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Alimentary > Immunology > Flashcards

Immunology Flashcards

1
Q

What are the 4 main mechanisms for protection from infection in the GI mucosa

A

Physical barrier - epithelium, glycocalyx, mucous, unstirred layer + peristalsis

Chemical barriers - enzymes from panted cells and acid

bacterial protection - commensal bacteria

Immunological - MALT, B and T cells and GALT + BALT

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2
Q

Describe GALT and what it can be split into

A

Gut-Associated lymphoid tissue (adaptive and innate response)

(organised) Peyer’s patches (SI), caecal patches (LI) and lymphocytes in the mesenteric lymph nodules (organised)
or
(disorganised) sites with lymphocytes in the lamina propria - mainly IgA secreting B cells and lymphocytes in the interstitial space below the basolateral membrane

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3
Q

Describe the Peyer’s patches

A

Found in the SI, most in the distal ileum
Aggregated lymphoid follicles covered with follicle associated epithelium (FAE)
Rich in B, T dendritic cells and macrophages
Monitors local bacteria

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4
Q

Describe Peyer’s patches development

A

Requires exposure to bacterial flora
Have 50 in the last trimester
Hit the maximum no. of 250 in the teenage years

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5
Q

Describe the M cells

A

The FAE contains specialised enterocytes/M cells
Transcytosis of luminal bacteria, antigens and proteins (uptake)
Express IgA receptors to transfer IgA bacteria complexes to the Peyer’s patches

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6
Q

Describe antigen uptake

A

Combined effort of M cells and dendritic cells (trans-epithelial)
Antigens are presented to lymphocytes for assessment and response
Activated cells develop gut homing markers and migrate to the mesenteric lymph nodes to proliferate

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7
Q

Explain the abundance of IgA

A

Most abundant antibody in the body (IgG most abundant circulating)
Highly prevalent in mucosal secretions due to MALT being associated with lots of IgA plasma cells
90% of gut B cells secrete IgA

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8
Q

What is SIgA

A

Dimeric form of IgA produced by lamina propria B cells
Binds to pathogens to prevent their adherence to the mucosal wall
Stimulated by M cells and dendritic cells
Made up of 2 IgA, j chain and secretory component

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9
Q

Describe the formation of SIgA

A
  1. In a plasma cells 2 IgA molecules are bound by a j-chain
  2. Secretion into the interstitial space
  3. Dimer binds to a receptor on the external basolateral surface of enterocytes (PIgR)
  4. Formation of SIgA
  5. endocytosis of SIgA into the epithelial cell
  6. transport via vesicle to the apical membrane
  7. exocytosis into the gut lumen
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10
Q

What are the functions of the secretory component of the SIgA

A

helps move IgA move through the enterocyte

Protects the antibody dimer from enzymatic and acid degradation

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11
Q

Describe lymphocyte circulation

A

Stimulated lymphocytes in the Peyer’s patches migrate into the local mesenteric lymph nodes to enter the lymphatic system
Drain into the thoracic duct
Lymphocytes then activated by tissue specific endothelial adhesion molecules which stimulates transmigration (requires HEV) to enter the blood
Lamina propria OR skin, tonsils, BALT

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12
Q

Explain the process of transmigration

A

L-selectin (lectin that binds to carbs) expressed on the surface of lymphocytes and mediates the interactions to allow leukocytes to roll in postcapilary venues and HEVs
L-selectin binds to mucosal addressing cell adhesion molecule-1 (MAdCAM-1)

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13
Q

What is MAdCAM-1 and where is it expressed

A

Enables lymphocyte recruitment in chronic gut inflammation
HEVs of Peyer’s patches and mesenteric lymph nodes
flattened endothelial cells
Activation via binding to integrin

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14
Q

What are the symptoms of irritable bowel syndrome

A

Recurrent abdominal pain
Abnormal bowel motility
Constipation and/or diarrhoea
(Does not involve inflammation, ulcers (IBD))

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15
Q

What are the risk factors of IBS and what is it caused by

A

stress
Gastroenteritis from norovirus and rotavirus
Visceral hypersensitivity

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16
Q

Describe the treatment of IBS

A

Diet modification - Avoiding certain foods such as apples, beans, cauliflowers.

Treatment of constipation - soluble fiber, stool softeners and osmotic laxatives

Treatment of spasms and pain - anti-diarrheals, anti-muscarinic

Management of stress, anxiety, depression

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17
Q

What are the symptoms of coeliac disease

A

Abdominal distension (bloating)
Diarrhoea
Sometimes dermititis herpetiformis

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18
Q

Explain the pathophysiology of coeliac disease

A
  1. Gliadin is not broken down in the stomach and binds to IgA at the mucosal membrane
  2. This binds to transferring receptor TFR and is transferred to the lamina propria
  3. tissue transglutaminase (tTG) cuts the amide group
  4. Deamidates gliadin is phagocytosed by macrophages and presented by MHC II
  5. Activation of the immediate system to destroy the epithelial cells
19
Q

How can coeliac disease be diagnosed

A

Antibody blood tests - anti-gliadin, anti-tTg, anti-endomysial (EMAs)
Biopsy test of duodenum

20
Q

What are the suggested dietary modifications suggested for coeliac disease

A

Gluten-free diet (wheat, barley, rye exclusion) and medication.
Factors affecting compliance are lifestyle, eating out, cross contamination at home and holidays.

