Endocrine Lecture Notes

Lipid Disorders

noreply@blogger.com (Anonymous) — Mon, 10 Feb 2014 22:28:00 +0000

Lipid Disorders-
-Hypercholesterolemia-

-Lipid disorders occur either as a result of one or more genetic abnormalities or secondary to underlying disease
-Family history of hypercholesterolemia is a major risk factor
-High levels of cholesterol have been shown to lead to atherosclerosis and lead to coronary heart disease
-the first line recommendation in the treatment of hypercholesterolemia is diet modification and exercise
-Low HDL is also an indication for instituting therapy
-Weight loss has been shown to lower LDL levels by 5-7 percent
-Statins can reduce the cardiovascular risk by 20-30 percent regardless of the baseline LDL
-Patients that are given a medication to lower LDL should be given a statin
-if patients have known coronary heart disease or have a similar risk should be treated with a higher dose of the statin (ex Lipitor 40-80 mg or Crestor 20-40 mg) regardless of the baseline LDL
-patients with acute coronary syndrome and those with similar risk Crestor 80 mg daily
-Patients with stable cardiovascular disease should get at least a 50 percent reduction of the LDL or a LDL level of less than 100 or have their dose increased
-If patients are on the high statin dose, a second LDL lowering medicine should be added

-Hypertriglyceridemia-

-Lipid disorders occur either as a result of one or more genetic abnormalities or secondary to underlying disease
-the primary dyslipidemias are associated with an overproduction or impaired removal of lipoproteins

-Normal triglycerides is less than 150
-Borderline high is 150-199
-High 200-499
-Very High over 500

-elevated triglyceride levels are independently associated with cardiovascular risk
-there is an association between elevated triglycerides and coronary heart disease
-non fasting triglyceride elevations have been showed to show increase risk for ischemic stroke
-many acquired disorders, conditions, and therapies raise serum triglycerides: obesity, diabetes mellitus, nephrotic syndrome, hypothyroidism, pregnancy, tamoxifen, beta blockers, immunosuppressive medications, HIV medications, retinoids, and estrogen replacement

-Family history is a strong risk factor for development of hypertriglyceridemia

-Mild to Moderate Hypertriglyceridemia (150-500) should be treated with lifestyle modifications. Cardiovascular risk reduction with statins is best accomplished when instituting medications

-Gemfibrozil has been shown to reduce triglyceride levels by 31 percent and raise HDL

-Severe Hypertriglyceridemia (>500) are at increased risk for pancreatitis. It is recommended to decrease level so there is no development of pancreatitis. This can be done with statins or Gemfibrozil

-Fibrates (Fenofibrate or Gemfibrozil) , Nicotinic Acid, and fish oil can also be used to help lower triglyceride levels

Diabetes Mellitus

noreply@blogger.com (Anonymous) — Mon, 10 Feb 2014 15:22:00 +0000

Diabetes Mellitus-

-Diabetes Mellitus Type I-

-DM Type IA is caused by autoimmune destruction of the insulin producing beta cells of the Islet of Langerhans
-DM Type IIB is just non autoimmune destruction of the insulin producing beta cells of the Islet of Langerhans
-it is a matter of insulin not being produced instead of our bodies not being able to utilize the insulin the body produces
-DM Type I is best managed with a long acting insulin such as Lantus to take manage basal needs and immediate acting to manage short term needs
-Typically presents with polydipsia, polyuria, and weightless with hyperglycemia and ketonuria
-May be asymptomatic
-Can present with Diabetic Ketoacidosis. Present with similar symptoms but with drowsiness, fruity smelling breath, and tachypnea, with vomiting.

-To diagnosis Diabetes, fasting glucose of >126, random glucose >200, post prandial glucose of >200 after two hours, or a Hgb A1C of >6.5%.

