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Endocrine System > Lecture 12: Clinical Calcium Homeostasis > Flashcards

Lecture 12: Clinical Calcium Homeostasis Flashcards

1
Q

list dietary sources of calcium

A
  • milk, cheese and oher dairy foods
  • green leafy vegetables: broccoli, cabbage and okra
  • soya beans
  • tofu
  • nuts
  • bread and anything made with fortified flour
  • fish where you eat the bones such as sardines and pilchards
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2
Q

list the functions of calcium

A
  • bone formation
  • cell division & growth
  • muscle contraction
  • neurotransmitter release
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3
Q

what is the normal range of plasma calcium?

A

2.20-2.60 mmol/l

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4
Q

describe the process of stimulating parathyroid hormone secretion

A
  • Chief cells respond directly to changes in calcium concentrations.
  • alterations in ECF Ca2+ levels are transmitted into the parathyroid cells via calcium-sensing receptor (CaSR).
  • PTH is secreted by chief cells in response to a fall in calcium.
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5
Q

What are the functions of parathyroid hormone?

A
  • PTH has direct effects that promote reabsorption of calcium from renal tubules and bone.
  • PTH mediates the conversion of vitamin D from its inactive to active form.
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6
Q

What bone problem
might lengthy exposure
to inappropriate levels of
PTH lead to?

A

osteoporosis

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7
Q

where in the body does the conversion of vitamin D from its inactive to active form take place?

A

kidney

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8
Q

what is considered hypocalcaemia?

A

serum calcium < 2.20

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9
Q

list the causes of hypocalcaemia

A
  • diruption of parathyroid gland due to total thyroidectomy, may be temporary or permanent.
  • following selective parathyroidectomy (usually transient and mild).
  • severe vitamin D deficiency
  • Mg2+ deficiency
  • cytotoxic drug-induced hypocalcaemia
  • pancreatitis, rhabdomyolysis and large volume blood transfusions
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10
Q

clinical features of hypocalcaemia

SPASMODIC E

A
  • Spasms (Trousseau’s sign)
  • Perioral parasthaesia
  • Anxiety/irritability
  • Seizures
  • Muscle tone increase (colic, dysphagia)
  • Orientation impairment (i.e. confusion)
  • Dermatitis
  • Impetigo herpetiformis
  • Chvostek’s sign
  • ECG shows prolonged QTc
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11
Q

what investigations are performed for suspected hypocalcaemia

A
  • ECG
  • serum calcium
  • albumin
  • phosphate
  • PTH
  • U&es
  • vitamin D
  • magnesium
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12
Q

causes of hypoparathyroidism

A
  • agenesis (e.g. DiGeorge syndrome)
  • destruction (neck surgery, autoimmune disease)
  • infiltration (e.g. haemochromatosis or Wilson’s disease)
  • reduced secretion of PTH (neonatal hypocalcaemia, hypomagnesaemia)
  • resistance to PTH
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13
Q

describe pseudohypoparathyroidism

A
  • refers to a group of heterogeneous disorders defined by target organ (kidney and bone) unresponsiveness to PTH.
  • characterised by hypocalcaemia, hypophosphatemia and, in contrast to hypoparathyroidism, **elevated rather than reduced PTH concentrations. **
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14
Q

features of Albright’s hereditary osteodystrophy (AHO)

A
  • obesity
  • short stature
  • shortening of metacarpal bones
  • can occur in patients with pseudohypoparathyroidism
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15
Q

what does Albright’s hereditary Osteodystrophy (AHO) alone without abnormalities of calcium or PTH indicate?

A

pseudo-pseudohypoparathyroidism

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16
Q

describe the treatment of ‘mild’ hypocalcaemia

asymptomatic, > 1.9mmol/L

A
  • commence oral calcium tablets
  • if post-thyroidectomy repeat calcium 24 hours later
  • if vitamin D deficient, start vitamin D
  • if low Mg2+, stop any precipitating drug and replace Mg2+
17
Q

describe the treatment of ‘severe’ hypocalcaemia

symptomatic or < 1.9mmol/L

A
  • medical emergency
  • administer IV calcium gluconate
  • Initial bolus (10-20ml 10% calcium gluconate in 50-100ml of 5% dextrose IV over 10 minutes with ECG monitoring)
  • The initial bolus can be repeated until the patient is asymptomatic and/or calcium levels significantly increased
  • A Calcium gluconate infusion can then follow (100ml of 10% calcium gluconate in 1litre of 0.9% saline or 5% dextrose and infuse at 50-100ml/h)
  • Aim to achieve normocalcaemia
  • Treat the underlying cause
18
Q

when would active vitamin D be prescribed?

A

Vitamin D requires
hydroxylation by the kidney
to its active form, therefore
the hydroxylated derivatives
alfacalcidol or calcitriol
should be prescribed if
patients with severe renal
impairment require vitamin
D therapy

19
Q

clinical features of hypercalcaemia
- renal, GI, musculoskeletal, neurological, cardiovascular

A

Renal:
- polyuria
- polydipsia
- nephrolithiasis

Gastrointestinal:
- anorexia
- nausea and vomiting
- bowel hypomotility and constipation

Musculoskeletal:
- muscle weakness
- bone pain
- oesteoporosis

Neurological:
- decreased concentration
- confusion

Cardiovascular
- shortening of QT interval
- bradycardia
- hypertension

20
Q

hypercalcaemia investigations

A
  • U&Es
  • Ca
  • PO4
  • Alk phos
  • Myeloma screen
  • serum ACE
  • PTH
  • consider ECG
21
Q

two main causes of hypercalcaemia

A
  • primary hyperparathyroidism (parathyroid adenoma - 85%, four gland hyperplasia - 15%)
  • hypercalcaemia of malignancy
22
Q

primary hyperparathyroidism investigations

A
  • Ca, PTH
  • U&Es: check renal function
  • abdominal imaging: renal calculi
  • DEXA (bone density scan): osteoporosis
  • spot urinary calcium/creatine ratio
  • 24hr urinary calcium
  • vitamin D
23
Q

primary hyperparathyroidism treatment

A
  • surgery
  • generous fluid intake
  • vitamin D replacement
  • cinacalcet (acts as a calcimetic, i.e. mimic the effect of calcium on the calcium sensin receptor on chief cells, this leads to a fall in PTH and subsequently calcium levels)
24
Q

describe familial hypocalciuric hypercalcaemia (FHH)

A
  • autosomal dominant disorder of the calcium sensing receptor.
  • benign, no therapy indicated
  • low levels of urinary calcium
25
Q

describe MEN type 1

A

Multiple endocrine neoplasia type 1 (MEN1) is a rare genetic disorder that causes tumours to develop in the:
- parathyroid glands (> hyperparathyroidism)
- pituitary gland
- pancreas

  • caused by MENIN mutation (chromosome 11)
26
Q

describe MEN type 2A

A

Multiple endocrine neoplasia ype 2A is a genetic disorder that can cause:
- primary hyperparathyroidism (due to hyperplasia or adenomas)
- medullary thyroid cancer
- phaeochromocytoma

RET mutation

27
Q

hypercalcaemia acute management

A
  • 0.9% saline 4-6 litres over 24 hours
  • monitor for fluid overload
  • consider dialysis if severe renal failure
  • after rehydration > IV bisphosphonates e.g. zolendronic acid
28
Q

second line management of hypercalcaemia

A
  • glucocorticoids
  • calcitonin
  • calcimimetics
  • parathyroidectomy

Endocrine System (29 decks)

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