. K., Kim, H. T., Cho, W. H., & Park, U. J. (2015). The Effects
of Normal Saline Solution versus Hartmann's Solution on the Acid-base and Electrolytes
Status and Renal Function after Kidney Transplantation. The Journal of the Korean
Society for Transplantation, 29(4), 194-199. doi:
https://doi.org/10.4285/jkstn.2015.29.4.194.
Nakagawa, N., Maruyama, H., Zaimoku, Y., Maruyama, K., Saito, C., Katagiri, T., ... & Nakao,
S. (2015). Evidence for a Common Immune Pathophysiology in Acquired Aplastic
Anemia and Ulcerative Colitis. doi: https://doi.org/.
Schniers, A., Goll, R., Pasing, Y., Sørbye, S. W., Florholmen, J., & Hansen, T. (2019).
Ulcerative colitis: functional analysis of the in-depth proteome. Clinical
proteomics, 16(1), 4. doi: https://doi.org/10.1186/s12014-019-9224-6.
Sroufe, I. A., Gardner, T., Bresnahan, K. A., Quarnberg, S. M., & Wiedmeier, P. R. (2017).
Insights into the pathophysiology of ulcerative colitis: interleukin‐13 modulates STAT6
and p38 MAPK activity in the colon epithelial sodium channel. The Journal of
physiology, 595(2), 421-422. doi: https://doi.org/10.1113/JP272492.
Stenson, W. F., Tremaine, W. J., & Cohen, R. D. (2016). Ulcerative Colitis: Clinical
Manifestations and Management. Yamada's Atlas of Gastroenterology, 216-224. doi:
https://doi.org/10.1002/9781118512104.ch28.
Weinberg, L., Chiam, E., Hooper, J., Liskaser, F., Hawkins, A. K., Massie, D., ... & Bellomo, R.
(2018). Plasma-Lyte 148 vs. Hartmann’s solution for cardiopulmonary bypass pump
prime: a prospective double-blind randomized trial. Perfusion, 33(4), 310-319. doi:
https://doi.org/10.1177%2F0267659117742479.
Kim, M. Y., Jeon, N. Y., Hyun, S. K., Kim, H. T., Cho, W. H., & Park, U. J. (2015). The Effects
of Normal Saline Solution versus Hartmann's Solution on the Acid-base and Electrolytes
Status and Renal Function after Kidney Transplantation. The Journal of the Korean
Society for Transplantation, 29(4), 194-199. doi:
https://doi.org/10.4285/jkstn.2015.29.4.194.
Nakagawa, N., Maruyama, H., Zaimoku, Y., Maruyama, K., Saito, C., Katagiri, T., ... & Nakao,
S. (2015). Evidence for a Common Immune Pathophysiology in Acquired Aplastic
Anemia and Ulcerative Colitis. doi: https://doi.org/.
Schniers, A., Goll, R., Pasing, Y., Sørbye, S. W., Florholmen, J., & Hansen, T. (2019).
Ulcerative colitis: functional analysis of the in-depth proteome. Clinical
proteomics, 16(1), 4. doi: https://doi.org/10.1186/s12014-019-9224-6.
Sroufe, I. A., Gardner, T., Bresnahan, K. A., Quarnberg, S. M., & Wiedmeier, P. R. (2017).
Insights into the pathophysiology of ulcerative colitis: interleukin‐13 modulates STAT6
and p38 MAPK activity in the colon epithelial sodium channel. The Journal of
physiology, 595(2), 421-422. doi: https://doi.org/10.1113/JP272492.
Stenson, W. F., Tremaine, W. J., & Cohen, R. D. (2016). Ulcerative Colitis: Clinical
Manifestations and Management. Yamada's Atlas of Gastroenterology, 216-224. doi:
https://doi.org/10.1002/9781118512104.ch28.
Weinberg, L., Chiam, E., Hooper, J., Liskaser, F., Hawkins, A. K., Massie, D., ... & Bellomo, R.
(2018). Plasma-Lyte 148 vs. Hartmann’s solution for cardiopulmonary bypass pump
prime: a prospective double-blind randomized trial. Perfusion, 33(4), 310-319. doi:
https://doi.org/10.1177%2F0267659117742479.
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7HEALTH CASE STUDY
Yadlapalli, J. S. K., Dogra, N., Walbaum, A. W., Wessinger, W. D., Prather, P. L., Crooks, P. A.,
& Dobretsov, M. (2017). Evaluation of Analgesia, Tolerance, and the Mechanism of
Action of Morphine-6-O-Sulfate Across Multiple Pain Modalities in Sprague-Dawley
Rats. Anesthesia and analgesia, 125(3), 1021-1031. doi:
https://dx.doi.org/10.1213%2FANE.0000000000002006.
Yam, M., Loh, Y., Tan, C., Khadijah Adam, S., Abdul Manan, N., & Basir, R. (2018). General
pathways of pain sensation and the major neurotransmitters involved in pain
regulation. International journal of molecular sciences, 19(8), 2164. doi:
https://doi.org/10.3390/ijms19082164.
Yangyang, R. Y., & Rodriguez, J. R. (2017). Clinical presentation of Crohn’s, ulcerative colitis,
and indeterminate colitis: Symptoms, extraintestinal manifestations, and disease
phenotypes. In Seminars in pediatric surgery (Vol. 26, No. 6, pp. 349-355). WB
Saunders. doi: https://doi.org/10.1053/j.sempedsurg.2017.10.003.
Yung, M., Letton, G., & Keeley, S. (2017). Controlled trial of Hartmann's solution versus 0.9%
saline for diabetic ketoacidosis. Journal of paediatrics and child health, 53(1), 12-17.
doi: https://doi.org/10.1111/jpc.13436.
Yadlapalli, J. S. K., Dogra, N., Walbaum, A. W., Wessinger, W. D., Prather, P. L., Crooks, P. A.,
& Dobretsov, M. (2017). Evaluation of Analgesia, Tolerance, and the Mechanism of
Action of Morphine-6-O-Sulfate Across Multiple Pain Modalities in Sprague-Dawley
Rats. Anesthesia and analgesia, 125(3), 1021-1031. doi:
https://dx.doi.org/10.1213%2FANE.0000000000002006.
Yam, M., Loh, Y., Tan, C., Khadijah Adam, S., Abdul Manan, N., & Basir, R. (2018). General
pathways of pain sensation and the major neurotransmitters involved in pain
regulation. International journal of molecular sciences, 19(8), 2164. doi:
https://doi.org/10.3390/ijms19082164.
Yangyang, R. Y., & Rodriguez, J. R. (2017). Clinical presentation of Crohn’s, ulcerative colitis,
and indeterminate colitis: Symptoms, extraintestinal manifestations, and disease
phenotypes. In Seminars in pediatric surgery (Vol. 26, No. 6, pp. 349-355). WB
Saunders. doi: https://doi.org/10.1053/j.sempedsurg.2017.10.003.
Yung, M., Letton, G., & Keeley, S. (2017). Controlled trial of Hartmann's solution versus 0.9%
saline for diabetic ketoacidosis. Journal of paediatrics and child health, 53(1), 12-17.
doi: https://doi.org/10.1111/jpc.13436.
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