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ECOS II Midterm > Approach To Endocrine Complaints II > Flashcards

Approach To Endocrine Complaints II Flashcards

1
Q

Describe the thyroid gland

A

Plays a major role in the metabolism, growth and development of the human body
Disorders include hypothyroidism (hormone deficiency) and hyperthyroidism (hormone excess)

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2
Q

What are some causes for hypothyroidism?

A

Worldwide = iodine deficiency

Developed world = autoimmune disease (Hashimoto’s thyroiditis) or iatrogenic cause (treatment of hyperthyroidism)

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3
Q

What is Hashimoto’s thyroiditis?

A

Autoimmune mediated process
Most common cause of hypothyroidism in the US
Initial sub clinical stage followed by overt hypothyroidism
Prevalence is greater in women
Insidious onset
+/- goiter (if present, feels irregular and firm)

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4
Q

What are the key sx for hypothyroidism?

A

Fatigue, weakness, dry skin, feeling cold, hair loss, constipation, weight gain, changes in menses (women)

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5
Q

What are the key signs for hypothyroidism?

A

Dry coarse, cool skin, puffy hands feet and face (myxedema), diffuse alopecia, edema and hyporeflexia

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6
Q

What labs are done to evaluate for hypothyroidism?

A

Elevated TSH
If abnormal, measure T4
Low T4 = primary hypothyroidism
Measuring thyroid peroxidase Abs differentiates autoimmune vs other

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7
Q

How is hypothyroidism managed?

A

Remember general rules - replace hormone ideally as physiologically as possible
Replace hormone with thyroxine (T4)

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8
Q

What are the primary causes for hyperthyroidism?

A

Grave’s disease, toxic multinodular goiter, toxic adenomas (benign, functional tumors of thyroid gland “hot nodules”)

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9
Q

What is Grave’s disease?

A

Accounts for 60-80%
Most common cause of hyperthyroidism in the US
Is an autoimmune disease that leads to a generalized overactivity of the entire thyroid gland

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10
Q

What are the key sx for Grave’s disease?

A

Hyperactivity/irritability, heat intolerance, palpitations, weight loss with increased appetite, decreased menses (women)

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11
Q

What are the key signs for Grave’s disease?

A

Tachycardia, tremor, goiter, warm most skin, eyelid retraction, hyper reflexia
Thyroid is usually diffusely enlarged, firm, not nodular

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12
Q

Which labs are done to evaluate for hyperthyroidism?

A

Suppressed TSH
Measure thyroid hormones
High T4 or T3 = primary hyperthyroidism
Are clinical features of Grave’s disease present? If not clinically Grave’s disease, then ultrasound and uptake scan are done

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13
Q

How is hyperthyroidism managed?

A

Block thyroid hormone synthesis with anti-thyroid drugs

Remove thyroid tissue with radioiodine ablation or thyroidectomy

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14
Q

What is a goiter?

A

Enlarged gland, usually the result of bio synthetic defects, iodine deficiency, autoimmune disease, etc
Leads to increased TSH which stimulates thyroid growth

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15
Q

What is nodular disease?

A

Disordered growth of thyroid cells
Enlargement may be benign growth vs malignant growth
Prevalence of nodules 3-7% by exam, up to 50% by ultrasound
-may be solitary vs multiple
-may be functional vs no function (termed toxic and nontoxic)

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16
Q

What is the most common malignancy of the endocrine system?

A

Thyroid cancer

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17
Q

Describe the parathyroid glands

A

PTH helps maintain an appropriate balance of Ca in the bloodstream and in tissues that depend on Ca for proper functioning
Increases bone resorption, increases intestinal Ca secretion via vitamin D, decreases Ca excretion in the kidney
Increased Ca decreases PTH, and vice versa

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18
Q

What are the primary causes of primary hyperparathyroidism (HPT)?

A

Autonomously functioning adenomas (80%) or hyperplasia (general enlargement)
Rarely may be cancer

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19
Q

What are the signs/sx for primary HPT?

A

Most asymptomatic

Incidentally discovered elevated Ca

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20
Q

What is the classic presentation for primary HPT?

