Endocrine Diagnosis and Treatment Flashcards
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
Low TSH
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
Treatment:
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
Causes:
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
Treatment:
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
- 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 - Low ACTH=adrenal tumor or hyperplasia (adrenal imaging should be done)
- 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)
Or - 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
Arteriography/venography
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
hypoglycemia, 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
Treatment goals of diabetes
Glycemic control-HbA1c less than 7%, fasting blood glucose less than 130, and peak postprandial blood glucose less than 180
BP control less than 130/85
LDL less than 100, HDL greater than 40
Smoking cessation
daily aspirin
Treatment of Diabetes
Diet and exercise
Glucose >240=insulin
Glucose 140-240=hypoglycemic agents (sulfonylureas, metformin, acrabose, thiazoldinediones)
Metformin is first agent of choice
Regular insulin give IV for ketoacidosis
Diabetic retinopathy complications and treatment
edema of the macula=leading cause of blindness
Vitreal hemorrhhage and retinal detachment can lead to blindness
Treatment is laser photocoagulation
Treatment of diabetic peripheral neuropathy
NSAIDs, gabapentin, tricyclic antidepressants or pregabalin
Treatment of diabetic gastroparesis
metoclopramide, exercise and low fat diet
Diagnosis and treatment of DKA
Diagnosis: Hyperglycemia (glucose >450)
Metabolic acidosis: ph less than 7.3 and serum HCO3- less than 15 increased anion gap
Ketonemia: acetoacetate, acetone and B-hydroxybutyrate
Hyperosmoalrity
Hyponatremia-total body sodium is normal
hyperkalemia: total body potassium is low
Phosphate and Mg are low
Treatment:
IV insulin immediately -make sure not hypokalemic
Continue insulin until anion gap closes and metabolic acidosis is corrected
Give SC insulin when anion gap less than 12, HCO3 >15 and eating again overlap by 1-2 hours
Fluid replacment: .9% immediately
Add 5% glucose once blood glucose reaches less than 250 to prevent hypoglycemia
Replace potassium with IV fluids if less than 5.2 (no insulin if K+ less than 3.3) -initiate within 1-2 hours of starting insulin
Bicaronate if ph less than 6.9
Assessment of anion gap and beta-hydroxy-butyrate indicate resolution from DKA
Diagnosis and treatment of hyperosmolar hyperglycemic nonketotic syndrome
Diagnosis: hyperglycemia >900 Hyperosmolarity >320 Serum pH>7.3 (no acidosis, no ketosis) HCO3->15 elevated BUN-prerenal azotemia
Treatment: fluid replacement is most important (normal saline): 1L in first hour another liter in the next 2 hours
When glucose reaches 250 mg/DL add 5% glucose
insulin-5 to 10 unit IV followed by continuous low dose infusion
Diagnosis and treatment of hypoglycemia
Diagnosis: blood glucose below 50
true hypoglycemia:
hypoglycemic symptoms brought on by fasting
blood glucose less than 50 during an attack
glucose admin reduces smptoms
Measure: insulin, C pepetide and glucose during fast
Treatment: Patient can eat give sugar containing foods
If can’t eat give D50W IV and switch to D10W as clinical condition improves and glucose level is >100
If alcoholic give thiamine first
