Approach To Endocrine Complaints II Flashcards
Describe the thyroid gland
Plays a major role in the metabolism, growth and development of the human body
Disorders include hypothyroidism (hormone deficiency) and hyperthyroidism (hormone excess)
What are some causes for hypothyroidism?
Worldwide = iodine deficiency
Developed world = autoimmune disease (Hashimoto’s thyroiditis) or iatrogenic cause (treatment of hyperthyroidism)
What is Hashimoto’s thyroiditis?
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)
What are the key sx for hypothyroidism?
Fatigue, weakness, dry skin, feeling cold, hair loss, constipation, weight gain, changes in menses (women)
What are the key signs for hypothyroidism?
Dry coarse, cool skin, puffy hands feet and face (myxedema), diffuse alopecia, edema and hyporeflexia
What labs are done to evaluate for hypothyroidism?
Elevated TSH
If abnormal, measure T4
Low T4 = primary hypothyroidism
Measuring thyroid peroxidase Abs differentiates autoimmune vs other
How is hypothyroidism managed?
Remember general rules - replace hormone ideally as physiologically as possible
Replace hormone with thyroxine (T4)
What are the primary causes for hyperthyroidism?
Grave’s disease, toxic multinodular goiter, toxic adenomas (benign, functional tumors of thyroid gland “hot nodules”)
What is Grave’s disease?
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
What are the key sx for Grave’s disease?
Hyperactivity/irritability, heat intolerance, palpitations, weight loss with increased appetite, decreased menses (women)
What are the key signs for Grave’s disease?
Tachycardia, tremor, goiter, warm most skin, eyelid retraction, hyper reflexia
Thyroid is usually diffusely enlarged, firm, not nodular
Which labs are done to evaluate for hyperthyroidism?
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
How is hyperthyroidism managed?
Block thyroid hormone synthesis with anti-thyroid drugs
Remove thyroid tissue with radioiodine ablation or thyroidectomy
What is a goiter?
Enlarged gland, usually the result of bio synthetic defects, iodine deficiency, autoimmune disease, etc
Leads to increased TSH which stimulates thyroid growth
What is nodular disease?
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)
What is the most common malignancy of the endocrine system?
Thyroid cancer
Describe the parathyroid glands
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
What are the primary causes of primary hyperparathyroidism (HPT)?
Autonomously functioning adenomas (80%) or hyperplasia (general enlargement)
Rarely may be cancer
What are the signs/sx for primary HPT?
Most asymptomatic
Incidentally discovered elevated Ca
What is the classic presentation for primary HPT?
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
What are some differential considerations of primary HPT?
Hypercalcemia of malignancy (2nd most common cause)
-usually symptomatic at discovery
-Ca usually markedly elevated
Other disorders with elevated Ca as a component
Which labs are done to evaluate for primary HPT?
Verify Ca, check PTH
If abnormally high measure Ca excretion in urine
Elevated = primary hyperparathyroidism
How is primary HPT managed?
Remove parathyroid glands surgically
Management of asymptomatic disease is less clear
What are the primary causes for hypoparathyroidism?
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)
What are the key sx for hypoparathyroidism?
Uncontrollable, painful spasms in face, hands, arms and feet
Pins and needles sensation in hands, feet and around mouth
What are key signs for hypoparathyroidism?
Hypotension, irregular heart beat, heart failure
Classical findings: Chvostek’s sign and trousseau sign**
What is Chvosteks sign?
Tapping the facial nerve elicits twitch of spasm or facial muscles
What is trousseau sign?
Spasm of the hand upon inflation of the BP cuff
What labs are done to evaluate for hypothyroidism?
Verify Ca, check PTH
If abnormally low, measure Ca excretion in urine
Decreased = hypoparathyroidism
What is the management for hypoparathyroidism?
No PTH preparations are approved for use for hormone replacement
Use medications and dietary modifications to increase Ca
Describe the adrenal glands
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
Describe the glucocorticoids
Regulated by CRH, ACTH and cortisol
Hormone deficiency = adrenal insufficiency (primary vs secondary)
Hormone excess = Cushing’s disease
Describe mineralocorticoids
Primarily controlled by RAAS regulatory cycle
Hormone deficiency = adrenal insufficiency (primary vs secondary)
Hormone excess = aldosteronism
What are the primary causes for hypoadrenalism (adrenal insufficiency)?
