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3a Notes AC > Paeds GI > Flashcards

Paeds GI Flashcards

1
Q

GORD Epidemiology

commonest cause of vomiting in infancy.

A
  • Starts off with reflux and 90% of infants stop having this by 1 year
  • If complications are present, reflux is referred to as gastro-oesophageal reflux disease
    Risk factors
  • preterm delivery
  • neurological disorders
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2
Q

GORD Pathophysiology

A
  • Functional immaturity of lower oesophageal spinchter causing it to relax
  • short intra-abdominal length of oesophagus increasing gastric pressure
  • Stomach contents refluxes through the lower oesophageal sphincter into the oesophagus then into mouth
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3
Q

GORD Signs And Symptoms

COMPLICATIONS
- Faltering growth due to severe vomiting
- Oesophagitis – haematemesis, discomfort on feeding, iron deficiency anaemia
- Recurrent pulmonary aspiration – recurrent pneumonia, cough or wheeze, apnoea in preterm infants
- aspiration
* frequent otitis media
* in older children dental erosion may occur

A

Features
* typically develops before 8 weeks
* vomiting/regurgitation following feeds
* Distress, crying or unsettled after feeding
* Reluctance to feed
* - Chronic cough
* Poor weight gain

Red flags in history:
- Not keeping any food down (pyloric stenosis/obstruction)
- Projectile/forceful vomiting (pyloric stenosis/obstruction)
- Bile staining (obstruction)
- Abdominal distension (obstruction)
- Reduced consciousness/bulging fontanelle/neurological signs (meningitis or raised ICP)
- Blood in stool (gastroenteritis or cows milk allergy)
- Signs of infection
- Rash, angioedema or other signs of allergy

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4
Q

GORD management

  • 24 hour oesophageal pH monitoring
  • Endoscopy including oesophageal biopsies to identify oesophagitis and exclude other causes of vomiting
A
  • Small, frequent meals, burping regularly to help milk settle, not over-feeding, and keeping baby upright after feeding. (30 degree head up)
    More problematic cases can justify treatment with:
  • Gaviscon mixed with feeds
  • Thickened milk or formula (anti-reflux available)
  • Omeprazole (if failure to thrive)
    Surgical fundoplication can be considered in very severe cases – rarely required or performed.

Dont use gaviscon and thickener together

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5
Q

What is Pyloric Stenosis?

More common in M. Family History

A
  • Hypertrophy of the circular muscles of the pylorus. leading to vomitting.
  • typically presents in the 2nd to 4th weeks of life
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6
Q

Signs And Symptoms Pyloric Stenosis

A
  • ‘projectile’ vomiting, typically 30 minutes after a feed
  • constipation and dehydration may also be present
  • a palpable mass may be present in the upper abdomen
  • hypochloraemic, hypokalaemic alkalosis due to persistent vomiting

peristalsis can be seen by observation of the abdomen

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7
Q

Management Pyloric Stenosis?

A

Diagnosis is most commonly made by ultrasound.

Management is with Ramstedt pyloromyotomy.
- After correction of Acid Base Balance

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8
Q

IBS Pathophyiology

around 5% of children between 4-18 have IBS.

AKA Functional gastrointestinal problem or functional abdominal pain disorder (FAPD).

A

disorder of visceral hypersensitivity and neurological hypervigilance in combination with psychosocial stressors. The gut is more sensitive to insults.

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9
Q

Signs & Symptoms IBS

pain oft peri-umbilical

A
  • Non-specific Abdo pain
  • Defecation
  • Alteration of stool frequency
  • Change in appearance of stool (diarrhoea or constipation)
  • Mucus in stools
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10
Q

Management IBS

A

try reassurance to child and parents, dietary changes, and behaviour modification to improve coping mechanisms and avoid reinforcement of pain

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11
Q

Gastroenteritis

Noro Virus most common. Rota virus protective due to vaccine

Campylobacter jejuni also common cause

A

Inflammation of stomach (Gastro) and intestines (enteritis)
* Viral cause most common (Faceal-Oral Route)
Signs & Symptoms
- Diarrhoea, Vomitting, Abdo cramps, fever, dehydration
Treatment
- Rehydration, preferably orally or NG tube; IV fluids may be used alternativel

