Endocrinology Flashcards
History: Two weeks generalized weakness, not eating
PE: Underweight, hyper-pigmented palmar creases, serum sodium 130, serum potassium 5.8
Dx?
Dx: Primary adrenal insufficiency (Addison’s)
ADDISON’s Mnemonic:
A - Autoimmune dz (primary cortical adrenal insufficiency)
D- Dark skin - hyperpigmentation
D - Drained - generalized weakness, tired, lethargic, emotional changes
I - Iatrogenic (possible cause)
S - starvation - anorexia (no appetite), weight loss,
O - hypOtenstion, hypoglycemia, hyper-K+
N - N/V/D, ABD pain, fever muscle/joint pain, severe debhdration- si adrenal crisis
Dx: Low cortisol, high ACTH - further testing w/ cosyntropin (synthetic acth) - normal person = cortisol level doubles - Addison = no inc
Tx: GC (Hydrocortisone)
Note: Hypo/hyperthryoidism does NOT cause electrolyte abnormalities - think issue with adrenal gland
Also hypothyroidism causes fatigue/lethargy with generalized weakness but causes weight GAIN, not loss & also causes edema, cold intolerance
Cushings = gushing cortisol
Conn syndrome = opposite = excess aldosterone
What is the best way to screen for diabetes mellitus?
Fasting plasma glucose = BEST WAY
>126 on TWO occasions
OR
Sx of DM + random plasma glucose >200
OR
Glucose >200 TWO hours after 75 g load of glucose during oral tolerance test
OR
HgA1c >6.5%
RF for DM
BMI >25 Age >45 Family Hx 1st deg rel HTN HLD Sedentary lifestyle
REVIEW PATIENT RISK FACTORS AND DO SCREENING ON ALL PATIENTS who have >1 RF ?
How often should patients be screened for DM?
Every 3 years
RAIU - increased diffuse uptake = ?
Hyperthryoid 2/2:
Graves disease
TSH-secreting pituitary adenoma
RAIU - decreased uptake = ?
Hypothyroid 2/2:
Thyroiditis (hashimoto’s, postpartum, dequervain)
RAIU - hot nodule
Toxic adenoma
RAIU - cold nodule
Rule out malignancy
RAIU - multiple nodules
Toxic multinodule goiter
Cretinism - = what? CP? Tx?
Cretinism = congenital hypothyroidism 2/2 maternal hypothyroidism or infant hypopituitarism
CP: Macroglossia, hoarse cry, coarse facial features, weight gain, umbilical hernia
**Mental development abnormalities if not corrected
Tx: Levothyroxine
Causes of hypothyroidism
Iodine deficiency Hashimoto's thyroiditis Postpartum thyroiditis Pituitary hypothyroidism Hypothalamic hypothyroidism Cretinism Reidel's thyroiditis
Sx of hypothyroidism
Dec BMR Cold intolerance Dry, tough skin Weight GAIN (despite being hungry) Non-pitting edema (myxedema) Loss of outer 1/3 eyebrow CNS hypoactivity (sluggish, fatigued, depression) Constipation Bradycardia, dec CO Mehorrhagia Hypoglycemia
**Think of all the different body systems - shuts down all of them!
Sx of hyperthyroidism
Increased BMR Heat intolerance Weight loss (even w/ inc appetite) Skin is warm, moist, soft, fine hair CNS hyperactivity (anxious, fine tremors, nervousness, fatigue) Diarrhea, hyperdefecation Tachycardia, palp, HOHF Scanty periods, gynecomastia Hyperglycemia
