Genitourinary 2 Flashcards

1
Q

What causes glomerulonephritis?

A

IgA nephropathy
Goodpasture’s disease
Post strep glomerulonephritis
Henoch Schoenlein purpura

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2
Q

What is IgA nephropathy?

A

Deposition of IgA into the mesangium of the kidney - results in inflammation and damage

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3
Q

How does IgA nephropathy present?

A

Asymptomatically with microscopic haematuria

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4
Q

How is IgA nephropathy treated?

A

Same as nephritic syndrome

Fish oil and steroids if persistent proteinuria after 3-6 months

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5
Q

How is IgA nephropathy diagnosed?

A

Biopsy

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6
Q

What is the most common cause of nephritic syndrome in high income countries?

A

IgA nephropathy

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7
Q

What causes Goodpasture’s disease?

A

Autoantibodies to type IV collagen in glomerular and alveolar membrane

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8
Q

How does Goodpasture’s disease present?

A

SOB and oliguria due to respiratory and renal damage

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9
Q

How is Goodpasture’s disease diagnosed?

A

Anti-GBM antibodies in bloods and biopsy

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10
Q

How is Goodpasture’s disease managed?

A

Plasma exchange, steroids and cyclophosphamide for immune suppression

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11
Q

What is Goodpasture’s disease a cause of?

A

Rapidly progressing glomerulonephritis leading to renal failure in days/weeks

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12
Q

What is post streptococcal glomerulonephritis?

A

Nephritic syndrome following infection 3-6 weeks prior

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13
Q

What causes post streptococcal glomerulonephritis?

A

Deposition of strep antigens in the glomeruli leading to inflammation and damage

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14
Q

How does post streptococcal glomerulonephritis present?

A

Haematuria - can present with acute nephritis

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15
Q

How is post strep glomerulonephritis diagnosed?

A

Evidence of strep infection

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16
Q

How is post strep glomerulonephritis treated?

A

Antibiotics to clear strep and supportive care

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17
Q

What is Henoch Schoenlein purpura?

A

Small vessel vasculitis that affects the kidney and joints due to IgA deposition

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18
Q

How does Henoch Schoenlein purpura present?

A

Purpuric rash on legs, nephritic symptoms and joint pain due to IgA deposition

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19
Q

How is Henoch Schoenlein purpura diagnosed?

A

Clinically, confimed with renal biopsy

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20
Q

How is Henoch Schoenlein purpura managed?

A

Corticosteroids and ACEi/ARB

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21
Q

What is nephrotic syndrome?

A

Issue with filtration barrier
Podocytes being implicated
Results in leaking of protein into urine

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22
Q

How does nephrotic syndrome present?

A

Proteinuria
Hypalbuminaemia
Oedema
Frothy urine

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23
Q

What causes nephrotic syndrome?

A

Minimal change disease
Focal segmental glomerulosclerosis
Membranous nephropathy

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24
Q

What are the secondary causes of nephrotic syndrome?

A

DDANI

Diabetes, drugs, autoimmune, neoplasia

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25
Q

How is nephrotic syndrome investigated?

A

Urinalysis
Urine protein:creatinine ratio
Blood tests
Renal biopsy

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26
Q

How is nephrotic syndrome managed?

A
Fluid and salt restriction
Loop diuretics - furosemide to manage oedema
Treat cause
ACEi/ARB to reduce protein loss
Manage complications
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27
Q

What are the complications of nephrotic syndrome?

A

Hyperlipidaemia - loss of albumin increases cholesterol formation (manage with statins)
VTE due to increased clotting factors - give heparin

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28
Q

How is minimal change disease diagnosed?

A

Biopsy

29
Q

How does minimal change disease present?

A

Nephrotic presentation

30
Q

How is minimal change disease treated?

A

High dose steroids - prednisolone

31
Q

What is the most common cause of nephrotic syndrome on renal biopsy?

A

Focal segmental glomerulosclerosis

32
Q

What causes focal segmental glomerulosclerosis?

A

Idiopathic

33
Q

How is focal segmental glomerulosclerosis diagnosed?

A

Presence of scarring of glomeruli i.e. focal sclerosis

34
Q

How is focal segmental glomerulosclerosis managed?

A

Steroids for idiopathic disease

All patients should receive ACEi/ARB for BP control

35
Q

How is membranous nephropathy diagnosed?

A

Renal biopsy = thickened glomerular basement membrane

Anti-phospholipase A2 receptor antibody 70-80% of patients

36
Q

How is membranous nephropathy managed?

