Parathyroid Disease Flashcards
calcium funciton
human skeleton
regulates degree of membrane excitability in nerve cells and muscle cells of GI and heart
nerve cells and hypercalcemia
cells are refectory to stimulation
hard to get the nerves excited
nerve cells and hypocalcemia
patients develop tetany or carpopedal spasm
nerves are very excitable
calcium levels in blood
9.5 mg/dL
half is bound to serum protein, half is ionized and active
calcium homeostasis maintained by
kidney, intestines, bones
hydroxylated vitamin D and parathyroid hormone
calcium palace in body
sensed by parathyroid and secretion of PTH increases
PTH immediate effects
stimulates kidney to hold on to calcium and bones to release calcium quickly bump up serum levels
PTH long term
PTH stimulates more absorption of calcium from gut by stimulating kidney to secrete vitamin D which acts at the gut receptor to increase calcium absorption
vitamin D
dietary intake or UV rays
biologically inert and must be hydrolyzed in body
vitamin D hydroxylation
skin/GI vitamin D
then goes to liver where it becomes 25-hydroxy-vitamin D (calcidiol)
finally goes to kidney where it goes to active 1,25-dihydroxy (calcitrol)
what do we use to measure vitamin D status
serum concentration of 25(OH)D
vitamin D toxicity
can cause non-specific s/s such as anorexia, weight loss, polyuria, and heart arrythmias
can raise blood levels calcium which leads to vascular and tissue calcification
calcium and the bones
bone balance is stimulated by exercise, anabolic, and anti-resorptive drugs
conditions that promote bone formation over bone resorption
effect of PTH (4)
- stops calcium excretion and promotes urinary phosphate excretion
- stimulates kidney to produce vitamin D
- activation of ostoeCLASTS
- stops activation of osteoBLASTS
normal calcium values
9-10.5 mg/dL
ionized levels - 4.5-5.6
severe calcium values
> 14 mg/dL
correct Ca
serum binding proteins (albumin) can cause falsely elevated levels
(Ca + 4) - albumin
what influences symptoms of high or low Ca
severity of derangement (farther from normal)
speed
hypercalcemia s/s
shortening of QT interval, HTN and bradycardia
hyperpolaziation of cell membrane
refractory to stimulation
skeletal muscle weakness
easy fatiguability and perceived muscle weakness
constipation, ileus, nausea, vomiting
increased GI acid production -PUD
volume depletion and renal failure
mental status change
workup of hypercalcemia
- confirm w/repeat lab, check albumin
2. check intact PTH
treatment of asymptomatic hypercalcemia
<12 mg/dL
hydration
avoidance of drugs that worsen (thiazides, lithium)
avoidance of factors that worsen it (bedrest, depletion)
treatment of severe hypercalcemia
> 14 mg/dL
aggressive IV normal saline to expand volume and IV bisphosphonate (Zometa)
hypocalcemia (nerve)
reduces ionic difference across cell membranes therefore making cells hyper excitable
hypocalcemia neuromuscular cell symptoms
- prolonged QT interval
- paresthesias
- seizures
- muscle spasms/tetany
hypocalcemia workup
begin with measurement of intact PTH
magnesium, creatinine, phosphate, and vitamin D metabolites
hypocalcemia treatment
depends on the cause, severity, presence of symptoms and how rapidly hypocalcemia developed
mild tx is asymptomatic, IV replacement is indicated to avoid severe arrhythmia
medications used in hypocalcemia
calcium gluconate (good!, gradually brings up Ca)
calcium chloride (crap, given in central line)
primary hyperparathyroidism
cause
mc of hypercalemia in healthy patients
typically results from single autonomous parathyroid adenoma
can be from multi-parathyroid gland hyperplasia
parathyroid cancer (<1%)
primary hyperparathyroidism
causes mild elevations of serum calcium
relatively asymptomatic
diagnosis of primary hyperparathyroidism
elevation in serum calcium and elevated intact PTH
if symptomatic primary hyperparathyroidism presents with
stones (kidney stones)
bones (osteoporosis and bone pain)