**Think of all the different body systems - puts all of them into overdrive!
Euthyroid sick syndrome
Abnormal findings on TFTs that occur in the setting of non-thyroidal illness, without pre-existing HPT dysfunction - common in MI, DKA, CRF, cirrhosis surgery, malignancies, sepsis,
Dx: Dec Free T4/3, Dec TSH
Note: Often resembles 2ry hypothyroidism lab-wise but it’s rare/weird to have 2ry thyroid disease that’s HYPO - so think of this if person is ill and has labs consistent w/ 2ry hypOOO-thyroidism
*T3 can also be low w/ increased reverse T3
Thyrotoxicosis (thyroid storm)
Happens after precipitating event like SURGERY, TRAUMA, INFECTION –> rare (1-2% of pt w/ hyperyhyroidism) but DEADLY (75% mortality rate)
CP: Hypermetabolic state - palp, tachy, afib, high fever, n/v, psychosis, tremors
Dx: Dec TSH (undetectable), and HIGH HIGH T4/T3
Tx: Anti-thyroid meds IV propylthiouracil (PTU) - inhibits thyroid hormone synthesis and prevents conversion of T4-> T3 peripherally or methimazole
Sx therapy: Tx palps w/ beta blockers
Supportive therapy: IV glucocorticoids, cardiac monitoring, IV fluids, cooling blankets, antipyretics (APAP)
Myxedema coma
Hypometabolic state = coma - so remember mxyedema coma = thyroid is CRITICALLY LOW
Extreme form of hypothyroidism a/w HIGH mortality rate
MC seen in elderly women with longstanding hypothyroidism in WINTER
Patho: 2/2 precipitating factor - infection, CVA< CHF - WITH long-standing undiagnosed hypothyroidism, discontinuation or noncompliance with levothyroxine therapy, failure to start levothyroxine after RAI ablation of thyroid patients w/ graves
CP: SEVERE sx of hypothyroidism- brady, obtunded, hypothermic, hypoventilation, hypoglycemia, hypotension, hyponatremia
Dx: HIGH serum TSH, LOW Free T4/3 (may be undetectable)
Tx: IV LEVOTHYROXINE, ICU admission, abx if infection, passive warming (blankets, warm room…RAPID WARMING C/I), IVF, IV corticosteroids if adrenal insufficiency is suspected
Grave’s disease - MC in? CP, Dx, tx?
Autoimmune disorder - body makes ab that activate the TSH receptor in the thyroid gland = inc thyroid hormone synthesis & thyroid gland growth
Worse w/ stress (pregnancy, illness)
CP:
Si/sx clinical hyperthyroidism
Diffuse enlarged thyroid
Thyroid BRUITS
Exophthalmos, proptosis, lid lag 2/2 hyalauronic acid deposition
Pretibial myxedema - (name = misnomer) = nonpitting edematous pink to brown plaques on shins
Dx: + TSH antibody, hyperthyroid TFTs (low TSH, high Free T4/3)
Tx: RAI ablation - destroys thyroid gland - needs replacement after - can also use PTU, Bb for tachy sx
Describe typical pt w/ Graves
Nancy Grave = 20-40 YO woman who smokes POT (pretibial myxdedema, ophthalmopathy, thyroid bruits/enlargement) to chill her out b/c she’s a nervous nelly w/ palp, hot all the time, skinny, losing weight, poops all over, skin shiny, hair fine
Nancy is a total hot mess
Toxic multinodular goiter and toxic adenoma
TMG = multiple autonomously functioning thyroid nodules
TA = one autonomously functioning nodule
CP = clinical hyperthyroidism (no skin or eye changes - exopthalmos = unique to graves)
PE = palpable nodule(s)
Dx = Dec TSH, Inc Free T4/3
RAIU TMG = patchy areas of both inc and dec uptake
RAIU TA = HOT nodule (inc local uptake in one area)
Tx TMG & TA = RAI ablation (MC) or meds (PTU - inhibits thyroid hormone synthesis, preferred in pregnancy )
TSH-secreting pituitary adenoma
MCC SECONDARY hyperthyroidism = autonomous TSH secretion by pituitary adenoma
CP/PE = clinical hyperthyroidism w/ diffuse enlarged thyroid, BITEMPORAL HEMIANOPSIA (bc tumor presses on optic chiasm), mental disturbances
Dx = HIGH TSH, HIGH FT4/3, RAIU = diffuse uptake
Suspect adenoma…get brain MRI
Tx = transsphenoidal surgery to remove pituitary adenoma
Hashimoto’s thyroiditis
AKA chronic lymphocytic
MCC hypothyroidism in the US 6x MC in women
Patho: AI antibodies against thyroid
CP: Clinical hypothyroidism, painless enlarged thyroid, may present euthyroid
