Endo exam 3 diagnoses/labs Flashcards

(79 cards)

1
Q

Addisons disease
labs only

A

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 +)

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2
Q

Addisons disease imaging only

A

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

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3
Q

Interfering factors of cortisol levels for cushings

A

Na+ intake, age, sex, race, pregnancy, meds, renal impairment, and menstrual phase

Menstrual. Then Salty racy, age appropriate sex
Then pregnant, whoops

+ renal

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4
Q

Cushings syndrome lab workup

step 1

A

CBC- leukocytosis w/ neutrophillia, lymphocytopenia, low eosinphils

CMP- increased glucose +/- hypernatremia, hypokalemia

Cortisol causes early release of neutrophils and less apoptosis of neutrophils

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5
Q

Cushing syndrome Source workup

step 2

A

Need 2 + tests of the following:

Dexamethasone suppression, 24 h urine free cortisol, late night salivary cortisol

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6
Q

What is low dose dexamethasone suppression test for cushings

A

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

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7
Q

24 h urine free cortisol cushings

A

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

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8
Q

cushings - What is salivary cortisol

and interfering factors

A

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

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9
Q

Determining the DIAGNOSIS for cushings disease after the 2 tests

step 3

A

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.

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10
Q

How to determine cause for hypercortisolism

step 4

A

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

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11
Q

What should the CT or MRI show

step 5

A
  • 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

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12
Q

Inferior petrosal sinus sampling

step 6

A

causes increased ACTH, and confirmes the pituitary cushings disease

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13
Q

Congenital Adrenal Hyperplasia workup

A

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

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14
Q

Primary aldosteronism workup initial

A

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!

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15
Q

Interfering meds for primary aldosteronism dx

A

Bad: spironolactone, ACEi, ARB, any direct renin inhib

Good: slow release verapamil, hydralazine, terazosin, doxazosin

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16
Q

Confirmatory Testing for primary aldosteronism

A

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

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17
Q

Determine cause of Primary aldosteronism

A

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

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18
Q

Pheochromocytoma workup

A

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.

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19
Q

Adrenal Adenoma Workup

A

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

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20
Q

Adrenal Carcinoma

A

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.

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21
Q

Hyperprolactinemia workup

A

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.

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22
Q

Growth hormone deficiency kid workup

A

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.

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23
Q

GH stim test children

A

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

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24
Q

GH adult deficiency workup, first step

A

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

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25
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
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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.
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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.
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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.
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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 ## Footnote if problem at the brain (secondary, then both pituitary and hypogonadism)
30
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
31
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.
32
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
33
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
34
Total Serum Ca2+
protein bound AND free calcium. 40-50% albumin bound ionionized free Ca is active
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False negative results from Total serum calcium
high false positive: hemo concentrated, high serum proteins low false positive: low serum proteins
36
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
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False results of phosphorus
high levels of lipid, protein, and bilirubin Billy is prosperous from high protein and fat
38
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
39
1,25 vit D calcitrol (serum)
end product of vitamen D.
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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.
41
Potential false results from vitamen D?
increased serum paraproteins (multiple myeloma)
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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
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Serum PTH
Dx hyperparathyroidism High sensitvity and specificity
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High/low calcium workup
PTH, vit D, albumin, Cr, Ca, P, Mg
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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. ## Footnote 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.
46
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
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Secondary hyperPTHism
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what makes calcium high or low
high- bone breakdown, supplements, kidney disease, meds. low- low PTH, low Vit D, kidney dz
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When do you correct calcium
use the calcuim and albumin. Use when abnormal albumin levels occur
50
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.
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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
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PTHrP- what makes it high
humoral hypercalcemia of malignancy
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Serum PTH
high hyperparathyroidism low hypoparathyroidism
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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
55
High TSH interpretation
not enough T3/T4. primary hypothyroidism. could be from inadequate medication dose, thyroiditis, large doses of iodine, overfunctioning pituitary gland
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Low TSH interpretation
too much T3/T4 Primary hyperthyroidism could be under fx pituit or hypothal
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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
58
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
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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
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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
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TRH stim tests
Released from the hypothalamus Assess pituitary rsp to TRH. to see if problem is hypothalamus.
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TRH interfering factors
exaggerated in women and pregnancy diminished in elderly and MDD patients
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What is normal TRH stim test?
2X increase in THS w/i 30 min of TRH IV bolus
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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)
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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
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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
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Subclinical Hypothyroidism
Normal FT4 with increased TSH trial of LT4 if symptomatic but otherwise resolves itself in 30% of cases within 2 years
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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
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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.
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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
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Subclinical hyperthyroidism Thyroid labs
Normal serum FT4 and T3 w/ low TSH If symptoms, treat
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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
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Subacute thyroiditis
elevated ESR low antithyroid atb titiers hyper or hypo thyroid labs
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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
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Ridel IgG4 thyroiditis
normal thyroid labs or signs of hyper/hypo thyroidism
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Sick Euthyroid Syndrome
labs are not accurate in severe causes due to the impaired deiodination of T4 to T3
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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.
78
Thyroid goiter/nodules | step 2
eval hyperfunctioning thyroid tissue. - RAI uptake CT scan - Fine needle aspiration biopsy
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