Bacterial: caused by Contamination has muscus,bloody diarrhoea, Tenesmus

Complications
- Dehydration leading to shock – most serious complication
- Secondary lactose intolerance
- Bacteraemia or secondary infection
- Reiter’s syndrome, typically with Shigella or Campylobacter
- Haemolytic uraemic syndrome – production of Shiga toxin that destroys red blood cells and leads to this syndrome, typically E. coli or Shigella
- Guillain-Barre syndrome, typically Campylobacter
- Haemorrhagic colitis

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12
Q

idiopathic

Constipation in Children

The frequency at which children open their bowels varies widely but generally decreases with age from a mean of 3 times per day for infants under 6 months old to once a day after 3 years of age.

A

Under 1

  • Fewer than 3 complete stools per week, Hard large stool or rabbit droppings
  • Distress on passing stool, Bleeding associated with hard stool, Straining

Above 1

  • Fewer than 3 complete stools per week, Overflow soiling, Smelly
  • Poor appetite that improves with passage of large stool, Abdo/anal pain, Evidence of retentive posturing: typical straight-legged, tiptoed, back arching

Other causes of constipation in children include:
dehydration
low-fibre diet
medications: e.g. Opiates
anal fissure
over-enthusiastic potty training
hypothyroidism
Hirschsprung’s disease
hypercalcaemia
learning disabilities

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13
Q

Red Flags of Constipation in Children

A
  • Passing meconium > 48 hours
  • ‘Ribbon’ stools
  • Faltering growth is an amber flag
  • Distension Abdo
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14
Q

Treatment Constipation

Prior to starting treatment, the child needs to be assessed for faecal impaction. Factors which suggest faecal impaction include:
symptoms of severe constipation
overflow soiling
faecal mass palpable in the abdomen (digital rectal examination should only be carried out by a specialist)

A

If faecal impaction is present
* polyethylene glycol 3350 + electrolytes (Movicol Paediatric Plain) using an escalating dose regimen as the first-line treatment
* add a stimulant laxative if Movicol Paediatric Plain does not lead to disimpaction after 2 weeks
NORMAL
* first-line: Movicol Paediatric Plain

AVOID IN INFANTS

do not use dietary interventions alone as first-line treatment although ensure the child is having adequate fluid and fibre intake

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15
Q

Appendicitis in Children

Symptoms, epidemiology, atypical?

Rosvings: palpation in the LIF causes pain in the RIF

A
  • Central abdominal pain radiating to RIF - may have guarding
  • Low grade pyrexia
  • minimal vomiting
  • On palpation there is tenderness in McBurney’s point.
  • Rosving’s Sign +ve

Younger children present in atypical way

Appendicitis uncommon in children under 4

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16
Q

Appendiciis Pathophysiology

A
  • Appendix becomes inflamed due to infection trapped within the appendix by obstruction; inflammation can quickly proceed to gangrene and rupture.
  • lumen often obstructed by faecolith

Can lead to peritonitis. if ruptured

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17
Q

Diagnosis and Management Appendicitis

A
  • raised inflammatory markers – raised WCC in around 80-90% of cases.
  • USS
  • Appendicectomy

Laparoscopic surgery associated with fewer risks and faster recovery compared to laparotomy.

Administration of prophylactic intravenous antibiotics reduces wound infection rates

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18
Q

OFTEN INDIRECT HERNIA

Paediatric Inguinal Hernia Causes

Inguinal hernias are a common disorder in children.

M>F

A
  • Persistently Patent Processus Vaginalis
  • Commoner in males as the testis migrates from its location on the posterior abdominal wall, down through the inguinal canal.
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19
Q

Paediatric Inguinal Hernia Signs And symptoms

A
  • Lump in groin, might extend to scrotum or labium
  • usually asymptomatic
  • Intermittent - only visible when straining or coughing
  • palpable lump in groin
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20
Q

Paediatric Inguinal Hernia
Complications and Treatments

Children presenting in the first few months of life are at the highest risk of strangulation and the hernia should be repaired urgentl

A
  • Contents may become incarcerated or testes strangulation
  • Progressive oedema due to venous and lymphatic obstruction - infarction of testes!
  • Gentle taxis into inguinal canal w/ analgesia
  • surgery perfromed electively in elder children and emergency for infants.

