Renal / Gu Flashcards

1
Q

How do urinary tract anomalies present

A
Uti - usually recurrent 
Recurrent abdo pain 
Palpable mass
Haematuria 
Failure to thrive
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2
Q

3 types of urinary tract anomalies

A

Renal abnormalities
Obstructive lesions of urinary tract
Vesicouretic reflux

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3
Q

Egs of renal anomalies

A
Renal agenesis
Ectopic kidney 
Duplex kidney 
Horseshoe kidney 
Cystic disease of kidney
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4
Q

What is renal agenesis and what does it result in

A

Absence of both kidneys

Potters syndrome - oligohydraminos (caused by lack of fetal urine)

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5
Q

What is associated with renal agenesis

A

Lung hyperplasia

Postural deformities

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6
Q

What is an ectopic kidney ?

Why about it makes pain misleading

A

Failure of kidney to ascend from pelvis / ascend too far to thorax
Pain depends on site

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7
Q

What is a duplex kidney

A

Premature division of ureteric bud -> duplex system

Kind of get extra bit of kidney on one / both sides which may have an extra ureter as well

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8
Q

What other abnormalities are associated with duplex kidney

A

Renal dysplasia

Vesicouretic reflux

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9
Q

Complications with extra ureter in duplex kidney

A

Often have abnormal drainage eg into urethra -> continuous urinary leakage / into wrong part of bladder -> reflux

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10
Q

What is horseshoe kidney ? Why?

A

Kidneys joined at lower poles

Abnormal migration and separation

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11
Q

4 types of kidney cystic disease

A

Muticystic dysplastic kidney
Autosomal recessive polycystic kidney disease
ADPKD
Tuberous sclerosis

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12
Q

Which cystic disease has no functional renal tissue

A

MCKD - large fluid filled cysts like grapes

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13
Q

ARPKD causes

A

Diffuse bilateral enlargement of kidneys

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14
Q

ARPKD causes

A

Separate cysts of varying sizes between normal renal parenchyma
Kidneys are enlarged

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15
Q

Ages of kidney failure in PKD

A

Recessive by around 15-20

Dominant by around 60

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16
Q

Locations of obstructive lesions in urinary tract

A

Pelviureteric junction, vesicouretic junction, the bladder, urethra

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17
Q

What causes obstruction in Pelviureteric obstruction (congenital hydronephrosis)?
Prognosis ?

A

Narrow lumen, compression by fibrous band / blood vessel.
Mild - often reduce spontaneously
Severe- surgery with conservation of renal tissue where possible

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18
Q

Prognosis of antenatal hydronephrosis? When to investigate ?

A

Often reduces after birth.

Investigate if bilateral ?urethral obstruction

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19
Q

Causes of vesicouretic obstruction? Where is the swelling ?

A

Stenosis, kinking / dilation of lower part of ureter (ureterocele)
Combination of hydroureter and hydronephrosis

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20
Q

Where do abnormal folds of urethral mucosa occur in males ? What do they cause?

A

Region of verumontanum.

Impede flow of urine with back pressure on bladder, ureters and kidneys

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21
Q

Prognosis of abnormal folds in posteriors urethral vales

A

Death in Utero from renal failure / after birth from potters syndrome
Uti, poor urinary stream, renal insufficiency

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22
Q

What causes primary vesicouretic reflux

A

Developmental anomaly of vesicouretic junction
Ureters enter directly into bladder rather than at an angle & the segment of ureter within bladder is abnormally short

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23
Q

What are the consequences of vesicouretic reflux

A

Reflux when voiding -> infection & exposing kidneys to bacteria & high pressure

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24
Q

Grading of vesicouretic reflux

A

I-V
Mild I- reflux into ureter only
Moderate III - dilation of ureter and renal pelvis
Severe V - gross dilation of ureter, renal pelvis and calyces

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25
Q

Features of VUR

A

Along with other GU anomalies & may be due to bladder pathology (eg. Neuropathic bladder)

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26
Q

Consequences of VUR

A

Predisposed to uti & pyelonephritis
Reflux nephropathy -tissue damage & scaring due to infection and back pressure -> hypertension and chronic renal failure

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27
Q

How is VUR diagnosed

A

Micturating cystourethrography (MCUG)

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28
Q

How does MCUG work ? What else can you look for

A

Bladder filled with contract medium via catheter -> bladder outlined and reflux detected
Obstruction can be demonstrated with views during voiding without catheter

