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ENT > Thyroid/Parathyroid > Flashcards

Thyroid/Parathyroid Flashcards

1
Q

List the parts of thyroid gland

A
  • 2 pear shaped lobes
  • isthmus
  • pyramidal lobe
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2
Q

Where are the superior parathyroids located?

A
  • Usually in the posterolateral aspect of the superior pole
  • 1cm above the intersection of the RLN and the inferior thyroid artery
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3
Q

Where are the inferior parathyroids located?

A
  • More variable, but most commonly 1-2cm from the entrance of the inferior thyroid artery into the lower thyroid pole
  • May also be associated with the superior thymus*
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4
Q

How much does the thyroid weigh, on average?

A

20 grams in males

17 grams in females

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5
Q

How much do the parathyroids weigh each?

A

20-40 mg

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6
Q

What is an average PTH level?

A

The average PTH level is 10-60 pg/ml

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7
Q

What ligament attaches the thyroid lobes to the trachea?

A

Lateral suspensory ligament, or Berry’s ligament

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8
Q

What cells are within the thyroid gland, and secrete calcitonin?

A

C-cells, or parafollicular cells

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9
Q

Describe the embryology of the thyroid

A

Endoderm between 1st and 2nd branchial arch on the floor of the pharynx (foramen cecum) invaginates at the 4th week and descends into mesenchymal tissue along thyroid duct (anterior to hyoid bone!)

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10
Q

Describe the embryology of the parathyroid

A

The 3rd dorsal branchial pouch leads to the inferior parathyroids AND the isthums

The 4th dorsal branchial pouch leads to the superior parathyroids AND C-cells of the thyroid

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11
Q

Where can an ectopic thyroid be found?

A

Anywhere along the thyroid duct from the tongue as a lingual thyroid to the sternal notch

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12
Q

Where is the most common location of aberrant parathyroids?

A

Anterior superior mediastinum

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13
Q

Describe a Thyroglossal Duct Cyst

A

Pathophysiology

failure of complete obliteration of thyroglossal duct
(created from tract of the thyroid descent from the foramen cecum down to midline neck)

Symptoms

midline neck mass with cystic and solid components, elevates with tongue protrusion (attached to hyoid bone), typically inferior to hyoid
bone and superior to thyroid gland, may have fibrous cord, dysphagia, globus sensation

Histopathology

lined with respiratory and squamous epithelium

Complications

rare malignant potential, secondary infection

Treatment

Sistrunk procedure (excision of cyst and tract with cuff of tongue base and mid-portion of hyoid bone, 3% recurrence)

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14
Q

What is the blood supply of the thyroid gland?

A
  • External carotid artery - superior thyroid artery - superior pole of thyroid
  • Innominate artery - thyroid ima artery - isthmus
  • Venous drainage from the superior, middle, inferior (largest) veins into the IJ
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15
Q

What is the blood supply of the parathyroids?

A

Subclavian artery ➝ thyrocervical trunk ➝ inferior thyroid artery ➝ lateral lobes of the thyroid and the inferior and superior parathyroid arteries

Superior parathyroid arteries may also arise from superior
thyroid artery

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16
Q

Thyroid blood supply

A
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17
Q

What nerve innervates the cricothyroid muscle?

A

External branch of SLN

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18
Q

What nerve provides the sensation to the larynx?

A

Internal branch of the SLN

Parallels the superior thyroid artery, pierces the thyrohyoid membrane

May anastomose with the RLN to form the loop of Galen

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19
Q

What are the prelaryngeal lymph nodes called?

A

Delphian nodes

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20
Q

Summarize Thyroid Hormone synthesis and release

A
  1. Anterior pituitary secretes TSH - increases thyroid iodide uptake
  2. Iodination of thyroglobulin forms monoiodotyrosine (MIT) and
    * *diiodotyrosine** (DIT) molecules (organification)
  3. MIT and DIT link together to form T3 or T4, stored in colloid
  4. Released into blood after endocytosis and fusion with lysosome to release T3 and T4 (T4 is 90% of thyroid output)
  5. Thyroid hormone transport via Thyroxine Binding Globulin (TBG, made from liver, increased in pregnancy, binds 75% of T4)
  6. Thyroxine Binding Pre-Albumin (TBPA) binds 15% of T4
  7. Albumin binds 5% of T4
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21
Q

Summarize Thyroid Hormone Regulation

A
  • Thyrotropin-Releasing Hormone (TRH) - released from supraoptic and paraventricular nuclei of hypothalamus (not affected by TH)
  • Thyroid Stimulating Hormone (TSH) - comes from anterior pituitary, inhibited by thyroid hormone for (-) feedback
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22
Q

What is the Wolff-Chaikoff Effect?

