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Year 4 PAEDS > Nutrition > Flashcards

Nutrition Flashcards

1
Q

What are the two forms of protein-energy malnutrition (PEM)?

A

Kwashiorkor

Marasmus

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2
Q

What is Kwashiorkor?

A

Fair-to-normal energy intake but inadequate protein

Associated with oedema and hepatomegaly

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3
Q

What is Marasmus?

A

Inadequate energy and protein intake

Associated with severe wasting

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4
Q

What is iron necessary for?

A

Haemoglobin

Myoglobin

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5
Q

What causes iron deficiency? (3)

A

1) Poor diet
2) Elevated need eg childhood
3) Parasitic infections

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6
Q

How does isolated iron deficiency manifest? (3)

A

1) Anaemia and fatigue
2) Impaired cognitive development
3) Reduced growth

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7
Q

How is iron deficiency managed?

A

1) Foods rich in iron
2) Iron-fortified weaning foods
3) Low-dose supplements

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8
Q

What is iodine necessary for?

A

Thyroid hormones

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9
Q

What causes iodine deficiency?

A

Most diets worldwide are deficient unless fortified salt or seafood are available

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10
Q

How does isolated iodine deficiency manifest? (3)

A

1) Goitre
2) Hypothyroidism
3) Growth restriction

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11
Q

How is iodine deficiency managed?

A

1) Iodine supplementation
2) Fortified salt
3) Seafood

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12
Q

What is vitamin A require for?

A

Eyes

Immune system

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13
Q

What causes vitamin A deficiency?

A

Diets poor in vegetables and animal products

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14
Q

How does isolated vitamin A deficiency manifest? (3)

A

1) Night blindness
2) Immune deficiency
3) Increased childhood illness and death

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15
Q

How is vitamin A deficiency managed?

A

1) Dark green leafy vegetables
2) Animal products
3) Fortification of oils/fats
4) Supplementation

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16
Q

What is zinc required for?

A

Many enzymes

Immune system

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17
Q

What causes zinc deficiency?

A

Diets based on refined cereals and lacking in animal products

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18
Q

How does isolated zinc deficiency manifest? (3)

A

1) Immune deficiency
2) Acrodermatitis
3) Increased childhood illness and death

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19
Q

How is zinc deficiency managed?

A

Zinc treatment for diarrhoea and malnutrition

Improved diet

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20
Q

How common is malnutrition?

A

Most important RF for illness and death

Direct cause of 300,000 deaths / year

Indirectly responsible for half all all deaths in young children, inc risk of death from:

  • Diarrhoea
  • LRTI
  • Malaria
  • Measles
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21
Q

What are some RF for malnutrition in children?

A

<5yrs - most vulnerable are premature babies and infants at time of weaning

Co-existing chronic illnesses / developmental delay

Neglect

Poverty

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22
Q

What is the WHO criteria for identifying children with severe malnutrition? (3)

A

1) Bipedal oedema
2) Visible severe wasting
3) Weight for height more than 3 standard deviations below the median

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23
Q

How does protein energy malnutrition present?

A

1) Poor weight gain
2) Slowed linear growth
3) Behavioural changes - irritability, apathy, anxiety, attention deficit

Classically apathetic and quiet when lying in their bed but cry when picked up with a typical monotonous bleat / loud groan

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24
Q

How does marasmus present?

A

1) Obvious loss of weight and muscle mass esp limb girdles, no SC fat
2) Thin, atrophic skin lies in folds
3) Pinched face that has appearance of old man / monkey
4) Alopecia and brittle hair
5) Sometimes lanugo hair

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25
Q

How does Kwashiorkor present?

A

1) Usually occurs in children 1-2 years with changing hair colour to red, grey or blonde
2) Moon face
3) Swollen abdo - pot belly
4) Hepatomegaly
5) Pitting oedema
5) Dry skin which splits where stretched over pressure areas to reveal pale areas

26
Q

What are the calorie requirements of:
0 - 1 year
1+ years

A

0-1 years: 110kcal/kg/day
1+ years: 1000 + (100x age)kcal/day

NB 150ml contains 110kcal

27
Q

How are maintenance fluids calculated?

