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Casey: Endocrine > Endocrine-Made Ridiculously Simple > Flashcards

Endocrine-Made Ridiculously Simple Flashcards

1
Q

When the thyroid itself over-secretes thyroid hormone (T3 & T4)

A

Primary Hyperthyroidism

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2
Q

When the pituitary over-stimulates the thyroid to secrete thyroid hormone (T3 & T4)

A

Secondary Hyperthyroidism

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3
Q

If the thyroid itself were to secrete lots of hormone “without being told to” this would increase negative feedback on the pituitary which would _____ TSH secretion?

A

Decrease

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4
Q

Primary hyperthyroidism, the TSH will be (High or Low)?

A

LOW

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5
Q

If the hyperthyroidism is secondary, i.e. caused by the over-secretion of TSH by the pituitary, the TSH will be (High or Low)?

A

HIGH

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6
Q

What is the key to distinguishing between primary and secondary hyperthyroidism?

A

TSH

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7
Q

A thyroid nodule that becomes independent of the pituitary and over-secretes thyroid hormone

A

Toxic nodule

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8
Q

Autoimmune disorder that causes hyperthyroidism; autoantibodies bind to the TSH receptors in the thyroid and act just like TSH, stimulating the thyroid to release thyroid hormone.

A

Graves’ Disease

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9
Q

The most common cause of hyperthyroidism

A

Graves’ Disease

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10
Q

Clinical features include Graves’ ophthalmology (inflammation of extra ocular muscles and periorbital tissue leading to bulging of eyes, ptosis), and pretibial myxedema (non-pitting edema on the anterior knee)

A

Graves’ Disease

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11
Q

An enlarged thyroid is also known as a….

A

goiter

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12
Q

High metabolism (weight loss), tachycardia (sometimes a-fib), dyspnea, heat intolerance, hot skin, increased appetite, tremor, and nervousness are some clinical signs of:

A

hyperthyroidism

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13
Q

Clinically, ophthalmology, pretibial myxedema, diffuse goiter, and/or thyroid bruit (rushing sound over thyroid on auscultation) will point toward a dx of:

A

Graves’ Disease

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14
Q

If the thyroid itself is the root of the problem and not producing any thyroid hormone, this DECREASES negative feedback on the pituitary, so in primary hypothyroidism, the TSH level will be ____?

A

INCREASED

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15
Q

In secondary hypothyroidism, the pituitary is the problem: the pituitary is not secreting an adequate amount of TSH, so the TSH will be ____?

A

DECREASED

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16
Q

The MC cause of hypothyroidism:

A

Hashimoto’s thyroiditis

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17
Q

autoimmune disease where the antibodies are directed against TPO and TG, resulting in lymphocyte infiltration of the thyroid gland which causes it to cease function

A

Hashimoto’s thyroiditis

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18
Q

____ deficiency causes hypothyroidism because ____ is necessary for thyroid hormone synthesis

A

Iodine

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19
Q

Symptoms include weight gain, cold intolerance, fatigue, weakness, bradycardia, hypoventilation, constipation, myalgias, arthralgias, and/or anemia; goiter may be present

A

hypothryoidism

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20
Q

Secretes aldosterone, glucocorticoids, sex hormones, norepinephrine, and epinephrine

A

Adrenal glands

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21
Q

Secretes epinephrine

A

adrenal medulla

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22
Q

Stress response hormones that increase BP and glucogenesis and decrease the immune response

A

glucocorticoids

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23
Q

Cortisol secretion is stimulated by secretion of ___ by the anterior pituitary which is triggered by secretion of ___ from the hypothalamus

A

1) ACTH

2) CRH

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24
Q

Clinical manifestations of cortisol ELEVATION:

A

Cushing’s Syndrome

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25
Q

Can cause hypernatremia, hypokalemia, and hypertension

A

Hyperaldosteronsim

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26
Q

One or both adrenal glands are hyperactive; causes include adrenal adenoma and adrenal carcinoma

