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Semester 4: Nutrition and Metabolism > PBL Topic 4 Case 4 > Flashcards

PBL Topic 4 Case 4 Flashcards

1
Q

What is the function of the ileocecal valve?

A
  • Prevents backflow of faecal contents from the cecum into the ileum
  • By closing when excessive pressure building up in cecum
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2
Q

What is the function of the ileocecal sphincter?

A
  • Remains constricted

- To slow emptying of ileal contents into cecum

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3
Q

Identify factors that affect the degree of contraction of the ileocecal valve and intensity of peristalsis in the terminal ileum

A
  • Distension of the cecum
  • Irritation in the cecum
  • Via the myenteric reflex in the gut wall and extrinsic autonomic nerves
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4
Q

Identify the functional anatomy of the colon

A
  • Proximal half is concerned with absorption of water and electrolytes
  • Distal half is concerned with storage of faecal matter
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5
Q

Outline the role of of serotonin on peristalsis in the colon

A
  • Released from neuroendocrine cells
  • In response to luminal distension
  • Which activates HT4 receptors
  • Which results in activation of sensory neurons (calcitonin gene-related peptide)
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6
Q

Outline the process of mixing movements in the colon

A
  • Combined contraction of circular muscles and longitudinal muscle
  • Causes unstimulated portion to bulge outward (haustration)
  • Disappears and reappears in a nearby area
  • Provides mixing and propulsion
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7
Q

What are mass movements?

A
  • Propulsive movements

- Which takes over propulsive role of haustrations

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8
Q

How frequently do mass movements occur?

A
  • One to three times per day

- For about 15 minutes at a time

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9
Q

Outline the process of mass movement

A
  • Constrictive ring occurs in response to distended or irritated point in transverse colon
  • Portion distal to ring loses its haustration and contracts as a single unit
  • Which propels faecal contents down the colon
  • Relaxes after 2-3 minutes and another mass movement occurs more distally
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10
Q

Identify two reflexes involved in the facilitation of mass movements

A
  • Gastrocolic reflex and duodenocolic reflex
  • Which arise from distension or irritation of stomach/duodenum
  • And are transmitted by way of autonomic nervous system
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11
Q

Why is the rectum typically empty of faeces?

A
  • Sphincter

- Sharp angulation

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12
Q

Outline the process of defecation

A
  • Mass movement forces faeces into rectum
  • Contraction of rectum
  • Relaxation of anal sphincters
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13
Q

Identify the two anal sphincters

A
  • Internal sphincter, composed of circular smooth muscle

- External anal sphincter, composed of striated voluntary muscle that surrounds the internal sphincter

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14
Q

Identify the innervation of the external anal sphincter

A
  • Pudendal nerve
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15
Q

What is the intrinsic reflex?

A
  • Distension of rectal wall
  • Initiates afferent signals through the myenteric plexus
  • To initiate peristaltic waves in the descending colon. sigmoid and rectum
  • And relaxation of the internal sphincter
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16
Q

What is the parasympathetic defecation reflex?

A
  • Stimulation of nerve endings in rectum
  • Which are transmitted into spinal cord
  • And then reflexly back to descending colon, sigmoid and rectum by way of pelvic splanchnic nerves
  • Which greatly intensify the peristaltic waves and relax the sphincters
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17
Q

Identify three factors that increase the intra-abdominal pressure and force faecal contents into rectum

A
  • Deep breath which moves the diaphragm downward
  • Closure of glottis
  • Contraction of abdominal wall muscles
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18
Q

What is the peritoneointestinal reflex?

A
  • Results from irritation of the peritoneum
  • Strongly inhibits the excitatory enteric nerves
  • To cause intestinal paralysis (especially in patients with peritonitis)
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19
Q

What are the renointestinal and vesicointestinal reflexes

A
  • Inhibition of intestinal activity

- As a result of kidney or bladder irritation

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20
Q

How do the crypts of Lieberkuhn in the large intestine differ to those in the small intestine?

A
  • No villi
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21
Q

How do the epithelial cells in the large intestine differ to those in the small intestine?

