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Phase3 3a > Paeds Gastro And Renal > Flashcards

Paeds Gastro And Renal Flashcards

1
Q

What is GORD?

A
  • Contents from the stomach reflux through the lower oesophageal sphincter into the oesophagus, throat and mouth.
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2
Q

What are signs of problematic reflux? (6)

A

-Chronic cough
-Hoarse cry
-Distress, crying or unsettled after feeding
-Reluctance to feed
-aspiration Pneumonia
-Poor weight gain

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3
Q

Management of GORD

A

Practical
-Small, frequent meals
-Burping regularly to help milk settle
-Not over-feeding
-Keep the baby upright after feeding (i.e. not lying flat)

Medical
-Gaviscon mixed with feeds
-Thickened milk or formula
-Proton pump inhibitors

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4
Q

What is sandifers syndrome

A

rare condition causing brief episodes of abnormal movements associated with gastro-oesophageal reflux in infants

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5
Q

Two features of sandifer syndrome

A

Torticollis: forceful contraction of the neck muscles causing twisting of the neck

Dystonia: abnormal muscle contractions causing twisting movements, arching of the back or unusual postures

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6
Q

Differential diagnosis of sandifers syndrome

A

-Infantile spasms (West syndrome)
-seizures.

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7
Q

What are some secondary causes of constipation in children

A

Hirschprungs disease
CF
Hypothyroidism
Cerebral palsy

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8
Q

Typical features of constipation

A

-Less than 3 stools a week
-Hard stools that are difficult to pass
-Rabbit dropping stools
-Straining and painful passages of stools
-Abdominal pain
-Holding an abnormal posture, referred to as -retentive posturing
-Rectal bleeding associated with hard stools
-Faecal impaction causing overflow soiling, with -incontinence of particularly loose smelly stools
-Hard stools may be palpable in abdomen
-Loss of the sensation of the need to open the bowels

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9
Q

What is encopresis

A
  • a sign of chronic constipation where the rectum become stretched and looses sensation

-the large hard stools remain but the loose stool sneak around and leak out

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10
Q

Causes of encopresis

A

Spina bifida
Hirschprung’s disease
Cerebral palsy
Learning disability
Psychosocial stress
Abuse

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11
Q

Lifestyle factors causing constipation

A
  • not regularly opening the bowels
    -low fibre diet
    -poor fluid intake and dehydration
    -sedentary lifestyle
    -abuse
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12
Q

Red flags that are serious when it comes to come constipation

A

Not passing meconium - may suggest CF or Hirschprungs

Vomiting - may suggest obstruction or Hirschprungs

-ribbon stool - anal stenosis

-neurological Sx - may suggest cerebral palsy or spinal cord lesion

-abnormal lower back - spina bifida

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13
Q

Managment of constipation in children

A
  • recommend high fibre diet and hydration
  • laxative - moviolas 1st line

-encourage going to the toilets - e.g using schedules and diaries

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14
Q

Faecal impaction tx

A

Disimpaction regimen with high laxative at first then slowly tapered off

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15
Q

What is the definition of constipation

A

the infrequent passage of dry, hardened faeces often accompanied by straining or pain

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16
Q

What is hirschprungs disease

A

Congential condition where nerve cells of the myentetic plexus are absent in the distal bowel and rectum resulting in narrowing of the bowel segment

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17
Q

What syndromes are associated with hirschsprungs

A

-Downs syndrome

-Neurofibromatosis

-Waardenburg syndrome (a genetic condition causing pale blue eyes, hearing loss and patches of white skin and hair)

-Multiple endocrine neoplasia type II

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18
Q

Presentation of Hirschprungs (5)

A

-Delay in passing meconium (more than 24 hours)

-Chronic constipation since birth

-Abdominal pain and distention

-Vomiting

-Poor weight gain and failure to thrive

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19
Q

What is Hirschprungs associated enterocolitis

A

Inflammation and obstruction of the intestine occur in gin 20% of children with hirschprungs

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20
Q

Presentation of HAEC

A

-fever
-abdominal distension
-diarrhoea ( can be with blood)

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21
Q

What are the complications of HAEC

A

-perforation of the bowel
-toxic megacolon
-death

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22
Q

Mx of HAEC

A

-ABX
-fluid resuscitation
-decompression of obstructed bowel

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23
Q

Diagnosis of Hirschprungs

A

GS
Suction rectal biopsy - to find absence of myenteric ganglion

Barium/ anaorectal manometry - to determine length of a ganglionic segment

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24
Q

MX of Hirschprungs

A

Colostomy - Removing the aganglionic part of the bowel

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25
Q

What is pyloric stenosis

A

-Hypertrophy (thickening) and narrowing of the pylorus preventing the food travelling from the stomach to the duodenum

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26
Q

Clinical features of pyloric stenosis (3)

A

• Vomiting, which increases in frequency and
forcefulness over time, ultimately becoming
projectile

• Hunger after vomiting until dehydration leads to
loss of interest in feeding

• Weight loss if presentation is delayed

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27
Q

How is pyloric stenosis diagnosed

A

-ultrasound

-test feed performed
may see gastric peristalsis from Left to right
Feel a pyloric mass like an olive

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28
Q

Management of pyloric stenosis

A

initial priority
-correct fluid and electrolyte balance with IV FLUIDS - potassium and dextrose

Then
-pyloromytomy - reducing the hypertrophic tissue

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29
Q

What metabolic imbalances occur in pyloric stenosis (3)

A

-hypochloreamic metabolic alkalosis
-hyponatraemia
-hypokalaemia

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30
Q

Presentation of pyloric stenosis

A

-failure to thrive
-projectile vomiting

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31
Q

What is gastroenteritis

A

Inflammation from the stomach to the intestines and presents with nausea, vomiting and diarrhoea.

