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
Q

What are the 4 main components of glomerulus

A

Endothelial cells, basement membrane, mesangium and podocytes

26
Q

Function and health is heavily dependant on structural integrity

A

T

27
Q

How can the glomerulus be damaged

A

Vascular disease, immunological disorders; complex deposits, deposition of foreign material: amyloid

28
Q

What are the 4 things all glomerular disease causes by at least one of?

A
  • 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
Q

Characteristics of congenital diseases of kidneys

A

Common clinical problems, often associated with after clinical or developmental abnormalities of kidney e.g, horseshoe or Agenesis

30
Q

Characteristics of poly cystic kidneys

A

Autosomal dominant
Progressively enlarge over time
Function deteriorated as cysts compress and replace functional tissue, chronic failure & hypertension

31
Q

Name the 5 types of glomerular disease

A
Acute Diffuse Proliferative GN (ADPGN)
Membranous Nephropathy (MN)
Membranous Proliferative GN (MPGN)
Focal Segmental Proliferative GN (FSPGN)
Minimal Change Disease (MCD)
32
Q

Characteristics of ARF

A

Majority of nephrons cease functioning. Reduced/no urine output (olig/anuria), electrolyte and fluid Imbalance.

33
Q

Where can the cause of ARF be found

A

Pre-renal, renal, post-renal - reversible

34
Q

Characteristics of CRF

A

progressive destruction of individual nephrons. Uraemia, failure of tubular function, polyuria, sometimes secondary to disease. Can —> Total renal failure

35
Q

Description of causes of CRF

A

Tubular & interstitial Disease, vascular disease, tubular disease
IRREVERSIBLE

36
Q

State 2 types of benign renal tumour and 1 malignant tumour

A

Renal Adenoma & Oncocytomas

Adenocarcinoma: majority of malignant Tumour’s, originate from renal tubular epithelium

37
Q

Describe some characteristics of congenital renal abnormalities

A

Glomerular (filtration), tubules (reabsorption), blood vessels (blood supply and carry blood to filter)

38
Q

What abnormalities can you get in the UT

A

?

39
Q

What are the two branches of partial renal failure

A

Nephrotic and Nephritic syndrome

40
Q

Where do stones (calculi) tend to originate

A

Usually develop in renal pelvis then move to UT & get stuck in narrow areas

41
Q

Brief description of calculi appearance and pathologies

A

Often large, spherical and laminated, subsequent to stasis or chronic infection
- can cause squamous metaplasia —> cancer

42
Q

Aetiology of renal tumours

A

Caused by environmental agents bring excreted in high concentrations in urine.
majority occur in bladder and arise from Translational cell epithelium

43
Q

Difference between high and low grade renal tumours

A

LG: only thickening of urothelial lining (overproliferation)
HG: architectural disorganisation, cytological atypia, loss of nuclear polarity, mitosis freq. disturbance

44
Q

80-85% of renal infections are caused by which organism?

A

E. Coli

45
Q

What common disease can be a predisposition to renal infections

A

Diabetes Mellitus

46
Q

Obstruction of the ureter/urethra can lead to:

A

Dilation of ureter - reabsorption of fluids by kidney

Dilation of bladder - hypertrophy of bladder wall —> outpouching

47
Q

What is the name of solid aggregates found in the bladder & pelvicalyceal

A

Calculi (pebble in Latin)

48
Q

Name some underlying causes for bladder stones

A

Low fluid/high salt intake, persistent UTIs or primary metabolic disturbances

49
Q

What process is used to treat calculi

A

Ultrasound with aid of CT to break into passable size

50
Q

Upper UT eliminates and the lower UT excretes

A

👌🏽

51
Q

Where does the lower UT extend from

A

Calyces to urethra

52
Q

Function of lower UT

A

Transmits urine from the kidney to exterior

53
Q

What type of epithelium is the lower UT lines with

A

Urothelium

54
Q

Name 2 pathologies of the UT

A

Infection and obstruction

55
Q

State 2 types of UT obstruction

A

Intrinsic e.g. stone formation

Extrinsic e.g. tumour, pregnancy

56
Q

True or False: polycystic kidneys are autosomal recessive

A

False, autosomal dominance