A
  • No enzymes

- Consist mainly of mucus secreting cells

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22
Q

Identify three causes of mucus secretion in the large intestine

A
  • Direct, tactile stimulation of the epithelial cells
  • Local nervous reflexes
  • Stimulation of the pelvic splanchnic nerves
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23
Q

Identify three protective functions of mucus in the large intestine

A
  • Excoriation by chyme
  • Bacterial activity
  • Faecal acids
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24
Q

Identify the mechanism of diarrhoea

A
  • Irritation of large intestine
  • Causes secretion of extra large quantities of water and electrolytes and viscid alkaline mucus
  • Which dilutes irritating factors
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25
Q

Identify one advantage and one disadvantage of diarrhoea

A
  • Causes rapid movement of irritating factor towards anus to be expelled
  • Loss of large quantities of water and electrolytes causing dehydration
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26
Q

How many mL of chyme pass through the ileocecal valve into the large intestine each day? How many mL of this remains in faeces?

A
  • 1500 ml

- 100 ml

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27
Q

How is the large intestine adapted to absorb sodium ions more completely?

A
  • No back-diffusion of ions
  • Due to tighter gap junctions
  • Allows for a steeper concentration gradient
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28
Q

What is the role of bicarbonate ion secretion in the large intestine?

A
  • Helps to neutralise the acidic end products of bacterial action
  • Provides an exchange transport process for chloride ions
  • Which helps to create an osmotic gradient for absorption of water
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29
Q

identify substances formed as a result of bacterial activity in the large intesitne

A
  • Vitamin K
  • Vitamin B12
  • Vitamin B1 (thiamine)
  • Vitamin B2 (riboflavin)
  • Flatus gases
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30
Q

Identify three gases that make up flatus

A
  • Carbon dioxide
  • Methane
  • Hydrogen gas
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31
Q

Identify the components of faeces

A
  • 3/4 water 1/4 solid
  • 30% dead bacteria
  • 40% undigested roughage
  • Dried constituents of digestive juices
  • Bile pigments
  • Inorganic matter
  • Protein
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32
Q

Why is faeces brown?

A
  • Stercobilin
  • Urobilin
  • Derivatives of bilirubin
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33
Q

Outline the four stages of the cell cycle

A
  • G1: Preparation for DNA synthesis
  • S phase: DNA synthesis
  • G2 phase: Preparation for division
  • M Phase: Mitosis
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34
Q

Which stages of the cell cycle constitute interphase?

A
  • G1
  • S
  • G2
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35
Q

Where are the two checkpoints located in the cell cycle? What is the importance of them?

A
  • Before S phase and M phase
  • Halts the cell cycle in response to DNA damage
  • To maintain genetic stability
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36
Q

What is G0?

A
  • Quiescent phase

- Where cells are not rapidly divide

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37
Q

What are positive and negative regulators?

A
  • Positive regulators control the changes necessary for cell division
  • Negative regulators control positive regulators
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38
Q

Identify two families of proteins that control the progress through the cell cycle, and the way in which they control this

A
  • Cyclins and cyclin dependent kinases
  • Cyclin activates CDK
  • Which allows CDK to phosphorylate the proteins necessary for a particular step in the cycle
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39
Q

How is cyclin degraded?

A
  • Ubiquitin / protease system
  • Enzymes add small molecules of ubiquitin to cyclin
  • Which directs the cyclin to a proteasome where it is degraded
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40
Q

Identify the main cyclins involved in the cell cycle and their associated CDK

A
  • Cyclin A: CDK1 + CDK2
  • Cyclin B: CDK1
  • Cyclin D: CDK4 + CDK6
  • Cyclin E: CDK2
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41
Q

Outline the role of Cyclin D in cell cycle control

A
  • Binds with CDK4 + CDK6
  • To phosphorylate retinoblastoma protein
  • Which allows passage of cells from G0 to G1
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42
Q

Which phases of the cell cycle are controlled by each cyclin?

A
  • G1-S: Cyclin E
  • S-G2: Cyclin E and Cyclin A
  • G2-M: Cyclin A and Cyclin B
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43
Q

Outline the process of mitosis

A
  • Prophase: Condensation of chromosomes, disintegration of nuclear membrane
  • Metaphase: Chromosomes align on equator of cell
  • Anaphase: Mitotic apparatus captures and draws chromosomes to opposite poles of cell
  • Telophase: Formation of nuclear membranes, cytokinesis
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44
Q

Identify two negative regulator of the cell cycle

A
  • Hypophosphorylated Rb

- CDK Inhibitors

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45
Q

Identify the two families of CDK inhibitors

A
  • CIP family: p21, p27, p57

- Ink family p16, p19, p15

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46
Q

How does the p53 gene induce DNA repair?

