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Phase 3A Medicine > Paediatrics - GI, nutrition, renal (4) > Flashcards

Paediatrics - GI, nutrition, renal (4) Flashcards

1
Q

Red flag: bile-stained vomit

Diagnosis you’re worried about?

A

Intestinal obstruction

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2
Q

Red flag: Haematemesis

Diagnoses you’re worried about?

A

Oesophagitis
Peptic ulcer
Oral/nasal bleeding
Oesophageal variceal bleeding

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3
Q

Red flag: Projectile vomiting in first few weeks of life

Diagnosis you’re worried about?

A

Pyloric stenosis

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4
Q

Red flag: Vomiting at end of paraoxysmal coughing

Diagnosis you’re worried about?

A

Whooping cough (pertussis)

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5
Q

Red flag: Abdominal tenderness

Diagnosis you’re worried about?

A

Surgical abdomen

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6
Q

Red flag: Abdominal distension

Diagnosis you’re worried about?

A

Intestinal obstruction

incl. strangulated inguinal hernia

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7
Q

Red flag: Hepatosplenomegaly

Diagnosis you’re worried about?

A

CLD, inborn error of metabolism

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8
Q

Red flag: Blood in stool

Diagnosis you’re worried about?

A

Intussusception, bacterial gastroenteritis

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9
Q

Red flag: Faltering growth

Diagnosis you’re worried about?

A

GORD, coeliac, chronic GI conditions

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10
Q

What are the two terms used to describe the non-forceful return of milk by babies?

A
  1. Posseting - small amounts of milk that accompany the return of swallowed air
  2. Regurgitation - larger more frequent losses of milk
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11
Q

Vomiting is more prominent in intestinal obstruction that is more proximal or distal?

A

Proximal

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12
Q

Abdominal distension is more marked in proximal or distal obstruction?

A

Distal

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13
Q

What causes GOR?

A

Inappropriate relaxation of the lower oesophageal sphincter as a result of functional immaturity

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14
Q

Give three factors that worsen GOR?

A
  1. Predominantly fluid diet
  2. Mainly horizontal posture
  3. Short intraabdominal length of oesophagus
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15
Q

By what age does all spontaneous reflux tend to resolve?

A

12 months

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16
Q

GORD is more common in which children (3)?

A
  1. CP patients or those with neurodevelopmental problems
  2. Preterm infants
  3. Following surgery for oesophageal atresia/ diaphragmatic hernia
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17
Q

How is GOR diagnosed?

A

Clinically

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18
Q

If history of GOR atypical or there is failure to respond to treatment what investigations may be done?

A
  1. 24 hr oesophageal pH

2. Endoscopy with biopsy to identify oesophagitis and exclude other causes

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19
Q

Management of GORD? (In stages)

A
  1. Feed thickeners (Carobel), smaller more frequent feeds
  2. Medication to suppress acid
    - Hydrogen receptor antagonists (ranitidine)
    - Proton pump inhibitor (omeprazole)
  3. Fundoplication
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20
Q

What are ranitidine and omeprazole and what do they do?

A 
Ranitidine = hydrogen receptro antagonist
Omeprazole = PPI

Reduce the volume of gastric contents and treat acid related oesophagitis

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21
Q

What does a fundoplication do and why is it used as a treatment of GORD?

A

Fundus of the stomach is wrapped around intraabdominal oesophagus. (Nissen fundoplication)

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22
Q

Which sphincter is involved in GORD?

A

Lower oesophageal sphincter

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23
Q

What is pyloric stenosis?

A

Hypertrophy of the pyloric muscle causing gastric outflow obstruction

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24
Q

When does pyloric stenosis present?

A

Week 2-8

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25
Q

In what gender is pyloric stenosis more common?

A

Boys (4:1) particularly firstborn

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26
Q

Clinical features of pyloric stenosis?

A

Vomiting (increases in frequency and focefulness over time)
Hunger after vomiting until dehydration leads to loss of interest in feeding
Weight loss
Hypochloraemic metabolic alkalosis (low plasma sodium and potassium)

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27
Q

How is pyloric stenosis investigated?

A

Baby given milk feed to calm
Observed for gastric peristalsis (wave moving from left to right across the abdomen)
Pyloric mass felt in right upper quadrant
Ultrasound can confirm diagnosis prior to surgery

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28
Q

What are the two main signs seen in pyloric stenosis?

A 
Gastric peristalsis
Pyloric mass (like an olive) in right upper quadrant)
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29
Q

Management of pyloric stenosis?

A
  • Correct fluid and electrolyte imbalance with IV fluid

- Pyloromyotomy (division of hypertrophied muscle down to the mucosa)

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30
Q

What is infant ‘colic’?

A

Term used to describe symptom complex that occurs during the first few months of life. Paraoxysmal, inconsolable crying or screaming is often accompanied by drawing up of knees and passage of excessive flatus.

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31
Q

At what age does colic typically resolve?

A

3-12 months

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32
Q

What is the treatment of colic?

A

Gripe water

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33
Q

If colic persists, what diagnoses are you concerned about?

A

Cow’s milk protein allergy

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34
Q

If colic persists what two investigations would you do?

