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NUTRITIONAL

PATHOLOGY
(Vitamins and Trace elements)
Presenter: Dr. Subira Matiku 
Facilitator: Dr.Kabyemela
OBJECTIVES 
 To describe vitamins and mineral elements

 To describe sources of various vitamins

 To determine problems associated with vitamin and


minerals deficiencies
Introduction

Vitamins and minerals/trace elements are essential


micronutrients needed by the body in very small amounts

However, their impact on a body’s health are critical, and


deficiency in any of them can cause severe and even life-
threatening conditions

An adequate diet should provide


 Energy in the form of carbohydrates
 Amino acids (Essential and non-essential) and fatty acids to be used as
building blocks
 Vitamins and minerals, which function as coenzymes or hormones in vital
metabolic pathways
VITAMINS
 “VITAMIN” means “vital for life”
* Nutrients required in very
small amounts - mg or µg

 VITAMINS are *Micronutrients 


 which are necessary for everyday healthy
functioning of the body
 13 vitamins are essential for health 
 Vitamins A, D, E, and K are fat soluble 
 Vitamin C and the 8 B-complex vitamins are water soluble 

 Deficiencies in a single vitamin are uncommon

 These vitamins must be supplied in the diet 

 Exceptions:
 Small amounts of D, K, biotin and niacin can be synthesized
endogenously 
 Vitamin D from UV light 
 Vitamin K and biotin from intestinal microflora
  Niacin from tryptophan (amino acid)
Lipid soluble and water soluble vitamins Trace elements

Thiamin
Niacin
Pantothenic acid
Vitamin A Copper Iron
Biotin
Selenium Iodine
Vitamin D Folate
Manganese Zinc
Vitamin E Riboflavin
Molybdenum Cobalt
Vitamin K Vitamin B6
Vitamin B12
Vitamin C

Essential Micronutrients
Water soluble Fat Soluble
 Cannot be stored in body -  Can be stored in body - regular
regular supply needed supply not needed

 Excess is excreted in urine -  Can accumulate to toxic levels


no danger of toxic levels if large amounts ingested

 Unstable to heat and light,  Fairly stable at normal cooking


leach into cooking liquids temperatures

 can only be absorbed


efficiently when there is
normal fat absorption
VITAMIN DEFICIENCY

Primary deficiency (common) due to


malnutrition

Secondary deficiency due to:


– Malabsorbation
– Storage disturbance
– Impaired metabolic conversion
– Distorted blood transport
FAT SOLUBLE VITAMINS
VITAMIN A
§ Vitamin A is a group of related natural
and synthetic compounds -Hormone like activity
§ Retinoids (Retinol, retinal, retinoic acid)
= Active forms of preformed vitamin A
§ The body can convert b-carotene to retinol, thus called
provitamin A.
§ Retinol is stored in the liver, which makes it available
to cells, which then convert it to the other two active
forms
RICH DIETARY SOURCES
Animal Foods Plant Foods
Cod liver oil Sweet potato
Liver & kidney Carrots, Spinach,
Egg yolk Cantaloupe
Butter palm oil
Milk & cheese Apricot
Fish oils & meat Papaya, mango
Vitamin A 
Normal function Deficiency state
 Maintain normal vision in  Impaired vision during
reduced light night (night blindness)
 Potentiate differentiation  ocular changes
of mucus producing
epithelial cells xerophthalmia

 Enhancing immunity to  Dryness of conjunctivae


infections (xerosis)
 Antioxidative effect  Vit A deficiency affect
 Photoprotective effect epithelium
VITAMIN A TOXICITY
 Acute toxicity 
  Headache, vomiting, stupor, death 

