Term
| Where are the endocrine and CNS connected? |
|
Definition
| The Hypothalamic-hypophyseal portal system. |
|
|
Term
| What are the 6 main functions of the endocrine system? |
|
Definition
1. Response to stress and injury.
2. Growth/development.
3. Reproduction.
4. Ionic homeostasis.
5. Energy Metabolism.
6. Immune response. |
|
|
Term
| How does the endocrine system control calcium homeostasis? |
|
Definition
|
|
Term
| How does the endocrine system maintain ionic homeostasis? |
|
Definition
|
|
Term
| Which hormone is primarily responsible for controlling the Basic Metabolic Rate? |
|
Definition
|
|
Term
| Which hormone is responsible for the control of cytokine release involved in cell-mediated immunity? |
|
Definition
|
|
Term
| Describe the 2 main classes of hormones (Steroids and Thyronines) and (Polypeptides and Catecholamines). Which ones last longer? |
|
Definition
| Steroids and thyronines are lipid soluble and polypeptides and catecholamines are water soluble. Lipid soluble hormones have a longer lasting effect. |
|
|
Term
| Give the class and examples of adrenocortical hormones. |
|
Definition
| Steroid class and examples are cortisol, aldosterone and androgens. |
|
|
Term
| Give the class and examples of Gonadal hormones. |
|
Definition
| Steroid hormones and examples are estradiol and testesterone. |
|
|
Term
| Give the class and examples of Thyronine hormones. |
|
Definition
| They are Thyronines and are Thyroxine (T4) and Triiodothyronine (T3). |
|
|
Term
| What are some examples of glycoprotein hormones? Are they lipid or water soluble? |
|
Definition
| TSH, FSH and LH. They are water soluble. |
|
|
Term
| What are some examples of catecholamine hormones? Are they lipid or water soluble? |
|
Definition
| Epi and Norepi. They are water soluble. |
|
|
Term
| Are insulin, parathyroid hormone, ACTH and glucagon water or lipid soluble? |
|
Definition
| They are all water soluble. |
|
|
Term
| Describe the function of the Hypothalamic-hypophyseal portal system? How does the pituitary system respond to the hormones that reach it through the Hypothalamic-hypophyseal portal system? |
|
Definition
| The Hypothalamic-hypophyseal portal system allows the transport of neurohormones (stimulating and inhibiting) from the hypothalamus to reach the pituitary gland. The pituitary gland responds to these hormones by secreting its hormones which travel through the bloodstream to the target organs. |
|
|
Term
| Explain the feedback system for oxytocin and breast feeding. |
|
Definition
| It is a positive feedback system where suckling from the baby causes the release of oxytocin which stimulates the release of milk from the mammary gland. (POSITIVE FEEDBACK). |
|
|
Term
| Which endocrine hormones are under circadian rhythm secretion? |
|
Definition
| ACTH, cortisol and gonadotropins (in women). |
|
|
Term
| How is hormone deficiency treated? |
|
Definition
| HRT (Hormone Replacement Therapy) |
|
|
Term
| How is a hormone excess condition treated? |
|
Definition
| Total/partial gland removal or medications that supress hormone production or antagonize the hormone. |
|
|
Term
| How are hormone target cell resistance conditions treated? |
|
Definition
| By enhancing the hormone-receptor interaction if possible. |
|
|
Term
| Where is the pituitary gland located? |
|
Definition
| In the sella turcica of the sphenoid bone. |
|
|
Term
| What are the anterior and posterior lobes of the pituitary also called? |
|
Definition
Anterior = Adenohypophysis.
Posterior = Neurohypophysis. |
|
|
Term
| Why might visual changes be a common symptom with pituitary tumors? |
|
Definition
| BC the pituitary gland is located right next to the optic chiasm so the tumor may grow and push against the optic chiasm. |
|
|
Term
| What supplies blood to the Pituitary? |
|
Definition
| The Hypothalamic-hypophyseal portal system. |
|
|
Term
| Which hormones are secreted by Eosinophils of the anterior pituitary? |
|
Definition
|
|
Term
| Which hormones are secreted by Basophils of the anterior pituitary? |
|
Definition
|
|
Term
| Which 7 hormones are secreted by the Anterior pituitary? |
|
Definition
| ACTH, GH, PRL (Prolactin), TSH, FSH, LH and MSH (Melanocyte stimulating hormone). |
|
|
Term
| Which 2 hormones are secreted by the posterior pituitary? |
|
Definition
|
|
Term
| What is the target tissue of ACTH? Action? How is it up and down regulated? |
|
Definition
Target is the adrenal cortex.