A

excess iodine inhibits thyroid hormone

(usually temporary)

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23
Q

List the effects of thyroid hormone

A
  1. Elevates metabolic rate (thermogenesis, increases oxygen consumption)
  2. Essential for normal neural and skeletal development (stimulates chondrocytes, bone reabsorption, growth of neuronal tissue)
  3. Increases sympathetic activity (increases heart rate and contractility)
  4. Releases steroid hormones
  5. Stimulates erythropoiesis
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24
Q

How do Propylthiouracil (PTU) and Methimazole work?

A

These inhibit T3 conversion and the oxidation and organification of iodine

Side effects: hepatitis, agranulocytosis, parotiditis

Methimazole contraindicated in pregnancy

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25
Q

How does Lugol’s solution work?

A

Excess iodine inhibits thyroid hormone

Wolff-Chaikoff Effect

Contraindicated in RA

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26
Q

Why do Glucocorticoids suppress thyroid activity?

A

suppress the hypothalamic-pituitary-thyroid axis

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27
Q

How are Propanolol and Metoprolol used in thyrotoxicosis?

A

Used to control peripheral manifestations of sympathetic overactivity

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28
Q

List the various Thyroid Function Tests

A
  1. Total T4: radioimmunoassay measures free and bound T4
  2. Free T4: measures unbound T4, more specific for hypo- and hyperthyroidism
  3. TSH: radioimmunoassay measures TSH, most sensitive test for primary hypo- and hyperthyroidism
  4. Total T3: radioimmunoassay measures free and bound T3, useful for toxic nodules and toxic multinodular goiters (higher increase in T3 than T4)
  5. TRH Stimulation Test: measures TSH after infusion of TRH, tests pituitary secretion of TSH and hypothalamic response
  6. Radioactive Iodide Uptake (RAIU): measures the percentage of
    radiolabeled iodine taken up by the thyroid, assess metabolic status
  7. Calcitonin: elevated in medullary thyroid carcinoma
  8. Resin T3 Uptake (RT3U): measures the binding capacity of existing
    TBG, indirect measurement of TBG, an increased RT3U suggests a
    decreased total TBG (pregnancy or estrogen from oral contraceptives
    increases TBP and therefore increases total T4, however will have a
    normal euthyroid state (normal free T4)
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29
Q

Why must an FNA showing follicular cells be investigated further?

A

You must do a hemithyroidectomy to examine architecture

Could be adenoma or carcinoma

Specifically, you are looking for extracapsular spread, LVI or vascular invasion, or metastasis

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30
Q

FNA shows Amyloid Deposits (stained with Congo Red) suggests what?

A

Medullary carcinoma

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31
Q

What percentage of “cold” nodules are malignant?

A

These are hypofunctioning nodules

Have a 5-20% malingancy rate

Consider lobectomy and isthmusectomy

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32
Q

What percentage of “hot” nodules are malignant?

A

These are hyperfunctioning

4% malignancy rate

Maybe be observed

33
Q

Describe the features of a Thyroid Cyst

A

Pathophysiology

typically arises from degenerated nodules, may result
from cystic degeneration of malignancy

Symptoms

smooth, round mass

Diagnosis

FNA, ultrasound, CT

Treatment

may observe for regression, fine needle aspirate relieves pain and acquires cells for cytology, may consider lobectomy for recurrent cysts
that are recalcitrant to drainage or bloody aspirates

34
Q

Describe the features of Euthyroid Goiter

A
  • More common in women
  • Pathophysiology: iodine deficiency ➝ TSH hypersecretion ➝ stimulates chronic thyroid hyperplasia and involution ➝multinodularity

Types
1. Endemic Goiter: iodine deficiency, extrinsic goitrogens (soybeans,
lithium, iodides, etc.)
2. Sporadic: uncertain etiology