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32
Q

Common cause of gastroenteritis

A

Viral

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33
Q

Key concern regarding gastroenteritis

A

Dehydration

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34
Q

Management of gastroenteritis

A

rehydration
-clinical dehydration - ORS
-shock - IV 0.9 sodium chloride solution an consult paediatrician

-if sepsis suspected then give abx

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35
Q

How is clinical dehydration managed in children

A

ORS
-give fluid deficit replacement (50ml/Kg) over 4 hours and maintenance fluids
-if vomiting give NG tube

If still not getting better
-IV therapy for rehydration 100ml/Kg if shocked
-give 0.9% nacl solution

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36
Q

Most common causative organism of gastroenteritis in developed countries

A

Rotavirus

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37
Q

DDX of gastroenteritis

A

-Infection (gastroenteritis)
-Inflammatory bowel disease
-Lactose intolerance
-Coeliac disease
-Cystic fibrosis
-Toddler’s diarrhoea
-Irritable bowel syndrome
-Medications (e.g. antibiotics)

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38
Q

Viral causes of gastroenteritis

A

-rotavirus
-norovirus
-adenovirus (less common)

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39
Q

Why should antibiotics not be given in E.coli gastroenteritis

A

-increases the risk of haemolytic uraemic syndrome

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40
Q

How does e.coli cause Haemolytic uraemic syndrome

A
  • releases shiga toxin
    -destroying blood cells
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41
Q

Which bacteria is responsible for travellers diarrhoea

A

Campylobacter Jejuni - most common cause of bacterial gastroenteritis worldwide

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42
Q

How is c.jejuni spread

A

Raw or improperly cooked poultry
Untreated water
Unpasteurised milk

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43
Q

Antibiotics used for for c.jejuni infection

A

-azithromycin
-cirpofloxacin

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44
Q

How is salmonella spread

A

-eating raw eggs or poultry, or food contaminated with the infected faeces of small animals

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45
Q

Sx of salmonella

A

-watery diarrhoae can be with mucus or blood
-abdo pain
-vomiting

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46
Q

How is bacillus cereus spread

A

-grows well on food not immediately refrigerated after cooking. The typical food is fried rice left out at room temperature.

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47
Q

Bacillus cereus infection symptoms

A

-abdo cramps
-vomiting
-watery diarrhoea

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48
Q

What is the course of a bacillus cereus infection

A

-vomiting within first 5 hours
-watery diarrhoea after 8 hours
-all Sx resolve within 24 hours

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49
Q

Post Gastroenteritis Complications (4)

A

-Lactose intolerance
-Irritable bowel syndrome
-Reactive arthritis
-Guillain–Barré syndrome

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50
Q

How due gardia lamiblia spread

A

faeco oral transmission
-lives in small intestine of mammals
-cysts released in stools of infected mammals
-which contaminate food or water

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51
Q

Tx of giardiasis infection

A

Metronidazole

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52
Q

Dx of gardiasis

A

Stool microscopy

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53
Q

Red flag signs of dehydration

A

-appears unwell
-sunken eyes
-tachycardia
-tachypnoea
-reduced skin turgor
-lethargy

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54
Q

What is appendicitis

A

Inflammation of the appendix

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55
Q

Peak age of appendicitis

A

10-20 year olds

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56
Q

Key presenting features of appendicitis (7)

A

-abdo pain - central moving down to the right iliac fossa and localising there

  • loss of appetite
  • nausea and vomiting

-rosvings sign - LIF palpation causes RIF pain

-rebound tenderness

-percussion tenderness

-Guarding

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57
Q

How to diagnose appendicitis

A
  • clinical presentation + diagnostic laparoscopy
  • inflammatory markers
  • CT scan - to confirm
  • Ultrasound in females to exclude ectopic pregnancy or other gynae pathology
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58
Q

Differential diagnosis of appendicitis

A

-ectopic pregnancy

-ovarian cyst/ torsion

-meckels diverticulum

-mesenteric Adenitis

-appendix mass

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59
Q

What do you do to exclude ectopic pregnancy

A

Serum / urine b HCG (pregnancy test)

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60
Q

What is mesenteric Adenitis

A

-inflamed abdominal lymph nodes, accompanied by abdo pain

-often associated with tonsillitis or URTI

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61
Q

Mx of appendicitis

A

-immediate admission under the surgical team

Appendectomy

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62
Q

Complications of appendicectomy

A

-bleeding and infection
-pain and scars
-damage to the bowel bladder
-removal of a normal appendix
-anaesthetic risk
-VTE (DVT and PE) from surgery

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63
Q

What is biliary atresia

A
  • congential condition where a section of the bile duct is either narrow or absent

-leads to cholestasis where the bile cannot be transported from liver to bowel

-prevents the excretion of conjugated bilirubin

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64
Q

Management of biliary atresia (2)

A

Kasai portoenterostomy
-attaching a section of small intestine to the liver

Full liver transplant

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65
Q

Presentation of babies with biliary atresia

A

-mild jaundice
-stools are pale
-urine dark
-hepatomegaly
-Splenomegaly

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66
Q

Diagnostic treatment of biliary atresia

A

Laparotomy by cholangiography - doesnt show the outline of biliary tree

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67
Q

What are choledochal cysts

A

-cystic dilatations of the bile ducts

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68
Q

Presentation of choledochal cysts

A

-abdo pain
-palpable mass
-Jaundice

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69
Q

Diagnosis of choledochal cyst

A

Ultrasound/ radionuclide scanning

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70
Q

Tx of choledochal cyst

A

-surgical excision

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71
Q

Complications for choledochal cyst

A

Cholangitis
Malignancy in biliary tree

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72
Q

What is intussusception

A

Condition where the bowel invaginates of proximal bowel into the distal part

-most commonly ileum passing into the caecum

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73
Q

What the most common cause of intestinal obstruction in infants

A

Intussusception

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74
Q

Presentation of intussusception (6)

A

-sudden, severe, colicky pain
-pallor
-refuse feeds
- vomiting (can be bilestained depending on site
-palpable sausage shaped mass
-redcurrant jelly stool comprising of blood stained mucus
-abdominal distension

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75
Q

Investigations for intussusception

A

X-ray
-distension of small bowel
-abscence of gas in distal colon

Abdo ultrasound
-TARGET SHAPED MASS

Contrast enema

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76
Q

In boys what should you always consider for acute abdo pain?

