SAQ Seen Part Flashcards
Difference between haemochromatosis and haemosiderosis
Haemochromatosis
- autosomal recessive disorder
- systemic iron deposition causing tissue damage around body
- no haemosiderin accumulation seen
Haemosiderosis
- not due to genetic defect, result of alcoholism or thalassaemia
- focal iron deposition that doesn’t cause tissue damage around body
- haemosiderin accumulation is seen
Principle of Perls reaction
- detects iron in haemosiderin
- iron is detected by potassium ferrocyanide
- produces dense blue precipitate (pigment Prussian blue)
- iron won’t react w/ ferrocyanide, must be released by acid hydrolysis
What is Perls reagent a mixture of?
- 2% potassium ferrocyanide
- 2% hydrochloric acid
Hexagonal-shaped “classical lobule” unit of the liver
- hexagonal plates of hepatocytes stacked on top of each other
- as hepatocytes extend towards periphery, they’re arranged into strips
- organized into irregular anastomosing plates that radiate towards a central vein
- portal triad; branches of portal vein, hepatic artery, bile ducts and small lymphatic vessels
- portal triad is surrounded by loose stromal connective tissue
What does Reticulin staining highlight in a liver biopsy?
- assesses liver architecture, mainly hepatic plates
- highlights reticulin fibers (type III collagen) in the space of Disse, shows thickness of hepatocyte plates
- fibres appear black against grey or light pink background
- makes it easier to visualize areas of hepatocyte loss (collapse) or regeneration (increased thickness)
- also shows compression of plates in nodular regressive hyperplasia and collapse of reticulin framework in necrosis
Principle of H&E staining
- Haematoxylin: basic dye,stains acidic and basophilic structures
- Haematoxylin: cell nucleus, ribosomes, rough ER stain blue/purple
- Eosin: acidic dye, stains basic and acidophilic structures
- Eosin: cytoplasm, cell walls, extracellular fibres stain pink
- gives diagnosis in 70% of clinical reports
How would be presence of “Cirrhosis” show in the liver?
- activation of hepatic stellate cells causes myofibroblasts to expand
- thick bands of mature fibrous tissue from expansion of myofibroblasts
- nodules of regenerative hepatocytes
- healthy liver cells replaced by scar tissue, loss of normal architecture
Mutation that gives rise to sickle cell anaemia
- mutation on HBB gene on chromosome 11
- results in production of abnormal version of beta-globin called haemoglobin S
Major symptoms of sickle cell anaemia
- anaemia: sickle cells are destroyed easily causing RBC shortage, body can’t get enough O2, fatigue and shortness of breath
- pain crises: extreme pain periods, can last up to a week
- frequent infections: can damage spleen, increasing vulnerability
- delayed growth/puberty: RBC shortage can slow growth
Why does it lead to sickling?
- HBB gene that codes for Hb production undergoes mutation
- abnormal Hb molecules stick to one another and form long, rod-like structures
- RBCs become stuff and misshaped, assuming a sickle shape
Events that lead to higher
monocyte/macrophage counts in the patient’s liver
- Kupffer cells: induce immune tolerance to antigens, repair tissue after injury, sense alterations in tissue integrity
- MoMOs: pro-inflammatory and anti-inflammatory, replenish KCs after injury
- liver failure can immunosuppress, highly susceptible to infections
- monocyte infiltration lead to local destruction, pro-inflammatory cytokines released
- liver cell injury - activation of hepatic stellate cells - KCs released mediators - myofibroblasts expansion - fibrosis - cirrhosis
Principles of the Complement Dependent Cytotoxicity
Antibody Screening technique
- most popular method of HLA Ab detection
- lymphocyte target cells used to detect complement-fixing IgG and IgM in serum after rabbit complement addition
- DTT differentiates IgM from IgG
- DTT reduces disulphide bonds in IgM pentamer, renders negative a reaction due to IgM
- serum samples are tested against lymphocyte panel either random or alternatively selected to represent spectrum of HLA types in donor population
Advantages of Antibody Screening Technique
- autoantibodies are frequently weak or non-reactive w/lymphocytes from patients w/B-cell chronic lymphatic leukaemia
- these cells can be useful in elucidating patient’s antibody profile
Disadvantages of Antibody Screening Technique
- while DTT can differentiate IgM + IgG, doesn’t indicate specificity of antibody
- potentially clinically relevant weak IgG HLA-specific antibodies may also be rendered negative after DTT addition