-Other causes of hyperglycemia include: critically ill patients (shock or sepsis), medications, and neonatal hyperglycemia (from stress, sepsis and drugs)

-Patients with diabetes need to be screened for complications-

-Patients need annual eye exams to screen for refractive errors, cataracts, glaucoma, and retinopathy

-Foot examination should be inspected at each routine visit to identify problems with nail care, poor fitting footwear, fungal infections, and to screen for neurologic and vascular disease
-Neuropathy and vascular complications put the patient at risk for ulcers which can cause infections and lead to amputations

-Measurement of urinary albumin excretion. Abnormal results should be repeated at least 2-3 times over a 3-6 month period because of high rate of false positives. ACE inhibitors or ARB's help this. The need for further monitoring after instituting these therapies are not certain

-screening for coronary heart disease. Clinicians obtain a fasting lipid profile, blood pressure, and smoking history to decrease risk factors. It is not recommended to perform routine stress tests on asymptomatic diabetic patients.

-patients over 50 staring an exercise program, a resting 12 lead EKG is recommended for screening.

-Goal Hgb A1C is less than 7. It is obtained with every routine office visit lab screen

-Diabetes Type 2-

-Patients with type 2 diabetes have different degrees of insulin resistance
-Hyperglycemia can impair pancreatic beta cell function and make insulin resistance worse
-Majority of therapies are targeted at either increasing pancreatic beta cell activity or to better utilize the insulin in the body

-Recommended routine screening tests for type 2 diabetics is the same as type 1 diabetes

-Therapy for Type 2 Diabetes includes: dietary modification, exercise, weight reduction and medications
-Lifestyle modifications are the first line in treatment
-Metformin should be the initial anti glycemic agent
-next step should include an oral sulfonylurea or basal insulin
-if this therapy fails intensive insulin should be used
-less well validated therapies include pioglitazone or a GLP agonist
-sulfonylureas can lower glucose by 20 percent but lose their effectiveness over time
-meglitinides are short acting glucose lowering drugs that act like sulfonylureas but are less effective
-Thiazolidinediones (Actos and Avandia) lower glucose by decreasing insulin sensitivity
-DPP Inhibitors-are common second line treatments who patients that do not respond to a sulfonylurea
-Glucagon Like Peptide Agonists (GLP-1)-these are administer subcutaneously. These are add on drugs to patients that are poorly controlled on maximal dose of one or two agents
-Alpha Glucosidase Inhibitors-have additive hypoglycemic effects in the patients receiving diet and already on sulfonylureas, metformin, or insulin therapy

Diseases of the Pituitary Gland

noreply@blogger.com (Anonymous) — Mon, 10 Feb 2014 01:28:00 +0000

Diseases of the Pituitary Gland-

-Acromegaly/Gigantism-
-Acromegaly is caused from excessive secretion of growth hormone (GH)
-most common cause of acromegaly is a somatotroph (GH) adenoma
-this causes fusion of the epiphyseal growth plates n a child or adolescent called pituitary gigantism
-metabolic effects include nitrogen retention, insulin antagonism, and lipolysis

-may get headache and/or vision loss
-if the macroademona is large, may get decreased secretion of other pituitary hormones
-may get skin overgrowth and skin thickening
-may get macroglossia
-many organs can become enlarged including thyroid, heart, liver, lungs, and kidneys. Prostate enlargement may occur
-patients may get HTN, left ventricular hypertrophy, and cardiomyopathy
-patients with acromegaly have an increased risk of colon cancer

-Patients that have a resectable microadenoma or macroadenoma, these should be resected
-Somatostatin analogue treatment is an option
-If adenoma increases in size radiotherapy or repeat surgery is indicated

-Diabetes Insipidus-

-polyuria is urinary output greater than 3 liters per day

-Types of Diabetes Insipidus: Central diabetes insipidus, nephrogenic diabetes insipidus

-Can also have primary polydipsia where it is characterized by increased water intake, usually seen in those with psychiatric illness. Can be seen ion those taking phenothiazine therapy which has a side effect of dry mouth

