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FOO > IMMUNE MEDIATED INTESTINAL DISEASES > Flashcards

IMMUNE MEDIATED INTESTINAL DISEASES Flashcards

1
Q

WHAT PERCENTAGE OF COELIAC DISEASE IS FAMILIAL?

A

10-20%

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2
Q

WHAT DOES COELIAC DISEASE CAUSE DAMAGE TO?

A

INTESTINAL VILLI

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3
Q

WHICH CELLS OF THE IMMUNE SYSTEM ARE ACTIVATED IN COELIAC DISEASE?

A

GLUTEN SPECIFIC T LYMPHOCYTES

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4
Q

WOMEN:MEN AFFECTED BY COELIAC?

A

2:1 (THERE COULD BE BIAS)

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5
Q

PEOPLE OF WHICH DESCENT ARE PARTICULARLY AFFECTED BY COELIAC?

A

NORTHERN EUROPEAN

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6
Q

WHAT PERCENTAGE OF UK POPULATION IS AFFECTED BY COELIAC?

A

1%

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7
Q

SYMPTOMS OF COELIAC, CHILDREN VS ADULTS?

A

CHILDREN: GASTROINTESTINAL SYMPTOMS (DIARRHEA, FATTY STOOL, CRAMPS, VOMITING..), FAILURE TO THRIVE (LOW HEIGHT AND WEIGHT)
ADULTS: INTESTINAL SYMPTOMS, BEHAVIOURAL ISSUES (DEPRESSION, ANXIETY, MEMORY LOSS, DIFFICULTY TO FOCUS..)

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8
Q

WHICH FUNCTION OF THE GI TRACT DOES THE COELIAC MOSTLY AFFECT?

A

ABSORPTION

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9
Q

WHICH PARTS OF THE SMALL INTESTINE DOES COELIAC AFFECT?

A

UPPER SMALL INTESTINE AND THE JEJUNUM

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10
Q

WHICH GLUTEN PROTEIN CAUSES THE IMMUNE REACTION IN COELIAC DISEASE?

A

GLIADIN (can also be glutenin)

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11
Q

PATHOPHYSIOLOGY OF COELIAC DISEASE:

A
  • GLIADIN PROTEINS FROM GLUTEN ARE BROKEN DOWN IN PIECES CALLED EPITOPES
  • EPITOPES ARE SMALL PEPTIDES RECOGNISED BY IMMUNE CELLS, 1ST BEFORE ENTRY IN THE ENTEROCYTES, AND THEN AFTER EXITING THE ENTEROCYTE (IN THE LAMINA PROPRIA)
  • THIS RECOGNITION PATTERN WILL OCCUR IN EVERYONE, BUT IT IS DEREGULATED IN COELIAC
  • MOLECULES PRODUCED DURING THE IMMUNE REACTION WILL ATTACK THE ENTEROCYTES AND THIS IS HOW VILLI WILL LOSE THEIR INTEGRITY
  • CRYPT STRUCTURE (WHERE CCK IS PRODUCED) WILL BECOME HYPERTROPHIC SO THE SECRETIONS OF CCK WILL BE IMPAIRED
  • ENTEROCYTE RENEWAL IS IMAPIRED
  • GOBLET CELLS THAT NORMALLY PRODUCE PROTECTIVE MUCUS WILL ALSO BE IMPAIRED
  • IMMUNE CELLS WILL BE PRESENT IN ENTEROCYTES
  • DESTRUCTION OF VILLI WILL LEAD TO DESTRUCTION OF THE WHOLE MUCOSA, SO TIGHT JUNCTIONS WILL NOT FUNCTION NORMALLY WHICH LEADS TO ‘LEAKY GUT’, WHICH ALLOWS MOLECULES TO TRAVEL DIRECTLY FROM THE LUMEN TO LAMINA PROPRIA, WHICH THEN SENDS MORE SIGNALS TO THE IMMUNE CELLS THAT SOMETHING IS WRONG
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12
Q

WHAT IS ‘LEAKY GUT’?

