15.8 Parathyroid Flashcards
Primary hyperparathyroidism
-Tx
surgical removal of affected parathyroid gland
-be careful of hypocalcemia post-op, which can kill pt too
PTH:
- what cells secrete?
- functions and their mechs (3)
- Chief cells, in parathyroid gland
1. Bone: increase bone resorption of Ca+ and PO4 (by increaseing osteoblast activity, which in turn activates osteoclasts)
2. Intestine/Kidney: increase intestinal Ca+ absorption, through 1,25 Vit D (stimulates 1 OHlation in kidney)
3. Kidney: increase Ca+ reabsorption in DCT and decrease PO4 reabsorption in PCT
Secondary hyperparathyroidism
- most common cause
- mech
- chronic renal failure. Leads to Renal Osteodystrophy:
- decreased PO4 excretion leads to increased PO4 binding of free Ca+
- this leads to decreased free Ca+, increasing PTH
Primary hyperparathyroidism
- what about pancreas to be concerned about
- what about kidney to be concerned about (other than stones)?
- acute pancreatitis–Ca+ is enzyme activator
- nephrocalcinosis–renal insufficiency from Ca+ deposition
You see a pt with shortened 4th and 5th fingers. Pt is also very short.
-think what
- Pseudohypoparathyroidism, auto dom form
- PTH receptor Gs mutation
Chronic renal failure
- lab findings:
- PTH
- Ca+
- PO4
- ALP
Chronic renal failure is most common cause of secondary hyperparathyroidism. (decreased PO4 excretion leads to free Ca+ binding, lower free Ca+, increasing PTH)
- high PTH
- low Ca+
- high PO4
- high ALP
Hypoparathyroidism
- clinical symptoms
- physical exam tests (2)
- numbness, tingling (esp circumoral)
- tetany (Chvostek sign, Trousseau sign)
- Chvostek–cheek
- Trousseau–triceps
Pt’s x-ray shows dark, hollow spaces.
-Suspect what endocrine problem?
- Osteitis fibrosa cystica, from primary hyperparathyroidism
- high PTH leads to excess resorption of bone
- this leads to fibrosis of bone and cystic spaces
Primary hyperparathyroidism
-If you suspect this, what distinctive abnormal lab finding to look for?
expected lab results for:
- ALP
- PTH
- Ca+
- PO4
-high urinary cAMP (PTH stimulates Gs, cAMP in renal tubular cells)
Note: you typically don’t assoc high urinary cAMP with secondary hyperparathyroidism b/c the most common cause for that is chronic renal failure.
- high ALP (sign of increased osteoblast activity, which activates osteoclast activity)
- high PTH
- high Ca+
- low PO4
Primary hyperparathyroidism
- clinical presentation (4 classic)
- 2 more important symptoms
hypercalcemia–“stones, bones, groans, and psychiatric overtones”
- Stones–Ca+ stones
- Bones–Osteitis fibrosa cystica–bone resorption leads to fibrosis and cystic spaces
- Groans–constipation, weakness
- CNS disturbances–depression, seizures
- acute pancreatitis (Ca+ is enzyme activator)
- Nephrocalcinosis–Ca+ deposition leads to renal insufficiency
Hypoparathyroidism
-causes include (3)
- autoimmune damage
- surgical excision
- DiGeorge syndrome (failure to develop pouches 3,4)
Pseudohypoparathyroidism
- labs reveal what?
- cause
- how does auto dom form present (2)
- etiology
- hypocalcemia with high PTH
- caused by resistance to PTH in organs
- Auto dom form presents with:
1. short stature
2. short 4th, 5th fingers - caused by Gs mutation in PTH receptor
Primary hyperparathyroidism
- most common cause
- other causes include (2)
- parathyroid adenoma (80%)
1. sporadic parathyroid hyperplasia
2. parathyroid carcinoma
urinary cAMP
-significance
- measures renal activity of PTH–PTH stimulates Gs, AC, cAMP in renal tubule cells. cAMP leaks out into urine, which can be measured
- High urinary cAMP suggests hyperparathyroidism.
- If you see low urinary cAMP but still high PTH, think:
1. secondary hyperparathyroidism caused by chronic renal failure (most common cause of secondary hyperparathyroidism)
2. pseudohypoparathyroidism
