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Endocrinology - Chapters > Chap. 74-Calcemia > Flashcards

Chap. 74-Calcemia Flashcards

0
Q

How does hypercalcemia present clinically??

-signs/symptoms of the patient

A

skeletal muscular weakness, smooth muscle hypoactivity with constipation and ileus, and the full spectrum of mental dysfunction, progressing from lassitude to mild confusion to deep coma.

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1
Q

_____ causes hyperpolarization of neuromuscular cell membrane and therefore refractoriness to stimulation.

A

hypercalcemia

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2
Q

What are some manifestations of hypercalcemia?

A

renal failure.
causes a reduction in the glomerulur filtration rate (GFR) through afferent arteriolar vasoconstriction, and through activation of the calcium receptor in the distal nephron, causes a form of nephrogenic diabetes insipidus, assocaited with polydipsia and polyuria.
*These events lower ECF volume and lower the GFR
*interstitial calcium phosphate crystal deposition in the kidney can occur in the kidney (Nephrocalcinosis or interstitial nephritis) & nephrolithiasis with obstructive uropathy

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3
Q

What will you see on an EKG with hypercalcemia?

A

shortening of the QTC interval

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4
Q

People with serum calcium values above ____ are normally symptomatic.

A

13 mg/dL

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5
Q

Whether a person develops symptoms to hypercalcemia depends on several factors. One of which is the degree of hypercalcemia, above 13 mg/dL usualy causes a patient to have symptoms. What are the other factors that cause a patient to have symptoms?

A
  • duration of hypercalcemia ( a gradual increase even into sever 15 to 17 mg/dL range may cause little symptoms)
  • overall health, age, and general status of person influences symptoms
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6
Q

What is the most common cause of hypercalcemia among hospitalized patients?

A

cancer

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7
Q

What is the most common cause of of hypercalcemia among health outpatient?

A

hyperparathyroidism

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8
Q

T/F Hypercalcemia occurs late in the course of cancer and rapid progression to more severe hypercalcemia and rapid death is the rule. The 50% survival rate among patients with cancer following the development of hypercalcemia is about 30 days.

A

true

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9
Q

What are the common tumors that cause hypercalcemia?

A

breast, renal, squamous, and ovarian cacrinomas

*as well as multiple mylenoma and lymphoma

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10
Q

What are the tumor cancers that are NOT commonly associated with hypercalcemia?

A

colon, prostate, and gastric carcinoma

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11
Q

_______ mimics the actions of parathyroid hormone (PTH) on the kidney to prevent calcium excretion and on the skeleton to activate osteoclasts and induce bone resorption.

A

PTHrP - parathyroid hormone-related protein

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12
Q

_______ accounts for the most common mechanism of cancer that leads to hypercalcemia; it accounts for about 80% of the patients with malignancy-associated hypercalcemia (MAHC) and is the result of PTHrP.

A

Humoral hypercalcemia of malignancy

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13
Q

Tumors classically associated with ______ mechanism are squamous carcinomas of any site (larynx, lung, cervix, and esophagus), renal carcinomas, ovarian carcinomas, and lymphomas associated with human T-Cell lymphotropic virus type I HTLV-I.

A

HHM - humoral hypercalcemia of malignancy

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14
Q

Does hypercalcemia in HHM occur in the absence or presence of skeletal metastases?

A

absence usually

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15
Q

Can hypercalcemia in HHM be reversed by tumor resection or albation?

A

yes!!!!!!!!

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16
Q

Patients with hypercalcemia caused by cancer through HHM mechanism, display what other symptoms aside from hypercalcemia?

A
  1. PTH reduction
  2. 1,25[OH]2D reduction
  3. PTHrP elevation
  4. Serum Phosphorus reduction
  5. Tubular maximum for phosphorus (TmP) reduction
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17
Q

Aside from Cancer that leads to hypercalcemia through HHM, _______ is a second form of MAHC that is caused by a local tumor invasion of the skeleton.
*MAHC = Malignancy-Associated Hypercalcemia

A

Local Osteolytic hypercalcemia (LOH)

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18
Q

In contrast to patients with HHM, patients with LOH the skeletal metastatic or primary tumor burden is ______, and the offending tumor is most often ______ or _____.

A

LARGE

breast cancer or a hematologic neoplasm such as multiple myeloma, leukemia, or lymphoma

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19
Q

Patients with LOH display what other symptoms, aside from hypercalcemia?

