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Veterinary Medicine Year 2 > ENI - Calcium and Phosphorous > Flashcards

ENI - Calcium and Phosphorous Flashcards

1
Q

What are the roles of bones in the musculoskeletal system?

A
  • Structural
  • Protection
  • Locomotion
  • Mineral reservoir
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2
Q

What are the anatomical regions of bones?

A
  • Condyles and tuberosities
  • Cortex
  • Medulla
  • Shaft
  • Metaphyses
  • Epiphyses
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3
Q

What cells are found in bone?

A
  • Osteocytes
  • Osteoblasts
  • Osteoclasts
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4
Q

Describe the organic component of bone

A
  • Osteoid (ground substance)
  • Synthesised by osteoblasts, secreted onto existing bone surface
  • made of collagen type I majority (some type V)
  • Fibrils embedded in water, glycoproteins, proteoglycans and bone sialoproteins
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5
Q

What glycoproteins are found in the ground substance of bone and what is their function?

A
  • Osteonectin
  • Osteocalcin
  • Binds collagen and mineral
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6
Q

What proteoglycans are found in the ground substance of bone and what is their function?

A
  • Biglycan
  • Decorin
  • Bind growth factors
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7
Q

What bone sialoproteins are found in the ground substance and what is their function?

A
  • Osteopontin
  • Thrombospondin
  • Associated with cell adhesion
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8
Q

Describe the inorganic component of bone

A
  • Bone mineral
  • 60-70% dryweight
  • Hardness and rigidity
  • Make bone radiopaque
  • Largely hydroxyapatite, carbonate and calcium phosphate crystals
  • Mineralisation ocurs as soon as osteod secreted and takes years to complete
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9
Q

What are the different fibre patterns (bone tissues)

A
  • Woven bone
  • Lamellar bone
  • Osteobnatal bone
  • Fibrolamellar bone
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10
Q

Describe the osteoblasts

A
  • Derived from mesenchymal stem cells
  • Synthesise and secrete osteoid
  • Active in mineralisation process
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11
Q

Describe the osteocytes

A
  • Scattered within matrix
  • Interconnected by dendritic processes
  • Derived from osteoblasts but stopped synthesis of matric and divisng
  • Residue within lacunae which are interconnected by canaliculi
  • Long lived and maintain matrix
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12
Q

Describe the osteoclasts

A
  • Responsible for bone resorption
  • Large cells, multiple nuclei
  • Release protons leading to acid environment for demineralisation
  • Secrete proteases that destroy organic matrix
  • Derived from bone marrow
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13
Q

Give the metabolic functions of bone

A
  • Mineral storage
  • Growth factor storage
  • Fat storage
  • Acid-base balance
  • Detoxification
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14
Q

Outline the role of bone as an endocrine organ

A
  • Controls phosphate metabolism by releasing fibroblast growth factor-23 (FGF-23)
  • Bone cells also release osteocalcin hormone
  • Osteocalcin increases insulin secretion and sensitivity
  • increases number of insulin producing cells, reduces stores of fat
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15
Q

Outline paracrine cell signalling within the bone

A
  • OSteobalsts and osteoclasts controlled by chemical factors - promote or inhibit activity
  • Control rate bone is made, destroyed, or changed in shape
  • Osteoblast stimulation: increase in osteoid levels and inhibition of osteoclasts ability to break down osseus tissue leading to increased bone mass
  • Osteoblasts secrete cytokines that promote resorption of bone by stimulating osteoclast acivity and differentiation from progenitor cells
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16
Q

How are osteoclasts inhibited?

A

Rate at which osteoclasts resorb bone is inhibited by calcitonin and osteoprotegrin

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17
Q

In what proportions is total calcium in the blood found?

A
  • 40% boudn to plasma proteins (albumin etc)
  • 10% complexed (citrate, phosphate)
  • 50% ionised (active) form
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18
Q

Where is the majority of calcium stored?

A

99% stored in bone as extrcellular matrix

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19
Q

When measuring calcium, which fraction should be measured?

A

Free, this is the active and reflects changes in the protein bound etc

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20
Q

What are the 2 mechanisms of reducing calcium fluctuations?

A
  • Buffering: exchangebale calcium in bone salts and mitochondria
  • Hormonal control
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21
Q

What are the homrones controlling calcium levels?

