Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/81

Click to flip

81 Cards in this Set

  • Front
  • Back
What is meant by the term malnutrition?
poor (suboptimal) nutrition
What constitutes an adequate diet?
energy - in the form of carbohydrate, lipids and proteins

Essential amino acide and fatty acids

Vitamins and minerals
In heads or flocks of animals that are malnourished, what factors influence the clinical sings of malnutrition present in individual animal?
-duration of deficiency
-severity of deficiency
-complexity of deficiency
-species
-breed
-age
-gender
-work load
-environment
Why is it often difficult to accurately diagnose nutritional deficiency?
-the lesions caused by some nutritional deficiencies may mimic some toxic, viral and genetic disorders

-when multiple nutrients are deficient, the syndromes that develop may differ from a simple combination of the effects of individual deficiencies
What is meant by the term primary malnutrition?
dietary deficiency of one or more nutrients is the cause of malnutrition
What are some potential causes of secondary malnutrition?
● decreased intake of nutrients (eg: tooth wear)
● degreased absoption of nutrition (eg. bile duct obstruction)
● interference with storage or utilization of nutritients (diabetes mellitus)
● increased excretion of nutrients (via milk, urine etc)
● increased nutrient requirements (pregnancy, lactation)
● inherited metabolic defects
What is meant by the term marasmus in human medicine? In what circumstances does it develop? What are the consequences of marasmus?
● Marasmus is malnutrition caused primarily by severe reduction in caloric intake.
● catabolism of the somatic protein compartment to provide the abody with amino acides as a source of energy
● atrophy of skeletal muscles, weight loss, decreased muscle mass, large appearance head, normal or only slightly decreased [serum albumin]
What is meant by the term kwashiorkor in human medicine?
In waht circumstances does it develop?
What are the consequences of kwashiorkor?
● Kwashiorkor is malnutrition in which protein deprivation is greater than the reduction in total caloric intake
● most common in Afrecan children who have been weaned and subsequently def an exclusively carbohydrate diet
●severe loss of the visceral protein compartment, generalised oedema (→less weight loss), skin lesion, hypopigmentation, fatty degeneration of the liver etc..
What are the clinical signs that may manifest in a herd or flock of animals with protein-energy malnutrition?
● Depravement of Appetite (Pica)
● Reduced physical activity and metabolic production
● Emaciation
● Skeletal muscle atrophy
● Hepatic cluconeogenesis
● Depletion of Fat Strores
● Hepatic lipidosis
● Ketoacidosis
● Retarded Growth of Juveniles
● Hepatic Atrophy
● Exocrine pancreatic atrophy
● Gonadal atrophy
● Osteoporosis/Osteopenia
● Intestinal Villous Atrophy
● Oedema.Anasarca
● Lymphoid atrophy and immunocompromise
● Anaemia
What is meant by the term cachexia? What are some examples of cachectic illness? Why does cachexia develop in these conditions?
Cachexia refers to wasting.
Cachectic illnesses may be malignant neoplasia, tuberculosis, Johne's disease, lymphoma. These condition lead to changese in energy metabolism
What are the physiological controls of energy intake and expenditure?
Neural and hormonal mechanisms
(afferent system - the arcuate nucleus of the hypothalamus - effector system)
In what circumstances does obesity develop?
When dietary energy chronically exceeds energy expenditure, storing excess calories as triglycerides in adipose tissue
What are the potential consequences of obesity in human?
Increases the risk of the following conditions
● non-insulin-dependent diabetes mellitus
● systemic hypertension
● coronary artery disease
● hepatic lipidosis, heapatitis and cirrhosis
pancreatic necrosis
●cholelithiasis
●hypoventilation syndromes
●degenerative joint disease
●ischaemic stroke
●venous hrombosis
●cancer
What are proven consequences of obesity in domestic animals?
type Ⅱ diabetes mellitus and degenerative joint disease
What are the normal functions of vitamin A?
● for function and integrity of retinal rods and cones
● for function of osteoclasts
● important in epithelial cell differentiation
What are the syndromes that may result from vitamin A deficiency in domestic animals?
● night blindness
● urinary tract mucosa, tracheal mucosa due to squamous metaplasia of mucosal epithelium
● hyperkeratosis of the skin and follicular keratosis
● impaired reproductiv performance
● developmental defect (cardiac anomalies etc.)
● deafness
● communicating hydrocephalus
● dentin and enamel hypoplasia
What is the source of vitamin B1 in ruminant?
the synthetic activity of ruminal bacteria
In what circumstances can thiamine deficiency develop in ruminants?
● destruction of thiamine within the gastrointestinal tract
● inactivation of thiamine by excess sulphate or sulphides or elemental sulphur
● production of inactive thiamine analogues
● decreased absorption or increased faecal excretion of thiamine
● cobalt deficiency
● excess dietary sulphur etc.
What are the consequences and characteristic lesions of thiamine deficiency in ruminants?
anorexia(食欲不振), dullness, head-pressing, central blindness, acute cerebral oedema, laminar necrosis of the grey matter of the cerebral cortex
What is the source of vitamin B1 in carnivores?
from diet
In what circumstances can thiamine deficiency develop in carnivores?
● being fed a deficient diet
● eating excessive fish which naturally contain a thiaminase
● excessive cooking of meat or excessive heating of tinned food during manufacture
● preservation of meat with sulphur dioxide
What are the consequences and characteristic lesions of thiamine deficiency in carnivores?
Clinical signs: salivation, anorexia, bradycardia, ataxia, opisthotonus, continual crying etc.
Lesion: CNS lesions (in the grey matter of the brainstem, especially in relay systems for ocular and auditory stimuli), myocardial necrosis
What does riboflavin (vitamin B2) deficiency cause in chicks?
Curled toe paralysis with demyelination of the brachial and especially sciatic nerve
What is meant by the term scurvy?
deficiency of Vitamin C (=scorbutus)
Which species are predisposed to scurvy and why?
● Primates, guineapigs, Indian fruit bats and Indian pipistrels

