Kwashiorkor, marasmus, hypo & hypervitaminoses

1. KWASHIORKOR
MARASMUS
HYPO VITAMINOSIS AND
HYPER VITAMINOSIS
1
DR.ARUNV
DEPT. OF ORALAND
MAXILLOFACIAL SURGERY

2. MALNUTRITION
A pathological state due to a relative or absolute deficiency or
excess of one or more essential nutrients; clinically manifested or
detected only by biochemical, anthropometric or physiological tests.
2

3. CLASSIFICATION
1.Undernutrition: Marasmus
2.Overnutrition: Obesity,Hypervitaminoses
3.Specific Deficiency: Kwashiorkor,Hypovitaminoses,
4.Mineral Deficiencies
5.Imbalance: Electrolyte Imbalance
3

4.  Marasmus: weight for age < 60% expected
 Kwashiorkor: weight for age < 80% + edema
 Marasmic kwashiorkor: wt/age <60% +
edema
4

5. Kwashiorkor
 CicelyWilliams – 1933
 Sickness of deposed child
5

6. Between 1-3 yrs old
Etiology:
 Very low protein intake - following abrupt
weaning.
 In places where starchy foods are main
staple
6

7. Clinical Manifestations:
A. Diagnostic Signs
1. Edema
2. Muscle wasting
3. Psychomotor changes
B. Common Signs
1. Hair changes
2. Diffuse depigmentation of skin
3. Moon face
4. Anemia
C. Occasional Signs:
1. Flaky-paint rash
2. Hepatomegaly
7

8. 8

9. Bio chemical and Laboratory findings:
1. Decreased serum albumin
2. Potassium deficiency – due to diarrhea
3. Iron & folic acid deficiencies
4. Liver biopsy - fatty changes or fibrosis may
occur
9

10.  Ketonuria , aminoaciduria ,
 Increased levels of G.H., epinephrine and
steroid .
10

11. Marasmus
 Means “to waste”
 Common in the 1st year of life
 characterized by emaciation.
 Marasmus represents the end result of
starvation where both proteins and calories
are deficient.
11

12.  Marasmus - an adaptive response to
starvation, whereas kwashiorkor
represents a maladaptive response to
starvation
 In Marasmus the body utilizes all fat stores
before using muscles
12

13. Etiology
 lack of breast feeding and the use of dilute
animal milk.
 Poverty or famine and diarrhoea
 Ignorance & poor maternal nutrition are
also contributory
13

14. Clinical Features
1. Weight for age < 60% expected
2. Wasting of muscles and s/c fats
3. Growth retardation
4. Old man’s face
5. Mental changes
6. No edema
7. Diarrhea
8. Dry atrophic skin
14

15. 15

16.  low creatinine
 Hypoglycemia
 Decreased to normal albumin
 Normal serum potassium
16

17. Complications of PEM
 Hypoglycemia
 Hypothermia
 Hypokalemia
 Hyponatremia
 Heart failure
 Dehydration & shock
 Infections (bacterial, viral & thrush)
17

18. Marasmic kwashiorkor
 State intermediate between marasmus
&kwashiorkor when a previously marasmic
child develops edema due to higher
nutritional requirement
18

19. 19

20. Treatment
 Step1:emergency phase:during 1st 24-48hr
 A.hypothermia due to less subcutaneous fat,
:gradual warming with blankets
 B.infection:emperical anti biotics
 C.hypoglycemia: should be treated
 D. dehydration : i.v fluid
 Step 2 : dietary support
 3-4 g protein & 200 Cal /kg body wt/day +
vitamins & minerals
20

21. Vitamins
 Fat soluble
 VitaminA
 Vitamin D
 Vitamin E
 Vitamin K
 Water soluble
 Non B complex –Vitamin C
 B complex
21

22. Vitamin A
 Fat soluble
 Present in foods of animal origin
 Pro vitamin beta carotene – found in plants
 Retinol
 Retinal
 Retinoic acid
 Beta carotene
22

23.  RDA : 3500 IU for men & 2500 IU for women
 Sources : Liver, Kidney, egg yolk, milk,
cheese, fish liver oil
 Yellow and dark green vegetables, carrots ,
spinach, pumpkin, mango, papaya 23

