Endo exam 3 diagnoses/labs Flashcards
Addisons disease
labs only
low cortisol, low aldosterone
CBC- eosinophillia, lymphocytosis
CMP- for hyponatremia and hyperkalemia
BUN /Cr
Plasma cortisol at 8 am (less than 3) and incresed ACTH to dx**
Plasma ACTH greater than 200
Rapid ACTH stim test - adm cosyntropin and measure cortisol 45 m later
Plasma Renin (should be elevated if +)
Addisons disease imaging only
CXR if TB or pneumo is expected
CT abdomen: small w/o calcification is autoimmune
Enlarged: TB, fungal, hemorrhage, metastatic
Calcifications: TB, fungal, hemorrhage, pheo, melanoma
Black calcification
Interfering factors of cortisol levels for cushings
Na+ intake, age, sex, race, pregnancy, meds, renal impairment, and menstrual phase
Menstrual. Then Salty racy, age appropriate sex
Then pregnant, whoops
+ renal
Cushings syndrome lab workup
step 1
CBC- leukocytosis w/ neutrophillia, lymphocytopenia, low eosinphils
CMP- increased glucose +/- hypernatremia, hypokalemia
Cortisol causes early release of neutrophils and less apoptosis of neutrophils
Cushing syndrome Source workup
step 2
Need 2 + tests of the following:
Dexamethasone suppression, 24 h urine free cortisol, late night salivary cortisol
What is low dose dexamethasone suppression test for cushings
1 mg PO at 11 pm and then take cortisol serum at 8 AM.
greater than 5 is +
high false positives
only do low dose dexamethasone ONCE
24 h urine free cortisol cushings
begin collection after 1st morning void, all the voids after that, + first void of next morning
test cortisol in urine
+ test is 3X more than UL of normal. do test twice
cushings - What is salivary cortisol
and interfering factors
Collected by patient at 11 PM. + if above 100.
Interfering factors- steroids, brushed teeth, oral intake, inadquate collection
Elevated levels are seen with erratic sleep schedule, preg, anticonvulsants, mental illness, alcoholism, stress
MUST HAVE 2! + abn to be included as ONE of the tests
SPAAM E
Determining the DIAGNOSIS for cushings disease after the 2 tests
step 3
2 negative means refer to endocrin d/t high index of suspicion
1/2 positive - repeat test & consider cyclic cushings
2 positive - refer to endocrinologist
Next determine cause for hypercortisolism
if not 2 positive tests then you are suspicious. everything after step 3 is just determining the cause.
How to determine cause for hypercortisolism
step 4
Serum ACTH –> determines if acth dependant vs other etiology
If ACTH low, its d/t adrenal gland and a CT of adrenal gland should be ordered
If ACTH high, its dependant on ACTH, therefore its a pitutiary tumor and you should order a MRI of the brain
What should the CT or MRI show
step 5
- CT should show adrenal gland greater than 4 cm for malignancy, in addition to growth of nodules, 10 HU density
- MRI w/ contrast should show pitutiary lesion. if greater than 5 mm, begin treatment.
If no lesion or lesion is less than 5 mm, proceed with inferior petrosal sinus sampling. They go into the brain to see whats in there.
After the inferior petrosal sinus sampling, If normal ACTH, look for ectopic sources of ACTH via CT chest/abd or a PET
yellow ottoman
Inferior petrosal sinus sampling
step 6
causes increased ACTH, and confirmes the pituitary cushings disease
Congenital Adrenal Hyperplasia workup
Newborn screening CYP21A2
Ambiguous genitalia: hormonal, genetic, chromosomal testing
BMP
Hormonal workup- CYP17 and serDHEA are increased in 21 hydroxy deficiency
imaging is NOT necessary
ABD CT done to rule out adrenal hemorrhage and pelvic US
Primary aldosteronism workup initial
BMP - hypernatremia +/- hypokalemia
metabolic acidosis
Plasma renin activity (PRA) and PAC (ald concentration)
obtain in AM in seated position. PAC/PRA ratio should be greater than 20 to 25 for dx
Do the PRA/PAC lab after 2 hrs out of bed and seated for 15-60m.
