Nutritional Disease
Chapter 4
Protein-energy Malnutrition
(PEM)
Definition
? PEM is a kind of malnutrition caused by
inadequate dietary intake or some diseases,
occurs commonly in children under 3 years
of age,
Kwashiorkor
Marasmus
Etiology
? The Primary PEM
Inadequate food intake
Children under 3 yrs
? The Secondary causes
Increased nutrient needs
Disorder in nutrient absorption
Increased body metabolism
Pathophysiology
? Metabolism disorder
? Protein metabolism
anabolism & catabolism ; hypoalbuminemia
? Fat metabolism
mobilized fat store,acetone body ;
metabolism acidosis; fatty liver
? Carbohydrate,low hepatin,hypoglycemia
? Fluid & electrolyte disorders
hypernatremia; edema; potassium disorder;
acid-base disturbances
Pathophysiology
? Disorders of Organ & Tissue function
? Failure to thrive
? Lower digested function,diarrhea
? Central nerve system,apathy,or irritability
? Cardiovascular system,pulse slow,Low BP
? lower renal function,urine amount decrease
? low immunologic function,easy to be infected
Clinical manifestations
? History,Feeding history
Nonedematous PEM
(marasmus)
Edematous PEM
(Kwashiorkor)
WHO Z-score
system? underweightchronic or acute malnutrition
X－ 3SD≤W/A<X － 2SD moderate
W/A<X－ 3SD severe
? stunting
long-term chronic malnutrition
X－ 3SD≤H/A<X － 2SD moderate
H/A<X－ 3SD severe
? wasting
recent acute malnutrition
X－ 3SD≤W/H<X － 2SD moderate
W/H<X－ 3SD severe
Physical measurement
Laboratory examination
? plasma albumin concentration
Normal,>35g/L; Diagnose:< 25g/L
? Serum Pre-albumin concentration
Normal,150～ 296mg/L;
Mild deficiency,100～ 150mg/L;
Moderate:50～ 100mg/L; Severe:<50mg/L
? Urine hydroxy-proling concentration
Diagnosis
? History
? Clinical manifestations
?Anthropometric indicators
? Laboratory examination
Treatment
?To treat the primary disease
?To provide adequate nutrients intakes
? To supply energy and protein
? To keep the Fluid & electrolyte balance
? To supply multi-vitamins
? To provide the accelerant for protein synthesize
? Support therapy
Prevention
? promotion the skills for breast-feeding
and the introduction of supplementary
? Food Nutrition education
? Growth monitoring
? Prevention and treatment of infectious
diseases
Childhood Obesity
Definition
?Body Mass Index (BMI) kg/m2
Overweight,BMI P85 ~ P95
Obesity,BMI > P95
?Degree of Obesity
W/H－ W/H(P50)
Degree of Obesity＝ × 100％
W/H(P50)
Overweight,10－ 19.9％
Mild Obesity,20－ 29.9％
Moderate Obesity,30－ 49.9％
Severe Obesity,50％ 以上
Prevalence
In USA,10~15%
Girls > Boys
In China,1986 0.91%; 1996 1.71 %
Girls < Boys
Etiology
? Genetic
? Genetic background
? Variation in metabolism
? Environmental stimuli
? Dietary habits
? Physical activity
? Psychological and
emotional
? Good appetite
? Low physical activity
? High Risk age,infancy,preschool age & adolescence
? Physical growth,Tall stature,slightly advanced bone
age,and somewhat early puberty
? Psychological disorders,Self-contempt,timidity,
lonely anxiety,discrimination in social life
? Laboratory examination,Plasma lipid profiles，
cholesterol↑,?－ lipoprotein↑
Clinical manifestations
Diagnosis
? Precluded other diseases
Hypothyroidism
Hypercortisolemia
? Anthropometric indicators
Weight,Height,BMI
