Nutritional Disorders
Protein Deficiency
Vs
Excessive Intake
Protein Deficiency
Low protein Intake
<0.4-0.6g/Kg body wt./Day
Poor quality protein having limiting AA
Adverse Effect on the Body
Reduce synthesis of all protein in body
Reduce synthesis of all Enzymes/Hormones
Reduce synthesis of Transport protein
Reduce digestion/absorption of nutrients in GIT
Protein Deficiency
Deficiency occurs during following condition-
Prolonged starvation
Prolonged fever/Infection
Injury
Burns
Surgery
Chronic blood loose
Protein mal absorption
Cancer
Deficiency occurs during following life stages-
Pregnant mother
Infant
Children
Adolescent
Adult
Consequences of Protein Deficiency
(1) Oedema-
Due to accumulation of fluid in interstitial spaces.
Unhealthy swelling of body
(2) Growth retardation-
Protein deficiency reduces tissue protein
It reduces tissue deposition of protein
It adversely influence the vital functioning of cell,
tissue and organs & eventually growth retardation
(3) Muscle wasting-
Muscle mass is reservoir of protein
Low protein intake trigger tissue breakdown
(4)Fatty liver-Liver become fatty
(5) Adversely affect brain growth /development/functioning
(6) Low Immunity-Person become more susceptible to infections
Determination of oedema
Forms of Protein Calorie Malnutrition
Severe form of PCM/PEM
(1)Marasmus
Severe growth retardation Skin on bones
Loss of subcutaneous fat Wrinkle skin
No edema Bony prominence
Weak muscles
(2) Kwashiorkor
Low body wt Muscle wasting
Edema moon face
Pitting oedema
(3) Marasmic
Kwashiorkor
Marasmus + Kwashiorkor= Oedema+ Muscle wasting
Lathyrism
1-Neurolathyrism-Human
2-Osteolathyrism-Animals
Neurolathyrism is caused by eating -Khesari Dal
Lathyrus sativus= Khesari Dal
Diet containing over 30% of this pulse over2-6 months
It affects 15-45 years of age
Toxin-BOAA-Beta Oxalyl Amino Alanine
Satges-
Latent stage-weak nesss of lower limb/leg muscles
No stick stage-Knee joint/ankle joint painful movement
One stick stage-inversion of foot/walk on toes
Two stick stage-marked inversion of foot/walk on toes
Crawler stage-joint bcm fixed/erect/walking not possible
Preventive Measures
1- Banning the crop
2-Removal of toxin-Steeping & parboiling
3-Education
4-Genetic approach
5-Socio-conomic changes
Dropsy
1-Epidemic dropsy-
Sanguinarine=Argemone maxicana oil adulteration
2-Endemic Dropsy-
Pyrrolizidine alkaloids=crotolaria seeds(jhunjhunia )
Mechanism=
Toxin Sanguinarine interferes with oxidation of pyruvic
acid which accumulates in blood and it may lead to
sudden non-inflammatory edema of bilateral lower
limbs,diarrhoea,dilation of skin capillaries,cardiac failure
and death.
Edema due to proteinuria (loss of albumin)
Aflatoxicosis
Toxin-Aflatoxin=Aspergillus flavus/parasiticus
Aflatoxins are a group of chemically similar toxic
fungal metabolites (mycotoxins) produced by certain
moulds of the genus Aspergillus growing on a number
of raw food commodities. Aflatoxins are highly toxic
compounds and can cause both acute and chronic
toxicity in humans and many other animals.
Sign/symptoms
Nausea, vomiting, and abdominal pain.
Pulmonary edema, which is fluid buildup in the lungs.
Cerebral edema, which is fluid buildup in the brain.
Blood abnormalities, such as an increased risk of
bleeding out, Severe damage to the liver, Death.
Fluorosis
Recommende fluorine(India)-0.5-0.8mg/lt of water
Major source-Drinking water
Fluorine is a double edged sword
Inadequate intake-----Dental caries
Excess intake-----------Dental/skeletal fluorosis
Level>1.5ppm=Dental fluorosis-Dental mottling
Level>6.0ppm=Skeletal fluorosis
Level>10.0ppm=Crippling fluorosis
Prevention
1- Nalgonda Technique-NEERI Nagpur
Used for defluoridation of water
It evolves addition of ….
1-Lime
2-Alum
3-Bleaching powder
4-Flocculation
5- Sedimentation
6- Filteration
2-Parshanti Technology-SSU,AP,India-
Activated alumina is used and water is passed through it
3-ICOH Technique-ICOH Bangkok & WHO-
Charred bone meal and charcoal column is used for
passing the water.
Vitamin-A deficiency
Classification of xerophthalmia
1. XN Night blindness
2. X1A Conjunctival Xerosis
3. X1B Bitot’s spot
4. X2 Corneal Xerosis
5. X3A Corneal ulceration/keratomalacia (<
1/3 corneal surface)
6. X3B Corneal ulceration/keratomalacia (≥
1/3 corneal surface)
7. XS Corneal scar
8. XF Xerophthalmic fundus
Night Blindness
Lack of vitamin A causes night
blindness or inability to see in
dim light.
night blindness occurs as a result
of inadequate pigment in the
retina.
It also called tunnel vision.
Night blindness is also found in
pregnant women in some
instances, especially during the
last trimester of pregnancy when
the vitamin A needs are
increased.
Night Blindness
Bitot’s Spot
These are foamy and whitish
cheese-like tissue spots that
develop around the eye ball,
causing severe dryness in the
eyes.
These spots do not affect eye
sight in the day light.
Conjunctival Xerosis
Conjunctiva becomes dry and
non wettable.
Instead of looking smooth
shiny it appears muddy
&wrinkled.
Keratomalacia
One of the major cause for
blindness in India.
Cornea becomes soft and may
burst.
The process is rapid.
If the eye collapses vision is
lost.
