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Cardio > Histopathology Renal Pathology > Flashcards

Histopathology Renal Pathology Flashcards

1
Q

Functions of the kidney

A

• Excretion of waste products
• Regulation of water/salt
• Maintenance of acid/base balance
Secretion of hormones

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2
Q

Nephrotic syndrome – chronic

A
  • Massive proteinuria (selective albumin)
  • Hypoalbuminaemia
  • Oedema
  • Hyperlipidaemia/ - uria
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3
Q

Nephritic Syndrome acute

A
  • Variable proteinuria (not selective)
  • Haematuria
  • Mild oedema
  • Oliguria
  • Azotaemia
  • Hypertension
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4
Q

Nephrotic Syndrome: Definition

A

Damage to the filtration of the glomerulus not accompanied by inflammation or proliferative response

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5
Q

Nephrotic Syndrome: Histological damage

A

Loss of foot processes

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6
Q

Nephrotic Syndrome: Triad

A

Hypoproteinaemia (hypoalbuminaemia)
Oedema
Hyperlipidaemia

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7
Q

Nephrotic Syndrome: Massive proteinuria

A

> 3.5 g/day

Hypoalbuminaemia

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8
Q

Nephrotic Syndrome: Children

A

Minimal damage disease

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9
Q

Nephrotic Syndrome: Adults

A

Systemic disease (diabetes)

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10
Q

Nephrotic Syndrome: Nephrotic disease type?

A

Minimal change disease
Focal segmental glomerulosclerosis
Membranous glomerulonephritis

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11
Q

Nephrotic Syndrome: Minimal change disease/glomerulopathy

A
  • Commonest cause of nephrotic syndrome in childhood
  • No detectable immune deposit but has, nonetheless an immune basis
  • Strong association with resp. infection and immunization
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12
Q

Nephrotic Syndrome: Minimal change disease/ glomerulopathy histological

A

Diffuse effacement of foot processes (fused)

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13
Q

Nephrotic Syndrome: Focal segmental glomerulosclerosis

A
  • Primary or Secondary
  • Some (focal) glomeruli show partial (segmental) hyalinization
  • Unknown pathogenesis
  • Poor prognosis
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14
Q

Nephrotic Syndrome: Membranous glomerulonephritis

A
  • Deposition of anti-glomerular basal membrane antibodies

* Thickened GBM and sub epithelial deposits/spikes

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15
Q

Nephrotic Syndrome: Membranous glomerulonephritis epi

A
  • Commonest causes of nephrotic syndrome in adults

* 85% idiopathic, 15% association with malignant tumours, SLE, drugs, chronic infection.

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16
Q

Nephritic Syndrome: Description

A

Expression of acute glomerular injury
• Inflammation
• Vascular and epithelial damage
• Plus or minus proliferation of glomerular cells

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17
Q

Nephritic Syndrome: Triad

A
  • Haematuria
  • Azotemia
  • Oliguria
  • Mild oedema (facial puffiness)
  • Variable proteinuria
  • Mild to moderate Hypertension
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18
Q

Nephritic Syndrome: Membranoproliferative (mesangiocapillary) glomerulonephritis

A
  • Diffuse mesangioproliferative glomerulonephritis
  • Crescentric glomerulonephritis
  • Lupus nephritis
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19
Q

Nephritic Syndrome: Glomerulonephritis

A
  • Primary or secondary to systemic disease

* Immunological aetiology (+++ deposition of immune complex in the glomerular/capillary wall).

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20
Q

Nephritic Syndrome: Glomerulonephritis features

A
  • Local deposition of circulating immune complexes
  • Anti-glomerular basal membrane antibodies
  • Antibodies against glomerular component
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21
Q

Nephritic Syndrome: Prognosis

A
  • Benign outcome in children

* Permanent compromised of renal function in adults

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22
Q

Nephritic Syndrome: The Major cause of acute nephritis in childhood

A

Acute proliferative Glomerulonephritis

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23
Q

Nephritic Syndrome: Acute proliferative Glomerulonephritis arises

A

Arises following a group A beta-haemolytic streptococcal infection

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24
Q

Nephritic Syndrome: Acute proliferative Glomerulonephritis features

A
  • Endocapillary hypercellularity with numerous neutrophils and closure of glomerular vessels
  • The glomeruli are increased in size and cellularity
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25
Q

Nephritic Syndrome: Glomerulonephritis – antibodies against glomerular component

A
  • Usually presents with a combined nephritis – nephrotic picture
  • Cresentic or rapidly progressing glomerulonephritis
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26
Q

Nephritic Syndrome: Glomerulonephritis – antibodies against glomerular component

A

Increase in mesangial substance. Localized capillary wall thickenings, increased cellularity and pronounced lobulation.