A

LEAKY GUT REFERS TO IMPAIRED FUNCTIONING OF TIGHT JUNCTIONS WHICH CONNECT ENTEROCYTES, LEADING TO PASSAGE OF MOLECULES STRAIGHT FROM THE INTESTINAL LUMEN TO THE LAMINA PROPRIA, WHICH INDUCES IMMUNE RESPONSE.
IT IS A RESULT OF VILLUS DESTRUCTION IN COELIAC DISEASE

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13
Q

WHAT ARE EPITOPES?

A

SMALL PEPTIDES FORMED AS A RESULT OF GLIADIN BREAK DOWN WHICH ARE RECOGNIZED BY IMMUNE CELLS

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14
Q

WHICH IMMUNE CELLS ARE EPITOPES RECOGNISED BY?

A

ANTIBODIES IgA

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15
Q

WHAT HAPPENS IN COELIAC DISEASE AFTER EPITOPES ARE RECOGNISED BY IgA ANTIBODIES UP UNTIL THEY REACH LAMIN PROPRIA?

A
  • THE IgA-GLIADIN COMPLEX IS NOT ELIMINATED (AS IT WOULD NORMALLY BE)
  • IT IS INSTEAD RECOGNIZED BY TRANSFERRING (TfR) RECEPTOR ON VILLI SURFACE
  • THE COMPLEX OF TfR, IgA AND GLIADIN MOVES THROUGH ENTEROCYTES
  • GLIADIN PROTEINS ARE RELEASED ON THE BASOLATERAL SIDE OF THE ENETROCYTES FACING THE LAMINA PROPRIA
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16
Q

WHAT HAPPENS TO GLIADIN PEPTIDES IN THE LAMINA PROPRIA?

A
  • THEY ARE FIRSTLY DEAMIDATED BY TRANSGLUTAMINASE 2 (TG2)
  • TG2 CONVERTS GLUTAMINE TO GLUTAMATE (NEGATIVE CHARGE)
  • NEGATIVE CHARGE INCREASES THE IMMUNOGENICITY OF THE GLIADINS (IMMUNE CELLS WILL BE EVEN MORE ATTRACTED BY THIS TYPE OF PEPTIDES)
  • MACROPHAGES WILL ‘EAT’ THESE PEPTIDES
  • ONCE INSIDE THE MACROPHAGES AKA PRESENTING MOLECULES, PEPTIDES WILL BE PROCESSED AND ASSOCIATED WITH MOLECULES OF MHC CLASS II
  • MHC (MAJOR HISTOCOMPATIBILITY COMPLEX) CALLED HLA (HUMAN LEUKOCYTE ANTIGEN) IN HUMANS
  • IN COELIAC DISEASE, THESE MOLECULES ARE ASSOCIATED WITH HLA DQ2 (MOSTLY) OR HLA DQ8 GENES
  • T CELLS RECOGNISE HLA DQ2 ASSOCIATED WITH GLIADIN PEPTIDES AND THEN GET ACTIVATED AND SECRETE HIGH LEVELS OF PROINFLAMMATORY CYTOKINES
  • AN ACTIVATION CASCADE WILL FOLLOW; CYTOKINES ACTIVATE MORE IMMUNE CELLS
  • B CELLS ARE ALSO ACTIVATED AND THEY WILL PRODUCE ANTIBODIES, MEANING THE IMMUNE RESPONSE WILL BE STRONGER AFTER ANOTHER EXPOSURE TO GLUTEN
17
Q

DIFFERENCE BETWEEN MAJOR HISTOCOMPATIBILITY COMPLEX (MHC) CLASS I AND II?

A

I: INVOLVED IN AUTOIMMUNE DISEASE
II: INVOLVED IN RECOGNITION OF PATHOGENS OF EXTERNAL ELEMENTS

18
Q

EVERYBODY HAS HLA MOLECULES EXPRESSED WHERE?

