12 introduction to nutritional deficiencies

1. Nutritional
deficiency diseases
Karima Al Salihi

2. Introduction
1.Minerals
(1) Major elements are essential for growth. Their deficiency
Include: Phosphorous deficiency, Rickets, Osteomalacia and
osteodystrophic fibrosis.
(2) Trace elements are essential for healthy growth. They
include: copper, iron, zinc, iodine, selenium, cobalt and
manganese.
2. Vitamins
(1) Fat soluble vitamins as vitamin A, D, E & K.
(2) Water soluble vitamins as Bb B2, B6, B12 & C.

3. Etiology of the disease
1. Evidence of existence of deficiency
(1)Diet:
1) The type of the soil affects the plant
growing on it.
2) Farming practices and marketing may
affect the presence of specific nutrients in
livestock.

4. (2) Abnormal absorption
Diet may contain adequate amounts or others
substances which can decrease the absorption
such as:
1) Excess phosphate reduce calcium absorption.
2) Excess calcium reduce the absorption of
iodine.
3) Absence of bile salts prevent absorption of fat
soluble vitamin.
4) Chronic enteritis reduces dietary digestion and
absorption.

5. (3) Abnormal utilization of ingested
nutrient
Ingested certain material may effect on the
development of the deficiency e.g.
molybdenum and sulphate reduce copper
absorption, metabolism and storage.
(4) Abnormal requirement
Stimulation of the growth rate of animals by
improved nutrition of other practices may
increase their requirement of specific nutrient
to the point where deficiency disease occurs.

6. Diagnosis of nutritional def.:
1.Evidence of a deficiency
As to the cause of disease (clinical signs & PM): e.g Night blindness indicate
vitamin A deficiency. Level of vitamins and minerals in the blood, urine, liver
biopsy and postmortem lesion help in diagnosis.
2. Evidence based on cure or prevention by correction of deficiency
By observing the effects of specific addition to the ration (diagnostic therapy).
Distribution of Calcium, phosphorus and magnesium:
(1) Ca, inorganic ph and Mg ions are all found ECF. Ca and ph constitute the
abundant cation after K in bone. Mg is abundant anion after K in all ICF.
(2) Bone contains 99% of ca, 85% of ph and 75% of Mg of the body. The
main function of the three ions is in the bone formation.
(3) Magnesium and to a lesser extend calcium are important cofactor for many
enzyme.
(4) Ca and Mg stabilize nerve and muscle membrane (control irritability of Ca
resulted in increased acetyle choline liberated at the site. While increase Mg
resulted in decrease acetyle choline liberation).

7. Forms of calcium and phosphorus:
(1) Calcium is found in two forms:
1) Ionic which is physiologically active
form
2) Non-ionized mainly as a potentiate to
a lesser extent as citrate or phosphorus.
(2) Phosphorus occurs at least in
three forms:
1) Inorganic ions
2) Lipid bound phosphorus
3) Organic ester phosphorus

8. Physiological function of calcium
(1) Formation of bone and milk.
(2) Participation in the clotting of blood
(3) Maintenance of neuromuscular excitability.
(4) Essential for muscle contraction.
Physiological function of inorganic phosphorus
(1) Mineralization of bones and teeth.
(2) Formation of phospholipid of the milk.
(3) Formation of proteins and tissue enzymes.
(4) Intermediary metabolism of carbohydrate and muscle
contraction (Creatinine phosphatase, AMP, ATP, etc).
(5) Phosphorus is important in energy storage and transfer:
(6) Role in reproduction.
(7) Prevent RBCs fragility (enter in phospholipids of cell wall).

9. Chronic Phosphorus Deficiency
Etiology
1.Most phosphorus (PO4 = phosphate) deficiency in animals
is primary' (absolute dietary deficiency)
2.secondary PO4 deficiency is mediated by other factors.
3.Diets high in calcium or low in vitamin D prevent efficient
absorption and decrease bioavailability of PO4.