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27
Q

Diseases affecting tubules and interstitium: types

A

Acute tubular necrosis

Tubulointerstitial nephritis

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28
Q

Acute tubular necrosis epi

A

Most common cause of ARF

Reversible tubular injury

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29
Q

Causes of acute tubular necrosis

A

Ischemia (shock)

Toxic (Drugs)

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30
Q

Prognosis Acute tubular necrosis

A

Most patients recover

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31
Q

Acute tubular necrosis histology

A

There is focal necrosis and desquamation of the cells into the tubular lumen.

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32
Q

Tubulointersitial nephritis

A

Acute pyelonephritis
Chronic pyelonephritis: and reflux nephropathy
Drugs and toxins – analgesic nephropathy

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33
Q

Urinary tract infections and Reflux nephropathy

A

Women, elderly
Patients with catheters or malformations
Dysuria, frequency

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34
Q

Urinary tract infections and Reflux nephropathy organisms

A

E. coli

Proteus

35
Q

Acute pyelonephritis

A

Acute pyelonephritis in a patient presenting with fever and elevated creatinine. There is an acute inflammatory infiltrate in the interstitium and tubular lamina.

36
Q

Chronic pyelonephritis

A
  • The surface of the kidney is irregular/ or geographically, depressed in the scarred area with pseudo bulging of the remaining intact parenchyma.
  • Chronic pyelonephritis can affect both kidneys simultaneously; however, the scarring is asymmetrical.
  • The cut surface would reveal dilated, blunted or deformed calyces.
37
Q

Chronic pyelonephritis features

A

• Many dilated “colloid” filled tubules are present – ‘thyroidisation of the kidney’.

38
Q

Diseases of the blood vessels:

A

Hypertensive kidney disease

Benign nephrosclerosis

39
Q

Hypertensive kidney disease

A

Benign nephrosclerosis

40
Q

Benign nephrosclerosis

A
  • Focal sclerosis of renal arterioles and small arteries > focal ischemia > cortical scarring.
  • Some degree of nephroscleosis is present at autopsy with increased age.
  • HTN and DM increased the severity of the lesion.
41
Q

More severe

A

Malignant HTN and accelerated nephrosclerosis

42
Q

Cystic Disease of the Kidney: Types

A

Malformative/congenital

Acquired

43
Q

Cystic Disease of the Kidney: Malformative/congenital

A

Multicystic renal dysplasia (most common causes of abdominal mass in newborn)
Medullary sponge kidney

44
Q

Cystic Disease of the Kidney: Acquired

A 
Acquired renal cystic disease (mostly post dialysis)
Simple cysts (most common abnormality of the kidney)
45
Q

Cystic Disease of the Kidney:Hereditary

A 
Autosomal dominant (adult) polycystic kidney disease (ADPKD)
Autosomal recessive  (infantile) polycystic kidney disease
Nephronophthisis – medullary cystic kidney disease complex
46
Q

Cystic Disease of the Kidney:Adult polycystic disease epi

A

Occurs in 1/500 people
AD inheritance:
• Bilateral
• Presents middle age

47
Q

Cystic Disease of the Kidney: Clinically

A

Haematuria
UTI
Abdo mass
HTN

48
Q

Cystic Disease of the Kidney: Associated with CRF

A

Cerebral aneurysms
Subarachnoid haem
Cysts in other organs (liver, pancreas, lung)

49
Q

Cystic Disease of the Kidney: Complications

A

CRF

50
Q

Cystic Disease of the Kidney: Management

A

Supportive
Treat HTN
Some will need dialysis/transplant

51
Q

Infantile polycystic disease: Epi

A

1/20000

AR inheritance

52
Q

Infantile polycystic disease: Clinically

A

Large abdominal masses (both kidneys affected) at birth

53
Q

Infantile polycystic disease: Possible

A

“Potter” phenotype

54
Q

Infantile polycystic disease: Associated with

A

Liver abnormalities (congenital hepatic fibrosis, biliary dysgenesia, bile duct ectasia).