A
  • strangulated inguinal hernia
  • torsion of testis
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77
Q

Treatment of intussusception (3)

A
  • immediate fluid resuscitation
  • reduction by rectal air insufflation
  • surgery if above unsuccessful
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78
Q

Complications of intussusception (4)

A

Venous Obstruction
Gangrenous bowel
Perforation
Death

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79
Q

What is meckels diverticulum

A

Failure of the obliteration of the vitelline ducts

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80
Q

How to diagnose meckels diverticulum

A

Technetium scan - shows ectopic gastric mucosa in RIF

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81
Q

Extra intestinal manifestation of Crohn’s disease in children?

A

-oral lesions like apthous ulcers
-perianal skin tags
-uveitis
-arthralgia
-erythema nodosum

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82
Q

Classic presentation of Crohn’s disease in child

A

-abdo pain
-diarrhoea
-weight loss
-fever
-lethargy
-growth failure
-delayed puberty

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83
Q

What is Crohn’s disease

A

A form of IBD
Characterised by transmural inflammation, skip lesions most commonly affecting terminal ileum due to T cell immune mediated response

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84
Q

Where does Crohn’s disease most commonly affects

A

-Where GI tract
-most commonly proximal colon/ terminal ileum

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85
Q

How to diagnose Crohn’s disease

A

-Biopsy + endoscopy
-raised faecal calcprotectin (in all IBD)
-ANCA -ve unlike UC
-CRP, ESR, platelet count raised
-iron deficiency present

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86
Q

What are the finding of biopsy and endoscopy in crohns diseases

A

Biopsy
-transmural inflammation (all 4 layers of gut)
-non caseating granuloma

Endoscopy
-skip lesions
-cobblestoning

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87
Q

Micro and macro features of Crohn’s disease

A

Macro
-skip lesions
-cobblestone appearance due to fissures and ulcers
-thickened and narrow

Micro
-transmural
-non caseating granulomas
-increased goblet cells

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88
Q

Pathology of Crohn’s disease

A

-Faulty GI epithelium allows pathogen to enter wall

-leading exaggerated inflammatory response

-formation of granulomas and destruction of GI tissue

-leading to transmural ulcers and skip lesion and cobblestone appearance

-as the wall heals adhesions and fistulae form

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89
Q

Treatment for Crohn’s disease

A

Initially
-polymeric diet (liquid) 6-8 weeks works in 75% of cases

Steroids (oral prednisolone/ IV hydrocortisone)

Relapse then add
1st - azathioprine
2nd - Methotrexate
3rd - infliximab/ adalinumab (anti TNF)

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90
Q

When is surgery used in crohns

A

to treat complications such as:
Fistulae
Obstruction
Abscess formation
When disease is localised

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91
Q

What is ulcerative colitis

A

A form of IBD
That is a recurrent, inflammatory and ulcerating disease involving the mucosa of the colon

Inflammation goes from rectum upwards but never going past ileoceacal valve

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92
Q

What genes are associated with UC

A

HLAb27

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93
Q

What antibody is associated with UC

A

Positive pANCA

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94
Q

Symptoms of UC

A

-Pain in LLQ
-tenesmus
-bloody, mucus and watery diarrhoea
-weight loss and growth failure - more common in crohns

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95
Q

Extra intestinal features in UC

A

-arthritis
-erythema nodosum
-PSC
-clubbing
-episcleritis
-aphthous ulcers

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96
Q

How is UC diagnosed

A

Endoscopy (upper and ileocolonscopy)
Biopsy - crypt abscesses
Barium enema

Bloods - raised CRP and ESR
- faecal calprotectin
-iron deficiency aneamia
-positive pANCA

Stool sample - rule out infective colitis

Abdo x-ray - check for toxic megacolon

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97
Q

Macro and micro features of UC

A

macro
-continuous inflammation
-ulcers
-pseudo polyps

Micro
-Mucosal inflammation
-no granulomata
-depleted goblet cells
-increased crypt abscesses

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98
Q

What’s the inflammation like in UC

A

-continuous inflammation of LARGE bowel
-only affecting mucosa and sub mucosa
-can lead to crypt abscesses

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99
Q

How does UC differ in adults compared to children

A

-the colitis is not confined to the distal colon and instead 90% of children have PANCOLITIS (all large bowel)

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100
Q

Treatment for UC

A

Mild UC
1st line -aminosalicylates (mesalazine/ balsalazide)

2nd line -topical steroids

Severe UC
1st line - IV corticosteroids (hydrocortisone) + azathioprine

2nd line - IV ciclosporin

GOLD - Colectomy with ileostomy

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101
Q

1st line TX for maintaining remission of UC

A

Aminosalicylate
-mesalazine
-azathioprine
-mercaptopurine

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102
Q

Complications of crohns

A

-peri anal abscess
-anal fissure
-anal fistula
-obstruction
-strictures (narrowing)
-anaemia
-malabsorption
-osteoporosis

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103
Q

Complications of UC

A

-toxic megacolon
-perforation
-colonic adenocarcinoma
-obstruction
-strictures

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104
Q

Score for UC

A

Truelove and WITTS score

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105
Q

What is coeliac disease

A

utoimmune condition where exposure to gluten causes an immune reaction that creates inflammation in the small intestine usually developing in childhood

106
Q

Pathophysiology of coeliac

A

-autoantibodies are created in response to exposure to gluten.
-These autoantibodies target the epithelial cells of the intestine and lead to inflammation.