BMI=Weight/Height2 Kg/M2
Treatment
?Good lifestyle
?Control dietary intake
?Physical exercise
?Psychological treatment
?Medications
Not approved for Children
Control energy intake
Increase energy expenditure
Food selection
肉松
香肠
猪油
植物油
腰果
花生米
瓜子
猪脚
猪大肠
鸡心
红豆
绿豆
鳕鱼
各类肉
螃蟹
吐司
馒头
油豆腐
葡萄干
鸡蛋
鲜奶
米饭
面条
番薯
黑枣
香蕉
红枣
蓝灯
猪血
脱脂奶
稀饭
马铃薯
豆腐
水果
蔬菜
Food not recommend
? Barbecue food
? Deepfry food
? Bloat food
? High sugar food
?Tin food
Prevention
? Prevent high-birth-weight babies born
? Nurture good lifestyle
Routinely exercise
Less TV watching
A well-balance diet
? Avoiding over- feeding
? Growth monitoring
Vitmain D deficiency
? Rickets
? Infantile tetany
Skin,7-dehydrocholesterol
Vitamin D3
(an inactive form)
25-hydroxy vitamin D3
Hydroxylation
In the
Liver:
Foods intake
1,25-hydroxy vitamin D3
(active form)
HydroxylationIn the kidneys:
Vitamin D Sources and Activation
Ultraviolet
Etiology
? Inadequate direct exposure to sunlight
? Inadequate vitamin D intake
? Higher requirement
? Disorder in vitamin D absorption,or
activation
? Others,genetic
Ca,P
Homeostasis
+1,25(OH)2D
+PTH
- CT
+1,25(OH)2D
- PTH
- CT
+1,25(OH)2D
Bone
Intestine
Kidneys
Parathormone
(PTH)
Calcitonin
(CT)1,25(OH)2D
Ca,P
Homeostasis
Pathogenesis
+PTH
Vitamin D deficiency
Osteoid tissue
failure to
mineralize
Osteoid tissue
accumulation
Ca absorbed from the intestine
Urine P
Parathormone secreted
Ca× P Value
Mobilized
bone Ca,P
Vitamin D-deficient
Rickets
Serum Ca concentration
Serum P
Disorder of Ca & P metabolism During Vit,D Deficiency
Serum Ca,Normal,or
Unmobilized
bone Ca,P
Serum Ca
Vitamin D-deficient
Infantile tetany
? Rare in industrialized countries
? Common in China,& developing Country
20% in South China
30-40% in North China
Epidemiology of Rickets
?General manifestations
? Irritability,Eclampsia at night,
? Sweaty,Unease sleep
? Delayed in teeth eruption &
anterior fontanel closure
Cliniacl manifestations
Bone manifestations
Chest
Beading of the ribs
Pigeon breast deformity
Harrison groove
Head
Craniotabes
Ping-Pong Ball
Caput quadratum
Limb
Thickening of the wrists
& ankles
Bow-legs,knock-knees
Pigeon breast
deformity
Biochemical changes
?Normal or low serum calcium
?Serum phosphorus level less than 4mg/dl
?Serum AKP level elevated
?Low serum 25-hydroxycholecalciferol
?Active rickets,Distal ends,cupping and
fraying of the radius and ulna
?Healing rickets,Zones of preparatory
calcificaiton (ZPC); rachitic metaphysis
calcification taken place
Radiographic findings
? Based on
? a history of inadequate intake of vitamin
D,inadequate exposure to sunlight
? Characteristic clinical signs of rickets.
? Confirmed by
Chemical and radiographic examination
Diagnosis
Differential Diagnosis
?Cretinism
?Chondrodystrophy
?Hydrocephalus
?Vitamin D-resistant Rickets
Vitamin D-resistant Rickets
? Familial Hypophosohatemia
(X-linked Hypophosphatemia)
?Vitamin D-Dependent Rickets
(Hypocalcemic Vitamin D-Resistant Rickets)
?Rickets Associated with Renal Tubular Acidosis
?Renal Rickets
Treatment
? Both natural and artificial light of the
appropriate wavelength are effective
therapeutically
?Oral adiministration of Vitamin D is
preferred,5,000-10,000IU/d
?300,000IU im; repeat one months later,if
needed.