Interfering meds!
Interfering meds for primary aldosteronism dx
Bad: spironolactone, ACEi, ARB, any direct renin inhib
Good: slow release verapamil, hydralazine, terazosin, doxazosin
Confirmatory Testing for primary aldosteronism
Sodium loading PO or IV
PO is 3 d of salt, and K should be assessed each day. If low K, switch to NaCl.
24 h urine collection for ald, Na, Cr at the end
Urine Na should be greater than 250.
Urine ald greater than 12 for dx
IV- 2L over 4 h, greater than 10 is dx
Determine cause of Primary aldosteronism
CT scan - abdomen for mass
(positive results)
1.unilateral - less than 4 cm is Conn. greater than 4 is carcinoma.
2.bilateral hyperplasia- gland thickening or micronodular changes.
If Negative CT – consider adrenal vein sampling if surgery is considered, ONLY if severe uncontrolled HTN AND adrenalectomy is being considered
Pheochromocytoma workup
first step - Plasma free metanephrines is most sensitive.
second step - urine fractioned metaenphrine and creatinine; clonidine suppression test
clonidine is plasma. adm clonidine, wait 3 hr and assess plasma for metanephrines. less than 40% drop is positive.
urine - 24h collection.
Both plasma and urine should be 3X the UL of normal to be dx.
third: imaging. non-contrast of CT of adrenal gland.
if CT negative, do a CT/MRI of the chest, abd, pelvis.
MRI pref in kids and preg.
PET scan to r/o malignancy.
Adrenal Adenoma Workup
CT of adrenal gland w/o contrast, and refer to surgeon
+related labs
functional adenoma have sx
non functioning will be asymptomatic
functional adenoma greater than 1 cm that secretes steroids independantly from ACTH
Adrenal Carcinoma
Hormonal evaluation - pheo, hyperald, hypercortisolism
hyperandrogenism - FSH, LH, DHEAS, prolactin, 17 ohp, total and free testosterone
Imaging: CT abd and pelvis w/ contrast (tiger)
PET = increased uptake of radiotracer
Fine needle aspiration. only to r/o metastasis. pheo must be r/o already
fine needle not greater due to risk of tumor seeding into retroperitoneum.
Hyperprolactinemia workup
Hx of HA and vision changes means order MRI- definitive test for chiamsal syndrome
Serum PRL - more than 20 is +. get in the morning.
May be falsely incr. due to sleep, exercise, stress, breast stimulation, high protein meals
TSH and T4 levels to r/o hypothyroidism
Serum hCG pregnancy test
CMP to r/o liver and kidney dz.
Men get total and free T, LH, FSH.
Women w/ amen are ordered serum estradiol, LH, FSH for potential hypogonadism
If suspect adenoma, MRI IS DEFINITIVE.
if mass is found on sella turcica, investigate secr of other hormones should be tried.
if normal, its idiopathic hyperprolactinoma.
Growth hormone deficiency kid workup
R/o chronic systemic dz, undernutrition, inflammation, hypothyroidism, turner syndrome, skeletal disorders). if r/oed, then order a STIM test.
GH stim x2, IGF-1, IGFBP-3, Bone age Xray of distal radius
MRI if GH does NOT increase with stim (+ result), test to r/o pituitary tumor.
a CT w/ contrast is done only if MRI not available. Refer to genetic test.
GH stim test children
random serum GH not helpful!
combine GH w/ measurments of IGF-1 and IGF-1BP3. physio X2 OR pharm stim X2.
Pharm stimuli are: L dopa, clonidine, propanolol, arginine, insulin induced hypoglycemia
Green appls n dope lol + adult meds
stim performed after an overnight fast.
