Case 14

Question 1

What are the main two functions of the large intestine

Answer 1

• Absorption of water and electrolytes
• Storage of faecal matter

Question 2

What is the order of the large intestine starting at the ileum to the anus

Answer 2

(Starting at the right side) Ileum –> Caecum –> Ascending colon –> transverse colon –> descending colon –> sigmoid colon –> rectum –> anus (going to the left side)

Question 3

What parts of the large intestine are on the left and what parts are on the right what are the the functional difference between them

Answer 3

The right colon includes the cecum, ascending colon, hepatic flexure, and the proximal two-thirds of the transverse colon.

The left colon includes the distal third of the transverse colon, splenic flexure, descending colon and the sigmoid colon

Right side is responsible for water and electrolyte absorption, left side is responsible for the storage of faecal matter

Question 4

What are the 4 structural adaptations of the large intestine

Answer 4

• Teniae coli - 3 bands of longitudinal muscle
• Epiploic appendages - fat filled sacs from the outer edge of intestine
• Haustra - Sacculations (Segmentations or sacs) in the wall of the intestine
• Transverse folds of the rectum (Houston’s valves):

Question 5

Describe the action or movement of the Ascending and the proximal 2/3rds of the Transverse colon

Answer 5

At the ascending and proximal transverse colon you have haustral contractions, the haustra unit contracts slowly and rhythmically to allow for mixing within the haustra, the goal isn’t to propel the contents but to mix which helps in water and electrolyte absorption. This is known as the mixing movements of the large intestine and occur every 30 minutes allowing time for absorption

Question 6

Describe the action or movement of the distal third of the transverse colon and the descending colon

Answer 6

At the distal third of the transverse colon and the descending colon you have propulsive movements which involve the contraction of the teniae coli to produce large, powerful waves of contraction that propel contents toward the rectum. These movements usually occur 1-3 times a day, often after meals, and are due to the gastrocolic reflex. This movement is referred to as Mass movement

Question 7

Describe the Gastrocolic reflex

Answer 7

The gastrocolic reflex is the primary stimulator of peristalsis and occurs during and after meals. It works by the stimulation of the stretch receptors in the stomach which activates the enteric nervous system, increasing the motility of the gut.

Question 8

Describe the Defecation reflex

Answer 8

Once faeces reach the sigmoid colon and the rectum, stretch receptor in the muscularis externa are activated, these stretch receptors send impulses down the sensory afferent pelvic splanchnic nerve which go to levels S2, 3 and 4, there it synapses and sends off as the motor efferent pelvic splanchnic which goes to the muscularis externa of the sigmoid colon and rectum and causes it to contract. The motor pelvic splanchnic nerve also goes to the internal anal sphincter and causes it to relax. The only think left to do now is relax the external anal sphincter which is skeletal muscle meaning we have voluntary control over it, once that happens defecation occurs

Question 9

What do the interstitial cells of Cajal do

Answer 9

They are the pacemaker cells of the GI tract that create slow waves leading to contraction of smooth muscle

Question 10

Where are enterochromaffin (EC) cells located? and what do they secrete

Answer 10

EC cells are found in the mucosa of the gastrointestinal tract, particularly in the stomach and intestines. EC cells primarily release serotonin (5-HT).

Question 11

What triggers the release of serotonin from EC cells?

Answer 11

Serotonin release is triggered by chemical stimuli (nutrients, pH changes, bile acids) and mechanical stimuli (stretch or distension of the gut wall).

Question 12

What is the general role of serotonin in the gut?

Answer 12

Serotonin stimulates intrinsic sensory nerves via 5-HT3 receptors which modulates peristaltic contractions, and regulates secretions from smooth muscles.

Question 13

How does serotonin influence peristalsis?

Answer 13

Serotonin is released and attaches to 5-HT receptors on intrinsic primary affereny neurons.