groans (constipation/abdominal pain)
moans (psychiatric illness)
primary hyperparathyroidism labs
serum calcium will be high (>10.5)
ionized serum calcium high (>5.4)
serum iPTH high
serum phosphate LOW
primary hyperparathyroidism
treatment
asymptomatic: monitored with large fluid intake, pts typically note improvement in anxiety, phobias and mood
significant symptoms- parathyroidectomy
following surgery for primary hyperparathyroidism
PTH levels rapidly fall and cause hypocalcemia
must measure calcium levels and supplement Ca and Magnesium
hyperthyroidism is common - give propranolol
hungry bones
following sx for 1 hyperparathyroidism PTH decreases and bone reabsorption falls
rate of bone formation increases so hypocalcemia bc eats up all the calcium
hungry bones symptoms
parasthesia
spasm
may have seizures
secondary hyperparathyroidism
found in patients with chronic kidney disease or vitamin D deficiency
kidney fails to normally excrete phosphorus and instead excretes calcium
pathophys of secondary hyperparathyroidism
hyperphosphatemia and hypocalcemia to stimulate PTH secretion
elevated PTH coinages phosphate loss and mobilizes Ca2+ from bone but kidney can’t do it
failing kidney can’t produce adequate vitamin D so intestinal Ca absorption
parathyroid glands become hyper plastic
renal osteodystrophy w/bone pain (can cause cardiovascular calcification)
labs of secondary hyperparathyroidism
serum calcium is LOW
ionized calcium LOW
serum PTH is HIGH
serum phosphate is HIGH
treatment of secondary hyperparathyroidism
reduce dietary intake of phosphates (liquids, diary, protein, other)
patient may be placed on phosphate binders
normalization of vitamin D
phosphate binders MOA
bind to ingested phosphates, letting them pass out of GI tract without absorption
phosphate binders used
calcium acetate (PhosLo)
Selevamer (renvela, renegel)
fosrenol (Lanthanum)
what medication is used to normalize vitamin D levels
calciarlo (rocaltrol)
doxercalciferol (Hectorol)
Paricalcitol (Zemplar)
stimulates to get more calcium from the gut
final tool in armamentarium to create secondary HPT caused by CKD
cinacalcet (sensipar)
enhances sensitivity of parathryoid calcium receptor
receptor is harder to stimulate
tertiary hyperparathyroidism pathophysiology
occurs in patients with long-standing CKD after renal transplant
after kidney is transplanted the parathyroid is excessively stimulated and doesn’t recognize serum calcium
autonomously produce excessive parathyroid hormones
treatment of tertiary hyperparathyroidism
resistant to calcimimetic
can deposit calcium in tissues
treatment is by total or partial parathyroidectomy
ddx of all hyperparathyroidism
hypercalcemia of malignancy
hypercalcemia of malignancy
caused by tumor PTrH
low/undetectable intact PTH
treatment options for hypercalcemia of malignancy
aggressive IV fluid w/saline
bisphosphate (zometa)
hypoparathyroidism etiologies
- iatrogenic
- autoimmune destruction
- hypomagnesemia
rare, but can be caused by irradiation/infiltrative disease, genetic defect
hypomagnesemia is in which population
alcoholics
s/s of hypoparathyroidism
muscular (laryngospasm and bronchospasm)
neurologic
GI
psychiatric
chvostek sign
trousseau sign
chovstek sign
trapping face causes face to twitch
trousseau sign
BP causes spasm of hand
lab abnormalities of hypoparathyroidism
Low PTH
Hypocalcemia
hypomagnesemia
hyperphosphatemia
exclude vitamin D deficiency
hypoparathyroidism treatment
IV calcium gluconate initially
high oral calcium intake and supplements
vitamin D to maintain
thiazide diuretics (block excretion in urine)
recombinant PTH (BBW - osteosarcoma)
pseudohypoparathyroidism
tissue insensitivity to PTH (NO underlying disease)
results in hyperphosphatemia and hypocalcemia
elevation in PTH levels to cause bone disease
pseudohypoparathyroidism treatment
normalizing serum calcium levels, prevent renal excretion of calcium and low PTH
