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204 Cards in this Set

  • Front
  • Back
Thyroid ca occurs most often subsequent to?
childhood irradiation of the head and neck, which was common between 1900-1950s.
Pt may not be aware of the exposure. Risk increases with?
-incidence of Thyroid ca increases with?
age with a positive history of neck
irradiation affects women over men?
2:1 and 7-9 % of population
Benign disease risks?
include living in an iodine deficient area of an increased intake of substances that increase thyroid such as lithium, turnips, or beets. When a pt has symptoms classic for hypo- or hyperthyroid states, benign disease is most likely.
There are 3 major types of tumors?
Localized papillary follicularanaplastic medullary
localized papillary?
Thyroid Ca which has a great survival rate
anaplastic tumors?
(10-12%) which lead rapidly to death
medullary tumors?
Calcitonin is a unique tumor marker for?
Some familiar forms of medullary CA , it often presents as a nodule in the upper half of the thyroid gland
Lymphoma may develop as a?
primary lesion in the thyroid gland in chronic lymphocytic thyroiditis and often spreads to local lymph nodes.
Adjacent lymph nodes need to be evaluated too: when these are + what do you do?
immediate referral in indicated.
Thyroid scan ?
is more sensitive, picking up 95% of masses, but cannot distinguish malignant vs benign state.
Single nodules?
more often indicate malignancy and are usually asymptomatic. These may occasionally become painful if they undergo rapid growth, inflammation, or hemorrhage.
Often lymphoma induces?
tenderness since it develops rapidly.
Definitive diagnosis is then made via?
fine needle biopsy and a cytologic exam.
Solitary nodules may be either?
benign adenomas, thyroid carcinomas, or indicate a multinodular condition in which only one nodule may be palpable.
The the most common, nonmalignant nodules are?
Benign adenomas and they have a capsule.
Types of nodules?
benign adenomas colloid or adenomatous nodules.
Both are slow growers, and don’t produce much thyroid hormone. They appear as cold nodules on scan?
colloid or adenomatous nodules.
A toxic adenomas ?
exceeds 3 cm in diameter, suppresses TSH, and causes thyroid gland to become atrophic.
Thyroid cancer is rare but the diagnosis is on the increase in young women in their 30s. It rarely arises in?
a multinodular gland.
Clinical features of thyroid ca include?
cervical adenopathy, hoarseness due to laryngeal nerve compression, dysphagia, or obstruction. Appears as a cold nodule on a thyroid scan.
Hashimotos’ disease?
is an autoimmune condition and the leading cause of multinodular goiter
Hashimotos dx affects about?
4% of the population, and 15% of women over age 65. Women are affected in a 3:1 ratio.
Antimicrosomal antibodies are found Hashimotos dx in?
What happens in Hashimoto's dx?
Chronic inflammatory cell infiltrates and fibrosis occur.
The second most common cause of multinodular gland in adults is?
Multinodular goiter
Prognosis of multinodular goiter?
About 1/3 of pts will become euthyroid, and 1/3 become hypothyroid. It is an advanced stage of focal autonomous hyperplasia beginning as a diffusely enlarged gland and eventually becomes a multinodular gland.
With multinodular goiter, the gland feels?
less firm than in Hashimoto’s disease. Free thyroxine level is usually normal and TSH may be slightly low.
In cases of malignancy, are lab markers such as an abnormal TSH common?
no
A high antimicrosomal antibody titer suggests?
Hashimotos, or subacute lymphocytic thyroiditis
An elevated ESR may indicate?
subacute lymphocytic thyroiditis
When there is a positive family history of thyroid CA, which lab should be checked?
Check serum calcitonin level
Thyroid sono can detect what lesions?
about 1 mm in size and can differentiate cystic vs solid lesions. Is also used to localize lesions for biopsy.
Fine needle biopsy is done where?
in endocrinology office. A radionucleide scan is done over 2 days in an imaging facility or hosp setting.
The thyroid uptake and scan measures?
the ability of the thyroid gland to concentrate and retain iodine.
Thyroid uptake and scan procedure and prep?
