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A. MLA Map Paediatrics > Coeliac disease > Flashcards

Coeliac disease Flashcards

1
Q

Coeliac disease is an immune response where the body initiates an immune response to gluten causing inflammation of the intestines. What % of the population are estimated to have coeliac disease?

1 - 1%
2 - 10%
3 - 25%
4 - 50%

A

1 - 1%

  • immune-mediated small intestinal (SI) enteropathy (intestinal disease)
  • triggered by exposure to dietary gluten in genetically predisposed individuals, leading to malabsorption
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2
Q

Coeliac disease is caused by a protein called gluten, which of the following common products is gluten least likely to be found in?

1 - wheat
2 - barley
3 - rye
4 - oats

A

4 - oats
- can be contaminated due to interactions with other gluten containing foods

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3
Q

Coeliac disease is caused by a protein called gluten, what specific part of gluten is associated with coeliac disease?

1 - gliadin
2 - glutenin
3 - heme
4 - avenalin

A

1 - gliadin
- umbrella term for a group of gluten peptides
- all share 33 amino acid sequence triggering immune response

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4
Q

Are men or women more susceptible to coeliac disease?

A
  • women are more susceptible
  • this may be because women are more likely to seek help then men
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5
Q

Where in the world is coeliac disease most common?

1 - south America
2 - USA and Europe
3 - Canada
4 - Australasia

A

2 - USA and Europe
- very common in Ireland and Scandanavia

  • can typically occur in childhood, but can occur at any age
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6
Q

Coeliac diseases induces and immune response. Patients diagnosed with coeliac disease are likely to have all or some of the the following conditions, EXCEPT which one?

1 - down’s syndrome
2 - Type 2 diabetes mellitus
3 - auto-immune hepatitis
4 - thyroid gland abnormalities.

A

2 - Type 2 diabetes mellitus
- not an immune response

  • type 1 diabetes is common
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7
Q

Are children of parents who have coeliac disease more likely to develop coeliac than the general population?

A
  • yes
  • 1st degree relatives of patients
  • greater concordance in monozygotic (identical) twins (75%)
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8
Q

Which 2 of the following genes that have been shown to correlate with coeliac disease?

1 - Human Leukocyte Antigen (HLA) DQ2 genes
2 - Human leukocyte antigen (HLA) DRB1 genes
3 - Human Leukocyte Antigen (HLA) DQ8 genes
4 - Human Leukocyte Antigen (HLA) B27 genes

A

1 - Human Leukocyte Antigen (HLA) DQ2 genes
3 - Human Leukocyte Antigen (HLA) DQ8 genes
- HLA genes encode MHC-II molecules and tell them what to bind with, such as gliadin

  • HLA DRB1 = RA
  • HLA B27 = spondylitis
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9
Q

Patients with coeliac disease typically present with all of the following symptoms, EXCEPT which one?

1 - diarrhoea
2 - steatorrhea (fatty floating stools)
3 - bloody stools
4 - weight loss.
5 - anaemia (iron, B12 and folate malabsorption)
6 - fatigue
7 - vague abdominal pains/bloating

A

3 - bloody stools

  • but 1/3 of patients can also be asymptomatic
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10
Q

What clinical signs can we often identify in patients with coeliac disease?

1 - mouth ulcers/glossitis
2 - dermatitis herpetiformis (itchy/blistering)
3 - raised autoantibodies
4 - all of the above

A

4 - all of the above

  • dermatitis herpetiformis (itchy/blistering) rash caused by IgA antibodies mistakenly bind to tissue transglutaminase in epidermis of the skin
  • common around umbilicus and knees
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11
Q

The most common symptoms that patients with coeliac disease present with include diarrhoea, steatorrhea (fatty floating stools), weight loss, anaemia, vague abdominal pains. Which part of the GIT is most commonly affected in coeliac disease?

1 - stomach
2 - jejunum
3 - ileum
4 - duodenum

A

2 - jejunum
- commonly affects duodenum as well

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12
Q

What is the name of the rash in the image below that patients with coeliac disease present with?