107
Q

Two antibodies involved in coeliac

A

anti-tissue transglutaminase (anti-TTG)
anti-endomysial (anti-EMA)

108
Q

How does coeliac lead to malabsorption

A

-inflammation affects the jejunum particularly

-constant inflammation causes atrophy of the villi

-causes decreased Surface area of gut wall causes decreased nutrient uptake

109
Q

Presentation of coeliac

A

-OFTEN ASX

-Failure to thrive in young children
-Diarrhoea
-Fatigue
-Weight loss
-Mouth ulcers
-Anaemia secondary to iron, B12 or folate deficiency
-**Dermatitis ** - is an itchy blistering skin rash that typically appears on the abdomen

110
Q

What condition is linked and always tested for alongside coeliac

A

Type 1 diabetes

111
Q

Genetic association with coeliac (2)

A
  • HLA-DQ2 gene (in 90%)
  • HLA DQ8 gene
112
Q

Why do you test for total IgA levels in coeliac

A

-because Anti-TTG and Anti-EMA are IgA
-so some patients have IgA deficiency
-so will be false negative even if they have coeliac

**so then you test for IgG version of anti-TTG/EMA

113
Q

Dx of coeliac (3)

A

-MUST BE DONE WHILE STILL ON GLUTEN DIET

-Check total immunoglobulin A levels to exclude IgA deficiency before checking for coeliac disease specific antibodies:
Raised anti-TTG antibodies (first choice)
Raised anti-endomysial antibodies

-Endoscopy and intestinal biopsy show:
Crypt hypertrophy
Villous atrophy

114
Q

Coeliac disease associations (6)

A

-type 1 diabetes
-thyroid disease
-autoimmune hepatitis
-PBC
-PSC
-Down’s syndrome

115
Q

Tx of coeliac

A

Lifelong gluten free diet

116
Q

Complications of coeliac

A

-Vitamin deficiency
-Anaemia
-Osteoporosis
-Ulcerative jejunitis
-Enteropathy-associated T-cell lymphoma (EATL) of the intestine
-Non-Hodgkin lymphoma (NHL)
-Small bowel adenocarcinoma (rare)

117
Q

What is intestinal obstruction

A

-physical obstruction prevents the flow of faeces through the intestines.

-This blockage will lead to a back-pressure through the gastrointestinal system, causing vomiting and absolute constipation

118
Q

Cause of intestinal obstruction

A

-meconium ileus
-hirschsprungs
-oesophageal atresia
-duodenal atresia
-intussusception
-malrotations with volvulus
-strangulated hernia
-imperforate anus

119
Q

Presentation of intestinal obstruction

A

-Persistent vomiting - may be bilious
-abdo pain
-distension
-failure to pass stools
-tinkling bowel sounds/ absent bowel sounds

120
Q

Dx of obstruction

A

abdo X-ray
-dilated loops of bowel before the obstruction (proximal)
-collapsed loops past the obstruction (distal)
-absence of air in the rectum

121
Q

Management of obstruction

A

-nil by mouth
-insert nasogastric tube
-IV fluids to prevent and correct dehydration
-antiemetics and analgesia

-surgery last resort

122
Q

Presentation of marasmus

A

-wasted wizened appearance
-skinfold thickness and mid arm circumference reduced markedly
-withdrawn personality

123
Q

What is marasmus

A

Severe caloric and Protein energy malnutrition

-child has heigh and weight 3 standard deviations below the average

124
Q

Tx for marasmus

A

1- rehydration and fix electrolyte imbalance
2- nutritional rehabiliton - use liquid formulas and tube feeding balances fats, carbs and protein
3- prevention

125
Q

Presentation of Kwashiokor (9)

A

-generalised oedema
-severe wasting
-**flaky paint skin rash and skin thickening **
-angular stomatitis
-sparse hair
-diarrhoea
-hypothermia
-bradycardia
-hypotension

126
Q

What problems can need to be treated with malnutrition (6)

A

-hypoglycaemia
-Hypothermia - wrap up the child
-dehydration - IV fluids
-electrolyte imbalance - correct deficiencies
-infection - give ABX
-initiate feeding - small volumes frequently

127
Q

Reasons for malnutrition in less economically developed countries

A
  • war
    -social disruption
    -famine
    -natural disasters
128
Q

Reasons for malnutrition in developed countries

A

-poverty
-parental neglect
-poor education
-Restrictive diets
-feeding disorders
-chronic illness
-anorexia

129
Q

What is the WHO definition of malnutrition (3)

A
  • weight for height - 3 SDs below the median
  • mid upper arm circumference - less than 115mm

-height for age - shows growth stunting and an indication of chronic malnutrition

130
Q

What is kwashiorkor

A

A manifestation of severe protein energy malnutrition particularly affecting children in the tropics

131
Q

What does failure to thrive mean

A
  • Sub optimal weight gain in infants and toddlers when plotted on a centipede chart

-is present if the infant weight falls across two centile lines

132
Q

Give 6 Causes of failure to thrive

A

Not extensive list
-feeding problems E.g insufficient breast milk
-lack of regular feeding times
-low socioeconomic status
-infant resists feed
-maternal depression
-lack of maternal education
-neglect
-cleft palate
-Crohn’s disease
-CF
-vomiting and GORD
-coeliac
-Down’s syndrome
-malignancy
-CHD

