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BVMS Module 3 > WEEK 3 > Flashcards

WEEK 3 Flashcards

1
Q

describe the CHO metabolic pathway?

A

CHO - monosaccarides transported into S.I then into blood
Liver - hepatocytes pass glucose into circulating system.
Remaining glucose transported round body
Glucose taken up by cells in response to insulin and glycolysis

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2
Q

describe Fatty Acid Metabolism?

A

matrix or mitochondria, free ferrety acids used when glucose is low.
RBCs cannot use FA, cannot cross blood/brain barrier.

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3
Q

what do fatty acids undertake when in mitochondria?

A

oxidation - transformed into Acetyl CoA and oxidised for energy.

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4
Q

what is the carnitine shuttle?

A

long chain of FA into cytoplasm of mitochondria.

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5
Q

where is the CoA and ATP converted into Acetyl CoA synthase?

A

cytoplasm of cell

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6
Q

how are Ketone made form FAs?

A

3 molecules bodies produced in liver with fatty acid broken down in excess.
depends on the levels of available CHO that occur in striving/fasting CHO restrictions.

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7
Q

what is ketongenesis?

A

prodution of ketones form fatty acids.

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8
Q

how are fatty acids converted into TCA cycle?

A

FA - Acetyl CoA - citrate - TCA cycle

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9
Q

name the state when excess ketone bodies accumulate?

A

ketosis

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10
Q

what is ketoacidosis?

A

absence of insulin induces liver to produce glucose at high rate.
Fatty acid oxidation results in acetyl CoA
Acetyl CoA converted to ketone bodies
ketone bodies cause ketoacidosis

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11
Q

amino acid catabolism?

A

1- removal of amine group
transfer of amine group from amino acid to receptor.
2- breakdown of carbon skeletal
Glutamate - NH3 - urea cycle

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12
Q

what is the equation for the Urea cycle?

A

NH3 ➡️ carbonyl phosphate

NH3 + CO2 + 2ATP ➡️ carbonyl phosphate + 2ADP + PI

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13
Q

what is the role of the urea cycle?

A

carbonyl group is transferred to ornithine forming citullive. carbonyl reacts with asparate.
cleavage of argininosuccinate to release arginine
arginine is hydrolysed to urea

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14
Q

summarise the steps involved in ruminant digestion?

A

food mixes with saliva - passed into rumen - passed into reticulum, broken down into cuds - partially digested food - regurgitated into animals mouth and re-chewed/re-swallowed back into rumen(chewing the cud) - cellulose breakdown occurs in rumen - moves into omasum - water and vitamins are absorbed into body, pH decreases, enzymes released to breakdown before entering abomasum - further breakdown, passed to small + large intestines, nutrients absorbed before extrection.

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15
Q

describe the structure of Cellulose?

A

Beta 1,4- glycolic bonds, non ruminants cannot digest Beta only alpha bonds. Ruminants can hydrolyse bonds called microbial fermentation.

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16
Q

what is the role of rumen microbes in digestion>

A

rumen provides an anaerobic environment.
Cellulocytic bacteria - provided cellulose eneymze with cleavage
Amylolytic bacteria - produce amylase enzyme which cleaves A-1,4 bonds in starch and sugars.

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17
Q

how do microbes function in the rumen? and how VFAs are synthesised?

A

secrete enzymes that digest to yield simple sugars. produce Glucose - converted into - volatile fatty acids (VFAs) by microbial fermentation. VFAs short fatty acids, provide energy fr ruminants.

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18
Q

give some empales of VFAs?

A

Butryate, Propinate, Acetate.

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19
Q

describe how VFAs are absorbed?

A

rumen squamous epithelium (functions similarly to small intestine epithelium of non-ruminants), papillae increase SA on rumen so continuous removal of VFA from rumen drops the pH of rumen fluid.
More papillae = greater uptake of VFAs.

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20
Q

describe how VFA are used for energy provision?