A

SURFACE OF MACROPHAGES

19
Q

CLASS II HLA MOLECULES IN PEOPLE WITH COELIAC DISEASE ARE ENCODED BY WHICH 2 GENES + PERCENTAGE FOR BOTH?

A

HLA-DQ2 (95% OF PATIENTS)

HLA-DQ8

20
Q

EXACT T CELL TYPE THAT RECOGNISES THE HLA-DQ2 MOLECULE ASSOCIATED WITH GLIADIN PEPTIDES?

A

CD4+ T CELLS

21
Q

WHAT IS ZONULIN AND WHAT HAPPENS TO IT IN COELIAC DISEASE?

A

ZONULIN IS A REGULATOR OF INTESTINAL TIGHT JUNCTIONS. IT IS OVEREXPRESSED AND THAT LEADS TO INCREASED PERMEABILITY OF THESE JUNCTIONS WHICH MASSIVELY IMPAIRS THE INTEGRITY OF THE MUCOSA (PATHOGENS CAN GO THROUGH, FURTHER INCREASING INFLAMMATION)

22
Q

WHAT IS INFLAMMATORY BOWEL DISEASE?

A

REFERS TO IMMUNE MEDIATED DISORDERS REGROUPING CROHN’S DISEASE AND ULCERATIVE COLITIS (UC)

23
Q

DIFFERENCE BETWEEN COELIAC DISEASE AND CROHN’S DISEASE?

A

COELIAC IS A FOOD ALLERGY; IMMUNE RESPONSE AGAINST GLUTEN PROTEINS
CROHN’S IS AN AUTOIMMUNE DISEASE

24
Q

DIFFERENCE BETWEEN CROHN’S AND ULCERATIVE COLITIS?

A

DIFFERENT LOCATIONS OF INFLAMMATION (CROHN’S AFFECTS THE ENTIRE GI TRACT AND UC ONLY AFFECTS THE LARGE INTESTINE) + DIFFERENT LAYERS OF THE GI TRACT AFFECTED (UC AFFECTS ATHE LINING ALL ALONG, CROHN’S PENETRATES THE WHOLE INTESTINAL WALL BUT DIFFERENT AREAS ARE AFFECTED TO DIFFERENT EXTENT)

25
Q

SYMPTOMS OF ULCERATIVE COLITIS?

A

DIARRHEA, BLOOD IN THE STOOL, ABDOMINAL PAIN, WEIGHT LOSS..

26
Q

WHICH INFLAMMATORY BOWEL DISEASE CAN SOMETIMES BE DESCRIBED AS ‘PATCHY’?

A

CROHN’S

27
Q

CROHN’S DISEASE MOST OFTEN AFFECTS WHICH PARTS OF THE GI TRACT?

A

THE JEJENUM AND THE COLON (45%)

28
Q

SYMPTOMS OF CROHN’S?

A

BLOATING, DIARRHEA, BLOOD IN STOOL, ULCERS, FISTULAS, FEVER, SKIN ISSUES, MOOD DISORDERS, SIGNS OF MALABSORPTION

29
Q

HOW MANY PEOPLE IN THE WESTERN WORLD ARE AFFECTED BY CROHN’S?

A

2.5 MILLION

30
Q

CROHN’S MANIFESTATIONS IN CHILDREN?

A

NO GI SYMPTOMS!!!!

- FEVER, ANEMIA, GROWTH RETARDATION

31
Q

DIFFERENCES IN SYMPTOMS BETWEEN CROHN’S AND UC?

A

BLOOD IN STOOL MORE COMMON IN UC
UC PAIN MOSTLY IN LEFT PART OF ABDOMEN
CROHN’S PAIN IN THE ENTIRE ABDOMEN OR MORE TO THE RIGHT

32
Q

POSSIBLE CAUSES OF CROHN’S DISEASE?

A
  • IDIOPATHIC CONDITION
  • ASSOCIATION WITH SMOKING + SOME MEDICINES AND ANTIBIOTICS
  • <15% OF PATIENTS HAVE FAMILY HISTORY
  • 30 GENES IDENTIFIED AS ASSOCIATED WITH THE DISEASE
33
Q

WHICH CELLS ARE DEREGULATED IN CROHN’S?

