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ENDO 2 Exam II (2017) > Pales calcium lecture > Flashcards

Pales calcium lecture Flashcards

1
Q

PTH is regulated by

A

ionized calcium levels. If Ca is high– thyroid releases calcitonin–> increased deposition in bones, decreased uptake in intestines and reabosorption from urine

If Ca levels low–> Parathyroid releases PTH–> increased CA release from bones, uptake in intestines and reabsorption from urine

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2
Q

What Does PTH Do to Osteoblasts

A

Thought to actually INCREASE osteoblastic activity, but not too much
Net effect is still resorption

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3
Q

PTH Feedback Mechanisms

A

PTH secretion is modulated by calcium sensing receptors on membranes of parathyroid cells

  • High ionized Ca+ causes reduced PTH secretion
  • Low Mag also decreases PTH secretion
  • – High Mag can depress PTH as well
  • Hypocalcemia increases secretion

PTH increases renal loss of phosphate
Decreases serum phosphate levels

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4
Q

Vitamin D Axis

A

Second important regulator of Calcium
Vitamin D3 derived from diet
UV light converts cholesterol precursors to Vitamin D3
Increases calcium and phosphate absorption in gut
Suppresses parathyroid cell function

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5
Q

Most common cause of hypercalcemia

A

Primary Hyperparathyroidism

Single parathyroid adenoma in over 80% of cases
Double adenoma or gland hyperplasia in 20%
Carcinoma less than 1%
– Up to 5% if patient is under 30 years

Multiple Endocrine Neoplasia (10% of cases)

  • Parathyroid hyperplasia seen in MEN 1, 2A, and 2B
  • Multiglandular hypothyroidism is prominent in MEN 1
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6
Q

Primary Hyperparathyroidism presentation

A

Usually presents as asymptomatic hypercalcemia or with renal stones
Phosphate and bicarbonate wasting
- Non-anion gap metabolic acidosis
- Cortical bone loss leading to osteoporosis

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7
Q

Tertiary Hyperparathyroidism

A

Reduced activation of Vitamin D in the setting of chronic renal disease leading to elevated PTH

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8
Q

renal osteodystrophy

A

chronic renal failure –> decreased calcitriol –> decreased ca absorption–> increased PTH –> osteitis fibrosa cystica

aluminum –> osteomalacia

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9
Q

Familial Benign Hypocalciuric Hypercalcemia

A

Easily mistaken for mild hyperparathyroidism
Autosomal dominant inherited disorder
- Causes loss-of-function mutation in CaSR
— Calcium Sensing Receptors on parathyroid glands (Reduced sensing of calcium = increased PTH secretion)
— Calcium Sensing Receptors on renal tubules (Reduced sensing of calcium = reduced calcium in urine)
Normal or mildly elevated PTH and magnesium
Diagnose with low urinary calcium clearance
Surgery does not help – treat medically

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10
Q

Signs and Symptoms - Hypercalcemia

A

Fatigue, polyuria, weakness, anorexia, nausea, vomiting, constipation, abdominal pain, lethargy, mental status changes
Severe – coma or arrhythmias
“Stones, bones, abdominal groans, psychic moans with fatigue overtones”

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11
Q

Osteitis Fibrosa Cystica

A

Excessive PTH causes

  • Chronic bone resorption
  • Demineralization
  • Pathologic fractures
  • Cystic bone lesions
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12
Q

Evaluation of Hypercalcemia

A

check PTH. If High or normal- parathyroid mediated. check 24-hour urinary calcium. Ca low- benign familial hypercalcemia.
Ca high- primary hyperparathyroidism, evaluate for surgical indications

if PTH is low, non-parathyroid mediated. Cancer? granulomatous disease? thyroid, adrenal diseases? Consider checking PTHrP, vitamin D metabolites

