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Flashcards in Endocrine Diagnosis and Treatment Deck (38)
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Diagnosis of pregnancy induced hyperthyroidism

High TBG
T3 uptake will decrease (by resin)


radionucleotide uptake of plummer's disease (multinodular toxic goiter)

Decreased TSH

Patchy uptake

Atrophy of thyroid gland


Radionucleatide uptake of toxic thyroid adenoma

Atrophy of rest of thyroid


increased uptake in one area


Treatment of hyperthyroidism

Immediate control: B blockers
sodium ipodate or iopanoic acid if don't respond to conventional therapy

Non pregnant:start metimazole
Taper B blocker after 4-8 weeks
Continue methimazole for 1-2 years then measure TBG IgG Ab at 12 months if absent can discontinue therapy, 1 more year of therapy if present

Pregnant: Endocrinology consult
PTU preferred

Elderly, solitary nodule, antithyroid therapy fails: radioactive iodine ablation therapy

Thyroidectomy: reserved for large goiters, allergic to antithyroid drugs or if they prefer surgery


Treatment of Thyroid storm

IV fluids, cooling blankets, and glucose

PTU every 2 hours followed by iodine to inhibit thyroid hormone release

B blockers for HR

Dexmethasone impairs T4 to T3 conversion and provides adrenal support


Diagnosis of Graves Disease

IgG binds to TSH receptors
Thyroid bruit

Low TSH level-initial test of choice
Next order-T4 level

Radioactive T3 uptake: (give radioactive T3 with resin testing to see if TBG is "filled" and uptake by resin)
Diffuse uptake of radioactive T3


Diagnosis and treatment of Hashimotos (chornic lymphocytic thyroiditis)

Goiter is rubbery, nontender and nodular

High TSH

Low free T4

Decreased/ irregular uptake of radionucleotide iodine-

Increased antimicrosomal Abs, antiperoxidase, antithyroglobulin Abs

Elevated LDL and decreased HDL, hypertriglyceridemia, increased AST and ALT, increased creatinine kinase

Treatment: levothyroxine

Anemia: nomracytic


Treatment and diagnosis of sublclincal hypothyroidism

TSH elevated with normal T4 level

Elevated LDL levels

Treat with thyroxine if: patient develops goiter, hypercholesterolemia, symptoms of hypthyroidism, or significantly elevated TSH level


Treatment and Diagnosis of subacute (viral) thyroiditis

Assoiciated with HLA;B35

painful, tender thyroid gland

Radioiodine uptake is low
Low TSH (transient hyperthyroid state)
High ESR

Treatment: NSAIDs and aspirin for mild symptoms
Corticosteroids for more severe pain

Most recover within a few months to one year


Treatment and diagnosis of subacute lymphocytic thyroiditis

Transient thyrotoxic phase of 2 to 5 months followed by hypothyroid phase

Low radioactive iodine uptake-differentiates it from Graves' disease
no pain or tenderness of thyroid gland


Pituitary adenoma diagnosis and treatment

Can release GH, prolactin, ACTH and TSH

Diagnosis: MRI, horomone levels

Treatment: transsphenoidal surgery (except prolactinomas)
Radiation therapy and medical therapy adjunct


Hyperprolactinemia diagnosis and treatment

Prolactinoma, psychiatric medications, H2 blockers, metoclopramide, verapamil, estrogen, pregnancy, hypothyroidism

Diagnosis: elevated serum prolactin level
order a pregnancy test and TSH level
CT scan or MRI to identify mass lesions

Treatment: bromocriptine or cabergoline for 2 years
transesphenoidal surgery if non responsive (recurrence is high)


Acromegaly diagnosis and treatment

Diagnosis: IGF-1 (somatomedin C) elevated
Oral glucose suppression test-glucose fails to suppress GH (as it should in healthy individuals)
MRI of pituitary
Hyperprolactinemia, hyperglycemia, hypertriglyceridemia, and hyperphosphatemia may be seen

Transspenoidal resection of pituitary adenoma-treatment of choice
radiation thearpy if IGF-1 remain elevated
Octreotide to suppress GH secretion