Dx:
+ Thyroid Ab present (thyroglobulin ab, antimicrosomial ab, thyroid peroxidase ab)
TFTs - hypothyroid
RAIU decreased (usually not needed for dx)
Tx:
Levothyroxine
Silent (Lymphocytic) thyroiditis
Autoimmune - anti-thyroid ab in 50% - occurs after exposure to certain drugs, such as IFN-alpha, IL-2, lithium etc
CP: Ranges from thyrotoxicosis (first) to hypothyroid (depends on when they present)
Dx: + Thyroid Ab present (thyroglobulin ab, antimicrosomial ab, thyroid peroxidase ab)
Tx: return to euthyroid state w/in 12-18 mo without tx –> NO ANTITHYROID meds - 20% will end up with permanent hypothyroidism (chronic lymphocytic thyroiditis AKA Hashimoto’s)
Postpartum thyroiditis
Literally the exact same as silent lymphocytic thyroiditis except the thyroiditis occurs postpartum - thought to be AI (+Ab in > 80%)
CP: Ranges from thyrotoxicosis (first) to hypothyroid (depends on when they present)
Dx: + Thyroid Ab present (thyroglobulin ab, antimicrosomial ab, thyroid peroxidase ab)
Tx: return to euthyroid state w/in 12-18 mo without tx –> NO ANTITHYROID meds
Recurrence rate high –> can turn into chronic lymphocytic thyroiditis AKA Hashimoto’s
Which two kinds of thyroiditis can turn into chronic lymphocytic thyroiditis if they progress instead of returning to euthyroid?
Silent lymphocytic thyroiditis
Postpartum thyroiditis
Literally exact same patho –> 20% of above cases will become recurrent or permanent = when you are considered to have chronic lymphocytic thyroiditis AKA hashimoto’s aka autoimmune thyroiditis
Two above can present as hyperthyroid, euthyroid or hypothyroid!!
If present hyperthyroid, are differentiated fro graves via absence of exopthalmos/ocular involvement
All three (silent, pospartum, chronic) = painless, enlarged thyroid vs dequervain’s thyroiditis = PAINFUL (see next card). All 4 kinds of thyroiditis have decreased RAIU on scan
De Quervain’s granulomatous thyroiditis
= PAINFUL SUBACUTE thyroiditis
MC POST-VIRAL or viral inflammatory reaction - think of it as a huge version of a painful enlarged LN in a viral illness
MC present in hyperthyroidism in acute phase –> can present in range of thyrotoxicosis to hypothyroid (like most causes of thyroiditis)
Dx: Inc ESR = HALLMARK, NO thyroid antibodies, TFTs usually HYPER-thyroid
Elevated inflammatory markers and absence of anti-thyroid ab = only way to separate it from other causes of thyroiditis (silent lymphocytic, postpartum)
Tx: No anti-thyroid meds - return to euthyroid state in 12-18 months. Aspirin for pain, inflammation
5% possible permanent hypothyroidism
Acute suppurative thyroiditis
MCC = bacterial = staph
CP: Painful, fluctuant thyroid - usually very ill, febrile
Dx: Inc WBC w/ left shift, usually euthyroid
Tx: Antibiotics - drainage if abscess present
Reidel’s thyroiditis
FIBROUS thyroid
Firm hard WOODY nodule (similar to anaplastic CA)
May develop hypothyroidism
Surgery may be needed
RF Thyroid CA
Radiation exposure
MEN (= medullary carcinoma)
Family hx
? iodine def = follicular
Age < 20 or age > 60 - extremes of age, be suspicious- esp w/ hx head/neck radiation (= follicular or anaplastic respectively)
Thyroid cancer - ominous characteristics of a nodule
Painless Firm Non-mobile Rapid growth (?anaplastic) Vocal cord paralysis (hoarse voice)
Cold on RAIU
Note: Most pt w/ thyroid CA are euthyroid
Thyroid CA in order of frequency
Papillary MC (70-90%)
Follicular
Medullary
Anaplastic
Papillary thyroid cancer characteristics
Most common thyroid CA
RF = RADIATION EXPOSURE
Epi = YOUNG FEMALES -
PR - per rectum - papillary 2/2 radiation exposure
Psammoma bodies (cleaved nuclei) - papillary = psammoma
Multifocal, invades locally - spreads via lymphatics (local mets common)
Slow growth, found early, excellent prognosis (least aggressive thyroid CA)
Papillary = “popular” = most common
Tx: Total vs subtotal thyroidectomy
Follicular thyroid cancer
2nd MC thyroid CA.
