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Calcium and phosphorous Flashcards

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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
What mechanisms does calcitriol use to exert its action?
- calcium binding protein (calbindin) | - Calcium ATPase pumps (basolateral)
26
What are the actions of calcitriol?
- Increases calcium absorption from the intestine - decreases calcium excretion by the kidneys - Needed for normal functioningof bone
27
Explain how calcitriol increases calcium absorption from the intestine
- 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
28
Describe the role of calcitriol in calcium excretion from the kidney
- Decreases calcium excretion - Affects renal tubular epithelial cells - increase calcium (and phosphorous) reabsorption from urine - Weak effect in comaprison with PTH
29
Describe the role of calcitriol in normal bone function
- 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)
30
Where is PTH secreted?
- Prinicpal (Chief) cells of parathyroid glands
31
Outline PTH synthesis
- Preprohormone of 110 AAs - Then porhormone of 90 AAs - The into secretory vesicles as PTH (84 AAs) - N-terminus (first 34 AAs) mediates actions
32
Where is PTH degraded? Half life?
- In the liver | - Short half life of 10 minutes
33
Describe PTH secretion
- 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
34
Outline bone formation
- 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
35
What is the function of the osteocytic membrane?
Provides physical barrier between bone and extracellular fluid of the body
36
What are the 4 actions of PTH?
- Bone: fast phase from bone fluid - Bone: slow phase from bone - Kidney: reabsorption within tubules - Intestine: indirect effect through activation of vitamin D
37
Describe the fast phase resorption from bone fluid
- 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)
38
Describe the slow phase resorption from bone
- 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
39
Describe the PTH in reabsorption of Ca from the kidney tubules
- 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
40
Describe PTH in the activation of calcitriol
- 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
41
Describe the control of calcium absorption within the GI tract
- Calcitriol increases absorption from intestine | - Calcitonin secretion stimulated by gastrointestinal hormone e.g. gastrin, secretin
42
What is the role of calcitonin?
- Stimulated by hypercalcaemia - Opposite effects to PTH on bone - Acts to reduce blood ionised calcium
43
Where is calcitonin secreted from?
Parafollicular cells of the thyroid gland
44
What stimulates calcitonin secretion?
- Increased iCa2+ in plasma | - Gastrointestinal hormones such as gastrin, secretin stimulate secretion
45
What are the effects of calcitonin?
- 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
46
What are the functions of magnesium?
- Co-factor for enzymes - Pumps depend on Mg (e.g. Na/K-ATPase) - ATP production and nucleic acid syntehsis
47
Outline the key poins of magnesium homeostasis
- 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
48
What would the effects of excess PTH secretion?
- Hypercalcaemia due to excess bone resorption - Demineralisation leading to fragile bones - Hypophosphataemia due to increased secretion into urine
49
What are the skeletal muscle signs of hypocalcaemia in the cow?
- Recumbency - Weakness when attempting to stand - S bend in neck
50
What are the reproductive tract signs of hypocalcaemia in the cow?
- 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
What are the gastrointestinal tract signs of hypocalcaemia in the cow?
- Reduced contractions and peristalsis - Reduced rumen turnover - Rumenal impaction - Constipation - Gassy bloat due to reduced eructation
52
What are the cardiocasulcar signs of hypocalcaemia in the cow?
- Redcued forve of contraction thus redued cardiac output adn reflex tachycardia - Peripheral vasoconstriction - Cold extremities, poor absorption of subcut medicines
53
What are the signs of hypocalcaemia in horses?
- Tetany e.g. thumps in endurance horses - Transport tetany, lactation tetany, eclampsia - Synchronous diaphragmatic flutter in extreme cases
54
How does thumps occur?
- 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
Describe the clinical signs of hypocalcaemia in the dog
- Eclampsia in dogs (lactation tetany) - usually post-partum - Tetany not paresis (stiff, whereas cows usually paretic/floppy)
56
Describe the clinical signs of hypocalcaemia in reptiles and birds
- 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
What are the roles of calciu in the body?
- Muscle contraction - Decreases neurone Na permeability (thus preventing overstimulation of NMJs) - Mediates Ach release
58
What are the physiological effects of hypocalcaemia?
- Increased neuromuscular irritability (more likely to overpolarise, more frequent contractions) - Decreased smooth muscle contraction - Decreased skeletal muscle contraction - Reduced cardiac muscle contractility
59
What are the sources of calcium in the body?
- Blood (fast) - Reabsorption from urine (fast) - Intestinal (moderate) - Bone fluid (fast) - Bone matrix (slow) -
60
What factors affect the secretion and response to PTH?
- Metabolic alkalosis at calving reduces reponse to PTH | - Insufficient Mg reduces PTH secretion and effect
61
Why does parturient paresis (milk fever) develop in dairy cows?
- 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
Where do physiological mechansms fail with milk fever?
- Not enough calcium taken in - Rapid increase in Ca demand at calving - Response to PTH ot strong enough
63
What are the functions of phosphate?
- 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
Describe the locations of phosphate
- 85% in bone | - Almost all of rest is intracellular organic, some ECF
65
Describe the buffering action of phosphate
(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
Descirbe the relationship between calcium and phosphate
- 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
Describe phosphate absorption
- Intestinal promoted by calcitriol | - Renal reabsorption 80-90% PCT, rest in DCT
68
Describe phosphate excretion
- 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
Describe dietary deficiency of phosphorous
- Herbivores grazing phosphorous deficient pasture without grain - Bone mineralisation affected (rickets, osteomalacia) - Pica
70
Describe dietary excess of phosphorous
- Assocaited with calcium deficiency - Ideally Ca:P ratio close to or >1 - All meat diets - High cereal diets high phosphates, low calcium)
71
What factors control phosphate in the body?
