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Immunology - Path > Malabsorption > Flashcards

Malabsorption Flashcards

1
Q

What are the causes of a low MCV?

A
  • Iron deficiency
  • Thalassemia trait
  • Anaemia of chronic disease
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2
Q

Describe what the following will be in Iron deficiency anemia:

  1. Hb
  2. Serum iron
  3. TIBC or transferrin
  4. Transferrin saturation
  5. Ferritin
A
  1. Hb - LOW
  2. Serum iron - LOW
  3. TIBC or transferri - RAISED
  4. Transferrin saturation - LOW
  5. Ferritin - LOW
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3
Q

What will be following be in Anemia of chronic disease?

  1. Hb
  2. Serum iron
  3. TIBC or transferrin
  4. Transferrin saturation
  5. Ferritin
A
  1. Hb - LOW
  2. Serum iron - LOW
  3. TIBC or transferrin - NORMAL/LOW
  4. Transferrin saturation - NORMAL
  5. Ferritin - NORMAL (high in acute phase)
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4
Q

Describe what the following would be like in Thalassemia trait:

  1. Hb
  2. Serum iron
  3. TIBC or transferrin
  4. Transferrin saturation
  5. Ferritin
A
  1. Hb - NORMAL/LOW
  2. Serum iron - NORMAL
  3. TIBC or transferrin - NORMAL
  4. Transferrin saturation - NORMAL
  5. Ferritin - NORMAL
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5
Q

What does this image show? What could this be?

A
  • Hypochromic RBC
  • Pale
  • Microcytic RBC

Iron deficiency anemia

Thalassemia trait

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6
Q

What are the irregular shaped cells in this blood film called?

What are they a sign of?

A
  • Poikilocytes - abnormally shaped red blood cells - ‘tear drop’ cell
  • Also a sign of hypochromic red cells
  • Signs of Iron deficiency anemia
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7
Q

What is anisopoikilocytosis? What can it be a sign of?

A

Anisopoikilocytosis

  • Variations in size (aniso)
  • and shape (poikilo)
  • of cells (cytosis)

Sign of iron deficiency

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8
Q
  1. What does the image show?
  2. What could this be a sign of?
A
  1. Basophillic stippling - aggregated ribosomal material
  2. Can be a sign of:
  • Beta thalassemia trait
  • Lead poisoning
  • Alcoholism
  • Sideroblastic anemia - form of anemia where the bone marrow produces ringed sideroblasts rather than normal erythrocytes
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9
Q
  1. What does this image show?
  2. What is the caused/what is it a sign of?
  3. What could this be a sign of?
A
  1. Hypersegmented neutrophil
  2. This is megaloblastic anemia, which reflects impaired DNA synthesis
  3. Can be a sign of B12 deficiency, Folate deficiency and Drugs
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10
Q
  1. What does this image show?
  2. What are they?
  3. What can they be a sign of?
A
  1. Target cells/Codocytes
  2. Codocytes have a relatively high surface area:volume ratio
  3. Can be a sign of:
  • Iron deficiency
  • Thalassemia
  • Hyposplenism
  • Liver disease
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11
Q
  1. What does this image show/what is the abnormality?
  2. What is this abnormality a sign of?
A
  1. Howell-Jolly bodies - signs of nuclear remnants visible in red cells
  2. Hyposplenism
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12
Q

EMQ

Which are the following features of iron deficiency anemia?

A. Howell Jolly bodies and codocytes (target cells)

B. Macrocytosis and hypersegmented neutrophils

C. Microcytic hpochromic red cells with anisopoikilocytosis

A

C- microcytic hypochromic red cells with anisopoikilocytosis

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13
Q

What are the causes of iron deficiency?

A
  • MAJOR CAUSE - blood loss
  • Poor diet
  • Malabsorption
  • Combinations of the above
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14
Q

What are the causes of a megaloblastic change?

A
  • B12 or folate deficiency
  • Poor diet
  • Malabsorption
  • Pernicious anemia
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15
Q

What are the causes of hyposplenism?

A
  • Absent spleen - theraputic or trauma
  • Poorly-functioning spleen
    • Inflammatory bowel disease
    • Coeliac disease
    • Sickle cell disease
    • SLE
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16
Q

EMQ

Blood results show:

Ca 2.00 (2.15-2.65umol/l)

Alk phos 400 (30-130 U/l)

Vitamin D 18 (70-150nmol/l)

PTH 14 (1.1-6.8pmol/l)

What is the diagnosis?

A. Primary hyperparathyroidism

B. Vitamin D deficiency and secondary hyperparathyroidism

C. Vitamin D deficiency and tertiary hyperparathyroidism

D. Hypoparathyroidism

E. Osteoporosis

A

B - Vitamin D deficiency and secondary hyperparathyroidism

17
Q

What deficiences will be seen with the following conditions?

  1. Coeliac disease
  2. Crohn’s disease
  3. Pancreatic disease
  4. Infective/post-infective
A
  1. Coeliac disease - Iron, B12, Folate, Fat and calcium
  2. Crohn’s disease - B12, bile salts
  3. Pancreatic disease - Fat, Ca, B12
  4. Infective/post-infective - Fat, Folate
18
Q

What investigations should be done if suspecting a GI malabsorption issue?