A
  • Codes for p53 protein
  • Which accumulates in cells
  • Activates transcription factors such as p21
  • Which inactivates cyclin / CDK complexes
  • Thus preventing Rb phosphorylation
  • Arresting cell at checkpoint 1
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47
Q

Which cyclin is thought to be involved in arresting the cell cycle at checkpoint 2?

A
  • Cyclin B
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48
Q

Outline the extrinsic pathway of apoptosis

A
  • Binding of TNF to the death domain of a Fas receptor (e.g. CD95)
  • Causing Fas receptors to trimerise
  • And activate an initiator caspase (caspase 8)
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49
Q

Outline the intrinsic pathway of apoptosis

A
  • p53 activates BCL-2 proteins e.g. Bax, Bak
  • Which promote release of cytochrome C from mitochondria
  • Which complexes with Apaf-1
  • This complex combines with procaspase 9 to activate it
  • Which orchestrates the effector caspase pathway
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50
Q

What is the apoptosome?

A
  • Complex of cytochrome C, Apaf-1 and procaspase 9
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51
Q

Outline the execution phase of apoptosis

A
  • Executioner caspases cleave DNA repair enzymes, protein kinase C and cytoskeleton components
  • DNAase cuts DNA between nucleosomes
  • Nucleus shrinks (pyknosis) and fragments (karyorrhexis)
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52
Q

What is the role of apoptotic initiating factor (AIF)?

A
  • Enters cell nucleus and triggers cell suicide
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53
Q

What is a polyp?

A
  • Protuberant growth
  • Divided into epithelial and mesenchymal polyps
  • Which are subdivided into benign and malignant categories
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54
Q

Identify four types of benign epithelial polyps

A
  • Adenomas
  • Hamartomatous
  • Hyperplastic
  • Inflammatory
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55
Q

What is the incidence of adenomas?

A
  • 20% of population
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56
Q

Identify the types of adenomas

A
  • Tubular: 75%
  • Villous: 10%
  • Tubulovillous: 15%
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57
Q

Identify three structural features of a tubular adenoma

A
  • Pedunculated
  • Smaller (<10 mm in diameter)
  • Crypts lined by mucus secreting epithelium
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58
Q

Describe the structure of a villous adenoma

A
  • Sessile
  • Larger (20 mm in diameter)
  • Villi lined by columnar epithelium showing dysplasia
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59
Q

Describe the structure of hyperplastic polyps

A
  • Sessile
  • Elongated crypts with serrated appearance
  • No dysplasia
60
Q

Which gene is defective in most instances of hyperplastic polyps?

61
Q

When do inflammatory polyps typically occur?

62
Q

Name a condition that results in widespread hamartomatous polyps. Which gene is defective in this condition?

A
  • Peutz-Jeghers syndrome

- STK11

63
Q

Outline a clinical feature of Peutz-Jeghers syndrome?

A
  • Melanin pigmentation in lips, mouth and digits
64
Q

Identify four types of benign mesenchymal polyps

A
  • Lipomas
  • Fibromas
  • Haemangiomas
  • Lymphangiomas
65
Q

Which gene is affected in familial adenomatous polyposis?

A
  • APC gene
  • A tumour suppressor gene
  • On 5q21
66
Q

What is the colorectal cancer risk in FAP?

67
Q

How is FAP inherited?

A
  • Autosomal dominant
68
Q

Which gene is affected in hereditary non polyposis colorectal cancer (Lynch 1 or 2)?

A
  • MSH2 and MLH1

- Which are mismatch repair genes

69
Q

What is the colorectal cancer risk in HNPCC?

70
Q

How is HNPCC inherited?

A
  • Autosomal dominant
71
Q

What is the mean age of adenoma development in FAP?

72
Q

What are the treatment options for FAP?

