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Rapid review > Uropathology > Flashcards

Uropathology Flashcards

1
Q

Painless haematuria Ddx?

A

Malignany
Glomerulonephritis

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2
Q

Drugs which cause urine discolouration?

A

Rifampicin, metronidazole, nitrofurantoin, warfarin, phenytoin

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3
Q

ACR > 70 ?

A

strongly suggestive of glomerular pathology.

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4
Q

Referals for haematuria?

A

MACROSCOPIC USUALLY = BLADDER

MICROSCOPIC USUALLY = RENAL

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5
Q

Haematuria - investigations not to forget?

A

SERUM CREATININE
PROTEINURIA (PCR OR ACR)

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6
Q

What are mesangial cells?

A

make up the vascular pole ‘stalk’. They sit between the capillaries. Mesangial cell nuclei are very heterochromatic and dark.

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7
Q

Glomerulonephritis - pathophysiology?

A

(1) Proliferation of glomerular cells (epithelial + mesangial cells)
(2) ==> leading to BM thickening or podocyte foot process effacement
(3) Associated tubulo-interstitial damage

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8
Q

Primary causes of GN?

A

Intrinsic to kidney: Membranous, minimal change, FSGS

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9
Q

Secondary causes of GN?

A
  • Infection - bacterial, viral, parasitic
  • Autoimmune disease -eg. lupus
  • Drugs
  • Malignancy - eg. multiple myeloma
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10
Q

Nephrotic syndrome?

A

Proteinuria (> 3 g/24 hr)
Hypoalbuminaemia (< 30 g/L)
Oedema

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11
Q

Nephritic syndrome?

A

Haematuria
Oligouria
Hypertension

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12
Q

What does nephrotic syndrome result it?

A
  • Hypercholestralaemia - predisposing to ACS and stroke
  • Increased risk of thrombosis due to loss of antithrombin III, protein C and S and associated rise in fibrinogen levels
  • Increased infections - renal loss of immunoglobulins
  • Hypocalcaemia due to vitD binding protein lost in urine
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13
Q

Nephrotic - type of GN?

A

Non-proliferative

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14
Q

Nephritic type of GN?

A

Proliferative

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15
Q

What presents with pure nephritic syndrome?

A

(all As)
ANCA+ve ones (Rapidly progressive GN/crescenteric)
IgAnephropathy
Alport’s syndrome
Lupus nephritis
Anti-GBM

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16
Q

Most common causes of nephrotic syndrome?

A

Children = minimal change disease.
Adults = focal segmental glomerulosclerosis.
Overall = Membranous GN

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17
Q

General approach to treating GN?

A

Steroids +/- cyclophosphamide
Reducing proteinuria: with an ACEi or ARB
Preventing VTEs: with aspirin, plus anticoagulation in anyone with albumin <20g/L
Treating hyperlipidaemia: with statins if indicated
If refractory / complications: consider dialysis

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18
Q

Minimal change disease?
- PP and Tx

A

fusion of podocytes and effacement of epithelial foot processes.
Treatment: steroids steroids and steroids.

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19
Q

Focal segmental glomerulosclerosis?
PP and Tx

A

Biopsy: scarring of some segments of some glomerulus (hence FOCAL and SEGMENTAL.
Treatment: ACEi/ARB and BP control, steroids

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20
Q

Membranous nephropathy
PP, biopsy and Tx?

A

Can by primary or secondary to malignancy, autoimmune disease, infection (hep B/C) etc.
Biopsy: diffusely thickened GBM due to Ig deposits, subepithelial deposits of immune complexes (under the podocytes), spike & dome pattern; anti-PLA2R positive
Treatment: ACEi/ARB and BP control; steroids + cyclophosphamide

21
Q

Membranoproliferative glomerulonephritis
PP and Tx?

A

proliferation of mesangial cells on light microscopy, may see immune complex deposition
Treatment: ACEi/ARB and BP control; steroids

22
Q

IgA nephropathy
PP and Tx:

A

Classically causes macroscopic haematuria just a few days post viral infection.
Biopsy: IgA and C3 deposition in the mesangium.
Treatment: if mild none, otherwise ACEi + steroids in progressive disease.

23
Q

Post-streptococcal (Diffusely Proflierative)
- What is it?
- Biopsy?
- Treatment?

A

Streptococcal infection 1-3 weeks before. Patients classically - Low C3, AntiStreptolysin O Test positive.
Biopsy: Immune complex deposition in glomeruli. Granular appearance.
Treatment: None needed usually. Monitor for hypertension.

24
Q

HSP (in children mostly)

A

Related to IgA. More systemic IgA vasculitis.
Presents with tetrad of non-blanching purpuric rash, abdominal pain, polyarthritis and renal impairment which manifests similarly to IgA nephropathy.
Treatment: usually supportive and analgesia for arthralgia
Prognosis: usually excellent. Monitor BP and urinalysis to detect progressive renal involvement. ⅓ can relapse.

25
Q

Rapidly progressive (e.g. Anti-GBM)

A

Manifestation of severe glomerular damage. Secondary to autoimmune disease (SLE, GPA) and infection.
Histology: hypercellularity (increase in mesangial, epithelial and endothelial cells and increased number of inflammatory cells).

Treatment: plasma exchange, steroids, cyclophosphamide and often dialysis.

26
Q

Henoch-Schonlein Purpura - Immunostaining

A

IgA
C3

27
Q

Lupus nephritis - Immunostaining?

A

IgM, IgG, C1q, C3

28
Q

ANCA- associated GN Immunostaining?