These neurons can either activate excitatory motor neurons which causes Acetylcholine (ACh) and Substance P to be secreted behind the food bolus causing contraction . (Excitatory transmitters)

OR they can active inhibitory motor neurons which causes the release of Nitric Oxide (NO) and VIP to be secreted ahead of the bolus, relaxing the muscle, facilitating its movement. (Inhibitory transmitters)

Question 14

How does serotonin contribute to vomiting? and how can medication be used to counter this

Answer 14

When the epithelium of the enterochromaffin cells get irritated by toxins or cytotoxic drugs they can release serotonin (5-HT) which can activate vagal afferent (sensory) neurons that send signals all the way up to the medulla and activate the vomiting center which triggers the vomiting reflex. and so 5-HT3 antagonists are used as anti-emetic drugs

Question 15

Does noradrenaline decrease or increase contraction of the gut

Answer 15

Noradrenaline causes hyperpolarisation of the muscularis externa muscles and so causes decreased contraction of the gut

Question 16

What are the hormones secreted in response to food stimulating the nerves in the gut and what do they do

Answer 16

• Motilin → depolarisation (= increase contraction)
• Secretin, G.I.P. → hyperpolarisation (= ↓ contraction)
• Adrenaline → hyperpolarisation (= ↓ contraction)

Question 17

Describe the Immunology of the gut

Answer 17

The upper layer of mucus is colonised by bacteria (gut microbiome) which can be useful to health

IgA antibody is a GI specific antibody responsible for primary defense against bacteria

Peyer patches are small clusters of lymphatic tissue found in the wall of the small intestine. Specifically, they reside within the lamina propria and extend into the submucosa of the ileum. Peyer’s patches act as the immune system’s first line of defense against microbial and dietary antigens. They have immune cells in them that secrete the IgA antibodies.

Paneth cells, which are located in base of crypts of villi of small intestine = produce alpha and beta defensins which help defend the intestine against bacteria (disrupts cell wall)

Question 18

What is the difference between atrophy and hypertrophy?

Answer 18

Atrophy: Decrease in the size of cells.

Hypertrophy: Increase in the size of cells.

Question 19

What is the difference between hyperplasia and aplasia?

Answer 19

Hyperplasia: Increase in the number of cells.

Aplasia: Complete absence of cell production.

Question 20

What is Metaplasia

Answer 20

Metaplasia: Reversible change where one cell type is replaced by another.

Question 21

What is Dysplasia

Answer 21

Dysplasia: Abnormal and disorganized growth of cells, often precancerous.

Question 22

What is Anaplasia

Answer 22

Anaplasia refers to the loss of structural and functional differentiation in cells, meaning that the cells have reverted to a more primitive, less specialized state. This is typically seen in cancerous cells, where the normal characteristics of the cells are lost, and they begin to resemble less-differentiated, undifferentiated cells.

Question 23

Describe the cell cycle

Answer 23

The cell begins in G1 where cellular contents, excluding the chromosomes, are duplicated.

It then goes on to to the S phase where each of the 46 chromosomes are duplicated by the cell

Then it goes to G2 where the cell double checks the duplicated chromosomes for any errors and makes any needed repairs

Finally it enters mitosis which has 5 phases and will have a seperate flashcard on it

Question 24

Describe the mitosis stage

Answer 24

Mitosis =
1. Prophase – chromosome becomes visible. 2 pairs of centriole separate, and nucleus disintegrates.

2. Metaphase – chromatids move to a midline
   (equator)
3. Anaphase – Chromatids are pulled Apart
4. Telophase – Chromosomes uncoil, two nuclei
   formed
5. Cytokinesis – Cytoplasmic division.

Question 25

Where are the 3 checkpoints located in the cell cycle and what do they check for?

