Intestines Flashcards
1
Q
Into where does the stomach empty chyme?
A
The duodenum
2
Q
What happens to chyme in the duodenum?
A
It is conditioned
3
Q
What features of chyme are modified in conditioning?
A
- Acidic
- Hypertonic
- Partly digested
4
Q
How is the acidity of chyme modified in conditioning?
A
It is corrected by HCO3-
5
Q
Where does the HCO3- used to correct the acidic nature of chyme in conditioning come from?
A
Secreted from the pancreas, liver, and duodenal mucosa
6
Q
When is the HCO3- used to correct the acidity of chyme in conditioning produced?
A
During the production of gastric acid
7
Q
How is hypertonicity of chyme modified in conditioning?
A
Corrected by the osmotic movement of water into the duodenum across its wall
8
Q
How is the partly digested nature of chyme modified in conditioning?
A
Digestion is completed by enzymes
9
Q
Where do the enzymes used to finish digestion of chyme in conditioning come from?
A
The pancreas and duodenal mucosa
10
Q
Other than enzymes, what is required from the completion of digestion of chyme in conditioning?
A
Bile acids from the liver
11
Q
What conditions does absorption require?
A
A large surface area, to which the luminal contents of the small intestine needs to be exposed to through gentle agitation for hours
12
Q
How is the surface area of the small intestine maximised?
A
- Very long
- Increased by millions of villi projecting into the lumen
13
Q
How do epithelial cells (enterocytes) arise?
A
By rapid division in the crypts between the villi, and migration towards the tips
14
Q
What happens to enterocytes at the tips of the villi?
A
They are shed
15
Q
What happens to newly formed enterocytes as they migrate to the tip?
A
They mature
16
Q
What covers the luminal surface of the enterocytes?
A
Microvilli
17
Q
What is the purpose of the microvilli present on the enterocytes?
A
- Further increase surface area
- Form the brush border
18
Q
What does the brush border form?
A
An ‘unstirred layer’
19
Q
What happens at the unstirred layer?
A
Nutrients meet and react with enzymes secreted by the enterocytes, completing digestion prior to absorption
20
Q
Label this diagram
A
- A - Muscle layers
- B - Villi
- C - Hepatic portal vein
- D - Lumen
- E - Capillary bed
- F - Lacteal
- G - Microvilli
- H - Villi
21
Q
What is the function of the large intestines?
A
Absorb water from the indigestible residues of chyme
22
Q
What do the large intestines do to the indigestible residues of chyme?
A
Convert them into semi-solid stool or faeces
23
Q
What happens to the faeces formed by the large intestines?
A
It is stored temporarily and allowed to accumulate until defecation occurs
24
Q
What are teniae coli?
A
The thickened bands of smooth muscle of the large intestines
25
What do the teniae coli constitute?
Most of the longitudinal coat of the large intestines
26
Where do the teniae coli run?
The length of the large intestine
27
What is the effect of the teniae coli on the part of the wall they are associated with?
They shorten it
28
Why do the teniae coli shorten the part of the wall they are associated with?
Because of their tonic contraction
29
What does the shortening of the wall due to teniae coli form?
Haustra
30
What are haustra?
Where the colon becomes sacculated, or 'baggy', between the teniae
31
Label this diagram
* A - Right colic (hepatic) flexure
* B - Transverse colon
* C - Superior mesenteric artery
* D - Haustrum
* E - Ascending colon
* F - Ileum
* G - Ileocecal valve
* H - Cecum
* I - Vermiform appendix
* J - Rectum
* K - Anal canal
* L - External anal sphincter
* M - Sigmoid colon
* N - Tenia coli
* O - Cut edge of mesentery
* P - Descending colon
* Q - Epiploic appendages
* R - Transverse mesocolon
* S - Left colic (splenic) flexure
32
What are the sections of the small intestine?
* Duodenum
* Jejenum
* Ileum
33
What functions are common between all sections of the small intestine?
* Secrete protease and carbohydrase enzymes to complete digestion
* Secrete hormones
34
What hormones are secreted by all sections of the small intestine?
* Secretin
* Gastrin
* Cholecystokinin
35
What are the functions of the duodenum?
* Addition of bile and pancreatic secretions
* Secretes HCO3- to neutralise chyme
* Osmotic movement of water into the duodenum, making chyme more hypotonic
* Absorption
36
Where in the duodenum are bile and pancreatic secretions added?
Ampulla of Vater
37
What is absorbed in the duodenum?
Iron
38
What are the functions of the jejunum?