10. Clinical signs
The earliest signs of chronic PO4 deficiency included:
(1) Decreased feed consumption, pica and weight loss.
(2) Retarded growth and poor milk production.
(3) Reproductive disturbances such as anestrus, irregular
estrus, reduced conception rate and delayed puberty.
(4) Oesteomalacia in adult (Characterized by emaciated,
dull, stiff and shifting lameness usually develop
spontaneous fractures that don’t heal).
(5) Rickets in young growing animals (Characterized by
enlarged, painful swelling of the epiphysis and metaphysis
of the long bones and the costo-chondral junctions. The
animal is stiff, the forelegs are bowed and the back is
arched).

11. Diagnosis
(1) History' (Diet contents).
(2) Clinical signs: Abnormal development of bone and teeth,
plays a part in the production of bloat, make RBCs fragile,
infertility, decrease milk, rough coat, pica and
osteodystrophy in late stages.
(3) Laboratory: Depressed serum P04 (1.5 to 3.5 mg/dl)
disturbance of Ca, P and vitamin D levels

12. Treatment
•Oral and daily supplement of
PO4 including sodium acid
phosphate (30-60 g), bone
meal (125 g daily) and bran
(5-10 Kg) and or ph injection
(See hypophosphatemia).

13. RICKETS
•A disease of chronic nature
affecting young growing animals. It
is a disease of young and rapidly
growing animals.
•Characterized by defective calcification of growing bones
leading to deformity of skeleton and disturbance in general
health.
•Essential lesion is failure of provisional calcification with
persistent hypertrophic cartilage and enlargement of epiphysis

14. Etiology
•Caused by factors disturbing
metabolism of calcium & phosphorus.
•Calcium metabolism is very much
dependent on phosphorus and vit.D ,
rickets may result from lack/deficiency
of any of these components i.e.
calcium , phosphorus or vit.D or their
disturbances in metabolism.

15. •Factors causing deficiency of
calcium
1) Deficiency in diet e.g. meat and by-products.
2) Deficiency due to improper absorption from gut due
to;
a) vit.D deficiency.
b) Alkaline pH of digesta.
c) formation of insoluble complexes like
oxalates,
ca-soaps with organic acids etc.
3) Improper Ca & P balance e.g excess phosphorus
in meat & by-products form insoluble Ca3(PO4)2
which is excreted in feaces.

16. 4)Steatorrhoea as in pancreatic and liver diseases.
Steatorrhea (or steatorrhoea) is the presence
of excess fat in feces.
5) Renal diseases :-
a) Less phosphorus excretion inhibiting Ca⁺⁺ absorption due
to formation of insoluble compounds.
b) Increased nitrogenous wastes in blood leading to acidosis for
which Ca⁺⁺ acts as base so is less available for mineralization
for other processes.
c) Reduced synthesis of 1,25(OH)2 vit. D or calcitriol.
6) Presence of endoparasites.

17. Factors causing deficiency of phosphorus
1) Deficiency in diet as in milk and diary products.
2) Formation of insoluble complexes as with Ca , Fe , & Al when
taken in excess.
3) Dogs having habit of ingesting grass containing phytic acid
forming insoluble complexes.

18. Factors causing deficiency of Vit. D.
1) Deficiency in diet like milk, cream, egg yolk & animal fat.
2) Deficiency of sunlight as in dogs retained indoors.
3) Steatorrhoea as in diseases of liver and pancrease.

19. CALCIUM PHYSIOLOGY: BLOOD CALCIUM
Calcium flux into and out of blood:
•
–“IN” factors: intestinal absorption, bone resorption
–
–“OUT” factors: renal excretion, bone formation (ca incorpation into
bone)
–Balance between “IN” and “OUT” factors maintained by :
•organ physiology of gut, bone, and kidney
•hormone function of PTH , Vit. D. and Calcitonin.

