Understanding Ulcerative Colitis and its Impact on the Body
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This article provides an in-depth understanding of ulcerative colitis, a chronic inflammatory bowel disease. It discusses the symptoms, causes, and effects of the disease, including its impact on the body and the potential for weight loss. The article also explores the role of the immune system and the enteric nervous system in the progression of the disease. Additionally, it explains the rationale behind the administration of Hartman's solution to maintain fluid balance in patients with ulcerative colitis.
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Answer no 1
It is reported from the case study; Eleanor a 48-year-old lady had been diagnosed
with ulcerative colitis 17 years ago and had suffered from severe symptoms of the disease.
She had several admissions to hospital because of uncontrolled symptoms of ulcerative
colitis-like severe diarrhoea with blood, occurrence of pus and pain in lower abdomen.
Later, with the progression of disease, she had painful and distended abdomen, her skin
becomes dry and cool with no turgor. On diagnosis with help of colonoscopy and MRI
scan, she has now developed Pancolitis with pseudopolyps is sigmoid colon. In last two
weeks, she lost 9 Kgs of weight as she was feeling too ill to eat and drink. As the impact of
this, she felt being fatigued and unable to do any activities. The transition of disease from
ulcerative colitis to pancolitis cause adverse changes in his body structure and function
which can be the primary cause for loss of appetite. Colitis causes inflammation in small
and large intestine specifically the colon (Hindryckx, Jairath & D'haens, 2016).
Ulcerative colitis tends to form ulcer in inner lumen of large intestine specifically in
rectum. Inner lining of large intestine is made of three-layer known as mucosa, submucosa
and muscle layer (Spoendlin et al., 2015). These ulcers are spot in the mucosa where tissue
get damaged and left behind with open sore (Tahara et al., 2015). Recent research on the
disease, says that ulcerative disease is an autoimmune disease where Cytotoxic T cell
present in the inner lining of epithelium of mucosa layer of colon is responsible for
ulceration (Ge et al., 2015). They degrade the inner lining of colon leaving behind the
eroded areas known as ulcer. The reason behind it is still unclear. It is also known that P-
ANCA antibodies present in the blood can mistakenly target antigens on neutrophils cell.
However, some theory says that it cross-react with healthy bacteria of gut, and attack the
It is reported from the case study; Eleanor a 48-year-old lady had been diagnosed
with ulcerative colitis 17 years ago and had suffered from severe symptoms of the disease.
She had several admissions to hospital because of uncontrolled symptoms of ulcerative
colitis-like severe diarrhoea with blood, occurrence of pus and pain in lower abdomen.
Later, with the progression of disease, she had painful and distended abdomen, her skin
becomes dry and cool with no turgor. On diagnosis with help of colonoscopy and MRI
scan, she has now developed Pancolitis with pseudopolyps is sigmoid colon. In last two
weeks, she lost 9 Kgs of weight as she was feeling too ill to eat and drink. As the impact of
this, she felt being fatigued and unable to do any activities. The transition of disease from
ulcerative colitis to pancolitis cause adverse changes in his body structure and function
which can be the primary cause for loss of appetite. Colitis causes inflammation in small
and large intestine specifically the colon (Hindryckx, Jairath & D'haens, 2016).
Ulcerative colitis tends to form ulcer in inner lumen of large intestine specifically in
rectum. Inner lining of large intestine is made of three-layer known as mucosa, submucosa
and muscle layer (Spoendlin et al., 2015). These ulcers are spot in the mucosa where tissue
get damaged and left behind with open sore (Tahara et al., 2015). Recent research on the
disease, says that ulcerative disease is an autoimmune disease where Cytotoxic T cell
present in the inner lining of epithelium of mucosa layer of colon is responsible for
ulceration (Ge et al., 2015). They degrade the inner lining of colon leaving behind the
eroded areas known as ulcer. The reason behind it is still unclear. It is also known that P-
ANCA antibodies present in the blood can mistakenly target antigens on neutrophils cell.
However, some theory says that it cross-react with healthy bacteria of gut, and attack the
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cells of inner lining of intestine thus changing digestion to serious infection (Dulai,
Sandborn & Gupta, 2016). In response to immune system, number of white blood cell
increases against the infection thus causing colitis in inner lining of rectum. Ulcerative
colitis is circumferential to lining of large intestine may increase proximally, sometimes
whole colon with numerous pseudopolyps hence, causing pancolitis (Pardi, 2017). Increase
in ulcerative from rectum to whole colon cause weak digestion, lower absorption of water
and anaemia thus, causing weight loss.
Answer no 2
Pain pathway is divided into three steps. 1. Transduction, 2. Transmission, 3.
