Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Liv vet med yr1 > Vitamins + minerals > Flashcards

Vitamins + minerals Flashcards

1
Q

Vitamins (definition)

A

Organic compounds required in very small quantities for normal body function

Absence from the diet results in signs of deficiency –> death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Which are the fat soluble vitamins?

A

A, D, E, K

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Chemical names of the fat soluble vitamins

A

A = retinol
D = calciferols
E = tocopherols
K = quinones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Which are the water soluble vitamins?

A

B complex, C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the names of the B complex vitamins?

A

B₁ = Thiamin
B₂ = Riboflavin
B₃ = Nicotinic acid/niacin
B₅ = pantothenic acid
B₆ = pyridoxine
B₇ = Biotin
B₉ = Folic acid
B₁₂ = Cyanobalamin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Sources of vitamins

A
  • Provitamins are compounds that act as vitamins after undergoing a chemical change to active forms in the body
  • Foods low in a vitamin may still contribute if consumed in large amounts/frequently
  • Many vitamins are destroyed by oxidation
  • How food is processed, stored and cooked can have a major influence on the level of vitamins it contains
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Metabolic functions of retinol

A

1) Formation + integrity of epithelia + mucous membranes

2) Retinal function - combines with opsin to form rhodopsin needed for night vision

3) Bone growth

4) Immune function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Pro-vitamin A: β carotene

A

Converted to retinol during absorption through the gut wall

This ability varies with:
- Age: young animals are poor converters
- Species: cats can’t convert β-carotene at all
- Breed: channel island cattle are very poor converters
- Health: diseases affecting the gut wall and liver function

Because retinol is stored in the liver, animals don’t require a daily supply

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Sources of retinol

A
  • Liver
  • Accumulates and stored in the liver
  • Egg yolk
  • Milk fat

β carotene: plants (grass)

Retinol deficient foods:
- Cereal grains
- Meat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Retinol deficiency in cattle

A
  • Mild deficiency - rough, scaly skin
  • Prolonged deficiency - night blindness, lachrymation, corneal opacity, retained placenta, still birth

Deficiency is rare in adults as carotenoids acquired at pasture replenish hepatic sores of vitamin A -> able to provide adequate retinol cover over winter periods

Intensively reared indoor beef cattle on cereal diets are prone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Retinol deficiency in dogs + cats

A

Can occur if fed all-meat diets without liver

Dogs:
- Scurvy
- Scaly skin (first sign)
- Night blindness
- Abnormal skeletal growth

Cats:
- Foetal defects are apparent + complete infertility can result

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Retinol deficiency in poultry

A

Symptoms appear quickly (2-3 wks)
- Pale comb/wattles
- Loss of condition
- Retarded growth
- Ruffled plumage
- General unthriftiness
- Susceptible to infectious diseases
- High mortality rate

Poutry feeds require vitamin A supplement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Hypervititamiosis A (dogs + cats)

A

EX fish liver oil/liver intakes

  • Abnormal bone deposition
  • lameness
  • Vertebral spondylosis
  • Gingivitis
  • Weight loss
  • Poor coat
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Hypervitaminosis A (Pigs)

A

Excessive intakes of retinol in pregnant sows may cause cardiac abnormalities in piglets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Vitamin D - the calciferols

A

All steroids qualitatively exhibiting the biological activity of cholecalciferol.

Two most important forms:
- Ergocalciferol (Vitamin D₂) -> derived from the provitamin ergosterol
- Cholecalfierol (Vitamin D₃) -> derived from the provitamin 7-dehydrocholesteral

The provitamins have no vitamin value.
- Must be converted into calciferols before it can be used in the animal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Sources of the calciferols (D)

A
  • Sunlight on skin
  • Fish (oily)
  • Egg yolk
  • Hay (sun dried roughages)
  • Colostrum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Metabolic functions of the calciferols (D)

A
  • Promotes Ca²⁺ absorption from digest in the gut lumen
  • When blood Ca²⁺ concentrations decrease it enhances intestinal absorption of Ca²⁺
  • Stimulates phosphorus uptake from gut + reabsorption of both Ca²⁺ and P from bone and kidney
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Calciferol deficiencies

A

Rickets - soft weak deformed bones in young growing animals.

