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AGPC3 > Endocrine Disorders > Flashcards

Endocrine Disorders Flashcards

1
Q

What is the pathway for thyroid regulation?

A

Hypothalamus - thyrotropin-releasing hormone (TRH) => anterior pituitary - thyroid stimulating hormone (TSH) => thyroid - T4 and T3 => plasma - T4 and free T4/T3 and free T4 => peripheral tissues - free T4/free T3/reverse T3

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2
Q

What is the condition with low TSH and low free T4?

A

secondary hypothyroidism

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3
Q

What is the condition with normal TSH and low free T4?

A

non-thyroid illness

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4
Q

What is the condition with high TSH and low free T4?

A

primary hypothyroidism

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5
Q

What is the condition with low TSH and normal free T4?

A

sub-clinical hyperthyroidism

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6
Q

What is the condition with normal TSH and normal free T4?

A

euthyroid state

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7
Q

What is the condition with high TSH and normal free T4?

A

sub-clinical hypothyroidism

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8
Q

What is the condition with low TSH and high free T4?

A

primary hyperthyroidism

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9
Q

What is the condition with normal TSH and high free T4?

A

non-thyroid illness or patient on Eltroxin (levothyroxine)

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10
Q

What is the condition with high TSH and high free T4?

A

secondary hyperthyroidism

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11
Q

What is the normal range for TSH?

A

0.5 - 5.0 mU/L (upper limit soon to be revised to 2.5 mU/L)

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12
Q

What is the normal range for free T4?

A

0.7 - 2.1 ng/dL

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13
Q

What do the parathyroid glands do?

A

Chief cells synthesize and secrete parathyroid hormone - polypeptide hormone

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14
Q

What are the roles of parathyroid hormone?

A

plays a major role in bone remodeling, calcium homeostasis, regulation of calcium levels, and bone mass; participates in renal excretion of phosphate and activation of vitamin D

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15
Q

How is parathyroid hormone regulated?

A

by serum ionized calcium via calcium-sensing receptors on the surface of parathyroid cells => high serum calcium levels suppress PTH secretion while low levels stimulate PTH release

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16
Q

How is primary hyperparathyroidism diagnosed?

A

patients exhibit elevated levels of serum calcium (10-11 mg/dL) and parathyroid hormone - may occur when patients are taking lithium or thiazide diuretics

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17
Q

What is primary hyperparathyroidism?

A

abnormal regulation of PTH secretion => hyper secretion of PTH relative to the serum calcium concentration

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18
Q

What are the effects of increasing levels of PTH?

A

stimulates bone resorption, leading to an increase in serum calcium levels and increased activation of vitamin D

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19
Q

What is the negative feedback loop relating to the parathyroid glands?

A

when serum calcium levels increase, PTH decreases (and vice versa) => when serum calcium levels decrease, PTH increases (and vice versa)

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20
Q

What are the clinical manifestations of primary hyperparathyroidism?

A

elevated PTH levels, hypercalcemia, hypercalciuria (and possible increased formation of kidney stones/urolithiasis), decrease serum phosphate levels (“stones, bones, abdominal groans, psychic moans”)

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21
Q

What is the normal range for parathyroid hormone?

A

10 - 60 pg/mL

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22
Q

What is the negative feedback loop in the thyroid gland?

A

As TSH increases, free T4 decreases => as TSH decreases, free T4 increases

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23
Q

What are some causes of hypercalcemia?

A

primary hyperparathyroidism, vitamin D intoxication, use of thiazide diuretics or lithium, hyperthyroidism, pheochromocytoma, adrenal insufficiency, immobilization

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24
Q

What are signs and symptoms of excess parathyroid hormone?

A

s/s of hypercalcemia (weakness and myalgia, confusion, lethary, parethesias), bone pain, osteoporosis, nephrolithiasis (kidney stones), hypophosphatemia, increased calcitriol, hyperuricemia, gout, anemia, HTN, abdominal pain, nausea, peptic ulcer, constipation, pancreatitis

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25
Q

What is the most common cause of secondary hyperparathyroidism?

A

chronic renal failure - normally, reduction in plasma vitamin D and moderate decreases in serum calcium lead to greater synthesis and secretion of PTH => in chronic renal disease, parathyroid expression of vitamin D and calcium receptors is reduced making the gland resistant to the usual negative feedback loop

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26
Q

What is a classic sign of hypoparathyroidism?

A

Chvostek sign - twitching or contraction of the facial muscles in response to tapping the facial nerve at a point anterior to the ear and above the zygomatic bone - due to hypocalcemic tetany

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27
Q

What is the mechanism of pseudohypoparathyroidism?

A

abnormal response to PTH due to a congenital defect in the G protein (NOT due to decreased PTH levels)

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28
Q

What are the classic features of pseudohypoparathyroidism type 1a?

A

generalized hormone (TSH, LH, FSH) resistance to PTH - abnormal physical features (round face), short stature, skeletal abnormalities (short metacarpals)

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29
Q

What are the classic features of pseudohypoparathyroidism type 1b?

A

renal resistance to PTH - low plasma calcium levels, high phosphate levels, elevated PTH levels with a normal appearance

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30
Q

What is the normal ionized calcium range?

A

8.5 - 10.5 mg/dL

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31
Q

What is the normal plasma phosphate range?

A

3 - 4.5 mg/dL

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32
Q

What is the normal plasma PTH range?

