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174 Cards in this Set

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Patient presents to ED with hypotension, fever, low Na, high K, hypoglycemia
-Consider __
-Dx and tx by _
Addison's disease:
-low aldosterone and glucocorticoids -> low Na, high K, hypoglycemia
-Crisis presents similar to sepsis with hypotension, fever
-Steroids are diagnostic and therapeutic
Phenylethanolamine N-methyltransferase (PNMT) in adrenal medulla converts __ to __
Phenylethanolamine N-methyltransferase (PNMT) in adrenal medulla converts NE to epi.
increased by cortisol (from adrenal cortex)
-S-adenosyl-L-methionine ('SAM') is a required cofactor
A 35 year-old carpenter presents with chronic abdominal pain. CT scan of abdomen is unremarkable, except for an adrenal mass, 9 cm in diameter. Next step in management would include:
ipsilateral adrenelectomy
In patients with non-functional adrenal masses, adrenalectomy should be performed if the tumor is more than 6 cm or if the CT and/or MRI scanning are atypical for an adenoma.
Non-functional lesions smaller than 4cm may be safely observed with interval CT or MRI scanning at 3 months and 1 year. Between 4 and 6 cm are controversial
Three years after undergoing treatment for breast cancer, a 64-year-old woman is asymptomatic. On routine follow-up examination, her serum calcium level is 12.8 mg/dl and the remainder of her metabolic profile is normal. A bone scan shows multiple metastases to her ribs and spine. The most appropriate initial management of her hypercalcemia is _
Breast cancer mets to bone release PTHrp -> hypercalcemia
-Sm cell lung ca, other non-hematologic cancers do this as well. Hyper-ca NOT 2/2 bone destruction.
-increased urine cAMP 2/2 effect of PTHrp on kidney (unlike low urine cAMP in hematologic malignancies, which increase Ca by bone destruction)
Parafollicular C cells:
-derived from _ in embryo
-produce hormone _
Parafollicular C cells:
-derived from neural crest
-produce calcitonin => decrease serum Ca
female presents c/ virilization, hypotension.
Suspect _
CAH: 21-hydroxylase defic (90%): high 17-OH progesterone -> high testosterone, salt wasting -> HYPOtension, precocious puberty (M), virilization (F). Tx = cortisol, genitoplasty
-11-hydroxylase defic: high 11-deoxycortisone -> salt saving, HYPERtension, precoc. puberty, virilization. Tx = same
-17-hydroxylase defic: ambiguous genitalia in males @ birth. salt saving
male presents c/ precocious puberty, chronic hypertension.
Suspect _
CAH: 21-hydroxylase defic (90%): high 17-OH progesterone -> high testosterone, salt wasting -> HYPOtension, precocious puberty (M), virilization (F). Tx = cortisol, genitoplasty
-11-hydroxylase defic: high 11-deoxycortisone -> salt saving, HYPERtension, precoc. puberty, virilization. Tx = same
-17-hydroxylase defic: ambiguous genitalia in males @ birth. salt saving
Newborn male has ambigious genitalia, hypertension.
-Suspect _
CAH:
21-hydroxylase defic (90%): high 17-OH progesterone ->
high testosterone, salt wasting ->
HYPOtension, precocious puberty (M), virilization (F).
Tx = cortisol, genitoplasty

11-hydroxylase defic: high 11-deoxycortisone ->
salt saving, HYPERtension, precoc. puberty, virilization.
Tx = same

17-hydroxylase defic: ambiguous genitalia in males @ birth.
salt saving
patient presents to endocrine clinic c/ HTN, low K, high Na, metabolic alkalosis
-Suspect __
- _% are 2/2 adenoma, _% are 2/2 hyperplasia
- what 3 tests are used to diagnose adenoma vs .hyperplasia?
(what does it mean if 18-OH corticosterone is high?)
Conn's syndrome = hyperaldosteronism
-Primary (low renin, A:R ratio >400): 80% adenoma, 20% bilateral hyperplasia (see with postural stimulation test)
-[Secondary (high renin): more common. CHF, renal artery stenosis, liver failure, pregnancy, diuretics, Barter's syn (renin-secreting tumor)]
-HTN, low K, high Na
-Captopril test =>aldosterone decreases if 2/2 hyperplasia (vs. tumor) or Upright sitting test (slight increase in aldosterone and renin if hyperplasia)
-18-OH corticosterone is high (>100 ug/dL) c/ cancer, low c/ hyperplasia
- if Adenoma => responds well to surgery.
- if Hyperplasia => 1st try spironolactone, Ca channel blocker, K
- needs postop fludrocortisone if bilat resection done
Cricothyroid muscle is ennervated by the _ nerve
Cricothyroid muscle is ennervated by the superior laryngeal nerve
#1 cause of Cushing's syndrome = __
Cushing's syndrome:
-#1 cause = iatrogenic
1. 24-hr urine cortisol = most sensitive
2. low-dose overnight dex supp test: low cortisol means pituitary adenoma is supressed = Cushing's dz
3. serum ACTH: high => ectopic ACTH or pituitary tumor not suppressed by low-dose test (go to #4). low=> hypercortisol 2/2 adrenal tumor or hyperplasia
4. high-dose overnight dex supp test. (+) = pituitary origin. (-) = ectopic ACTH. if can't tell, proceed to CRH test (pituitary adenoma will make increased ACTH but ectopic production won't respond.)
-MRI useful. NP-59 scintigraphy localizes adrenal tumors, differentiates from hyperplasia
70% of non-iatrogenic Cushing's syndrome is 2/2 _
-lesion is in which organ?
-ACTH is low or high?
-what result of dexamethasone supression?
Cushing's syndrome:
1.24-hr urine cortisol = most sensitive
2. low-dose overnight dex supp test: low cortisol means PITUITARY ADENOMA (high ACTH) is supressed = CUSHING'S DZ
3. serum ACTH: low=> hypercortisol 2/2 adrenal tumor or hyperplasia. high => ectopic ACTH or pituitary tumor not suppressed by low-dose test (go to #4).
4. high-dose overnight dex supp test. (+) = pituitary origin. (-) = ectopic ACTH. if can't tell, proceed to CRH test (pituitary adenoma will make increased ACTH but ectopic production won't respond.)

