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P2 - Gastrointestinal system > Large intestine, fluid and electrolyte balance, diarrhoea > Flashcards

Large intestine, fluid and electrolyte balance, diarrhoea Flashcards

1
Q

What is coeliac disease?

A

Gluten-sensitive enteropathy/small intestinal villous atrophy that resolves when gluten is withdrawn from the diet/inappropriate T cell-mediated immune response

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2
Q

What are the risk factors for coeliac disease?

A

Female, relative with coeliac disease and HLA-DQ2

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3
Q

What is α-gliadin?

A

Component of gluten which seems to be the most reactive

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4
Q

Describe the infectious hypothesis of coeliac disease

A

Infection with Adenovirus 12 in genetically susceptible individuals leads to immune system recognizing α-gliadin as it is similar to portion of the virus (E1b), this causes cross-reactivity with α-gliadin and ultimately coeliac disease

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5
Q

How is α-gliading recognized by the immune system?

A

Digested products of α-gliadin are absorbed into the lamina propria, deamination of glutamine residues by TTG which leads to bonding to HLADQ2 and activation of pro-inflammatory T-cell response

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6
Q

What is the clinical presentation of coeliac disease in infants?

A

Present after introduction of cereals with impaired growth, diarrhoea, vomiting, abdominal distension

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7
Q

What is the clinical presentation of coeliac disease in older children?

A

Anaemia, short stature, pubertal delay, recurrent abdominal pain or behavioural disturbance

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8
Q

What is the clinical presentation of coeliac disease in adults?

A

Diarrhoea, bloating, flatulence, abdominal discomfort; may be provoked by infection, pregnancy or surgery; chronic or recurrent, nutritional deficiency, reduced fertility, osteoporosis, unexplained raise in AST/ALT, neurological and psychiatric symptoms

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9
Q

Describe the histological findings in coeliac disease

A

Mucosal inflammation, loss of villous height - villi may be flat or short and broad, no change in total mucous thickness due to crypts elongation, patchy mucosal damage and increased plasma cells and intraepithelial lymphocytes

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10
Q

What are the consequences of villous damage in coeliac disease

A

Reduced surface area and thus reduced absorptive capacity leading to diarrhoea, malabsorption, weight loss, abdominal pain and vomiting

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11
Q

Discuss the effects of coeliac disease on iron homeostasis

A

As iron absorption occurs predominantly in duodenum and jejunum the damaged epithelium does not take enough iron in, thus people with coeliac disease will often also have iron deficiency

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12
Q

How is coeliac disease diagnosed?

A

Serology (IgA tTG - specific and sensitive; IgA EMA - 1% less specific); endoscopy (scalloping of the folds, prominent submucosal blood vessels, nodulat pattern to the mucosa)

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13
Q

What is the management for coeliac disease/

A

Gluten-free diet

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14
Q

What is the definition of diarrhoea?

A

3 or more loose or water stools per day

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15
Q

Name the 3 pathogenic mechanisms of diarrhoea

A

Toxin mediated, damage to intestinal epithelial cells, invasion across intestinal epithelial barrier

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16
Q

Name the bacteria that cause diarrhoea with the first one being the most common

A

Campylobacter sp; salmonella sp, shigella sp, E. coli, clostridium difficile….

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17
Q

Name the viruses that cause diarrhoea with the first one being the most common

A

Norovirus, sapovirus, rotavirus, adenovirus

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18
Q

Name the parasites that cause diarrhoea

A

Cryptosporidium (from lambs, causes cramps and large volume water diarrhoea),
giardia (in water from deceased animals),
entamoeba histolytica, cyclospora, isospora

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19
Q

What is a common source of campylobacter?

A

Chicken

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20
Q

What is the infecting dose and the incubation period of cambylobacter?

A

9 000 organisms, incubation period 3 days

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21
Q

How does campylobacter cause diarrhoea?

A

Attaches and invades the intestinal epithelial cells, it is sensitive to stomach acidity

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22
Q

What are the clinical features of campylobacter?

A

Frequent high volume diarrhoea, may be bloody;

Severe abdominal pain, nausea, fever

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23
Q

What is the course of infection with campylobacter?

A

Self-limiting, about 7 days

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24
Q

Describe the use of antibiotics in campylobacter infection

A

High rates of resistance and develop resistance on treatment, rarely indicated

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25
Q

What are the late complications of campylobacter

A

Reactive arthritis and Guilian-Barre syndrome

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26
Q

What is the main source of salmonella and how is it transmitted?

