arises as an outpouching of the primitive foregut around the third week of gestation

originates at the base of the tongue at the foramen cecum

During its descent, the anlage remains connected to the foramen cecum via an epithelial-lined tube known as the thyroglossal duct

paired lateral anlages originate from the fourth branchial pouch and fuse with the median anlage at approximately the fifth week of gestation. The lateral anlages are neuroectodermal in origin (ultimobranchial bodies) and provide the calcitonin producing parafollicular or C cells

Thyroglossal Duct Cyst and Sinus may occur anywhere along the migratory path of the thyroid 80% are found in juxtaposition to the hyoid bone usually asymptomatic but occasionally become infected by

oral bacteria, prompting the patient to seek medical advice midline neck mass that moves upward with protrusion of

the tongue. Sistrunk = which consists of en bloc cystectomy and

excision of the central hyoid bone Lingual Thyroid

failure of the median thyroid anlage to descend normally Intervention necessary for obstructive symptoms such as

choking, dysphagia, airway obstruction, or hemorrhage Surgical excision rarely needed should be preceded by

an evaluation of normal thyroid tissue in the neck to avoid inadvertently rendering the patient hypothyroid.

TSH is only necessary testThyrotropin-Releasing Hormone to

evaluate pituitary functionThyroid antibodiesRadionuclide ImagingUltrasound CT or MRI scans

Diffuse Toxic Goiter (Graves' Disease) Antibodies against TSH receptor MCC of hyperthyroidism in US Strong familial predisposition Conditions such as the postpartum state, iodine excess, lithium therapy, and

bacterial and viral infections have been suggested as possible triggers Sx: palpitations, nervousness, fatigue, emotional lability, hyperkinesis, GI

complaints Suppressed TSH with elevated T3, T4 Tx: antithryroid drugs, radioactive idoine, ablation, surgery when others fail

or contraindicated or suspicious nodule Toxic Multinodular Goiter

often have a prior history of a nontoxic multinodular goiter thyroid nodules become autonomous to cause hyperthyroidism. See suppressed TSH level and elevated free T4 or T3 levels RAI uptake also is increased, showing multiple nodules with increased

uptake and suppression of the remaining gland. Subtotal thyroidectomy is the gold standard

Hyperthyroidism accompanied by fever, central nervous system agitation or depression, cardiovascular dysfunction

Beta blockers reduce peripheral T4 to T3 conversion decrease the hyperthyroid symptoms.

Oxygen supplementation and hemodynamic support

Lugol's iodine decrease iodine uptake and thyroid hormone

secretion. PTU blocks the formation of new thyroid

hormone

= Suppurative Thyroiditis Infectious agents can seed it from the

hematogenous or lymphatic route via direct spread from persistent pyriform sinus

fistulae or thyroglossal duct cysts penetrating trauma to the thyroid gland due to immunosuppression.

Streptococcus and anaerobes account for about 70% of cases;

Acute suppurative thyroiditis is more common in children preceded by an upper respiratory tract infection or

otitis media Treatment consists of IV antibiotics and

drainage of abscesses.

Painful or painless forms Painful thyroiditis thought to be viral in

origin Thyroiditis most commonly occurs in 30-

to 40-year-old women History of a preceding upper respiratory

tract infection often can be elicited. In the early stages of the disease, TSH is

decreased, and T4 , and T3 levels are elevated due to the release of preformed thyroid hormone from destroyed follicles.

Painless thyroiditis is considered to be autoimmune in origin

The most common inflammatory disorder of the thyroid and the leading cause of hypothyroidism.