Ovaries can descend into hernia if it becomes incarcerated and this will be difficult to manage.

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21
Q

Crohns V UC

IBD in children

Incidence has markedly increased in children in the last 2 decades.

A

Crohns
is transmural, granulomatous inflammation that may affect any part of the GI tract, but most common sites are terminal ileum and proximal colon. Bowel involvement is non-continous – skip lesions of normal bowel present where there is no inflammation
Ulcerative Colitis
involves the colon only; variable distance from the rectum proximally. 90% of children have pancolitis. Terminal ileum may also be affected (‘backwash ileitis’). Only the mucosa is affected in this condition.

Pancolitis: inflammation of whole colon

22
Q

IBD Symptoms

A
  • Perfuse diarrhoea (bloody/mucus)
  • urgency
  • Abdo cramps
  • weight loss
  • Anaemia
    CD
  • Oral ulcers, RIF mass, perianal disease
    UC
  • abdominal tenderness and distension
    Can also lead to faltering growth, delayed puberty and nutritional deficiencies i.e. vitamin B12.

Extra-intestinal manifestations include:
- Finger clubbing
- Erythema nodosum
- Pyoderma gangrenosum
- Episcleritis and iritis
- Inflammatory arthritis
- Primary sclerosing cholangitis (UC)

23
Q

Investigations IBD

A
  • Faecal calprotectin – released by intestines in response to inflammation; useful in screening.
  • Endoscopy – colonoscopy and biopsy is gold standard for diagnosis; may need OGD for CD to visualise upper GI tract.
  • Radiological imaging with ultrasound, CT and MRI can be used to look for complications such as fistula, abscesses and strictures.

Complications include:
- Toxic megacolon (UC>CD)
- GI perforation or strictures
- Pseudo-polyps
- Massive GI haemorrhage
- Colon carcinoma (UC: 50% risk after 10-20 years disease)
- Fistula involving bowel only, bowel and skin, vagina or bladder (CD)
- Abscesses (CD)

24
Q

Management IBD

A

CD
* Steroids IV
* aminosalciylates if contr’d
* Maintenance of remission is tailored to individuals, and they may decide to not use medications. First line medications are azathioprine or mercaptopurine; methotrexate is an alternative if these are not suitable. Corticosteroids not used for remission maintenance.

UC
* aminosalicylates 1st line
* with corticosteroids as second line. In severe disease, IV corticosteroids used first line, with IV ciclosporin as second line.

25
Q

Autoimmune

Coeliac Disease Pathophysiology

Coeliac disease is caused by sensitivity to the protein gluten.

Children present around 3y ( when cereal is usually introduced)

A
  • Inflammation that occurs affects the small bowel, particularly the jejunum.
  • Causes atrophy of the intestinal villi, leading to malabsorption of nutrients and disease related symptoms.

Gluten is found in found in wheat, barley and rye

it is strongly associated with HLA-DQ2 (95% of patients) and HLA-DQ8 (80%)

26
Q

Coeliac Disease Signs & Symptoms

A
  • failure to thrive
  • diarrhoea
  • abdominal distension
  • older children may present with anaemia
  • many cases are not diagnosed to adulthood

Can also be dermatitis herpetiformis – this is an itchy, blistering rash that typically appears on the abdomen.

27
Q

Coeliac Disease Investigations

Total immunoglobulin A should be checked first to exclude IgA deficiency before checking for coeliac disease specific antibodies

A
  • Raised anti-tissue transglutaminase (TTG) antibodies IgA
  • Raised anti-endomysial (EMA) antibodies
  • To confirm jejunal biopsy showing subtotal villous atrophy

All children with type 1 diabetes are tested due to the high incidence in these patients.

28
Q

Coeliac Disease Management and Complications

Solids should be introduced to baby’s diet at 6mths. breastfeeding and milk

A
  • Treatment is a lifelong gluten-free diet with correction of any vitamin deficiencies that may be present

Pneumococcal vaccination given due to the association with hyposplenism.

