Gastrointestinal Flashcards

1
Q

What is the surgical sieve?

A

A mnemonic used to think of differential diagnoses of problems.

VITAMIN D

Vascular
Infective / inflammatory
Trauma
Autoimmune
Metabolic
Iatrogenic / idiopathic
Neoplastic
Developmental
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2
Q

Differential diagnosis of vomiting?

A

V: vascular - intracranial haemorrhage

I: infection - UTI, gastroenteritis, meningitis

T: trauma

A: autoimmune - IBD, Coeliac

M: metabolic - GORD, pyloric stenosis, intussusception

I: iatrogenic / idiopathic - overfeeding

N: neoplasia

D: developmental - malrotation, Hirschprung’s

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3
Q

If a child projectile vomits, what are you immediately thinking of?

A

Pyloric stenosis

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4
Q

What is pyloric stenosis? What’s the pathogenesis?

A

Hypertrophy and hyperplasia of the pylorus (sphincter) and the antrum of the stomach

Causing narrowing of exit from stomach to duodenum

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5
Q

At what age does pyloric stenosis usually present?

A

3-8 weeks

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6
Q

Presentation of patients with pyloric stenosis?

A

Vomiting occurring minutes after feeds which worsens until it is projectile (a good few metres)

Non-bilious vomit

Constipation, few stools

Do not appear too ill, but are hungry and grumpy

Dehydration

Poor weight gain

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7
Q

On examination what would you find on a patient with pyloric stenosis?

A

Olive shaped mass which is the hypertrophic pylorus. Felt in RUQ or epigastrium

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8
Q

Investigation of suspected pyloric stenosis?

A

Bloods: the usual, U+E to look for signs of dehydration, electrolyte imbalance

USS

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9
Q

What would U+E and blood gas results show in pyloric stenosis?

A

U+E:
hypernatraemia (due to dehydration)
hypokalaemia (due to vomiting)
High creatinine + urea + albumin (due to dehydration)

Blood gas:
You’d see metabolic alkalosis due to loss of HCl when vomiting

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10
Q

Management of pyloric stenosis?

A

Stabilise before surgery: rehydrate, correct electrolyte imbalance

Surgery: open up pylorus pyloromyotomy

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11
Q

What is Hirschprung’s disease? (simply)

A

Simply put, it’s an absence of nerve supply to the rectum and sometimes the end of the colon

This leads to the rectum becoming stiff and unable to do peristalsis, so it becomes an obstruction and stool can’t move through

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12
Q

What’s the pathophysiology of Hirschprung’s disease?

A

Absence of parasympathetic ganglion cells in the myenteric and submucosal plexus of the rectum (and possibly into the colon)

The nerve supply never develops during gestation

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13
Q

Is it parasympathetic or sympathetic nervous system that’s lost in Hirschprung’s disease? What happens as a result?

A

Parasympathetic supply is lost.

Parasympathetic system initiates digestion, so peristalsis of gut. In Hirschprung’s you have loss of peristalsis

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14
Q

Presentation of Hirschprung’s disease in neonates?

A

Delayed (after 48 hrs) or no passage of meconium. Sometimes meconium passage is normal though

Vomiting

Distended abdomen

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15
Q

Presentation of Hirschprung’s disease in infants and children?

A

Chronic constipation resistant to usual treatments

Early satiety, abdominal discomfort, poor nutrition and weight gain

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16
Q

Investigation of suspected Hirschprung’s disease?

A

Bloods

Abdominal X-ray: you’d see obstruction, a dilated lower bowel

Anorectal manometry

Rectal biopsy (diagnostic)

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17
Q

What on earth is anorectal manometry?!

A

Detects the pressures of the anal sphincter muscles

Sensation in the rectum

Neural reflexes that are needed for normal bowel movements.

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18
Q

Patients with Hirschprung’s disease are at higher risk of developing what? How would you manage in that situation?

A

Enterocolitis, infection of intestinal tract

Broad spectrum antibiotics, fluid rehydration

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19
Q

List some broad spectrum antibiotics?

A

Amoxicillin
Streptomycin
Chloramphenicol
Levofloxacin

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20
Q

Non-surgical management of Hirschprung’s disease?

A

IV rehydration

Cessation of oral feeding

Decompress obstruction: NG tube, DRE, saline enema

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21
Q

Surgical management of Hirschprung’s disease?

A

Pull-through: remove aganglionic part of bowel and attach two ends together

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22
Q

What does atresia mean? List some types.

A

When an orifice or passage is closed off

Oesophageal atresia: when the oesophagus is blind ended and doesn’t connect to the rest of the oesophagus and into stomach. Like two sausages in a line.

Biliary atresia: atresia in ducts of biliary tree

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23
Q

What other structural abnormality is often seen with oesophageal atresia?

A

Tracheo-oesophageal fistula

The second half of the oesophagus is looking for somewhere to attach to so it attaches to the trachea.

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24
Q

What is intesussception?

A

Invagination of a proximal bit of bowel into a distal bit, ‘telescoping’

Causing obstruction

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25
Q

Which part of the bowel is most commonly involved in intesussception?

A

The ileum goes into the caecum through the ileocaecal valve

26
Q

Presentation of intusussception? Common age range?

A

3 months to 2 years

Paroxysmal episodes of severe colicky pain and pallor, they draw up their legs in pain

Refusing feeds

Vomiting, may be bilious if below sphincter of oddi

Redcurrant jelly stool, blood + mucus

Abdominal distension and shock

27
Q

What’s the cause of intusussception?

A

No known cause

Thought that there could be a link with viral infection

28
Q

Why does intusussception lead to shock? What type of shock?

A

Hypovolaemic shock

Because fluid pools in the gut? So less in circulation? Not too sure

29
Q

Investigations of suspected intusussception?