Hashimoto's thyroiditis = autoimmune process that activation of CD4+ T (helper) lymphocytes with specificity for

thyroid antigens T cells can recruit cytotoxic CD8+ T cells to the thyroid autoantibodies, which lead to complement fixation and killing

by natural killer cells More common in women between the ages of 30 and 50

years old. An elevated TSH and the presence of thyroid

autoantibodies FNAB is indicated in patients who present with a solitary

suspicious nodule or a rapidly enlarging goiter. Treatment

Thyroid hormone replacement therapy is indicated in overtly hypothyroid patients, with a goal of maintaining normal TSH levels.

replacement of all or part of the thyroid parenchyma by fibrous tissue

etiology of this disorder is controversial predominantly in women between the ages

of 30 to 60 years old presents as a painless, hard anterior neck

mass, which progresses over weeks to years to produce symptoms of compression, including dysphagia, dyspnea, choking, and hoarseness.

Patients may present with symptoms of hypothyroidism and hypoparathyroidism as the gland is replaced by fibrous tissue

Surgery is mainstay of treatment

4% of individuals in the United States Assess symptoms Determine family history

risk factor for the development of both medullary and nonmedullary thyroid cancer

Do PE best palpated from behind the patient

and with the neck in mild extension. Then proceed to further tests…

80% of all thyroid malignancies predominant thyroid cancer in children and individuals

exposed to external radiation. Lymph node metastases are common, Orphan Annie nuclei Psammoma bodies Excellent prognosis with a >95% 10-year survival rate. AGES scoring system

Age, histologic Grade, Extrathyroidal invasion metastases and tumor Size Low versus High risk patients

If any high-risk factors total or near-total thyroidectomy. If minimal papillary thyroid carcinoma in removed for other

reasons, unilateral thyroid lobectomy and isthmusectomy is usually enough.

10% of thyroid cancers Limitations inherent to FNAB diagnosis Usually are solitary lesions, and the

majority are surrounded by a capsule. Treatment

Thyroid lobectomy because at least 80% of these patients will have benign adenomas.

Intraoperative frozen-section examination usually is not helpful

Total thyroidectomy should be performed when thyroid cancer is diagnosed

Stop T4 therapy for 4-6 weeks Radioactive Iodine Scan look for hot spot Adjuvant treatment with radioactive iodine Then resume thyroid replacement therapy,

will help supress Can follow thyroglobulin measurement as

marker Screening ultrasound periodically to

evaluate central and lateral neck compartments

5% of thyroid malignancies and arises from the parafollicular or C cells of the thyroid,

25% occur within the spectrum of several inherited syndromes such as familial MTC, MEN2A, and MEN2B. germline mutations in the RET proto-oncogene.

Present with neck mass, lymphadenopathy in 15-20% Hematogenous spread Unilateral if sporadic, multifocal if familial Amyloid on slides Screen for MEN!

Treat pheochromocytoma first Total thyroidectomy with bilateral central neck

dissection Followup measure calcitonin and cEA 10 yr survival 80% Perform prophylactic thyroidectomy for MEN2 with

RET

1 % of thyroid malignancies in US Women more common Classic: long standing neck mass that rapidly enlarges

and becomes painful Sx: dysphonia, dysphagia, and dyspnea May be fixed to surrounding structures or may be

ulcerated with areas of necrosis Confirmed by FNA Isthmusectomy with or without a tracheostomy may

be needed to alleviate tracheal obstruction. Treatment and Prognosis

most aggressive thyroid malignancy few patients surviving 6 months Combined radiation and chemotherapy in patients with

resectable disease has been associated with prolonged

Superior glands from the fourth branchial pouch (also thyroid gland)

Inferior glands form third branchial pouch (also thymus)

The position of normal superior parathyroid glands is more consistent with 80% of these glands being found near the

posterior aspect of the upper and middle thyroid lobes,

Approximately 15% of inferior glands are found in the thymus.

Undescended inferior glands may be found near the skull base, angle of the mandible, frequency of intrathyroidal glands is about 2%.

Rely on a G-protein coupled membrane receptor to regulate PTH secretion by sensing extracellular calcium levels

PTH secretion also stimulated by low levels of 1,25-dihydroxy vitamin D, catecholamines, and hypomagnesemia.

Secreted PTH has a half-life of 2 to 4 minutes. PTH functions to regulate calcium levels via its actions on three

target organs: Bone Kidney Gut

Calcitonin produced by thyroid C cells antihypercalcemic hormone inhibits osteoclast-mediated bone resorption.

