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Veterinary medicine year 2 > Nutrition > Flashcards

Nutrition Flashcards

1
Q

Where is phosphate used in the Body

A

DNA and RNA
NADP
ATP
Phosphate esters
Receptor and intracellular messenger function
Hydroxyapatite

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2
Q

What are the locations of phosphate in the body?

A

Bone
Intracellular organic molecules
Extracellular fluid

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3
Q

How does the law of mass action apply to calcium and PO4

A

High concentrations of either or both in a solution will form insoluble precipitates
Homeostasis aims to keep Ca and PO4 at levels suitable for mineralisation of bone but not soft tissue mineralisation

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4
Q

How is phosphate controlled?

A

Absorb more phosphate by calcitriol
Intestinal pho abs promoted by 1,25 Dihydroxy vitamin D (calcitriol)
Renal absorption PCT and DCT

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5
Q

How is phosphate excreted by the body?

A

PTH promotes renal PO4 losses
Salivary losses and recycling by cattle
FGF-23

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6
Q

What is FGF-23?

A

Fibroblast growth factor 23
Phosphophaeteamic peptide secreted by the bone in response to circulating phosphate
Phosphaturetic - promotes loss of phosphate

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7
Q

FGF-23 effect on calcitriol

A

Anti alpha 1 hydroxylase (inhibits the release of calcitriol)

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8
Q

Effect of FGF-23 on PTH

A

Anti PTH so stops the release of PTH

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9
Q

How can phosphate deficiencies occur and how does this present?

A

Herbivores grazing pasture without grain
Bone mineralisation and Pica

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10
Q

What occurs if there is an excess of dietary phosphate?

A

Associated with calcium deficiency
Ideally Ca:P ratio is Ca>P

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11
Q

Which factors control phosphate release?

A

Dietary intake and absorption
Calcitriol
PTH
Renal tubular resorption
Phosphatonins

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12
Q

How does Hyperphosphataemia occur?

A

Reduced GFR
Calcitriol = intestinal absorption (vit D toxicity)
Hypoparathyroidism
Increased bone turnover

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13
Q

Clinical presentation of hyperphosphataemia

A

Decrease calcitriol
Secondary renal hyperparathyroidism
Osteopenia, Osteomalacia, rubber jaw
Soft tissue mineralisation
Can cause hypocalcaemia as PO4 binds to calcium

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14
Q

How does increase phosphate = secondary renal hyperparathyroidism?

A

dec GFR-> red PO4 clearance-> inc serum PO4= FGF-23 release
Complex Ca inc but ionised Ca decrease
Ionised Ca dec = inc PTH so bone resorption
Tubular damage+ FGF23 = Dec calcitriol
Polyuria
Poor appetite and decreased calcitriol = poor uptake of calcium

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15
Q

How can secondary renal hyperparathyroidism be treated?

A

Therapeutic calcitriol

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16
Q

What Bran- disease?

A

Equine secondary hyperparathyroidism

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17
Q

What is the pathophysiology of Bran disease?

A

Low Ca and High phosphorus graind
Low Ca:P ratio
FGF23 decreases calcitriokl
Ionised Ca dec so ~PTH inc = bone resorption
Bone loss from the skull = swelling

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18
Q

How can PO4 be restricted?

A

PO4 restricted diets
PO4 binders - oral antacids - lanthanum carbonate

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19
Q

What is ruminant urolithiasis?

A

At risk - sheep, goats and fattening beef
High grain diets with high Phosphorus
Uroliths contain Struvite and apatite
Causes alkaline urine
Surgical treatmetn

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20
Q

Where do ruminant urolithiasis occur?

A

Urethral diverticulum

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21
Q

How does hypophosphotaemia occur?

A

Increased PTH
Dietary deficiency in PO4
Milk fever and eclampsia
Lack of calcitriol
Insulin promotes uptake into cells

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22
Q

Faconi syndrome

A

PCT defect

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23
Q

What is the clinical presentation of hypophosphataemia?

A

Muscle weakness and pain
Haemolytic anaemia, ATP dependent membrane
Inc oxygen binging -> hypoxia
Poor growth
Poor milk yields
Low fertility

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24
Q

What is the treatment for down cows?

A

IV phosphorous
often treatment with calcium alone will correct via PTH and GI function

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25
Q

How can phosphate levels be diagnosed?

