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USMLE Step 2 CK
Figure 2-7. Pathways for Synthesis and Secretion of Thyroid Hormones
Hypothalamus
Anterior Pituitary
● Internal Medicine
TRH
+
+
Thyroid
TBG +
I+
–
TSH
T
4
T
3
I–
IPO
2
Proteases
peptidases
MIT
DIT
+
IPO
Organic iodine
in thyroglobulin
Colloid
Transport
Oxidation
Organification
Release
–
: inorganic iodide
I
T
4
T
3
IPO: iodide peroxidase
MIT: monoiodotyrosine
DIT: di-iodotyrosine
RAIU ( thyroid-reactive iodine uptake) varies directly with the functional state of the thyroid.
After 24 hours, normal uptake is 5–30% of administered dose. RAIU is increased in Graves’
disease or toxic nodule and decreased in thyroiditis or surreptitious ingestion of thyroid
hormone.
Note
The answers to Diagnosis
column can be found at the
end of the chapter.
Table 2-2. Evaluating Thyroid Function
Thyroid Hormones and TSH RAI Uptake Scan Diagnosis
↓ TSH; free ↑ T4, ↑ T
↓ TSH; free ↑ T4, ↑ T
↓ TSH; free ↓ T4, ↓ T
3
3
3
20
↑ RAIU
↓ RAIU
↓ RAIU
Other tests include antimicrosomal and antithyroglobulin antibodies, which are detected
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in Hashimoto thyroiditis. In Graves’ disease, thyroid-stimulating immunoglobulin (TSI) is
found. Serum thyroglobulin concentration can be used to assess the adequacy of treatment
and follow-up of thyroid cancer, and to confirm the diagnosis of thyrotoxicosis factitia.
Chapter 2
l Endocrinology
Hyperthyroidism (Thyrotoxicosis)
A wide range of conditions can cause hyperthyroidism; Graves’ disease, an autoimmune dis-
order, is the most common. Graves’ causes the production of antibodies (thyroid stimulating
immunoglobulin [TSI]), which stimulate the thyroid to secrete T4 and T3.
Intrinsic thyroid autonomy can also result from a hyperfunctioning adenoma (toxic adenoma) or it can be caused by toxic multinodular goiter (Plummer disease), a non-autoimmune
disease of the elderly associated commonly with arrhythmia and CHF and sometimes the
consequence of simple goiter.
Transient hyperthyroidism results from subacute thyroiditis (painful) or lymphocytic thyroiditis (painless, postpartum). For treatment purposes, it is important to distinguish primary
hyperthyroidism (Grave’s disease or toxic adenoma) from thyroiditis.
Drugs such as amiodarone, alpha interferon, and lithium can induce thyrotoxicosis. Excess
iodine, as may occur in people taking certain expectorants, or iodine-containing contrast
agents for imaging studies may cause hyperthyroidism. Extrathyroid source of hormones
include thyrotoxicosis factitia and ectopic thyroid tissue (struma ovarii, functioning follicular
carcinoma). Rarely, hyperthyroidism can result from excess production of TSH (secondary
hyperthyroidism).
Clinical Pearl
Physical Examination of the
Hyperthyroid Patient
Painless & diffuse
enlargement = Graves’
Painless & nodules = Plummer
Painful & diffuse enlargement =
subacute thyroiditis
No thyroid enlargement
or thyroid not palpated =
factitious
Courtesy of Tom D. Thacher, M.D.
Figure 2-8. Pretibial Myxedema, a Manifestation of Graves’ Disease
21
USMLE Step 2 CK
l Internal Medicine
Graves’ disease
Graves’ disease (toxic diffuse goiter = hyperthyroidism + diffuse goiter + exophthalmos + dermopathy) deserves a special mention. In Graves’ there is formation of autoantibodies which bind
to the TSH receptor in thyroid cell membranes and stimulate the gland to hyperfunction (TSI).
• Commonly affects patients age <50
• Women > men
• Significant genetic component, i.e., a person is more likely to be affected if they have
family member with the disease
• Commonly triggered by stress, infection, and pregnancy
• Patients with another autoimmune disease such as type 1 diabetes or pernicious anemia are more likely to be affected
• Smoking causes increased risk of disease and may make the exopthalmos worse
Wikimedia, Jonathan Trobe, MD/University of Michigan Kellogg Eye Center
Figure 2-9. Proptosis and Lid Retraction from Graves’ Disease
Clinical Findings. Graves’ is associated clinically with diffuse painless enlargement of the
thyroid. Nervous symptoms predominate in younger patients, whereas cardiovascular and
myopathic symptoms are more common in older patients. Atrial fibrillation can also be seen.
