Endocrine System Flashcards
pituitary gland - basics
pea-sized gland in brain
- below optic chiasm
Anterior lobe:
- secretes TROPHIC hormones (other flags are target - adrenal cortex, thyroid, ovaries, testes)
- secretes GH and prolactin
Posterior lobe:
- secretes vasopressin / ADH and oxytocin
HPA axis: hypothalamic pituitary adrenal axis
- negative feedback loop
neoplastic disease (adenoma) of pituitary - sxs
benign growth in pituitary gland
- adenoma is most common
s/sx (general):
- HA, bitemporal hemianopsia/visual field defect, CN III
Presenting sxs relate to cell type of adenoma
- prolactin secreting
- GH secreting
- ACTH secreting
neoplastic disease (adenoma) of pituitary - s/sx
- prolactin secreting
- GH secreting
- ACTH secreting
- Prolactinoma
- M: hypogonadism
- F: oligomenorrhea, infertility, galactorrhea - GH excess (somatotroph)
- gigantism before puberty
- acromegaly after puberty (esp. hands, feet, face) - ACTH (corticotroph)
- Cushing disease: HTN, central obesity, moon face, buffalo hump
acromegaly/gigantism
due to excess growth hormone
- can be from pituitary adenoma
- GH converted to IGH (insulin-like GH) in liver)
- gigantism before puberty
- acromegaly after puberty
s/sx:
- extremity enlargement
- thick skin
- course facial features (prominent mandible, brow, lips)
- organomegaly
pituitary adenoma - dx (for each type)
MRI: image pituitary
Labs: depend on type of adenoma
Prolactinoma: high prolactin so eval testosterone (M) and estradiol, FSH, LH (F)
GH excess (somatotroph): serum IGF high, NO suppression of GH w/ glucose tolerance test - eval TSH, T4, glucose
ACTH (corticotroph): elevated 24 hr cortisol
- suppression w/ high dose dexamethasone suppression test
- CRH stimulation test differentiates from other adrenal cortex pathology
pituitary adenoma - tx (for each type)
- prolactinoma
- prolactin secretion from ant. pituitary is inhibited by dopamine
- dopamine agonist medication (cabergoline, bromocriptine)
- surgery - GH secreting (somatotroph)
- surgery
- may need medication post-surgery for hormone management - ACTH secreting (corticotroph)
- surgery
- may need medication post-surgery for hormone management
hypopituitarism - definition, causes
not enough secretion from pituitary
can original from hypothalamus with releasing hormones or pituitary
causes:
- congenital
- acquired: surgery, radiation, trauma
- infarction: sheehan syndrome (post partum)
- mass in hypothalamus or ant. pituitary
hypopituitarism - s/sx
depend on which hormone(s) are deficient:
- prolactin - inhibition of post part lactation
- GH - short stature (meds), strength loss, central obesity (adults)
- ACTH - reduction of adrenal cortisol = Addison dz
- TSH - secondary hypothyroidism
- FSH/LH - hypogonadism and infertility
dwarfism - definition, clinical features, dx, tx
GH deficiency during childhood
- short stature (height 2.25 SDs blow mean (1%))
- growth failure
Dx:
- IGF low
- hypoglycemia as infant
- eval genetic conditions
Tx:
- synthetic GH injections
vasopressin/ADH and hypothalamus
hypothalamus sensitive to osmolality
- high: inc. thirst, triggers post. pituitary to inc. ADH release which effects kidneys (inc. H2O absorption)
- low: ADH low resulting in diuresis
diabetes insipidus - definition, s/sx, 2 forms, tx
defect or deficiency in vasopressin (aka ADH)
s/sx:
- intense thirst (polydipsia)
- excessive urination (polyuria)
2 forms:
- Central: dec. pituitary secretion of ADH (trauma, neoplasm, infection, iatrogenic after surgery)
- tx: replace vasopressin with analog called desmopressin (DDAVP) - Nephrogenic: failure of response to ADH in kidneys (drugs - lithium, hypercalcemia)
- Tx: thiazide diuretics, indomethacin
hypothalamic-pituitary-thyroid axis
hypothalamus: release TRH –>
anterior pituitary: release TSH –>
thyroid gland: release T3 and T4
- negative feedback on both hypothalamus (TRH) and ant. pituitary (TSH)
- T3 and T4 have systemic effect of increasing metabolism
thyroid gland hormones
thyroxine (T4): 91%
- only produced in thyroid gland