Action is to increase the secretion of glucocorticoids.
It is upregulated by CRH (corticotropin releasing hormone) and downregulated by excess glucocorticoids. |
|
|
Term
| What is the target tissue of GH? Action? How is it up and down regulated? |
|
Definition
Target is most body tissues.
Action is growth, lipolysis and protein synthesis.
It is upregulated by GHRH (Growth Hormone Releasing Hormone) and downregulated by somatostatin. |
|
|
Term
| What is the target tissue of PRL? Action? How is it down regulated? |
|
Definition
Target is the mammary glands.
Main action is to increase milk production.
It is downregulated by PIH (Prolactin Inhibiting Hormone). |
|
|
Term
| What is the target tissue of TSH? Action? How is it up and down regulated? |
|
Definition
Target is the thyroid gland.
Action is to increase the secretion of thyroid hormones.
It is upregulated by TRH (Thyrotropin releasing hormone) and downregulated by excess thyroid hormones. |
|
|
Term
| What is the target tissue of FSH? Action? How is it up and down regulated? |
|
Definition
Target is the gonads.
Action is to increase the production of gametes and estrogen production.
It is upregulated by GnRH and downregulated by inhibin and excess sex hormones. |
|
|
Term
| What is the target tissue of LH? Action? How is it up and down regulated? |
|
Definition
Target is the gonads.
Action is to increase the secretion of sex hormones.
It is upregulated by GnRH and inhibited by inhibin and excess sex hormones. |
|
|
Term
| Where does ACTH stimulate the adrenal gland? What does it stimulate it to produce? |
|
Definition
| It stimulates the cortex of the adrenal gland. It stimulates the production of corticosteroids, mainly glucocorticoids (Cortisol). |
|
|
Term
| What is another name for GH? What can stimulate the synthesis of GH? What can inhibit the synthesis of GH? |
|
Definition
| Somatomedian. GH synthesis can be stimulated by GHRH, hypoglycemia, fasting, exercise, ADH, dopamine and alpha-adrenergic drugs. GH can be inhibited by somatostatin, hyperglycemia, cortisol, pregnancy, obesity and beta-adrenergic drugs. |
|
|
Term
| What hormones does somatostatin inhibit? |
|
Definition
| It inhibits the secretion of GH, Prolactin and TSH. |
|
|
Term
| How will hypothyroidism present with respect to T3, T4 and TSH? |
|
Definition
| TSH will be high but T3 and T4 will be low. |
|
|
Term
| How does follicular growth inhibit FSH and LH secretion? |
|
Definition
| As the follicle grows it releases inhibin, which shuts off the FSH and LH production. |
|
|
Term
| Which hormone is critical for spermatogenesis via stimulation of Sertoli cells in the testes? |
|
Definition
|
|
Term
| Which hormone is responsible for production of testosterone via Leydig cell stimulation? |
|
Definition
|
|
Term
| Which hormone triggers ovulation in women? |
|
Definition
| It is triggered by a surge of LH. |
|
|
Term
| What is the major action of Oxytocin? What can inhibit Oxytocin? |
|
Definition
| Major action is to stimulate milk let-down during breast feeding. It can be inhibited by stress, sympathetic activity and alcohol. |
|
|
Term
| What are oxytocin's actions during labor? |
|
Definition
| Cervical dilation before birth and contraction during the 2nd and 3rd stages of labor. |
|
|
Term
| What are the common causes of hypopituitarism? |
|
Definition
| Pituitary tumors, vascular thrombosis leading to necrosis of pituitary, or autoimmune. |
|
|
Term
| Describe the order of loss of hormones seen with Hypopituitarism. |
|
Definition
| GH is usually lost first then FSH/LH then TSH and then ACTH. |
|
|
Term
| When does ADH deficiency Hypopituitarism occur? |
|
Definition
| ADH deficiency is rare in primary pituitary disease but is common with stalk and hypothalamic lesions. |
|
|
Term
| What is Sheehan’s Syndrome? S&S? |
|
Definition