A

Serum/ plasma phosphorus (cells might burst w hypo so could create false increase)
Urea, creatine as evidence of renal dysfunction
Total calcium , ionised calcium and albumin

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26
Q

Where is calcium found in the blood?

A

Bound to plasma proteins
Complexes (citrate)
Ionised calcium

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27
Q

How should the interpretation of total plasma calcium change with hypoproteinemia?

A

Total lower but ionised unchanged
Dont interpret low ca as hypocalcaemia
Ignore if low ca = Low albumin

28
Q

What are the 4 major actions of the parathyroid hormone?

A

Bone - fast phase get ca from bone fluid
Bone - slow phase gets Ca from bone
Kidney - reabsorption in tubules for more Ca
Intestine- indirect effect through activation of vit D to get calcium

29
Q

Calcitonin

A

Hormone with opposite actions to PTH
Secreted from thyroid cells

30
Q

Describe the effects of PTH on phosphorous homeostasis

A

Promotes Renal loss of phosphorous
Promotes absorption of phosphorous from the GI tract and release from bone

31
Q

How would a parathyroid tumour affect different structures of the body?

A

Fast and slow bone resorption
High plasma Ca
Low plasma phosphorous
In the urine calcium is retained and phosphorus will be excreted

32
Q

What would be the outcome of an animal on a high phosphorous diet with little Ca?

A

Nutritional secondary parathyroidism, increased FGF bine resorption, rubber jaw and big head

33
Q

Describe the process of calcitriol stimulated absorption by intestinal cells

A

Calcium channel proteins (luminal)
Calcium binding protein (calbindin)
Calcium ATPase pumps (basolateral)

34
Q

What role calcium play in nerve conduction?

A

Depolarisation - Membrane is permeable to Na ions which flow inwards
Repolarisation- Na channels close, K chanels more perm so K outwards = normal negative resting membrane potential

35
Q

What effect would a calcium deficit have on nerve conduction?

A

Sodium voltage gated channels open very easily because calcium binds to exterior channel to change electrical state

nerve fibre excitable
Nerves fire repetitively without stimulation

All occurs when ionised calcium drops below 50%

36
Q

Muscle tetany

A

Tetanic contraction of the muscles
When occurs in resp system can be fatal

37
Q

What role does calcium play in the neuromuscular synapse?

A

AP opens voltage gated Ca channels at NM synapse
Incr Ca conc in terminal
Inc rate of ACh vesicles fusion
Exocytosis of ACh into synaptic terminal
ACh binds to ACh gated ion channels in post sy
Influx of Na+ = end plate potential = AP

38
Q

What mechanism contracts skeletal muscles

A

Excitation contraction coupling

AP from Muscle surface-> transverse tubules
Ca released in myofibrils from SR
Ca binds to troponin C = contraction
Inhib affect of troponin tropomyosin complex on actin inhibited by Ca= musc contraction

39
Q

What mechanism contracts smooth muscle?

A

Similar to skeletal muscle contraction
Initiation is increase in intracellular Ca+
Nerve or hormonally regulated
No troponin instead calmodulin
Calmodulin binds with 4 Ca ions
Calmodulin Ca complex activated myosin kinase
Myosin kinase phosphorylates reg chain on myosin head which binds actin filament

40
Q

What is the mechanism by which cardiac muscle contracts?

A

Excitation contraction coupling
AP spreads over muscle membrane via T tubules
T tubule AP acts on longitudinal sarcoplasmic tbules = release of Ca from SR into musc sarcopalsm
Ca -> myofibrils
Myosin -> actin = muscle contraction

41
Q

How do structural differences between skeletal and cardiac muscle affect response to ECF calcium concentrations?

A

Skeletal musc have closed T tubules so Ca is released from SR so not affected as much by ECF ca conc
Cardiac musc- Open T tubules so ECF into interstitium to T tubules
Cardiac calcium directly related to ECF calcium conc

42
Q

How is calcium involved in inc cardiac contractility induced by catecholamines?

A

Norepinephrine = cardiac musc fibre to be more permeable to ca
Inc contractile strength

43
Q

What clinical signs would be seen in skeletal muscle of a bitch with eclampsia?

