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Endocrine > 190. Ca/PTH/Bone Pathophys > Flashcards

190. Ca/PTH/Bone Pathophys Flashcards

1
Q

Hypercalcemia

  • Etiologies
  • Clinical Features
  • Therapy
A

E: PTH-dependent: primary hyperPTH, hereditary (MEN I, IIA, FHH)
PTH-independent: malignancy, thiazides, vit D toxicity, hyperthyroidism, milk-alkali syndrome (ingest too many antacids)

CF: stones, bones, groans, psychologic overtones
Stones - nephrolithiasis and nephrocalcinosis, induced nephrogenic DI (polyuria)
Bones - arthralgias, myalgias, weakness
Groans (GI) - abd pain, constipation, N/V
Psychologic - neuro impairment
Shortened QT interval

Tx: Loop Diuretics, Bisphosphonates, Calcitonin, GCs

  1. Stop meds/supplements
  2. Hydration (due to polyuria/dehydration)
  3. Add loop diuretic (flush system)
  4. IV Bisphosphonates
  5. Calcitonin or GCs
  6. Dialysis
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2
Q

Primary Hyperparathyroidism

  • what is it
  • prevalence, age of pt
  • gross
  • pathophys
  • dx
  • sx: renal and bone
  • tx
A

Most common outpt cause of hyperCa, rising prevalence due to Ca being checked routinely on labs
Childhood onset = hereditary disorder (MEN I, IIA)
most commonly seen in pts >50yo

Gross: 85% benign solitary parathyroid adenoma, 5% 2 adenomas present, 10% multiple gland hyperplasia (sporadic and MEN I/IIA)

PPhys: high PTH = increased bone resorption (high Ca, PO4), increased Ca reabsorption and PO4 excretion and vit D activation = increased Ca/PO4 absorption [HIGH CA, PO4 LOW OR NORMAL]

Dx: need high Ca with normal or low PTH (not suppressed) with high/normal urine Ca (due to spillover, distinguished from FHH)

Sx: Renal - polyuria, nephrolithiasis/nephrocalcinosis
Bone: osteoporosis, fractures, low BMD - more cortical bone loss than trabecular [ex: salt + pepper skull]

Tx:
if asx - observe
if sx - surgery (well tolerated)
if cant have surgery - cinacalcet - lower serum Ca by binding CaSR = decreasing PTH

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3
Q

FHH (Familial Hypocalciuric Hypocalcemia)

  • what is it/signs
  • genetics
  • dx
  • tx
A

mildly high serum Ca, PTH normal-to-high, hypocalciuria
genes: AD disorder, 1 allele CaSR inactivated!
Dx: LOW urine Ca!! usually with +FamHx of relative with hyperCa or hyperCa known in infancy
tx: observation = NO SURGERY (benign condition)

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4
Q

Humoral Hypercalcemia of Malignancy

- three different mechanisms

A
  1. PTHrp: binds PTH receptor, expressed in fetus, breast, milk, SQUAMOUS CELL CARCINOMA of lung, head/neck, carcinoma of kidney and ovary
    Dx: measure PTHrp level in blood
  2. Local Bone Resorption: via tumor cell production of osteolytic factors in MULTIPLE MYELOMA, LYMPHOMA, BREAST/PROSTATE CANCER
    dx: check imaging/DXA
  3. Ectopic Vitamin D: due to ectopic production of 1a-hydroxylase = in LEUKEMIA, LYMPHOMA, RENAL CELL CANCER, SARCOIDOSIS, TB
    dx: measure vit D levels
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5
Q

Hypocalcemia

  • how to correct for low albumin
  • clinical features (what is Chvostek’s and Trousseau’s signs)
  • tx
A

Correction: for every point albumin is under four, add 0.8 to Ca (low albumin causes low total serum Ca but normal free active Ca)

CF: neuromuscular irritability, paresthesias
Chvostek: facial twitch when tap below zygomatic arch
Trousseau: wrist/finger flexion when inflate and hold BP cuff above systolic BP
Laryngospasm, bronchospasm, prolonged QT, seizures, tetany

tx: 1. Ca (IV, oral)
2. Vit D (check if deficient and correct)
3. Calcitriol (1,25-diOH vit D - good for VDRR, renal failure, hypoPTH)
4. PTH approved for hypoparathyroidism