A

10 - 65 pg/mL

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33
Q

What are the major causes of Cushing’s syndrome?

A

iatrogenic (pharmacologic doses of glucocorticoids), ectopic ACTH (small-cell lung cancer), pituitary ACTH-dependent (benign and malignant adrenal tumors)

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34
Q

What are the common signs and symptoms of Cushing’s syndrome?

A

*supraclavicular fat pads (and dorsocervical fat pad - “buffalo hump”), *skin atrophy and loss of subcutaneous fat (skin peels after being covered with adhesive tape), *wide purplish striae, *proximal muscle weakness, centripetal obesity (face, neck, trunk, abdomen most common feature), facial plethora (“moon face”), depression, insomnia, glucose intolerance, HTN, easy bruisability, hirsutism, amenorrhea/impotence, acne - none are pathognomonic => important clinical clue is simultaneous development and increasing severity of several symptoms

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35
Q

What is factitious Cushing’s syndrome?

A

surreptitious intake of glucocorticoids - clue to diagnosis is low or erratic values for urinary cortisol

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36
Q

What are the diagnostic tests for hypercortisolism?

A

late-night salivary cortisol (> 7.5 mcg/dL), 24-hour urinary free cortisol excretion (basal urinary cortisol excretion more than three times the upper limit of normal), overnight 1 mg dexamethasone suppression test (> 1.8 mcg/dL)

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37
Q

What are some physiologic causes of hypercortisolism that should be excluded in a diagnosis of Cushing’s syndrome (pseudo-Cushing’s syndrome)?

A

pregnancy, severe obesity (visceral obesity or PCOS), psychological stress (severe depression), malnutrition/anorexia nervosa/intense chronic exercise, poorly controlled diabetes mellitus, chronic alcoholism

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38
Q

What is the rationale for the late-night salivary cortisol test?

A

the normal evening nadir in serum cortisol is preserved in obese and depressed patients but not in those with Cushing’s syndrome - not a good test for patients with erratic sleep schedules or shift work

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39
Q

What is the use of low-dose dexamethasone suppression tests?

A

used to distinguish patients with Cushing’s disease (caused by pituitary hypersecretion of ACTH) from patients with ectopic ACTH (caused by nonpituitary ACTH-secreting tumors) - not good test for patients with abnormally high levels of corticosteroid-binding globulin (e.g., estrogen-containing drugs - stop oral contraceptives 6 weeks prior)

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40
Q

What are common causes of ACTH-dependent Cushing’s syndrome (associated with bilateral adrenocortical hyperplasia)?

A

pituitary hypersecretion of ACTH (Cushing’s disease), ectopic secretion of ACTH (non-pituitary tumors), ectopic secretion of corticotropin-releasing hormone by non-hypothalamic tumors, iatrogenic due to administration of exogenous ACTH (not glucocorticoids)

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41
Q

What are the common causes of ACTH-independent Cushing’s syndrome?

A

iatrogenic due to exogenous administration of glucocorticoids (most commonly, prednisone), adrenocortical adenomas/carcinomas, primary pigmented nodular adrenocorical disease, bilateral macronodular adrenal hyperplasia

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42
Q

What are the two most common causes of Cushing’s syndrome?

A

iatrogenic Cushing’s due to exogenous administration of glucocorticoids and pituitary tumoral hypersecretion of ACTH

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43
Q

What is the treatment for Cushing’s syndrome?

A

treat the underlying cause (e.g., stop glucocorticoids with exogenous therapy causing Cushing’s syndrome, transsphenoidal microadenomectomy for microadenoma)

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44
Q

How long does it take for physical signs and symptoms of Cushing’s syndrome to resolve after effective cure?

A

two to 12 months - HTN, osteoporosis, and glucose intolerance improve but may not disappear

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45
Q

What are some common triggers of acute adrenal insufficiency?

A

serious infection, major stress, persistent vomiting, failure to take extra glucocorticoid during infection/major illness

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46
Q

What are the manifestations of adrenal crisis?

A

shock, anorexia, N/V, abdominal/flank/back/lower chest pain, abdominal rigidity/rebound tenderness, weakness, fatigue, lethargy, fever, salt craving, confusion, coma, hyponatremia, hyperkalemia, hypoglycemia, hyperpigmentation, weight loss, electrolyte abnormalities, calcification of auricular cartilages (men only), vitiligo

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47
Q

What is the major hormonal factor precipitating adrenal crisis?

A

mineralocorticoid (not glucocorticoid)

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48
Q

What is the major clinical problem with adrenal crisis?

A

hypotension (SBP < 110 mmHg)

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49
Q

What differentiates primary from secondary/tertiary adrenal insufficiency?

A

in secondary/tertiary adrenal insufficiency, mineralocorticoid function is preserved

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50
Q

What are the most common features of adrenal insufficiency?

A

chronic malaise, lassitude, fatigue (worse with exertion and improved with bed rest), weakness (generalized), anorexia, weight loss, N/V, constipation, flank pain, orthostatic hypotension, arthralgias, salt craving

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51
Q

What are the causes of hyponatremia in patients with adrenal insufficiency?

A

sodium loss and volume depletion due to mineralocorticoid deficiency and increased vasopressin secretion (due to cortisol deficiency) - may lead to massive salt ingestion “chased” with lemon juice and thirst for iced liquids

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52
Q

What are the features of hyperpigmentation in adrenal insufficiency?