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13
Q

Management of Hypercalcemia

A

Intravenous fluids
Loop diuretic medications (such as furosemide) to help flush excess calcium from the system and keep the kidneys functioning
Intravenous bisphosphonates, a group of drugs that includes pamidronate (Aredia) and zolendronate (Zometa), to prevent bone breakdown
Calcitonin, a hormone produced by the thyroid gland, to reduce bone reabsorption and slow bone loss
Glucocorticoids (corticosteroids) to help counter the effects of too much vitamin D in the blood caused by hypercalcemia
Cinacalcet (Sensipar), a calcimimetic that activates CaSR. Primarily used to treat secondary hyperparathyroidism in renal disease or hypercalcemia with parathyroid carcinoma.
Hemodialysis or peritoneal dialysis to remove excess waste and calcium from the blood if the kidneys are damaged and there is no response to other treatments

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14
Q

Acquired Hypoparathyroidism- postoperative

A 
S/P thyroidectomy 
- Usually transient but can be permanent
S/P multiple parathyroidectomies
S/P removal of parathyroid adenoma
- Transient – due to suppression of remaining glands
S/P neck irradiation
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15
Q

causes of Acquired Hypoparathyroidism- Parathyroid damage

A 
Exposure to heavy metals
- Copper (Wilson’s Disease)
- Iron (Hemochromatosis, transfusion hemosiderosis)
Granulomas
Sporadic immunity
Tumors
Infection
Riedel’s thyroiditis
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16
Q

Acquired Hypoparathyroidism- functional

A 
Magnesium deficiency (malabsorbtion, alcoholism)
Prevents the secretion of PTH
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17
Q

Acquired Hypoparathyroidism- PGA Type 1: Autoimmune polyendocrinopathy

A

AKA Autoimmune Polyendocrinopathy Candidiasis ectodermal dystrophy (APECED)

Presents in childhood with two of the following:
- Candidiasis
- Hypoparathyroidism
- Addison disease
May have cataracts, uveitis, alopecia, vitiligo or autoimmune thyroid disease

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18
Q

Congenital Hypoparathyroidism- 3 types

A

Abnormal calcium-sensing receptors suppress the parathyroid glands

  • Hypocalcemia without elevated PTH
  • Autosomal dominate hypocalcemia with hypercalciuria
  • Affects 1 in 70,000 infants with seizures

Barakat or HDR Syndrome

  • Hypoparathyroidism, Deafness, Renal dysplasia
  • Autosomal dominant mutation of GATA3
  • Hypocalcemia and high frequency deafness from birth
  • Later mental retardation & hypocalcemic tetany

DiGeorge’s Syndrome
- Congenital cardiac and facial anomalies
- Deletion of Chromosome 22
- Hypocalcemia with tetany
Usually in infancy, but sometimes not until adulthood

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19
Q

DiGeorge’s Syndrome

A 
Cardiac Abnormalities
- (tetrology of Fallot)
Abnormal fascies
Thymic aplasia
Cleft palate
Hypocalcemia
Autoimmune hypoparathyroidism
20
Q

Pseudohypoparathyroidism

A 
End-organ resistance to PTH
- Several subtypes
Hypocalcemia
- Tubular resistance to PTH = hypercalciuria
Hyperphosphatemia
Increased circulating PTH
Normal PTH receptors in bone
- Boney changes of hyperparathyroidism present

Pseudopseudohypoparathyroidism
- Phenotypic abnormalities without hypocalcemia

21
Q

Albright Heredetary Osteodystrophy

A

a form of pseudohypoparathyroidism

Short stature, obese
Bradydactyly, round faces
Dermal ossifications
Mental retardation

22
Q

Vitamin D Deficiency in kids

A

Rickets
signs: soft spot on baby’s head is slow to close, bony necklace, curved bones, big, lumpy joints, bowed legs

lack of vitamin D, calcium or phosphate

23
Q

Osteomalacia

A

Soft bones’
Remodeled bone does not mineralize
pain in the bones and hips, bone fractures, and muscle weakness