1 - dermatitis herpetiformis
2 - excema
3 - dermatomyositis
4 - psoriasis

A

1 - dermatitis Herpetiformis
- an itchy, vesicular rash on extensor surfaces

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13
Q

In the image below are 3 signs of coeliac disease. From left to right match the labels with the symptoms?

  • angular stomatitis (iron/vit B12 deficiency)
  • glosittis (iron deficiency)
  • pallor (anaemia)
A
  • far left = pallor (anaemia)
  • middle = angular stomatitis (iron/vit B12 deficiency)
  • far right = glosittis (iron deficiency)
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14
Q

Gliadin is able to be absorbed by the small intestines and enter the lamina propria, what are the 2 ways gliadin is able to cross epithelial cells in the small intestines?

A
  • paracellular (between cells and tigh junctions)
  • transcellular (through cells)
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15
Q

Gliadin is able to be absorbed by the small intestines, either paracellular (between cells and tight junctions)or transcellular (through cells) where it comes into contact with the lamina propria. Once into the lamina propria what is the 1st thing that happens to the gliadin?

1 - macrophage engulfs gliadin and presents it on its MHC-II complex
2 - enzyme tissue transglutaminase (tTG) removes amide group forming deaminated gliadin
3 - B cells produce antibodies against gliadin and tTG
4 - CD4 T-helper cell bind to MHC-II complex and releases cytokines (interferon gamma and TNF-a)

A

2 - enzyme tissue transglutaminase (tTG) removes amide group forming deaminated gliadin

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16
Q

Gliadin is able to be absorbed by the small intestines and enter the lamina propria. Once into the lamina propria the enzyme tissue transglutaminase (tTG) removes amide group producing deaminated gluten protein. What happens to the deaminated gluten proteins?

1 - macrophage engulfs gliadin and presents it on its MHC-II complex
2 - CD8 T cells bind and induce apoptosis in inflamed epithelial cells
3 - B cells produce antibodies against gliadin and tTG
4 - CD4 T-helper cell bind to MHC-II complex and releases cytokines (interferon gamma and TNF-a)

A

1 - macrophage engulfs gliadin and presents it on its MHC-II complex

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17
Q

Once deaminated gluten proteins have been phagocytosed by macrophages and presented on MHC-II. What immune cells bind to MHC-II?

1 - CD4 T helper cells
2 - CD8 cytotoxic t cells
3 - natural killer cells
4 - eosinophils

A

1 - CD4 T helper cells

18
Q

Once deaminated gluten proteins have been phagocytosed by macrophages and presented on MHC-II CD4 T helper cells bind to the MHC-II. What happens after this?

1 - macrophage engulfs epithelial cells
2 - CD8 T cells bind and induce apoptosis in inflamed epithelial cells
3 - B cells produce antibodies against gliadin and tTG
4 - CD4 T-helper cell bind to MHC-II complex and releases cytokines (interferon gamma and TNF-a)

A

4 - CD4 T-helper cell bind to MHC-II complex and releases cytokines (interferon gamma and TNF-a)

  • inflammatory cytokines can damage intestinal lumen
19
Q

Once deaminated gluten proteins have been phagocytosed by macrophages and presented on MHC-II CD4 T helper cells bind to the MHC-II and secrete inflammatory cytokines that can damage intestinal lumen. What 2 other cells are activated by T-helper cells?

1 - neutrophils
2 - CD8 cytotoxic t cells
3 - natural killer cells
4 - eosinophils

A

2 - CD8 cytotoxic t cells
3 - natural killer cells

20
Q

Once CD8 cytotoxic t cells and natural killer (NK) cells have been activated by T-helper cells in coeliac disease, what do the NK cells go on to do?

1 - engulfs gliadin entering lamina propria
2 - bind and induce apoptosis in inflamed epithelial cells
3 - produce antibodies against gliadin and tTG
4 - all of the above

A

2 - bind and induce apoptosis in inflamed epithelial cells

21
Q

Once B cells have been activated by CD4 T helper cells, they can produce 3 things. Which of the following is NOT one of these things?

