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Endocrinology > Calcium and Parathyroid Disorders > Flashcards

Calcium and Parathyroid Disorders Flashcards

1
Q

How do parathyroid hormones increase serum Calcium?

A
  1. Kidney: PTH inc Ca and dec PO reabsorption and inc active vit D.
  2. Bone: PTH causes bone resorption>bone formation, so Ca is released into blood.
  3. Small intestines: Inc Ca absorption due to active vit D (PTH indirect effect).
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2
Q

Describe how PTH regulates Ca homeostasis (starting with low Ca levels)

A
  1. Low Ca levels results in more PTH secreted
  2. This targets tissues in the body to: (i) Inc bone resorption, (ii) inc Ca reabsorption in kidneys, (iii) inc Ca absorption in gut (via active vit D).
  3. This feedback allows serum Ca to return to set point.
  4. PTH controls Ca balance to keep serum Ca in a narrow normal range.
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3
Q

How may low Ca levels impact cellular processes (neurones)? And what signs and symptoms would you see in a pt with low Ca levels?

A
  1. Resting state of Na-channels are stabilised by Ca.
  2. Low Ca would mean Na channels are unstable and so cells will depolarise more easily (more excitable)
  3. Tetany (involuntary muscle contraction), Chvostek’s, Trousseau;s sign, muscle cramps, abdominal pain, perioral tingling, seizures
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4
Q

How and when would you perform Chvostek sign?

A

Remember CHvostek = CHeek

  1. Neurological examination for hypocalcaemia and hypoparathyroidism
  2. Tapping of CN7 causes contraction of facial muscles
  3. Look for spasm of facial nerve - tetany, hyper-relexia.
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5
Q

How and when would you perform Trousseau’s sign?

A
  1. Test for hypocalcaemia and hypoparathyroidism
  2. Inflate BP cuff to systolic pressure for 5mins
  3. Hand spasm seen (carpo-predal spasm).
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6
Q

What is hypocalcaemia? RF?

A
  1. Lower than normal calcium levels that may be due to too little calcium entering or too much leaving the blood
  2. RF = vit D or Mg deficiency, Hx of GI disorders, pancreatitis, kidney failure, liver failure, anxiety disorders
  3. Note: mild hypocalcaemia pt can be asymptomatic
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7
Q

What are the causes of hypocalcaemia?

A
  • Hypoparathyridism
  • Low vitamin D
  • Kidney failure - reduced Ca absorb
  • Tissue injury
  • Too many blood transfusions
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8
Q

Describe presentation of hypocalcaemia

A
  • CATS
  • Convulsion (uncontrolled muscle spasms)
  • Arrythmias
  • Tetany and Tingling (Paresthesia)
  • Stridor and Spasms.
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9
Q

Ex + Investigation of hypocalcaemia

A
  1. Chvostek and Toursseau sign
  2. Bloods
    - Serum Ca must be done w/o tourniquet as venous stasis can result in falsely raised Ca
    - PTH, Vit D, Mg
  3. ECG - look for prolonged ST, AT, arrythmias
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10
Q

Treatment and Management of Hypocalcaemia (Main goal, acute, chronic, hypomagnesaemic)

A
  1. Main goal is to normalise Ca level by (i) Calcium gluconate, (ii) Vit D supplementation
  2. Acute = Oral/IV Ca gluconate if pt symptomatic or risk of complications
  3. Chronic = Ca and vit D supps, Calcitriol (renal impairment). Monitor serum and urine conc.
  4. If hypomagnesaemic = correct Mg level before as hypocalcaemia will resolve
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11
Q

Complication of hypocalcaemia

A
  1. CVD = Cardiovascular collapse, hypotension, dysrhythmias.

2. Neuro = Seizures, basal ganglia calcification, parkinsonism

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12
Q

Pseudohypoparathyroidism - What is it? Symptoms and Signs? Clinical features?

A
  1. Resistance to PTH that arises from Type 1 Albright hereditary osteodystrophy. Body produces appropriate PTH h/e tissues do not respond to its effect.
  2. Short stature, round face, short neck, short metacarpals, mild learning difficulties, other hormone resistance, diabetes mellitus
  3. High or normal PTH (NOTE: tissues don’t respond to this so it’s like there’s no PTH), hypocalcaemia, hyperphosphatemia
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13
Q

Hypoparathyroidism - what is it? RF? Causes (5)?

