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PANCE Review > Endocrine System > Flashcards

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
Q

hyperparathyroid - definition, clinical

A

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
Q

hyperparathyroid - dx, tx

A

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
Q

hypoparathyroidism - definition, s/sx

A

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
Q

hypoparathyroidism - dx, tx

A

Dx:

  • low PTH
  • low ca++
  • elevated phosphate

Tx:
- replace doses of calcium and vit D

29
Q

vitamin D (1,25-dihydroxycholecalciferol) - basics

A
  • 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
Q

disorders related to vitamin D

A

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
Q

adrenal glands - what do they produce

A

adrenal cortex (outer layer)

  • aldosterone
  • cortisol**
  • androgens

adrenal medulla (inner layer)

  • epinephrine (80%)
  • norepinephrine (20%)
32
Q

glucocorticoids - general systemic effects

A

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
Q

Cushing syndrome - definition, causes, s/sx

A

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
Q

Cushing Syndrome - dx

A
  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
  1. 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
  2. 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
  3. Imaging: only for mass identification
35
Q

Cushing disease

A

when high cortisol is due to pituitary ademona

36
Q

Cushing syndrome - tx

A 
Pituitary adenoma (Cushing dz)
 - surgery

Adrenal adenoma
- surgery

Ectopic ACTH

  • resect hormone-producing tumor
  • meds to suppress hypercortisolism

Exogenous glucocorticoids
- taper steroid meds

37
Q

Addison disease - definition, causes, s/sx

A

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
Q

Addison disease - dx, tx

A

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

  1. mineralocorticoids: fludrocortisone
39
Q

Addisonian crisis

A

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
Q

pheochromocytoma

A

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
Q

Diabetes Mellitus - screening and types

A

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
Q

DKA

A

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
Q

Diabetes Mellitus - diagnosis

A
  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
Q

Diabetes Mellitus - Type 1 tx

A

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
Q

Diabetes Mellitus - Type 2 tx

A

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
Q

DM medications - mechanisms of action

A

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
Q

DM - management beyond medications

A

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
Q

hypercholesterolemia - defintion, screening, dx

A

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
Q

hypercholesterolemia - management

A

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
Q

hypertriglyceridemia

A

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

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