Pituitary adenoma: mostly MICROadenomas. Need petrosal sampling to figure out which side. MRI also helpful. Vertical incision to find adenoma. Most resected c/ transsphenoidal approach. XRT if unresectable.
__ type of Cushing's syndrome:
-low ACTH
-cortisol not supressed by dexamethasone test
Cushing's syndrome:
1. 24-hr urine cortisol = most sensitive
2. low-dose overnight dex supp test: low cortisol => pituitary adenoma = Cushing's dz
3. serum ACTH: high => ectopic ACTH or pituitary tumor (go to #4). low=> hypercortisol 2/2 ADRENAL ADENOMA OR HYPERPLASIA (15% of cases, low ACTH)
4. high-dose overnight dex supp test. (+) = pituitary origin. (-) = ectopic ACTH. if can't tell, proceed to CRH test (pituitary adenoma will make increased ACTH but ectopic production won't respond.)
-MRI useful. NP-59 scintigraphy localizes adrenal tumors, differentiates from hyperplasia
_ type of Cushing's syndrome
-high ACTH
-not supressed by dexamethasone test
Cushing's syndrome:
1. 24-hr urine cortisol = most sensitive
2. low-dose overnight dex supp test: low cortisol => pituitary adenoma = Cushing's dz
3. serum ACTH: high => ectopic ACTH or pituitary tumor (go to #4). low=> hypercortisol 2/2 adrenal adenoma or hyperplasia
4. high-dose overnight dex supp test. (+) = pituitary origin. (-) = ECTOPIC ACTH (most commonly sm cell ca). if can't tell, proceed to CRH test (pituitary adenoma will make increased ACTH but ectopic production won't respond.)
-MRI useful. NP-59 scintigraphy localizes adrenal tumors, differentiates from hyperplasia
A 35 yo female presents with development of hirsutims. Patient has negative history of exogenous steroid administration. Further examination reveals hypertension, fatigue, depression, and amenorrhea. The most likely diagnosis is:
Cushing's Syndrome = central obesity, glucose intolerance, hypertension, plethora, hirsutism, osteoporosis, nephrolithiasis, menstrual irregularity, muscle weakness, and emotional lability.
The most common cause of non-iatrogenic Cushing syndrome is Cushing disease, ACTH secreting pituitary adenoma (68%).
Adrenal adenoma accounts for 10% of non-iatrogenic cases.
Ectopic CRH syndrome accounts for <1%.
Pt presents c/ PTH 30-60, serum Ca 9-11, low urine Ca.
-Suspect _
-Tx is _
Familial hypercalcemic hypocalciuria:
-2/2 increased binding of PTH to defective PTH receptor in distal convoluted tubule -> increased Ca resorption
-Tx: do nothing. NO parathyroidectomy (Ca not very elevated)
Pt c/ asymptomatic thyroid mass, normal TFTs.
FNA => follicular cells
-Next step..
Thyroid mass c/ FNA (+) for follicular cells:
5-10% malignancy risk => lobectomy (or thyroidectomy)
Pt c/ asymptomatic thyroid mass, normal TFTs, FNA (+) for follicular cells
-Found to have follicular CA 1.9 cm on lobectomy
Next step…
Thyroid lobectomy (+) for follicular CA => proceed to total thyroidectomy if >1 cm or extrathyroidal disease (capsule invasion, clinical or pos. nodes, mets)
-Clinically (+) cervical LNs or extrathyroidal dz => ipsilateral MRND
-Lesion >1 cm or capsular invasion => I-131 x 6 weeks post-op
-Microinvasive (<1 cm), rare nodal spread (<10%), then usually incidental finding on path and lobectomy is sufficient as long as margins (-)
-Thyroid hormone replacement postop to reduce TSH, suppress future growth
-70% 5-yr survival, prognosis depends on stage
Follicular cell thyroid ca:
-_ to _ % metastatic @ presentation
-Spreads via __ (#1 site = _)
Follicular thyroid CA:
-50-60% metastatic @ presentation, more aggressive than papillary CA
-Hematogenous spread (BONE most common)
-Typicaly age 50's-60's, F:M 3:1
-If FNA shows follicular cells => 10% malignancy risk
-Path (+) for adenoma or follicular hyperplasia => lobectomy only
-typically requires total thyroidectomy + postop RI ablation
-Follicular Ca >1 cm or extrathyroidal dz => total thyroidectomy
-Clinically (+) cervical nodes or extrathyroidal dz => ipsilateral MRND
-Lesion >1 cm or extrathyroidal dz/capsular invasion => I-131 x 6 weeks post-op
-Microinvasive (<1 cm), rare nodal spread (<10%), then usually incidental finding on path => lobectomy suffiicient as long as margins (-)
-70% 5-year survival, prognosis based on stage
Pt has thyroid nodule, then undergoes FNA which demonstrates follicular cells.
next step is _
FNA can't distinguish malignant/benign with follicular or Hurthle cell (subtype of follicular) => need TISSUE
-10% cahnge of malignancy if FNA shows follicular cells
Why do patient’s with gastrinomas often suffer from severe diarrhea?
Excess gastrin production
Excess acid inactivation of small bowel enzymes causes malabsorption leading to diarrhea.
A 65 yo female with history of living in area endemic for iodine deficiency presents with an anterior neck nodule. Examination reveals a 4 cm firm, mobile thyroid nodule. No lymphadenopathy was noted. Patient was taken to the OR for resection. Intraoperative frozen section of the tumor reveal Hurthle cell tumor. Which is the course of action for this patient.
Total thyroidectomy
-Hurthle cell ca = subtype of follicular thyroid ca.
-Similar tx, prognosis
-early nodal spread if malignant
-mets to bone, lung
-< 2cm + contained in 1 thyoid lobe => lobectomy or isthmectomy.
-2-4 cm + high risk patient (e.g. advanced age) => total thyroidectomy
- > 4cm => total thyroidectomy must be done b/c 50% risk of cancer.
-MRND if clinically (+) nodes
Treatment for hypercalcemia
Hypercalcemia:
-Confusion, somnolence, shortened QT
-Tx: NS @ 200-300/hr, Furosemide
-NO LR or thiazides!
what type of diuretic causes hypercalcemia
THIAZIDES cause hypercalcemia
#1 cause of persistant hyperparathyroidism after parathyroidectomy =
1% rate of persistant hyperparathyroidism after parathyroidectomy
-Usually 2/2 missed adenoma in the neck
Hyperthyroid in pregnancy:
-1st line med = _ (does not cross placenta)
-Persistant sx-=> _
-Can beta blocker be used for sx?
Hyperthyroid in pregnancy:
-1st line = propylthiouracil (does not cross placenta)
-Persistant sx-=> thyroidectomy in 2nd trimester (decreased risk of adverse events, premature labor)
-I-131 would ablate fetal thyroid
-Methimazole causes cretinism
-Don't mask sx c/ beta blocker b/c hyperthroidism still present, still increased risk of stillbirth, cause fetal growth retardation in 3rd trimester
#1 cause of hypoparathyroidism = _
Hypoparathyroidism:
#1 cause = previous thyroid surgery
-Numbness/tingling in cirumoral area, fingers -> anxiety, confusion -> Tetany (carpopedal spasms, convusions, laryngospam which can be deadly
-Concomitant hypo-Mg can make correction of Ca difficult
Give thyroid hormone replacement following I-131 for papillary or follicular thyroid ca
-Suppresses TSH -> suppress growth of residual cancer tissue
Give thyroid hormone replacement following I-131 for papillary or follicular thyroid ca
-Suppresses TSH -> suppress growth of residual cancer tissue
Radioactive iodine is used for _ type thyroid tumors
Radioactive I:
-for well-differentiated tumors (papillary, follicular)
what should be done c/ patient's synthroid in preparation for I-131 scan?
must be hypothyroid for I-131 scan =>
stop levothyroxine (T4) 6 weeks before, liothyroxine (T3) 3 weeks before
what is the #1 endocrine pancreatic tumor
insulinoma = #1 endocrine pancreatic tumor overall
(but not part of a MEN subgroup; gastrinoma = #1 endocrine pancreatic tumor in MEN)
Medullary thyroid ca:
-from _ type cells. The _t proto-oncogene = diagnostiic
-_% have MEN2 (tend to be bilat, younger, worse prognosis)
Path: _ is pathognomonic
-Provocative test: administer _ -> increases calcitonin
-Tx: total thyroidectomy. add neck dissection if node (+)
Medullary thyroid ca:
-from parafollicular C cells. Ret proto-oncogene = diagnostiic
-20% have MEN2 (tend to be bilat, younger, worse prognosis)
Path: AMYLOID pathognomonic
-Provocative test: administer GASTRIN -> increases calcitonin
-Tx: total thyroidectomy. add neck dissection if node (+)
order of treatment for pt c/ MEN 1 and gastrinoma
MEN I syndrome include parathyroid hyperplasia (causing hypercalcemia), pancreatic and duodenal neuroendocrine tumors, and pituitary tumors.
1. total parathyroidectomy or 3 1/2 with autotransplantation for hypercalcemia. If pt has ZE syn, should improve the symptoms. 2. gastrinoma resection if sx not improved c/ PPIs and parathyroidectomy
MEN 1 = ...
MEN 1:
Pancreatic islet cell tumor (Gastrinoma = #1, 50% multiple, 50% malignant, #1 morbidity of MEN 1)
Pituitary tumor (Prolactinoma = #1)
hyper-Parathyroidism (usually 1st to have sx, fix this 1st)
MENIN gene
What is the major source of morbidity from MEN 1?
MEN 1: MENIN gene, from APUD cells, autosomal D, 100% penetrance, variable expressivity
-Parathyroid hyperplasia => urinary sx, usually the 1st part to be symptomatic, needs to be corrected before the others. Tx = 4-gland resection c/ autotransplantation
-Pancreatic islet cell tumors => the major MEN1 morbidity. Gastrinoma = #1. 50% multiple, 50% malignant.
-Pituitary adenoma. Prolactinoma = #1
MEN 1 pt has parathyroid hyperplasia and a gastrinoma.
1st step of treatment is _
MEN 1: MENIN gene, from APUD cells, autosomal D, 100% penetrance, variable expressivity
-Parathyroid hyperplasia => urinary sx, usually the 1st part to be symptomatic, needs to be corrected before the others. Tx = 4-gland resection c/ autotransplantation
-Pancreatic islet cell tumors => the major MEN1 morbidity. Gastrinoma = #1. 50% multiple, 50% malignant.
-Pituitary adenoma. Prolactinoma = #1
MEN 1 is most likely to present with symptoms of _
MEN 1: MENIN gene, from APUD cells, autosomal D, 100% penetrance, variable expressivity
-Parathyroid hyperplasia => urinary sx, usually the 1st part to be symptomatic, needs to be corrected before the others. Tx = 4-gland resection c/ autotransplantation
-Pancreatic islet cell tumors => the major MEN1 morbidity. Gastrinoma = #1. 50% multiple, 50% malignant.
-Pituitary adenoma. Prolactinoma = #1
Pt presents c/ hyperparathyroidism, found to have MEN 1 and a pituitary mass.
-Pituitary mass is most likely to be a _
MEN 1: MENIN gene, from APUD cells, autosomal D, 100% penetrance, variable expressivity
-Parathyroid hyperplasia => urinary sx, usually the 1st part to be symptomatic, needs to be corrected before the others. Tx = 4-gland resection c/ autotransplantation
-Pancreatic islet cell tumors => the major MEN1 morbidity. Gastrinoma = #1. 50% multiple, 50% malignant.
-Pituitary adenoma. PROLACTINOMA = #1
MEN 2a = ...
MEN 2a:
hyper-Parathyroidism
Medullary thyroid ca (in nearly all pts, 1st to be symptomatic - usually diarrhea, #1 cause of death in MEN 2a)
Pheochromocytoma (often bilateral, almost always benign, fix this 1st)
-RET protooncogene
MEN 2a is most likely to present with symptoms of _
MEN 2a: RET proto-oncogene, from APUD cells, autosomal D, 100% penetrance, variable expressivity
-Parathyroid hyperplasia in 5-20%
-Pheochromocytoma in 10-60%. Often bilateral, benign but needs to be corrected 1st.
-Medullary ca of thyroid in ~100%, often bilateral. #1 cause of death in MEN2. Usually 1st part to be symptomatic = diarrhea 2/2 calcitonin
What is the major source of morbidity from MEN 2a?
Inheritance? What gene?
What type of cells?
MEN 2a: RET proto-oncogene, from APUD (amine precursor uptake decorboxylase) cells, autosomal D, 100% penetrance, variable expressivity
-Parathyroid hyperplasia in 5-20%
-Pheochromocytoma in 10-60%. Often bilateral, benign. corrected 1st.
-Medullary ca of thyroid in ~100%, often bilateral. #1 cause of death in MEN2. 1st to be symptomatic usually: => diarrhea 2/2 calcitonin most common.
Pt presents c/ pheochromocytoma, found to have MEN 2a and hyperparathyroidism.
1st step of treatment is _
MEN 2a: RET proto-oncogene, from APUD cells, autosomal D, 100% penetrance, variable expressivity
-Parathyroid hyperplasia in 5-20%
-Pheochromocytoma in 10-60%. Often bilateral, benign but needs to be corrected 1st.
-Medullary ca of thyroid in ~100%, often bilateral. #1 cause of death in MEN2. Usually 1st part to be symptomatic: => diarrhea 2/2 calcitonin most common.
MEN 2b:
#1 cause of death = _
MEN 2b:
mucosal neuromas, Marfan's habitus, musculoskel abnormalities
Medullary thyroid ca (in nearly all pts, 1st to be symptomatic - usually diarrhea, #1 cause of death in MEN 2a)
Pheochromocytoma (often bilateral, almost always benign, fix this 1st)
RET protooncogene
MEN 2b is most likely to present with symptoms of _
MEN 2b: RET proto-oncogene, from APUD cells, autosomal D, 100% penetrance, variable expressivity
-Mucosal neuromas (gut), ganglioneuromatosis in 100%
-Marfanoid habitus, musculoskel abnormalities
-Pheochromocytoma in 50%. Often bilateral, benign but needs to be corrected 1st.
-Medullary ca of thyroid in~100%, often bilateral. #1 cause of death in MEN2, more aggressive in MEN2b. Usually 1st part to be symptomatic = diarrhea 2/2 calcitonin
What is the major source of morbidity from MEN 2b?
MEN 2b: RET proto-oncogene, from APUD cells, autosomal D, 100% penetrance, variable expressivity
-Mucosal neuromas (gut), ganglioneuromatosis in 100%
-Marfanoid habitus, musculoskel abnormalities
-Pheochromocytoma in 50%. Often bilateral, benign but needs to be corrected 1st.
-Medullary ca of thyroid in~100%, often bilateral. #1 cause of death in MEN2, more aggressive in MEN2b. Usually 1st part to be symptomatic => diarrhea most common.
Pt presents c/ pheochromocytoma, found to have MEN 2b and medullary ca of thyroid.
1st step of treatment is _
MEN 2b: RET proto-oncogene, from APUD cells, autosomal D, 100% penetrance, variable expressivity
-Mucosal neuromas (gut), ganglioneuromatosis in 100%
-Marfanoid habitus, musculoskel abnormalities
-Pheochromocytoma in 50%. Often bilateral, benign but needs to be corrected 1st.
-Medullary ca of thyroid in~100%, often bilateral. #1 cause of death in MEN2, more aggressive in MEN2b. Usually 1st part to be symptomatic => diarrhea most common.
how does methimazole work?
Methimazole:
-Prevents peripheral conversion of T4-> T3
(unlike PTU, doesn't also prevent creation of thyroid hormone in gland)
-high relapse rate => continue x6 mo before stopping, or before starting radioactive iodine
what is the diagnostic test of choice for solitary neck mass
solitary neck mass => do FNA (don't need to get imaging 1st)
Pt develops increased pigmentation, amenorrhea, and vision change after adrenalectomy
-Tx = _
Nelson syndrome:
-after bilateral adrenalectomy (10%)
-Increased CRH -> pituitary enlargement ->
ACTH, amenorrhea, pigmentation (2/2 beta-MSH = melanocyte stim. hormone = peptide byproduct of ACTH), bitemporal hemianopsia
-Tx = steroids
60F presents c/ muscle weakness, myalgia, bone pain.
Imaging shows nephrolithiasis and bone lesions
-Must consider ...
Primary hyperparathyroidism
-PTH >40 pg/mL, Ca >10.5, Cl:PO4 ratio >33, +/-hyperchloremic met acidosis,
-PRAD-1 oncogene, radiation exposure increase risk of adenoma
-Older women
-OSTEITIS FIBROSA CYSTICA (brown tumors) = bone lesions 2/2 Ca resorption
-Most pts asymptomatic
-Sx: muscle weakness, myalgia, nephrolithiasis, pacreatitis, PUD, depression, bone pain, pathologic fx, MS change, constipation, N/V, anorexia
-Can get HTN 2/2 renal impairment
_ = #1 endocrine pancreatic tumor overall
Insulinoma = #1 endocrine pancreatic tumor overall
(but not part of a MEN subgroup)
5 indications for total thyroidectomy for papillary thyroid ca
Papillary thyroid ca:
-Total thyroidectomy for: >1 cm, bilateral lesions, multicentricity, hx XRT, extra-thyroidal dz (capsular invasion, (+) margins, mets, clincal or (+) LNs)
most common type of thyroid ca = _
-_% of adults, _% of children are node (+) on presentation
-F:M ratio is _:_
_% before age 40
Papillary thyroid ca = most Popular = 85% of thyroid cancer
-Lymphatic spread but nodes don't predict survival
-20% of adults, 80% of children are node (+) on presentation, 80% are multicentric.
-F:M 3:1. 50% before age 40
-Path:PSAMMOMA bodies represent deposited Ca
-RF = radiation exposure
-MACIS criteria: Mets, Age M>50 or F>40, Completeness of resection, Invasiveness, Size >1.5 cm
what artery supplies the parathyoid glands
inferior thyroid artery supplies the parathyroids
#1 explanation for persistent post-op hyperparathyroidism = _
missed adenoma = #1 reason for persistent primary hyperparathyroidism
-5% of pts have multiple adenomas @ time of surgery
#1 location for a missed parathyroid gland @ reexploration = _
#1 location for a missed parathyroid gland @ reexploration =
normal anatomic position
_ artery = blood supply to superior and inferior parathyroid glands
INFERIOR THYROID artery = blood supply to superior and inferior parathyroid glands
Superior parathyroids: from _th pharyngeal pouch
Inferior parathyroids + thymus: from __th pharyngeal pouch
Superior parathyroids: 4th pouch, ass'd c/ thyroid complex. lateral to RLN. above inf thyroid art.