A
  • PTH (parathyroid hormone)
  • Calcitonin (from parafollicular/C-cells)
  • Calcitriol (active vit D)
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22
Q

What is the hormonal response to hypocalcaemia?

A
  • Low blood calcium
  • Increase PTH
  • Produce more calcitriol
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23
Q

What is the hormonal response to hypercalcaemia?

A
  • Decrease PTH

- Increase calcitonin

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24
Q

What stimulates activation of calcitriol?

A
  • PTH

- low blood phosphorous

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25
Q

What mechanisms does calcitriol use to exert its action?

A
  • calcium binding protein (calbindin)

- Calcium ATPase pumps (basolateral)

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26
Q

What are the actions of calcitriol?

A
  • Increases calcium absorption from the intestine
  • decreases calcium excretion by the kidneys
  • Needed for normal functioningof bone
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27
Q

Explain how calcitriol increases calcium absorption from the intestine

A
  • Increases active transport of calcium
  • Enters intestinal epithelial cells
  • Increases synthesis of calbindin
  • Takes approx 48 hours
  • Calcium uptake via facilitated diffusion
  • Accelerated by calcitriol activated calcium ATPase pumps on basolateral membranes (secondary active transport)
  • Calbindin ferries calcium from apical region to ATPase pumps on basolateral side
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28
Q

Describe the role of calcitriol in calcium excretion from the kidney

A
  • Decreases calcium excretion
  • Affects renal tubular epithelial cells
  • increase calcium (and phosphorous) reabsorption from urine
  • Weak effect in comaprison with PTH
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29
Q

Describe the role of calcitriol in normal bone function

A
  • Osteoblast and osteoclast functions
  • Both absorption and deposition of bone
  • Without vit D, is not resorbed in response to PTH
  • THorugh that vit D permits calcium transport across membranes
  • Excess vit D causes osseus proliferation (calcium deposition)
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30
Q

Where is PTH secreted?

A
  • Prinicpal (Chief) cells of parathyroid glands
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31
Q

Outline PTH synthesis

A
  • Preprohormone of 110 AAs
  • Then porhormone of 90 AAs
  • The into secretory vesicles as PTH (84 AAs)
  • N-terminus (first 34 AAs) mediates actions
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32
Q

Where is PTH degraded? Half life?

A
  • In the liver

- Short half life of 10 minutes

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33
Q

Describe PTH secretion

A
  • Continual, but increases as ECF ionised calcium levels decrease
  • Direct negative feedback system
  • Membrane receptors on principle cells
  • Coupled to G-protein, controls exocytosis of PTH containing vesicles
  • Secretion increases when iCa2+ falls (<1mmol/L) and decreases when it increases (1.25mmol/L)
  • Very responsive
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34
Q

Outline bone formation

A
  • Ongoing
  • Osteoclasts (multinucleated) erode bone and incorporate calcium into ECF
  • Osteoblast initially forms bone matrix and then becomes osteocyte
  • Continuous layer of osteocytes and osteoblasts that covers bone surface (osteocytic membrane)
  • Bone fluid between osteocytic memrbane and bone
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35
Q

What is the function of the osteocytic membrane?

A

Provides physical barrier between bone and extracellular fluid of the body

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36
Q

What are the 4 actions of PTH?

A
  • Bone: fast phase from bone fluid
  • Bone: slow phase from bone
  • Kidney: reabsorption within tubules
  • Intestine: indirect effect through activation of vitamin D
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37
Q

Describe the fast phase resorption from bone fluid

A
  • Minutes, increases for hours
  • Acts on existing osteocytes and blasts
  • Cells connected by osteocytic membrane system
  • Bone fluid between membrane and bone
  • Increased calcium uptake into ECF to restore calcium levls
  • PTH interacts with membrane receptors on osteoblasts and clasts
  • Increases permeability of Ca on bone fluid side of membrane
  • Increased Ca uptake from bone
  • Bone fluid calcium levels drop
  • Calcium phosphate crystals replace calcium in bone fluid (osteolysis)
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38
Q

Describe the slow phase resorption from bone

A
  • Activation of osteocalsts
  • No receptors for PTH, signal fromm activated osteocytes and blasts
  • 2 stages: existing osteoclasts activated, new ones formed
  • Progressive depletion of bone mineral via bone resorption
  • Multinucleated osteoclasts attach to bone, forms reaction chamber, bone resorption by release of organic acids nad proteolytic enzymes
  • Released Ca and P transported across osteoclast to blood
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39
Q