A
  1. Under production or lack of function of PTH
  2. RF = Fx, thyroid surgery, radiation, autoimmunity, low Mg
  3. (i) Parathyroidectomy (most common),
    (ii) Autoimmune polyendocrine syndrome type 1 - destroys PTG,
    (iii) Genetic conditions: DiGeorge syndrome - PTG can’t produce enough PTH, Autosomal dominant hypoparathyroidism - mutation in PTG cell’s Ca sensing receptor, Pseudohypoparathyroidism Type 1A - PTH isn’t a problem, tissues don’t respond to PTH
  4. Radiation or Drugs
  5. Mg deficiency
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14
Q

Symptoms of Hypoparathyroidism

A
  1. Hypocalcamia Sx (think CATS = Convulsions, arrhythmia, tetany, stridor)
  2. Hyperphosphatemia
  3. Calcification of basal ganglia, lens of eye (due to elevated serum calcium-phosphorus)
  4. Seizures
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15
Q

Presentation and History of Hypoparathyroidism

A
  1. Hx = Fx, thyroid surgery, radiation, autoimmunity, low Mg

2. Hypocalcaemia Sx, Bone pain, Abdo pain, Muscle pain, lethargy, headaches, brittle nails, dry hair and skin.

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16
Q

Examination of Hypoparathyroidism

A
  1. Chvostek sign
  2. Trousseau’s sign
  3. Physical examination
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17
Q

Investigation of Hypoparathyroidism

A
  1. Blood - low Ca, high PO, low PTH, normal ALP, Mg may be low, low active vitamin D.
  2. U&E (to exclude CKD)
  3. If autoimmune suspected look for TSH, thyroxine, thyroid autoantibodies, ACTH and adrenal antibodies
  4. 24h urine test - low Ca
  5. Other tests if required: ECG, MRI, renal ultrasound, hand radiography, genetic studies.
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18
Q

Treatment of Hypoparathyroidism

A
  1. Calcium and/or Vit D supplements
  2. IV Ca (severe hypocalcaemia)
  3. Stop medications that cause low Ca e.g. diuretics, PPIs
  4. Dietary - low PO, Ca and vit D diet e.g. diary
  5. Long term PTH replacement therapy.
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19
Q

What is hypercalcaemia? What are RF associated with it?

A
  • Higher than normal Ca levels
  • RF = (i) hormone related: PTH problems, adrenal insufficiency, acromegaly. (ii) Medication: lithium, excess vitamin D/A supps, diuretics. (iii) Medical conditions: sarcoidosis, TB, hodgkins lymphoma, renal impairment. (iv) Cancer treatment.
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20
Q

What causes hypercalcaemia (6)?

A
  1. COMMON: Osteoclastic bone resorption - Release of calcium into blood
  2. COMMON: Metastatic malignant tumour
  3. COMMON: Primary hyperparathyroidism
  4. Excess vitamin D via diet, supplements
  5. Medications - thiazide diuretics which inc Ca reabsorb
  6. More rare causes:
    • Thyrotoxocosis
    • Sarcoidosis
    • Familial hypocalciuric / benign hypercalcaemia
    • Immobilisation
    • Milk-alkali
    • Adrenal insufficiency
    • Phaeochromocytoma
21
Q

Describe how hypercalcemia impacts cellular processes (neurons and kidney)

A

Neurons

  1. Na-channels are stabilised by Ca
  2. High Ca makes it less likely for Na-channels to open
  3. Harder for cell to depolarise (less excitable)
  4. Causes slower or absent reflexes
  5. Slower muscle contractions - constipation, muscle weakness.

Kidneys

  1. Tries to excrete excess Ca - hypercalciuria
  2. H/e excess fluid leaves and pt feels dehydrated
  3. If long standing hypercalcaemia: Combination of dehydration and hypercalciuria –> formation of calcium oxalate kidney stones
22
Q

Clinical features, signs, symptoms of hypercalcaemia

A
  1. Skeletal = bone pain, osteoporosis, fractures
  2. neuro = fatigue, lethargy, muscle weakness, confusion, cognitive impairment, depression, GAD
  3. GI = nausea, vomiting, weight loss
  4. Renal = renal stones, thirst, polyuria, polydipsia, dehydration
  5. CV = hypertension, shortened QT interval, arrthymias
23
Q

Investigation of hypercalcaemia

A
  1. Blood:
    - corrected Ca levels
    - PTH, Mg, Phosphate, Vit D
    - U&E (assess hydration status, AKI, CKD)
    - 9am serum cortisol (if Addison’s suspected)
    - LFTs (exclude liver metastases or chronic liver failure)
    - TFTs (exclude thyrotoxicosis)
  2. ECG - shortening of QT interval
  3. Other tests: urine Ca, Phosphate, ACR, protein electrophoresis
24
Q

Treatment of hypercalcaemia (3 ways).