A

generalization but most conspicuous in areas exposed to light, chronic friction, or pressure; patchy pigmentation of lips, buccal mucosa, under tongue, on gingival border, on hard palate; scars acquired during primary insufficiency are permanently pigmented; hair/nails become darker with longitudinal bands of darkening - begins to fade within several days and disappears with months of adequate glucocorticoid therapy (scars never fade - melanin is trapped in fibrous connective tissue)

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53
Q

Which clinical manifestations are similar in all types of adrenal insufficiency?

A

weakness, fatigue, myalgia, arthralgia, psychiatric symptoms (caused by glucocorticoid deficiency)

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54
Q

What features differ between primary and secondary/tertiary adrenal insufficiency?

A

in secondary/tertiary insufficiency: hyperpigmentation does not occur, dehydration is not present, hypotension less prominent, hyperkalemia not present, GI symptoms uncommon, hypoglycemia more common

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55
Q

What is the most common cause of adrenal insufficiency (generally)?

A

prolonged administration of pharmacologic doses of synthetic glucocorticoids causing corticotropin (ACTH) deficiency

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56
Q

What are the types of adrenal insufficiency?

A

primary, secondary (pituitary), tertiary (hypothalamic)

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57
Q

How is adrenal insufficiency demonstrated clinically?

A

(1) inappropriately low cortisol secretion, (2) determine whether cortisol secretion is dependent on or independent of corticotropin (ACTH) deficiency, (3) seek treatable cause

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58
Q

What is the most common cause of primary adrenal insufficiency?

A

autoimmune adrenalitis

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59
Q

What are the four stages of adrenal insufficiency in patients with autoimmune adrenalitis?

A

(1) high plasma renin activity and normal/low serum aldosterone, (2) impaired serum cortisol response to ACTH stimulation, (3) increased morning plasma ACTH with normal serum cortisol, (4) low morning serum cortisol and overt clinical adrenal insufficiency (adrenal destruction essentially complete)

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60
Q

What early morning (6 am) level of serum cortisol concentration is suggestive of adrenal insufficiency?

A

less than 3 mcg/dL

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61
Q

What early morning (8 am) salivary cortisol concentration is suggestive of adrenal insufficiency?

A

less than 1.8 ng/mL

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62
Q

Why should cortisol levels be checked in the early morning?

A

this is the time when cortisol levels are usually higher - levels are at their lowest one hour after usual hour of sleep

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63
Q

What type of adrenal insufficiency is present when serum cortisol is inappropriately low and plasma ACTH is very high (may be > 4000 pg/mL)?

A

primary adrenal disease - both mineralocorticoid and cortisol deficiency

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64
Q

What type of adrenal insufficiency is present when both serum cortisol and ACTH concentrations are inappropriately low (ACTH 20 to 52 pg/mL)?

A

secondary (pituitary disease) or tertiary (hypothalamic disease)

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65
Q

What is the short ACTH stimulation test?

A

test performed to determine the type (primary or secondary/tertiary) of adrenal insufficiency

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66
Q

What is a normal response to the ACTH stimulation test?

A

rise in serum cortisol concentration after 30 to 60 minutes to a peak of > 18 to 20 mcg/dL after a 250 mcg IV bolus of ACTH - excludes primary and most cases of secondary adrenal insufficiency

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67
Q

What is the pathology of primary adrenal insufficiency?

A

inability to secrete cortisol (adrenal glands partially or completely destroyed and unable to respond to ACTH) but intact ability to secrete ACTH

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68
Q

What is the pathology of secondary/tertiary adrenal insufficiency?

A

patients have normal but atrophic adrenal glands that are capable of producing cortisol but fail to do so due to deficient ACTH secretion

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69
Q

Which test can differentiate between secondary and tertiary adrenal insufficiency?

A

administration of corticotropin-releasing hormone (CRH) - patients with tertiary adrenal insufficiency lack CRH from hypothalamus and have exaggerated and prolonged ACTH response

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70
Q

What is Addison’s Disease?

A

most common cause of primary adrenal insufficiency in the U.S. - autoimmune process that destroys the adrenal cortex

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71
Q

Which infectious processes can lead to adrenal insufficiency?

A

tuberculosis, fungal infections, cyotmegalovirus, syphilis, opportunistic infections with HIV

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72
Q

What is Graves’ disease?

A

autoimmune disease characterized by hyperthyroidism caused by thyroid-stimulating hormone-receptor antibodies (TRAb) that activate the receptor and stimulate thyroid synthesis and secretion - presence of TRAb distinguishes Graves’ disease from other causes of hyperthyroidism

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73
Q

What is the treatment for Graves’ disease?

A

beta blocker (atenolol 25-50 mg/day) to ameliorate common symptoms (palpitations, tachycardia, tremulousness, anxiety, and heat intolerance) and measures to decrease thyroid synthesis (thionamide, radioiodine ablation, or thyroidectomy)

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74
Q

What are the thionamides used to treat Graves’ disease?

A

methimazole (used almost exclusively) and propylthiouracil (preferred in the first trimester of pregnancy and in patients with drug reactions to methimazole)

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75
Q

What is the initial dose of methimazole for treatment of Graves’ disease?

A

small goiters and mild hyperthyroidism (free T4 1-1.5X upper limit of normal) = 10 mg daily; larger goiters and more severe hyperthyroidism (free T4 2X upper limit of normal) = 20-30 mg daily

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76
Q

When should thionamides be administered prior to radioiodine ablation in patients with Graves’ disease?