Osteomalacia in adults (weak bones)

Poor egg shell quality and weak bones in poultry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Metabolic functions of Vitamin E - ⍺-tocopherol

A
  • Biological antioxidant
  • Acts with an Se containing enzyme to protect cells from oxidative damage caused by free radicals
  • Important for normal reproductive function, muscular function and capillary integrity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Sources of ⍺-tocopherol

A
  • Little body reserve so dietary intake is important
  • Greed fodder
  • Cereals - but decreases rapidly during storage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

⍺-tocopherol deficiencies

A

Nutritional myopathy
- White muscle disease (calves)
- Staff lamb diseases

Cardiac disease
- Mulberry heart disease - pigs/calves

Brain damage - crazy chick disease

Lameness + muscle stiffness
- Tying up (horses)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Vitamin K - quinones

A

Several forms exist e.g
- Phylloquinone
- Menaquinone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Metabolic functions of the quinones (K)

A
  • Essential for the normal clotting of blood
  • Bone + kidney function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Sources of the quinones (K)

A
  • Green, leafy materials
  • Egg yolk, liver + fish
  • Gut bacteria synthesis vitK

Rapidly destroyed by heat + exposure to sunlight

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Quinone deficiency (K)

A

Unlikely to occur in cattle, horses or pigs

Usually no dietary requirement for ruminants as microbial population of the rumen can synthesise

Chicks - anaemia + delayed blood clotting

26
Q

B complex vitamins

A

Water soluble
- Minimal body reserves
- Signs of deficiency: sudden onset

Rumen bacteria can synthesise B vitamins in sufficient quantities - deficiency only in pre-ruminant young, sick animals

Metabolism - pathways of cellular respiration + energy transfer; co-enzymes

27
Q

Sources of B complex vitamins

A
  • Liver
  • Yeasts
  • Green foods
  • Cereals
  • MIlk
28
Q

Thiamine - B₁

A

Metabolism - initiation + propagation of nerve impulses

Signs of deficiency:
- Progressive dysfunction of the nervous system
- Paralysis
- Blindness
- Muscular dysfunction
- Loss of appetite
- Emaciation

Ruminants: Bacterial thiaminases produced in disturbed rumen microflora destroy ingested + bacterial thiamine -> deficiency

29
Q

Riboflavin - B₂

A

Cereals a poor source

Metabolism:
- Vital for oxidative phosphorylation and H⁺ transport

Signs of deficiency:
- Pigs: poor appetite + growth, skin eruptions, vomiting, eye abnormalities, infertility + abortion
- Chicks: curled toe paralysis
- Ruminants: inappetence, diarrhoea, mouth lesions

30
Q

The pyridoxines - B₆

A

Deficiency is rare due to wide distribution in many foods + gut microbial synthesis

Signs of deficiency:
- Chicks: neural degeneration + jerky gait

31
Q

Cyanocobalmin - B₁₂

A

Chemical nature - centred around a cobalt atom

Sources:
- Foods of animal origin are primary nutritional source
- Exclusively microbial in origin as long as cobalt present in diet

Metabolism - important coenzyme in cellular respiratory pathways

Signs of deficiency
- Mostly in young animals -> poor growth

32
Q

Metabolic functions of ascorbic acid (C)

A
  • Normal collagen formation
  • Metabolic oxidation + reduction pathways
  • Iron transport
  • Antioxidant
33
Q

Sources of ascorbic acid (C)

A
  • Citrus fruits
  • Green leafy vegetables
  • Synthetic

Destroyed by exposure to light + alkali
Only essential in the diet of primates, guinea pigs, fruit bats
Other species synthesis it from glucose

34
Q

Deficiency of ascorbic acid

A
  • Scurvy
  • Muscle/joint pain -> reluctance to move
  • Lethargy
  • Red dots on the skin
  • Bleeding/swelling of gums
  • Diarrhoea
  • Weight loss
  • Rough coat
  • Reduced immune function
35
Q

Essential minerals

A

Essential dietary minerals are divided int o2 groups according to the quantities required by animals:
- Macrominerals (g/d)
- Microminerals (trace elements) (mg/d)

36
Q

Major elements

A
  • Calcium (15 g/kg)
  • Phosphorus (10 g/kg)
  • Potassium (2 g/kg)
  • Sodium (1.6 g/kg)
  • Chlorine (1.1 g/kg)
  • Sulphur (1.5 g/kg)
  • Magnesium ( 0.4 g/kg)
    1.5 Ca: 1P
37
Q