Modulation (Descalzi et al., 2017). Nociceptors present in the tissue are sensitized by
prostaglandin and bradykinin, to activation by the stimuli, and the information is passed by
the receptor via electrical signal and is transferred from the peripheral nervous system to
central nervous system through axons. Nociceptors have two type of fibre called A delta
and C fibres, these penetrate in the dorsal horn of spinal cord (Price & Inyang, 2015).
Passage of the pain information is often control by at this point by mean of
neurotransmitter. Neurotransmitters transmit the signal to the synaptic cleft of spinal cord
neuron, and then modulation event takes place. The information goes to thalamus through
motor neuron and sends to sensory cortex of brain which receive the information as pain
(Yarnitsky, 2015).
Morphine antagonize the opioid receptor present in the brain. They block the release
of neurotransmitter by inhibiting Ca2+ ion influx into the presynaptic end. (Bao et al., 2015).
Or they can open the potassium channels, cause hyperpolarization of the neuron thus create
efflux of potassium ion and prevent the release of neurotransmitter. These steps thus block
Sandborn & Gupta, 2016). In response to immune system, number of white blood cell
increases against the infection thus causing colitis in inner lining of rectum. Ulcerative
colitis is circumferential to lining of large intestine may increase proximally, sometimes
whole colon with numerous pseudopolyps hence, causing pancolitis (Pardi, 2017). Increase
in ulcerative from rectum to whole colon cause weak digestion, lower absorption of water
and anaemia thus, causing weight loss.
Answer no 2
Pain pathway is divided into three steps. 1. Transduction, 2. Transmission, 3.
Modulation (Descalzi et al., 2017). Nociceptors present in the tissue are sensitized by
prostaglandin and bradykinin, to activation by the stimuli, and the information is passed by
the receptor via electrical signal and is transferred from the peripheral nervous system to
central nervous system through axons. Nociceptors have two type of fibre called A delta
and C fibres, these penetrate in the dorsal horn of spinal cord (Price & Inyang, 2015).
Passage of the pain information is often control by at this point by mean of
neurotransmitter. Neurotransmitters transmit the signal to the synaptic cleft of spinal cord
neuron, and then modulation event takes place. The information goes to thalamus through
motor neuron and sends to sensory cortex of brain which receive the information as pain
(Yarnitsky, 2015).
Morphine antagonize the opioid receptor present in the brain. They block the release
of neurotransmitter by inhibiting Ca2+ ion influx into the presynaptic end. (Bao et al., 2015).
Or they can open the potassium channels, cause hyperpolarization of the neuron thus create
efflux of potassium ion and prevent the release of neurotransmitter. These steps thus block
the synaptic transmission (Kesavan, 2015). As a result of this, a number of nociceptive
receptors becomes limited and does not reach the thalamus. Hence, pain pathway is
blocked.
Answer no 3
Mr Eleanor diagnosed with ulcerative colitis showed high frequency of diarrhoea
with blood. Associated symptoms include pain in lower abdomen, cramps, abdominal
bloating and she also feel fatigued. The manifestation of her is progressive over numerous
years. Currently, on physical examination, following thing was noted; Low haemoglobin,
high number of white blood cell, elevated ESR, high C-reactive protein and low albumen.
Earlier she was having large number of pseudopolyps in the descending and sigmoid colon.
On MRI test, the result disclosed that she had developed pancolitis. With progression of
disease, now she had distended abdomen, skin became pale and dry. She faces the problem
of slow capillary refill and has flat neck veins. The illness of Mr Eleanor has got
deteriorated day by day.
The reason for deterioration of disease can be linked to enteric nervous system. All
component of human gut is connected to CNS and regulates all the functionality of it.
Clinical observation facts the reason for spreading of colitis to non-inflamed area includes
GI innervation. These include imbalance of GI function and neurological pathway. There is
prolonged hyperexcitation of sympathetic ganglion due to IPAN activation. This cause
hyperactivation of afferent neuron and release neuropeptide substance, somatostatin
proteins, adrenergic and serotoninergic neurotransmitter (Goverse, Stakenborg, & Matteoli,
2016). The signal is passed to whole of intestine. This structural change involves neuronal
receptors becomes limited and does not reach the thalamus. Hence, pain pathway is
blocked.
Answer no 3
Mr Eleanor diagnosed with ulcerative colitis showed high frequency of diarrhoea
with blood. Associated symptoms include pain in lower abdomen, cramps, abdominal
bloating and she also feel fatigued. The manifestation of her is progressive over numerous
years. Currently, on physical examination, following thing was noted; Low haemoglobin,
high number of white blood cell, elevated ESR, high C-reactive protein and low albumen.
