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ED fellowship paeds > GIT > Flashcards

GIT Flashcards

1
Q

Discuss neonatal jaundice

A

Formed by the breakdown of haem – unconjucated hyperbilrubinaemia is common to almost all neonates – physical signs appear at 5 mg/gl –. usually benign and slef limiting termed physiological jaundice of the newborn which occurs in 50% of cases

At levels great than 20-25mg/gl there is an increased risk of bilrubin induced neurological dysfunction(BIND). Early potentially reversible signs and symptoms includ somnolence, poor feeding, hypertonia or hypotonia –> if untreated progress to chronic long term sequalue Kernicterus

Sympoms of Kernicterus includ CP, sensorineural hearing lose and gaze abnormalilties

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2
Q

Discuss risk factors for the development of neonatal jaundice

A

Prematurity
isoimmune mediated haemolysis (ABO incompatibility)
Sepsis
Cephalohaematomas
Dehydration
Inhereted abnormailites (G6PD), spherocystosis

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3
Q

Discuss DDX of neonatal unconjugated hyperbylirbunaemia

A

Benign

  • Physiological
  • Breast milk jaundice

Haemolysis

  • ABO incompatibility
  • Physiological breakdown of birth trauma haematoma
  • Intracranial/ventricular haemoarrahge
  • spherocytosis
  • Sickle cell
  • Thalassaemia
  • G6PD
  • Pyruvate kinse defiency

Infectious

  • TORCH infections
  • UTI
  • Sepsis

Obstrucrive

  • Meconium ileus
  • Hirschsprung;s diseaes
  • Duodenal atresia
  • Pyloric stenosis

Metabolic

  • Glactosemia
  • congenital hpotheroidism
  • Crigler-Najjar syndrome
  • Gilbert syndrome
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4
Q

Discuss DDX of neonatal conjugated hyperbylirbunaemia

A

Much rarer than unconjugated

Infectious 
-TORCH 
-UTI 
-sepsis 
-TB 
-heb B 
-Coxsackie 
-ECHO 
HIV 
Obstructive 
-Bilary atresia 
-choledochal cyst
-Bile duct stricutres
_inspissated bile syndrome 
-neonatal hepatitis 
-Alagille syndrome 
-Byler idsaes 
-Congential hepatic firbosis

Metabolic
- Glycogen storage sdisease
-A1 antitrypisn
CF

Misc

  • drugs and toxins
  • Parenteral nutrition
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5
Q

Discuss clinical features of neonatal jaundice

A

Healthy infants are born with normal levels of bilirubin which peak on the 3rd day of life and than decline to normal levels in 2 weeks

Physiological jaundice rarely occurs within the first 24 hours. Breast milk jaundice has the same gradual increase seen with physiological jaundice but levels continue to increase and peak at around 10-21 days

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6
Q

Discuss management options and disposition of neonatal jaundice

A

Normogram depending on risk stratification -> phototherapy, nurse child in nappy only, protect eys

Exchange transfusion indicated if bilirubin continuing to rise despite intesive phototherapy or if approaching normogram levels for transfusions

IVIG evidence in inconlusive in neonates with severe haemolytic disease

Disposition
- all children with bilirubin levels greater than 18-20mg/dl or with conjugated hyperbilirubinaemia need admission for treatment/investigation

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7
Q

Discuss exchange transfusion

A

Infants with severely elevated bilirubin not responding to treatment are at the greatest risk of BIND
Exchange tranfusion are indicate for these infants
Time consuming procedure which should be completed in the NICU
A double volume transfusion replaces approximatly 85% of an infants blood volume and reduces the total bilirubin by at least 50%
It is performed serially taking small amounts of the infants blood and transfusion a similar volume of PRBC