Describe the PTH in reabsorption of Ca from the kidney tubules

A
  • Increases calcium reabsorption in late distal tubules and collecting ducts
  • Results in retention of Ca and Mg
  • Decreases phosphorous reabsorption in renal proximal tubule
  • Results in rapid loss of phosphorous but retention of calcium
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40
Q

Describe PTH in the activation of calcitriol

A
  • Vitamin D from diet or skin
  • Final conversion in teh kidney
  • Catalysed by 1-alpha-hydroxylase activated by PTH
  • Rise in PTH leads to a ris ein calcitriol
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41
Q

Describe the control of calcium absorption within the GI tract

A
  • Calcitriol increases absorption from intestine

- Calcitonin secretion stimulated by gastrointestinal hormone e.g. gastrin, secretin

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42
Q

What is the role of calcitonin?

A
  • Stimulated by hypercalcaemia
  • Opposite effects to PTH on bone
  • Acts to reduce blood ionised calcium
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43
Q

Where is calcitonin secreted from?

A

Parafollicular cells of the thyroid gland

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44
Q

What stimulates calcitonin secretion?

A
  • Increased iCa2+ in plasma

- Gastrointestinal hormones such as gastrin, secretin stimulate secretion

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45
Q

What are the effects of calcitonin?

A
  • Fast phase bone response (inhibit osteoclast absorptive activities)
  • Slow phase one response (reduce formation of new osteoclasts)
  • Slight (insignificant) effects on kidney and intestinal tract
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46
Q

What are the functions of magnesium?

A
  • Co-factor for enzymes
  • Pumps depend on Mg (e.g. Na/K-ATPase)
  • ATP production and nucleic acid syntehsis
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47
Q

Outline the key poins of magnesium homeostasis

A
  • Not hormonally controlled
  • Whole body mg level is balance beween inflow and outflow
  • outflow via urine (affected by PTH), saliva (importnat in ruminants), milk (during lactation)
  • Excess inflow handled easily via excretion
  • Excess outflow not easily remedied
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48
Q

What would the effects of excess PTH secretion?

A
  • Hypercalcaemia due to excess bone resorption
  • Demineralisation leading to fragile bones
  • Hypophosphataemia due to increased secretion into urine
49
Q

What are the skeletal muscle signs of hypocalcaemia in the cow?

A
  • Recumbency
  • Weakness when attempting to stand
  • S bend in neck
50
Q

What are the reproductive tract signs of hypocalcaemia in the cow?

A
  • Poor uterine contraction leadign to uterine inertia, dystocia, still birth
  • Poor uterine involution leading to reatined foetal membranes, increased risk of metritis and increased risk of uterine prolapse
51
Q

What are the gastrointestinal tract signs of hypocalcaemia in the cow?

A
  • Reduced contractions and peristalsis
  • Reduced rumen turnover
  • Rumenal impaction
  • Constipation
  • Gassy bloat due to reduced eructation
52
Q

What are the cardiocasulcar signs of hypocalcaemia in the cow?

A
  • Redcued forve of contraction thus redued cardiac output adn reflex tachycardia
  • Peripheral vasoconstriction
  • Cold extremities, poor absorption of subcut medicines
53
Q

What are the signs of hypocalcaemia in horses?

A
  • Tetany e.g. thumps in endurance horses
  • Transport tetany, lactation tetany, eclampsia
  • Synchronous diaphragmatic flutter in extreme cases
54
Q

How does thumps occur?

A
  • Neuromuscular junction irritability increases with decreased calcium
  • Nerves controlling diaphragm dpolarise with each heart beat, as run close to the heart
  • Contraction of the diaphragm with each beat, leading to thumping respiratory effort
55
Q

Describe the clinical signs of hypocalcaemia in the dog

A
  • Eclampsia in dogs (lactation tetany)
  • usually post-partum
  • Tetany not paresis (stiff, whereas cows usually paretic/floppy)
56
Q

Describe the clinical signs of hypocalcaemia in reptiles and birds

A
  • Metabolic bone disease
  • Secondary to nutritional hyperparathyroidism (not enough UV, inappropriate diet, too much phsophate, not enough calcium, metabolise bone, weakens bone amtrix)
  • Pathological fracture
  • Tetany
57
Q

What are the roles of calciu in the body?

