Step Up- Endocrine Flashcards

1
Q

Most common cause of hyperthyroidism

A

Graves disease

-IgG to TSH receptor (TSIg)

Young women

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2
Q

Three signs of hyperthyroidism that are specific to graves disease

A

Exopthalmos

Pretibial myxedema

Thyroid bruit

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3
Q

What is the purpose of a radioactive T3 uptake test?

A

The T3 can either be taken up by free TBG or by the resin that is given to the patient.

If the resin takes up the T3 as seen on the scan, then the TBG is likely saturated with T3 and therefore hyperthyroidism is a likely diagnosis.

This helps to diagenose true hyperthyroidism with elevated TBG

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4
Q

Normal free thyroxine index?

A

4-11

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5
Q

First line management of hyperthyroidism? Major side effect?

A

PTU and methimazole

Agranulocytosis

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6
Q

Contraindications to radioactive iodine treatment

A

Breastfeeding and pregnancy

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7
Q

Treatment of thyroid storm…

A

B-blocker for HR control

PTU

Dexamethasone to impair peripheral conversion of T4 to T3

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8
Q

Patients with hasimotos have increased risk of these cancers

A

thyroid lymphoma

thyroid carcinoma

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9
Q

Elevated TSH with normal T4

A

Subclinical hypothyroidism

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10
Q

antimicrosomal antibodies are increased in this form of hypothyroidism

A

Hashimoto’s

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11
Q

Subacute, or viral, thyroiditis is associated with this human leukocyte antigen…

A

HLA-B35

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12
Q

What is one of the defining physical finidings in subacte granulomatous thyoiditis?

A

PAINFUL thyroid

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13
Q

Ab present in chronic lymphocytic thyroiditis

A

antiperoxidase antibodies (90%)

antithyroglobulin antibodies (50%)

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14
Q

progressive replacement of the thyroid with fibrous tissue. Presents as painless hardened thyroid

A

Reidel’s thyroiditis

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15
Q

Characteristics that suggest malignancy in a thyroid nodule

A
  • Fixed
  • unusually firm
  • solitary
  • Hx of radiation
  • Rapid growth
  • Vocal cord paralysis
  • Cervical adenopathy
  • FMHx
  • Elevated Serum Ca
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16
Q

First step in thyroid nodule evaluations

A

FNA (95% Sen and Sp.)

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17
Q

Which thyroid cancer is FNA NOT reliable for?

A

Follicular

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18
Q

Syndromes associated with thyroid cancer

A

Gardner’s syndrome and Cowden’s syndrome–> Papillary

MEN type II for meduallary thyroid cancer

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19
Q

Most common form of thyroid cancer

A

Papillary (also least aggressive)

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20
Q

Papillary thyroid cancer is most commonly associated witht his risk factor

A

radiation exposure

(Papillary is Pounded by radiation)

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21
Q

This form of thyroid cancer commonly matastasizes to distant organs (brain, bone, lung, liver)

A

Follicular

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22
Q

How does papillary thyroid cancer spread?

A

Via lymphatics

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23
Q

MEN II is associated with this form of thyroid cancer

A

Medullary

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24
Q

Medullary thyroid cancer is associated with this electrolyte distubance

Why?

A

Hypercalcemia

Cancer derived from parafollicular (c cells) which produce calcitonin

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25
Q

Worst form of thyroid cancer

A

anaplastic

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26
Q

What is the tx for most thyroid cancers?

A

Lobectomy (papillary) or total thyroidectomy (all others) with adjuvent radioiodine therapy

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27
Q

Medications associated with hyperprolacinemia

A

Psychiatric medications

H2 blockers

metoclopromide

verpamil

estrogen

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28
Q

Treatment of prolactinoma

A

bromocroptine (dopamine agonist)

Continue tx for 2 years before considering sugery unless otherwise indicated

Cabergoline may be better tolerated

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29
Q

Most common cause of death in patients with acromegaly

A

Hypertrophic cardiomyopathy (heart disease)

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30
Q

Levels of this are significantly elevated in acromegaly

A

Somatomedin C (IGF-1)

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31
Q

How does an oral glucose suppression test work?