* Absorption
* Uptake of things small enough to soak through the villi
39
What is absorbed in the jejenum?
* Carbohydrates
* Amino acids
40
What substances are small enough to soak through the villi?
* Fatty acids
* Vitamins
* Minerals
* Electrolytes
* Water
41
What is the function of the ileum?
Absorption
42
What is absorbed by the ileum?
* Vitamin B12
* Bile
* Anything not absorbed by the jejenum
43
Label this diagram
* A - Duodenum
* B - Ileocecal junction
* C - Cecum
* D - Appendix
* E - Duodenojejunal junction
1. Jejunum
2. Ileum
44
How long does the large intestine take to finish the digestion of food?
About 16 hours
45
What are the functions of the large intestine?
* Absorption
* Sends indigestible matter to the rectum
46
What does the large intestine absorb?
* Water
* Any remaining absorbable nutrients
* Vitamins created by colonic bacteria
47
What vitamins are created by colonic bacteria?
* Vitamin K
* B12
* Thiamine
* Riboflavin
48
What is the function of the rectum?
Stores and compacts faecal matter
49
In what form are carbohydrates ingested in the small intestime?
In the form of amyloses, amylopectins, or dissacharides *such as sucrose*
50
What is the structure of amylose?
Straight chain with α-1,4 bonds
51
What is the structure of amylopectin?
Branched, with α-1,6 bonds at branches
52
What do α-amylases act on?
α-1,4 bonds
53
Where are α-amylases secreted?
* In saliva
* By pancreas
54
What do α-amylases yield?
* Glucose and maltose from amyloses
* α-limit dextrins from amylopectins
55
What completes the breakdown of glucose?
Brush border enzymes
56
What enzymes are found in the brush border?
* Isomaltase
* Maltase
* Sucrase
* Lactase
57
What does isomaltase do?
Breaks down branched molecules at α-1,6 bonds
58
What does maltase do?
Converts maltose to glucose
59
What does sucrase do?
Converts sucrose to glucose and fructose diamer
60
What does lactase do?
Converts lactose to glucose and galactose diamer
61
Where does the energy from the active absorption of glucose come from?
The Na+ gradient set up by Na/K/ATPase in the basolateral membrane
62
Where does glucose enter the epithelial cell?
Across its apical membrane
63
What transport is required to move glucose across the epithelial apical membrane?
Na+/Glucose Symporter, **SGLT1**
64
Other than glucose, what does SGLT1 transport?
Galactose
65
Where does glucose leave the epithelial cell into the bloodstream?
Across the basolateral membrane
66
How does glucose leave the epithelial cell across the basolateral membrane?
Via facilitated diffusion through the **GLUT2** transporter
67
How does fructose enter the epithelial cell from the lumen?
Via facilitated diffusion
68
What are proteins digested to?
Oligopeptides
69
What is an oligopeptide?
Short peptides, 10-20 AA's long
70
Where are proteins first digested?
In the stomach
71
What digests proteins in the stomach?
Pepsin
72
What secretes pepsin in the stomach?
Chief cells
73
What enzymes digest proteins in the duodenum?
Peptidases
74
What secretes the peptidases in the duodenum?
The pancreas
75
How do different peptidases vary?
They 'prefer' breaking different bonds
76
What peptidases are present in the duodenum?
* Pepsin
* Trypsin
* Chymotrypsin
* Carboxypeptidase
77
What bonds does pepsin prefer to break?
Bonds near aromatic AA side chains
78
What bonds does trypsin prefer to break?
Bonds near basic AA side chains
79
What bonds does chymotrypsin prefer to break?
Bonds near aromatic AA side chains
80
What bonds does carboxypeptidase prefer to break?
C-terminal AA's with basic side chains
81
In what form can proteins be absorbed by the small intestine?
Both amino acids and small peptides *(2/3 AA's)*
82
How does absorption of proteins by the small intestine differ in neonates?
In neonates, the gut is 'open', so in addition to amino acids and small proteins, they are able to pick up whole proteins
83
What is the clinical importance of the 'open' gut in neonates?
It allows breast milk to confer passive immunity on babies via IgA absorption
84
What transporter is required for the active uptake of amino acids?
Na+/Amino acid co-transporters
85
How many types of Na+/Amino acid co-transporters are there?
At least 5
86
How do Na+/Amino acid transporters get the energy required for the active uptake of amino acids?