A

Chicken and reptiles, person to person infection

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27
Q

What is the infectious dose of salmonella and how is risk increased within the host?

A

10 000 organisms; increased risk with decreased stomach acid and diminished gut flora

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28
Q

What is mechanism of salmonella infection?

A

Invasion of enterocytes with subsequent inflammatory response; onset within 72 hours of ingestion

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29
Q

What are the symptoms of salmonella related diarrhoea?

A

Nausea, diarrhoea, abdominal cramps and fever

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30
Q

What are the complications of salmonella infection?

A

Secondary infection - endocarditis, osteomyelitis, mycotic aneurysm; and bacteraemia (bacteria in blood)

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31
Q

What is the use of antibiotics in salmonella?

A

Non-significant reduction in duration, self-limiting to 10 days and antibiotics are only given in severe disease

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32
Q

What is the pathogenesis of E.coli infection?

A

Attachment and production of shiga toxin that causes enterocyte death, bacteria also enters the systemic circulation

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33
Q

What is the infectious load and incubation period of E. coli?

A

10 organisms, sporadic outbreaks with incubation period 3 to 4 days

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34
Q

What are the symptoms of E. coli infection?

A

Bloody diarrhoea and abdominal tenderness

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35
Q

What is haemolytic uraemic syndrome caused by E.coli?

A

Systemic effect of shiga toxin, triad: microangiopathic haemolytic anaemia, acute renal failure, thrombocytopenia; 10% of patients, up to 5% mortality

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36
Q

What is the management or E. coli infection?

A

Supportive

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37
Q

How can E. coli infection be prevented?

A

Strict infection control for healthcare workers, screening of contacts, appropriate butchering of meat, public health measures in outbreaks

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38
Q

What are the risk factors associated with Clostridium difficile infection?

A

Antibiotic exposure, older age, hospitalisation

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39
Q

What is the pathogenesis of Clostridium difficile infection?

A

Decreased colonisation resistance, colonic colonisation leads to toxin production

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40
Q

What are the signs of Clostridium difficile infection?

A

Loose stools and colic, fever, leukocytosis, protein losing enteropathy

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41
Q

What is the diagnosis of Clostridium difficile?

A

Toxin detection by tissue culture assay and toxin detection by c. diff antigen

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42
Q

What is the treatment of diarrhoea in infection with Clostridium difficile?

A

Stop causative antibiotic if possible, Metronidazole/Vancomycin and recolonise with normal flora

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43
Q

What does norovirus causes?

A

Common epidemics of gastroenteritis

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44
Q

How is norovirus transmitted?

A

Faecal-oral route, difficult to disinfect

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45
Q

What are the clinical features of norovirus infection?

A

Acute explosive diarrhoea and vomiting, 24 to 48 hours, no lasting immunity

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46
Q

Name the symptoms of gastroenteritis

A

Vomiting, nausea, diarrhoea,

non-intestinal manifestations: botulism, Guillain-Barre syndrome

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47
Q

What is the onset of vomiting in gastroenteritis and what is vomiting associated with?

A

Sudden onset 6-12 hour of food ingestion, suggests pre-formed toxin for example - S aureus, B cereus or norovirus

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48
Q

Describe the typical diarrhoea caused within the small intestine

A

Large volume watery diarrhoea, cramps, bloating, wind, weight loss; fever and blood in stool are rare

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49
Q

Describe the typical diarrhoea caused within the large intestine

A

Frequent small volume, painful stool, fever and blood common

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50
Q

List the main investigations in diarrhoea

A

History, Faecal leukocytes/occult blood, stool examination/culture, endoscopy

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51
Q

What are the main points to ask in diarrhoea history

A

Food history, onset and nature of symptoms, residence, occupation, travel, pets/hobbies, recent hospitalisations/antibiotics, co-morbidity

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52
Q

What is occult blood and what causes in terms of diarrhoea?

A

Blood in the faeces that is not visibly apparent, bacterial cause

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53
Q

What presence of faecal leukocytes indicates and what are the tests characteristics in terms of diarrhoea?

A

Indicates colonic or inflammatory cause; poor sensitivity and specificity so not used clinically

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54
Q

What is done within stool culture?

