Surgical Endocrinology

University of Virginia Clinical

Clerkship in Surgery
Peter I. Ellman M.D.
 Plan for Talk
• Review the objectives as outlined by the
Lawrence text.
• Discuss the anatomy, physiology,
pathophysiology, diagnosis and treatment
of thyroid, parathyroid and adrenal gland
disorders.
• Discuss the MEN syndromes.
Objectives for the Thyroid Gland
1. Discuss the evaluation and differential dx
of a patient with a thyroid nodule.
2. List the different types of thyroid cancer,
their cell types of origin, and the
appropriate theraputic strategy for each.
3. Major risk factors for carcinoma of the
thyroid gland and prognostic variables
that dictate therapy.
4. SX of Hyperthyroidism, DDX and TX
 Objectives for the Parathyroid Glands
1. Understand the role of the parathyroid glands in the
physiology of calcium hemostasis.
2. List the causes, symptoms, and signs of
hypercalcemia.
3. Know the difference between 1°, 2°, 4°
hyperparathyroidism.
4. Discuss the evaluation and ddx of a paitent with
hypercalcemia.
5. Understand the management of acute and severe
hypercalcemia.
6. Surgical indications for hyperparathyroidism
7. Complications of parathyroid surgery.
 Objectives for the Adrenal Glands
1. Describe the clinical features of Cushing’s syndrome and discuss
how lesions in the pituitary, adrenal cortex and extraadrenal sites
are distinguished diagnostically.
2. Med and surg mgmt of patients with adrenal adenoma, pituitary
adenoma causing adrenal hyperplasia, and with ACTH producing
neoplasm.
3. Path, clinical features, lab findings, W/U, mgmt. of pt with 1°
aldosteronism.
4. Discuss pheochromocytoma, signs and symptoms, W/U, mgmt.
5. Discuss adrenal cortical carcinoma, assoicated signs and
symptoms, W/U managment.
6. Mgmt. and evaluation of incidentally discovered adrenal mass.
7. Causes of adrenal insufficiency in surgical setting, as well as
clinical and laboratory findings (RECENT JAMA ARTICLE)
 Thyroid Anatomy
• Two lobes in neck, connected by
isthmus at second tracheal ring.
• Embryologic origin at site of
foramen cecum on tongue—
migrates ventral to the hyoid
bone– why people get thyroglossal
duct cyst.
• Arerial supply 2: Superior thyroid
artery via the external carotid and
Inferior thyroid artery via the
Thyrocervical trunk (off the
subclavian).
• Venous drainage 3: through the
superior, middle and inferior
thryoid veins.
 Thyroid Physiology
• Two groups of
hormone producing
cells
– 1: Follicular cells
produce, store and
release T4 and T3
– 2: Parafollicular cells
secrete calcitonin.
 Follicular cells
• Capture iodide from the circulation and
concentrate it and then oxidize it (organification,
occuring in the apical membranes of the cells)
• Tyrosine residues of thyrogolbulin are then
iodinated by oxidized iodides, forming
monoiodotyrosine and diiodotyrosine which then
couple to form T4 and T3-which is then stored.
• When thyroid stimulating hormone (TSH)
stimulates the thyroid, the iodinated
thyroglobulin then is taken into the cell and is
hydrolized to T4 and T3-which is then released
into the circulation.
 TSH
• Besides stimulating the release of T3 and T4,
TSH can stimulate the cell to increase
production of thyroid hormones.
• TSH production is stimulated by Thyrotropin-
releasing hormone (TRH) which is secreted by
the hypothalamus. This intern is controlled by a
feedback mechanism. Increased T3 and T4
have a negative feedback mechanism on TRH
as well as TSH
 The parafollicular (aka C cells)
• Secrete calcitonin which is stimulated by
high serum calcium levels, which inhibits
osteoclast activity, which in turn decreased
calcium levels.
• Total absence of these cells produces no
demonstrable negative physiologic effect!
 Objective T1:W/U of Thyroid Nodule

• Always a thorough H & P (remember for

oral exam).
– Hx of irradiation to the head or neck?
– Family history of MEN syndrome (will get to
this later)
– Carefully palpate the thyroid and regional
lymph nodes.
– How long has nodule been present? Any
associated pain, hoarseness, dysphagia,
dyspnea, or hemoptysis?
 Objective T1:W/U of Thyroid Nodule