Using the Na+ gradient set up by Na/K/ATPase
87
Give 5 types of Na+/Amino acid co-transporters
Those that take up -
* Small, neutral AA's
* Neutral AA's, basic AA's, and cysteine
* Acidic AA's
* Imuno-AA's
* ß AA's *(mainly taurine)*
88
What facilitates some AA uptake?
Passive diffusion
89
How are dipeptides and tripeptides taken up?
By an active mechanism associated with pumping H+ into the lumen, which then returns by co-transport with the peptide
90
What is the result of fats being relatively insoluble in water?
They tend to aggregate into large globules
91
What is the result of fats tending to aggregate into large globules?
It prevents effective action of digestive enzymes
92
What excerbates the aggregation of fat into large globules?
Acid in the stomach
93
What happens to fats in the duodenum?
They are incorporated into micelles
94
What allows fats to be incorporated into micelles in the duodenum?
Bile acids
95
How big are the micelles formed by fats and bile acids in the duodenum?
4-6nm
96
Describe the structure of the fat micelles formed in the duodenum?
Fats in the middle and polar components of bile acids on the outside
97
What is the function of the fat micelles?
* Generate a high surface area for the action of lipases
* Carry products into the 'unstirred layer'
98
What is the effect of lipases on the fat micelles?
They cleave the fatty acids from glycerol
99
Where is the 'unstirred layer' located?
Immediately next to the mucosa
100
What happens to micelles in the unstirred layer?
Fatty acids can be released to slowly diffuse into the epithelial cells
101
What happens to the fatty acids from micelles once inside epithelial cells?
They are reconstituted into triacylglycerols and re-expelled as chylomicrons
102
What are chylomicrons?
Structured small particles
103
What are chylomicrons made up of?
Lipids covered in phospholipids
104
What do chylomicrons do?
Facilitate the transport of fat in the lymphatic system from the gut to systemic veins
105
How is sodium taken up by the small intestine?
Via diffusion into the cell, and actively transported across the basolateral membrane by Na-K-ATPase
106
What is the importance of sodium uptake by the small intestine?
It provides the driving force for the majority of absorption
107
What ion follows the movement of Na+?
Chloride
108
What does the movement of Na+ and Cl-, coupled with all of absorption, give?
An osmotic gradient
109
What does the osmotic gradient in the small intestine do?
Leads to the uptake of water
110
What minerals are taken up by the small intestine?
* Calcium
* Iron
* Vitamins
111
How much calcium is absorbed from the small intestine each day, compared to how much is consumed?
700mg/day absorbed out of 6g consumed - *\>10%*
112
How does Ca2+ enter the epithelial cell?
Facilitated diffusion
113
What allows Ca2+ to be taken up into the small intestinal epithelial cell by facilitated diffusion?
There is a low intracellular concentration
114
How is Ca2+ pumped out of the basolateral membrane?
By Ca2+-ATPase
115
What does both the facilitated diffusion of calcium and transport through the basolateral membrane require?
Vitamin D
116
What is the uptake of calcium by the small intestine stimulated by?
Parathyroid hormone (PTH)
117
How much iron is consumed per day?
20mg
118
What constitutes most of the iron consumed?
Haem
119
In what form can iron be absorbed?
Only its ferrous form **(Fe2+)**
120
How is iron made into its ferrous form?
Gastric acid solubises iron complexes, making them ferrous
121
What happens to ferrous iron once it has been formed in the stomach?
Gastroferrin binds iron and keeps it ferrous
122
What secretes gastroferrin?
The stomach
123
What secretes transferrin?
Intestinal mucosal cells
124
What does transferrin do?
Finds ferrous ions in the lumen
125
What happens once transferrin has found ferrous iron in the lumen?
The complex is taken into cells by endocytosis, spplit, and the iron is exported to the blood
126
What happens once the iron split from transferrin is exported to the blood?
It binds again to transferrin
127
How are water-soluble vitamins absorbed in the small intestine?
Via passive diffusion
128
What vitamins are water soluble?
* Vitamin C
* B vitamins
129
What is vitamin B12 absorbed with?
A co-factor
130
Where is vitamin B12 absorbed?
In the terminal ileum only
131
When does the intrinsic factor bind to vitamin B12?
In the stomach
132
What is the purpose of the intrinsic factor binding to vitamin B12?
To keep in soluble
133
What secretes the intrinsic factor that binds to vitamin B12?
The stomach mucosa
134
What occurs with vitamin B12 deficiency?
Pernicious anaemia
135
What causes pernicious anaemia?
Damage to the stomach, preventing it from secreting the intrinsic factor, or when the terminal ileum has been damaged or removed
136
When may the terminal ileum be damaged?
