Paeds Renal + Urology Flashcards

1
Q

What is a UTI

A

infections anywhere along urethra, bladder, ureters and kidneys pathway

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2
Q

What is cystitis

A

inflammation of the bladder

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3
Q

What are symptoms of UTI in babies

A

Fever ** may be only sign
Lethargy
Irritability
Vomiting
Poor feeding
Urinary frequency

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4
Q

What are symptoms of UTI in older infants and children

A

Fever
Abdominal pain, particularly suprapubic pain
Vomiting
Dysuria (painful urination)
Urinary frequency
Incontinence

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5
Q

How is UTI investigated

A

clean catch urine sample or urine collection pad
urine dipstix

aspirate bladder
catheter

US
Micturating cystourethrogram
DMSA scan

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6
Q

What findings on urine dipstick suggest UTI

A

Nitrites
Leukocytes

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7
Q

which is more indicative of UTI leukocytes or nitrites

A

leukocytes

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8
Q

How is UTI managed under 3 months

A

referred immediately to a paediatrician

start immediate IV antibiotics (e.g. ceftriaxone)

have a full septic screen, including blood cultures, bloods and lactate.

A lumbar puncture should also be considered.

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9
Q

How is UTI managed over 3 months

A

Lower UTI = 3 days of Oral antibiotics can be considered if they are otherwise well.

Upper UTI = consider admission w IV Abx or oral ABx for 7-10 days

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10
Q

What children with UTIs are followed up

A

All children under the age of 3 months
Children of any age who are systemically unwell
Children with recurrent UTI

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11
Q

what is bacteriological criterion for UTI Diagnosis

A

10^5 organisms/ml of single bacteria on a CCU/MSU

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12
Q

What are typical Abx choices for UTIs in children

A

Lower:

  • Trimethoprim
  • Nitrofurantoin
  • Cefalexin
  • Amoxicillin

Upper:

  • cephalosporin
  • co-amoxiclav
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13
Q

what is the investigation all children under 6 months with their first UTI

A

abdominal ultrasound within 6 weeks, or during the illness if there are recurrent UTIs or atypical bacteria

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14
Q

what is the investigation for children with recurrent UTIs

A

abdominal ultrasound within 6 weeks

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15
Q

what is the investigation for children with atypical UTIs

A

an abdominal ultrasound during the illness

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16
Q

How is renal damage assessed

A

DMSA (Dimercaptosuccinic Acid) Scan

injecting a radioactive material (DMSA) and using a gamma camera to assess how well the material is taken up by the kidneys

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17
Q

what are causes of increases interstitial fluid

A

obstruction of Lymph drainage
obstruction of venous drainage
Lowered oncotic pressure - low albumin/protein
salt and water retention

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18
Q

How does DMSA scan assess damange

A

Where there are patches of kidney that have not taken up the material, this indicates scarring that may be the result of previous infection.

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19
Q

What is Vesico-ureteric reflux (VUR)

A

backflow of urine from the bladder into the ureter and kidney

found in around 30% of children who present with a UTI.

associated dilatation, clubbing


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20
Q

What does Vesico-ureteric reflux (VUR) predisposes a patient to

A

developing upper urinary tract infections and subsequent renal scarring

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21
Q

How is Vesico-ureteric reflux (VUR) diagnosed

A

micturating cystourethrogram (MCUG).

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22
Q

How is Vesico-ureteric reflux (VUR) managed

A

Avoid constipation
Avoid an excessively full bladder
Prophylactic antibiotics
Surgical input from paediatric urology

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23
Q

What is micturating Cystourethrogram (MCUG) used to investiagte

A
  • atypical or recurrent UTIs in children under 6 months
  • family history of vesico-ureteric reflux
  • dilatation of the ureter on ultrasound
  • poor urinary flow
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24
Q

How does micturating Cystourethrogram (MCUG) work

A

catheterising the child, injecting contrast into the bladder and taking a series of xray films to determine whether the contrast is refluxing into the ureters.

Children are usually given prophylactic antibiotics for 3 days around the time of the investigation.

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25
Q

what pyelonephritis

A

inflammation of the kidney resulting from bacterial infection

the inflammation affects the renal pelvis (join between kidney and ureter) and parenchyma (tissue).