Complications of untreated disease includes:
- Osteoporosis
- Enteropathy-associated T-cell lymphoma of the intestine
- Non-Hodgkin lymphoma
- Small bowel adenocarcinoma (rare)
Rarely may present with neurological complications:
- Peripheral neuropathy
- Cerebellar ataxia
- Epilepsy

29
Q

Define Marasmus & Treatment

Severe Malnutrition

A
  • Inadequate Protein + Calorie intake
  • Leads to insufficient energy balance -> -ve energy balance + Redeuce Basal metabolic rate.
  • Wizened Faces, disproportionate head size.
  • Severe Muscle Wasting and Subcut fat loss
  • Hypotension, Hypothermia, Hypoglucaemia, Anaemia, Hyponateremia with other electrolyte imbalance
  • Prone to infections

Wizened: Having a shriveled, thin, withered face.

Treatment
- Prophylactic Abx - malnutrition induced immunodeficieny compensation
- Correct Glycemic, electrolyte, hydration abnormalities
- Protein refeeding

30
Q

Define Kwashiokor and Treatment

Common in children in food-scarce environments who are weaned of breast milk and given carb-rich diets.

A
  • Sufficient Calorie intake BUT inadequate protein intake.
  • Bilateral Pitting Oedema. Distendeded stomach.
  • Muscle Wasting, Hepatomegaly.
  • Hypoglycaemia, Decreased lipids, hypoalbuminaemia, hypoproteinemia, Anaemia, Electrolyte depletion.
    Pathophysiology
  • Extreme protein deficiency leads to decreased liver synthesis, osmotic imbalance leading to oedema: cause of distension

DISTENTION: BLOATING

Treatment
- Prophylactic Abx - malnutrition induced immunodeficieny compensation
- Correct Glycemic, electrolyte, hydration abnormalities
- Protein refeeding

31
Q

Transmitted by Inheritance

Hirschsprung’s Disease Pathophysiology

* Down’s syndrome association. M>F

Hirschsprung’s disease is caused by an aganglionic segment of bowel due to a developmental failure of the parasympathetic

A
  • Failure of development of nerves in one part of the bowel while baby is in the womb. = narrowed segment of bowel (aganglionic)
  • The aganglionic section of colon does not react causing it to become constricted
  • Parasympathetic neuroblasts fail to migrate from the neural crest to the distal colon → developmental failure of the parasympathetic Auerbach and Meissner plexuses → uncoordinated peristalsis → functional obstruction
32
Q

Hirschsprung’s Disease Signs and Symptoms

Meconium: cells, protein, fats, and intestinal secretions, like bile

A
  • Unable to pass meconium within 24h of Life
  • older children: constipation, abdominal distension
  • Rectal examination may reveal a narrowed segment and withdrawal of examining finger often releases a gush of liquid stool and flatus
33
Q

Hirschsprung’s Disease Investigations & Management

A
  • abdominal x-ray
  • rectal biopsy: gold standard for diagnosis acetyl-cholinesterase +ve
  • Management initially: rectal washouts/bowel irrigation then surgical and usually involves an initial colostomy followed by anastomosis of normally innervated bowel to the anus.

Complications below

Occasionally infants present with severe, life-threatening Hirschsprung entercolitis during the first few weeks of life – inflammation and obstruction of the intestine. Can lead to toxic megacolon and perforation of the bowel – required urgent antibiotics, fluid resuscitation and decompression of obstructed bowel.
In later childhood presentation with chronic constipation usually profound and associated with abdominal distension without soiling.
Growth faltering may also be present.

34
Q

linked to viral infections

Intussusception Pathophysiology

Intussusception describes the invagination of one portion of bowel into the lumen of the adjacent bowel, most commonly around the ileo-caecal region.

A
  • Invagination thickens the overall size of the bowel and narrows the lumen at the folded area, leading to a palpable mass in the abdomen and obstruction to the passage of faeces through the bowel.

Intussusception usually affects infants between 6-18 months old. Boys are affected twice as often as girls

35
Q

Intussuception Features

A
  • paroxysmal abdominal colic pain
  • during paroxysm the infant will characteristically draw their knees up and turn pale
  • vomiting
  • bloodstained stool - ‘red-currant jelly’ - is a late sign
  • sausage-shaped mass in the right upper quadrant

ultrasound is now the investigation of choice and may show a target-like mass

36
Q

Intussuception Management

Therapeutic enemas can be used to try and reduce intussusception

A
  • the majority of children can be treated with reduction by air insufflation under radiological control
  • If signs of peritonitis then surgery will be performed.

complications below

Most serious complication is stretching and constriction of the mesentery resulting in venous obstruction, causing engorgement and bleeding from the bowel mucosa, fluid loss and subsequently bowel perforation, peritonitis and gut necrosis.

