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Phase 3a Finals > Paediatric GI > Flashcards

Paediatric GI Flashcards

1
Q

GORD IN CHILDREN

MC cause of what in infancy?

Risk factors

A

vomiting

infants regurgitate their feeds.

preterm delivery
neurological disorders

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2
Q

features of GORD in children

A

before 8 weeks

vomiting/regurgitation - milk vomits after feeds and could be after laid flat.

excessive crying - esp whilst feeding

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3
Q

diagnosis of GORD in children

A

clinical

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4
Q

mx of GORD in kids

A

30 degree head up during feed.

sleep on back - reduce cot death risk

ensure not overfed , trial smaller feed

trial thickened formula eg:
- rich starch
- cornstarch
-locust bean gum
-carob bean gum

  • trial alginate therapy - gaviscon. not at same time as thickened formula.

NO PPI.

prokinetic if specialist: metoclopramide

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5
Q

when could you give a ppi in gord in kids

A

1 or more of:
- unexplained feeding difficulties like refusing, gagging/choking

  • distressed behaviour
  • faltering growth
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6
Q

complications of gord in kids

A

distress
failure to thrive
aspiration
frequent otitis media
in older kids dental erosion.

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7
Q

GORD kid has severe comp like failure to thrive what to do?

A

if med tx ineffective do fundoplication

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8
Q

adults: indications for upper gi endoscopy

A

over 55
sx over 4 weeks or persistent sx despite tx

dysphagia
relapsing sx
weight loss

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9
Q

what to do in gord suspected adult if endoscopy negative

A

24hr oesophageal ph monitoring (gold standard)

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10
Q

adults: mx of gord

endoscopy proven oesophagitis

endoscopically negative reflux disease

A

proven:
- full dose ppi 1-2 mths
- if response, low dose tx when needed
- if not double dose ppi 1 month

negative:
- full dose ppi 1 mth
- response: low dose tx, when needed
- if no response: H2RA (famotidine) or prokinetic 1 mth

stop nsaids
antacids like gavison - short term

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11
Q

complications adult gord

A

oesophagitis
ulcers
anaemia
benign strictures
barrett’s oesophagus
oesophageal carcinoma

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12
Q

what is GORD?

A

acid from stomach flow through lower oesophageal sphincter and into oesophagus

irritates lining and causes sx.

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13
Q

why does the acid affect oesophagus more than stomach?

A

squamous epithilial lining in oesophagus more sensitive to acid than columnar epithelial lining in stomach.

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14
Q

causes of gord in adults

A

greasy spicy foods
coffe tea
alcohol
nsaids
stress
smoking
obesity
hiatus hernia

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15
Q

how does gord present in adults

A

dyspepsia :

  • heart burn
  • acid regurg
    -bloating
    -nocturnal cough
    -hoarse voice
  • retrosternal/epigastric pain
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16
Q

red flags with GORD - adults

A

2 week wait referral.
- urgent direct-acess endoscopy.

dysphagia - any age - 2 week wait refer

  • over 55
    -weight loss
    -upper abdo pain
    -reflux
  • tx-resistant dyspepsia
    -n+v
  • upper abdo mass on palpation
    -low hb (anaemia)
  • raised platelet count.
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17
Q

what is a oesophago-gastro-duodenoscopy?

assess for what?

A

camera through mouth down to oesophagus, stomach and duodenum.

used to assess:

  • gastritis
    -peptic ulcers
    -upper gi bleed
    -oesopageal varices (liver cirrhosis)
  • barrets oesophagus
  • oesophageal stricture
  • malignancy of oesophagus/stomach
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18
Q

pt comes in with upper gi bleeding ie melaena or coffee ground vomiting what to do ?

A

admission
urgent endoscopy

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19
Q

what is fundoplication?

A

laparoscopic fundoplication - tie the fundus of the stomach around lower oesophagus to narrow LOS.

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20
Q

What is a hiatus hernia?

4 types?