A

2 week trial of protein hydrolysate formula (cow’s milk free)

if symptoms persist then

Trial of GOR treatment

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35
Q

Give 5 causes of acute abdominal pain

A
  1. Appendicitis
  2. Lower lobe pneumonia
  3. Diabetic ketoacidosis
  4. UTI
  5. Pancreatitis
  6. Testicular torsion / strangulated inguinal hernia
  7. Obstruction
  8. Peritonitis (nephrotic syndrome/ liver disease)
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36
Q

What are the symptoms of appendicitis?

A

Nausea, vomiting, abdo pain

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37
Q

Describe the pain associated with appendicitis

A

Begin central and colicky then localises to the right iliac fossa

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38
Q

What are the signs of appendicitis?

A

Abdo pain aggravated by movement

Persistent tenderness with guarding in the right iliac fossa

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39
Q

What is the point called at which there is tenderness and guarding in appendicitis?

A

McBurney’s point

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40
Q

What are the signs and symptoms of a retrocaecal appendix?

A

All of above but localised guarding may be absent

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41
Q

Why may white blood cells or organisms in the urine be seen in appendicitis?

A

Inflamed appendix may be adjacent to the ureter or bladder

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42
Q

How is appendicitis diagnosed?

A

Regular clinical review every few hours

Laparoscopy is available to see whether or not the appendix is inflamed

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43
Q

What is the treatment of appendicitis?

A

Appendicectomy

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44
Q

Give a sign of a perforated appendix?

A

Generalised guarding

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45
Q

Treatment of a perforated appendix?

A

Fluid resuscitation
IV abx
Laparotomy

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46
Q

Palpable mass in RIF but no signs of generalised peritonitis. Management?

A

Elect for conservative management.
IV abx
Elective appendicectomy a number of weeks later

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47
Q

What is a complicated appendicitis?

A
  1. Appendix mass
  2. An abscess
  3. Perforation
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48
Q

What is non-specific abdominal pain?

A

Pain that resolves in 24-48 hours

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49
Q

What is intussusception?

A

Invagination of proximal bowel into distal segment

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50
Q

What part of the bowel is typically affected in intussusception?

A

Ileum into caecum through ileocaecal valve

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51
Q

Peak age of presentation for intussusception?

A

3 months - 2 years

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52
Q

How does intussusception cause bowel perforation/ gut necrosis?

A

Stretching and constriction of the mesentery
Resulting in venous obstruction, causing engorgement and bleeding from the mucosa
Fluid loss and bowel perforation

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53
Q

Presentation of intussusception?

A

Paraoxysmal colicky pain w/pallor
Refusal of feeds, vomiting (can be bile stained)
Sausage shaped mass palpable in abdomen
Redcurrant jelly stool (blood stained mucus)
Abdominal distension and shock

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54
Q

What is thought to cause intussusception?

A

Viral infection leading to enlargement of Peyer’s patches which forms the lead point

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55
Q

What is the management of intussusception?

A

Fluid resuscitation (hypovolaemic shock if don’t as fluid pools in the gut)

Rectal air insufflation under supervision of paediatric surgeon

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56
Q

What will an xray of a child with intussusception show?

A
  1. Distended small bowel

2. Absence of gas in distal colon or rectum

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57
Q

What is the investigation of a child with suspected intussusception?

A

Abdo ultrasound

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58
Q

What sign is often seen on abdo ultrasound of a child with intussusception?

A

Doughnut sign/ target sign

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59
Q

If rectal air insufflation of an intussuscepted bowel fails, what is the subsequent management?

A

Operative reduction

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60
Q

Give a complication of intussusception

A

Hypovolaemic shock

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61
Q

Give a contraindication of rectal air insufflation as the management for intussusception

A

Presence of peritonitis

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62
Q

What is a Meckel diverticulum a remnant of ?

A

Vitello-intestinal duct

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63
Q

How may a Meckel diverticulum present? (4)

A 
Severe rectal bleeding
Intussusception 
Volvulus
Diverticulitis
Acute reduction in haemoglobin

or/ asymptomatic

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64
Q

What blood result is often seen in a patient with Meckel diverticulum?

A

Acute reducation in haemoglobin

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65
Q

What is the investigation for suspected Meckel diverticulum? (And what does it show?)

A

Technetium scan - increased uptake by gastric mucosa of Meckel diverticulum

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66
Q

Treatment of Meckel diverticulum?

A

Surgical resection

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67
Q

What is the prevalence of Meckel diverticulim?

A

2/100

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68
Q

At what age does malrotation typically present?

A

1-3 days of life

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69
Q

What is the typical presentation of malrotation?

A

Obstruction with bilious vomiting

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70
Q

What is the investigation required in a child with dark green vomiting?

A

Urgent upper gastrointestinal contrast study to asess intestinal rotation unless signs of a vascular compromise are present

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71
Q

If dark green vomiting and signs of vascular compromise to the bowel, what is the management?

A

Urgent laparotomy

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72
Q

What blood supply is often compromised in malrotation or a volvulus?

A

Superior mesenteric artery to small intestine and proximal large intestine

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73
Q

Treatment of malrotation?