A

Consider microscopy for ova and cysts, document a pathogen for public health implications and indications for treatment; low rate positive stool cultures

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55
Q

Why use endoscopy in diarrhoea?

A

If another than infectious cause suspected, can determine colitis

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56
Q

What are the main treatments for diarrhoea?

A

Oral rehydration solution, IV fluid replacement, antibiotics, symptomatic treatment

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57
Q

Name one oral rehydration solution

A

Dioralyte

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58
Q

Describe use of antibiotics in diarrhoea

A

Diarrhoea is usually self-limiting illness, reduce duration by 1 day, can worsen outcome in E. coli; used in severe cases (sepsis or bacteraemia), in significant co-morbidity, and in c. difficile associated diarrhoea

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59
Q

Name antibiotics that are used to treat diarrhoea

A

Metronidazole (c diff), and quinolones like ciprofloxacin

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60
Q

Describe options for symptomatic treatment

A

Generally not indicated, imodium - slows down movement and thus no clearing of the GI, may not be beneficial, little evidence for exclusion diets, yakult - probiotic

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61
Q

Describe the water balance in normal physiology

A

Oral intake about 2 L, turnover of 9 L in small intestine, 150 ml to 2 L absorbed in large intestine; 100 ml excreted

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62
Q

Outline the role of small intestine in electrolyte balance

A

Secreted: Cl-, H20
Absorbed: Na+, Cl- and H20 (more than secreted)
Most water and nutrients absorbed

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63
Q

Outline the role of large intestine in electrolyte balance

A

Secreted: K+, HCO3-
Absorbed: larger quantities of those secreted
Conservation of water, electrolytes and short-chain fatty acids

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64
Q

What is the primary transport of absorption?

A

Active transport of sodium out on the basolateral pole of the cell by Na+/K+-ATPase

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65
Q

Describe the secondary transport of absorption

A

Passive transport on the apical pole driven by decreased Na+ conc in the cell; sodium contransporters for amino acids, peptides, bile salts, vitamins; antiporter (Na+ for H+), Na+ channels, Cl-/HCO3- - exchange carrier

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66
Q

Name the main types of membrane transporters for absorption

A

ATP-driven pump, co-transporter/symporter, exchange carrier/antiporter, ion channel

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67
Q

Outline the role of sodium in nutrient absorption

A

Drives absorption of water, sodium gradient provides energy for active transport of many minerals, vitamins and metabolites

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68
Q

What are the main processes that lead to fluid and electrolyte loss?

A

Fluid circuit hypothesis, loss of potassium with loss of cells, loss of K+ and HCO3- in the stool (hypokalaemia and acidosis), loosened tight junctions or increased vasodilation

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69
Q

What is the fluid circuit hypothesis?

A

Loss of fluid absorption capacity through damage, cell immaturity or challenge by bacterial and viral enterotoxins reverses net absorption to secretion

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70
Q

Identify the main electrolytes that may be lost through GI tract

A

Na+, Cl-, K+, HCO3-

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71
Q

Understand the mechanism of intestinal transport of glucose and apply this knowledge to treatment of dehydration

A

Absord with Na+ by SGLT1 transporter on the apical pole and then by GLUT2 transporter on the basolateral pole; oral rehydration therapy - give NaCl solution with glucose

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72
Q

Understand the mechanism of intestinal secretion of chloride ion

A

By Chloride channel = CTFR

  • In intestine, pancreatic ducts and lungs
  • Part of cAMP signalling system
  • secretes Cl- back to the lumen, Na+ and K+ follow
  • creates layer of H20 close to the cells
  • Moistens the epithelia
  • Can be activated by enterotoxins
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73
Q

How is CTFR/chloride channel activated by cAMP

A

Beta2-adrenergic receptor activates cAMP through G proteins, this activates protein kinase A which causes ATP binding to Cystic fibrosis transmembrane conductance regulator (CFTR) and Cl- secretion into the lumen

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74
Q

What is the role of chloride ion secretion in the development of severe diarrhoea

A

Enterotoxins of Vibrio cholerae and Escherichia coli activate intracellular cAMP/PKA and activate CFTR on the apical plasma membrane leading to massive Cl- secretion

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75
Q

Describe the cycle of increased water secretions in the small intestine leading to diarrhoea

A

Fluid secretion –> more fluid in the lumen and more rapid propulsion —> decreased absorption –> more fluid –> diarrhoea