Answer 25

G1/S Checkpoint (Restriction Point) is located at the end of G1 phase and checks for: - Cell size. - Nutrient availability. - DNA damage. - External growth signals. G2/M Checkpoint is located at the end of G2 phase and it checks for: - Complete and accurate DNA replication. - DNA damage repair. Metaphase (Spindle Assembly) Checkpoint is located in the metaphase of mitosis and checks for: - Proper chromosome alignment. - Correct attachment of chromosomes to spindle fibers.

Question 26

How is progression through the cell cycle done and what proteins drive it

Answer 26

Progression through cell cycle is driven by CDK’s (cyclin dependant kinases) and Cyclins Remember 4/6, 2, 2, 1, 1 AND DEAAB (Don't even ask anymore bro) Now starting at G1 you have CDK4/6 that binds to Cyclin D and drives the cell cycle from early G1 to late G1 Then you have CDK2 that binds with Cyclin E and prepares the cell to enter S phase Then you have CDK2 that binds with Cyclin A which Initiates and regulates DNA replication. Then you have CDK1 that binds to Cyclin A which prepares the cell for mitosis. And finally you have CDK1 which binds to Cyclin B and drives the cell into Mitosis

Question 27

What are the two types of genes that mediate cancer

Answer 27

(Proto-)oncogenes and Tumor Suppressor Genes

Question 28

What are proto-oncogenes and list an example of some

Answer 28

Proto-oncogenes are the genes necessary to help a cell grow, they have the potential to cause cancer if mutated as it leads to uncontrollable growth. Oncogenes are dominant meaning only one mutated allele is needed for it to be activated Examples include KRAS, MYC and HER2 genes

Question 29

What are the types of receptor found in the gut lumen and what do they sense

Answer 29

- Mechanoreceptors that sense distension - Osmoreceptors that sense osmolaity - Chemoreceptors that sense acidity and others that sense digestive products

Question 30

What allows muscles in the gut to contract as a unit

Answer 30

Gap junctions

Question 31

Describe the membrane potential of the gut and why they are like this

Answer 31

Membrane potential is unstable (5-15mV) (slow waves) and these slow waves determine the frequency of contractions (e.g. stomach = 3/min while duodenum is up to 12/min), this is controlled by the interstitial cells of Cajal

Question 32

Food stimulates nerve and hormonal activity which can increase or decrease maximum depolarisation. List these hormones and nerve secretions and what they do

Answer 32

VIP = Vasoactive intestinal peptide and it decreases contractions

Question 33

Useful gut hormone pictures that shows when gut hormones are released and their levels in each level

Answer 33

Question 34

What is the hormone released during fasting periods and it responsible for the hunger pangs

Answer 34

Motilin

Question 35

95% of Serotonin found in the body is in the gut: TRUE or FALSE

Answer 35

True

Question 36

How does vomitting occur after the vomiting centre in the medulla is stimulated

Answer 36

The medulla stimulates the gut to undergo retrograde peristalsis from the terminal ileum which causes the contents to move towards the stomach, the distension of the upper tract re-enforces the urge to vomit. Abdominal muscles contract which increases intra-abdominal pressure (IAP) which pushes the diaphragm up and increases intra-thoracic pressure (ITP) and this increase in IAP and ITP forces stomach contents through the oesophagus and upper oesophageal sphincter

Question 37

What receptors can be influenced in anti-emetic drugs

Answer 37

Question 38

How do opioids affect the gut and their MOA

Answer 38

Mu, kappa and delta receptors are expressed in the GI tract with Mu receptors being especially important Activation of these receptors causes G protein activation which activates K+ channels and inhibits Ca2+ channels which decreases synaptic transmission and fluid secretion. A decrease in synaptic transmission means that GI motility is decreased so the gut content stay in the gut for longer meaning more water is absorbed from them leading to constipation. Opioids also prevent the relaxation in front of the gut content so the food becomes trapped Opioids can be used as antidiarrheal drugs E.g. Loperamide (Imodium) which decreases peristalsis and gastric emptying

Question 39

Explain how Clostridium Difficile infection happens after you take antibiotics and what u can do to fix it