A
  • Prophylactic colectomy
  • With ileorectal anastomosis
  • Often before the age of 20
73
Q

Describe the activation of oncogenes in the development of colorectal cancer

A
  • KRAS: increased proliferation and reduced apoptosis through MAPK pathway
  • c-MYC: increased DNA synthesis through encoding of a phosphoprotein
74
Q

Identify the loss of function mutations of tumour suppressor genes in the development of colorectal cancer

A
  • Point mutation of APC with subsequent loss of healthy allele
  • MCC mutation whose gene product is involved in cell cycle control
  • DCC involved in control of apoptosis
  • T43 involved in DNA repair
  • NME1 involved in metastasis
75
Q

Describe the defects in DNA repair in the development of colorectal cancer

A
  • Defects in DNA repair genes manifest as microsatellite instability
  • Including hMLH1 and hMSH2 (in HNPCC)
76
Q

Identify the role of the more recently discovered beta-catenin oncogene in the development of colorectal cancer

A
  • Typically phosphorylated by GSK3 which causes its degradation
  • Mutation allows WNT to bind to frizzled protein
  • Which inhibits phosphorylation of beta catenin
  • Which can now enter nucleus where it interacts with transcription factors
  • Changing gene expression and increasing cellular proliferation
77
Q

Outline the epidemiology of colorectal cancer

A
  • Third most common worldwide
  • More common in Western countries
  • Second most common cancer in UK
  • Incidence increases with age (average at diagnosis = 60-65)
78
Q

Identify six factors that increase the risk of colorectal cancer

A
  • Increasing age
  • Saturated fats and red meat
  • Colorectal polyps
  • Obesity
  • Smoking
  • Acromegaly
79
Q

Identify three factors that decrease the risk of colorectal cancer

A
  • Vegetables, garlic, milk and calcium
  • Exercise
  • Aspirin and other NSAIDs
80
Q

Identify a condition implicated in the development of colorectal cancer

A
  • Ulcerative colitis
81
Q

What percentage of cancers occur in the rectum?

82
Q

What percentage of cancers occur in the sigmoid colon?

83
Q

What type of cancers are most commonly found in the rectum? What symptoms is this associated with?

A
  • Ulcerating type
  • Rectal bleeding
  • Mucus discharge
  • Feeling of incomplete emptying
84
Q

What type of cancers are most commonly found in the descending and sigmoid colon? What symptoms is this associated with?

A
  • Stenosing type

- Producing obstruction

85
Q

What type of cancers are most commonly found in the right colon? What symptoms is this associated with?

A
  • Polypoid / Fungating
  • Occult bleeding
  • Patient develops iron deficiency anaemia
86
Q

Why are cancers in the cecum and ascending colon more likely to be advanced at the time of presentation?

A
  • Distensibility of cecum and fluid bowel contents
87
Q

What is the gold standard investigation for colorectal cancer? Identify two advantages of this method

A
  • Colonoscopy
  • Allows for biopsy and removal of polyps
  • Higher sensitivity and specificity
88
Q

Identify a non-invasive investigation for colorectal cancer that has replaced double contrast barium enema

A
  • CT colnography
89
Q

Identify two investigations useful for detecting hepatic metastasis

A
  • Intraoperative ultrasound

- CT

90
Q

Name an antigen that can be raised in colorectal cancer

A
  • Serum carcinoembryonic antigen (CEA)
91
Q

Identify a surgical intervention for rectal cancer

A
  • Total mesorectal excision with a low rectal anastomosis
92
Q

Identify a surgical intervention for colonic cancer

A
  • Segmentation resection with restorative anastomosis

- Removal of lymph nodes as far as the root of the mesentery

93
Q

Identify a treatment that has increased the proportion of advanced colorectal tumours that can be resected?

A
  • Cisplatin and 5-fluorouracil

- With radiotherapy

94
Q

Why are Dukes C and Duke B rectal cancers given postoperative radiotherapy? Why is this not helpful for colic cancers proximal to the descending colon?

