SAQ Flashcards

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1
Q

1a) What are the implications and potentials of this disease for the patient?

A
  • Inflammation and damage to the filtering part of the kidneys
  • Quick/slow onset
  • Toxins/metabolic waste/excess fluids are NOT properly filtered (build up, causing swelling and fatigue)
  • Haematuria (loss of RBC, due to inflammatory response)
  • Azotemia (too much waste product in blood, i.e., nitrogen, creatine)
  • Proteinuria (loss of proteins in blood)
  • High blood pressure (due to inflammation/scarring)
  • Dialysis may be needed (to clean blood and remove excess fluid/toxins)
  • Kidney failure requires transplant
  • May result in end-stage renal disease (ESRD)
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2
Q

1b) What would a positive result for the congo red method mean for the patient?

A
  • Congo Red differentiates between amyloidosis and fibrillary glomerulonrphritis (FGN)
  • They usually share similar electron microscope signatures and similar clinical signs
  • Positive result indicates amyloidosis
  • Detects the amyloid structure of protein aggregates
  • Blue-green birefringence and bright orange areas of amyloid deposition
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3
Q

1c) What is the principle of the PAS method?

A
  • A histochemical reaction
  • Demonstrates polysaccharides, glycogen, etc. in carbohydrates
  • Periodic acid oxidases carbohydrates to release aldehyde, making it an oxidised compound which fixes to the colourless Schiff’s reagent
  • Magenta colour localized at site of aldehyde formation
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4
Q

1d) How would the presence of “malignant hypertension” show as in the tissue?

A
  • Visible areas of thrombosis (blood clots in vessels) and necrosis
  • Glomerular lesions
  • Smaller glomeruli, varying degrees of hyalinization
  • Tubular atrophy (injury with thickened tubular basement membrane)
  • Periglomerular fibrosis (hardening/scarring of tissue)
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5
Q

1e) What type of glomerulonephritis is suggested in the photographic results above?

A
  • Crescentic/rapidly progressing glomerulonrphritis
  • Renal biopsy PAS shows: formation of crescent, composed of parietal epithelial cells, macrophages, fibrin
  • Fibrin found between proliferated cells
  • Compressed capillary loops
  • Segmental fibrinoid necrosis of glomerular tuffs
  • > 50% crescent formation in glomeruli
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6
Q

1f) What potential treatment and lifestyle changes would the patient need to consider with the disease?

A
  • Diet changes: less salt/protein (reduces strain on kidneys, reduced sodium retention and lowers blood pressure)
  • Dialysis for acute kidney failure
  • Angiotensin-converting enzyme (ACE) inhibitors (lower blood pressure)
  • Kidney transplant
  • Diuretics (remove excess fluid and increase urine production)
  • Corticosteroids (decrease inflammation)
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7
Q

2a) Describe and explain the significance of the indicated features from the haematology results, biochemistry results and any other aspects you consider significant to the diagnosis/patient symptoms. You may use features from the patient and normal blood films for comparison.

A
  • Burr cells: Little significance, common in population
  • Acanthocytosis cells: presence indicates glomerular bleeding as usually trapped and destroyed in spleen
  • Normochromic: indicates sufficient iron supply
  • Pale skin: indicates low RBC count (low oxygen and haemoglobin)
  • High blood pressure: strains organs, increasing risk of heart disease/attacks
  • Haematuria/Proteinuria: suggests advanced kidney damage
  • Low RBC count: issues in production or regularion (destroys quicker than produces) or blood loss somewhere
  • High total bilirubin: indicates liver/bile duct issues, or increase in RBC destruction
  • High blood urea: Suggests urea nitrogen not properly filtered by kidneys. Or due to dehydration
  • High total protein and albumin count in urine: dehydration or inflammation/chronic infection. Albumin leaks through damaged kidneys
  • High erythrocyte sedimentation rate: suggests inflammation/infection
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8
Q

2b) Explain what is meant by the tern extravascular haemolysis and the mechanisms by which RBCs are removed by macrophages.

A
  • Erythrophagocytosis in spleen
  • Filters blood to remove debris, old/damaged RBC and microorganisms
  • RBC usually have ~120 day lifespan
  • Many reticular fibres in spleen to support macrophages and dendritic cells
  • Blood carries microorganisms to spleen, where they are filtered out and phagocytosed by macrophages and DCs, then exposed to B/T lymphocytes to initiate adaptive immune response
  • Macrophages recognise RBCs by range of senescence markers
  • Destruction is antagonistically controlled by effects of CD47 and Phosphatidylserine
    1. Activation of phagocytes via inflammatory mediators
    2. Chemotaxis of phagocytes
    3. Attachment (enhanced with IgG)
    4. Ingestion of cell
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9
Q

2c) Because of these findings the patient was indicated to be in need of a Renal transplant. A kidney became available and a cytotoxic cross-match was undertaken to ensure donor/patient compatibility. Illustrate the principles of the complement dependant cytotoxicity cross match technique (8 marks) and demonstrate some of the advantages and disadvantages of this technique (2 marks)

A
  • Mechanism of host defence where antibodies induce target cell lysis via activation of complement system
  • CDC induced when C1q protein binds to Fc region of an antibody-opsinised (covered) cell
  • Leads to formation of C1 complex and eventually the complement membrane attack complex (MAC) which firms pores in cell membranes, leading to lysis
  • CDC is tightly regulated, using several monoclonal antibodies to attack target cells
  • Powerful screening platform used in HLA typing
  • CDC-HLA typing uses anti-HLA antibodies from monoclonal antibodies, incubates them with patient/donor’s lymphocytes
  • Amount of dead cells is measured
  • CDC assay: Incubate the patient’s serum with the donor’s lymphocytes, and second incubate after adding the rabbit complement
  • Dead cells indicate an unsuitable donor
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