37
Q

Congenital condition

Meckel’s diverticulum Pathophysiology

Rule of 2s
* occurs in 2% of the population
* is 2 feet from the ileocaecal valve
* is 2 inches long

A
  • Congenital diverticulum of the small intestine
  • Ileal remnant of the vitello-intestinal duct which contains ectopic gastric mucosa or pancreatic tissue. Normally involutes during late foetal development but in these patients there is failure of this process.
38
Q

Meckel’s diverticulum Signs and Symptoms

present before the age of 2

idiopathic congenital abnormality

A
  • Majority of patients remain asymptomatic
  • abdominal pain mimicking appendicitis
  • rectal bleeding
  • Meckel’s diverticulum is the most common cause of painless massive GI bleeding requiring a transfusion in children between the ages of 1 and 2 years
  • intestinal obstruction
  • secondary to an omphalomesenteric band (most commonly), volvulus and intussusception

Rectal bleeding is neither malena or bright red.

39
Q

Meckel’s diverticulum Investigations and management

A
  • if the child is haemodynamically stable with less severe or intermittent bleeding then a ‘Meckel’s scan’ should be considered
  • uses 99m technetium pertechnetate, which has an affinity for gastric mucosa
  • mesenteric arteriography may also be used in more severe cases e.g. transfusion is required
    Management
  • removal if narrow neck or symptomatic
  • options are between wedge excision or formal small bowel resection and anastomosis
40
Q

Chronic

Toddler’s Diarrhoea Features

  • Toddler’s diarrhoea is a chronic non-specific diarrhoea seen in small children, between about one and four years. This condition accounts for a large proportion of children with chronic diarrhoea, but should be regarded as a diagnosis of exclusion
A
  • Frequent, poorly formed brown and slightly offensive stools
  • food material easily recognisable in the stools is a hallmark feature
  • Repeated parental reassurance and avoidance of full-strength fruit juices are usually sufficient

Child: Normal Behaviour, apetite, growth & active

Stool anaylysis and examinations are unremarkable.
DD: Coealiac, infective diarrhoea, Giardiasis
Dietary investigation may reveal a very high intake of fruit juices and cordials,

41
Q

. Mainly in infants under 5 months of age

Infantile Colic

do not recommend the use of simeticone (such as Infacol®) or lactase (such as Colief®) drops.

A
  • Self-limiting condition which is defined clinically as repeated episodes of excessive and inconsolable crying & pulling-up of the legs, often worse in the evening.
  • In an infant that otherwise appears to be healthy and thriving.

Tests done to rule out abnormality, urinalysis, cxr, bloods, xrays

Acknowledgement and support of the parents concerns is key part of the management.
Can give advice on strategies that may help soothe an infant – holding the baby, gentle motion, white noise, warm bath and winding technique
Kangaroo Mother care may be helpful (skin to skin contact for multiple hours a day)

42
Q

Cow’s Milk Protein Allergy Pathophysiology

typically presents in the first 3 months of life in formula-fed infants, although rarely it is seen in exclusively breastfed infants.

A
  • Both immediate (IgE mediated) and delayed (non-IgE mediated) reactions are seen. The term CMPA is usually used for immediate reactions and CMPI for mild-moderate delayed reactions.

I: Intolerance. A:Allergy

43
Q

Cow’s Milk Protein Allergy
Features

A
  • regurgitation and vomiting
  • diarrhoea
  • urticaria, atopic eczema
  • ‘colic’ symptoms: irritability, crying
  • wheeze, chronic cough
  • rarely angioedema and anaphylaxis may occur

Diagnosis is often clinical (e.g. improvement with cow’s milk protein elimination). Investigations include:
skin prick/patch testing
total IgE and specific IgE (RAST) for cow’s milk protein

44
Q

Cow’s Milk Protein Allergy Management

If the symptoms are severe (e.g. failure to thrive) refer to a paediatrician.