Other clinical findings include emotional lability, inability to sleep, tremors, frequent bowel
movements, excessive sweating, and heat intolerance. Weight loss (despite increased appetite)
and loss of strength also are seen. Proximal muscle weakness may be a prominent symptom
in many cases and can be the primary reason why the patient sees a physician. Dyspnea, palpitations, angina, or cardiac failure may occur. The skin is warm and moist, and palmar erythema is present along with fine and silky hair in hyperthyroidism. Ocular signs include staring, infrequent blinking, and lid lag. Menstrual irregularity such as oligomenorrhea occurs.
Osteoporosis and hypercalcemia can occur from increases in osteoclast activity.
Diagnosis. The diagnosis of Graves’ is made on history and physical examination. Lab studies
include suppressed TSH and high serum free T4 and T3 (Note, in secondary hyperthyroidism,
TSH is elevated). The RAIU is increased (Note, in subacute thyroiditis and factitious hyperthyroidism, RAIU is decreased). TSI, antithyroglobulin and antimicrosomal antibodies are elevated.
22
Treatment. Treatment involves relief of symptoms and correction of the thyrotoxic state.
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Adrenergic hyperfunction is treated with beta-adrenergic blockade (propranolol). Correcting
the high thyroid hormone levels can be achieved with an anti-thyroid medication (methimazole or propylthiouracil) which blocks the synthesis of thyroid hormones and/or by treatment
with radioactive iodine. Methimazole is preferred, as it has a longer half-life, reverses hyperthyroidism more quickly, and has fewer side effects than propylthiouracil.
• Methimazole requires an average of 6 weeks to lower T4 levels to normal and is often
given before radioactive iodine treatment; it can be taken 1x/ day.
• Because of its potential for liver damage, propylthiouracil is used only when methimazole is not appropriate; it must be taken 2−3x/ day.
Antithyroid drugs during pregnancy. Propylthiouracil was the traditional drug of choice
during pregnancy because it is associated with less severe birth defects than methimazole. But
experts now recommend that propylthiouracil be given during the first trimester only. This
is because there have been rare cases of liver damage in people taking propylthiouracil. After
the first trimester, women should switch to methimazole for the rest of the pregnancy. For
women who are nursing, methimazole is probably a better choice than propylthiouracil (to
avoid liver side effects). Both drugs can cause agranulocytosis.
The most commonly used ‘permanent’ therapy for Graves’ disease is radioactive iodine.
Indications for its use (overusing antithyroid agents alone) include:
• Large thyroid gland
• Multiple symptoms of thyrotoxicosis
• High levels of thyroxine
• High titers of TSI
Chapter 2
l Endocrinology
Because of the high relapse rate (>50%) associated with antithyroid therapy, many physicians
in the United States prefer to use radioactive iodine as first-line therapy. Patients currently
taking antithyroid drugs must discontinue the medication at least 2 days prior to taking
the radiopharmaceutical since pretreatment with antithyroid drugs reduces the cure rate
of radioiodine therapy in hyperthyroid diseases. With radioactive iodine, the desired result
is hypothyroidism due to destruction of the gland, which usually occurs 2-3 months postadministration, after which hormone replacement treatment is indicated.
Subtotal thyroidectomy (and rarely total thyroidectomy) is indicated only in pregnancy (second trimester), in children, and in cases when the thyroid is so large that there are compressive symptoms.
Thyroid Storm
Thyroid storm is an extreme form of thyrotoxicosis. This is an endocrine emergency. It is
precipitated by stress, infection, surgery, or trauma. It is manifested by extreme irritability,
delirium, coma, tachycardia, restlessness, vomiting, jaundice, diarrhea, hypotension, dehydration, and high fever.
Treatment. The treatment of thyroid storm involves supportive therapy with saline and
glucose hydration, glucocorticoids, and oxygen cooling blanket. Therapy for hyperthyroidism is also used and includes first, propylthiouracil. Next, iodine should be given to inhibit
hormone release. This should be followed by adrenergic antagonists (e.g., b-adrenergic blockers). Finally, dexamethasone is given to provide adrenal support. Antithyroid drugs should be
Clinical Pearl
Wolff–Chaikoff Effect
When large quantities of iodide
are ingested by patients with
hyperthyroidism, the result is
thyroid hormone suppression
(Wolff-Chaikoff effect).