A

1- sliding
2- rolling
3 - combo of sliding and rolling
4- large opening with additional abdo organs entering thorax

hernation of stomach through diaphragm.

  • normally diaphragm opening at los level and fixed.
  • narrow opening helps maintain the sphincter and stop acid and stomach contents refluxing up.
  • when its wider, stomach enters through diaphragm and contents reflux up.
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21
Q

how can a hiatus hernia be seen?
ix

A

cxr
ct
endoscopy
barium swallow

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22
Q

explain
sliding hiatus hernia
rolling hiatus hernia
type 4

A
  • sliding:
  • stomach slides up through diaphragm, gastro-oesopageal junction pass up into thorax.
  • rolling:
  • seperate portion of stomach folds around and enters through diaphragm opening alongside oeso.

4:
- large hernia
- bowel pancreas or omentum pass up through diaphragm.

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23
Q

What is pyloric stenosis caused by ?

when does it present and how?

A

2nd to 4th week of life - projectile vomiting - 30 mins after feed.

rarely upto 4 months.

cause: hypertrophy of circular muscles of pylorus.

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24
Q

epidemiology of pyloric stenosis

A

males : 4* more
10-15% infants positive fhx
1st borns - more affected.

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25
Q

features of pyloric stenosis

A

projectile vomiting - 30 mins after feed

constipation and dehydration

palpable mass - upper abdomen - poss (hypertrophic muscle of pylorus)

  • hypochloraemic, hypokalaemic alkalosis due to persistent vomiting.
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26
Q

how would you diagnose pyloric stenosis?

how would you manage pyloric stenosis?

A

uss - thickened pylorus

ramstedt pyloromyotomy. - laparoscopic pyloromyotomy :

  • incision into smooth muscle of pylorus
  • widen canal allowing food to pass from stomach to duodenum as normal.

blood gas: hypochloric (low chloride) met alkalosis. - baby vomits the hcl from stomach.

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27
Q

presentation of pyloric stenosis pt

A

1st few weeks of life

hungry baby thin pale failing to thrive.

projectile vomiting.

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28
Q

what is the pyloric sphincter?

A

ring of smooth muscle forms canal between stomach and duodenum.

hypertrophy and narrowing of pylorus causes the stenosis.

food cant travel.

then you get powerful peristalsis in stomach as it tries to push food into duodenum but it cant so goes other way: oeseophagus - projective vomit.

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29
Q

What is zollinger ellison syndrome?

what is gastrin?
sx

gastrinoma associated with?

A

rare condition.

duodenal or pancreatic tumour secretes excessive quantities of gastrin.

gastrin: hormone stimulates acid secretion in stomach.

=
severe dyspepsia
diarrhoea
peptic ulces

gastrin-secreting tumours - gastrinomas associated with MEN1 - autosomal dominant. - can cause parathyroid and pituitary tumours

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30
Q

What is hirschsprung’s disease?

A

CONGENITAL

caused by aganglionic segment of bowel due to developmental failure or parasympathetic (MYENTERIC) auerback and meissner plexuses.

RARE.
important for childhood constipation!!

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31
Q

associations of hirschsprungs disease

A

3 times mc in males
downs syndrome
neurofibromatosis

MEN type II
Waardenburg syndrome: pale blue eyes, hearing loss and patches of white skin and hair)

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32
Q

pathophysiology of hirschsprungs disease

A

parasympathetic neuroblasts fail to migrate from neural crest to the distal colon and rectum. - section at end of colon left without parasympathetic ganglion cells.

therefore : developmental failure of parasympathetic auerback and miessner plexuses

therefore uncoordinated peristalsis

therefore functional obstruction

aganglionic section doesnt relax - constriction. - loss of movement of faeces and obstruction in bowel.

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33
Q

possible presentation of hirschsprungs disease

A

neonatal period: failure or delay to pass meconium more than 24 hrs.

chronic constipation since birth
vomiting
poor weight gain/failure to thrive

older children:
constipation
abdo distention

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34
Q

ix for hirschsprungs disease

A

abdo x ray

rectal biopsy - gold : bowel histology: abscence of ganglionic cells.