A

If glucose load fails to suppress GH, this can confirm diagnosis of acromegaly

32
Q

Normal serum osmolality

A

250-290

33
Q

How to diagnose diabetes insipidis (neuro v. nephro v. psychiatric issue)

A

water deprivation test

34
Q

Treatment for central DI

A

Desmopressin (nasal, oral, IM)

or Chlorpropamide and tx underlying cause

35
Q

Tx for nephrogenic DI

A

discontinue offending agent

Sodium restriction and thiazide diuretic (depletes sodium leading to increased absorbtion in the proimal tubule of water and Na which decreases urine volume)

36
Q

Is edema seen in SIADH? Why or why not?

A

NO

Despite hyponatremia, naturesis is occuring due to the increased release of atrial naturitic peptide and the inhibition of the Renin-angiotensin-aldosterone system

37
Q

Treatments for SIADH id patient is asymptomatic

A

Water restriction

Loop diuretic

Lithium carbonate or demeclocycline (inhibit ADH in the kidney)

38
Q

Danger of raising Na too quickly in SIADH?

A

Central pontine myelinolysis (replacement should no exceed 0.5meq/L/hr)

39
Q

After establishment of cushing syndrome and high ACTH (or no suppression with low dose), how does the high dose dexamathasone suppression test work?

A

If the high dose dexamethasone does no suppress the production of ACTH the tumor is most likely and ectopic ACTH producing tumor–> Chest CT, abdominal CT and octreotide scan

If the suppression test does suppress then the tumor is most likely pituitary in origin–> head MRI

40
Q

Pheochromocytomas are most commonly found here

A

adrenal medulla– arising from chromaffin cells

41
Q

Rule of 10s for pheochromocytoma

A

10% familial

10% bilateral

10% malignant

10% multiple

10% in children

10% extra adrenal

42
Q

How to diagnose pheo

A

Urine screen for metanepherine, VMA, HMA, and normetenepherine

43
Q

Drug used to pretreat in removal of pheo

A

alpha blockade with phenoxybenzamine 10-14d prior to surgery

propanolol 2-3d prior

(alpha blockade for BP abd Beta for HR)

44
Q

MEN type I is composed of these abnormalities

A

Parathyroid hyperplasia

pancratic islet tumors

pituitary tumors

45
Q

MEN IIA is composed of these clinical findings

A

(MPP)

Medullary thyroid carcinoma

Pheochromocytoma

Pharathyroid abnormalities

46
Q

MEN IIB is composed of…

A

“MMMP”

Mucosal neuromas

Medullary thyroid tumors

Marfanoid body

Pheo

47
Q

electrolyte disturbance present in hyoeraldosteronism

A

Sodium retention

Hypokalemia

Metabolic alkylosis (loss of H+ in the mudullary collecting tubules)

48
Q

Most common cause of hyperaldosteronism

A

Adrenal adenoma– conn syndrome most common

Adrenal hyperplasia (almost always bilateral)

Rarely adrenal carcinoma

49
Q

laboratory study to evaluate for hyperaldosteronism

A

plasma adosterone:renin ratio >30

inappropriately elevated aldosterone with a decrease in renin activity

50
Q

Confirmatory test for hyoperaldosteronism (there are two)

A
  1. Saline infusion test

Infusion of saline should result in decrease in plasma aldosterone in normal patients. It will not in patient with hyoperaldosteronism

  1. Oral sodium loading
    - should result in decreased aldosterone. Increased aldosterone in the setting of increased urine sodium confirms the diagnosis
51
Q

How can venous versus arterial blood elucidate the cause of hyperaldosteronism

A

Aldosterone high on venous side= adenoma

Aldosterone high on venous and arterial side= hyperplasia

52
Q

Tx for aldosterone producing adeoma

Tx for bilateral hyperplasia

A

Resection for adenoma

Spironolactone for bilateral hyperplasia

53
Q

Most common infectious cause of primary adrenal insufficiency worldwide? Industrialized nations?