Answer 39

A healthy gut microbiome keeps C. Difficile at bay, once you start taking antibiotics, the useful bacteria in your gut die off which allows C. Difficile to thrive and for its spores to bloom leading to an infection. This can cause pseudomembranous colitis which is life-threatening, you then take antibiotics for this but when exposed to new C. Diff spores the cycle continueS. So to solve this issue you can have a faecal transplant (faecal transplant therapy) which provides you with a new healthy gut micro biome which can keep C. Diff at bay

Question 40

IgA antibodies show evidence of only binding to colitis causing bacteria: TRUE or FALSE

Answer 40

True

Question 41

Where do u find stems cells in the gut and what do they do

Answer 41

Stem cells are found in the bottom of the crypt next to the paneth cells. These do not come from the bone marrow, you are born with them. They are responsible for replacing the epithelium within their respective crypt and around it which is good because you can repair local damage from a local supply of stem cells. What’s special is that the differentiated cells can also sometimes revert back to being stem cells (plasticity)

Question 42

What happens to the lining of the epithelium in coeliac disease

Answer 42

You get crypt hyperplasia and villis atrophy which means that the villus gets smaller and the crypt gets bigger because the proliferation of the crypt zone gets larger

Question 43

What two immune cells are especially important in the gut

Answer 43

Dendritic cells and Macrophages

Question 44

What Interleukins are very important for gut health and what innate lymphoid cell creates it

Answer 44

- ILC3 is very important for gut health it makes IL17 and IL22 which is also very important - IL 22 is a key factor for epithelial barrier maintenance - ILC3 is also both pro and anti-tumorigenic

Question 45

What are the main T cell types found at mucosal surfaces and what do they do

Answer 45

T-regs are T-regulatory cells and are essential for regulating immune cell homeostasis, tissue repair, barrier integrity, inflammation control etc.

Question 46

What happens when mucosal homeostasis is lost

Answer 46

You get inflammatory bowel disease (IBD) and can present in different diseases such as Ulcerative Colitis and Crohn’s disease

Question 47

What’s the difference between Ulcerative colitis and Crohn’s disease

Answer 47

They are both inflammatory bowel diseases but Crohn's disease can affect any part of the digestive tract, from the mouth to the anus, often with patchy inflammation and skip lesions (healthy tissue between inflamed areas). Ulcerative colitis, on the other hand, is limited to the colon (large intestine) and rectum, and the inflammation is continuous throughout the affected area Crohn’s disease also affects all layers of the bowel wall (transmural) while UC typically only affects the innermost lining (mucosa)

Question 48

What are crohn's disease and ulcerative colitis symptoms

Answer 48

Abdominal pain and cramping: Common in both conditions, often related to inflammation and ulceration of the intestinal lining. Diarrhea: Often with urgency, sometimes bloody, and can be severe, especially in acute flare-ups. Fatigue: Chronic inflammation and malabsorption can lead to tiredness and weakness. Weight loss: Due to malabsorption and loss of appetite during flare-ups. Fever: Often during flare-ups or infections. Anemia: Caused by blood loss (especially in ulcerative colitis) or chronic inflammation, leading to a lack of red blood cells. Rectal bleeding: Can occur in both diseases, especially during flare-ups when ulcers in the intestines cause blood to appear in the stool.

Question 49

What causes inflammatory bowel disease

Answer 49

Question 50

People with IBD have double the risk of developing colorectal cancer (CRC) and type 2 diabetes also can increase risk of CRC: TRUE or FALSE

Answer 50

True

Question 51

How long does food spend in each part of the digestive system?

Answer 51

Mouth and Esophagus: Seconds to minutes. Stomach: 2 to 4 hours (depends on food type). Small Intestine: 4 to 6 hours (majority of digestion and nutrient absorption). Large Intestine (Colon): 10 to 72 hours (water absorption, stool formation). Total Time: 24 to 72 hours (varies based on diet, metabolism, and health conditions).