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76
Q

Name the possible mechanisms of diarrhoea

A

Non-absorbable solutes, failure to digest or absorb nutrients, secretory agonists, inflammation

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77
Q

Name the 3 basic classifications of diarrhoea

A

Secretory diarrhoea, inflammatory diarrhoea and osmotic/malabsorptive

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78
Q

Describe the causes of secretory diarrhoea

A

Acute infections, failure of bile salt absorption, laxative abuse, carcinoid syndrome, Zollinger-Ellison syndrome

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79
Q

Describe the mechanism of secretory diarrhoea

A

Secreted: Na+, K+, Cl-, HCO3-
- decreased absorption and increased secretion, results in high volume faeces, bacteria destroy tight junctions and cause leakage of water

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80
Q

Describe the causes of inflammatory diarrhoea

A

Inflammatory bowel disease, Crohn disease, ulcerative colitis, infectious disease: Shigella, salmonella; irritable colon

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81
Q

What is the mechanism of inflammatory diarrhoea

A

Increased secretion and propulsive activity of the bowel, results in low volume excretion

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82
Q

Describe the causes of osmotic diarrhoea

A

Laxative, antacids, acarbose (alpha-glucosidase inhibitor), orlistat (lipase inhibitor), digestive enzymes deficiencies, inflammatory disease, short bowel syndrome

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83
Q

Describe the mechanism of osmotic diarrhoea

A

Decreased intestinal absorption, results in high volume faeces

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84
Q

Describe the importance of child diarrhoea in terms of public health

A

Major cause of child deaths worldwide

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85
Q

What is bloody diarrhoea?

A

Intestinal damage and nutrient loss, commonly caused by Shigella

86
Q

What is persistent diarrhoea?

A

More than 14 days, happens in undernourished children, often with other diseases

87
Q

What is the treatment for children’s diarrhoea?

A

Fluid replacement, zinc supplements, continue feeding

88
Q

What are the most common causes of child diarrhoea?

A

Unsafe water, poor sanitation, poor hygiene

89
Q

What are the public health interventions to prevent child diarrhoea

A

Rotavirus and measles vaccinations, early breastfeeding and vit A supplements, hand washing with soap, improved water quality, community-wide sanitation promotion

90
Q

Understand the role of osmolality changes in determining water movement between intracellular and extracellular fluid

A
  • High osmolality draws water into a compartment –> high plasma osmolality = cellular dehydration
  • Low osmolality means water movement out of a compartment –> low plasma osmolality = cellular overhydration and oedema
  • Osmolality is determined by non-absorbable nutrients
91
Q

How is osmolality relevant to treatment of fluid and electrolyte disorders

A

The composition of solution given needs to change depending on the problem
- UNICEF ORS - reduced osmolality ORS decreases stool output and dehydration aby 20-30% compared to the original formula

92
Q

What is the osmolality of standard ORS vs reduced osmolality ORS solution?

A 
Standards = 311 mmol/l
Reduced = 251 mmol/l
93
Q

What is normal blood osmolality?

A

275–295 mmol/kg

94
Q

What are the main types of intravenous fluids

A

Blood products, colloids, crystalloids, saline, dextrose, lactate-containing intravenous fluids

95
Q

Describe properties of colloids

A

Large molecular; albumin, hydroxyethyl starch, haemocoel

96
Q

Describe properties of crystalloids

A

Water plus electrolytes –> sodium chloride, sodium lactate, potassium chloride, and calcium chloride in water: Saline, dextrose, ringer-lactate, Hartmann’s

97
Q

Give an example of hypoosmotic solution

A

Saline 0.45%

98
Q

Give an example of hyperosmotic solution

A

Sodium bicarbonate 8,4%

99
Q

Give an example of isosmotic solution

A

Saline 0.9% or dextrose 5%

100
Q

What is the caloric value of 5% dextrose solution?

A

5 g/100 ml

101
Q

Describe properties of lactate-containing intravenous fluids

A

Bicarbonate is produced during lactate metabolism, normal saline may contribute to metabolic acidosis, but ringer-lactate may increase cerebral oedema

102
Q

What factors determine the rate of fluid replacement

A

Age, cardiovascular status, renal function, severity of existing dehydration, time it took to develop

103
Q

What is the regime of emergency re-hydration

A

500 ml bag each 2 hours

104
Q

What is the standard regimen of rehydration?

