Parathyroid Disease Flashcards

1
Q

What is the function of the parathyroid?

A

Controls serum calcium levels

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2
Q

What 4 components are involved in calcium homeostasis

A
  1. Serum calcium
  2. Serum Phosphate
  3. 1,25-dihydroxyvitamin D-3
  4. Parathyroid Hormone (PTH)
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3
Q

What percentage of the total body calcium is stored in bone?

A

99%

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4
Q

What percentage of body’s calcium that is not stored in bone is bound to plasma membranes?

A

50% (of 1%)

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5
Q

What percentage of the body’s calcium that is not stored in bone is free or ionized and ready for use in physiologic functions?

A

40% (of 1%)

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6
Q

What is the most essential element in our bodies, and is the only element in the body that has its own regulating system?

A

Calcium

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7
Q

What are the primary functions of calcium?

A

Nerve conduction (electrical energy for our NS)
Muscle contraction (electrical energy for our muscular sx)
Bones and teeth (strength to skeletal sx)
Enzymatic co-factor for blood clotting
Required for hormone secretion and fx of cell receptors
Plasma membrane permeability and stability

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8
Q

What is the single most important factor in regulation of serum calcium?

A

Parathyroid hormone

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9
Q

What is PTH regulated by?

A

the level of ionized plasma calcium

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10
Q

Where is PTH secreted from?

A

the parathyroid gland in response to low calcium levels

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11
Q

What are the major targets for PTH action?

A

Kidney and bone

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12
Q

What does PTH do in the Kidney?

A

Increases renal calcium resorption in tubules (keeps it from being excreted in the urine)
Increases phosphate excretion by blocking reabsortption in the tubules
Increases conversion of Vitamin D to active form in kidney-this increases GI absorption of calcium

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13
Q

What are the two phases of PTH action on the bone?

A
Rapid phase (minutes)
Slow phase (days)
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14
Q

What occurs during the rapid phase of PTH action in the bones?

A

PTH bind to receptors on osteoblasts and clasts

membrane pumps Ca from bone fluid which is transported into the blood stream

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15
Q

What occurs during the slow phase of PTH action in the bones?

A

Osteoclasts are activated and breakdown formed bone
this results in increased osteoclastic activity causing Ca to be released into blood stream increasing serum calcium levels

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16
Q

What is vitamin D-3 formed by?

A

skin w/ exposure to sunlight

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17
Q

What is vitamin D-2 formed by?

A

it is absorbed by our diet.

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18
Q

What activates Vitamin D-3

A

25-hydroxylation in liver and 1-hydroxylation in kidney into bioactive form. (needs to be activated in kidneys in response to PTH stim. (due to low Ca.) and low phosphate levels

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19
Q

What is the primary action of D3?

A

promotes intestinal absorption of calcium and phosphate and enhances bone absorption of Ca

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20
Q

As Ca levels increase PTH secretion _____, renal vitamin D activation _____, intestinal Ca absorption ___ and ___ in renal phosphate reabsorption.

A

As Ca levels increase PTH secretion decreases, Renal Vit D activation decreases, intestinal Ca absorption decreases and increases in renal phosphate reabsorption

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21
Q

What percent of phosphate is found in the bone?

A

85%

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22
Q

What form does phosphate take in serum?

A

Phospholipids, phosphate esters, inorganic phosphate (ionized).

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23
Q

What are the major functions of phosphate in the body?

A

Regulation of acid-base balance

Energy for muscle contraction (ATP)

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24
Q

What is the opposing hormone of potassium?