• On physical exam:
– Nodule should be carefully examined to
assess size, consitency, extension and
fixation. Single or multiple?
– Is there cervical lymphadenopathy?
– Is there a rapid pulse, tremor, exopthalmos?
– Direct laryngoscopy is important in
preoperative evaluation to assess for vocal
cord paralysis.
 DDX of thyroid nodule
• Benign • Malignant
– Toxic thyroid adenoma – Papillary CA
– Cyst – Follicular CA
– Papillary adenoma – Hürthle Cell CA
– Follicular adenoma – Medullary CA
(most common – Anaplastic CA
adenoma) – Thyroid Lymphoma
• Colloid (macrofollicular)
• Fetal (microfollicular)
– Metastatic
• Embryonal
Carcinoma to the
Throid Gland.
– Hürthle cell adenoma
 FNA
• Fine needle aspiration is the single most important study
in evaluating a thyroid mass.
– Only 3% of patients with a benign dx on FNA have thryoid
cancer, and 85% of nodules identified as malignant on FNA are
cancers at resection.
• 68% to 98% sensitive and 56% to 100% specific.
• Approx 75% are classified as “benign”, 25% as “suspicious” and
5% as “malignant.
• Follow patients with benign dx closely
• Follicular adenomas cannot be distinguished from
follicular carcinoma by FNA and warrants a surgical
exploration--most likely total thyroidectomy.
– do not do frozen section! It has been shown to be notoriously
inaccurate!)
 Other imaging modalities
• Not required for the routine evaluation of the
vast majority of thyroid nodules.
• It is important to try and avoid the use of
iondinated contrast materials preperatively.
– This can impair postoperative tx.
• Hot vs. Cold nodules.
– A technicium thyroid scan may show a “cold” or
hypofunctioning nodule. While it is c/w cancer, it could
also be benign solid or cystic nodule that could be
diagnosed with or even treated with FNA.
 Use of ultrasound
• Good for determining the size, number
and location of thyroid nodules accurately.
• Questionable use as a “screening tool”.
Can increase the rate of finding
incidentalomas.
 Objective T2: List 7 Thyroid
Carcinomas, Cell Types, and Tx.
1. Papillary CA
2. Follicular CA
3. Hürthle Cell CA
4. Medullary CA
5. Anaplastic CA
6. Thyroid Lymphoma
7. Metastatic Carcinoma to the Throid
Gland.
 Papillary CA
• Divided into the papillary, mixed
papillary/follicular and follicular variant of
papillary.
• Most Common Thyroid Malignancies!
• Arises from Follicular Cells
– Histologically associated with fibrosis,
calicifications, squamous metaplasia,
psammoma bodies, lymphatic invasion.
 Papillary CA TX
• Tx is somewhat controversial. At the very least
pt needs ipsilateral lobectomy and
isthmusectomy. Some surgeons recommend
total thyroidectomy. It is important to know that
you don’t just take out the nodule!
• LND for clinically significant nodal disease.
• Surgery is followed by scanning with radioactive
iodine to detect residual normal thyroid tissue as
well as metastatic disease (lungs and bones).
 Follicular CA- Overview

• Increased in regions of the world where

iodine is deficient.
• Dx of malignancy requires that either
vascular or capsular invasion by tumor be
demonstrated.
• Again, FNA and Frozen Section cannot be
trusted. Dx is deferred pending histologic
review.
 Follicular CA—Cell origins
• Come from follicular cells (not surprising)
• On histologic exam there is a paucity of
colloid associated with follicular cells.
• Extra points for knowing that follicular
carcinomas that demonstrate only minor
capsular invasion have a relatively benign
course.
• Vascular invasion indicates more
aggressive behavior.
 Follicular CA- Tx
• Total thyroidectomy is recommended by
many for virtually all patients, particularly
those with lesions larger than 4cm. Some
surgeons may elect to do just lobectomy
and isthmusectomy.
• Adjuvant therapy with radioactive iodine,
as with papillary CA
 Hürthle Cell CA-Overview

