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Surgery Clerkship > Surgical Management of Endocrinopathies > Flashcards

Surgical Management of Endocrinopathies Flashcards

1
Q

Gastrinoma

A
  • Pres: Many peptic ulcers, unusually distal peptic ulcers, or peptic ulcers refractory to PPIs
  • Dx: Elevated gastrin (must be taken off of PPIs) for screening. If gastrin in 4 digits, it is cancer. If it is more mildly elevated, confirm diagnosis with secretin challenge (should turn off healthy gastrin, in cancer gastrin elevates instead). Somatostatin receptor scintillography to locate tumor.
  • Tx: Resect
    • Note: We don’t cut it out because it is milignant, we cut it out because #1 it causes refractory PUD and #2 it can produce other gastric cancers that are malignant.
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2
Q

Insulinoma

A
  • Dx: Wait for quantitative or symptomatic hypoglycemia, then draw labs: insulin, c-peptide, and sulfonylurea screen. If insulin and c-peptide are elevated, you have your diagnosis. Follow-up with CT scan for localization and staging.
  • Tx: IV glucose after taking diagnostic bloodwork. Surgical resection.
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3
Q

“Migratory necrolytic dermatitis”

A

Glucagonoma buzz word

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4
Q

Primary hyperparathyroidism

A
  • Presentation: Elevated Ca, low phos, may present w/ osteofibrosis cystica (aka Brown tumor) and/or bone pain
  • Dx: Sestanibi scan (to tell you which parathyroid is hot)
  • Tx: Cut it out. Then, carefully monitor Ca post-operatively, since other parathyroids may take time to recover. Give IV calcium when necessary until parathyroids recover.
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5
Q

Thyroid nodule management algorithm

A

Note: If first FNA indeterminate, wait 6-12 weeks and repeat (to avoid false positives from reactive changes caused by first FNA)

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6
Q

Parathyroid autofluorescence

A
  • Parathyroid glands possess a unique autofluorescence in the near-infrared spectrum (~820 nm emission)
  • Can be visualized via: Storz laparoscopic near-infrared/indocyanine green (NIR/ICG) imaging system with minor modifications to the xenon light source (filtered to emit 690 nm to 790 nm light, less than 1% in the red and green above 470 nm and no blue light)
  • Post-processing may be utilized to enhance the signal to noise ratio on the display and improve detection
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7
Q

Follicular adenoma vs follicular carcinoma

A
  • Follicular adenoma is a benign thyroid nodule
  • They are quite common in adults
  • Unfortunately, they cannot be differentiated from follicular carcinoma on the basis of cytology (aspiration) alone. This requires a core needle biopsy showing architecture.
    • Note: The same is true of Hurthle cell adenoma vs carcinoma
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8
Q

MEN syndromes

A
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9
Q

Thyroid nodules greater than ___ in size are clinically significant and require further evaluation

A

Thyroid nodules greater than 1 cm in size are clinically significant and require further evaluation

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10
Q

If a biopsy result for thyroid mass returns as medullary thyroid cancer, the next step is. . .

A

. . . MEN2 testing

If MEN2 testing is positive, urine metanephrines should be run to screen for pheochromocytoma. If present, this cancer takes precidence and should be dealt with prior to the medullary carcinoma.

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11
Q

If a patient’s FNAB results are nondiagnostic, the next step is to. . .

A

. . . try FNAB again!

Repeat biopsy will obtain an adequate specimen the second time in 50% of cases

If this second biopsy failed, the surgery is recommended.

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12
Q

Routine tests performed in a patient with a thyroid nodule who is clinically euthyroid

A

TSH and FNA biopsy

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13
Q

The presentation of multiple subcentimeter cystic nodules in the thyroid is. . .

A

. . . common, typically seen in women

These are probably macrofollicles. They can be safely observed with serial ultrasound if TSH is normal.

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14
Q

Most important risk factor for thyroid cancer

A

History of head/neck irradiation

GREATLY increases odds that any thyroid nodule is cancerous

MEN2 A or B is also an important risk factor.

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15
Q

Role of thyroid uptake scan

A

Principally used in the scenario of nodule + hyperthyroidism

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16
Q

Initial step in treatment of a thyroid neoplasm after diagnosis

A

Diagnostic thyroid lobectomy

This is necessary for local staging, which cannot be determined by FNA

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17
Q

Chloride phosphate ratio

A

Cl : Phos > 33 : 1 suggests hyperparathyroidism

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18
Q

Diagnosis and management of FHH

A

Diagnosis is by demonstrating elevated PTH in the context of low urinary calcium plus family history

Management is. . . nothing. It is a benign condition.