Radioactive iodine is administered as either I 131 of I 123. Pt should be fasting. Amount of radioactivity is measured after 2, 6, and 24 hours. Painless procedure. It is contraindicated during pregnancy, in children, or those with a history of iodine allergy.
Pts taking a number of meds need to discontinue these prior to thyroid uptake and scan, per schedule: check with radiologist. Interfering meds include?
thyroid replacement or suppressive therapy, sulfonamides, corticosteroids, nitrates, INH, aspirin, Coumadin, orinase
Other OTC meds include iodine containing?
expectorants, cough suppressants, and vitamins. Dietary sources of iodine should be restricted for one week following testing.
Most malignant nodules appear as ____ nodules on scan?
“cold
,Though a warm nodule does not R/O malignancy?
About 15-20% of cold nodules are malignant. A hot nodule has low malignancy potential.
A pt with a multinodular gland only needs biopsy if there is a history of ?
neck irradiation, a rapid growth of a single nodule occurs, there is onset of recurrent laryngeal nerve palsy, or cervical adenopathy is present.
Sono should be regularly done to monitor?
multinodular glands, if a goiter markedly enlarges while a pt is on suppressive therapy, or an enlarging tender gland occurs.
Benign adenomas are monitored how ofter and why?
annually for size and hormone levels.
Which nodules require biopsy?
A mass under 2 cm rarely becomes problematic. Single nodules require biopsy.
Mixed papillary/follicular and papillary account for____% of tumors?
60-70% of tumor
On PE, a palpable nodule is found only 4-7% of the time. If a nodule is detected, document?
its size, consistency and number of nodules.
PE findings suggestive of CA include?
a solitary, hard nodule with irregular borders that is fixed and does not move with swallowing.
A soft nodule does not R/O cancer, it often represents ?
papillary CA
A benign solitary nodule in a pt otherwise healthy and euthyroid may be given?
a trial of exogenous thyroid hormone to shrink size of gland: it works in up to 30% of pts if TSH is suppressed.
For a trial of exogenous thyroid hormone to shrink size of gland, start with?
dose levothyroxine 50 mcg and work up to 100-150 mcg to drop TSH to 0.05-0.3.
A trial of exogenous thyroid hormone to shrink size of gland: doesn’t work with which nodules? It's contra in which pts?
colloid nodules, and is contraindicated in the elderly or those with underlying CAD.
Ablation is recommended for?
toxic nodules and functioning solitary adenomas over 3 cm and increased serum T3. Young pts are the best surgical candidates.
Radioiodine is best for which pts?
the elderly: a palpable nodule may remain after treatment.
Pt's with radioiodine must be monitored for?
post treatment hypothyroidism.
Small cysts in multinodular goiter can be treated by being?
aspirated, large ones surgically removed.
A pt with a multinodular goiter may need what med?
a beta blocker for 10 days before any contrast study is done.
Thyroid hormone stimulates?
calorigenesis and catabolism.
T3?
free T4?
(thyroxine)
.
Thyroid hormone stimulates calorigenesis and catabolism& it accounts for the production of T3&T4 inducing excessive circulating amounts which can occur transiently in ?
chronic lymphocytic Hashimoto’s thyroiditis, and subacute granulomatous thyroiditis.diffuse toxic goiter (Graves disease), toxic multinodular goiter, toxic uninodular goiter (toxic nodule), or in pts taking excessive levothyroxine.
Increased thyroid hormone is a common condition affecting women more than men and most often over age?
60.
Clinical presentation of hyperthyroidism in the elderly can be?
atypical.
The mechanism responsible for excess circulating hormone can be?
increased TSH production, stimulation of thyroid TSH receptors by immunoglobulins, autonomous thyroid hormone production, increased release of thyroid hormone without increased production, or intake of exogenous hormone.
Clinical presentation of hyperthyroidism?
heat intolerance, nervousness, tremor, increased appetite, weight loss, excessive sweating, lid lag, stare, muscle weakness, frequent defecation.
With hyperthyroidism,the elderly may become?
apathetic, develop a fib, wt loss, or no symptoms. Apathy may be mistakenly diagnosed as depression.