• Less common than follicular ca and is often considered a

subset of follicular ca.
• More aggressive
– Higher incidence of metastasis
– Lower survivial rate
• Similar difficulties in preoperative dx like follicular cell
CA, but there may be a linear relationship between
lesion size and malignancy.
– In a study of 57 patients, th chance of malignancy when lesions
are >4cm was 65%, and it was 17% when <1cm
• Cell type is still of follicular cell origin.
 Hurthle Cell CA Tx
• For lesions >4cm, total thyroidectomy
• For lesions <1cm, thyroid lobectomy and
isthmusectomy, with completion
thyroidectomy if the permanent histology
proves to be cancer.
• Follow up radioactive iodine??
 Medullary CA (MTC)- Overview
• Slow growing, but aggressive neuroendocrine
tumor.
– Metastasizes early to lymph nodes, then to liver,
lungs and bones.
• Originates from the parafollicular C cells!!
• 80% of pateints with medullary CA have
sporadic MTC, while in 20% people have an
autosomal mutation in the RET protooncogene.
– RET protooncogene abnormalities are assocated with
the MEN-IIA, MEN-IIB and familial medullary thyroid
cancer (FMTC)
 Presentation and Dx of MTC
• FNA can be diagnostic, especially when
the slides are assayed for calcitonin and
CEA activity. Both are elevated.
• Up to 75% presenting with sporadic MTC
have lymph node mets.
 Tx of Sporadic MTC
• Screen for pheochromocytoma and
hyperparathyroidism (rule out MEN
syndrome)
• Total thyroidectomy with central lymph
node dissection (remember that 75%) and
ipsilateral modified radical neck dissection.
• No role for radioactive iodine.
 Tx of familial forms of MTC
• Got RET?
– Sam Wells, a famously mean surgeon from Duke,
then Wash U. famously showed that there is a role for
prophylactic thyroidectomy could be beneficial after
DNA testing of patients at risk.
– Children with MEN IIA should undergo thyroidectomy
at 5-6 years of age.
• Routine central neck dissection has been advocated, but no
lateral LND.
– Children with MEN IIB have the most aggressive form
of MTC. Total thyroidectomy should be performed
ASAP, preferably before the age of 2.
 Post surgical care for MTC
• Often have persistently high levels of calcitonin.
• This often will necessitate repeated aggressive
neck dissection to root out any residual tissue.
However, only 38% of these patients will
eventually be normalized. These patients often
have occult distant mets. Laparoscopic
evaluation of the liver has been recently adopted
prior to neck dissection.
• Note that this is a slow growing tumor and
patients with incurable metastatic disease can
often live for decades.
• Radiation may have a role, chemo does not.
 Anaplastic CA
• Rare– BAD NEWS
• Patients present with rapidly expanding neck
mass, often with aggressive invasion of local
structures, often with airway compromise.
• Derive from de-differentiated follicular
adenoma/carcinoma.
• Surgery is often not possible, and thus
Chemotherapy and Radiation is the current
treatment.
 Thyroid Lymphoma

• Like anaplastic ca, presents as a rapidly

enlarging neck mass.
• FNA combined with flow cytometry shows
a monoclonal population of lymphocytes.
• Tx is radiotherapy and chemotherapy.
• Studies involving surgical debulking have
failed to show any benefit.
Metastatic Carcinoma to the Throid
Gland
• Not as uncommon as you might think.
• Autopsy series demonstrate 1% to 24% of
patients who die of extrathyroidal
malignancies. 5-7% are clinically
significant.
• Most often from Renal Cell CA (50% of
cases)
• There is a role for resection of these mets
in some patients.
 Objective T3-Risk factors for Thyroid CA