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29
Q

Issues with MCUG

A

Radiation dose is high and there is risk of infection

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30
Q

Management of VUR

A
Mild VUR resolves spontaneously (10%/year) but,
Prophylactic Abx (eg trimethoprim) 

Surgery if the prophylaxis fails / VUR in stages IV / V

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31
Q

How long is prophylactic Abx given to kids with VUR

A

Until free of infection, regained bladder control and is older than 5

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32
Q

Types of radiological investigation of kidney and urinary tract

A

Ultrasound

Functional scanning - static nuclear medicine scanning / dynamic nuclear medicine scanning

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33
Q

How does static nuclear medicine scanning work? What is is particularly good at identifying ?

A

An isotope labeled substance (eg DMSA) that is incorporated into renal tissue is used.

Identifying renal scaring

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34
Q

How does dynamic nuclear medicine scanning work? What does it give information on? When can it be used to detect VUR ?

A

An isotope labeled substance usually MAG3 that is excreted at PCT is used
Info on Blood flow, renal functioning & drainage

In an older child who can cooperate by stopping & starting micturition on command

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35
Q

What are the key Inguinal scrotal disorders

A

Undescended testis
Inguinal hernia and hydrocele
Acute scrotum

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36
Q

Where do testis develop? When do the go into scrotum? Who has undescended testis more commonly?

A

Intraabdominally via Inguinal canal in third trimester therefore preterm more frequently

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37
Q

2 types of undescended testis

A

Incompletely descended - lying along normal pathway (20%)

Maldescended/ectopic - deviated from normal path agree emerging from superficial Inguinal ring

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38
Q

When are testis checked ? When referee to a surgeon?

A

Birth, 6/12, 18/12

If impalpable or ectopic testis found at 6/52

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39
Q

Further investigations for undescended testis

A

Uss, MRI, laparoscopy to determine existence and location

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40
Q

Management of undescended testis

A

Orchidopexy - best between 1-2 years

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41
Q

What are the benefits of orchidopexy

A

Decreased risk of torsion & malignancy, increased fertility.
Psychological and cosmetic benefits

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42
Q

When the testis descend into scrotum what do they take and what can this cause ?

A

Connecting fold of peritoneum (process vaginalis) - failure to close -> Inguinal hernia / hydrocele

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43
Q

Who gets more Inguinal hernias

A

Boys, preterm, FHx

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44
Q

How does Inguinal hernia present

A

Parents note intermittent swelling in groin or scrotum

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45
Q

What are the danger signs of irreducible hernia? What are you worried about?

A

Hard , tender, vomiting

.Strangulation

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46
Q

Treatment of hernia

A

Surgery

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47
Q

When does a hydrocele form rather than hernia?

A

If process vaginalis is small

48
Q

How to differentiate hydrocele from hernia

A

Possible to get above and trans illuminates

49
Q

Treatment of hydrocele

A

Reassurance - usually spontaneously reduces by 1 year

50
Q

Acute swelling and pain in scrotum is what until proven otherwise

A

Torsion

51
Q

What causes torsion

A

Inadequate fixation of tunica vaginalis allows testis to rotate and occlude its blood supply

52
Q

Treatment of torsion

A

Surgical exploration without delay

Often affects both testis as Defect commonly bilateral

53
Q

DD of torsion

A

Torsion of testicular appendix (hydratid of morgani) - vestigigial remnant of Müllerian duct
Epididymo-orchitis
Idiopathic scrotal odema

54
Q

What is hypospadias? Severe forms associated with?

A

Congenital abnormalities of the position of the urethral meatus .
Chordee (ventral curvature of penis)

55
Q

What is phimosis ? How can mild be managed ?

A

Adhesion of foreskin to glans penis after 3 years .

Mild - periodic gentle retraction

56
Q

Is a none retracting foreskin and ballooning / preputial adhesions indications for circumcision

A

No they are normal and common in small boys

57
Q

Indications for circumcision

A

Balanitis xerotrica obliterans
Recurrent balanitis
Sometimes- recurrent uti

58
Q

What is balanitis xerotica obliterans

A

Thickens scarred white prepuce adherent to glans (caused by recurrent infection )

59
Q

Why is uti in childhood important

A

Up to half have structural abnormalities.