+ if it stays the same or changes less than 7
GH adult deficiency workup, first step
Prerequsities for diagnostic tests-
Pituitrary surgery, pituitary or hypothalamic tumor, hx cranial infection, evidence of pituitary lesion, childhood GH replacement tx, unexplained low age and sex matched IGF-1 levels
P- STL , HT
Brain infected, low IGF, replace therapy from childhood
GH adult def workup 2nd step
Pharm GH stim test - insulin +/- physiologic stimuli.unable to produce GH hormone.
under 3 is severe, 5 moderate
for diabetics, use GHRH + arginine test. its alternative to insulin. +/- physiologic stimuli
Acromegaly - adult
age and sex matched serum IGF1
Dx of acromegaly is confirmed w/ failure of GH suppression to less than 0.4 w/in 1-2 hours of PO glucose load.
Gigantism
age and sex matched serum IGF1
Dx of acromegaly is confirmed w/ failure of GH suppression to less than 0.4 w/in 1-2 hours of PO glucose load.
Hypogonadism males
Males - check testosterone in the morning (free T and serum T). low if under 240. free t low if under 35.
Verify with repeat test + serum LH/FSH and PRL.
Hypogonadism females
hCG, serum PRL, FSH/LH and TSH
stimulation w/ GnRH causing increased LH/RSH should get a normal response if intact pitutiary and hypothalmic working. If so then order MRI b/c of secondary hypogonadism
MRI of the brain. if pituitary and hypothalamic is abn
if problem at the gland, primary
if problem at the brain (secondary, then both pituitary and hypogonadism)
SIADH workup
diagnosis of exclusion
R/o first - HF, cirrhosis, CKD
Hyponatremia w/ serum hypoosmol (dilute)
Continued renal excretion of salt w/ high urine osmosles
Absence of volume depletion - normal skin turgor and normal BP
**Corrected by fluid restriction! **
+ order BMP to check renal function
Diabetes Insipidus workup
1st step- 24 h urine collection to check the total volume of urine and Cr
Urine must be 2L/24h at least to continue
2nd step- water restriction test. patients can’t drink water. urine will remain dilute if positive. (also r/o psychogenic)
3rd step- vasopressin challenge test. Desmopressin acetate is given. urine volume is measured 12 hrs before desmo is given, and 12 hrs after desmo is given.
Pts with nephrogenic DI will have NO CHANGE
Pts w/ central DI will get better from this. If we know its not genetic, or inherited from their family, then..
4th step- MRI of pituitary and hypothalamus.
MRI skull for mass lesions.
Ddx in diabetes insipitus
polyuria is caused by many things….
psychogenic polydipsia, DM, cushings, corticosteroids, lithium, hypercalcemia, noctural polyuria of parkinsons
L PP CCC D
Pituitary adenoma workup
from expanding cranial mass which causes HA and vision changes. it can also manifest as a deficiency of 1 or more pituitary hormones.
MRI of the brain
Opthalmologic exam
labs
Look for bitemporal hemianopia. 40% of tumors found on autopsies are prolactinomas
Total Serum Ca2+
protein bound AND free calcium.
40-50% albumin bound
ionionized free Ca is active
False negative results from Total serum calcium
high false positive: hemo concentrated, high serum proteins
low false positive: low serum proteins
Serum phosphorus
highest in the AM, low in the PM
varies with time of year and food+antacids, renal functions, menopause, pregnancy, bedrest
Sleep, & eat
Bleed born
Renal
False results of phosphorus
high levels of lipid, protein, and bilirubin
Billy is prosperous from high protein and fat
Vit D inactive (serum)
what is its name?
D3 animal derived and synth in skin.
D2 plant derived.
Absorb D3 and D2 or synthesize some D3.
This is called serum 25-hydroxy vit D
1,25 vit D calcitrol (serum)
end product of vitamen D.
How does vit D get processed
serum 25-hydroxy vit D is not active. its synthesized in skin or absorbed from plant or animal. next, it gets sent to the liver and turns into OH 25 vit. After that it gets processed at the KIDNEY and PTH stimulates its synthesis. Then it goes straight back to the gut to help Ca get absorbed into the GI.