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26
Q

What are RF for pyelonephritis

A
  • Female sex
  • Structural urological abnormalities
  • Vesico-ureteric reflux (urine refluxing from the bladder to the ureters – usually in children)
  • Diabetes
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27
Q

What is the MC causative organism for pyelonephritis

A

Escherichia coli

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28
Q

What type of bacteria is E. coli

A

gram-negative, anaerobic, rod-shaped bacteria

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29
Q

Other than E. coli what are causative organisms of pyelonephritis

A

Klebsiella pneumoniae (gram-negative anaerobic rod)
Enterococcus
Pseudomonas aeruginosa
Staphylococcus saprophyticus
Candida albicans (fungal)

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30
Q

What are the triad of pyelonephritis symptoms

A

similar presentation to lower urinary tract infections (i.e. dysuria, suprapubic discomfort and increased frequency)

PLUS

  • Fever
  • Loin or back pain (bilateral or unilateral)
  • Nausea / vomiting
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31
Q

How is pyelonephritis investigated

A

Urine dipstick –> nitrities, leukocytes & blood
Midstream urine (MSU) for microscopy, culture and sensitivity
Blood tests –> WBC and CRP

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32
Q

how is pyelonephritis managed

A

1st line Abx 7-10 days
- cephalosporin or co-amoxiclav

refer to hospital of sepsis suspect

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33
Q

What are the three tests for sepsis

A

Blood lactate level
Blood cultures
Urine output

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34
Q

What are the treatments tests for sepsis

A
  • Oxygen to maintain oxygen saturations of 94-98% (or 88-92% in COPD)
  • Empirical broad-spectrum IV antibiotics (according to local guidelines)
  • IV fluids
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35
Q

What are two things to keep in mind in patients not responding to treatment for pyelonephritis

A
  • Renal abscess
  • Kidney stone –> obstructing the ureter, causing pyelonephritis
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36
Q

What can recurrent pyelonephritis lead to

A

scarring of the renal parenchyma, leading to chronic kidney disease (CKD).

It can progress to end-stage renal failure.

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37
Q

what is enuresis

A

‘involuntary discharge of urine by day or night or both, in a child aged 5 years or older, in the absence of congenital or acquired defects of the nervous system or urinary tract’

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38
Q

what is nocturnal enuresis

A

Bed wetting

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39
Q

what is diurnal enuresis

A

Inability to control bladder function during the day

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40
Q

what is average age for children to get control of daytime and nighttime urination

A
  • daytime urination by 2 years
  • nighttime urination by 3 – 4 years.
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41
Q

what is primary nocturnal enuresis

A

where the child has never managed to be consistently dry at night.

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42
Q

What is the most common cause of primary nocturnal enuresis

A

variation on normal development

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43
Q

What are other causes of primary nocturnal enuresis

A

Overactive bladder
Fluid intake
Failure to wake
Psychological distress

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44
Q

What are secondary causes of primary nocturnal enuresis

A
  • chronic constipation
  • urinary tract infection
  • learning disability
  • cerebral palsy
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45
Q

What is the initial step in management of primary nocturnal enuresis

A

establish the underlying cause.

2 week diary of toileting, fluid intake and bedwetting episodes.

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46
Q

What does the management of primary nocturnal enuresis involves

A
  • Reassure parents of children under 5 years that it is likely to resolve without any treatment
  • Lifestyle changes: reduced fluid intake in the evenings, pass urine before bed and ensure easy access to a toilet
  • Encouragement and positive reinforcement. Avoid blame or shame.
  • Treat any underlying causes or exacerbating factors, such as constipation
  • Enuresis alarms
  • Pharmacological treatment
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47
Q

What is Secondary nocturnal enuresis

A

where a child begins wetting the bed when they have previously been dry for at least 6 months

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48
Q

What are causes of Secondary nocturnal enuresis

A

Urinary tract infection ** MC
Constipation ** MC
Type 1 diabetes
New psychosocial problems (e.g. stress in family or school life)
Maltreatment

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49
Q

What should always be considered in cases of Secondary nocturnal enuresis

A

abuse and safeguarding

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50
Q

What are two main types of Incontinence

A

Urge incontinence is an overactive bladder that gives little warning before emptying
Stress incontinence describes leakage of urine during physical exertion, coughing or laughing.

