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Y4 SA - urinary & endocrine disease > Calcium disorders > Flashcards

Calcium disorders Flashcards

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1
Q

What facilitates calcium being taken out of the gut? What does this mean?

A
  • calcitriol
  • dogs, cats & people need vitamin d for calcium absorption
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2
Q

Where does vitamin d come from for most species?

A
  • diet rather than sunlight
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3
Q

What has to happen to the liver for it to not convert vitamin d?

A
  • it has to be almost non-existent
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4
Q

Where can problems occur in the formation of active vitamin d (calcitriol)?

A
  • in the kidneys
  • need to have enough renal tubules available for this
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5
Q

What hormone is anti-calcitriol? What does this work in response to?

A
  • FGF23: prevents calcitriol being made
  • in response to high phosphate concentrations
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6
Q

What is the calcium level in the blood ultimately controlled by?

A
  • Parathyroid hormone
  • PTH increases calcium levels if low
  • PTH control/monitors ionised calcium in the blood
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7
Q

EDTA contamination impact on calcium

A
  • makes it low
  • EDTA holds onto calcium in a blood sample to stop the blood from clotting
    – Calcium is a coag factor in most of the coag cascade
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8
Q

How does albumin affect calcium?

A
  • albumin/protein bound calcium
  • hypoalbuminaemia = low protein bound calcium
    – As long as ionised calcium is fine the animal with be physiologically fine i.e. not worried re specific calcium problem
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9
Q

What conditions/things can affect lab reading of calcium?

A
  • lipaemia
  • icterus
  • haemolysis
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10
Q

Calcium in the circulation - different components

A
  • ~50% ionised calcium
  • ~45% bound calcium
  • ~5% complexed calcium
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11
Q

How does phosphorus affect calcium?

A
  • with renal dz there is more phosphate in the blood
    – holds onto calcium
    – therefore, increased complexed calcium fracture
    – draws calcium out of the ionised calcium pool
    – so total calcium can look high but ionised calcium is lower
  • the body can recognise this and try to get the ionised calcium back to normal
    – if it succeeds can get an even higher total but normal or low ionised calcium
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12
Q

Renal secondary hyperparathyroidism

A
  • FGF-23, decreased calcitriol and reduced calcium absorption → ↑PTH
  • Hyperphosphatemia → increased complexed fraction of calcium
  • serum total calcium normal or high
  • ionised calcium low or low-normal
  • high serum parathyroid hormone
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13
Q

What can go wrong to cause hypercalcaemia?

A

Increased PTH activity
▪ Primary hyperparathyroidism

Activity of PTH-like substances
▪ Humoral hypercalcaemia of malignancy
– Parathyroid hormone related peptide (PTHrP)

Increased Vitamin D activity
▪ Dietary/toxin
▪ Granulomas

Osteolysis
▪ Local destruction of bone (neoplasia)

Other/unclear mechanism
▪ Hypoadrenocorticism
▪ Feline idiopathic hypercalcaemia
▪ Raisin toxicity

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14
Q

Causes of total hypercalcaemia in dogs (decreasing in prevalence)

A
  1. Malignancy
  2. Hypoadrenocorticism
  3. Primary hyperparathyroidism
  4. Chronic renal failure
  5. Vitamin D toxicosis
  6. Granulomatous diseases
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15
Q

Causes of total hypercalcaemia in cats (decreasing in prevalence)

A
  1. Idiopathic hypercalcaemia
  2. Renal failure (total mainly, occ iCa)
  3. Malignancy (lymphoma and squamous cell carcinoma)
  4. Primary hyperparathyroidism
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16
Q

HARD IONS/ HOGS IN YARD

A

▪H - Hyperparathyroidism
▪A - Addison’s
▪R – Renal (total Ca, horses)
▪D - Vitamin D
▪I - Idiopathic
▪O - Osteolysis
▪N - Neoplasia
▪S - Spurious

▪ H - HYPERPARATHYROIDISM
▪ O - OSTEOLYSIS
▪ G – GRANULOMATOUS DISEASE
▪ S – SPURIOUS (ALBUMIN?)
▪ I - IDOPATHIC
▪ N - NEOPLASIA
▪Y - YOUNG
▪ A – ADDISON’S DISEASE
▪ R – RENAL DISEASE (total Ca, horses)
▪ D – VITAMIN D TOXICITY

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17
Q

Principal differentials for hypercalcaemia

A

Parathyroid dependent (Primary hyperparathyroidism):
- Parathyroid adenoma
- Parathyroid adenocarcinoma
- Parathyroid hyperplasia
- Calcium sensor defect (FHH; theoretical)

Parathyroid independent:
- Humoral hypercalcaemia of malignancy
- Vitamin D excess
- Granulomatous disease
- Osteolysis
- Feline idiopathic hypercalcaemia
- Hypoadrenocorticism