1 - anti-tissue transglutaminase (tTG) IgA
2 - anti-gliadin IgA
3 - anti-CD8 cytotoxic T cells
4 - anti-endomysial (smooth muscle bundles of many tissue)

A

3 - anti-CD8 cytotoxic T cells

22
Q

All of the following are common histological signs of coeliac disease in GIT biopsies, EXCEPT which one?

1 - cobblestone appearence
2 - villus atrophy
3 - infiltration of inflammatory cells
4 - crypt hyperplasia

A

1 - cobblestone appearance
- this is common in crohns disease

23
Q

When trying to diagnose a patient with coeliac disease, what is really important?

1 - they must have a bowel prep
2 - free from gluten in diet for >24h
3 - free from gluten in diet for >48h
4 - remain on gluten diet until after diagnosis

A

4 - remain on gluten diet until after diagnosis
- if not consuming gluten then the disease may not be active
- at least 6 weeks prior to endoscopy

24
Q

What is typically the gold standard for diagnosing a patient with coeliac disease?

1 - measuring serum antibodies
2 - clinical history
3 - endoscopy with biopsy
4 - MRI scan

A

3 - endoscopy with biopsy
- can also measure antibodies in the biopsy

25
Q

Endoscopy is the gold standard for coeliac disease, where we can identify:

  • villus atrophy
  • crypt hyperplasia
  • inflammatory cell infiltration (lymphocytes)

Which scoring tool is used to identify the severity of the above in coeliac disease?

1 - blatchford score
2 - CURB-65 score
3 - DUKEs score
4 - Marsh criteria

A

4 - Marsh criteria

26
Q

When diagnosing coeliac disease we are able to measure antibodies in the plasma, which of the following antibodies should be tested?

1 - anti-endomysial (tissue surrounding smooth muscle)
2 - anti-tissue transglutaminase
3 - anti-gliadin antibodies
4 - all of the above

A

4 - all of the above

  • 6-22% of patients have serology negative coeliac disease so no detection of antibodies
  • anti-tissue transglutaminase = 1st choice
27
Q

When diagnosing coeliac disease we are able to measure antibodies in the plasma, we can measure the following antibodies

  • anti-endomysial (tissue surrounding smooth muscle)
  • anti-tissue transglutaminase
  • anti-gliadin antibodies

Which antibodies are these?

1 - IgA
2 - IgE
3 - IgM
4 - IgD

A

1 - IgA

28
Q

How do we treat coeliac disease?

1 - remove gluten from the diet
2 - lose weight
3 - bowel surgery
4 - corticosteroids

A

1 - remove gluten from the diet

29
Q

If we fail to treat a patient with coeliac disease the following complications can occur. Which of the following is NOT a complication of coeliac disease?

1 - vitamin deficiency
2 - anaemia
3 - osteoporosis
4 - RA
5 - ulcerated jejunum
6 - small bowel adenocarcinoma
7 - non-Hodgkin lymphoma

A

4 - RA

30
Q

When treating patients with coeliac disease why is it important to provide supplement vitamins and minerals?

A
  • increased risk of malabsorption
  • B12 (intrinsic factor), folate and calcium are often taken
  • annual bloods to monitor levels
31
Q

Re-feeding syndrome is often associated with all of the following, EXCEPT which one?

1 - hypokalemia
2 - hypomagnesemia
3 - hypophosphatemia
4 - hyponatraemia

A

4 - hyponatraemia

  • hypophosphatemia causes most of the associated symptoms of re-feeding syndrome
32
Q

If patients who have been starved for a period of time in a catabolic (breaking down amino acids, glycogen, lipoids etc for energy) state are re-fed to aggressively, this can lead to re-feeding syndrome and cause hypokalemia, hypomagnesemia and hypophosphatemia. Why does this occur?

1 - kidneys go into overdrive and increase urine output
2 - blood glucose levels drop and electrolytes flood out of cells
3 - blood glucose increases, insulin increases as dose anabolic processes
4 - all of the above

A

3 - blood glucose increases, insulin increases as dose anabolic processes

  • increased insulin drives anabolic process
  • electrolytes flood into cells to aid this metabolic process
33
Q

In addition to electrolyte disturbances in patients with re-feeding syndrome, which vitamin is particularly low?