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51
Q

What are other causes of diurnal enuresis other than stress and urge incontinence

A
  • Recurrent urinary tract infections
  • Psychosocial problems
  • Constipation
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52
Q

Name three medications for nocturnal enuresis

A

Desmopressin
Oxybutinin
Imipramine

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53
Q

What is Desmopressin

A

analogue of vasopressin (also known as anti-diuretic hormone).

It reduces the volume of urine produced by the kidneys. It is taken at bedtime with the intention of reducing nocturnal enuresis.

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54
Q

What oxybutinin

A

anticholinergic medication that reduces the contractility of the bladder.

It can be helpful where there is an overactive bladder causing urge incontinence.

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55
Q

What is Imipramine

A

tricyclic antidepressant.

It is not clear how it works, but it may relax the bladder and lighten sleep.

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56
Q

What is AKI

A

rapid drop in kidney function, diagnosed by measuring the serum creatinine.

Acute kidney injury is most common in acutely unwell patients (e.g., infections or following surgery).

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57
Q

What is criteria for diagnosing AKI

A
  • Rise in creatinine of more than 25 mm/L in 48 hours
  • Rise in creatinine of more than 50% in 7 days
  • Urine output of less than 0.5 ml/kg/hour over at least 6 hours
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58
Q

What are RF for predispose developing AKI

A
  • Older age (e.g., above 65 years)
  • Sepsis
  • CKD
  • Heart failure
  • Diabetes
  • Liver disease
  • Cognitive impairment (leading to reduced fluid intake)
  • Medications (e.g., NSAIDs, gentamicin, diuretics and ACE inhibitors)
  • Radiocontrast agents (e.g., used during CT scans)
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59
Q

What are pre renal causes of AKI

A

MC - Insufficient blood supply (hypoperfusion) to kidneys

  • Dehydration
  • Shock (e.g., sepsis or acute blood loss)
  • Heart failure
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60
Q

What are renal causes of AKI

A

intrinsic disease in the kidney

  • Acute tubular necrosis
  • Glomerulonephritis
  • Acute interstitial nephritis
  • Haemolytic uraemic syndrome
  • Rhabdomyolysis
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61
Q

What are post renal causes of AKI

A

obstruction to the outflow of urine away from the kidney, causing back-pressure into the kidney and reduced kidney function

  • Kidney stones
  • Tumours (e.g., retroperitoneal, bladder or prostate)
  • Strictures of the ureters or urethra
  • Benign prostatic hyperplasia (benign enlarged prostate)
  • Neurogenic bladder
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62
Q

what is acute tubular necrosis

A

refers to damage and death (necrosis) of the epithelial cells of the renal tubule

MC of AKI

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63
Q

What are two causes of damage to kidney cells

A

Ischaemia due to hypoperfusion (e.g., dehydration, shock or heart failure)
Nephrotoxins (e.g., gentamicin, radiocontrast agents or cisplatin)

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64
Q

What can be seen on urinalysis for acute tubular necrosis

A

Muddy brown casts

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65
Q

How long does recovery from acute tubular necrosis take

A

1-3 weeks

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66
Q

what is Acute interstitial nephritis

A

acute inflammation of the interstitium (the space between the tubules and vessels).

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67
Q

What is cause of acute interstitial nephritis

A
  • Drugs (e.g. NSAIDs or antibiotics)
  • Infections (e.g., E. coli or HIV)
  • Autoimmune conditions (e.g., sarcoidosis or SLE)
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68
Q

What is Nephritis

A

inflammation within the nephrons of the kidneys

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69
Q

What does Nephritis cause

A
  • Haematuria: invisible or visible amounts of blood in the urine
  • Proteinuria: although less than in nephrotic syndrome
  • Oliguria (significantly reduced urine output)
  • Fluid retentions
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70
Q

What are two most common causes of Nephritis in children

A

post-streptococcal glomerulonephritis and IgA nephropathy (Berger’s disease).

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71
Q

What precipitates post-streptococcal glomerulonephritis

A

occurs 1 – 2 WEEKS after a β-haemolytic streptococcus infection, such as tonsillitis caused by Streptococcus pyogenes

72
Q

what is pathophysiology of post-streptococcal glomerulonephritis

A

immune complex (IgG, IgM and C3) deposition in the glomeruli and cause inflammation.