• Hx of irradiation to the head and neck in

childhood (used to be for tonsils, enlarged
adenoids or thymus, even acne!), nuclear
accidents
• Iodine deficiency (goiter)
• Female predominance 3:1
• More virulent in elderly patients
• Genetic (MEN syndromes, FMTC)
• Hashimoto’s thyroiditis (lymphoma)
• Previous ca (particularly RCC)
 Objective T4 Sx and Tx of
Hyperthyroidism
• Causes
– Exogenous hormone
– Subacute thyroiditis
– Postpartum thyroiditis
– Iodine induced hyperthyroidism
– Struma ovarri
– Functional metastatic thyroid carcinoma
– Three that are Surgically Treated ARE:
1. Grave’s disease
2. Toxic multinodular goiter
3. Autonomously functioning toxic adenoma
 Grave’s disease
• Autoimmune disease
• Clinical symptoms (of hyperthyroidism)
– Palpitations, sweating, intolerance to heat,
irritability, insomnia, nervousness, weigh loss,
fatigue
• Signs
– Bruit over the gland, tremors, arrhythmias
• Exopthalmos, edema of eyelids, pretibial
edema.
 Toxic Multinodular Goiter
• Enlargement of the thyroid glands over a
long period of time.
• Treatment is medically initially, but the
preferred treatment is surgical.
• In setting of bilateral multiple nodules, total
or near total thyroidecomy is indicated.
• If nodules are predominantly on one side,
then ipsilateral lobectomy and
ithmusectomy are probably adequate.
 Solitary Toxic Adenoma
• Patients presenting with thyrotoxicosis and
a dominant thyroid nodule.
• Elevated T3, T4 and a suppressed TSH
level.
• Tx is administration of 131I or surgery.
• Surgery is recommended for younger
patients with moderate size to large
nodules.
• Lobectomy is usually adequate
 Grave’s disease Tx
• Medical for initial treatment.
– Antithyroid drugs (propylthiouricil, iodine)
– Recurrence is high if drugs are stopped
• Surgical treatment
– Bilateral total or near-total thyroidectomy
– Pts will now need thyroid replacement for the
rest of their life.
 Parathyroid Gland Anatomy
• Paired organs, normally with 2
on the posterior surface of
each thyroid lobe.
• Embryologic development from
3rd (inferior parathyroid gland
with thymus) and and 4th
(superior parathyroid gland
and C cell precursors)
pharyngeal pouches.
• Art supply from inferior thryoid
arteries.
• Superior gland is usually
posterior and lateral to the
recurrent laryngeal nerve.
• Inferior is anterior and medial
to the recurrent laryngeal
nerve.
Ob P1- parathyroid glands and the physiology of calcium hemostasis.

• Synthesize and secret parathyroid hormone,

which along with vitamin D maintains calcium
hemostasis.

Calcium PTH

Bone resorption, Renal resorption

urine phosphorus
 List the causes, symptoms, and signs of hypercalcemia.

• Stones
– Nephrolithiasis
• Bones
– Painful resorption of bone
• Moans and Psychatric overtones
– Fatigue, depression, confusion
• Abdominal groans
– Peptic ulcer and pancreatitis
 Know the difference between 1°, 2°, 4°
hyperparathyroidism.

• Primary Hyperparathyroidism
PTH calcium (normal renal function)
–83% parathyroid adenoma, 15% parathyroid
hyperplasia, carcinoma is rare 1-2%
• Secondary Hyperparathyroidism
poor renal function calcium, PO4 PTH
normal Ca
• Tertiary Hyperparathyroidism
Hyperplastic parathyroids from chronic
stimulation continue post renal transplant
 Discuss ddx of a paitent with hypercalcemia.
• Hyperparathyroidism
• Malignancy
– Hematologic
– PTHrP producer
• Hyperthyroidsm
• Multiple myeloma
• Sarcoidosis
• Milk-alkili syndrome
• Vit D or A intoxication
• Paget’s disease
• Immobilization
• Thiazide diuretics
• Addisonian Crisis
• Familial hypocalcuric
hypocalcemia
• Neonatal severe
hyperparathyroidism.
 Evaluation of Hypercalcemia
• Send off PTH levels to diagnose primary
versus other causes.
• 24 hour urine calcium measurement and
chloride to phosphate ratio (>33)
• X-rays are diagnostic for Paget’s disease
• EKG– will classically show shortened QT
and prolonged PR interval. Check rate for
bradycardia.
 Understand the management of acute and severe hypercalcemia.