Epi: MC 40-60YO
RF: Iodine def = Foll-I-cular
Spread:
via bl vessels - distant mets COMMON (lung, brain, bone, liver, skin) & local mets rare - dx later than papillary = worse prognosis but still slow-growing
Poor prognostic indicators: HURTHE cells (FH in alphabet), > 4 cm, distant mets, vascular invasion
Tx: Total vs subtotal thyroidectomy
Medullary thyroid CA
2nd most aggressive form (anaplastic worst)
Greatest RF = MEN 2a, 2b(a/w pheo) (Medullary=Men), not a/w radiation exposure
Arises from para-follicular “C-cells” that secrete CALCITONIN (= hypocalcemia)
Local invasion early, distant mets late (brain, bone, liver, adrenal medulla)
Tx: surgical - total thyroidectomy. Calcitonin levels used to monitor for residual disease present after tx or for recurrence
Anaplastic
Least common, most aggressive
RAPID GROWTH
MC in males > 65 YO
Poorly differentiated, early mets to nodes and distant sites - may invade trachea
Poor prognosis
2/2 uncommon inactivation of p53 TSG
SO…older patient with rapidly enlarging mass….think anaplastic
Tx: External beam radiation, chemotherapy (not amenable to surgical resection b/c poorly differentiated)
Two on outside of (PfmA) may be related to radiation exposure & they’re at the extremes of ages
Thyroid nodule workup
Most nodules in men & children are malignant, esp if at extremes of age
Most nodules in women are benign (follicular adenoma or cyst)
Benign characteristics:
Smooth, firm, irregular, sharply outlined, discrete
Malignant characteristics:
Rapid growth, fixed in one place, no movement w/ swallowing
Dx: Most pt are euthyroid. Get FNA w/ Bx = best initial test to eval a nodule
How to decide whether to biopsy a nodule
Goal = not biopsy if you don’t need to
+ RF = increases your pretest probability that this is cancer
Patient characteristics: Prior radiation of head & neck (HL survivor) Family hx of thyroid CA Nodule + hoarseness Age (< 20 YO, > 60YO)
Physical exam findings:
Fixed, firm, hard, nodule, w/ non-tender LAD = likely a malignancy. Painful = less likely to be cancer. Painless doesn’t help b/c could be a lot of things.
Ultrasound findings: Solid mass Hypo-echogenic Size > 2 cm (DO BX!!!) Micro-calcifications Irregular borders
**If you have multiple of these elements then they are pushing you to get the biopsy!!! If you have all of these elements absent, then they’re asking you what you can do to avoid getting a FNA w/ bx
Find nodule - get TSH - if hyperfunctioning nodule (low TSH) = LOW RISK NODULE probably - get a RAIU to make sure that it’s the nodule that’s hypersecreting! Tx = treat hyperthyroidism (RAI ablation)
Find nodule - get TSH - if low, you’re thinking the nodule must be hyperfunctioning - but if you get the RAIU & it’s a COLD nodule then eventually you will need a FNA w/ bx - could get US next but will need to Bx eventually
If you get TSH & it’s elevated (low free T4/3) then doing the RAIU is useless b/c you know it’s not a hot nodule - so what you do here is get the ULTRASOUND - next steps based on risk & size:
If US shows nodule > 1 cm then get an FNA w/ Bx
If US shows nodule < 1 cm, it’s small and you can repeat US in 6 months - if growing, get FNA w/ bx
If FNA = cancer, get surgery. If FNA is not cancer, repeat US every 6-12 mo. If ???? FNA - repeat FNA - or remove w/ surgery to get the bx after two fails
MCC primary hyper-parathyroidism
Parathyroid adenoma (80%)
Also:
Parathyroid hyperplasia
Lithium
MEN I & IIA
MCC secondary hyper-parathyroidism, labs, tx
Chronic kidney disease
= no activation of vitamin D = no calcium absorption = hypocalcemia so body keeps pumping out
What does parathyroid hormone do? When released?