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USMLE Step 2 CK
l Internal Medicine
stopped several days (1–2 weeks) before and after the RAI treatment. The antithyroid medications, such as PTU, block the uptake of the radioactive iodine.
Hypothyroidism
Etiology. The etiology of hypothyroidism results from the thyroid in 95% of cases (primary).
Primary hypothyroidism can occur secondary to chronic thyroiditis (Hashimoto disease); this
is the most common cause of goitrous hypothyroidism and is associated with antimicrosomal
antibodies. Postablative surgery or radioactive iodine, heritable biosynthetic defects, and
iodine deficiency can lead to primary hypothyroidism. Drugs such as lithium and acetylsalicylic acid can elicit primary hypothyroidism. Amiodarone, interferon, and sulfonamides can
cause hypothyroidism.
Suprathyroid causes of hypothyroidism include pituitary induced (secondary hypothyroidism) or hypothalamic induced (tertiary hypothyroidism).
Amiodarone, an antiarrhythmic drug used in the treatment of ventricular and supraventricular tachyarrhythmia, is structurally similar to T4 and contains approximately 40% iodine. It is
highly lipid-soluble and is concentrated in the adipose tissue, muscle, liver, lung, and thyroid
gland. Its elimination half-life is high (50−100 days) and thus total body iodine stores can
remain increased for up to 9 months after discontinuation of the drug. Thyroid abnormalities
have been noted in up to 20% of patients receiving long-term amiodarone therapy. However,
a meta-analysis suggested that with the lower doses of amiodarone, incidence of thyroid
dysfunction is around 4%. The effects range from abnormal thyroid function test findings
(without clinical hyper- or hypothyroidism) to overt thyroid dysfunction, which may be amiodarone-induced thyrotoxicosis or amiodarone-induced hypothyroidism (both can develop in
apparently normal thyroid glands or in glands with preexisting abnormalities).
• Amiodarone-induced thyrotoxicosis
– Ty p e 1 occurs in patients with underlying thyroid pathology such as autonomous
nodular goiter or Graves’; treatment is anti-thyroid therapy
– Ty p e 2 is a result of amiodarone causing a subacute thyroiditis, with release of pre-
formed thyroid hormones into the circulation; treatment is a trial of glucocorticoids
• Amiodarone-induced hypothyroidism due to inhibition of peripheral conversion of
T4 to T3
Clinical Findings. In the newborn, signs and symptoms of hypothyroidism include cretinism
(in 1/5,000 neonates) and juvenile hypothyroidism. Persistent physiologic jaundice, hoarse
cry, constipation, somnolence, and feeding problems are also seen. In later months, delayed
milestones and dwarfism, coarse features, protruding tongue, broad flat nose, widely set eyes,
sparse hair, dry skin, protuberant abdomen, potbelly with umbilical hernia, impaired mental
development, retarded bone age, and delayed dentition are also seen.
Signs and symptoms of hypothyroidism in the adult in the early stages include lethargy, constipation, cold intolerance, stiffness and cramping of muscles, carpal tunnel syndrome, and
menorrhagia. Later in the course of disease intellectual and motor activity slows, appetite
decreases and weight increases, hair and skin become dry, voice gets deeper and hoarse, and
deafness may occur. Slow deep tendon reflexes with prolonged relaxation phase are noted on
examination. Cholesterol levels in the blood may be elevated. Ultimately, myxedema appears
with an expressionless face, sparse hair, periorbital puffiness, large tongue, and pale, cool skin
that feels rough and doughy. Hyponatremia and anemia also occur.
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Diagnosis. Diagnosis of hypothyroidism is made by symptoms and physical findings.
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Laboratory tests are also used to confirm diagnosis (Table 2-3).
Table 2-3. Confirmation of Hypothyroid Diagnosis*
Primary Hypothyroidism 2° or 3° Hypothyroidism
↑ TSH Normal or ↓ TSH
↓ T
, ↓ FT
4
4
↓ T4, ↓ FT
4
T3 decreases in lesser extent Accompanied by decreased secretion of
other hormones
*Also seen: hypercholesterolemia, elevation of CPK, AST, hyponatremia, LDH; 12% associated to
pernicious anemia
Management. The goal in management of hypothyroidism is to restore metabolic state with
levothyroxine. This has to be done gradually in the elderly and patients with coronary artery
disease. Levothyroxine (T4) should be administered with monitoring of TSH/T3, T4 levels (it
takes 6 weeks after dosing changes for TSH to equilibrate).
