1. Pathology of the kidney, ureters and bladder 1 Flashcards

1
Q

4 roles of the kidney?

A
  1. Fluid and electrolyte balance
  2. Resorption of solutes
  3. Excretion e.g. of conjugated xenobiotics
  4. Endocrine
    - Renin for bp control
    - Erythropoietin for RBC production
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2
Q

4 examples of congenital renal abnormalities?

A
  1. Hypoplasia (possibly due to RA stenosis)
  2. Potter syndrome (bilateral renal agenesis)
  3. Vesicoureteric reflux (from bladder back up ureters, leading to irritation and infection)
  4. Renal artery stenosis cyst
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3
Q

Genetic renal abnormalities?

A
  1. Autosomal dominant polycystic disease (leads to chronic renal failure and dialysis)
  2. Simple cyst (common, not worry)
  3. Familial mediterranean fever
  4. Alport’s syndrome
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4
Q

Glomerular disease:
Mediated by? There associated to..
Examples of primary and secondary?

A

Medicated by Immunological processes therefore HLA association

Primary: Glomerulonephritis
Secondary: Vascular, autoimmune e.g. SLE, amyloid, diabetes, acquired.

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5
Q

SLE stands for?

A

Systemic lupus erythematosus

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6
Q

What is the consequence of type II hypersensitivity in the glomerulus?
Features?
Appearance?

A
  1. Anti-GBM antibodies and Complement fixation (by antibodies IMG and IGG)
  2. Diffuse damage and fibrin leakage

Features

  • Proliferated parietal endothelial cells due to fibrin
  • Focal disruption of BM
  • Increased mesangial cells
  • Focal loss of foot processes
  • Fibrin present on parietal cells.

Appearance: Crescent due to proliferation of parietal epithelium and inflammatory cells. Forms scar so glomerulus is lost.

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7
Q

What is good pastures syndrome?

A

Goodpasture disease is a term used to describe glomerulonephritis (type II hypersensitivity), with or without pulmonary hemorrhage, and the presence of circulating anti–glomerular basement membrane (anti-GBM) antibodies.

Leads to characteristic proliferation of parietal epithelium and inflammatory cells –> Crescents

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8
Q

Clinical effects of type 2 hypersensitivity in the glomerulus?

A
Fast
Haematuria: Yes
Proteinuria: Yes but not a lot 
Less urine due to nephron comprise, oliguria 
Lung involvement
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9
Q

What is the consequence of type III hypersensitivity in the glomerulus?

Features?

A

Immune complex deposition
Size determines where deposition occurs
+/- complement fixation

Features:

  • Proliferated endothelial cells
  • Increased mesanglial cells
  • Immune complexes present
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10
Q

Causes of type 2 hypersensitivity in the glomerulus?

A

Goodpastures-autoimmune
Vasculitis - ANCA (Anti-neutrophil cytoplasmic antibodies)
SLE
Organic solvent

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11
Q

Clinical effects and causes of type 3 hypersensitivity in the glomerulus?

A

Clinical effects:
-Fast or slow. depends on immune complex formation
-Haematuria: Yes
-More or less urine
-Proteinuria: Little
-Pain: yes due to inflammation and swelling
=Nephritic syndrome

Causes:

  • Post infection e.g. strep.
  • Vasculitis e.g. ANCA
  • SLE
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12
Q

Membranous GN:
What is it?
Clinical effects?
Causes?

A

What is it?
An immunologically mediated disease in which immune complexes deposit in the subepithelial space

Clinical effects:
Slow process
Haematuria: A little 
More urine initially
Proteinuria: YES
Pain: No, due to to active inflammation
=Nephrotic syndrome

Causes:

  • Males>females
  • Adults
  • Hep B
  • Idiopathic
  • Penicillamine
  • SLE
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13
Q
Minimal lesion GN:
Who?
Treat with?
Clinical effect?
Causes?
Type of hypersensitivity?
A

Who: Children
Treat with steroids
Clinical effect: Marked proteinuria
Causes: Hodgkins lymphoma, remission with measles

Type 4 HS= Foot processes fuse leads to proteinuria, nephrotic syndrome, high lipids, cell mediated.

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14
Q

Consequence of glomerular damage?

A

Glomerular damage
–>
Increased permeability of glomerular capillaries to protein
–> Proteinuria
–> Hypoproteinemia
1. Compesatory synthesis of proteins by liver (increasing lipoproteins) –> HYPERLIPIDEMIA
2. Decrease plasma oncotic pressure –> Edema

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15
Q

Difference between nephritic and nephrotic syndrome?

A

Nephrotic syndrome involves the loss of a lot of protein

Nephritic syndrome involves the loss of a lot of blood.

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16
Q

Clinical features of nephritic syndrome?

A

Blood
Pain
Less proteinuria
Oliguria

17
Q

Causes of proteinuria apart from nephritic and nephrotic syndrome?

A

Diabetes

Amyloidosis

18
Q

Causes of focal and segmental necrotising GN?

A

Proliferative GN
Vasculitiis
SLE

19
Q

Tubulointerstitial disease

A

Cause: Drug hypersensitivity *, also due to ischaemia and SLE

Leads to acute tubular necrosis and ascending infection

20
Q

TTTIS classification of renal pathology

A

TRAUMA
-Trauma

TUMOUR

  • Non-neoplastic
  • Benign
  • Malignant (primary/secondary)

TUBERCLE
-Chronic inflammatory

INFLAMMATION

  • Infection
  • Acute inflammation
  • Immunological

STONE

  • Genetic
  • Metabolic
21
Q

What is the effect of kidney hypoplasia due to renal artery stenosis on bp?

A

Leads to hypertension and the failure kidney thinks it’s ischaemic leading to renin release

22
Q

3 components of glomerulus filter?

A
  1. Fenestrated endothelial cells
  2. Charge of BM
  3. Foot processes of podocytes which forms slit diaphragm
23
Q

Examples of nephritic and nephrotic syndrome?

A

Nephrotic syndrome: Minimal change, FSGS, membranous

Nephritic syndrome: Proliferative GN, mesangiocapillary GN

24
Q

Common vascular diseases affecting the kidneys

A
  • Hypertension
  • Vasculitis
  • Mesangial IgA disease
  • TTP
  • HUS