Pyelonephritis may scar growing kidney predisposing to hypertension and chronic renal failure if scarring is bilateral

60
Q

Causes of urinary stasis

A

VUR
Obstructive uropathy - ureterocele, urethral valves
Neuropathic bladder - eg. Spina bifida
Behavioural infrequent voiding & constipation

61
Q

Commonest organism(s) causing uti

A

E. coli

Proteus, pseudomonas

62
Q

Who is more likely to get proteus infection? Predisposes to?

A

Boys

Phosphate stone formation

63
Q

What does pseudomonas infection possibly indicate

A

Structural abnormality in the urinary tract affecting drainage

64
Q

Uti features infancy

A

Fever, lethargy, vomiting & diarrhoea, poor feeding / failure to thrive, prolonged neonatal jaundice, septicaemia, febrile convulsions

65
Q

Uti features childhood

A

Dysuria & frequency, fevers (+/- rigors), lethargy & anorexia, V&D, febrile convulsion, recurrence / secondary enuresis

66
Q

Investigations for uti

A

Urine sample - dipstick (nitriles, leukocyte), M,C&S (microscopy, culture and sensitivity)

67
Q

Diagnosis of uti

A

Culture of pure growth of a single pathogen at at least 105 colony forming units per L of urine

68
Q

Methods for collecting urine and when used

A

Suprapubic aspirate - all babies

69
Q

Why do you treat UTIs quickly

A

Reduce risk of scarring

70
Q

How do you treat most UTIs ? Eg?

A

Oral Abx

eg. Coamoxiclav for 5/7, 10/7 if systemically unwell (adjusting according to sensitivity on urine M,C&S

71
Q

Uti treatment for infants / severely unwell ? Eg?

A

IV Abx

Ampicillin / cefotaxime plus gentamicin

72
Q

In severe why is augmentin given for 48hrs ? Switched to?

A

Reduce fever and risk of meningitis - then switch to trimethoprim

73
Q

Further investigation post uti

A

Imaging to assess for anatomical / functional abnormalities eg VUR and for renal scarring.
Initial uss to identify a) presence of 2 kidneys, b) obstructions with urinary tract dilutions

74
Q

Management of infants post uti ? When is it done ? What else is done?

A

Initial uss and MCUG (looking for VUR) + static radioisotope scan (DMSA) to identify renal scars
Defer until 3/12 after acute infection to avoid detecting transient abnormalities
Abx prophylaxis in interim

75
Q

Management of 1-5 year olds post uti

A

Uss & static radioisotope scan (MCUG reserved for abnormality on DMSA scan, recurrent infections, FHx of reflux)

76
Q

When is risk of renal scarring with uti less

A

With increasing age (uncommon after 5 years old )

77
Q

Advise to prevent uti recurrence

A

High fluid intake, regular unhurried voiding, lactobacillus, cranberry juice, good perineal hygiene

78
Q

When might transient proteinuria occur and not warrant investigation

A

During febrile illness / after exercise

79
Q

How can you measure persistent proteinuria ? What should it not exceed ?

A

24 HR urine or a timed collection.

Not exceed 4mg/h per m2

80
Q

What is a more useful urine sample than 24 HR collection in young children ? Why? What should it be?

A

Early morning protein:creatine ratio - early morning to exclude orthostatic changes
Protein should be

81
Q

What characterises nephrotic syndrome ? Levels?

A

Gross proteinuria 300-400 mg/mmol

Hypoalbuinaemia (

82
Q

Usual cause of nephrotic syndrome (others)?

A

Idiopathic
Can secondary to systemic disease eg. HSP & other vasculitis (SLE…), infections (eg. Malaria), allergens (eg. Bee stings)

83
Q

Features of nephrotic syndrome ? Earliest?