Prevention
? Adequate exposure to ultraviolet light
? Oral administration of Vitamin D
400IU daily
Tetany of Vitamin D Deficiency
(infantile tetany)
? Accompaning rickets
? Serum ionized calcium concentration falls
below 3-4mg/dl
? Muscular irritability
? Diagnosis based on the combined presence of
rickets,low serum calcium concentration,and
symptoms of tetany
Hypervitaminosis D
? Excessive amounts of Vitamin D intake,usually develop
after 1-3 mo of excessive intake
? Anorexia,irritability,constipation,polydipsia
? Chemical examination,Hypercalcemia and
hypercalciuria
? radiographs,metastatic calcification and generalized
osteopetrosis in long bone
? Treatment,discontinuing vitamin D intake and
decreasing calcium intake
谢 谢 ！
Chapter 4
Protein-energy Malnutrition
(PEM)
Definition
? PEM is a kind of malnutrition caused by
inadequate dietary intake or some diseases,
occurs commonly in children under 3 years
of age,
Kwashiorkor
Marasmus
Etiology
? The Primary PEM
Inadequate food intake
Children under 3 yrs
? The Secondary causes
Increased nutrient needs
Disorder in nutrient absorption
Increased body metabolism
Pathophysiology
? Metabolism disorder
? Protein metabolism
anabolism & catabolism ; hypoalbuminemia
? Fat metabolism
mobilized fat store,acetone body ;
metabolism acidosis; fatty liver
? Carbohydrate,low hepatin,hypoglycemia
? Fluid & electrolyte disorders
hypernatremia; edema; potassium disorder;
acid-base disturbances
Pathophysiology
? Disorders of Organ & Tissue function
? Failure to thrive
? Lower digested function,diarrhea
? Central nerve system,apathy,or irritability
? Cardiovascular system,pulse slow,Low BP
? lower renal function,urine amount decrease
? low immunologic function,easy to be infected
Clinical manifestations
? History,Feeding history
Nonedematous PEM
(marasmus)
Edematous PEM
(Kwashiorkor)
WHO Z-score
system? underweightchronic or acute malnutrition
X－ 3SD≤W/A<X － 2SD moderate
W/A<X－ 3SD severe
? stunting
long-term chronic malnutrition
X－ 3SD≤H/A<X － 2SD moderate
H/A<X－ 3SD severe
? wasting
recent acute malnutrition
X－ 3SD≤W/H<X － 2SD moderate
W/H<X－ 3SD severe
Physical measurement
Laboratory examination
? plasma albumin concentration
Normal,>35g/L; Diagnose:< 25g/L
? Serum Pre-albumin concentration
Normal,150～ 296mg/L;
Mild deficiency,100～ 150mg/L;
Moderate:50～ 100mg/L; Severe:<50mg/L
? Urine hydroxy-proling concentration
Diagnosis
? History
? Clinical manifestations
?Anthropometric indicators
? Laboratory examination
Treatment
?To treat the primary disease
?To provide adequate nutrients intakes
? To supply energy and protein
? To keep the Fluid & electrolyte balance
? To supply multi-vitamins
? To provide the accelerant for protein synthesize
? Support therapy
Prevention
? promotion the skills for breast-feeding
and the introduction of supplementary
? Food Nutrition education
? Growth monitoring
? Prevention and treatment of infectious
diseases
Childhood Obesity
Definition
?Body Mass Index (BMI) kg/m2
Overweight,BMI P85 ~ P95
Obesity,BMI > P95
?Degree of Obesity
W/H－ W/H(P50)
Degree of Obesity＝ × 100％
W/H(P50)
Overweight,10－ 19.9％
Mild Obesity,20－ 29.9％
Moderate Obesity,30－ 49.9％
Severe Obesity,50％ 以上
Prevalence
In USA,10~15%
Girls > Boys
In China,1986 0.91%; 1996 1.71 %
Girls < Boys
Etiology
? Genetic
? Genetic background
? Variation in metabolism
? Environmental stimuli
? Dietary habits
? Physical activity
? Psychological and
emotional
? Good appetite
? Low physical activity
? High Risk age,infancy,preschool age & adolescence
? Physical growth,Tall stature,slightly advanced bone
age,and somewhat early puberty
? Psychological disorders,Self-contempt,timidity,
lonely anxiety,discrimination in social life
? Laboratory examination,Plasma lipid profiles，
cholesterol↑,?－ lipoprotein↑
Clinical manifestations
Diagnosis
? Precluded other diseases
Hypothyroidism
Hypercortisolemia
? Anthropometric indicators
Weight,Height,BMI
BMI=Weight/Height2 Kg/M2