• Mainstay of management is:

1. admittnance to hospital (severe is considered
asymptomatic with >3.2mmol/L, or
symptomatic patient)
2. Expand Volume with NSS or LR (500 ml bolus
STAT)
3. Diurese with loop diuretics
4. Other meds may be started (bisphosponates,
calcitonin, mithramycin ect.)
 Indications for surgery
• Nephrolithiasis, bone disease, and
neuromuscular symptoms respond well to
surgery.
• Primary hyperparathyroidism due to adenoma is
cured surgically by excision of the adenoma. All
four glands must be identified though!
• Primary hyperparathyriodism due to parathyroid
hyperplasia is treated with subtotal
parathyroidectomy (3 1/2) or total
parathyroidectomy with autotranspantation into
the arm.
 Surgical indications for
asymptomatic hyperparathyroidism
• On initial evaluation • Following asymptomatic
– Markedly elevated CA pt
– Pt becomes symptomatic
– Hx of life threatening
– Ca 1-1.6 mg/100 ml above
hypercalcemia (??) normal
– Reduced Cr CL. – Nephrolithiasis
– Nephrolithiasis – Decline in bone mass
– Markedly elevated – Neuro or psych problems
24hr U Ca – Pt desire to fix.

– Substantially reduced
bone mass
 Complications of parathyroid surgery.

• Hypocalcemia
• Persistent hypercalcemia
• Recurrent laryngeal nerve injury
 Adrenal anatomy
• Paired structures living superior to the kidneys.
They are flat and triangular, about 5 grams
• Arterial supply (3 each)
1. Superior adrenal off inf. phrenic A.
2. Middle adrenal off the aorta
3. Inferior adrenal arising off the enal A.
• Venous supply (one major on each)
1. Right adrenal vein drains into vena cava.
2. Left adrenal vein drains into the left renal vein
 Cortex and Medulla
• Cortex- mesodermal in origin
– Zona glomerulosa
• Production site of aldosterone
– Zona fasiculata
• Production site of cortisol and sex steroids
– Zona reticularis
• Production site of cortisol, androgens and estrogens.
• Medulla-ectodermal in origin
– Production center of catecholemines epinephrine and
norepinephrine.
Describe the clinical features of Cushing’s syndrome and discuss how
lesions in the pituitary, adrenal cortex and extraadrenal sites are
distinguished diagnostically.

• Cushing’s syndrome (not to be confused with Cushing’s disease!

(you know this)
– muscle wasting
• Steroidal proteolysis
– truncal obesity
• differential insulin and steroid receptors
– Htn
• Glucocorticoid effects on the heart, kidneys ect.
– ostoporosis
• Steroidal effects on bone growth
– infection
• immunosuppression
– striae and poor wound healing
• Suppresion of scar contraction and inflammatory response
– Hyperglycemia
• decreased peripheral use of glucose and increased gluconeogenesis.
 DDX of Cushing’s Syndrome
• Iatrogenic
• Cushing disease (pitutary ACTH excess—
70% of Cushing’s syndrome)
• Ectopic ACTH production-15%
• Adrenal adenoma or carcinoma- 15%
• Micronodular pigmented hyperplasia
• Macronodular pigmented hyperplasia
• Steroid dependent adrenal hypeplasia
 How lesions in the pituitary, adrenal cortex and
extraadrenal sites are distinguished diagnostically

• First confirm that the patient has

hypercortisolism.
– Start with plasma cortisol on multiple venous
samplings (get at 6am and 8pm)
– Diurnal variation in pituitary adenomas and
adrenal tumors.
– Can also get 17-OH corticosteroid
measurments in the urine.
– Measurment of urinary free cortisol
How lesions in the pituitary, adrenal cortex and extraadrenal sites are
distinguished diagnostically-CONT
Plasma ACTH levels can be helpful in determining

Type of ACTH after high CRH

Plasma dose
Cushing’s Dexamethasone stimulation
ACTH Level
syndrome Test test
Highly increased
Pituitary NL to cortisol compared to
normal
increased
Adrenal Low or
undetactable
Ectopic ACTH Increased
producing
tumor
 How lesions in the pituitary, adrenal cortex and
extraadrenal sites are distinguished diagnostically-CONT

• CT and MRI of head can image pituitary tumors

• Ectopic Cushings syndrome represents
approximately 15% of the cases and is more
common in men
– Most commonly oat cell ca of lung (thus chest film
can be diagnostic), but can also occur with bronchial
carcinoids, thymomas, and tumors of the pancreas.
• CT of adrenals is a good first imaging study of
the adrenals.
– Other fancier tests exist
 Med and surg mgmt of patients with adrenal adenoma, pituitary
adenoma causing adrenal hyperplasia, and with ACTH producing
neoplasm