A

patients with moderate or severe orbitopathy - to achieve euthyroid (radioiodine ablation can cause or worsen Graves’ opthalmopathy)

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77
Q

How does radioiodone ablation work for treatment of hyperthyroidism?

A

radioiodine is administered in capsule or oral solution, which is rapidly absorbed from the GI tract and concentrated in thyroid tissues - results in ablation of thyroid within 6 to 18 weeks

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78
Q

When is surgery recommended for treatment of Graves’ disease?

A

severe hyperthyroidism and large goiter, pregnant women allergic to antithyroid drugs, patients with allergies to antithyroid drugs who refuse radioiodine

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79
Q

What other medications can be used in treatment of Graves’ disease?

A

glucocorticoids (inhibit peripheral T4 to T3 conversion), lithium (blocks thyroid hormone release), cholestyremine with methimazole (lowers serum T4 and T3 concentrations more rapidly than methimazole alone), carnitine (has naturally occurring peripheral antagonist of thyroid hormone action), rituximab (may induce sustained remission in patients with low TRAb levels)

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80
Q

What are the common clinical feature of hypothyroidism?

A

fatigue, cold intolerance, weight gain, constipation, dry skin, myalgia, menstrual irregularities, goiter, bradycardia, HTN, delayed relaxation of deep tendon reflex, slowed mental processing, yellow skin (due to elevations in beta-carotene), carpal tunnel syndrome, coarse hair

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81
Q

What is the treatment for primary hypothyroidism?

A

replacement of T4 (levothyroxine/Synthroid)

82
Q

What is central hypothyroidism?

A

hypothyroidism due to insufficient stimulation of thyroid gland by TSH caused by secondary (pituitary) or tertiary (hypothalamic) disease

83
Q

What is the most common cause of primary hypothyroidism in iodine sufficient areas?

A

Hashimoto’s thyroiditis - pathologic feature = lymphocytic infiltration; serologic feature = presence of high serum concentrations of antibodies to thyroid peroxidase (TPO) and thyroglobulin

84
Q

Which patients should be screened for hypothyroidism?

A

those with symptoms, laboratory abnormalities that could be caused by hypothyroidism, those with risk factors, taking drugs that may impair thyroid function (thionamides, lithium, amiodarone, interferon alpha, interleukin-2)

85
Q

Which conditions should trigger testing of thyroid function?

A

substantial hyperlipidemia, hyponatremia, high serum muscle enzyme concentrations, macrocytic anemia, pericardial/pleural effusions, previous thyroid injury, pituitary/hypothalamic disorders, Hx of autoimmune disease

86
Q

What conditions can cause transient hypothyroidism?

A

lymphocytic thyroiditis, postpartum, subtotal thyroidectomy, radioiodine ablation, withdrawal of suppressive doses of thyroid hormone

87
Q

What is Hashimoto’s thyroiditis?

A

chronic autoimmune thyroid inflammation that is the most common cause of hypothyroidism in iodine sufficient areas of the world - characterized by gradual thyroid failure (with or without goiter) due to autoimmune mediated destruction of the thyroid gland (apoptosis of thyroid epithelial cells)

88
Q

What are the common signs of Hashimoto’s thyroiditis?

A

high serum concentrations of antibodies against thyroid antigens (thyroid peroxidase [TPO], thyroglobulin [Tg], TSH receptor), diffuse lymphocytic infiltration of the thyroid, and follicular destruction

89
Q

What are features of hypothyroidism in children and adolescents?

A

declining growth velocity/short stature, altered school performance, sluggishness, lethargy, cold intolerance, constipation, dry skin, brittle hair, facial puffiness, muscle aches/pains, goiter, overweight (due to fluid retention), dull/placid expression, bradycardia, pseudohypertorphy of the muscles, delayed deep tendon reflexes

90
Q

What is the most common cause of hypothyroidism worldwide?

A

iodine insufficiency

91
Q

What is the pathway of thyroid hormone production?

A

hypothalamus secretes thyrotropin-releasing hormone (TRH) => triggers release of TSH from anterior pituitary => stimulates thyroid to release T4/T3 (which inhibits TSH and TRH) => T4 converted to T3 in peripheral tissues => increase levels of free T4/T3 induced negative feedback cycle

92
Q

What are the common clinical manifestations of central hypothyroidism?

A

fatigue, cold intolerance, muscle cramps, headache, weight gain, lack of goiter, Hx of hypothalamic/pituitary disease

93
Q

What are the common neurologic manifestations of hypothyroidism?

A

myxedema coma (decreased mental status, bradycardia, hypothermia), cognitive impairment (slowed mentation, poor concentration/short-term memory), cerebellar ataxia (gait disturbance), carpal tunnel syndrome, peripheral neuropathy, myopathy, depressed mood, apathy, psychosis

94
Q

When should treatment be initiated in hypothyroidism?

A

any patients with symptoms or when TSH levels are persistently greater than 10 mU/L

95
Q

What is the adult dosage of levothyroxine to treat hypothyroidism?

A

1.6 mcg/kg/day - for subclinical hypothyroidism consider starting at 50% to 75% of predicted full replacement dosage

96
Q

What is the target goal for TSH in treatment of primary hypothyroidism?

A

0.5 to 2.0 mU/L

97
Q

What is thyrotoxicosis?