Treatment
?Good lifestyle
?Control dietary intake
?Physical exercise
?Psychological treatment
?Medications
Not approved for Children
Control energy intake
Increase energy expenditure
Food selection
肉松
香肠
猪油
植物油
腰果
花生米
瓜子
猪脚
猪大肠
鸡心
红豆
绿豆
鳕鱼
各类肉
螃蟹
吐司
馒头
油豆腐
葡萄干
鸡蛋
鲜奶
米饭
面条
番薯
黑枣
香蕉
红枣
蓝灯
猪血
脱脂奶
稀饭
马铃薯
豆腐
水果
蔬菜
Food not recommend
? Barbecue food
? Deepfry food
? Bloat food
? High sugar food
?Tin food
Prevention
? Prevent high-birth-weight babies born
? Nurture good lifestyle
Routinely exercise
Less TV watching
A well-balance diet
? Avoiding over- feeding
? Growth monitoring
Vitmain D deficiency
? Rickets
? Infantile tetany
Skin,7-dehydrocholesterol
Vitamin D3
(an inactive form)
25-hydroxy vitamin D3
Hydroxylation
In the
Liver:
Foods intake
1,25-hydroxy vitamin D3
(active form)
HydroxylationIn the kidneys:
Vitamin D Sources and Activation
Ultraviolet
Etiology
? Inadequate direct exposure to sunlight
? Inadequate vitamin D intake
? Higher requirement
? Disorder in vitamin D absorption,or
activation
? Others,genetic
Ca,P
Homeostasis
+1,25(OH)2D
+PTH
- CT
+1,25(OH)2D
- PTH
- CT
+1,25(OH)2D
Bone
Intestine
Kidneys
Parathormone
(PTH)
Calcitonin
(CT)1,25(OH)2D
Ca,P
Homeostasis
Pathogenesis
+PTH
Vitamin D deficiency
Osteoid tissue
failure to
mineralize
Osteoid tissue
accumulation
Ca absorbed from the intestine
Urine P
Parathormone secreted
Ca× P Value
Mobilized
bone Ca,P
Vitamin D-deficient
Rickets
Serum Ca concentration
Serum P
Disorder of Ca & P metabolism During Vit,D Deficiency
Serum Ca,Normal,or
Unmobilized
bone Ca,P
Serum Ca
Vitamin D-deficient
Infantile tetany
? Rare in industrialized countries
? Common in China,& developing Country
20% in South China
30-40% in North China
Epidemiology of Rickets
?General manifestations
? Irritability,Eclampsia at night,
? Sweaty,Unease sleep
? Delayed in teeth eruption &
anterior fontanel closure
Cliniacl manifestations
Bone manifestations
Chest
Beading of the ribs
Pigeon breast deformity
Harrison groove
Head
Craniotabes
Ping-Pong Ball
Caput quadratum
Limb
Thickening of the wrists
& ankles
Bow-legs,knock-knees
Pigeon breast
deformity
Biochemical changes
?Normal or low serum calcium
?Serum phosphorus level less than 4mg/dl
?Serum AKP level elevated
?Low serum 25-hydroxycholecalciferol
?Active rickets,Distal ends,cupping and
fraying of the radius and ulna
?Healing rickets,Zones of preparatory
calcificaiton (ZPC); rachitic metaphysis
calcification taken place
Radiographic findings
? Based on
? a history of inadequate intake of vitamin
D,inadequate exposure to sunlight
? Characteristic clinical signs of rickets.
? Confirmed by
Chemical and radiographic examination
Diagnosis
Differential Diagnosis
?Cretinism
?Chondrodystrophy
?Hydrocephalus
?Vitamin D-resistant Rickets
Vitamin D-resistant Rickets
? Familial Hypophosohatemia
(X-linked Hypophosphatemia)
?Vitamin D-Dependent Rickets
(Hypocalcemic Vitamin D-Resistant Rickets)
?Rickets Associated with Renal Tubular Acidosis
?Renal Rickets
Treatment
? Both natural and artificial light of the
appropriate wavelength are effective
therapeutically
?Oral adiministration of Vitamin D is
preferred,5,000-10,000IU/d
?300,000IU im; repeat one months later,if
needed.
Prevention
? Adequate exposure to ultraviolet light
? Oral administration of Vitamin D
400IU daily
Tetany of Vitamin D Deficiency
(infantile tetany)
? Accompaning rickets
? Serum ionized calcium concentration falls
below 3-4mg/dl
? Muscular irritability
? Diagnosis based on the combined presence of
rickets,low serum calcium concentration,and
symptoms of tetany
Hypervitaminosis D
? Excessive amounts of Vitamin D intake,usually develop
after 1-3 mo of excessive intake
? Anorexia,irritability,constipation,polydipsia
? Chemical examination,Hypercalcemia and
hypercalciuria
? radiographs,metastatic calcification and generalized
osteopetrosis in long bone
? Treatment,discontinuing vitamin D intake and
decreasing calcium intake
谢 谢 ！
