Urology disorders Flashcards

1
Q

What are the results of kidney dysfunction?

A

Filtration failure - haematuria, proteinuria, low serum protein, low albumin

Hypertension water retention

metabolic acidosis

anaemia

vit D deficiency and secondary hyperparathryroidism

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2
Q

Inflammatory reasons?

A

Cystitis infection

Metabolic diabetic nephropathy

Immunological Nephritic syndrome / nephrotic sundrome

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3
Q

Obstructive reasons?

A

Stones, benign prostatic hypertrophy

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4
Q

neoplastic reasons?

A

Kidney, balder, prostatic, testicular cancer

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5
Q

Developmental / genetic reasons?

A

Polycystic kidneys, horseshoe kidney

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6
Q

Where are the locations for infection and what pathogen?

A

Bladder: cystitis
Kidney: pyelonephritis
Consider other contributing factors e.g. obstruction, stones, prostatic hypertrophy, cancer.

Bacteria: most common
Virus: immunocompromised patients
Fungal: immunocompromised patients

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7
Q

URI for infectious condition management?

A

2+ leucocytes + nitrate, trace of blood in dipstick

urine microscopy, culture and sensitivity

Give antibiotics, pain control, hydration

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8
Q

Clinical presentation of immunological cause?

A

Nephritic syndrome

Proteinuria

Nephrotic syndrome

Immunostaining of inflammatory cells - brown stains - in biopsy

Potential mechanisms : antibody, neutrophils, monocytes, macrophages, t cells

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9
Q

Nephritic syndrome signs?

A

Haematuria
Variable amount of proteinuria
May have hypertension, reduced urine output, increased urea and creatinine

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10
Q

What is IgA nephropathy?

A

The most common primary glomerulonephritis world-wide.
Very high prevalence in Far East.
Deposition of IgA antibody in the kidney (detected by immunohistochemistry).
Inflammation and scarring.
About 30% progress to kidney failure.

treat the hypertension and reduce proteinuria

  • : angiotensin receptor inhibitor (ARB) (e.g. irbesartan) or angiotensin converting enzyme inhibitor (ACEI) (e.g. ramipril)
    Reduce sodium intake

Immunotherapy: (Many different choices, ongoing clinical trials)
Renal replacement therapy: when reaching late stage kidney disease
Kidney transplantation
Dialysis

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11
Q

What is Goodpasture’s disease

A

Anti-glomerular basement membrane (GBM) antibody mediated: Goodpasture’s disease.
Shared common antigen between lung and kidney: α3chain of type IV collagen.

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12
Q

SLE?

A

Systemic lupus erythematosus (SLE): autoantibodies: antinuclear factor, anti-dsDNA.
Vasculitis: antineutrophil cytoplasm antibody (ANCA).

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13
Q

Nephrotic syndrome signs?

A
Peripheral oedema
Severe proteinuria
Low serum albumin
Variable amount of microscopic haematuria
Associated with hyperlipidaemia

Facial and leg swelling with frothy urine

Low BP

No blood but yes protein in urine

on biopsy - very minimal change to glomerulopathy

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14
Q

Causes of nephrotic syndrome?

A
Minimal change glomerulopathy
Membranous nephropathy
Focal segmental glomerulosclerosis
Lupus nephritis
Others

treat : corticosteroids, cyclophosphamide

Recent development: tacrolimus, antibody therapy targeting B cell pathway.
Diuretics: to reduce the peripheral oedema.
Prevention of thrombosis: anticoagulation.

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15
Q

What is minimal change glomerulopathy?

A

Most common in children, also affect other age groups
Normal light microscopy
Electron microscopy: podocyte effacement- abnormal flatten appearance (figure below)
Complication: high risk of thrombosis

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16
Q

Clinical presentation of stones causing kidney failure?

A

Pain (abdomen, back-loin).
Blood in urine.
Associated with urine infection.
About 90% of kidney stone are radio-opaque.

Tenderness of loin and lower abdomen.

17
Q

how to treat stones

A

pain and hydration

Shockwave Lithotripsy: High energy sound waves to break up large kidney stones into smaller one.

Ureteroscopy: Through urethra, bladder and ureter.

Percutaneous nephrolithotomy: Small percutaneous incision. Insertion of nephroscope. Stone is removed (may need to broken in smaller pieces).

18
Q

tumour examples?

A

Benign prostatic hypertrophy

Malignant:
Kidney: Renal cell carcinoma
Ureter and bladder: Transitional cell carcinoma
Prostatic cancer
Testicular cancer
19
Q

Clinical presentation of tumours?

Investigations?

A

Asymptomatic (incidental finding during other investigation).
Haematuria.
Pain.

Imaging (ultrasound, CT scan and/or MRI)
Urine cytology
Blood test for marker: prostatic specific antigen (PSA)
Kidney function
Histological diagnosis: biopsy or excised tumour
Staging studies: any evidence of metastasis

20
Q

Types of polycystic kidney disease?

A

Neonatal: autosomal recessive
Adult onset: autosomal dominant
Some patients without family history

21
Q

consequences of polycystic kidney disease?

A
Loss of kidney function
Pain
Bleeding into the renal cysts
Infection of renal cysts
Asymptomatic in some patients
22
Q

How to treat polycystic kidney disease?

A

New medication: Tolvaptan (a vasopressin receptor 2 antagonist) to slow down the cysts formation.
Treat hypertension, infection.
Pain control.
Renal replacement therapy (transplantation, dialysis).

23
Q

Consequences of horsehoe kidney?

A

Increased risk of:
Obstruction
Stone
Infection