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MSRA Content > Urinary System - Level 3 > Flashcards

Urinary System - Level 3 Flashcards

1
Q

Type of polycystic kidney disease - autosomal dominant?

A

o 85% mutations in PKD1 (c16), 15% have PKD2 (c4) with slower course, PKD3 also described
o Mutations in polycystin 1/2/3 which regulate tubular and vascular development in kidneys and other organs

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2
Q

Type of polycystic kidney disease - autosomal recessive?

A

o Chromosome 6 encoding fibrocystin

o Less common than ADPKD

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3
Q

Epidemiology of polycystic kidney disease?

A
  • AD – 1 in 1000 individuals, 10% of people on dialysis
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4
Q

Symptoms of autosomal dominant polycystic kidney disease?

A

 Loin pain
 Hypertension
 Haematuria

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5
Q

Signs of autosomal dominant polycystic kidney disease?

A 
	Renal enlargement with cysts
	Haematuria
	Cyst infection
	Renal calculi
	Hypertension
	Progressive renal failure
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6
Q

Extra-renal signs of autosomal dominant polycystic kidney disease?

A 
	Liver cysts
	Subarachnoid haemorrhage (SAH)
	Mitral valve prolapse
	Ovarian cysts
	Diverticular disease
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7
Q

Symptoms of autosomal recessive polycystic kidney disease - category 1 - perinatal?

A

 Large abdomen, renal enlargement
 Severe renal impairment in utero – oligohydramnios and pulmonary hypoplasia
 75% result in death within a week of birth

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8
Q

Symptoms of autosomal recessive polycystic kidney disease - category 2 - neonate?

A

 Palpable kidneys at birth and kidney disease progresses
 Liver involvement
 Usually causes death within few months

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9
Q

Symptoms of autosomal recessive polycystic kidney disease - category 3 - infancy?

A

 Enlarged kidneys, hepatosplenomegaly

 Develop ESKD

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10
Q

Symptoms of autosomal recessive polycystic kidney disease - category 4 - childhood?

A

 Marked liver disease
 <10% develop ESKD
 Renal enlargement and hepatosplenomegaly
 Mortality is lowest in this category

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11
Q

Investigations in autosomal dominant polycystic kidney disease - screening for people with family affected?

A

Abdominal USS

Diagnosis when FHx &:

<30 - at least 2 unilateral or bilateral cysts

30 to 59 - 2 cysts in each kidney

> 60 - 4 cysts in each kidney

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12
Q

Investigations in autosomal dominant polycystic kidney disease - other investigations?

A

Bloods
• FBC (high Hb)
• U&E
• Bone profile

Imaging
• USS & CT

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13
Q

Investigations in autosomal dominant polycystic kidney disease - screening for SAH?

A

 MR angiography

 1st degree relatives with SAH + ADPKD

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14
Q

Investigations for autosomal recessive polycystic kidney disease?

A

o USS in perinatal period
o CT and MRI in older children
o Genetic Testing if one diagnosed case in family

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15
Q

Management of polycystic kidney disease - general advice?

A

o Advise against contact sport
o Avoid smoking
o Maintain healthy diet and BMI
o Regular exercise

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16
Q

Management of polycystic kidney disease - monitoring?

A

Annual
o BP
o U&E
o USS

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17
Q

Management of polycystic kidney disease - BP?

A

o Target BP <130/80

o Use ACEi/ARBs

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18
Q

Management of polycystic kidney disease - drug treatment?

A

Tolvaptan
o Slow progression of cysts development and renal insufficiency if CKD stage 2/3 at start of treatment and evidence of rapidly progressing disease

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19
Q

Management of polycystic kidney disease - in end-stage renal failure?

A

Dialysis or transplant

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20
Q

Prognosis of polycystic kidney disease?

A

o 50% will be in ESRD requiring dialysis or transplant by age of 60 in PKD1 and 75 in PKD2

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21
Q

Definition of polycystic ovary disease?

A

o Hyperandrogenism, oligomenorrhoea and polycystic ovaries on US without other causes of polycystic ovaries

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22
Q

Epidemiology of polycystic ovary disease?

A
  • Prevalence = 10% of women at childbearing age.

- Responsible for ~80% of anovulatory subfertility.

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23
Q

Pathogenesis of polycystic ovary disease?