In thyrotoxicosis what labs may be abnormal?
alk phos elevates, and ACE level. These may persist after treatment
Graves disease?
is an autoimmune condition that accounts for about 90% of hyperthyroidism seen in pts under 40 years
What may trigger excess hormone production?
an environmental link is being explored. It begins as a deficiency of thyroid-specific suppressor T cell lymphocytes allowing formation of thyroid stimulating IgG antibodies which bind to thyrotropin on thyroid cell surfaces and trigger excess hormone production.
Ophthalmopathy affects about 40% of pts with hyperthyriodism?
Eye changes occur concurrently with hyperthyroidism development and usually remain after treatment. With mild occurrence, there is mild periorbital edema and conjunctival inflammation to extraocular muscle dysfunction, corneal injury and optic nerve damage. Other symptoms can include eye pain, diplopia, proptosis, and blurred vision.
When the thyroid gland is diffusely enlarged, a bruit can be heard. Classic s/sx thyrotoxicosis include?
velvety skin, hair becoming silky in texture, vitiligo, gynecomastia, and reversible cardiomyopathy (a decreased ejection fraction with exercise).
What seems to be a factor re: incidence of development of thyrotoxicosis?
Exposure to contrast media seems to be a factor
Toxic multinodular goiter, or Plummer’s disease, accounts for most cases of hyperthyroidism in?
elderly and middle aged patients. Often assoc with long term goiter and presents with cardiac symptoms such as new onset a fib, heart failure, or angina, often due to coexisting disease in elderly pts.
Exopthalmos with hyperthyroidism is unlikely in this population?
Several transient forms of hyperthyroidism occur?
postpartum thyroiditis, Subacute thyroiditis
Postpartum thyroiditis?
(subacute lymphocytic)
Postpartum thyroiditis (subacute lymphocytic) affects about?
5% of women with onset 3-6 months post-partum
With Postpartum thyroiditis (subacute lymphocytic), the gland is?
nontender. Anti thyroid antibody level may be slightly positive. Resolves after several months. Tends to recur with subsequent pregnancies.
Subacute thyroiditis?
often follows a viral infection and induces a tender, multinodular gland.
Rarely, a ___________ may be responsible for an extreme TSH elevation?
pituitary adenoma
In pituitary adenoma the thyroid gland becomes?
diffusely enlarged similar to in Graves disease, but no exopthalmos develops.
A hydatiform mole when massive produces ?
hyperthyroidism and some thyroid stimulating activity via HCG.
A dermoid ovarian tumor may also rarely induce ?
hyperthyroidism.
What's needed to confirm hyperthyroidism since in many cases the clinical presentation is not clear ?
Lab tests (e.g. in the elderly, pregnant, or those with mild symptoms).
The hallmark result in hyperthyroidism?
is an elevated free T4, or free T3 which = serum T4 x T3 resin uptake.
Serum TSH must be very low or absent to diagnose ?
hyperthyroidism.
When serum levels are equivocal, it is sometimes helpful to obtain ?
thyrotropin releasing hormone stimulation testing (TRH). If hyperthyroidism is real, the TSH response to TRH is minimal to absent.
During history, for hyperthyroidism, ask about ?
recent pregnancy or viral illness, history of goiter or thyroid nodule, use of thyroid hormone, eye changes, and known ovarian, pituitary or thyroid tumor.
During PE, check the thyroid gland for?
size and nodularity
Look for extra-thyroid findings such as eye changes?
true proptosis = more than 20 mm of eye protrusion from the orbital bone and pretibial myxedema is noted.
Nonspecific findings
Nonspecific eye findings with hyperthyroidism include?
lid lag and stare
Consider pelvic and visual field testing to R/O?
ovarian or pituitary etiologies.
What diagnostic tests should be ordered?
Order thyroid sono/scan.
Blood work includes ?
antithyroid antibody level (elevated), on CBC see mild anemia, granulocytosis, lypmhocytosis
Hyperthyroidism treatment?
Antithyroid drugs, radioiodine, or thyroidectomy are usual therapies. All pts with hyperthyroidism are referred to endocrinologist for management.