= AKI

73
Q

When is diagnosis of post-streptococcal glomerulonephritis considered

A

evidence of recent tonsillitis caused by streptococcus

74
Q

How is post-streptococcal glomerulonephritis investigated

A

immunology - anti-streptolysin antibody titre & low C3
urine dipstick
urinalysis
throat swab

75
Q

How is post-streptococcal glomerulonephritis managed

A

majority supportive
Fluid balance
correction of other imbalances
antihypertensive medications and diuretics if complications (oedema and hypertension)
Abx for strep infection - penicillin

76
Q

How are IgA nephropathy and post-strep glomerulonephritis differentiated

A

IgA = 1-2 days after + macroscopic haematuria
Post Strep = 1-2 weeks + proteinuria + lower complement levels

77
Q

what is IgA nephropathy

A

Mesangial deposition of IgA immune complexes in the nephrons of the kidney causes inflammation

IgA vasculitis

78
Q

How condition does IgA nephropathy have a degree of overlap with

A

Henoch-Schonlein Purpura

79
Q

what is shown in a renal biopsy of IgA nephropathy

A
  • IgA & complement deposits on the basement membrane
  • glomerular mesangial proliferation
80
Q

How is IgA nephropathy managed

A

minimal proteinuria and a normal glomerular filtration rate (GFR)

  • no treatment needed, other than follow-up to check renal function

persistent proteinuria & a normal or only slightly reduced GFR

  • initial treatment is with ACE inhibitors

falling GFR or failure to respond to ACE inhibitors

  • immunosuppression with corticosteroids
81
Q

WHat is Henoch-Schonlein Purpura (HSP)

A

IgA mediated small vessel vasculitis.

Inflammation occurs in the affected organs due to IgA deposits in the blood vessels.

82
Q

what triggers HSP

A

haematuria proteinura
acute nephritis
renal impairment
hypertension

83
Q

what are 4 classic features of HSP

A
  • palpable purpuric rash (with localized oedema) over buttocks and extensor surfaces of arms and legs
  • abdominal pain
  • polyarthritis
  • features of IgA nephropathy may occur e.g. haematuria, renal failure
84
Q

What should be monitored in HSP

A

blood pressure and urinanalysis

85
Q

what is Nephrotic syndrome

A

the basement membrane in the glomerulus becomes highly permeable, resulting in significant proteinuria.

86
Q

What is the classic triad of Nephrotic syndrome

A

Low serum albumin (< 25 g/l)
High urine protein content (>3+ protein on urine dipstick)
Oedema

87
Q

what are symptoms of Nephrotic syndrome

A

frothy urine, generalised oedema and pallor.

88
Q

What are signs of Nephrotic syndrome

A
  • Deranged lipid profile, with high levels of cholesterol, triglycerides and low density lipoproteins
  • High blood pressure
  • Hyper-coagulability, with an increased tendency to form blood clots
  • predisposition to infection (due to loss of immunoglobulins)
89
Q

What are initial investigation for nephrotic syndrome

A

urine dipstick

90
Q

What is MC of Nephrotic syndrome in children

A

minimal change disease

90% of cases in children under 10
peak incidence btwn 2 and 5 years of age

91
Q

what intrinsic kidney disease can cause Nephrotic syndrome

A

Focal segmental glomerulosclerosis
Membranoproliferative glomerulonephritis

92
Q

What systemic illness can cause Nephrotic syndrome

A

Henoch schonlein purpura (HSP)
Diabetes
Infection, such as HIV, hepatitis and malaria

93
Q

What does biopsy for minimal change disease show on light microscope

A

no change

94
Q

What does ECM show for minimal change disease

A
  • diffuse loss of podocyte foot processes
  • vacuolation
  • appearance of microvilli.
95
Q

What does urinalysis for minimal change disease show

A

small molecular weight proteins and hyaline casts.

96
Q

How is minimal change disease managed

A

High dose corticosteroids (i.e. prednisolone) for 4 weeks and then gradually weaned over the next 8 weeks

97
Q

Other than steroids how is nephrotic syndrome managed

A

Low salt diet
Diuretics may be used to treat oedema
Albumin infusions may be required in severe hypoalbuminaemia
Antibiotic prophylaxis may be given in severe cases (penicillin V)
Immunisations

98
Q

What is alternative to steroids in steroid resistant children for Nephrotic syndrome

A

ACE inhibitors and immunosuppressants such as cyclosporine, tacrolimus or rituximab

99
Q

What are complications of Nephrotic syndrome

A

Hypovolaemia (oedema and low BP)
Thrombosis
high cholesterol
Infection - peritonitis
AKI or CKD
Relapse

