Clinical assessment

1. Clinical
Assessment
Md . Sajib Reza
Lecturer
Department of Food technology and Nutritional Science
Mawlana Bhashani Science and Technology university
Tangail-1902, Bangladesh
Email: sajib.ftns2010@gmail.Com

2. Clinical assessment … …
“Clinical examination consists of a routine medical history and a physical
examination to detect physical signs (observation made by a qualified examiner)
and symptoms (manifestations reported by the patients) associated with
malnutrition”
• Medical history and Physical examination are the clinical methods
• Used to detect signs (i.e., observations made by a qualified examiner) and
symptoms (i.e., manifestations reported by the patient) associated with
malnutrition
• Normally used in community nutrition surveys.
• Signs and symptoms are often nonspecific
• Only develop during the advanced stages of nutritional depletion, when diseases
are present.
• Diagnosis should not rely exclusively on clinical methods
• Laboratory methods should also be included as an adjunct to clinical assessment

3. Some Common Clinical Signs …. ….
• Hair: Lack of lusture, thinness & sparseness, straightness, dyspigmentation, flag
sign, can be easily plucked due to PEM.
• Face: Diffuse depigmentation, moon face and old man face due to PEM.
• Eyes: Conjuctival xerosis, corneal xerosis, bitot’s spot, corneal scars due to
vitamin-A deficiency. Pallor of eyes due to iron deficiency.
• Lips: Angular stomatitis, angular scars, cheiliosis due to riboflavin deficiency.
• Tongue: Raw or scarlet tongue, edema of tongue, fissures due to niacin deficiency.
Patchy glossitis, magenta tongue due to riboflavin deficiency.
• Neck: Different stages of goiter due to iodine deficiency.
• Skin: Follicular hyperkeratosis, perifollicular hemorrhage, pretichial hemorrhage
due to vitamin C & other vitamins. flaky paint dermatosis due to PEM.
• Teeth: Gray or black spots (fluorosis), dental caries.
• Nails: Spoon-shape (koilonychia), brittle.

4. Difference between healthy child and
malnourished child: … … Sajib Reza

5. Protein Energy Malnutrition (PEM) ….
….
• PEM: “Protein energy malnutrition is a form of malnutrition describes as a range of
clinico-pathlogical condition arising from co-incidental lack of protein and calories, in
varying proportions occurring mostly in infant and young children, and commonly
associated with infection”. (WHO-1973)
• It is the leading cause of death in children in developing countries.
• Types of PEM:
* KWASHIORKOR:
Mainly due to lack of protein intake
* MARASMUS:
Mainly due to lack of primarily calorie/energy intake and secondarily protein intake.
* MARASMIC KWASHIORKOR:
• Children have both features of kwashiorkor and marasmus.

6. Causes … …

7. KWASHIORKOR … … …. ….
• Mainly protein deficiency
• Serious forms of PEM
• It effects children more than one year.
• But it may occur at any age.
• Mainly characterized by edema and moon face.
CAUSES:
1. Early weaning with low protein diet (mainly carbohydrate, starchy diet no protein, milk)
2. Repeated infections. E.g. communicable disease like diarrhea.
3. Ineffective weaning
Sajib Reza

8. Clinical features of Kwashiorkor …. ….
Kwashiorkor is relatively easy to diagnose based on the child’s history, the symptoms
reported and the clinical signs observed
1. Edema
2. Moon face
3. Skin changes / flaky paint dermatitis
4. Hair changes
5. Fatty infiltration in liver
6. Diarrhea
7. Poor growth
8. Wasting
9. Anemia
10. Apathetic / lethargic

9. Examples of kwashiorkor …. ….

10. 1. Edema …. ….
• Accumulation of fluid causes swelling
• Starts with a light swelling in the feet and spread up to
the legs.
• Later hands and face also swell.
Detection procedure:
• Pressing the skin with fingers.
• A depression can be seen at the place where pressure is
applied.

