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

Calcium disorders Flashcards

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

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

Investigation - history

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

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)

A
  • calcium + phosphorus complex/precipitate leading to mineralisation in the tissues that damages organs + stops function (kidney, GI mucosa)
25
Q

Clinical review - LN

A

▪ Palpation/Imaging

26
Q

Clinical review - masses other than anal sac masses - what could they be?

A

▪ Neoplasia
▪ Granulomas

26
Q

Clinical review - anal sac masses

A

▪ Rectal examination may be required
▪ Sublumbar lymph nodes on imaging

27
Q

Parathyroid imaging

A
  • US
28
Q

Clinical review - angiostrongylus

A

▪ Imaging, faecal examination
▪ Haematomas, bleeding

29
Q

Clin path

A

▪ 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
Q

PTH/PTHrP excess findings: total calcium, ionised calcium and phosphorus

A

Total calcium: increased
Ionised calcium: increased
Phosphorus: decreased or normal

31
Q

Vitamin D dependent findings: total calcium, ionised calcium and phosphorus

A

Total calcium: increased
Ionised calcium: increased
Phosphorus: increased

32
Q

Renal secondary hyperparathyroidism findings: total calcium, ionised calcium and phosphorus

A

Total calcium: increased
Ionised calcium: decreased or normal
Phosphorus: normal (early) increased (late)

33
Q

Azoteamic hypercalcaemia - which came first?

A

▪Renal dysfunction → elevated total calcium: ionised calcium normal or decreased
▪Elevated calcium → renal dysfunction: ionised calcium increased

34
Q

PTH dependent hypercalcaemia

A
  • PTH increased
  • Calcium increased
35
Q

PTH independent hypercalcaemia

A
  • PTH decreased
  • Calcium increased
36
Q

Further Investigations beyond PTH and iCa

A

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
Q

PTHrP

A

▪present in many humoral hypercalcemia of malignancy cases ▪Special shipping - very labile
▪Positive result helpful

38
Q

25 hydroxy vitamin D

A

▪ 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
Q

1, 25 dihydroxy vitamin D

A

▪ 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
Q

Generic treatment for hypercalcaemia

A

▪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
Q

More specific treatment

A

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
Q

Parathyroid adenoma - peri- & post-surgical consideration

A
  • 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
Q

Causes of hypocalcaemia

A

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
Q

Hypoparathyroidism/hypocalcaemia clinical presentation

A

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
Q

Hypocalcaemia diagnosis

A

▪ History
▪Routine lab results, e.g., phosphorus
▪Rarely PTH, iCa and Mg measurements

46
Q

Hypocalcaemia - Short term/acute therapy

A

▪IV calcium
– Gluconate, e.g. 0.5-1.5ml/kg over 20-30 minutes
– Borogluconate
– Chloride
▪Monitor for bradycardia

47
Q

Hypocalcaemia - Long-term therapy

A

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
Q

Primary hyperparathyroidism (CS, what is it, tx)

A

▪ Clinical signs of hypercalcaemia
▪ Excess (inappropriately high) PTH with hypercalcaemia
▪ Therapy by surgical removal (temporary medical by bisphosphonates)

49
Q

Secondary hyperparathyroidism (types, CS, tx)

A

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 (17 decks)

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