100
Q

What are features that can accompany AKI

A

Rash
Fever
Flank pain
Eosinophilia

101
Q

How is AKI investigated

A

Urinalysis assesses for protein, blood, leucocytes, nitrites and glucose:

US of Urinary tract for obstruction

102
Q

what does Leucocytes and nitrites in urine suggest

A

infection

103
Q

what does Protein and blood and nitrites in urine suggest

A

acute nephritis (but can be positive in infection)

104
Q

what does glucose and nitrites in urine suggest

A

diabetes

105
Q

how can AKI be prevented

A

Avoiding nephrotoxic medications where appropriate
Ensuring adequate fluid intake (including IV fluids if oral intake is inadequate)
Additional fluids before and after radiocontrast agents

106
Q

How is AKI treated

A
  • IV fluids for dehydration and hypovolaemia
  • Withhold medications that may worsen the condition (e.g., NSAIDs and ACE inhibitors)
  • Withhold/adjust medications that may accumulate with reduced renal function (e.g., metformin and opiates)
  • Relieve the obstruction in a post-renal AKI (e.g., insert a catheter in a patient with prostatic hyperplasia)
  • Dialysis may be required in severe cases
107
Q

Are ACE inhibitors nephrotoxic

A

incorrect

ACE inhibitors should be stopped in an acute kidney injury, as they reduce the filtration pressure.

However, ACE inhibitors have a protective effect on the kidneys long-term.

They are offered to certain patients with hypertension, diabetes and chronic kidney disease to protect the kidneys from further damage.

108
Q

What are complications of AKI

A
  • Fluid overload, heart failure and pulmonary oedema
  • Hyperkalaemia
  • Metabolic acidosis
  • Uraemia (high urea), which can lead to encephalopathy and pericarditis
109
Q

what is CKD

A

chronic reduction in kidney function sustained over three months.

It tends to be permanent and progressive.

110
Q

What causes CKD

A

Diabetes
Hypertension
Medications (e.g., NSAIDs or lithium)
Glomerulonephritis
Polycystic kidney disease

111
Q

How does CKD present

A

most asymptomatic

Fatigue
Pallor (due to anaemia)
Foamy urine (proteinuria)
Nausea
Loss of appetite
Pruritus (itching)
Oedema
Hypertension
Peripheral neuropathy

112
Q

What is estimated glomerular filtration rate (eGFR) based on

A

based on the serum creatinine, age and gender

113
Q

what is glomerular filtration rate

A

the rate at which fluid is filtered from the blood into Bowman’s capsule

114
Q

How is Proteinuria quantified in CKD

A

urine albumin:creatinine ratio (ACR).

115
Q

what can Haematuria indicate

A

infection
malignancy (e.g., bladder cancer)
glomerulonephritis
kidney stones.

116
Q

How is CKD investigated

A

estimated glomerular filtration rate (eGFR
Proteinuria
Haematuria
Renal US

117
Q

What investigations can be ordered to ID RF for CKD

A

Blood pressure (for hypertension)
HbA1c (for diabetes)
Lipid profile (for hypercholesterolaemia)

118
Q

What is CKD diagnoses criteria

A

Over 3 months of

  • Estimated glomerular filtration rate (eGFR) is sustained below 60 mL/min/1.73 m2 (G score)
  • Urine albumin:creatinine ratio (ACR) is sustained above 3 mg/mmol (A Score)
119
Q

what are units of eGFR

A

mL/min/1.73 m2

120
Q

what are units for ACR

A

mg/mmol

121
Q

What is Accelerated progression in eGFR

A

sustained decline in the eGFR within one year of either 25% or 15 mL/min/1.73 m2.

122
Q

What are complications of CKD

A

Anaemia
Renal bone disease
Cardiovascular disease
Peripheral neuropathy
End-stage kidney disease
Dialysis-related complications

123
Q

What is the Kidney Failure Risk Equation

A

to estimate the 5-year risk of kidney failure requiring dialysis.

