Parathyroid Flashcards
(38 cards)
What is the role of parathyroid glands?
- secrete PTH
- regulates serum calcium - promoting calcium reabsorption from bone and kidne yand gut absorption with vitamin D
- inhibits phosphourous reabsorption
- promotes activation of vitamin D
Hypocalcemia - neuromuscular irritability with perioral numbness, paresthesia of hands or feet, myalgias, muscle cramping, generalized muscle spasm with tetany, hyperactive reflexes, laryngospasm
Bradycardia, ventricular arrhythmias, impaired ventricular EF, seizures, depression, psychiatric changes, irritability, fatigue, cognitive impairment, Parkinson symptoms, papilledema, kidney disease (nephrolithiasis/calcinosis)
Dry, rough skin, dry hair, scalp and eyebrow hair loss, brittle fingernails (transverse grooves)
hypoparathyroidism
Underproduction of parathyroid hormone –
MC: from removal of parathyroid glands during surgery (acquired - transient or permanent)
Autoimmune polyendocrine syndrome, genetic causes (DiGeorge syndrome, autosomal dominant), pseudohypoparathyroidism, magnesium deficiency (profound)
hypoparathyroidism
+Chvostek sign
+Trousseau sign
LABS: low PTH, low calcium (albumin, magnesium, vitamin D can be low with phosphorus high as well)
Hypoalbuminemia → need serum ionized calcium/corrected value
EKG: arrhythmias (torsades, afib), prolonged ST and QT intervals
IMAGING: non-contrast CT of kidneys, CT scan of brain may reveal calcifications
Slit-lamp → posterior cataract formation
hypoparathyroidism
hypocalcemia + decreased PTH + increased phosphate
hypoparathyroidism
How do you treat hypoparathyroidism?
Prophylaxis against severe: calcitriol (Vitamin D)+ calcium carbonate (Ca<8 with PTH <10-15 = high risk)
EMERGENCY: hypoparathyroid tetany
Airway
+ IV calcium gluconate (slowly)
+ oral calcium ASAP
+ vitamin D preparations (calcitriol)
+ magnesium (IV if severe)
what monitoring needs to be done for hypoparathyroidism?
Close monitoring: therapy with Ca<8, vitamin D, calcium, Mg
-Urine calcium <30 ideal
-Ca 800-1000 PO daily
-Recombinant PTH for refractory
Hypercalcemia - asymptomatic or with mild symptoms - decreased deep tendon reflexes
“Bones, stones, abdominal groans, psychic moans, with fatigue overtones”
Arthralgia and bone pain, osteitis fibrosa cystica, skeletal fractures, depression, constipation, fatigue, headache, insomnia, irritability, psychosis, depression, HTN, palpitations, prolonged PR interval, polyuria, polydipsia, N/V/C/WL
Small vessel thrombosis
In pregnancy = preeclampsia, fetal complications
Fatigue with normocalcemic
Carcinoma = large, palpable neck mass, vocal cord paralysis from recurrent laryngeal nerve palsy (FNA not recommended!!!)
hyperparathyroidism
hyperparathyroidism is more common in
7th decade
women
blacks
Overproduction of parathyroid hormones: primary - (single parathyroid adenoma), secondary, or tertiary (often with kidneys; CKD with long-term/chronic hypocalcemia from another disease process causing shift and continuous activation) 3-calcium malabsorption→ excessive excretion of calcium and phosphate by kidneys → hypercalcemia
MCC of hypercalcemia
Genetic testing recommended for those with documented primary hyperparathyroidism, <40, family history, multiglandular disease
hyperparathyroidism
Hypercalcemia
Serum adjusted Ca >10.5
Confirm diagnosis with urinary calcium excretion + serum levels of intact PTH
1 = calcium excretion is normal or high, serum phosphate low, increased Ca/P ratio, ALP elevation in bone disease only
2 = low bone density, low-normal serum Ca, elevated PTH → look for causes/deficiencies
Elevated PTH → Ca, Phos, Vitamin D → differentiate
IMAGING: not required for dx, but for surgery – US to located any adenomas
SPECT, PET/MRI
hyperparathyroidism
How do you treat asymptomatic primary hyperparathyroidism?
check kidneys, closely monitored
– postmenopausal women = ERT
– hypercalciuria or calcium nephrolithiasis (thiazide)
Avoid large doses of thiazides, vitamin A, calcium antacids/supplements
MONITOR: Ca, albumin (2x/year), kidney function (1x/year), bone density (q2y) – (rising = concern)
How do you treat primary symptomatic hyperparathyroidism?
fluids – IV saline
CaSR activations – cinacalcet (decreases PTH secretion) increase slowly until normocalcemic
Carcinoma/bone disease → + bisphosphonate, zoledronic acid
Consider denosumab if severe
Vitamin D/vitamin D analogs
Beta blockers to avoid cardiac issues
parathyroidectomy ! remove adenoma!
How do you treat severe primary hyperparathyroidism?
IV bisphosphonates (pamidronate and zoledronic acid) Calcitonin + IV saline with hypercalcemia
→Parathyroidectomy recommended for those who have nephrolithiasis or parathyroid bone disease and asymptomatic patients with considerable symptoms/considerations
How do you treat secondary hyperparathyroidism?
treat deficiency/supplement
– CKD: sevelamer, calcium, Vitamin D
– Vit. D deficiency = supplement
Bone and proximal muscle pain, pathologic fractures, chondrocalcinosis
Bone disorder associated with CKD – not proper elimination of phosphate, poor vitamin D synthesis, hypocalcemia → increased PTH
renal osteodystrophy
Low Ca, high phosphate, high PTH (SECONDARY)
IMAGING: periosteal erosions, bony cysts with thin trabeculae and cortex, “salt and pepper” appearance of skull
Biopsy = cystic brown tumors (hemosiderin)
renal osteodystrophy
How do you treat renal osteodystrophy?
Phosphate binders, vitamin D, cinacalcet
delayed fontanel closure, delayed growth, dentition, costal cartilage enlargement, bowing of long bones
asymptomatic → diffuse bone pain, muscular weakness proximally, hip pain (antalgic gait), bowing of long bones, hypocalcemia
osteomalacia/rickets
Defective mineralization causing low bone density – from deficiency in Ca, P, low ALP
childhood or adolescence before fusion
= adults with fused epiphyses
Vitamin D deficiency, Ca deficiency, phosphate deficiency (genetic, tumor, alcoholism nutrition, prolonged parenteral nutrition), aluminum toxicity, hypophosphatasia (low ALP)
rickets/osteomalacia
LABS: low Vitamin D, Ca, P
Increased ALP
IMAGING: looser lines, transverse pseudo-fracture lines (osteoids)
rickets/osteomalacia
how do you treat rickets/osteomalacia?
Vitamin D (ergocalciferol)
Autosomal dominant trait causing predisposition to development of tumors in 2+ endocrine glands
MEN
3Ps: pancreas, pituitary, parathyroid
Pituitary: Hypercalcemia usually age 14-18 with clinical manifestations in 30s or 40s, Hyperparathyroidism is first clinical manifestation
Pancreatic: GEP-NETS, gastrinomas - stimulates gastrin + worsens secretion in duodenum (abdominal pain, ulcers, vomiting)
Insulinomas, glucagonoma
Extrapancreatic neuroendocrine tumors
Pituitary adenomas - PRL, GH – headaches, vision problems
MEN1