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35
Q

mx of hirschsprungs

A

initially: rectal washouts/bowel irrigation

fluid resus

definitive: surgery to affected segment of colon

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36
Q

RELEVANCE OF myenteric plexus in hirschprungs disease

A

the myenteric plexus or the auerbachs forms the enteric nervous system - brain of gut.

its not there for hirschsprungs.

this nerve plexus run along bowel in bowel wall.
- stimulates peristalsis of large bowel. - without it the bowel loses mobility and cant pass food along length.

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37
Q

what is hirschsprung - associated entercolitis?

presentation

lead to what?

tx?

A

inflammation and obstruction of intestine.

2-4 weeks of birth with :
- fever
-abdo distention
-diarrhoea(often with blood)
- features of sepsis

life threatening.

lead to : - toxic megacolon an perforation of the bowel.

tx:
- abx
-fluid resus
-decompression of obstructed bowel

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38
Q

What is biliary atresia?

A

CONGENITAL

obliteration or discontinuity within extrahepatic biliary system : obstruction in bile flow.

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39
Q

3 types of biliary atresia

A

1: proximal ducts patent, common duct obliterated

2: atresia of cystic duct and cystic structures found in porta hepatis

3: atresia of left and right ducts to level of porta hepatis.

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40
Q

pt presenting with biliary atresia?

A

1st few weeks of life

jaundice - extending beyond phsyiological 2 weeks.

darkin urine and pale stools.

appetite and growth disturbance. - could be normal in some

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41
Q

signs of biliary atresia

A

jaundice

hepatomegaly with splenomegaly

abnormal growth

cardiac murmurs if associated cardiac abnormalities present.

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42
Q

ix of biliary atresia

A

Serum Billirubin : conjugated and total. conjugated high total normal

LFT: serum bile acids, aminotransferases raised.

serum alpha 1 antitrypsin: deficiency

sweat chloride test: CF involves biliary tract

uss of biliary tree and liver: poss distention and tract abnormalities

percutaneous liver biopsy with intraoperative cholangioscopy

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43
Q

mx of biliary atresia

A

surgery only definitive: dissection of abnormalities into distinct ducts and anastomosis creation.

medical: abx and bile acid enhancers after surgery

KASAI PROTOENTEROSTOMY: attack section of SI to liver opening where bile ducts normally attaches.

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44
Q

complications of biliary atresia

A

unsuccessful anastomosis formation

progressive liver disease

cirrhosis with eventual HCC

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45
Q

prognosis of biliary atresia

A

good if surgery successful

if fails: liver transplant needed in 1st 2 yrs of life

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46
Q

What is marasmus?

A

Severe malnutrition caused by an overall deficiency in caloric intake (protein and energy). Usually kids under 5, in developing countries.

Results in extreme fat and muscle loss, causing stunted growth, severe weight loss and immunodeficiency.

Common in areas of famine or severe malnutrition

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47
Q

presentation of marasmus

A

Severe weight loss
Emaciation
Prominent bones, sunken eyes, thin, dry skin
Irritability
Growth failure
Weakness

48
Q

Mx of marasmus

A

Rehydration
Gradual intro of calories
Micronutrient supplementation
Long term nutritional rehabilitation and infection management

49
Q

comps of marasmus

A

Immunodeficiency leading to severe infection
Electrolyte imbalance (hypokalaemia)
Hypoglycaemia
Growth retardation

50
Q

What is kwashiorkor?

A

Severe protein malnutrition that occurs despite sufficient caloric intake. Often areas where diet is primarily starchy or carbohydrate heavy with little protein.

Children often appear puffy due to generalised oedema (hypoalbuminaemia), especially in legs and face.