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18
Q

Further differentials for hypercalcaemia - PTH independent

A

Malignancy:
- Lymphoma (T-cell)
- Anal sac apocrine gland adenocarcinoma
- Other carcinoma
- Myeloma
- Osteosarcoma
- Bone metastases
- Histiocytic neoplasia

Vitamin D excess:
- Over-supplementation
- Incorrect dietary formulation
- Rodenticide
- Vitamin D analogue (Dovobet/Dovonex)
- Plants
- Granulomatous disease
- Immunological (e.g. polyarthritis)

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19
Q

Hyperadrenocorticism causing hypercalcaemia

A

▪Usually mild hypercalcaemia but other signs are used to diagnose the disease
▪Present in ~30% of Addisonian dogs
▪Usually only affects total calcium; ionized calcium is normal (?)
▪Exact mechanism unknown
▪Dehydration and increased protein concentration
▪Decreased renal calcium excretion

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20
Q

Idiopathic hypercalcaemia (signalment, degree of hypercalcaemia, aetiology)

A

▪Young to middle-aged cats
▪Mild to moderate hypercalcaemia
▪No obvious etiology
–Hypercalcaemia (total and ionized)
–Normal phosphorus concentration
–Intact PTH normal or decreased
–PTHrp undetectable
–Normal vitamin D3 concentration
–?Association with acidifying diets

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21
Q

Presenting signs of hypercalcaemia

Study These Flashcards
A
  • Polyuria/polydipsia
  • dehydration
  • Vomiting
  • Anorexia
  • Muscle weakness
  • (consequences of urinary calculi)
  • (rubber jaw/ osteopenia)
  • (lymphadenopathy)
22
Q

Investigation - history

Study These Flashcards
A

Diet
▪ Supplements
▪ Unusual or unfamiliar brand
▪ Access to grapes/raisins

Access to vitamin D
▪ Supplements
▪ Rodenticide (cholecalciferol; not EU)
▪ Psoriasis medication (Dovonex/Dovobet)
▪ Certain plants

23
Q

Investigation - signalment

Study These Flashcards
A

▪ Primary hyperparathyoidism is middle-age to geriatric disease
▪ Breed predisposition (Keeshond)

24
Q

Issues when both phosphorus + calcium are high in hypercalcaemia (renal secondary hyperparathyroidism)