A

Ionised Ca in blood drops
Ca deficit = permeability changes to voltage gated Ca2+ and Na+
Inc influx of Na+ so excitable cells
means lower threshold and more musc contractions = tetanic muscle contractions

Tremors, twitching, musc spasm, stiffness, ataxia

44
Q

role of FGF23

A

Promotes renal losses of phosphorus

45
Q

High blood phosphorous leads to what parathyroid state?

A

Secondary hyperparathyroidism

46
Q

What can go wrong to cause hypercalcaemia?

A

Inc PTH activitt
Activity of PTH like substances
Increased Vit D activity
Osteolysis
HyperAC

47
Q

How is calcium homeostasis maintained?

A

PTH negative feedback - inc when low Ca dec when high Ca
Active vitamin D3 (calcitriol)- promoted by PTH, Inhibited by FGF-23

48
Q

What is PTH related peptide?

A

PTH related protein - same biological activity as PTH
Peptide hormone that shares 60% homology with PTH

49
Q

What is PTH rp produced by?

A

Cartilage
Bone
Muscle
Epithelium
CNS
Specific tumours

50
Q

What are the differential diagnoses for hypercalcaemia?

A

HARD IONS
Hyperparathyroidism
Addisons
Renal
Vit D
Idiopathic
Osteolysis
Neoplasia
Spurious

51
Q

What are the causes of HyperCa in dogs?

A
  1. Malignancy
  2. hypoadrenocorticism
  3. Primary hyperparathyroidism
  4. Chronic renal failure
  5. Vitamin D toxicosis
  6. Granulomatous diseases
52
Q

What are the causes of HyperCa in cats?

A
  1. Idiopathic hypercalcaemia
  2. Renal failure
  3. Malignancy
  4. Primary hyperparathyroidism
53
Q

What are the causes of total hyperCa in horses?

A

Chronic renal failure
Vitamin D toxicosis
Hypercalcaemia of malignancy
Primary HyperPT

54
Q

What are the clinical signs of hyperCa?

A

PUPD
Weakness
Anorexia, vomiting constipation
Musc twitching, shiverign seizures
Bradycarda, cardiac arrhythmias (inc cont, dec excitability)

55
Q

How is palpation carried out with suspicion for hyperCa?

A

lymph nodes
Anal sac masses
Other masses - neoplasia and granulomas
Angiostrongylus - imaging and faceal exam
Haematomas

56
Q

What are the lab tests for hypercalcaemia?

A

Total calcium
Ionised calcium
Phosphorus
PTH
PTH rp
Vitamin D

57
Q

What is hypervitaminosis D?

A

Increased Ca x P product causes soft tissue mineralisation

58
Q

How is PTH independent hyperCa investigated?

A

Low PTH and high iCa
No initial clinical appearance of neoplasia

Tests
PTHro
25 hydroxyvitamin D (calcidiol)
1, 25 dihydroxy vitamin D (calcitriol)

59
Q

Calcidiol

A

25 hydroxy vitamin D

60
Q

Calcitriol

A

1,25 dihydroxy vitamin D

61
Q

What is the role of calcium?

A

Muscle contraction
Decrease neurone sodium permeability
Mediate ACh release

62
Q

What pathology is associated with hypocalcaemia?

A

Inc iritability
Dec smooth musc contraction
reduced cardiac musc contraction
Decreased skeletal muscle contraction

63
Q

What are the clinical signs of milk fever?

A

Reduced muscle contractions
- Skeletal affects posture adn gait
- Smooth - repro tract and GI tract
- Cardiac - heart and circulation

64
Q

What is the pathophysiology of milk fever?

A

In dairy cows calving Ca demand rapidly increases
Ca loss through milk
Ca in plasma to PTH
PTH increase - inc Ca resorption from bone
Calcitriol increase to SI
more Ca absorption

65
Q

Why does metabolic alkalosis predispose to milk fever?

A

High cation diets can cause milk fever as they induce metabolic alkalosis
Reduced the ability of cow to maintain calcium

Metabolic alkalosis blocks binding of Ca to albumin and decreases ionised calcium

66
Q

How can milk fever be prevented?

A

Calcium restriction during close up transition dry period
Dietary cation anion balance
Oral supplementation with calcium at calving

Veterinary medicine year 2 (23 decks)

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