-Central Diabetes Insipidus-is characterized by deficient secretion of antidiuretic hormone (ADH). Common causes include trauma, pituitary surgery, and hypoxic or ischemic encephalopathy

-Nephrogenic Diabetes Insipidus-has normal ADH but the kidney has varying degrees of resistance to its renal retaining effects. If seen during childhood is due to inherited defects. Adults is usually acquired and secondary to lithium use and hypercalcemia

-low plasma sodium concentration an low urine osmolality is due to overload from primary polydipsia

-a high to normal plasma sodium concentration and low urine osmolality is less than plasma, points to diagnosis of diabetes insipidus

-a normal plasma sodium concentration with a urine osmolality more than 600 excludes the diagnosis of diabetes insipidus

-water restriction test is raising the plasma osmolality by either water restriction or administration of hypertonic saline (0.05 mL/kg/min) for no more than 2 hours.
-raising plasma osmolality leads to progressive ADH release and increase in urine osmolality in normal patients
-once the plasma osmolality reaches 295-300 or the plasma sodium is 145 or higher, the effect of endogenous ADH is maximal. Administering ADH at this point will not elevate urine osmolality unless ADH release is impaired (except patients with central diabetes insipidus)
-the water restriction tests involves measurement of the urine volume and osmolality every hour and the plasma sodium concentration and osmolality every 2 hours. The patient should not drink 2-3 hours before the test

-End point for the water restriction test is when the urine osmolality reaches normal value above 600 (means normal ADH release)
-also when the urine osmolality is stable on 2 or 3 consecutive measurements, with a rising plasma osmolality
-also when the plasma osmolality exceeds 295-300 or the plasma sodium is over 145.
-desmopressin is administered
-plasma and urine ADH levels should be measured if the response to the water restriction test is equivocal

-Central DI-ADH release and urine and plasma osmolality may rise submaximally. Desmopressin will rise urine osmolality

-Nephrogenic DI-has a submaximal rise in urine osmolality in response to water restriction. The plasma osmolality stimulates ADH release. This will produce a modest increase in urine osmolality due to resistance to ADH

-Patients with Central DI or Nephrogenic DI present with polyuria, polydipsia, and nocturia

-Treatment of Central Diabetes Insipidus involves Desmopressin which is the preferred medication
-A low solute and sodium diet should be instituted
-Desmopressin has little effect on nephrogenic diabetes insipidus

-Dwarfism-

-Dwarfism is defined as usually a height less than 4 feet 10 inches
-It is caused by multiple medical condition
-Achondroplasia accounts for 70-80 percent of the cases
-Turner syndrome and growth hormone deficiency can be traced to some of the cases of dwarfism
-Three to thirty percent of children with growth hormone deficiency have a parent, sibling or child affected
-Short stature is a term applied to child who is two standard deviation below the mean
-Idiopathic short stature is when there is no endocrine, metabolic, or other diagnostic cause
-Intrinsic short stature is a normal family variant
-Delayed growth and puberty usually is due to under nutrition
-Attenuated growth usually results from metabolic or endocrine disorders or severe systemic illness
-Endocrine causes include Vitamin D deficiency or resistance, growth hormone deficiency, growth hormone insensitivity, and hypothyroidism
-Glucocorticoid therapy long term effects endogenous growth hormone secretion
-Autoimmune Diabetes Mellitus can cause attenuated growth
-Growth hormone deficiency results from deficiency of the growth hormone releasing hormone (GHRH) but can be because of sellar and presellar tumors
-Treatment is targeted at finding the cause and reversing what can be reversed

-Neoplastic Disease-

-There are other sellar lesions that are not adenomas, but cannot be differentiated from other adenomas until biopsy.

-Craniopharyngiomas are mixed solid and cystic lesions that arise from remnants of Rathke's pouch. It is a benign lesion

-Meningioma-usually benign lesion that comes from the meninges and can be anywhere in the head

-Pituicytoma-uncomon glioma that arises from the posterior pituitary. Has no known hormonal function.