Crohn's
137
How is the uptake of Na+ related to the uptake of water?
It generates an osmotic gradient, which water follows
138
What does glucose uptake do?
* Stimulates Na+ uptake
* Generates its own osmotic gradient
139
What will stimulate maximum water uptake?
A mixture of glucose and NaCl
140
What is the mixture of glucose and NaCl known as?
Oral rehydration fluid
141
What must happen to the intestinal contents for effective absorption?
It must move very slowly *(transit time in hours)*, whilst being gently agitated
142
How is the slow movement and agitation of intestinal contents achieved?
By a pattern of motility called segmenting
143
Are segmenting and perilstalsis the same thing?
No, they are very different
144
How is the small intestine divided?
Into sections
145
What does each section of the small intestine have?
A pacemaker
146
How does the frequency of the pacemaker change through the small intestine?
It gets less from the duodenum to the terminal ileum *(12 times a minute to 8)*
147
What is the decrease in pacemaker frequency phenomenom known as?
The intestinal gradient
148
What does each pacemaker drive?
A small section of intestine
149
What does the pacemaker driving of the section of small intestine cause?
Intermitted contraction of the smooth muscle along its length
150
What is the result of the intermittent smooth muscle contraction caused by the pacemaker?
It seperates the intestine into segments where the muscle is not contracted
151
What happens to the intestinal contents at each segment?
It is effectively mixed by movement from the portions that do contract
152
What happens after a few seconds of contraction of a segment?
The contractions relax, and the next pacemaker fires to make different areas contract
153
What is the purpose of segmenting?
Mixes the contents of the intestine
## Footnote
*Segmenting itself does not proper contents*
154
What does the intestinal gradient result in?
## Footnote
*In terms of movement*
There is a net movement, albeit slow, in a caudal direction
155
What is the large intestine naturally divided into?
Segments known as Haustra
156
How are Haustra formed?
The circular muscles are more complete than the longitudinal, which have been reduced to taenia coli
157
Describe the structure of taenia coli
* Thick circular muscle
* Thin longitudinal muscle
* Only 3 layers
158
What is the effect of contraction of hte smooth muscle in the walls of the Haustra?
It shuffles the contents back and forth
159
What happens as the intestinal contents is being shuffled back and forth by the Haustra?
There is slow absorption of the remaining water and salts, forming faeces
160
Where does the intestinal contents progress too from the Haustra?
The sigmoid colon
161
How is Haustral shuffling controlled?
Segmenting like control
162
What happens in mass movement of the colon?
Once or twice a day, there is a perilstaltic propelling pattern from the transverse through to the descending colon
163
What is the result of mass movement?
It forces faeces rapidly into the rectum
164
What happens when faeces is forced into the rectum?
It induces the urge to defecate
165
Why does faeces being forced into the rectum induce the urge to defecate?
Because the rectum is normally empty
166
What is mass movement often triggered by?
The gastro-colic reflex, *triggered by eating*
167
Does mass movement occur at certain times of the day?
Often does, *because people 'like to be regular'*
168
How many anal sphincters are there?
Two, *internal and external*
169
What kind of muscle is present in the internal anal sphincters?
Smooth
170
What control is the internal anal sphincter under?
Parasympathetic
171
What happens to the internal anal sphincter when it recieves parasymphathetic stimulation?
It relaxes
172
What kind of muscle is present in the external anal sphincter?
Voluntary striated muscle
173
What control is the external anal sphincter under?
Voluntary *(normally)*
174
What happens once both anal sphincrers are relaxed?
Intra-abdominal pressure is increased, forcing expiration
175
What is the result of the increase in intra-abdominal pressure caused by the relaxation of the internal and external anal sphincters?
There is an expulsion of faeces
176
When is the voluntary control of the external sphincter overriden?
If rectal pressure becomes too high
177
What are the types of inflammatory bowel disease?
* Ulcerative colitis
* Crohn's disease
* Diversion Colitis
* Diverticular colitis
* Radiation
* Drugs
* Infections
* Ischaemic colitis
178
What is ulcerative colitis?
An inflammatory disorder
179
Where does ulcerative colitis affect?
The rectum, and extends proximally in continuity to affect a variable extent of the colon
180
What is meant by UC extending in continuity?
There are no breaks in the inflammation
181
Where is there a high incidence of UC?
* US, UK and northen Europe
* Young adults
* More commonly in females
182
What is the mucosa of UC patients dominated by?
Th2 (T-helper) cells
183
What do Th2 cells produce?