• Medical management
– Metyrapone and aminoglutethimide inhibit enzymes of
the adrenal steroidogenic pathway. Not satisfactory
for long term.
– Mitotane is a chemotheraputic that is effective 30 to
70 percent of the time in decreasing steroid output in
malignant functioning adrenocortical lesions.
– Nonoperative treatment for congenital adrenal
hyperplasia (steroid dependent)
• Cortisone acetate is sufficient.
• If mineralocorticoid is needed, Florinef works.
 Surgical treatment
• Pituitary Cushings
– Transsphenoidal resection for pituitary adenoma is
treatment of choice.
– Pituitary irradiation has been shown to effective in
80% of children.
• Adrenal Cushings
– Total adrenalectomy of the affected gland
• Ectopic Cushings
– Tx is directed towards the underlying neoplasm
secreting ACTH
 Path, clinical features, lab findings, W/U, mgmt. of pt with
1° aldosteronism

Effects of Aldosterone Secretion

Tubular Action Normal amounts Excessive Amts

resorption protects against low •positive sodium

of Na+ volume states balance
•hyporeninemia
•met alk
• htn
•hyperglycema
•noctura
protects against •muscle weakness
resorption hyperkalemia
of K+
 Primary aldosteronism DDX and
DX

• DDX
– adenoma
– Primary hyperplasia of the zona glomerulosa
– Adrenal carcinoma
 Dx of Aldosteronism
• Serum tests
– Potassium is low, Renin is Low
• Urine tests
– Potassium excretion is high
– Aldosterone exretion is high
• Confirming tests—plasma and urinary
aldosterone suppression tests.
– 2,000 ml NSS over 4 hour period should
suppress.
 DX of Aldosteronism cont.
• Very important to distinguish aldosterone
producing adenoma from hyperplasia of Zona
glomerulosa since surgery only works for one!
– Postural stimulation
• Aldosterone and renin are measured in recumbent position
and then 2-4 hours after ambulating
– Renin remains suppressed in adenomas
– 18-hydroxycorticosterone is increased in patients with
adenomas but remains normal in those with
hyperplasia.
– Venous sampling, CT scan may lateralize
 Tx of Aldosteronism
• Medical
– Spironolactone
• Inhibits sodium-postassium exchange in the distal
tubule, normalizes serum K and may lower blood
pressure.
• Surgical
– Total adrenalectomy of involved gland
– It is important to resore potassium levels
preoperatively.
Discuss pheochromocytoma, signs
and symptoms, W/U, mgmt
• Overview
– Funcionally active tumors- producing epinephrine and
norepinephrine
– 90% are benign, 10% are malignant
• 10% Rule
– Malignant, bilateral, extra-adrenal, multiple, familial, children.
– 90% are found in the adrenal medulla
– Of extra-adrenal, most are found in the organs of
Zuckerkandl, extra-adrenal paraganglia, urinary
bladder, and mediastinum
 Signs and symptoms of pheo
• Hypertension
– 50% sustained
• Can have paroxysms of more severe hypertension
superimposed.
– 50% intermittent
• Sweating, headiaches, palpitations,
tremor, nervousness, weight loss, fatigue,
abdominal or chest pains, polydipsia and
polyuria, convulsions
 Workup of pheochromocytoma
• Urinary metanephrines and VMA are
elevated in 90% to 95% of cases.
• Fractionated urinary and plasma
catecholamine levels can increase the
accuracy of the dx to nearly 100%
• CT and MRI (accurate in 95%)
• Scintigraphy and vena cava sampling for
that extra hard to find lesion
 Preparation for surgery
• Adrenergic blockade
– Preop control of htn
– Reduces risks of dramatic pressure swings
– Provides vasodilation, allowing restoration of
normal blood volume
• Alpha blockade with Phenoxybnzamine 2
weeks prior to surgery. (40mg/day)
• Beta blockade with propranolol 3 days
prior to surgery (40mg/day)
 Operation of pheo
• Arterial and Central venous monitoring
• Transabdomial approach.
• Total adrenalectomy
Discuss adrenal cortical carcinoma, assoicated signs and
symptoms, W/U managment