● Because they cannot synthesise Vitamin C and must obtain Vitamin C from fresh fruit or green vegetables
What are the typical lesions of scurvy?
● retarded fibroplasia
● abnormal ossification of bone
● failure of wound healing
● gingivitis (歯肉炎)
● bleeding gums
How do domestic animals obtain Vitamin D?
● from diets
● Vitamin D3 can be formed in the skin by exposure to UV light
What is the normal function of vitamin D?
● maintain normal blood calcium levels

● mineralisation of osteoid and growth cartilage → increases osteoblast number and activity
What are the characteristic lesion of vitamin D deficiency in juvenile and adult animals?
●In juvenile, rickets (骨軟症): deposition of osteoid on the cartilage, shortening of bones, expansion of the growth cartilage, joint enlargement, soft bones

●In adults, osteomalacia: softening of bones, excessibe deposition of unmineralised osteoid at sites of mechanical stress, pathological bone fractures, bone deformities, collapse etc.
What is the normal function of vitamin E and selenium?
act extracellularly and intracellularly as an antioxidant, scavenging free radicals
What are the syndromes that develop in domestic animals due to vitamin E and/or selenium deficiency? In which species do they occur?
● white muscle disease esp. in ruminants
● mulberry (暗紅色)heart disease (pigs)
● hepatosis dietetica (pigs)
● mutritional steatitis = "yellow fat disease" (cats, horses, pigs and rabbits)
● encephalomalacia (pigs & chicken)
● exudative diathesis (pigs & poultry)
What is the normal function of vitamin K?
synthesis of coagulation factors Ⅱ, Ⅶ, Ⅸ, Ⅹ
How do animals obtain vitamin K?
Vitamin K1 & K2: from diets (green plants and animal tissues) or synthesized by gut microbes
Vitamin K3: synthetic compound
In what circumstances does vitamin K deficiency develop?
● antagonism of vitamin K by coumarin anticoagulant poisons
● lipid maldigestion/malabsorption
● bile duct obstruction
● prolonged use of antibiotics (which interfere with gut microbial synthesis)
What is the expected consequence of deficiency?
haemorrhage due to inability to generate fibrin
In what circumstances does dietary calcium deficiency develop in domestic animals?
●dietary deficiency: food with low Ca level, meat (rich in S but low in Ca)
●decreased absorption of Ca due to formation of complexes with phytate or oxalate or formation of soaps with lipids
What are the potential consequences of Ca deficiency in domestic animals?
● osteoporosis
● secondary nutritional hyperparathyroidism
● milk fever (parturient paresis)
Why is it important not to feed high Ca diets during gestation to domestic animals? What are the potential consequences of supplementing Ca during gestation
To keep their Ca homeostasis under the fine control of the parathyroid glands
feeding high Ca diet increases the incidence of milk fever (complex metabolic disorder with hypocalcaemia )

a high Ca diet during gestation stimulates thyroid C cell which leads to Ca-induced decrease in bone remodelling and decreased numbers of osteoclasts + inactivity of parathyroid chief cells. This causes decrease in parathyroid hormone synthesis and secretion
What is the normal function of cobalt? How does cobalt deficiency manifest in ruminants?
● for gastrointestinal synthesis of vitamin B12 in most herbivores