A

1st 10kg = 100mls/kg/day
2nd 10kg = 50mls/kg/day
3rd and thereafter = 20mls/kg/day

28
Q

What conditions cause malabsorption?

A 
Severe GORD
Immunodeficiency
Chronic infection
Coeliac
IBD
Parasitic infection
29
Q

Over what % weight loss in 3 months suggests impaired nutritional status?

A

> 10% in 3 months

30
Q

What can be assessed to monitor malnutrition and weight?

A

Serial height and weight:
- Falling across 2 centile lines or below 3rd centile implies impairment

<90% expected weight for height

BMI

Mid-arm circumference divided by hand circumference

Serum albumin

31
Q

What is refeeding syndrome?

A

In starvation the secretion of insulin is decreased in response to a reduced intake of carbohydrates. Instead fat and protein stores are catabolised to produce energy. This results in an intracellular loss of electrolytes, in particular phosphate. Malnourished patients’ intracellular phosphate stores can be depleted despite normal serum phosphate concentrations. When they start to feed a sudden shift from fat to carbohydrate metabolism occurs and secretion of insulin increases. This stimulates cellular uptake of phosphate, which can lead to profound hypophosphataemia

This phenomenon usually occurs within four days of starting to feed again. It can lead to arrhythmias and death

32
Q

Is malnutrition in the first year of life concerning?

A

Yes malnutrition in the first year of life is associated with permanent mental handicap even if subsequently corrected

33
Q

How does severe vit D deficiency manifest in:

1) Adults
2) Children

A

1) Adults = osteomalacia

2) Children = rickets

34
Q

What is the pathophysiology of rickets?

A

Caused by inadequate mineralisation of bone matrix

Vit D deficiency causes low calcium and phosphate, which lead to secondary hyperparathyroidism

Osteomalacia = loss of skeletal mass caused by inadequate mineralisation of the normal osteoid tissue after closure of the growth plates

Rickets = same process which occurs before the growth plates have closed

35
Q

List some clinical signs of hypocalcaeamia

A

Increased neuromuscular excitability:

  • Muscle spasms
  • Tetany
  • Cardiac dysfunction
36
Q

List some clinical signs of hypercalcaemia

A

Leads to diffuse precipitation of calcium phosphate in tissues, leading to widespread organ dysfunction and damage

Bones, stones, groans and moans

Bones = painful bone condition eg osteitis fibrous crystica

Groans = GI symptoms such as n&v, constipation, indigestion

Moans = NS groans such as lethargy, fatigue, memory loss, psychosis, depression

37
Q

What are the 3 stores of calcium in the body

A

Intracellular
Extracellular and blood
Bone

38
Q

Where is dietary calcium absorbed?

A

Small intestine

39
Q

What is the role of parathyroid hormone?

A

To increase blood concentrations of calcium

40
Q

How does parathyroid hormone increase blood levels of calcium?

A

1) Stimulates production of biologically-active vit D within kidney

2) Facilitates mobilisation of calcium and phosphate from bone
- To prevent detrimental increases in phosphate, PTH also has potent effect on kidney to eliminate phosphate

3) Maximises tubular reabsorption of calcium within the kidney

41
Q

What is the role of vit D?

A

Also acts to increase blood levels of calcium

Most important effect is to facilitate absorption of calcium from small intestine

Also enhances flexes od calcium out of bone

42
Q

What is calcitonin?

A

A hormone that functions to reduce blood calcium levels

Secreted in response to hypercalcaemia

43
Q

How does calcitonin work?

A

Suppresses renal tubular reabsorption of calcium (enhances excretion of calcium into urine)

Inhibits bone resorption, which minimises fluxes of calcium from bone into blood

44
Q

How is vitamin D supplied to the body?

A

1) Sunlight (90%) - skin exposure of ultraviolet light
- Vit D3 derived from hydroxylation of vit D in liver and kidneys

2) Dietary intake eg oily fish, liver, egg yolks, fortified foods

45
Q

What are some causes of vit D deficiency?