Increases blood levels of calcium
It is released in response to low calcium levels in the blood (receptors in parathyroid can tell how much calcium is floating thru there or hitting their receptors)
PTH =
Inc osteoclast activity
Inc GUT absorption Ca2+
Inc excretion of phosphate
Calcium level consistent with primary hyper-parathyroidism
HYPER-calcemia
Remember in primary you have an ectopic source (parathyroid adenoma, hyperplasia) or cause (MENI, IIA) causing totally unregulated release of parathyroid hormone - totally abherent
Tons of random PTH = VERY HIGH calcium levels
Hypercalcemia = stones bones, abd groans, psychic moans, decreased DTRs
Labs consistent w/ 2ry hyper-parathyroidism
Secondary Hyper-PTH is when the body is stimulating tons of PTH release due to low levels of blood calcium
So there’s no issue with the parathyroid itself (as in primary dz). There is just something causing very low levels of calcium so a lot of PTH is released and it’s actually doing its job correctly
Causes:
CKD (No vit D = no Ca ab)
Severe hypocalcemia
Severe vit D def
Dx of primary hyper-PTH
Triad of primary hyper-PTH & other labs supporting dx
Triad:
- High intact PTH (ectopic focus)
- High Calcium as a result
- Low phosphate
Other:
- Inc 24-hour urine Ca excretion
- Osteopenia on bone scan
- Imaging studies to look for parathyroid adenoma
Tx primary hyper -pth
Parathyroidectomy
Tx secondary hyper-pth
Vitamin D & Ca2+ supplementation
Hypoparathyroidism - etiology
RARE - either low PTH or insensitivity to PTH…
Two MCC = post-surgical or autoimmune
- Accidental damage/removal of PT gland during neck or thyroid surgery
- AI destruction of the PT gland
- Radiation therapy
- Hypomagnesemia (Mg required for production of PTH)
Diagnosis of hypo-PTH:
Triad of hypoparathyroidism
Low Ca2+
Decreased intact PTH
Increased phosphate
AKA exact opposite of primary hyper PTH triad
CP & Dx, Tx hypo-PTH
CP: Hypocalcemia si/sx (trosseau & chvostek’s signs, increased DTRs
Dx: Triad (low Ca, low PTH, high phosphate)
Tx: Calcium supplementation & vitamin D
Hypocalcemia causes increased or decreased DTR?
Increased - they don’t have the calcium they need to have smooth controlled muscle contraction = hyperreflexic & trossesau & chovstek’s
Hypercalcemia causes increased or decreased DTR?
Decreased DTRs
Stones, bones, moans, groans too!`
Hypocalcemia w/ dec PTH, increased phosphate
Post-surgical destruction of parathyroid or AI
Hypercalcemia w/ inc PTH, decreased phosphate
Parathyroid adenoma
Increased PTH w/ low calcium
Low calcium is causing body to appropriately secrete more & more PTH to try to raise serum Ca2+ levels
MCC = CKD = secondary hyper-PTH
> 90% of cases of hypercalcemia are 2/2?
Primary hyperparathyroidism or malignancy!!!
Hypercalcemia 2/2 malignancy a/w which other lab abnl?