-Germ Cell Pituitary Tumors-they are also ectopic pinealomas that are malignant and present with headache, nausea, vomiting, and lethargy, diplopia, and can have diabetes insipidus. These usually respond well to radiation. Human Beta HCG and alpha fetal protein can be increased.

-Chordomas-locally aggressive tumors that metastasize from the Pituitary gland. They present with headaches, vision disturbances, and anterior pituitary hormone abnormalities. It is a malignant tumor

-Primary Central Nervous System Lymphoma-sometimes involves both the pituitary any hypothalamus. It is a malignant tumor

-One to two percent of sellar masses involve metastasis from a distant site. Most commonly it occurs with breast cancer in women and lung cancer in men.

-Adenomas-

-Lactotroph Pituitary Adenoma- dopamine agonist should be used for decreasing adenoma size. These can be very large and cause visual defects

-Somatotroph Pituitary Adenomas-cause acromegaly. They are confined to the sella. If these tumors impair vision, surgical removal is recommended. Surgery offers a rapid cure of acromegaly.

-Corticotroph Pituitary Adenomas-no matter if they are micro or macro adenomas surgery is recommended first line. Before surgery you want to confirm Cushing Syndrome and demonstrate the adenoma is the source of the excessive ACTH secretion

-Thyrotrph Pituitary Hyperplasia-can be do to long standing hypothyroidism and primary hypogonadism

Diseases of the Adrenal Glands

noreply@blogger.com (Anonymous) — Sun, 09 Feb 2014 11:05:00 +0000

Diseases of the Adrenal Glands-

-Corticoadrenal Insufficiency-

-The symptoms of adrenal insufficiency depend on the amount of adrenal function loss and the rate of which it is lost
-common symptoms of adrenal insufficiency are malaise, lassitude, fatigue, generalized weakness, anorexia, abdominal pain, nausea, vomiting, diarrhea, and weight loss
-may have postural hypotension or syncope
-hyponatremia is common, hyperkalemia and hypoglycemia are common
-hyperpigmentation is seen in almost all patients
-decreased axillary and pubic hair loss, loss of libido are common in women. Amenorrhea may be present
-may have psychosis, depression, impairment of memory, or mild organic brain syndrome

-can come from prolonged administration of glucocorticoids. This is the most common causes of adrenal insufficiency

-initial workup should include CBC, Chem 7, ACTH, renin, cortisol, aldosterone
-ACTH stimulation test is good for helping establishing the diagnosis
-Abdominal CT scan may show enlarged adrenal glands or adrenal calcification

-causes of adrenal insufficiency include: destruction of adrenal cortex (from autoimmune adrenalitis), polyglandular autoimmune syndrome type 1 and 2, infectious, tuberculosis, fungal infections, HIV, hemorrhagic infarction of the adrenal gland, metastatic disease, and drugs

-Adrenal Insufficiency can come from 3 different mechanisms-

-Primary Adrenal Insufficiency (Addison's Disease)-an inadequate serum cortisol response to ACTH stimulation shows adrenal insufficiency but does not show if primary, secondary or tertiary.

-A Pituitary Disorder resulting from deficiency of ACTH

-A Hypothalamic Disorder resulting from CRH deficiency and leads to low ACTH

-Treatment of Chronic Primary Adrenal Insufficiency includes supplement of dexamethasone or prednisone, fludicortisone, liberal salt intake, androgen replacement and patient medication

-Fever should be examined for etiology and treated

-Adrenal crisis usually presents as shock. Abdominal tenderness and fever may be present. Fever would be do to infection and needs to be treated.