A

general term for presence of increased levels of thyroxine (T4), triiodothyronine (T3) or both, from any cause

98
Q

How is hyperthyroidism defined?

A

thyrotoxicosis in which the thyroid is actively overproducing thyroid hormone

99
Q

How does radioactive iodine uptake test differentiate different causes of hyperthyroidism?

A

diffuse/uniform uptake = Grave’s disease; patchy distribution = toxic multinodular goiter; unifocal activity limited to a single nodule = toxic adenoma

100
Q

What are the common presentations of hyperthyroidism?

A

palpitations, anxiety, restlessness, insomnia, impaired concentration, emotional lability, weight loss, heat intolerance, exertional dyspnea, fatigue, menstrual disorders, hair thinning, warm/moist skin, hyperreflexia, lid lag/retraction, tachycardia, preorbital myxedema, goiter

101
Q

What is adrenal insufficiency?

A

inadequate production of glucocorticoids, mineralocorticoids, or both by the adrenal glands

102
Q

How is adrenal insufficiency categorized?

A

primary (dysfunction or complete destruction of the adrenal cortex), secondary (inadequate adrenocorticotropic hormone [ACTH] production by pituitary), or tertiary (inadequate corticotropin-releasing hormone [CRH] by hypothalamus)

103
Q

What is the most common cause of primary adrenal insufficiency?

A

autoimmune adrenalitis (Addison’s disease) - associated with increased levels of 21-hydroxylase antibodies

104
Q

What is the most common cause of central (secondary or tertiary) adrenal insufficiency?

A

withdrawal of glcucorticoids after long-term use

105
Q

What are common laboratory abnormalities in adrenal insufficiency?

A

hyperkalemia (due to mineralocorticoid deficiency) and hyponatremia (due to glucocorticoid deficiency - related to elevated vasopressin, free water retention, shift of free sodium into cell)

106
Q

What are the signs and symptoms of adrenal crisis?

A

severe hypotension, weakness, fatigue, N/V, abdominal pain, fever, altered mental status, hypoglycemia

107
Q

What is the treatment for adrenal crisis?

A

dexamethasone initially (4 mg IV), IV hydrocortisone (100 mg IV p8h), IV saline

108
Q

What is the treatment of chronic adrenal insufficiency?

A

hydrocortisone (has been glucocorticoid and mineralocorticoid activity) 10-15 mg in a.m. and 5-10 mg in p.m.

109
Q

What is the recommendation for glucocorticoid therapy for patients with adrenal insufficiency during times of stress?

A

dosages of glucocorticoids should be doubled or tripled for mild to moderate infections and during labor and delivery

110
Q

What is a pheochromocytoma?

A

adrenal medullary (central part of the adrenal gland) tumor composed of chromaffin cells and capable of secreting epinephrine, norepinephrine, and dopamine

111
Q

What is the classic triad of a pheochromocytoma?

A

sudden severe headaches, diaphoresis, palpitations - HTN, tremor, pallor, and anxiety are also common

112
Q

Why are BP effects so variable in pheochromocytoma?

A

the tumors may cause secretion of different biogenic amines - those that secrete epinephrine (a beta-andrenergic stimulatory vasodilator) will cause hypotension while those that secrete norepinephrine (an alpha-andrenergic stimulatory vasoconstrictor) will cause hypertension

113
Q

How is pheochromocytoma diagnosed?

A

test for plasma free metanephrine - fourfold elevations are nearly 100% predictive of a tumor

114
Q

What is the treatment for pheochromocytoma?

A

surgical resection

115
Q

What is the role of cortisol and other glucocorticoids in healthy people?

A

increase glucose production and protein breakdown, inhibit protein synthesis, stimulate lipolysis, affect immune and inflammatory responses, maintain BP

116
Q

How are cortisol levels normally regulated?

A

hypothalamus produces corticotropin-releasing hormone (CRH) and vasopressin (antidiuretic hormone), which stimulate the pituitary gland to produce the hormone adrenocorticotropin (ACTH), which, in turn, stimulates the adrenal glands to produce cortisol => cortisol feeds back to hypothalamus and pituitary glands to suppress ACTH and CRH => cortisol production normally follows circadian rhythm (higher in the early morning and lower in the late evening)

117
Q

What are the clinical symptoms of excessive cortisol production (Cushing’s syndrome)?

A

obesity, wasting of extremities, moon facies, supraclavicular fat pads, buffalo hump, thinning of skin, easy bruising, violaceous striae, HTN, atherosclerosis, CHF, edema, muscular weakness, gonadal dysfunction, depression, insomnia, emotional lability, osteoporosis, increased infections, poor wound healing, acne, hirsutism

118
Q

What is Nelson syndrome?

A

appearance, sometimes years after adrenalectomy (to treat Cushing’s syndrome), of an aggressive corticotrophic pituitary tumor - pituitary gland continues to grow and secretes ACTH => key characteristic is dark skin color

119
Q

What is band keratopathy?

A

irregular region of calcium phosphate deposition at the medial and lateral limbic margins of the outer edges of the corneas

120
Q

What are the classic radiographic findings in hyperparathyroidism?

A

subperiosteal bone resorption along the radial aspect of the middle and distal phalanges and distal clavicles; salt-and-pepper skull; bone cysts; brown tumors on long bones

121
Q

What is the primary differential diagnosis of hyperparathyroidism?

A

hypercalcemia

122
Q

What are the laboratory findings in different types of hyperparathyroidism?