Increase PTH-related protein (PTHrp) & Decreased intact PTH
Note: If this was parathyroid gland mediated you’d have hypercalcemia with INCREASED intact PTH
Signs of low serum calcium
EKG
Tx
Chvostek’s sign
Trosseau’s sign
GI: Diarrhea, cramps
Neuromuscular: Cramping, increased DTR, finger paresthesias
Cardio: CHF, arrhythmias
EKG: Prolonged QT interval
Tx:
Mild: Oral Ca & vit D
Severe: IV Ca gluconate
- *May need K+ & Mg2+ repletion as well
- *Remember if serum albumin is low, Ca2|+ will look even lower
Signs hypercalcemia
Labs
EKG
Tx
Most are ASX! Stones (kidney) Bones (painful, fx) Abd groans (ileus, constipation) Psychic moans (weakness, fatigue, ams, dec DTR, depression or psychosis)
Labs: Inc Ca2+ (may look normal if low albumin)
EKG: Shortened QT interval, prolonged PR interva., QRS widening
Tx:
Severe/symptomatic: IV saline, fursosemide, avoid thiazides (= inc Ca), calcitonin, bisphosphonates (in severe cases)
Mild: No tx necessary
Signs hypercalcemia
Labs
EKG
Tx
Most are ASX! Stones (kidney) Bones (painful, fx) Abd groans (ileus, constipation) Psychic moans (weakness, fatigue, ams, dec DTR, depression or psychosis)
Labs: Inc Ca2+ (may look normal if low albumin)
EKG: Shortened QT interval, prolonged PR interva., QRS widening
Tx:
Severe/symptomatic: IV saline, fursosemide, avoid thiazides (= inc Ca), calcitonin, bisphosphonates (in severe cases)
Mild: No tx necessary
Renal osteodystrophy = ?, labs = ?, dx? management?
R. osteodystrophy = bone disorders related to chronic kidney disease:
- Osteomalacia
- Osteitis fibrosis cystica
Labs: Pooped out kidney = Can't excrete Phos = Inc Phos No active Vit D = LOW Calcium = Increased intact PTH
Dx:
Above labs
Xray osteitis fibrosis cystica = periosteal erosions, bony cysts, “salt & pepper” skull, “cystic brown tumors” on bx
Tx:
Phosphate binders: calcium carbonate, Vitamin D (active form - calcitriol), Cinacalcet (lowers PTH)
Labs in osteoporosis
NORMAL levels of Ca2+, Phos, PTH & ALP = one way of telling apart from renal osteodystrophy (osteitis fibrosis cystica, also osteomalacia if vit d low 2/2 CKD) if just low vit D in general then general osteomalacia
Pathologic fx more common in OP b/c bones are BRITTLE
Labs in osteoporosis
NORMAL levels of Ca2+, Phos, PTH & ALP = one way of telling apart from renal osteodystrophy (osteomalacia & osteitis fibrosis cystica)
Pathologic fx more common in OP b/c bones are BRITTLE
xray appearnace osteoporosis vs osteomalacia vs renal osteodystrophy
OP - GET DEXA scan - will be <2.5 SD from mean
Osteomalacia = LOOSER LINES (zones)
Renal osteodystrophy (osteitis fibrosis cystica) = cystic brown tumors
How to tell if osteomalacia is 2/2 CKD or just generalized low Vitamin D (intake)
Phosphate will be retained in CKD b/c kidney’s are pooped out & can’t secrete it anymore
Will be increased if 2ry hyper PTH 2/2 low calcium blood levels & kidneys are okay b/c Phos is in inverse relationship w/ PTH (PTH = inc phos excretion)
Primary adrenal insufficiency = ?