21
Q

What are the symptoms of Crohn’s disease

A

Pain in affected area, most commonly in right lower quadrant.
Diarrhea and blood in stool.

22
Q

What is inflammatory bowel disease

A

Ulcerative colitis, Crohn’s disease

23
Q

What is the pathophysiology of Crohn’s disease

A

Immune-related
Mycobaterium paratuberculosis, pseudomonas and listeria
Unregulated immune response and GI tract is destroyed
associated with NOD2 gene mutation

24
Q

Describe the treatment of Crohn’s disease

A 
Anti-inflammatory drugs and antibiotics
Immunosuppressants e.g. corticosteroids
Surgical removal of the affected tissue
Liquid diet 
Low fibre
Decrease obstruction pain and gas production
25
Q

What are the symptoms of ulcerative colitis

A

Pain in left lower quadrant due to ulcers along the inner surface of large intestine, including the colon and rectum.
Severe and frequent diarrhea (sometimes bloody).

26
Q

Describe the pathophysiology of ulcerative colitis

A

Autoimmune disorder - T cells destroy the cells lining the walls of large intestine
Secondary cause - Diet and stress

27
Q

Describe the treatment for ulcerative colltis

A

Anti-inflammatory drugs (sulasalazine and mesalamine)
immunosuppressants (corticosteroids, azathioprine, cyclosporine)
Colectomy
Dietary manipulation
Pre/probiotics to treat pouchitis

28
Q

How can diarrhoea be treated

A 
Drink fluid
Nutritious drinks
Replace salt
Eat soluble fibre
Avoid gas producing foods, fibre, alcohol and caffeine
29
Q

What are the symptoms of cholera infection

A

Vomiting, nausea
Abdominal pain
Severe dehydration and diarrhoea (watery)

30
Q

Describe the pathophysiology of cholera infections

A

vibrio cholerae transmitted through the feral-oral route and spreads through contaminated water and food
Reaches the SI
On contact with the epithelial cells it releases toxins
Na+, K+ and Cl- (+ water) exits

31
Q

Describe FAE

A

follicle associated epithelium
No goblet cells
No secretory IgA
Little microvilli

32
Q

Describe the dual role of the GI tract in immunology

A

Restrained activation
Tolerance to food antigens and commensal bacteria
Immunoreactivity to pathogens

33
Q

What makes up the gut microbiota

A

10^14 gut bacteria
4 phyla of bacteria (bacteroidetes, firmicutes, actinobacteria, proteobacteria)
Viruses and fungi

34
Q

What is Dysbiosis

A

Altered microbiota composition

Infection, diet, xenobiotics, hygiene and genetics contribute to either microbiota or dysbiosis

35
Q

Describe MALT

A

Mucosa associated lymphoid tissue
Found in the submucosa below the epithelium
Lymphoid mass with lymphoid follicles
Follicles surrounded by HEV
Oral cavity is rich in these e.g. tonsils

36
Q

Describe B cell adaptive response

A
  1. Mature naive B cells express IgM
  2. upon antigen presentation class switch to IgA
  3. T cells and dendritic cells influence B cell maturation via cytokine release
  4. B cells mature to become IgA secreting cells
  5. Population of the lamina propria
37
Q

Describe the diagnosis of cholera infection

A

Bacterial culture from stool sample on selective agar

Rapid dipstick also available

38
Q

What are some causes of infectious diarrhoea

A 
Cholera
E. Coli
Salmonella
Shigella
Clostridium difficile

Rotavirus (children)
Norovirus

Giardia lamblia
Entamoeba histolytica

39
Q

Describe rotavirus infection

A

RNA virus that replicates in enterocytes
Infects children
Treated by oral rehydration
Vaccination = rotarix

40
Q

Describe norovirus infection

A

RNA virus
acute gastroentiris
Faecal-oral

41
Q

Describe campylobacter infection

A

Undercooked meat, untreated water, unpasteurised milk
Low infective dose
Most common cause of food poisoning
Azithromycin (macrolide)

42
Q

What are the types of E. coli associated with diarrhoea

A

ETEC - cholera like, watery
EHEC/STEC - most dangerous
EIEC - shigella like, bloody
3 other types

43
Q

Describe clostridium difficile infection management

A 
Isolation
Stop antibiotics
Vancomycin, metronidazole
Increasingly difficult to treat after recurrence 
Faecal microbiota transplantation

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