A
  1. reduction in PTH, PTHrP, and 1,25[OH]2D

2. normal or elevated serum phosphorus levels

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20
Q

The 3rd form of MAHC is due to secretion of 1,25[OH]2D by _______ or ______.

A

lymphomas or dysgerminomas

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21
Q

Lymphomas are particularly interesting in that they may cause hypercalcemia through an HHM mechanism with systemic PTHrP secretion through a local skeletal invasion mechanism and through systemic production of 1,25[OH]2D. Recently the syndrome has been observed in association with ____.

A

ovarian dysgerminomas

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22
Q

Although most instances of HHM are due to PTHrP, several well documented case reports of _________ have come to light. These case reports have included colon carcinoma, a squamous carcinoma of the lung, a small cell carcinoma of the ovary, and a neuroendocrine tumor.

A

ectopic secretion of authentic PTH

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23
Q

T/F A single parathyroid adenoma causing Hyperparathyroidism is most commonly cause of Hypercalcemia in a healthy outpatient.

A

true

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24
Q

How does a single parathyroid adenoma cause hyperparathyroidism?

A

overproduces PTH

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25
Q

What confirms the diagnosis of hypercalcemia caused single parathyroid adenoma?

A

*****Elevated PTH
(hypophosphatemia, a reduction in the TMP, increased plasma 1,25[OH]2D, an increase in serum chloride, and a reduction in serum bicarbonate are also typical features.

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26
Q

Most often, primary HPT is asymptomatic. However, some patients develop ________ and ________, most often as a result of calcium oxalate, and less often as a result of calcium phosphate stones.

A

hypercalciuria and calcium nephrolithiasis

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27
Q

Patients with sever hyperparathyroidism experience a reduction in bone mineral density called ______.

A

Osteitis fibrosa cystica

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28
Q

Osteopenia, hypercalciuria, kidney stones, reduced renal function, and a serum calcium greater than 1 mg/dL is considered an indication for _______.

A

parathyroidectomy

***know what is an indication for parathyroidectomy!!!!!!

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29
Q

_____, ______, and _____ are SOFT indications for surgery at best.

A

Cognitive dysfunction, peptic ulcers, hypertension

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30
Q

HPT can occur as part of one of the multiple endocrine neoplasia (MEN) syndromes. ______ = (MEN-1) ; ______ = (MEN-2)

A 
MEN-1 = pituitary and islet tumors
MEN-2 = pheochromocytomas and medullary carcinoma of the thyroid
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31
Q

Secondary HPT, by definition, is an appropriate increase in ________ associated with eucalcemia or hypocalcemia, occurring in an attempt to correct hypocalcemia, occurring in an attempt to correct hypocalcemia resulting for example from vitamin D deficiency or chronic renal failure.

A

circulating PTH

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32
Q

What is tertiary HPT?

A

HPT associated with hypercalcemia that appears in the setting of prolonged stimulation of parathyroid glands, such as chronic renal failure with hypocalcemia or chronic vitamin D deficiency resulting from malabsorption.

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33
Q

Chronic parathyroid stimulation leads to parathyroid hyperplasia adn at times adenomas, and these may, if they fail to suppress with the development of hypercalcemia, cause hypercalcemia. The classic example is the development of _______ following successful _______.

A

PTH-dependent hypercalcemia following successful renal transplantation.

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34
Q

_____ = autosomal dominant inherited disorder that is due to heterozygous inactivating mutations in the calcium receptor. Thus parathyroid glands that bear this receptor on their surface inappropriately perceive circulating calcium concentrations to be low, therefore behaving as though the patient is hypocalcemic and inappropriately secrete additional PTH. This action causes the serum calcium to rise, and with an elevated calcium,PTH returns to a high-normal level.

A

Familial Hypocalciuric Hypercalcemia

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35
Q

What are the effects on the kidney In familial hypocalciuric hypercalcemia?

A

the kidney innapropriately conserves calcium, leading to hypocalciuria and contributing to hypercalcemia

36
Q

What is the effect on the CNS in Familial Hypocalciuric Hypercalcemia?

A

the hypercalcemia goes unperceived by the CNS and affected individuals are therefore asymptomatic

37
Q

What is important about a patient who is familial hypocalciuric hypercalcemia in regard to parathyroidectomy?