51
Q

Presentation of Kwashiorkor

A

Oedema (legs, face)
Moon face
Depigmented hair
Enlarged, fatty liver

52
Q

RF of kwashiorkor

A

Sudden breastfeeding cessation
Poverty
Insufficient protein, high carbohydrate
Food insecurity/scarcity

53
Q

comps of kwashiorkor

A

High mortality if untreated
Heart failure (due to severe oedema)
Sepsis
Severe diarrhoea
Refeeding syndrome if not treated properly

54
Q

mx of kwashiorkor

A

Electrolyte and fluid imbalance correction (slow, prevent osmotic demyelination syndrome)
Gradual nutritional rehabilitation, protein rich etc

55
Q

What is neonatal hepatitis syndrome?

A

Inflammation of liver of newborns usually in first months of life. Can be due to viral infection, genetic disorders, or may be idiopathic.

Inflammation leads to impaired bile flow, damaging liver

56
Q

Causes of neonatal hepatitis syndrome

A

Viral (cytomegalovirus, hepatitis B)
Metabolic disease (galactosemia, tyrosinaemia)
Genetic disorders (alpha 1 antitrypsin deficiency)

Family history and prematurity are RF

57
Q

How does neonatal hepatitis syndrome present

A

Jaundice >first 2 weeks, prolonged
Hepatomegaly
Dark urine and pale stools
Poor feeding, failure to thrive

58
Q

Management of NH Syndrome

A

Treatment of underlying cause
Fat soluble vitamin supplementation (ADEK)
Ursodeoxycholic acid to aid bile flow
Liver transplant if severe

59
Q

What is meckel’s diverticulum?

A

Congenital diverticulum of the small intestine. Remnant of omphalomesenteric duct and contains ectopic ileal, gastric or pancreatic mucosa

Usually asymptomatic but can present with abdominal (RLQ) pain, rectal bleeding or intestinal obstruction. It is the biggest cause of painless massive GI bleeding between 1 and 2y.

60
Q

How is meckel’s diverticulum ix and mx?

A

Meckels scan
- 99m Technetium pertechnetate scan, which has an affinity for gastric mucosa

Managed
- Laparoscopic surgery or diverticulectomy.
- Small bowel resection and anastomosis.

61
Q

rule of 2’s

meckels diverticulum

A

Meckel’s diverticulum
- 2% of population
- 2 inches long
- 2 feet from ileocaecal valve
- 2x as likely in boys
- 2yo when it causes GI bleed
- 2 types of ectopic tissue (pancreatic and gastric (susceptible to ulcer))

62
Q

possible causes of intestinal obstruction

A

Meconium ileus
Hirschprung’s disease
Oesophageal/duodenal atresia
Intussusception
Intestinal malrotation

63
Q

presentation of intestinal obstruction

A

Persistent vomiting
Abdominal pain/distention
Failure to pass stool/wind
Bowel sounds (tinkling early and absent later)

64
Q

ix in bowel obstruction

A

Abdominal X ray
- Dilated loops of bowel proximal to obstruction and collapsed distal.
- Absence of air in rectum

65
Q

mx of bowel obstruction

A

NBM
NG Tube and draingage
IV fluids
Surgical definitive

66
Q

What is toddlers diarrhoea?

A

Chronic, non specific diarrhoea, between 1 and 4 years of age. Is a diagnosis of exclusion

67
Q

features of toddlers diarhoea?

A

Frequent, poorly formed, offensive stools
Food material easily recognisable

Child is normally well, active and has unimpaired growth. Normal appetite and normal/increased fluid intake.

No positive findings on examination or lab investigations

68
Q

Mx of toddlers diarhoea

A

Paternal reassurance, avoidance of full strength fruit juice.

Faeces normally becomes firm when child is toilet trained or by 3 years

69
Q

What is failure to thrive?