A
  • Excess androgens
    o Hypersecretion of LH (increased frequency and amplitude of LH pulses).
    o LH stimulates androgen secretion from ovarian thecal cells
  • Androgens are steroid hormones (e.g. testosterone) that stimulates or controls the development and maintenance of male characteristics
    o Increased androgens in the ovary disrupt folliculogenesis lead to excess small ovarian follicles (hence the cysts) and irregular/absent ovulation.
    o  peripheral androgens cause hirsutism (acne/body hair).
  • Insulin resistance leads to hyperinsulinemia:
    o Reduced sex hormone binding globulin (SHBG) in liver so increased free testosterone
    o Increased androgen production
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24
Q

Aetiology of polycystic ovary disease?

A
  • Unknown

* Genetic (there is familial clustering of PCOS)

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25
Q

Symptoms of polycystic ovary disease?

A

o Asymptomatic
o Oligomenorrhoea (irregular periods, <9 per year) or amenorrhoea (no periods)
o Signs of hyperaldosteronism: acne, hirsutism, alopecia.
o Obesity
o Psychological: mood swings, depression, anxiety
o Sub/infertility
o Recurrent miscarriage

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26
Q

Signs of polycystic ovary disease?

A

o Male-pattern baldness, alopecia
o Obesity (usually central)
o Acanthosis nigricans (areas of increased velvety skin pigmentation which occur in the axillae and other flexures)
o Clitoromegaly, increased muscle mass, deep voice - severe

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27
Q

Investigations of polycystic ovary disease - bloods?

A 
	Total testosterone (normal or slightly raised)
	Free testosterone (may be raised if >5nmol/L – exclude androgen-secreting tumours and CAH – 17-hydroxyprogesterone)
	SHBG (normal or low in PCOS)
	LH (elevated)
	FSH (normal)
	TFTs
	Prolactin
•	To exclude a prolactinoma
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28
Q

Investigations of polycystic ovary disease - imaging and screening?

A

o USS
o Screen for diabetes (OGTT) and abnormal lipids
o BMI

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29
Q

What is the Rotterdam criteria for diagnosing polycystic ovary disease?

A

Requires the presence of 2 out of 3 of:
• Polycystic ovaries on US (12 or more follicles or ovarian volume >10 on USS)
• Oligo-ovulation or anovulation
• Clinical/biochemical features of hyperandrogenism (Acne, excess body hair, alopecia OR raised serum testosterone)

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30
Q

Management of PCOS - general advice?

A 
o	Weight loss
o	Diet 
o	Exercise
o	Stop smoking
o	Sleep apnoea advice
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31
Q

Management of PCOS - women not planning pregnancy - improving insulin resistance?

A

 Metformin (not licensed so risks and benefits weighed up)

32
Q

Management of PCOS - women not planning pregnancy - hormonal control?

A

 COCP cyclical
 IUS
 If not taking pill (norethisterone 5mg TDS PO for 10 days)

33
Q

Management of PCOS - women not planning pregnancy - hirsutism control?

A 
	Co-cyprindol 2mg/d
	Waxing, shaving
	Eflornithine facial cream
	Spironolactone
•	Avoid in pregnancy, teratogenic
34
Q

Management of PCOS - women presenting with subfertility and wishing to conceive?

A

Clomifene citrate
 Induces ovulation
 Use for <6 cycles
 Need US monitoring

Metformin added on

Laparoscopic Ovarian Drilling
 Needlepoint diathermy in 4 places per ovary to reduce steroid production
 When clomifene not working

35
Q

Complications of PCOS?

A
  • Infertility
  • Endometrial hyperplasia and cancer
  • CVD risk
  • T2DM – screening offered if obese, FHx, >40
  • GDM – screen in pregnancy 24-28 weeks
36
Q

Definition of urethral stricture?

A
  • Narrowing of urethra due to scar tissue developing in tissues
  • Men common
37
Q

Causes of urethral stricture?

A

o Iatrogenic (catheter, endoscope, prostatectomy, TURP)
o BPH
o Trauma (pelvic fracture, straddle injury)
o Infection (UTIs, gonorrhoea, chlamydia)
o Congenital
o Cancer (rare)

38
Q

Symptoms and signs of urethral stricture?

A
  • Reduced urine flow
  • Straining to pass urine
  • Spraying of urine or double stream
  • Incomplete bladder emptying
  • UTIs
  • Reduced force of ejaculation
39
Q

Investigations of urethral stricture?