Question 52

What are the hallmarks of cancer

Answer 52

- Evading apoptosis - Self-sufficiency in growth signals - Insensitivity to anti-growth signals - Tissue invasion and metastasis - Limitless replicative potential - Sustained angiogenesis

Question 53

What is Tumor Heterogeneity

Answer 53

Tumor heterogeneity refers to the diversity and variation that exists within a tumor or between tumors in the same individual

Question 54

Explain Knudson’s 2 hit hypothesis and what tumour suppressor genes are

Answer 54

Tumour suppressor genes are RECESSIVE. For a cancer to develop, both copies of a tumor suppressor gene must be inactivated through mutations, meaning that two separate "hits" are required to occur on the same gene before a cell can become cancerous In Familial cancers, individuals that INHERIT a mutated copy of a tumour suppressor gene (first hit) have a higher risk of developing cancer as they only require one additional mutation (second hit) to trigger tumour formation.

Question 55

What are some examples of tumor suppressor genes that are commonly mutated in colorectal cancer

Answer 55

APC and p53

Question 56

What are oncogenes and give some general examples of some

Answer 56

Oncogenes are genes necessary to help a cell grow, they have the potential to cause cancer if mutated as it leads to uncontrollable growth. Oncogenes are dominant meaning only one mutated allele is needed for it to be activated Examples include RAS, MYC and SRC genes

Question 57

What are some examples of Oncogenes that are commonly mutated in colorectal cancer

Answer 57

Beta-Catenin and KRAS

Question 58

What does p53 do

Answer 58

p53 (TP53): A tumor suppressor gene, often called the "guardian of the genome." Functions: Regulates cell cycle, DNA repair, apoptosis, senescence, and inhibits angiogenesis. Mechanism: p53 is a transcription factor that gets activated by DNA damage, once this happens it allows for the transcription and translation of certain proteins like p21 for cell arrest (works by stopping CDK and cyclin action) and BAX for cell apoptosis. Cancer Link: Mutated in >50% of cancers; leads to uncontrolled cell growth and tumor progression.

Question 59

Higher tumor heterogeneity means the chance of tumor relapse and lack of response to treatment is higher: TRUE or FALSE

Answer 59

True

Question 60

Explain Wnt signalling and how it can lead to cell growth

Answer 60

Wnt is a ligand molecule that binds to receptors outside cells that causes growth. Inside the cell you have a complex of proteins consisting of, GSK-3beta, APC and B-catenin, with APC driving the complex to stay together. When this complex is all together B-catenin gets phosphorylated and degraded meaning it can't cause cell growth When Wnt doesn't bind to its receptor this happens and B-catenin is degraded. When Wnt does bind to its receptor the complex gets dismantled which causes GSK-3beta and APC to be inactivated, this means B-Catenin no longer gets phosphorylated and degraded so it enters the nucleus and causes the expression of Cyclin D and myc which drives the the cell into the cell cycle and causes it to divide

Question 61

What are the function of crypts in the gut and how does it link in with wnt signalling

Answer 61

Intestinal crypts are invaginations in the gut lining housing stem cells and progenitor cells responsible for regenerating the intestinal epithelium. Cells in the crypt proliferate and differentiate as they migrate up the villi, and eventually undergo apoptosis at the villus tip. The Wnt Pathway maintains stem cell proliferation in the crypt base. With high levels of Wnt in the bottom of the crypt and lowering levels as it goes up to the villi tip, forming a wnt gradient. Wnt signaling activates β-catenin, promoting transcription of genes for cell division (e.g., MYC, Cyclin D1).