Symptoms

multiple nodules of varying size,may present with compressive symptoms (stridor, dysphagia)

Diagnosis

FNA of a prominent nodule, TFT to confirm euthyroid state (may be hypothyroid), consider radionuclear scanning to evaluate functional status

Treatment

iodine replacement (reverses goiter), hormonal suppression (controversial), radioactive iodine therapy or surgical excision (subtotal thyroidectomy) may be considered for cosmesis, decompression,
 concern of malignancy, or toxicosis
35
Q

Describe the features of a Mediastinal Goiter

A

Pathophysiology

intrathoracic extension of thyroid gland (inferior
extension is the path of least resistance)

Symptoms

dyspnea, stridor, dysphagia, choking, superior vena cava syndrome

Diagnosis

CT/MRI of neck and chest, radionuclear scanning

Treatment

surgical excision, typically accessed from collar incision although a sternotomy may be required

36
Q

What are the symptoms of hyperthyroidism?

A
  1. Elevated Metabolic Rate: weight loss, fatigue, sweating, heat
    intolerance
  2. Increased Sympathetic Activity: palpitations, tachycardia, tremor
  3. Increased Protein Degradation: weakness, fine hair
  4. Neurologic Effects: increased deep tendon reflex, nervousness
  5. Reproductive Effects: abnormal menstrual cycle, decreased libido
37
Q

List the most common cause of hyperthyroidism

A
  • Graves’ Disease
  • Multinodular Toxic Goiter
  • Subacute Thyroiditis
  • Exogenous from medications, iodine induced
  • Uninodular Toxic Goiter
  • Thyroid Cancer
  • Pituitary tumors
38
Q

Describe the features of Graves’ Disease

A

Pathophysiology

thyroid receptor autoantibody (IgG) ➝ stimulates
glandular hyperplasia via TSH receptor ➝ goiter and increased T3 and T4 secretion

Risks

radiation exposure, women (adolescence or 30-40), genetic disposition

Histopathology

hyperplasia, increased colloid material, papillary
projections

Symptoms

diffuse goiter, hyperthyroid symptoms (see above), infiltrate dermopathy, exophthalmos (autoimmune ➝ extraocular muscle deposition), blindness from optic neuropathy, pre-tibial myxedema

Diagnosis

thyroid-stimulating autoantibodies; elevated T3, T4, RAIU, and thyroglobulins; decreased serum TSH; radioactive iodine scan reveals
diffuse uptake

39
Q

Describe the treatment of Graves’ Disease

A
  1. Propylthiouracil and Methimazole may be considered forsmall goiter and moderate disease
  2. Propanolol: may be supplemented for severe symptoms
  3. Radioactive Iodine (131I): indicated for more severe symptoms or failed medical therapy; there is risk of hypothyroidism and is contraindicated in pregnancy
  4. Subtotal Thyroidectomy: indicated for failed medical therapy, pregnancy (especially in second trimester), noncompliance, suspicious nonfunctioning (“cold”) nodule, compressive symptoms
40
Q

What are the symptoms of hypothyroidism?

A
  • Reduced Metabolic Rate: weight gain, cold intolerance, lethargy
  • Decreased Sympathetic Activity: bradycardia, constipation
  • Decreased Protein Degradation: weakness, fine hair, hoarseness
  • Decreased Neurologic Response: slowed deep tendon reflex, depression
  • Myxedema: nonpitting edema
  • Creatinism: hypothyroidism in children; mental retardation, impaired physical growth, macroglossia, protruberant abdomen
  • Myxedema Coma: severe hypothyroidism; hypothermia, hypoglycemia, hypoventilation, ileus, death; Rx: parenteral levothyroxine, corticosteroids
41
Q

What are the causes of hypothyroidism?