  Chronic toxicity 
  Weight loss, vomiting, dryness of lips 
 Bone and joint pain, hyperostosis, hepatomegaly with
fibrosis 
  Predisposition to bone fractures (due to stimulation of
osteoclasts) 
  Congenital malformations 
 Synthetic retinoids for acne (Accutane™)
contraindicated during pregnancy 
  Cause CNS, cardiac and craniofacial defects
CAROTENEMIA
 Excess vitamin A precursors 
 Usually from eating too many carrots, or
artificial “suntanning” pills 
 Yellow-orange colored skin (mainly palms
and soles) 
Sclera remain white (vs. real jaundice) 
 Not associated with toxicity, even in large
amounts
Vitamin D
Sources of vitamin D
Two possible sources :
1)endogenous synthesis in skin 
2)DIET
Sunlight converts 7,dehydrocholesterol to vit D3
 Fish liver oil
 Fish & sea food (herring & salmon)
 Eggs
Plants do not contain vitamin D3, but contain its precursor
ergosterol, which can be converted to vit D2
FUNCTIONS OF VITAMIN D
The maintenance of  of normal plasma levels
of calcium and phosphorus
Is required for normal mineralisation of
epiphyseal cartilage and osteid matrix
Favours differentiation of osteoclasts from
their precursors(monocytes)helps in
resorptive function of bone
Increases synthesis of calcium binding proteins
like osteocalcin and osteonectin
Vitamin D deficiency leads to
Rickets in small children.
 Osteomalacia in adults
 Osteoporosis
SKELETAL CHANGES IN RICKETS
Non ambulatory stage: head and chest
sustain greatest stresses
 Occipital bone become flattened
 Parietal bone can be buckled in by pressure,
which recoil back with the release of pressure
(craniotabes)
 An excess of osteoid frontal
 Bossing and squared appearance of head
 Chest deformities
 Overgrowth of cartilage or osteid tissue at the
costochondral junctionrichitic rosary

 Weakened metaphyseal areas of the ribs are subject to


pull of respiratory musclespigeon Breast
deformity

 Inward pull at the margin diaphragmHarrison’s


groove

 Ambulating child: lumbar lordosis, bowing of legs


VITAMIN E
 The term vitamin E describes a family of 8
antioxidants

 4 tocopherols (alpha, beta,gamma and


delta)
 4 tocotrienols

 Alpha tocopherol is the active form of


vitamin  E in the human body
Vitamin E Dietary sources

Vegetable oils

Almonds and peanuts

Avocado

Spinach

Carrots(least)
FUNCTIONS
 It intercepts free radicals and prevents destruction of
cell membranes

 Prevents LDL oxidation and risk for atherosclerosis

 Needed for normal nerve development

 May play a role in immune function

 Prevents the alteration of cell’s DNA and risk for


cancer development
VITAMIN E DEFICIENCY
 Neurological symptoms (impaired
coordination and muscle weakness)

 Increased risk of cardiovascular disease

 Hemolytic anemia in children


Risk factors
Severe PEM

Genetic defects affecting the


transfer protein of alpha tocopherols

Fat malabsorption
Therapeutic uses
 Prevention of cardiovascular disease

 Diabetes mellitus

 Cancer prevention

 Boost immunity

 Dementia 
VITAMIN K
 The main type is called phylloquinone, found in green leafy
vegetables like collard greens, kale, and spinach. 

 The other type, menaquinones, are found in some animal foods


and fermented foods.

 Menaquinones can also be produced by bacteria in the human


body

 Required for functional activity of clotting factors II, VII, IX, X


and protein C and S
SOURCES
 Green leafy vegetables including collard and turnip greens,
kale, spinach, broccoli, Brussels sprouts, cabbage, lettuces.

 Soybean and canola oil.

 Salad dressings made with soybean or canola oil.

 Fortified meal replacement shakes.


