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Gluten-sensitive enteropathy/small intestinal villous atrophy that resolves when gluten is withdrawn from the diet/inappropriate T cell-mediated immune response
2
Q
What are the risk factors for coeliac disease?
A
Female, relative with coeliac disease and HLA-DQ2
3
Q
What is α-gliadin?
A
Component of gluten which seems to be the most reactive
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
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
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
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
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
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
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
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
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)
13
Q
What is the management for coeliac disease/
A
Gluten-free diet
14
Q
What is the definition of diarrhoea?
A
3 or more loose or water stools per day
15
Q
Name the 3 pathogenic mechanisms of diarrhoea
A
Toxin mediated, damage to intestinal epithelial cells, invasion across intestinal epithelial barrier
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….
17
Q
Name the viruses that cause diarrhoea with the first one being the most common
A
Norovirus, sapovirus, rotavirus, adenovirus
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
19
Q
What is a common source of campylobacter?
A
Chicken
20
Q
What is the infecting dose and the incubation period of cambylobacter?
A
9 000 organisms, incubation period 3 days
21
Q
How does campylobacter cause diarrhoea?
A
Attaches and invades the intestinal epithelial cells, it is sensitive to stomach acidity
22
Q
What are the clinical features of campylobacter?
A
Frequent high volume diarrhoea, may be bloody;
Severe abdominal pain, nausea, fever
23
Q
What is the course of infection with campylobacter?
A
Self-limiting, about 7 days
24
Q
Describe the use of antibiotics in campylobacter infection
A
High rates of resistance and develop resistance on treatment, rarely indicated
25
What are the late complications of campylobacter
Reactive arthritis and Guilian-Barre syndrome
26
What is the main source of salmonella and how is it transmitted?
Chicken and reptiles, person to person infection
27
What is the infectious dose of salmonella and how is risk increased within the host?
10 000 organisms; increased risk with decreased stomach acid and diminished gut flora
28
What is mechanism of salmonella infection?
Invasion of enterocytes with subsequent inflammatory response; onset within 72 hours of ingestion
29
What are the symptoms of salmonella related diarrhoea?
Nausea, diarrhoea, abdominal cramps and fever
30
What are the complications of salmonella infection?
Secondary infection - endocarditis, osteomyelitis, mycotic aneurysm; and bacteraemia (bacteria in blood)
31
What is the use of antibiotics in salmonella?
Non-significant reduction in duration, self-limiting to 10 days and antibiotics are only given in severe disease
32
What is the pathogenesis of E.coli infection?
Attachment and production of shiga toxin that causes enterocyte death, bacteria also enters the systemic circulation
33
What is the infectious load and incubation period of E. coli?
10 organisms, sporadic outbreaks with incubation period 3 to 4 days
34
What are the symptoms of E. coli infection?
Bloody diarrhoea and abdominal tenderness
35
What is haemolytic uraemic syndrome caused by E.coli?
Systemic effect of shiga toxin, triad: microangiopathic haemolytic anaemia, acute renal failure, thrombocytopenia; 10% of patients, up to 5% mortality
36
What is the management or E. coli infection?
Supportive
37
How can E. coli infection be prevented?
Strict infection control for healthcare workers, screening of contacts, appropriate butchering of meat, public health measures in outbreaks
38
What are the risk factors associated with Clostridium difficile infection?
Antibiotic exposure, older age, hospitalisation
39
What is the pathogenesis of Clostridium difficile infection?
Decreased colonisation resistance, colonic colonisation leads to toxin production
40
What are the signs of Clostridium difficile infection?
Loose stools and colic, fever, leukocytosis, protein losing enteropathy
41
What is the diagnosis of Clostridium difficile?
Toxin detection by tissue culture assay and toxin detection by c. diff antigen
42
What is the treatment of diarrhoea in infection with Clostridium difficile?
Stop causative antibiotic if possible, Metronidazole/Vancomycin and recolonise with normal flora
43
What does norovirus causes?
Common epidemics of gastroenteritis
44
How is norovirus transmitted?
