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Surgery Shelf Study Guide > Endocrine Surgery > Flashcards

Endocrine Surgery Flashcards

0
Q

What is a thyroglossal duct cyst?

A

Remnant of thyroglossal duct as a mobile midline neck mass
dx at 1-2 yo due to neck fat
tx Sistrunk operation (take out cyst, trunk, and medial portion of hyoid bone)

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1
Q

What is the embyrology of the thyroid?

A

Derivative of foramen cecum from the base of the tongue

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2
Q

How do you manage a thyroid nodule?

A

First get TSH levels
If euthyroid, get FNA for cancer Dx
Otherwise, work up for hypo or hyperthyroidism

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3
Q

What is a risk for malignancy for thyroid nodules?

A

Solid nodules, cold nodules (lack of radioiodine uptake), size >1.5 cm

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4
Q

What are the main causes of hyperthyroidism?

A

1) Graves’ disease
2) toxic adenoma
3) toxic multinodular goiter

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5
Q

What is Graves’ disease?

A

Autoimmune disease due to IgG against TSH-R causing exophtalmos, pretibial myxedema, and hyperthyroidism

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6
Q

How do you treat a thyroid storm?

A

Beta blockers and antithyroid drugs (PTU and methimazole block peroxidase)

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7
Q

What is a toxic adenoma?

A

Dx hot nodule on scan with peripheral suppression

tx is lobectomy if >2 cm, radio-iodine if <2 cm

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8
Q

What are the main causes of hypothyroidism?

A

Hashimoto thyroiditis
Subacute/De Quervain thyroiditis
acute bacterial thyroiditis

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9
Q

What is Hashimoto thyroiditis?

A

Autoimmune disease with lymphocytic infiltration, tx with Synthroid

anti-TSH, anti-microsomal, anti-thyrogolbulin, anti-peroxidase antibodies

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10
Q

What is De Quervain thyroiditis?

A

Subacute, painful granulomatous inflammation following viral URI
Tx with observation (self-resolving)

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11
Q

What are the types of thyroid cancers?

A 
Papillary (80%)
Follicular (10%)
Medullary (4%)
Anaplastic (1%)
FNA can be used to dx papillary and medullary but not follicular (must see capsular invasion to DDx adenoma vs. carcinoma)
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12
Q

How is papillary cancer treated?

A

Associated with radiation, lymphatic spread, best px overall, bx shows “Orphan Annie nuclei” with psamomma bodies
Tx with total thyroidectomy with central LN excision–> modified radical neck dissection if LN are positive for cancer

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13
Q

How is follicular cancer treated?

A

Endemic to iodine-deficient regions, hematogenous spread, 2nd best px
Tx with hemilobectomy with biopsy because 80% are benign adenomas, total thyroidectomy if bx reveals malignant carcinoma

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14
Q

How is medullary cancer treated?

A

Medullary cancer AD inheritance with MEN 2A/2B syndromes, delta ret proto-oncogene, both lymphatic and hematogenous spread
bx amyloid deposits, third best prognosis
tx with total thyroidectomy for both cancer and ret + prophylaxis with central LN excision –> modified radical neck dissection if LN are positive for cancer

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15
Q

How do you treat anaplastic cancer?

A

Rare, worst px

tx is palliative only

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16
Q

What is post-thyroidectomy follow up?

A

Take patient off T4 for six weeks (T3 instead), increase TSH level, and make sure total thyroidectomy was performed; give radioactive iodine exam after six weeks to check if any metastases will light up
Continue to follow thyroglobulin levels
For medullary cancer, 24 hour urine for VMA or metanephrines (MEN syndrome can present with pheochromocytoma), follow calcitonin levels

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17
Q

What is a modified radical neck dissection?

A

Like radical neck dissection, but spares sternocleidomastoid muscle, CN XI, and internal jugular vein

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18
Q

What are the risk factors for thyroid cancer?

A

Superior laryngeal nerve (soft/deep voice)
Recurrent laryngeal nerve (hoarseness if unilateral, dyspnea if bilateral)
Parathyroid glands (hypoparathyroidism)

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19
Q

What is the embryology of the parathyroid gland?

A

Third branchial pouch becomes inferior glands and thymus, 4th becomes superior glands

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20
Q

What is DiGeorge syndrome?

A

Congenital absence of both 3rd and 4th branchial pouches, leading to hypocalcemia and thymic aplasia

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21
Q

What is PTH?

A

Secreted from chief cells; three functions: increases renal calcium and decreases phosphorous
increases bone calcium and phosphorous
stimulates 1-alphahydroxylase to activate vitamin D for indirect GI resorption of calcium

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22
Q

What is osteitis fibrosa cystica?

A

Rapid, painful loss of bone due to HPTH; “moth eaten skull”

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23
Q

What is calciphylaxis?

A

Calcium deposition in soft tissue due to HPTH

24
Q

What happens to the bone in multiple myeloma?

A

Punched out lesions of bone due to a B-cell neoplasm

25
Q

What are the symptoms of hypercalcemia?

A

kidney stones, painful bones, abdominal groans (peptic ulcers, pancreatitis, cholelithiasis), psychic overtones (decreased MS)

26
Q

What is the differential for hypercalcemia?

A

paratyroid adenoma, metastases to bone

27
Q

What happens in primary HPTH?

A

Increased PTH/increased Ca/ decreased P

Most sensitive test is Cl:P ratio >33:1; 90% adenoma

28
Q

How is primary HPTH managed?