Question 62

Explain how the mutation of the APC gene can cause tumor formation in the gut

Answer 62

APC is a tumor suppressor gene, meaning both copies have to be mutated for it to stop doing it function. At the base of the crypt you have high levels of Wnt and so high levels of proliferation meaning cells proliferate. As you go up the crypt Wnt levels should decrease and so should proliferation levels as B-Catenin starts to get degraded again. As Wnt levels decrease as you go up the crypt this function of B-catenin should cease but because of the APC mutation, Wnt signalling means nothing and the cell continue to proliferate and a tumor is formed. This is because loss of APC function means that the GSK-3B, APC, B-catenin complex can no longer be kept together which means that B-catenin is free to go and influence cell growth as it doesn't get degraded.

Question 63

Explain how the mutation of the Beta-catenin can cause tumor formation in the gut

Answer 63

B-Catenin is the fundamental factor that leads to cell growth and proliferation and so it is an Oncogene. This means that one mutation of the B-catenin gene can lead B-catenin being constantly produced and so constant cell proliferation which leads to tumor formation.

Question 64

What is usually the main mutation in Familial adenomatous polyposis (FAP) and on what chromosome is it located

Answer 64

APC gene mutation, the gene is located on chromosome 5q21

Question 65

How can u remember GSK-3Beta and Beta-catenin

Answer 65

Remember GSK-3Beta by thinking of BSK but the b for beta is at the end instead of the start and you add a G For Beta-catenin just remember the beta part and for the Catenin think of cats having nine lives but the e in nine is in the middle instead of in the end so catenin

Question 66

Explain how RAS/KRAS mutation can cause tumor formation

Answer 66

KRAS is specific member of the RAS family. The RAS gene is an oncogene that codes for the RAS protein which has GTPase activity. KRAS mutation is what contributes specifically colon cancer RAS is like a switch. Normally, Ras is bound to GDP (guanosine diphosphate) and is inactive. Upon binding to GTP (guanosine triphosphate), it becomes active. Once in the active form, Ras can initiate signalling cascades to cause: ○ Inhibition of apoptosis ○ Cell growth ○ Protein synthesis Once you don't need growth of the cell anymore RAS hydrolyses GTP and turns it into GDP which returns it to its inactive state When a KRAS mutation occurs it prevents it from being able to hydrolyse GTP to GDP meaning it constantly stays active leading to colon cancer KRAS mutations are very specific and occur at specific sites of the gene often in codons 12, 13, or 61 with a mutation in codon 12 being the most common.

Question 67

What is Hereditary non-polyposis colon cancer (HNPCC) also known as and what is it

Answer 67

HNPCC is also known as Lynch syndrome and is an inherited condition increasing the risk of colorectal and other cancers (e.g., endometrial, ovarian). It has very few polyps but when they do form the progression into cancer is fast (2-3 years) compared to FAP (8-10 years)

Question 68

What mutation occurs in Hereditary non-polyposis colon cancer (HNPCC) and how does it work, and what gene is affected

Answer 68

The mutation that occurs that causes HNPCC is in a mismatch repair gene. Usually in a cell you have TGF-Beta receptors that respond to TGF-beta, which is a growth inhibitor. Mutations in a mismatch repair gene causes deletion of AA bases in the TGF-Beta receptor meaning the cell can no longer respond to TGF-beta, this means the cell can longer have its growth inhibited and so the cell keep proliferating The gene affected is SMAD2 / SMAD4

Question 69

What are the two colon cancers you need to know

Answer 69

- FAP (Familial adenomatous polyposis) - HNPCC (Hereditary non-polyposis colon cancer)

Question 70

What are the main mutations you need to know for colon cancer

Answer 70

- Mutation in the APC tumor suppressor gene which acts Wnt signalling and B-catenin - Mutation in the oncogene KRAS - Mutation in the inhibitory growth signal receptor TGF-Beta (can be considered an tumor suppressor gene)

Question 71

What does cancer -omics analyses

Answer 71

DNA, RNA and proteins

Question 72

Picture on pathophysiology of colon cancer

Answer 72

Question 73

How does right-sided colon cancer present

Answer 73

* Weight loss * Anaemia (Reduced haemoglobin) * Occult bleed (hidden bleeding) * No bowel obstruction * Late diagnosis