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8
Q

Discuss indications for evaluation of jaundice infacts and exchange transfusions

A
  • Jaundice within the first 24 horus of life
  • elevated conjugated bilirubin level
  • Rapidly rising total serum bilirubin unexplained by history or physical examination
  • Total serum bilirubin approaching exchange leve or not responding to phototherapy
  • jaundice persisting past 3 weeks of age
  • sick appearing child
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9
Q

Discuss TORCH infections

A 
Infections acquired in utero or during the birthing process 
T- toxiplasmosis 
O- other (syphilis, VZV, parvovirus) 
R- Rubella 
c- CMV
-H HSV

They include hepatosplenomegaly (enlargement of the liver and spleen), fever, lethargy, difficulty feeding, anemia, petechiae, purpurae, jaundice, and chorioretinitis.

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10
Q

Discuss hypertrophic pyloric stenosis

A

Most common cause of infantile GI obstruction past the first month of life.
Boys are affected more than 4:1
Risk factors include prematurity and exposure to erythromycin or azithromycin.
Infants are born with a normal sized pylorus which hypertrophies over time. As the pylorus enlarges progressive gastric outlet obsturction develops and vomiting ensures.
Vomiting causes loss of fluid, hydrogen and chloride. As the kidney attempts to correct this K is exchanged for H leading to the classic hypochloremic-hypokalaemia metabolic alkalosis

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11
Q

Discuss Clinical features of pyloric stenosis

A

Present aged 2-6 weeks with progressive vomiting that becomes projectile but remains non bilious.
Early in the course the children remain vigourous with a ravenous appetite. Quickly finish an entire bottle only to regurg contents
Later stages is characterised by dehydration, FTT and malnurition.

Children may have a palpable pyloris in the right epigastrium commonly referred to as an olive.

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12
Q

Discuss IX of pyloric stenosis

A

Labs as above with hypochloremic, hypokalaemia alkalosis and dehydration picture

US is gold standard with spec and sens of 95% – US finding include a thickened pyloric muscles and in some cases the string sign showing small amounts of contrast material through the pyloric sphincter

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13
Q

Discuss DDX of pyloric stenosis

A

Main DDX is GORD – usually present quickly after birth and static in severity
Pyloric stenosis usual begins with vomiting at around 2-3 weeks with progressive symtpoms

patients who present with sudden onset severe vomiting or bilious in nature should be evaluarted for malrotation , duodenal atresia and NEC

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14
Q

Discuss Malrotation with midgut volvulus

A

Occurs in a 1:500 live births with a 1:2 male predominance
Occurs in the first month of cases in 1/3 of cases, in the first yuear in 50% and before age of 5 in 75%
Bilious emesis is the hallmark of presentation – mortality is 3-15%

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15
Q

Discuss clinical features of midgut volvulus

A

Sudden onset bilious emesis and abdominal distention
Colour of bile yellow or green is not indicative of surgical vs non surgical pathology only of time and oxidation

Children usually present unwell and can be shocked

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16
Q

Discuss IX of midgut volvusus

A

AXR - air fluid levels suggestive of obstruction, abnormally dilated bowel loops overlying the liver and a paucity of small bowel gas distally –> can show double bubble signs

US- Abnormal orientation of mesenteric artery and vein
-Whirlpool sign caused by twisting of the vessels around the mesenteric stalk

Fluroscopy - limited upper GI contrast series is the exam of choice, not only will it identify the volvus but in instances where the spont reduction has occured the underlying malrotation will be eveident

  • corkscrew sign
  • tapering or beaking of the bowel in complete obstruction
  • malrotated bowel configration

CT is usually not recommeneded as carries incrased radiation exposure

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17
Q

Discuss management of malrotation and volvulus

A

Surgical review should be obtained for any child with bilious vomiting
In acute midgut volvulus operitve intervention must be rapid to save the bwoel from necrosis

IV access and labs for glucose and electrolye, UEC and LFT
20ml/kg fluid boluse until adequate circulation has been re-establisehd
If ill appearing broad emperical antibtiocs should be given