A
  • Radiation Therapy
  • Chronic Thyroiditis
  • Idiopathic Atrophy
  • Hashimoto’s Thyroiditis
  • Surgical or Radioiodine Ablation Therapies
  • Secondary Hypothyr oidism (pituitary or hypothalamic dysfunction)
  • Iodine Deficiency
  • Congenital Hypothyroidism: from maternal iodine expectorants, anti-thyroid medications, and anti-thyroid antibodies
42
Q

Describe the features of Subacute Thyroiditis (de Quervains)

A

Pathophysiology

viral (mumps, Coxsackivirus) ➝ decreased iodine
uptake (unlike Grave’s)

Symptoms

painful enlarged thyroid, self limiting, malaise, associated upper respiratory infection

Diagnosis

clinical history, TFT (may be transient hyperthyroid)

Treatment

symptomatic therapy, observation

43
Q

Describe the features of Hashimoto‘s Thyroiditis (Chronic Autoimmune Thyroiditis)

A

associated with lymphoma, neoplasms, other autoimmune disease

Pathophysiology

anti-thyroglobulin & anti-microsomal Ab ➝ anti-TSH receptor ➝ transient hyperthyroid then hypothyroidism

Risks

women, genetic susceptibility (HLA-DR3), Sjögren’s, DM, pernicious anemia

Histopathology

fibrosis, lymphocytic infiltration

Symptoms

slowly enlarging goiter, painless

Diagnosis

antimicrosomal antibodies, ESR, TFT (may have elevated, normal, or low serum levels of T4 and TSH), FNA only for prominent nodules suspicious of carcinoma or lymphoma that do not resolve with medical therapy)

Treatment

long term thyroxine therapy with TFT monitoring; surgical excision for compressive symptoms, suspicious nonfunctioning (“cold”) nodule, and pregnancy

44
Q

This type of thyroiditis is like subacte (self-limited hyperthyroid) but painless, common in women postpartum

A

Painless thyroiditis

45
Q

Describe Riedel’s Thyroiditis

A
  • thyroid fibrosis of unknown origin, “rock hard” thyroid, produces local pressure and hypothyroidism;
  • hormone replacement, may consider surgical release at isthmus
46
Q

What is Acute Supporative Thyroiditis?

A
  • uncommon infection
  • Rx: systemic antibiotics, consider drainage for abscess formation
47
Q

What are the High Risk AMES criteria?

A
  1. Age: males ≥41 years old, females ≥51 years old
  2. Metastasis: presence of metastasis suggests malignancy
  3. Extent: extrathyroidal, major capsular involvement
  4. Size: nodule ≥5 cm
  5. Other: radiation therapy, autoimmune thyroiditis, more common in women (children and males have a higher risk of malignancy if presents with a thyroid nodule)

Staging: I: thyroid only; II: nonfixed cervical node; III: fixed cervical node; IV: metastasis

48
Q

Describe features of Thyroid Adenomas

A
  • 70% of solitary nodules
  • follicular adenomas are the most common
  • papillary adenomas are exceedingly rare
49
Q

Describe features of Papillary Carcinoma

A
  • most common
  • more common in young females

Risks

radiation exposure, Gardner’s syndrome

30% palpable regional nodes (70% occult nodes)

Diagnosis

FNA

Histopathology

papillary and follicular structures, psammoma bodies
(calcific), intranuclear vacuoles (“Orphan Annie” eyes), multicentric

Prognosis

95% 5-year survival; poor prognostic indicators include
tumors >1.5 cm or extracapsular spread (cervical metastases have increased cervical recurrence rates without affecting survival)

Treatment

  1. Total or near total thyroidectomy (multicentric)
  2. Lobectomy and isthmusectomy (hemithyroidectomy) with radioactive iodine (I131) may be considered if <1.5 cm or in younger patients
  3. Modified neck dissection (MND) for palpable nodes only (elective neck dissection [END] has not been shown to improve survival)
  4. Thyroid suppression therapy
50
Q

Describe the features of Follicular Carcinoma

A
  • more common in the elderly and in females
  • 50% hematogenous spread with distant metastasis (lymphatic spread rare)

Diagnosis

requires open biopsy (unable to distinguish adenoma from carcinoma from FNA)

Histopathology

unifocal; extracapsular spread, invasion of lymphatics
or vasculature, or metastasis required for diagnosis

Prognosis

70–85% 5-year survival (20% with distant metastasis),
worse prognosis for angioinvasion, extracapsular spread

Treatment

  1. Lobectomy and isthmusectomy (hemithyroidectomy) for low risk groups (may consider intraoperative frozen section with completion total thyroidectomy (or subtotal) for carcinoma)
  2. Subtotal or total thyroidectomy with radioactive iodine (I131) for high-risk groups (angioinvasion, extracapsular spread)
  3. Lateral neck dissection for clinical nodes thyroid suppression therapy
51
Q