11. 2. Moon face…. ….
• Puffy or swollen face because of accumulation of
fluid/edema or fatty tissue.
• Appears round like so called moon face.
Sajib Reza

12. 3. Flaky paint dermatosis / skin change …. ….
• Characterized by extensive flaking and pigmentation mostly in
sun unexpected areas.
• The skin becomes thick and varnished.
• It gets peeled off.
• The skin lesion first occur in areas subject to friction or
pressure. eg The groin, behind the kness, on the buttocks, and
at the elbows.
• Darkly pigmented patches form and these may peel rather like
sun baked blistered paint.
• This has leading to the term peeling paint or flaky paint
dermatosis.

13. 4. Hair change …. ….
• Hair of normal asian child is dark, black, coarse in
texture and reflects light.
• In kwashiorkor hair become –
- thin
- lack of luster
- dull and lifeless
- Easily pluckable without pain
- Change to raddish color

14. 5. Fatty infiltration in liver …. ….
• Liver becomes enlarged (hepatomegaly)
• Fatty liver has yellow greasy appearance
and is often enlarged and swollen with fat.
• Fatty liver occurs when excess fat
accumulates inside liver cell.
• The healthy liver replaced with fatty tissue.
• Cause: the liver burns fat less efficiently
resulting the liver to enlarged.

15. 6. Diarrhea …. ….
• Stools are frequently loose.
• Contain undigested particle of food.
• Have offensive smell
• Have watery and tinged with blood
7. Poor growth … …..
• A child loses weight and fails to grow.
• Loss in weight is less severe than in
marasmus.
• Weight loss and growth failure can not
marked due to edema.

16. 8. Wasting …. ….
• Muscle wasting is present but not be evident
because of edema.
• Childs arm and legs are thin because of muscle
wasting.

17. Marasmus …. ….
• Mainly primarily calorie / energy deficiency and secondarily protein deficiency
• It effects children less than one year. (up to about three and a half years)
• Mainly characterized by muscle wasting/ emaciated (skin & bone) and monkey face / simian.
CAUSES:
1. Early weaning with very low calorie diet (rice water, jaggary, dilute milk)
2. Deficiency in one of food in general – energy rich
3. A form of starvation
4. Repeated infections and parasitic diseases of childhood. eg. communicable disease like diarrhea,
measles, whooping cough, malaria, tuberculosis etc
5. common causes are premature birth, and digestive upsets such as malabsorption or vomiting
6. Ineffective weaning
7. Child does not get adequate supplies of breast milk or of any alternative food.
8. A very common cause is early cessation of breastfeeding.
Sajib Reza

18. Clinical features of marasmus …. ….
1. Wasting
2. Appetite
3. Poor growth
4. Alertness/irritable
5. Diarrhea
6. Anemia
7. Skin sores/wrinkles
8. Hair changes

19. Example of marasmus …. ….

20. 1. Muscle Wasting …. ….
• The loss of flesh is obvious. so skin becomes wrinkled
• The belly is contrast to the rest of the body
• Looks highly emaciated with all skin & bone appearance sunken eyes, prominent ribs.
• Hence it is called wasting disease.
• The face has a characteristics simian (monkey like) appearance.

21. 2. Appetite …. ….
• The child has a good/increased appetite.
• Children violently suck their hands or clothing or noises.

22. 3. Alertness/ irritable … … …
• Child becomes irritable.
• The child cries continuously due to extremely weakness.

23. 4. Poor growth … …
* In all cases the Childs fails to grow properly due to protein and energy deficiency.
* Weight will be found to be extremely low by normal due to loss of muscle.

24. 5. Diarrhea … …
• A marasmus child has frequent watery stools.
• Child gets dehydrated.
6. Skin sores/wrinkles … ….
• There is no flaky pain dermatosis.
• Skin are wrinkled.
• There may be pressure sores over bony prominence.

25. 7. Hair change … …
• Hair are normal in child of marasmus.
• Marked change in texture than of color.