- Dietary intake and absorption - Calcitriol - PTH - Renal tubular reabsorption - Phosphatonins FGF-23)
72
How may hyperphosphataemia occur?
- 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
Outline the role of FGF-23 on hyperphosphataemia
- Decreased calcitriol, feedback to parathyroid to stimulate PTH production - Secondary renal hyperparathyroidism - OSteopaenia, osteomalacia, rubber jaw - Soft tissue mmineralisation if calcium also high
74
Outline acute hyperphosphataemia
- Leads to hypocalcaemia - Quick increase in phsophate will suck out all calcium possible, binds out leading to hypocalcaemia - Tetany
75
Describe secondary renal hyperparathyroidism in hyperphosphataemia
- 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
Describe the effects of hyperphosphataemia on calcium
- 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
What is rubber jaw?
Demineralisation of jaw bone due to over-resorption of bone stimulated by PTH (often due to hyperphosphataemia)
78
Outline Bran disease in horses
- 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
Describe the clinical consequences of hypophosphataemia
- 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
Outline hypophosphataemia in downer cows
- 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
Describe ruminant urolithiasis as a phosphorous disorder
- 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
Describe hypophosphataemia
- 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
List the diagnostic tests used to differentiate phosphorous disorders
- Serum/plasma phosphorous - Urea, creatinine - Total calcium, ionised calciu, albumin - Fractional excretion of phosphorous - PTH, 25OH vit D, calcitriol - FGF-23
84
Describe the use of serum/plasma phosphorous in the diagnosis of phosphorous disorders
- 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
Describe the use of urea and creatinine in the diagnosis of phosphorous disorders
Give evidence of renal dysfunction which may be the cause of phosphate problems
86
Describe the use of fractional excretion of phosphorous in the diagnosis of phosphorous disorders
- Ratio of serum and urine phosphorous and creatinine | - Can measure reabsorption/secretion
87
Describe the role of calcium in the neuromuscular junction
- 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
Explain the role of calcium in skeletal muscle contraction
- 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
Explain the role of calcium in smooth muscle contraction
- 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
Explain the role of calcium in cardiac muscle contraction
- 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
Explain why hypocalcaemia leads to tachycardia
- 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
Why might high AST and creatinine be found in hypocalcaemic cows?
- Muscle injury - Lots of muscle damage from lying on them, reduced blood flow to muscles - Damage due to pressur
93
Why might CO2 be high and Cl be low in hypocalcaemic cows?
- 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
Explain how metabolic alkalosis predisposes cows to hypocalcaemia
- 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
What is the main risk when infusing calcium to a hypocalcaemic cow?
- 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
How does parity affect the risk of hypocalcaemia?
- 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
What is the effect of dehydration on total calcium?
- High albumin - Thus increase in total calcium - But ionised calcium will be normal
98
List the potential causes of hypercalcaemia
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
List the common causes of total hypercalcaemia in dogs
- malignancy (tumour) - Hypoadrenocorticism (Addison's) - Primary hyperparathyroidism - Chronic renal failure - Vitamin D toxicosis - Granulomatous diseases
100
List the common causes of total hypercalcaemia in cats
- Idiopathic - Renal failure - Malignancy (lymphoma and squamous cell carcinoma) - Primary hyperparathyroidism
101
List the common causes of total hypercalcaemia in horses
- Chronic renal failure - Vitamin D toxicosis - Hypercalcaemia of malignancy - Primary hyperparathyroidism
102
Explain how PTH-related protein can cause hypercalcaemia
- 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
What are the 3 mechanisms of hypercalcaemia of malignancy?
- PTHrp production by neoplasia (humoral hypercalcaemia of malignancy) - Direct neoplasia-induced bone damage - Indirect neoplasia induced bone damage
104
Explain how humoral hypercalcaemia of malignancy (PTHrp production by neoplasia) leads to hyperphosphataemia and low PTH
- 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
Describe the common laboratory abnormalities with hypercalcaemia of malignancy
- Hypophosphataemia or normal phosphorous - Elevated (abnormal) THrp (majority of cases) - Normal or low PTH (negative feedback loop)
106
Explain how indirect neoplasia induced bone damage leads to hypercalcaemia
- Cytokines released from tumours | - Effect on osteoclasts leading to bone resorption
107
Explain how primary hyperparathyroidism can lead to hypercalcaemia
- 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
What are some laboratory abnormalities seen with primary hyperparathyroidism leading to hypercalcaemia?
- Hypophosphataemia or normal phosphorous - PTH normal or increased - PTHrp decreased to 0
109
How is primary hyperparathyroidism leading to hypercalcaemia diagnosed?
- Simultaneous iCa2+ and PTH concentrations (both high) - Ultrasound neck for enlarged parathyroid gland - Cervical exploratory surgery
110
Explain secondary renal hyperparathyroidism
- 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
What are the typical laboratory findings in secondary renal hyperparathyroidism?
- 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
Describe idiopathic hypercalcaemia
- 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
List the clinical signs of hypercalcaemia
- 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
How does hypercalcaemia lead to PUPD?
- Ca antagonises ADH in kidney - Medullary washout - Secondary to renal damage - Secondary nephrogenic diabetes insipidus
115
How does hypercalcaemia cause bradycadia and carrhythmias?
- Increased contractility, increases cardiac output so reflex rate decreases - Decreased myocardial excitability
116
Where does soft tissue mineralisation often occur in hypercalcaemia and what is the effect of this?
- 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
What are some lower urinary tract signs that may occur with hypercalcaemia?
- Pollakiuria - Stranguria - Dysuria
118
What are some common tumours that cause hypercalcaemia?
- Lymphoma - Leukaemia - Anal gland tumours - Do this by producing PTHrp

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