Potential false results from vitamen D?
increased serum paraproteins (multiple myeloma)
Serum PTHrP
naturally found in tooth enamel and mammary gland development.
Pathologically secreted by cancer and attaches to PTH-R
“lima beans”. caues PTH effect.
High means humoral hypercalcemia of malignancy
Mama’s lima bean dinner
Serum PTH
Dx hyperparathyroidism
High sensitvity and specificity
High/low calcium workup
PTH, vit D, albumin, Cr, Ca, P, Mg
Primary hyperparathyroidism labs
Calcium is elevated. It correlates with adenoma size. If 14 mg, carcinoma
**PTH **- elevated CONFIRMS diagnosis.
If 5X UL of normal, carcinoma.
Serum 25-OH vit D - low d/t excessive conversion of 25-OH vit D into 1,25 vit D
**Serum Cr and eGFR **- determine presence of renal dysfxn
If PTH is normal compared to a high calcium, check 24hr urine Ca. helps to assess for familiar hypocalciuric hypercalcemia FHH
24 h urine Ca - assess for primary hyperparathyroidism vs FHH. less than 200 Ca is FHH or primary vit D def.more than 200 excludes FHH. Cannot be on a loop or thiazide diuretic for test.
Serum phosphorus - differentiates primary from secondary hyperPTH.
normal to low = primary.
high = secondary.
FHH is a rare autosomal dominant causing decreased fxn of Ca-sensing receptors on parathyroid and renal cells. broken receptor. Higher than normal Ca exists to cause PTH to back down.
Primary hyperPTHism imaging
NOT NECESSARY FOR DX BUT
only if SURGERY tx is an option
Neck US good for adenomas
Radioactive nuclear medicine for hyperfuncting parathyroid glands, brighter on image
CT-4D: captures rapid uptake and washout of parathyroid adenomas
Secondary hyperPTHism
what makes calcium high or low
high- bone breakdown, supplements, kidney disease, meds.
low- low PTH, low Vit D, kidney dz
When do you correct calcium
use the calcuim and albumin.
Use when abnormal albumin levels occur
Serum phosphorus
What causes it to be high or low naturally
high - hypoPTH, kidney dz, acidosis, cell lysis (15% of P is in ICF)
low - hyperPTH, malabs, meds, low vit D.
need D to absorb Ca and P.
Vitamen D, what causes it to be high or low naturally
high - supplements, PTH high, extrarenal prouduction (lymphoma)
low- CKD, severe vit D deficiency, heritable dz, tumor induced osteomalacia, HIV protease inhitor
PTHrP- what makes it high
humoral hypercalcemia of malignancy
Serum PTH
high hyperparathyroidism
low hypoparathyroidism
What interferes with TSH
high = antithyroid meds, lithium, iodine, severe illness
low= heparin, NSAID, ASA, dopamine, steorids, severe illness
A lowly horse on steroids is dope, except when hes ill, then use aspirin and NSAIDS
Diurnal variation : peak TSH at 10 PM and trough at 10 AM
TSH is high because the thyroid hormone is too low
High TSH interpretation
not enough T3/T4. primary hypothyroidism.
could be from inadequate medication dose, thyroiditis, large doses of iodine, overfunctioning pituitary gland
Low TSH interpretation
too much T3/T4
Primary hyperthyroidism
could be under fx pituit or hypothal
T3/T4 test interfering factors
high= high TBG (estrogen, pregnancy, methadone)
low = low TBG (estrogen, pregnancy, methadone), protein bound drugs (NSAID, phenytoin), androgens, lithium
* T3 is less stable than T4 d/t lower binding protein
* neonates have higher levers of Free T4. screen them use T4
High levels of T3/T4 causes
excess thyroid hormones
hyperthyroid states
acute thyroiditis
excess dosing of thyroid meds
ectopic thyroid tissue
increased serum proteins, including TBG
Low levels of T3/T4
Insufficient thyriod hormone
hypothyroid states
iodine insufficiency
Inadequte dosing of meds
protein depleted state. - malnutrition, nephrotic syndrome
T3 and Free T3 could be low d/t decr conversion of T3. caused by liver dz or severe illness.