| It is pituitary necrosis occurring from hypovolemia and shock from childbirth. S&S include lactation that does not start after childbirth, fatigue and loss of pubic/axillary hair. |
|
|
Term
| What is Pituitary Apoplexy? S&S? Complications? |
|
Definition
| It is a condition caused by a hemorrhagic infarction of a normal pituitary gland or a pituitary tumor. S&S include a severe headache, stiff neck, visual field defects and oculomotor palsies. Complications include coma from edema compressing the hypothalamus. |
|
|
Term
| How will a Pituitary Apoplexy present on Spinal Tap and MRI? |
|
Definition
| Spinal Tap will have blood in the CSF and MRI will show hemorrhage. |
|
|
Term
| What is the difference between Pituitary Gigantism and Acromegaly? |
|
Definition
| They are both due to hypersecretion of GH but Gigantism will result if the hypersecretion begins before the closure of the epiphyses and Acromegaly will result in the hypersecretion begins after closure of the epiphyses. |
|
|
Term
| What is the most common cause of Pituitary Gigantism and Acromegaly? |
|
Definition
| Pituitary Adenoma (Somatotropic adenoma) |
|
|
Term
| How Pituitary Gigantism and Acromegaly diagnosed and treated? |
|
Definition
| Diagnosed by clinical/x-rays/GH levels. Treatment is removal/destruction of the adenoma. |
|
|
Term
| What are the S&S for Acromegaly? |
|
Definition
| Increase in coarse body hair, skin thickening and hyperpigmentation, mandible overgrowth, excessive sweating, offensive body odor, a deep husky voice, arthritis, barrel chested, peripheral neuropathies, headaches, bitemporal hemianopsia (if tumor compresses optic chiasm) and enlargement of most organs. |
|
|
Term
| What other conditions can Acromegaly increase a patient risk for? |
|
Definition
| HTN (1/3 of patients), cancer (especially GI), hyperphosphatemia, impaired glucose tolerance that can lead to DM, Galactorrhea (milk discharge unrelated to breast feeding) and erectile dysfunction. |
|
|
Term
| What blood marker can be used to diagnose and monitor response to therapy in individuals with Acromegaly? |
|
Definition
| Plasma insulin-like growth factor 1 (IGF-1). (It is better than GH bc GH levels fluctuate but IGF-1 levels do not). |
|
|
Term
| What are the 3 types of pituitary tumors? Which one is most common in children? |
|
Definition
| Pituitary adenomas, Craniopharyngiomas, and Meningiomas. Craniopharyngiomas are the most common in children. |
|
|
Term
| Will pituitary tumors cause excess or insufficient hormone production? |
|
Definition
| Could be either. Pituitary adenomas can increase hormone production and other tumors can cause destruction of gland cells and lead to insufficient hormone production. |
|
|
Term
| What is the most common type of pituitary tumor that comprises 30% of all pituitary tumors? |
|
Definition
|
|
Term
| What are the typical S&S of a prolactinoma? |
|
Definition
| Women complain of amenorrhea and galactorrhea. |
|
|
Term
| What does a pituitary Corticotropic Adenoma secrete? |
|
Definition
|
|
Term
| What is the difference between Cushing's disease vs. Cushing's syndrome? |
|
Definition
| Disease is due to a corticotropic adenoma of the pituitary that hypersecretes ACTH which results in excess Cortisol. Syndrome is due to excess ACTH production by a tumor or by administration of excess corticosteroids such as in treatment for another condition. |
|
|
Term
| What are the S&S and sequela of Cushing's Disease? |
|
Definition
| S&S include central obesity, moon face, buffalo hump, purple striae, osteoporosis, growth retardation and HTN / decreased glucose tolerance. |
|
|
Term
| How is a Corticotropic Adenoma / Cushing's Disease diagnosed? |
|
Definition
| Dexamethasone suppression test |
|
|
Term
| What condition is described by a deficiency of ADH due to a hypothalamic-pituitary disorder? |
|
Definition
| Central diabetes insipidis |
|
|
Term
|
Definition
| Syndrome of inappropriate secretion of ADH |
|
|
Term