Faecal-oral route, difficult to disinfect
45
What are the clinical features of norovirus infection?
Acute explosive diarrhoea and vomiting, 24 to 48 hours, no lasting immunity
46
Name the symptoms of gastroenteritis
Vomiting, nausea, diarrhoea,
non-intestinal manifestations: botulism, Guillain-Barre syndrome
47
What is the onset of vomiting in gastroenteritis and what is vomiting associated with?
Sudden onset 6-12 hour of food ingestion, suggests pre-formed toxin for example - S aureus, B cereus or norovirus
48
Describe the typical diarrhoea caused within the small intestine
Large volume watery diarrhoea, cramps, bloating, wind, weight loss; fever and blood in stool are rare
49
Describe the typical diarrhoea caused within the large intestine
Frequent small volume, painful stool, fever and blood common
50
List the main investigations in diarrhoea
History, Faecal leukocytes/occult blood, stool examination/culture, endoscopy
51
What are the main points to ask in diarrhoea history
Food history, onset and nature of symptoms, residence, occupation, travel, pets/hobbies, recent hospitalisations/antibiotics, co-morbidity
52
What is occult blood and what causes in terms of diarrhoea?
Blood in the faeces that is not visibly apparent, bacterial cause
53
What presence of faecal leukocytes indicates and what are the tests characteristics in terms of diarrhoea?
Indicates colonic or inflammatory cause; poor sensitivity and specificity so not used clinically
54
What is done within stool culture?
Consider microscopy for ova and cysts, document a pathogen for public health implications and indications for treatment; low rate positive stool cultures
55
Why use endoscopy in diarrhoea?
If another than infectious cause suspected, can determine colitis
56
What are the main treatments for diarrhoea?
Oral rehydration solution, IV fluid replacement, antibiotics, symptomatic treatment
57
Name one oral rehydration solution
Dioralyte
58
Describe use of antibiotics in diarrhoea
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
59
Name antibiotics that are used to treat diarrhoea
Metronidazole (c diff), and quinolones like ciprofloxacin
60
Describe options for symptomatic treatment
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
61
Describe the water balance in normal physiology
Oral intake about 2 L, turnover of 9 L in small intestine, 150 ml to 2 L absorbed in large intestine; 100 ml excreted
62
Outline the role of small intestine in electrolyte balance
Secreted: Cl-, H20
Absorbed: Na+, Cl- and H20 (more than secreted)
Most water and nutrients absorbed
63
Outline the role of large intestine in electrolyte balance
Secreted: K+, HCO3-
Absorbed: larger quantities of those secreted
Conservation of water, electrolytes and short-chain fatty acids
64
What is the primary transport of absorption?
Active transport of sodium out on the basolateral pole of the cell by Na+/K+-ATPase
65
Describe the secondary transport of absorption
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
66
Name the main types of membrane transporters for absorption
ATP-driven pump, co-transporter/symporter, exchange carrier/antiporter, ion channel
67
Outline the role of sodium in nutrient absorption
Drives absorption of water, sodium gradient provides energy for active transport of many minerals, vitamins and metabolites
68
What are the main processes that lead to fluid and electrolyte loss?
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
69
What is the fluid circuit hypothesis?