Inferior parathyroids + thymus: 3rd pharyngeal pouch. inferior more variable position.. medial to RLN. below inf thyroid art #1 ectopic site = tail of thymus.
#1 location for ectopic parathyroid gland = _
#1 location for ectopic parathyroid gland =
inferior parathyroids in TAIL OF THYMUS, can migrate to the anterior mediastinum
-Other ectopic sites: intrathyroid, mediastinum, near tracheoesophageal groove
What is the order of where to look intraop if there is a missing parathyroid gland and you are doing parathyroidectomy for 4-gland hyperplasia?
4-gland parathryoid hyperplasia is treated c/ 4-gland resection + forearm re-implant or 3.5-gland resection
(only do reimplant into the SCM if parathryroid accidentally injured during thyroidectomy)
1. inside carotid sheath + look there
2. tracheoesophageal groove
3. transcervical thymectomy
4. ipsilateral thyroid lobectomy

-if intra-op PTH being measured, can confirm that 4th parathryoid is out (should drop 50% in 10-15 min)
The arterial blood supply to parathyroids come from...
The vascular supply to the parathyroid glands is mainly from the inferior thyroid artery. However, it can also arise from superior thyroid artery (20% of superior parathyroids), the lowest thyroid artery (thyroidea ima), and the arteries of larynx, trachea, esophagus or mediastinum
patient presents c/ primary hyperparathyroidism, palpable neck mass, Ca >15
-What surgery should you plan to do?
Parathyroid carcinoma:
-Rare. Presents c/ similar sx to parathyroid adenoma (hyper-Ca)
-Suspect if Ca >15 or palpable neck mass + primary hyperparathyoid
-Unlike adnenoma, more likely to be locally invasive (not "shell out") on excision
-Tx: en bloc resection of gland c/ surrounding structures (usually ipsilateral thyoid lobectomy)
normal parathyroid hormone level = _ to _ pg/mL
Parathyroid hormone:
-Normal level 5-40 pg/mL (also sae 10-60 pg/mL)
1/2 life 18 min
Ca reabsorbtion in DCT, PO4 secretion
-Increases osteoclasts in bone to release Ca, Po4
N terminal active, C terminal inactive (like insulin)
-1-OH-hydroxylation of VitD in kidney -> more Ca-binding protein in intestine
Parathyroid hormone increases _ levels by 3 mechanisms ...
Decreases _ levels by 1 mechanism
Parathyroid hormone:
increases 1-OH hydroxylation of vit D in kidney -> increases Ca binding protein -> increases Ca and PO4-absorption in gut
-increases Ca absorption in DCT of kidney, decreases PO4 absorption
-promotes Ca and PO4- release by osteoclasts
Pheochromocytoma:
Hypotension following removal is 2/2 _
-Treat c/ _
Pheochromocytoma:
Hypotension following removal is 2/2 hypovolemia
-Treat c/ IV fluid bolus