A

Because affected individuals are asymptomatic and do not develop adverse sequelae from the syndrome, its primary importance is that affected individuals be properly identified and protected from UNNECESSARY PARATHYROIDECTOMY. PARTIAL or SUBTOTAL parathyroidectomy has NO effect on these individuals, BUT TOTAL parathyroidectomy causes HYPOTHYROIDISM.

38
Q

In some patients, two defective alleles of the calcium sensor are inherited. These individuals have complete inability to sense calcium and therefore develop severe symptomatic hypercalcemia. Should you do a parathyroidectomy?

A

YES! homozygous individuals require UREGENT TOTAL PARATHRYOIDECTOMY

39
Q

Almost all granulomatous disorders can lead to hypercalcemia. What are the 3 prototypes?

A

sarcoidosis, TB, and the fugal diseases

40
Q

Granulomas have the ability to convert ______.

A

inactive 25-hydroxyvitamin D to the active metabolite, 1,25[OH]2D.
**Thus individuals with these disorders, when exposed to sunlight, ultraviolet radiation, or relatively trivial quantities of dietary vitamin D, may develop mild to severe hypercalcemia.

41
Q

What are the other 4 endocrine disorders that cause hypercalcemia besides parathyroidism?

A
  1. hyperthyroidism - increase in osteoclast activity
  2. pheochromocytoma - primary Hyperparathyroidism occuring as part of the MEN-II Syndrome
  3. hypoadrenalism - w/hypotension = so-called Addisons Crisis
  4. VIPomas - islet cell tumors that produce vasoactive intestinal polypeptide … VIPomas lead to the watery diarrhea, hypokalemia, achlorhydria (WDHA) syndrome, also referred to as pancreatic cholera.
42
Q

What drugs cause hypercalcemia?

A

**thiazide diuretics and lithium - increase renal tubular calcium reabsorption

  • aminophylline & theophlline - phosphodiesterase inhibitors
  • Vitamin D - stimulates intestinal calcium absorption; but can stimulate osteoclastic bone resorption
  • Vitamin A - stimulates bone resorption
  • Foscarnet - antiviral agent
  • ESTROGEN & TAMOXIFEN = breast cancer with extensive skeletal metastasis - so called estrogen flare
43
Q

______ = ingesting large quantities of calcium carbonate or other calcium -containing antacids for peptic disease. In general for hypercalcemia to occur, calcium intake must exceed 4 grams per day and is often in the 10-20 grams per day range.

A

Milk-Alkali Syndrome

44
Q

What is the basis of the immobilization syndrome?

A

immobilization activates osteoclastic bone resorption and at the same time inhibits osteoblastic activity, producing a severe upcompling of bone resorption from formation, with rapid and enormous net losses of calcium from the skeleton into the ECF.

45
Q

What is the best treatment for immobilization causing hypercalcemia?

A

active weight bearing, hydration, antiresorptive drugs such as the bisphosphates may be used

46
Q

T/F Chronic and acute renal failure has been associated with hypercalcemia. The more common initial abnormality is hypocalcemia induced by a reduction in kidney-derived 1,25[OH]2D or paracalcitol treatment to prevent renal osteodystropy. Immobilization in the setting of chronic renal failure resulting from *rhabdomyolysis (crush injury), transient rebound hypercalcemia has been described as renal failure resolves and serum phosphate concentrations decline.

A

true

47
Q

About 50% of circulating calcium is bound to serum albumin and other proteins. Thus, ____ in serum proteins will naturally lead to an increase in total, but not ionized serum calcium concentrations. When do you see this?

A

increase; this increase is commonly observed in settings of volume depletion and dehydration and may account for the hypercalcemia observed in patients with ADDISON CRISIS.

48
Q

A more unusual form of hypercalcemia caused by *hyperproteinemai occurs in patients with myeloma or Waldenstrom macroglobulinemia. What is unusual about this?

A

abnormal immunoglobulin found in these diseases specifically binds calcium and leads to an increase in total, but NOT ionized serum calcium
**this scenario is not the norm for patients with myeloma and hypercalcemia, who have increases in the ionized component of serum calcium. Patients with this syndrome DO NOT display features typical of authentic hypercalcemia: reduced mental status, prolonged QTC interval on EKG, and hypercalciuria

49
Q

T/F Patients with end stage liver disease awaiting transplantation have been described as being hypercalcmic.