Loss of fluid absorption capacity through damage, cell immaturity or challenge by bacterial and viral enterotoxins reverses net absorption to secretion
70
Identify the main electrolytes that may be lost through GI tract
Na+, Cl-, K+, HCO3-
71
Understand the mechanism of intestinal transport of glucose and apply this knowledge to treatment of dehydration
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
72
Understand the mechanism of intestinal secretion of chloride ion
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
73
How is CTFR/chloride channel activated by cAMP
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
74
What is the role of chloride ion secretion in the development of severe diarrhoea
Enterotoxins of Vibrio cholerae and Escherichia coli activate intracellular cAMP/PKA and activate CFTR on the apical plasma membrane leading to massive Cl- secretion
75
Describe the cycle of increased water secretions in the small intestine leading to diarrhoea
Fluid secretion --> more fluid in the lumen and more rapid propulsion ---> decreased absorption --> more fluid --> diarrhoea
76
Name the possible mechanisms of diarrhoea
Non-absorbable solutes, failure to digest or absorb nutrients, secretory agonists, inflammation
77
Name the 3 basic classifications of diarrhoea
Secretory diarrhoea, inflammatory diarrhoea and osmotic/malabsorptive
78
Describe the causes of secretory diarrhoea
Acute infections, failure of bile salt absorption, laxative abuse, carcinoid syndrome, Zollinger-Ellison syndrome
79
Describe the mechanism of secretory diarrhoea
Secreted: Na+, K+, Cl-, HCO3-
- decreased absorption and increased secretion, results in high volume faeces, bacteria destroy tight junctions and cause leakage of water
80
Describe the causes of inflammatory diarrhoea
Inflammatory bowel disease, Crohn disease, ulcerative colitis, infectious disease: Shigella, salmonella; irritable colon
81
What is the mechanism of inflammatory diarrhoea
Increased secretion and propulsive activity of the bowel, results in low volume excretion
82
Describe the causes of osmotic diarrhoea
Laxative, antacids, acarbose (alpha-glucosidase inhibitor), orlistat (lipase inhibitor), digestive enzymes deficiencies, inflammatory disease, short bowel syndrome
83
Describe the mechanism of osmotic diarrhoea
Decreased intestinal absorption, results in high volume faeces
84
Describe the importance of child diarrhoea in terms of public health
Major cause of child deaths worldwide
85
What is bloody diarrhoea?
Intestinal damage and nutrient loss, commonly caused by Shigella
86
What is persistent diarrhoea?
More than 14 days, happens in undernourished children, often with other diseases
87
What is the treatment for children's diarrhoea?
Fluid replacement, zinc supplements, continue feeding
88
What are the most common causes of child diarrhoea?
Unsafe water, poor sanitation, poor hygiene
89
What are the public health interventions to prevent child diarrhoea
Rotavirus and measles vaccinations, early breastfeeding and vit A supplements, hand washing with soap, improved water quality, community-wide sanitation promotion
90
Understand the role of osmolality changes in determining water movement between intracellular and extracellular fluid
- 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
How is osmolality relevant to treatment of fluid and electrolyte disorders
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
What is the osmolality of standard ORS vs reduced osmolality ORS solution?
```
Standards = 311 mmol/l
Reduced = 251 mmol/l
```
93
What is normal blood osmolality?
275–295 mmol/kg
94
What are the main types of intravenous fluids
Blood products, colloids, crystalloids, saline, dextrose, lactate-containing intravenous fluids
95
Describe properties of colloids
Large molecular; albumin, hydroxyethyl starch, haemocoel
96
Describe properties of crystalloids
Water plus electrolytes --> sodium chloride, sodium lactate, potassium chloride, and calcium chloride in water: Saline, dextrose, ringer-lactate, Hartmann's
97
Give an example of hypoosmotic solution
Saline 0.45%
98
Give an example of hyperosmotic solution
Sodium bicarbonate 8,4%
99
Give an example of isosmotic solution
Saline 0.9% or dextrose 5%
100
What is the caloric value of 5% dextrose solution?
5 g/100 ml
101
Describe properties of lactate-containing intravenous fluids
Bicarbonate is produced during lactate metabolism, normal saline may contribute to metabolic acidosis, but ringer-lactate may increase cerebral oedema
102
What factors determine the rate of fluid replacement
Age, cardiovascular status, renal function, severity of existing dehydration, time it took to develop
103
What is the regime of emergency re-hydration
500 ml bag each 2 hours
104
What is the standard regimen of rehydration?
500 mL bag every 6 hours - 2 L in 24 hours
105
What is the slow rehydration regimen?
500 mL bag every 8 hours - 1.5 L in 24 hours
106
What are the principles of safe potassium replacement?
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
When do you use cardiac monitoring in terms of potassium supplementation?
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
What are the cardiac effects of hypokalaemia?
ST depression.
T wave inversion.