Phenoxybenzamine will worsen vasodilation, hypotension
Epi (alpha 1, beta 1/2), phenylephrine (alpha 1 agonist) will work only transiently
Pheochromocytoma pre-op prep:
1. Drug _ x _-_ weeks
2. Fluid loading (pt should gain fluid weight)
3.Drug _ (beta blockade) x _ hrs AFTER _ confirmed by _
Pheochromocytoma pre-op prep:
1. PHENOXYBENZAMINE or prazosin (long-acting alpha blockade) x 1-3 weeks
2. Fluid loading (pt should gain fluid weight)
3.Propranolol (beta blockade) x 48 hrs

-Start beta blockade AFTER alpha blockade confirmed by normal orthostatic changes, fluid loading complete.
-Unopposed alpha adrenergic activity can cuase MI, hypertensive crisis, pulm edema-
#1 location for extra-adrenal pheochromocytoma = _
Pheochromocytoma: -
Rare, slow-growing, R>L
-CHROMAFFIN cells: symp ganglia or neural crest cells
-10% rule: malignant, bilateral, in children, familial, extra-adrenal
-EXTRAadrenal more likely malignant, don't make epi. #1 location = Organ of Zuckerkandl @ aortic bifurcation
-Ass'd c/ MEN2a/b, von Recklinghausen's, tuberous sclerosis, Sturge-Weber
-Sx: episodic HT, headache, diaphoresis, palpitations
-Dx: 24-hr urine VMA (most sensitive), metanephrines = breakdown products of epi, NE
-MIBG scan (131-metaiodobenzylguanine = NE analogue) (or CT, MRI) => locate. Still can't localize => laparotomy
-Clonidine supression test (a tumor doesn't respond)
-DON'T do venography => can cause hypertensive crisis
Malignant pheochromocytoma is clearly identified by which anatomic attributes?
Diagnosis of malignant pheochromocytoma is often difficult. It generally established when there is invasion of adjacent structures or by documenting nodal or distant metastases
Posterior pituitary makes 2 hormones..
Posterior pituitary =neurohypophysis: ADH, oxytocin
Anterior pituitary = adneohypophysis: GH, ACTH, TSH, LH, FSH, prolactin
-Chromophobe pit. adenoma: non-functional. decreased GH, FSH, LH, TSH, ACTH
-Prolactinoma = #1 pituitary adenoma (tx: bromocriptine or transsphenoidal resection)
#1 pituitary adenoma = _
What are the main treatments for prolactinoma?
Posterior pituitary =neurohypophysis: ADH, oxytocin
Anterior pituitary = adneohypophysis: GH, ACTH, TSH, LH, FSH, prolactin
-Chromophobe pit. adenoma: non-functional. decreased GH, FSH, LH, TSH, ACTH

-Prolactinoma = #1 pituitary adenoma
Tx: bromocriptine.
MICROadenomas (most cases): transsphenoidal resection if failure of med mgmt. Pregnancy not an indication.
MACROadenomas: resect if hemorrhage, visual loss, pregnancy, CSF leak
Chromophobe pituitary adenoma: 5 hormones that may be made
Posterior pituitary =neurohypophysis: ADH, oxytocin
Anterior pituitary = adneohypophysis: GH, ACTH, TSH, LH, FSH, prolactin
-Chromophobe pit. adenoma: non-functional. decreased GH, FSH, LH, TSH, ACTH
-Prolactinoma = #1 pituitary adenoma (tx: bromocriptine or transsphenoidal resection)
65F presents c/ hyperthyoid sx, neck mass, no opthalmologic changes
-Hyperfunctioning nodule identified
-This syndrome is called _
-Tx is _
Plummers syndrome:
-hyper-functioning nodule develops within a longstanding goiter ->
-Hyperthyroidism without ophthalmologic sx
-Toxic multi or uni-nodular goiters
-Typical population: women over the age of 60
-Indication for thyroidectomy (doesn't respond to meds)
Pt has Ca 11, PTH 200, elevated urine Ca
What type of hyperparathyroidism is this?
Primary hyperparathyroidism
-Hyperchloremic metabolic acidosis
-PTH >40 pg/mL
-Ca >10.5
-High renal cAMP (effect on PTH R in kidney)
Cl:PO4 ratio >33
-High urine Ca in 70% (normal in 30%)
acid/base change associated with primary hyperparathyroidism is _
PTH > _pg/mL
Cl: PO4 ratio > _

What oncogene increases risk of adenoma?
Primary hyperparathyroidism
-PTH >40 pg/mL, Ca >10.5, high renal cAMP (effect on PTH R in kidney), Cl:PO4 ratio >33, +/- HYPERCHLOREMIC METABOLIC ACIDOSIS,
-PRAD-1 oncogene increases risk for adenomas
-Older women
-Osteitis fibrosa cystica (brown tumors) = bone lesions 2/2 Ca resorption
-Most pts asymptomatic
-Sx: muscle weakness, myalgia, nephrolithiasis, pacreatitis, PUD, depression, bone pain, pathologic fx, MS change, constipation, N/V, anorexia
-Can get HTN 2/2 renal impairment
Primary hyperparathyrodism:
_% have single adenoma
_% have multiple adenomas
_% have diffuse hyperplasia
_% have parathryroid adnenocarcinoma
Primary hyperparathyrodism:
80-85% have single adenoma => resect adenoma, inspect other glands to r/o hyperplasia or another adenoma
4%% have multiple adenomas
15% have diffuse hyperplasia (MEN 1 ot 2a have 4-gland hyperplasia) => don't biopsy all glands b/c risk of hemorrhage, hypo-PTH. resect 3.5 glands or parathyroidectomy + reimplantation
<1% have parathyroid adnenocarcinoma (very high Ca levels) => radical parathyroidecomy including ipsilateral glands
primary hyperparathyroidism:
-ass'd c/ __ oncogene and history of environmental exposure to __
Primary hyperparathyroidism
-PTH >40 pg/mL, Ca >10.5, Cl:PO4 ratio >33, +/-hyperchloremic met acidosis,
-PRAD-1 oncogene, RADIATION exposure increase risk of adenoma
-Older women
-Osteitis fibrosa cystica (brown tumors) = bone lesions 2/2 Ca resorption
-Most pts asymptomatic
-Sx: muscle weakness, myalgia, nephrolithiasis, pacreatitis, PUD, depression, bone pain, pathologic fx, MS change, constipation, N/V, anorexia
-Can get HTN 2/2 renal impairment
5 indications for surgery for hyperparathryoidism
Primary hyperparathyroidism - 5 indications for surgery:
1.Symptomatic dz
2.Asymptomatic + Ca>13
3. Decreased Cr clearance
4. Nephrolithiasis
5. Significantly decreased bone mass

Adenoma (84%). PRAD-1 increases risk => resection; inspect other glands to r/o hyperplasia or multiple adenomas (4%)
-Hyperplasia (15%) => resect 3.5 glands or total parathyroidectomy + autoimplantation (don't biopsy all glands 2/2 risk of hemorrhage + hypoparathyroid)
-Parathyroid adenocarcinoma (<1%) => radical parathyroidectomy (c/ ipsilateral thyroid)
-Pregnancy => surgery in 2nd trimester to avoid risk of 3rd trimester stillbirth
Lab changes with primary hyperparathyroidism...