A

Renal stones
Abnormal bones - osteitis fibrosis cystica (rare) - now osteoporosis
Abdominal moans - pain, N/V, constipation
Psychic groans - anxiety, depression, confusion, stupor, coma
Neuromuscular sx - proximal muscle weakness, easy fatigability, atrophy

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21
Q

What are some differential considerations of primary HPT?

A

Hypercalcemia of malignancy (2nd most common cause)
-usually symptomatic at discovery
-Ca usually markedly elevated
Other disorders with elevated Ca as a component

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22
Q

Which labs are done to evaluate for primary HPT?

A

Verify Ca, check PTH
If abnormally high measure Ca excretion in urine
Elevated = primary hyperparathyroidism

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23
Q

How is primary HPT managed?

A

Remove parathyroid glands surgically

Management of asymptomatic disease is less clear

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24
Q

What are the primary causes for hypoparathyroidism?

A

Most commonly occurs after inadvertent damage or removal of parathyroid glands during neck surgery
It can occur years after neck surgery
Autoimmune parathyroid destruction
Can rarely have tissue resistance to PTH (pseudohypoparathyroidism)

25
Q

What are the key sx for hypoparathyroidism?

A

Uncontrollable, painful spasms in face, hands, arms and feet
Pins and needles sensation in hands, feet and around mouth

26
Q

What are key signs for hypoparathyroidism?

A

Hypotension, irregular heart beat, heart failure

Classical findings: Chvostek’s sign and trousseau sign**

27
Q

What is Chvosteks sign?

A

Tapping the facial nerve elicits twitch of spasm or facial muscles

28
Q

What is trousseau sign?

A

Spasm of the hand upon inflation of the BP cuff

29
Q

What labs are done to evaluate for hypothyroidism?

A

Verify Ca, check PTH
If abnormally low, measure Ca excretion in urine
Decreased = hypoparathyroidism

30
Q

What is the management for hypoparathyroidism?

A

No PTH preparations are approved for use for hormone replacement
Use medications and dietary modifications to increase Ca

31
Q

Describe the adrenal glands

A

Play a major role and have multiple functions
Secrete mineralocorticoids which help regulate Na and K handing in the kidney which affects BP and fluid volume
Also secretes glucocorticoids which are responsible for aiding in glucose metabolism, inflammatory and immune response to illness
Also catecholamines, adrenal androgens

32
Q

Describe the glucocorticoids

A

Regulated by CRH, ACTH and cortisol
Hormone deficiency = adrenal insufficiency (primary vs secondary)
Hormone excess = Cushing’s disease

33
Q

Describe mineralocorticoids

A

Primarily controlled by RAAS regulatory cycle
Hormone deficiency = adrenal insufficiency (primary vs secondary)
Hormone excess = aldosteronism

34
Q

What are the primary causes for hypoadrenalism (adrenal insufficiency)?

A

Autoimmune destruction of adrenal gland (Addison’s disease)*
Destruction of gland by infection, hemorrhage, infiltration, metastasis
Genetic diseases - cause distinct enzymatic blocks in steroidogenesis

35
Q

What are secondary causes of hypoadrenalism (adrenal insufficiency)?

A

Suppression of HPA axis from exogenous glucocorticoids (most common*)
Hypothalamic/pituitary failure (usually from tumors, surgery, or irradiation; rarely from infarction)

36
Q

What are the key signs/sx for glucocorticoid deficiency?

A

Fatigue, weight loss/anorexia, hypoglycemia, low BP, postural hypotension

37
Q

What are the key signs/sx for mineralocorticoid deficiency?

A

Salt craving, low BP, postural hypotension, hyponatremia and hyperkalemia, hyperpigmentation (primary adrenal insufficiency only)

38
Q

What are some signs for Addison’s disease?

A

Hyperpigmentation in areas of increased friction including palmar creases, dorsal foot, nipples and axillary region, patch hyperpigmentation of the oral mucosa

39
Q

What labs emulate for adrenal insufficiency?