Prominent U waves.
Long QU interval.
109
Describe the systemic approach to the assessment of a patient with suspected fluid/electrolyte disorder
Assess the clinical state --> assess intake/output --> electrolyte shifts --> replace --> daily need, anticipate loss, previous deficit
110
What are the measurements needed in suspected fluid/electrolyte disorder
Electrolyte profile, blood gases, glucose, albumin, urea, creatinine, plasma osmolality
111
Define cholecystitis
Inflammation of gallbladder
112
Define cholelithiasis
Gallstone within gallbladder
113
Define cholecystectomy
Removal of gallbladder
114
Define choledocholithiasis
Gallstone within bile duct
115
What is MRCP
MRI cholangiopancreatography
116
What is ERCP
Endoscopic retrograde cholangionpancreatography
117
What is PTC
Percutaneous transhepatic cholangiography
118
Describe the biliary tree
Biliary canaliculi -> interlobular bile ducts -> septal bile ducts -> intrahepatic ducts -> R/L hepatic duct -> common hepatic duct -> common bile duct
119
Describe the function of the gallbladder and what is its bile capacity
Concentrates bile by absorbing H20 and salts; 30 to 50 ml surface
120
Describe the anatomical relations of the gallbladder
Lies in GB fossa on inferior surface of right liver lobe and is connected to common bile duct by cystic duct
121
What are the 3 anatomical regions of the gallbladder and what is its epithelium?
Fundus, body and neck (connects to duct)
| Columnar epithelial lining
122
What is Hartmann's pouch and where it is?
Lies on the inferior side of gallbladder on the junction between body and neck; may be a site of gallstone impact
123
What is Calot's triangle?
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
What are the components of bile?
Bile acids, water, electrolytes, cholesterol, phospholipids, conjugated bilirubin
125
Describe bile acid synthesis
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
How are secondary bile salts produced?
By action of intestinal bacteria de-hydroxylation,
127
How much of bile acids is reabsorbed and where?
95% of bile acids
| Reabsorbed mainly in the ileum/terminal ileum by active transport
128
How do the bile acids travel back to liver?
Bound to albumin
129
Outline the regulation of gallbladder contraction
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
What are the 3 main types of gallstones?
Cholesterol stone, bile pigment stone, mixed stones
131
Describe cholesterol stone
Usually solitary, oval and large
132
Describe bile pigment stones
Multiple, irregular, hard, associated with chronic haemolysis
133
What are the risk factors for gallstones
5 F's - female, fair, fertility, forty and fat; + inflammatory bowel disease and fam history
134
Name the 3 main events that lead to gallstone formation
Cholesterol supersaturation, biliary stasis, increased secretion of bilirubin
135
What is cholesterol supersaturation?
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
What is biliary stasis?
Occurs during periods of fasting and starvation, observed during prolonged total parenteral nutrition
137
How does increased secretion of bilirubin lead to gallstones?
Increased RBC breakdown - esp. haematological conditions, malaria, valvular heart disease, post chemo
- failure of hepatic conjugation
138
What are the causes of obstructive jaundice?
Common: choledocholithiasis, pancreatic cancers - head of pancreas compressing CBD
Less common:
Pancreatitis - swelling compressing
Cholengiocarcinoma, portal lymphadenopathy, benign bile duct stricture
139
Outline pancreatic cancer
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
What are the LFTs like in obstructive jaundice?
```
ALP increased up to 10x
GGT rise - often
Bilirubin - steadily increases
AST/ALT - can be elevated but little
in prolonged - coagulopathy
```
141
Name the general characteristics of the large intestine
Large internal diameter, omental appendices/epiploic appendages, taenia coli, haustra of the colon
142
What is cecum?
Beginning of large intestine in the right groin, changes into ascending colon at the ileocecal opening, contains the appendix
143
Describe the appendix
Narrow, blind ended tube with large aggregations of lymphoid tissue in its walls
Suspended from the terminal by the mesoappendix
144
How can you identify the origin of appendix and what are its possible locations?