High urine ca in _%
Primary hyperparathyroidism
-Hyperchloremic metabolic acidosis
-PTH >40 pg/mL
-Ca >10.5
-High renal cAMP (effect on PTH R in kidney)
Cl:PO4 ratio >33
-High urine Ca in 70% (normal in 30%)
Mechanism of propylthiouracil is …
Propylthiouracil (thionamide, along with methimazole):
-INHIBITS PEROXIDASES, which connect iodine to tyrosine to form DIT, MIT
-PTU, propranolol, and Prednisone also inhibit peripheral conversion of T4 -> T3
-SE: aplasic anemia, AGRANULOCYTOSIS (rare)
-crosses placenta. preferred over methimazole definitely during FIRST trimester, most review books says all of pregnancy
Pt being treated for hyperthyroidism develops aplastic anemia, agranuocytosis.
-Suspect medication _ or _
Propylthiouracil:
-Inhibit peroxidases -> prevents DIT, MIT coupling
-SE: aplasic anemia, agranulocytosis (rare)
-PTU preferred in 1st trimester; may change to methimazole in 2nd-3rd trimester. can cause cretinism.
Pt s/p total thyroidectomy complains of loss of voice pitch
Most likely 2/2 injury to the _ nerve
Recurrent laryngeal nerve injury (e.g. during total thyroidectomy) -> hoarseness
(R injury more common than L but R less likely to be recurrent)
_ nerve innervates all of the larynx except for the _
Recurrent laryngeal nerve:
-Innervates all of larynx except CRICOTHYROID muscle
-Run posterior to thyroid lobes in tracheoesophageal groove
-Can tract c/ inferior thyroid artery, but variable
-L RLN loops around aorta
-R RLN loops around R subclavian = innominate artery, but R is more lateral, more likely than L to be non-recurrent (e.g. 2/2 replaced R subclavian off the descending aorta)
-Risk of injury to non-recurrent laryngeal nerve during surgery
-Unilateral injury -> hoarseness; Bilat injury -> airway obstruction 2/2 medialization of cords, requires emergent tracheostomy
what is the most common explanation for a non-recurrent laryngeal nerve?
replaced R subclavian off the descending aorta
where are the recurrent laryngeal nerves recurrent?
RIGHT recurrent laryngeal nerve => loops around R subclavain (or innominate) artery. More likely than L to not be recurrent
LEFT recurrent laryngeal nerve = loops around aorta
Pt is s/p total thyroidectomy, gets extubated, then experiences severe resp stridor, possible impending resp arrest. No sign of hematoma
Suspect _ -> do _
Bilateral recurrent laryngeal nerve injury during total thyroidectomy -> medialization of cords -> severe resp stridor, possibe resp arrest, very difficult to reintubate
-Do TRACHEOSTOMY via the COLLAR INCISION that was used for thyroidectomy
Adrenal cortical ca:
_% are functioning tumors
typical presentation
medication used to treat
Adrenal cortical ca:
-bimodal age distribution: before age 5, after age 50. F >M
-50% functioning tumors: cortisol, aldosterone, sex steroids
-children have virilization in 90%. feminization in men. masculinization in women
CT findings: heterogeneous enhancement, slow washout. MRI hypointense on T1, high-intermediate signal on T2. if >4 cm, likely malignant
-Sx: abn pain, wt loss, weakness
-80% have advanced dz @ time of diagnosis
-Tx: radical adrenalectomy. Mitotane (AKA Op-DDD = adrenal-lytic) for residual or recurrent dz
-20% 5-yr survival
Renal osteodystrophy causes hyper-parathryroidism by 2 mechanisms:
1. Kidney loses __, retains __.
2. Decreased ____ (chemical rxn)
Renal osteodystrophy causes hyper-parathryroidism by 2 mechanisms:
1. Kidney loses Ca2+, retains PO4-. (main mechanism)
2. Decreased vitamin D 1-hydroxylation
Renin-angiotensin-aldosterone system:
low NaCl -> sensed by the ___ -> produces __ ->
converts __ to __ -> which is converted to __ in the _ -> A-2 = vasoconstrictor, increases Aldosterone ->
retains ___, loses __ and __ in urine
Renin-angiotensin-aldosterone system:
low NaCl -> sensed by the macula densa -> produces renin ->
converts angiotensinogen to A-1 -> which is converted to A-2 in the lung ->
A-2 = vasoconstrictor, increases Aldosterone ->
retains Na, loses K and H+ in urine
RET proto-oncogene is ass'd c/ 3 disorders...
RET proto-oncogene
-60% have MEN 2a
-5% have MEN 2b
-35% have familial medullary thyroid ca
Pt presents c/ Ca 8, PTH 200, Cr 7, and bone pain.
-Suspect _
-Tx is _
Secondary hyperparathyroidism:
-Usually dialysis pts c/ chronic Ca loss
-Elevated PTH, normal Ca
-Rarely requires surgery
-Most common surgery indication = bone pain 2/2 Ca resorption
post-partum patient is not lactating and has persistent amenorrhea.
Must consider...
Sheehan syndrome: post-partum lack of lactation, persistent amenorrhea
+/- adrenal insuff, hypothyroidism
-2/2 pituitary ischemia 2/2 hemorrhage, hypotension
most common tumor to cause paraneoplastic hypercalcemia = _
-primary tx _
-how can you tell this from primary hypoparathryroid?
Small cell lung ca = most common tumor to cause paraneoplastic hyper-Ca
(distinguish from parathryroid dz by normal/low PTH)
-primary tx = osteoclast inhibitor = bisphosphonate
What syndrome?
Bridging veins absent on one side of brain
Sturge-Weber = cephalotrigeminal angiomatosis:
-NOT inherited, presents by age ~2
-Bridging veins absent on one side of brain -> that side develops central venous drainage -> venous HTN after birth -> increased risk of thrombosis, multiple tiny infarcts -> atrophy, calcification of one hemisphere

Port-wine angioma can trigger w/up, especially if it involves medial canthus (but is an isolated finding in 90% of cases)
-increased risk of pheochromocytoma
After an upper respiratory infection a patient develops fever and a tender thyroid. The most appropriate treatment would be:
This is a typical presentation of Subacute Thyroiditis, the exact cause of which is unknown. This is generally a self-limiting process, however, treatment with corticosteroids or NSAIDS is effective in relieving symptoms.
Pt s/p total thyroidectomy complains of loss of voice pitch
Most likely 2/2 injury to the _ nerve
Superior laryngeal nerve injury (e.g. during thyroidectomy) -> loss of pitch
(motor to cricothyroid. Injury => loss of projection, high pitch)
What nerve supplies the cricothyroid muscle?
-What are the symptoms of nerve injury?
Superior laryngeal nerve:
Vagus -> Sup laryngeal nerve -> internal + external branches -> EXTERNAL branch travels c/ SUP. THYROID ARTERY to CRICOTHYROID muscle
(only laryngeal muscle innervated by the nerve)
-injury (e.g. during thyroidectomy) -> weak voice, loss of voice quality @ higher ranges
T3: more or less active than T4?
1/2 life is _
T3: 3x as active as T4
-1/2 life = 3 days
indications for thyroidectomy to treat hyperthyroid
Thyroidectomy for hyperthyroid if:
-Pregnant (beta block then operate)
-Plummer's syndrome = autonomously functioning nodule
-Compressive sx
-Failed medical tx
patient is s/p thyroidectomy that day, extubated in PACU and has severe resp stridor and impending resp arrest. No hematoma on exam.
-Next step is ..
open wound and place emergent trach,
-Very difficult to intubate c/ bilateral RLN injury and medialization of both cords
Pt c/ thyroid mass + palpable LN's pre-op is found to have thyroid CA on lobectomy.
Next step…
Thyroid CA + palpable LNs =>
total thyroidectomy + modified radical neck dissection

Indications for MRND = extra-thyroidal dz: capsule invasion, clinical or (+) nodal dz, or mets
How is the Wolff-Chaikoff effect used to treat thyroid storm?
Thyroid storm:
-Sx: increased HR, numbness, irritability, vomiting, diarrhea
High-output cardiac failure = #1 cause of death
-Post-op pt c/ undiagnosed GRAVE'S > precipitated by anxiety, excessive gland palpation, adrenergic stimulants
-Inital tx: beta blockers (ESMOLOL drip), PTU, Lugol's soln (KI), cooling blanketsl O2, lucose, fluid
-Emergent thyroidectomy rarely indicated
-WOLFF-CHAIKOFF effect = give pt high doses of I (Lugol's soln, KI) -> inhibit TSH action on thyroid -> inhibit organic coupling of iodide -> less T3, T4 release
Initial therapy for thryoid storm is _
Thyroid storm:
-Sx: increased HR, numbness, irritability, vomiting, diarrhea
High-output cardiac failure = #1 cause of death
-Post-op pt c/ undiagnosed GRAVE'S > precipitated by anxiety, excessive gland palpation, adrenergic stimulants
-Inital tx = beta blockers (ESMOLOL drip) -> PTU, Lugol's soln (KI), cooling blanketsl O2, lucose, fluid
-Emergent thyroidectomy rarely indicated
-WOLFF-CHAIKOFF effect = give pt high doses of I (Lugol's soln, KI) -> inhibit TSH action on thyroid -> inhibit organic coupling of iodide -> less T3, T4 release
4 main prognostic factors for thyroid ca..
(remember acronym)
Thyroid ca worse prognostic factors: AGES
Age: women >50, men >40
Grade (poorly diff)
Extebnt: extracapsular extension, regional LN dz
Size >4 cm or Sex Male
I-131 is indicated for 2 types of thyroid ca...
I-131 - for PAPILLARY & FOLLICULAR thyroid ca. Indications:
-recurrent dz
-primary inoperable tumors 2/2 local invasion
-Papillary c/ extranodal dz
-Follicular >1 cm OR extranodal dz
-For metastatic dz, thyroidectomy facilitates entry of I-131 into metastatic lesions