A

Main goal is to lower Ca levels with medication

  1. Inc Urinary Excretion - rehydrate (more Ca filtered out), loop diuretics (inhibit Ca reabsorb)
  2. Increase Gi excretion - glucocorticoids (dec Ca absorption)
  3. Prevent bone resorption by inhibiting osteoclasts - biphosphonates, calcitonin
25
Q

Treatment and management of hypercalcaemia (severe, acute, chronic, PTH-mediated)

A
  1. Urgent 2ww referral if malignancy
  2. Discontinue medications known to worsen it
  3. 0.9% saline will inc circulating volume and help inc Ca U/O
  4. Loop diuretic (furosemide) for fluid overload DOES NOT reduce serum Ca
  5. Rehydration
  6. IV Bisophonates - pamidronate, zolendronic acid (reduces bone turnover)
  7. Glucocorticoids - useful if vit D toxicity, sarcoidosis, lymphoma
  8. Calcitonin may be given

PTH-mediated hypercalcaemia

  1. Asymptomatic = monitor bone density, renal function and serum and urinary Ca levels.
  2. Symptomatic = dietary Ca reduced - minimise dairy products and leafy vegetables.
  3. If PTH raised and symptomatic refer for parathyroidectomy.
26
Q

What is hyperparathyroidism?

A

Overproduction of PTH

27
Q

What is primary hyperparathyroidism? Causes? Clinical features?

A
  1. Abnormal active PTG. Excess PTH made independently of Ca levels

Causes

  1. 80% Parathyroid adenoma
  2. Hyperplasia (parathyroid cells divide excessively -> growth of glands)
  3. <0.5% Maligant, parathyroid carcinoma

Clinical features?

  1. Hypercalcaemia - neurons less excitable, slower muscle contractions
  2. Hypophosphatemia
  3. Hypercalciuria and dehydration - as too much Ca is reabsorbed by kidney and excess loss in urine
28
Q

What is secondary hyperparathyroidism? Causes (3) ?

A
  1. PTG is normal but over production of PTH made in response to chronic hypocalcaemia.

Causes
1. CKD: At level of kidneys - less PO excreted, not enough active vitamin D made. Low Vit D, low Ca absorption at gut so PTH rise in response to low Ca

  1. Vit D deficiency: Chronic lack of vitamin D due to lack of sunlight, poor intake
  2. Hyperphosphatemia reduces amount of free calcium ions in blood as PO binds to Ca.
29
Q

What is tertiary hyperparathyroidism? Causes?

A

Individuals who have had secondary hyperparathyroidism (sHPT) for years and develop primary hyperthyroidism where parathyroid glands make PTH independent of Ca levels.

Clinical features

  • Hypercalcemia as result of untreated sHPT
  • Phosphate levels can vary depends on if individual has:
  • CKD = high PO
  • Kidney transplant = low PO (‘new kidneys’ are working and responding to Ca levels’)
30
Q

Symptoms of PRIMARY hyperparathyroidism

A

‘Stones, thrones, bones, groans, psychiatric overtones’

  1. Kidney, gallbladder stones
  2. Thrones: Polyuria, polydipsia
  3. Bone pain
  4. Groans: Constipation, abdo pain, and muscle weakness
  5. Depressed mood, confused
31
Q

Symptoms of SECONDARY hyperparathyroidism

A
  1. Often presents with CKD symptoms if primary cause
  2. Renal osteodystrophy (bone disease)
  3. Calcification in blood vessels of soft tissue due to high PO sticks to Ca and from bone-like crystals
32
Q

Symptoms of TERTIARY hyperparathyroidism

A
  1. Symptoms same as primary/hypercalcaemia:
    - Kidney, gallbladder stones
    - Polyuria
    - Bone pain
    - Constipation and muscle weakness
    - Depressed mood, confused
  2. PO-Ca calcification of blood vessel of soft tissues due to elevated PO levels
33
Q

Investigations and results for primary, secondary, tertiary hyperparathyroidism?

A
  1. Blood test:
    - Confirm PTH levels
    - serum levels of Ca, PO, Vit D
  2. Primary = high Ca, Low Po.
    Secondary = Low Ca, High Po, Low Vit D.
    Tertiary = high Ca but distinguished from primary if CKD present. PO depends if pt has CKD (high PO) or kidney transplant (low PO)
34
Q

Treatment of primary, secondary, tertiary hyperparathyroidism

A

Primary and tertiary

  1. Parathyroidectomy
  2. Cinacalcet - If unable for surgery or tertiary, these reduce PTH released from PTG
  3. Correct dehydration w/ IV fluids
  4. Fluids and balanced diet - avoid high Ca meals
  5. Avoid diuretics
  6. Consider bisphosphonates

Secondary - depends on cause

  1. Oral vitamin D (colecalciferol) = low vitamin D is the most common cause and can be corrected with this.
  2. Kidney disease = transplant if there’s kidney failure
35
Q

describe the three types of HYPO-PARA-thyroidism

A
  1. Hypoparathyroidism - Due to gland failure – causes reduced calcium with normal/raised phosphate and normal alkaline phosphatase
  2. Secondary Hypoparathyroidism - Due to an external cause - commonest cause is surgical damage leading to the same biochemical abnormalities as above
  3. Pseudohypoparthyroidism - Peripheral resistance to parathyroid hormone – causes reduced calcium, raised phosphate, normal or raised alkaline phosphatase
36
Q

Common clinical symptoms of hypercalcaemia.

