Renal/ GU Flashcards

1
Q

What is the aetiology of nephritic syndrome?

A
  • Most common cause is IgA nephropathy
  • Bacterial infection (e.g. MRSA)
  • Hepatitis B and C
  • Schistomiasis
  • Malaria
  • Post-streptococcal infection
  • Infective endocarditis
  • SLE
  • Systemic sclerosis
  • ANCA associated vasculitis
  • Goodpastures disease
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2
Q

What is the presentation of nephritic syndrome?

A
  • Haematuria
  • Proteinuria
  • Hypertension and oedema
  • Oliguria
  • Uraemia with symptoms (anorexia, pruritus, lethargy and nausea)
  • Deteriorating kidney function
  • Moderate-severe decrease in GFR
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3
Q

How is nephritic syndrome diagnosed?

A
  • History to determine cause
  • Measure eGFR, proteinuria, serum U&E and albumin
  • Swab from throat of infected skin
  • Urine dipstick for proteinuria and haematuria
  • Renal biopsy is necessary
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4
Q

How is nephritic syndrome managed?

A

Treat underlying cause

  • Post-strep = antibiotics
  • SLE = steroids, immunosuppression, cyclophosphamide, rituximab
  • ANCA-associated vasculitis = immunosuppression, steroids, cyclophosphamide, rituximab, plasma exchange
  • Goodpastures = remove antibody via plasma exchange, immunosuppression, steroids/ cyclophosphamide
  • IgA nephropathy = BP control with ACEi
  • Hypertension = salt restriction and loop diuretics
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5
Q

What is the aetiology of nephrotic syndrome? (Primary and secondary causes)

A

PRIMARY CAUSES:

  • Minimal change disease – most common cause in children
  • Membranous neuropathy (can be idiopathic or secondary e.g. drugs, autoimmune, infection, neoplasia)
  • Focal segmental glomerulosclerosis

SECONDARY CAUSES:

  • Diabetes mellitus
  • Amyloid
  • Infections (Hep B, C, HIV)
  • SLE, RA
  • Drugs
  • Malignancy
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6
Q

What is the pathophysiology of nephrotic syndrome?

A
  • Basement membrane of the glomerulus is damaged
  • Increased permeability to serum protein causing proteinuria
  • Leads to low serum protein
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7
Q

What is the presentation of nephrotic syndrome?

A
  • Triad of proteinuria, hypoalbuminemia and oedema
  • Normal/mild increase BP
  • Normal/mild decrease GFR
  • Frothy urine
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8
Q

What are the differential diagnosis of nephrotic syndrome?

A
  • Congestive heart failure

- Cirrhosis

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9
Q

How is nephrotic syndrome diagnosed?

A
  • Establish cause with renal biopsy
  • Urine dipstick – high protein
  • CXR or CUUS – pleural effusion/ ascites
  • Low serum albumin
  • Serum creatinine, eGFR, lipids and glucose
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10
Q

How is nephrotic syndrome managed?

A
  • Treat underlying cause
  • TO REDUCE OEDEMA: loop diuretics, thiazide diuretics, fluid and salt restriction
  • TO REDUCE PROTEINURIA: prophylactic anticoagulation with warfarin, statins for cholesterol, treat infections and vaccinate
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11
Q

What is the aetiology of polycystic disease?

A
  • Mutations in PKD1 genes on chromosome 16

- Mutations in PKD2 genes on chromosome 4

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12
Q

What is the pathophysiology of polycystic disease?

A
  • PKD1 encodes polycystin 1 which is involved in cell-cell and cell-matrix interactions (regulated tubular and vascular development in kidneys)
  • PKD2 encodes polycystin 2 (a calcium ion channel)
  • Polycystin complex occurs in cilia responsible for sensing tubule flow
  • Disruption in this causes reduced cytoplasmic Ca2+, resulting in cyst formation
  • Rate of renal function decline is dependent on size and growth of cysts
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13
Q

What are the risk factors of polycystic disease?

A
  • Family history – commonest inherited kidney disease
  • FHx of ESRF
  • FHx of hypertension
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14
Q

What is the presentation of polycystic disease?