Describe the features of Hurthle Cell Tumors

A
  • variation of follicular carcinoma (Hürthle cells predominate)
  • difficult to distinguish adenoma from carcinoma (assume malignancy)

Histopathology

Hürthle cells (large granular eosinophilic cells,
trabecular pattern)

Treatment

same as follicular carcinoma

52
Q

Describe the features of Medullary Thyroid Carcinoma

A

Pathophysiology

derived from parafollicular or C-cells (produce calcitonin)

Types

  1. Familial: 20%, Multiple Endocrine Neoplasia IIA/B, multicentric, bilateral
  2. Sporadic: 80%, unifocal, unilateral, worse prognosis,

50–60% lymph node involvement (late vascular involvement), approximately 8% distant metastasis

secretory granules of malignant C-cells release calcitonin and also secrete **gastrin**, adrenocorticotropin hormone (**ACTH**), **substance P**,
 carcinoembryonic antigen (**CEA**), and others

Prognosis

50–80% survival; worse prognosis if unilateral, sporadic type, younger patient, or with metastasis

Diagnosis

FNA or biopsy, elevated serum calcitonin, elevated CEA, presence
of Ret-3 oncogene

Histopathology

small round cells, amyloid stroma, may have
calcification and fibrotic strands

Treatment

  1. Patient and family should be screened for MEN syndrome), examine for mucosal neuromas, marfanoid habitus, serum calcium levels, urine catecholamines and metabolites (vanillylmandelic acid, metanephrine)
  2. Total thyroidectomy with elective or modified neck dissection and medical thyroid suppression therapy
  3. Screen with calcitonin levels to monitor for recurrence
53
Q

Why is RAI (I131) not active agains medullary thyroid cancer?

A

Parafollicular cells do not take up I131

54
Q

Describe the feature of Anaplastic Carcinoma

A

• most commonly seen in the elderly

Pathophysiology

may be from transformation of a well-differentiated
carcinoma (may find coexistent follicular or papillary carcinoma)

uniformly fatal (5-year survival), often found with metastatic disease

Histopathology

giant and spindle cells variation, undifferentiated
“bizarre cells”

Treatment

no adequate therapy, tracheotomy (protect airway), consider radiation and chemotherapy, surgical resection may be considered (controversial)

55
Q

Describe the features of Thyroid Lymphoma

A

• associated with chronic lymphocytic thyroiditis and Hashimoto’s thyroiditis

Diagnosis

difficult to distinguish lymphoma from chronic lymphocytic thyroiditis by FNA alone, therefore a conformational open biopsy is
required along with lymphoma staging work-up

Treatment

Radiotherapy to neck and superior mediastinum, surgical excision considered if tumor is confined to the thyroid

56
Q

Why would you guve preoprerative potassium iodine?

A

Used in Graves disease, to decrease vascularity of gland and therefore decrease blood loss (in theory)

57
Q

Reasons to perform a Thyroidectomy?

A
  1. Cancer
  2. Compression (SOA, dysphagia)
  3. Cosmesis
  4. Failed medical management for Graves or hyperthyroidism
  5. Pregnancy in Graves disease or Hashimoto’s thyroiditis
58
Q

What are some post op complications of thyroidectomy?

A
  • Hematoma
  • VF paralysis - RLN or SLN injury (SLN more common), avoid ligation of inferior thyroid artery
  • Transient or permanent hypocalcemia - may reimplant parathyroid into SCM. Prevent by avoiding ligation of inferior thyroid artery
  • Thoracic duct injury - rare, leads to chyle leak
59
Q

What are the progressive symptoms of hypocalcemia?

A

Less calcium means lower threshold of depolarization

CATS go numb

Convulsions, Arrhythmias, Tetany and numbness/parasthesias in hands, feet, around mouth and lips.

Chvostek’s sign - tapping of the inferior portion of the zygoma will produce facial spasms

Trousseau sign - eliciting carpal spasm by inflating the blood pressure cuff and maintaining the cuff pressure above systolic

Intermittent QT prolongation leading to Torsades de Pointes

Treatment

Give 2 amps of IV Calcium Gluconate

60
Q

What are the features of Thyroid Storm?

