Inflammatory Bowel Disease Flashcards

1
Q

What effect does cholecystokinin (‘bile sac move’) have?

A

Contraction of gall bladder
Pancreas releases enzyme rich secretions
Bile produced
Inhibits gastric emptying

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2
Q

What is CCK stimulated by?

A

Presence of fats in chyme in duodenum

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3
Q

What releases CCK?

A

I cells (in duodenum and jejenum)

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4
Q

Large intestine start to end

A

Caecum to anal canal

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5
Q

Epithelia in colon

A

Columnar - produce lots of mucus due to high levels of bacteria in colon

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6
Q

Function of large intestine

A

Remove the water from all the indigestible gut contents
Turns chyme into semi solid
Produces certain vitamins
Temporary storage until defecation (distal)

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7
Q

What doe colon contain?

A

Microbiome - important as contains lots of commensal bacteria, disease is worse if this is altered

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8
Q

Where does colonic mucosa get nutrients from?

A

Majority is not from blood
Mainly from short chain fatty acids derived from fermentation of dietary fibre
By products of fermentation - CO2, methane, hydrogen gas

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9
Q

Peritoneum in relation to colon

A

Ascending and descending is retroperitoneal
Transverse and sigmoid has it’s own mesentery (transverse mesocolon for transverse)

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10
Q

Rectum in relation to peritoneum

A

Upper 1/3 - intraperitoneal
Middle 1/3 - retroperitoneal
Lower 1/3 - no peritoneum

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11
Q

Diameters of colon vs SI

A

SI - 3cm
Colon - 6cm
Caecum - 9cm

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12
Q

What is created by ascending and descending retroperitoneal structures?

A

Paracolic gutters (left and right)

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13
Q

Which is longer, ascending or descending?

A

Descending - ascending is often shortened if caecum only descends a short amount in embryological development

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14
Q

Arterial supply to midgut component of colon

(midgut is distal duodenum to proximal 2/3 transverse colon)

A

Superior mesenteric artery branches:

Ileo-colic supplies caecum (7pm)
Right colic supplies ascending colon (9pm)
Middle colic supplies transverse colon (10pm)

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15
Q

Arterial supply of hindgut component of colon

(hindgut is distal 1/3 transverse colon to rectum)

A

Inferior mesenteric artery branches:

Left colic - descending colon
Sigmoid - sigmoid colon
Superior rectal artery - upper 1/3 rectum (IMA just renamed to this when enters pelvis)

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16
Q

Venous drainage of midgut

A

Superior mesenteric vein

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17
Q

Venous drainage of hindgut

A

Inferior mesenteric vein

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18
Q

Rectum venous drainage

A

Upper 1/3 - drains into superior rectal vein
Middle and lower 1/3 drain into systemic venous system via inferior rectal vein to internal iliac vein

(site of varices as porto-systemic anastomoses)

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19
Q

Large intestine vs small

A

Large - wider (6cm vs 3)
Large - shorter (6ft vs 20ft)
Large - has crypts not villi (liks SI)

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20
Q

Outer structure of large bowel

A

Has incomplete layers of longitudinal muscle Instead has bands called teniae coli - three of them

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21
Q

What are haustra?

A

Sacculations caused by contraction of teniae coli (sections between indentations)

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22
Q

What channel allows H2O reabsorption in colon?

A

ENaC - induced by aldosterone

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23
Q

Water absorption per day and where

A

1500mls enters colon per day
ONLY 100mls exits

Most in proximal colon

24
Q

What structure between epithelia is different in colon?

A

Tighter tight junctions - allows bigger gradient to form and less back diffusion of ions

25
Q

What is inflammatory bowel disease?

A

Group of conditions characterised by idiopathic inflammation of GI tract

26
Q

2 most common types of inflammatory bowel disease

A

Crohns disease
Ulcerative collitis

(if cannot determine between two its called indeterminate collitis)

27
Q

Age peaks for IBD

A

20s
60s

28
Q

Crohns disease 5 key points

A

Affects anywhere in GI tract - ileum usually involved
Transmural - full thickness
Skip lesions (affected then unaffected sections)
Get granulomas on histology
Perianal disease?