A

Poor physical growth and development

Faltering growth if they fall in centile spaces (e.g. distance between 75th and 50th centile)

1 if birthweight <9th centile
2 if birthweight 9-91st centile
3 if birthweight above 91st centile

70
Q

causes of failure to thrive

A

Inadequate intake
- Maternal absorption
- Neglect
- Poverty
Difficulty feeding
- Poor suck (cerebral palsy)
- Cleft lip/palate
- Pyloric stenosis
Malabsorption
Increased energy requirements
- Hyperthyroid
- Cystic fibrosis, heart disease
- Chronic infection
Inability to process nutrition

71
Q

how do BMI and MID parental height suggest inadequate growth?

A

Height more than 2 centiles below mid parental height centile
BMI below 2nd centile

72
Q

What is cows milk protein allergy/intolerance?

A

Usually seen in the first 3 months of formula fed children,

can rarely be seen in exclusively breastfed infants.

CMPA for immediate (<2 hours, IgE mediated)
CMPI if mild/moderate and delayed (several days, non IgE mediated)

73
Q

features of cows milk protein intolerance/allergy

A

Occurs in first 3 months of life:
- Regurgitation and vomiting
- Diarrhoea
- Urticaria
- Colic symptoms (crying, irritability)
- Wheeze, chronic cough
- Rarely anaphylaxis

Cows milk protein intolerance has the bloating, wind, diarrhoea and vomiting, but no rash, angio-oedema, sneezing or coughing.

74
Q

How is cows milk protein intolerance/allergy ix?

A

skin prick/patch testing
total IgE and specific IgE (RAST) for Cows milk protein

Avoiding cows milk should fully resolve issues

75
Q

mx of cows milk protein intolerance/allergy

A

Avoid cow’s milk

If formula fed
- Extensive hydrolysed formula first line replacement
- If intolerance, can be started on milk ladder

Breast feeding
- Breast feeding mother should avoid dairy products
- May need maternal calcium supplements
- Hydrolysed formula milk when breastfeeding stops until 12 months, for at least 6 months

76
Q

What is coeliac disease?

A

A sensitivity to the gluten protein. Repeated exposure leads to villous atrophy causing malabsorption. Children normally present before 3yo. Normally affects small bowel, particularly the jejunum

77
Q

How does coeliac present?

A

Often asymptomatic, low threshold for testing
- Failure to thrive
- Diarrhoea
- Abdominal distention
- Anaemia
- Mouth ulcers

Dermatitis herpetiformis - itchy, blistering skin rash that typically appears on the abdomen

78
Q

genetic association with coeliac disease

A

HLA-DQ2 (90%)
HLA-DQ8

79
Q

Ix for coeliac

A

Antibodies
- Anti-TTG and Endomysial antibodies (IgA - undetectable if IgA deficiency)
- Anti-DGPs (Deaminated Gliadin Peptides)

Endoscopy and intestinal
- Crypt hyperplasia
- Villous atrophy
- Increased intraepithelial lymphocytes
- Lamina propia infiltration

Gluten free diet trial

80
Q

tx of coeliac

A

gluten free diet

81
Q

disease associations with coeliac

A

Autoimmune
- T1DM
- Thyroid disease
- Autoimmune hepatitis
- PBC/PSC
- Down’s

82
Q

Possible complications of untreated coeliac

A

Malnutrition/vitamin deficiency
Anaemia
Osteoporosis
Non hodgkins lymphoma
Small bowel adenocarcinoma

83
Q

What is irritable bowel syndrome, how does it present and how long should symptoms last?

A

Abdominal pain or
Bloating or
Change in bowel habit and stool constitution (watery, loose, hard, mucus)
Pain relieved with defecation.

> 6 months.

Diagnosed through exclusion and if
- Altered stool passage
- Abdominal bloating
- Symptoms made worse by eating
- Passage of mucus

84
Q

Red flags in bloody diarrhoea

A

Rectal bleeding
Unexplained weight loss
FH of bowel or ovarian cancer
> 60y onset

85
Q

Ix in ibs, including cancers that mimic it (not necessarily in kids)

A

FBC (check anaemia)
Inflammatory markers
Coeliac serology
Faecal calprotectin
CA125 (ovarian cancer) CA19/9 (pancreatic)
*Ovarian presents similar, just much older. E.g. 50yo woman with bloating, abdo pain. Non specific

86
Q

non medical mx of ibs

A

Lifestyle advice
- Fluids
- Regular small meals
- Low FODMAP diet
- Limit caffeine, alcohol, fatty foods
- Reduce stress
- Change fibre depending if constipation or diarrhoea

CBT may be used

87
Q

Medical management of IBS

A

Loperamide for diarrhoea (slows down bowel)
Linaclotide for constipation (laxative)

88
Q

What is bowel intussusception, what age does it normally affect?

