Renal Pathology Flashcards

1
Q

What is H&E staining used for

A

To look at histological structure e.g. thickening of a membrane

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2
Q

What is periodic Acid-Schiff (PAS) used for

A

To stain carbohydrates and proteins

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3
Q

What is Masons trichrome used for

A

To stain collagen (blue) and look for connective tissues

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4
Q

What is Jones silver stain used for

A

Look for lacy membranes in conjunction with PAS or H&E

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5
Q

How is a Glomerular disease classified

A

By histological changes e.g. ADPGN

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6
Q

What are the characteristics of Crescentic Glomerulonephritis

A

Proliferation of epithelial cells
Enlargement and compression of glomerular rift causing it to shrivel and lose func.
Hard to treat

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7
Q

What could be a cause of crescentic glomerulonephritis

A

Diffuse GN
ADPGN
MPGN
Focal Segmented GN

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8
Q

Describe some clinical features and histological findings of renal disease

A

Increased proliferation of endo/epi/mesangial cells —> haematuria/nephritic
Changes to BM sensitivity —> proteinuria
Possible —> ARF

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9
Q

Name 4 methods of diagnosis for renal pathologies

A
  • Renal biopsy
  • Light microscopy (H&E, PAS, Jones & Trichrome)
  • immunofluorescence microscopy If electron microscopy
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10
Q

Characteristics of Focal Segmented GN

A

Cellular proliferation affecting one segment of glomerular tuft
Only affects portion of glomeruli (focal)

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11
Q

Difference between primary and secondary

A

Primary - caused by disease Incl. IgA mesangial disease and good pastures syndrome
Secondary - associated with systematic diseases

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12
Q

What can Minimal Change Disease cause

A

Most common nephrotic disease in children, proteinuria, fusion of podocyte feet altering specificity

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13
Q

What are the characteristics of Minimal change disease

A

Most common nephrotic disease in children, proteinuria, fusion of podocyte feet altering specificity

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14
Q

How can minimal change disease be treated

A

Typically with steroids to bring about remission

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15
Q

Characteristics of Membranous Nepropathy

A

Immune complex deposition in BM if all segments of Glom (Global)
No inflammation of epi/endothelial cells or proliferation
Origin of complexes unknown

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16
Q

Describe the process of the affect of Membranous Nepropathy

A

Immune complexes in Basal Membrane epithelial side —> new basal membrane forms around it —> complexes disappear leaving holes behind —> lacy BM affects specificity —> proteinuria —> nephrotic syndrome

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17
Q

Describe the difference between Type 1 and Type 2 MPGN

A
Type 1 (90%) lobularity by proliferation of mesangial cells, capillaries thicken due to immune complexes 
Type 2 (10%) less prominent proliferation, thickening of GNM, dense deposits of C3 in BM (no immune complexes, just compliment)
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18
Q

What can Membranous Proliferative GN cause

A

Haematuria, nephrotic syndrome or mixed nephrotic nephritic syndrome

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19
Q

What is nephrotic syndrome

A

Disturbance in glomerular structure.

  • reduces blood flow through glom —> leakage of RBCs to urine, haematuria
  • retention of waste products (uraemia, particularly nitrogenous waste)
  • activation of RAA system for fluid retention and mild hypertension
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20
Q

What is nephritic syndrom

A

Glom loses ability to retain protein (proteinuria).

  • conseq. Albumin decrease —> hypoalbuminaemia
  • oedema, result of abnormality in glomerular BM
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21
Q

What are the 4 patterns in glomerular disease

A

Deposition of immune complex
Proliferation of endothelial cells
Neutrophil polymorphism
Mildd mesangial cell Proliferative

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22
Q

Characteristics of Global, Segmental, Diffuse & Focal

A

Global - Whole glom and glom capillaries affected
Segmental - only part of glomeruli affected
Focal - some glomeruli affected
Diffuse - All glomeruli affected

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23
Q

How does ADPGN affect you

A
  • Blockage of capillaries —> less blood flow —> less filtration —> oliguria —> haematuria
  • Low BP —> hypertension —> (RA system) —> increase in BP
24
Q