26. Marasmic kwashiorkor … …
• Children with features of both nutritional
marasmus and kwashiorkor are diagnosed
as having marasmic kwashiorkor.
• Found to have both oedema and a weight
for age below 60 percent of child’s age.
• Features of nutritional marasmus
including - severe wasting, lack of
subcutaneous fat and poor growth, and in
addition to oedema, which is always
present.
• Features of kwashiorkor - flaky-paint
dermatosis, hair changes, mental changes
and hepatomegaly

27. Continue … …

28. Difference between kwashiorkor & marasmus … …
…
Sajib Reza

29. Continue … …

30. Xerophthalmia
Vitamin - deficiency
Sajib Reza

31. Anatomy
of eye

32. Anatomy
of eye

33. Vitamin A
• Pre-formed vitamin A / Biologically active vitamers: Retinol/ Retinal/ Retinoic acid ►
Found only in animals
(human milk, liver, especially fish liver oil such as cod, shark, mackerel, egg yolk, milk and dairy product
such as butter, ghee, cheese, curd, fortify processed foods include sugar, fats, oils, condiments)
• Occurs as retinylesters of fatty acids in membrane bound cellular lipid and fat-containing
storage cells.
---------------------------------------------------------------------------------------------------
• Pro-vitamin A: Carotenoids (α-carotene, β-carotene, xanthophyl, lycopene, chlorophyll)
► Found only in plants
(dark green leafy vegetables like spinach, amaranth; yellow and red fruits and vegetables like pumpkins,
carrots, tomatoes, squash, drumstick, peaches, papaya, mangoes, apricots, jackfruit, banana, oranges)
• Occurs in cellular lipids, embedded in chloroplasts or the pigment containing portion of
chromoplast.

34. Nomenclature … ….
Provitamin A : β-Carotene
Vitamin A1 : Retinol ( Vitamin A alcohol)
Vitamin A2 : 3 –Dehydro-retinol
Vitamin A aldehyde : Retinal
Vitamin A acid : Retinoic acid
Vitamin A ester : Retinyl ester
Neo vitamin A : Stereoisomer of Vitamin A1, has
70 –80% of biological activity of Vitamin A1.
Sajib Reza

35. Vitamin A absorption, transport and storage.
☻Pro-vitamin A, carotenoids are converted to retinol by a cleavage enzyme in the intestinal mucosa.
☻Absorption of retinol and β-carotene by mucosal cells.
☻Retinol is re-esterified with fatty acids and unconverted carotenoids incorporated into chylomicrons in the
intestine.
☻ Chylomicrons enter into the blood.
☻ All retinylesters are present in the chylomicrone are taken by the liver and stored as retinyl palmitate.
☻ Retinylesters are broken down and re-synthesized in the liver.
☻ Free retrinol bound to retinol binding protein (RBP).
☻ The retinol is bound to cellular retinol binding protein (CRBP) by RBP.
☻More than 90% of body supply of vitamin A is stored in liver cells and secretes vitamin A in the form of
retinol, which is bound to retinol-binding protein.
Hydrolysis in intestine
Pancreatic esterase
Retinylesters of diet
Presence of bile salt
Retinol + Free fatty
acids

36. Storage of Vitamin A … …
• Liver (in stellate cell) has an enormous capacity for storing Vitamin A in the
form of retinol palmitate.
• Under normal conditions, a well fed person has sufficient Vitamin A reserves to
meet his needs for 6-9 months or more
• Free retinol is Highly active but toxic, so it is transported in the blood stream by
combining with retinol binding protein (RBP) (produced in the liver)
• So, in severe protein deficiency, production of retinol binding protein prevents
mobilization of liver retinol reserves.
Sajib Reza

37. Functions of Vitamin A … …
 For normal vision in dim light.
 Maintaining the integrity and normal functioning of glandular and epithelial tissues
which lines intestinal, respiratory and tracts as well as skin and eyes.
 Supports growth (skeletal growth)
 Retinol and retinoic acid function as steroid hormones. They regulate the protein synthesis
thus involved in cell growth and differentiation.
 Synthesis of certain glycoproteins.
 Essential for the maintenance of
proper immune system
 Carotenoids function as antioxidants and reduce the risk of cancers. May protect against
some epithelial cancers.