A
  • Post-void bladder US
  • Urine flow tests
  • Retrograde urethrogram (antegrade cystourethrogram if suprapubic catheter in place)
40
Q

Management of urethral stricture?

A
  • Dilating and stretching
  • Stenting (work best for short strictures)
  • Internal urethrotomy (endoscopic)
  • Urethroplasty
41
Q

Definition of vesicoureteric reflux?

A
  • Reflux of urine from bladder into ureter
  • Usually due to primary maturation abnormality of vesicoureteral junction which leads to impairment of normal pinch-cock action of VUJ in micturition
  • Can be unilateral or bilateral
42
Q

Epidemiology of vesicoureteric reflux?

A

Females common

  • 25% of children <6 with first-time URI have VUR and 25% have significant VUR
  • 1-3% prevalence in general population
  • Most common cause of chronic pyelonephritis
43
Q

Associated conditions of vesicoureteric reflux?

A

o Congenital obstructive posterior urethral membrane (COPUM)
o Bulbar urethral obstruction (Cobb collar)
o Ureteral partial obstruction
o Duplex collecting system

44
Q

Symptoms of vesicoureteric reflux?

A 
-	Recurrent UTIs
o	Dysuria
o	Frequency
o	Offensive smelling urine
o	Abdominal pain
o	Fever
45
Q

Investigations of vesicoureteric reflux?

A
  • US KUB

- Micturating cysto-urethrogram (MCUG)

46
Q

What is MCUG and how is it graded in vesicoureteric reflux?

A

Micturating cysto-urethrogram (MCUG)

o Bladder catheterised, then filled with dye and x-ray

o Graded:
 1 – limited to ureters
 2 – renal pelvis
 3 – mild dilatation of ureter and pelvicalyceal system
 4 – tortuous ureter with moderate dilatations, blunt fornices
 5 - severe dilatation of ureter and pelvicalyceal system, loss of fornices

47
Q

Further testing of vesicoureteric reflux?

A
  • Mercapto acetyl tri-glycine reflux test (MAG3)
    o Injection of special dye is given and pictures taken when passing urine
  • Dimercapto succinic acid (DMSA) to assess kidneys
48
Q

Management of vesicoureteric reflux - general measures?

A

o Ensure good fluid intake
o Pass urine regularly (women after sexual intercourse)
o Avoid constipation

49
Q

Management of vesicoureteric reflux - medication?

A

o Low-dose prophylactic antibiotics at night

 Trimethoprim/Nitrofurantoin/Amoxcillin

50
Q

Management of vesicoureteric reflux - surgery?

A

o Cystoscopy and injection of Deflux

o Open/Keyhole ureteric re-implantation

51
Q

Complications of vesicoureteric reflux?

A
  • Renal scarring
  • Recurrent UTIs
  • Acute pyelonephritis
52
Q

Definition of glomerulonephritis?

A
  • Increased glomerular cellularity restricts glomerular blood flow and therefore filtration is decreased
  • Leads to:
    o Decreased urine output and volume overload
    o Hypertension
    o Oedema
    o Haematuria and proteinuria
53
Q

Epidemiology of glomerulonephritis?

A
  • Peak age 7 years
54
Q

Aetiology of nephritic syndrome - primary causes?

A

IgA Nephropathy
o Visible haematuria
o Most common glomerulonephritis

Mesangiocapillary glomerulonephritis
o Episodes of macroscopic haematuria, commonly associated with URTIs

55
Q

Aetiology of nephritic syndrome - secondary causes?

A

Post-infectious (streptococcal most common, staph aureus)
o Usually presents 7-21 days to streptococcal throat infection
o Cola-coloured urine
o High anti-DNAse

Vasculitis (HSP, SLE, Wegeners granulomatosis)
o HSP is vasculitis disease, see HSP
o SLE mainly affect adolescent girls and presents with multiple antibodies and haematuria/proteinuria

SLE

Goodpasture syndrome
o Anti-GBM positive
o Auto-antibodies to type 1 collagen – renal and lung disease

56
Q

Aetiology of nephrotic syndrome - primary causes?