NP may prescribe?
low dose beta blocker for short term hyperadrenergic symptom management such as tremor, heat intolerance, palpitations, or nervousness: these work within a few days. This may be adequate monotherapy for transient hyperthyroidism, and minimize major cardiac complications of hyperthyroid disease such as a fib or angina
Beta blockers must be used with extreme caution in?
the elderly or those with pre-existing heart disease.
Which BB can you use for hyperthyroidism?
Propanolol 80 mg, atenolol 50 mg daily and educating pt to monitor resting and exercise heart rate needed.
When beta blockers are prescribed surgery can proceed in?
1-2 weeks, vs using antithyroid drugs require 6-8 weeks of pre-op therapy. Sometimes potassium iodide is added to regimen.
Antithyroid drugs include?
methimazole and propylthiouracil (PTU). Younger pts are more often treated with one of these.
Methimazole is potent, dosed at?
PTU MOA? for which pts? dose?
blocks peripheral conversion of T4 to T3 and helps many Graves pts achieve remission. Dose is usually 100 mg three times a day.
Both PTU and methimazole drugs?
suppress thyroid auto-immunity and decrease thyroid stimulating antibodies.
Clinical response with PTU and methimazole evident in?
Pts are usually treated with PTU and methimazole for?
Usually pts are treated for 1-2 years.
After 1-2 yrs of tx with PTU and methimazole?
D/C therapy and check whether still needed.
Common adverse effects with PTU and methimazole are?
skin rash, fever, and arthralgias and agranulocytosis is a rare
agranulocytosis with PTU and methimazole is a rare but a very significant risk, especially if pt is?
over 40.
When would agranulocytosis occur with PTU and methimazole?
it usually does so after 2-4 months of therapy.
With PTU and methimazole how long do you monitor blood work?
If leucocytes drop below what #, do you D/ C PTU or methimazole?
Mild leucopenia is common: D/c drug if drops below 1500/mm3.
What tx is used more often in elderly pts?
Radioactive iodine is used more often in elderly pts.
Who else is radioactive iodine indicated for?
those with Graves dx, after antithyroid therapy is not effective, in noncompliant pts, those with solitary toxic nodules, those with contraindications for or reluctance to undergo surgery.
What is the most common complication of tx for hyperthyroidism?
is the development of hypothyroidism, (70% in the first year) after high dose, but it does provide good therapeutic response.
After radioactive iodine/ hyperthyroid tx, how often do pts need to monitored? Why?
every 6 months. About 20% of Graves pts experience worsening ophthalmopathy after treatment:need prednisone.}
Dose of steroids to decrease opthalmopathy after tx?
sometimes oral prednisone (20-40 mg/day) for several months after radioactive iodine with dose taper can minimize symptoms, but then pt needs to deal with steroid side effects and risks.
Surgery risks include?
1) permanent hypothyroidism, 2) laryngeal paralysis, 3) hypoparathyroidism, and 4) recurrence of hyperthyroidism.
Surgery for hyperthyroidism is the treatment of choice during?
pregnancy, with refractory disease, when necessary to relieve esophageal
Surgery risks include ?
1) permanent hypothyroidism, 2) laryngeal paralysis, 3) hypoparathyroidism, and 4) recurrence of hyperthyroidism.
Surgery is the treatment of choice during?
pregnancy, with refractory disease, when necessary to relieve esophageal obstruction, in cases of ineffective therapy with antithyroid therapy, pt who refuse radioiodine, or young pts with severe disease.
What is less invasive and expensive then surgery?
I 131 is less expensive and less invasive
Monitoring treatment?
1.Note weight changes, degree of heat intolerance, appetite, anxiousness, energy level, resting heart rate, skin temp/texture, eye exam.
What labs should be measured?
serum TFTs and monitor change in serum free T4 and TSH, which provides the best measure of treatment status and first sign of overtreatment which can induce hypothyroidism
Pt with Graves disease, monitor which labs?
serum level of antibodies to TSH receptors
If on PTU, monitor ?
leukocyte count if on PTU or over 30 mg/day methimazole every 2-4 weeks during the first 4 months.
Educate pt to report?
s/sx of hypothyroidism or agranulocytosis such as fever, chills. Follow up with ophth if diplopia or decreased vision develops.
The most common form of hypothyroidism in the US is?