133
Q

How are inguinal hernia normally caused

A

Patent Processus vaginalis

134
Q

how does an inguinal hernia normally present

A

-an irreducible lump in the groin or scrotum
-irritability
-vomiting
-pain on straining or coughing

135
Q

Biggest risk in inguinal hernias

A

Strangulation of the hernia (blood supply compromised to area)

136
Q

Treatment for inguinal hernias

A
  • opioid analgesia and sustained gentle compression

-surgery urgently to avoid strangulation

137
Q

Assessment for failure to thrive includes? (7)

A

-pregnancy, birth, development and social history
-feeding or eating history
-observe feeding
-mums physical and mental health
-parent and child interaction
-HEIGHT,WIEGHT AND BMI and plot on growth chart
-mid parental height

138
Q

What is the mid parental height

A

Calculate mean of parental heights

-add 7cm for male infants
-subtract 7cm for female infant s

139
Q

What is includes in a feeding shitory

A

Ask about:
-breast/ bottle fed
-feeding times, volume and frequency
-difficulty with feeding
-food choices
-meal time routines
-appetite of child
-food aversion

140
Q

how to calculate BMI

A

Weight Kg/height m2

141
Q

Outcomes that suggest inadequate nutrition/ growth disorder

A

-Height more than 2 centile spaces BELOW the mid-parental height centile

-BMI below the 2nd centile

142
Q

Initial investigations with faltering growth

A

-urine dipstick for UTI
-coeliac screen (anti TTG/ Anti EMA)

143
Q

How to manage failure to thrive if inadequate nutrition is the cause

A

-nutritional supplemental drinks

-dietician review

-energy dense foods to boost calories

-reduce milk consumption to improve appetite for other food

-encourage regular mealtimes

144
Q

What is cows milk protein allergy

A

A hypersensitivity reaction to the protein in cows milk can be IgE mediated or non IgE mediated

145
Q

Difference between IgE mediated and non IgE mediated cows milk protein allergy

A

IgE mediated - rapid reaction to cows milk occurring within 2 hours

Non IgE mediated -slowly over several days

146
Q

In who are cows milk protein allergy more common

A
  • formula fed babies
  • family history of atopic conditions
147
Q

Presentation of cows milk protein allergy

A

GI symptoms
-bloating and wind
-abdo pain
-diarrhoea
-vomiting

Allergic symptoms
-urticarial rash
-angio oedema
-cough or wheeze
-watery eyes
-Eczema

Severe - anaphylaxis

148
Q

Mx of cow milk protein allergy

A

Avoid cows milk
-breast feeding mothers avoid dairy products
-replace formula with hydrolysed formula designed for cows milk protein allergy

-normally children outgrow the allergy at 3 years old

149
Q

Ix for cows milk protein allergy

A

-full history and examination
-Skin prick testing

150
Q

How does hydrolysed formulas help cows milk protein allergy

A

-Hydrolysed formulas contain cow’s milk

-however the proteins have been broken down so that they no longer trigger an immune response.

151
Q

Difference between cows milk intolerance and cows milk allergy

A

-with allergy children will not be able to tolerate it at all, in tolerance will just suffer GI symptoms

-they both have GI symptoms but allergy will have rash, angio oedema, sneezing and coughing

152
Q

Differential diagnosis of toddlers diarrhoea

A

-lactose intolerance
-fructose/sucrose intolerance
-infective causes - rotavirus, norovirus, gastroenteritis
-IBD

153
Q

How can diarrhoea be helped

A

4F’s

-low fat diet
-6-8 cups of fluid
-regulate the amount of fruit due to fructose not being as easily absorbed at a young age
-fibre intake - 12/18g per day

154
Q

What is toddlers diarrhoea

A

-benign diarrheal disorder that presents with 6-8 watery stools per day for more than 3 weeks without evidence of systemic illness

155
Q

What is a UTI

A

An infection of anywhere along the urinary tract including the urethra, bladder, ureters and kidneys

156
Q

What is cystitis

A

Imflammation of the bladder

157
Q

What is pyelonephritis

A

Infection of the kidneys can lead to scarring and reduced kidney function

158
Q

Symtoms of UTI in babies

A

Babies:
FEVER
Lethargy
Irritability
Vomiting
Poor feeding
Increase frequency

159
Q

Symptoms of UTI in older children

A

FEVER
Abdo pain - particularly suprapubic
Vomiting
dysuria - pain on urination
Urinary frequency
Incontinence

160
Q

Diagnostic criteria for acute pyelonephritis (2)

A

-temp greater than 38
-loin pain/ tenderness

161
Q

Methods to get urine from a child (5)

A

-clean catch sample into a waiting clean pot when nappy is removed - GS

-adhesive plastic bag applied to perineum that has been washed

-urethral catheter if urgency needed

-suprapubic aspiration - fine needle inserted directly into the bladder

-older children - can use midstream sample

162
Q

When should a urine sample always be collected and tested

A

-patient has temperature of 38 or above

163
Q

Bacterial and host factors that predispose to UTI (4)

A

-the infecting organism (hygiene) - E.coli comes from bowel flora

-constipation

-antenatal diagnosed renal or urinary tract abnormality

-incomplete bladder emptying

-vesicouteric reflux - backflow of urine into renal pelvis

164
Q

What do nitrites and leukocytes suggest in a urine dipstick

A

Nitrites - gram negative bacteria break down nitrates to nitrites - so suggest bacteria in the urine

Leukocytes - raised number can suggest an infection or inflammation - urine dipstick test for leukocyte esterase

165
Q

Management of UTI

A

All children under 3 months with a fever
- start immediate IV Abx e.g cefotaxime
- AND full septic screen

Over three months - pyelonephritis/ UUTI
- oral antibiotics usually co amoxiclav 7-10 days unless sepsis suspected then IV Abx