24. functions
 Vision – rhodopsin cycle orWald’s visual cycle
 Protein synthesis
 Epithelial tissue health
 Immune system function
 Carotenoids – anti oxidant
 Transferrin – iron transport protein
24

25. Hypo Vitaminosis A
 Eyes :
 Night blindness (nyctalopia)
 Xerophthalmia
 Bitot’s spots – white triangular plaques in certain
areas of conjunctiva
 Keratomalacia – destruction of cornea due to
prolonged xerophthalmia and can even lead to
blindness
25

26. Hypo Vitaminosis A
 Growth :
 Growth retardation
 Impaired skeletal formation
 Reproduction :
 Degeneration of germinal epithelium in males
 Skin and epithelium:
 Rough and dry skin
 Keratinization of epithelial cells of GIT, urinary tract
and respiratory tract(squamous metaplasia)
 Increased susceptibility to infections
26

27. 27

28. Hypervitaminosis A
 Dermatitis
 Enlargement of liver
 Skeletal decalcification
 Tenderness of long bones
 Loss of weight
 Loss of hair
 Joint pain
28

29. Vitamin D
 Anti rachitic vitamin
 Sun shine vitamin
 Calciferol
 Ergo calciferol (D2) – plant sources
 Chole calciferol (D3) –animal sources
29

30.  7 dehydrocholesterol is converted to chole
calciferol on exposure to sunlight
 hydroxylated in the kidney & the liver
to the active form 1,25
Dihydroxycholecalciferol
 Concentration of 1,25 DHCC regulated by
plasma levels of calcium and phosphate
30

31.  Milk, fatty fish and eggs
 RDA – 200 – 400 IU
31

32. Functions
Intestine:
 Increases calcium binding protein
 Phosphorus ions absorption through specific
phosphate carrier
 Alkaline phosphatase (AP) synthesis
 Muscles
 Tonicity and the normal contraction of the
muscles
32

33. Functions
 Promotes renal calcium re-absorption
 Stimulates renal phosphate absorption
 Calcium homeostasis: together with
PTH it mobilises calcium from skeletal
stores
 In the osteoblasts stimulates calcium
uptake and aids in Mineralisation of
the growth plate & osteoid
33

34.  At risk populations
 Breastfed infants
 Older adults
 People with limited sun exposure
34

35. Deficiency
 Rickets
 Osteomalacia
 Osteoporosis
35

36. Rickets
 Most common during the first year of life.
 The first signs of hypocalcaemia are CNS
changes- excitation, restlessness,
excessive sweating, tremors of the chin
and extremities.
36

37. Rickets
 Skin and muscle changes- pallor, occipital
alopecia, fragile nails and hair, muscular
hypotony, motor retardation.
 hypocalcemia and hypophosphatemia.
37

38. ACUTE SIGNS
 Craniotabes –osteolyses detected by pressing
firmly over the occipital or posterior parietal
bones,a ping-pong ball sensation will be felt.
38

39. SUBACUTE SIGNS
 frontal and temporal bossing
 False closure of sutures ,in the X-ray
craniosynostosis is absent.
 Maxilla in the form of trapezium, abnormal
dentition.
 Late dental evolution, enamel defects in
the primary and permanent dentition.
39

40. In the chest, knobby deformities results in
the rachitic rosary along the costochondral
junctions.
 The weakened ribs pulled by muscles also
produce flaring over the diaphragm, which
is known as Harrison groove.
 The sternum may be pulled into a pigeon-
chest deformity
40

41. 41

42. Sub acute signs
 Spinal column- scoliosis, kyphosis.
 Extremities- bowlegs or knock kness legs.
 Deformities of the spine, pelvis and legs
result in reduced stature, rachitic
dwarfism.
42

43.  At the ankle, palpation of the tibial
malleolus gives the impression of a
double epiphysis (Marfan sign).
 greenstick fracture of long bones
43

44. 44

45. LABORATORY DATA
Decreases
in serum calcium,
serum phosphorus,,
calcitriol, urinary
calcium.
Parathyroid hormone,
alkaline phosphatase,
urinary phosphorus
levels are elevated.
45