A

ACTH stimulation, then measure cortisol response
If abnormally low measure plasma ACTH, renin and aldosterone
Need those labs to distinguish primary vs secondary disease

40
Q

What is the management for adrenal insufficiency?

A

Hormone replacement
Primary -> replace glucocorticoid and mineralocorticoid
Secondary -> replace glucocorticoid

41
Q

What is Cushing’s syndrome (hypercortisolism)?

A

Constellation of clinical features that result from chronic exposure to excess glucocorticoids of any etiology
Causes: ACTH dependent or independent

42
Q

Describe ACTH dependent hypercortisolism

A

Pituitary adenoma which produces ACTH (Cushing’s disease)*

Ectopic secretion of ACTH by non-pituitary tumor

43
Q

Describe ACTH independent hypercortisolism

A

Adrenocortical adenoma or carcinoma (rare)

44
Q

What is the iatrogenic cause of hypercortisolism?

A

Medical use of glucocorticoids for immunosuppression or tx of inflammatory disorders (most common)

45
Q

What are the key sx for Cushing’s syndrome?

A 
Weight gain (around the abdomen) 
Easy bruising, acne, hirsutism 
Weakness (especially proximal muscleS) 
Abnormal menses (women), decreased libido 
Emotional lability, depression
46
Q

What are the key signs for Cushing’s syndrome?

A

Central obesity, purple stretch marks (striae), moon face, brittle skin in an elderly pt, hyperpigmentation of knuckles in pt’s with ATCH excess, buffalo hump, bruise easily, thin arms and legs, red cheeks, increased facial hair growth in women

47
Q

What labs are done to evaluate for Cushing’s syndrome?

A

Dexamethasone (glucocorticoid) suppression test - then measure cortisol
Measure cortisol directly with 24 hour urine excretion, midnight plasma cortisol
If cortisol abnormally high -> measure plasma ACTH
-trying to localize disease establish why

48
Q

How is Cushing’s disease managed?

A

Remove tumor in adrenal gland, pituitary, etc surgically

Block cortisol synthesis with medication

49
Q

What are the causes for mineralocorticoid excess (aldosteronism)?

A

Primary aldosteronism

Most common = adrenal adenomas (Conn’s syndrome), bilateral adrenal hyperplasia

50
Q

What is the clinical hallmark for aldosteronism?

A

HTN with low K (hypokalemia)

Na usually normal

51
Q

What labs are done to evaluate for aldosteronism?

A

Consider in severe/poorly controlled/early HTN, hypokalemia, etc
Measure plasma renin and aldosterone
If abnormal, image adrenal glands

52
Q

How is aldosteronism managed?

A

Remove unilateral lesions surgically

Block excess aldosterone with mineralocorticoid antagonist (for bilateral hyperplasia)

53
Q

Describe adrenal masses

A

Usually incidentally discovered
Benign -> majority are endocrine inactive
Malignant -> account for less than 3-7% of adrenal masses

54
Q

What is the evaluation/management for adrenal masses?

A

<1cm = monitor for change over time
>1cm requires diagnostic evaluation (benign vs malignant)
-does it secrete hormones that could detrimentally effect healthy? Ex. Pheochromocytoma*

55
Q

What is pheochromocytoma?

A

Catecholamine producing tumors derived from the sympathetic or parasympathetic NS
Classic sx triad: palpitations, HA, profuse sweating, sx highly variable, paroxysmal
Dominant sign = HTN (often episodic)

56
Q

What is the evaluation/management for pheochromocytoma?

A

Measure catecholamines/metanephrines in urine or plasma
Localize tumor with imaging
Remove tumor surgically

57
Q

Describe pituitary tumors

A

Often incidentally discovered on imaging studies
Usually pituitary adenomas
Common features: HA, visual loss, individual/features based on hormone being secreted

58
Q

What is the evaluation/management for pituitary tumors?

A

Screen for endocrine function with appropriate biochemical testing based on clinical presentation
Remove symptomatic tumors surgically
Block hormones excess with specific medical therapy
Small, non functional adenomas may be monitored with serial imaging

ECOS II Midterm (10 decks)

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