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18
Q

Discuss differential of vomiting in infancy

A 
Mechanical 
-GORD 
-Malrotation with midgut volvulus 
-Pyloric stenosis 
-Meckels diverticulum 
-Intussusception 
-bowel obstruction 
-Incarcerated hernia 
_tracheooesophaegeal fistula 
Inflammatory or infection 
-NEC 
-gastroenteritis 
-sepsis 
-HSP 
-Menigitis 
0Pneumonia 
-ottits media

Genurinary
- UTS

CNS

  • hydrocephalus
  • intracranial haemorrhage
  • intracranial tumor

Metbaolic

  • DKA
  • Congential adrenal hyperplasia
  • Urea cycle defects
  • organic acidurias
  • amino acidopathies
  • fatty oxidation disorders

OIther

  • NAI
  • Toxins
  • Munchausen syndrom by proxy
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19
Q

Discuss NEC

A

Most common GI emergency in neonates,and most common cause of intestinal perforation in neonates
Prematurity is the most common risk factor with 90% of cases being premature

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20
Q

Discuss differential of vomiting in Children

A

Mechanical

  • Constipation
  • incarcerated hernia
  • Meckel’s diverticulum
  • bowel obstruction

Inflammatory or infectious

  • gastritis or gastroenteritis
  • OM
  • Appendicitis
  • pancreatitis
  • HSP
  • biliarty tract diseaes

Genurinary
-UTI

CMS

  • migraine
  • hydrocephalus
  • ICH
  • intracnrial tumor
  • Reye’s - intracranail and hepatic oedema

Metabolic

  • DKA
  • Urea cycle defect
  • fatty acid oxidation disorders
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21
Q

Discuss differential of Bilious vomiting

A

1) intestinal atreasia
2) anorectal anomalies
3) meconium ileus
4) hirschsprungs
5) malrotation with volvulus
6) irreducible inguinal hernia
7) intussusception
8) inflammatory
9) Meckel’s diverticulum
10) adhesions
11) non surgical

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22
Q

Discuss clinical features of NEC

A

Feeding intolerance with either bilary or non bilary vomiting - advancing to shocked children with haematemisis, haematochezia, fever and shock.

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23
Q

Discuss IX of NEC

A

AXR is the imaging modality of choice in NEC – radiograph show nonspecific dilated loops of bowel with intramural air - pneumoatosis is present in 75% of NEC cases

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24
Q

Discuss management of NEC

A

ABCD - often unstable
secure airway if needed
C: IV or IO access with fluid bolusing to maintina MAP, UO conisder tropes if not winning

Neonates suspected of NEC should be NBM with placement of an orogastric or nasogastric tube for decompression

Broad spectrum antibiotics should also be given
Pip taz 25mg/kg IV QID + Gentamycin 2.5mg/kg

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25
Q

Discuss GORD

A

One of the msot common causes of vomiting during infancy, occurs as a result of an incompetent LES. Chronic reflux can lead to oesophagitis, aspiration and failure to thrive

26
Q

Discuss clinical features of GERD

A

Begins shortly after birth and resolves with time usually by the age of 1.
Range in severity from asymptomatic to occasional episdoes of spitting up to persistant severe vomiting.

27
Q

Discuss management of GORD

A

Most infants respond to conservative lifestyle modifications such as smaller feeds, frequent burping, formula thickened and a semi upright position after feeding

28
Q

Discuss intussuscpetion

A

Refers to invagination of part of the intestine into itself.
Most common presentation is between 6-36 months with 60% of cases under a year of age and 80-90% below 2 years of age. 10% of cases occur in children over the age of 5

In younger children lead points for the development of intussessuption are usually due to enlarged Peyers patches. Approximately 75% of cases especially those in older children have a pathological lead point inclduing

  • HSP vasculitis,
  • Meckel’s diverticulum,
  • lymphoma,
  • polyps,
  • postsurgical scares,
  • celiac disaes
  • CF.