29
Q

Ulcerative colitis 5 key points

A

Begins in rectum and can extend to involve entire colon (BUT NO MORE)
Continuous pattern (no skip)
Mucosal (superficial) inflammation
Blood in stool

30
Q

Extra intestinal problems associated with IBD

A

MSK pain - arthritis

Skin - psoriasis, erythema nodosum, pyoderma gangrenosum

Liver/biliary tree - primary sclerosing cholangitis

Eye problems

31
Q

Causes of IBD

A

Genetic - identical twins had 70% concordance
Gut organisms (microbiome)
Immune response
Triggers - abx, infections, smoking diet

32
Q

Smoking effects on crohns and UC

A

Crohns - worsens inflammation
Ulcerative collitis - supresses and eases inflammation

33
Q

Presentation of crohns

A

Young female/male
5x loose stools a day - non-bloody
Weight loss
Joint pain
RLQ pain
Smoker

34
Q

Signs of crohns found on further signs/exams

A

Tender mass RLQ
Mild perianal inflammation/ulceration - this is externally visible (in UC YOU DO NOT GET THIS)
Low grade fever
Mildly anaemic

35
Q

Gross pathological appearance of crohns

A

Skip lesions
Hyperaemia (red)
Mucosal oedema
Discrete superficial ulcers and deeper ulcers
Transmural inflammation
Thickening of bowel wall, narrowing of lumen
Cobblestone
Fistulae - bowel and bowel, bowel and bladder, bowel and vagina

36
Q

What does cobblestone appearance of crohns mean?

A

Linear ulcers criss-cross and oedematous tissue bulges between

37
Q

Microscopic appearance of crohns

A

Granuloma formation - epithelioid macrophages

38
Q

Investigations for crohns

A

Bloods - anaemia?

CT/MRI - see external effects as is transmural eg fistula, bowel thickening, obstruction

Barium enema/swallow - used less now, but can see structures/fistulae. (radioopaque fluid with fluroscopy)

Colonoscopy - would see gross patho changes as mentioned above

39
Q

Presentation of ulcerative collitis

A

Young f/m
6x BLOODY stools per day with MUCUS (superficial mucosa layer only remember)
Weight loss
Mild lower abdo pain/cramping
Painful red eye

40
Q

Signs found on exam for UC

A

Mildly tender abdomen
NO perianal disease
Normal temp

41
Q

Histological changes in UC

A

Chronic inflammatory infiltrate into lamina propria

Crypt abscesses - neutrophilic exudate here

Crypt distortion - irregular glands with distortion, darker nuclei

Reduced goblet cells

NOOOO GRANULOMA - only in crohns

42
Q

Larger pathological changes seen in UC

A

Pseudopolyps - from inflammation then healing, ulcerations around normal tissue, not true polyps

Loss of haustra - inflammation reduces appearance

43
Q

Investigating UC

A

Bloods - anaemia?

Stool culture - blood/mucus

Colonoscopy - ulcers link (continuous)

Plain abdo X-rays

Barium enema

44
Q

Why not CT/MRI in UC

A

It is only within GI tract as is not transmural just affecting mucosal layer
CT is more useful in seeing the outside effects eg fistula formation in crohns

45
Q

Is malnutrition possible in crohns or UC?

A

Yes - in crohns if affects SI as absorption affected

No in UC - only affects colon, weight loss is more due to lack of appetite due to pain etc

46
Q

Does crohns involve rectum?

A

NO
But UC does

47
Q

Is fibrosis common in crohns?

A

Yes - but not in UC

48
Q

Crypt abscesses?

A

Rare in crohns
YESSS for UC

49
Q

Do you get ulcers (amphtous or linear) in ulcerative collitis?

A

No - only in crohns

50
Q

Friable mucosa

A

Friable in UC but not in crohns (see table in pg 27 of this lecture to summarise all)

51
Q

Radiolofy of crohns

A

See strictures/narrowings

52
Q

Radioloy of UC

A

Loss of haustra - ‘featureless’ just looks like smooth sausage
Continuous
Granular appearance from mucosal inflammation

53
Q

Treatments for IBD medical

A

Aminosalicylates - flare ups and remission

Corticosteroids - flare ups only

Immunomodulators

Faecal matter transplant?

54
Q

Crohns surgical treatment

A

Not curable as can affect all of GI tract - cannot remove all
Can remove small parts of bowel with strictures/fistulas

55
Q

UC surgical treatment

A

Curable - can have colectomy (colon removed)
If the inflammation does not settle or if there are precancerous changes
Can plug terminal ileum into a bit of rectum if they leave it
= continence

BUT rectum can still have UC but it easier to manage

56
Q

Problem with surgery to resolve IBD

A

Risk adhesions causing bowel obstruction

In crohns - if keep removing small parts of bowel can become too short and cause permanent diarrhoea due to not enough contact time