38. Role of vitamin A in vision
• Retinal helps in dim and bright light visions.
• Rods for: Normal vision (Black & ) + vision in
(present in retina)
• Cones for: Colour vision + visual acuity (present in retina)
• Rod contain rhodopsin (made up of 11-cis retinal + opsin)

39. Role of vitamin A in vision
:Normal vision/dim light vision:
• When light strikes 11-cis retinal opsin convert to All trans
retinal.
• At the same time opsin is dissociates.
• The conversion of rhodopsin to opsin and all trans retinal occurs
through many intermediates reaction.
• 1st stage: a light signal is converted into atomic motion.
• 2nd stage: this atomic motion is converted into nerve impulse.
• 3rd stage: this impulse is transmitted by the optic nurve to the
brain.
• This is followed by Dissociation of all trans retinal from opsin.
• Immediately isomerized by retinal isomerase to 11-cis retinal.
• This 11 cis retinal combines with opsin to regenerate rhodopsin
to complete visual cycle.

40. Role of vitamin A in vision
:::::::::::::COLUOR vision: ::::::::::::
■ Cone cells contain 3 different reninal which produce color
vision
- Porphyropsin ▬►Red
- Iodopsin ▬► Blue
- Cyanopsin ▬► Green
■ When light strikes the retina, it bleaches one or more
pigments depending on the color quality of the light.
■ These pigments are converted/splits to all trans retinal and
opsin.
■ Red if porphyropsin is split, green if iodopsin is split, blue
if cyanopsin is split.
■ If mixtures of the three are converted the color read out on
the proportion of the three splits.

41. Causes of xerophthalmia … …
PRIMARY CAUSES OF DEFICIENCY – Vitamin A deficiency
SECONDARY CAUSES OF DEFICIENCY:
• PEM
• Infections
• Measles virus commonly affects the eyes.
• Fat malabsorption.
• Liver disorders effects storage of Vitamin A.
• Failure to synthesize chylomicrons and RBP.
• Xerophthalmia arises when the diet contains practically no whole milk and dairy product such
as butter, cheese, curd etc.
• Diet contains very limited amounts of fresh fruits and vegetables.
• Xerophthalmia and keratomalacia both occur in the first year of life amongst artificially fed
infants.
Sajib Reza

42. Classification of Xerophthalmia (WHO
classification)…
► XN, XIA, XIB, X2 can usually heal back to normal with good treatment.
► In stage X2 is an emergency that must be treated immediately because in a few days could turn into X3.
► X3B X3A and if untreated can heal but by leaving defects that can even lead to total blindness if the lesion
(abnormality) of the cornea is extensive enough to cover the entire cornea (cornea optical zone).

43. XN - NIGHT BLINDNESS … …
• First evidence and symptom of vitamin A deficiency.
• It is not a disease itself but a symptom of several eye diseases.
• Lack of Vitamin A first causes Night blindness or nyctalopia
• It is the inability to see in dim light especially in late evening.
• It occurs due to impairment in dark adaptation.
• The condition may get worse if Vitamin A is not taken,
especially if they suffer from diarrhoea and other infections.
Rods contain a receptor-protein called rhodopsin. When light falls on rhodopsin, it undergoes a
series of conformational changes ultimately generating electrical signals which are carried to the
brain via the optic nerve. In the absence of light, rhodopsin is regenerated. The body synthesizes
rhodopsin from vitamin A, which is why a deficiency in vitamin A causes poor night vision.

44. X1A - CONJUNCTIVAL XEROSIS ... ...
• It is the first sign of Vitamin A deficiency.
• The conjuctiva becomes dry and non-wettable.
• It appears muddy, thickened, pigmented and wrinkled
(instead of clear, smooth and shiny)
• The pigmentation gives the conjunctiva a “smoky”
appearance.
• Caused by deficiency of tears or conjunctival secretions.
• These reflects a past deficiency of vitamin A.