Earlier she was having large number of pseudopolyps in the descending and sigmoid colon.
On MRI test, the result disclosed that she had developed pancolitis. With progression of
disease, now she had distended abdomen, skin became pale and dry. She faces the problem
of slow capillary refill and has flat neck veins. The illness of Mr Eleanor has got
deteriorated day by day.
The reason for deterioration of disease can be linked to enteric nervous system. All
component of human gut is connected to CNS and regulates all the functionality of it.
Clinical observation facts the reason for spreading of colitis to non-inflamed area includes
GI innervation. These include imbalance of GI function and neurological pathway. There is
prolonged hyperexcitation of sympathetic ganglion due to IPAN activation. This cause
hyperactivation of afferent neuron and release neuropeptide substance, somatostatin
proteins, adrenergic and serotoninergic neurotransmitter (Goverse, Stakenborg, & Matteoli,
2016). The signal is passed to whole of intestine. This structural change involves neuronal
degeneration which is followed by several soreness in the GI tract causing pancolitis in
whole large intestine.
Answer no 4
The fluid given to Mr Eleanor is 1000ml Hartman’s solution. Hartman’s solution is
also known as Ringer lactate solution is the mixture of several salt dissolved in sterile water
that is used to create isotonic solution in relation with human body fluid. The composition
of Hartman’s solutions per litre are: sodium- 130nmol, potassium- 5nmol, chloride-
112nmol, calcium- 2nmol and bicarbonate- 28nmol. These solutions are isotonic in nature,
sterile and non-pyrogenic (Zochios & Valchanov, 2018). It is majorly used for electrolyte
replacement in the body. This fluid contain lactate so cannot be given to diabetic patients,
however, it is beneficial for other patient as it does not cause acidosis (Feuerstein &
Fitzpatrick, 2018).
The rationale for administration of Hartman’s solution is to maintain the fluid
balance in him as he has lost large amount of water and sodium due to diarrhoea. This has
caused because ulcerative colitis has resulted soreness in the wall of intestine, hence the
absorption of water does not take place leads to loss of water and disruption of osmotic
gradient inside the body. The Hartman solution is given Mr Eleanor to replenish the lost
water and ions, therefore, maintaining the specific fluid balance inside the body.
whole large intestine.
Answer no 4
The fluid given to Mr Eleanor is 1000ml Hartman’s solution. Hartman’s solution is
also known as Ringer lactate solution is the mixture of several salt dissolved in sterile water
that is used to create isotonic solution in relation with human body fluid. The composition
of Hartman’s solutions per litre are: sodium- 130nmol, potassium- 5nmol, chloride-
112nmol, calcium- 2nmol and bicarbonate- 28nmol. These solutions are isotonic in nature,
sterile and non-pyrogenic (Zochios & Valchanov, 2018). It is majorly used for electrolyte
replacement in the body. This fluid contain lactate so cannot be given to diabetic patients,
however, it is beneficial for other patient as it does not cause acidosis (Feuerstein &
Fitzpatrick, 2018).
The rationale for administration of Hartman’s solution is to maintain the fluid
balance in him as he has lost large amount of water and sodium due to diarrhoea. This has
caused because ulcerative colitis has resulted soreness in the wall of intestine, hence the
absorption of water does not take place leads to loss of water and disruption of osmotic
gradient inside the body. The Hartman solution is given Mr Eleanor to replenish the lost
water and ions, therefore, maintaining the specific fluid balance inside the body.
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References
Bao, Y., Gao, Y., Hou, W., Yang, L., Kong, X., Zheng, H., ... & Hua, B. (2015).
Engagement of signaling pathways of protease‐activated receptor 2 and μ‐opioid
receptor in bone cancer pain and morphine tolerance. International journal of
cancer, 137(6), 1475-1483.
Descalzi, G., Ikegami, D., Ushijima, T., Nestler, E. J., Zachariou, V., & Narita, M. (2015).
Epigenetic mechanisms of chronic pain. Trends in neurosciences, 38(4), 237-246.
Dulai, P. S., Sandborn, W. J., & Gupta, S. (2016). Colorectal cancer and dysplasia in
inflammatory bowel disease: a review of disease epidemiology, pathophysiology,
and management. Cancer Prevention Research, 9(12), 887-894.
Feuerstein, G., & Fitzpatrick, G. M. (2018). U.S. Patent Application No. 15/735,196.
Ge, J., Zhang, X., Liu, J., Fu, Z., Shi, X., Li, Q., ... & Zhu, Q. (2015). Elevated expression
of interleukin-21 and its correlation to T-cell subpopulation in patients with
ulcerative colitis. Central-European journal of immunology, 40(3), 331.