Vitamin D refers to vitamin D2 and vitamin D3 , both produced by photolysis of naturally occurring sterol precursors Vitamin D is metabolized in the liver to its primary circulating form, 25-

hydroxyvitamin D. Further hydroxylation 1,25-dihydroxy vitamin D most metabolically

active Vitamin D stimulates the absorption of calcium and phosphate from the gut

and the resorption of calcium from the bone.

Most cases of PHPT are sporadic. Occurs within the spectrum of a number o inherited

disorders such as MEN1, MEN2A, isolated familial HPT Hyperplasia, Adenoma, Carcinoma PHPT is the earliest and most common manifestation of

MEN1 80 to 100% of patients by age 40 years old

Sx: kidney stones, painful bones, abdominal groans, psychic moans, and fatigue overtones

More likely to be asymptomatic and picked up on blood tests

Measure PTH to decide between the 2 causes of hypercalcemia

Surgery for complications, classic symptoms, age < 50 Total versus focused

Localization studies: ultrasound, Sestamibi scan

1% of PHPT cases. Suspect by preoperatively by the

presence of severe symptoms serum calcium levels >14 mg/dL significantly elevated PTH levels (5 x normal) palpable parathyroid gland

Local invasion is most common Treatment

bilateral neck exploration, with en bloc excision of the tumor and the ipsilateral thyroid lobe.

Modified radical neck dissection if lymphadeonopathy

Uncontrolled PTH secretion, worsened by polyuria, dehydration, and

reduced kidney function Treatment consists of therapies to

lower serum calcium levels followed by surgery

The mainstay of therapy involves rehydration

diuresis with furosemide Further bisphosphonates, etc

Asymptomatic Patient Serum Ca > 1 mg/dl Above upper limits

of normal Life threatening hypercalcemic episode Reduced creatinine clearance Renal stones on xray Markedley elevated 24 hour urine Ca Substantially decreased bone mineral

density

commonly occurs in patients with chronic renal failure but also may occur in those with hypocalcemia secondary to inadequate calcium or vitamin D intake, or malabsorption.

The pathophysiology related to hyperphosphatemia, deficiency of 1,25-dihydroxy vitamin D due to loss of renal tissue, low calcium intake, decreased calcium absorption, and abnormal parathyroid cell response

generally hypocalcemic or normocalcemic. treated medically with a low-phosphate diet, phosphate

binders, adequate intake of calcium and 1,25-dihydroxy vitamin D and a high calcium, low-aluminum dialysis bath.

Surgery if: bone pain, pruritus, calcium >11 mg/dL with markedly

elevated PTH, calciphylaxis A bilateral neck exploration is indicated Consider subtotal resection with autotransplant

some patients develop autonomous parathyroid gland function and tertiary HPT after renal transplant

pathologic fractures, bone pain, renal stones, mental status changes.

Surgery if persists 1 year after transplant

Hypocalcemia Vocal cord paralysis HypoparathyroidismPermanent if > 6 mths

Outer cortex and an inner medulla The cortex originates from mesodermal

tissue near the gonads Ectopic adrenocortical tissue may be found

in the ovaries, spermatic cord, and testes. Adrenal medulla is ectodermal in origin

and arises from the neural crest. Most extra-adrenal neural tissue regresses

but may persist at several sites. The largest of these ia left of the aortic

bifurcation near the inferior mesenteric artery origin and is designated as the organ of Zuckerkandl.

Secondary causes from stimulation of the renin-angiotensin system from renal artery stenosis and to low-flow states such as congestive heart failure and cirrhosis.

Primary hyperaldosteronism results from autonomous aldosterone secretion which, I leads to suppression of renin secretion. 1% of hypertension cases. Hypokalemia Causes:

▪ Adenoma 70%▪ Hyperplasia 30%▪ Carcinoma rare

Sx: hypertension difficult to control despite multiple-drug therapy, muscle weakness, polydipsia, polyuria, nocturia, headaches, and fatigue.