A

Tuberculosis

Idiopathic (likely autoimmune) addison disease

54
Q

Most common cause of secondary adrenal insufficiency?

A

Long term steroid therapy

55
Q

Symptoms of lack of cortisol?

A

GI pain

Hypoglycemia

Hyperpigmentation (due to increased ACTH and melanocyte stimulating hormone)

hypotension and shock

Hyponatremia and hypovolemia

Hyperkalemia

56
Q

How do the treatements for primary and secondary adrenal insufficiency difffer?

A

Primary: both glucocorticoid (prednisone/hydrocortisone) need to be replaced due to low cortisol and low aldosterone

Secondary: Glucocorticoid replacement is necessary but mineralocorticoid is not because aldosterone is normal

57
Q

This enzyme is the most commonly deficient enzyme in congenital adrenal hyperplasia

A

21-hydroxylase

58
Q

High levels of this enzyme are present in individuals with 21-hydroxylase deficiency

A

17-hydroxyprogesterone

59
Q

What is the pathophysiology of congential adrenal hyperplasia and how it causes virilization?

A

As precursors to 21-hydroxylase build up they are shunted to synthesis of androgens (DHEA and Testosterone)

–Females born with ambiguous genitalia but normal uterus and ovaries

60
Q

What major electrolyte disturbance is associated with congenital adrenal hyperplasia?

A

Hyponatremia and hyperkalemia dye to lack of mineralocorticoid

61
Q

Difference betwen dawn phenomenon and symogyi effect

A

Dawn phenomenon: morning hyperglycemia in response to growth hormone

Symogyi effect: morning hyperglycemia in response to nocturnal hypoglycemia

62
Q

This hyperglycemic agent is contraindicated in patients with renal failure

A

Metformin

63
Q

Hyaline deposition in one area of the kidney (nodular glomerular sclerosis) is pathognomonic for this….

A

Diabetic nephropathy

64
Q

Why may ketones be falsely negative in ciruclatory collapse?

A

The production of lactate shifts the production of ketones to B-hydroxybtyrate over acetoacetate. Acetoacetic acid is normally the one that is measured.

65
Q

Sodium correction in DKA

A

Add 1.6 to measured Na for every 100 mg/dL increase in glucose.

66
Q

What causes the need for Na correction in DKA

A

glucose causes osmotic shift of fluid from ICF to ECF thus diluting the Na.

67
Q

Describe the changes in potassium that are caused by DKA

A

Initially hyperkalemia due to shift from acidosis

Insulin and overall loss in the urine causes intracellular shift of K leading to dangerous hyperkalemia

ALWAYS A TOTAL DEFICIT

68
Q

Findings in hyperosmolar, hyperglycemic, non-ketotic state?

A

Hyperosmolarity– due to osmotic diuresis

Hyperglycemia

non-ketotic– due to enough basal insuline to suppress ketogenisis

69
Q

This should always be given before or with glucose in hypoglycemia

A

Thiamine to avoid wenicke encephalopathy

70
Q

Insulinoma is assocaited with this syndrome

A

MEN1

71
Q

Gastrinoma, also known as

A

zollinger-ellison syndrome– a pacreatic islet cell tumor that secrets gastrin

Leads to high gastric acid levels and ulcers

72
Q

Gastrinoma triangle

A

cystic duct superiorly, second and third portion of duodenum inferiorly, and neck of pancreas medially

73
Q

In zollinger-ellison syndrome, gastrin increases substantially after administration of this…

A

secretin

74
Q

Glucagonoma is associated with this dermatologic manifestation

A

necrotizing migratory erythema

75
Q

watery diarrhea, achlorhydria, hyperglycemia and hypercalcemia

A

VIPoma