A

Pauci-immune

29
Q

Anti GBM disease Immunostaining?

A

Linear IgG

30
Q

Post-infectious GN Immunostaining?

A

IgG and C3 in chunky, irregular mesangial and capillary wall pattern (Stary sky)

31
Q

Bladder cancer types?

A

Benign - uncommon (Urothelial papilloma, nephrogenic adenoma)

Cancer- 90% carcinoma, 5% squamous cell carcinoma and adenocarcinoma

32
Q

Bladder cancer histology?

A

Finger-like projections
High grade cellular features: cellular atypia
High grade nuclear features: nuclear pleomorphism, hyperchromatic nuclei, high N:C ratio, frequent mitotic figures

33
Q

What goes into a histopathology report?

A

PATIENT INFORMATION:
CLINICAL INFORMATION:
MACROSCOPIC description:
MICROSCOPIC description:
CLINICAL DIAGNOSIS:

34
Q

What staging criteria for prostate cancer?

A

Gleason grading - based on architecture and predominant patterns

35
Q

Most common histological subtype of renal cancer?

A

renal clear cell carcinoma (usually from cells of the PCT)

36
Q

Genetics of clear cell renal adencarcinoma?

A
  • Most are sporadic
  • 60% patients withvon Hippel-Lindau syndrome(autosomal dominant) develop bilateral multiple RCCs
37
Q

Pathophysiology of Type 1 diabetes?

A

Some trigger (could be infection, cross-reactivity)  APC present beta-islet or insulin peptides to CD4+ TH cells
CD4+ TH cells activate CD8 T cells and B cells (class switching, antibody production) = CD8 T cell-mediated death of pancreatic beta islet cells, or antibody-mediated destruction

38
Q

Autoantibodies to beta cell antigens?

A
  • Insulin autoantibodies (anti IAA)
  • Glutamic acid decarboxylase (Anti-GAD65)
  • Antibodie to protein tyrosine phophatase (anti IA-2A)
  • Antibody to zinc transporter 8 (anti ZnT8)
39
Q

How to manage DKA?

A
  • Start IV FLUIDS first – 1L of 0.9% saline (no potassium) to run over 1 hr
  • Start continuous FIXED RATE IV insulin infusion
  • CONTINUE long acting insulin (e.g. Insulatard, Glargine, Levemir) at usual dose and usual time

If this is a new diagnosis of diabetes, prescribe 10 units subcutaneous long-acting Glargine at 22.00 hrs

Infusion instructions: 50 units Actrapid insulin made up to 50ml with 0.9% saline (1 unit per ml), to be administered via syringe driver at rate of 0.1 units/kg/hr

Ongoing assessment and corrections
Aims:
- Correct fluid and electrolyte imbalance
- Maintain plasma potassium between 4.0-5.0 mmol/L
- Deliver enough insulin to clear blood of ketones, aiming for blood ketone level of < 0.3 mmol/L

40
Q

Classify the complication of diabetes mellitus?

A
  • Macrovascular disease = accelerate atherosclerosis
  • Microvascular disease = basement membrane dysfunction
  • Infection = ischaemia, immune dysfunction and hyperglycaemia
41
Q

Macrovascular disease in DM?

A

Accelerated atherosclerosis
- Aorta, coronary and renal arteries
- PVD
- Stroke

42
Q

Microvascular disease in DM?

A

Basement membrane dysfunction
- Retinopathy
- Diabetic nephropathy
- Peripheral nephropathy

43
Q

Infection in DM?

A
  • Soft tissue
  • Upper and lower urinary tract
  • Respiratory tract
44
Q

Atherosclerotic lesion formation?

A

I. Isolated macrophage foam cells

II. Cells filled with intracellular lipid forming fatty streaks

III. Small extracellular lipid pools

IV. Smooth muscle and collagen surrounding a core of extracellular lipid

V. Fibrotic calcified plaques with a lipid core

VI. High risk plaque with ulceration, haematoma or thrombosis

45
Q

Advanced diabetic nephropathy - histology

A

1) light increase in mesangial matrix and arteriolar hyalinosis surrounding artery
2) hyaline material grows to form nodular protein aggregates within the capillary loops - Kimmelstiel-Wilson nodules
3) Structural changes result in microaneyrusm formation ) and eventually complete sclerosis and loss of function

46
Q

Acute pyelonephritis in DM Histology?

A

Macro: presence of multiple subcortical abscesses with surrounding hyperaemia
Micro: lneutrophils infiltrating the tubules and interstitium (Note that pyelonephritis usually spares the glomeruli). There is some necrosis of tubular epithelial cells and in this particularly severe cases, colonies of bacteria within the kidney

47
Q

Appropriate investigations into DI?

A
  • Paired morning and plasma urine sample
  • Water deprivation test – abstain from fluid and food for 8hrs
    At baseline t=0, empty bladder, record body weight and measre U&Es, plasma and urine osmolality
    Record hourly urine output
    At t=2/4/6/7/8 hours, weight patient and repeat blood and urine samples
    At 8 hours gives demopressin
48
Q

Cranial DI - Ix and Mx?

A
  • MRI head
  • Desmopressin + underlying condition
49
Q

Nephrogenic DI - Ix and Mx?

A
  • Renal studies (USS kidneys, urine dip, uni analysis, uACR, U&Es)
  • Correct metabolic disturbances
    Remove causal drugs (if possible…)
    Consider trial of high dose desmopressin
    Consider trial of thiazides or NSAIDs

Rapid review (7 decks)

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