A

true

50
Q

______ , individuals who drink water form contaminated wells, can be described as being hypercalemic.

A

Manganese intoxication

51
Q

______ leads to a reduction in the potential difference across cell membranes, which leads to hyperexcitability, particularly of cells of the neuromuscular class.

A

Hypocalcemia

52
Q

What are some of the symptoms associated with hypocalcemia in regards to the neuromuscular cells?

A
  • neuromuscular cells spontaneously fire and produce
    1. spontaneous seizures
    2. paresthesias
    3. skeletal muscle contraction (carpal spasm, pedal spasm, or tetany)
53
Q

What are the names of the two physical signs that you observe with hypocalcemia?
Can you describe them?

A
  1. Trousseau sign = spontaneous contraction of the forearm muscles in response to application of a blood pressure cuff around the upper arm and inflation to above systolic pressure
  2. Chvostek sign- twitching of the facial muscles with gentle tapping of the facial nerve as it exits the parotid gland
54
Q

What will an EKG show with hypocalcemia?

A

prolonged QTc interval

55
Q

Does hypocalcemia have an effect on the heart?

A

Rarely, severe hypocalcemia has been reported to cause hypocontractility of the myocardium and congestive heart failure because calcium is required for muscle contraction

56
Q

Prolonged hypoparathyroidism may be associated with basal ganglia calcification, which is asymptomatic. How could you view this in a patient?

A

IMPRESSIVE :) on a CT Scan and PLAIN X-RAY of the SKULL

57
Q

What are the five general mechanisms that may result in hypocalcemia?

A
  1. reduction in serum binding proteins (albumin)
  2. increase in serum phosphate with a resultant increase in calcium phosphate solubility product
  3. Increase in renal calcium excretion
  4. reduction in intestinal calcium absorption
  5. loss of calcium from the ECF into the Skeleton.
58
Q

In practice several of the factors that cause hypocalcemia are operative in several disorders. For example:
_____ = reduction in intestinal calcium in hypoparathyroidism combines with an inability to reabsorb calcium from the distal tubule to cause hypocalcemia.
_____ = extensive osteoblastic metastases, increase in osteoblast activity remove calcium from the ECF
_____ = a reduction in intestinal calcium intake.

A
  1. hypoparathyroidism
  2. breast cancer
  3. anorexia
59
Q

How does hypoparathyroidism cause hypocalcemia?

A

1 & #2 combined cause hypocalcemia

  1. decrease in intestinal calcium absorption - a result of low circulating 1,25[OH]2D concentrations, which are a result of low circulating PTH
  2. Reduced calcium reabsorption in the distal tubule - a result of decreased circulating PTH
60
Q

Hypoparathyroidism may be idiopathic or autoimmune. Can you name some autoimmune diseases hypoparathyroidism could be associated with?
Any other ways hypoparathyroidism could occur?

A
  • *Hypoparathyroidism may be idiopathic or autoimmune, occuring in isolation or as part of the *polyglandular failure syndrome in association with
  • Graves hyperparathyroidism, Hashimoto thyroiditis, Addison’s disease, type 1 diabetes, vitiligo, musculocutaneous candidiasis, and others.
  • ***Hypoparathyroidism is COMMONLY encountered as SURGICAL HYPOPARATHYROIDISM in patients who have undergone thyroid, parathyroid, or laryngeal surgery for multinodular goiter or Graves Disease, for parathyroid hyperplasia, or for carcinoma of larynx or esophagus.
61
Q

What are 4 less common causes of hypoparathyroidism?

RARE

A
  1. DiGeorge Syndrome
  2. isolated parathyroid failure
  3. activating mutations in the calcium receptor gene (autosomal dominant hypoparathyroidism), the PTH gene, or the glial cell missing-B (GCMB) gene.
  4. tissue infiltrative diseases such as breast cancer, Wilson’s disease (copper deposition), hemochromatosis (iron deposition), or sarcoidosis may destroy or replace normal parathyroid tissue RARELYYYYY
62
Q

How will you diagnose Hypoparathyroidism?

-LAB TEST Results

A
  • low serum ionized calcium level in patients with an inappropriately reduce PTH concentration
  • phosphorus concentration is high-normal or frankly elevated
  • plasma 1,25[OH]2D concentrations are reduced
63
Q

What are the treatment options for Hypoparathyroidism?