A
  • To reduce the risk of local recurrence if operate resection margins are involved
  • Difficulties delivering a sufficient dose without toxicity to adjacent structures
95
Q

Identify two follow-up investigations following surgical removal of colorectal cancesr

A
  • Colonoscopy

- CEA measurements

96
Q

Outline the staging and survival for colorectal cancer

A
  • Stage 1 / Duke’s A: T1/T2 90% 5 year survival rate
  • Stage 2 / Duke’s B: T3/T4 65% 5 year survival rate
  • Stage 3 / Duke’s C: N1/N2 35% 5 year survival rate
  • Stage 4 / Duke’s D: M1 7% 5 year survival rate
97
Q

In the pathological sequence of the development of colorectal cancer:

Identify the changes that cause the formation of a small polypoid adenoma from normal epithelium

A
  • APC mutation
  • MCC mutation
  • 5q mutation
  • c-MYC activation
  • ‘Susceptibility gene’ 8q24
98
Q

In the pathological sequence of the development of colorectal cancer:

Identify the changes that cause the formation of a large polypoid adenoma from a small polypoid adenoma

A
  • KRAS mutation
99
Q

In the pathological sequence of the development of colorectal cancer:

Identify the changes that cause the formation of an invasive carcinoma from a large polypoid adenoma

A
  • p53 mutation

- 18q deletion

100
Q

In the pathological sequence of the development of colorectal cancer:

Identify the changes that cause the metastasis in invasive adenocarcinoma

A
  • NME1 deletion
101
Q

What percentage of cancers are familial and what percentage are sporadic?

A
  • Familial: 1%

- Sporadic: 99%

102
Q

What is the difference between chromosomal and microsatellite instability?

A
  • Chromosome instability causes chromosome breaks due to numerical and structural abnormalities
  • Microsatellite instability due to defective DNA mismatch repair
103
Q

What is a gatekeeper gene?

A
  • Inhibits proliferation of, or promote death of, cells with damaged DNA
104
Q

What is a caretaker gene?

A
  • Maintain the integrity of the genome by repairing DNA damage
105
Q

Identify a gatekeeper gene that is a transcription factor that responds to DNA damage

106
Q

Identify a gatekeeper that controls the cell cycle at the G1/S checkpoint

107
Q

Identify a gatekeeper that regulates the beta catenin function in the WNT pathway

108
Q

Identify a caretaker that is involved in DNA repair and is susceptible to mutation in pancreatic cancer?

109
Q

Identify a caretaker gene involved in DNA mismatch repair that is susceptible to mutation in Lynch syndrome

A
  • MSH2

- MLH1

110
Q

Identify four methods of oncogene activation

A
  • Translocation of oncogene to an actively transcribed site
  • Point mutation causing it to be hyperactive
  • Amplification by insertion of multiple copies of an oncogene
  • Insertion of promotor sequences of a retrovirus
111
Q

Identify an oncogene that is a platelet derived growth factor

112
Q

Identify an oncogene that is a a receptor for epidermal growth factor

113
Q

Identify two oncogenes involved in intracellular signalling (protein-tyrosine kinase)

114
Q

Identify an oncogene that is a transcription factor for driving proliferation and regulating apoptosis

115
Q

Identify an oncogene that is involved in intracellular signalling (GTP-binding, binary switch)

116
Q

How are chemotherapy drugs combined together?

A
  • Based on differing mechanisms and non-overlapping toxicities
  • To avoid resistance and minimise adverse effects
117
Q

How are chemotherapy drugs administered (timings)?

A
  • Given over a period of days

- Followed by a rest of a few weeks

118
Q

Identify 4 alkylating agents

A
  • Cyclophosphamide
  • Cisplatin
  • Busulfan
  • Oxaliplatin
119
Q

Outline the mechanism of action of alkylating agents

A
  • Formation of a carbonic ion with only six electrons in outer shell
  • React with nucleophiles in DNA (e.g. N7 of guanine)
  • Causing intra-chain cross linking or interchain cross linking (if bifunctional)
  • Resulting in transcription interference and chain breakage
120
Q

Identify four adverse effects of alkylating agents

A
  • Bone marrow depression
  • GI disturbances
  • Sterility
  • Increased risk of leukaemia
121
Q

Identify two examples of antimetabolites

A
  • Methotrexate

- Fluorouracil

122
Q

Outline the mechanism of action of methotrexate

A
  • Higher affinity for DHFR than DHF
  • Reducing intracellular THF
  • Which is required for carrying methyl groups for conversion of DUMP to DTMP by thymidylate synthase
  • Which is essential for DNA synthesis
123
Q

Outline the mechanism of action of fluorouracil

A
  • Converted into a fraudulent nucleotide, FDUMP
  • Which interacts with thymidylate synthase
  • But is not converted into DTMP
  • Which is essential for DNA synthesis
124
Q

