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Phase 3a - Arun&Erin > Paeds - GI & Renal > Flashcards

Paeds - GI & 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 - movicols 1st line, senna

-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 most commonly responsible for travellers diarrhoea

A

Enterogenic e.coli

2nd is campylobacter jejuni

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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/clarithromycin
-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

How to diagnose 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 - first line
-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

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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.

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107
Q

Two antibodies involved in coeliac

A

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

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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

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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

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110
Q

What condition is linked and always tested for alongside coeliac

A

Type 1 diabetes

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111
Q

Genetic association with coeliac (2)

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

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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

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114
Q

Coeliac disease associations (6)

A

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

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115
Q

Tx of coeliac

A

Lifelong gluten free diet

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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)

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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 centile 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 history

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 + urgency
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

-Immunosuppression

-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 in children

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 cefalexin or co amoxiclav 7-10 days unless sepsis suspected then IV Abx

Over three months cystitis/ LRTI
- oral antibiotics for 3 days 1st line trimethoprim 2nd line amoxicillin/ nitrofurantoin

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 releasing into the ureters - checking for reflux

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 advice to prevent UTIs (3)

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

Classic triad of nephrotic syndrome

A

Hypoalbuminaemia < 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) + PPI
  • 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
  • cyclosporine
    -tacrolimus
    -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 dominant/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 type of 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 of RBC

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 e.g quinines
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
Bleeding
Ulceration

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) AKA: lichen sclerosis

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 of management 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 for nocturnal enuresis

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 moved 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 sides 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 process 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

What is Prolonged neonatal jaundice
What are some causes of

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

-FBC
-TFT
-blood and urine cultures
-G6PD levels

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)

262
Q

What is oesophageal atresia?

A

A congenital condition where the oesophagus and trachea don’t separate normally meaning the food doesn’t pass from mouth to stomach as upper and lower oesophagus dont connect

263
Q

What condition is also normally present with oesophageal atresia?

A

tracheal fistula

264
Q

Risk factors for oesophageal atresia

A

Maternal use of alcohol
Smoking
Uncontrolled diabetes
Increased maternal age
VACTERL syndrome
Trisomy’s - Down syndrome (21), patau (13), edwards(18)

265
Q

What is a tracheal fistula

A

Where the trachea fuses with either the upper/lower/both parts of the oesophagus in oesophageal atresia

266
Q

Complications of oesophageal atresia with tracheal fistula (6)
-Preoperative
-Postoperative

A

Preoperative due to aspiration
Bronchiectasis
Lung abcess
Aspiration pneumonia

Posteroperative
-strictures
-recurrence of fistula
-leaking at the site of joining

267
Q

Why does oesophageal atresia cause polyhydramnios prenatally

A

Fetus doesn’t swallow amniotic fluid normally so it builds up

268
Q

Signs of oesophageal atresia (3C’s) (9)

A

-coughing
-cyanosis
-choking
-Frothy Salivation from mouth and nose
-excess drooling
-inability swallowing feeds
-abdo distension
-vomiting
-resp distress - aspiration pneumonia

269
Q

Ix of oesophageal atresia

A

-examination - nasogastric/ orogastric tube cant pass all the way

-Abdo x rays - may see gastric bubbles of air (if lower oesophagus connects to trachea)

Chest x-ray with contrast - diagnostic

270
Q

Tx of oesophageal atresia

A

Surgery

271
Q

What is gastroschisis

A

when a baby is born with the intestines sticking out through a hole in the belly wall near the belly button

272
Q

Difference between omphalocele and gastroschisis

A

Omphalocele is where the abdominal contents protrude into the umbilical cord meaning they are SEALED by a peritoneal layer of the cord

273
Q

Risk factors for gastroshcisis

A

Increased Maternal age

Alcohol + Tobacco during pregnancy

274
Q

Diagnosis of gastroschisis before birth

A

Ultrasound
Blood test raised alpha feta protein is associated with abdo wall defects

275
Q

Treatment of gastroschisis (3)

A

Surgery - where the intestines are placed back in the body and closure of the defect

IV nutrients

ABx for potential infection

276
Q

What is kernicterus

A

brain damage caused by excessive bilirubin levels as bilirubin can cross the blood brain barrier

277
Q

What is the presentation of kernicterus

A

-non responsive baby
-floppy
-drowsy
-poor feeding

278
Q

What is the complications of kernicterus (3)

A

Cerebral palsy
Learning disability
Deafness

279
Q

What are treatment threshold charts for neonatal jaundice

A

Charts that measure total bilirubin levels based on their gestational age neonatal jaundice

If it passes the first threshold then give phototherapy
If it passes the second threshold then give exchange transfusion

280
Q

How does phototherapy work for jaundice

A

Converted unconjugated bilirbin into isomers that can be excreted without undergoing conjugation inj the liver

-blue light is best + protect the eyes with an eye patch

-monitor bilirubin levels for further 18 hours to make sure it doesn’t spike again

281
Q

Investigations for UTIs in children

A

URINE DIP NOT VIABLE IN UNDER 3 MONTHS
Urine culture
Blood culture

LP- for meningitis for any child under 1 with fever

Kidney ultrasound -look for renal malformation

282
Q

If resistant strain of bacteria for UTI which Abx do you move to

A

Meropenem

283
Q

Posterior urethral valve presentation

A

Difficulty urinating
Weak urinary stream
Chronic urinary retention
Palpable bladder
Recurrent urinary tract infections
Impaired kidney function
Bilateral hydrnephrosis
Oligohydramnios
Underdeveloped fetal lungs

284
Q

Posterior urethral valve Ix

A

Abdominal ultrasound - enlarged, thickened bladder and bilateral hydronephrosis

MCUG -location of the extra urethral tissue and reflux of urine back into the bladder

Cystoscopy involves a camera inserted into the urethra to get a detailed view of the extra tissue. Cystoscopy can be used to ablate or remove the extra tissue.

285
Q

Posterior urethral valve mx

A

Mild cases - observed and monitored. temporary urinary catheter inserted to bypass the valve whilst awaiting definitive management.

Definitive management- ablation or removal of the extra urethral tissue, usually during cystoscopy.

286
Q

What is posterior urethral valve

A

where there is tissue at the proximal end of the urethra (closest to the bladder) that causes obstruction of urine output

287
Q

What is DMSA used to assess

A

Kidney scarring and function comparatively to each kidney

288
Q

Sx of alports syndrome

A

-sensorineural hearing loss - bilateral
-vision problems - lenticonus
-pregoressive renal failure
-microscopic haematuria

289
Q

Treatment for c.diff infection

A

1st line- oral vancomycin
2nd line - oral fidaxomicin
3rd line/ life threatening - Oral Vancomycin + IV metronidazole

290
Q

Risk factors for c.diff infection

A

PPI use

Cephalosporins

Phase 3a - Arun&Erin (15 decks)

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