A

500 mL bag every 6 hours - 2 L in 24 hours

105
Q

What is the slow rehydration regimen?

A

500 mL bag every 8 hours - 1.5 L in 24 hours

106
Q

What are the principles of safe potassium replacement?

A

Maximum concentration for peripheral administration: 40 mmol/L
Maximum rate: 10 mmol/L or with cardiac monitoring
Indicate the final volume of the solution

107
Q

When do you use cardiac monitoring in terms of potassium supplementation?

A

Baseline ECG required if K<3 mmol/L
Cardiac monitoring if K<2.5 mmol/L
Or if K is given faster than 10 mmol/L

108
Q

What are the cardiac effects of hypokalaemia?

A

ST depression.
T wave inversion.
Prominent U waves.
Long QU interval.

109
Q

Describe the systemic approach to the assessment of a patient with suspected fluid/electrolyte disorder

A

Assess the clinical state –> assess intake/output –> electrolyte shifts –> replace –> daily need, anticipate loss, previous deficit

110
Q

What are the measurements needed in suspected fluid/electrolyte disorder

A

Electrolyte profile, blood gases, glucose, albumin, urea, creatinine, plasma osmolality

111
Q

Define cholecystitis

A

Inflammation of gallbladder

112
Q

Define cholelithiasis

A

Gallstone within gallbladder

113
Q

Define cholecystectomy

A

Removal of gallbladder

114
Q

Define choledocholithiasis

A

Gallstone within bile duct

115
Q

What is MRCP

A

MRI cholangiopancreatography

116
Q

What is ERCP

A

Endoscopic retrograde cholangionpancreatography

117
Q

What is PTC

A

Percutaneous transhepatic cholangiography

118
Q

Describe the biliary tree

A

Biliary canaliculi -> interlobular bile ducts -> septal bile ducts -> intrahepatic ducts -> R/L hepatic duct -> common hepatic duct -> common bile duct

119
Q

Describe the function of the gallbladder and what is its bile capacity

A

Concentrates bile by absorbing H20 and salts; 30 to 50 ml surface

120
Q

Describe the anatomical relations of the gallbladder

A

Lies in GB fossa on inferior surface of right liver lobe and is connected to common bile duct by cystic duct

121
Q

What are the 3 anatomical regions of the gallbladder and what is its epithelium?

A

Fundus, body and neck (connects to duct)

Columnar epithelial lining

122
Q

What is Hartmann’s pouch and where it is?

A

Lies on the inferior side of gallbladder on the junction between body and neck; may be a site of gallstone impact

123
Q

What is Calot’s triangle?

A

Boundaries: cystic duct, common hepatic duct and inferior edge of the liver
Contents: right hepatic artery, cystic artery, cystic lymph node (of Lund), connective tissue, lymphatics, occasionally accessory hepatic ducts and arteries
Needs to be dissected in cholecystectomy

124
Q

What are the components of bile?

A

Bile acids, water, electrolytes, cholesterol, phospholipids, conjugated bilirubin

125
Q

Describe bile acid synthesis

A

Synthesised from cholesterol in hepatocyte –> cholic acid and chenodeoxycholic acid = primary bile acids;
Conjugated to secondary bile acids by taurine or glycine, actively transported out of hepatocytes

126
Q

How are secondary bile salts produced?

A

By action of intestinal bacteria de-hydroxylation,

127
Q

How much of bile acids is reabsorbed and where?

A

95% of bile acids

Reabsorbed mainly in the ileum/terminal ileum by active transport

128
Q

How do the bile acids travel back to liver?

A

Bound to albumin

129
Q

Outline the regulation of gallbladder contraction

A
  1. Vagal stimulation promotes GB contraction
  2. Cholecystokinin (CCK) released from duodenum in response to presence of luminal fat
  3. CCK mediated GB contraction and relaxation of sphincter of Oddi (SO) -> release of bile juice in to duodenum
  4. GB relaxation and closure of SO mediated by sympathetic nerves and gut hormones vasoactive intestinal polypeptide (VIP) and somatostatin
130
Q

What are the 3 main types of gallstones?

A

Cholesterol stone, bile pigment stone, mixed stones

131
Q

Describe cholesterol stone

A

Usually solitary, oval and large

132
Q

Describe bile pigment stones

A

Multiple, irregular, hard, associated with chronic haemolysis

133
Q

What are the risk factors for gallstones

A

5 F’s - female, fair, fertility, forty and fat; + inflammatory bowel disease and fam history

134
Q

Name the 3 main events that lead to gallstone formation

A

Cholesterol supersaturation, biliary stasis, increased secretion of bilirubin

135
Q

What is cholesterol supersaturation?