Describe glomerulus function

A

Specialised capillary system, highly selective filtration barrier responsible for urine filtration
- ultrafiltration gets collected in B capsule —> drains into tubules

25
What are the 4 main components of glomerulus
Endothelial cells, basement membrane, mesangium and podocytes
26
Function and health is heavily dependant on structural integrity
T
27
How can the glomerulus be damaged
Vascular disease, immunological disorders; complex deposits, deposition of foreign material: amyloid
28
What are the 4 things all glomerular disease causes by at least one of?
- Proliferation of endothelial/mesangial cells —> block lumen —> decreases blood flow - BM thickening —> altered by specificity —> proteinuria - capillary wall necrosis (toxic substance) - crescent formation (ep cell prolif)
29
Characteristics of congenital diseases of kidneys
Common clinical problems, often associated with after clinical or developmental abnormalities of kidney e.g, horseshoe or Agenesis
30
Characteristics of poly cystic kidneys
Autosomal dominant Progressively enlarge over time Function deteriorated as cysts compress and replace functional tissue, chronic failure & hypertension
31
Name the 5 types of glomerular disease
``` Acute Diffuse Proliferative GN (ADPGN) Membranous Nephropathy (MN) Membranous Proliferative GN (MPGN) Focal Segmental Proliferative GN (FSPGN) Minimal Change Disease (MCD) ```
32
Characteristics of ARF
Majority of nephrons cease functioning. Reduced/no urine output (olig/anuria), electrolyte and fluid Imbalance.
33
Where can the cause of ARF be found
Pre-renal, renal, post-renal - reversible
34
Characteristics of CRF
progressive destruction of individual nephrons. Uraemia, failure of tubular function, polyuria, sometimes secondary to disease. Can —> Total renal failure
35
Description of causes of CRF
Tubular & interstitial Disease, vascular disease, tubular disease IRREVERSIBLE
36
State 2 types of benign renal tumour and 1 malignant tumour
Renal Adenoma & Oncocytomas | Adenocarcinoma: majority of malignant Tumour’s, originate from renal tubular epithelium
37
Describe some characteristics of congenital renal abnormalities
Glomerular (filtration), tubules (reabsorption), blood vessels (blood supply and carry blood to filter)
38
What abnormalities can you get in the UT
?
39
What are the two branches of partial renal failure
Nephrotic and Nephritic syndrome
40
Where do stones (calculi) tend to originate
Usually develop in renal pelvis then move to UT & get stuck in narrow areas
41
Brief description of calculi appearance and pathologies
Often large, spherical and laminated, subsequent to stasis or chronic infection - can cause squamous metaplasia —> cancer
42
Aetiology of renal tumours
Caused by environmental agents bring excreted in high concentrations in urine. majority occur in bladder and arise from Translational cell epithelium
43
Difference between high and low grade renal tumours
LG: only thickening of urothelial lining (overproliferation) HG: architectural disorganisation, cytological atypia, loss of nuclear polarity, mitosis freq. disturbance
44
80-85% of renal infections are caused by which organism?
E. Coli
45
What common disease can be a predisposition to renal infections
Diabetes Mellitus
46
Obstruction of the ureter/urethra can lead to:
Dilation of ureter - reabsorption of fluids by kidney | Dilation of bladder - hypertrophy of bladder wall —> outpouching
47
What is the name of solid aggregates found in the bladder & pelvicalyceal
Calculi (pebble in Latin)
48
Name some underlying causes for bladder stones
Low fluid/high salt intake, persistent UTIs or primary metabolic disturbances
49
What process is used to treat calculi
Ultrasound with aid of CT to break into passable size
50
Upper UT eliminates and the lower UT excretes
👌🏽
51
Where does the lower UT extend from
Calyces to urethra
52
Function of lower UT
Transmits urine from the kidney to exterior
53
What type of epithelium is the lower UT lines with
Urothelium
54
Name 2 pathologies of the UT
Infection and obstruction
55
State 2 types of UT obstruction
Intrinsic e.g. stone formation | Extrinsic e.g. tumour, pregnancy
56
True or False: polycystic kidneys are autosomal recessive
False, autosomal dominance