-Treatment of adrenal crisis includes IV fluids 1-3 liters of NS or D5 NS within the first 12-24 hours. Hypotonic saline could make the hyponatremia worse
-Dexamethasone 4 mg IV should be given

-Cushing Syndrome-

-Cushing Syndrome may be either ACTH dependent or independent
-The most common cause of Cushing Syndrome is from administration of glucocorticoids

-If the cause is ACTH dependent will see adrenal cortical hyperplasia on imaging studies

-If the cause is ACTH independent, it is most commonly iatrogenic. Can see it also from adrenal adenomas or carcinomas

-Most patients with Cushing Disease will have a pituitary adenoma

-There may be ectopic ACTH from benign neuroendocrine tumors (carcinoid) or from malignant sources like Oat Cell carcinoma

-There may ectopic CRH where the tumor causes hyperplasia and hypersecretion of pituitary corticotrophs

-To establish the diagnosis of Cushing Syndrome want to exclude the presence of exogenous steroid ingestion

-Patients with other disorders may have high cortisol levels and not have Cushing Syndrome, these disorders are: physical stress, severe bacterial infection, severe obesity, polycystic ovarian syndrome, major depression, and chronic alcoholism. These patients are sometimes referred to as having pseudo Cushing Syndrome.

-Need two first line tests to confirm the presence of Cushing Syndrome
-Should use late night salivary cortisol, urinary cortisol, and low dose dexamethasone suppression test as the first line tests
-urine and saliva cortisol tests should be obtained twice
-urine cortisol excretion should be 3 times the upper limit of normal to rule in Cushing Syndrome

-Treatment of Cushing Syndrome includes reveres clinical manifestations by normalizing cortisol levels, remove any tumors causing, avoid permanent dependence on medications, and avoid hormone deficiency

-Need to discontinue exogenous glucocorticoids
-Need to treat pituitary adenomas with transsphenoidal microadenomectomy
-Adrenal enzyme inhibitors can be used if surgery is delayed or contraindicated
-Pituitary irradiation can be done on patients where fertility is a concern
-Bilateral adrenalectomy with lifelong glucocorticoid and mineralocorticoid replacement is a final definitive cure
-Patients with ectopic ACTH or CRH syndromes the tumor should be removed
-Somatostatin Analogues rapidly reduces ACTH secretion by non pituitary tumors

-Neoplastic Disease-

-Unilateral tumors or masses of the Adrenal Gland are considered functional (hormone secreting) or silent
-Adrenal tumors are also classified as either benign or malignant
-Most adrenal tumors are benign, silent tumors known as adrenal incidentalomas
-There are other benign functional tumors that cause Cushing Syndrome, Primary Hyperadosteronism, and virlization
-Adrenocortical Carcinomas are aggressive tumors that can be functional and cause Cushing Syndrome or can be non functional and just present as an abdominal mass
-Pheochromocytomas are catecholamine producing tumors that arise from the adrenal medulla. They can be benign or malignant. They cause high blood pressure and catecholamine related physiologic changes

-Adrenocortical Adenomas are begin neoplasms that can secrete steroids independently from ACTH or the renin angiotensin mechanism

-Aldosteronemas are adrenal incidentalomas that can cause primary aldosteronism

-The maximum diameter is predictive of malignancy, most adrenal adenomas are less than 4 cm in diameter

Diseases of the Thyroid Gland

noreply@blogger.com (Anonymous) — Fri, 07 Feb 2014 11:00:00 +0000

Disease of the Thyroid Gland-

-Hyperparathyroidism-

-should be suspected when high serum calcium levels are detected

-Primary hyperthyroidism occurs due to PTH activation of osteoclasts leading to more bone reabsorption causing elevated calcium levels

-This also causes increased intestinal absorption of calcium

-Most common cause of primary hyperthyroidism is due to parathyroid adenoma

-Diagnosis of primary hyperparathyroidism is made with a high PTH or one that is in the normal range but elevated inappropriately given the elevated given the patients hypercalcemia

-Patients with primary hyperparathyroidism are usually asymptomatic

-Elevated isolated serum calcium level should be repeated.
-Malignancy is another cause for hypercalcemia. Malignancy and Primary Hyperparathyroidism account 90 percent of cases of hypercalcemia

