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year 2 > Inflammation Of The Gut > Flashcards

Inflammation Of The Gut Flashcards

1
Q

What are the components of the small intestine?

A

Duodenum, jejunum and ileum which are responsible for enzymatic digestion of food and absorption of nutrients.

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2
Q

Where are Peyer’s patches located?

A

ONLY in the ileum of the small intestine (occasionally in the distal jejunum)

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3
Q

How do muscular contractions occur in the GI system?

A

Stimulated by the pacemaker cells of the GI tract which are interstitial cells of Cajal that cause slow wave action potentials in the muscularis externa, into either tonic or phasic contraction.

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4
Q

What are tonic contractions?

A

Maintained contraction of the smooth muscle for minutes to hours, occurring in the sphincters and the stomach.

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5
Q

What are phasic contractions?

A

Rapid transient contractions without obvious changes, which is carried out by the muscularis externa in the posterior stomach and small intestine.

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6
Q

What is peristalsis?

A

Contractions occur in waves directly behind the bolus.

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7
Q

What is segmentation?

A

Pattern of GI contraction which occurs in short lengths, carried out by the longitudinal muscle. There is alternating contraction of the inner circular muscle and in other segments, relaxation of the outer longitudinal muscles in order to mix food.

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8
Q

What is the general composition of the small intestine?

A

Simple columnar epithelia lined with microvilli and a mucous layer. Contains goblet cells, Paneth cells and a crypt for proliferation of stem cells for renewal of the intestinal layer.

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9
Q

What are the unique features of the duodenum?

A

Microvilli are longer and slender. It contains Brunner’s glands in the sub mucosa which produce alkaline rich mucous fluid in response to parasympathetic stimulation.

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10
Q

Where are Brunner’s glands located?

A

Submucosa of Duodenum and Oesophagus.

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11
Q

What is the role of the large intestine?

A

Storage and elimiation of food residues, absorption of water.
Bacterial degradation of nutrients like fibre into short-chain fatty acids via fermentation.

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12
Q

What is the histology of the large intestine?

A

Simple columnar epithelium which is numerous in goblet cells. It contains absorptive enterocytes and enteroendocrine cells such as chromaffin and L cells. Contains no villi.

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13
Q

What are enterochromaffin cells?

A

Endocrine cells found in the colon that produce serotonin to stimulate gastric mucus production.

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14
Q

What are L cells?

A

Produce:
Glucagon-like peptide 1 which inhibits gastric acid secretion and promote satiety
Peptide YY cells to slow intestinal motility for satiety

They are found in the ileum and colon.

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15
Q

Where are Paneth cells located in the large intestine?

A

Only found in the right colon and limited in number compared to small intestine to limit potential damage against digestive enzymes.

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16
Q

Which cells are present in the lamina propia?

A

Inflammatory cells and fibroblasts.

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17
Q

What are the histological layers of the intestine?

A

Mucosa
Submucosa
Muscularis mucosae
Muscularis propia
Subserosa
Serosa

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18
Q

What is the mucosa of the intestine?

A

Contains the epithelial cells and the lamina propia, a layer of loose connective tissue rich in immune cells. It contains lymphoid follicles and Muscularis mucosae.

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19
Q

What is the Muscularis mucosae?

A

Thin layer of smooth muscle which controls movement of the mucosa.

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20
Q

What is the Submucosa?

A

Contains loose connective tissue of collagen, smooth muscle and adipose tissue. The enteric plexus of Meissner’s and Henle’s is found here in the jejunum and ileum.

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21
Q

What are Meisser’s plexus?

A

Enteric plexus in the Submucosa jejunum and ileum which provides parasympathetic innervation to the goblet cells for secretion.

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22
Q

What is the Muscularis propia?

A

Consists of outer longitudinal muscle and inner circular muscle for peristalsis of food. Between these layers is the Auerbach plexus.

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23
Q

What is the Auerbach plexus?

A

Responsible for innervation of the gut which lies between layers of the Muscularis propia for stimulating peristalsis.

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24
Q

What is the serosa?

A

Contains simple squamous epithelia which is high vascularised and contains lymphatic vessels and is covered by visceral peritoneum

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25
Q

What are the interstitial cells of Cajal?

A

Pacemakers of the GI tract for action potentials for slow wave phasic peristalsis, located in the Submucosa and the gap between the Submucosa and circular muscle layer.

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26
Q

What are the symptoms of IBD?

A

Pain, swelling, bloody diarrhoea, weight loss and lethargy.

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27
Q

How does disease present in the small intestine?

A

Severe abdominal pain, vomiting, weight loss due to malabsorption, and water diarrhoea.

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28
Q

How are abdominal symptoms assessed in history?

A

Changes in bowel habit
Pain or discomfort
Any wind?
Stomach distention/bloating.

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29
Q

How is diarrhoea assessed in a history?