45. X1A - CONJUNCTIVAL XEROSIS continue ... ...

46. X1B - BITOT’S SPOTS ... ...
• They are triangular shape, greyish white or yellowish, foamy spots or plaque on
the bulbar conjuctiva on either side of the cornea.
• Look like a fine foam with many tiny bubbles.
• Due to its increased thickness.
• Usually bilateral
• In young children, it indicates Vitamin A deficiency.
Sajib Reza

47. X1B - BITOT’S SPOTS CONTINUE ... ...

48. X2 - CORNEAL XEROSIS ...
• The cornea appears dull, dry and non-wettable and eventually
opaque.
• First appears hazy & then granular.
• This stage is very serious.
• In more severe deficiency, there maybe corneal ulceration
• The ulcer may heal leaving a corneal scar which may affect vision.
Cause: This is because glands in the conjunctiva no longer function
normally.
• This leads to loss of tears and also loss of mucous, which acts as a
‘wetting agent’.
• The lack of mucous together with lack of tears not only leads to
the dry appearance but also increases the risk of infection.
Concequences: The drying is followed by a softening/melting of the
cornea with ulceration and areas of necrosis.

49. X3A – Corneal Ulceration … …
• It is the liquefaction of the cornea. This is an medical
emergency.
• The cornea (a part or the whole) may become hazy, soft and
may burst open.
• Corneal ulcer are usually circular and punched out in
appearance.
• Rapid necrosis, corneal melting/softening, perforation,
prolapsed of intracellular contents.
• Red or look surprisingly white, swollen,
• Epithelial defects in periphery of cornea.
• This process is rapid and if the eye collapses, vision is lose.

50. X3B – Corneal Ulceration/Keratomalacia … …
• The most severe form of xerophthalmia is keratomalacia in
which more than one-third of the cornea is affected.
• The whole of the cornea may become soft and melt.
• Melting and clouding of the cornea (the clear layer in front
of the iris and pupil)
• Ulceration may lead to – perforation of the cornea, prolapsed
of the iris, loss of ocular contents.
• Destruction, inflammation, lesion, abrasion, injury of the eye
content and iris, a condition called KERATOMALACIA.
• The cornea may become edematous and thickened, and then
melt away.
• Ulcers may extend to centrally.
• This occurs because the structure of the collagen in the
cornea is affected by a process known as necrosis.

51. Difference btween X3A & X3B … …
Sajib Reza

52. XS - Corneal Scar
• The end result of corneal ulceration and
keratomalacia is corneal scarring.
• Result: ►Forward bulging of a badly damaged
cornea
► An eye that has shriveled up.
• Depending on the degree of scarring, Scar tissue
may develop vision problems such as
to total blindness.
• Cause: This is because the corneal scar may
, s c a t t e r or block light from refracting
onto the lens and retina properly.

53. XF - XEROPTHALMIA Fundus … …
• The retina has white dots around the periphery of the
fundus.
• Characterized by typical
► seed like
► raised,
► whitish/yellow
► scattered uniformly over the part of the fundus
► at the level of optic disks.
• Pale yellow spots near the course of the retinal vessels and in
the retinal periphery.

54. Iodine Deficiency Disorder
Sajib Reza

55. The Thyroid gland … …
• The thyroid is a small, butterfly- shaped gland inside the neck,
just below the Adam’s apple.
• The thyroid gland produces two hormones that are secreted into
the blood which control the body’s metabolism.

56. The Hypothalamic-Pituitary-Thyroid Axis … …
• In response to thyroid realeasing hormone (TRH) secretion by the hypothalamous, the pituitary gland secretes Thyroid Stimulation
Hormone (TSH). TSH stimulates iodine trapping and thyroid hormone synthesis by the thyroid glsnd snd the release of T3
(Triiodothyronine) and T4 (thyroxine) into the circulation.
• When dietary iodine is sufficient, the presence of adequate serum T4 and T3 concentrations feeds back at the level of both the
hypothalamous and pituitary gland, decreasing TRH and TSH production.
• When circulating T4 concentrations decrease, the pituitary gland increases its secretion of TSH, stimulating iodine trapping and
production and release of both T3 and T4. In the case of iodine deficiency persistently elevated TSH levels may lead to hypertrophy of
the thyroid gland, also known as goiter.

