Endocrine System Flashcards

1
Q

pituitary gland - basics

A

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

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2
Q

neoplastic disease (adenoma) of pituitary - sxs

A

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
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3
Q

neoplastic disease (adenoma) of pituitary - s/sx

  • prolactin secreting
  • GH secreting
  • ACTH secreting
A
  1. Prolactinoma
    - M: hypogonadism
    - F: oligomenorrhea, infertility, galactorrhea
  2. GH excess (somatotroph)
    - gigantism before puberty
    - acromegaly after puberty (esp. hands, feet, face)
  3. ACTH (corticotroph)
    - Cushing disease: HTN, central obesity, moon face, buffalo hump
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4
Q

acromegaly/gigantism

A

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
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5
Q

pituitary adenoma - dx (for each type)

A

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
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6
Q

pituitary adenoma - tx (for each type)

A
  1. prolactinoma
    - prolactin secretion from ant. pituitary is inhibited by dopamine
    - dopamine agonist medication (cabergoline, bromocriptine)
    - surgery
  2. GH secreting (somatotroph)
    - surgery
    - may need medication post-surgery for hormone management
  3. ACTH secreting (corticotroph)
    - surgery
    - may need medication post-surgery for hormone management
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7
Q

hypopituitarism - definition, causes

A

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
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8
Q

hypopituitarism - s/sx

A

depend on which hormone(s) are deficient:

  1. prolactin - inhibition of post part lactation
  2. GH - short stature (meds), strength loss, central obesity (adults)
  3. ACTH - reduction of adrenal cortisol = Addison dz
  4. TSH - secondary hypothyroidism
  5. FSH/LH - hypogonadism and infertility
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9
Q

dwarfism - definition, clinical features, dx, tx

A

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

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10
Q

vasopressin/ADH and hypothalamus

A

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
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11
Q

diabetes insipidus - definition, s/sx, 2 forms, tx

A

defect or deficiency in vasopressin (aka ADH)

s/sx:

  • intense thirst (polydipsia)
  • excessive urination (polyuria)

2 forms:

  1. Central: dec. pituitary secretion of ADH (trauma, neoplasm, infection, iatrogenic after surgery)
    - tx: replace vasopressin with analog called desmopressin (DDAVP)
  2. Nephrogenic: failure of response to ADH in kidneys (drugs - lithium, hypercalcemia)
    - Tx: thiazide diuretics, indomethacin
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12
Q

hypothalamic-pituitary-thyroid axis

A

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
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13
Q

thyroid gland hormones

A

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

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14
Q

hyperthyroidism - definition, causes, s/sx, dx

A

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
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15
Q

Grave’s disease - definition, sxs, dx, tx

A

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)
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16
Q

thyroid storm - definition, causes, s/sx, dx

A

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

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17
Q

hypothyroidism - definition, causes

A

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
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18
Q

hypothyroidism - s/sx, dx

A

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
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19
Q

hypothyroidism - tx

A

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
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20
Q

myxedema coma

A

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
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21
Q

thyroid cancer - s/sx, dx, tx

A

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)
22
Q

thyroiditis - definiton, causes

A

inflammation of thyroid

Causes:

  • commonly due to autoimmune process: Hashimoto thyroiditis
  • multinodular goiter: elderly
  • subacute
  • infectious
23
Q

thyroiditis - sxs, dx, and tx (for each cause)

A

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
24
Q

parathyroid - location and role

A

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
25
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
26
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
27
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
28
hypoparathyroidism - dx, tx
Dx: - low PTH - low ca++ - elevated phosphate Tx: - replace doses of calcium and vit D
29
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
30
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
31
adrenal glands - what do they produce
adrenal cortex (outer layer) - aldosterone - cortisol** - androgens adrenal medulla (inner layer) - epinephrine (80%) - norepinephrine (20%)
32
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
33
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
34
Cushing Syndrome - dx
1. 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 2. 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 3. 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 4. Imaging: only for mass identification
35
Cushing disease
when high cortisol is due to pituitary ademona
36
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
37
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
38
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 2. mineralocorticoids: fludrocortisone
39
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
40
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
41
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
42
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
43
Diabetes Mellitus - diagnosis
1. classic sxs + random glucose > 200 2. HgbA1C > 6.5 (prediabetes: 5.7-6.5) 3. fasting glucose (x2) > 126 (prediabetes: 100-125) 4. 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
44
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
45
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) ```
46
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
47
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
48
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
49
hypercholesterolemia - management
diet: low in saturated fats - not effective if genetic cause Meds: 1. HMG-CoA reductase inhibitors (Statins): reduce formation of cholesterol - SE: myopathy, myalgia 2. Niacin: reduce VLDL and LDL; dec. TG - SE: flushing rx 3. Bile acid binding resins: Lower LDL 4. Fibric acid: inc. HDL (and lowers LDL); dec. TG 5. Ezetimibe: reduces LDL
50
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