A
  • Muscle contraction
  • Decreases neurone Na permeability (thus preventing overstimulation of NMJs)
  • Mediates Ach release
58
Q

What are the physiological effects of hypocalcaemia?

A
  • Increased neuromuscular irritability (more likely to overpolarise, more frequent contractions)
  • Decreased smooth muscle contraction
  • Decreased skeletal muscle contraction
  • Reduced cardiac muscle contractility
59
Q

What are the sources of calcium in the body?

A
  • Blood (fast)
  • Reabsorption from urine (fast)
  • Intestinal (moderate)
  • Bone fluid (fast)
  • ## Bone matrix (slow)
60
Q

What factors affect the secretion and response to PTH?

A
  • Metabolic alkalosis at calving reduces reponse to PTH

- Insufficient Mg reduces PTH secretion and effect

61
Q

Why does parturient paresis (milk fever) develop in dairy cows?

A
  • Maintenance calcium is 25g/day (650kg, 20kg DMI cow)
  • Late pregnancy needs extra 13.9g/day
  • 12 litres of colostrum needs extra 30g/day
  • 40 litres of milk needs extra 73g/day
  • Huge cacium requirement, unable to eat enoguh to meet this demand
62
Q

Where do physiological mechansms fail with milk fever?

A
  • Not enough calcium taken in
  • Rapid increase in Ca demand at calving
  • Response to PTH ot strong enough
63
Q

What are the functions of phosphate?

A
  • DNA/RNA
  • NADP
  • ATP/ADP (oxidative phosphorylation)
  • Phosphate esters e.g. glucose-6-phosphae, phoslolipids
  • receptros and intracellular messenger function (phosphorylatings, protein kinase actions etc)
  • Hydroxyapatite of bon and teeth
  • Buffer
64
Q

Describe the locations of phosphate

A
  • 85% in bone

- Almost all of rest is intracellular organic, some ECF

65
Q

Describe the buffering action of phosphate

A

(HPO4)2- (weak alkali) and H2PO4- (weak acid) can move between various forms allowig it to acts as buffer and keep appropriate concentration of phosphate in EC

66
Q

Descirbe the relationship between calcium and phosphate

A
  • Law of mass action
  • High concetrnates of either or both in soluble give insoluble precipitates
  • Aim to keep levels at suitable point for bone minerallisation but not soft tissue
  • Food high in phos usually low in calcium e.g. meat
  • Connected control mechanisms
67
Q

Describe phosphate absorption

A
  • Intestinal promoted by calcitriol

- Renal reabsorption 80-90% PCT, rest in DCT

68
Q

Describe phosphate excretion

A
  • Renal loss increased by PTH
  • Salivary losses and recycling (cattle)
  • FGF-23 secreted by bone in response to phosphate is phosphaturetic and anti alpha1-hydroxylase, anti PTH (aim is to reduce phsophate in ECF, FGF-23 encourages loss through urine)
69
Q

Describe dietary deficiency of phosphorous

A
  • Herbivores grazing phosphorous deficient pasture without grain
  • Bone mineralisation affected (rickets, osteomalacia)
  • Pica
70
Q

Describe dietary excess of phosphorous

A
  • Assocaited with calcium deficiency
  • Ideally Ca:P ratio close to or >1
  • All meat diets
  • High cereal diets high phosphates, low calcium)
71
Q

What factors control phosphate in the body?

A
  • Dietary intake and absorption
  • Calcitriol
  • PTH
  • Renal tubular reabsorption
  • Phosphatonins FGF-23)
72
Q

How may hyperphosphataemia occur?