Identify phase specific agents that act in S phase

A
  • Methotrexate

- Fluorouracil

125
Q

Outline the mechanism of action of doxorubicin

A
  • Inhibits DNA and RNA synthesis

- Through interference with topoisomerase II

126
Q

Outline the mechanism of action of bleomycin

A
  • Causes fragmentation of DNA chains
127
Q

Identify two types of resistance to anticancer drugs

A
  • Primary resistance: present when drug is first given

- Acquired: developed during treatment with drug

128
Q

Outline the role of P-glycoprotein (P-gp/MDR1) in resistance to anticancer drugs

A
  • Decreases accumulation of drugs in cells

- By picking up foreign chemicals (e.g. drugs) and expelling them

129
Q

Identify five main side effects of chemotherapy and how they are managed

A
  • Vomiting (metoclopramide)
  • Hair loss (scalp cooling)
  • Tiredness (nutrition and hydration)
  • Myelosuppression (give molgramostim)
  • Mucositis (antiseptic mouthwash)
130
Q

Outline the mechanism of action of cinnarizine

A
  • H1 receptor antagonist

- Vestibular nuclei

131
Q

Outline the mechanism of action of metoclopramide / domperidone

A
  • D2 receptor antagonist

- Chemoreceptor trigger zone

132
Q

Outline the mechanism of action of ondansetron

A
  • 5-Ht3 receptor antagonist

- Chemoreceptor trigger zone

133
Q

Identify an antispasmodic drug

A
  • Hyoscine butyl-bromide
134
Q

Identify 8 psychological factors in the initiation and promotion of cancer

A
  • Behavioural factors
  • Stress
  • Life events
  • Control
  • Coping styles
  • Depression
  • Personality
  • Hardiness
135
Q

Describe a type C personality

A
  • Helpless
  • Passive
  • Appeasing
136
Q

Describe the components of hardiness

A
  • Control
  • Commitment
  • Challenge
137
Q

Identify psychologicla consequences of cancer

A
  • Depression
  • Anxiety
  • Anger
  • Fighting spirit
138
Q

Identify the components of a fighting spirit

A
  • Searching for meaning (cause of their cancer)
  • Gaining a sense of mastery (medication and positive thinking)
  • Self-enhancement through social downward comparison
139
Q

Identify how psychology can be used to alleviate symptoms of cancer

A
  • Pain management through biofeedback and hypnosis
  • Treating nausea and vomiting through relaxation and desensitisation
  • Social support interventions to reduce denial and promote hope
  • Body image counselling
  • Cognitive adaptation strategies to increase well-being and decrease distress
140
Q

Describe a whole person approach in the psychological alleviation of cancer symptoms

A
  • Relaxation
  • Mental imagery
  • Exercise
141
Q

Identify the three basic mechanisms needed to transform a normal cell into a neoplastic cell

A
  • Immortalisation by telomerase expression
  • Removal of growth inhibition by Inactivation of both copies of a tumour suppressor gene
  • Autocrine growth stimulation by mutation of proto-oncogenes to produce oncogenes
142
Q

Identify four nuclear changes in neoplastic cells

A
  • Enlargement of nucleus
  • Dark staining (hyperchromasia)
  • Variability in shape and size
  • Chromatin clumping (pleomorphism)
143
Q

What is molgramostim? What is its mechanism of action and what is it used to treated?

A
  • Recombinant GM-CSF
  • Which functions as an immune stimulator
  • Used to manage myelosuppression with chemotherapy
144
Q

What is the role of ALT?

A
  • Aminotransferase
  • Transfer of amino group of alanine to alpha-ketoglutarate
  • To produce pyruvate and glutamate
145
Q

What is the role of AST?

A
  • Aminotransferase
  • Transfer of amino group of aspartate to alpha-ketoglutarate
  • To produce oxaloacetate and glutamate
146
Q

What are ABC transporters?

A
  • (A)TP (B)inding (C)assette Transporter Pumps
  • Which are depending on hydrolysis of ATP to transport molecules
  • Examples include BSEP2 and MRP2 which secrete bile salts from hepatocytes into bile canaliculi

Semester 4: Nutrition and Metabolism (17 decks)

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