Hashimotos thyroiditis
Less common causes of hypothyroidism, include?
neck irradiation, iodine administration, use of lithium, or para-aminosalicylic acid. Condition also occurs in a pt taking inappropriate dose of thyroid replacement.
Increased incidence of hypothyroidism found in?
among women, and with aging.
Primary hypothyroidism occurs secondary to?
impaired thyroid function and secondary disease secondary to hypothalamic-pituitary function disorders. [
In primary hypothyroidism disease, the hypothalamus response is to ?
increase thyrotropin releasing hormone, which triggers pituitary thyrotropin (TSH) secretion, which stimulates thyroid gland enlargement, goiter formation, and synthesis of T3 (triiodothyronine) over T4 (thyroxine).
In secondary hypothyroidism disease?
TSH response is inadequate, gland is normal or diminished in size and synthesis of both T3 and T4 is decreased.
Forms of primary hypothyroid include?
Hashimoto's, Post partum thyroiditis, Radiation induced hypothyroidism, Subacute thyroiditis, Subtotal thyroidectomy
Hashimotos’ ?
an immune-mediated disease. Monitor antimicrosomal antibodies. Gland enlarges, with or without nodule development.
Post partum thyroiditis?
is a variant of Hashimotos. Affects 5% of post partum women
Postpartum thyroiditis resolves over?
2-3 months but tends to recur in subsequent pregnancies.
Radiation induced hypothyroidism is?
either consequence of I 131 therapy, or neck irradiation for lymphoma and head and neck cancer
Subacute thyroiditis follows ?
a viral infection inducing a tender, enlarged gland which is often asymmetric. First hyperthyroid then hypothyroid occur. Takes weeks to months to resolve.
Subtotal thyroidectomy occurs why? and when?
half of pts treated develop hypothyroid within one year. Also about 5% of pts using lithium become hypothyroid over time.
Subclinical or borderline TSH elevation would give what lab result? Clinical manifestations would show when?
(slightly elevated, 6-14 with other TFTs remaining normal). Clinical manifestations usually develop within 5 years if TSH remains over 6. If TSH over 20, 100% likelihood of hypothyroid development.
S/Sx of hypothyroidism?
gradual onset fatigue, dry skin, heavy periods, slight weight gain, cold intolerance. Later, very dry skin, coarse hair texture, hoarseness, more weight gain, slightly impaired cognition, depression, constipation. Later, myxedematous changes occur, facial edema, tongue enlargement, dull expression, carpal tunnel syndrome, decreased hearing, weak muscles, arthralgias.
On PE hypothyroidism would present as ?
+/- goiter
With secondary hypothyroidism would present as?
signs of ovarian/adrenal insufficiency (e.g. loss axillary and pubic hair, amenorrhea, postural hypotension, low luteinizing hormone, follicle stimulating hormone, and ACTH.
Patho of hypothyroidism?
Increased TSH precedes clinical findings, then TRH increases. Later free T4 drops and hypercholesterolemia with LDL increases and lower HDL assoc with anemia (normochromic, normocytic) or microcystic secondary iron deficiency from heavy menses.
Diagnosis is confirmed of hypothyroidism by?
increased TSH and low free T4.
TSH?
is the test of choice, and most sensitive indicator.
Presence of antimicrosomal antibodies most strongly suggests ?
Hashimotos.
TRH stimulation can confirm?
secondary disease.
Treatment indicated for clinically hypothyroid patients?
do gradual replacement with (DAW) synthroid (levothyroxine) at 0.025 -0.05 mg per day for older pts especially with known cardiac disease. Younger patients can start at 0.10 mg/day.
Recheck blood work with thyroid replacemnt?
in 4-6 weeks to assess progress
May take TSH up to how much time to normalize?
12 months to normalize.
Once TSH is stable, check patient every?
6 months via TSH
Drug absorption is adversely affected by concurrent?
ferrous sulfate.
To evaluate a new patient on long term replacement?
discontinue the drug for 4 weeks and recheck blood work 4-6 weeks after discontinuing.
With recheck in 4-6 wks, If pt appears clinically hypothyroid and blood work suggests hypothyroid but TSH is not elevated, look for?
pituitary insufficiency.