A

calcitonin

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25
Where is calcitonin produced?
the thyroid gland
26
What is the function of calcitonin in the body?
Decrease plasma (ECF) calcium levels (much lesser degree than PTH and Vitamin D)
27
What are the target tissues of calcitonin
Bone: inhibits ca resorption by inhibiting osteoclasts Kidney: Stimulates calcium (and phosphate) excretion in renal tubules
28
What 3 hormones regulate calcium phosphate balance?
PTH, Cacitonin, Vitamin D
29
What do PTH, calcitonin, and Vitamin D do synergistically?
- control Ca/P absorption in intestines - Controls deposition and absorption of Ca/P from bone - Controls the renal reabsorption and excretion of Ca/P by the kidney
30
Define hyperparathyroidism
Abnormal hyper secretion of PTH | -results in hypercalcemia, and hypophosphatemia (hallmark)
31
What can excessive PTH cause?
``` cortical demineralization fractures cystic bone lesions kidney stones d/t hypercalciuria slowing of NS MSK symptoms ```
32
MC cause of elevated PTH and hypercalciuria?
Primary hyperparathyroidism.
33
What is the epidemiology of Hyperparathyroidism?
Common in poly >40yo | MC in females (75%)
34
What is the MC cause of Hyperparathyroidism?
85%-parathyroid adenoma
35
What is the etiology of hyperparathyroidism?
Adenoma diffuse parathyroid hyperplasia <1%-parathyroid carcinoma RARE-parathyroid cyst, multiple endocrine neoplasia (MEN)
36
What is the hallmark of secondary hyperparathyroidism?
Elevated PTH, normal to low Ca levels, and high (renal disease) to low (Vit. D/absorption d/o) phosphate levels
37
Does hypercalcemia occur with secondary hyperparathyroidism?
NO
38
Define hyperparathyroidism
Compensatory hyper-functioning of the parathyroid gland caused by hypocalcemia or peripheral resistance to PTH
39
Which one is reversible by tx underlying cause-Primary or secondary Hyperparathyroidism?
Secondary!
40
Etiology of secondary hyperparathyroidism
-Chronic renal insufficiency/failure is MC cause (hyperparathyroidism is the least of their problem) -Vit D deficiency 2nd mc -calcium malabsorption -medications that accelerate met of Vit D or decrease absorb. of Ca (phenytoid, phenobarbital, laxative)
41
signs and sx. of primary hyperparathyroidism
Hypercalcemia is usually an incidental finding on routine blood work most pt's are asymptomatic bones, stones, abdominal groans, psychiatric moans, and fatigue overtones.
42
What is the term Bones, Stones, Abdominal Groans, Psychiatric Moans, and Fatigue Overtones relative to?
Primary hyperparathyroidism: Bones-bone loss, fx, pain, weakness, myalgia, arthralgia Stones-kidney stones Abd groans-Peptic dz, pancreatitis, cholelithiasis, n/v, loss of appetite, constipation, and pain Psychic Moans: depression, nervousness, cog. dysfx., CV: HTN arrhythmias
43
Signs and symptoms of secondary hyperparathyroidism
Presentation is often that of renal failure weakening of bones, fx, pain hyperphosphatemia-heart
44
Primary labs for hyperparathyroidism
Hypercalcemia >10.5mg/dL (HALLMARK) Serum phosphate LOW <2.5 mg/dL PTH elevation confirms dx.
45
Secondary labs for hyperparathyrodism
Serum phos is HIGH in kidney failure and LOW if d/t absorption Elevated serum PTH Normal serum Ca.
46
Imaging for Hyperparathyroidism
US gold standard Not necessary for diagnosis- can also identify adenoma with CT or MRI Non-contrast CT assess for stones DEXA scan-for bone loss
47
DDX for hypercalcemia
``` parathyroid Malignancy Vitamin D/Calcium Idiopathyic hypercalcemia in infancy High bone turnover Renal Adrenal insuff. (addison's) ```
48
First line tx for primary hyperparathyroidism
Parathyroidectomy-for adenomas, hyperplasia, ca, cysts | and for all pt's with symptomatic hyperparathyroidism, kidney stones ,bone dz, pregnancy
49
Second line tx for primary hyperparathyroidism
``` Pt's who are not a candidate for surgery Medical management: Fluids for hypercalcemia Bisphosphonates IV Vit D supp. Cinacalcet Estrogen Raloxifen Avoid thiazide diuretics, calcium sup. Frequent lab monitoring of Ca, albumin, renal fx. and DEXA scan Encourage activity, avoid immobilization stay well hydrated. ```
50
tx of secondary hyperparathyroidism
``` tx underlying condition Medical Tx is MAINSTAY Vit. D suppl. Phosphate binders Calcimimetics IF medical tx. fails-surgical tx. ```
51
Prognosis of Primary hyperparathyroidism
- sx pts will worsen until treated. - 1/3 of asympt pt's will develop worsening hypercaclemia, hypercalciuria, and reduced bone density-careful monitoring is required - Surgical removal of single adenoma is 94% successful
52
Prognosis of secondary hyperparathyroid
medical therapy is successful in most | if surgery performed 10% risk of recurrence
53
Definition of hypoparathyroidism
Condition where body does not produce enough PTH | -presents with hypocalcemia
54
What is the etiology of hypoparathyroidism?
Acquired-post thyroidectomy (usually transient) Autoimmune-Isolated or combined w/ other d/o s.a. lupus Functional-D/t malabsorption, alcoholism, Vit D def. Congenital Other-damage from heavy metals, iron, granulomas, infections, tumors
55
What is Chvostek's sign
Facial contraction on tapping facial nerve in front of the ear.
56
Trousseau's phenomenon
Carpal spasm after application of a BP cuff.
57
Labs for hypoparathyroidism
``` Serum calcium-low Serum phosphate-low PTH levels-low Urinary Ca.-low Alk phos.-normal ```
58
Imaging/special tests for hypoparathyroidism
XR, CT-skull ma show basal ganglia calcification, bones may be denser, cutaneous calcifications. Slit lamp-early cataract formation ECG-Prolonged QT and T wave abnormalities DEXA-bone density
59
Complications of hypoparathyroidism
Acute tetany w/ stridor-resp. obstruction Cataract parkinsonian sx. Ossiviation of paravert. ligaments w/ second nerve root compression seizures
60
DDX for hypoparathyroidism
``` Resp alkalosis idiopath epilepsy, choreathetosis, brain tumor asthma malabsorption medications Psuedohypoparathyroidism ```
61
Emergency tx (acute attack) hypoparathyroidism
Usually occurs after surgery-emergent tx required - maintain open airway - IV Ca. Gluconate - Oral Ca - Vit D - Magnesium (if hypo magnesium) - Transplantation of cryopreserved parathyroid tissue restores normocalcemia 23% of time.
62
Maintenance tx for hypoparathyroidism
Maintain serum calcium bw 8-8.6mg/dL -slightly lower than normal to minimize hypercalciuria and decrease risk of overdose and risk of hypercalcinemia Vit D suppl. PTH-subq injection (expensive not great option) Avoid or minimize calcium depleting drugs (furosemide,)
63
Prognosis for hypoparathyroidism
Good outcome Dental changes, cataracts brain calcifications-permanent Frequent monitoring of blood work to follow lights, and urine for Ca. is necessary