57. Iodine … …
 Iodine is essential for human health as it is a constituent of thyroid hormones, which play an
important role in physical and mental development.
 Iodine is one of the leading causes of preventable mental retardation and brain damage in the
world. Iodine deficiency not only leads to goiter and cretinism but also to a much broad spectrum
of disorders
 The Iodine deficiency has an immediate effect on child learning capacity, women's health, the
qualities of life in communities and economic productivity.
 Normal requirement : 150 μg per person per day.
 Total quantity present in body is (15-20 mg) mostly in thyroid gland
 However, very low iodine intakes can reduce ↓ thyroid hormone production with ↑ elevate TSH
levels.
 If iodine intake falls below approximately 10–20 mcg/day, hypothyroidism occurs.
 Goiter is the earliest clinical sign of iodine deficiency.
• Thyroxine: Contain four atoms of iodine + Tyrosine.
• Triiodothyronine: Contain three atoms of iodine + Tyrosine.
• In body cells and tissues the T4 is converted to T3
• Plasma iodine: 4 – 10 mg/dl.
• RDA: 150 - 200 µg/day
• The total body contains about 20 mg of iodine.
• 80% is present in the thyroid gland. In the organic form as iodothyroglobulin.
Sajib Reza

58. Definition of IDD... ...
• Iodine Deficiency Disorders refer to a BROAD SPECTRUM of health
consequences resulting from inadequate intake of iodine. The adverse
consequences of iodine deficiency lead to a wide spectrum of problems ranging
from abortion and still birth to mental and physical retardation and deafness,
which collectively known as Iodine Deficiency Disorders (IDDs)
• TWO MAIN DEFICIENCY DISORDER OF IODINE ARE -

59. Causes/Risk factors … …
Following is a list of potential risk factors that may lead to iodine deficiency:
• Low dietary iodine
• Iron and selenium deficiency (iron, selenium are contained in proteins that are important for synthesis of thyroid
hormones, for example peroxidases)
• Pregnancy
• Exposure radiation
• Increased intake of goitrogens (calcium, lithium), such as some drugs and antibiotics (substances that interfere with
iodine uptake in the thyroid gland) (cassava, lima beans, maize, bamboo shoots, and sweet potatoes)
• Gender (higher occurrence in women)
• Oral contraceptives
• High consumption of conserved, pickled foods that contain thyrostatics
• Smoking tobacco (Thyocyanate)
• Age (for different types of iodine deficiency at different ages)

60. Consequences … …
Most important consequences of the spectrum of IDD are:
• Goiter
• Mental retardation (Fetal stage up to 3rd month of birth)
• Hypothyroidism
• Cretinism
• Increased morbidity and mortality of infants and neonates

61. Complaints/Consequences of Iodine Deficiency
Fetus/Neonates:
• Cretinism (commonly characterised by mental
deficiency, deafness, squint, disorders of stance
and gait, stunted growth and hypothyroidism)
• Increased prenatal and infantile mortality
• Increased risk of deaf-mutism
• Retarded bone growth
Children
• Goiter
• Physical development delays
• Mental development delays
• Impaired sense of hearing and problems with
speech
• Paralysis of limbs
Pregnant women and women of child bearing
age
• Congenital anomalies
• Reduced fertility
• Irregular menstrual cycle
• Increased incidence of spontaneous abortions
• Still birth
Adults
• Goiter
• Reduced IQ (about 10-15 points)
• Risk of compression of the upper airways
• Increased risk of thyroid cancer
• Hypothyroidism
• Constipation
• Dry, flaky skin
• Generally inactive and sleepy
• Cold intolerance
Sajib Reza

62. Broad Spectrum of disease ... ...
Table 1. The Spectrum of Iodine Deficiency Disorders, IDD.
Fetus Abortions Stillbirths
Congenital anomalies
Increased perinatal mortality
Endemic cretinism
Neonate Neonatal goiter Neonatal hypothyroidism
Endemic mental retardation
Increased susceptibility of the thyroid gland
to nuclear radiation
Child and Goiter adolescent (Subclinical) hypothyroidism
Impaired mental function
Retarded physical development
Increased susceptibility of the thyroid gland
to nuclear radiation
Adult Goiter with its complications Hypothyroidism
Impaired mental function
Spontaneous hyperthyroidism in the elderly
Iodine-induced hyperthyroidism
Increased susceptibility of the thyroid gland
to nuclear radiation
Adapted from Hetzel (1), Laurberg et al. (52, 171) and Stanbury et al. (158).