90% of cases are ileocolic in nature

29
Q

Discuss clinical finding in intussusception

A

The classic triad of abdominal pain, palpable sausage shaped abdominal mass and bloody stools (current jelly).

Abdominal is the most common symptom- cycic episodes of severe abdominla pain as waves of peristalsis cayse bowel dilation
Episode typically last 10-15 minutes and occur in intervals of 15-30 minutes.

During episode the child may be irritable and inconsolable often described as drwaing the legs up and screaming

30
Q

Discuss IX of intussuscpetion

A

AXR

1) absence of air in the right upper quadrant
2) a right sided soft tissue shadow giving an impression of an intracolonic mass or crescent sign
3) absence of intestinal air or fluid levels in the caecum
4) distal intestinal obstruction with dilated intestinal loops
5) intra peritoneal free air
6) unremarkable gas intestinal pattern

US is the diagnostic modality of choice. Highly specific and sensitive.

  • Target sign is classic
  • Pseudo kidney sign
31
Q

Discuss management of intussuspceiton

A

ABCD

IV fluid boluses 20ml/kg should be given until adequate intravscular volume has beenachieved
NPO + NGT
Prompt surgical referral

Air contrastenema or barium enema has a 90% success rate in decompression of intussusception

recurs in 12% of radiographic reductions – 50% present of these recurrences represent in the first 48 hours

Factors that reduce the likleyhood of successful reduction with air enema or increase risk of perforation

1) patients age: <3 months or older than 5 years
2) long duration of symptoms more than 48 hours
3) passage of rectal blood
4) dehydration significant
5) small bowel obstruction
6) presence of dissection sign on contrast study

32
Q

Discuss Hirschsprung disease

A

Account for approxiamtly 20% of cases of parital intestinal obstruction in early infacny.

Congential aganglionosis of the colin - in the myenteric plexus of the dsital colun. The anus is invariably involved with aganglionic bowel usually extending proximally 4-25 cm. The absence of ganglion causes a functional obstruction

33
Q

Discuss clinical features of Hirschprung disease

A

Often seen in neonates with inability to pass meconium however spectrum of disease is identified and can present in infants presenting to the ED with chronic constipation

34
Q

Discuss Meckel’s Diverticulum

A

Meckels are remanants of the omphalomesenteric duct and contain bowel wall with 60% containing heterotopic tissue usually gastric mucosa. . Bleeding occurs when aicd secretion form the ectopic gastric mucosa causes ulceration and erosions.

Follows the so called rule of 2s. The diverticulum is 2 cm wide, 2cm long and located with 2 feet of the ileocaecal valve.
Occurs in 2% of the population and only 2% of patient become symptomatic

35
Q

Discuss clinical feature

A

Classically present with massive painless rectal bleeding. Some children complain of cramping abodminla pain

Examination is usually NAD
Blood often described as brick red but may range from melena to bright fresh blood

36
Q

Discuss IX of Meckles

A

Technetium 99m scan is the diagnostic modality of choice and has an accuracy of 90% when ectopic gastric mucosa is present

37
Q

Discuss management of Meckles

A

ABCD

Replace haemorrhage

38
Q

Discuss HSP

A

Also known as anaphylactoid purpura is a hypersensitivity vasculitis with immune complex deposition of IGA – affect arterioles and capillaries

most well known for its petechial to purpuric rash HSP is a systemic vasculitis affecting any vessel

Most common in children 4-11 year of age and occurs during the spring season after URTI

39
Q

Discuss clinical features of HSP

A

In contrast to many other forms of systmeic vasculitis IgAV is self limited in the marjoity of ccases
It has a classic tetrad of clinical manifestations:

1: Palpable purpura in patients with netiher thrombocytopenia or coagulpathy - usually located on buttocks and lower limbs
2: arthirtis/arthralgia - transient migratory