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19
Q

Parathyroid hyperplasia vs parathyroid adenoma

A

Parathyroid adenoma is one hot nodule.

Parathyroid hyperplasia involves all four parathyroids.

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20
Q

PTH on renal electrolyte handling

A

PTH increases the excretion of phosphate and bicarb

To maintain electrical neutrality, more chloride is reabsorbed

Hence, elevated chloride : phosphate ratio

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21
Q

Hypercalcemia of malignancy vs primary hyperparathyroidism on electrolytes alone

A

Primary hyperparathyroidism is associated with elevated chloride, while hypercalcemia of malignancy (ectopic 1 alpha hydroxylase) is not.

Both produce hypercalcemia and can produce hypophosphatemia.

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22
Q

Most common metabolic complication of primary hyperparathyroidism

A

Kidney stones!

~1/5 of patients with primary hyperparathyroidism present this way

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23
Q

While primary hyperparathyroidism is the #1 cause of hypercalcemia in the general outpatient population, ___ is the #1 cause of hypercalcemia in hospitalized patients.

A

While primary hyperparathyroidism is the #1 cause of hypercalcemia in the general outpatient population, malignancy is the #1 cause of hypercalcemia in hospitalized patients.

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24
Q

Surgical management of parathyroid hyperplasia

A

Total parathyroidectomy with reimplantation (of 1/2 gland)

OR

Subtotal parathyroidectomy

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25
Q

Surgical management of parathyroid carcinoma

A

En-bloc ipsilateral removal of with thyroid lobectomy and excision of involved soft tissue

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26
Q

Types of acquired parathyroid disease that can cause hypercalcemia

A
  • Primary hyperparathyroidism
  • Tertiary hyperparathyroidism
  • Parathyroid hyperplasia
  • Parathyroid carcioma
    • While most thyroid cancers do not secrete thyroid hormone, most parathyroid cancers do secrete PTH
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27
Q

R and L adrenalectomies are. . .

A

. . . completely different surgeries

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28
Q

Which surgery is higher risk? R or L adrenalectomy?

A

R, because if you accidentally nick the adrenal vein or IVC, the IVC will pour blood into the abdomen

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29
Q

Mnemonic for zones of the adrenal gland

A

GFR

Granulosa, fasciculata, reticularis

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30
Q

Up to __ of adrenal incidentalomas are functional

A

Up to 1/3 of adrenal incidentalomas are functional

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31
Q

Any adrenal incidentaloma ____ needs an evaluation – unless it is ___.

A

Any adrenal incidentaloma > 1 cm needs an evaluation – unless it is an obvious myelolipoma (fatty on imaging).

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32
Q

Best rule out test for Cushing’s

A

1 mg dexamethasone suppression test

Take pill at 11:00, come in for blood test next morning

Then follow with high dose supression test if positive

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33
Q

Assessment of physiologic derangements in Cushing’s

A
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34
Q

Best rule out test for Conn’s

A

Renin:aldosterone ratio

> 30 indicates positive screening

Can’t be measured while on mineralocorticoid receptor antagonists

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35
Q

Pheochromocytoma testing

A

Rule out with plasma metanephrines (> 2x normal is positive)

If positive, confirm with 24 hour urinary metanephrines

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36
Q

Adrenocortical carcinoma

A
  • Poor prognosis
  • No biochemical markers to detect malignancy – criteria for cancer based on imaging findings
    • < 4 cm, can monitor, low risk malignancy
    • > 4 cm, higher risk malignancy, remove by open adrenalectomy
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37
Q

You should NEVER biopsy a patient with an adrenal mass without ruling out. . .

A

. . . pheochromocytoma

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38
Q

Pheochrocytoma rule of 10’s

A
39
Q

Unlike most adrenal masses, pheochromocytomas are ___ on MRI

A

Unlike most adrenal masses, pheochromocytomas are T2 bright on MRI

Since they are so vascular

40
Q

When the diagnosis of pheochromocytoma is made

A
  1. If on a beta blocker, stop it
    • Want to alpha block first
  2. Put on phenoxybenzamine (alpha blocker)
41
Q

In the case of hyperaldosteronism, many patients with adrenal nodule. . .

A

. . . have an incidental adrenal nodule and a non-surgical source of hyperaldosteronism

Might be bilateral hyperplasia, might be familial syndrome, might be myofibrosis, etc.