Hypopituitarism causes, diagnosis and treatment

causes: radiation therapy, sheehans syndrome, infiltrative processses-sarcoidosis, hemochromatosis, head trauma, caernous sinus thrombosis, surgery

Diagnosis: low levels of target hormones with normal trophic hormones
MRI of the brain

Treatment: replacement of hormones
if want to conceive refer to endocrinologist


Central Diabetes insipidus causes, diagnosis and treatment

idiopathic, trauma, sarcoidosis, Tb, syphilis, encephaltiis

Diagnosis: colorless urine, thirst and polydipsia, polyuria, hypernatremia
Low urine specific gravity, low osmolality
Plasma osmolality: 280-310
Low ADH level

water deprivation test: no increase in urine osmalality above 280 mOsm/kg after 24 dehydration
Increase in urine osmolality after ADH given

Treatment: Desmopressin
Chlorpropamide increases ADH secretion


Nephrogenic Diabetes insipidus causes, diagnosis and treatment

Causes: lithium, hypercalcemia, pyelo, demeclocyline, or congenital

Diagnosis: colorless urine, thirst and polydipsia, polyuria, hypernatremia
Low urine specific gravity, low osmolality
Plasma osmolality: 280-310
High ADH level

water deprivation test:
No increase in urine osmolality above 280 mOsm/kg with dehydration
No response to ADH after 24 hour dehydration

Treatment: sodium restriction and thiazide diuretics
Increased reabsorption of sodium and water in proximal tubule leading to decreased urine volume


SIADH causes, diagnosis and treatment

Causes: neoplasms, lymphomas, leukemia
CNS disorders (stroke, head trauma, infection)
Pulmonary disorders (pneumonia, TB)
Venitilators with positive pressure, vincristine, SSRIs, chlorpropamide, oxytocin, morphine, desmopressin, NSAIDs potentiate ADH action, postoperative state

diagnosis: inappropriately concentrated urine, low plasma osmolality (less than 280) and increased urine osmolality (>100-150)
low serum uric acid level
Low BUN and creatinine
Absence of hypervolemia

asymptomatic: water restriction or normal saline with a loop diuretic if need faster results
Lithium carbonate or demecolcycline

symptomatic: restrict water intake, give isotonic saline\
raise .5 mEq/L per hour


Pseudohypoparathyrodism diagnosis

hypocalcemia, hyperphosphatemia, high PTH, low urinary cAMP


Hypoparathyroidism diagnosis and treatment

Diagnosis: prolonged QT on ECG
low serum calcium, high serum phosphage, serum PTH inappropriately low, low urine cAMP

Treatment: IV calcium gluconate in severe cases
oral calcium in mild to moderate cases
Vitamin D supplementation
Avoid hypercalciuria by keeping serum calcium at 8.0 to 8.5


Primary hyperparathyroidism diagnosis and treatment

Diagnosis: HTN, shrotened QT weight loss, polydipsia, polyuria

Hypercalcmia (ionized fraction or ionized Ca level)
PTH elevated relative to serum calcium levels

Hypophosphatemia, hypercalciuria, urine cAMP is elevated

Chloride/phosphorus ratio >33 is diagnostic

Radiographs: subperiosteal bone resorption (radial aspect of second and third phalanges), osteopenia

Treatment: 3D sestambi scintography and US localize before surgery
Surgery indications: age less than 50, marked decrease in bone mass, nephrolithiasis, episode of severe hypercalcemia, urine calcium >400 mg in 24 hours

Due to hyperplasia: all four glands removed and small amount of parathyroid tissue is placed in forearm to retain parathyroid function
Due to adenoma: surgical removal of adenoma
Due to carcinoma: remove the tumor, ipsilateral thyroid lobe and all enlarged lymph nodes

Encourage fluids, give diuretics (furosemide) to enhance calcium excretion if hypercalcemia is severe NOT THIAZIDES


Dexmethasone suppression test

1. give 1 mg of dexmetasone at 11 p.m. and measure serum cortisol level at 8 a.m.
If the serum cortisol is less than 5 than Cushing syndrome is ruled out
Cortisol greater than 5 means check ACTH level
2. Low ACTH=adrenal tumor or hyperplasia (adrenal imaging should be done)
3. High ACTH leads to high dose dexmethasone test
Greater than 50% suppression=pituitary (MRI)
less than 50% suppression=ectopic source (chest and abdominal CT, ocretreotide scan)
4. CRH stimulation test
+ equals pituatry
- equals ectopic source