A
  • subcutaneous injection is a potential treatment but NOT approved
    1. NORMALLY treatment is giving pt large doses of calcium about 2000 mg per day = to increase intestinal calcium absorption
    2. w/ #1 also give Active form of Vitamin D about .25 to 1 microgram a day
64
Q

What is the goal of treating hypoparathyroidism?
What are the risks?
What should you do to prevent the risks?

A
  • induce sufficient intestinal calcium hyperabsorption to overwhelm the ability of the kidney to excrete it
  • risks for inducing significant hypercalciuria and therefore nephocalcinosis and nephrolithiasis
  • 24 hour urinary calcium must be measured regularly and hypercalciuria minimized, which generally means maintaining the serum calcium in the low normal range about 8.5-9 mg/dL
65
Q

In some instances, calcium and vitamin D alone may be ineffective or may induce hypercalciuria when treating a patient with hypoparathyroidism. What should the PA do then?

A

addition of thiazide diuretic such as hydrochlorothiazide, which stimulates renal calcium reabsorption, may be effective in preventing hypercalciuria and at the same time raising serum caclium

66
Q

**What is the most common form of the pseudohypoparathyroid syndrome?

pseudohypoparathyroid = a group of disorders that have in common resistance to the actions of PTH. In most cases, the resistance is due to different types of inactivating mutations in the signal transducing protein Gs-alpha.

A

Type Ia = multiple hormone resistance and a phenotype ALBRIGHT HEREDIATARY OSTEODYSTROPHY

67
Q

What are the signs/symptoms of Albright Hereditary Osteodystrophy?

A
  • short stature, shortened fourth and fifth metacarpals, obesity, mental retardation, subcutaneous calcifications, and cafe-au-lait spots
  • because the disorder is hereditary a clear family history of this phenomenon is often present, as well as family history of hypocalcemia or siezures
68
Q

How can you make and confirm the diagnosis of Albright hereditary osteodystrophy?

A
  • diagnosis is made by findings of an elevated circulating PTH in a patient with hypocalcemia and hyperphosphatemia in whom others causes of hypocalcemia and secondary hypothyroidism have been excluded.
  • The diagnosis can be CONFIRMED by infusing PTH and filaing to observe the normal phophaturic, cyclic adenosine monophosphate, and calcemic responses.

*treat similiar to hypoparathyroidism

69
Q

What is required in order to absorb calcium from the intestine?

A

active vitamin D (1,25[OH]2D)

70
Q

What is required for activation of Vitamin D?

A
  1. exposure to sunlight or diet
  2. intact liver with which to convert vitamin D to 25-hydroxyvitamin D, and an intact kidney to convert 25-hydroxyvitamin D to 1,25(OH)2D.
71
Q

Developing ____ and ____, or ______ occurs when one or more of the activation pathways of vitamin D is disrupted.

A

hypocalcemia and osteomalacia, or rickets

72
Q
  1. Specifically, malabsorption syndromes such as short bowel syndrome and celiac sprue lead to hypocalcemia as a result of _____ and ______.
  2. Chronic liver diseases particularly primary biliary cirrhosis, lead to _____ and ____.
  3. Chronic renal insufficiency leads to failure to produce _____, with reductions in _____ and _____.
A
  1. hypocalcemia and Vitamin D malabsorption
  2. hypocalcemia and osteomalacia
  3. 1,25[OH]2D ; serum calcium and inefficient absorption of intestinal calcium
73
Q

Certain genetic syndromes occur in which the enzyme vitamin D 1-alpha-hydroxylase is mutated (_____ syndrome) or in which the vitamin D receptor is mutated (______ syndrome).
*What 4 signs/symptoms occur in these patients?

A

vitamin D-dependent rickets type I
vitamin D - dependent rickets type II
- Affected individuals have severe hypocalcemia, alopecia, severe rickets, and dental abnormalities
*EASY TO RECOGNIZE & CONFIRM DIAGNOSIS

74
Q

What drugs can cause hypocalcemia and osteomalacia?

A

high doses with anticonvulsants such as phenytoin or phenobarbital or their derivatives

75
Q

Reduction in serum albumin, as occurs in burn patients, the nephrotic syndrome, malnutrition, and cirrhosis, lead to reductions in ______ without a reduction in ______.