A

primary (high-normal parathyroid hormone and high calcium), secondary (high parathyroid hormone and low-normal calcium), tertiary (very high parathyroid hormone and high calcium)

123
Q

What are the indications for parathyroidectomy in patients with primary hyperparathyroidism?

A

patients with confirmed hyperparathyroidism who present with symptomatic disease (polydipsia, polyuria, nephrolithiasis, osteoporosis, fragility fractures, pancreatitis, peptic ulcer disease, GERD, neurocognitive dysfunction); patients with asymptomatic hyperparathyroidism but with serum calcium > 1.0 mg/dL above the upper normal limit, GFR < 60 mL/min, DEXA T-score < -2.5, age < 50 years with mild hypercalcemia, calcium nephrolithiasis

124
Q

What are the recommendations for health management among patients with hyperparathyroidism?

A

adequate hydration (> 8 glasses of water daily), exercise, normal-calcium diet, avoid thiazide diuretics and lithium

125
Q

What is parathyroid crisis?

A

severe hypercalcemia (> 15 mg/dL) in patients with primary hyperparathyroidism - CNS dysfunction, change in mental status (confusion and coma), bone disease, nephrolithiasis, severe abdominal pain, N/V, peptic ulcer, pancreatitis

126
Q

What is the meaning of the phrase “bones, stone, abdominal groans, and psychic moans” in hyperparathyroidism?

A

common symptoms of disease: bone pain and resorption (decreased bone density at cortical sites [forearm and hip] than trabecular sites [spine]); nephrolithiasis; nausea and constipation; lethargy, depression, psychosis, decreased social interaction, cognitive dysfunction

127
Q

What is the Wolff-Chaikoff effect?

A

iodine excess inhibits T4 and T3 synthesis in patients with abnormal thyroid glands, leading to hypothyroidism

128
Q

What are the contraindications to parathyroid surgery?

A

relative contraindications: (1) contralateral recurrent laryngeal nerve injury/vocal cord dysfunction and (2) symptomatic cervical disc disease; absolute contraindication: familial hypocalciuric hypercalcemia (persistent, mildly elevated serum calcium level due to higher renal setpoint for calcium excretion)

129
Q

What are the two mechanisms of hyperthyroidism?

A

(1) de novo synthesis of hormone (normal or high radioiodine uptake - treat with thionamides) and (2) hyperthyroidism due to inflammation/destruction of thyroid tissue/extrathyroidal source of thyroid hormone (low/near absent radioiodine uptake - near absent common only with amiodarone)

130
Q

What are the causes of de novo synthesis of thyroid hormone in hyperthyroidism?

A

(1) Graves’ disease - autoimmune disorder due to TSH-receptor antibodies which stimulate thyroid gland growth and thyroid hormone synthesis/release; (2) toxic adenoma/toxic multinodular goiter; (3) iodine-induced hyperthyroidism; (4) TSH-producing pituitary adenomas

131
Q

What are the causes of hyperthyroidism with near absent radioiodine uptake?

A

(1) thyroiditis (amiodarone, radiation, interferon alpha, lithium, palpation thyroiditis) => treat with beta blockers and anti-inflammatory drugs (aspirin) and (2) exogenous or ectopic sources of thyroid hormone (Synthroid overdose, struma ovarii [thyroid tissue in an ovarian neoplasm], thyroid cancer metastases)

132
Q

What are the changes induced by lack of thyroid hormone that lead to manifestations of hypothyroidism?

A

(1) generalized slowing of metabolic processes (fatigue, slow movement/speech, cold intolerance, constipation, weight gain, delayed relaxation of deep tendon reflexes, bradycardia) and (2) accumulation of matrix glycosaminoglycans in interstitial spaces (coarse hair and skin, puffy facies, enlargement of tongue, hoarseness)

133
Q

What are skin manifestations of hypothyroidism?

A

skin is cool and pale (decreased blood flow), dry/rough skin (due to hyperkeratosis), decreased sweating, carotenemia, hair loss, coarse hair, brittle nails, myxedema, vitiligo, alopecia areata

134
Q

What is the dosage requirement for levothyroxine in the elderly?

A

<= 75% of the dosage needed for younger people

135
Q

A “cold spot” in a thyroid scan of a PT with a thyroid mass is most likely to be?

A

a thyroid cyst - fluid filled mobile mass

136
Q

What is the effect of taking levothyroxine at the same time as iron, calcium, aluminum-containing antacids, sucralfate, or daily products?

A

reduced absorption of levothyroxine - take at the same time very day on an empty stomach with a glass of water and separate these other medications by several hours

137
Q

What is the effect of taking levothyroxine at the same time as rifampin, phenytoin, carbamazepine, and phenobarbital?

A

its metabolism can be increased, with resulting reduction of free T4 - take at the same time very day on an empty stomach with a glass of water and separate these other medications by several hours

138
Q

What is the likely diagnosis of a patient with painless thyroid mass and TSH level of < 0.1 IU/mL?

A

autonomously functioning adenoma

139
Q

What are the signs and symptoms of a thyroid malignancy?

A

very high free T4 level, fixed/painless thyroid mass, hoarseness, dysphagia

140
Q

What is a possible consequence of excessive levothyroxine use?

A

bone thinning

141
Q

How often should TSH be reassessed after levothyroxine dosage adjustment?

A

every 6-8 weeks (effects of a dosage adjustment would not cause a change in TSH for 5-6 drug half-lives)

142
Q

What are risk factors for thyroid dysfunction?