A
  • Reduced GFR leading to reduced clearance
  • Calcitriol promotes intestinal absorption (vitamin D toxicity)
  • Hypoparathyroidism
  • Young and growing (growth hormone at renal tubules, also in acromegaly)
  • increased bone turnover e.g. hyperadrenocorticism, hyperthyroidism
73
Q

Outline the role of FGF-23 on hyperphosphataemia

A
  • Decreased calcitriol, feedback to parathyroid to stimulate PTH production
  • Secondary renal hyperparathyroidism
  • OSteopaenia, osteomalacia, rubber jaw
  • Soft tissue mmineralisation if calcium also high
74
Q

Outline acute hyperphosphataemia

A
  • Leads to hypocalcaemia
  • Quick increase in phsophate will suck out all calcium possible, binds out leading to hypocalcaemia
  • Tetany
75
Q

Describe secondary renal hyperparathyroidism in hyperphosphataemia

A
  • Renal disease leading to reduced GFR, reduced PO4 clearance
  • Increased serum PO4 stimulating FGF-23
  • Complexed Ca fraction increases, ionised calcium fraction decreases
  • Leads to increased pTH secretion, increased bone resorption
  • Tubular damage
  • FGF-23 leads to decreased calcitriol
  • Polyuria leads to increased calcium losses
  • Poor appetite and decreased calcitriol meanpoor calcium uptake
76
Q

Describe the effects of hyperphosphataemia on calcium

A
  • Complexed fraction of calcium increases, albumin stays the same, ionised depleted to bind to phos
  • Increased total Ca butionised decreased
  • So total calcium is not accurate reflection of wha is going on in the body as the useable fraction has been decreased even if toal has increased
77
Q

What is rubber jaw?

A

Demineralisation of jaw bone due to over-resorption of bone stimulated by PTH (often due to hyperphosphataemia)

78
Q

Outline Bran disease in horses

A
  • Hyperphosphataemia in horses
  • Low calcium grasses (e.g. oxalates, bind to calcium)
  • High phosphorous grains
  • Low dietary Ca:P ratio
  • FGF-23 leads to decreased calcitriol
  • Ionised fraction decreases, increased PTH in response, eads to bone resorption
  • Bone loss from skull leads to swelling
79
Q

Describe the clinical consequences of hypophosphataemia

A
  • Relatively uncommon
  • Long term: osteomalacia, deformity, pain
  • muscle weakness, pain, decreased myocardial output, rhabdomyolysis
  • Haemolytic anaemia (ATP dependent membrane), increased oxygen binding leading to hypoxia (decreased diphosphoglycerate)
80
Q

Outline hypophosphataemia in downer cows

A
  • Often hypocalcaemic and hypophosphoataemic
  • Similar mechanism caused by high demand
  • Treatment with calcium alone will often correct via PTH and GI function, increased uptake
81
Q

Describe ruminant urolithiasis as a phosphorous disorder

A
  • High grain diets, high phos
  • Phosphate containing uroliths promoted (struvite, apatite)
  • Alkaline urine
  • reduced water intake
  • +/- obstruction of distal sigmoid flexure, near insertion of retractor penis muscle and at vermiform appendage
82
Q

Describe hypophosphataemia

A
  • Increased PTH or PTH related protein, promote P clearance
  • Dietary deficiency
  • Milk fever and eclampsia
  • lack of calcitriol
  • Insulin promotes uptake into cells
  • Diuresis
  • Fanconi syndrome (tubular cells unable to reabsorb phosphate, lose P)
83
Q

List the diagnostic tests used to differentiate phosphorous disorders

A
  • Serum/plasma phosphorous
  • Urea, creatinine
  • Total calcium, ionised calciu, albumin
  • Fractional excretion of phosphorous
  • PTH, 25OH vit D, calcitriol
  • FGF-23
84
Q

Describe the use of serum/plasma phosphorous in the diagnosis of phosphorous disorders

A
  • Haemolysis leading to release of P from RBCs
  • Can give false increase in serum P
  • Coccygeal/tail vein used in cattle as jugular runs from salivary glands which have a lot of P so would give falsely low P
85
Q

Describe the use of urea and creatinine in the diagnosis of phosphorous disorders

A

Give evidence of renal dysfunction which may be the cause of phosphate problems

86
Q

Describe the use of fractional excretion of phosphorous in the diagnosis of phosphorous disorders

A
  • Ratio of serum and urine phosphorous and creatinine

- Can measure reabsorption/secretion

87
Q

Describe the role of calcium in the neuromuscular junction

A
  • Action potential reaches axon terminal
  • Voltage gated Ca channels open
  • Ca in
  • Stimulates reelase of vesicles containing neurotransmitters via exocytosis
  • Ach binds to Ach gated ion chanels on post-synaptic side
  • Influx of Na generates end plate potential
  • Initiates action potential along muscle membrane
88
Q

