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PATH FINAL > Histo: Renal Pathology > Flashcards

Histo: Renal Pathology Flashcards

1
Q

Outline which kidney pathology affects the glomerulus, tubulues / interstitium and blood vessels

A

Glomerulus
Nephrotic syndromes
Nephritic syndromes

Tubules and Interstitium
Acute tubular necrosis
Tubulointerstitial nephritis

Blood vessels
Thrombotic microangiopathies (HUS, TTP)

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2
Q

Define nephrotic syndrome

A

Several renal diseases which cause increased glomerular permeability.

Characterised by triad:
1. proteinuria (>3g/24hrs / “frothy urine”)
2. Hypoalbuminaemia
3. Oedema (peri-ocular in children)

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3
Q

Primary causes of nephrotic syndrome

A
  • Minimal change disease
  • Membranous Glomerular Disease
  • Focal Segmental Glomerulosclerosis
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4
Q

Secondary causes of nephrotic syndrome

A

Diabetes
Amyloidosis

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5
Q

Differentiate between the epidemiology of the primary causes of nephrotic syndrome
* Minimal change disease
* Membranous Glomerular Disease
* Focal Segmental Glomerulosclerosis

A
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6
Q

Differentiate between the aetiological processes behind the primary causes of nephrotic syndrome
* Minimal change disease
* Membranous Glomerular Disease
* Focal Segmental Glomerulosclerosis

A

Minimal change disease
Idiopathic - possible trigger being recent allergic reaction as associated with eczema and asthma

Membranous Glomerular Disease
Primary = antibodies against phospholipase A2 present in 75% of cases. commonest
Secondary = SLE, infection, drugs, malignancy

FSGs
Primary = idiopathic
Secondary = obesity, HIV, drugs (lithium, heroin), lymphoma

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7
Q

Differentiate between the changes seen on light microscopy between the primary causes of nephrotic syndrome
* Minimal change disease
* Membranous Glomerular Disease
* Focal Segmental Glomerulosclerosis

A
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8
Q

Differentiate between the changes seen on electron microscopy between the primary causes of nephrotic syndrome
* Minimal change disease
* Membranous Glomerular Disease
* Focal Segmental Glomerulosclerosis

A

ALL show loss of podocyte foot processes

membranous glomerular disease shows subepithelial deposits described as “spikey”

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9
Q

Differentiate between the changes seen on immunofluroescence between the primary causes of nephrotic syndrome
* Minimal change disease
* Membranous Glomerular Disease
* Focal Segmental Glomerulosclerosis

A
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10
Q

Outline the response to steroids between between the primary causes of nephrotic syndrome
* Minimal change disease
* Membranous Glomerular Disease
* Focal Segmental Glomerulosclerosis

A
  • Minimal change disease = good
  • Membranous Glomerular Disease = poor
  • Focal Segmental Glomerulosclerosis = 50% respond
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11
Q

Outline the management of the primary causes of nephrotic syndrome
* Minimal change disease
* Membranous Glomerular Disease
* Focal Segmental Glomerulosclerosis

A
  • Minimal change disease = 1) steroids 2) cyclosporin
  • Membranous Glomerular Disease = steroids and ACEi/ARB to control HTN
  • Focal Segmental Glomerulosclerosis= steroids and ACEi/ARB to control HTN
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12
Q

Differentiate between the histological findings of the secondary causes of nephrotic syndrome
* Diabetes
* Amyloidosis

A
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13
Q

What are the 2 common types of Amyloidosis which can lead to nephrotic syndrome

A

AA Amyloidosis = acut ephase protein amyloidosis, associated with chronic inflammation

AL Amyloidosis = light chain amyloidosis commonly secondary to multiple myeloma

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14
Q

Outline what the trends in the following investigation would be like in nephrotic syndrome
* Urine dip
* Urine PCR
* Serum albumin
* Total cholesterol
* Immunoglobulins

A

note: renal biopsy is investigation of choice in adults but avoided in children

Urine dip = proteinuria but NO haematuria
Urine PCR = >300mg/mmol
Serum albumin = low
Total cholersterol = high
Immunoglobulins = low

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15
Q

Define nephritic syndrome

What is it characterised by

A

Disorders involving glomerular inflammation

Characterised by: PHAROH
Proteinuria (less than nephrotic)
Haematuria
Azootemia (high urea and creatinine)
Red cell casts in urine
Oliguria
Hypertension