A

Formula Fed
* extensive hydrolysed formula (eHF) milk is the first-line replacement formula for infants with mild-moderate symptoms
* amino acid-based formula (AAF) in infants with severe CMPA or if no response to eHF
Breast fed
* continue breastfeeding
* eliminate cow’s milk protein from maternal diet. Consider prescribing calcium supplements for breastfeeding mothers whose babies have, or are suspected to have, CMPI, to prevent deficiency whilst they exclude dairy from their diet
* use eHF milk when breastfeeding stops, until 12 months of age and at least for 6 months

CMPI usually resolves in most children
* in children with IgE mediated intolerance around 55% will be milk tolerant by the age of 5 years
* in children with non-IgE mediated intolerance most children will be milk tolerant by the age of 3 years
* a challenge is often performed in the hospital setting as anaphylaxis can occur.

45
Q

Umbilical hernia in children

A

Umbilical hernia are relatively common in children and may be found during the newborn exam. Usually no treatment is required as they typically resolve by 3 years of age

Associations
* Afro-Caribbean infants
* Down’s syndrome
* mucopolysaccharide storage diseases

46
Q

unique to neonatal children

Biliary Atresia Pathophysiology

Extrahepatic biliary atresia is more common in females than males

Biliary atresia is a paediatric condition involving either obliteration or discontinuity within the extrahepatic biliary system, results in an obstruction in the flow of bile

A

Type 1: The proximal ducts are patent, however, the common duct is obliterated
Type 2: There is atresia of the cystic duct and cystic structures are found in the porta hepatis
Type 3: There is atresia of the left and right ducts to the level of the porta hepatis, this occurs in >90% of cases of biliary atresia

Untreated, chronic liver disease develops and death occurs within 2 years.
Can lead to growth failure, vitamin D deficiency/fractures, GI bleeding and cholangitis.

47
Q

Biliary Atresia Symptoms

A

Patients typically present in the first few weeks of life with:

  • Jaundice extending beyond the physiological two weeks
  • Dark urine and pale stools
  • Appetite and growth disturbance, however, may be normal in some cases
  • Cardiac murmurs if associated cardiac abnormalities present
  • Hepatomegaly with splenomegaly
48
Q

Biliary Atresia Management

A
  • Surgical intervention is the only definitive treatment for biliary atresia: Intervention may include dissection of the abnormalities into distinct ducts and anastomosis creation
  • Medical intervention includes antibiotic coverage and bile acid enhancers following surgery

Untreated, chronic liver disease develops and death occurs within 2 years.
Can lead to growth failure, vitamin D deficiency/fractures, GI bleeding and cholangitis.

49
Q

Biliary Atresia Investigations

A
  • Serum bilirubin including differentiation into conjugated and total bilirubin: Total bilirubin may be normal, whereas conjugated bilirubin is abnormally high
  • Raised LFTs
  • Serum alpha 1-antitrypsin: Deficiency may be a cause of neonatal cholestasis
  • Ultrasound of the biliary tree and liver: May show distension and tract abnormalities
    Percutaneous liver biopsy with intraoperative cholangioscopy
50
Q

Choledochal Cyst

Five varieties have been described. The most common type is a fusiform

are caused by a specific weakness in a part or the whole of the wall of the common bile duct, and usually presents in neonates or children.

A
  • The cyst may contain up to 1 to 2 litres of bile. In adult life they often contain gallstones.
  • The classical presentation of abdominal pain, jaundice and right upper quadrant mass occurs in about 33% of patients. There may be acute cholangitis - fever, right upper quadrant tenderness, jaundice and leukocytosis, biliary cirrhosis or diffuse peritonitis following rupture of the cyst.
51
Q

Inflammation of liver in newborns (1-2mths after birth)

Neonatal hepatitis features

Rubella, CMV, Alpha a1 antitrypsin deficiency

if untreated - 6mths - chronic liver disease - heapatic cirrhosis - Liver failure

A
  • Jaundice, pruritus, rashes, dark urine, pale stools, hepatamegaly
  • decreased intestinal bile flow - impaired fat digestion, vit absorption, failure to grow
  • USS used w/biopsy of liver cells
  • Serum bilirubin raised
  • Ursodeoxycholic acid for iincreased bile formation
  • Vit supplements
  • may need liver transplant

3a Notes AC (20 decks)

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