-can cure bone and lung mets
-done 6 weeks post-op
-SE: sialoadenitis, GI sx, infertility, BM suppression, parathyroid dysfx, leukemia
Best lab test for picking up recurrent papillary or follicular thyroid ca
Follow serum THYROGLOBULIN levels s/p total thyroidectomy for papillary or follicular thyroid ca to detect recurrence
Thyroid hormone binds a receptor located at the cell _
Thyroid hormone binds a receptor located at the NUCLEUS
Evaluation of a 17-year-old boy with an asymptomatic mass in his neck discloses a "hot" thyroid nodule that is 3 cm in diameter. He is clinically and chemically euthyroid with a very low level of thyroid-stimulating hormone. The most appropriate management is
thyroid lobectomy
thyroid storm:
-tachycardia, fever, numbness, irritability, N/V, diarrhea
-#1 cause of death = high output cardiac failure
-most common post-op in pt c/ undiagnosed Grave's. also 2/2 anxiety, excess palpation of gland, adrenergic stimulants
-Tx: beta blocker, PTU, Lugol's (KI), steroids, cooling, oxygen, glucose, fluid
Rarely need emergent thyroidectomy
-Wolff-Chaikoff effect: give high doses of Lugols= KI to inhibit TSH action -> inhibit organic coupling of iodide ->less T3, T4
What syndrome? "Zits, Fits, + Nitwits"
-Skin lesions, hamartomas, myoclonic seizures , mental retardation
Tuberous sclerosis = Bourneville's Dz: autosomal D neurocutaneous dz, xsomes 9,11
-"Zits, Fits, + Nitwits"
-Skin lesions, hamartomas
-Myoclonic seizures (90%, start at age 1-2)
-Mental retardation (50%)
what syndrome?: multifocal and recureent renal cell ca, renal cysts, CNS tumors, pheochromocytoma
Von Hipple Lindau:
multifocal and recureent renal cell ca, renal cysts, CNS tumors, pheochromocytoma
what is the endocrine malignancy associated with von recklinghausen's dz?
von Recklinghausen's = Neurofibromatosis type 1 = #1 phakomatosis.
-Autosomal D, xsome 17. Defined by 2/7 criteria
Cutaneous lesions: 1. CAFE-AU-LAIT SPOTS, 2. neurofibromas, schwannomas, 3. axillary/inguinal/intertriginous freckling
PERIPHERAL NEURAL TUMORS: 4. optic glioma, 5. lisch nodules
Skeletal deformaties: 6. sphenoid dysplasia, long bone cortical thickening
7. 1st deg relative c/ NF1
also have PHEOCHROMOCYTOMA
What is Waterhouse-Friedrickson syndrome?
Waterhouse-Friderichsen syndrome:
-adrenal hemorrhage 2/2 meningococcal sepsis -> can cause adrenal insuff
How is the Wolk Chaikoff effect used in thyroid storm?
Wolk Chaikoff effect:
-High I-doses (lugol's, KI) inhibit TSH
-Useful in thyroid storm
Parafollicular C cells:
-derived from _ in embryo
-produce hormone _
Parafollicular C cells:
-derived from neural crest
-produce calcitonin => decrease serum Ca
Cricothyroid muscle is ennervated by the _ nerve
Cricothyroid muscle is ennervated by the superior laryngeal nerve
Pt presents c/ PTH 30-60, serum Ca 9-11, low urine Ca.
-Suspect _
-Tx is _
Familial hypercalcemic hypocalciuria:
-2/2 increased binding of PTH to defective PTH receptor in distal convoluted tubule -> increased Ca resorption
-Tx: do nothing. NO parathyroidectomy (Ca not very elevated)
Pt c/ asymptomatic thyroid mass, normal TFTs.
FNA => follicular cells
-Next step..
Thyroid mass c/ FNA (+) for follicular cells:
5-10% malignancy risk => lobectomy or thyroidectomy
Pt c/ asymptomatic thyroid mass, normal TFTs, FNA (+) for follicular cells
-Found to have follicular CA on lobectomy
Next step…
Thyroid lobectomy (+) for follicular CA => proceed to total thyroidectomy if >1 cm or extrathyroidal disease
-Extrathyroidal involvement or clinically (+) cervical LNs => ipsilateral MRND
-Lesion >1 cm or capsular invasion => I-131 x 6 weeks post-op
-Microinvasive (<1 cm), rare nodal spread (<10%), then usually incidental finding on path and lobectomy is sufficient as long as margins (-)
-70% 5-yr survival, prognosis depends on stage
- 50% metastatic on presentation. bone mets most common.
Follicular thyroid CA:
-_% metastatic @ presentation
-spread by LNs or blood? #1 site for mets? (
- indications for total thyroidectomy? for MRLND? for I-131?
Follicular thyroid CA:
-50-60% metastatic @ presentation, more aggressive than papillary CA
-Hematogenous spread (BONE most common)
-Typically age 50's-60's, F:M 3:1
-If FNA shows follicular cells => 10% malignancy risk
-Path (+) for adenoma or follicular hyperplasia => lobectomy only
-typically requires total thyroidectomy + postop RI ablation
-Follicular Ca >1 cm or extrathyroidal dz => total thyroidectomy
-Clinically (+) cervical nodes or extrathyroidal dz => ipsilateral MRND
-Lesion >1 cm or extrathyroidal dz/capsular invasion => I-131 x 6 weeks post-op
-Microinvasive (<1 cm), rare nodal spread (<10%), then usually incidental finding on path => lobectomy suffiicient as long as margins (-)
-70% 5-year survival, prognosis based on stage
Pt has thyroid nodule, then undergoes FNA which demonstrates follicular cells.
next step is _
FNA can't distinguish malignant/benign with follicular or Hurthle cell (subtype of follicular) => need TISSUE
-10% cahnge of malignancy if FNA shows follicular cells
A 65 yo female with history of living in area endemic for iodine deficiency presents with an anterior neck nodule. Examination reveals a 4 cm firm, mobile thyroid nodule. No lymphadenopathy was noted. Patient was taken to the OR for resection. Intraoperative frozen section of the tumor reveal Hurthle cell tumor. Which is the course of action for this patient.
Total thyroidectomy
-Hurthle cell carcinoma of the thyroid is a subtype of follicular ca
- Tx, prognosis are similar with small differences (Sabiston, p619). Most are benign. Usually older pts
- <2 cm, contained in 1 lobe=> lobectomy or isthmectomy.
- MOST CASES: 2-4 cm and patient is high risk (e.g. advanced age)=> TOTAL THYROIDECTOMY
- > 4cm => total thyroidectomy for sure - 50% risk of cancer.
Treatment for hypercalcemia
Hypercalcemia:
-Confusion, somnolence, shortened QT
-Tx: NS @ 200-300/hr, Furosemide
-NO LR or thiazides!
#1 cause of persistant hyperparathyroidism after parathyroidectomy =
1% rate of persistant hyperparathyroidism after parathyroidectomy
-Usually 2/2 missed adenoma in the neck
Hyperthyroid in pregnancy:
-1st line = propylthiouracil (does not cross placenta)
-Persistant sx-=> thyroidectomy in 2nd trimester (decreased risk of adverse events, premature labor)
-I-131 would ablate fetal thyroid
-Methimazole causes cretinism
-Don't mask sx c/ beta blocker b/c hyperthroidism still present, still increased risk of stillbirth, cause fetal growth retardation in 3rd trimester
Hyperthyroid in pregnancy:
-1st line = propylthiouracil (does not cross placenta)
-Persistant sx-=> thyroidectomy in 2nd trimester (decreased risk of adverse events, premature labor)
-I-131 would ablate fetal thyroid
-Methimazole causes cretinism
-Don't mask sx c/ beta blocker b/c hyperthroidism still present, still increased risk of stillbirth, cause fetal growth retardation in 3rd trimester
#1 cause of hypoparathyroidism = _
Hypoparathyroidism:
#1 cause = previous thyroid surgery
-Numbness/tingling in cirumoral area, fingers -> anxiety, confusion -> Tetany (carpopedal spasms, convusions, laryngospam which can be deadly
-Concomitant hypo-Mg can make correction of Ca difficult
Why give thyroid hormone replacement following I-131 for papillary or follicular thyroid ca?
Give thyroid hormone replacement following I-131 for papillary or follicular thyroid ca
-Suppresses TSH -> suppress growth of residual cancer tissue
Radioactive iodine is used for _ type thyroid tumors
I-131 if:
- starts 6 weeks post-op
- (I-131 scan to r/o mets also best done 4-6 wks postop when PTH highest)
- Papillary, follicular ca only
- can cure bone and lung mets