●cobalt deficiency = "coast disease" "wasting disease" "enzootic marasmus" leading to poor appetite, emaciation, weakness, normocytic normochromin anemia, hepatic lipidosis(white liver disease)
In what circumstances can dietary copper deficiency develop?
● fed milk for prolonged periods
● copper-deficient soils
● inadequate intake from forage
● interference with absorption due to antagonism
What are the potential consequences of dietary copper deficiency in domestic animals?
● swayback(脊柱湾曲症)
● enzootic ataxia(運動失調)
● achromotrichia (色素欠乏症)
● steely wool
● osteoporosis
● anaemia
● falling disease
Why is iodine an essential dietary component?
iodine is essential for production of thyroid hormones
In what circumstances can iodine deficiency develop?
● in high mountain and inland area (seawater is rich in iodine)
● consumption of goitrogenic compounds that interfere with normal thyroid hormone synthesis (e.g.thiocyanates)
What are the potential consequences of iodine deficiency?
●offspring are likely to develop severe diffuse hyperplastic goitre and signs of hypothyroidism
●offspring may be sparesly haired or hairless, myxoedematous, stillborn or born weak
●slightly prolonged gestation
●dystocia (難産)due to large goitres
●tendency to retain the palcenta
Why is iron an essential component of the diet?
It is an essential component of haemoglobin, myoglobin, cytochromes

also essential to the function of several enzymes
In what species can dietary iron deficiency develop?
● mainly in humans and piglets
● occasionally in kittens, foals and calves due to the low iron content of milk
What are the potential consequences of iron deficiency?
● ill thrift
● paller
● haemic murmur
● pulmonary oedema
What are the syndromes seen in domestic animals due to magnesium deficiency?
● milk tetany (due to prolonged feeding of low Mg milk)
● winter tetany (due to poor quality hay)
● grass tetany (due to lush succulent grasses or wheat or cereal crops
What does manganese deficiency cause in domestic animals?
● impaired synthesis of proteoglycans and cartilage matrix
● chrondrodysplasia in calves
● testicular degeneration
● failure to come on heat
● perosis in checkens
Why is phosphorus deficiency common in ruminants?
for ruminants, plants are the only source of phosphorus
What are the potential consequence of phosphorus deficiency?
generalised weakness, weight loss, rickets in young, osteomalacia in older, osteoporosis, pronounced pica
Why are herbivores prone to sodium chloride deficiency?
they only gain sodium chloride from plants which may be low in sodium. (carnivores obtain sufficient sodium chloride from their prey)
What are the potential consequences of chroride deficiency?
● licking of objects and sweat of other animals
● weakness
● loss of appetite
● weight loss
●reduced growth rate etc.
In what circumstances does zinc deficiency develop?
● excess dietary calcium or phytate
● dietary deficiency
What are the potential consequences of zinc deficiency in pigs, ruminants and dogs?
Pigs: parakeratosis
Ruminants: parakeratosis, testicular atrophy
Dogs: parakeratosis,
What are the exogenous pigments that can be found in the tissues of domestic animals?
●carbon
●dusts
●metals
●tattoo ink & dyes
●carotenoids
What is meant by the term anthracosis?
accumulation of carbon in tissues
Where an in what circumstances does carbon accumulate in domestic animals?
●inhalation of polluted air ●inhaled carbon is phagocytosed by alveolar macrophages and transported by macrophages to tracheobronchial lymph nodes and occasionally other organs
What does accumulated carbon look like grossly and microscopically? Is it of significance of veterinary medicine?
●microscopically black pigment
●if the quantity is large, grossly black or grey speckling of the lungs
●carbon is relatively non-toxic, and significant problem in human rather than animals
Where an in what circumstances does silica accumulate in domestic animals?
●working in rock quarries and mines or wherever rock is being cut or sandblasted
●desert-dwelling animals, especially those that forage in the ground
→silica-induced pulmonary lesions
What do inhaled silicates look like microscopically? What are the consequences of inhalation of silica?
●appear microscopically as fine needle-like crystals that are clear or almost colourless