A

Volume and consistency of stools
Number of stools per day
Acute diarrhoea vs chronic diarrhoea
Small bowel diarrhoea vs large bowel diarrhoea.

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30
Q

What is diarrhoea?

A

Passing 3 or more loose stools in one day, more frequent than usual for an individual.

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31
Q

What is acute diarrhoea?

A

Diarrhoea lasting less than 4 weeks which typically occurs due to infection.

32
Q

What is chronic diarrhoea?

A

Diarrhoea lasting over 4 weeks due to organic causes or functional causes.

33
Q

What are organic causes of chronic diarrhoea?

A

Conditions such as Coeliac’s disease. Inflammatory bowel disorders such as Crohn’s disease or ulcerative colitis

Typically large volume of stools containing blood and is associated with cramping pain and weight loss. Extra symptoms include fever , arthritis and skin lesions.

34
Q

What are the functional causes of Crohn’s disease?

A

Inflammatory Bowel disease, related to stress.

Typically, smaller volumes of stool with no blood and occurs in the morning. There will be no change in weight.

35
Q

How does small bowel diarrhoea present?

A

Issue in the small intestines that causes stools to be less frequent but of a larger volume of loose stools that are green/gray in colour.

36
Q

How does large bowel diarrhoea present?

A

Issue in the colon that causes a higher frequency of loose stools of a smaller volume than the small intestine. It may contain blood or mucous.

37
Q

What are the causes of diarrhoea in developing countries?

A

Infections from bacteria and parasites.

38
Q

What are the causes of diarrhoea in developed countries?

A

Malabsorption syndromes, IBD, IBS or chronic infections.

39
Q

What is the pathophysiology of diarrhoea?

A

Disturbance to motility
Osmotic diarrhoea
Defective absorption
Abnormal mucosal secretion
Permeability defect.

40
Q

How is osmosis involved in diarrhoea?

A

Osmotically active solutes in the lumen promote secretion of water and electrolytes out of the intestine and lead to loose stools.

41
Q

How does mucus secretion affect the bowels?

A

Increased mucus secretion due to infection or inflammation causes looser stools and diarrhoea.

42
Q

What are the deficiencies in inflammation of the bowel?

A

Bone disease due to malabsorption of Vitamin D or calcium
Anaemia due to malabsorption of folate/B12 or blood loss in stools.
Less blood clotting due to deficiency of Vitamin K, as a result of fat malabsorption

43
Q

What are the signs and symptoms of vitamin deficiency in inflammatory bowel conditions?

A

Glossitis (Macrocytic anaemia)
Pallor (Anaemia)
Skin pigmentation and Petechia (Vitamin K deficiency)
Muscle pain and Neuropathy (Ca2+ deficiency)

44
Q

What are the features of general ill health?

A

Anorexia/ Weight loss
Oedema
Lethargy
Dehydration
Amenorrhea/infertility/impotence

45
Q

What is Coeliac’s disease?

A

Inflammatory condition characterised by the intolerance to the protein gliadin in gluten that commonly presents in childhood, which affects more women than men. It is more common in Ireland than the UK.

This autoimmune response results in intraepithelial T lymphocytes that increase the risk for lymphoma malignancy.

46
Q

What is the Pathophysiology of coeliac’s disease?

A

Gluten is broken down into a fragment of gliadin which is taken up by absorptive enterocytes. It is broken down by tissue glutaminase dehydrogenase to demainated gliadin peptides. These are taken up by dendritic cells in individuals with the HLA for HLA-DQ2 or HLA-DQ8 on the human major histocompatibility complex. This is presented to T cells in the Peyer’s patches and induce formation of major antibodies.

47
Q

What are the antibodies in coeliac’s disease?

A

Anti-tissue transglutaminase IgA antibody
Anti-endomysial IgA antibodies which damage the intestines and cause swelling and inflammation
Anti-deaminated gliadin peptide IgA antibodies.

48
Q

Which antibody is best used for diagnosis of Coeliac’s disease?

A

Anti-transglutaminase antibody because it has a higher sensitivity and negative predictive value.
-> Endomysial antibodies are more labour intensive to examine and anti-deaminated gliadin antibodies have only been introduced recently.

49
Q

What are the histological features of Coeliac’ disease?

A

Main site affected is the jejunum.

Crypt hyperplasia/hypertrophy

Blunting and atrophy of mucosa

Increased numbers of intraepithelial lymphocytes which increases the risk of lymphoma.

Lamina propia will have an increased number of chronic inflammatory cells

Deficiency in IgA antibodies

50
Q

What are the complications of coeliac’s disease?

A

Bone disease due to malabsorption of calcium and vitamin D in the small intestine.

Malignancy with a 4x greater risk of developing enteropathy associated T cell lymphoma and non-Hodgkin’s lymphoma compared to the general population. This occurs due to intraepithelial lymphocytes deposition.

Adenocarcinomas in the lung or breast or GI tract

51
Q

What are the symptoms for Coeliac’s disease?