With excessive doses (TSH < 0.5) what may be induced?
osteoporosis may be induced.
With secondary hypothyroidism dx, therapy, do ACTH stimulating test to assess adrenal reserve if low, give?
cortisone acetate before adding thyroid replacement.
Hypercalcemia often an incidental finding noted during routine blood work, suggests?
parathyroid dysfunction.
Hypercalcemia may signal?
Normal calcium range is about ?
8.5-10.4 mg/dL.
When level is 20% above normal, (around 13), symptoms include /
fatigue, difficulty concentrating, headache, constipation, muscle weakness.
At Calcium levels of 14-15?
psych symptoms appear, nausea, vomiting, stupor, coma, myalgias, polyuria, nephrolithiasis.
Hypercalcemia due to malignancy usually presents at level ?
over 14, with increased alk phos level, hypochloremic acidosis, and a more acute onset.
What drugs may temporarily increase calcium level?
Thiazide diuretics
Hypercalcemia occurs during when? and in who?
4th-6th decade of life. women > men, 2:1
Calcium level is controlled by/
bone metabolism renal excretion and intestinal absorption via calcitonin, parathormone, and cholecalciferol (vitamin D3).
Calcitonin lowers the serum calcium via?
bone formation
PTH raises serum calcium via?
Next blood test to order is?
an intact PTH level. Refer to endocrinologist for follow up
. Eventual treatment may include surgery. Surgery more often recommended when?
kidney stone formation becomes recurrent, creatinine clearance drops, or significant bone loss is noted.
Limiting dietary calcium often recommended, and drinking?
at least 2 liters of decaf fluid daily.
Blood work up should include?
repeat serum calcium level, with serum albumin and globulin too. Can check 1,25 dihydroxy vitamin D.Sometimes increase is due to prolonged tourniquet application during venipuncture. Consider DEXA, since spine measures trabecular bone.
R/O signs of malignancy, look for?
breast mass, bone tenderness or lymphadenopathy, and sarcoid (check for lymphadenopathy) and run and ACE level
Hyperparathyroidism?
does not induce clear clinical signs.
Hirsuitism in women, is caused by an increase in?
androgenic activity with increased growth of hormone dependent pubic, axillary, abdominal, chest, and facial hair.
An endocrinology evaluation is needed for women with concurrent ?
Source of increased androgen is either the?
testosterone metabolite 5-alpha-dihydrotestosterone, which is produced at the hair follicle, via DHEA and androstenedione, a testosterone precursor for the ovaries and adrenals.
Hirsuit women usually have an increased?
testosterone level or increased DHEA/ androstenedione level. Hyperinsulinemia due to insulin resistance has been linked with the development of obesity and hirsuitism.
There are ethnic and racial patterns noted. Hair growth in 9 androgen dependent body areas can be ranked on a scale from?
zero (no hair growth) to 4 (frankly virile) and a total score over 8 = hirsuitism.
Ovarian sources?
most women with non-virulizing hirsuitism have oligomenorrhea or amenorrhea have PCOS.
Ovarian tumors can induce testosterone levels over?
200 ng/dl.
Adrenal sources:?
late onset congenital adrenal hyperplasia, occurs with menstrual irreg and hirsuitism
Hirituism could be caused by?
Ovarian sources, Adrenal sources, Cushing’s syndrome with adrenocortical CA, Androgen excess with hyperporlactinemia, Idiopathic, drug use
Drug induced via?
anabolic steroids, Danazol (for endometriosis), some OCPs, glucocorticoids, cyclosporine, minoxidil.
Evaluation for hirituism includes?
careful hx, FH, PE, refer to endocrinologist. On history, ask about voice changes, recession of hair at temples, acne, increased muscle mass, sudden increased hair growth after age 25, amenorrhea or menstrual changes, galactorrhea
Hirituism on PE?
normal findings include terminal hair on face, areola, lower abdomen. Abnormal findings include new hair growth on upper abdomen, upper back, sternum, shoulders.
With oligomenorrhea, what diagnostic tests should been done?
pelvic sono, LH, FSH ratios (increase), testosterone (free serum level increases), prolactin.