46. R/F
1. Osteoporosis of clavicle, costal bones,
humerus.
2. widening of the distal epyphysis,
fraying and widening of the
metaphysis, and angular deformities of
the arm and leg bones.
3. Thinning of the cortex, diaphysis and the
cranial bones
46

47. 47

48. Types of Rickets
 Nutritional
 Nutritional rickets results from
inadequate sunlight exposure or
inadequate intake of dietary vitamin D,
calcium, or phosphorus
48

49. Vitamin D dependent
 Vitamin D-dependent rickets, type I is
secondary to a defect in the gene that
codes for the production of renal 25(OH)D3-
1-alpha-hydroxylase.
 Vitamin D-dependent rickets, type II is a
rare autosomal disorder caused by
mutations in the vitamin D receptor.Type II
does not respond to vitamin D treatment;
elevated levels of circulating calcitriol
differentiate this type from type I
49

50. Vitamin D resistant
 Rickets refractory to vitamin D treatment
 Hereditary in nature
 also known as familial hypophosphatemic
rickets.
 Normal levels of calcitriol are found in this
disorder.
50

51.  1-2% of calcium chloride in milk- 4-6g/day
for the first 2 days; after that
 1-3g/day continued for1-2wk.
51

52. 1 STAGE
 VITAMIN D –2000 IU OD 30 DAYS
2 STAGE
 VITAMIN D –3500 IU OD 40 DAYS
3 STAGE
 VITAMIN D –- 5000 IU OD 45 DAYS
Then prophylactic dose – 500 IU till the end
of the second – third year of life
52

53. HYPERVITAMINOSIS D
 hypotonia, anorexia, vomiting, irritability,
constipation, polydipsia, polyuria, sleep
disorder, dehydration
Joint & muscle pains
Disorientation & coma.
renal damage and calcification
53

54. VITAMIN E
 AlphaTocopherol
 Naturally occuring anti oxidant
 Prevents oxidation of RBC
 Prevents sterility
 Increases synthesis of heme
 Helps in storage and synthesis of creatine,
nucleic acids etc
 Anti cancer vitamin- prevents free radical
formation
54

55.  Increased vitamin E intakes associated
with decreased risk of coronary heart
disease
 Vitamin E delayed or minimized cataract
development
 Increased vitamin E intakes or blood levels
associated with reduced risk of
Alzheimer’s disease
55

56.  Vegetable oils
 Almonds
 Meat
 Milk
 butter
 RDA : 10 mg per day
56

57. Hypovitaminosis E
 Neurological symptoms – impaired
coordination
 Muscle degeneration & weakness
 Increased risk for sterility
 Increased fragility of erythrocytes
 Hyper vitaminosis E - least toxic vitamin and
hence rarely causes overdose effects
57

58. Vitamin K
 German word Koagulation
 Phylloquinone: Green leafy vegetables
 Menaquinone: Intestinal bacteria
 Intestinal bacterial synthesis meets the daily
requirement of vitamin K even without dietary
supplement
 Menadione: synthetic form
 RDA – 70-120 ug/ day
58

59. Functions
 Coenzyme for the synthesis of prothrombin and
blood clotting factorsVII, IX,X in the liver
 carboxylation of glutamic acid residues on vitamin
K-dependent proteins. involved in:

1) Coagulation
2) Bone Mineralization and
3) Cell growth
59

60. Deficiency
 Uncommon.
 seen in breast fed infants – can lead to
hemorrhagic disease of new born
long-term antibiotic treatment
(loss of colonic bacteria).
60

61.  Hemorrhagic disease of the newborn
 Bruising tendency, ecchymotic patches
 Gingival bleeding, epistaxis, hematuria,
melena
 Post-traumatic bleeding / internal bleeding
 Prolonged prothrombin time
61

62.  Osteoporosis due to failed carboxylation
of osteocalcin and decreased activity of
osteoblasts
62

63. Vitamin C
 Ascorbic acid
 Not synthesized by human body
 citrus fruit and juices ( lemons, oranges,
peaches, strawberries etc)
 Also in cabbage, broccoli, cauliflower, leaf
lettuce, tomatoes, potatoes, and beans.
 90-100 mg/day
63