3: abdominal pain + other GIT complaints –> can lead to ileoileal intussuscpetion
- can range from mild (nausea, vomiting, abdominal pain) to severe ( GIT haemorrhage, bowel ischaemia and necrosis)

4:renal disease - microscopic haematuria

Relapsing and remitting for several weeks

40
Q

Discuss management and dispostion of children with HSP

A

Most require only supportive care. Mild to moderate pain is usually well controlled with anti-inflamatory drugs or paracetamol.
Prednisone at a dose of 1mg/Kg is reserved for those with severe symptoms

Most pateint can be managed symptomatically with a close OPD follow-up. Indications for hospitalisation include

  • Orchitis
  • Moderate to severe pain,
  • polyarthritis
  • GI bleeding
  • inability to ambulate
  • uncertain diagnosis
  • singificant renal involvement
41
Q

Discuss DDX of GI bleeding in infants

A

Factitious

Upper GIT

  • PUD
  • oesophagitis’
  • mallory weis tear
  • vascular malforation
  • oesophageal varices and portal hypertensive gastropathy
Lower 
- NEC
-Intussuscpetion 
-Gastroenteritis 
Mil allergy 
-vascular malformation 
-hirshprungs
-meckles 
HSP
HUS

Rectal
-fissue

Other

  • bleeding dyscrasia
  • NAI
  • Toxin
42
Q

Discuss GI foreign bodies

A

Commonly pass the entire GIT without complication

  • classically get lodged in three areas
    1) Upper oesophageal sphincter
    2) Thoracic inlet
    3) LES
43
Q

Discuss clincial features of GI fFB

A

Most asymptomatic and go unoticed
If inhaled persistent coughing, wheezign and WOB may be present.
Swalloed button batteries warrant special mention – these lodge in the oesophagus and cause severe mucosal erosions, severe burns and mediastintiis in as little as 2 horus as a result of the elvtrical current dsicharged from lithium abtters. Once in the stomach batteries will still usually pass without complciaton

44
Q

Discuss Indication for removal of GIT foreign bodies

A
  • Signs of respiratory distress
  • evidence of oesophageal obsturction (inability to swallow secretion)
  • Button batteries in the oeosphagus – 2 hours time limit for removal
  • Sharp or long (>5cm) objects in the oesophagus or stomach
  • high powered magnets
  • signs or symptoms of intestinal inflammation, obsturction or perforation
  • oesophageal foreing bodies impacted for >24 hours or for an unknown amount of time
45
Q

Discuss appendicitis

A

Peak age of incidence is between 9 and 12 years of age and it is uncommon in children younger tahn 5 years of age. Thoes who develop appendicits at a younger age have marked increase in risk of perforation
-neonates 83 percent
-young children <5 51-100 percent
In adults a thicker appendiceal wall resists perforation and a well developed omentum aids in walling off infection to prevent spread – chioldren have neither so rupture tends to occur earlier and diffus peritonitis develops more readily

46
Q

Discuss clinical features of appendicitis

A

Symptoms are generally progressive over the first 24 hours. Classically abdominal pain, nausea and vomiting and anorexia
Abdominal pain is usually first described as a vague crampy and periumbilical.
Pain than becomes more severe constant and localized to the RLQ
Fever usually develops later or not at all

Peritonism in the RLQ worst at Mcburneys poitn
Rovsing, psoas and obturator signs are difficult to asses in young children

47
Q

Discuss IX of appendicitis

A

Most children with appendicits will have elevated WBC and CRP – especially if symptoms have been present for longer than 24 hours
Usually will cause a sterile pyruria

US is the most commonly used first line imaging modality. Finding include
- Enlarged non compresible appendix with thick wall (>2mm wall thickness and >6mm total diameter of appendix)
-Ring of fire on doppler
- Painful to probe pressure
_sens and spec of 90% when visualised