A

Steatorrhea and strong-smelling stools due to fat malabsorption.
Glossitis due to B12 and folate malabsorption
Failure to thrive/Weight loss and anorexia
Failure to thrive
Apolthous ulcers
Anaemia

52
Q

Which deficiencies occur in Coeliac’s disease?

A

Iron deficiency
Folate and B12 deficiency
Ca2+ deficiency

53
Q

Which gene has the strongest association with Coeliac’s disease?

A

HLA-DQ2.

54
Q

What is inflammatory bowel disease?

A

Chronic inflammation of the GI tract caused by 2 disorders: ulcerative colitis and Crohn’s disease.

55
Q

What is ulcerative colitis?

A

Superficial inflammation which primarily begins in the sigmoid colon and rectum. It is progressive and moves up the colon to the left descending (left-sided colitis) and to the transverse colon (extensive colitis)

It is more common than Crohn’s. Smoking is a protective factor and onset is 15-40 years old..

56
Q

What are the consequences of ulcerative colitis?

A

Toxic megacolon (enlarged colon)
Severe bleeding
Rupture of bowels
Abscess formation
Colon cancer

57
Q

What is Crohn’s disease?

A

Transmural inflammation from mouth to anus but most commonly in the distal ileum or colon. It is characterised by skip lesions, patchy areas of inflammation with undamaged areas. Mouth ulcers can iccur

Onset is 15-40 years old and smoking is an aggravating factor. Rectum is only affected in half of patients.

58
Q

What are the complications with Crohn’s disease?

A

It can cause:
Stricture of the colon that causes stenosis of faeces
Fistula Formation.
Colon cancer.

59
Q

Which part of the colon is affected in Crohn’s disease?

A

Occurs anywhere from mouth to anus but typically in the terminal ileum and the colon. Smoking is aggravating factor.

60
Q

Which part of the colon is affected in ulcerative colitis?

A

Sigmoid colon and rectum, where smoking is a protective factor.

61
Q

What is the incidence of Crohn’s disease?

A

More women are affected than men and incidence fluctuates. May be caused by a genetic defect that means the immune response against a causative agent is uncontrolled. It typically affects the small intestine.

62
Q

Which infections trigger Crohn’s disease?

A

Mycobacterium and measles virus.

63
Q

What is the incidence of ulcerative colitis?

A

More common than Crohn’s disease, and it affects more men, with incidence being stable and decreasing after 20 in women. Men have lowest incidence at 45 but it increase after.

64
Q

What is the cause of IBD?

A

Theoritetical causes such as:
—>Autoimmune response to epithelial cell components like glycoproteins or Molecular mimicry
—>Toxic response to pathogens, abnormal luminal contents or increased absorption of luminal macromolecules
—>Medications

65
Q

Which medications increase the risk of IBD?

A

Antibiotics
NSAIDs
Oral contraceptives

66
Q

What infections increase the risk of IBD?

A

Measles virus
Mycobacterium tuberculosis
Microbiome constituents.

67
Q

What is the presentation of ulcerative colitis?

A

BLOODY diarrhoea, frequency and urgency of defaecation. Cramping abdominal pain and FEVER, waking in night.

NO WEIGHT LOSS. Compared to Crohn’s, there is more blood and diarrhoea.

68
Q

What is the presentation of Crohn’s disease?

A

WEIGHT loss, abdominal PAIN, bleeding, fever and perianal disease.

Compared to UC, there is more pain and less fever, diarrhoea and blood.

69
Q

How is the histology of bowel affected in ulcerative colitis?

A

Affects distal colon and always involves the rectum. Inflammation is superficial and mucous membrane is raw. Abscess formation occurs in the crypts of the epithelia.

70
Q

How is the histology of bowel affected in Crohn’s disease?

A

Increased abdominal thickness with cobblestone mucous membrane and granuloma formation.

Affects all layers and lymphocyte infiltration always occurs with fistula being common. Pyloric metaplasia and muscular hypertrophy occurs.

71
Q

What are the complications with Crohn’s disease?

A

Anal lesions
Malabsorption due to resectioning of the bowel as a treatment.

72
Q

Which part of the gut is most commonly affected in Crohn’s?

A

Small intestine.

73
Q

What are the systemic complications of IBD?

A

Arthritis,
Aphthous stomatitis: oral ulcers

Sclerosing cholangitis: narrowing of the bile duct
Iritis

Pyoderma gangrenosum: large painful sores on the shins

74
Q

What is the risk of colorectal cancer in IBD?

A

Greater lifetime risk in Crohn’s disease; Risk is higher at a younger age in ulcerative colitis, peaking at 30-40 years old.

75
Q

What is fulminant colitis?

A

Severe complication of ulcerative colitis that leads to toxic megacolon.

76
Q

What is inanities?

A

Exhaustion due to lack of nourishment.

77
Q

How is IBD diagnosed?

A

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