A

Down syndrome (hypo); elderly (either); use of iodide (hypo), amiodarone, lithium (either), interferon-alpha, interluken-2; female (either); postpartum (hypo); personal/family Hx of autoimmune disease; Hx of head/neck irradiation or surgery (hypo)

143
Q

What is dessicated thyroid (Armour)

A

natural thyroid replacement that contains T4 and T3 - animal derived (porcine or bovine thyroid)

144
Q

What is the role of aldosterone in homeostasis?

A

a mineralocorticoid hormone produced in the adrenal cortex that regulates sodium and potassium balance

145
Q

What are the common causes of primary adrenal insufficiency?

A

autoimmune response (Addison’s), infections (TB, HIV, fungal infections), hemorrhage/blood loss, tumors, use of anticoagulants

146
Q

What are the common causes of secondary adrenal insufficiency?

A

pituitary disease (produces ACTH, which stimulated adrenal gland to produce its hormones) and abrupt cessation of systemic corticosteroids taken for chronic conditions for a protracted period of time

147
Q

What are some medications that can be used to control cortisol production?

A

mitotane (Lysodren), metyrapone (Metopirone), and mifepristone (Korlym) - blocks the effects of cortisol on tissues

148
Q

After subtotal thyroidectomy it is crucial to assess?

A

speaking ability - risk for laryngeal nerve damage

149
Q

What is myxedema?

A

abnormal deposits of mucin in the skin and other tissues due to deficiency of thyroxine (T4) - causes a dry/waxy swelling in the skin and nonpitting edema in the pretibial and facial area (more common in hypothyroidism) => untreated, can cause severe atherosclerosis attributed to increase in serum cholesterol (especially LDL)

150
Q

What is the therapeutic approach for a benign thyroid nodule?

A

watchful waiting with annual follow-up - surgery may be indicated if the nodule increases in size and interferes with breathing

151
Q

Why is parathyroid hormone increased during pregnancy?

A

to meet the increased requirements for calcium and vitamin D for fetal skeletal growth

152
Q

What is Trousseau’s sign?

A

carpal spasm in hand and fingers (flexed elbow and wrist, adducted thumb over palm, flexed metacarpophalangeal joints, adduction of hyperextended fingers, extended interphalangeal joints) in response to occlusion of the blood supply to the arm (using a BP cuff - inflated to 20 mmHg above level of SBP and maintained for 3 minutes) secondary to ulnar and median nerve ischemia - often preceded by muscle cramps in the legs and feet

153
Q

What are the two common signs for hypocalcemia?

A

Trousseau’s and Chvostek’s

154
Q

Which hormones are secreted by the posterior pituitary gland?

A

antidiuretic hormone (ADH - targets kidneys) and oxytocin (targets uterus and breasts)

155
Q

What is the common treatment for Graves’ ophthalmopathy?

A

prednisone to decrease swelling

156
Q

Why should a patient with pheochromocytoma void in small amounts?

A

avoid a full bladder

157
Q

What laboratory testing should a woman undergo prior to radioactive iodine therapy for Graves’ disease?

A

beta human chorionic gonadotropin - to rule out pregnancy

158
Q

What are the requirements for levothyroxine Tx during pregnancy?

A

dosage increase (by around 30%) - needs to be monitored throughout the pregnancy and dosage adjusted accordingly (natural increase in thyroid hormone generally occurs after delivery)

159
Q

What is apathetic hyperthyroidism of the elderly?

A

atypical presentation of hyperthyroidism - atrial fibrillation, depression, anorexia, and weight loss

160
Q

What are the typical findings in hypoparathyroidism?

A

elevated serum phosphate, decreased PTH and serum calcium, increased neuromuscular activity, decreased bone resorption, hypocalciuria, hypophosphaturia

161
Q

What is the most common cause of hypercalcemia?

A

primary hyperparathyroidism

162
Q

What accounts for the easy bruising in a PT with Cushing’s disease?

A

protein wasting and collagen loss

163
Q

What is the most common autoimmune disease in the United States?

A

Graves’ diseas

164
Q

What are common laboratory findings in a PT with Cushing’s disease?

A

increased cortisol, increased sodium, decreased potassium

165
Q

What is the appropriate response to a patient with hyperthyroidism who presents with a gritty feeling in her eyes, diminished visual acuity, change in ability to see colors, and feeling of pressure behind the eyes?

A

emergency referral to an ophthalmologist - PT is at risk for compression of the optic nerve and blindness

166
Q

After establishing clinical and biochemical euthyroid following thyroidectomy, how often should TSH be assessed?

A

annually

167
Q

What does a thyroid bruit indicate?

A

increased thyroid vascularity associated with hyperthyroidism (“thrill” is a palpable increase in vascularity)

168
Q

What is the mechanism of action of saturated solution of potassium iodide?

A

blocks thyroid hormone production and release

169
Q

What is the mechanism of action of propylthiouracil and methimazole

A

block peripheral conversion of T4 to T3

170
Q

What is the mechanism of action of type II calcimimetics (e.g., Cinacalcet)?

A

bind to calcium-sensing receptors on the surface of the parathyroid glands, which increases sensitivity to extracellular calcium and reduces excess secretion of PTH - used to treat secondary hyperparathyroidism (not PHPT)

171
Q

Which hormones are secreted by the anterior pituitary gland?