-If malignancy is present, the PTH level is usually normal or low, where as in primary hyperparathyroidism the levels are usually high

-Familial hypocalciuric hypercalcemia (FHH) is due to an inactivating mutation of the calcium sensing receptor in the kidneys. See a hypercalcemia with a mildly elevated PTH concentration
-Family history of hypercalcemia that is symptomatic is helpful for coming up with the diagnosis

-Thiazide diuretics reduce calcium urine excretion and can cause mild hypercalcemia
-Lithium decreases parathyroid gland sensitivity to calcium, and decreases urinary excretion.
-Some patients on lithium develop hypercalcemia and hypocalciuria

-Secondary Hyperparathyroidism is when the parathyroid appropriately responds to a reduced level of calcium. This causes elevated PTH, the calcium absorption from the intestines to increase and increase bone reabsorption.
-Secondary Hyperparathyroidism has an elevated PTH and a low or normal calcium
-Secondary hyperparathyroid may come from renal failure and impaired calcitrol production and inadequate calcium uptake. Vitamin D Deficiency can cause.

-Normocalcemic Primary Hyperparathyroidism-secondary hyperparathyroid causes need to be ruled out. Normal calcium and elevated PTH. Vitamin D deficiency can cause

-Clinically most the time hyperparathyroidism can be asymptomatic

-Classic symptoms if present "bones, stones, abdominal moans, and psychic groans." Anorexia, nausea, constipation, polydipsia, bone pain, kidney stone, muscle weakness, polyuria, and psychiatric psychosis.

-Hypoparathyroidism-

-most common cause is neck surgery on the thyroid or parathyroid
-after surgery hypoparathyroidism may be transient or may be permanent
-clinically will see a low PTH and low serum calcium
-calcium and vitamin D supplementation are the mainstays of hypoparathyroidism treatment
-symptoms of hypoparathyroidism include: tingling in hands and feet, involuntary muscle movements, muscle cramps, fatigue, irritability, anxiety, and depression
-long term hypoparathyroidism can cause cataracts, dry skin, coarse hair, and brittle fingernails

-Hyperthyroidism-

-many disorders can cause hyperthyroidism: Graves Disease, Hashiomotos Thyrotoxicosis, Toxic Adenoma, Toxic Multiple Nodular Goiter, Iodine Induced Hyperthyroidism, Trophoblastic Disease from Germ Cell Tumors, TSH mediated hyperthyroidism, Thyroiditis, and exogenous and ectopic hyperthyroidism
-Graves Disease is the most common cause of hyperthyroidism.
-Graves Disease is an autoimmune disorder that causes thyrotropin (TSH) receptor antibodies, which stimulate thyroid gland growth and thyroid hormone synthesis and release.

-Hashimoto's Thyroiditis is an autoimmune disease that causes patients initially to present with hyperparathyroidism and high radio iodine uptake similar to Graves disease but eventually go hypothyroid
-hypothyroid develops because of the infiltration of the thyroid gland with lymphocytes

-Toxic adenoma and multinodular goiter result from focal or diffuse hyperplasia of the thyroid follicular cells whose functional capacity is independent regulation of TSH.
-Toxic multinodular goiter tends to be more common in areas where iodine uptake is low
-Thyroid adenomas are not related to iodine uptake

-Iodine Induced Hyperthyroidism can occur after an iodine load such as IV contrast for CT scan, or amiodarone administration.
-Iodine Induced Hyperthyroidism is rare

-Trophoblastic or germ cell tumors can be rare causes of hyperthyroidism
-Can occur as a hydatidiform mole in women
-Can occur in Choriocarcinoma in men with testicular germ cell tumors via direct stimulation of the TSH receptors

-TSH mediated hyperthyroidism is when there is a pituitary adenoma producing TSH. Therapy is directed at removing the tumor

-Thyroiditis is a group of heterogenous disorders that result from inflammation of thyroid tissue with transient hyperthyroidism
-Thyroiditis has hyperthyroid phase, then hypothyroid phase and then a recovery of thyroid function

-Exogenous and ectopic hyperthyroidism occurs from taking too much thyroid hormone or it being produced by other parts of the body.
-exogenous thyroid hormone can be produced by struma ovarii, which is from a functioning ovarian neoplasm.