A

proponiate - glucose synthesis
acetate - milk fat synthesis
butyrate - derived form acetate and used for ketone body synthesis.

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21
Q

describe how VFA are used in the rumen for energy provision?

A

proponiate converted into GNG which is converted into glucose
Butyrate converted into B-hydroxybutyrate which is converted into acetyl CoA - TCA or Triacyglycerol (TAG)
Acetate converted into acetyl CoA - TCA or Triacyglycerol (TAG) (Fatty acid synthesis)

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22
Q

how the lipid equations that are metabolised in ruminants?

A

triglycerols ➡️(microbial lipase) fatty acids and glycerol

polyunsaturated fatty acids ➡️(shift of the double bond by rumen bacteria) saturated fatty acids

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23
Q

describe the formations of micelles in SI?

A

single layer phospholipid + cholertsol outer shell

non polar lipids in core. hydrophilic head and hydrophobic body.

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24
Q

how are triglucerols transformed into chylomicrons?

A

they are resynthesised in enterocyte and packaged with cholesterol + phospholipids into chylomicrons.
Chylomicrons enter into lymphatics and ultimately emptying into veins.

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25
Q

how do chylomicrons leave the enterocyte intestinal cell?

A

exocytosis into the lymph vessels.

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26
Q

describe how fatty acids are used for energy?

A

fatty acids taken up by LIVER for energy via b-oxidation to form acetyl CoA, enters TCA cycle for ATP synthesis.

OR

FA are converted into ketones bodies in LIVER, ketone bodies then transited into tissue.
As rate of fat metabolism ⬆️, circulating fee FA levels ⬆️.

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27
Q

what is required for the metabolism of fat?

A

glucose

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28
Q

what is ketosis?

A

occurs in dairy cattle in early lactation, high glucose levels demand + intense adipose utilisation.
it occurs when animal feed intake is NOT sufficient for the animal. it burns fat and makes things called ketones, which it can use for fuel

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29
Q

describe how ketosis causes ketone bodies in milk and urine?

A

not enough glucose intake- metalosation of FA and G, FA and G oxidised to acetyl CoA, excess acetyl CoA is convertedto ketone bodies acetotacetae and B-hydroxybutyrate.
ketosis occurs, ketone bodies build up in urine and milk supplies.

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30
Q

describe protein microbal digestion in ruminanats?

A

uses hydrolysis - cleave peptides bonds
and deamination. - removal of AA groups releasing NH3 and C isolation.
NH3 detoxified by urea cycle to form urea
microbes can therefore synthesise ALL amino acids .

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31
Q

how is pepsinogen to pepsin conversion stimulated?

A

in abomasum, chemical breakdown of protein occurs, preside of food stimulates HCL secretion, causing stimulation of pepsinogen to pepsin.

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32
Q

describe how the ruminant milk synethsis is actiavted?

A

Food is broken down into cellulose into VFAs (propionate, butyrate, acetate) in rumen leads to glucose in liver from GNG being produced and leading to lactose being produced.
Milk fat produced from acetate and butyrate via FA synthesis and protein made form microbial digestion.

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33
Q

describe the stomach in ruminants?

A

Rumen, reticulum, omasum and abomasum.

Forestomach - non-glandular. not produce digestive enzymes. able to house food for later, store energy

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34
Q

describe the reticulum?

A

reticular papillae, HONEYCOMB pattern, grazing animals have larger papillae, contains 3 layers; gas layer (methane + CO2) solid layer(fresh forage), liquid layer(fluoride present)

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35
Q

describe the reticulum motility in ruminant?

A

mixing of food with rumen microorganism, prevent accuminaltion of VFAs, mixing the cud with saliva

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36
Q

describe the 3 contraction patterns in reticulum of ruminants?

A

mixing (primary) contractions - dorsal ruminal sac contraction
eructing (secondary) contritions - gas bubbles move crainally, cause-dorsal sac contracts
Rumination - thorax expands epigoliattis closes yje larynx, antiperstailic oesophageal wave starts and move the bolus chewing the cud in the mouth.

