Approach To Endocrine Complaints II

Question 1

Describe the thyroid gland

Answer 1

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

Question 2

What are some causes for hypothyroidism?

Answer 2

Worldwide = iodine deficiency

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

Question 3

What is Hashimoto’s thyroiditis?

Answer 3

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)

Question 4

What are the key sx for hypothyroidism?

Answer 4

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

Question 5

What are the key signs for hypothyroidism?

Answer 5

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

Question 6

What labs are done to evaluate for hypothyroidism?

Answer 6

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

Question 7

How is hypothyroidism managed?

Answer 7

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

Question 8

What are the primary causes for hyperthyroidism?

Answer 8

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

Question 9

What is Grave’s disease?

Answer 9

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

Question 10

What are the key sx for Grave’s disease?

Answer 10

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

Question 11

What are the key signs for Grave’s disease?

Answer 11

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

Question 12

Which labs are done to evaluate for hyperthyroidism?

Answer 12

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

Question 13

How is hyperthyroidism managed?

Answer 13

Block thyroid hormone synthesis with anti-thyroid drugs

Remove thyroid tissue with radioiodine ablation or thyroidectomy

Question 14

What is a goiter?

Answer 14

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

Question 15

What is nodular disease?

Answer 15

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)

Question 16

What is the most common malignancy of the endocrine system?

Answer 16

Thyroid cancer

Question 17

Describe the parathyroid glands

Answer 17

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

Question 18

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

Answer 18

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

Question 19

What are the signs/sx for primary HPT?

Answer 19

Most asymptomatic

Incidentally discovered elevated Ca

Question 20

What is the classic presentation for primary HPT?

Answer 20

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

Question 21

What are some differential considerations of primary HPT?

Answer 21

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

Question 22

Which labs are done to evaluate for primary HPT?

Answer 22

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

Question 23

How is primary HPT managed?

Answer 23

Remove parathyroid glands surgically

Management of asymptomatic disease is less clear

Question 24

What are the primary causes for hypoparathyroidism?

Answer 24

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)

Question 25

What are the key sx for hypoparathyroidism?

Answer 25

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

Question 26

What are key signs for hypoparathyroidism?

Answer 26

Hypotension, irregular heart beat, heart failure | Classical findings: Chvostek’s sign and trousseau sign**

Question 27

What is Chvosteks sign?

Answer 27

Tapping the facial nerve elicits twitch of spasm or facial muscles

Question 28

What is trousseau sign?

Answer 28

Spasm of the hand upon inflation of the BP cuff

Question 29

What labs are done to evaluate for hypothyroidism?

Answer 29

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

Question 30

What is the management for hypoparathyroidism?

Answer 30

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

Question 31

Describe the adrenal glands

Answer 31

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

Question 32

Describe the glucocorticoids

Answer 32

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

Question 33

Describe mineralocorticoids

Answer 33

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

Question 34

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

Answer 34

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

Question 35

What are secondary causes of hypoadrenalism (adrenal insufficiency)?

Answer 35

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

Question 36

What are the key signs/sx for glucocorticoid deficiency?

Answer 36

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

Question 37

What are the key signs/sx for mineralocorticoid deficiency?

Answer 37

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

Question 38

What are some signs for Addison’s disease?

Answer 38

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

Question 39

What labs emulate for adrenal insufficiency?

Answer 39

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

Question 40

What is the management for adrenal insufficiency?

Answer 40

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

Question 41

What is Cushing’s syndrome (hypercortisolism)?

Answer 41

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

Question 42

Describe ACTH dependent hypercortisolism

Answer 42

Pituitary adenoma which produces ACTH (Cushing’s disease)* | Ectopic secretion of ACTH by non-pituitary tumor

Question 43

Describe ACTH independent hypercortisolism

Answer 43

Adrenocortical adenoma or carcinoma (rare)

Question 44

What is the iatrogenic cause of hypercortisolism?

Answer 44

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

Question 45

What are the key sx for Cushing’s syndrome?

Answer 45

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

Question 46

What are the key signs for Cushing’s syndrome?

Answer 46

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

Question 47

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

Answer 47

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

Question 48

How is Cushing’s disease managed?

Answer 48

Remove tumor in adrenal gland, pituitary, etc surgically | Block cortisol synthesis with medication

Question 49

What are the causes for mineralocorticoid excess (aldosteronism)?

Answer 49

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

Question 50

What is the clinical hallmark for aldosteronism?

Answer 50

HTN with low K (hypokalemia) | Na usually normal

Question 51

What labs are done to evaluate for aldosteronism?

Answer 51

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

Question 52

How is aldosteronism managed?

Answer 52

Remove unilateral lesions surgically | Block excess aldosterone with mineralocorticoid antagonist (for bilateral hyperplasia)

Question 53

Describe adrenal masses

Answer 53

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

Question 54

What is the evaluation/management for adrenal masses?

Answer 54

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

Question 55

What is pheochromocytoma?

Answer 55

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)

Question 56

What is the evaluation/management for pheochromocytoma?

Answer 56

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

Question 57

Describe pituitary tumors

Answer 57

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

Question 58

What is the evaluation/management for pituitary tumors?

Answer 58

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