A

Minimal change disease – 85% in children
o Idiopathic, NSAIDs, Hodgkin’s lymphoma
o Biopsy – normal under light microscopy
o Steroids usual course of treatment

Focal segmental glomerulonephritis (FSGN) – most common in adults
o Segmental areas of mesangial collapse and sclerosis
o Due idiopathic, HIV, SCD, Alport’s, obesity, reflux nephropathy

Membranous nephropathy – common in older adults
o Due to – malignancy, hepatitis B, gold, penicillamine, NSAIDs, thyroid, SLE
o Thickened GBM

Membranoproliferative glomerulonephritis

57
Q

Aetiology of nephrotic syndrome - secondary causes?

A
  • Infection – HIV, HepB/C, syphilis, malaria
  • SLE, HSP, Lupus
  • Diabetes – MC secondary cause
  • Alport’s syndrome
  • Malignancies
  • Toxins (snake bites, bee stings) and heavy metals
58
Q

Symptoms of nephritic syndrome?

A

o Haematuria, raised BP, oliguria, reduced EGFR

59
Q

Symptoms of nephrotic syndrome?

A

o Proteinuria, oedema, hypoalbuminaemia

60
Q

Symptoms of uraemia?

A

o Malaise, anorexia, fever

61
Q

Investigations in glomerulonephritis - what bloods to do to find cause??

A

o FBC, CRP, U&Es (creatinine, K, bicarbonate, calcium, phosphate, albumin)
o Complement (low C3, normal C4)
o ANA and anti-DNA antibodies (SLE suspected), Anti-GBM (Goodpastures), ANCA (if vasculitis suspected – Wegeners, polyangiitis)
o Blood cultures
o Glucose
o Viral Serology (HepB/HepC)

62
Q

Investigations in glomerulonephritis - other investigations?

A

Mid-stream urine M, C & S
o Count RBCs, WBCs, hyaline, granular casts, red cell casts means glomerular bleeding in post-infectious glomerulonephritis
o Urine culture and specific gravity

Urine dipstick

Urine PCR

Renal US

Renal biopsy

63
Q

Management of glomerulonephritis?

A

Early referral to nephrologist

Supportive treatment
o Attention to fluid balance
o Keep BP <130/80 or <125/75 if proteinuria >1g/d
 ACEi/ARB – useful as reduce proteinuria and preserve renal function
o Treat Oedema
 Loop diuretics

Nitroprusside for encephalopathy

HSP and IgA nephropathy require long term follow-up

SLE needs immunosupression

64
Q

What is normal daily urine protein excretion in a day?

A
  • Average daily urine protein excretion in adults is 80mg/day
  • Normal <150mg/day
65
Q

Definition of orthostatic proteinuria?

A

o Normal urinary protein excretion during night but increased excretion during the day, associated with activity and upright posture
o Due to increased renal dynamics
o Mostly albumin

66
Q

Epidemiology of orthostatic proteinuria?

A
  • Most common in children and young adults, males more

- 22% of school males

67
Q

Symptoms of orthostatic proteinuria?

A
  • Transient symptoms – recent strenuous exercise
68
Q

Other causes of proteinuria?

A

o Physical Exercise, fever, pregnancy, UTI, Nephrotic syndrome, renal tubular disease, CKD
o Nutcracker Phenomenon – compression of left renal vein between aorta and superior mesenteric artery

69
Q

Investigations of orthostatic proteinuria?

A
  • Urinalysis
  • Bloods
  • Urine ACR/PCR EMU (first-void) & random sample in day
  • 24-hour urine collection
70
Q

Investigations of orthostatic proteinuria -urinalysis findings?

A

o Positive protein dipstick during day
o Negative EMU protein sample
o Exclude UTI, diabetes

71
Q

Investigations of orthostatic proteinuria -bloods findings?

A

o U&Es normal

o Glucose normal

72
Q

Investigations of orthostatic proteinuria -urine ACR/PCR findings?

A

o Absence of proteinuria in morning sample and presence in daytime confirms orthostatic proteinuria

73
Q

Investigations of orthostatic proteinuria -24-hour urine collection findings?

A

Protein, creatinine clearance – split into day and night collections

74
Q

Investigations of orthostatic proteinuria -diagnosing nutcracker phenomenon?

A

o US KUB normal

o CT

75
Q

Management of orthostatic proteinuria?

A
  • Rule out other causes – may require referral to nephrologist
  • No specific treatment – may persist but no clinical significance

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