Over three months cystitis/ LRTI
- oral antibiotics for 3 days

166
Q

Typical antibiotics of choice for UTI in child (4)

A

Trimethoprim
Nitrofurantoin
Cefalexin
Amoxicillin

167
Q

What is a DMSA scan

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

-where some parts of the kidney have not taken the material indicates scarring from previous infection

168
Q

What is a micturating cysturethrogram (MCUG)

A

-catheterise the child
-inject contrast into the bladder
-take x-rays to determine wether the contrast is relaxing into the ureters

169
Q

How is vesico uteric reflux diagnosed

A

Micturating cystourethrogram (MCUG)

170
Q

Management of vesico uteric reflux

A

-Avoid constipation

-Avoid an excessively full bladder

-Prophylactic antibiotics

-Surgical input from paediatric urology

171
Q

When should children have abdo ultrasound scans for UTIs (3)

A
  • all children under 6 months with their first UTI within 6 weeks
  • children who have recurrent UTIs within 6 weeks
  • children with atypical UTIs during illness
172
Q

What is nephrotic syndrome

A

When the basement membrane in the glomerulus become highly permeable to protein, allowing leakage of proteins from blood to urine

173
Q

Clinical signs of nephrotic syndrome (4)

A

-periorbital oedema - especially on waking

-scrotal or vulval, leg and ankle oedema

-ascites

-breathlessness - due to pleural effusion and abdo distension

-foamy urine - due to excess protein

174
Q

Pyelonephritis triad of symptoms

A
  • loin pain
    -fever
    -nausea and vomiting
175
Q

Investigations for pyelonephritis

A

-urine dipstick And MC+S
-if recurrent then abdo ultrasound

176
Q

Medical measures to prevent UTIs (3)

A
  • high fluid intake
  • regular voiding
    -ensure complete bladder emptying
177
Q

Classic triad of nephrotic syndrome

A

Low serum albumin < 3.4 g/dL
High urine protein content >3 on urine dipstick (frothy urine)
Oedema

178
Q

Other than the classic triad what are three other features that occur in patients with nephrotic syndrome:

A

Deranged lipid profile, with high levels of cholesterol, triglycerides and LDLs

High blood pressure

Hyper-coagulability, with an increased tendency to form blood clots

179
Q

Most common cause of nephrotic syndrome in children

A

Minimal change disease (90%) in under 10s

180
Q

What are some causes of nephrotic syndrome (6)

A

Isolated
- minimal change

Secondary to intrinsic kidney disease
- focal segmental glomerulosclerosis
- membranoproliferative glomerulonephritis

Secondary to systemic illness
- henoch schonlein purpura
- diabetes
- infection

181
Q

What infections can cause nephrotic syndrome

A

HIV
Malaria
Hepatitis

182
Q

What is minimal change disease

A

Most common cause of nephrotic syndrome in children That can occur in otherwise healthy children without any clear reason

183
Q

Investigations in minimal change disease

A

Urinalysis - small molecular proteins and hyaline casts

Renal biopsy - no abnormality

184
Q

Management of minimal change disease

A

Corticosteroids (prednisolone)

185
Q

Management of nephrotic syndrome

A
  • high dose steroids for 4 weeks and then weaned over 8 weeks (prednisolone)
  • low salt diets
  • diuretics for oedema
  • albumin infusions for hypoalbuminaemia
  • antibiotic prophylaxis in severe cases
186
Q

What is steroid sensitive nephrotic syndrome

A

Children that shows the proteinuria resolves with corticosteroid therapy

187
Q

Management for steroid resistant nephrotic syndrome

A
  • referred to paediatric nephrologist
    -given diuretics for oedema
    -salt restriction
    -ACE inhibitors
    -sometime NSAIDS
188
Q

Complications of nephrotic syndrome

A

-hypovolaemia
-thrombosis
-infection
-hypercholesteroleamia
-acute renal failure

189
Q

Why can hypovolaemia occur in nephrotic syndrome

A

fluid leaks from the intravascular space into the interstitial space causing oedema and low blood pressure.

190
Q

Why can thrombosis occur in nephrotic syndrome

A
  • proteins that normally prevent blood clotting are lost in the kidneys (antithrombin)

-liver responds to the low albumin by producing pro-thrombotic proteins.

  • lead to PE and DVT
191
Q

Why can infection be a complication in nephrotic syndrome

A

-kidneys leak immunoglobulins, weakening the capacity of the immune system to respond.

-This is exacerbated by treatment with medications that suppress the immune system, such as steroids.

-most common infection is pneumococcus and seasonal influenza

192
Q

What would be seen on light and electron microscopy for minimal change, FSGS, membranous nephropathy

A

Minimal change:
Light microscope - no change
Electron microscope - podocyte effacement and fusion

Focal segmental glomerulosclerosis
Light microscope - segmental sclerosis less than 50%
Electron microscopy - podocyte effacement

Membranous nephropathy
Light microscope - thickened GBM
Electron microscope - sub podocyte immune complex deposition

193
Q

What inheritance pattern of congenital nephrotic syndrome

A

Autosomal Recessive

194
Q

Which groups are more likely to get congenital nephrotic syndrome

A

-Finnish people
-consanguineous families

195
Q

Tx for congenital nephrotic syndrome

A
  • unilateral nephectomy to control albuminuria
    -then dialysis for renal failure
    -until old and fit enough for kidney transplant
196
Q

Causes of acute nephritis

A

-Post-infectious (including streptococcus)

-Vasculitis Henoch–Schönlein purpura, SLE, Wegener granulomatosis, microscopic poly-
arteritis, polyarteritis nodosa)

-IgA nephropathy and mesangiocapillary
glomerulonephritis

-Goodpasture syndrome – very rare.