Autoimmune destruction of adrenal gland (Addison’s disease)*
Destruction of gland by infection, hemorrhage, infiltration, metastasis
Genetic diseases - cause distinct enzymatic blocks in steroidogenesis
What are secondary causes of hypoadrenalism (adrenal insufficiency)?
Suppression of HPA axis from exogenous glucocorticoids (most common*)
Hypothalamic/pituitary failure (usually from tumors, surgery, or irradiation; rarely from infarction)
What are the key signs/sx for glucocorticoid deficiency?
Fatigue, weight loss/anorexia, hypoglycemia, low BP, postural hypotension
What are the key signs/sx for mineralocorticoid deficiency?
Salt craving, low BP, postural hypotension, hyponatremia and hyperkalemia, hyperpigmentation (primary adrenal insufficiency only)
What are some signs for Addison’s disease?
Hyperpigmentation in areas of increased friction including palmar creases, dorsal foot, nipples and axillary region, patch hyperpigmentation of the oral mucosa
What labs emulate for adrenal insufficiency?
ACTH stimulation, then measure cortisol response
If abnormally low measure plasma ACTH, renin and aldosterone
Need those labs to distinguish primary vs secondary disease
What is the management for adrenal insufficiency?
Hormone replacement
Primary -> replace glucocorticoid and mineralocorticoid
Secondary -> replace glucocorticoid
What is Cushing’s syndrome (hypercortisolism)?
Constellation of clinical features that result from chronic exposure to excess glucocorticoids of any etiology
Causes: ACTH dependent or independent
Describe ACTH dependent hypercortisolism
Pituitary adenoma which produces ACTH (Cushing’s disease)*
Ectopic secretion of ACTH by non-pituitary tumor
Describe ACTH independent hypercortisolism
Adrenocortical adenoma or carcinoma (rare)
What is the iatrogenic cause of hypercortisolism?
Medical use of glucocorticoids for immunosuppression or tx of inflammatory disorders (most common)
What are the key sx for Cushing’s syndrome?
Weight gain (around the abdomen) Easy bruising, acne, hirsutism Weakness (especially proximal muscleS) Abnormal menses (women), decreased libido Emotional lability, depression
What are the key signs for Cushing’s syndrome?
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
What labs are done to evaluate for Cushing’s syndrome?
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
How is Cushing’s disease managed?
Remove tumor in adrenal gland, pituitary, etc surgically
Block cortisol synthesis with medication
What are the causes for mineralocorticoid excess (aldosteronism)?
Primary aldosteronism
Most common = adrenal adenomas (Conn’s syndrome), bilateral adrenal hyperplasia
What is the clinical hallmark for aldosteronism?
HTN with low K (hypokalemia)
Na usually normal
What labs are done to evaluate for aldosteronism?
Consider in severe/poorly controlled/early HTN, hypokalemia, etc
Measure plasma renin and aldosterone
If abnormal, image adrenal glands
How is aldosteronism managed?
Remove unilateral lesions surgically
Block excess aldosterone with mineralocorticoid antagonist (for bilateral hyperplasia)
Describe adrenal masses
Usually incidentally discovered
Benign -> majority are endocrine inactive
Malignant -> account for less than 3-7% of adrenal masses
What is the evaluation/management for adrenal masses?
<1cm = monitor for change over time
>1cm requires diagnostic evaluation (benign vs malignant)
-does it secrete hormones that could detrimentally effect healthy? Ex. Pheochromocytoma*
What is pheochromocytoma?
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)
What is the evaluation/management for pheochromocytoma?
Measure catecholamines/metanephrines in urine or plasma
Localize tumor with imaging
Remove tumor surgically
Describe pituitary tumors
Often incidentally discovered on imaging studies
Usually pituitary adenomas
Common features: HA, visual loss, individual/features based on hormone being secreted
What is the evaluation/management for pituitary tumors?
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