24
Q

Hypo-magnesemia

A 
Cofactor for PTH secretion
Required for release of stored hormone from secretory granules. 
Participates in the PTH affect on the bone and kidneys
Common in 
- chronic gastrointestinal disease
- nutritional deficiency
- Alcoholism
- cis-platinum therapy
25
Q

Clinical Findings of Hypocalcemia- acute and chronic

A 
acute:
Muscle cramps
Tetany
Irritability
Carpopedal spasm
Convulsions
Perioral tingling
Tingling in hands/feet
chronic:
Lethargy
Personality changes
Anxiety state
Blurred vision (cataracts)
Parkinsonism
Mental retardation
26
Q

Signs of Hypocalcemia

A

Chvostek sign
- Facial muscle contraction on tapping the facial nerve in front or ear

Trousseau phenomenon

  • Carpal spasm after application of BP cuff due to tetany
  • – Specific and sensitive for hypocalcemia

Nonspecific signs

  • Candidiasis, brittle nails, dry skin
  • Cararacts, loss of eyebrows
  • Hyperactive DTRs
  • Papilledema (rare)
27
Q

Paget’s Disease of Bone

A

Osteitis Deformans

Focal disorder of bone remodeling that leads to greatly accelerated rates of bone turnover.

  • Disruption of normal architecture
  • Gross deformities
  • — Enlargement of skull, bowing of long bones
  • Etiology unknown – probably osteoclast abnormality (? viral, ? Genetic)
28
Q

Paget’s Disease Symptoms

A 
Often asymptomatic
- Only 27% have symptoms at time of diagnosis
Headache
Bone pain and deformity
Warmth of skin over involved bone
High output cardiac failure
Entrapment neuropathies (hearing loss)
Kyphosis
Fracture with only slight trauma
Affected bones develop high blood flow
Increased vascularity may cause:
- Warmth of skin over involved bone
- High output cardiac failure
- Vascular ‘steal’ from spinal cord - paralysis
29
Q

Radiographic Findings in Paget’s Disease

A

Osteolytic phase
- Advancing, wedge-shaped resorption front at either end of long bones or circumscribed osteolytic lesions in the skull (osteoporosis circumscripta)

Mixed phase

  • Less bone remodeling, more sclerosis
  • Enlarged bone, ? Bowing, fractures

Osteoblastic phase

  • “Cotton wool” appearance with patchy increase in bone density
  • Bone scan shows osteoblastic uptake and can help identify the extent of the disease
30
Q

Treatment of Paget’s Disease

A

Treatment controversial if asymptomatic
- Does tend to progress without treatment

No cure, but can decrease the rate of osteoclastic bone resorption

  • Bisphosphonates – Treatment of choice
  • Calcitonin (SQ, IM, nasal) – shorter lived suppression
  • – Can develop neutralizing antibodies
  • – Not as potent as the bisphosphonates
  • Symptomatic therapy
31
Q

Laboratory Findings in Paget’s

A

Serum alkaline phosphatase usually elevated

  • Can be used to follow activity of disease
  • Bone-specific alk phos if near normal levels

Other bone markers

  • Serum C-telopeptide (high)
  • Urinary hydroxyproline (high in active disease)
  • Serum calcium (usually high)
  • Serum 25-OH vitamin D
  • – Screen for vitamin D deficiency
32
Q

Osteoporosis

A

Silent skeletal disorder characterized by compromised bone strength and increased predisposition to fracture

33
Q

Risk Factors for Osteoporosis

A

genetic: female, white, asian, FmHx of osteoporosis, small body size or weight
hormonal: menopause (natural, premature, or surgical)
lifestyle and nutrition; inadequate calcium intake, smoking, excessive alcohol consumption, eating disorders, excessive physical activity causing amenorrhea
medications: glucocorticoids, anticonvulsants, heparin
medical conditions