A

High levels of cholesterol lead to supersaturation, occurs in high levels of oestrogen (obesity, pregnancy, liver disease); also in low bile acid levels e.g. in Crohns disease, small bowel resection -> ineffective enterohepatic circulation

136
Q

What is biliary stasis?

A

Occurs during periods of fasting and starvation, observed during prolonged total parenteral nutrition

137
Q

How does increased secretion of bilirubin lead to gallstones?

A

Increased RBC breakdown - esp. haematological conditions, malaria, valvular heart disease, post chemo
- failure of hepatic conjugation

138
Q

What are the causes of obstructive jaundice?

A

Common: choledocholithiasis, pancreatic cancers - head of pancreas compressing CBD
Less common:
Pancreatitis - swelling compressing
Cholengiocarcinoma, portal lymphadenopathy, benign bile duct stricture

139
Q

Outline pancreatic cancer

A

Most commonly in head of pancreas, compresses CBD as it passes through pancreatic tissue, painless jaundice, often presents late, ERCP and stent provides drainage of bile, relief of jaundice, bridge to chemo

140
Q

What are the LFTs like in obstructive jaundice?

A 
ALP increased up to 10x
GGT rise - often
Bilirubin - steadily increases
AST/ALT - can be elevated but little
in prolonged - coagulopathy
141
Q

Name the general characteristics of the large intestine

A

Large internal diameter, omental appendices/epiploic appendages, taenia coli, haustra of the colon

142
Q

What is cecum?

A

Beginning of large intestine in the right groin, changes into ascending colon at the ileocecal opening, contains the appendix

143
Q

Describe the appendix

A

Narrow, blind ended tube with large aggregations of lymphoid tissue in its walls
Suspended from the terminal by the mesoappendix

144
Q

How can you identify the origin of appendix and what are its possible locations?

A

The taenia coli lead towards the base of appendix

Retrocecal, paracecal, subcecal, pelvic, subileal, postileal, preileal

145
Q

Is the colon peritoneal structure and what holds it in place?

A

Yes, intraperitoneal; suspended by mesentery

146
Q

What is the cecal blood supply and what is its origin?

A

Anterior and posterior cecal artery from the ileocolic a, appendicular artery
All from superior mesenteric artery

147
Q

What is the venous drainage of the cecum?

A

Ileocolic vein and appendicular vein

148
Q

What are the potential spaces between the colon and the abdominal wall laterally called?

A

Left and right paracolic gutters

149
Q

As ascending colon bends below the liver it forms ___ ___/__ __ __.

A

Right hepatic flexure or just hepatic flexure

150
Q

What is the supply of the ascending colon?

A

The marginal artery which is supplied by right colic artery and ileocolic artery; both of which originate in the superior mesenteric artery

151
Q

What is the venous drainage of the ascending colon?

A

Right colic and ileocolic veins drain to the superior mesenteric

152
Q

Which parts of the colon are intraperitoneal?

A

The transverse colon; ascending and descending are retroperitoneal

153
Q

The tranverse colong bends below the spleen downwards forming __ __/__ __ __.

A

Left colic flexure or splenic flexure

154
Q

To what and by what is the transverse colon attached?

A

To diaphragm by phrenico-colic ligament

155
Q

What is the arterial supply of the transverse colon?

A

Marginal artery supplied by right colic and middle colic from sup mesenteric, and left colic from inferior mesenteric

156
Q

How is the transverse colon drained?

A

By middle colic vein to sup mesenteric vein

157
Q

What is the blood supply and drainage of descending colon?

A

Left colic artery feeding into marginal, from inferior mes a

Left colic vein

158
Q

What is the sigmoid mesocolon?

A

Structure that suspends the sigmoid colon

159
Q

What defines the pelvic inlet?

A
  1. superior margin of pubic symphysis
  2. pubic crest
  3. Iliopectineal line
  4. Anterior border of ala sacrum
  5. Sacral promontory
160
Q

What is the blood supply and drainage of sigmoid colon?

A

Sigmoid arteries and vein, both into the inferior mesenteric vessels

161
Q

What is mesentery?