20. CALCIUM HOMEOSTASIS
CALCIUM HOMEOSTASIS
DIETARY CALCIUM
INTESTINAL ABSORPTION
ORGAN PHYSIOLOGY
ENDOCRINE PHYSIOLOGY
dietary habits,
supplements
BLOOD CALCIUM
BONE
KIDNEYS
URINE
THE ONLY “IN”
THE PRINCIPLE “OUT”
ORGAN PHYS.
ENDOCRINE PHYS.
ORGAN,
ENDOCRINE

21. PATHO-PHYSIOLOGY OF RICKETS
…………….RICKETS……………..
Disturbance in bone metabolism & mineralization leading
to weak & thin bones
Negative calcium and phosphorus balance
Mobilization of Ca from bone, dec. phosphorus resorption from kidney leading
to phosptaturia & hypophosphatemia
2º hyperparathyroidism
Hypocalcaemia / hypocalciuria
Decreased absorption of Ca from gut.
Deficiency of vit D / def. of Ca in diet

22. PATHOGENESIS
INTERUPTION OF ENDOCHONDRIAL OSSIFICATION AT EPIPHYSIAL PLATE OF LONG
BONES WHILE FORMATION OF MATRIX & PROLIFERATION OF CARTILAGE CELLS PROCEED
NORMALLY
CAPILLARY INSHOOTS FROM METAPHYSIS INVADE EPIPHYSIS REGION
FORMING OSTEIOD TISSUE HAVING PROTEIN BASE IN WHICH CA & P
DEPOSITION HAS FAILED
ENORMOUS ACCUMULATION OF OSTEIOD & CARTILAGE
WIDENED AND IRREGULAR EPIPHYSEAL LINE OF RADIOLUCENCY
AND APPARENT SWELLING OF BONE EXTREMITIES

23. THICK LAYERS OF OSTEIOD LAID DOWN IN
METAPHYSIS & EPIPHYSIS ABOUT THIN OLD
RESIDUAL BONE FRAGMENTS AND ENLARGED
HAVERSIAN CANALS
CHARACTERISTIC GLOBULAR ENLARGEMENTS
FORMED AT TYPICAL SITES LIKE COSTO-CHONDRIAL
JUNCTION OF RIBS (rachitic rosary)
MARROW DISPLAYS A MODERATE DEGREE OF
VASCULARITY & FIBROSIS

24. BONES BECOME WEAK WITH
THIN SHAFTS LEADING TO
BENDING ON WEIGHT
BEARING(bow-legs)
DEFORMED SKELETON &
FAILURE OF BODY
GROWTH

25. CLINICAL FINDINGS
a) Stunted growth.
b) “Bow legs” condition due to abnormal curvature of long
bones usually forward and outward at the knee.
c) Enlargement of limb joints mostly distal ends of radius & ulna.
d) Enlargement of costochondrial junctions appearing as string of
beads(rachitic rosary).

26. Stiffness of joint, lameness and tendency to lay
down.
Narrowing of chest cavity due to abnormal
bending of ribs(pigeon chest)
Flat toe appearance’ due to flattening of bones
and relaxation of muscles & tendons
Impaired muscular activity leading to lameness
Animal very much susceptible to fracture of
bone.
Arched back condition.
Pot bellied appearance of abdomen.
Deformity of pelvic bones will later cause
maternal dystocia.

27. Eruption of teeth is delayed
and irregular ,
often badly aligned
and wear rapidly &
unevenly.
General condition is poor .
There is unthriftiness , pica
& occasional diarrhoea

28. Clinical pathology
v There may be decreased serum & phosphorus level.
v Increased level of alkaline phosphatase enzyme.
v Confirmatory diagnosis by radiological examination of bone
(lack of density , wide epiphyseal plate & epiphyseal line which
are very much pathogonomic , wooly & moth eaten appearance
of epiphyseal ends of long bones)

29. Diagnosis
Dietary
history of low
Ca ,
phosphorus
or vit. D
• Clinical
findings
• Clinical
pathology
Confirmation
by
radiography

30. Treatment
• Change of diet to major commercial balanced dog or cat foods
which contain sufficient vit.D content. Animal may respond
within 3 week otherwise vit.D therapy can be recommended.
• Vit.D therapy at a suggested level of 10-12 times, the daily
requirement on alternate days for 1 week (daily req. of dog is
700 I.U.
• Supplementation of Calcium by oral feeding( bone meal ,
limestone powder, mineral mixtures) and injections.
• Adequate exposure to sunlight.

31. •Feeding some organic meals such as liver, kidney, heart, &
cod liver oil to pups will correct the condition( rich source of
vit.D).
•Massaging of bones with oil and then putting the animal in
sunlight proves useful.
•Correction of other disease conditions indirectly affecting
bone metabolism.