T4 and free T4 low due to only T3 medications
TBG labs high and low
released from the liver. Thyroxine binding globulin.
High:
increased estrogen (preg, ocp, menopause hormone replacement) , infectious hepatitis
Low:
Hypoproteinemia - nephrotic syndrome, liver dz, malabs/malnutrition, ovarian failure, incr Testost levels, major stress
TRH stim tests
Released from the hypothalamus
Assess pituitary rsp to TRH. to see if problem is hypothalamus.
TRH interfering factors
exaggerated in women and pregnancy
diminished in elderly and MDD patients
What is normal TRH stim test?
2X increase in THS w/i 30 min of TRH IV bolus
Abnormal TRH- primary hypo, secondary, tertiary
Primary - negative feedback on TSH d/t maximal pituitary suppression by T3 T4
Secondary - no TSH increase
Tertiary - delayed increase in baseline TSH (60-120 m)
Hypothyroidism workup labs
Screen w/ serum TSH
Primary: TSH increased and FT4 decreased
+/- anemia, lipid panel shows high lipids, low salt, low sugar, high PRL
Hashimotos: + anti-TPO and/or +anti-Tg
Hypothyroidism imaging
NOT indicated in SIMPLE cases
Consider if thyromegaly or thyroid nodule
Thyroid US
other: CT, MRI (visualize gland)
Enlarged thymus - AI thyroiditis
Enlarged pituitary - Hyperplasia of TSH secreting cells occurs
Subclinical Hypothyroidism
Normal FT4 with increased TSH
trial of LT4 if symptomatic but otherwise resolves itself in 30% of cases within 2 years
Thyrotoxicosis workup
Screen with serum TSH, +/- FT4
Possible hypercalcemia
high alk phosphates
anemia
decreased granulocytes
If Graves: + TSH, anti-TPO, anti-Tg
If thyroiditis: high ESR (antithyroid atb)
If thyrotoxicosis Factitia: low serum TGs
+imaging
Thyrotoxicosis imaging for etiology
Radioactive iodine RAI uptake and screening - determine etiology
Increased RAI uptake means graves, toxic solitary nodule, toxic multinodular goiter, type 1 amiodarone tox
Decreased RAI uptake means thyroiditis, iodine induced tox, type 2 amiodarone tox
can’t use in pregnant women
can’t use to determine if CA or not. requires exposure to radiation so some risk.
Thyrotoxicosis Thyroid imaging - for enlarged thyroid
ultrasound of thyroid
Color flow doppler sonography - identifies if increased blood flow
Does not diffentiate b/w benign or CA lesion
Subclinical hyperthyroidism Thyroid labs
Normal serum FT4 and T3 w/ low TSH
If symptoms, treat
Hashimoto disease
thyroiditis subtype
+ anti-TPO
+ anti-Tg
US - diffuse hetergenous density
could have Serum atb for celiac dz
FNA biopsy - nodules carry 8% risk of CA
Subacute thyroiditis
elevated ESR
low antithyroid atb titiers
hyper or hypo thyroid labs
Suppurative infectious thyroiditis
increased ESR, leukocytes
US- ID presence of abcess
normal thyroid function, normal atb
FNA biopsy with gram stain and cx 100% required
Ridel IgG4 thyroiditis
normal thyroid labs or signs of hyper/hypo thyroidism
Sick Euthyroid Syndrome
labs are not accurate in severe causes due to the impaired deiodination of T4 to T3
Thyroid Nodules/Goiters
step 1
TSH on ALL patients with nodule/goiter
+/- FT4, AI labs
For size/characteristics - thyroid US
If thyroid US is benign- cystic lesions.
When thyroid US is concerning - irregular margins, solid lesions, microcalcifications, abn vascularity greater than 1 cm.
Thyroid goiter/nodules
step 2
eval hyperfunctioning thyroid tissue. - RAI uptake
CT scan -
Fine needle aspiration biopsy