A

Surgical correction through laparotomy

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74
Q

Clinical features of malrotation?

A

Bilious vomiting
Abdo pain
Tenderness from peritonitis or ischaemic bowel

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75
Q

What are the name of the bands of peritoneum that often obstruct the duodenum in malrotation?

A

Ladd bands

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76
Q

What is the definition of recurrent abdominal pain?

A

Pain sufficient to interrupt normal activities that lasts for at least 3 months

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77
Q

Give some common causes of recurrent abdominal pain

A

Largely due to functional abnormalities of gut motility

  • IBS
  • Constipation
  • Coeliac disease
  • Abdominal migraine
  • Functional dyspepsia
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78
Q

Give two tests that should be carried out on a child with recurrent abdominal pain to exclude organic causes

A
  1. Thyroid function tests

2. Coeliac antibodies

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79
Q

Treatment of abdominal migraine?

A

Anti-migraine medication

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80
Q

Risk factors for IBS

A
  1. Family history
  2. Previous recent history of GI infection
  3. Stress and anxiety
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81
Q

What are the typical characteristic symptoms in a patient with IBS?

A
  1. Non-specific abdominal pain often peri-umbilical
  2. Pain relieved by defecation
  3. Explosive, loose or mucousy stools
  4. Bloating
  5. Feeling of incomplete defecation
  6. Constipation
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82
Q

If a child is suspected of having IBS, what is an important diagnosis to exclude prior to this?

A

Coeliac disease - check coeliac antibody serology

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83
Q

Give a predisposing factor to duodenal ulcers

A

H.pylori infection

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84
Q

Give 4 factors that indicate the presence of a duodenal ulcer

A
  1. Epigastric pain
  2. Pain radiates through the back
  3. Woken at night with pain
  4. Family history of peptic ulceration in first-degree relative
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85
Q

What disease does H.pylori typically cause?

A

Nodular antral gastritis

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86
Q

What are the typical symptoms of a H.pylori infection

A

Abdo pain

Nausea

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87
Q

How is H.pylori infection identified?

A

Gastric antral biopsy

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88
Q

What product does H.pylori produce and what tests are used to detect this product?

A

Urease

Detected through 13C breath test (administration of 13C labelled urea by mouth)
Stool antigen for H.pylori

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89
Q

a) What is the treatment for peptic ulceration

b) What is the treatment if ulceration suspected of being a result of H.pylori infection

A

a) PPI - omeprazole

b) add eradication therapy e.g. amox/metronidazole/ clarithromycin

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90
Q

What is the management of a child who has failed to respond to peptic ulcer treatment?

A

Upper GI endoscopy

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91
Q

If upper GI endoscopy in child with suspected peptic ulcer disease which did not respond to treatment is normal, what is the diagnosis?

A

Functional dyspepsia

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92
Q

Symptoms of functional dyspepsia?

A
  1. Same as those of PUD (abdo pain and nausea)
  2. Early satiety
  3. Bloating
  4. Post prandial vomiting
  5. Delayed gastric emptying
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93
Q

What is the treatment of functional dyspepsia?

A

Hypoallergenic diet

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94
Q

What is eosinophilic oesophagitis?

A

Inflammatory condition affecting the oesophagus caused by activation of eosinophils within the mucosa and submucosa

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95
Q

Presentation of eosinophilic oesophagitis?

A
  1. Vomiting
  2. Discomfort on swallowing
  3. Bolus dysphagia (food sticking)
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96
Q

What is the pathophysiology of eosinophilic oesophagitis?

A

Allergic

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97
Q

Eosinophilic oesophagitis is more common in which children?

A

Those with other features of atopy (asthma, eczema, hay fever)

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98
Q

How is eosinophilic oesophagitis diagnosed?

A

Endoscopy

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99
Q

What signs are seen on endoscopy of a child with eosinophilic oesophagitis?

A
  1. Linear furrows
  2. Trachealisation
  3. Microscopically - eosinophilic infiltration
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100
Q

What is the treatment of eosinophilic oesophagitis

A

Swallowed corticosteroids
(Fluticasone/ viscous budesonide)

Or exclusion diet

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101
Q

What is the most frequent cause of gastroenteritis in developed countries?

A

Rotavirus

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102
Q

Presence of blood in stool generally suggests what about the cause of the infection, in a child with gastroenteritis?

A

Bacterial cause

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103
Q

Clinical features of a shigella/salmonella infection? (4)

A
  1. Dysenteric infection with blood and pus in stool
  2. Pain
  3. Tenesmus
  4. Shigella - high fever
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104
Q

Clinical features of a cholera/ e.coli infection?

A
  1. Profuse, rapidly dehydrating diarrhoea
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105
Q

Give two protozoan causes of gastroenteritis?

A
  1. Giardia

2. Cryptosporidium

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106
Q

Clinical dehydration typically relates to what percentage loss of body weight?

A

5-10%

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107
Q

When a child is shocked due to dehydration, what is the typical loss of body weight?

108
Q

What are the consequences of hyponatraemic dehydration and how does it occur?