CT

48
Q

Disccus DDX of appendicitis

A

Mesonteric adenitits is the msot common DDX of appendicitis usually differentiated on US

Girls of reproductive age merit consideration of gynecological pathology including pregnancy, ovarian torsions and cyst and PID

49
Q

Discuss Paediatric appendicits score

A 
8 factors includein 
-anorexia --1
nausea or vomitng -1 
migration of pain -1 
Fever >38 -1 
pain with cough, percussion or hopping  -2
RLQ tenderness -2 
WBC >10 -1
Neutrophils >7.5 -1

PAS of <3 suggestive of low risk ofr appendicitis may be discharged home if carers happy

PAS of >7 indicate high risk for appendicitis and should have surgical review

50
Q

Discuss Alvarado score (MANTRELS) and its utility in children

A 
10 point score from 8 components 
-migratory RLQ pain -1 
ANorexia -1 
nausea and vomitni -1 
tenderness in the RLQ-2 
Rebound tenderness in the RLQ -1 
T >37.5 -1 
Leukocytosis -2
Shift of the WBC -1

Not validated in paeds as has inadequate accurate for appendicits - overestimates severity of intermediate group

51
Q

Define poor weight gain (previously failure to thrive)

A

1) Weight less than the 2nd centile for gestation corrected age and sex or
2) decreased velocity of weight gain that is disproportionate to growth in length
3) a rate of weight change that causes a decrease of tow or mare major centile lines

52
Q

Discuss aetiology of poor weight gain (previously failure to thrive)

A

1) inadequate nutrient intake
- poor feeding technique
- disturbed caregiver/child relationship
- Economic deprivation
- inappropriate nutrient intake (e.g excess fruit juice, factitious food allegery, inappropriate preparation)
- inappropriate parental knowledge of appropraite diet for infants and toddlers
- insufficient lactation in mother
- picky eater
- GORD
- psychosocial
- mechanical problems ( cleft palate, nasal obstruction, adenoidal hypertrophy, dental lesions)

2) inadequate appetite or inability to eat large amounts
- oral aversion problems with certain textures
- psychosocial problems
- cardiopulonary disease
- hypotnoia, muscle weakness, or hypertonia
- anorexia of chornic infection or immune defieincy
- CP
- CNS pathology
- genetic syndrome
- anaeamia
- chronic consitpation

3) inadequtne nutrient absorption or increased losses
- malabsorption (lactose intolerance, CF, cardiac disease, malrotation, IBD milk allergy)
- biliary atresia, cirrhosis
- vomiting or spitting up (related to infectious gastro, increased ICP, adrenal insufficiency or durgs)
- intestinal tract obstruction (pyloric stneosis, hernia, malrotation, intussuscpetion)
- infectious diarrhoea
- NEC

4) increased nutrient requirement
- hyperthyroidism
- malignancy
- chronic IBD
- chronic systemic disease (Juvenile idiopathic arthritis)
- Chronic or recurrent systemic infection
- chroncic metabolic problems ( storage diseaes, inborn error of metabolis)
- chronic respi insufficiency (CF)
- congential or acquired heart disease

53
Q

Define acute liver failure

A

1) Biochemical evidence of liver injury (usually of less than 8 weeks duration)
2) no history of chronic liver disease
3) coagulopathy that it not corrected with vitamin k
4) an INR greater than 1.5 if accompanied by encpehalopathy or greater than 2 if not

Less emphasis on encephalopathy compared to adults as can be difficult to diagnose in children

54
Q

List causes of ALF in children

A

1) Cholestasis
- bilary atresia
- choledochal cyst
- intrahepatic bile duct paucity
- inspissated bile syndrome

2) Idiopathic neonatal hepatitis
3) CF
4) encodcrine
5) neonatal haemochromatosisi

6) infection CMV, HSV, VZV, EBV,
- bacterial sepsis, UTI, TB syphilis
- parasiste toxoplasma