42
Q

Risks for poor improvement of hyperaldosteronism with surgery on adrenal aldosteronoma

A
  • Male
  • Old
  • Overweight
43
Q

Diagnosis of a gastrinoma

A

Secretin stimulation and serum gastrin measurement

44
Q

Pancreatic neuroendocrine neoplasm syndromes

A
  • Insulinoma: Refractory hypoglycemia with high C peptide and no history of sulfonylurea use.
  • Gastrinoma: Refractory peptic ulcer disease and a metabolic alkalosis
  • Glucagonoma: Diabetes, stomatitis, anemia, and necrolytic migratory erythema
  • VIPoma: Watery diarrhea, hypokalemia, achloyhydria
  • Somatostatinoma: Steatorrhea, cholelithiasis, and diabetes
45
Q

Patient presents with new onset weakness. Weakness is increased upon repetitive motion. What are you likely to find on imaging of this patient?

A

A thymoma

This patient has myasthenia gravis, and 50% of patients with myasthenia gravis have a thymoma, and thymectomy improves MG symptoms in up to 60% of patients with myasthenia gravis

46
Q

Most common anterior mediastinal mass by age and gender

A

Women under age 40: Hodgkin’s and Non-Hodgkin’s lymphoma

Men under age 40: Non-seminomatous germ cell tumors, followed by Hodgkin’s and Non-Hodgkin’s lymphoma

Over age 40: Thymoma

47
Q

Tumor markers for male germ cell malignancies

A

Seminomas tend to be relatively tumor marker poor, while nonseminomatous germ cell tumors having significantly elevated tumor markers (AFP, beta-HCG)

Rather than having tumor markers, seminomas often present with anterior mediastinal mass, so imaging should be performed if suspected.

48
Q

Substernal goiters

A

Thyroid goiters that extend from cervical goiter (or rarely originate in the mediastinum) may present as anterior mediastinal masses

Those which develop de-novo in the mediastinum often have bloodflow directly from the aortic arch and are highly vascular, while those that extend from above are supplied by the typical thyroid vessels.

49
Q

Posterior mediastinal tumors

A

~15% of mediastinal masses in adults, but ~50% in children

Often of neurogenic origin

50
Q

Middle mediastinal masses

A

Often associated with lymphoproliferative disorders such as lymphoma or Castleman’s disease

51
Q

Thymectomy in non-thymomatous myasthenia gravis

A

Utility still unclear.

Some of these patients have thymic hyperplasia on post-surgcial pathology and it is believed that they may benefit. Modest benefits have been shown for certain populations, particularly young female patients with mild disease, however the evidence is not high quality.

52
Q

Diagnosis and treatment for common mediastinal masses

A
53
Q

Staging of thymomas

A

Based upon surgical pathology of margins. As such, surgical resection is necessary for tumor staging and cannot be done prior to surgery.

54
Q

Diagnosis of mediastinal mass

A

FNAs are often preformed first, but are unlikely to yield diagnosis.

Diagnosis is usually made at the time of surgery or based on surgical pathology.

55
Q

Thymoma paraneoplastic syndromes

A
  • Myasthenia gravis
  • Red cell dysplasia
  • Immunodeficiency (Good’s syndrome w/ hypogammaglobulinemia)
  • Collagen vascular disease
    • These are often not resolved with thymectomy
56
Q

Aldosterone and cortisol producing lesions require ___ in order to confirm the utility of surgical resection

A

Aldosterone and cortisol producing lesions require hormone lateralization studies in order to confirm the utility of surgical resection

57
Q

Utility of PET scan in evaluation of an adrenal mass

A

In someone with known metastatic disease, PET can tell you whether an adrenal mass is primary adrenal or a metastasis

58
Q

Etiologies of adrenal incidentaloma that can be ruled out based on CT criteria alone

A
  • Myelolipoma
  • Cyst
  • Hematoma
59
Q

Criteria for adrenalectomy

A
  • Any functional adrenal tumor
  • Nonfunctional adrenal tumors > 4 cm
  • Adrenal tumors that grow by 0.8 cm or more over 1 year
  • Tumors with imaging characteristics suspicious for adrenocortical carcinoma
    • Irregular margins, heterogeneous density, scattered areas of deattenuation, local invasion
  • Suspected oligometastatic disease to the adrenal gland
60
Q

Recommended management for adrenal incidentalomas < 4.0 cm that are proven nonfunctional and nonmetastatic

A
  • Repeat imaging at 3 months and again at 15 months
    • Increase in size by 1 cm is an indication for prompt adrenalectomy
  • In the absence of change during this period, follow annually with history, physical exam.
    • Repeated biochemical testing is reserved for the context of abnormal historical or physical findings
61
Q

Plasma vs urine metanephrines

A

Plasma is more sensitive, but less specific than urine metanephrines

62
Q

When you have an adrenal mass and you are not sure whether or not it is a pheochromocytoma after CT and metanephrines, what can you do?

A

I-131 metaiodobenzylguanidine scan

Used for confirmation or evaluation of nonlocalized pheochromoctyomia. Has specificity of 90-100% for pheos, but is not entirely sensitive.

63
Q

Perioperative evaluation and management for pheochromoctyoma

A
  • CXR (pheos often metastasize to the lungs)
  • EKG and Echo (to rule out cardiomyopathy secondary to chronic catecholamine excess)
  • Manage catecholamine balance:
    • Take off of beta blocker if already on one
    • Add alpha blocker at least 2 weeks prior to surgery (phenoxybenzamine is preferred)
    • Add alpha-methyl-p-tyrosine (competitive inhibitor of tyrosine hydroxylase)
    • Add back additional beta blockade if necessary
64
Q

Intraoperative hemodynamic management of a patient with pheochromocytoma

A
  • They come in already on phenoxybenzamine and alpha-methyl-p-tyrosine
  • Continuous IV nitroprusside drip to control hypertension
  • Esmolol (short acting beta blocker) as needed to control tachycardia
  • After excision when hypotension ensues, continuous IV norepinephrine when fluids are insufficient
65
Q

If a serum metanephrine level comes back mildly elevated, the next step is. . .

A

. . . 24 hour urine metanephrine, normetanephrine, and VMA to confirm elevation.

66
Q

PEDIS for evaluation of diabetic foot wounds

A
  • Perfusion
  • Extent
  • Depth
  • Infection
  • Sensation
67
Q

Initial empiric workup for classic uncomplicated diabetic foot ulcer

A
  • Wound culture
  • Blood culture
  • Empiric antibiotics covering Staph aureus and GAS
    • Pseudomonas as well if necrotic or blue-tinged wound
    • 7-14 day course is recommended in absence of osteomyelitis
    • 4-6 weeks if osteomyelitis present
  • Bed rest
  • Glycemic control
  • Local wound care:
    • ​Sharp debridement
    • Larval therapy
    • Topical agents
68
Q

Motor neuropathy and autonomic neuropathy in diabetic foot disease

A

In addition to the effects of sensory neuropathy, motor and autonomic neuropathy may contribute to the development of diabetic foot ulcers

Imbalance between flexor and extensor groups may cause resting foot deformities or poor fine motor control which increases vulnerability to injuries.

Autonomic neuropathy may cause loss of sweat gland function, skin cracking, soft tissue edema, and osteopenia.

69
Q

Any wound with a visible biofilm generally requires ___

A

Any wound with a visible biofilm generally requires debridement

70
Q

Bunion

A
  • aka Hallux valgus
  • Enlargement of the bony tissue at the base of the big toe
  • Generally associated with angulation of the first toe toward the other toes.
  • Usually in women and related to wearing tight, pointed, confining shoes.
  • Predisposes to injuries in the overlying skin and soft tissue.
71
Q

Hammertoe

A
  • Contracture of the toes (often sparing the big toe)
    • Upward bend of the second to fifth toes at the metatarsal-proximal phalangeal joint
    • Downward bend of the distal toes
  • Produces “clawed toes”
  • Deformity occurs uniformly in women and is due to muscle-tendon imbalance produced by tight shoes with heels
72
Q

Charcot foot

A
  • Type of neuropathic osteoarthropathy
    • occurs mostly in diabetic patients
  • Often difficult to differentiate from diabetic foot infection with osteomyelitis
  • Neurally mediated vascular reflex causes inflammation, increases blood flow and metabolic cahnges in bones in the foot/ankle
    • Risk for fractures and soft tissue trauma
  • Late-stage disease produces “rocker-bottom” deformity (pictured)
  • Treatment involves offloading
73
Q

Offloading

A

Form of treatment strategy for Charcot foot

Affected foot is immobilized in a contact cast to rest injuries and prevent progression of injuries to permanent deformity

74
Q

Diabetic foot ulcers at the tips of the toes are likely to be ___ in origin.

A

Diabetic foot ulcers at the tips of the toes are likely to be vascular in origin.

75
Q

Diabetic foot disease screening by risk stratification

A
  • Low risk: Intact sensation and pulses. Annual exams.
  • Moderate risk: Neuropathy OR absent pulses. Exams every 3-6 months.
  • High risk: Anything more than the above or history of prior ulcers. Exam every 1-3 months.
76
Q

If you suspect that a diabetic foot ulcer may involve osteomyelitis, you should preform ____ for diagnosis

A

If you suspect that a diabetic foot ulcer may involve osteomyelitis, you should preform a gallium scintigraphy scan for diagnosis

Gallium-67 is a radionuclide that binds to acute phase reactants such as transferrin and accumulates in areas of infection and inflammation.

77
Q

Signs of deep space infection in diabetic foot ulceration

A
  • Pain
  • Swelling
  • Wound drainage
    • The above are all indications for imaging studies/wound exploration in the appropriate clinical context
78
Q

Claudication in a diabetic patient

A

May be absent as a clinical indicator of peripheral arterial disease due to diabetic neuropathy!

Therefore, these patients should have screening ABIs or toe-brachial indices at every visit. Keep in mind that these may be falsely elevated due to arterial calcifications.

79
Q

ABI and chronic ulcers

A

In the setting of PAD with ABI less than 0.5, it is highly unlikely that a chronic foot ulcer distal to the involved vessel will heal without revascularization.

If revascularization is not an option, amputation may be required.

80
Q

Recurrent diabetic foot ulcers after antibiotic therapy are highly likely to be ___, even if the first was not.

A

Recurrent diabetic foot ulcers after antibiotic therapy are highly likely to be polymicrobial, even if the first was not.

So if the first one got better with vancomycin, you still have to pull out broad spectrum antibiotics (piperacillin-tazobactam) when it comes back.

81
Q

Brown tumor

A
  • Bone lesion that arises in settings of excess osteoclast activity, such as hyperparathyroidism
    • Consists of mostly fibrous tissue with a high degree of hemosiderin
    • The high level of hemosiderin colors the tumors brown, hence the name
  • They are a form of osteitis fibrosa cystica
  • Most commonly affects the maxilla and mandible, though any bone may be affected
  • Associations:
    • Hyperparathyroidism
    • ESRD osteodystrophy
82
Q

Carcinoid syndrome

A
  • Hallmarks:
    • Episodic flushing
    • Secretory diarrhea
    • Cutaneous telangiectasias
    • Bronchospasm
    • Tricuspid regurgitation
  • Pathophysiology:
    • Tumor (usually in terminal ileum, colon, or lung) that secretes histamine, serotonin, or VIP.
84
Q

Milk-Alkali syndrome

A
  • Hypercalcemia symptoms: Abdominal pain, constipation, polydipsia
  • Due to excessive intake of calcium and absorbable alkali
  • Hypercalcemia causes renal artery vasoconstriction and nephrogenic diabetes insipidus
    • This may be so severe as to cause AKI
  • Often in patients being treated for osteoporosis
85
Q

Extra-osseus manifestations of Paget’s disease

A
  • All due to bone growth/obstruction
    • Headaches
    • Cranial nerve palsies
    • Hearing loss (involvement of ossicles)
86
Q

Paget’s disease on CXR

A
  • May present with osteolytic lesions or mixed osteolytic-osteoblastic lesions, but NEVER osteoblastic lesions
87
Q

Addison’s is sometimes associated with ___ on blood labs

A

Addison’s is sometimes associated with normocytic anemia and eosinophilia on blood labs

89
Q

Labs in Paget’s disease

A
  • High ALK
  • High urine hydroxyproline
  • Relatively normal calcium and phosphate
90
Q

Labs in osteomalacia

A
  • PTH will be high
  • Calcium can be low OR normal
  • Phosphate will be low
  • Vitamin D will be low
91
Q

Hurthle cells

A

Cells found among follicular thyroid cancer OR instead of typical follicular cells (as a subtype of follicular carcinoma)

The cells are large and highly “oxyphilic”, with copious eosinophilic cytoplasmic granules. They also have prominent nucleoli.

92
Q

Medullary thyroid cancer histology

A
  • Stroma contains large amounts of amyloid, and thus stains with Congo red
  • Neuroendocrine appearance with packages of uniform cells
93
Q

Thyroid storm

A
  • Goiter, tremors, and lid lag are specific features
94
Q

Bethesda classification

A
95
Q

Another name for “euthyroid sick syndrome”

A

Low T3 syndrome

Basically describes the main abnormality

96
Q

Mutations that are basically 100% for thyroid malignancy

A

BRAF-V600E mutation (differentiated thyroid cancer)

RET (medullary thyroid cancer)

Surgery Clerkship (42 decks)

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