A

Occurs when an infant with diarrhoea drinks large quantities of water or other hypotonic solutions and thus plasma sodium drops

Consequences are seizures as a result of intracellular volume and therefore brain volume. And a greater degree of shock as the extracellular volume decreases as water moves into cells.

109
Q

Give 7 clinical features of shock from dehydration in an infant

A
  1. Pale or mottled skin
  2. Hypotension
  3. Decreased consciousness
  4. Sunken fontanelle
  5. Dry mucous membranes
  6. Eyes sunken and tearless
  7. Tachypnoea
  8. Tachycardia
  9. Cap refill >2s
  10. Weak peripheral pulses
  11. Reduced urine output
  12. Reduced tissue turgor
  13. Cold extremities
110
Q

If a child has hypernatraemic dehydration, their plasma sodium should be reduced slowly to prevent cerebral oedema and seizures. At what rate should it be reduced?

A

Less than 0.5mmol/l per hour

111
Q

Give 3 indications for the use of antibiotics in a child with gastroenteritis?

A
  1. Suspected or confirmed sepsis
  2. Extraintestinal spread of infection
  3. Salmonella in a child under 6 months
  4. Malnourished or immunocompromised children
  5. Specific infections e.g. C.diff
112
Q

Management of gastroenteritis

A

Rehydrate!

113
Q

Malabsorptive disorders generally manifest in three ways, what are they?

A
  1. Abnormal stool
  2. Poor weight gain/ faltering growth
  3. Specific nutrient deficiencies
114
Q

What is coeliac disease and what substance is it that causes a problem?

A

Enteropathy in which the gliadin fraction of gluten in wheat, barley and rye provoke a damaging immune response in the proximal small intestinal mucosa.

115
Q

What are the mucosal architecture changes seen in coeliac disease?

A 
Crypt hyperplasia
Villous atrophy
Thickening of basement membrane
Increased intraepithelial lymphocytes 
Reduced goblet cells
116
Q

What are the symptoms of coeliac disease in a 8-24 month old ?

A
  • Faltering growth
  • Abdominal distension
  • Buttock wasting
  • Abnormal stools
  • General irritability
117
Q

The general presentation of coeliac disease is now highly variable. Give 3 common presenting clinical features.

A
  1. Mild, non-specific GI symptoms
  2. Anaemia (iron/folate)
  3. Growth faltering

OR on screening of at risk children (T1 diabetes, autoimmune thyroid disease, downs) and first degree relatives of somebody with coeliac disease

118
Q

What children would be classed as at risk for coeliac disease?

A
  1. T1 diabetics
  2. Autoimmune thyroid disease
  3. Children with down’s syndrome
  4. First degree relatives of somebody with coeliac
119
Q

Give the name of the two highly specific and sensitive serological screening tests for coeliac disease

A
  1. Anti-tTG (immunoglobulin A tissue transglutaminase antibodies)
  2. EMA (endomysial antibodies)
120
Q

How is coeliac disease diagnosed?

A
  1. Strongly suggested by positive serology
  2. Confirmation depends upon mucosal changes on small intestinal (duodenal) biopsy and followed up by the resolution of symptoms and catch up growth upon gluten withdrawal
121
Q

Management of coeliac disease

A

Remove all products containing wheat, rye and barley from the diet

122
Q

What are the risks of a coeliac not following a gluten free diet?

A
  1. Micronutrient deficiency (osteopenia)

2. Small but definite increase in bowel malignancy (small bowel lymphoma)

123
Q

Short bowel syndrome is usually a consequence of what?

A

Surgical resection due to congenital anomalies (congenital atresia) or necrotising enterocolitis, malrotation with volvulus, or trauma.

124
Q

What type of malabsorption is seen in short bowel syndrome?

A

Nutrient, water and electrolyte

125
Q

If short bowel syndrome is severe what is the management?

A

Supplemental paraenteral nutrition

126
Q

What is the most common cause of persistent loose stools in preschool children?

A

Chronic non-specific diarrhoea (toddler’s diarrhoea)

127
Q

Before diagnosing toddler’s diarrhoea, what other conditions would you want to rule out?

A
  1. Coeliac disease

2. Cow’s milk protein allergy (can be temporary following gastroenteritis)

128
Q

What is the typical stool associated with toddler’s diarrhoea

A

Varying greatly - sometimes well formed and sometimes explosive and loose.
Often undigested vegetables

129
Q

Which form of IBD is more common in children?

130
Q

Which parts of the GI tract are affected in Crohn’s?

A

Any from mouth to anus, it’s patchy. Most commonly distal ileum and proximal colon.

131
Q

Which parts of the GI tract are affected in UC?

A

Inflammation confined to colon

132
Q

What are the 3 typical presenting factors in Crohn’s disease

A
  1. Abdominal pain
  2. Diarrhoea
  3. Weight loss
133
Q

Give 3 signs of Crohn’s disease that may be used for diagnosis or to identify a relapse

A
  1. Raised inflam markers (platelet count, ESR, CRP)
  2. Iron deficiency anaemia
  3. Low serum albumin
134
Q

How is Crohn’s diagnosed? The presence of what is termed the histological hallmark?