- Indications: recurrent pr metastatic papillary/follicular ca (if mets, do total thyroidectomy 1st), primary inoperable tumors 2/2 local invasion, papillary + extrathyroidal dz, follicular >1 cm + extrathyroidal dz
Medullary thyroid ca:
-from _ type cells. The _t proto-oncogene = diagnostiic
-_% have MEN2 (tend to be bilat, younger, worse prognosis)
Path: _ is pathognomonic
-Provocative test: administer _ -> increases calcitonin
-Tx: total thyroidectomy. add neck dissection if node (+)
Medullary thyroid ca:
-from parafollicular C cells. Ret proto-oncogene = diagnostiic
-20% have MEN2 (tend to be bilat, younger, worse prognosis)
Path: AMYLOID pathognomonic
-Provocative test: administer GASTRIN -> increases calcitonin
-Tx: total thyroidectomy. add neck dissection if node (+)
MEN 1 = ...
MEN 1:
Pancreatic islet cell tumor (Gastrinoma = #1, 50% multiple, 50% malignant, #1 morbidity of MEN 1)
Pituitary tumor (Prolactinoma = #1)
hyper-Parathyroidism (usually 1st to have sx, fix this 1st)
MENIN gene
What is the major source of morbidity from MEN 1?
MEN 1: MENIN gene, from APUD cells, autosomal D, 100% penetrance, variable expressivity
-Parathyroid hyperplasia => urinary sx, usually the 1st part to be symptomatic, needs to be corrected before the others. Tx = 4-gland resection c/ autotransplantation
-Pancreatic islet cell tumors => the major MEN1 morbidity. Gastrinoma = #1. 50% multiple, 50% malignant.
-Pituitary adenoma. Prolactinoma = #1
MEN 1 pt has parathyroid hyperplasia and a gastrinoma.
1st step of treatment is _
MEN 1: MENIN gene, from APUD cells, autosomal D, 100% penetrance, variable expressivity
-Parathyroid hyperplasia => urinary sx, usually the 1st part to be symptomatic, needs to be corrected before the others. Tx = 4-gland resection c/ autotransplantation
-Pancreatic islet cell tumors => the major MEN1 morbidity. Gastrinoma = #1. 50% multiple, 50% malignant.
-Pituitary adenoma. Prolactinoma = #1
MEN 1 is most likely to present with symptoms of _
MEN 1: MENIN gene, from APUD cells, autosomal D, 100% penetrance, variable expressivity
-Parathyroid hyperplasia => urinary sx, usually the 1st part to be symptomatic, needs to be corrected before the others. Tx = 4-gland resection c/ autotransplantation
-Pancreatic islet cell tumors => the major MEN1 morbidity. Gastrinoma = #1. 50% multiple, 50% malignant.
-Pituitary adenoma. Prolactinoma = #1
Pt presents c/ hyperparathyroidism, found to have MEN 1 and a pituitary mass.
-Pituitary mass is most likely to be a _
MEN 1: MENIN gene, from APUD cells, autosomal D, 100% penetrance, variable expressivity
-Parathyroid hyperplasia => urinary sx, usually the 1st part to be symptomatic, needs to be corrected before the others. Tx = 4-gland resection c/ autotransplantation
-Pancreatic islet cell tumors => the major MEN1 morbidity. Gastrinoma = #1. 50% multiple, 50% malignant.
-Pituitary adenoma. PROLACTINOMA = #1
MEN 2a = ...
MEN 2a:
hyper-Parathyroidism
Medullary thyroid ca (in nearly all pts, 1st to be symptomatic - usually diarrhea, #1 cause of death in MEN 2a)
Pheochromocytoma (often bilateral, almost always benign, fix this 1st)
-RET protooncogene
MEN 2a is most likely to present with symptoms of _
MEN 2a: RET proto-oncogene, from APUD cells, autosomal D, 100% penetrance, variable expressivity
-Parathyroid hyperplasia in 5-20%
-Pheochromocytoma in 10-60%. Often bilateral, benign but needs to be corrected 1st.
-Medullary ca of thyroid in ~100%, often bilateral. #1 cause of death in MEN2. Usually 1st part to be symptomatic: => diarrhea 2/2 calcitonin most common.
What is the major source of morbidity from MEN 2a?
MEN 2a: RET proto-oncogene, from APUD cells, autosomal D, 100% penetrance, variable expressivity
-Parathyroid hyperplasia in 5-20%
-Pheochromocytoma in 10-60%. Often bilateral, benign but needs to be corrected 1st.
-Medullary ca of thyroid in ~100%, often bilateral. #1 cause of death in MEN2. Usually 1st part to be symptomatic: => diarrhea 2/2 calcitonin most common.
Pt presents c/ pheochromocytoma, found to have MEN 2a and hyperparathyroidism.
1st step of treatment is _
MEN 2a: RET proto-oncogene, from APUD cells, autosomal D, 100% penetrance, variable expressivity
-Parathyroid hyperplasia in 5-20%
-Pheochromocytoma in 10-60%. Often bilateral, benign but needs to be corrected 1st.
-Medullary ca of thyroid in ~100%, often bilateral. #1 cause of death in MEN2. Usually 1st part to be symptomatic: => diarrhea 2/2 calcitonin most common.
MEN 2b = ..
MEN 2b:
mucosal neuromas, Marfan's habitus, musculoskel abnormalities
Medullary thyroid ca (in nearly all pts, 1st to be symptomatic - usually diarrhea, #1 cause of death in MEN 2a)
Pheochromocytoma (often bilateral, almost always benign, fix this 1st)
RET protooncogene
MEN 2b is most likely to present with symptoms of _
MEN 2b: RET proto-oncogene, from APUD cells, autosomal D, 100% penetrance, variable expressivity
-Mucosal neuromas (gut), ganglioneuromatosis in 100%
-Marfanoid habitus, musculoskel abnormalities
-Pheochromocytoma in 50%. Often bilateral, benign but needs to be corrected 1st.
-Medullary ca of thyroid in~100%, often bilateral. #1 cause of death in MEN2, more aggressive in MEN2b. Usually 1st part to be symptomatic => diarrhea most common.
What is the major source of morbidity from MEN 2b?
MEN 2b: RET proto-oncogene, from APUD cells, autosomal D, 100% penetrance, variable expressivity
-Mucosal neuromas (gut), ganglioneuromatosis in 100%
-Marfanoid habitus, musculoskel abnormalities
-Pheochromocytoma in 50%. Often bilateral, benign but needs to be corrected 1st.
-Medullary ca of thyroid in~100%, often bilateral. #1 cause of death in MEN2, more aggressive in MEN2b. Usually 1st part to be symptomatic => diarrhea most common.
Pt presents c/ pheochromocytoma, found to have MEN 2b and medullary ca of thyroid.
1st step of treatment is _
MEN 2b: RET proto-oncogene, from APUD cells, autosomal D, 100% penetrance, variable expressivity
-Mucosal neuromas (gut), ganglioneuromatosis in 100%
-Marfanoid habitus, musculoskel abnormalities
-Pheochromocytoma in 50%. Often bilateral, benign but needs to be corrected 1st.
-Medullary ca of thyroid in~100%, often bilateral. #1 cause of death in MEN2, more aggressive in MEN2b. Usually 1st part to be symptomatic => diarrhea most common.
60F presents c/ muscle weakness, myalgia, bone pain.
Imaging shows nephrolithiasis and bone lesions
-Must consider ...
Primary hyperparathyroidism
-PTH >40 pg/mL, Ca >10.5, Cl:PO4 ratio >33, +/-hyperchloremic met acidosis,
-PRAD-1 oncogene, radiation exposure increase risk of adenoma
-Older women
-OSTEITIS FIBROSA CYSTICA (brown tumors) = bone lesions 2/2 Ca resorption
-Most pts asymptomatic
-Sx: muscle weakness, myalgia, nephrolithiasis, pacreatitis, PUD, depression, bone pain, pathologic fx, MS change, constipation, N/V, anorexia
-Can get HTN 2/2 renal impairment
_ = #1 endocrine pancreatic tumor overall
Insulinoma = #1 endocrine pancreatic tumor overall
(but not part of a MEN subgroup)
5 indications for total thyroidectomy for papillary thyroid ca
Papillary thyroid ca:
-Total thyroidectomy for: >1 cm, bilateral lesions, multicentricity, hx XRT, extra-thyroidal dz (capsular invasion, (+) margins, mets, clincal or (+) LNs)
most common type of thyroid ca = _
-_% of adults, _% of children are node (+) on presentation
-F:M ratio is _:_
_% before age 40
Papillary thyroid ca = most Popular = 85% of thyroid cancer
-Lymphatic spread but nodes don't predict survival
-20% of adults, 80% of children are node (+) on presentation, 80% are multicentric.
-F:M 3:1. 50% before age 40
-Path:PSAMMOMA bodies represent deposited Ca
-RF = radiation exposure
-MACIS criteria: Mets, Age M>50 or F>40, Completeness of resection, Invasiveness, Size >1.5 cm
#1 location for a missed parathyroid gland @ reexploration = _
#1 location for a missed parathyroid gland @ reexploration =
normal anatomic position
Superior: lateral to RLN. above inf thyroid artery
Inferior: medial to RLN. more anterior and below inf thyroid artery. more likely to be ectopic. occasionally in tail of thymus, can migrate to anterior mediastinum (other ectopic sites: intrathyroid, mediastinal, near TE groove)
_ artery = blood supply to superior and inferior parathyroid glands
INFERIOR THYROID artery = blood supply to superior and inferior parathyroid glands
Superior parathyroids: from _th pharyngeal pouch
Inferior parathyroids + thymus: from __th pharyngeal pouch
Superior parathyroids: 4th pouch, ass'd c/ thyroid complex. lateral to RLN. above inf thyroid art.

Inferior parathyroids + thymus: 3rd pharyngeal pouch. inferior more variable position.. medial to RLN. below inf thyroid art #1 ectopic site = tail of thymus.
#1 location for ectopic parathyroid gland = _
#1 location for ectopic parathyroid gland =
inferior parathyroids in TAIL OF THYMUS, can migrate to the anterior mediastinum
-Other ectopic sites: intrathyroid, mediastinum, near tracheoesophageal groove
normal parathyroid hormone level = _ to _ pg/mL
Parathyroid hormone:
-Normal level 5-40 pg/mL
1/2 life 18 min
Ca reabsorbtion in DCT, PO4 secretion
-Increases osteoclasts in bone to release Ca, Po4
N terminal active, C terminal inactive (like insulin)
-1-OH-hydroxylation of VitD in kidney -> more Ca-binding protein in intestine
Parathyroid hormone increases _ levels by 3 mechanisms ...
Decreases _ levels by 1 mechanism
Parathyroid hormone:
increases 1-OH hydroxylation of vit D in kidney -> increases Ca binding protein -> increases Ca and PO4-absorption in gut
-increases Ca absorption in DCT of kidney, decreases PO4 absorption
-promotes Ca and PO4- release by osteoclasts
Pt has Ca 11, PTH 200, elevated urine Ca
What type of hyperparathyroidism is this?
Primary hyperparathyroidism
-Hyperchloremic metabolic acidosis
-PTH >40 pg/mL
-Ca >10.5
-High renal cAMP (effect on PTH R in kidney)
Cl:PO4 ratio >33
-High urine Ca in 70% (normal in 30%)
acid/base change associated with primary hyperparathyroidism is _
Primary hyperparathyroidism
-PTH >40 pg/mL, Ca >10.5, high renal cAMP (effect on PTH R in kidney), Cl:PO4 ratio >33, +/- HYPERCHLOREMIC METABOLIC ACIDOSIS,
-PRAD-1 oncogene increases risk for adenomas
-Older women
-Osteitis fibrosa cystica (brown tumors) = bone lesions 2/2 Ca resorption
-Most pts asymptomatic
-Sx: muscle weakness, myalgia, nephrolithiasis, pacreatitis, PUD, depression, bone pain, pathologic fx, MS change, constipation, N/V, anorexia
-Can get HTN 2/2 renal impairment
Primary hyperparathyrodism:
_% have single adenoma
_% have multiple adenomas
_% have diffuse hyperplasia
_% have parathryroid adnenocarcinoma
Primary hyperparathyrodism:
80-85% have single adenoma => resect adenoma, inspect other glands to r/o hyperplasia or another adenoma
4%% have multiple adenomas
15% have diffuse hyperplasia (MEN 1 ot 2a have 4-gland hyperplasia) => don't biopsy all glands b/c risk of hemorrhage, hypo-PTH. resect 3.5 glands or parathyroidectomy + reimplantation
<1% have parathyroid adnenocarcinoma (very high Ca levels) => radical parathyroidecomy including ipsilateral glands
primary hyperparathyroidism:
-ass'd c/ __ oncogene and history of environmental exposure to __
Primary hyperparathyroidism
-PTH >40 pg/mL, Ca >10.5, Cl:PO4 ratio >33, +/-hyperchloremic met acidosis,
-PRAD-1 oncogene, RADIATION exposure increase risk of adenoma
-Older women
-Osteitis fibrosa cystica (brown tumors) = bone lesions 2/2 Ca resorption
-Most pts asymptomatic
-Sx: muscle weakness, myalgia, nephrolithiasis, pacreatitis, PUD, depression, bone pain, pathologic fx, MS change, constipation, N/V, anorexia
-Can get HTN 2/2 renal impairment
5 indications for surgery for hyperparathryoidism
Primary hyperparathyroidism - 5 indications for surgery:
1.Symptomatic dz
2.Asymptomatic + Ca>13
3. Decreased Cr clearance
4. Nephrolithiasis
5. Significantly decreased bone mass