Addison’s disease
Etio primary adrenal insufficiency
- Autoimmune (MC in industrualized nations) = ADRENAL ATROPHY
Autoimmune = atrophy
- Infection (MC worldwide) - Tb, HIV, etc = ADRENAL CALCIFICATION
InfeCtion = Calcification
Main clinically significant difference between primary and secondary adrenal insufficiency
Primary = NO MINERALOCORTICOID FUNCTION - lack of cortisol AND aldosterone b/c adrenal gland is destroyed
Secondary = lack of cortisol only 2/2 no ACTH - but adrenal gland itself is functioning & still responds & makes mineralocorticoids when prompted (RAAS –> ald release)
Main clinically significant difference between primary and secondary adrenal insufficiency
Primary = NO MINERALOCORTICOID FUNCTION - lack of cortisol AND aldosterone b/c adrenal gland is destroyed
Secondary = lack of cortisol only 2/2 no ACTH - but adrenal gland itself is functioning & still responds & makes mineralocorticoids when prompted (RAAS –> ald release)
CP secondary adrenal insufficiency (remember caused by exogenous steroid use = HPA axis shut down –> LOOK FOR IN HISTORY / MEDS
WEAKNESS & Muscle cramps in 99% of patients!!!
Nonspecific GI sx:
N/V/D, Abd pain, Weight loss, Anorexia
Fatigue, headache, sweating, abnl menstrual periods
Notice: secondary adrenal insufficiency only has sx of low cortisol (still has aldosterone - so has decreased energy, fatigue, muscle aches, myalgias, fatigue, dec appetite, weight loss, anorexia, nausea, vom, abd pain) but does not have the sx of low aldosterone (electrolyte abnl - mild if present, hypotension) - one thing is that hypoglycemia more common in secondary!
Remember person who went into adrenal crisis at NWH b/c didn’t continue home meds (steroids) correctly! :(
Cortisol functions
Energy
Increases blood sugar
Blood pressure
Cortisol functions
Energy
Increases blood sugar
Blood pressure
Weakness, muscle cramps & nonspecific GI sx (N/V/D/ abd cramps)
LOW CORTISOL - adrenal insufficiency (1ry or 2ry)
+ LOW Na, HIGH K+, hypotension = primary
Dx adrenal insufficiency - screening test
High dose ACTH (cosyntropin) stimulation test
Blood or urine cortisol measured before & ofter IM injection of ACTH
Normal response = rise in cortisol levels after ACTH given
Adrenal insufficiency = little or no increase in cortisol levels (adrenal gland atrophied (adison’s) or shut off b/c of exogenous steroids - 2ry) - so no response
Tx primary vs secondary adrenal insufficiency
Primary: replace glucocorticoids (hydrocortisone) AND mineralocorticoids (fludrocortisone)
Secondary: Hydrocortisone alone (RAAS/aldosterone intact)
Tx primary vs secondary adrenal insufficiency
Primary: replace glucocorticoids (hydrocortisone) AND mineralocorticoids (fludrocortisone)
Secondary: Hydrocortisone alone (RAAS/aldosterone intact)
What’s the primary manifestation of acute adrenal insufficiency?
SHOCK - hypotension, hypovolemia
Hyponatremia, hyperkalemia, hypoglycemia
MCC = abrupt withdrawal of glucocorticoids, also undiagnosed addison’s & person in stress/illness, or exacerbation of known addison’s (forgot to triple steroids in time of stress)
What’s the primary manifestation of acute adrenal insufficiency?