63. Broad Spectrum of IDD ... ...
• Foetus changes: Abortions, still birth, congenital anomalies
• Increased perinatal mortality
• Increased infant mortality
• Neurological cretinism: Mental deficiency, deaf-mutism, spastic diplegia and
• squint.
• Myoedematous cretinism: Dwarfism, mental deficiency, psychomotor defect &
• Foetal hypothyroidism.
• Neonatal Changes: Neonatal hypothyroidism and neonatal goiter.
• Child & adolescent: Juvenile goiter, hypothyroidism, impaired mental function and
retarded physical development.
• Changes of Adult: Goiter with its complications, hypothyroidism and impaired mental
function.

64. Pathophysiology of Endemic goiter … …
Iodine
deficieny
Low level of T4
and T3
No inhibition of
TSH production
Too much TSH
production
Hyperplasia in thyroid
gland
Goitr
e

65. Goiter
• “Goiter can be defined as the swelling of the thyroid gland due to dysfunction of
thyroid homeastasis resulting from iodine deficiency”.
• “A low amount of thyroxine (one of the two thyroid hormones) in the blood, due to
lack of dietary iodine to make it gives rise to high levels of thyroid stimulating
hormones (TSH), which stimulates the thyroid gland to increased many
biochemical processes, the cellular growth and proliferation can result in the
characteristics swelling or hyperplasia of the thyroid gland or goiter”.

66. Classification of Goitre … …
• Classification of goiter:
• Grade O: No goiter lobes smaller than end joint of thumb.
• Grade IA: Thyroid lobes larger than ends of thumbs.
• Grade IB: Thyroid gland visible with head bent back.
• Grade 2: Thyroid gland visible with head in normal position.
• Grade 3: Thyroid gland visible from about 10 meters.
• In a community survey:
• Grade 2 and 3 are called visible goiter.
• Grade 1A, IB with grades 2 and 3 are called total goiter.
• Clinical classification:
• Grade O- Only absence of goiter.
• Grade 1- only palpable, not visible in normal neck position.
• Grade 2- visible in normal position.

67. Nutritional Anemia
• Common nutritional; anaemia:
• Iron deficiency Anaemia: Iron deficiency anaemia is the most common type
of anaemia overall. Iron deficiency anaemia is due to insufficient dietary
intake or absorption of iron to meet the body’s needs. Iron is an essential part
of hemoglobin, low iron level result in decreased incorporation of hemoglobin
into red blood cells.
• Megaloblastic anaemia: The most common cause of macrocyte anaemi, is due
to deficiency of either vitamin B12, folic acid or both. Deficiency in folate or
vitamin-B12 can be due to inadequate intake or in sufficient absorption of
vitamin-B12.

68. Classification of Anemia by severity
1. Mild=110 g/L to normal-[For men:135 to 175 g/L; Women: 120 to 155 g/L]
2. Moderate= 80 g/L to 110 g/L
3. Severe= Less than 80 g/L [Hemoglobin]
* For adult male & adult pregnant female.
• WHO hemoglobin threshold used to define anemia. (g/L)
Age or gender group Hb threshold (g/L)
Children (0.5-5.0 y) 110
Children (5-12 y) 115
Teens (12-15 y) 12
Women, non-pregnant (>15 y) 12
Women, Pregnant 11
Men (>15 yrs 13
Sajib Reza

69. Clinical Consequences of IDA (Iron
Deficiency Anaemia)
• In pregnant women- anemia results in retardation of intrauterine growth, low birth weights, increased
perinatal mortality and increased maternal mortality.
• Mothers - are less able to care for their children at home.
• Infants - suffer permanent impairment of cognitive development. lower cognitive and IQ performance.
These effects do not improve when the anemia is corrected.
• Children - susceptible to poisoning from heavy metals (including lead).
• For all types of persons-
 morbidity from infectious diseases is increased because anemia adversely affects the immune system.
 Severe anemia reduces the body’s ability to monitor and regulate body temperature when exposed to
cold.
 impair cognitive performance at all stages of life
 physical work capacity is significantly reduced.
 reduced muscle function, physical activity, workplace and school productivity, mental acuity and
concentration in older children and adults.

70. Thank you