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6
Q

Hypoparathyroidism
- etiology

Hypocalcemia in Renal Failure

  • what is it
  • effects
A

E: destruction (surgical MOST COMMON, autoimmune, ionizing radiation, infiltration), congenital (DiGeorge), functional (HYPOMG - need Mg for PTH)

SECONDARY HYPERPARATHYROIDISM
Renal: loss of PTH response = increase urine Ca loss and decrease urine PO4 excretion (hyperPO4 reduces Ca solubility) = secondary hyperPTH (lowering Ca)
also decreased 1a-hydroxylase = less active vit D = secondary hyperPTH

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7
Q

Rickets + Osteomalacia

  • what is it, cause
  • pathogenesis
  • CM
  • causes, dx of vit D deficiency
  • tx
A

Defect of bone mineralization due to low vit D, low Ca, or low PO4
PGen: Chronic low vit D = low gut Ca absorption = low serum Ca = high PTH (2’ HPTH) = increase bone resorption; low Ca and low PO4 only seen in severe cases - run out of bone
CM: skeletal deformities, bone pain/fragility/fractures, muscular hypotonia, weakness

VIT D
Source: sun, diet (fatty fish, eggs, mushrooms, fortified milk or yogurt), limited by Northern climate, clothes, sunscreen, age, skin cancer risk, dark skin tone
Cause of deficiency: low intake, low skin synthesis (clothes, sunscreen), low bioavailability (obesity, malabsorption), high intestinal losses
Dx: MEASURE STORAGE FORM (25-OH D) should be low (body keeps active form in normal range)

Tx: D2 (ergocalciferol, Rx), D3 (cholecalciferol, OTC), Ca (diet supplements), Calcitriol (1,25-diOH D, Rx), Phosphate if indicated

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8
Q

Osteoporosis

  • what is it
  • classification
  • pathogenesis
  • RFs
  • dx
  • prevention
  • tx
A

compromised bone strength leading to high risk of fractures (less bone density (thinning) and less bone quality (structural defects))
Class: T-score (compare to healthiest population): osteopenia b/w -1 + -2.5 SDs, osteoporosis blasts = bone loss = low BMD
RF: Sex (W>M), Age, Body Size (slender more risk due to lower peak BMD), race, FamHx
Change to hormone levels (menopause, hypogonadism)
Lifestyle (sedentary, tobacco, alcohol)
Nutrition (Ca/Vit D Deficiency, anorexia)
PMHx: malabsorption, thyrotoxicosis, HPTH, hypogonadism, renal disease
Drugs: GCs, anti-epileptics, cancer tx

Dx: DXA reports T score and Z score (age/sex matched control)

Prevention: maximize peak BMD in adolescence with physical activity and nutrition (Ca/Vit D); minimize other RFs (hypogonadism, tobacco, alcohol, meds, EDs), healthy lifestyle interventions at any age

Tx: Anti-resorptive (bisphosphonates, denosumab, calcitonin, SERMs/Estrogen), Anabolic (teriparatide, abaloparatide, romosozumab)

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9
Q

Paget’s Disease

  • what is it
  • pt population
  • etiology
  • dx - ddx
  • CM
  • tx
A

hyperdynamic bone remodeling in certain areas, high osteoclast and osteoblast activity
Pt: 1-3% population, most >55yo
Etio: VIRAL (paramyxovirus)

Dx: Elevated ALK PHOS or incidental XRAY

  • need fractionated ALK PHOS to see high in bone (not liver)
  • shows state of high turnover: Paget’s, HyperPTH, fractures, bone malignancy/mets

CM: bone scan missing landmarks, areas looking thinner/thicker, microfractures
Degenerative changes: pain, nerve compression, hearing loss (ear canal bony overgrowth)
Labs: normal Ca/PO4/PTH, HIGH ALK PHOS
bony deformities (leg bowing), pathologic fracture, high output CHF (due to increased bone vascularity)

tx: relieve sx and prevent complications
- NSAIDS/PT for pain
- BISPHOSPHONATES - normalize alk phos and diminish disease progression
- CALCITONIN - may decrease disease progression

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