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37
Q

what control the reticulrumen rumination?

A

central NS innvertaion of reticulum, vagus nerve branches

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38
Q

explain the modulation of motility of reticulumreumen rumination?

A

external stimuli
response - excitatory
inter stimuli

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39
Q

describe some of the external stimuli for reticulum rumination>

A

temperature
hormonal
inhibitory LPS

40
Q

describe an internal stimuli for reticulum rumination>

A

rumen VFAs

41
Q

explain what endocrine regulation of glucose metabolism is for?

A

brain,liver and blood cells dn NOT have insulin receptors

reply on simple diffusion of glucose for correct glucose levels

42
Q

describe how the pancreas is used in endocrine regulation of glucose?

A

2% of pancreas = islets of langerhans, essential for digestion. contains discrete groups of cells 4 main cell types all in a capsule

43
Q

what are the 4 cell types in pancreas for endocrine regulation?

A

beta cells - insulin 60% location - centre of islets
alpha cells - glucagon 25% outer regions of islets
Delta cells - somatasatin
F cells - pancreatic polypeptide

44
Q

describe Insulin?

A

lower blood glucose level, hepatocytes, muscle cells, adiopocytes.

45
Q

how does insulin stimulate anabolic reactions?

A

glycneogenesis liver, skeletal muscle + adipose, protein synthesis (storage)

46
Q

when was insulin discovered and who by?

A

1922, by Banting + Bert

47
Q

describe insulin secretion?

A

constant from B-cells can be up or down regulated.
modulated by hyperglycaemia and stimulates insulin release.
Glucose present in plasma
⬇️
through carrier protein
⬇️
metabolical to ATP
⬇️
reduced K+ permeability to membrane
⬇️
Ca2+ come into cells via extracellular fluid
⬇️
increased in Ca2+ causes insulin to move by exocytosis out of cell

48
Q

what is Glucagon?

A

single chain of 29AA - produced in stomach and a similar molecule glicentin in produced in S.I,
RAISES blood glucose levels/slows drop in plasma glucose. TARGETS- hepatocytes and adipocytes.

49
Q

describe Glucagon secretion?

A

hypoglycaemia stimulates glucagon synthesis and release.
Sympathetic NS - increase glucagon release and inhibits insulin.
Amino acids (especially alanine and arginine) stimulate glucagon release (also stimulates insulin) .
Somatostatin inhibits Glucagon release (also insulin).
generally opposite of insulin.

50
Q

what effect does adrenaline/noroadrenaline have on circulating glucose?

A

Physical activity ➡️ SNS - insulin (storage) glucagon, direct effect (liver and adipose glycogenlysis)

51
Q

what effect does low plasma glucose and stress have on the adrenal gland?

A

causes metabolism of AA from all cells except hepatocytes - hepatic gluconeogensis
OR
hormone sensitive lipase - metabolisation of FA and glycerol for adipose tissue.

52
Q

explain hypoglycaemia?

A

low blood glucose - excessive insulin production due to an insulin producing tutor
OR
excessive administration of insulin
symptoms - increase HR, sweating, tremor, panting

53
Q

explain hyperglycaemia?

A

raised blood glucose levels - glucose secreted in urine (glycosuria)
osmotic diuresis leading to secondary polyuria and consequent polydipsia.
Diabetes Mellitus - release or total absence of insulin, tissues are unable to use glucose despite high plasma concentration

54
Q

describe Type 1/2 diabetes Mellitus?

A

types1 - failure of insulin secretion (most common in dogs)

type 2 - reduced insulin tissue sensitivity followed by beta cell failure (most common in cats)

55
Q

how can diabetes cause ketoacidosis?

