Hair

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Hair

Lack of Luster – Kwashiorkor
development of dull, brittle hair

Thin, sparse hair – Kwashiorkor

Dyspigmentation – Kwashiorkor

Easy Pluckability – Kwashiorkor

Severe malnutrition presenting as kwashiorkor or marasmus is still a significant health problem in
developing countries. Kwashiorkor is caused by a protein deficiency characterized by irritability, hair

changes, edema, hepatomegaly, and dyspigmentation. Metabolic features include hypoalbuminemia,
hepatic steatosis, and hypoglycaemia. (Bandsma, 2010)
The hair of a normal Asian, African or Latin American child is usually dark black and coarse in
texture and has a healthy sheen that reflects light. In kwashiorkor, the hair becomes silkier and thinner.
African hair loses its tight curl. At the same time it lacks lustre, is dull and lifeless and may change in
colour to brown or reddish brown. Sometimes small tufts can be easily and almost painlessly plucked out.
On examination under a microscope, plucked hair exhibits root changes and a narrower diameter than
normal hair. The tensile strength of the hair is also reduced. In Latin America bands of discoloured hair
are reported as a sign of kwashiorkor. These reddish-brown stripes have been termed the "flag sign" or
"signa bandera". (Human Nutrition in the Developing World) Hypoalbuminemia indicates a severe
derangement in the child's metabolic system, reflecting a disturbance in protein metabolism (37,41),
potentially cytokine-mediated inhibition of albumin synthesis (42), or, alternatively, cytokine-mediated
capillary leak and redistribution of albumin to the extravascular space. (Bandsma, 2010)
Face

Nasolabial Dyssebacia –
Riboflavin Deficiency

Moon Face – Kwashiorkor
 The cheeks may appear to be swollen with either
fatty tissue or fluid, giving the characteristic appearance
known as "moonface".

Eyes

Pale Conjunctiva – Anemia

Bitot’s Spot – Vitamin A Deficiency
• whipped up meibomian secretions and
conjunctival debris with bacteria that adhere to a xerotic
patch of conjunctiva.


usually but not always located temporally.



can be removed with a Q-tip to reveal the

underlying xerosis. It quickly reforms.


appear as grayish-white triangular plaques, firmly adherent to the conjunctiva due to increased
thickness of conjunctiva in certain areas
Conjunctival Xerosis – Vitamin A Deficiency


Xerosis is the term used to describe dryness.

• loss of mucus-secreting goblet cells and
eventually to squamous cell metaplasia of the
conjunctival epithelial cells.
• Conjunctiva becomes dry, thick, and wrinkled.
It gets keratinized, loses its normal transparency, and acquires a smoky appearance


Conjunctival xerosis typically is found on the temporal and interpalpebral bulbar conjunctiva.

Corneal Sclerosis – Vitamin A Deficiency
 Band Keratopathy
 degeneration of the cornea seen in eye
with a chronically damaged cornea, resulting in
opacification of the cornea



Keratomalacia – Vitamin A Deficiency
• a full-thickness liquefactive necrosis of the
cornea.
• these ulcers are small, partial, or of full
thickness, located in the periphery in the early stages.
• they can extend to obscure the pupillary axis
and develop secondary bacterial infection
associated with a preceding systemic stressor, such as measles, diarrhea, or respiratory infection,
or with concurrent severe protein-energy malnutrition.

Ocular manifestations of vitamin A deificiency are collectively called xerophthalmia and range
from conjunctival xerosis to severe blinding complications such as keratomalacia. In the eye, vitamin A
has a pivotal role in the functioning of the retina and the conjunctiva.
Vitamin A is the backbone of the visual pigments for the rods and the cones, responsible for
vision in dim or low light and color vision and vision in bright light, respectively. In rod cells, the
aldehyde form of vitamin A (retinal) and the protein opsin combine to create rhodopsin, which is the
photosensitive pigment. When light hits the rod cells, the pigment isomerizes, which leads to the nerve
impulse and results in the visual signal. The pigment is broken down to opsin and the stereoisomer of
retinal (all-trans configuration). The correct geometrical form of retinal has to be reconstituted to combine
with opsin to reform the pigment. However, in this process, some of the retinal is always lost, so a
constant source of vitamin A must be available for adequate levels of rhodopsin and optimal rod function.
The mechanisms of stimulation, breakdown, and regeneration of visual pigments are thought to be similar
in rod and cone cells.
In the conjunctiva, vitamin A is necessary for the maintenance of the specialized epithelial
surface. A lack of vitamin A leads to atrophic changes in the normal mucosal surface, with loss of goblet
cells, and replacement of the normal epithelium by an inappropriate keratinized stratified squamous
epithelium. In addition, the substantia propria of the cornea breaks down and liquefies (colliquative
necrosis), resulting in keratomalacia.

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