Goverse, G., Stakenborg, M., & Matteoli, G. (2016). The intestinal cholinergic anti‐
inflammatory pathway. The Journal of physiology, 594(20), 5771-5780.
Hindryckx, P., Jairath, V., & D'haens, G. (2016). Acute severe ulcerative colitis: from
pathophysiology to clinical management. Nature Reviews Gastroenterology &
Hepatology, 13(11), 654.
Kesavan, K. (2015). Neurodevelopmental implications of neonatal pain and morphine
exposure. Pediatric annals, 44(11), e260-e264.
Bao, Y., Gao, Y., Hou, W., Yang, L., Kong, X., Zheng, H., ... & Hua, B. (2015).
Engagement of signaling pathways of protease‐activated receptor 2 and μ‐opioid
receptor in bone cancer pain and morphine tolerance. International journal of
cancer, 137(6), 1475-1483.
Descalzi, G., Ikegami, D., Ushijima, T., Nestler, E. J., Zachariou, V., & Narita, M. (2015).
Epigenetic mechanisms of chronic pain. Trends in neurosciences, 38(4), 237-246.
Dulai, P. S., Sandborn, W. J., & Gupta, S. (2016). Colorectal cancer and dysplasia in
inflammatory bowel disease: a review of disease epidemiology, pathophysiology,
and management. Cancer Prevention Research, 9(12), 887-894.
Feuerstein, G., & Fitzpatrick, G. M. (2018). U.S. Patent Application No. 15/735,196.
Ge, J., Zhang, X., Liu, J., Fu, Z., Shi, X., Li, Q., ... & Zhu, Q. (2015). Elevated expression
of interleukin-21 and its correlation to T-cell subpopulation in patients with
ulcerative colitis. Central-European journal of immunology, 40(3), 331.
Goverse, G., Stakenborg, M., & Matteoli, G. (2016). The intestinal cholinergic anti‐
inflammatory pathway. The Journal of physiology, 594(20), 5771-5780.
Hindryckx, P., Jairath, V., & D'haens, G. (2016). Acute severe ulcerative colitis: from
pathophysiology to clinical management. Nature Reviews Gastroenterology &
Hepatology, 13(11), 654.
Kesavan, K. (2015). Neurodevelopmental implications of neonatal pain and morphine
exposure. Pediatric annals, 44(11), e260-e264.
Pardi, D. S. (2017). Diagnosis and management of microscopic colitis. The American
journal of gastroenterology, 112(1), 78.
Price, T. J., & Inyang, K. E. (2015). Commonalities between pain and memory mechanisms
and their meaning for understanding chronic pain. In Progress in molecular biology
and translational science (Vol. 131, pp. 409-434). Academic Press.
Spoendlin, J., Karatas, G., Furlano, R. I., Jick, S. S., & Meier, C. R. (2015). Rosacea in
patients with ulcerative colitis and Crohn's disease: a population-based case-control
study. Inflammatory bowel diseases, 22(3), 680-687.
Tahara, T., Shibata, T., Kawamura, T., Okubo, M., Ichikawa, Y., Sumi, K., ... & Nakagawa,
Y. (2015). Fusobacterium detected in colonic biopsy and clinicopathological
features of ulcerative colitis in Japan. Digestive diseases and sciences, 60(1), 205-
210.
Yarnitsky, D. (2015). Role of endogenous pain modulation in chronic pain mechanisms and
treatment. Pain, 156, S24-S31.
Zochios, V., & Valchanov, K. (2018). Fluid Administration. Core Topics in Cardiothoracic
Critical Care, 116.
journal of gastroenterology, 112(1), 78.
Price, T. J., & Inyang, K. E. (2015). Commonalities between pain and memory mechanisms
and their meaning for understanding chronic pain. In Progress in molecular biology
and translational science (Vol. 131, pp. 409-434). Academic Press.
Spoendlin, J., Karatas, G., Furlano, R. I., Jick, S. S., & Meier, C. R. (2015). Rosacea in
patients with ulcerative colitis and Crohn's disease: a population-based case-control
study. Inflammatory bowel diseases, 22(3), 680-687.
Tahara, T., Shibata, T., Kawamura, T., Okubo, M., Ichikawa, Y., Sumi, K., ... & Nakagawa,
Y. (2015). Fusobacterium detected in colonic biopsy and clinicopathological
features of ulcerative colitis in Japan. Digestive diseases and sciences, 60(1), 205-
210.
Yarnitsky, D. (2015). Role of endogenous pain modulation in chronic pain mechanisms and
treatment. Pain, 156, S24-S31.
Zochios, V., & Valchanov, K. (2018). Fluid Administration. Core Topics in Cardiothoracic
Critical Care, 116.
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