-Thyroid hormone effects almost every organ system in the body.

-Skin-hyperthyroidism causes increased sweating due to increased caloric burning
-Hyperthyroidism causing softening of nails, thinning of hair, and can cause hyperpigmentation

-Stare and lid lag occur in patients with hyperthyroidism because of sympathetic overactivity
-Patients with graves disease can get exophthalmus because of inflammation of the extraocular muscles and orbital fat and connective tissue.

-Hyperthyroidism patients have increased cardiac output and increased peripheral oxygen needs and increased cardiac contractility. Can cause systolic hypertension
-Atrial fib occurs in 10-20 percent of the patients with hyperthyroidism

-Hyperthyroid patients have lower serum total and HDL cholesterol
-Hyperthyroid patient can have impaired glucose tolerance if untreated
-Hyperthyroidism can result in lower serum cortisol concentrations

-Dyspnea can occur with hyperthyroidism because oxygen consumption and CO2 production increase
-can be tracheal obstruction due to large goiter
-respiratory muscle weakness can cause dyspnea with hyperthyroidism

-Weight loss with hyperthyroidism is due to increased metabolic rate and increased gut motility.
-Dysphagia may occur because of goiter

-RBC mass index is increase with hyperthyroidism
-may have a noromchromic normocytic anemia
-hyperthyroidism can be associated with ITP

-Urinary frequency and nocturia are common with hyperthyroidism
-Woman with hyperthyroid may see high serum estradiol, high LH, and may get oligomenorrhea and anovulatory infertility

-Thyroid hormone stimulaters bone reabsorption, bone loss
-May see increased urinary calcium excretion

-Hyperthyroidism can cause psychosis, agitation and depression

-Treatment of hyperthyroidism includes beta blockers, PTU or methimazole, or radioactive iodine
-Beta Blockers are for symptomatic treatment of hyperthyroidism
-PTU or methimazole are thyroid hormone antagonists
-Radioactive iodine is indicated for graves disease
-surgical removal of thyroid gland is an option if necessary

-Hypothyroidism-

-Several different causes of hypothyroidism

-Primary hypothyroidism is when there is decreased secretion of T3 and T4 which results in a increase int TSH secretion

-Chronic autoimmune (Hashimotos) Thyroiditis- most common cause of hypothyroidism. When there is cell and antibody mediated destruction of thyroid tissue

-Iatrogenic Hypothyroidism-caused by thyroidectomy radio iodine treatment, or external radiation and there is less secretion of T3 and T4 as a result of it

-Iodine related hypothyroidism-excess or iodine deficiency can cause hypothyroidism. Iodine excess causes the inhibition of iodide organification from T4 to T3 synthesis. Iodine deficiency causes the inability to synthesize thyroid hormone.

-Drugs such as PTU and methimazole can cause hypothyroidism. Lithium, Amiodarone and Ethionamide have been known to cause hypothyroidism.

-Infiltrative disease such as fibrous thyroiditis, hemochromatosis, scleroderma, leukemia, and cystinosis are rare causes of hypothyroidism

-Hypothyroidism in infants and children are caused by agenesis and dysgenesis of the thyroid

-Transient hypothyroidism can be caused by post partum thyroiditis, subtotal thyroidectomy, or patients post radioactive iodine therapy with Graves disease

-Secondary Hypothyroidism is caused by lack of TSH secretion from the anterior pituitary gland

-Tertiary (Central) is caused by lack of TRH secretion form the hypothalamus

-Hypothyroidism affects essentially every organ system

-Hypothyroidism causes decreased sweating, skin discoloration, hair to be coarse, non pitting edema (myxedema), vitiligo, and alopecia