A

glucose high BUT… unavailable to cells, glucagon raised.
protein catabolism and AA release for liver glucaneogensis. FA converted to acetyl CoA rather than triglycerides.
hepatic conversion of acetyl CoA to ketones and acetate.

56
Q

what is CATCH 22?

A

ketone and lactic acid in blood, leads to loss of electrolytes + H20 = dehydration.
Stress hormones increase = hyperglycaemia.
vicious speed of effect can lead to death

57
Q

what does an abrupt change to a diet cause in horses?

A

increased risk of colic/laminitis

58
Q

what are some key consideration of equine nutrition management?

A

eat grass little an often, 16hr/day
2%BW of food a day.
Hieracrhy is a thing and reduced fighting.
non ruminant herbivores, 200 litres. with foregut and hind gut. and magus pilicuts separating. saliva in horse is non-digestible

59
Q

what effects does an abrupt change to diet cause?

A

affects microbial populations, GIT disturbance

⬇️ diet digestability, ill health (colic)

60
Q

what can be done to change the diet in a horse gradually?

A

change to forage fraction less of a risk :)
DONT - Rapid increase in cereal grains :(
- rapid ⬇️ conc and ⬆️ forage :(
- rapid ⬆️ lush pasture :(

61
Q

what is good husbandry for an equine owner?

A 
adepuate housing
inspect for injury/disease often
routine grooming 
routine dental care 
infectious disease prevention 
programme control parasite burden
62
Q

what is lameness and how can it be controlled?

A

poor shoeing, prolonged intervals between shoeing, port foot, trauma, posture, ostertheimits. use a fairer to come and look at feet and replace old shoes etc/

63
Q

laminitis

A

pedal bone attachment to lamanae, failure to acctach instead. front feet, complex aetiopathogenesis. common in ponies

64
Q

how should the environment of a horse be respiratory disease free?

A

good clean housing, good ventilation, good drainage, low respirate dust environments within breathing zone of horse. (asthma/disease)

65
Q

what is severe equine asthma?

A

allergy to organic particles, inhaled dust/spores, cough/nasal discharge, repsirty rate and effect.

66
Q

what is infections diseases in equine?

A

UK and USA viruses, equine influenza, strangles, equine herpes, tetanus, parasites
prevention- vaccination/biosecurity.

67
Q

what is involved in biosecurity for animals?

A

isolation in NEW/CLEAN yard - 2 weeks

deworming, hygiene, manage horses in smaller groups, individual grooming kits

68
Q

name some UK vaccinations in equine?

A

Tetanus + Flu - essential, equien influenza, equine herpes aswell,

69
Q

what is equien influenza?

A

fever, nasal discharge, highly contagious, costly disease to racing world, <50% of UK is vaccinated

70
Q

what is tetanus prophylaxis?

A

lock jaw
produces neurotoxins with infected tissue,
vaccination for all horses.
two vaccines 1 month apart - booster 2-3 years.

71
Q

equine influenza A?

A

orthomyxovidae (RNAvirus) (two subtypes)
H7N7 - equine-1 (UK + Europe, North America)
H3N8 - equine-2 (china, uk, europe)

72
Q

explain the influenza vaccination regimen?

A
  1. vaccination - influenza + tetanus, 1 month
  2. vaccination - influenza + tetanus, 6 months
  3. vaccination - influenza, 1 year
    yearly boosters after that
73
Q

name some UK exotic disease in equine health?

A 
anthrax 2006
contagious equine metritis 2012
equine viral arteritis 2012
rabies 1920
warble fly 1990
piroplasmosis
74
Q

what are equine intestinal parasites?

A

lifelong succeptabulty to certain parasite species including tapeworms etc
infected when grazing, into stomach,
foals secceptiable to ascarid worm infection.

75
Q

Ascarids?

A

Parascaris equrorum, LARGEST nematode of horse, in S.I , larvae can carve tissue damage during migration
CAUSE COLIC

76
Q

Ascarids lifecycle?