A

Straight to surgery if symptomatic (4-gland exploration)

29
Q

What is 4-gland exploration?

A

Open exploration of neck area
Adenoma– remove
Hyperplasia – take 3 1/2 glands out, or take all 4 our and auto-transplant 1/2 back in
Carcinoma – en bloc resection of parathyroid and ipsi thyroid lobe

30
Q

What is secondary HPTH? How is it managed?

A

Increased PTH/ decreased Ca/ increased P due to renal failure
Managed medically or 3 1/2 gland excision if complications exist

31
Q

What is tertiary HPTH? How is it managed?

A

Increased PTH/ increased Ca/ decreased P, found in renal transplant patient whose parathyroid glands work autonomously
managed by 3 1/2 gland excision if HPTH persists for 1 year following transplant

32
Q

What is a Sestamibi scan?

A

“lighting up” in parathyroid gland is 85% accurate for dx of parathyroid adenoma

33
Q

What is a hypercalcemic crisis?

A

Ca > 15 indicating carcinoma; tx flush with NS, then drain with furosemide, then treat underlying cause
Median sternotomy is indicated if life-threatening

34
Q

What is MEN1 (Wemer)?

A

Pituitary adenoma, pancreatic endocrine cancer (MC gastrinoma), parathyroid hyperplasia

35
Q

How do you treat MEN1?

A

Excise parathyroid first since hypercalcemia can cause an increase in gastrin levels; if ZE ca’t be controlled with PPIs –> total gastrectomy since MEN gastrinomas are multifocal

36
Q

What is MEN2A (Sipple)?

A

Parathyroid hyperplasia, pheochromocytoma, thyroid medullary cancer

37
Q

What is MEN 2B?

A

Pheochromocytoma, thyroid medullary cancer, mucosal neuromas, Marfanoid habitus

38
Q

How do you treat MEN 2A/2B?

A

Excise pheochromocytoma first since it can be life-threatening

39
Q

How do you treat a gastrinoma?

A

Give PPIs, if acid persists, get serum gastrin levels
500 present
200-500 indeterminate, requires secretin stimulation test
if paradoxical increase in gastrin with secretin, present
get CT scan to localize and cut it out

40
Q

How does an insulinoma present?

A

Hypoglycemia

Dx increase in C-peptide levels or monitored fasting (to see if they’re “faking it”); get CT scan and cut it out

41
Q

How does a glucagonoma present?

A

Presents as new-onset diabetes and migratory rash from lower body upwards
dx glucose challenge test; get CT scan and cut it out
if metastatic, give somatostatin and streptozocin since surgery is contraindicated

42
Q

How does nesidioblastosis present?

A

Presents as hypersecretion of insulin a newborn

Tx pancreatectomy

43
Q

What are the types of pituitary adenomas?

A 
Prolactinoma
Null cell tumor
ACTH
GH
May present as bitemporal hemianopsia due to optic chiasm compression
44
Q

What does a prolactinoma present with?

A

Galactorrhea and amenorrhea, tx with bromocriptine

45
Q

How does Cushing syndrome present?

A

Truncal obesity, abdominal striae, buffalo hump, hyperglycemia, osteoporosis, HTN, and immunosuppression due to increased cortisol

46
Q

What causes Cushing syndrome?

A

MCC cause is exogenous steroid use

intrinsic causes include pituitary adenoma, adrenal adenoma, and ectopic secretion of ACTH

47
Q

What is pituitary Cushing?

A

Due to increased ACTH secretion
Suppressable by high dose dexamethasone
Dx by MRI
Tx transsphenoid hypophysectomy

48
Q

What is adrenal Cushing?

A

Due to increased cortisol secretion (causes decreased ACTH); Dx CT scan, Tx adrenalectomy

49
Q

What is ectopic Cushing?

A

Due to increased ACTH secretion usually from SCLC, not suppressable by high dose dexamethasone

50
Q

What are the adrenal gland tumors?

A

Aldosteronoma, cortisoloma, sex hormone-secreting tumor, pheochromocytoma, incidentaloma

51
Q

What is an aldosteronoma?

A 
Presents as increased Na, decreased K, decreased H, decreased renin; dx CT for mass (if no mass present of increased renin, think RA stenosis)
tx adrenalectomy (adenoma) or aldactone (hyperplasia)
52
Q

What is a cortisoloma?

A

Presents as adrenal Cushing’s

Tx adrenalectomy

53
Q

How do you treat a sex hormone-secreting tumor?

A

Adrenalectomy

54
Q

What is a pheochromocytoma?

A

Presents with HA, HTN, palpitations, etc.
Dx 24 hour urinary VMA or metanephrines
Tx alpha blockers (phenoxybenzamine) then beta blockers then adrenalectomy

55
Q

How do you treat an incidentaloma?

A

Make sure it’s not secreting hormones, then work-up based on size
If >5 cm, resect and check other organs since adrenals are common site of metastasis

56
Q

What is renovascular hypertension?

A

Presents as HTN + abdominal bruits, secondary to fibromuscular dysplasia (young women) or atherosclerosis (old men) of the renal arteries; get a doppler of renal vessels, then either balloon dilation or surgical correction

57
Q

How does aortic coarctation present?

A

Presents as HTN in arms but normal BP in legs; get CXR (scalloping or ribs) then confirm with spiral CT, then surgical correction

Surgery Shelf Study Guide (13 decks)

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