A
  1. Endoscopy

2. Histology - non-caseating epitheliod cell granulomata

135
Q

Small bowel imaging in a patient with Crohn’s disease will reveal what?

A
  1. Narrowing
  2. Fissuring
  3. Mucosal irregularities
  4. Bowel wall thickening
136
Q

What is the treatment of Crohn’s?

A 
Nutritional therapy - normal diet replaced by whole protein modular feeds for 6-8 weeks 
If ineffective (25%) systemic steroids required
137
Q

What medication is used in a relapse of Crohn’s disease?

A

Immunosuppressants (azathioprine, mercaptopurine, methotrexate)

After that anti-TNF (infliximab/adalimumab)

138
Q

Presentation of Ulcerative Colitis

A
  1. Rectal bleeding
  2. Diarrhoea
  3. Colicky pain
139
Q

Give two extra-intestinal complications of UC

A
  1. Arthritis

2. Erythema nodosum

140
Q

How is the diagnosis of UC made?

A

Endoscopy (upper and ileocolonoscopy)

141
Q

How is UC in children different to that in adults?

A

90% of children have pancolitis whereas in adults, inflammation is typically confined to the distal colon

142
Q

What is seen on histology in UC?

A
  1. Mucosal inflammation
  2. Crypt damage
  3. Ulceration
143
Q

How would you differentiate between UC and Crohn’s?

A

You would do small bowel imaging to ensure that extra-colonic inflammation was not present

144
Q

What is the treatment of mild UC?

A

Aminosalicylates (mesalazine)

145
Q

What is the treatment of extensive UC?

A

Systemic steroids for acute exacerbations and immunomodulatory therapy e.g. azathioprine, can give in combination with low-dose corticosteroid therapy.

146
Q

Management of treatment resistant UC?

A

Biological therapies e.g. infliximab/ ciclosporin, then surgery

147
Q

Treatment of severe fulminating UC?

A

Medical emergency
IV fluids and steroids
Followed by colectomy

148
Q

There is an increased risk of what in adults who had UC as a child?

A

Adenocarcinoma

149
Q

Why do patients with UC receive screening after 10 years of diagnosis?

A

For adenocarcinoma

150
Q

What is the definition of constipation?

A

Infrequent passage of dry, hardened faeces often accompanied by straining or pain and bleeding associated with hard stools.

151
Q

Symptoms of constipation

A

Abdominal pain (waxes and wanes)
Overflow soiling
Hard faeces
Rectal bleeding

152
Q

Give two factors which may precipitate constipation

A
  1. Dehydration

2. Anal fissure

153
Q

Although rare, give 3 potential underlying causes for a child with constipation

A
  1. Hirschprung disease
  2. Lower spinal cord problems
  3. Anorectal abnormalities
  4. Hypothyroidism
  5. Coeliac disease
  6. Hypercalcaemia

Or idiopathic - main

154
Q

How would you investigate constipation?

A

Investigations usually not required. Do not carry out DRE

155
Q

What happens to the rectum in long-standing constipation?

A

Becomes distended and loss of feeling the need to defecate, which causes involuntary soiling

156
Q

How is constipation managed?

A

Evacuate the overloaded rectum using disimpaction regimen of stool softeners

  • Initially with macrogel laxative e.g movicol
  • Administer increasing dose regimen over 1-2 weeks until impaction resolves
  • If unsuccesful use stimulant laxative e.g. senna/ sodium picosulphate
  • If movicol not tolerated use osmotic laxative e.g. lactulose
157
Q

What is the maintenance treatment for constipation?

A

Polyethylene glycol is the treatment of choice (movicol)

Dose should be gradually decreased over months

158
Q

If not treatment for constipation has worked what is the management?

A

Enema or manual evacuation under general

159
Q

How do children with Hirshsprung disease typically present? (ie. signs and symptoms)

A

Usually in neonatal period with intestinal obstruction made clear by a failure to pass meconium within the first 24 hours of life

Abdominal distension and bile stained vomiting then occur

160
Q

What is Hirschprung disease?

A

Absence of ganglion cells from the myenteric and submucosal plexuses of the large bowel, resulting in a narrow, contracted segment.

161
Q

What part of the colon is typically affected in Hirschprung disease?

A

Abnormal bowel extends from the rectum for a variable distance.

75% is confined to rectosigmoid
10% entire colon affected

162
Q

What would the investigations for suspected Hirschprung’s disease consist of?

A

Rectal examination - narrowed segment and gush of liquid stool and flatus released after removal

163
Q

What are the clinical features of Hirschprung disease in a child?

A

Profound chronic constipation
Abdominal distension
Growth failure

164
Q

How is Hirschprung disease diagnosed?

A

Suction rectal biopsy
- Demonstrates the absence of ganglion cells with the presence of large, ACh positive nerve trunks on a suction rectal biopsy

Barium studies or anorectal manometry can give the surgeon an idea of length of aganglionic segment

165
Q

Management of Hirschprung disease?

A

Colostomy followed by anastomozing normally innervated bowel to the anus/

166
Q

How are the majority of structural abnormalities of the kidneys and UT identified?