VITAMIN K DEFICIENCY
 Increased risk with 
  Fat malabsorption syndromes 
 Diffuse liver disease 
  Absence of vitamin K-synthesizing bacterial flora 
 Broad spectrum antibiotics can destroy it
 Not fully developed in neonates (vitamin K given
prophylactically to all newborns)
 Deficiency causes bleeding diathesis (skin, gums,
umbilicus, viscera, intracranial) 
 Coumarin (warfarin) induces deficiency 
 Desirable in thromboembolic disease
WATER SOLUBLE
VITAMINS
VITAMIN C (ASCORBIC ACID)
 Functions: 
 Formation of normal collagen
 Antioxidant
 Neurotransmitter synthesis
 Modulating the immune response

 Deficiency disease is called scurvy 


 Those most at risk are elderly who live
alone, alcoholics, infants fed exclusively processed
milk
 Used to be seen with long sea voyages 
 Symptoms reversible almost immediately with vitamin
C
SCURVY (VITAMIN C
DEFICIENCY)
 Poor wound healing – poor collagen synthesis
 Ecchymoses and purpura in skin and gingival
mucosa (small vessels have defective collagen)
 Secondary gum infections 
 Papular rash 
 Skeletal changes due to insufficient osteoid matrix
SCURVY (VITAMIN C
DEFICIENCY)...
 Growing children: bowing of long bones,
depression of the sternum with outward projection
of the ends of the ribs

 Sub-periosteal hematomas and hemarthrosis after


minimal trauma 

 Retrobulbar, subarachnoid and intracerebral


hemorrhages (can be fatal
VITAMIN DEFICIENCY COMPARISON
Vit  C
Vit D
1. Poor osteoid
production 1. Poor mineralization
(calcification of bone)
2. Bowing of long
bones of lower legs 2. Bowing of long bones of
lower legs
3.  Depression of
sternum with outward 3.  Protrusion of sternum
projection of ribs with overgrowth of
cartilage at costochondral
junction “rachitic rosary
B-COMPLEX VITAMINS
 B1 (thiamine), B2 (riboflavin), B3 (niacin), B5
(pantothenic acid), B6 (pyridoxine), B7 (biotin), B12
and B9 (folate) 

 All function as coenzymes, and needs are tied to


energy intake 

 Not much is present in polished rice, white flour, white


sugar
THIAMINE(B1)
 Functions as a catalyst in the generation of energy through
decarboxylation of branched-chain amino acids and alpha-
ketoacids
 Acts as a coenzyme for transketolase reactions in the form of
thiamine pyrophosphate. 
 Also plays an unidentified role in propagating nerve impulses
and taking part in myelin sheath maintenance
 This water-soluble vitamin is present in meat, beef, pork,
legumes, whole grains, and nuts
 Thiamine deficiency can affect the cardiovascular, nervous, and
immune systems, as commonly seen in wet beriberi, dry
beriberi, or Wernicke-Korsakoff syndrome
THIAMINE (B1 ) DEFICIENCY
 Usually symptoms appear 4 weeks after stopping intake
 Deficiency results in ;
 Dry beriberi
 Wernickle encephalopathy and  kosarkoff syndrome
 Wet beriberi
 Common in alcoholics (25% of those admitted) 
 Dry beriberi occurs when the CNS is involved
 The neurological features include impaired reflexes and
symmetrical motor and sensory deficits in the extremities.
  Loss of myelin is seen without any acute inflammation.
BERIBERI (THIAMINE DEFICIENCY)
 Wernicke encephalopathy is a variation of dry beriberi
 Starts with nausea and vomiting, followed by
horizontal nystagmus, ocular nerve palsy, fever, ataxia,
and progressive mental impairment, eventually leading
to the Korsakoff syndrome
 Wet beriberi is present when the cardiovascular
system is involved. 
 The heart fails to function, leading to edema and fluid
retention.
 The key reason for heart dysfunction is an overuse injury
Risks for deficiency
 Poor intake
 Diets primarily high in polished rice/processed grains
 Chronic alcoholism
 Parenteral nutrition without adequate thiamine supplementation
 Gastric bypass surgery

 Poor absorption
 Malnutrition
 Gastric bypass surgery
 Malabsorption syndrome

 Increased loss 
 Diarrhea
 Hyperemesis gravidarum
 Diuretic use
 Renal replacement therapy