A
  • Can be clinically silent for many years, so family screening is essential
  • Loin pain, haematuria from haemorrhaging into cyst
  • Excessive water and salt loss
  • Nocturia
  • Bilateral kidney enlargement
  • Renal colic due to clots
  • Hypertension
  • Renal stones
  • Progressive renal failure
  • Polycystic liver disease
  • Pancreatitis
  • Ovarian cysts
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15
Q

What are the differential diagnoses of polycystic disease?

A
  • Acquired and simple cysts of the kidneys
  • Autosomal recessive PKD
  • Medullary sponge kidney
  • Tuberous sclerosis
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16
Q

How is polycystic disease diagnosed?

A
  • Personal history
  • Family history
  • BP may be raised
  • USS (diagnostic if ≥ 3 cysts aged 15-39y; ≥2 aged 40-59y; ≥4 aged >60y)
  • Genetic testing for PKD1 and PKD2
17
Q

How is polycystic disease managed?

A
  • No treatment to slow disease progression
  • BP control with ACEi
  • Treats stones and give analgesia
  • Laparoscopic removal of cysts to help with pain and nephropathy
  • Renal replacement therapy for ESRF
  • Disease progression monitored by serial progression of serum creatinine
18
Q

What is an epididymal cyst?

A

Smooth, extra testicular, spherical cyst in the head of the epididymis that lies above and behind the testes

19
Q

What is the presentation of an epididymal cyst?

A
  • Normally present having noticed a lump
  • Often multiple and may be bilateral
  • Small cysts may remain undetected and asymptomatic
  • May be painful when large
  • Well defined and will trans -luminate since fluid-filled
  • Testis is palpable quite separately from cyst
20
Q

What are the differential diagnoses of an epididymal cyst?

A
  • Spermatocele (fluid and sperm filled cyst)
  • Hydrocele
  • Varicocele
21
Q

How are epididymal cysts diagnosed?

A

Scrotal USS

22
Q

How are epididymal cysts managed?

A
  • Usually not necessary

- Surgical excision is painful and symptomatic

23
Q

What is a hydrocele?

A

Abnormal collection of fluid within the tunica vaginalis so surrounded entire testicle

24
Q

What is the aetiology of a hydrocele? (Primary and secondary)

A
  • PRIMARY: more common and larger, usually in younger men, associated with a patent processus vaginalis
  • SECONDARY: rare are present in older boys and men, secondary to testis tumour, trauma, infection, TB, testicular torsion, generalised oedema
25
Q

What is the pathophysiology of a hydrocele? (Simple and communicating hydroceles)

A
  • SIMPLE hydrocele: overproduction of fluid in the tunica vaginalis
  • COMMUNICATING hydrocele: processus vaginalis fails to close, allowing peritoneal fluid to communicate freely with the scrotal portion
26
Q

What is the presentation of a hydrocele?

A
  • Scrotal enlargement with a non-tender, smooth cystic swelling
  • No pain unless infected
  • Testes are usually palpable but may be difficult to palpate in large hydrocele
27
Q

What are the differential diagnoses of a hydrocele?

A
  • Testicular torsion

- Strangulated hernia

28
Q

How are hydroceles diagnosed?

A
  • Testicular USS

- Serum alpha-fetoprotein and human chorionic gonadotrophin to exclude malignant teratomas or germ cell tumours

29
Q

How are hydroceles managed?

A
  • May resolve spontaneously
  • Many of infancy resolve by 2y
  • Therapeutic aspiration or surgical removal
30
Q

What is a varicocele?

A

Abnormal dilation of the testicular veins in the pampiniform venomous plexus, caused by venous reflux

31
Q

What is the aetiology of a varicocele?

A
  • More common on the left
  • Increased reflux from the compression of the renal vein
  • Lack of effective valves between testicular and renal veins
32
Q

What is the presentation of a varicocele?

A
  • Often visible as distended scrotal blood vessels (feels like a ‘bag of worms’)
  • May complain of a dull ache or scrotal heaviness
  • Scrotum hangs lower on the side of the varicocele
33
Q

What are the differential diagnoses of a varicocele?

A

Secondary to other pathological processes blocking the testicular vein e.g. kidney tumours and other retroperitoneal tumours

34
Q

How is a varicocele diagnosed?

A
  • Venography

- Colour doppler USS to see blood flow

35
Q

How is a varicocele managed?

A
  • Surgery (if pain, infertility of testicular atrophy)