Labs: K+. Measure renin-aldosterone CT scan can localize with sensitivity of 90% Selective venous sampling Txs:

spironolactone (aldosterone antagonist) amiloride (a potassium-sparing diuretic that blocks sodium channels in the distal

nephron nifedipine Captopril Unilateral tumors producing aldosterone are best managed by adrenalectomy

Hypercortisolism Most common cause iatrogenic 70% are pituitary tumor, 20% adrenal tumor, 10% ectopic ACTH

producing tumor Sx: wt gain, buffalo hump, central obesity, striae, acne,

hypertension, neurologic or pyschiatric disorders elevated glucocorticoid levels that are not suppressible by

exogenous hormone administration and loss of diurnal variation overnight low-dose dexamethasone suppression test. In this test

Cushing's syndrome patients do not suppress Measure ACTH to determine if ACTH dependent; If ACTH dependent do high dose dexamethoasone test; if no supression then

likely ectopic Laparoscopic adrenalectomy is the treatment of choice for

patients with adrenal adenomas. Open adrenalectomy for large tumors (≥6 cm) or those suspected

to be adrenocortical cancers Cushing disease treatment is transsphenoidal excision May need mineralocorticoid and glucocorticoid replacement

therapy

Deficiencies or complete absence of enzymes involved in adrenal steroidogenesis.

21-Hydroxylase deficiency is the most common enzymatic defect (>90% of cases) overproduction of adrenal androgens and corticosteroid precursors

such as 17-hydroxyprogesterone and androstenedione. converted to testosterone in the peripheral tissues, thereby

leading to virilization. Complete deficiency of 21-hydroxylase presents at birth with:

virilization, diarrhea, hypovolemia, hyponatremia, hyperkalemia, and hyperpigmentation.

Dx: karyotype and measurement of plasma and urinary steroids

Tx: traditionally have been managed medically with cortisol and mineralocorticoid replacement to suppress the hypothalamic-pituitary-adrenal axis.

teroids required often are supraphysiologic lead to iatrogenic hypercortisolism lap adrenalectomy gaining momentum

Disorders of the Adrenal Medulla; paraganglioma if extra adrenal

10 percent tumor because 10% are bilateral, 10% are malignant, 10% occur in

pediatric patients, 10% are extra-adrenal, and 10% are familial.

Pheochromocytomas occur in families with MEN2A and MEN2B

Sx: Headache, palpitations, and diaphoresis Dx: 24 hr urine for catecholamines and plasma

metanephrines CT to localize tumor Need alpha blocker first, titrate to orthostatic

hypotension Adrenalectomy is treatment of choice 12-29% are malignant, and these tumors are

associated with decreased

May be primary, resulting from adrenal disease, or secondary, due to a deficiency of ACTH

The most commonly encountered causes of primary adrenal insufficiency are autoimmune disease, infections, and metastatic deposits.

fulminant meningococcal septicemia (Waterhouse-Friderichsen syndrome).

Bilateral adrenal hemorrhage also can occur secondary to trauma, severe stress, infection, and coagulopathies and, if unrecognized, is lethal.

Suspect in stressed patients with any of the relevant risk factors

laboratory findings: hyponatremia, hyperkalemia, fasting or reactive hypoglycemia

ACTH stim test Peak cortisol levels <20 g/dL suggest adrenal insufficiency

Replace glucocorticoids and mineralocorticoids

Postoperative hemodynamic instability pheochromocytomas

Nelson's syndrome from progressive growth increased ACTH levels hyperpigmentation, extraocular muscle palsies.

You are seeing a postop total parathyroidectomy patient who complains of SOB. What do you do?

A patient is diagnosed with medullary thyroid cancer, what should you do prior to surgery?

An FNA shows follicular cells, what should you recommend

What are the complications of thyroidectomy or parathyroidectomy?

How do your prepare a pheochromocytoma patient for surgery?