 Increased thiamine utilization


 Pregnancy
 Lactation
 Hyperthyroidism
 Refeeding syndrome
RIBOFLAVIN (B2 )
 Sources: meat, dairy, vegetables 

 Absorbed in upper GI tract

 Converted to coenzymes flavin mononucleotide and


flavin adenine dinucleotide, cofactors for many enzymes
in intermediary metabolism

 Ariboflavinosis(The signs and symptoms of riboflavin deficiency)


 Persons in economically deprived developing countries 
  Alcoholics, chronic infections, advanced cancer and other
debilitating diseases, anorexics and individuals who avoid milk
Sign and symptoms

Cheliosis (cracks and fissures at angles


of mouth) 

Glossitis (atrophic tongue) 

Corneal opacities and ulcerations 

Dermatitis
NIACIN (B3 )
 Sources 
 Grains, legumes, seed oils (small quantities in meats) 
  Niacin in corn is in a bound form and unabsorbable 

 Deficency can be seen where corn is most of the diet 

 Can be synthesized endogenously from tryptophan 

 Incorporated into nicotinamide adenine dinucleotide


(NAD) and NAD phosphate, involved in a variety of
redox reactions

  Alcoholics, chronic debilitating diseases (e.g., HIV)


NIACIN (B3 ) DEFICIENCY (PELLAGRA)
 A deficiency of tryptophan can mimic
niacin deficiency  (pellagra) .Three D’s: 
 Dermatitis 
 Thickened red rough skin, bilaterally symmetric on
exposed areas of the body 

 Diarrhea 
 Atrophy of columnar epithelium of GI tract

 Dementia
NIACIN DEFICIENCY
PYRIDOXINE (B6 )
 Derivatives serve as coenzymes in many intermediary
reactions

 Clinically overt deficiency of vitamin B6 is rare in humans 

 Deficiency  leads to cheilosis, glossitis, dermatitis,


peripheral neuropathy  and Maintenance  syndromes of
myelinization of spinal cord tracts
FOLATE
 Sources 
  Whole-wheat flour, beans, nuts, liver, green leafy vegetables 

 Essential for transfer and use of one-carbon units in DNA synthesis

 Depleted in cooked and processed foods

 Folate requirement is increased during pregnancy! 

 Deficiency can predispose to fetal neural tube defects and


megaloblastic anemia
VITAMIN B12 DEFICIENCY
 Required for normal folate metabolism and DNA
synthesis
 Good sources of vitamin B12 include meat, fish, milk,
cheese, eggs and some fortified breakfast cereals.
 Deficiency can lead to;
 Sub-acute combined degeneration of the spinal cord 
 Potentially reversible 
 Numbness and tingling in the lower extremities progressing to
spastic weakness and then paraplegia
 Degeneration of both ascending and descending tracts of the
spinal cord
 Megaloblastic anemia
MINERAL DEFICIENCIES
/TRACE ELEMENTS
 Many trace minerals are found within the body

 Deficiencies can occur due to;-

  Inadequate supplementation in total parenteral nutrition


(TPN) 

 Interference with absorption by dietary constituents 

 Inborn errors of metabolism leading to abnormal absorption


MINERAL
DEFICIENCIES
 5 minerals are associated with well characterized deficiency states

 Iron, zinc, copper, selenium and iodine 

 Iron deficiency is most common in U.S. 

 In children, usually inadequate intake 

 In adults, usually blood loss or pregnancy

 Hypochromic microcytic anemia (defective heme synthesis


ZINC DEFICIENCY
 Abundant in the diet: meat, shellfish, fish, wholegrain cereals,
legumes

  Deficiency usually due to 


 TPN unsupplemented by zinc
  Congenital zinc deficiency (auto recessive, rare)

  Findings 
 Acrodermatitis enteropathica 
 Rash around eyes, nose mouth and anus
  Anorexia, diarrhea, growth retardation, impaired night vision, depressed
mental function
ZINC DEFICIENCY
TRACE ELEMENTS.
THANK YOU

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