• Poor prognosis
• 5 year survival rate of 20% to 25%
• Signs and symptoms would be related to
adenomatous precursor or asymptomatic.
 Mgmt. and evaluation of incidentally discovered adrenal
mass

• Adrenal incidentalomas <5cm do not

require resection.
• Negative predictive value for primary
adrenal carcinoma in adrenal masses
<6cm as measured on CT scans ranges
from 96% to 99%.
• Additional tests are not necssary.
 Causes of adrenal insufficiency in surgical setting, as well as clinical
and laboratory findings (RECENT JAMA ARTICLE)
• Causes of postoperative primary adrenal insufficiency include
– Autoimmune disease, TB, fungal disease, malignancy,
AIDS, and drug suppression. Hemmorhage is a common
cause in the ICU
• Secondary causes (decreased ACTH) include:
– suppresion by glucocorticoid therapy, ACTH secreting
tumors, pituitary operation, irradiation, head trauma.
• Clinical findings– anorexia, malaise, hypoglycemia,
hypotension:
– Low CO and high SVRI or High CO and low SVRI
• Dx is by measuring free cortisol and cosyntropin stim.test
• Tx is with fluids and steriods (dexamethasone followed by
hydrocortisone)
• Recent study in JAMA
 MEN Type I (Wermer’s syndrome)
• Hyperparathyroidism
– 90% of patients, mostly hyperplasia of multiple
glands.
• Pituitary tumors
– 65%--Usually chromophobe adenomas
• Producing acromegaly, galactorrhea, anmenorrhea, or
Cushing’s
• Pancreatic tumors
– 80% of cases
• Non-beta islet cell tumors causing the Zollinger-Ellison
Syndrome
 MEN IIA (Sipple’s syndrome)
• Hyperparathyroidsim
– 60% of patients (shares this in common with
MEN I)
• Medullary thryoid carcinoma
– Occurs in ALL PATIENTS
• Pheochromocytomas
– Occur in 40%, are usually bilateral,
occasionally are malignant.
 MEN IIB
• Medullary thyroid carcinoma (like II A)
• Pheochromocytoma (like IIA)
• No hyperparathyroidism
• Addition of mucosal neuromas on tongue,
eyelids, lips, pharynx.
• Presents at a much earlier age
• Marfanoid habitus, kyphosis, pectus excavatum
• Hirshprung’s disease
Objectives for the Thyroid Gland
1. Discuss the evaluation and differential dx
of a patient with a thyroid nodule.
2. List the different types of thyroid cancer,
their cell types of origin, and the
appropriate theraputic strategy for each.
3. Major risk factors for carcinoma of the
thyroid gland and prognostic variables
that dictate therapy.
4. SX of Hyperparathyroidism, DDX and TX
 Objectives for the Parathyroid Glands
1. Understand the role of the parathyroid glands in the
physiology of calcium hemostasis.
2. List the causes, symptoms, and signs of
hypercalcemia.
3. Know the difference between 1°, 2°, 4°
hyperparathyroidism.
4. Discuss the evaluation and ddx of a paitent with
hypercalcemia.
5. Understand the management of acute and severe
hypercalcemia.
6. Surgical indications for hyperparathyroidism
7. Complications of parathyroid surgery.
 Objectives for the Adrenal Glands
1. Describe the clinical features of Cushing’s syndrome and discuss
how lesions in the pituitary, adrenal cortex and extraadrenal sites
are distinguished diagnostically.
2. Med and surg mgmt of patients with adrenal adenoma, pituitary
adenoma causing adrenal hyperplasia, and with ACTH producing
neoplasm.
3. Path, clinical features, lab findings, W/U, mgmt. of pt with 1°
aldosteronism.
4. Discuss pheochromocytoma, signs and symptoms, W/U, mgmt.
5. Discuss adrenal cortical carcinoma, assoicated signs and
symptoms, W/U managment.
6. Mgmt. and evaluation of incidentally discovered adrenal mass.
7. Causes of adrenal insufficiency in surgical setting, as well as
clinical and laboratory findings (RECENT JAMA ARTICLE)
 To really get it down
• Have a “friend” pimp you mercilessly on
the oral exam questions they have at the
end of the chapter (tonight preferably)
That’s it. Thanks for listening!