197
Q

What is nephritis

A

Inflammation within the nephrons of the kidneys causing
-reduction in kidney function leading to hypertension
-haematuria
-proteinuria (less than in nephrotic)

198
Q

How does post strep glomerulonephritis occur

A
  • 1- 3 weeks after a beta haemolytic strep infection such as tonsillitis (strep pyogenes)

-immune complex made up of strep antigens, antibodies and complement proteins get stuck in the glomeruli

-leading to inflammation and deterioration of kidney function

199
Q

Management of post strep glomerulonephritis

A

-antihypertensive for HTN
-diuretics for oedema

200
Q

What is IgA nephropathy

A

-IgA deposits in the nephrons of the kidney causing inflammation
-closely related to henoch schonlein purpura

201
Q

Mx of IgA nephropathy

A

antihypertensives
-ACE inhibitors
-ARBs

immunosuppressants
-Steroids
-Cyclophosphamide

202
Q

How does henoch schonlein purpura lead to nephritis

A

-causes increased circulating IgA antibodies and disrupt IgG antibodies

-causes production of complexes that activate complement and are deposits Ed in organs like the kidney

-leading to inflammatory response

203
Q

What is Alport syndrome

A

-an X-linked recessive disorder due to mutation of COL4A5 that progresses to end-stage renal failure by early adult life in males

-associated with nerve deafness and ocular defects and kidney disease

204
Q

Management of alport syndrome

A

Slow the progression
- ACE inhibitors - BP
- ARBs - BP
- diuretics - oedema

Kidney Transplant IS CURE

Hearing aid for hearing loss

205
Q

Treatment for vasculitis related nephritis (3)

A
  • Steroids
  • plasma exchange
  • IV cyclophosphamide
206
Q

Symptoms of vasculitis

A
  • fever
  • Malaise
  • weight loss
  • skin rash
  • arthropathy
207
Q

Findings of post strep GN under:
Light microscope
Electron microscope
Immunofluorescence

A

Light microscope - hyper cellular glomeruli

Electron microscope - subendothelial immune complex deposition

Immunofluorescence - starry sky appearance of IgG, IgM and C3 deposits along GBM

208
Q

How to diagnose lupus

A

Anti DsDNA antibodies
ANA +ve

209
Q

Management of SLE related nephritis (3)

A
  • Steroids
  • Hydroxychlorquine
  • Cyclophosphamide
210
Q

Difference in findings between HSP and IgA nephropathy

A

IgA nephropathy - will only see IgA deposition in the kidneys

HSP - will see it all over organs such s kidney, liver, skin

211
Q

What are hypersensitivity reactions are most causes of nephritic syndrome

A

Type 3 (except goodpastures)

212
Q

Classic triad of haemolytic Uraemic syndrome

A
  • Microangiopathic haemolytic anaemia
  • Acute kidney injury
  • Thrombocytopenia (low platelets)
213
Q

What is microangiopathic haemolytic aneamia

A

-destruction of red blood cells due to pathology in small vessels
-Tiny blood clots partially obstruct the small vessels and cause rupturing

214
Q

What is haemolytic uraemic syndrome

A
  • involves thrombosis in small blood vessels throughout the body

-often affects children following an episode of gastroenteritis

215
Q

Which bacteria often lead to HUS

A

Shiga toxins released from

  • E.coli 0157
  • shigella
216
Q

What medications can increase the risk of developing HUS (2)

A

Antibiotics
Anti motility meds (loperamide)

217
Q

Presentation of HUS

A

First Sx - Diarrhoea that turns bloody after 3 days

Then:
Fever
Abdominal pain
Lethargy
Pallor
Reduced urine output (oliguria)
Haematuria
Hypertension
Bruising
Jaundice (due to haemolysis)
Confusion

218
Q

How to treat HUS (5)

A

Usually self limiting with supportive care

  • Stool culture to establish causative organ and give Appropraite Abx

Hospital admission to treat:
Hypovolaemia (e.g., IV fluids)
Hypertension
Severe anaemia (e.g., blood transfusions)
Severe renal failure (e.g., haemodialysis)

219
Q

What is a hypospadia

A

-a congenital condition where the opening of the urethra is abnormally displaced to the bottom side of the penis toward the scrotum

220
Q

Management of hypospadias

A
  • Mild cases may not require any treatment

-Surgery performed after 3 – 4 months of age,
aims to correct the position of the meatus and straighten the penis

221
Q

Complications of hypospadias (3)

A

Difficulty directing urination
Cosmetic and psychological concerns
Sexual dysfunction

222
Q

Why are parents of children with hypospadias warned to not get their children circumsized?

A

Because it is often needed for the reconstructive surgery

223
Q

What is a Chordee

A

Ventral curvature of the shaft of the penis (downwards) particularly seen during erection

224
Q

What is phimosis

A

The inability to retract the foreskin which at first is physiological, but can then be pathological

225
Q

which disease causes pathological phimosis

A

Local skin disease called Balanitis xerotica obliterans (BXO)

226
Q

Management of phimosis

A

Circumcision - to reduce risk of UTI

227
Q

How to diagnose alport sydrome (2)

A

-Genetic testing

-Biopsy
Skin
Kidney - review of Glomerular basement membrane

228
Q

Alport syndrome clinical features (5)

A
  • microscopic haematuria in childhood
  • proteinuria
  • hypertension due to renal impairment
  • sensorineural hearing loss
  • ocular pathology
229
Q

What are the ocular effects that Alport syndrome can cause

A

Anterior lenticonus: protrusion of the lens due to weakness of the lens capsule.

Retinal granulations: white / yellow granulations seen on the retina.

Cornea: recurrent corneal erosions.