Adenoma (84%) => resection; inspect other glands to r/o hyperplasia or multiple adenomas (4%)
-Hyperplasia (15%) => resect 3.5 glands or total parathyroidectomy + autoimplantation (don't biopsy all glands 2/2 risk of hemorrhage + hypoparathyroid)
-Parathyroid adenocarcinoma (<1%) => radical parathyroidectomy (c/ ipsilateral thyroid)
-Pregnancy => surgery in 2nd trimester to avoid risk of 3rd trimester stillbirth
Lab changes with primary hyperparathyroidism
Primary hyperparathyroidism
-Hyperchloremic metabolic acidosis
-PTH >40 pg/mL
-Ca >10.5
-High renal cAMP (effect on PTH R in kidney)
Cl:PO4 ratio >33
-High urine Ca in 70% (normal in 30%)
Mechanism of propylthiouracil is …
Propylthiouracil (thionamide, along with methimazole):
-Inhibits peroxidases, which connect iodine to tyrosine to form DIT, MIT
-PTU, Propranolol, and Prednisone (steroid) inhibit peripheral conversion of T4 -> T3
-SE: aplasic anemia, agranulocytosis (rare)
-crosses placenta. preferred over methimazole during FIRST trimester only
Pt being treated for hyperthyroidism develops aplastic anemia, agranuocytosis.
-Suspect medication _ or _
Propylthiouracil, Methimazole (thionamides):
-Inhibit peroxidases -> prevents DIT, MIT coupling
-SE: aplasic anemia, agranulocytosis (rare)
-PTU preferred in 1st trimester; may change to methimazole in 2nd-3rd trimester. can cause cretinism.
Pt s/p total thyroidectomy complains of loss of voice pitch
Most likely 2/2 injury to the _ nerve
Recurrent laryngeal nerve injury (e.g. during total thyroidectomy) -> hoarseness
_ nerve innervates all of the larynx except for the _
Recurrent laryngeal nerve:
-Innervates all of larynx except CRICOTHYROID muscle
-Run posterior to thyroid lobes in tracheoesophageal groove
-Can tract c/ inferior thyroid artery, but variable
-L RLN loops around aorta
-R RLN loops around R subclavian = innominate artery, but R is more lateral, more likely than L to be non-recurrent (e.g. 2/2 replaced R subclavian off the descending aorta)
-Risk of injury to non-recurrent laryngeal nerve during surgery
-Unilateral injury -> hoarseness; Bilat injury -> airway obstruction 2/2 medialization of cords, requires emergent tracheostomy
Pt is s/p total thyroidectomy, gets extubated, then experiences severe resp stridor, possible impending resp arrest. No sign of hematoma
Suspect _ -> do _
Bilateral recurrent laryngeal nerve injury during total thyroidectomy -> medialization of cords -> severe resp stridor, possibe resp arrest, very difficult to reintubate
-Do TRACHEOSTOMY via the COLLAR INCISION that was used for thyroidectomy
RET proto-oncogene is ass'd c/ 3 disorders...
RET proto-oncogene
-60% have MEN 2a
-5% have MEN 2b
-35% have familial medullary thyroid ca
Pt presents c/ Ca 8, PTH 200, Cr 7, and bone pain.
-Suspect _
-Tx is _
Secondary hyperparathyroidism:
-Usually dialysis pts c/ chronic Ca loss. Renal osteodystrophy = Al accumulates in bones -> osteomalacia after dialysis x several yrs.
-Elevated PTH, normal Ca
-Rarely requires surgery (subtotal thyroidectomy or total parathyroidectomy + autotransplant)
-Most common surgery indication = bone pain 2/2 Ca resorption
-Tx: control PO4, Ca supplement, vit D. l
After an upper respiratory infection a patient develops fever and a tender thyroid. The most appropriate treatment would be:
This is a typical presentation of Subacute Thyroiditis, the exact cause of which is unknown. This is generally a self-limiting process, however, treatment with corticosteroids or NSAIDS is effective in relieving symptoms.
Pt s/p total thyroidectomy complains of loss of voice pitch
Most likely 2/2 injury to the _ nerve
Superior laryngeal nerve injury (e.g. during thyroidectomy) -> loss of pitch
(motor to cricothyroid. Injury => loss of projection, high pitch)
T3: more or less active than T4?
1/2 life is _
T3: 3x as active as T4
-1/2 life = 3 days
Pt c/ thyroid mass + palpable LN's pre-op is found to have thyroid CA on lobectomy.
What are the indications for MRND?
Thyroid CA + palpable LNs =>
total thyroidectomy + modified radical neck dissection

Indications for MRND = extra-thyroidal dz: capsule invasion, clinical or (+) nodal dz, or mets
How is the Wolff-Chaikoff effect used to treat thyroid storm?
Thyroid storm:
-Sx: increased HR, numbness, irritability, vomiting, diarrhea
High-output cardiac failure = #1 cause of death
-Post-op pt c/ undiagnosed GRAVE'S > precipitated by anxiety, excessive gland palpation, adrenergic stimulants
-Inital tx: beta blockers (ESMOLOL drip), PTU, Lugol's soln (KI), cooling blanketsl O2, lucose, fluid
-Emergent thyroidectomy rarely indicated
-WOLFF-CHAIKOFF effect = give pt high doses of I (Lugol's soln, KI) -> inhibit TSH action on thyroid -> inhibit organic coupling of iodide -> less T3, T4 release
Initial therapy for thryoid storm is _
Thyroid storm:
-Sx: increased HR, numbness, irritability, vomiting, diarrhea
High-output cardiac failure = #1 cause of death
-Post-op pt c/ undiagnosed GRAVE'S > precipitated by anxiety, excessive gland palpation, adrenergic stimulants
-Inital tx = beta blockers (ESMOLOL drip) -> PTU, Lugol's soln (KI), cooling blanketsl O2, lucose, fluid
-Emergent thyroidectomy rarely indicated
-WOLFF-CHAIKOFF effect = give pt high doses of I (Lugol's soln, KI) -> inhibit TSH action on thyroid -> inhibit organic coupling of iodide -> less T3, T4 release
I-131 is indicated for 2 types of thyroid ca...
I-131 - for PAPILLARY & FOLLICULAR thyroid ca. Indications:
-recurrent dz
-primary inoperable tumors 2/2 local invasion
-Papillary c/ extranodal dz
-Follicular >1 cm OR extranodal dz
-For metastatic dz, thyroidectomy facilitates entry of I-131 into metastatic lesions

-can cure bone and lung mets
-done 6 weeks post-op
-SE: sialoadenitis, GI sx, infertility, BM suppression, parathyroid dysfx, leukemia
Best lab test for picking up recurrent papillary or follicular thyroid ca
Follow serum thyroglobulin levels s/p total thyroidectomy for papillary or follicular thyroid ca to detect recurrence
what is the endocrine malignancy associated with von recklinghausen's dz?
von Recklinghausen's = Neurofibromatosis type 1 = #1 phakomatosis.
-Autosomal D, xsome 17. Defined by 2/7 criteria
Cutaneous lesions: 1. CAFE-AU-LAIT SPOTS, 2. neurofibromas, schwannomas, 3. axillary/inguinal/intertriginous freckling
PERIPHERAL NEURAL TUMORS: 4. optic glioma, 5. lisch nodules
Skeletal deformaties: 6. sphenoid dysplasia, long bone cortical thickening
7. 1st deg relative c/ NF1
also have PHEOCHROMOCYTOMA
How is the Wolk Chaikoff effect used in thyroid storm?
Wolk Chaikoff effect:
-High I-doses (lugol's, KI) inhibit TSH
-Useful in thyroid storm