124
Q

When should a patient be referred to a renal specialist

A
  • eGFR less than 30 mL/min/1.73 m2
  • Urine ACR more than 70 mg/mmol
  • Accelerated progression (a decrease in eGFR of 25% or 15 mL/min/1.73 m2 within 12 months)
  • 5-year risk of requiring dialysis over 5%
  • Uncontrolled hypertension despite four or more antihypertensives
125
Q

What medications slow progression of CKD

A

ACE inhibitors (or angiotensin II receptor blockers)
SGLT-2 inhibitors (specifically dapagliflozin)

126
Q

What medications reduce the risk of complications of CKD

A

Exercise, maintain a healthy weight and avoid smoking
Atorvastatin 20mg for primary prevention of cardiovascular disease (in all patients with CKD)

127
Q

What management to treat metabolic acidosis

A

Oral sodium bicarbonate

128
Q

What management to treat anaemia

A

iron and erythropoietin

129
Q

What management to treat renal bone disease

A

Vitamin D, low phosphate diet and phosphate binders

130
Q

what does management of end-stage renal disease involve

A

Special dietary advice
Dialysis
Renal transplant

131
Q

When is short-term dialysis indicated

A

A – Acidosis (severe and not responding to treatment)
E – Electrolyte abnormalities (particularly treatment-resistant hyperkalaemia)
I – Intoxication (overdose of certain medications)
O – Oedema (severe and unresponsive pulmonary oedema)
U – Uraemia symptoms such as seizures or reduced consciousness

132
Q

What is long-term dialysis indicated

A

End-stage renal failure

133
Q

What are two options for long-term dialysis

A

Haemodialysis
Peritoneal dialysis

134
Q

What is Haemodialysis

A

4 hours a day, three days per week.

Blood is taken out of the body, passed through the dialysis machine, and pumped back into the body. The blood passes along a series of semipermeable membranes inside the dialysis machine.

135
Q

what are two options of longer term access for Haemodialysis

A

Tunnelled cuffed catheter
Arteriovenous fistula

136
Q

what is AV fistula

A

artificial connection between an artery and a vein.

It bypasses the capillary system and allows blood to flow under high pressure from the artery directly into the vein

This provides a permanent, large, easy-access blood vessel with high-pressure arterial blood flow

137
Q

What are options for AV fistula

A
  • Radiocephalic fistula at the wrist (radial artery to cephalic vein)
  • Brachiocephalic fistula at the antecubital fossa (brachial artery to cephalic vein)
  • Brachiobasilic fistula at the upper arm (less common and a more complex operation)
138
Q

what are complications of an AV fistula

A

Aneurysm
Infection
Thrombosis
Stenosis
STEAL syndrome
High-output heart failure

139
Q

what is Peritoneal dialysis

A

Uses the peritoneal membrane to filter the blood.

A special dialysis solution containing dextrose is added to the peritoneal cavity

Ultrafiltration occurs from the blood, across the peritoneal membrane, into the dialysis solution.

The dialysis solution is replaced, taking away the waste products that have filtered out of the blood.

140
Q

what are two types of Peritoneal dialysis

A

Continuous ambulatory peritoneal dialysis (CAPD) - dialysis always in peritoneal cavity
Automated dialysis - overnight

141
Q

What are complications of Peritoneal dialysis

A
  • Bacterial peritonitis (infections in the high-sugar environment are common and serious)
  • Peritoneal sclerosis (thickening and scarring of the peritoneal membrane)
  • Ultrafiltration failure (the dextrose is absorbed, reducing the filtration gradient, making ultrafiltration less effective)
  • Weight gain (due to absorption of the dextrose)
  • Psychosocial implications
142
Q

What is Hypospadias

A

congenital condition

the opening of the urethra is abnormally displaced to the ventral side (underside) of the penis

143
Q

What is Epispadias

A

the opening of the urethra is displaced to the dorsal side (top side) of the penis

144
Q

when is Hypospadias diagnosed

A

examination of the newborn.

145
Q

How is Hypospadias managed

A

Do not circumsise until indicates ok

referral to specialist
mild = no treatment required
surgery at 3-4 months
surgery to correct position and straighten penis

146
Q

What are complications of Hypospadias

A

Difficulty directing urination
Cosmetic and psychological concerns
Sexual dysfunction

147
Q

What is Haemolytic uraemic syndrome

A

thrombosis in small blood vessels triggered by shiga toxins from E.coli 0157 or shigella

148
Q

Who does Haemolytic uraemic syndrome commonly affect and what increases the risk of developing HUS

A

following an episode of gastroenteritis.

Antibiotics and anti-motility medication (e.g., loperamide) used to treat gastroenteritis increase the risk of HUS.