A

Antenatal ultrasound screening

167
Q

What are the two main serious sequelae of pyelonephritis in children?

A

CKD

Hypertension

168
Q

Triad of UTI symptoms?

A

Dysuria
Frequency
Loin pain

169
Q

Dysuria alone is indicative of what?

170
Q

Symptoms of pyelonephritis?

A

Fever

Systemic involvement

171
Q

Symptoms of UTI in infant?

A 
Fever
Vomiting
Lethargy
Anorexia
Offensive urine
Febrile seizure
172
Q

How are urine samples in infants collected? (4)

A
  1. Clean catch
  2. Adhesive bag to perineum
  3. Urethral catheter
  4. Suprapubic aspiration
173
Q

How are urine samples in children collected?

A

Midstream sample

174
Q

What is the testing done for a UTI?

A
  1. Nitrite stick test
  2. Leucocyte esterase stick testing
  3. Urine culture unless 1 and 2 negative
175
Q

In what children with suspected UTI is a urine culture indicated?

A

All <3 years

If recurrent, if atypical

176
Q

What result is indicative of a UTI on a urine culture?
(90% confidence)

And how is 95% confidence achieved?

A

More than 10^5 colony forming units (CFU) per ml of a SINGLE organism

Result achieved twice on two separate samples

177
Q

What result is indicative of UTI on a urine culture or a catheter or suprapubic sample?

A

Any bacterial growth of a single organism

178
Q

What are the 4 most common organisms causing UTI in children?

A
  1. E.coli
  2. Klebsiella proteus
  3. Pseudomonas
  4. Streptococcus faecalis
179
Q

Finding of what organism in the urine is suggestive of a structural abnormality of the urinary tract?

A

Pseudomonas

180
Q

What organism causing a UTI is more commonly seen in boys and predisposes to formation of phosphate stones?

A

Klebsiella proteus

181
Q

Give 5 causes of incomplete bladder emptying in children

A
  1. Infrequent voiding = bladder enlargement
  2. Obstruction (constipation)
  3. Neuropathic bladder
  4. Vulvitis
  5. VESICOURETERIC REFLUX
182
Q

Give 4 causes of VESICOURETERIC REFLUX

A
  1. Developmental anomaly due to inheritance
  2. Caused by a neuropathic bladder
  3. Urethral obstruction
  4. Temporary after UTI
183
Q

What is the chance of a first degree relative of somebody with vesicoureteric reflux, also having displaced ureters?

184
Q

Give three ways in which VESICOURETERIC REFLUX damages the bladder

A
  1. Urine drains from ureters post void = incomplete emptying and therefore predisposes to infection
  2. Intrarenal reflux = infected kidney
  3. Bladder voiding pressure transmitted to papillae = increased renal pressure and therefore damage
185
Q

What is the treatment of vesicoureteric reflux?

A

Same as that for recurrent UTI

Tends to resolve with age

186
Q

Give the circumstances under which an ultrasound would be performed to investigate a UTI

A
  1. Recurrent infection

2. Atypical infection

187
Q

Give 3 examples of atypical UTIs

A
  1. Septic
  2. Mass
  3. Decreased urinary flow
  4. Increased creatinine
  5. No response to ABx in 48 hours
  6. Atypical infections
188
Q

What is the medical management advised to parents of a child with a UTI

A
  1. Increase fluids
  2. Void regularly/ double void
  3. Treat constipation
  4. ABx prophylaxis
  5. Give lactobacillus acidophilus
189
Q

Give three examples of antibiotics that may be prescribed as prophylaxis for UTI

A
  1. Trimethoprim
  2. Nitrofurantoin
  3. Cephalexin
190
Q

What is the management of a child with recurrent UTI/ scarring/ reflux?

(Including long term management)

A
  1. Long term low dose ABx
  2. Circumcision in boys
  3. Anti VUR surgery
  4. Check BP annually
  5. Urinalysis (check for proteinuria) –> CKD
  6. Regularly assess renal function and growth (ultrasound)
191
Q

What is the management of a suspected UTI in a child of under 3 months of age?

A
  1. Refer to hosp
  2. IV ABx (co-amox 5-7 days)
  3. Oral ABx
192
Q

What is the management of a suspected pyelonephritis in a child of over 3 months?

A
  1. Oral ABx (trimethoprim) 7 days OR

2. IV ABX 4 days followed by 7-10 days oral (co-amox)

193
Q

What is the management of a child of over 3 months with suspected cystitis?

A

Oral ABx 3 days (nitrofurantoin or trimethprim)

194
Q

What would make you think that a child may have pyelonephritis as opposed to lower UTI?

A
  1. Bacteruria and fever >38 degrees

2. Bacteruria and loin pain

195
Q

What additional scans would be organised for a child

a) <1 year post UTI
b) 1 year - 3 years post UTI?

A

a) MCUG and DMSA (micturating cystourethrogram)

b) DMSA (dimercaptosuccinic acid)

196
Q

What is a MCUG and what does it do?

A

Micturating cystourethrogram

Detects obstruction and vesicoureteric reflux

197
Q

What is a DMSA and what does it do?