SHOCK - hypotension, hypovolemia
Hyponatremia, hyperkalemia, hypoglycemia
MCC = abrupt withdrawal of glucocorticoids, also undiagnosed addison’s & person in stress/illness, or exacerbation of known addison’s (forgot to triple steroids in time of stress)
Cushing’s syndrome vs. disease
Syndrome = the signs and symptoms related to cortisol excess (any cause)
Disease = high cortisol 2/2 ACTH-secreting pituitary adenoma
Cushing’s syndrome
= Si/sx cortisol excess =
Fat redistribution =
Central adiposity &
Muscle/proximal wasting
Thinning of skin, striae, acanthosis nigrans
Buffalo hump
Moon facies, weight gain
Osteoporosis
Hypokalemia
Hyper-pigmentation in causes w/ increased ACTH
Cushing’s disease - etio, si/sx, dx, tx
Cushings DISEASE = too much cortisol 2/2 ACTH-secreting pituitary adenoma
Si/sx: cortisol excess
Dx:
Cushing’s syndrome dx w/ LOW dose dexamethasone suppression test - positive is no suppression of cortisol levels (cortisol > 5) - normally increased GC would depress cortisol levels b/c dex is 4x stronger than cortisol
Cushing’s DISEASE dx - use HIGH dose dexamethasone suppression test - suppression = cushing’s disease (a ton of dexmeth is enough to decrease the pituitary tumor from secreting some ACTH)
Tx: Transsphenoidal surgery to remove pituitary adenoma
Low dose dexamethasone suppression test results:
+ Suppression of cortisol release
No cushing’s syndrome (normal bodily response to dexamethasone release)
Low dose dexamethasone suppression test results:
+ Suppression of cortisol release
No cushing’s syndrome (normal bodily response to dexamethasone release)
Low dose dexamethasone suppression test results:
Cortisol level: 7.5
NO suppression of cortisol if level is > 5.0
Means person has cushing’s syndrome….now we just have to figure out the cause…
Order a HIGH dose dexamethasone suppression test & ACTH level now to see if it’s cushing’s disease
Low dose dexamethasone suppression test results: No suppression of cortisol
High dose dexamethasone suppression test results:
+ suppression of cortisol levels
ACTH HIGH
Cushing’s disease!
ACTH-secreting pituitary adenoma!
Low dose dexamethasone suppression test results: No suppression of cortisol
High dose dexamethasone suppression test results:
No suppression of cortisol levels
ACTH LOW
No suppression with HIGH dose = issue outside HPA axis
Low ACTH means you have an adrenal adenoma secreting cortisol
Low dose dexamethasone suppression test results: No suppression of cortisol
High dose dexamethasone suppression test results:
No suppression of cortisol levels
ACTH HIGH
No suppression with HIGH dose = issue outside HPA axis
HIGH ACTH means you have a tumor outside the HPA axis secreting ACTH
AKA paraneoplastic syndrome - Small cell lung cancers are known for doing this!!
SCLC = SVC syndrome, SIADH, Lambert eaton, Cushing’s
Etio secondary hyperaldosteronism
2/2 Increased renin production (renin-dependent)
(1ry is renin dependent)
MCC = Renal artery stenosis = RAAS activated all the time = high aldosterone levels!
Or decreased renal perfusion (CHF, hypovolemia etc)
CP hyperaldosteronism
Mostly ASX
Low K+
HIGH Na+
Metabolic alkalosis (2/2 dumping of K+ & H+ to retain Na+)
Fluid retention = HYPERTENSION
Most sensitive test to distinguish primary from secondary hyperaldosteronism
Ald: Renin ratio (ARR)
ARR > 20
(high Ald & low renin) = 1ry hyperaldosteronism (renin-independent)
Low ARR (high renin levels) = 2ry hyperaldosteronism (renin-dependent)
Labs of hyperaldosteronism
Low K+
High Na+
Metabolic alkalosis (body dumps K+/H+ ions to retain the Na+ ion)
Tx Conn syndrome
Remove the mass on the adrenal gland that is secreting aldosterone
AND
Spirinolactone (ald antagonist)
Tx adrenal hyperplasia
Spirinolactone (ald antagonist)
Treatment secondary hyperaldosteronism
(remember that is 2/2 RAS = inc renin = RVHTN)
Angioplasty = definitive tx
ACEI - blocks ald
Pheochromocytoma - what? CP? Dx? Tx?
Pheo = catecholamine-secreting adrenal tumor - secretes NE & epi autonomously & intermittently
CP: HYPERTENSION + “PHE” = Palpitations, Headaches (paroxysmal) & Excessive sweating
Dx: 24 hour urinary catecholamine (w/ breakdown products - metanephrine)
Tx: Total adrenalectomy - MUST initiate alpha blockade 2 weeks before surgery w/ PHEnoxybenzamine or PHEntolamine & followed by beta blockade
Note: Think “PHE” for CP and treatment
First line treatmnet prolactinoma
MEDICAL management - dopamine agonists (cabergoline (less S/E than bromo), bromocriptine,)
Decreases PRL release
2nd line = trans-sphenoidal surgery