A

ACEi/ARB in all

High risk of progression = prednisolone and cyclophosphamide

37
Q

What are the key clinical features of nephritic syndrome?

A
Proteinuria ++
HTN
Haematuria visible/non-visible
Oedema +
GFR ↓↓
Rash? N+V? Abdo pain?
38
Q

What is the most common GU tract malignancy?

A

Bladder cancer - M>F

39
Q

What is the epidemiology of bladder cancer?

A

3% of all cancer deaths and 10th most common cancer

40
Q

What makes up the majority of bladder cancers?

A

90% are urothelial carcinoma and spreads to iliac and para-aortic nodes, liver and lungs

41
Q

What causes bladder cancer?

A
Smoking - 2-4x risk, accounts for half of male cases of bladder cancer
>55
Pelvic radiation
Exposure to occupational carcinogens
Bladder stones - chronic inflammation
42
Q

How does bladder cancer present?

A

Painless haematuria

UTI symptoms without bacteriuria

43
Q

How is bladder cancer investigated?

A

Urinalysis - sterile pyuria
Cytoscopy and biopsy - diagnostic
CT urogram - allows staging

44
Q

How is bladder cancer managed?

A

T1: transurethral resection or local diathermy
T2-3: radical cystectomy
T4: palliative chemo and radio

45
Q

What are the majority of renal cancers found to be?

A

90% of cancers are found to be arising from the proximal tubular epithelium and are classes of carcinomas

46
Q

What is the epidemiology of renal cancer?

A

Mean age of diagnosis is 55 with M:F = 2:1

47
Q

How is renal cancer picked up?

A

50% are picked up incidentally with 30% having mets on diagnosis

48
Q

Where can renal cancer spread to?

A

Bone, liver and lungs

49
Q

What are the risk factors for renal cancer?

A

Haemodialysis
Smoking
HTN

50
Q

How does renal cancer present?

A

Haematuria
Flank pain
Palpable abdominal mass

51
Q

How is renal cancer investigated?

A
Bloods - polycythaemia from EPO secretion
Raised BP - renin secretion
US
CT/MRI
CXR - shows cannon ball mets
52
Q

What score is used to predict survival from renal cancer?

A

Mayo prognostic risk score

53
Q

How is renal cancer treated?

A

Stage 1: partial or radical nephrectomy
Stage 2: radical nephrectomy
Stage 3: radical nephrectomy and adrenalectomy
Stage 4: systemic treatment

54
Q

What is a UTI?

A

Presence of microorganisms in the urinary tract and produces clinical features

55
Q

What do UTIs affect?

A

Lower tract causing cystitis (bladder), urethritis and prostatitis, and upper causing pyelonephritis

56
Q

What can untreated urolithiasis lead to?

A

UTI

57
Q

What causes a UTI?

A

KEEPS

Klebsiella
E. Coli - most common causing 50% of cases
Enterococci
Proteus
Staphylococcus coagulase -ve
58
Q

How does a UTI present?

A

Voiding symptoms - FUNDS

Frequency
Urgency
Nocturia
Dysuria

59
Q

What is pyelonephritis?

A

Infection and inflammation of kidney, most often due to ascending UTI

60
Q

How does pyelonephritis present?

A

Loin pain, fever and pyuria
Costovertebral joint pain and tenderness
Septic shock in advanced disease

61
Q

How is pyelonephritis investigated?

A

Urinalysis
Midstream urine and culture - gold standard
Bloods
Renal US

62
Q

How is pyelonephritis treated?

A

Antibiotics - cefalexin for 7-10 days
Trimethoprim or amoxicillin if sensitive
Paracetamol for analgesia

63
Q

What is cystitis?

A

Infection of the urinary bladder and is most common in young sexually active women

64
Q

What are the risk factors of cystitis?

A

History of UTI
Diabetes
Frequent sexual intercourse
Pregnancy

65
Q

How does cystitis present?

A
Dysuria - discomfort pain, burning on urination
Frequency
Urgency
Cloudy smell urine
Suprapubic tenderness/discomfort
66
Q

How is cystitis investigated?

A

Urine dipstick - if positive for nitrites or WBCs and RBCs then UTI likely (unreliable in women over 65 so don’t bother)
Urine culture and sensitivity - gold standard

67
Q

How is cystitis managed?

A

3 days of trimethoprim (avoid if pregnant) or nitrofurantoin (avoid at term pregnancy)

68
Q

What are the secondary causes of focal segmental glomerulosclerosis?

A

HIV, heroin or lithium

69
Q

How does minimal change disease present on microscopy?

A

Normal appearance upon microscopy but there is abnormal function