* Transforming Growth Factor (TGF)
* IL-5
184
How does ulcerative colitis present?
* Rectal bleeding
* Diarrheoa
* Abdominal pain
185
Where does extensive colitis affect?
Entire colon and rectum
186
What is extensive colitis also known as?
Pancolitis or total colitis
187
What is affected in distal colitis?
* Rectum
* Sigmod colon
* Descending colon
188
What is affected in proctitis?
Rectum only
189
What is Crohn's disease?
A condition of chronic inflammation
190
Where does Crohn's Disease affect?
Potentially any location of the GI tract from mouth to anus
191
When does CD have the highest incidence?
Two peaks-
* 15-30 years
* 60 years
192
What is the mucosa of CD patients dominated by?
Th1 (T-helper) cells
193
What do Th1 cells produce?
* Interferon Gamma (IFN-γ)
* IL2
194
What does the presentation of CD depend on?
The diseases location
195
What is the presentation of CD with upper GI involvement?
* Nausea and vomiting
* Dyspepsia
* Small bowel obstruction
* Anorexia
* Weight loss
* Loose stools
196
What is the presentation of CD when its a colonic disease?
* Diarrhoea
* Passage of obvious blood
197
What may occur when there is termianal ileum involvement in CD?
Anaemia
198
Why may terminal ileum involvement in CD cause anaemia?
Because of poor absorption of vitamin B12
199
What causes inflammatory bowel disease?
* May have genetic predisposition
* Environmental factors
200
What genes may give genetic predisposition to inflammatory bowel disease?
* IBD1
* NOD2/CARD15
201
By how much does having one copy of a risk allele increase the risk of Crohns?
2-4x
202
By how much does having two copies of a risk allele increase the risk of Crohn's?
20-40x
203
What environmental factors may increase the risk of inflammatory bowel disease?
* NSAIDs
* Early appendectomy
* Smoking
204
Why does NSAIDs increase the risk of IBD?
May be the altered intestinal barrier
205
What is an early appendectomy linked to?
Increased UC incidence
206
What is the effect of smoking on the risk of IBD?
* Protects against UC
* Increases risk of CD
207
What are the triggers for inflammatory bowel disease?
* Antibiotics
* Diet
* Acute infections
* NSAIDs
* Smoking
* Stress
208
How deep is the inflammation in UC?
Mucosal
209
How deep is the inflammation in CD?
Transmural
210
What is the difference in the pattern of disease between UC and CD?
In UC it is continuous. In CD, it may skip area
211
What is the location of UC?
Colorectum
212
What is the location of CD?
Mouth to anus
213
Is there rectal involvement in UC?
Usually
214
Is there rectal involvement in CD?
Can be, *but less common than in UC*
215
What kind of ileal disease is sometimes present with UC?
Backwash ileitis
216
What % of UC patients also have backwash ileitis?
15-20%
217
Does Crohn's disease present with ileal disease?
Yes, it is common
218
Does UC cause fistulas?
Rarely
219
Does CD cause fistulas?
Commonly
220
Does UC cause perianal disease?
Rarely
221
Does CD cause perianal disease?
Commonly
222
Does UC cause granulomas?
Unlikely
223
Does CD cause granulomas?
Yes, *in 50-60% of patients*
224
Does UC cause overt bleeding?
It is unusual
225
Does CD cause overt bleeding?
It is less common
226
Does UC cause malnutrition?
It is unlikely
227
Does CD cause malnutrition?
It is more common
228
What cancer risk does UC confer?
Colorectal cancer
229
What cancer risk does CD confer?
Colorectal cancer or small bowel cancer, *depending on location*
230
What will be seen on a radiograph in UC?
Collar button ulcers
231
What will be seen on a radiograph in CD?
String sign of Kantor
232
What methods are commonly used for investigating inflammatory bowel disease?
* Colonoscopy
* Stool analysis
* Barium radiographs
* CT scan
* Capsule endoscopy
* Plain X-ray
233
How is a colonoscopy used to investigate IBD?
* Biopsies of involved mucosa
* Ulceration
234
What will be looked for in stool analysis?
* Parasites
* Clostridium difficile toxin
235
How is a stool analysis conducted?
Using a culture
236
When will a plain X-ray be used to investigate IBD?
If bowel obstruction or perforation suspected
237
What is this image showing?
Crohn's disease
238
What macroscopic changes will be seen in CD?