A

Bloods

X-ray: distended small bowel, can sometimes see intusussception

USS

30
Q

Management of suspected intusussception?

A

Fluid resuscitation if in shock

Air enema with USS guidance: blow air up through the rectum

If this fails surgery to reduce

31
Q

Describe the pathophysiology of malrotation?

A

During fetal development, the bowel comes out of the abdomen and then folds back in a particular way.

In malrotation, the bowel folds back in abnormally and is not fixed correctly.

Sometimes this causes no problems
Sometimes it leads to increased risk of obstruction and volvulus

32
Q

Why does malrotation lead to obstruction?

A

Bowel is not fixed so more likely to twist

There are ‘Ladd bands’ which cross the duodenum which contribute to obstruction

33
Q

Presentation of malrotation?

A

Bilious vomiting

Abdominal pain, paroxysmal, drawing up legs

Not passing faeces, or very little

If bowel blood supply is lost, necrosis leading to peritonitis: abdo distention, toxic

Dehydration

34
Q

What is bilious vomiting, what should you immediately think of?

A

Green vomit

Malrotation, investigate urgently

35
Q

Investigations of suspected malrotation?

A

Urgent upper GI tract contrast study

Also bloods etc.

36
Q

What age does malrotation usually present?

A

Often in first few months of life

But can be any time

37
Q

What’s the most common type of malrotation?

A

Duodenojejunal flexure is further right than it should be

Caecum is high in RUQ

38
Q

Management of malrotation?

A

Surgery to fix bowel into (pretty) normal place

If you think blood supply could be compromised, urgent laparotomy

39
Q

Draw out a picture of volvulus and malrotation?

A

https://www.google.co.uk/search?q=volvulus&source=lnms&tbm=isch&sa=X&ved=0ahUKEwjLmcafssbWAhXBD8AKHSbyDaYQ_AUICigB&biw=1536&bih=723#imgrc=mj6fGKmXpzkKiM:

40
Q

What is volvulus?

A

When the bowel twists round itself and the mesentery causing a blockage

41
Q

What is toxic megacolon? What’s the usual cause?

A

When the colon becomes very dilated and can lead to shock

Usually IBD, most often ulcerative colitis

42
Q

What’s the pathophysiology of toxic megacolon?

A

Inflammation and damage to the colon wall caused by toxins

Breakdown of mucosal layer, destruction of the nerve supply and damage to colonic musculature

Leads to a pretty much paralysed colon

Pressure builds up in the colon due to faecal stasis

This can lead to sepsis and perforation

43
Q

Clinical features of suspected toxic megacolon?

A

Abdo pain, tenderness
Bloating
Fever
Shock

44
Q

Management of toxic megacolon?

A

Decompress with suction

Colectomy

45
Q

What is coeliac disease?

A

Dietary gluten causes autoimmune reaction which causes inflammation of the small bowel

46
Q

Which part of the gluten are coeliac patients intolerant to?

A

Peptide, called alpha-gliadin

47
Q

Presentation of coeliac disease? What age?

A

Any age, but commonly infancy when weaning and 5th decade

Can be non specific:

  • malaise
  • fatigue

Small bowel disease:

  • diarrhoea, Steatorrhoea
  • abdominal pain
  • anorexia, weight loss

Malabsorption:

  • anaemia
  • nutritional deficiency
48
Q

What deficiencies are commonly seen in coeliac disease?

Why?

A

Folate
Vitamin B12
Iron deficiency

The body is not able to absorb these very well via small bowel

49
Q

Investigations for coeliac disease?

A

Serum antibodies
Anti-gliadin
Anti-endomysial
Tissue transglutaminase

50
Q

Differential diagnosis of diarrhoea?

A

Gastroenteritis

Systemic infection: UTI, pneumonia, meningitis

IBD

Intolerance: lactose, milk protein

Malabsorption: coeliac, CF

Surgical problem

Encopresis: constipation with overflow

Hyperthyroidism

Toddler’s diarrhoea

Psychological (IBS)

51
Q

Describe pathophysiology of encopresis?

A

When faeces stay in the bowel for a long time, water is drawn out of them making them hard.

The hard faeces stretches and weakens bowel wall

Liquid stool from higher up leaks around it and out. Patient is unaware they’re passing stool

52
Q

Which age group are susceptible to encopresis?

A

up to age 4

53
Q

How do patients with encopresis present?

A
Constipation
Leaking of stool
Explosive diarrhoea
Nausea + vomiting
Dizziness
Tachycardia
54
Q

Management of encopresis?

A

Disimpaction regime (laxatives)

Or use a clean prep (like used for colonoscopy) during a hospital stay

Advise on diet (more fibre, fruit and veg)

55
Q

When do children usually grow out of Toddler’s diarrhoea?

A

By age 4

56
Q

List some causes of proteinuria in children?

A

UTI
Nephrotic syndrome
Renal dysplasia and reflux
Nephritis

57
Q

What is nephrotic syndrome? What’s the diagnostic criteria (in children)?

A

A set of symptoms/signs (see below) with different causes

Diagnostic criteria:

  • proteinuria
  • low serum albumin
  • clinical evidence of peripheral oedema
58
Q

List some causes of nephrotic syndrome?

A

Congenital nephrotic syndrome

Idiopathic
Glomerulosclerosis
Glomerulonephritis
SLE
Diabetes
59
Q

Management of nephrotic syndrome?

A

Steroids! Prednisolone

Fluid restriction, low salt diet

Diuretics

Others: cyclophosphamide, cyclosporin

60
Q

What’s the prognosis of nephrotic syndrome?

A

1/3 resolve
1/3 have infrequent relapses
1/3 have frequent relapses