A

hatching of third larvae (L3) in stomach + SI
larvae reach liver via portal vein migration.
leave reach lung via vena cava + right heart pervallatum into lung acerlarions as migration via tracheas + pharynx to SI

77
Q

Large Strongyles?

A

adult nematode resides in caecum and ventral colon.
Stronglye eggs, -easily detached by faeces.
associated with Colic - L4 larvae migrate in arteriole calls + cargocyte near cranial. messater root
life cycle - eggs in faeces grow in grass into L3 on grasses, eaten by h0rses, into adult adult stages.

78
Q

Cyathostomins?

A

leading nematode parthogn in horses, over 50 species!
resides in caecum and large colon, eggs easily detected
L3 larvae invade mucosal lining, form encysted larvae that may develop into L4 and erupt cyst and enter lumen.

79
Q

Gasterophilus?

A

Anthrapod - Bot fliles, most common - gastrophilus intestines, not general with disease.

80
Q

tapeworm?

A

resides in caecum, adjacent to ileocaecal valve, cause inflammation on site.
difficult to detect in eggs in faeces. serum/saliva, ELISA test more sensitive
associated with colic

81
Q

Colic?

A

clinical syndrome associated with abdominal pain, 7.19 colics/100 per year in horses.
No surgery required
causes - may involve GIT and other body systems. abstraction to normal gut motility diet + management- stabbing + excerise. Parasites
Dental care
stereotypes

82
Q

what is Gastric Ulceration Syndrome

A

High prevalence in thoroughbred racing horses
Stubbled for log period of time.
less forage/pasture
high intensity exercise

83
Q

what are geriatric horses?

A

old horses, >15 y/o

25-29% of UK.

84
Q

how is Digestible energy measured?

A

DE = GE - faeces energy

85
Q

how is metabolisable energy measured?

A

ME = DE - urine energy - gaseous energy

86
Q

how to calculate ME? in ruminants?

A

ME = 0.8 x DE (20% apparent DE is excreted)

87
Q

how does the Nitrogen balance raise and decrease in ME?

A

Nitrogen balance - excess of N in food - ⬆️ urea - ⬆️ urine - ⬇️ ME

88
Q

how is Net energy measured?

A

NE = ME - heat increment

heat increment includes - mastication, salivation, swallowing, 3-6% ME intake

89
Q

how is NE utilised for maintenance and production?

A 
utilisation of NE = ME x K(efficient factor) 
Km - mainatnce 
Kc - conceptes 
Kl - lactation 
Kg or Kf - growth
90
Q

what is the relevance of protein?

A

major source of nuturion/rations - dietary, endogenous

20 AA supplies in diet

91
Q

what is protein required for?

A 
tissue maintenance
protein in tissue 
wool and hair
milk
growth
gestation
92
Q

how do ruminants and non muminats get protein?

A

ruminants - from complex system of degradation and synthesis in rumen
non-ruminants - from AA from digestion of feed in S.I

93
Q

how is biological value measured?

A 
Biological value (BV) - direct measure of dietary protein that can be utilised by animal 
BV = N intake - (faeced N - MFN) - (urinary N - EUN) / N intake - (faeced N - MFN)

MFN - metallic faecal N
EUN - endogenous urianry N

94
Q

how is protein produced in Ruminants?

A

protein hydrolysed - AA and peptides
AA degreaded to NH3
NH3 utilised by rumen microbes to synthesis proteins
Microbes synthesise essential and non-essenal aa

95
Q

synthesis of protein in ruminants?

A

⬇️P = ⬇️NH3 ➡️ ⬇️NH3 = ⬇️microbial growth = ⬇️CHO digestion and intakes
⬆️P = ⬆️NH3 ➡️⬆️NH3 = converted into urea (via liver) = microbial P = NH3 requires CHO soluble.
most urea is excreted in urine some enter rumen via saliva.
EXCESS NH3 = TOXIC

BVMS Module 3 (3 decks)

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