What indicates the presence of weight faltering in infants?
If an infant’s weight falls across two centile spaces.
What is the final common pathway for weight faltering?
Inadequate food intake.
1/69
p.1
Weight Faltering in Children

What indicates the presence of weight faltering in infants?

If an infant’s weight falls across two centile spaces.

p.1
Weight Faltering in Children

What is the final common pathway for weight faltering?

Inadequate food intake.

p.1
Weight Faltering in Children

What is the significance of a child's weight being below the second centile?

The likelihood of weight faltering increases the further the weight is below the second centile.

p.1
Investigations for Weight Issues

What are common investigations for weight faltering?

Full blood count, serum electrolytes, liver function tests, thyroid function tests, and more.

p.1
Investigations for Weight Issues

What does a low ferritin level indicate?

Iron-deficiency anaemia.

p.1
Malnutrition Causes and Consequences

What is the impact of malnutrition on children under 5 years of age?

It is responsible for about a third of all deaths in this age group.

p.1
Malnutrition Causes and Consequences

What factors contribute to malnutrition in developed countries?

Poverty, parental neglect, or poor education.

p.1
Malnutrition Causes and Consequences

What percentage of children in specialist hospitals experience moderate/mild malnutrition?

20–40%.

p.1
Assessment of Nutritional Status

What are the components of nutritional status assessment?

Dietary intake, anthropometry, and laboratory assessments.

p.1
Weight Faltering in Children

What is weight faltering?

A description of inadequate weight gain in infants, not a diagnosis.

p.7
Nutritional Deficiencies in Developed Countries

What are some clinical features of hypocalcaemia and rickets?

Poor growth, frontal bossing, delayed closure of anterior fontanelle, bowing of weight-bearing bones, and seizures.

p.4
Management of Nutritional Disorders

What is the role of ready-to-use therapeutic food (RUTF) in managing severe acute malnutrition?

It provides a nutrient-rich diet based on peanut butter, dried skimmed milk, vitamins, and minerals.

p.6
Malnutrition Causes and Consequences

What is the primary cause of rickets during the early twentieth century?

Nutritional vitamin D deficiency due to inadequate intake or insufficient exposure to direct sunlight.

p.4
Severe Malnutrition Types: Marasmus and Kwashiorkor

What characterizes Kwashiorkor?

Severe protein-energy malnutrition with symptoms like oedema, hyperkeratosis, and skin depigmentation.

p.7
Management of Nutritional Disorders

How long does healing from rickets typically take?

2–4 weeks, but complete reversal of bony deformities may take years.

p.6
Severe Malnutrition Types: Marasmus and Kwashiorkor

What are the clinical manifestations of rickets?

Symptoms include cranio-tabes, rachitic rosary, widened wrists and ankles, Harrison’s sulcus, and bowed legs.

p.6
Assessment of Nutritional Status

What blood test results are indicative of rickets?

Low or normal serum calcium, low phosphorus, high plasma alkaline phosphatase, low 25-hydroxyvitamin D, and elevated parathyroid hormone.

p.3
Severe Malnutrition Types: Marasmus and Kwashiorkor

What defines severe acute malnutrition?

Weight for height more than 3 standard deviations below the median, MUAC less than 115 mm, or bilateral oedema.

p.1
Assessment of Nutritional Status

How can dietary assessment be conducted?

By asking parents to record the food the child eats over several days.

p.4
Management of Nutritional Disorders

What is the mortality rate for complicated severe acute malnutrition?

Up to 30%.

p.2
Enteral and Parenteral Nutrition

What is enteral nutrition used for?

When the digestive tract is functioning, as it maintains gut function and is safe.

p.2
Assessment of Nutritional Status

What does skinfold thickness of the triceps reflect?

Subcutaneous fat stores.

p.6
Severe Malnutrition Types: Marasmus and Kwashiorkor

What is the earliest sign of rickets?

A sensation similar to pressing a ping-pong ball over the occipital or posterior parietal bones (cranio-tabes).

p.3
Assessment of Nutritional Status

What is the WHO's recommended measure for assessing acute malnutrition?