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16
Q

Outline the main causes of nephritic syndrome

A
  • Post streptococal glomerulonephritis
  • IgA nephropathy (Berger’s Disease)
  • Rapidly progressive glomerulonephritis
  • Hereditary nephritis
  • Thin basement membrane disease (benign familial haematuria)
17
Q

Key features of post streptococcal nephritis
(sx onset, pathophysiology, sx, bloods, biopsy findings, management)

A
  • Occurring 1-3 weeks after strep throat infection or impetigo
  • immune complex deposition = damage
  • Main symptoms = haematurai, proteinuria, oedema, HTN
  • Bloods = ASOT titre elevated, low C3
  • Biopsy = increased cellularity of glomeruli (light micro), granular IgG deposits and C3 in GM (immunofluro), subendothelial humps (electric micro)
  • Management = supportive
18
Q

Key features of IgA nephropathy
(epidemiology, pathophysio, symptoms and onset, bloods, biopsy)

A
  • Commonest cause of GN worldwide
  • IgA immune complexes in glomeruli
  • Presents 1-2 days after URTI with painless frank haematuria (earlier than post-strep!!) - sometimes with vasculitic rash
  • Raised IgA in bloods
  • Biopsy = granular deposition of igA and C3 in mesangium
19
Q

How is Rapid progressive (Crescentic) glomerulonephritis different from other causes of nephritic syndrome

A

Most agressive form of glomerulonephritis - can cause end stage renal failure in weeks

Oliguria and renal failure more common alongisde other features of nephritic syndrome

Crescents in glomeruli on light microscopy (crescents = proliferation of macrophages, parietal cells in bowman’s space)

20
Q

Differentiate between the 3 different types of Rapidly progressive glomerulonephritis
(pathogenesis, causes, light microscopy, fluroescence microscopy, additional organ involvement)

A
21
Q

Key features of hereditary nephritis (Alport’s Syndrome)

A
  • X-linked hereditary glomerular disease caused by mutation in type4 collagen alpha 5 chain
  • Nephritic syndrome + sensorineural deafness + eye disorders
  • 5-20yrs old
22
Q

Key features of Thin Basement Membrane Disease (Benign Familial Haematuria)

A
  • Very rarely a cause of nephritic syndrome - normally results in asymptomatic haematuria alone
  • Autosomal dominant mutation causing diffuse thinning of GBM due to mutation to type4 collagen
23
Q

3 main differentials in asymptomatic haematuria

A

Thin basemenet membrane disease IgA nephropathy
Alprot syndrome

24
Q

Pathophysiological mechanism of acute tubular injury

A

Damage to tubular epithelial cells is commonly due to ischaemia

25
Q

Causes of Acute Tubular Injury

A

Ischaemia of Nephrons (arising from pre-renal AKI causes)

Nephrotoxins (e..g drugs such as aminoglycosides or NSAIDs, myoglobin, heavy metals, contrast agents)

26
Q

Histopathological findings consistent with acute tubular injury

A

necrosis of short segments of tubules showing loss of brush border and loss of tubular cells (necrosis of tubular cells)

27
Q

Key features of acute interstitial nephritis
(definition, symptoms, histology)

A
  • Hypersensitvity reaction usually to drugs - hence symptoms starting days after drug exposure
  • Symptoms = fever, skin rash, haematuria, proteinuria, eosinophilia
  • Histology = inflammatory infiltrarte with tubular injury and presence of granulomas and eosinophils
28
Q

Differentiate between the two types of thrombotic microangiopathies
(HUS, TTP)

A
29
Q

Inheritence pattern of Adult Polycystic Kidney Disease and named mutation & chromosome

A

autosomal dominant - mutation in PKD1 chromosome 16

30
Q

What is the pathognomic feature of Adult Polycystic Kidney disease

A

Large multicystic kidneys with destroyed renal parenchyma

31
Q

Clinical features of adult polycystic kidney disease

A

note berry aneurysms are common vascular complication to be aware

32
Q

types of renal cell carcinoma

A
33
Q

Waxy Casts in urine suggests what?

A

Chronic Kidney Disease

34
Q

Fatty casts in urine suggest what?

A

Nephrotic syndrome

35
Q

What protein is deficient in Polycystic Kidney disease

A

Polycystin 1

PATH FINAL (36 decks)

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