7) metabolic
- a1 antitrypsin
- bile acid metabolis
- urea cycle abnormaltiies

8) Toxin
- paracetamol

9) Tumor
- intra or extra hepatic

55
Q

Discuss classification of acute liver failure

A

Hyper acute - <7days
Acute - 8-28 days
Subacute - 5-12 weeks

56
Q

Discuss classification of acute liver failure

A

Hyper acute - <7days
Acute - 8-28 days
Subacute - 5-12 weeks

57
Q

Discuss aspirin and Reye’s syndrome

A

Mitochondrial dysfunction leading to acute encephalopathy selective hepatic dysfunction and visceral fatty infilitration has been called Reye

Mitochondrial oxidative phosphorylation and fatty acid B oxidation are the metabolic pathways affected in Reye’s syndrome.

Preceding viral infection (classically VZV) immune mediators and aspirin (or its metabolites) can limit normal functioning of these pathways

58
Q

Describe biliary atresia

A

Complete absence of the extrahepatic biliary structure leads to cholestasis and a clinical picture of jaundice, pale stools and dark urine

Three categories

1) biliary atresia without associated anomalies
- 70-85% of infants with biliary atresia
- gradual onset of jaundice pale stools and dark urine within 2 month of birth
2) biliary atresai with laterality malformation
- 10-15% of biliary atresia
- situs invertis, asplenia, malrotation and certain cardiac and VC anomalies
3) biliary atresia associated with other malforation
- 5-10% of infants with biliary atresia
- associations include - intestinal atresia, imperforate anus, renal anomalies and certain cardiac anomalies.

Jaundice is usually the presenting feature and conjugated hyperbilirubinaemia on blood test. Usually leads to acute on chronic liver failure and transplant

59
Q

Describe biliary atresia

A

Complete absence of the extrahepatic biliary structure leads to cholestasis and a clinical picture of jaundice, pale stools and dark urine

Three categories

1) biliary atresia without associated anomalies
- 70-85% of infants with biliary atresia
- gradual onset of jaundice pale stools and dark urine within 2 month of birth
2) biliary atresai with laterality malformation
- 10-15% of biliary atresia
- situs invertis, asplenia, malrotation and certain cardiac and VC anomalies
3) biliary atresia associated with other malforation
- 5-10% of infants with biliary atresia
- associations include - intestinal atresia, imperforate anus, renal anomalies and certain cardiac anomalies.

Jaundice is usually the presenting feature and conjugated hyperbilirubinaemia on blood test. Usually leads to acute on chronic liver failure and transplant

60
Q

Discuss pathophys of hepatic encephalopathy

A

1) reduction in synthesis of substances essential for normal brain function
2) production of substances that are neurotoxic
3) reduced elimination of neurotoxins

Contributions from ammonia, inflammatory cytokines, benzodiazepine like compounds and manganese lead to neuronal dysufnction and altered interation of astrocytes with neurons.

The balance of inhibitory vs excitatory neurotransmission is altered in hepatic encephalopathy - Ammonia seems to augment inhibitory neurotransmission.

61
Q

Discuss stages of hepatic encephalopthy

A

Grade 0 - normal
Grade 1- lethargy euphoria poor consentration, reduced cognitive performance
Grade 2 - drowsiness erratic behaviour disorienation - asterixis incontience fetor hepaticus

Grade 3 - stuporous but rousable, incoherent speech, asterixis, hyperreflexia, rigidity

Grade 4 coma - no asterixis, areflexia, flaccidity
a- response to pain
b- no response to pain

62
Q

Discuss IX for liver disease

A

Bloods - FNC, LFT, glucose, coag, renal function, blood gas, serum ammonia,

Potential post discussion with hepatologist

  • viral serology
  • copper
  • caeruloplasmin level
  • alpha 1 antitrypsin
  • lactate
  • drug screen
  • urine metabolic screen

Relevent imaging

ED fellowship paeds (15 decks)

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