Explain the role of calcium in skeletal muscle contraction

A
  • AP transmitted from muscle surface to transverse tubules
  • Ca ions releases close to myofibrils from SR
  • Binds to troponin C
  • Causes conformational change, tropomyosin changes position and exposes binding site for myosin heads
  • Sliding filament theory
89
Q

Explain the role of calcium in smooth muscle contraction

A
  • Increased intacellular calcium initiates contraction
  • 4 calcium ions bind to calmodulin, activates enzyme myosin kinase
  • kinase transfers phosphate from ATP to myosin head
  • Alters conformation and activates, allowing binding to actin
90
Q

Explain the role of calcium in cardiac muscle contraction

A
  • Calcium ion release from SR to muscle sarcoplasm
  • Bind to troponin C, moves away from actin binding site so actin and myosin can bind
  • Sliding filament model
91
Q

Explain why hypocalcaemia leads to tachycardia

A
  • Reduced contractility
  • But increased frequency of contractions due to increased irritability of NMJ
  • Reduced cardiac output due to reduced contractility so reflex increase in heart rate
92
Q

Why might high AST and creatinine be found in hypocalcaemic cows?

A
  • Muscle injury
  • Lots of muscle damage from lying on them, reduced blood flow to muscles
  • Damage due to pressur
93
Q

Why might CO2 be high and Cl be low in hypocalcaemic cows?

A
  • Total Co2 primarily composed of bicarb, is a measure of acid base balance
  • Bicarb major base
  • High levels suggest metabolic alkalosis
  • Plasma Cl low because metabolic alkalosis is present, to maintain electroneutrality Cl- will decrease when bicarb is high
94
Q

Explain how metabolic alkalosis predisposes cows to hypocalcaemia

A
  • Alkalosis leads to increase in albumin binding to calcium, ionised calcium levels low
  • PTH activates vit D
  • In metabolic alkalosis, prevents response to PTH
  • Less mobilisation from bone, less absorption at renal tubules, less absorption at intestines via calcitriol
  • More likely to become hypocalcaemic
95
Q

What is the main risk when infusing calcium to a hypocalcaemic cow?

A
  • Need to go slow as too much too fast may lead to dysrhyhmias and arrhythmias
  • Cardiac arrest and death possible
  • May also cause haematoma/blow vein
96
Q

How does parity affect the risk of hypocalcaemia?

A
  • Increased parity means more lactations
  • With each lactations, milk production increases
  • Thus in each lactation, there is increased energy and calcium requirement, more difficult for cow to keep up
97
Q

What is the effect of dehydration on total calcium?

A
  • High albumin
  • Thus increase in total calcium
  • But ionised calcium will be normal
98
Q

List the potential causes of hypercalcaemia

A

HOGS IN YARD

  • H = hyperparathyroidism
  • O = osteolysis
  • G = granulomatous disease
  • S = spurious (albumin, increased total ionised normal)
  • I = idiopathic
  • N = neoplasia
  • Y = young (normal physiology)
  • A = Addison’s disease
  • R = renal disease
  • D = vitamin D toxicity
99
Q

List the common causes of total hypercalcaemia in dogs

A
  • malignancy (tumour)
  • Hypoadrenocorticism (Addison’s)
  • Primary hyperparathyroidism
  • Chronic renal failure
  • Vitamin D toxicosis
  • Granulomatous diseases
100
Q

List the common causes of total hypercalcaemia in cats

A
  • Idiopathic
  • Renal failure
  • Malignancy (lymphoma and squamous cell carcinoma)
  • Primary hyperparathyroidism
101
Q

List the common causes of total hypercalcaemia in horses

A
  • Chronic renal failure
  • Vitamin D toxicosis
  • Hypercalcaemia of malignancy
  • Primary hyperparathyroidism
102
Q

Explain how PTH-related protein can cause hypercalcaemia

A
  • Same biological activity as PTH
  • Leads to bone resorption and thus increased blood calcium
  • Produced in utero or embryo bby cartilage, bone, muscle epithelium, CNS
  • Specific tumours secrete PTHrps and increase serum calcium
103
Q

What are the 3 mechanisms of hypercalcaemia of malignancy?