Weight for height, plotted against a standard growth chart to determine z-scores.

p.7
Management of Nutritional Disorders

What is a significant risk for obese children?

They are likely to become obese adults.

p.6
Management of Nutritional Disorders

How is nutritional rickets managed?

By advising a balanced diet, correcting risk factors, and administering vitamin D3.

p.2
Malnutrition Causes and Consequences

What are the consequences of severe malnutrition?

Impaired immunity, delayed wound healing, increased operative morbidity and mortality.

p.2
Management of Nutritional Disorders

What is the role of intensive nutritional support for malnourished children?

To help them grow better when they have long-term disorders.

p.7
Assessment of Nutritional Status

What is the Body Mass Index (BMI) formula for children?

Weight in kg divided by height in meters squared.

p.4
Management of Nutritional Disorders

What are the essential steps in the acute management of severe malnutrition according to WHO?

Treat hypoglycaemia, hypothermia, dehydration, correct electrolyte imbalance, treat infection, and correct micronutrient deficiencies.

p.2
Enteral and Parenteral Nutrition

How are feeds typically administered in enteral nutrition?

Nasogastrically, by gastrostomy, or via a feeding tube in the jejunum.

p.4
Stunting in Children

What are the long-term risks associated with stunting in children?

Increased susceptibility to illness, poor academic performance, and higher risk of obesity and non-communicable diseases in adulthood.

p.3
Enteral and Parenteral Nutrition

What is the purpose of parenteral nutrition (PN)?

To provide a nutritionally complete feed via intravenous fluid, either exclusively or as an adjunct to enteral feeds.

p.5
Vitamin D Deficiency and Rickets

What can develop if Vitamin D is not supplied in adequate amounts during childhood?

Rickets and osteomalacia.

p.7
Severe Malnutrition Types: Marasmus and Kwashiorkor

What is Harrison’s sulcus?

An indentation of the softened lower ribcage at the site of attachment of the diaphragm.

p.7
Severe Malnutrition Types: Marasmus and Kwashiorkor

What are the diagnostic features of rickets?

Low serum calcium, low phosphorus, greatly increased alkaline phosphatase, low 25-hydroxyvitamin D, and elevated parathyroid hormone.

p.3
Severe Malnutrition Types: Marasmus and Kwashiorkor

What are the three classifications of severe protein-calorie malnutrition?

Marasmus, kwashiorkor, and marasmic kwashiorkor.

p.3
Severe Malnutrition Types: Marasmus and Kwashiorkor

What are some symptoms of kwashiorkor?

Generalized oedema, flaky-paint skin rash, distended abdomen, and low plasma levels of various nutrients.

p.3
Enteral and Parenteral Nutrition

What are the components of parenteral nutrition?

Glucose, fat emulsion, synthetic amino acids, electrolytes, vitamins, and trace elements.

p.4
Severe Malnutrition Types: Marasmus and Kwashiorkor

What is Marasmus?

A form of severe malnutrition in infants, often due to inability to establish breastfeeding.

p.4
Management of Nutritional Disorders

What are the signs that indicate complicated severe acute malnutrition?

No appetite, severe oedema, medical complications, or being less than 6 months old.

p.6
Assessment of Nutritional Status

What dietary history is significant in diagnosing rickets?

Prolonged breastfeeding.

p.4
Stunting in Children

What target did the World Health Assembly set for reducing stunting by 2025?

A 40% reduction in the number of stunted children.

p.6
Malnutrition Causes and Consequences

What factors increase the risk of nutritional rickets?

Living in northern latitudes, dark skin, decreased sunlight exposure, maternal vitamin D deficiency, and diets low in calcium, phosphorus, and vitamin D.

p.5
Vitamin D Deficiency and Rickets

What are the main functions of Vitamin D?

Regulation of calcium and phosphate metabolism, essential for bone health and regulation of the immune system.

p.5
Vitamin D Deficiency and Rickets

What usually causes Vitamin D deficiency?

Inadequate UVB exposure, deficient intake, or defective metabolism of Vitamin D.

p.5
Vitamin D Deficiency and Rickets

What is the most important source of Vitamin D in most countries?