A

Double layer of visceral peritoneum that attaches its associated structure to the posterior abdominal wall

162
Q

The rectum and sigmoid colon are joined by ___.

A

Rectosigmoid junction

163
Q

What is the arterial blood supply to the rectum and anal canal?

A

Superior rectal artery (from inferior mes)
Middle rectal artery (from internal iliac)
Inferior rectal a (from internal pudendal a)

164
Q

Name the nerves innervating the large intestine

A

Pelvis nerves, vagal input and enteric nervous system, pudendal nerves

165
Q

Which nerves control the external anal sphincter?

A

Pudendal

166
Q

Which nerves control the inner anal sphincter?

A

Vagal and enteric nervous system

167
Q

What is characteristic of the mucosa of colon?

A

Crypts of Lieberkühn

168
Q

What are the epithelia of the large intestine?

A

Surface simple columnar epithelium and glandular epithelium in the crypts

169
Q

Name the cell types of the glandular epithelium

A

Enterocytes, goblet cells, stem cells, enteroendocrine cells, paneth cells (only in cecum)

170
Q

Describe the cells of the surface simple columnar epithelium

A

Absorptive enterocytes - have short apical microvilli, controlled by aldosterone
Goblet cells - secrete mucous to form protective barrier

171
Q

What is contained within the muscularis mucosae?

A

Isolated lymphoid follicles that penetrate to submucosa

172
Q

Describe the muscularis of the large intestine

A

Bundles of longitudinal muscle fuse to form the taeniae coli - 3 ribbon like structure
Inner layer of circular muscle

173
Q

How is the rectum divided?

A

Upper part - rectum proper

Lower part - anal canal which is further divided by pectinate line into upper and lower

174
Q

Describe the features above the pectinate line

A

8 - 10 longitudinal anal columns connected by valves at their bases
Sinuses behind the valves and anal mucous glands open into each sinus

175
Q

Describe the epithelial transformation zone in the anal canal

A

At the level of the pectinate line

Change of epithelium from simple columnar to stratified squamous epithelium with sebaceous and sweat glands

176
Q

Where and how is the internal anal sphincter formed?

A

At the lower anal canal, it is thickening of the circular inner layer of the muscularis; longitudinal smooth muscle layer extends over the sphincter and attaches to connective tissue

177
Q

Describe the external anal sphincter

A

Skeletal muscle, and supported by the levator ani muscle

178
Q

How does the anal canal end?

A

With the anal orifice

179
Q

What are the functions of the large intestine?

A

Digestion and absorption
Reabsorption of remaining fluid
Faeces storage
Vitamins K, B1, B2, B6, B12 and biotin

180
Q

What is the gastrocolic reflex?

A

Long arc reflex activated by stomach filling to increase the gut motility resulting in colon emptying

181
Q

How is the gastrocolic reflex regulated?

A

By chemosensitive and mechanosensitive components; by release of 5-HT and acetylcholine

182
Q

What is the orthocolic reflex?

A

Activated on rising from bed, promotes morning urge to defecate

183
Q

How are the local colonic reflexes regulated?

A

Generated by filling of the lumen and activation of stretch receptors
Passing of food stimulates short bursts of Cl- and fluid secretion mediated by 5-HT from enteroendocrine cells and Ach from enteric secretomotor nerves

184
Q

What bioactive peptides are released to control colonic motility and by what cells?

A

Enterochromaffin cells - 5HT

Enteroendocrine cells - peptide YY

185
Q

Why is peptide YY released and what are its effects?

A

Released in response to lipid in the ileum and colon, decreases gastric emptying and intestinal propulsive motility, reduces Cl- and thus fluid secretion

186
Q

Name the 3 patterns of colonic motility

A

Short-duration contractions, long-duration contractions and high-amplitude propagating contraction

187
Q

What is the role of short-duration contractions?

A

Mixing by circular muscle, stationary pressure waves lasting for about 8 seconds

188
Q

What is the role of long-duration contractions?

A

By taeniae coli, last from 20 to 60 seconds, may propagate over short distancs

189
Q

What is the role of high-amplitude propagating contractions?