To R/O late onset congenital adrenal hyperplasia, do?
ACTH stimulation test (performed by a specialist). Obtain baseline plasma 17-hyroxyprogesterone level and then 30-60 minutes after pt given 25 micrograms synthetic ACTH IV. Pretest level >300 ng/dl suggests disease and post test level > 1200 ng/dl at 30 minutes confirms.
In a pt with a Cushingoid appearance, what diag tests should be done? What's the procedure?
a dexamethasone suppression test. Pt takes 1 mg dexamethasone PO at midnight, then measure plasma cortisol at 8 AM. Normally, cortisol is suppressed to <5 micrograms/dl. Can also measure urinary 24 hour free cortisol level: abnormal if over 100 micrograms/dl.
A pt with an adrenocortical CA, what would be eleveated?
urinary 17-ketosteroids are elevated.
Virilization refers to the?
biological development of sex differences, changes that make a male body different from a female body. Most of the changes of virilization are produced by androgens.
In a pt with virilization, check?
serum testosterone (level >200 ng/dl suggests adrenal or ovarian neoplasm) and urinary 17-ketosteroids: elevated adrenal androgens suggest + adrenal cortical CA. Serum DHEA 0ver 800 micrograms/dl suggests adrenal tumor, follow up with sono or CT.
With hirituism, R/O surreptitious use of ?
androstenedione, especially in athletes to enhance performance.
Treatment?
supportive measures include electrolysis, bleaching, waxing. OCPs to suppress ovarian and adrenal androgen production at estrogen levels 35-50 micrograms.
Glucocorticoids given for?
congenital adrenal hyperplasia
Gynecomastia may be a result of?
adrenal or testicular CA, cirrhosis, hyperthyroidism.
Estradiol ?
(growth hormone of the breast)
Estradiol increases occurs secondary to?
decreased androgen production, increased estrogen production, or increased availability of estrogen precursors.
One third of the time Gynecomastia presents?
unilaterally, bilat in 2/3. Affects about 1% adult men, most common as a phase in puberty (70%), or in cases of CA as above.
Gynecomastia may follow?
androstendione use, dig, synthetic estrogen, ketoconazole, marijuana, cimetidine.
In Klinefelter’s syndrome, which is noted at puberty, presents with?
long limbs, small testes, infertility, normal or deformed secondary sexual characteristics. May occas occur after a recovery from a long illness.
With gynecomastia labs to check out for possible causes listed above, include?
LH & FSH levels (increase in Klinefelter’s)
Galactorrhea is discharge of?
of milk or colostrums form the breast in the absence of nursing. May be secondary to hyperprolactinemia or pituitary tumor (prolactin levels exceed 1000).
About 20% of pts with galactorrhea have ?
hyperporlactinemia. Persistant galactorrhea after childbirth responsible for about 10% of cases.
Women with hyperprolactinemia could also have?
menstrual irregularities, amenorrhea, infertility, osteoporosis
Pts with a sellar mass often have a?
headache and visual field disturbances.
With galactorrhea and hyperprolactinemia, ask whether pt takes ?
OCPs, phenothiazine, heroin, reserpine, methyldopa, haloperidol.
With galactorrhea and hyperprolactinemia, check which labs?
check serum prolactin level, TFTs.
If pt has galctorrhea, irreg menses, and an increased serum prolactin level, what do you do?
send for MRI with contrast, attn: sellar region (microadenomas may be difficult to detect). Check visual fields.
ACE levels can be used in the evaluation of ?
sarcoidosis and some other diseases. People with sarcoidosis may have their ACE levels tested regularly to check the severity of the disease and to monitor the response to therapy.
ACE test also helps confirm?
Gaucher's disease and leprosy.
Elevated serum calcium levels have increased with wider use of calcium and vit D supplements for osteoporosis, when amounts of ___________ are consumed daily?
50,000 IU vit D and 3-5 grams calcium
Cushings syndrome presents as?
include centripetal obesity, violaceous striae, muscle wasting, and myopathy. Gyn exam look for enlarged ovaries, adnexal masses.
Labs for hirituism?
none for familial forms when hirsuitism occurs at puberty.