• If there is a strong suspicion of suprathyroid hypothyroidism of hypothalamic or pituitary origin, give hydrocortisone with thyroid hormones.
• In patients with suprathyroid hypothyroidism, T4 level rather than TSH is used to
guide treatment.
• Levothyroxine should be taken on an empty stomach with no other drugs or vitamins;
multivitamins, including calcium and iron, can decrease its absorption.
• If a patient has coronary heart disease that needs intervention, do the intervention
(CABG or stent placement) before thyroid hormone replacement is initiated.
Chapter 2
l Endocrinology
During pregnancy, demand for thyroid hormones may increase and thus close monitoring of
TSH and T4 should be done. Hypothyroidism during pregnancy should be treated with levothyroxine, with serum TSH goal to be kept in the lower reference range. Serum TSH should
be measured at 4−6 weeks’ gestation, then every 4−6 weeks until 20 weeks’ gestation.
Myxedema coma can result if severe, long-standing hypothyroidism is left untreated. Patients
develop a hypothermic, stuporous state that is frequently fatal. It is associated with respiratory
depression (CO2 retention). Myxedema coma is precipitated by cold exposure, trauma, infections, and CNS depressants. Treatment includes very high doses of T4 along with T3.
Thyroiditis
Thyroiditis includes disorders of different etiologies characterized by inflammation of the thyroid. They have different clinical courses, and each can be associated at one time or another
with euthyroid, thyrotoxic, or hypothyroid state.
Subacute Thyroiditis. Subacute thyroiditis includes granulomatous, giant cell, or de Quervain
thyroiditis. This can occur at any age, although most commonly in the fourth and fifth
decades. Subacute thyroiditis is probably of viral origin and follows upper respiratory infection symptoms including malaise, fever, pain over the thyroid, and pain referred to the lower
jaw, ears, neck, or arms. The thyroid gland is enlarged and firm in this setting. Laboratory
Clinical Pearl
• Hashimoto thyroiditis
presents more commonly
as hypothyroidism.
• Subacute (de Quervain)
thyroiditis presents
more commonly as
hyperthyroidism.
25
USMLE Step 2 CK
l Internal Medicine
findings in subacute thyroiditis include elevated erythrocyte sedimentation rate (ESR),
decreased radioactive iodine uptake, initial elevation in T4 and T3 (caused by leak of hormone
from the gland), followed by hypothyroidism as the hormone is depleted.
The differential diagnosis of subacute thyroiditis includes mostly Graves’ disease. Treatment
is symptomatic with NSAIDs, prednisone, and propranolol. The disorder may smolder for
months but eventually subsides with return to normal function.
Hashimoto Thyroiditis. Hashimoto thyroiditis is a chronic inflammatory process of the thyroid
with lymphocytic infiltration of the gland, and is thought to be caused by autoimmune factors.
• Etiology. Hashimoto thyroiditis is a common disorder occurring most frequently in
middle-aged women, and is the most common cause of sporadic goiter in children.
Autoimmune factors are implicated as evidenced by lymphocytic infiltration, presence
of increased immunoglobulin, and antibodies against components of thyroid tissue
(antithyroglobulin Abs).
• Clinical findings. Clinical findings include agoiter that is painless, which is the
main feature of this disease. The goiter is rubbery and not always symmetrical.
Hypothyroidism occurs.
• Diagnosis. The diagnosis of Hashimoto thyroiditis is suggested by finding a firm,
nontoxic goiter on examination. Laboratory values in the early stages are metabolically normal, then TSH increases, and T4 and T3 decrease. High titers of antithyroid
antibodies, namely antimicrosomal antibodies, are present. Histologic confirmation
is made by needle biopsy, but it is usually not needed. Antithyroperoxidase antibodies
are found as well.
• Management. Hashimoto thyroiditis is managed by replacement with l-thyroxine.
Lymphocytic (Silent, Painless, or Postpartum) Thyroiditis. Lymphocytic thyroiditis is a self-
limiting episode of thyrotoxicosis associated with chronic lymphocytic thyroiditis. It is more
common in women of any age. The thyroid is nontender, firm, symmetrical, and slightly to
moderately enlarged. T4 and T3 are elevated, RAIU is low, and ESR normal. If antithyroid
antibodies are present, they are only in a low titer. Etiology and pathogenesis of lymphocytic
thyroiditis is unclear. This disease may last for 2–5 months and be recurrent (as in postpartum thyroiditis). Treatment is symptomatic with propranolol.