The taenia coli lead towards the base of appendix
| Retrocecal, paracecal, subcecal, pelvic, subileal, postileal, preileal
145
Is the colon peritoneal structure and what holds it in place?
Yes, intraperitoneal; suspended by mesentery
146
What is the cecal blood supply and what is its origin?
Anterior and posterior cecal artery from the ileocolic a, appendicular artery
All from superior mesenteric artery
147
What is the venous drainage of the cecum?
Ileocolic vein and appendicular vein
148
What are the potential spaces between the colon and the abdominal wall laterally called?
Left and right paracolic gutters
149
As ascending colon bends below the liver it forms ___ ___/__ __ __.
Right hepatic flexure or just hepatic flexure
150
What is the supply of the ascending colon?
The marginal artery which is supplied by right colic artery and ileocolic artery; both of which originate in the superior mesenteric artery
151
What is the venous drainage of the ascending colon?
Right colic and ileocolic veins drain to the superior mesenteric
152
Which parts of the colon are intraperitoneal?
The transverse colon; ascending and descending are retroperitoneal
153
The tranverse colong bends below the spleen downwards forming __ __/__ __ __.
Left colic flexure or splenic flexure
154
To what and by what is the transverse colon attached?
To diaphragm by phrenico-colic ligament
155
What is the arterial supply of the transverse colon?
Marginal artery supplied by right colic and middle colic from sup mesenteric, and left colic from inferior mesenteric
156
How is the transverse colon drained?
By middle colic vein to sup mesenteric vein
157
What is the blood supply and drainage of descending colon?
Left colic artery feeding into marginal, from inferior mes a
| Left colic vein
158
What is the sigmoid mesocolon?
Structure that suspends the sigmoid colon
159
What defines the pelvic inlet?
1. superior margin of pubic symphysis
2. pubic crest
3. Iliopectineal line
4. Anterior border of ala sacrum
5. Sacral promontory
160
What is the blood supply and drainage of sigmoid colon?
Sigmoid arteries and vein, both into the inferior mesenteric vessels
161
What is mesentery?
Double layer of visceral peritoneum that attaches its associated structure to the posterior abdominal wall
162
The rectum and sigmoid colon are joined by ___.
Rectosigmoid junction
163
What is the arterial blood supply to the rectum and anal canal?
Superior rectal artery (from inferior mes)
Middle rectal artery (from internal iliac)
Inferior rectal a (from internal pudendal a)
164
Name the nerves innervating the large intestine
Pelvis nerves, vagal input and enteric nervous system, pudendal nerves
165
Which nerves control the external anal sphincter?
Pudendal
166
Which nerves control the inner anal sphincter?
Vagal and enteric nervous system
167
What is characteristic of the mucosa of colon?
Crypts of Lieberkühn
168
What are the epithelia of the large intestine?
Surface simple columnar epithelium and glandular epithelium in the crypts
169
Name the cell types of the glandular epithelium
Enterocytes, goblet cells, stem cells, enteroendocrine cells, paneth cells (only in cecum)
170
Describe the cells of the surface simple columnar epithelium
Absorptive enterocytes - have short apical microvilli, controlled by aldosterone
Goblet cells - secrete mucous to form protective barrier
171
What is contained within the muscularis mucosae?
Isolated lymphoid follicles that penetrate to submucosa
172
Describe the muscularis of the large intestine
Bundles of longitudinal muscle fuse to form the taeniae coli - 3 ribbon like structure
Inner layer of circular muscle
173
How is the rectum divided?
Upper part - rectum proper
| Lower part - anal canal which is further divided by pectinate line into upper and lower
174
Describe the features above the pectinate line
8 - 10 longitudinal anal columns connected by valves at their bases
Sinuses behind the valves and anal mucous glands open into each sinus
175
Describe the epithelial transformation zone in the anal canal
At the level of the pectinate line
| Change of epithelium from simple columnar to stratified squamous epithelium with sebaceous and sweat glands
176
Where and how is the internal anal sphincter formed?
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
Describe the external anal sphincter
Skeletal muscle, and supported by the levator ani muscle
178
How does the anal canal end?