Treatment of Cushing's syndrome

Iatrogenic: tapering of glucocorticoid
Pituitary Cushing's syndrome: surgery (treanssphenoidal ablation)
Adrenal adenoma or carcinoma: adrenalectomy


Diagnosis and treatment of pheochromocytoma

Diagnosis: urinary metanephrine, Vanillylmanndelic acid, homovanillic acid normetanephrine
Plasma metanephrines
Urine/serum epi and NE-if epi is elevated tumor must be adrenal or near the adrenal gland
Tumor localization: CT or MRI

Treatment: surgical tumor resection with early ligation of venous drainage
Patients treated with a-blockade (phenoxybenzamine) for 10-14 days prior to surgery (BP control) and B blockade 2-3 days (HR control) prior to surgery
Possible adrenalectomy


Diagnosis and treatment of MEN syndrome

Screen with PCR on blood sample and DNA testing

Treatment: total thyroidectomy


Primary Hyperaldosteronism diagnosis and treatment

HTN, weakness, polydipsia, noncturnal polyuria
hypernatremia and hypokalemia (metabolic alkalosis)

Diagnosis: plasma aldosterone:renin ratio is >30

Saline infusion test:
infusion of saline will decrease aldosterone levels in normal patients but not with hyperaldosteronism
Aldosterone levels are less than 8.5 after saline infusion then primary aldosteronism is ruled out

Oral sodium loading:
high salt diet for 3 days-high urine aldosterone in setting of high urine sodium confirms diagnosis

Diagnose cause:
Adrenal venous sampling: high levels of aldosterone on one side=adenoma, bilateral=hyperplasia
Renin aldosterone stimulation test
CT/MRI of adrenals: adenoma or hyperplasia anatomically
Iodocholesterol scanning: functional approach to differentiation

Treatment: adenoma-surgical resection
Adrenal incidentaloma-resection if greater than 6 cm
bilateral hyperplasia: spironolactone (NOT surgery)


Adrenal crisis diagnosis and treatment

severe hypotension and cardiovascular collapse

Treatment: IV hydrocortisone, IV fluids (several liters of normal saline with 5% dextrose)


Adrenal insufficiency diagnosis and treatment

low aldosterone (primary only)-hyponatremia, hyperkalemia and hypovolemia

Diagnosis: decreased plasma cortisol
Plasma ACTH-low implies a secondary adrenal insufficiency

ACTH test: give IV infusion of ACTH and measure cortisol-cortisol does not increase in primary every
Cortisol will increase after 4 to 5 days in secondary (aldosterone and renin will also be normal)

treatment: primary: daily oral glucocorticoid (hydrocortisone or prednisone) daily fludrocortisone (mineralcorticoid)
Secondary: no mineralcorticoid necessary


21 hydroxylase deficiency congenital adrenal hyperplasia diagnosis and treatment

Diagnosis: increased 17-hydroxyprogesterone

Treatment: cortisol and mineralcorticoid (shuts off ACTH secretion)
Surgically: correct female genital abnormalities


Diabetes diagnosis

Two fasting glucose measurements greater than 125 mg/dL-preferred (recheck if between 100-126)

Single glucose level of 200 mg/dL with symptoms

Increased (>200) glucose level on oral glucose tolerance testing (after administration of equivalent of 75 g glucose load

hemoglobin A1c>6.5%


Diabetes Outpatient management

Monitor HbA1c every 3 months (keeping it below 7.0 is the goal)

Check blood glucose levels before meals and at bedtime. Monitor 90 to 120 minutes after meals

Screen for microalbuninema once a year (prescribe ACE inhib or ARB)

Check BUN and Cr once a year

Eye screening yearly

Check feet at every visit-encourage patient to do so

Check cholesterol once a year: Statin if LDL >100

ACE or ARB if BP >130/80

Daily aspirin in all diabetics over age 30

Pneumoccocal vaccine