A

Results of both local influences and long reflex arcs, 10 times per day, wave along the whole colon, only in aboral direction

190
Q

Describe the process of defacation

A
  1. Filling of the rectum causes relaxation of the internal anal sphincter via the release of the vasoactive intestinal polypeptide and the generation of NO
  2. Anal sampling to prevent faecal incontinence by distinguishing solid, liquid or gas
  3. Sensory nerve endings generate contraction or relaxation of the external anal sphincter
  4. If proceeding with defecation move to the right position to straighten the exit
  5. Relaxation of puborectalis muscle
  6. Rectal contractions, assisted by muscles like diaphragm increase abdominal pressure
191
Q

Outline the normal microflora of the gut

A

Commensal bacteria or enteric bacterial ecosystem
Symbiotic relationship established after birth
In large intestine and bit in distal small intestine

192
Q

Name the functions of commensal bacteria

A

Fermentation of undigested products, metabolism of bile acids and bilirubin, xenobiotics detoxification, protect from invasive pathogens, may generate toxic or carcinogenic compounds from dietary substrates,
Help development of gut epithelium and its differentiation

193
Q

Describe how is useful fermentatin by commensal bacteria

A

Metabolize components that were not digested previously e.g. dietary fibre
Vitamin B7, B9; magnesium, calcium and iron synthesis
Production of short chain fatty acids

194
Q

What are the main short chain fatty acids produced by fermentation by the commensal bacteria?

A

Acetic acid - energy and substrate for fat synthesis
Propionic acid - energy, gluconeogenesis, reduction of cholesterol synthesis
Butyric acid - fuel for colonic cells, affect differentiation, apoptosis of cancer cells

195
Q

What are the main bacterial types in the colon?

A
  1. 9% anaerobes
    - non-sporing
    - Sporing
    - Sporing aerobes
    - Micriaerophilis
196
Q

Give example of Non-sporing anaerobes in the colon

A

Bacteriodes spp, Bifido bacterium spp, eubacterium spp

197
Q

Give example of sporing anaerobes

A

Clostridium spp

198
Q

Give example of microaerophilis in the colon

A

Lactobacillus, Streptococcus

199
Q

What are the metabolic effects of enteric bacteria on urea?

A

Acted on by urease to give ammonia, which can be absorbed or secreted as ammonium

200
Q

What are the metabolic effects of enteric bacteria on Bilirubin?

A

By reducteases to give stercobilinogen and urobilinogen

201
Q

What are the metabolic effects of enteric bacteria on primary bile acids?

A

By dehydroxylase to give secondary bile acids to be reabsorbed

202
Q

What are the metabolic effects of enteric bacteria on conjugated bile acids?

A

By deconjugases to give secondary bile acids

203
Q

What are the metabolic effects of enteric bacteria on fiber?

A

By glycosidases to give short chain fatty acids, H+, CO2, CO

204
Q

What are the metabolic effects of enteric bacteria on amino acids?

A

By decarboxylases and deaminases to give ammoniaand bicarbonate

205
Q

What are the metabolic effects of enteric bacteria on cysteine, methionine?

A

By sulfatases to give hydrogen sulfide, to be excreted in flatus

206
Q

What is the effects of antibiotics on the fut microflora?

A

Wide-spectrum antibiotics can disrupt the coloic miroflora

  • diminish levels of bacterial diversity
  • stereotypic declines
  • expansion of certain taxa
  • usually recovers but may have persistent consequences
207
Q

Name 2 antibiotics which have effect on the gut flora

A

Clyndamycin, ciproflaxin, clarithromycin, metronidazole

208
Q

What are the measures for benefit of the uninfected when gastroenteritis is detected?

A

Isolation of patients with C. dificile
Notify the local authority proper officer
- in cholera, bloody diarrhoea, food poisoning and haemolytic uraemic syndrome
Increase hygiene
Wash contaminated surfaces
Limit exposure up to 48 h of symptom relief
No public swimming for 2 weeks (cryptosporidiosis)

209
Q

What is the most common antibiotic used in adult acute bacterial gastroenteritis?

A

Ciprofloxacin 500 mg twice daily

210
Q

What is antibiotic of choice for gastroenteritis caused by Colstridium difficile?

A

Metronidazole 400 mg 3x day

211
Q

What is the special consideration when treating patient infected by E. coli O157:H7?

A

Antibiotic use may induce toxin production and increase risk for development of hemolytic-uremic syndrome

212
Q

What is hemolytic-uremic syndrome?

A

Triad of hemolytic anemia, acute kidney failure and low platelet count (thrombocytopenia)

P2 - Gastrointestinal system (5 decks)

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