Reidel Thyroiditis. Reidel thyroiditis results from intense fibrosis of the thyroid and surrounding structures (including mediastinal and retroperitoneal fibrosis).
Neoplasia of the Thyroid
Classification. Thyroid adenomas may be nonfunctioning or hyperfunctioning. They are slow
growing over many years. Management for hyperfunctioning adenomas includes ablation
with radioactive iodine. The types of thyroid adenomas are follicular (which is most common and highly differentiated, autonomous nodule), papillary, and Hürthle.
Types of thyroid carcinomas
Papillary Carcinoma. Papillary carcinoma is the most common thyroid cancer. It is associated
with history of radiation exposure. 60–70% of all thyroid cancers are papillary. Women are
affected by papillary carcinoma 2–3 times more than men. There is a bimodal frequency and
peaks occur in the second and third decades and again later in life. This tumor is slow growing
26
and spreads via lymphatics after many years. The treatment is surgery when the tumor is small
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and limited to a single area of the thyroid. TSH suppression therapy with levothyroxine is also
used. With large tumors, radiation therapy is used with surgery.
Follicular Carcinoma. Follicular carcinoma accounts for 15–20% of all thyroid cancers. It is
more common in the elderly and in women rather than men. This tumor is more malignant
than papillary carcinoma. Follicular carcinoma spreads hematogenously with distant metastasis to the lung and bone. Treatment requires near total thyroidectomy with postoperative
radioiodine ablation.
Chapter 2
l Endocrinology
Anaplastic Carcinoma. Anaplastic carcinoma accounts for 1–2% of all thyroid cancer. It
occurs mostly in elderly patients. Women are affected more than men with this tumor.
Anaplastic carcinoma is highly malignant with rapid and painful enlargement. Eighty percent
of patients die within 1 year of diagnosis. This cancer spreads by direct extension.
Medullary Carcinoma. Medullary carcinoma accounts for 5% of all thyroid cancers. It occurs
as a sporadic form or familial form. This tumor arises from parafollicular cells of the thyroid and is more malignant than follicular carcinoma. The tumor often produces calcitonin.
Medullary carcinoma is the component of two types of MEN (multiple endocrine neoplasia). In type IIa (Sipple syndrome), pheochromocytoma, medullary thyroid carcinoma, and
(in one-half of cases) parathyroid hyperplasia occur. In MEN type IIb, pheochromocytoma,
medullary carcinoma, and neuromas occur. Medullary carcinoma may also occur in families
without other associated endocrine dysfunctions. The only effective therapy is thyroidectomy.
Calcitonin levels can also be increased from cancer of the lung, pancreas, breast, and colon.
The only thyroid cancer with an elevated calcitonin level is medullary cancer.
When to suspect a thyroid carcinoma
Suspect a thyroid carcinoma when there is recent growth of thyroid or mass with no tenderness or hoarseness. Patients with a history of radiation therapy of the head, neck, or upper
mediastinum in childhood average 30 years to develop thyroid cancer. The presence of a
solitary nodule or the production of calcitonin are also clues to malignancy. Calcifications on
x-rays such as psammoma bodies suggest papillary carcinoma; increased density is seen in
medullary carcinoma. Do thyroid function tests first; cancer is never hyperfunctioning.
Clinical Pearl
RET mutations are the
mutations associated with
MEN2 and familial medullary
thyroid carcinomas.
Diagnostic approach to solitary nonfunctioning nodule
Fine-needle aspiration (FNA) for cytology is the initial procedure of choice in the evaluation of
most patients. Five percent of nonfunctioning thyroid nodules prove to be malignant; functioning nodules are very seldom malignant. The first test to do in a patient with a thyroid nodule is
TSH; if this is normal, then proceed to FNA. U/S is useful to distinguish cysts from solid nodules.
PARATHYROID GLANDS
Generalities. The function of parathyroid hormone (PTH) is to maintain extracellular fluid
calcium concentration. PTH acts directly on the bone and kidney, and indirectly on intestine
(through its effects on synthesis of 1,25-dihydroxycholecalciferol [1,25(OH)2D3]) to increase
serum calcium. It is closely regulated by the concentration of serum-ionized calcium. PTH
increases osteoclast activity, which releases calcium. PTH also inhibits phosphate reabsorption
in the kidney tubule. This also favors bone dissolution and calcium release from bones. PTH
activates vitamin D, which increases the GI absorption of calcium.