A

Peri orbital oedema (particularly on walking) - earliest sign
Scrotal / vulval, leg & ankle oedema
Ascities
Breathlessness due to plwural effusions &abdominal distension

84
Q

Investigations for nephrotic syndrome

A
Urine dipstick (+++protein) 
FBC & ESR (inflam / infection) 
U&E, creatine, albumin
Compliment levels (c3/c4) 
Urinary sodium concentration 
Antistreptolysin titre (ASOT) & throat swab 
Urine microscopy &a culture 
Hepatitis serology 
Anti DNAse B (?group A strep)
85
Q

What’s more common steroid sensitive or steroid resistant nephrosis

A

90% steroid sensitive

86
Q

Usual demographic for steroid sensitive nephrosis

A
87
Q

Histology of steroid sensitive

A

Minimal change

88
Q

Management of steroid sensitive

A
Oral corticosteroids (60mg/m2/day prednisolone) for 4 weeks then 49mg/m2 every other day for 4 weeks then stop. 
Manage hypovolaemia
89
Q

When is nephrosis defined as steroid resistant

A

No remission on 4 weeks of steroid therapy

90
Q

Usual demographic for steroid resistant nephrosis

A

Age 12, elevated BP, heamaturia, decreased renal function, features of nephritis

91
Q

Histology of steroid resistant nephrosis

A

Various, underlying glomerulonephropathy (eg. Focal segmental glomeruloscerosis, membrano-proliferative glomerulonephritis)

92
Q

Management of steroid resistant

A

Refer t paediatric nephrologist

93
Q

Complications of nephrosis

A

Hypovolaemia
Thrombosis
Secondary infection
Hypercholesterolaemia

94
Q

Features of hypovolaemia

A

Increased packed cell volume (PCV), hypotension, peripheral vasoconstriction, urinary sodium

95
Q

Why does nephrosis -> thrombosis ?

What can add to this?

A

Hypercoagulable state due to urinary losses of antithrombin.

thrombocytosis may be exaggerated by steroid therapy

96
Q

Why do you get secondary infections with nephrosis ? What is usual cause? What can happen? And what is the prophylaxis

A

High risk of infection with capsulated bacteria (especially pneumococcus). Peritonitis may occur. Penicillin prophylaxis in acute phase

97
Q

Why do you get hypercholesterolaemia in nephrosis

A

Inversely correlated with albumin

98
Q

How many people with nephrosis relapse

A

2/3

99
Q

What can be done for frequent relapses of nephrosis

A

Further immunosuppression eg cyclophosphamide, levamisole or cyclosporin A

100
Q

Characteristics of nephritis

A

Salt & retention - (hypertension, oedema), decreased urine output (+seizures)
Heamaturia - often macroscopic “smokey” coloured
Proteinuria - varying degree
Impaired GFR - rising creatinine (variable)

101
Q

Causes of nephritis

A

Post infectious
Vasculitis
IgA nephropathy & mesangiocapillary glomerulonephritis
Anti GBM disease

102
Q

Usual infection for secondary nephritis

A

Skin/ throat with group A b-haemolytic strep

103
Q

Egs of vasculitis -> nephritis

A

Henoch-schlonlein purpura, SLE, Wegners granulomatosis

104
Q

Other name for anti GBM disease? Other feature

A

Goodpastures syndrome

Heamoptysis

105
Q

General investigations for nephritis

A

Urine - blood, protein, red cell casts (microscopy)

AXR - exclude other causes

106
Q

Diagnosis of post strep glomerulonephritis

A

Evidence / Hx of recent (~10/7) infection (culture of organism, increased ASOT)
Low complement c3 levels

107
Q

What is ASOT

A

Anti streptolysin O

108
Q

Demographic of who gets henoch - schonlein purpura

A

Aged 3-10, males 2x, peaks during winter months & often preceded by LRTI

109
Q

Features of nephritis (4 things)

A

Rash - over buttocks, extensor surfaces of legs and arms ; purpuric
Joint and pain swelling - knees and ankles (large joints)
Abdo pain - haematemesis / malaena, intussusception
Renal - nephritis

110
Q

Management of nephritis

A

Fluid balance - measure urine output, low/moderate fluid intake, diuretics, decrease salt
Treat hypertension
Correct other imbalances (potassium / acidosis)
Penicillin (to treat underlying strep infection)

111
Q

What is the most common cause of paediatric acute renal failure

A

Haemolytic ureamic syndrome

112
Q

What is HUS associated with

A

Diarrhoea caused by E. coli 0157:H7 which produces a verocytotoxin

113
Q

How does a verocytotoxin cause damage

A

Released from GI tract & causes fragmentation of RBCs, microangiopathic haemolytic anaemia & thrombocytopenia
-> kidney vasculature becomes thrombosed and infarcted

114
Q

Management of HUS

A

Supportive and 90% regain full renal function

115
Q

What is contraindicated in HUS

A

Abx