Triiodothyronine (T3): 7%
- 4x as potent as T4
- T4 –> T3 conversion
NOTE: iodine required for production of thyroid hormones
hyperthyroidism - definition, causes, s/sx, dx
too much thyroid hormone (aka thyrotoxicosis)
causes:
- Grave’s disease
- toxic nodules
- thyroiditis
- iodine induced
- exogenous hormone
s/sx: high metabolism
- weight loss
- tachycardia, anxiety, sweating, brittle hair
- thyroid goiter
Grave’s disease - definition, sxs, dx, tx
autoimmune dz where antibodies bind to and activate TSH receptor, mincing effects of TSH
- TSH is actually low (no negative feedback)
- most common cause of hyperthyroidism
s/sx
- weight loss
- tachycardia, anxiety, sweating, brittle hair
- eye sxs: swelling, inflammation, exophthalmos (bulging)
Dx:
- low TSH, high T4 and T3
- positive thyrotropin-receptor antibodies (diagnostic)
- thyroid U/S shows diffuse uptake of radioactive iodine (endogenous source = Graves)
Tx:
- symptomatic: propranolol (beta blocker)
- anti thyroid drugs (block thyroid peroxidase): methimazole, PTU
- radioactive iodine ablated thyroid fx (this can result in hypothyroid)
- surgery (can result in hoarseness, hypoparathyroidism)
thyroid storm - definition, causes, s/sx, dx
very high level of thyroid hormones
- rare complication w/ high mortality
causes: serious illness, thyroid surgery, infection, radio-active iodine admin
clinical: tachycardia, delirium, high fever, V/D, dehydration
tx:
- beta blocker
- PTU
- iodide
- glucocorticoids
hypothyroidism - definition, causes
low thyroid hormones
causes:
- autoimmune thyroiditis (Hashimoto) - most common
- no thyroid: after thyroidectomy, post RAI
- meds: amiodarone, lithium
- secondary hypothyroidism: pituitary dysfx, postpartum necrosis (Sheehan), neoplasm
hypothyroidism - s/sx, dx
s/sx: slow metabolism
- fatigue, weakness, weight gain
- cold intolerance, constipation
- dry, course skin
- enlarged thyroid/goiter: Hoshimoto)
- congenital: growth failure, mental retardation (checked on NB screen)
Dx: Primary hypothyroidism: - serum TSH high - Serum T4/T3 low Subclinical hypothyroidism: - serum TSH high - Serum T4/T3 normal
hypothyroidism - tx
daily levothyroxine (synthetic T4)
monitor with TSH levels
- check every 4-6 wks
- normal range: 0.4-4.2
- close monitoring w/ wt change, med change, pregnancy
myxedema coma
VERY low T4 and T3 levels
- often in elderly women
- boggy eyes, swollen face, non-pitting edema, pericardial effusion, AMS
- ICU admit, thyroxine IV, glucocorticoids IV
thyroid cancer - s/sx, dx, tx
papillary is most common and least aggressive (slow-growing)
thyroid lymphoma in Hoshimotos
s/sx:
- firm, palpable non-tender nodule
- hoarseness, dysphagia
Note: not all nodules are cancerous
Dx:
- U/S showing nodules w/ irregular borders, complex cyst, micro calcifications
- fine-needle aspiration if suspicious
- tx varies from monitoring to thyroidectomy (w/ T4 replacment)
thyroiditis - definiton, causes
inflammation of thyroid
Causes:
- commonly due to autoimmune process: Hashimoto thyroiditis
- multinodular goiter: elderly
- subacute
- infectious
thyroiditis - sxs, dx, and tx (for each cause)
Clinical:
- Hashimoto: rubbery firmness, diffusely enlarged goiter
- Subacute: painful goiter, dysphagia
- Infectious: painful, enlarged thyroid, systemic sxs
Dx:
- Hashimotos: high TSH, pos. TPO antibodies
- subacute: ESR high, antibodies negative
- infectious: ESR and leukocytes high
Note: fine-needle aspiration is rapid growth, painful nodule
Tx:
- Hashimoto: levothyroxine
- subacute: aspirin, supportive care
- infectious: ABX, drainage
parathyroid - location and role
located in posterior poles of thyroid gland
- 4 glands
Role:
- controls Ca++ homeostasis
- low calcium, causes inc. PTH release
- PTH target organs are bone and kidney
- PTH also activates vit D which stimulates Ca++ reabsorption in gut
Feedback on parathyroid glands:
- positive: low serum Ca++
- negative: high serum Ca++, high vit D
hyperparathyroid - definition, clinical
PTH excess results in elevated Ca++
causes:
- parathyroid adenoma, meds (lithium), chronic renal failure
s/sx:
- can be asymptomatic
- bones: cortical bone loss, pain
- stones: kidney stones
- abd groans: abd pain, N/V
- psychic moans: depression, weakness, memory issues
hyperparathyroid - dx, tx
Dx:
- serum Ca++ elevated
- serum PTH elevated
Note: Imaging to guide surgery
Tx:
- remove adenoma
- maintain normal vit D and calcium diet
- encourage fluids to avoid kidney stones
- avoid thiazides and lithium
hypoparathyroidism - definition, s/sx
PTH deficiency resulting in low serum Ca++
cause:
- thyroidectomy
- parathyroid adenoma
s/sx: think hypocalcemia (“neuromuscular irritability”)
- weakness, fatigue, muscle spasm, paresthesias of hands/lip
- Chvostek sign: twitching of facial muscle when facial nerve tapped
- Trousseau sign: carpal spasm when arm is compressed with BP cuff for 3-5 min
hypoparathyroidism - dx, tx
Dx:
- low PTH
- low ca++
- elevated phosphate
Tx:
- replace doses of calcium and vit D
vitamin D (1,25-dihydroxycholecalciferol) - basics
- obtained through diet and sunlight
- converted to active for (1,25) in kidney
- active vit D binds GI receptors to allow Ca++ absorption
chronic renal dz:
- dec. vit. D since cannot be converted to active form
- results in low Ca++ levels which result in secondary hyperparathyroidism
disorders related to vitamin D
rickets: low vit. D (and calcium) in children
osteomalacia: decrease bone mineralization
osteoporosis: caused by reduced osteoblastic activity due to lack of estrogen and/or physical activity
- results in dec. bone mineralization and matrix formation
adrenal glands - what do they produce
adrenal cortex (outer layer)
- aldosterone
- cortisol**
- androgens
adrenal medulla (inner layer)
- epinephrine (80%)
- norepinephrine (20%)
glucocorticoids - general systemic effects
inc. plasma glucose levels
inc glycogen synthesis
catecholamine effects
maintain vascular integrity and response to pressers / fluid volume
inc RBC
Inc. anti-inflammatory cytokine production, dec. inflammation
Cushing syndrome - definition, causes, s/sx
hypercortisolism (high cortisol)
Causes:
- ACTH-secreting pituitary adenoma (Cushing disease)
- adrenal adenoma
- ectopic ACTH (lung cancer)
- too much exogenous glucocorticoid (meds)
s/sx:
- weakness, easy bruising
- central obesity, hirsutism, round face (moon facies), supraclavicular fat pads
- HTN, inc. infections, bone loss
Cushing Syndrome - dx
- establish that you have high cortisol
- overnight low dose dexamethasone suppression test
- if no suppression (cortisol > 5) = + for Cushing
24-hr urinary free cortisol
- 3x normal = + for Cushing
- confirmatory test
late-night salivary cortisol
- high (>250) = + for Cushing
- confirmatory test
- identify source of high cortisol by measuring ACTH
- low ACTH: cortisol is turning off HPA –> adrenal source
- high ACTH: HPA feedback not responding –> pituitary or ectopic source - if ACTH is high, is it pituitary or ectopic - do high dose dexamethasone test
- if low: pituitary adenoma since high cortisol is turning off HPA = Cushing disease
- if high: ectopic source since HPA feedback not responding - Imaging: only for mass identification
Cushing disease
when high cortisol is due to pituitary ademona
Cushing syndrome - tx
Pituitary adenoma (Cushing dz) - surgery
Adrenal adenoma
- surgery
Ectopic ACTH
- resect hormone-producing tumor
- meds to suppress hypercortisolism
Exogenous glucocorticoids
- taper steroid meds
Addison disease - definition, causes, s/sx
too little cortisol
causes:
- autoimmune: anti adrenal antibodies (most common)
- infection (TB)
- iatrogenic (adrenalectomy)
- secondary: pituitary failure, stop exogenous steroids
s/sx:
- malaise, fatigue (worse with exertion and relieved with rest), weakness, pain/arthralgia
- N/V, weight loss, abd pain
- irritable, depression
- hypotension, hypoglycemia
Addison disease - dx, tx
Labs:
- low plasma cortisol
- high ACTH
Indicates corticoadrenal insufficiency
Do Cosynotropin stimulation test (synthetic ACTH)
- normal: serum cortisol inc.
