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Clin Med I - Endocrine > Parathyroid Disease > Flashcards

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
Q

Where is calcitonin produced?

A

the thyroid gland

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26
Q

What is the function of calcitonin in the body?

A

Decrease plasma (ECF) calcium levels (much lesser degree than PTH and Vitamin D)

27
Q

What are the target tissues of calcitonin

A

Bone: inhibits ca resorption by inhibiting osteoclasts
Kidney: Stimulates calcium (and phosphate) excretion in renal tubules

28
Q

What 3 hormones regulate calcium phosphate balance?

A

PTH, Cacitonin, Vitamin D

29
Q

What do PTH, calcitonin, and Vitamin D do synergistically?

A
  • 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
Q

Define hyperparathyroidism

A

Abnormal hyper secretion of PTH

-results in hypercalcemia, and hypophosphatemia (hallmark)

31
Q

What can excessive PTH cause?

A 
cortical demineralization
fractures
cystic bone lesions
kidney stones d/t hypercalciuria
slowing of NS 
MSK symptoms
32
Q

MC cause of elevated PTH and hypercalciuria?

A

Primary hyperparathyroidism.

33
Q

What is the epidemiology of Hyperparathyroidism?

A

Common in poly >40yo

MC in females (75%)

34
Q

What is the MC cause of Hyperparathyroidism?

A

85%-parathyroid adenoma

35
Q

What is the etiology of hyperparathyroidism?

A

Adenoma
diffuse parathyroid hyperplasia
<1%-parathyroid carcinoma
RARE-parathyroid cyst, multiple endocrine neoplasia (MEN)

36
Q

What is the hallmark of secondary hyperparathyroidism?

A

Elevated PTH, normal to low Ca levels, and high (renal disease) to low (Vit. D/absorption d/o) phosphate levels

37
Q

Does hypercalcemia occur with secondary hyperparathyroidism?

A

NO

38
Q

Define hyperparathyroidism

A

Compensatory hyper-functioning of the parathyroid gland caused by hypocalcemia or peripheral resistance to PTH

39
Q

Which one is reversible by tx underlying cause-Primary or secondary Hyperparathyroidism?

A

Secondary!

40
Q

Etiology of secondary hyperparathyroidism

A

-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
Q

signs and sx. of primary hyperparathyroidism

A

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
Q

What is the term Bones, Stones, Abdominal Groans, Psychiatric Moans, and Fatigue Overtones relative to?

A

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
Q

Signs and symptoms of secondary hyperparathyroidism

A

Presentation is often that of renal failure
weakening of bones, fx, pain
hyperphosphatemia-heart

44
Q

Primary labs for hyperparathyroidism

A

Hypercalcemia >10.5mg/dL (HALLMARK)
Serum phosphate LOW <2.5 mg/dL
PTH elevation confirms dx.

45
Q

Secondary labs for hyperparathyrodism

A

Serum phos is HIGH in kidney failure and LOW if d/t absorption
Elevated serum PTH
Normal serum Ca.

46
Q

Imaging for Hyperparathyroidism

A

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
Q

DDX for hypercalcemia

A 
parathyroid
Malignancy
Vitamin D/Calcium
Idiopathyic hypercalcemia in infancy
High bone turnover
Renal
Adrenal insuff. (addison's)
48
Q

First line tx for primary hyperparathyroidism

A

Parathyroidectomy-for adenomas, hyperplasia, ca, cysts

and for all pt’s with symptomatic hyperparathyroidism, kidney stones ,bone dz, pregnancy

49
Q

Second line tx for primary hyperparathyroidism

A 
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
Q

tx of secondary hyperparathyroidism

A 
tx underlying condition
Medical Tx is MAINSTAY
Vit. D suppl. 
Phosphate binders
Calcimimetics
IF medical tx. fails-surgical tx.
51
Q

Prognosis of Primary hyperparathyroidism

A
  • 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
Q

Prognosis of secondary hyperparathyroid

A

medical therapy is successful in most

if surgery performed 10% risk of recurrence

53
Q

Definition of hypoparathyroidism

A

Condition where body does not produce enough PTH

-presents with hypocalcemia

54
Q

What is the etiology of hypoparathyroidism?

A

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
Q

What is Chvostek’s sign

A

Facial contraction on tapping facial nerve in front of the ear.

56
Q

Trousseau’s phenomenon

A

Carpal spasm after application of a BP cuff.

57
Q

Labs for hypoparathyroidism

A 
Serum calcium-low
Serum phosphate-low
PTH levels-low
Urinary Ca.-low
Alk phos.-normal
58
Q

Imaging/special tests for hypoparathyroidism

A

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
Q

Complications of hypoparathyroidism

A

Acute tetany w/ stridor-resp. obstruction
Cataract
parkinsonian sx.
Ossiviation of paravert. ligaments w/ second nerve root compression
seizures

60
Q

DDX for hypoparathyroidism

A 
Resp alkalosis
idiopath epilepsy, choreathetosis, brain tumor
asthma
malabsorption
medications
Psuedohypoparathyroidism
61
Q

Emergency tx (acute attack) hypoparathyroidism

A

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
Q

Maintenance tx for hypoparathyroidism

A

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
Q

Prognosis for hypoparathyroidism

A

Good outcome
Dental changes, cataracts brain calcifications-permanent
Frequent monitoring of blood work to follow lights, and urine for Ca. is necessary

Clin Med I - Endocrine (6 decks)

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