A

Etiology

surgery, trauma, childbirth, infection

  • 50% mortality

Symptoms

fever, profuse sweating, tachycardia, nausea, abdominal pain, tremors, restless, psychosis, coma, stupor

Diagnosis

clinical history and exam

Treatment

  1. Immediate administration of inorganic iodine, propylthiouracil, propanolol, and corticosteroids
  2. Supportive measures (glucose-containing IV fluids, cooling blanket, supplemental oxygen, pyrogens)
  3. Intensive care admission (cardiac monitoring)
61
Q

Features of Primary Hyperparathyroidism?

A
  • Elevated serum PTH
  • Benign Adenoma: most common, single adenomatous gland
  • Parathyroid Hyperplasia: associated with MEN I & IIA
  • Familial hypocalciuric hypercalcemia (autosomal dominant, increased renal calcium absorption), familial hyperparathyroidism
  • Carcinoma of the Parathyroid Gland: rare tumor, suspect with a palpable, gray mass, vocal fold paralysis, or severe hypercalcemia; Rx: en bloc resection including thyroid lobectomy, monitor for recurrence with serial serum calcium levels
  • Must differentiate hyperparathyroidism from other causes of hypercalcemia
62
Q

List the causes of hypercalcemia

A

CHIMPANZEES

  • Calcium (exogenous)
  • Hyperparathyroidism
  • Immobility
  • Metastasis to bone
  • Paget’s disease
  • Addison’s disease
  • Neoplasms (prostate, lung, colon, breast)
  • Zollinger-Ellison syndrome (hypergastrinemia)
  • Excess: vit A or D, thiazides, lithium, estrogens, milk-alkali syndrome
  • Endocrine disorders: FHH, hyperthyroidism, pheochromocyoma
  • Sarcoidosis and Tuberculosis
63
Q

Features of Secondary Hyperparathyroidism?

A
  • Compensatory parathyroid hyperplasia secondary to malfunction of other organ system
  • decreased 1 hydroxylase in the kidney
  • patients are hypocalcemic

Causes

  • chronic renal disease, osteogenesis imperfecta, Paget’s disease, multiple myeloma, bone metastasis
64
Q

Features of Tertiary Hyperparathyroidism?

A
  • Autonomous or irrepressible PTH production (parathyroid hyperplasia from secondary parathyroidism, persistent hyperfunction despite correction)
  • May have normal or low calcium
65
Q

Important questions to ask in the History and Physical in a patient with hyperparathyroidism

A
  • Contributing Factors: family history of MEN disorders, radiation exposure
  • “Stones, bones, groans:” nephrolithiasis, osteitis fibrosa cystica, cholelithiasis
  • Renal: polyuria, nephrolithiasis, nephrocalcinosis
  • Gastrointestinal: constipation, dyspepsia, pancreatitis
  • Musculoskeletal: muscle weakness, bone and joint pain (osteitis fibrosa cystica, calcific tendonitis)
  • Central Nervous System: slow mentation, fatigue, depression, poor memory, psychosis
  • Cardiovascular: heartblock, hypertension
66
Q

How do you diagnose Hyperparathyroidism?

A
  • Serum Electrolytes: ionized calcium (should be elevated at 3 different times), magnesium (usually low), chloride (usually elevated from PTH induced bicarburia), and phosphate (usually low)
  • PTH levels: immunoradiometric assay
  • Plain Films: brown tumors (osteitis fibrosis cystica), loss of lamina, resorption of terminal phalanges, soft-tissue calcification, chest x-ray (granulomatous diseases or metastasis), abdominal film (renal calculi)
  • Others: alkaline phosphatase (suggests bone disease), BUN/creatinine (renal function), urine calcium (elevated in primary hyperparathyroidism, low levels with familial hypocalciuric hypercalcemia), TFT, ACE levels (sarcoidosis), serum prolactin and gastrin and urine catecholamines and metabolites (evaluate for MEN syndromes)
  • Think “CHIMPANZEES” for other causes of hypercalcemia
67
Q

How do you localize hyperparathyroidism?