-Hypothyroidism cans cause periorbital edema

-Hypothyroidism can cause normochromic normocytic anemia

-Hypothyroidism causes decrease cardiac output and reduction of heart rate and cardiac contractility. Hypertension can be caused from an increased in peripheral vascular resistance. Increased cholesterol can be seen from decreased cholesterol metabolism

-Fatigue, shortness of breath on exertion and rhinitis can be caused by respiratory muscle weakness with hypothyroidism

-Hypothyroidism causes decreased gut motility, constipation, and decreased taste sensation, and gastric atrophy

-Hypothyroidism can cause oligomenorrhea, amenorrhea, or hypermenorrhea. This can lead to infertility. Decreased libido, erectile dysfunction, and delayed ejaculation are possible in hypothyroidism

-Hypothyroidism left untreated can cause hashimotos encephalopathy, myxedema coma, and carpal tunnel syndrome

-Hypothyroidism can also cause joint pain, aches, and stiffness. There is an increased incidence of gout with hypothyroid patients.

-Hypothyroidism can cause hyponatremia

-Standard treatment of hypothyroidism is replacement therapy. Synthetic thyroxine (T4) or combination T3 and T4 therapy. There is also T3 alone therapy

-Neoplastic Disease-

-Thyroid Cancer is divided into 4 categories: papillary follicular, medullary, and anaplastic
-Papillary and follicular cancers are differentiated tumors and are basically treated the sam
-Anaplastic cancer appear to arise from other cancers
-Other cancers include primary thyroid lymphoma, multiple endocrine neoplasia type 2, familial medullary cancer, or mets from breast, colon, renal cancer, or melanoma

-Initial staging is done with TMN (Tumor Node Metastasis)

-Surgery is the initial treatment for differentiated thyroid cancer. It is recommended if the primary tumor is at least 1-2 cm in diameter or if mets are present

-Radioiodine therapy is used post thyroidectomy for adjuvant ablation on residual thyroid tissue and possible microscopic residual cancer, treatment of residual or metastatic thyroid cancer, and distant metastasis

-After thyroidectomy levothyroxine is need in all patients to prevent hypothyroidism.

-Radiation therapy may be needed for patients with differentiated thyroid cancer who have metastatic disease that is not responsive to radioiodine or patients with tumors that do not concentrate radioiodine

-Diagnosis is made by biopsy usually on fine need aspirate.
-This is done after Iodine 129 scan nuclear scan
-serum thyroglobulin is used to monitor patients with differentiated thyroid cancer

-Parathyroid Cancer-
-It is rare cause of hyperparathyroidism
-most patients have hypercalcemia or normal calcium and present with a neck mass
-Multiple glands being affected are extremely rare
-Surgery is the mainstay in treatment of parathyroid carcinoma
-Radiation and Chemotherapy have poor results and should only be considered when patient not a candidate for surgery

-Thyroiditis-

-Thyroiditis refers to a group of disorders that cause thyroid inflammation

-Subacute thyroiditis is characterized by neck pain, tender goiter, and elevated T3 and T4. Usually has hyperthyroidism followed by hypothyroidism

-Infectious Thyroiditis can be acute or chronic. Acute infections may cause abscess formation. Staph or strep may cause.

-Radiation Thyroiditis happens when a patient with Graves Disease develops thyroid pain and tenderness 5-10 days after radiation therapy

-Palpation or trauma induced thyroiditis can happen from a vigorous exam or manipulation of the thyroid during biopsy or neck surgery. Can also be from seat belt during auto accident

-Post Partum Thyroiditis occurs within a year after childbirth. It is usually painless

-Drug Induced Thyroiditis can occur with patients taking interferon alpha, amiodarone, lithium, or intraleukin 2.

-Fibrous Thyroiditis is when there is fibrous from macrophage or eosinophil infiltration and extends to adjacent tissues