A

primary hyperaldosteronism

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27
Q

The adrenal glands are over-stimulated ; causes include hyperkalemia, hyponatremia, and hypotension

A

secondary hyperaldosteronism

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28
Q

Responsible for sodium reabsorption and potassium excretion

A

Aldosterone

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29
Q

Can lead to hyponatremia and hyperkalemia

A

Hypoaldosteronism

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30
Q

Refers to a pathological elevation of cortisol

A

Cushing’s syndrome

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31
Q

Over-stimulation of the adrenal glands by an ACTH-secreting tumor in the pituitary

A

Cushing’s Disease

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32
Q

Truncal obesity, a moon face, a buffalo hump on back, easy bruising, purple striae, hypertension, edema, weakness, osteoporosis and/or osteonecrosis, hirsuitism, acne, virilization, diabetes, immunosuppression, and/or cognitive effects

A

Cushing’s syndrome

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33
Q

If one or both adrenal glands are autonomously hyper-secreting, this hyper-secretion, this hypersecretion will increase negative feedback on pituitary, thus ACTH will be ___

A

LOW

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34
Q

Test that relies on the principal of negative feedback to localize the source of ACTH

A

Dexamethasone Suppression Test

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35
Q

A steroid that mimics cortisol and exert negative feedback on the pituitary, decreasing ACTH output from the pituitary.

A

Dexamethasone

36
Q

If a low dose dexamethasone suppression test does NOT suppress ACTH, this indicates:

A

Cushing’s syndrome exists

37
Q

When localizing the ACTH source in Cushing’s syndrome the pituitary ____ (does/does not) respond to negative feedback and ectopic sites____ (do/do not)

A

1) does

2) do not

38
Q

Pathology of one or both adrenal adrenal glands; primary adrenal insufficiency aka=

A

Addison’s Disease

39
Q

Lack of ACTH stimulation from the pituitary=

A

secondary adrenal insufficiency

40
Q

Lack of CRH from from the hypothalamus

A

Tertiary adrenal insufficiency

41
Q

Symptoms can include weakness, fatigue, lightheadedness, weightless, dehydration, hair loss, vomiting, hypoglycemia, and/or anemia; hyponatremia and hyperkalemia

A

Adrenal Insufficiency

42
Q

Can occur when a pt goes through withdrawal after abrupt termination of steroid treatment:

A

Adrenal insufficiency

43
Q

If both cortisol and aldosterone are low,and ACTH is high this suggests:

A

Primary adrenal insufficiency

44
Q

Is a rare but extremely dangerous cause of HTN

A

Pheochromocytoma

45
Q

Catecholamine-secreting tumor that most commonly occurs in the adrenal medulla–> the catecholamines (i.e., norepinephrine and epinephrine) cause vasoconstriction, thus HTN

A

Pheochromocytoma

46
Q

Dx of this is confirmed by elevated urine levels of catecholamines and their metabolic by-products, called metanephrines.

A

Pheochromocytoma

47
Q

Follow the “rule of 10s”: 10% are bilateral ,10% are not in adrenal gland, and 10% are malignant

A

Pheochromocytoma

48
Q

What should never be given to a pt with a pheochromocytoma?

A

Beta blocker

49
Q

ACTH-secreting_____ adenomas lead to increased cortisol secretion (Cushing’s Disease)

A

Pituitary

50
Q

TSH-secreting_____adenomas can cause secondary hyperthyroidism

A

Pituitary

51
Q

Stimulates release of insulin-like growth factor (IGF)

A

Growth hormone (GH)

52
Q

What inhibits growth hormone?

A

Somatostatin

53
Q

Inhibits GnRH secretion from the hypothalamus:

A

Prolactin

54
Q

Decreased GnRH secretion from the hypothalamus leads to reduced secretion of ___ & ___ from the pituitary?

A

FSH/LH

55
Q

What is released from the hypothalamus that inhibits prolactin release from the anterior pituitary?