A

growth hormone (targets bones and organs), adrenocorticotropic hormone (ACTH - targets adrenal cortex), TSH (targets thyroid), follicle-stimulating hormone (FSH - targets testes and ovaries), luteinizing hormone (LH - targets ovaries), prolactin (targets breasts)

172
Q

What are the signs of hypocalcemia?

A

positive Chvostek’s sign, positive Trousseau’s sign, tetany, carpopedal spasms, tingling of lips/hands, muscular/abdominal cramps, low serum calcium, high serum phosphate, reduce urine calcium excretion

173
Q

Which laboratory tests should be order prior to initiation of (and monitored throughout treatment) antithyroid drugs?

A

WBC count (risk for agranulocytosis) and liver function tests (risk of liver failure)

174
Q

What are signs of virilization in women exposed to increased levels of androgens?

A

increased muscle mass, clitoral enlargement, lowered voice, behavioral changes

175
Q

What are some common clinical manifestations of hypercalcemia in hyperparathyroidism?

A

HTN, left ventricular hypertrophy, peptic ulcer disease, pancreatitis, fatigue, anxiety, bone loss

176
Q

What does the TSH test do?

A

measures the pituitary gland’s response to peripheral levels of thyroid hormone

177
Q

How does smoking increase the risk of ophthalmopathy in Graves’ disease?

A

use of tobacco increases inflammatory cytokines within the orbit - smoking is the most important known risk factor for the development or worsening of Graves’ ophthalmopathy

178
Q

How is serum thyroglobulin used?

A

to monitor for recurrence of thyroid cancer and to diagnose destructive thyroiditis

179
Q

What is Job-Basedown phenomenon?

A

iodine-induced thyrotoxicosis following exposure to large quantities of iodine (e.g., radiographic contrast agents)

180
Q

What are the markers for Hashimoto’s?

A

antiperoxidase and antithyroglobulin

181
Q

What are the potential sequelea of thyroiditis?

A

thyrotoxicosis - but can resolve spontaneously with brief hypothyroid phase

182
Q

When is treatment of hyperthyroidism recommended?

A

any PT with TSH < 0.1 mU/L

183
Q

What is methiomazole embropathy?

A

reflects the teratogenic effects of methiomazole

184
Q

Which lab tests are most sensitive to the functioning of antithyroid drugs?

A

T4 and T3 should be assessed about 4 weeks after initiation - TSH can remain suppressed for several months

185
Q

What are the extrathyroidal manifestations of Graves’ disease?

A

ophthalmopathy, dermopathy (pretibial myxedema - hyperpigmented orange peel texture to skin), thyroid acropachy (digital clubbing and edema)

186
Q

What is the most sensitive assay to confirm the diagnosis of thyrotoxicosis?

A

3rd generation assay to detect TSH within 0.01 mU/mL

187
Q

What is thyrotoxicosis?

A

Presence of increase serum levels of T4 (thyroxine) and T3 (triiodothyronine), regardless of the cause

188
Q

What is the most common cause of hyperparathyroidism?

A

single parathyroid adenoma (85% of the time)

189
Q

What are the effects of parathyroid hormone on calcium and phosphate?

A

serum calcium increases and serum phosphate decreases

190
Q

What are the clinical symptoms of excessive cortisol?

A

inhibition of bone formation (osteoporosis), HTN, proteolysis (muscular weakness), increased lipolysis (thinning of skin), gonadal dysfunction, depression

191
Q

What are the normal functions of cortisol?

A

BBIIG - maintains BP, Bone formation inhibition, anti-Inflammatory, decrease Immune function, increase Glucose production

192
Q

What is the most common sign of adrenal insufficiency?

A

weight loss

193
Q

What are the signs and symptoms of adrenal insufficiency?

A

STEROID - Sodium/Sugar low, Tiredness/fatigue/weakness, Electrolyte imbalance (hyperkalemia, hyponatremia), Reproductive changes, lOw BP (vascular collapse/shock), Increased pigmentation, Diarrhea/N/V and Depression

194
Q

What is the cosyntropin (man-made/synthetic portion of the natural hormone corticotropin/ACTH) stimulation test?

A

used to determine whether adrenal glands can respond appropriately to maximal stimulation by synthetic ACTH

195
Q

What distinguishes primary from central adrenal insufficiency?

A

in primary adrenal insufficiency ACTH is elevated - in central adrenal insufficiency ACTH abnormally normal (not elevated in response to low cortisol) or frankly low

196
Q

What is ostitis fibrosa cystica?

A

classical manifestation of primary hyperparathyroidal bone disease: salt and pepper skull, bone resorption in phalanges, bone cysts (excess osteoclast activity), brown tumors (due to hemosiderin deposition) of long bones => due to hypercalcemia

197
Q

What is T3 toxicosis?

A

greater increase in T3 than T4 - seen in Graves’ disease and multinodular goiter => due to increased T3 secretion and increased conversion of T4 to T3

198
Q

What are the three clinical criteria for diagnosing Graves’ disease?

A

new onset ophthalomopathy, non-nodular enlarged thyroid, severe hyperthyroidism

199
Q

What is suggested by hyperthyroidism in the setting of high RAI uptake?

A

de novo synthesis of hormone

200
Q

What is suggested by hyperthyroidism in the setting of limited RAI uptake?

A

inflammation and destruction of thyroid tissues or extrathyroidal source of thyroid hormone

AGPC3 (19 decks)

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