149
Q

What is classic triad for Haemolytic uraemic syndrome

A

Microangiopathic haemolytic anaemia
Acute kidney injury
Thrombocytopenia (low platelets)

150
Q

How does Haemolytic uraemic syndrome present

A

Diarrhoea is the first symptom, which turns bloody within 3 days

Around a week after the onset of diarrhoea

  • Fever
  • Abdominal pain
  • Lethargy
  • Pallor
  • Reduced urine output (oliguria)
  • Haematuria
  • Hypertension
  • Bruising
  • Jaundice (due to haemolysis)
  • Confusion
151
Q

How is Haemolytic uraemic syndrome investigated

A

Stool culture is used to establish the causative organism.

152
Q

Haemolytic uraemic syndrome managed

A

medical emergency

  • Hypovolaemia (e.g., IV fluids)
  • Hypertension
  • Severe anaemia (e.g., blood transfusions)
  • Severe renal failure (e.g., haemodialysis)
153
Q

What are structures of urinary track

A
  • Kidneys
  • Ureters
  • Bladder (with the detrusor muscle)
  • Urethra
  • Internal urethral sphincter (smooth muscle under autonomic control)
  • Prostate (in males)
  • External urethral sphincter (skeletal muscle under voluntary control)
154
Q

From outside in what are structures of the kidney

A
  • Cortex
  • Medulla
  • Pyramids and columns
  • Major and minor calyx (pleural: calyces)
  • Renal pelvis
  • Pelviureteric junction (PUJ)
  • Ureter
155
Q

What is hydronephrosis

A

swelling of the renal pelvis and calyces in the kidney

156
Q

How is obstructive uropathy diagnosed

A

ultrasound of KUB

157
Q

What are common causes of upper urinary tract obstruction?

A

Kidney stones
Tumours
Ureter strictures
Retroperitoneal fibrosis
Bladder cancer
Ureterocele

158
Q

What are common causes of lower urinary tract obstruction?

A

Benign prostatic hyperplasia
Prostate cancer
Bladder cancer
Urethral strictures
Neurogenic bladder

159
Q

How is upper urinary tract obstruction managed

A

nephrostomy used to bypass an obstruction

160
Q

How is lower urinary tract obstruction managed

A

urethral or suprapubic catheter used to bypass an obstruction

161
Q

What are complications of obstructive uropathy

A
  • Pain
  • Acute kidney injury (post-renal)
  • Chronic kidney disease
  • Infection
  • Hydronephrosis
  • Urinary retention and bladder distention
  • Overflow incontinence of urine
162
Q

What is intravenous urogram

A

x-ray with IV contrast collecting in the urinary tract

163
Q

What are Undescended Testes

A

testes have not made it out of the abdomen by birth

aka cryptorchidism

164
Q

Where may undescended testes be palpable from

A

inguinal canal

165
Q

What do undescended testes in older children or after puberty hold a higher risk of

A

torsion, infertility and testicular cancer.

166
Q

what are RF for undescended testes

A

Family history of undescended testes
Low birth weight
Small for gestational age
Prematurity
Maternal smoking during pregnancy

167
Q

How are undescended testes managed before 6 months

A

Watching and waiting is appropriate in newborns. In most cases the testes will descend in the first 3 – 6 months

168
Q

How are undescended testes managed after 6 months

A

should be seen by a paediatric urologist.

Orchidopexy (surgical correction of undescended testes) should be carried out between 6 and 12 months of age.

169
Q

when may testes retract back into inguinal canal

A

when it is cold or the cremasteric reflex is activated

170
Q

What is Orchiopexy

A

correcting the position of the testicles and fixing them in place

171
Q

What is Orchidectomy

A

removing the testicle) if the surgery is delayed or there is necrosis

172
Q

What are examination findings for testicular torsion

A

Firm swollen testicle
Elevated (retracted) testicle
Absent cremasteric reflex
Abnormal testicular lie (often horizontal)
Rotation, so that epididymis is not in normal posterior position

173
Q

What can delay in treatment for testicular torsion lead to

A

increases the risk of ischaemia and necrosis of the testicle, leading to sub-fertility or infertility.

174
Q

what is testicular torsion

A

twisting of the spermatic cord with rotation of the testicl

urological emergency

175
Q

What is bell-clapper deformity

A

the fixation between the testicle and the tunica vaginalis is absent.