64.  Protects against immune system deficiencies,
cardio vascular disease, prenatal health
problems, eye disease, and skin wrinkling.
 Helps form collagen in bones, cartilage,
muscle, and blood vessels.
 Helps in wound healing
 Helps absorb iron.
64

65. Deficiency –Scurvy
Early Symptoms
 Appetite loss, weight loss, diarrhea, rapid breathing, fever,
irritability, bleeding, and feeling of numbness
Progressed Symptoms
 Bleeding of the gums, loosened teeth, petechial hemorrhage of
the skin and mucous membranes, bleeding in the eye,
65

66. Hypervitaminosis C
 Haemochromatosis
 Renal calculi
 Erosion of enamel
66

67. Vitamin B1 - Thiamine
 Anti beri-beri / anti neuritic vitamin
 Sources :
 Cereals, pulses, oil seeds
 Pork, liver, heart,kidney
 RDA : 1-1.5mg/day
 Polishing of cereals removes 80% of thiamine
67

68. Functions
 Important coenzyme in energy metabolism
 It acts as coenzyme in the production of
ribose
 TPP – transmission of nerve impulse
68

69. Deficiency
 Occurs where polished rice is the only staple
 Beriberi (I can’t I can’t)
 Weakness, nerve degeneration, irritability, poor
arm/leg coordination, peripheral neuropathy, pins
and needles sensation in legs.
 Edema, heart failure
69

70. Wet Beri Beri
 Edema of the legs, circulatory disturbances,
hypertrophic cardiomyopathy systolic
murmurs and dyspnea may develop.
 BP is elevated
 The pulse is rapid and irregular, and the neck
veins are distended
70

71. Dry Beri Beri
 Edema does not occur
 A condition consisting of paresthesia
(prickling or burning) and numbness of the
feet and cramps in the legs is present
 Muscles become progressively weak
71

72. Infantile beri beri
 Caused by inadequate thiamin in the breast
milk
 Characterized by sleeplessness, restlessness,
vomiting, convulsions, dyspnea, cyanosis and
cardiac failure
 Bouts of screaming that resemble abdominal
colic
72

73. Wernicke Korsakoff Syndrome
 Severe deficiency of thiamin in the alcoholic
individual
 Characterized by confusion, paralysis of eye
muscles, and loss of memory
 Peculiar gait and foot and wrist drop are seen
in advanced cases
73

74. Vitamin B2 (Riboflavin)
 flavin mononucleotide (FMN)
 flavin adenine dinucleotide (FAD)
 Sources :
 Milk, liver, heart, and kidney
 Cheese
 Eggs
 Leafy green vegetables
 RDA – 1.2-1.7 mg/day
74

75. Functions
 Co enzyme in Oxidation reduction reactions –
energy production
 Assist in the metabolism carbohydrates,
protein and fats
 Oxidation of most drugs (called the drug
vitamin)
75

76. Deficiency symptoms
 Gastrointestinal disease that causes vomiting
and hypermotility of the gastrointestinal tract
 Angular stomatis
 Glossitis
76

77. Niacin (Vit. B3)
 Nicotinamide adenine dinucleotide (NAD)
 And NAD-phosphate (NADP)
 can be synthesized in body (via tryptophan)
 Sources :
 Enriched grains, ready to eat cereals
 Beef, chicken, turkey, fish
 Asparagus, peanuts
 RDA – 15-20 mg/day
77

78. Deficiency
 Pellagra
 In people whose staple diet is corn
 characterized as the disease causing 4D’s
 Dermatitis
 Diarrhea
 Dementia
 Death
 Dermatitis – in sun exposed areas
 Dementia – anxiety,irritability, poor
memory, insomnia
 Glossitis and stomatitis
78

79. Over doses
 Over doses can lower LDL andTG and
increase HDL
79

80. Pantothenic acid
 Chick anti dermatitis factor
 Metabolic role as co enzyme A
 Sources :
 Egg
 Liver
 Meat
 Milk
 RDA – 5-10 mg/day
80

81. Functions
 co enzyme A – central molecule in all
metabolic pathways and integrates different
pathways
 initiates the Krebs cycle and releases ATP
 It is the starting substance for the
biosynthesis of cholesterol
81

82. Deficiency
 Rare – due to wide distributed sources
 Fatigue
 Malaise
 Burning foot syndrome - Burning, prickling
sensations (paresthesia) of the hands and
feet, cramping of the leg muscles and
impaired coordination
82