A

DENDRITIC CELLS (TYPE OF ANTIGEN PRESENTING CELL)

34
Q

MECHANISM OF CROHN’S

A
  • DENDRITIC CELLS RECOGNIZE GUT BACTERIA OR PATHOGENS AND PRESENT ANTIGENS; HLA CLASS II MOLECULES
  • CD4+ TELL CELLS RECOGNISE THESE ANTIGENS AND PRODUCE CYTOKINES
  • CYTOKINES ACTIVATE SUB POPULATIONS OF T CELLS WHICH CONTINUE PRODUCING EVEN MORE INFLAMMATORY ENVIRONMENT
  • DENDRITIC CELLS ALSO ACTIVATE MACROPHAGES
  • MACROPHAGES SECRETE MORE CYTOKINES AS WELL AS PROTEASES
  • PROTEASES WILL ATTACK LINING OF THE INTESTINE

+

  • LAMINA PROPRIA CONTAINS VASCULAR CONNECTIONS; THERE ARE INACTIVE T CELLS IN THE BLOOD
  • BECAUSE THE INFLAMMATORY SIGNALS ARE HIGH, AN INTEGRIN PROTEIN MadCAM1 IS OVEREXPRESSED AND WILL ANCHOR THOSE T CELLS
  • THIS RECRUITMENT OF T CELLS IS BELIEVED TO BE THE CAUSE OF TRANSMURAL DESTRUCTION IN CROHN’S (DESTRUCTION OF ALL LAYERS OF THE GI SYSTEM)
  • THESE LEADS TO PRESENCE OF GRANULOMAS (ACCUMMULATIONS OF IMMUNE CELLS) AND IT IS ONE OF CROHN’S CHARACTERISTICS
35
Q

GRANULOMAS ARE A CHARACTERISTIC OF WHICH DISEASE?

A

CROHN’S

36
Q

HOW IS CROHN’S ABLE TO AFFECT DEEPER LAYERS OF THE GI TRACT TO ACHIEVE ITS TYPICAL TRANSMURAL DESTRUCTION?

A

INFLAMMATION LEVEL IN THE INTESTINES ARE HIGH IN CROHN’S DISEASE, AND THIS LEADS TO OVEREXPRESSION OF INTEGRIN PROTEIN MadCAM1 WHICH ANCHORS T CELLS FROM BLOOD IN VASCULAR CONNECTIONS OF THE LAMINA PROPRIA, SO THE IMMUNE RESPONSE/INFLAMMATION REACHES DEEPER LAYERS (BEYOND MUCOSA)

37
Q

POSSIBLE TREATMENTS FOR CROHN’S?

A

DEPENDING ON SYMPTOM SEVERITY:

  • ANTI INFLAMMATORY AGENTS (SALICYLATE)
  • ANTIBIOTICS (TO CONTROL GUT BACTERIA)
  • IMMUNO-SUPPRESSANTS (BUT LEAVES THE PATIENTS MORE PRONE TO OTHER INFECTIONS)
  • SURGERY (NOT ALWAYS SUCCESSFUL BECAUSE THE DISEASE CAN BE PATCHY)
38
Q

WHICH ANTI INFLAMMATORY THERAPY CAN BE USED IN CROHN’S?

A

SALICYLATE THERAPY

39
Q

IBD VS IBS

A

IBS - NO IMMUNE SYSTEM INVOLVEMENT, NO VISIBLE CHANGES OR ALTERATION OF THE GUT WALL, AFFECTS 15% OF PEOPLE WORLDWIDE, FOOD AND STRESS ARE MAJOR TRIGGERS
IBD - CHANGES SEEN IN MEDICAL IMAGING, CAN GET PROGRESSIVELY WORSE, RISK OF SURGERY AND HOSPITALIZATION, FEVER, BLOOD IN STOOL, ANEMIA….

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