2.2 Infant & child malnutrition Flashcards

1
Q

what is the definition of malnutrition?

A

deficiency of one/several nutrients essential for healthy growth and development (technically covers obesity but not usually used this way)

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2
Q

How does severe acute malnutrition (global malnutrition/ protein-energy malnutrition / marasmus) present

A
  1. Mid-upper arm circumference (MUAC) < 11.5cm
    • MUAC changes very little between 6 months – 5 years → same cut-off is used for all
    • Accurately predicts the risk of death
  2. Low weight-for-height (wasting) → z-score ≤ 3
    • Less accurately predicts risk of death than MUAC
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3
Q

How does Kwashiorkor (protein malnutrition) present?

A

Presence of nutritional bilateral pitting oedema

• Occurs not due to low albumin/oncotic effects (body has relatively normal albumin)

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4
Q

How does chronic malnutrition present?

A

Based on low height-for-age (stunting)

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5
Q

How is severe acute malnutrition managed?

  1. Emergency management
  2. Metabolic stabilisation (done slowly)
  3. Catchup growth
    * HIV management
A

1) Emergency management
• For hypoglycaemia (oral/IV glucose infusion, glucagon)
• For hypothermia (remove thermal stimulus, gentle rewarming

  1. Metabolic stabilisation (done slowly)
    • Low protein, low energy, low osmolarity feeds with micronutrient supplementation but no iron (feeding too much too early increases risk of overloading the liver that cannot detoxify reactive metabolites)
    • Treatment of infections with routine broad-spectrum antibiotics for children with SAM (infections may be subclinical in SAM) + anti-helminthic treatment and HIV/malaria testing (depending on local epidemiology)
    • Careful management of fluid & electrolyte balance (hypokalaemia and hypernatraemia predominate → due to poor function of Na+/K+ ATPase → total body sodium is high)
  2. Catchup growth
    • High protein, high energy feeds with iron

HIV management
• Must be considered carefully as immunosuppression increases mortality) → HIV testing is important

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6
Q

The introduction of iron into the diet for children with SAM should be delayed as early introduction results in excess mortality:
• Iron must be transported in blood while complexed to ____________ as it is highly reactive, and sequestration limits microbial replication (iron is required)
• Children with SAM have ______________ albumin levels but __________ transferrin levels (which take several days to improve) → plasma transferrin correlates with overall mortality risk

A

transferrin;

relatively normal;

very low

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7
Q

What is environmental enteropathy? What are it’s driving factors?

A

Environmental enteropathy is a chronic T cell-mediated inflammatory enteropathy, which is driven by environmental factors which are not well characterised:
• Driving factors: poor sanitation, undernutrition, specific GI infections (e.g. Giardia)

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8
Q

What are the clinical features of environmental enteropathy?

A

o Histological changes (indistinguishable from other forms of IBD): intestinal villous flattening, inflammatory infiltrate, crypt hyperplasia and abscesses o Small intestinal bacterial overgrowth (SIBO)
o Decreased microbial barrier function → chronic microbial translocation
o Reduced enteric absorptive capacity → growth faltering and anaemia of chronic disease

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9
Q

There are ~100 trillion commensal microorganisms in the human body, with the largest concentration in the ________, where they perform many functions (e.g. breaking down certain carbohydrates for which humans lack metabolic activity):
• Altered microbiome may play important roles in the development of malnutrition or obesity (metabolism of fat load)
• Management of malnutrition and GI diseases involving the microbiome includes faecal transplantation and enteric vaccination

Faecal transplantation: Transplantation of faecal material (containing commensal bacteria from the donor’s GI tract) via nasogastric tube:
• Proven efficacy as a treatment for _________________
• Likely to be an established therapeutic option in future for multiple indications (e.g. IBD, IBS)
• Much more complex intervention than pro/prebiotic supplementation and with technical challenges

Enteric vaccines (e.g. Rotavirus, polio) have markedly reduced efficacy in \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_, but these are the places which require vaccines the most → reasons are unclear (likely to be a combination of all the problems highlighted so far)
• Huge potential roadblock to healthy growth and development
A

gut;

recurrent C. difficile infection;

impoverished settings

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10
Q

Vitamin A is a nutritional immunomodulator with diverse immunologic effects:
• Downregulation of monocyte production of _____________
• Promotion of _____________
• Improvement of some _______________
• Engenders gut-homing phenotype of lymphocytes

A

TNF-α and IL-6;

lymphopoiesis and Th1 function;

vaccine responses

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11
Q

What are the effects of vitamin A deficiency?

A
  • Eyes: night blindness, xerophthalmia (dryness of conjunctiva and cornea with inflammation and ridge formation)
  • Others: increased risk of infectious diseases (especially measles, pneumonia, diarrhoea)
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12
Q

What is the management of vitamin A deficiency

A

Vitamin A supplementation: associated with 24% reduction in mortality in low/middle income countries → 6-monthly vitamin A supplementation is important in preventive paediatric medicine in tropics
• Beneficial effect seems to be more pronounced in Asia than Africa
• Currently begins at 6 months → trials of neonatal supplementation (earlier than 6 months) may cause more harm (especially in girls)
• Impact on vaccination responses and potential interference is very controversial
• Supplementation in kwashiorkor increases mortality

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13
Q

What are the effects of the anemia?

A
  • Cognitive impairment: Hb mediates oxygen delivery to the brain → widely speculated that anaemia may mediate cognitive impairment
  • Iron deficiency anaemia: microcytic hypochromic anaemia
  • Malaria protection: mild anaemia (sickle cell trait) protects from malaria
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14
Q

How should iron deficiency be managed?

A
Iron supplementation (excess mortality from supplementation is limited to those who were iron replete at the point of supplementation): 
• Likely to cause black stools (unabsorbed iron), changes in bowel habits (constipation/diarrhoea

Hepcidin may be the key to safer iron supplementation → master regulator of iron metabolism produced by the liver (reduces serum iron levels) → upregulated by nutritional feedback cues and by innate immune activation (sequester iron away from pathogens)

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15
Q

What is the function of zinc?

A

Zinc is an important nutrient which has many biological and immunological functions, including facilitating many enzyme processes (able to accept electron pair) and stabilising zinc finger protein motifs (important in transcription factor structure)

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16
Q

What of the effects of zinc definition?

A
  • Strong association with diarrhoea
  • Acrodermatitis enteropathica: Due to congenital deficiency in zinc absorptive capacity:
    • Characterised by eczematous lesions around the mouth and anus and chronic diarrhoea
17
Q

How should zinc deficiency be managed?

A

Zinc supplementation is recommended (10 – 20mg daily for 10 – 14 days) for all children with diarrhoea in areas where zinc deficiency is prevalent (not in Singapore):
• Supplementation during diarrhoeal illnesses reduces severity, duration, consequences and reduces the risk of new onset diarrhoea in the following 3 months, and may have additional benefits versus treatment (e.g. on pneumonia)