83. Pyridoxine (Vit. B6)
 Pyridoxal phosphate co enzyme
 Meat, fish, poultry
 Enriched cereals
 Potatoes,cabbage
 Milk
 RDA – 2-2.2 mg/day
83

84. Functions
 Activate enzymes needed for metabolism of
CHO, fat , protein
 Synthesize amino acid via transamination
 Synthesize neurotransmitters – serotinin,
GABA and histamine
 Synthesize hemoglobin and WBC
84

85. Deficiency
 Neurological symptoms
 Depression
 Irritability
 Convulsons
 Confusions
 Peripheral neuropathy
 Microcytic hypochromic anemia
85

86. Drug induced B6 deficiency
 Isoniazid – combines with pyridoxal
phosphate and inactivates PLP dependent
enzymes – leading to B6 deficiency –
peripheral neuropathy
86

87. Biotin
 Anti egg white injury factor
 Vitamin B7
 Rats fed with large quantity of raw egg white-
dermatits, neurological symptoms and
growth retardation – due to egg white injury
factor or avidin- reversed by biotins
87

88. Functions
 Carrier of CO2 in carboxylation reactions
 Metabolism of CHO and fat
 Synthesis of glucose, fatty acids, DNA
 Help break down certain amino acids
88

89.  liver, kidney, milk, egg yolk and yeast
 RDA – 100-300 mg
 Synthesised by intestinal flora, hence
deficiency is rare
 But can be seen in prolonged anti biotic
therapy
89

90.  Dermatitis
 Glossitis
 Loss of appetite and sleep
 Nausea
 Muscular pains
 Hyperesthesia (increased skin sensitivity
 Paresthesia (burning and prickling sensation)
 Alopecia
90

91. Folic Acid (Vit. B9)
 Active form is tetra hydrofolates
 Sources :
 Liver
 Kidney
 Dark green leafy vegetables
 Asparagus
 Brocolli
 Soybeans and nuts
 RDA – 200 ug
 Pregnancy and lactation 400 ug
91

92. Functions
 Amino acid and nucleic acid metabolism
 maturation of blood cells
 Necessary for the normal functioning of the
hematopoietic system
 Prevent anemia, some birth defects and heart
disease
92

93. Deficiency
 Most common vitamin deficiency
 Pregnant and lactating women
 Megaloblastic anemia of pregnancy
 Paresthesia
 Angular cheilosis and gingivitis
93

94. Neural tube defects
 Spina bifida
 Spinal malformation
 Paralysis
 Anencephaly
 No brain cortex
 Stillborn or die within hours
 Government requires folate enrichment of flour
and cereal
 May prevent 50% neural tube defects
94

95. Cobalamin (Vitamin B12 )
 Anti pernicious anemia vitamin
 Synthesized only by micro organisms and not by humans
 Contains the mineral cobalt
 Animal sources and no plant sources
 Curd
 Pork
 Fish
 Liver
 RDA – 3 ug/day
95

96.  Role in folate metabolism
 Maintenance of the myelin sheaths
 RBC formation
96

97. Deficiency
 Pernicious anemia – low Hb levels, decreased
number of erythrocytes and neurologiclal
manifestations
 etiology –
 Destruction of intrinsic factor needed for
absorption
 Hereditary malabsorption
 Gastrectomy
 Insufficient gastric HCl production (achlorhydria)
 Dietary deficiency as seen in pure vegetarians
97

98.  weakness, numbness and tingling in the
extremities, demyelination of nerves
 Patients may have difficulty in walking and
coordination of movements
 Patient may have a lemon-yellow complexion as a
result of jaundice caused by red cell destruction,
early graying of hair, fast heartbeat, ankle swelling
and peripheral neuritis
98

99. References
 Textbook of Pathology By Harsh Mohan – 6th
edition
 Robbins Basic Pathology – by Vinay Kumar,
Abul K. Abbas, Jon C. Aster - 9th edition
 Biochemistry By U Satyanarayana – 4th
edition
 Textbook of Biochemistry for Medical
Students By D M.VASUDEVAN – 7th edition

99

100. THANK YOU
100