A

Most commonly due to insufficient exposure to sunlight and nutritional deficiency

Other causes include:

  • GI malabsorption eg CF, biliary disease such as biliary atresia or PBC, IBD
  • Renal disease
  • Drug causes

NB severe calcium deficiency can cause rickets despite adequate vit D

46
Q

What drugs may cause vit D deficiency?

A

Anticonvulsants - phenytoin, carbamazepine, phenobarbital

Rifampicin
HAART
Colestyramine
Cadmium

47
Q

What are some risk factors for vit D deficiency? (5)

A

1) Routine covering of face / body
2) Infant who is exclusively breastfed, esp beyond 6 months of age
3) Poverty
4) High latitude countries
5) FH

48
Q

How may vit D deficiency present? (7)

A

1) Hypocalcaemia seizures or tetany, esp in neonatal period and during periods of rapid growth in adolescence
2) Rickets: bony deformity (from 6 months)
3) Irritability, reluctance to weight bear
4) Impaired growth
5) Increased susceptibility to infections and respiratory symptoms from ‘rachitic lung’ = reduced lung expansion and muscle weakness
6) Pectus carinatum
7) Severely = cardiomyopathy and potentially fatal HF

49
Q

What bony abnormalities are found in rickets?

A
  • Genu varum (bowing) is typical, but genu valgum (knock kneed) can also occur
  • Anterior bowing of femur and internal rotation of the ankle frequently
  • Softening of skull (carniotabes) and frontal bossing in the first few months of life, delayed closure of fontanelles
  • Tender swollen joints
  • Enlargement of ends of ribs (‘rachitic rosary’) due to expansion of costochondral junction in 3-6 month child
  • Delayed walk or waddling gait
  • Impaired growth
  • Fractures if severe
  • Dental deformities = delayed formation of teeth, enamel hypoplasia and dental caries

Child miserable due to bone and joint pain

50
Q

Ddx of rickets (4)

A

Hyper PTH
Osteitis fibrosa
Paget’s disease of bone
Myeloma

51
Q

What investigations are done for rickets?

A

Blood biochem: renal function, electrolytes, LFTS inc alk phos, PTH,
- Secondary hyperPTH classic

Vit D levels

Wrist x-ray required to diagnose rickets

Investigate underlying cause eg CF / coeliac

52
Q

What definitively shows rickets on a radiograph?

A

Radiography of a long bone which shows:

  • Cupping
  • Splaying
  • Fraying of metaphysis

Eg champagne glass wrist

53
Q

How are vit D levels measured?

A

Assay of serum 25-hydroxyvitamin D (25-OHD)

Symptomatic is less than 25nmol/L (10 micograms/L)

54
Q

How is vit D deficiency managed?

A

Diet
Inc exposure to sunlight
Vit D supplementation:
- PO calciferol either as ergocalciferol or colecalciferol

Children <6months: 3,000 IU calciferol daily

> 6 months: Inc to 6,000 IU calciferol daily

12-18 years: 10,000 IU

Calcium supplementation during first few weeks of therapy for growing child

Maintenance of 400 IU for child of any age

55
Q

What are the two different types of rickets?

A

1) Vitamin D dependent rickets type 1

2) Vitamin D dependent rickets type 2

56
Q

What is vitamin D dependent rickets type 1?

A

Autosomal recessive condition

Enzyme deficiency of enzyme needed to convert vit D to active form

57
Q

When does vitamin D dependent rickets type 1 usually present?

A

Within first 24 months of life

58
Q

How is vitamin D dependent rickets type 1 treated?

A

Required replacement dose of 1,25 dihydroxyvitamins-D3 = calcitrol

59
Q

What is vitamin D dependent rickets type 2?

A

Autosomal recessive condition

Due to mutations in vit D receptor gene

Leads to end-organ resistance to vit D

60
Q

When does vitamin D dependent rickets type 2 usually present?

A

Present at birth or during 1st year of life

Sparse body hair development or total alopesia

61
Q

How is vitamin D dependent rickets type 1 treated?

A

Supraphysiological doses of calcitriol

62
Q

What are the two main forms of vit D?

A

Vit D3 - synthesised in the skin by the action of sunlight

Vit D3 and D2 - obtained from food

Year 4 PAEDS (23 decks)

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