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
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
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
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
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
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
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
8
Q
What are the differential diagnosis of nephrotic syndrome?
A
- Congestive heart failure
- Cirrhosis
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
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
11
Q
What is the aetiology of polycystic disease?
A
- Mutations in PKD1 genes on chromosome 16
- Mutations in PKD2 genes on chromosome 4
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
13
Q
What are the risk factors of polycystic disease?
A
- Family history – commonest inherited kidney disease
- FHx of ESRF
- FHx of hypertension
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
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
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
What is the pathophysiology of a hydrocele? (Simple and communicating hydroceles)
- 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
What is the presentation of a hydrocele?
- 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
What are the differential diagnoses of a hydrocele?
- Testicular torsion
| - Strangulated hernia
28
How are hydroceles diagnosed?
- Testicular USS
| - Serum alpha-fetoprotein and human chorionic gonadotrophin to exclude malignant teratomas or germ cell tumours
29
How are hydroceles managed?
- May resolve spontaneously
- Many of infancy resolve by 2y
- Therapeutic aspiration or surgical removal
30
What is a varicocele?
Abnormal dilation of the testicular veins in the pampiniform venomous plexus, caused by venous reflux
31
What is the aetiology of a varicocele?
- More common on the left
- Increased reflux from the compression of the renal vein
- Lack of effective valves between testicular and renal veins
32
What is the presentation of a varicocele?
- 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
What are the differential diagnoses of a varicocele?
Secondary to other pathological processes blocking the testicular vein e.g. kidney tumours and other retroperitoneal tumours
34
How is a varicocele diagnosed?
- Venography
| - Colour doppler USS to see blood flow
35
How is a varicocele managed?
- Surgery (if pain, infertility of testicular atrophy)