Trace elements

A

Iron (20-60 mg/kg)
Zinc (10-50 mg/kg)
Copper (1-5 mg/kg)
Molybdenum (1-4 mg/kg)
Selenium (1-2 mg/kg)
Iodine (0.3-0.6 mg/kg)
Manganese (0.2-0.5 mg/kg)
Cobalt (<0.1 mg/kg)

38
Q

Calcium and phosphorus

A

Most important mineral constituents of bone and teeth

Physiological regulation of calcium + phosphorus uptake, storage function + excretion are inter related

39
Q

Calcium

A

~99% of body calcium is locked in the structure of bones and teeth

Of the remaining 1%
- 0.9% is contained within the cells of ICF
- 0.1% is contained outside of cells (ECF)
- Of this 0.1%, a small proportion is present in blood plasma

40
Q

Functions of calcium

A
  • Structural component of skeleton
  • Controls cell excitability (nerve/muscle)
  • Regulates muscle contraction
  • Regulates blood coagulation
  • Many enzyme actions
41
Q

Sources of calcium

A

Must take relative availability Ca:P into account - should be in the range of 1:1 to 1:2

Foods which supply an ideal Ca:P ratio:
- Leafy greens
- Hay/silage
- Animal products

Foods containing more P than Ca, requiring artificial ration balancing:
- Bran
- Cereals
- Roots
- Legume + oil seeds

Corrective sources of calcium:
- Limestone flour
- Poultry: soluble grit

Dietary absorption of calcium:
- Milk ~90%
- Other sources ~60%

42
Q

Factors affecting calcium absorption

A
  • Much plant Ca is bound as phyla’s
  • Oxalates bind to Ca to form insoluble salts -> bound in this form, calcium can’t be absorbed by animals
  • Total absorption of dietary Ca+P decreases as dietary concentration becomes excessive
  • High fat diets -> XS dietary free fatty acids bind Ca to form insoluble soaps
  • Enteritis - inflamed mucosa won’t absorb calcium
43
Q

Hypocalcaemia

A

Sudden decrease in blood calcium concentrates -> homeostatic control sluggish to correct

Acute form:
- Female mammals at the onset/peak of lactation -> high demands of mammary gland for calcium to synthesise milk
- Laying hands -> high calcium demands of eggshell production

44
Q

Hypocalcaemia - milk fever

A
  • Commonly from 1 day before calving to 3 days postpartum
  • High demand for Ca -> lactation
  • High yielding cows in their 3rd and subsequent lactations most susceptible
  • Slow homeostatic adaptation to increased Ca demand -> mechanisms unable to prevent a sudden decrease in blood Ca levels

Signs:
- Flaccid paralysis -> general uneasiness, dullness, paddling, inability to stand, coma, death
- Recumbenecy
- Rumen stasis
- Pupil dilation

45
Q

Chronic hypocalcaemia in growing animals

A

High rate of skeletal growth (^Ca/P demand)

Osteodystrophy = abnormal bone growth
- Deficiencies of Ca, P, vitamin D
- Accompanied with osteoporosis -> loss of Ca+P from bones making hem thinner

Rickets = failure of bone to ossify
- Vitamin D deficiency
- In ruminants a deficiency of either vitamin D or P can cause rickets

46
Q

Causes of chronic hypocalcaemia in growing animals

A

Puppies/kittens:
- Excessive P (secondary Ca deficiency)

Foals:
- Poor artificial rearing
- Gut parasites
- Low hay + high cereal diets (secondary deficiency)

Calves/lambs:
- Failure to supplement dietary Ca, P, vitamin D

47
Q

Hypocalcaemia in adults

A

Except in late pregnancy/lactation, skeletal Ca/P reserves are high -> can be withdrawn if temporary imbalance.