A

When a portion of the bowel invaginates into the lumen on the adjacent bowel, most commonly around the ileo-caecal region. This increases bowel size and narrows lumen, causing ostruction.

Usually affects infants 6-24 months. Boys 2x as often

89
Q

Presentation of intussuception. what does the infant do during attacks?

A

Intermittent severe crampy progressive abdo pain
Inconsolable crying
During attack the infant will raise knees up and turn pale
Vomiting
Bloodstained stools “red-currant jelly” late sign
Sausage shaped mass in upper right quadrant
May present with viral URTI preceding illness

90
Q

Ix and Mx of bowel intussusception

A

Ultrasound is investigation of choice - target like mass

Managed with reduction by air insufflation.
OR Barium enema

91
Q

comps of intussusception

A

obstruction
gangrene
perforation
death

92
Q

Pathophys of appendicits

A

Appendix sits at end of caecum. Trapped stool or other obstruction causes infection and inflammation, which quickly causes gangrene and rupture. Rupture releases contents into abdomen, causing peritonitis and possibly sepsis.

93
Q

How does appendicitis present?

A

Severe central abdominal pain that moves to RIF over time.
Tenderness in McBurney’s point (2/3 of the distance from belly button to ASIS (Anterior Superior Iliac Spine))
Rovsing’s sign (palpation of left iliac fossa causes pain in RIF)
Guarding
Rebound tenderness and percussion tenderness if progression to peritonitis

94
Q

How is appendicitis diagnosed?

A

Usually made clinically:
- Pain moving centrally to RIF
- low grade pyrexia
- minimal vomiting

CT GOLD Standard
Ultrasound in women (rule out ovarian cancer and gynae pathology)

Diagnostic laparoscopy if negative, with appendectomy in same procedure

95
Q

key appendicitis differentials

A

Ectopic pregnancy - bHCG will be raised (test to rule out)

Ovarian cysts - Pelvic and IF pain, not always right, can rupture or torsion

Meckels diverticulum - Malformation of distal ileum, usually asymptomatic but can inflame, rupture, bleed, volvulus, intussusception.

Mesenteric adenitis - Inflamed lymph nodes. Often associated with tonsilitis or URTI

Appendix mass - Omentum surrounds and sticks to inflamed appendix. Treated with abx and supportively. Appendectomy once acute infection resolves

96
Q

Complications of appendectomy

A

Bleeding, infection, pain scars
Bowel adhesions, causing obstruction
Damage to nearby organs
Veneous thromboembolism

97
Q

What is chrons

A

Chronic inflammation of the entire GI tract (mouth to anus). Terminal ileum and colon most commonly affected. Affects white people more

98
Q

rf of chrons

A

Family history
Smoking
White people
OCP
Diet low in fibre
NSAID

99
Q

Genetic association with chrons

A

NOD2/CARD15 gene mutation

100
Q

Inflammatory pattern of chrons

A

Transmural inflammation with areas of healthy bowel in between known as skip lesions, giving a cobblestone appearance.