Study These Flashcards
A
  • calcium + phosphorus complex/precipitate leading to mineralisation in the tissues that damages organs + stops function (kidney, GI mucosa)
25
Clinical review - LN
▪ Palpation/Imaging
26
Clinical review - masses other than anal sac masses - what could they be?
▪ Neoplasia ▪ Granulomas
26
Clinical review - anal sac masses
▪ Rectal examination may be required ▪ Sublumbar lymph nodes on imaging
27
Parathyroid imaging
- US
28
Clinical review - angiostrongylus
▪ Imaging, faecal examination ▪ Haematomas, bleeding
29
Clin path
▪ Ionised Calcium** ▪ Albumin ▪ Phosphorus ▪ Chloride -- Cl:P >150 (in mmol/L) high specificity for 10 HPTH and AGASAC, low sensitivity ▪ Urea and creatinine ▪ Na:K ratio (+/- ACTH stimulation)
30
PTH/PTHrP excess findings: total calcium, ionised calcium and phosphorus
Total calcium: increased Ionised calcium: increased Phosphorus: decreased or normal
31
Vitamin D dependent findings: total calcium, ionised calcium and phosphorus
Total calcium: increased Ionised calcium: increased Phosphorus: increased
32
Renal secondary hyperparathyroidism findings: total calcium, ionised calcium and phosphorus
Total calcium: increased Ionised calcium: decreased or normal Phosphorus: normal (early) increased (late)
33
Azoteamic hypercalcaemia - which came first?
▪Renal dysfunction → elevated total calcium: ionised calcium normal or decreased ▪Elevated calcium → renal dysfunction: ionised calcium increased
34
PTH dependent hypercalcaemia
- PTH increased - Calcium increased
35
PTH independent hypercalcaemia
- PTH decreased - Calcium increased
36
Further Investigations beyond PTH and iCa
Most common requirement is: ▪Characterise parathyroid independent hypercalcaemia ▪Low PTH and high iCa ▪No initial clinical appearance of neoplasia/granuloma Relevant lab tests: ▪Parathyroid related peptide (PTHrP) ▪25 hydroxy-vitamin D (calcidiol) ▪1, 25 dihydroxy-vitamin D (calcitriol)
37
PTHrP
▪present in many humoral hypercalcemia of malignancy cases ▪Special shipping - very labile ▪Positive result helpful
38
25 hydroxy vitamin D
▪ 25 hydroxylation occurs in liver ▪ Excellent indicator of dietary sufficiency and excess ▪ Use for suspected cholecalciferol intoxication ▪ Rule out dietary mis-formulation ▪ Will not detect analogues ▪ Recognition of intestinal, cardiac and neoplastic risk ▪ UV adequacy
39
1, 25 dihydroxy vitamin D
▪ 1 α hydroxylation occurs in renal tubules ▪ 1 α hydroxylation occurs in macrophages/granulomata ▪ Lower when reduced renal tubular mass ▪ Implicated in pathogenesis of renal 20hyperPTH ▪ Will not detect analogues: Calcipotriene etc ▪ May be helpful in hypocalcaemia investigation
40
Generic treatment for hypercalcaemia
▪Determine urgency by Ca x P ▪ Fluids/diuresis --5ml/kg/hr NaCl --Furosemide 2mg/kg BID-TID – only once hydrated -- Care – check impact on potassium ▪ Glucocorticoids -- Pred 1mg/kg or equivalent ▪ Bisphosphanates -- Alendronate, clodronante, etidronate (oral) -- Pamidronate, zolendronate (IV) Caution: impact on future diagnostics if normalise iCa or e.g. impact lymphoma with glucocorticoid
41
More specific treatment
Depends on cause, treat directly: ▪Neoplasia (surgery/chemotherapy) ▪Toxicities – remove and generic Tx ▪Addison’s (DOCP, Florinef) ▪Idiopathic (diet, generic therapy (bisphosphonates, glucocorticoids)) ▪Primary hyperparathyroidism (surgery, percutaneous ablation) ▪Granulomatous (surgery/antimicrobials/antifungals) ▪Immune-mediated - immunosuppression
42
Parathyroid adenoma - peri- & post-surgical consideration
* Hyperactive nodule → hypercalcaemia * Hypercalcaemia→ negative feedback→atrophy of normal tissue * Remove nodule → HYPOcalcaemia * ?”hungrybones” * Monitor calcium post-surgically * Support with IV calcium (any point in oral?) * Vitamin D therapy (Calcitriol, Alfacalcidiol) * Aim for subclinical hypocalcaemia–provide stimulus for remaining tissue to regain function
43
Causes of hypocalcaemia
Parathyroid dependent ▪ Primary hypoparathyroidism -- spontaneous immune mediated -- functional hypomagnesaemic -- post-surgical e.g. feline hyperthyroidism Demand exceeds supply or mobilization ▪ periparturient tetany (eclampsia) ▪ nutritional deficiency of calcium or vitamin D -- e.g. all meat diets, severe GI disease ▪ pancreatitis with fat necrosis [PTH and Calcitriol resistance syndromes]
44
Hypoparathyroidism/hypocalcaemia clinical presentation
Signs associated with neuromuscular excitability: - muscle fasciculaton/tremors - face rubbing - biting & licking paws/body - hypersensitivity to external stimuli - stiff, stilted gait - ataxia - tetanic seizures - resp arrest - weakness Behavioural changes: - agitation - anxiety - vocalisation - aggression Other: - panting - hyperthermia - cataracts - lengthening or ST segment & QT interval on ECG - 3rd eyelid prolapse in cats
45
Hypocalcaemia diagnosis
▪ History ▪Routine lab results, e.g., phosphorus ▪Rarely PTH, iCa and Mg measurements
46
Hypocalcaemia - Short term/acute therapy
▪IV calcium -- Gluconate, e.g. 0.5-1.5ml/kg over 20-30 minutes -- Borogluconate -- Chloride ▪Monitor for bradycardia
47
Hypocalcaemia - Long-term therapy
Aim for subclinical or low-normal hypocalcaemia ▪ Post –thyroidectomy: want to stimulate remaining tissue ▪ Primary hypoparathyroidism: reduce risk of iatrogenic Vit D toxicosis Oral calcium supplement only if diet insufficient ▪ Sometimes used in early therapy Vitamin D to promote Calcium uptake ▪Initially short acting (lower risk, higher cost) - Calcitriol ▪Wean to intermediate/longer acting (higher risk lower cost) - Alfacidol, dihydrotachysterol
48
Primary hyperparathyroidism (CS, what is it, tx)
▪ Clinical signs of hypercalcaemia ▪ Excess (inappropriately high) PTH with hypercalcaemia ▪ Therapy by surgical removal (temporary medical by bisphosphonates)
49
Secondary hyperparathyroidism (types, CS, tx)
Renal ▪ Signs relating to renal disease, ?rubber jaw in extreme ▪Plasma phosphate, iCa, ?FGF-23 ▪ Tx phosphate restriction, ?calcitriol Nutritional ▪ Pathological fractures ▪ Correct nutritional deficiency (avoid all-meat diets)

Y4 SA - urinary & endocrine disease (16 decks)

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