A
  • reductions in serum total calcium without a reduction in the ionized serum calcium
  • therefore, measuring ionized calcium directly is important if the authentic ionized serum calcium concentration level is needed.
76
Q

T/F Gram positive and gram negative sepsis have been associated with hypocalcemia that is generally mild.

A

true

77
Q

Magnesium is a divalent cation, in very high concentrations may therefore mimic what?
What will this cause?

A
  • mimics the actions of calcium to suppress PTH and in doing so leads to functional type of hypoparathyroidism and hypocalcemia.
  • calcium is a divalent cation also ;)
78
Q

In what patients do you see hypermagnesemia?

A

-sever hypermagnesemia (serum magnesium concentration in the 10-mg/dL range) caused by renal failure accompanied by magnesium antacid ingestion or following the treatment of eclampsia with large doses of intravenous magnesium

79
Q

______ is one of the most common causes of hypocalcemia. It is encountered in patients with alcoholism, malnutrition, cisplatin therapy for cancer, and intestinal malabsorption syndromes.

A

Hypomagnesium

80
Q

How does hypomagnesemia cause hypocalcemia?

A
  1. inhibits PTH secretion - a magnesium adenosine triphosphate is required for PTH secretion
  2. prevents the calcemic actions of PTH on the kidney and skeleton.
    * *Thus hypomagnesemia causes a functional form of hypoparathyroidism as well as resistance to PTH
81
Q

________ = increased rates of bone mineralization, out of proportion to the rate of bone resorption, will lead to net calcium entry into the skeleton and, if these rates are large, hypocalcemia.

A

Rapid Bone Formation

82
Q

_______ may follow parathyroidectomy. Patients usually with severe primary or secondary Hyperparathyroidism, undergoes parathyroidectomy. Preoperatively, the rates of bone turnover, both resorption and formation are very high but are approximately coupled. What is the problem postoperatively??

A

Hungry Bone Syndrome

  • postoperatively, the rate of osteoclastic bone resorption abruptly declines, with the decline in PTH, but the elevated rate of mineralization of previously formed osteoid remains the same as it was preoperatively for days or weeks or more.
  • the skeleton becomes a sink for calcium and hypocalcemia ensues
83
Q

What are two other examples of rapid bone formation causing hypocalcemia?

A
  1. vitamin D deficiency who have severe osteomalacia or rickets and large amounts of unmineralized osteoid. When these patients are treated with vitamin D, rapid mineralization of unmineralized osteoid occurs, and again, the skeleton becomes a sink for calcium and hypocalcemia ensues.
  2. extensive osteoblastic metastases = prostate cancer or breast cancer
84
Q

______ can be caused by rhabdomyolysis (from crush injuries), renal failure, and the tumor lysis syndrome, resulting in hypocalcemia. Can be seen in preparation for colonoscopy. One of the first sign of this is a SIEZURE.

A

Hyperphosphatemia

85
Q

What are some medications that cause hypocalcemia?

A
  1. mithramycin (plicamycin) = treatment of hypercalcemia
  2. biphosphonates (pamidronate, zoledronate)
  3. calcitonin
  4. Fluoride
  5. Calcium Chelator (Ethylenediaminetetraacetic acid IV, Citrate - used for citrated blood for transfusion)
  6. Radiographic IV contrast agents
  7. Antiviral Drug - Foscarnet
86
Q

_____ commonly causes hypocalcemia. The classic mechanism is the formation of calcium-free fatty acid soaps.

A

Pancreatitis

87
Q

What is the mechanism of hypocalcemia caused by pancreatitis?

A
  1. Pancreatitis occurs and releases lipase into the retroperitoneum and peritoneum, which leads to the autodigestion of retroperitoneal and omental fat.
  2. This action releases free fatty acids, such as palmitate, linoleate, and stearate, form triglyceride fat stores, and these negatively charged ions tightly bind (chelate) calcium in the ECF.
  3. THis binding leads to the formation of insoluble calcium-free fatty acid salts in the retroperitoneum and rapidly depletes the extracellular calcium, causing hypocalcemia.
88
Q

T/F Hypocalcemia caused by pancreatitis is reversible and should be diagnosed by elimination of hypocalcemia caused by hypoalbuminemia, hypomagnesemia, and vitamin D deficiency FIRST!

A

true

Endocrinology - Chapters (20 decks)

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