A
  • PTHrp production by neoplasia (humoral hypercalcaemia of malignancy)
  • Direct neoplasia-induced bone damage
  • Indirect neoplasia induced bone damage
104
Q

Explain how humoral hypercalcaemia of malignancy (PTHrp production by neoplasia) leads to hyperphosphataemia and low PTH

A
  • PTHrp leads to high blood calcium
  • negative feedback to parathyroid gland so reduce production of PTH
  • PTH needed for phosphate excretion, so end up with hig phosphate
105
Q

Describe the common laboratory abnormalities with hypercalcaemia of malignancy

A
  • Hypophosphataemia or normal phosphorous
  • Elevated (abnormal) THrp (majority of cases)
  • Normal or low PTH (negative feedback loop)
106
Q

Explain how indirect neoplasia induced bone damage leads to hypercalcaemia

A
  • Cytokines released from tumours

- Effect on osteoclasts leading to bone resorption

107
Q

Explain how primary hyperparathyroidism can lead to hypercalcaemia

A
  • Abnormality of principle cells
  • Gland functions autonomously, no response to negative feedback
  • Solitary adrenoma in 85-0% of cases
  • Or hyperplasia or carcinoma
  • Atrophy of unaffected glands
108
Q

What are some laboratory abnormalities seen with primary hyperparathyroidism leading to hypercalcaemia?

A
  • Hypophosphataemia or normal phosphorous
  • PTH normal or increased
  • PTHrp decreased to 0
109
Q

How is primary hyperparathyroidism leading to hypercalcaemia diagnosed?

A
  • Simultaneous iCa2+ and PTH concentrations (both high)
  • Ultrasound neck for enlarged parathyroid gland
  • Cervical exploratory surgery
110
Q

Explain secondary renal hyperparathyroidism

A
  • Chronic renal failure leads to increased phosphate retention (reducced excretion)
  • Decreased free Ca as binds to P
  • Decreased production of calcitriol as kidney damaged
  • Increased PTH to maintain iCa2+
  • Fast and slow retrieval from bone
  • Mineralisation in kidney worsens situation
  • Increased retrieval from bone and reduced excretion (high PTH) means high total Ca but low iCa2+
111
Q

What are the typical laboratory findings in secondary renal hyperparathyroidism?

A
  • Hyperphosphataemia
  • Hypercalcaemia (total)
  • Ioninsed calcium within normal limits
  • PTH normal to increased
  • Azotaemia increased BU and creatinine due to decreased reanl function)
  • PTHrp normal
112
Q

Describe idiopathic hypercalcaemia

A
  • Young to middle-aged cats
  • Mild to moderate hypercalcaemia
  • No obvious aetiology: hyperCa (total and ionised), normal P, intact PTH normal or decreased, PTHrp undetectable, normal calcitriol
  • No azotaemia, normal parathyroids
  • Calcium oxalate urinary stones secondary to increased Ca loss in urine
  • renal disease may develop as complication (obstruction, repeated UTIs)
113
Q

List the clinical signs of hypercalcaemia

A
  • PUPD
  • Weakness, depression, mental dullness
  • Anorexia, vomiting, constipation
  • Muscle twitching, shivering, seizures
  • Bradycardia, arrhythmias
  • Soft tissue mineralisation
  • Lower urinary tract signs
  • Bladder stone formation
  • +/- UTI
114
Q

How does hypercalcaemia lead to PUPD?

A
  • Ca antagonises ADH in kidney
  • Medullary washout
  • Secondary to renal damage
  • Secondary nephrogenic diabetes insipidus
115
Q

How does hypercalcaemia cause bradycadia and carrhythmias?

A
  • Increased contractility, increases cardiac output so reflex rate decreases
  • Decreased myocardial excitability
116
Q

Where does soft tissue mineralisation often occur in hypercalcaemia and what is the effect of this?

A
  • Kidneys, (can be any soft tissue)
  • Leads to progressive renal failure
  • Ca:P ratio dependent (high Ca but normal or low P less likely to get mineralisation)
117
Q

What are some lower urinary tract signs that may occur with hypercalcaemia?

A
  • Pollakiuria
  • Stranguria
  • Dysuria
118
Q

What are some common tumours that cause hypercalcaemia?

A
  • Lymphoma
  • Leukaemia
  • Anal gland tumours
  • Do this by producing PTHrp

Veterinary Medicine Year 2 (30 decks)

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