1 - B12
2 - folate
3 - thiamine (B1)
4 - vitamin K

A

3 - thiamine (B1)
- low already but in re-feeding syndrome this is required for cells to function so thiamine floods into cells

34
Q

Low thiamine (B1) in re-feeding syndrome can cause wernicke-korsakoff syndrome. Which of the following are symptoms of this syndrome?

1 - confusion
2 - ataxia
3 - ophthalmoplegia (eye muscle weakness)
4 - psychosis
5 - confabulations (lies without any intent)
6 - amnesia (retro and antegrade)
7 - all of the above

A

7 - all of the above

  • wernicke = acute with confusion, ataxia and ophthalmoplegia (eye muscle weakness)
  • korsakoff = chronic neurological condition with psychosis, confabulations (lies without any intent) and amnesia
35
Q

Hypophosphatemia can occur in re-feeding syndrome. Which of the following does NOT occur due to hypophosphatemia?

1 - muscle weakness
2 - stroke
3 - rhabdomyolysis
4 - seizures
5 - arrhythmias
6 -paresthesia (burning, pins and needle feeling in hands)

A
36
Q

Hypokalemia can occur in re-feeding syndrome. Which 2 of the following typically occur due to hypokalaemia?

1 - ECG changes
2 - AKI
3 - pleural effusions
4 - muscle weakness

A

1 - ECG changes
- T wave flattening and U waves
- increased risk of arrhythmias

4 - muscle weakness
- typically begins in lower limbs

37
Q

Which of the following is NOT a risk factor when trying to identify patients at risk of re-feeding syndrome?

1 - BMI < 25 kg/m2
2 - unintentional weight loss >15% over 3-6 months
3 - little nutritional intake > 10 days
4 - hypokalaemia, hypophosphataemia or hypomagnesaemia prior to feeding (unless high)

A

1 - BMI < 25 kg/m2
- typically <16 kg/m2

38
Q

In a patient at risk of re-feeding syndrome patients should initially be fed on 50% of their requirements over what time period before an increase?

1 - 2 hours
2 - 12 hours
3 - 16 hours
4 - 24 hours

A

4 - 24 hours

39
Q

A 35 year old female presents to her GP with fatigue and a new itchy vesicular rash over her knees and is found to have iron deficiency. Her GP checks her bloods which confirm she is positive for anti-tissue transglutaminase. What is the name for the rash?

1) Eczema
2) Shingles
3) DermatitisHerpetiformis
4) Impetigo
5) Bullous Pemphigoid

A

3) DermatitisHerpetiformis

40
Q

Coeliac Disease is diagnosed by a combination of positive serology and positive histology. What histological findings would confirm coeliac disease?

1) Gastric crypt hyperplasia, flattened gastric villi, intraepithelial lymphocytes
2) Gastric crypt hypoplasia, enlarged gastric villi, helicobacter pylori
3) Duodenal crypt hyperplasia, enlarged duodenal villi, intraepithelial lymphocytes
4) Duodenal crypt hyperplasia, flattened duodenal villi, intraepithelial lymphocytes
5) Duodenal crypt hypoplasia, flattened duodenal villi, intraepithelial neutrophils

A

3) Duodenal crypt hyperplasia, enlarged duodenal villi, intraepithelial lymphocytes

41
Q

Refeeding syndrome is associated with which one of the following abnormalities:

1) HighPhosphate
2) LowPhosphate
3) HighThiamine
4) Hypovolaemia
5) Hyperkalaemia

A

2) LowPhosphate

42
Q

A 65 year old is admitted with vomiting and weight loss and on her radiology is confirmed to have a gastric outlet obstruction from a resectable pancreatic cancer compressing the duodenum. She describes 5% weight loss in the last 2 months. An OGD is performed and a very tight impassable stricture confirmed. What is her best feeding option?

1) A nasogastrictube
2) A nasojejunaltube
3) A PEG
4) A RIG
5) Parenteral Nutrition

A

5) Parenteral Nutrition
- there is an impassable stricture
- no matter what other option is tried, the food cannot pass and get to the rest of the GIT

A. MLA Map Paediatrics (61 decks)

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