A
  • Inflammatory markers - CRP and ESR
  • Serological tests
  • Upper GI endocscopy and distal duodenal biopsies
  • Faecal elastase, pancreolauryl test, CT scanning
  • MRI of small bowel
19
Q
  1. What is coeliac disease?
  2. What is the form of inheritance?
  3. Which HLA is it associated with?
A
  1. Coeliac disease is a polygenic auto-immune disease, causing an intolerance to gluten
  2. 75% concordanxe in monozygotic twins. 40% heritability maps to MHC complex gene loci
  3. 90% patients carry HLA DQ2
20
Q

What happens during coeliac disease when gluten is present?

A
  • Coeliac disease is T cell response to gluten
  • Peptides from gliadin are demaidated by tissue transglutaminase and presented by APCs
  • CD4 T cells recognise deamidated peptides presented by HLA DQ2 or DQ8
  • T cell activation leads to the secretion of IFN-gamma and may indirectly increased the release of IL-15
  • Cytokines produced promotes activation of the intra-epithelial lymphocytes
  • Intra-epithelial lymphocytes kill epithelial cells in a NKG2D dependent manner. Therefore damage in coeliac is mediated by gamma and delta T cell receptors expressing IEL (intra-epithelial lymphocytes)
21
Q

What are the antibodies in coeliac disease

A
  • Anti- Tissue transglutaminase
  • Endomysial antibodies
  • Deamidated gliadin peptide antibodies
22
Q

What does tissue transglutaminase do?

A

Tissue transglutaminase deamidates gliadin. Gliadin is component of gluten

23
Q

Describe how the body can produce anti-gliadin antibodies and their role in the pathophysiology of coeliac disease

A
  • Stimulation of T cells specific for gliadin peptides - APC presents a gliadin peptide complex (HLA DQ2 or 8)
  • T cells specific for gliafin provide help for B cells whose surface receptors recognise gliadin
  • B cells specific for gliadin mature to form plasma cells secreting antibodies specific for gliadin
  • antibodies for anti-gliadin attack gliadin produced when gluten is broken down and cause an immune response in the body when gluten is ingested
24
Q

Describe the production of antibodies against transglutaminase

A
  • T cells specific for gliadin can also provide help for B cells whose surface receptors recognise the transglutaminase part of the transglutaminase/gliadin complex
  • B cells for transglutaminase mature to for plasma cells secreting antibodies specific for transglutaminase
  • antibodies recognise surface tissue transglutaminase on the endomysial cells
25
Q

Describe the different serological tests for coeliac disease including sensitivity and specificity and when they appear

A
  • IgA anti-transglutaminase antobody - sensitivity = 90-94%, specificity =95%. Antibody appears within several months after insitution of gluten free diet
  • IgA anti-endomysial antibody - sensitivity 85-94%, specificity = 95%. Antibody disappears within several months after insitution of gluten free diet
  • IgA or IgG anti-gliadin antibody - sensitivity = 57-80%, specificity =30-50%. Most persistent, may be detectable up to 12 months after institution of a gluten-free diet. Not used often as a poor test
26
Q

What is the gold-standard for diagnosis of coeliac disease and why?

A
  • duodenal biospy and histology is gold standard
  • otherwise, there is major implications of the diagnosis including having to follow a gluten-free diet and complications of having coeliac disease
27
Q

What is the histopathology of coeliac disease from a duodenal biopsy?

A
  • Villous atrophy
  • Normal villous:crypt ratio is 2-4:1. In coeliac disease, the villous height is reduced and crypts become hyperplastic, resulting in reduced villous:crypts ratio
  • mucosal thickness remains the dame due to crypt hyperplasia
  • villous atrophy results in decreased surface area leading to malabsorption
28
Q
  1. What are intraepithelial lymphocytes?
  2. How many are there in people with coeliac disease?
  3. What else can cause an increase in IELs?
A
  1. Normal duodenal villi contain less than 20 IELs per 100 epithelial cells. These lymphocytes are 𝛄ƍ T cells
  2. In coeliac disease, this is increased to more than 20 IELs oer 100 epithelial cells
  3. Other causes include: dermatitis herpetiformis, giardiasis, cows milk protein sensitivity, IgA deficiency etc.
29
Q

Apart from coeliac disease, what are other causes of villous atrophy?

A
  • Giardiasis - parasitic infection
  • tropical sprue
  • Crohn’s disease
  • Radiation/chemotherapy
  • Bacterial overgrowth
  • Nutritional deficiencies
  • Graft vs host disease
  • Microvillous inclusion disease
  • Common variable immunodeficiency
30
Q

A diagnosis of coeliac disease was made in someone, what needs to be done now?

A
  • Dietary management - avoidance of gluten
  • Advice long term about complications
  • Implications for family
  • Sources of patient information
  • Ongoing monitoring
31
Q

What are the complications of coeliac disease?

A
  • Malabsorption
  • Osteomalacia and osteoporosis
  • Neurological disease - epilepsy and cerebral calcification
  • Lymphoma - EATL
  • Hyposplenism
32
Q

What are the possible complications of undiagnosed coeliac disease?

A
  • Undiagnosed deficiencies - iron, folate, B12, Vitamin D and K
  • Dietary compliance protects against malignancy
  • Often feel better physically and psychologically when treated
  • mortality rate of untreated coeliacs is x2-3 of general popultion - lymphomas and infection
33
Q

What other automimmune conditions is coeliac disease associated with?

A
  • Dermatitis herpetiformis = 100%
  • Type 1 diabetes mellitus = 7%
  • Autoimmune thyroid disease
  • Down’s syndrome
34
Q

In which patients is it useless in looking for antibodies for coeliac disease?

A

Patients who are IgA deficient

35
Q
A

Immunology - Path (9 decks)

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