A

Dimercaptosuccinic acid - checks for renal scarring 3 months after UTi

198
Q

Give 5 causes of acute nephritis

A
  1. Post-infectious
  2. Vasculitis (HSP, SLE, Wegener granulomatosis, microscopic polyarteritis)
  3. IgA nephropathy
  4. Antiglomerular basement membrane disease (Goodpasteur’s syndrome)
199
Q

Pathophysiology of nephritis (why you get the symptoms you get)

A

Increased glomerular cellularity
Restricted glomerular blood flow
Reduced glomerular filtration –> leads to symptoms

200
Q

What are the clinical features of nephritis

A
  1. Decreased urine output and volume overload
  2. Hypertension (can cause seizures)
  3. Oedema (periorbital initially)
  4. Haematuria
  5. Proteinuria
201
Q

Haematuria or proteinuria or both?

a) Nephrotic syndrome
b) Acute nephritis

A

a) Proteinuria

b) Both

202
Q

What is the treatment of nephritis?

A
  1. Manage water and electrolytes
  2. Diuretics
  3. Biopsy and immunosuppression / plasma exchange if continues as can cause irreversible CKD within weeks to months
203
Q

What cause of acute nephritis is unlikely to cause rapid deterioration in renal function? (rapid progressive glomerulonephritis)

A

Post-streptococcal

204
Q

Is streptococcus most commonly a cause of nephritis in developed or developing countries?

A

Developing

205
Q

What are the clinical features of a child with HSP?

A
  1. Symmetrical rash over buttocks, extensor surfaces off arms and legs and ankles (trunk sparing). Initially urticarial but can become maculopapular and purpuric, palpable and recurs over several weeks.
  2. Arthralgia of knees and ankles
  3. Periarticular oedema
  4. Colicky abdo pain –> haematemesis, melaena, intussuseption
  5. Renal involvement (glomerulonephritis) - Microscopic or macroscopic haematuria/ mild proteinuria (nephrotic syndrome rare).
206
Q

What is the most common first feature of HSP?

A

Maculopapular rash

207
Q

What percentage of children with HSP will have persisting haematuria or proteinuria after a year?

208
Q

Which children require long term follow up for HSP?

Why?

A
  1. If haematuria or proteinuria persists after a year
  2. Required treatment for HSP nephritis

Because hypertension and progressive CKD may develop after several years

209
Q

Describe the rash seen in a child with HSP

Including where it is seen and where is spared

A

Symmetrical rash over buttocks, extensor surfaces off arms and legs and ankles (trunk sparing). Initially urticarial but can become maculopapular and purpuric, palpable and recurs over several weeks.

210
Q

What is HSP?

A

Combination of features caused by a vasculitis

211
Q

What is the cause of HSP?

A

Unknown. circulating IgA due to genetics and antigen exposure increase, interacts with IgG and deposits in organs. Interacts with complement and precipitates inflammatory response in organs

212
Q

In what age group does HSP typically present?

A

3-10 years

213
Q

In what gender is HSP most commonly seen?

214
Q

At what time of the year does HSP peak?

215
Q

What is the common precipitating factor for HSP?

A

Upper respiratory tract infection

216
Q

IgA nephropathy often presents with what?

A

Macroscopic haematuria with a URTI

217
Q

Management of IgA nephropathy

A

Same as HSP

218
Q

How is HSP diagnosed?

A

Clinically

219
Q

What is the most common vasculitis to involve the kidney

A

Henoch-Schonlein purpura

220
Q

Treatment of any vasculitis with renal involvement?

A
  1. Corticosteroids
  2. Plasma exchange
  3. IV cyclophosphamide
221
Q

What are the most common causes of symptomatic hypertension in children?

A
  1. Renal
  2. Cardiac
  3. Endocrine
222
Q

Definition of hypertension in children?

A

BP above the 95th percentile for height, age and sex

223
Q

Presentation of hypertension in children? (6)

A

Vomiting, headache, facial palsy, hypertensive retinopathy, convulsions, proteinuria

224
Q

How do you investigate an abdominal mass?

225
Q

What is the most common cause of bilaterally enlarged kidneys in early life?

226
Q

ARPKD is associated with what other conditions?

A
  1. Hypertension
  2. Hepatic fibrosis
  3. Progression to CKD
227
Q

Which is the more severe from ARPKD or ADPKD?

228
Q

Give 3 renal causes of hypertension?

A
  1. Renal artery stenosis
  2. PKD
  3. Renal parenchymal disease
  4. Renal tumours
229
Q

Give 3 endocrine causes of hypertension?

A
  1. Congenital adrenal hyperplasia
  2. Cushings
  3. Hyperthyroidism
230
Q

Give two causes of hypertension linked to catecholamines?

A
  1. Neuroblastoma

2. Phaechromocytoma

231
Q

Give the main cardiac cause of hypertension in children

A

Coarctation of aorta

232
Q

Give 3 causes of renal calculi in children

A
  1. UTI
  2. Structual abnormalities of tract
  3. Metabolic abnormalities
233
Q

What are the most common type of renal stones seen in children?

A

Phosphate - due to infection with Proteus

234
Q

Presentation of renal calculi?