●activation of pulmonary macrophages and subsequently fibrosis which lead to firm coalescing granulomatous nodules and fibrosis
What do inhaled asbestos fibres cause in humans?
●iron-coated asbestos bodies may participate in redox reactions → tissue injury
●induces pulmonary macrophage activation → chronic granulomatous pneumonia and pulmonary and pleural fibrosis
●may induce malignant neoplasia
What might you find at necropsy in an animal that has died from acute copper poisoning?
●acute gastroenteritis
●acute hepatic necrosis
●intravascular anaemia
●haemoglobinaemina/haemoglobinuria
●jaundice
●renal tubular injury
●green-blue intestinal contents
What is the pathogenesis of chronic copper poisoning in sheep?
●chronic excess dietary intake of copper
(the excess copper is stored in lysosomes of hepatocytes and is gradually excreted into bile)
What abnormalities are expected at necropsy in a sheep that has died from chronic copper poisoning?
●paler liver due to hepatocyte apoptosis, anemia, hypoxic damage to hepatocytes
●dark kidney due to haemoglobinaemia
●big gull bladder
Of what significance is copper in dogs?
chronic copper storage in hepatocytes occurs as an inherited condition in some dog breeds, and may lead to chronic hepatitis and liver failure
Horses and some cattle breeds(esp. Guernsey and Jersey cattle) often have very yellow fat. Why is this so? How would you distinguish this from jandice at necropsy?
●Accumulation of lipochrome pigments (carotenoid pigment) which originate from plats
●Horses and cattle are relatively inefficient in converting beta carotene to vitamin A and in rejecting carotenoids in ingesta that are not required for vitamin A synthesis
●the yellow pigment is disappear in histological tissue preparation because the pigments is soluble in the organic solvents
What can be a consequence of administration of tetracyclines to juvenile animals?
●stains bones and teeth grossly yellow
Which cells produce melanin an how?
●synthesised by melanocytes
●within melanocytes, melanin is formed from the amino acid tyrosine within small membrane-bound Golgi vesicles (=premelnosomes and melanosomes)
Which other cells may contain melanin without producing it?
●basal layers of the epidermis
●the follicular epithelium
●epidermal keratinocytes
●cotex f hairs
What is the purpose of melanin production?
protection against solar
UV radiation by absorption of radiant energy and free radicals generated during UV injury
What does melanin look like in H&E-stained histological sections?
●histologically fine brown-black cytoplasmic granules in melanocytes
●if phagocytosed by macrophages, cytoplasmic melanin granules apppear coase
Which conditions in domestic animals are associated with localised increases in melanin pigment?
●hyperpigmentation of skin (due to ↑'d amounts of melanin w/in basal keratinocytes or endocrinophathies)
●lentige due to localised hyperplasia of melenocytes
●melanocytoma
●malignant melanoma
Which conditions in domestic animals are associated with localised or generalised decreases in melanin pigment? Which of these conditions are congenital and which are acquired? What are the potential consequencs of decreased melanin pigment?
●hypomelanosis (congenital) → predisposed to sunburn and skin cancer
●albinism (congenital defect in tyrosinase) → predisposed to sunburn and skin cancer
●Achromotrichia (acquired due to Cu deficiency)
●vitiligo (acquired)
●acquired hypopigmentation and pigmentary incontinence (due to displacement of melanin from epidermal +/- follicular keratinocytes
Why do ceroid and lipofuscin pigments accumulate in cells?
Lipofuscin farms within lysosomes. And ceroid is variant of lipifuscin.
From what are ceroid and lipofuscin derived?
Lipofuscin is formed by peroxidation & polymerisation of unsaturated fatty acids derived from phospholipid membranes of organelles that have undergone autophagocytosis
Ceroid is a variant of lipofuscine that is formed ealier in cell membrane degradation
What do lipofuscin and ceroid look like in H&E-stained histological section?
appears as fine golden-brown to dark brown cytoplasmic granules.
Histochemically lipofuscin and ceroid are indistinguishable except for lipofuscin being weakly acid-fast whereas ceroid being strongly acid-fast
Which cells commonly accumulate ceroid-lipofuscin?
Macrophages and hepatocytes, neuron, cardiac myocytes etc.
What abnormalities might you find at necropsy in a ruminant with environmental lipofuscinosis?
dull grey to uniform black pigmentation of the liver +/- hepatic lymph nodes, lungs and renal cortexs
What is thought to be the source of the pigment?
an insoluble residue from ingested foliage of the mulga tree
In what circumstances do harmoglobinaemia and haemoglobinuria develop?
Chronic copper poisoning, immune-mediated haemolytic anaemia