* Involved bowel usually thickened, often narrowed
* Deep ulcers and fissures in mucosa may produce **cobblestone apperance**
* Fistulae and abscesses may be seen
239
What does the presence of fistulae and abscesses in CD reflect?
Penetrating disease
240
What macroscopic changes will be seen with UC?
* Mucosa looks reddened, inflamed and bleeds easily
* In severe disease, there is extensive ulceration with the adjacent mucosa appearing as inflammatory (pseudo) polyps
241
What microscopic changes will be seen with CD?
* Inflammation through all layers of the bowel *(transmural)*
* Increase in chronic inflammatory cells
* Lymphoid hyperplasia
* Granulomas
242
Why can you see granulomas microscopically with CD?
TH1 response
243
What microscopic changes will be seen with UC?
* Superficial inflamamtion
* Chronic inflammatory cells infiltrate in the lamina propria
* Crypt abscesses
* Goblet cell depletion
244
How can differentation be made between UC and CD?
* Clinical data
* Radiological data
* Histological differences in rectal and colonic mucosa
245
How are samples of rectal and colonic mucosa obtained?
By biopsy
246
When may it not be possible to distinguish between UC and CD?
If the biopsies are obtained in the acute phase
247
What are patients considered to have when their disease cannot be distinguished between CD and UC?
Colitis of Undetermined Type and *a*Etiology (CUTE)
248
What may be of value when determining between CD and UC?
Serological testing for anti-neutrophil cytoplasmic antibodies (ANCA) in UC, and anti-*Saccharomyces cervisiae* antibodies (ASCA) in CD
249
What may be required to make an exact diagnosis sometimes?
Examination of a surgical colectomy specimen
250
When is a colonscopy performed with CD?
If colonic involvement is suspected
251
What will be seen on a colonscopy with CD?
Mild, patchy surface ulceration to cobblestoning
252
When is an upper GI endoscopy required with CD?
To exclude oesophageal and gastroduodenal disease in patients with relevant symptoms
253
When is small bowel imaging mandatory?
In patients with suspected Crohn's
254
How is small bowel imaging conducted?
* Barium follow through
* CT scan with oral contrast
* Small bowel ultrasound
* MRI
255
What will be seen in small bowel imaging in a patient with CD?
* Asymmetrical alteration in the mucosal pattern with deep ulceration, and areas of narrowing or structuring
* String sign of Kantor
256
When is a perianal MRI or endoanal ultrasound used in patients with CD?
To evaluate perianal disease
257
When is a capsule endoscopy used in Crohn's disease patients?
When they have a normal radiological examination
258
What is the 'gold standard' investigation for the diagnosis of UC?
Colonscopy with biopsy
259
What is a colonscopy used for in UC?
To assess the disease activity and extent
260
Why is a plain abdominal X-ray used in UC?
To exclude colonic dilation
261
Why are other imaging techniques rarely used in UC?
As endoscopy is preferred
262
What is often seen on imaging with UC patients?
Collar Button Ulcers
263
What are Collar Button Ulcers?
Ulcer through the bowel mucosa to the muscle, then up and down in a 'T' shape
264
What treatment options are available for CD?
* Induction of remission
* Maintenance of remission
* Treatment of perianal disease
* Surgical management
265
How is remission induced in CD patients?
* Oral or IV glucocorticosteroids
* Enteral nutrition
* Anti-TNF antibodies
266
What is the name of the anti-TNF antibodies given in CD?
Infliximab
267
How is remission maintained in CD?
* Methotrexate
* Azathioprine
* Anti-TNF antibodies
268
How is perianal disease treated?
* Ciprofloxacin and Metrronidazole
* Azathioprine
* Anti-TNF antibodies
269
How do anti-TNF antibodies treat CD?
They bind to membrane bound TNF-α and induce immune cell apoptosis
270
When is surgical management required for CD?
* Failure of therapy with acute or chronic symptoms
* Complications
* Failure to grow in children, despite children
271
272
What complications of CD may necessitate surgical management?
* Dilation
* Obstruction
* Perforation
* Abscesses
273
What surgical management may be performed in patients with CD?
* Colectomy
* Ileorectal anastomosis
274
What is used to treat distal UC *(proctitis)*?
Topical or suppository corticosteroids
275
What is used to treat left sided UC?
Topical corticosteroid enema
276
What is used to treat extensive UC?
* Oral corticosteroids
* Infliximab
277
When is surgical management required in patients with UC?
* Patients with complications
* Patients with corticosteroids dependence
278
What is the favoured surgical management in patients with acute UC?
Subtotal colectomy with end ileostomy and preservation of the rectum