A
  1. Weakness
  2. Tiredness
  3. Dehydration
  4. Renal Stones
  5. Fractures due to osteopaenia/osteoporosis
  6. Abdominal pain (constipation/pancreatitis)
  7. Depression/confusion
37
Q

What is the most common causes of HYPOparathyroidism

and primary HYPERparathyroidism

A
  1. Hypoparathyroidism = surgical removal of PTG during thyroidectomy
  2. Hyperparathyroidism = pituitary adenoma
38
Q

Where do we get Vitamin D from?

A

(1. ) Diet: Oily fish, red meats, liver, egg yolks, fortified foods - margarine, cereals
(2. ) Supplements
(3. ) Sunlight exposure

39
Q

Describe vitamin D metabolism to make active vitamin D

A

(1. ) Vitamin D is obtained and synthesized from diet and sun exposure to our skin.
(2. ) Two forms = D2 and D3 (cholecalciferol), these are biologically inactive
(3. ) In the liver and kidney, it undergoes a series of hydroxylation: Vitamin D –> 25(OH)D –> 1,25(OH)D (active)

40
Q

What is the importance of vitamin D?

A

(1. ) Ca homeostasis: Vitamin D promotes Ca and phosphate gut absorption
(2. ) Bone mineralisation & growth: Depends on adequate Ca and phosphate and this is maintained by vitamin D
(3. ) Immune system functioning

(4. ) Anti-tumour properties:
- Inhibits proliferation
- Induce differentiation
- Inhibits angiogenesis

41
Q

Vitamin D deficiency clinical features:

A

Low vit D = LOW CA, LOW PHOSPHATE

  • Hypocalcemia
  • Secondary hyperparathyroidism
  • Bone demineralization
  • Osteomalacia, osteoporosis,
    Rickets
  • Inc fracture risks
42
Q

What is osteomalacia ?

A

softening of bone due to insufficient minerals in the bone

43
Q

Osteomalacia vs Osteoporosis

A
  • Inosteoporosis, the bones are porousandbrittle, whereas inosteomalacia, the bones are soft.
  • This difference in bone consistency is related to the mineral-to-organic material ratio
44
Q

Aetiology of Vitamin D deficiency

A

(1. ) Insufficient dietary intake of vitamin D
(2. ) Lack of sunlight exposure
(3. ) Medications
(4. ) Malabsorption e.g. IBD, coeliac disease

(5.) Impaired active vitamin D synthesis:
Cirrhosis, renal failure, CKD

(6.) Obesity:
Vitamin D is fat soluble and can be sequestered and stored into adipose tissue

(7.) Increased need vitamin D:
Pregnancy, lactation

(8.) Genetics

45
Q

Risk Factors of Vitamin D deficiency

A

(1.) Dec sunlight exposure

(2. ) Reduced ability to absorb sunlight:
- Older age
- Darker skin = inc melanin, reduced ability absorb vitamin D

(3. ) Medications
(4. ) GI, liver, kidney conditions that cause malabsorption or impairs conversion of vitamin D
(5. ) High BMI
(6. ) Pregnancy

(7.) Vegan and vegetarian diet
Not eating fish, eggs

46
Q

Presentation of vitamin D deficiency

A
  • Asymptomatic
  • Low-mood, fatigue
  • Pain and muscle weakness
  • Infection
  • Bone and joint pain & tenderness
  • Hypocalcaemia related sx: Tetany, carpopedal spasm, O/E Trousseau, Chvostek’s sign
  • Fractures
47
Q

Ix of vitamin D deficiency (8)

A

Bloods

  1. Serum 25(OH)D
  2. Serum Ca, phosphate
  3. LFT: ALP, bone disease?
  4. PTH level: hyperparathyroidism?
  5. FBC: Anaemia may suggest malabsorption?
  6. Renal function: CKD, renal failure?

Further investigations if required:

  1. Wrist Xray: for Dx of rickets
  2. DEXA Scanning: osteoporosis?
48
Q

Treatment and Management of vitamin D deficiency

A

(1. ) Prevention and Education
- Dietary advice.
- Encourage exposure to sunlight.
- Vitamin D supplementation.

(2. ) Calciferol treatment
(a. ) if there is a deficiency
(b. ) Or has normal vit D but has:
- Osteoporosis, hi risk fracture, fragility fracture
- Antiresorptive drug
- Raised PTH
- Drugs known to causes vitamin D deficiency (antiepileptic, oral corticosteroids etc)
- Malabsorption disorder

Endocrinology (9 decks)

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