A

Dopamine

56
Q

Drives glucose INTO cells

A

Insulin

57
Q

Used for when glucose is “gone”; it causes release of glucose into the blood for the tissues that need it

A

Glucagon

58
Q

Released from beta cells of the pancreas after a big meal

A

insulin

59
Q

Stimulates glucose uptake into cells and its storage as glycogen, fat, and protein

A

insulin

60
Q

Goal of this is to reduce blood sugar levels, so it promotes both glucose storage and its breakdown

A

Insulin

61
Q

Secreted during a fast when blood sugar is low

A

Glucagon

62
Q

Decreases glycolysis and increases gluconeogenesis (glucose formation) & glycogenolysis (breakdown of glycogen to release glucose):

A

Glucagon

63
Q

Goal is to mobilize glucose stores from the liver so that glucose can be sent to the brain and heart and used for energy production in these organs

A

Glucagon

64
Q

In this disorder, there is either a decreased insulin secretion or insensitivity to insulin

A

Diabetes Mellitus

65
Q

Without insulin’s effects, glucose cannot be moved into the cells, and ____ can occur

A

Hyperglycemia (increased blood sugar)

66
Q

An autoimmune process that destroys the beta cells of the pancreas, leading to LOSS of insulin production

A

Type 1 DM

67
Q

Underlying pathophysiology is insulin RESISTANCE

A

Type 2 DM

68
Q

Increases insulin secretion to compensate for peripheral tissue resistance but eventually this mechanism fails

A

Type 2 DM

69
Q

3 hormones that regulate calcium concentration

A

PTH, Vitamin D, & Calcitonin

70
Q

2 hormones that RAISE serum calcium levels:

A

PTH & Vitamin D

71
Q

Hormone that DECREASES serum calcium levels:

A

Calcitonin

72
Q

Secrete PTH in response to LOW blood calcium levels:

A

Parathyroid gland(s)

73
Q

Increases blood calcium by stimulating osteoclasts to break down bone, increase reabsorption of calcium by kidneys, and increase conversion of inactive vitamin D to active vitamin D

A

PTH

74
Q

Causes elevated blood calcium & decreased blood phosphate (but increased urine phosphate)

A

PTH

75
Q

Increases absorption of calcium and phosphate by the gut; increases bone resorption and increases phosphate reabsorption in the kidneys

A

Vitamin D

76
Q

Antagonist hormone to PTH & Vitamin D

A

Calcitonin

77
Q

Decreases blood calcium by using calcium to build bone, and decreases renal reabsorption of calcium

A

Calcitonin

78
Q

Secreted by C-cells in the thyroid in response to high calcium levels

A

Calcitonin

79
Q

Excess secretion of PTH by parathyroid gland(s); MC cause is parathyroid adenoma; Incr in PTH will raise serum calcium levels

A

Hyperparathyroidism

80
Q

Labs: incr. Ca, PTH, decr. phosphate; incr urine phosphate and urine calcium

A

Hyperparathyroidism

81
Q

NOT related to pituitary; A decrease in serum calcium causes an increase in PTH secretion; can occur secondary to Vit. D deficiency or renal failure; result of hypOcalcemia

A

Secondary hyperparathyroidism

82
Q

Decrease in bone mass; common in elderly (from estrogen deficiency), and pts with elevated cortisol (Cushing’s, exogenous steroid tx); calcium and Vit D intake can help prevent

A

Osteoporosis

83
Q

Thickened, weakened bones; repeated bone resorption & bone formation leading to a disorganized/weaker bone

A

Paget’s Disease

84
Q

Phase of Paget’s disease: overactivity of osteoclasts and massive bone resorption

A

Lytic (hot) phase

85
Q

Phase of Paget’s disease: compensatory osteoblast response mixed with continued osteolytic activity in which bone is reformed in unorganized fashion

A

Intermediate phase

86
Q

Phase of Paget’s disease: continued disorganized bone formation

A

Sclerotic (cold) phase

87
Q

Management of osteoporosis & Paget’s disease

A

bisphosphonates

Casey: Endocrine (5 decks)

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