101
Q

Signs and symptoms of Crohns

A

Aphthous mouth ulcers
Abdominal tenderness and diarrhoea
Perianal lesions- skin tages, fissures, abscesses, ulcers, etc
Weight loss and failure to thrive

102
Q

Extra intestinal manifestations of chrons

A

Skin
- Perianal/mouth ulcers
- Erythema nodosum
- Pyoderma gangrenosum

MSK
- Arthritis
- Seronegative spondyloarthropathy
- Clubbing

Eyes:
- Conjunctivitis
- Iritis

103
Q

Ix in chrons

A

Faecal calprotectin raised

Serology
- pANCA Negative (more in UC)
- ASCA positive (more in Crohns)

Endoscopy + Biopsy
- Endoscopy: Skip lesions, cobblestoning, strictures
- Biopsy: Transmural inflammation, non caseating granulomas, goblet cells present

Small bowel enema
- High sensitivity/specificity for examination of terminal ileum
- Stricturs (Kantor’s string sign)
- Proximal bowel dilation
- Rose thorn ulcers
- Fistulae

104
Q

Tx in chrons

A

Stop smoking, NSAID

Induce remission
- Glucocorticoids: Budesonide (mild), prednisolone (moderate), IV hydrocortisone (very severe)
- Immunosuppressant: Azathioprine or methotrexate
- AntiTNF (infliximab)

Maintain remission:
- Azathioprine

105
Q

indications for surgery in chrons

A

80% of patients
- Sticturing terminal ileus disease (ileocaecal resection)
- Perianal fistulae (Diagnosed with MRI, treated surgically and draining seton left in to prevent abscess formation)
- Perianal abscess (Surgical incision and drainage)

106
Q

comps of chrons

A

Small bowel cancer
Colorectal cancer
Osteoporosis
Perianal fissure/fistula/abscess
Anaemia/malnutrition

107
Q

define uc

A

Relapsing and remitting bowel disease that usually involves rectum and can extend up large bowel, up to ileocaecal valve (does not affect anus).

3X more common in non smokers (smoking protective)

108
Q

rf for uc

A

Family History
HLAB27
NSAIDs
Infections
Not smoking
Chronic stress/depression

109
Q

UC Pattern of inflammation, what course does it follow, and how does damage lead to one of its characteristic features

A

Continuous inflammation affecting only the mucosal layers. Usually starts at rectum, working its way proximally, never past the ileocaecal valve.

Relapsing remitting course (flares with new damage, followed by healing)

Regenerating mucosa forms a scar that looks like polyps (pseudopolyps)

110
Q

sign of uc

A

LLQ and tenesmus
Bloody, mucusy diarrhoea
Abdominal pain, urgency, weight loss and malnutrition
Extraintestinal manifestations
- Uveitis
- Colorectal cancer
- Erythema nodosum
- Pyoderma gangrenosum
- Arthritis
- PSC!

111
Q

ix in uc

A

Colonoscopy
- Avoid colonoscopy if severe (perforation risk)
- Red, raw mucosa
- Continuous inflammation
- Loss of haustrations

Biopsy
- Pseudopolyps, crypt abscesses, goblet cell depletion, inflammation limited to mucosal layers

112
Q

What is the most common extra-intestinal manifestation of Crohns and UC

A

Arthritis

PSC and uveitis more common in UC

113
Q

classification of uc

A

Mild <4 stools/day, small amount of blood
Moderate 4-6 stools/day, varying amounts of blood
Severe 6+ bloody stools/day

114
Q

mx of uc

A

Induce remission

Rectal (topical) aminosalicylate - mesalazine/sulfasalazine. Add high dose oral aminosalicylate, and then oral corticosteroid, if extensive or if remission not achieved in 4 weeks.

Maintain remission

Aminosalicylate + azathioprine.

If severe/non responsive,
Colectomy is curative

115
Q

comps of uc

A

PSC
Bowel perforation
Toxic megacolon
Colonic adenocarcinoma
Strictures and bowel obstruction

116
Q

What if fulminant uc and what is its treatment?

A

Sudden, acute, severe UC flareup

> 10 bowel movements
Continuous bleeding
Abdominal tenderness
Toxicity
Colonic dilation

Managed in hospital
- IV corticosteroid
- IV ciclosporin or infliximab

Consider colectomy

117
Q
A

Phase 3a Finals (25 decks)

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