Mobilisation of skeletal Ca/P long term:
- Osteomalacia
- Increased incidence of osetoarthritis

Decreased milk yields

Urethral calculi in male lambs fed high concentrate diet

Horses, goats + pigs -> demineralisation of bones of skull + compensatory collagen deposition causing thickening of the bones

48
Q

Phosphorus

A

Close relationship with Ca in bone metabolism

Sources are the same as calcium

Factors affecting absorption:
- Oxalates + phytates -> much plant P is organically bound as salts of physic acid - in simple stomached animals, little of the phytate is available
- XS dietary Ca or P inhibit the absorption of P or Ca

Signs of deficiency (hypophosphataemia):
- Abnormal bone growth + osteomalacia
- Reduced growth rates
- Pica
- Infertility

49
Q

Magnesium

A

Closely associated with Ca + P

Functions:
- ~70% total body magnesium is present in bone;
- Most common enzyme activator
- Muscle contraction
- Propagation of nerve impulses

Body reserves + NONE + no homeostatic regulation -> dependant on dietary intake to maintain function

50
Q

Sources of magnesium

A
  • All green plants (chlorophyll)
  • Meat + bone
  • Colostrum
  • Magnesite + calcined magnesite

Absorption:
- 20-30% of dietary Mg
- Decreased by high copper + high phytate P intakes

51
Q

Hypomagnesaemia

A

4 major presentations:
1) Calves fed all milk diets
- Milk is a poor source of Mg
- Mg absorption decreases with age
2) Beef cattle + sheep fed on low quality roughage or fodder crops
- Symptoms may occur over several days
- Dullness, hyperasestesia, convulsions, death
3) Lactating cattle + sheep
- Grass staggers = emergency
- Signs: Recumbency, convulsions
4) Subclinical hypmagnesaemia
- Possibility a cause of reduced fertility + milk production in dairy cattle

52
Q

Hypomagnesaemia - grass staggers

A

Predisposing factors:
- Spring:
- Rapid grass growth = Mg uptake by plant
- Grass diarrhoea = faster passage of digest via the gut decreases Mg uptake
- Bad weather -> grass intake reduced as cows shelter
- Fertilesers
- Autumn - gradual decrease in gras Mg
- Year round - stresses which decrease food intake

53
Q

Control/prevention of hypomagnesamia

A

Provide shelter
Introduce to spring grass slowly
Use fertilisers with care + avoid K fertiliser in spring
Provide mineral licks
Top dress pastures
Increase clover in swards
Supplement diet or water with Mg
Mg rumen boluses
Avoid stress

54
Q

Functions of copper

A
  • Important in formation of some plasma proteins
  • Component of other blood proteins + plays role in oxygen metabolism
  • Vital role in may enzyme systems
  • Essential for normal hair, wool + feather pigmentation + crimp in wool
  • Essential for immune function
55
Q

Copper absorption

A
  • CuSO₄ is the most reality absorbed copper salt
  • Metalic copper is poorly absorbed
56
Q

Copper transport + tissue use

A
  • Loosely bound to albumin in the plasma
  • Stored + released from the liver to meet body requirements
57
Q

Copper deficiency

A
  • Anaemia
  • Abnormal bone growth
  • Abnormal hair, feather + wool growth
  • Loss of hair pigmentation
  • Cardiovascular disease

Most common in sheep + cattle

58
Q

Copper deficiency - swayback

A

Affects lamb born to Cu²⁺ deficient ewes.
Failure/degeneration of neural development in the lamb

a) Congenital - stillborn, weak -> ataxia -> paresis + death. Irreversible
b) Delayed onset - normal at birth -> depressed growth rate, rapid onset hindlimb weakness, ataxia -> paresis + death
Can be prevented by parenteral injection of small doses of Cu complexes

59
Q

Copper deficiency in cattle

A

Common 3-9 months of age especially in suckler calves where the dam may not be Cu deficient
Signs:
- Failure to thrive
- Poor growth
- Stiff gait/lameness
- Loss of hair pigment

60
Q

Copper and molybdenum

A
  • Certain pastures are known to cause scouring + unthriftiness in grazing cattle
  • The molybdenum concentration in teart pastures can be 10-50 fold greater than normal
  • Rumen microbes form sulphides which combine with Mo to form thiomolybdate
  • Thiomolybdate binds copper to form copper thiomolybdate - which decreases Cu absorption + causes signs of Cu deficiency, despite adequate dietary Cu provision
61
Q

Copper toxicity

A

Tolerance: Pigs>horses>cattle>sheep

Copper accumulates in liver -> cell necrosis

Signs:
- Jaundice
- Appetite loss
- Hepatic coma + death

62
Q

Copper toxicity in sheep

A

Different copper tolerance between breeds

While sharing a common pasture, North Ronaldsay sheep may demonstrate copper toxicity while the Scottish blackface breed are copper deficient

Liv vet med yr1 (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions