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GENSURG ROTATION > Endocrine Surgery > Flashcards

Endocrine Surgery Flashcards

1
Q

Most common pitutiary adenoma

A

prolactinoma

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2
Q

What mass effects can a pitutitary macroadenoma have?

A

Mass effects (e.g., headache, bitemporal hemianopsia due to compression of the optic chiasm, diplopia)

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3
Q

Acromegaly is a condition in which benign pituitary adenomas lead to an excess secretion of _____________________ and ______________________

A

Acromegaly is a condition in which benign pituitary adenomas lead to an excess secretion of growth hormone (GH) and insulin-like growth factor 1 (IGF-1).

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4
Q

The first step in diagnosing acromegaly is to measure__________________.

A

IGF-1 levels

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5
Q

An anabolic polypeptide hormone produced primarily by the liver in response to growth hormone. Stimulates cell growth and proliferation.

A

Insulin-like growth factor 1

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6
Q

Action of IGF-1in acromegaly

A

Binding to IGF-1 and insulin receptors → stimulation of cell growth and proliferation, inhibiting programmed cell death
Proliferative effects especially on bone, cartilage, skeletal muscle, skin, soft tissue, and organs
Impaired glucose tolerance caused by binding to insulin receptors

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7
Q

What diagnostics do we use to help dx acromegaly?

A

Serum IGF-1, oral glucose tolerance test, pitutitary MRI

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8
Q

What are some etiologies of goiter?

A

Iodine deficiency (leading cause of goiter worldwide)

Inflammation (e.g., Hashimoto thyroiditis, subacute granulomatous thyroiditis)

Graves disease

Thyroid cysts (e.g., thyroglossal cyst)

Thyroid adenomas

Thyroid carcinomas

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9
Q

What are some major causes of toxic goiter?

A

Graves and toxic multinodular goiter

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10
Q

What are some causes of hypothyroid goiter?

A

Hashimotos and congenital hypothyroid goiter

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11
Q

Three major causes of hyperthyroid

A

graves, toxic multinodular goiter, toxic adenoma

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12
Q

A transient and self-resolving patchy inflammation of the thyroid gland that is associated with granuloma formation. Often occurs after a viral upper respiratory infection and is more common among women. The clinical course is typically triphasic, beginning with hyperthyroidism, followed by hypothyroidism, and finally a return to the euthyroid state. Classically presents with tender goiter, elevated ESR, and jaw pain.

A

Subacute granulomatous thyroiditis

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13
Q

How would a thyroid impacted by graves present on iodine uptake scan?

A

Diffuse uptake of radioactive iodine

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14
Q

What are the anti-thyroid meds?

A

Methimazole and propylthiouracil, we use propylthiouracil for thyroid storm or first trimester pregnancy

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15
Q

TSH receptor autoantibodies stimulate the thyroid gland

A

Graves disease

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16
Q

B and T cell-mediated autoimmunity → production of stimulating immunoglobulin G (IgG) against TSH-receptor (TRAb; type II hypersensitivity reaction) →

A

↑ thyroid function and growth → hyperthyroidism and diffuse goiter

This is the pathophys of graves

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17
Q

What is this autoimmune reaction mostly associated with:
TSH autoantibodies are present in the orbital cavity (eye socket) → bind TSH receptor antigen (autoimmune reaction) on cells → lymphocytic infiltration into the orbital tissues → inflammation and release of cytokines from CD4+ T cells → stimulates fibroblasts to secrete glycosaminoglycans (hyaluronic acid), which also pulls water into the interstitial space (osmotic effect) ; → expansion of retro-orbital tissue

A

This is thyroid associated orbitopathy and it is often associated with graves, note that the presentation is not due to hyperthyroidism

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18
Q

What antibody markers do we look for in graves disease?

A

elevated TSH receptor antibodies or TRAbs

Other antibody markers of thyroid disease include anti-TPO and thyroglobulin antibodies (TgAbs), note that Antithyroid peroxidase antibodies (anti-TPO) and thyroglobulin antibodies (TgAbs) can be elevated in all forms of autoimmune thyroid disease and are not specific to Graves disease.

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19
Q

Secondary hypothyroid and tertiary hypothyroid can be caused by…

A

secondary–> think pituitary disorders like an dadenoma

tertiary–_ think hypothalamic disorders like a TRH deficiency

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20
Q

Red flags fro thyroid cancer?

A

male sex, hx of radiation to head or neck, fam hx of MEN2 or diffreentited thyroid cancer (papillary, follicular, or medullary). In addition to red flags for thyroid cancer, a solid nodule on thyroid ultrasound or a cold nodule on thyroid scintigraphy should raise suspicion for thyroid cancer.

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21
Q

Is the following likely to be benign or malignant:

A

Malignancy is rare in hyperfunctioning (hot) nodules.

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22
Q

How common are thyroid nodules and how likely are they to be benign or malignant?

A

50% of the population has nodules, 95% are benign % are malignant

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23
Q

Most common type of thyroid cancer

A

Papillary thyroid carcinoma

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24
Q

Thyroid cancer type seen in MEN2

A

medullary carcinoma

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25
Q

___________________________ is the most Prevalent type of thyroid cancer, it features Palpable lymph nodes, and it has the best Prognosis compared to all other types of thyroid cancer.

A

Papillary carcinoma

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26
Q

Calcitonin is a marker for which thyroid cancer?

A

Medullary, calcitonin secreted by parafollicular cells, which is the tissue of origin of medullary carcinoma

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27
Q

Dysphonia (hoarseness) and/or dysphagia: as a result of transection of the __________________ and ___________________

A

superior and recurrent laryngeal nerve

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28
Q

What structures do we have to keep in mind for thyroid surgery?

A

superior and recurrent laryngeal nerve, superior laryngeal artery and inferior thyroid artery

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29
Q

What are some complications of thyroid surgery?

A

Transient/permanent postoperative hypoparathyroidism (most common)

Transient/permanent RLN palsy

Superior laryngeal nerve palsy

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30
Q

In the evaluation of thyroid nodules, what is the next step after thirough hx and PE?

A

TSH

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31
Q

In the evaluation of thyroid nodules, if TSH is subnormal, what is the next step?

A

Scintigraphy

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32
Q

In the evaluation of thyroid nodules, if TSH is normal or elevated, what is the next step?

A

FNA if criteria met or monitor

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33
Q

second most common type of thyroid cancer

A

follicular thyroid cancer

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34
Q

____________thyroid cancer is characterized by hematogenous spread (most commonly to the lungs and bones) and lymph node involvement is rare

A

Follicular

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35
Q

Fine-needle aspiration findings of Psammoma bodies and “Orphan Annie” nuclei (clear, ground-glass, empty nuclei) in a thyroid nodule indicate a _______________

A

papillary microcarcinoma.

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36
Q

_____________________arise from a gain-of-function mutation in the TSH receptor gene that causes autonomous functioning of the TSH receptor independent of hypothalamic-pituitary regulation. Without negative feedback, the thyroid follicular cells become hyperplastic and eventually form…

A

Toxic adenoma/s

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37
Q

60% of pts with acromegaly get cardiovascular complications such as ______________________, ____________________, and __________________.

A

Cardiovascular complications such as hypertension, concentric ventricular hypertrophy, and arrhythmias are the most common complications and the cause of death in ∼ 60% of patients with acromegaly.

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38
Q

___________________ is the most common cause of hypothyroidism in the US and a risk factor for primary thyroid lymphoma.

A

Hashimoto thyroiditis

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39
Q

Among the treatment options for Graves disease, ______________ has the lowest recurrence rate.

A

radioactive iodine ablation (RAIA)

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40
Q

is a catecholamine-secreting tumor that typically develops in the adrenal medulla.

A

Pheochromocytoma

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41
Q

increased blood Pressure, head Pain (headache), Perspiration, Palpitations, and Pallor

A

Pheocrhomocytoma

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42
Q

Presentation of pheochromocytoma

A

3rd-5th decade of life, episodic blood pressure crises with paroxysmal headaches, diaphoresis, heart palpitations, and pallor. Pheochromocytomas may also be asymptomatic or manifest with persistent hypertension.

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43
Q

What is primary hyperaldoteronism?

A

is an excess of aldosterone caused by autonomous overproduction. It is typically due to adrenal hyperplasia (most commonly bilateral) or adrenal adenoma (typically unilateral).

44
Q

How does hyperaldosteronism lead to electrolyte abnormalities?

A

High systemic aldosterone levels result in increased renal sodium reabsorption and potassium secretion, which lead to water retention and hypokalemia.

45
Q

What are the signs/manifestations of hypokalemia that you might be looking for in a pt with primary hyperaldosteronism?

A

headache, muscle weakness, and polyuria

46
Q

How does hyperaldosteronism impact renin?

A

It results in low plasma renin activity

47
Q

What are some pharmacotherapies we can use in hyperaldosteronism?

A

Spironolactone and eplerenone (aldosterone antagonists)

48
Q

is caused by autonomous overproduction of aldosterone in the zona glomerulosa of one or both adrenal glands

A

Primary hyperaldosteronism (Conn syndrome)

49
Q

How does primary aldosteronism lead to hypertension?

A

↑ Aldosterone → ↑ open Na+ channels in principal cells of luminal membrane at the cortical collecting ducts of the kidneys → ↑ Na+ reabsorption and retention → water retention → hypertension

its a hyptertensive hormone!

50
Q

How does hyperaldosteronism lead to a metabolic alkalosis?

A

↑ Na+ reabsorption → electronegative lumen → electrical gradient through open K+ channels → ↑ K+ secretion → hypokalemia
Hypokalemia → metabolic alkalosis via two mechanisms (both of which decrease extracellular H+, thereby increasing extracellular pH):
Efflux of K+ from intracellular to extracellular space in exchange for H+
↑ H+ secretion in the kidney in order to enable ↑ K+ reabsorption

51
Q

Hypokalemia and drug resistant hypertenison is the hallmark of…

A

primary hyperaldosteronism

which is caused by idipathic adrenal hyperplasia or an aldosteronoma

52
Q

How might you be able to tell the difference between primary or secondary hyperaldoseronism?

A

The relationship between plasma aldosterone concenrtration and plasma renin activity (aldostereone-renin-ration ARR)

Primary: primary hyperaldosteronism have elevated aldosterone levels (PAC) that cause decreased renin activity (PRA), resulting in an elevated ARR. [(↑ PAC/↓ PRA) = ↑↑ ARR]

Secondary: ↑ PAC and ↑ PRA

53
Q

Defective HFE gene leading to defective binding of transferrin to its receptor and then decreased hepcidin synthesis by the liver

A

Hemochromatosis type 1

54
Q

This has little to do with endocrine surgery but I just learned this and its cool: what leads to anemia of chronic disease?

A

Hepcidin is an acute phase reactant released by the liver that decreases iron absorption by binding and degrading ferroportin on intestinal mucosal cells and macrophages, which inhibits iron transport. Levels are increased in patients with chronic inflammation, which causes anemia of chronic disease.

more hepcidin means less iron transport

55
Q

What liver, heart, and endocrine problems does hemochromatosis cause?

A

Liver: cirrhosis
Heart: restrictive cardiomyopathy
Endocrine: pitutitary dysfuntion, diabetes mellitus

56
Q

What labs help us dx hemochromatosis?

A

↑ Serum ferritin
↑ Transferrin saturation
↑ Serum iron
↓ Total iron-binding capacity

57
Q
A

Hemosiderin (normally golden yellow on microscopy) appears blue with the Prussian blue stain.

Seen in pts w/iron overload, hemochromatosis

58
Q

How do we treat hemochromatosis?

A

therapeutic phlebotomy, iron chelating therapy (Chelating agents: deferoxamine, deferasirox, or deferiprone)

59
Q

_____________ are small, slow-growing neuroendocrine tumors. They are most commonly located in the gastrointestinal tract and can synthesize a variety of hormones (especially serotonin).

A

Carcinoid tumors

60
Q

Why are most carcinoid tumors asymptomatic?

A

Carcinoid tumors produce hromones but the tumors tend to be located in the GI trat so the hormones they produce get shunted to the liver and are matabolized by first pass effect in the liver.

61
Q

What are the features/symptoms/signs of carcinoid syndrome?

A

diarrhea, flushing, dyspnea, wheezing

62
Q

If a pt is experiencing carcinoid syndrome, what does this tell you about the location of the tumor?

A

It has likely metastasized to the liver so now the hormones bypass first pass metabolism

63
Q

What marker is commonly lookd for in carcinoid tumors?

A

5-HIAA (A degradation product of serotonin metabolism. Elevated levels in 24-hour urine are seen in carcinoid tumor)

64
Q

What are somatostatin analogs used to treat?

A

A group of drugs that are used to treat acromegaly, carcinoid syndrome, and esophageal variceal bleeding. Examples include octreotide and lanreotide.

65
Q

The most common cause of endogenous hyperinsulinism and are benign in 90% of pts

A

insulinoma

66
Q

Insulinomas arrise from

A

pancreatic beta cell tumors

67
Q

What would you expect to see in insulin and c-peptide levels in a hypoglycemic pt w/an insulinoma?

A

Insulin and c-peptide elevated

68
Q

What would you expect to see in a 72 hr fasting test in a pt w/ an insulinoma in terms of insulin and glucose?

A

LOW glucose, HIGH insulin!

69
Q

a gastrin-secreting neuroendocrine tumor and is most often located in the duodenum and pancreas

A

This would be a gastrinoma also called zollinger ellison syndrome

70
Q

Hypergastrinemia → stimulation of parietal cells → gastric acid hypersecretion, which leads to:
Peptic ulcer disease
Inactivation of pancreatic enzymes → diarrhea, steatorrhea → malabsorption

This describes….

A

zollinger-ellison (gastrinoma)

71
Q

How may a gastrinoma lead to peptic ulcers and malabsorption?

A

Hypergastrinemia → stimulation of parietal cells → gastric acid hypersecretion, which leads to:
Peptic ulcer disease
Inactivation of pancreatic enzymes → diarrhea, steatorrhea → malabsorption

72
Q

To confirm a gastrinoma, what would we expect on fasting serum gastrin and gastric pH?

A

FSG > 1000 pg/mL and gastric pH < 2: gastrinoma is confirmed

73
Q

Are gastrinomas malignant?

A

50% are

74
Q

is caused by an altered menin protein expression and presents with primary hyperparathyroidism, often in association with endocrine pancreatic tumors and/or pituitary adenomas.

A

MEN1

75
Q

__________ and _________are caused by a mutated RET proto-oncogene and both present with medullary thyroid carcinoma and sometimes pheochromocytoma.

A

MEN2A and MEN2B

76
Q

MEN that presents with primary hyperparathyroidism

A

MEN1

77
Q

MEN that presents with Medullary throid carcinoma

A

MEN 2 a and b

78
Q

Which MEN: Medullary thyroid carcinoma, Pheochromocytoma, Parathyroid

A

2A

79
Q

Which MEN: Medullary thyroid carcinoma, Marfanoid habitus/Multiple neuromas, Pheochromocytoma

A

2B

80
Q

Which MEN: Parathyroid, Pancreas, Pituitary gland

A

MEN 1 (the 3P’s)

81
Q

. pHPT is characterized by elevated PTH and calcium levels and is usually caused by _______________, __________________, and _____________________.

A

parathyroid adenomas or hyperplasia, or, in rare cases, parathyroid carcinomas

82
Q

Stones, bones, abdominal groans, thrones, and psychiatric overtones!

A

Hyperparathyroidism

83
Q

When diagnosis primary hyperparathyroidism, we would expect hgih PTH or inappropriately normal. What do we mean by inappropriately normal?

A

PTH is released when calcium is high, so if calcium is high then PTH should be low not normal or high

84
Q

How does chronic kidney disease lead to secondary hyperparathyroidism?

A

Chronic kidney disease → impaired renal phosphate excretion → ↑ phosphate blood levels→ ↑ PTH secretion

In addition, CKD → ↓ biosynthesis of active vitamin D → ↓ intestinal calcium resorption and ↓ renal calcium reabsorption → hypocalcemia → ↑ PTH secretion

85
Q

Why is calcitonin elevated in medullary carcinomas?

A

Used as a marker because….
Calcitonin: A hormone secreted by parafollicular cells, which is the tissue of origin of medullary carcinoma
supportive diagnostic marker
monitor response to therapy

86
Q

Pts with medullary thyroid carcinoma, we should also look for what?

A

Pheochromocytoma because MEN2

87
Q

Before you even think about taking out that phechromocytoma, what do you need to give the patient?

A

Give that *itch some phenoxybenzamine to inhibit the effects of catecholamines to prevent hypertensive crisis

88
Q

In an adult patient with a family history of hepatocellular carcinoma, the presence of generalized fatigue, diabetes mellitus, cutaneous hyperpigmentation, hepatomegaly, laboratory evidence of iron overload (serum ferritin > 200 ng/mL among men or > 150 ng/mL among women, serum transferrin saturation ≥ 45%) suggests

A

Hemachromatosis bitches

89
Q

What gene do we need to know for MEN2?

A

RET

90
Q

This patient’s multiple lesions that developed into painful and pruritic crusty patches with areas of bronze-colored induration, and with a centrifugal distribution, are characteristic of necrolytic migratory erythema (NME). Lesions in NME tend to resolve and then reappear in a different location. NME, anemia, hyperglycemia, and chronic diarrhea (with associated weight loss) are characteristic symptoms of a disease process that affects the pancreas.

A

Glucagonoma apparently

91
Q

Glucagonoma

A

Increased fasting glucagon levels indicate a glucagonoma, a pancreatic α-cell neuroendocrine tumor. Excess glucagon increases gluconeogenesis and inhibits glycolysis, causing hyperglycemia and/or mild diabetes. Anemia may be a result of chronic illness or directly related to the inhibitory effect of glucagon on erythropoiesis. Patients with glucagonoma can also present with neuropsychiatric symptoms (e.g., depression, dementia, ataxia). NME is a paraneoplastic syndrome associated with tumors that secrete glucagon. Patients with suspected glucagonoma should undergo imaging (CT and/or MRI) to determine the location and size of the tumor and assess for possible metastases.

92
Q

Necrolytic migratory erythema, normocytic normochromic anemia, chronic diarrhea, and elevated glucose levels are characteristic clinical features of …..

A

glucagonoma

93
Q

What do we give patients to help w/symptoms of a gluconoma?

A

Octreotide, a somatostatin analog, reduces the secretion of glucagon to control the symptoms resulting from hypersecretion of glucagon (hyperglycemia, diarrhea, necrolytic migratory erythema, neurologic symptoms). In addition to supportive care (e.g., control of hyperglycemia), octreotide is the preferred initial therapy to bring these symptoms under rapid control.

94
Q

Exposure to ionizing radiation during childhood is associated with the formation of what thyroid cancer?

A

Exposure to ionizing radiation during childhood is associated with the formation of papillary thyroid carcinoma.

95
Q

What deficiency are patients with carcinoid syndrome at risk for?

A

B3 deficiency/niacin deficiency aka pellagra

96
Q

dermatitis, diarrhea, and glossitis are hallmarks of…

A

pellagra

97
Q

Watery diarrhea, crampy abdominal pain, episodic cutaneous flushing triggered by eating or emotional events, asthma-like attacks, and a murmur indicative of tricuspid regurgitation are highly suggestive of…..

A

Watery diarrhea, crampy abdominal pain, episodic cutaneous flushing triggered by eating or emotional events, asthma-like attacks, and a murmur indicative of tricuspid regurgitation are highly suggestive of carcinoid syndrome.

98
Q

a year-long history of diarrheal episodes, recently characterized by light brown, watery bowel movements, with mild abdominal pain and episodic cutaneous flushing. Together with hypokalemia, hypercalcemia, hyperglycemia, and achlorhydria/hypochlorhydria, this presentation is consistent with…

A

VIPoma

99
Q

What are some differences that can help you differentiate a VIPoma from carcinoid syndrome?

A

VIP (vasoactive intestinal peptide) inhibits gastric acid secretion, increases bone resorption, and stimulates gluconeogenesis, leading to achlorhydria/hypochlorhydria, hypercalcemia, and hyperglycemia, respectively. The cutaneous flushing seen in this patient is a result of VIP-induced vasodilation; this finding is seen in approx. 20% of patients with VIPoma.

100
Q

Why do patients with zollinger ellison have foul smelling floaty stools?

A

Inactivation of pancreatic enzymes

A gastrinoma (Zollinger-Ellison syndrome) causes a large volume of gastric acid to be produced, which decreases intestinal pH. Pancreatic lipases, which require an alkaline environment to function, are inactivated and can no longer emulsify fats. This may result in a deficiency of fat-soluble vitamins (e.g., vitamin E), causing neuromuscular disorders, such as ataxia. In addition, increased gastric acid leads to the development of PUD. Finally, gastrin acts directly on the intestine and prevents sodium and water reabsorption, resulting in secretory diarrhea. Treatment of gastrinoma (Zollinger-Ellison syndrome) includes proton pump inhibitors (e.g., omeprazole) and H2 antagonists (e.g., ranitidine) in order to reduce acid production. Octreotide (a somatostatin analog) may be used in refractory cases.

101
Q

What physical exam findings might be helpful in differentiating carcinoid from VIPoma on a test?

A

telangiectasias are found in carcinoid tumor pts NOT in VIPomas

102
Q

Why might we see hypokalemia in cushing syndrome?

A

Hypokalemia is due to the aldosterone-like effects of cortisol, which stimulates the excretion of potassium and hydrogen ions, causing metabolic alkalosis.

103
Q

When differentiating between primary and secondary hyporcortisolism, what mgiht be a tip off?

A

ACTH
PRIMARY hypercortisolism should have a negative feedback on the pit gland so LOW ACTH

Secondary hypercortisolism result from toooo much ACTH as in a pitutiary adenoma

Wither presents with cushings syndrome though

104
Q

Why might we see darkening of the mucous membranes and skin creases in cushings?

A

His hyperpigmentation (e.g., darkening of mucous membranes and skin creases) is a unique feature of Cushing disease that results from increased production of ACTH, which is cleaved from the same precursor as melanocyte-stimulating hormone.

105
Q

___________________is the treatment of choice for primary hyperaldosteronism caused by bilateral adrenal hyperplasia.

A

Eplerenone, an aldosterone receptor antagonist

In contrast to spironolactone, eplerenone does not block androgen or progesterone receptors, which decreases certain side effects (e.g., gynecomastia and decreased libido); however, eplerenone is only half as potent at blocking the mineralocorticoid receptor and is less effective at lowering blood pressure.

106
Q

51 yo female with symmetric arthralgias affecting the second and third metacarpophalangeal joints, skin hyperpigmentation, and diabetes mellitus suggests…

A

hemochromatosis. In premenopausal women, iron loss from menstruation can delay disease progression. In a menopausal woman like this patient, however, hemochromatosis will cause iron accumulation in multiple organs, causing symptoms as seen here.

GENSURG ROTATION (31 decks)

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