A
  • Thallium-Technetium Subtraction: thallium uptake by thyroid and parathyroid, technetium uptake by thyroid gland only, parathyroid glands identified by computer subtraction; up to 90% accurate (less accurate for multiple gland hyperplasia, associated thyroid disease, or small glands)
  • High-resolution Ultrasound: can not locate mediastinal, retrotracheal, retroesophageal, or small nodes
  • Selective Venous Catheterization for PTH: reserved after exploration has failed
  • CT/MRI: poor resolution, MRI more useful in identification of glands
68
Q

Can you give someone Technetium if they have a sulfur allergy?

A

NO

Sulfur colloid is a component of this radioactive material

69
Q

Surgical management of hyperparathyroidism

A
  • Surgery is the only definitive cure, avoids long-term complications of nephrocalcinosis and bone demineralizations
  • Parathyroidectomy is indicated for symptomatic (bone pain, pathological fractures, ectopic calcifications, intractable itching, etc) or persistently elevated serum calcium
  • Surgical Theory: must first remove pathologic gland (adenoma), hyperplasia versus adenoma can not be distinguished grossly, therefore, must identify one “normal” gland to evaluate hyperplasia, if other gland is also hyperplastic then assume parathyroid hyperplasia and perform a subtotal (31/2 glands) or total parathyroidectomy with autotransplantation, if gland is normal may either assume adenoma and terminate case or further biopsy other contralateral glands (controversial)
  • Autotransplantation requires 20 mg into muscle bed (usually to forearm)
  • Pregnant women should undergo surgery during second trimester to avoid miscarriage
70
Q

Complications of parathyroid surgery?

A
  • Persistent Hypercalcemia: most commonly from missed adenoma (the most commonly missed location is the posterior mediastinum), also from supernumerary gland, second adenoma, failed recognition of parathyroid hyperplasia, incorrect diagnosis, and residual adenoma
  • Postoperative Hypocalcemia and Hypomagnesmia: usually temporary until replacement of low bone calcium stores (increased risk with elevated alkaline phosphatase)
  • Nerve Injury and Hematomas
71
Q

What is the medical management of Hypercalcemia?

A
  • Saline Diuresis: restores extracellular fluid volume and promotes calcium excretion, loop diuretics can also be given (thiazides impair calcium excretion)
  • Biphosphonates: inhibit bone resorption, calcium serum levels reduce over several days
  • Plicamycin: inhibits bone resorption; toxic side effects include thrombocytopenia, hepatic dysfunction, and renal failure, therefore used only for malignant hypercalcemia
  • Calcitonin: rapid onset (serum calcium falls within hours)
  • Glucocorticoids: inhibit calcium intestinal absorption, may be effective for hypercalcemia secondary to malignancy
  • Gallium Nitrate: inhibits bone resorption, used for parathyroid carcinoma
  • Hemodialysis: indicated for life-threatening conditions
72
Q

What is Zuckerkandl’s tubercle?

A
  • A pyramidal extension of the thyroid gland, present at the most posterior side of each lobe
  • The structure is important in thyroid surgery as it is closely related to the recurrent laryngeal nerve, the inferior thyroid artery, Berry’s ligament and the parathyroid glands.
  • The structure is subject to an important amount of anatomic variation
73
Q

What is the most common cause of hypercalcemia in the non hospitalized patient?

A

Hyperparathyroidism (adenoma)

In hospitalized patients, think malignancy!

74
Q

What is “hungry bone syndrome”?

A

Postop hypocalcemia can occur following parathyroidectomy.

The chronic stimulation of the bone with PTH results in the skeletal depletion of calcium

The normalization of PTH causes the bone reuptake of calcium, with a resultant fall in serum calcium

75
Q

Features of hyperparathyroidism in pregnancy

A
  • Rare disorder
  • Surgical exploration should occur in 2nd trimester
  • Should perform total parathyroidectomy with autotransplant
  • After birth, neonates serum calcium level can drop quickly
  • 7-10 days for babys parathyroids to secrete PTH
76
Q

Where is the thyroid ima artery?

A
  • arises from the brachiocephalic trunk and ascends in front of the trachea to the lower part of the thyroid gland, which it supplies.
  • It is only present in approximately 3-10% of the population
77
Q

What is the relationship of the parathyroids to the recurrent laryngeal nerve?

A

Superior parathyroids are posterior to the RLN

Inferior parathyroids are anterior to the RLN

78
Q

Where does the RLN enter the larynx?

A

The caudal end of the cricopharyngeus muscle (cricothyroid membrane)

ENT (17 decks)

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