With the anal orifice
179
What are the functions of the large intestine?
Digestion and absorption
Reabsorption of remaining fluid
Faeces storage
Vitamins K, B1, B2, B6, B12 and biotin
180
What is the gastrocolic reflex?
Long arc reflex activated by stomach filling to increase the gut motility resulting in colon emptying
181
How is the gastrocolic reflex regulated?
By chemosensitive and mechanosensitive components; by release of 5-HT and acetylcholine
182
What is the orthocolic reflex?
Activated on rising from bed, promotes morning urge to defecate
183
How are the local colonic reflexes regulated?
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
What bioactive peptides are released to control colonic motility and by what cells?
Enterochromaffin cells - 5HT
| Enteroendocrine cells - peptide YY
185
Why is peptide YY released and what are its effects?
Released in response to lipid in the ileum and colon, decreases gastric emptying and intestinal propulsive motility, reduces Cl- and thus fluid secretion
186
Name the 3 patterns of colonic motility
Short-duration contractions, long-duration contractions and high-amplitude propagating contraction
187
What is the role of short-duration contractions?
Mixing by circular muscle, stationary pressure waves lasting for about 8 seconds
188
What is the role of long-duration contractions?
By taeniae coli, last from 20 to 60 seconds, may propagate over short distancs
189
What is the role of high-amplitude propagating contractions?
Results of both local influences and long reflex arcs, 10 times per day, wave along the whole colon, only in aboral direction
190
Describe the process of defacation
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
Outline the normal microflora of the gut
Commensal bacteria or enteric bacterial ecosystem
Symbiotic relationship established after birth
In large intestine and bit in distal small intestine
192
Name the functions of commensal bacteria
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
Describe how is useful fermentatin by commensal bacteria
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
What are the main short chain fatty acids produced by fermentation by the commensal bacteria?
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
What are the main bacterial types in the colon?
99. 9% anaerobes
- non-sporing
- Sporing
- Sporing aerobes
- Micriaerophilis
196
Give example of Non-sporing anaerobes in the colon
Bacteriodes spp, Bifido bacterium spp, eubacterium spp
197
Give example of sporing anaerobes
Clostridium spp
198
Give example of microaerophilis in the colon
Lactobacillus, Streptococcus
199
What are the metabolic effects of enteric bacteria on urea?
Acted on by urease to give ammonia, which can be absorbed or secreted as ammonium
200
What are the metabolic effects of enteric bacteria on Bilirubin?
By reducteases to give stercobilinogen and urobilinogen
201
What are the metabolic effects of enteric bacteria on primary bile acids?
By dehydroxylase to give secondary bile acids to be reabsorbed
202
What are the metabolic effects of enteric bacteria on conjugated bile acids?
By deconjugases to give secondary bile acids
203
What are the metabolic effects of enteric bacteria on fiber?
By glycosidases to give short chain fatty acids, H+, CO2, CO
204
What are the metabolic effects of enteric bacteria on amino acids?
By decarboxylases and deaminases to give ammoniaand bicarbonate
205
What are the metabolic effects of enteric bacteria on cysteine, methionine?
By sulfatases to give hydrogen sulfide, to be excreted in flatus
206
What is the effects of antibiotics on the fut microflora?
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
Name 2 antibiotics which have effect on the gut flora
Clyndamycin, ciproflaxin, clarithromycin, metronidazole
208
What are the measures for benefit of the uninfected when gastroenteritis is detected?
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
What is the most common antibiotic used in adult acute bacterial gastroenteritis?
Ciprofloxacin 500 mg twice daily
210
What is antibiotic of choice for gastroenteritis caused by Colstridium difficile?
Metronidazole 400 mg 3x day
211
What is the special consideration when treating patient infected by E. coli O157:H7?
Antibiotic use may induce toxin production and increase risk for development of hemolytic-uremic syndrome
212
What is hemolytic-uremic syndrome?
Triad of hemolytic anemia, acute kidney failure and low platelet count (thrombocytopenia)