Sunlight.

p.7
Management of Nutritional Disorders

What is the most common nutritional disorder affecting children in high-income countries?

Obesity.

p.2
Malnutrition Causes and Consequences

How can malnutrition affect a child's recovery from illness?

It can worsen the outcome, such as delaying weaning from mechanical ventilation due to respiratory muscle weakness.

p.7
Vitamin D Deficiency and Rickets

What dietary sources are typically supplemented with vitamin D in Europe?

Milk, dairy products, margarine, breakfast cereals, and fruit juice.

p.3
Assessment of Nutritional Status

What does MUAC stand for and how is it used?

Mid-upper-arm circumference; it uses color coding for identifying moderate and severe malnutrition.

p.4
Stunting in Children

What is the estimated number of stunted children under 5 in 2015?

About 156 million.

p.6
Malnutrition Causes and Consequences

What can cause rickets in extremely preterm infants?

Dietary deficiency of phosphorus, along with low stores of calcium and phosphorus.

p.6
Malnutrition Causes and Consequences

Which drugs can interfere with vitamin D metabolism and cause rickets?

Anticonvulsants such as phenobarbital and phenytoin.

p.5
Severe Malnutrition Types: Marasmus and Kwashiorkor

What is Marasmus characterized by?

Wasted, wizened appearance and apathy.

p.3
Severe Malnutrition Types: Marasmus and Kwashiorkor

What are the key characteristics of marasmus?

Wasted appearance without oedema; affected children are often withdrawn and apathetic.

p.2
Assessment of Nutritional Status

What is the purpose of measuring mid-upper-arm circumference (MUAC) in children?

To screen for malnutrition, especially in children aged 6 months to 5 years.

p.5
Vitamin D Deficiency and Rickets

What are the two main sources of Vitamin D?

Synthesis in the skin (Vitamin D3) following UV light exposure and dietary sources (Vitamin D2 or D3).

p.2
Investigations for Weight Issues

What can laboratory investigations detect in relation to malnutrition?

Early physiological adaptation to malnutrition, but clinical history and anthropometry are more valuable.

p.5
Severe Malnutrition Types: Marasmus and Kwashiorkor

What are the symptoms of Kwashiorkor?

Generalized edema, sparse and depigmented hair, skin rash, angular stomatitis, distended abdomen, enlarged liver, and diarrhea.

p.3
Enteral and Parenteral Nutrition

What are common reasons for needing long-term parenteral nutrition?

Short bowel syndrome, enteropathies, or motility disorders.

p.5
Vitamin D Deficiency and Rickets

What are the classical symptoms of Vitamin D deficiency?

Bony deformity and the classical picture of rickets.

p.2
Assessment of Nutritional Status

What is a key measurement in nutritional assessment?

Weight, height, mid-upper-arm circumference (MUAC), and skinfold thickness.

p.2
Malnutrition Causes and Consequences

What is a consequence of prolonged and profound malnutrition?

Permanent delay in intellectual development.

p.5
Vitamin D Deficiency and Rickets

What dietary sources are rich in Vitamin D?

Fish liver oil, fatty fish, and egg yolk.

p.3
Enteral and Parenteral Nutrition

What are potential complications of central venous catheter (CVC) use in PN?

CVC sepsis, blockage, venous thrombosis, and intestinal failure-associated liver disease.

p.5
Vitamin D Deficiency and Rickets

What happens to Vitamin D production when the sun's rays enter the atmosphere at an acute angle?

The atmosphere blocks the UVB rays, reducing Vitamin D3 production.

p.5
Vitamin D Deficiency and Rickets

What triggers the secretion of parathyroid hormone in response to low serum calcium?

Low serum calcium levels due to Vitamin D deficiency.

p.5
Vitamin D Deficiency and Rickets

How is Vitamin D metabolized in the body?

It is hydroxylated in the liver and kidney to produce 1,25-dihydroxyvitamin D, the most active form.

Study Smarter, Not Harder
Study Smarter, Not Harder