27
USMLE Step 2 CK
l Internal Medicine
Calcium Regulation—Overview. Calcium regulation involves 3 tissues, namely, the bone,
kidney, and intestine. It involves 3 hormones: PTH (hypercalcemic), calcitonin (hypocalcemic), and activated vitamin D (hypercalcemic).
Hypercalcemia
Hypercalcemia represents an increase in the total or free calcium level. About 98% of calcium
is stored in bone. Calcium is absorbed from the proximal portion of the small intestine, particularly the duodenum. About 80% of an ingested calcium load in the diet is lost in the feces,
unabsorbed. Of the 2% that is circulating in blood, free calcium is 50%, protein bound is
40%, with only 10% bound to citrate or phosphate buffers.
Etiology. The most common cause of hypercalcemia is primary hyperparathyroidism.
Hyperparathyroidism, which is usually asymptomatic, comes to light because of routine
office-based testing. The hypercalcemia of malignancy is due to a PTH-like protein produced
by squamous cell carcinoma of the lung or metastatic disease to the bone. Granulomatous
diseases such as sarcoidosis, tuberculosis, berylliosis, histoplasmosis, and coccidioidomycosis
are all associated with hypercalcemia. Neutrophils in granulomas have their own 25-vitamin
D hydroxylation, producing active 1,25 vitamin D. Rare causes include vitamin D intoxication, thiazide diuretics, lithium use, and Paget disease, as well as prolonged immobilization.
Hyperthyroidism is associated with hypercalcemia because there is a partial effect of thyroid
hormone on osteoclasts. Acidosis results in an increased amount of free calcium. This is
because albumin buffers acidosis. Increased binding of hydrogen ions to albumin results in
the displacement of calcium from albumin.
Familial hypocalciuric hypercalcemia (FHH) is a benign form of hypercalcemia. It presents
with mild hypercalcemia, family history of hypercalcemia, urine calcium to creatinine ratio
<0.01, and urine calcium <200 mg/day (hypocalciuria). Most cases are associated with loss of
function mutations in the CaSR gene, which encodes a calcium sensing receptor (expressed in
kidney and parathyroid tissue). The perceived lack of calcium levels by the parathyroid leads to
high levels of parathyroid hormone. FHH is indicated by the presence of hypercalcemia at the
same time with hypocalciuria. (In all other causes of hypercalcemia, elevated calcium levels
in the blood are correlated with elevated calcium urine levels, as a properly sensing kidney
works to excrete calcium.) No treatment is generally required, since patients are most com-
monly asymptomatic.
Clinical
• Neurologic: Hypercalcemia results in decreased mental activity such as lethargy and
confusion.
• GI: Hypercalcemia results in decreased bowel activity such as constipation and anorexia
but commonly gives nausea and vomiting as well. Pancreatitis occurs because of the
precipitation of calcium in the pancreas. Severe pancreatitis, however, is associated with
hypocalcemia because of binding of calcium to malabsorbed fat in the intestine. Ulcer
disease is caused by hypercalcemia for unclear reasons.
• Renal: Hypercalcemia results in polyuria and polydipsia because of the induction of
nephrogenic diabetes insipidus. Calcium also precipitates in the kidney, resulting in
both kidney stones as well as nephrolithiasis.
• Cardiovascular: Hypertension occurs in 30–50% of patients with hypercalcemia. The
EKG will show a short QT.
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PTH
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+
–
Calcitonin
Ca
free
+ –
2+
Ca
400 mg Ca
Absorption: 30–35%
+
Vit D Abs Ca/PO
Ca2+ + prot Plasma
Chapter 2
2+
/d
4
● Endocrinology
+
PTH
• Stimulates osteoclasts
• ↑ distal tubular
reabsorption of Ca
2+
• ↓ PO4 reabsorption
• ↑ production of
1,25 (OH)2 Vit D
1,25 (OH)
Vit D
2
Vit D
• ↑ CaPO4 intestinal absorption
• ↑ proximal tubular reabsorption
of PO
4
Calcitonin
• Inhibition of bone resorption
• Secreted by parafollicular
cells of thyroid gland
• Physiologic role incompletely
understood
Dietary
endogenous
Vit D
3
25-OH-Vit D
Figure 2-10. Calcium Regulation
29
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