230
Q

Symptoms of nephritic syndrome (7)

A

Lethargy

Recent infection: fever, sore throat, coryzal symptoms. Typical of poststreptococcal glomerulonephritis and IgA nephropathy

Haematuria

Oliguria: reduce urine output

Oedema: peripheral or periorbital

Shortness of breath: due to fluid overload

Haemoptysis: due to pulmonary haemorrhage (e.g. Anti-GBM, ANCA-vasculitis)

231
Q

Pathophysiology of lupus nephritis

A

-Immune complexes form due to anti-double-stranded DNA and deposit within the renal glomeruli.

-compliment proteins also activated

-leading to immune reaction

232
Q

What are ANCA associated vasculitis

A

Microscopic polyangiitis (MPA)

Wegener’s granulomatosis

Eosinophilic granulomatosis with polyangiitis (EGPA)

233
Q

How do ANCA associated vasculitis lead to glomerulonephritis

A

-the positive ANCAs which are antibodies target small blood vessels

-causes inflammation of small blood vessels and affects the glomeruli leading to poor filtration

234
Q

Treatment of ANCA glomerulonephritis

A

-corticosteroids
-cyclophosphamide

235
Q

Causes of AKI

A

Pre renal the most common cause in children: Hypovolaemia caused by infections such as gastroenteritis, burns, sepsis, haemorrhage and nephrotic syndrome

Renal: HUS, vasculitis, renal vein thrombosis, acute tubular necrosis, glomerulonephritis, pyelonephritis

Post renal: obstructions such as posterior urethral valves, blocker catheters, stones

236
Q

What is enuresis

A

Involuntary bed wetting

237
Q

What is primary nocturnal enuresis

A

Child has never managed to be consistently dry at night.

238
Q

Causes of primary nocturnal enuresis

A

-family history of delayed dry nights
-overactive bladder
-fluid intake prior to bedtime e.g caffeine as is a diuretic
-failure to wake
-psychological distress - school stress and low self esteem
-secondary causes - constipation, UTI, cerebral palsy

239
Q

Initial step in primary nocturnal enuresis

A

2 week diary of:
-toileting
-fluid intake
-bed wetting episodes

240
Q

Management of primary nocturnal enuresis

A

-reassurance to parents and children under 5 years is normal

-lifestyle changes - less fluid before bed/ pass urine before bed

-positive reinforcement and encouragement and avoid punishment

-treat underlying factors such as constipation

-enuresis alarms

-pharmacological treatment

241
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

-more indicative of underlying illness

242
Q

causes of secondary nocturnal enuresis (5)

A

-Urinary tract infection

-Constipation

-Type 1 diabetes

-New psychosocial problems (e.g. stress in family or school life)

-Maltreatment - always think abuse

243
Q

What is diurnal enuresis

A

Daytime incontinence, dry at night but still has episode of urinary incontinence during the day

-more frequent in girls

244
Q

Two main types of diurnal 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

245
Q

Pharmacological treatment

A

Nocturnal enuresis
Desmopressin - analogue vasopressin (ADH)

Urge incontinence
Oxybutinin - anticholinergic reducing the contractility of the bladder

Imipramine is a TCA - relax the bladder and lighten sleep

246
Q

What is the definition of malrotation

A

-condition where bowel twists abnormally in utero

247
Q

What is volvulus

A

Twisting of the bowel loops which leads to intestinal obstruction

248
Q

Presentation of volvulus or malrotation

A

-abdo pain
-bilious vomiting
-abdo distension
-tachycardia with HTN due to severe abdo pain

249
Q

Ix for malrotation/ volvulus

A

Barium enema
Abdo x- ray with contrast

250
Q

Treatment for malrotation

A

Laparotomy- small incisions to get into abdo cavity

251
Q

Treatment for volvulus

A

Ladds procedure
-intestine is straightened out and divided where small intestine superheated to right and colon to the left

252
Q

What is necrotising entercolitis

A

Acute inflammatory disease affecting preterm neonates leading to bowel necrosis and multisystem organ failure

253
Q

Risk factors for necrotising enterocoltiis

A

-low birth weight
-most common surgical emergency in neonates
-prematurity
-Abx Therapy for longer than 10 days

254
Q

Clinical presentation of necrotising entercolitis

A

-feeding intolerance
-vomiting (can be bilious)
-fresh blood in stools
-abdo distension
-reduced bowel sounds

255
Q

Ix for necrotising entercolitis

A

Bloods - thrombocytopenia, neutropenia
Blood gas - acidotic
X ray - riglers sign- both slides of bowel are visible due to gas in the cavity

256
Q

Mx for necrotising entercolitis

A

-nil by mouth
-bowel decompression by NG tube
-IV cefotaxime

-surgery to remove necrotic bowel

257
Q

What is neonatal physiological jaundice

A

-Breakdown of in utero heamaglobin by the baby
-the immature liver cannot high concentrations of bilirubin
-starts at 2-3 days of life

258
Q

What is pathological neonatal jaundice

A

-when it comes on less than 24 hours after birth
-indicates G6PD deficiency, spherocytosis, rhesus diseases, blood group incompatibility

259
Q

Prolonged neonatal jaundice

A

Jaundice for longer than 14 days in term infants

Causes:
-biliary atresia
-hypothyroidism
-breast milk jaundice
-UTI

260
Q

Investigations for neonatal jaundice (3)

A

-TCB - transcutaneous bilirubinometry non invasive test to determine the need for serum bilirubin

-Coombs test - detects antibodies
-infection screen

261
Q

Mx for neonatal jaundice

A

-use of treatment threshold graphs specific for gestational age

-phototherapy if above threshold and repeat serum bilirubins every 4-6 hours
-if levels reach second threshold then exchange transfusion
(See TCBM measurement)

Phase3 3a (8 decks)

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