Question 74

How does left-sided colon cancer present

Answer 74

* PR bleed (Stands for per rectum bleeding and refer to the passage of fresh blood through the anus.) * Tenesmus (continual feeling of needing to evacuate bowel) * Obstruction

Question 75

How many types in the bristol stool chart and what do they mean

Answer 75

7 Types

Question 76

How is screening done for colon cancer and how often

Answer 76

The NHS has a national screening programme offering screening every 2 years to all men and women aged 60 to 74 years in England, 50 to 74 years in Scotland. Faecal immunochemical tests (FIT) look very specifically for the amount of human haemoglobin in the stool If the results come back positive → colonoscopy. People with risk factors eg. FAP, HNPCC or inflammatory bowel disease are offered a colonoscopy at regular intervals to screen for bowel cancer.

Question 77

Who does NICE recommend a FIT test for

Answer 77

* People aged 40 and over with unexplained weight loss and abdominal pain, or * Aged under 50 with rectal bleeding and either of the following unexplained symptoms: * abdominal pain * weight loss, or * Aged 50 and over with any of the following unexplained symptoms: * rectal bleeding * abdominal pain * weight loss, or *Aged 60 and over with anaemia even in the absence of iron deficiency

Question 78

What investigations are done for colon cancer

Answer 78

- Gold standard is a Colonoscopy with biopsy and involves the endoscope reaching the entire length of the colon to the ileocecal valve - Can also do a sigmoidoscopy by the endoscope only reaches to the top of the descending colon - CEA tumor marker blood test which stands for Carcinoembryonic Antigen and is a tumor marker produced by some colorectal cancer cells. - Barium Enema test which is when a liquid containing barium is placed in the colon via the rectum, Apple core sign indicates a constricting tumor in the colon indicating colon cancer

Question 79

What is the TNM staging for colon cancer

Answer 79

Tumour (T) Tis - in situ (grown into mucosa) T1 - grown into submucosa T2 - grown into muscular layer T3 - grown into serosa T4 - grown through serosa Node (N) N0 - no nodes involved N1 - 3 nodes involved N2 - 4+ nodes involved Metastasis (M) M0 - no mets M1 - distant mets

Question 80

What 3 drugs are used in chemotherapy treatment for colon cancer

Answer 80

Chemotherapy is usually done for stage 3 or, stage 4 colon cancer (stage 4 meaning that it has metastasized) - Oxaliplatin - Fluorouracil - Folinic acid

Question 81

How does Oxaliplatin work and its side effect

Answer 81

It is a platinum based chemotherapy agent which selectively inhibits DNA synthesis - at high concentrations, RNA and protein synthesis are also suppressed. * Side effect – peripheral neuropathy

Question 82

How does Fluorouracil work (5-FU) and what is its side effects

Answer 82

It is a pyrimidine analogue and it stops DNA synthesis it does this by blocking thymidylate synthase which is an enzyme that converts uracil → thymidylate, this means thymidine (pyrimidine) can’t be incorporated into DNA * Side effects = nausea, diarrhea, and vomiting

Question 83

How does folinic acid work and what is it usually given with

Answer 83

* Given in combination with 5-FU (Fluorouracil) it enhances the action of 5-FU by making it stay in the cancer cell longer and exert its anti-cancer effect.

Question 84

What are the different surgical treatments for colon cancer and what do they involve removing.

Answer 84

Right hemicolectomy - The right side of the colon in removed Left hemicolectomy - The left side of the colon is removed Sigmoid colectomy - the sigmoid colon is removed Subtotal or Total colectomy - Most or all of the colon is removed (Total usually leaves behind the rectum) Proctocolectomy - All of the colon and the rectum are removed

Question 85

What the surgery called where all of the colon and rectum are removed

Answer 85

Proctocolectomy