34
Q

Indications for Measuring BMD

A

women age > 65
postmenopausal women under 65 who have at least one risk factor for osteoporosis other than menopause
postmenopausal women who present with fractures
women who are considering therapy for osteoporosis and for whom bone mineral densitometry test restults would influence this decision
women who have been receiving hormone replacement therapy for a prolonged period
radiographic findings suggestive of osteoporosis or vertebral deformity
corticosteroid therapy for more than 3 months
primary hyperparathyroidism
treatment for osteoporosis (to monitor therapeutic response)

35
Q

BMD Assessment

A

Dual energy X-ray absorbtiometry is the gold standard for measuring bone mass

  • Best correlation with fracture risk
  • Short scanning time
  • Low exposure to radiation
  • Can measure in all areas of skeleton

Other methods:

  • Quantitative CT, single-photon absorbtiometry
  • Quantitative ultrasound
36
Q

DEXA Scan Results

A

T-Score

  • Standard deviation from the mean BMD of a young healthy population
  • Primarily used to diagnose osteoporosis
  • T-Score of -1 = 10% bone loss

Z-Score

  • Standard deviation from the BMD of an age and sex matched group
  • Used for younger men, children, and premenopausal women
37
Q

WHO Definition of Bone Mass

A

Normal: T score > - 1
osteopenia: T score -1 to -2.5
Osteoporosis: T score less than -2.5
Established osteoporosis: T score under -2.5 and osteoporotic fracture

38
Q

Prevention of Osteoporosis

A

calcium intake

Postmenopausal women with T-Score less than -1 and risk factors:
Vitamin D supplementation (400-800 IU daily)
Exercise
Cessation of smoking
Fall prevention
Limitation of alcohol and caffeine
? Medications

39
Q

Exercise and physical activity

for osteoporosis

A

No consensus on how much or what type

30 minutes of weight bearing or resistance exercise at least 4 times per week

40
Q

Bisphosphonates

A

Pyrophosphate derivatives that bind to boney surface and inhibit osteoclastic bone resorption
- Poorly absorbed – must take fasting
- Alendronate and risedronate
— Significant anti-fracture efficacy at spine, hip and other sites.
— Alendronate more effective in reducing fractures with severe osteoporosis than osteopenia
— Optimal duration of treatment is not known
(Continued improvement after 5-7 years with no cumulative negative effects.)

41
Q

Zoledronate (Zometa)

A

Newer bisphosphonate

Single injected dose suppressed bone turnover for a full year and induced significant gains in BMD.

42
Q

Hormone Replacement Therapy

A

Women’s Health initiative
- HRT increased risk of CV disease, breast cancer, stroke, DVT, and PE.

SERMs – Raloxifene

  • Estrogen-like effect on bone but inhibits effects of estrogen on breast and uterus
  • Increased BMD, decreases risk of vertebral fractures, but not hip fractures
  • No increased risk of CV disease and decreases breast cancer risk. Increases risk for DVT/PE.
43
Q

Calcitonin

A

Nasal spray
Increases BMD in spine and decreases vertebral fractures.
- Does not affect incidence of hip fractures
Indicated for women 5 years postmenopausal
Analgesic effect on bone pain

44
Q

Teriparatide (rPTH)

A

Only anabolic agent
Stimulates osteoblastic bone formation
SQ injections
- No more than 2 years duration
Increases BMD and decreases fracture risk
Indicated for patients with high fracture risk and are intolerant of other medications
Avoid with Paget’s hx of radiation involving bone, or skeletal cancer – possible osteosarcoma.

45
Q

Denosumab (Prolia, Xgeva)

A

Approved by FDA in 2010
Monoclonal antibody that inhibits osteoclastic activation
Binds to RANKL
- Receptor Activator of Nuclear factor Kappa B
Subcutaneous dosing every 6 months

ENDO 2 Exam II (2017) (19 decks)

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