3. Paeds [GE and nutrition] Flashcards

1
Q

If weight / growth faltering is identified, what should be included in the dietary history?

A

History of milk feeding, including current volumes if infant.

Age at weaning.

Range and type of foods now taken.

Mealtime routines and eating and feeding behaviours.

3 day food diary.

Preterm / IUGR?
Other systemic symptoms e.g. diarrhoea, vomiting, cough, lethargy?
Development normal?

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2
Q

What features should be looked out for on examination of a child presenting with weight / growth faltering?

A

Dysmorphic features, for genetic conditions.

Koilonychia / angular stomatitis as evidence of nutritional deficiencies.

Chronic respiratory disease.

Heart murmur / signs of heart failure from congenital heart disease.

Distended abdomen, thin buttocks in malabsorption.

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3
Q

Causes of growth faltering can be split into 5 categories. What are they, and give examples.

A

Inadequate intake

Inadequate retention; vomiting due to CMPA, GORD, gastroenteritis etc.

Increased requirements; congenital heart disease, chronic infection e.g. HIV, hyperthyroidism, CF, malignancy, CKD

Malabsorption; CF, coeliac disease, CMPA, cholestatic liver disease, short gut syndrome, post NEC.

Failure to utilise nutrients; genetic disorders e.g. Down syndrome, IUGR, extreme prematurity, congenital infection, hypothyroidism, metabolic disorders.

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4
Q

Inadequate intake is a big cause of faltering growth. It can be split into environmental and pathological causes; discuss factors involved in each of these categories.

A

Environmental;
Inadequate feeding, from poor technique / insufficient milk / food etc.

Psychosocial deprivation / poor interaction / maternal mental illness

Neglect / child abuse, including factitious illness from underfeeding to generate weight faltering.

Pathological;
Impaired suck / swallow e.g. tongue tie / cleft palate, oromotor dysfunction in CP.
OR
Chronic illness leading to anorexia, e.g. Crohn’s, CKD, CF, liver disease

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5
Q

Why is it normal for babies to reflux feeds?

A

Immaturity of the LOS, allowing stomach contents to easily reflux into the oesophagus.

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6
Q

It’s normal for babies to have some reflux after larger feeds. What are some signs of more problematic reflux though?

A

Chronic cough
Hoarseness
Distress / crying / unsettled after every feed
Reluctance to feed
Pneumonia
Poor weight gain

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7
Q

Vomiting in babies is very non-specific and often has no underlying pathology. However, there are some pathological causes; give 8.

A

overfeeding
GORD
Pyloric stenosis (projectile)
Gastritis / gastroenteritis
Appendicitis
Infections
Intestinal obstruction
Bulimia

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8
Q

In cases of GORD, sometimes explanation, reassurance and practical advice is all that is needed. What advice would you give to a worried parent?

A

Small, frequent meals
Burping regularly to help milk settle
Not overfeeding
Keep baby upright after feeding i.e. not lying flat

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9
Q

You have provided adequate advice for the initial presentation of GORD. The parents represent and say that none of that advice has helped. What are 3 options you could think about now?

A

Gaviscon mixed in with feeds

Thickened milk or formula

PPI if other methods are inadequate

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10
Q

What is Sandifer’s syndrome?

A

A rare condition causing brief abnormal movements, associated with GORD in infants.
Infants are often neurologically normal.

Key features:
Torticollis; forceful contraction of neck muscles causing twisting of neck.
Dystonia; abnormal muscle contractions causing twisting movements, arhcing of back or unusual postures.

Consider referral, even though it usually resolves as reflux is treated, as the differentials include more serious conditions such as infantile spasms and seizures.

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11
Q

What is biliary atresia?

A

Congenital condition

Section of bile duct is either narrowed or absent

Results in cholestasis, where the bile cannot be transported from the liver to the bowel

Conjugated bilirubin excretion is prevented, as it is usually excreted in bile

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12
Q

When does biliary atresia present, and what are the clinical signs?

A

Shortly after birth

Significant jaundice is seen, due to high conjugated bilirubin

Persistent jaundice lasting >14 days in term babies, and >21 days in preterm

Pale stools
Dark urine
Hepatomegaly

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13
Q

There are many causes of jaundice in the neonate; give some examples, and how lab investigations are used to rule out / in biliary atresia.

A

Breast milk jaundice
Infection, esp UTI
Congenital hypothyroidism

Levels of conjugated and unconjugated bilirubin must be measured; in biliary atresia, the hyperbilirubinaemia is conjugated. In the causes above, it would be unconjugated.

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14
Q

What is the name of the procedure used to treat biliary atresia, and what does it involve?

A

Kasai portoenterostomy

A section of the small intestine is attached to the opening of the liver, where the bile duct normally attaches.
Often patients require a full liver transplant later down the line (20% by age 20).

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15
Q

What are some long term complications of biliary atresia?

A

Faltering growth
Portal hypertension
Ascending bacterial cholangitis
Ascites

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16
Q

What are the classification types of biliary atresia?

A

I; only obliteration of CBD

II; obliteration extends to the common hepatic duct

III; obliteration of entire hepato-biliary tree (most common!)

17
Q

Blood tests with conjugated Br are indicated. What other investigations are warranted and what would they show if biliary atresia was present?

A

HPB US showing absent gallbladder or irregular outline.

Radionucleotide imaging with HIDA scan; no excretion = ?biliary atresia

Liver biopsy

18
Q

Definitive of biliary atresia is via Kasai procedure, however some pharmacological interventions can be started in the interim. What are these?

A

Ursodeoxycholic acid
Vitamins A,D,E & K
Nutritional support
Antibiotics for prevention of cholangitis

19
Q

Which antibodies are implicated in coeliac disease, and how do they relate to disease activity?

A

anti-TTG
EMAs
(both are IgA - when you test for these, you must do a matched IgA level, as some patients will have IgA deficiency)

(+anti-DGPs)

They correlate with disease activity, and rise in more active disease / may disappear with effective treatment.

20
Q

Complications of untreated coeliac disease:

A

Osteoporosis / osteopenia (*all patients should be on calcium and vitamin D supplementation)
Osteomalacia
Abnormal LFTs
Hyposplenism
Dermatitis herpetiformis
NHL
Enteropathy-associated T-cell lymphoma (EATL) of the intestine
Small bowel adenocarcinoma

21
Q

Give 3 differentials for coeliac disease:

A

Crohn’s disease / UC
Malignancy e.g. GI or haematological cancers
PUD
IBS
CMPA
Non-coeliac gluten insensitivity

22
Q

What bloods are routinely checked with suspicion of coeliac disease?

A

FBC
Iron
B12
Folate
Calcium
IgA and anti-TTG
EMA if ttg is unavailable or weakly positive
Small intestine biopsy is diagnostic; crypt hyperplasia and villous atrophy

23
Q
A