55
Q

Infantile polycystic disease: Evolves into

A

Death shortly after birth in severe forms
Renal failure
Hypertension
Portal Hypertension

56
Q

Simple renal cysts

A

Common autopsy findings. No clinical significance.

57
Q

Other cysts

A

Dialysis associated cystic disease

58
Q

Chronic Renal Disease: Description

A

Abnormal kidney function/ structure –end result of a number different renal diseases.
• Frequently unrecognised and/or coexisting with other conditions
• Can be asymptomatic till it progresses into end stage renal disease.

59
Q

Chronic Renal Disease: Causes

A

Diabetes

Hyperternsion

60
Q

Glomerulonephritis 40%

A

Chronic Pyelonephritis (20%)

61
Q

Polycystic disease 9%

A

Multisystem diseases 9%

62
Q

Acute Renal Failure → Description

A

Rapid reduction of in renal excretory function ( within 48 hr)

63
Q

Acute Renal Failure → Clinically

A

Absolute increase in serum creatinine >=m0.3 mg/dl serum urea, CR, K with anuria/ oliguria (<15ml/hr)
Reduction urine output (oliguria) less than 0.5 ml/kg per hour for more than 6 hr

64
Q

Acute Renal Failure → Clinical presentations

A

Oliguric phase – metabolic acidosis, increased Urea]Recovery pahse – polyuria

65
Q

Acute Renal Failure → Prerenal (renal perfusion)

A

Shock, Renal artery stenosis

66
Q

Acute Renal Failure → Renal causes (parenchyml structures)

A

ATN
Acute GN
Acute inst nephritis
CRF

67
Q

Acute Renal Failure → Post Renal (urine output)

A

Obstructive lesions
Stones
Tumours

68
Q

Nephrolithiasis: Description

A

Stone formation either in the kidney or renal tract

69
Q

Nephrolithiasis: Epi

A
  • 20-30 yrs M>F
  • 5% of population
  • Reoccurrence - 40 to 70%
  • Symptomatic – 50% will cause some problem with 5 years of discovery
70
Q

Nephrolithiasis: Stone types

A
  • Calcium oxalate
  • Triple phosphate (magnesium ammonium calcium phosphate)
  • Urate
  • Cystine
71
Q

Nephrolithiasis: Calcium oxalate

A

Hypercalcaemia/Idiopathic hypercalciuria 75%

72
Q

Nephrolithiasis: Triple phosphate (magnesium ammonium calcium phosphate)

A

Proteus infection which splits urea into ammonium (Staghorn calculus) 15%

73
Q

Nephrolithiasis: Urate

A

Hyperuricaemia (GOUT) 6%

74
Q

Nephrolithiasis: Cystine

A

In born error of metabolism 1%

75
Q

Nephrolithiasis:Predisposition to conditions

A

Dehydration
Sarcoidosis hypercalcaemia (Granuomas produce VitD)
Cushing disease hypercalcemi
Oxalate rich food broccoli, celery
Bladder obstruction urine stasis, stagnant urine
Polycystic disease congenital disorder
Medullary sponge kidney congenital disorder
Calycael diverticula congenital disorder
Urinary diversions crystallation on exposed metallic surgical clips
Stents, catheters crystallisation on foreign substances

76
Q

Renal Tumours: Types

A

Childhood –Wilm’s tumour

77
Q

Renal Tumours: Benign

A

Papillary adenomas. Fund at autopsy (<5mm), Fibroma

78
Q

Renal Tumours:Malignant -

A

Renal cell Carcinoma (80%) TCC (20%)

79
Q

Renal Tumours: Renal cell carcinoma risk factors

A

Smoking
HTN
Obesity
Heavy Metals

80
Q

Renal Tumours:Von Hippel Lindau syndrome

A

Haemangioblastoma of cerebellum
Retina
Renal cyst
Bilateral RCC

81
Q

Renal Tumours:Clinical presentation of Renal tumours

A 
Paraneoplastic conditions
e.g.
•	Polycythemia
•	Hypercalcaemia
•	Liver
•	Dysfunction
•	Cushing syndrome
•	Amyloidosis
Palpable mass
Haematuria
Backpain
82
Q

Renal Tumours: Histotypes

A

Clear cell

Papillary and chromophobe

83
Q

Renal Tumours:Survival

A

5 yrs 70% if no mets, 45% if mets

84
Q

Renal Tumours: Microscopic findings

A

Clear cytoplasm and sharply outlined cell membrane

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