A
  1. Haematuria
  2. Loin or abdo pain
  3. UTI
  4. Passage of stone
235
Q

What is Fanconi syndrome?

A

Generalised proximal tubule dysfunction

236
Q

What are the cardinal features of fanconi syndrome?

A

Excessive urinary loss of

  • amino acids
  • glucose
  • phosphate
  • bicarbonate
  • sodium
  • calcium
  • potassium
  • magnesium
237
Q

How does a child with fanconi syndrome present?

A
  1. Polydipsia and polyuria
  2. Salt depletion and dehydration
  3. Hyperchloaemic metabolic acidosis
  4. Rickets
  5. Faltering growth
238
Q

What are the three main causes of fanconi syndrome?

A
  1. Idiopathic
  2. Secondary to inborn errors of metabolism e.g. Glycogen storage disorders, Wilsons disease
  3. Acquired - heavy metals, drugs and toxins, vit D deficiency
239
Q

What is the most common type of Acute Kidney Injury in children?

240
Q

What is the main symptom of AKI?

A

Oliguria = <0.5ml/kg/hr

241
Q

What would suggest a renal cause of AKI?

A

Salt and water retention

Blood protein and casts in the urine

242
Q

What is the cause of postrenal AKI?

A

Obstruction

243
Q

What is the main cause of prerenal failure?

A

Hypovolaemia

244
Q

How is prerenal failure managed?

A

Correct fluid depletion

Circulatory support

245
Q

How is renal failure managed?

A

Restrict fluids

Challenge with diuretics

246
Q

What are the two most common renal causes of acute renal failure?

A
  1. HUS
  2. Acute tubular necrosis

Others: glomerulonephritis, pyelonephritis

247
Q

How is postrenal failure managed?

A

Assess site of obstruction

Nephrostomy or bladder catherisation

248
Q

Give two example causes of postrenal failure

A

Obstruction

  • posterior urethral valves
  • blocked urinary catheter
249
Q

Give three indications for the use of dialysis in AKI?

A
  1. Hyperkalaemia
  2. Hypo or hypernatraemia
  3. Pulmonary oedema or hypertension due to volume overload
  4. Metabolic acidosis
  5. Multisystem failure
250
Q

What are the main principles of managing AKI?

A
  1. Treat underlying cause
  2. Treat metabolic abnormalities
  3. Dialysis if necessary
251
Q

What is the triad seen in Haemolytic Uraemic Syndrome?

A
  1. Acute renal failure
  2. Microangiopathic haemolytic anaemia
  3. Thrombocytopenia
252
Q

HUS is typically secondary to what?

A

Gastrointestinal infection with Ecoli O157:h7 . Acquired through contact with farm animals, eating uncooked beef or unpasteurised milk

or Shigella

253
Q

HUS usually follows what symptom?

A

Bloody diarrhoea

254
Q

What is the prognosis for typical HUS?

A

Good.

Long term follow up required incase persistent proteinuria. hypertension and CKD

255
Q

What is the difference between atypical and typical HUS

A
  1. Atypical can be familial
  2. Atypical has no diarrhoeal prodrome
  3. Atypical has frequent relapses
  4. Atypical much worse prognosis
256
Q

Give some examples of causes of atypical HUS

A

Infection, medication, autoimmune, genetics

257
Q

What is the pathophysiology of HUS?

A

Glomerular endothelium gets damaged and clots form in the kidneys

258
Q

How is HUS diagnosed?

A
  1. Signs of kidney damage
    - proteinuria, haematuria, increased urea and creatinine
  2. Schistocytes/ helmet cells on blood smear
  3. Cultured ecoli
259
Q

Treatment of HUS? (D +/ typical)

A

Supportive

Don’t prescribe abx

260
Q

Stage 5 CKD is defined by a GFR of less than what?

A

15ml/min per 1.73m2

261
Q

What are the clinical features of stage 4 or 5 CKD? (5)

A
  1. Anorexia and lethargy
  2. Polydipsia and polyuria
  3. Faltering growth
  4. Bony deformities (renal rickets/osteodystrophy)
  5. Hypertension
  6. Proteinuria
  7. Normochromic, normocytic anaemia
262
Q

What are the three most common causes of CKD in children?

A
  1. Renal dysplasia+- reflux
  2. Obstructive uropathy
  3. Glomerular disease or congenital nephrotic syndrome
263
Q

What is renal osteodystrophy and why is it seen in patients with CKD?

A

Phosphate retention and hypocalcaemia occur due to decreased activation of vit D by kidney

Therefore get secondary hyperparathyroidism

Causes efflux of calcium from bone and results in osteitis fibrosa and osteomalacia of bones

264
Q

Management of renal osteodystrophy

A
  1. Minimise phosphate intake e.g. restrict milk products
  2. Calcium carbonate as phosphate binder
  3. Activated vit D supplements
265
Q

Give 3 complications of CKD on other systems

A
  1. Renal osteodystrophy
  2. Anaemia (EPO)
  3. Hormonal abnormalities - growth hormone resistance
266
Q

When are most cases of CKD picked up?

A

Antenatal US

Phase 3A Medicine (12 decks)

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