- if serum cortisol stays low = corticoadrenal insufficiency
- if also anti adrenal antibodies = Addison’s
- if not autoimmune, image adrenal glands for source
tx: replace hormones
1. glucocorticoids: hydrocortisone
- mineralocorticoids: fludrocortisone
Addisonian crisis
emergent insufficient cortisol
causes:
- stress, surgery (adrenalectomy), destruction of pituitary, infection
s/sx:
- N/V, dehydration
- severe hypotension
- SHOCK
tx:
- IV hydrocortisone ASAP
- infection: broad ABX
- fluid manage, electrolyte manage
pheochromocytoma
tumor of adrenal medulla
- secretes epinephrine and norepinephrine
- rare
s/sx:
- palpitations
- diaphoresis
- headaches
- refractory HTN
dx:
- plasma and urine metanephrines high
- CT or MRI of abdomen to locate tumor
tx:
- BP comtrol: alpha blockers, beta blockers, Ca++ channel blockers
- surgical resection
Diabetes Mellitus - screening and types
metabolic abnormalities due to hyperglycemia
Screening:
- if overweight (BMI > 25) w/ additional risk factor (age, sedentary, ethnicity, FH DM, PCOS, HTN, hyper-lipids)
- anyone over age 45
Type 1: do not produce insulin
- autoimmune disease of pancreatic beta cells
- s/sx: polyuria, polydipsia, polyphagia (wt loss). DKA
Type 2: loss of insulin production and/or insulin resistance
DKA
can be presenting sxs of type I diabetic
- body is acidotic and using ketones for energy
s/sx:
- fruity breath
- abdominal pain
- Kussmaul breathing (deep) - breath off CO2
- confusion, lethargy
- tachycardic, hypotension
tx:
- ICU: IV insulin, glucose, fluids, monitor electrolytes
Diabetes Mellitus - diagnosis
- classic sxs + random glucose > 200
- HgbA1C > 6.5 (prediabetes: 5.7-6.5)
- fasting glucose (x2) > 126 (prediabetes: 100-125)
- 2-hr oral glucose tolerance test >200 (prediabetes: 140-199)
Note: will see GAD antibodies in type 1 (autoimmune dz)
- blood glucose tes preferred over HgBA1C in type 1
Diabetes Mellitus - Type 1 tx
goal: manage hyperglycemia (target A1C <7%)
basal and prandial insulin therapy
- rapid: lispro, glulisine, aspart
- intermediate: NPH
- long-acting: deter, glargine
OP monitoring of glucose by fingerstick glucometer
Diabetes Mellitus - Type 2 tx
goal: manage hyperglycemia (target A1C <7%)
#1 lifestyle: - wt loss, exercise, management of chronic dz
Meds: stepwise 1st line: biguanide (Metformin): reduces glucose produced by liver, inc. cell sensitivity to insulin - add second agent - add third agent - add insulin (basal 1st)
DM medications - mechanisms of action
Biguanide (Metformin): reduces glucose produced by liver, inc. cell sensitivity to insulin
Sulfonlyureas (glipizide, glyburide): stimulate insulin production from pancreas
Meglitinides (secretagogue) (Repaglinide, Nateglinide): stimulates beta cells of pancreas to inc. insulin secretion
Thiazolidinediones (Pioglitazone, Rosiglitazone): decrease insulin resistance of muscle cells and adipocytes (glucose taken up and used as energy or stored as fat)
DPP-4 Inhibitors (Sitagliptin, Saxagliptin, Linagliptin, Alogliptin) (aka incretin-based therapy): increase levels of “native”, active GLP-1 by inhibiting DPP-4 (enzyme that inactivates GLP-1)
- GLP-1 is hormone, called an incretin, that enhances insulin secretion and reduces glucagon secretion from pancreas
- only active in setting of high glucose – regulates itself (only works after eating)
Incretin (GLP-1) Mimetics: non-insulin injectable agent (aka incretin-based therapy)
- GLP-1 is hormone, called an incretin, that enhances insulin secretion and reduces glucagon secretion from pancreas
DM - management beyond medications
Patient education: smoking cessation, BP, nutrition
- macrovascular complications: CHD, PAD, CVD (cerebrovascular dz)
Routine labs: yearly fasting lipid panel, A1C every 3 months, check kidney and liver fx
- diabetic nephropathy (ACE-I)
Yearly eye exam
- retinopathy
Yearly foot exam
- peripheral neuropathy
Vaccines / immunizations
- tx as immunocompromised
hypercholesterolemia - defintion, screening, dx
total = HDL+VLDL+LDL
- high LDL is CV risk factor
- high HDL protective
screening:
- based on ASCVD risk factor calculation
dx: measure fasting levels
- LDL>100
- total>200
- HDL<60
hypercholesterolemia - management
diet: low in saturated fats
- not effective if genetic cause
Meds:
- HMG-CoA reductase inhibitors (Statins): reduce formation of cholesterol
- SE: myopathy, myalgia - Niacin: reduce VLDL and LDL; dec. TG
- SE: flushing rx - Bile acid binding resins: Lower LDL
- Fibric acid: inc. HDL (and lowers LDL); dec. TG
- Ezetimibe: reduces LDL
hypertriglyceridemia
causes:
- familial presentations can have elevations into 1000s
- can be secondarily caused by DM or pancreatitis
dx:
- elevated triglycerides w/ fasting specimen (>150)
tx:
- Fibrates, niacin, fish oil, statins