| What are the clinical features for Diabetes Insipidis? |
|
Definition
| Polyuria, Polyphagia and Polydipsia. |
|
|
Term
| How is diabetes insipidis diagnosed? |
|
Definition
| Diagnosed by the water deprivation test. |
|
|
Term
| How is diabetes insipidis managed? |
|
Definition
| Desmopressin (synthetic ADH) and thiazide diuretics. |
|
|
Term
| What is the cause of nephrogenic diabetes insipidis? |
|
Definition
| ADH production is normal but there is a resistance of the kidney to ADH. |
|
|
Term
| How can central diabetes insipidis and nephrogenic diabetes insipidis be distinguished? |
|
Definition
| ADH levels will be higher and there will not be a response to ADH supplementation with nephrogenic DI. |
|
|
Term
| How will the Water Deprivation Test distinguish between central and nephrogenic DI? |
|
Definition
| Neither of them will show an ability to concentrate urine but CDI will be able to after ADH administration and NDI will not. |
|
|
Term
| What is the etiology of SIADH? |
|
Definition
| Excessive ADH secretion due to: stroke, head injury, encephalitis or drugs. |
|
|
Term
| What are the S&S for SIADH? |
|
Definition
| Headache, seizures, nausea, vomiting, agitation and hyponatremia. |
|
|
Term
|
Definition
| It is diagnosed by daily urinary sodium excretion of more than 20 mEq/L. |
|
|
Term
| Which thyroid cells initiate the synthesis of thyroid hormones and activate their release? |
|
Definition
|
|
Term
| Which thyroid cells synthesize and store the thyroid hormones? |
|
Definition
| Colloid material (Thyroglobulin) |
|
|
Term
| Which thyroid hormone is produced at concentrations 10x greater than the other? Which one is 3-4 times more potent? |
|
Definition
| T4 is produced 10 times more than T3 but T3 is 3-4x as potent as T4. |
|
|
Term
| Explain how T3 and T4 are circulated in the bloodstream. In what state is it biologicall active? |
|
Definition
| They are circulated bound to plasma proteins and only the free fractions (unbound) are biologically active. **Alterations of binding protein levels will affect total T3/T4 levels but not free T3/T4 levels. |
|
|
Term
| What is Congenital Cretinism? |
|
Definition
| A congenital absence of or rudimentary Thyroid gland or a thyroid gland that is present but congenitally defective in hormone secretion. |
|
|
Term
| What is Acquired Cretinism? |
|
Definition
| AKA Juvenile Hypothyroidism, is atrophy of the thyroid gland or defective function that is not congenital. |
|
|
Term
| How can cretinism be treated? |
|
Definition
| Can be treated with Thyroid hormone replacement. |
|
|
Term
| What are some characteristics of Cretinism on physical exam and labs? |
|
Definition
| Dwarfism, mental retardation, dry/yellow/cold skin, pot belly, stippling of the epiphyses, low thyroid hormone levels and elevated serum cholesterol. |
|
|
Term
| What is the most sensitive and reliable indicator of thyroid function? |
|
Definition
| TSH levels. High = decreased thyroid function. Low = increased thyroid function. |
|
|
Term
| Explain the results for RAI uptake (radioiodine uptake test), Serum thyroxine, Free thyroxine and Serum TSH for hyper- and hypo- thyroidism. |
|
Definition
| RAI uptake, serum thyroxine and free thyroxine will be increased with hyperthyroidism and will be decreased with hypothyroidism. Serum TSH will be decreased with hyperthyroidism and will be increased with hypothyroidism. |
|
|
Term
| :state of thyroid hormone excess |
|
Definition
|
|
Term
| :state of thyroid hormone excess resulting from excess thyroid gland function |
|
Definition
|
|
Term
| What are some common examples of primary hyperthyroidism? |
|
Definition
| Graves disease, toxic nodular goiter, thyroid adenoma, functioning thyroid cancer and iodine excess. |
|
|
Term
| What are 2 common examples of secondary Hyperthyroidism? |
|
Definition
| TSH-secreting pituitary adenoma and ovarian tumor containing ectopic thyroid tissue. |
|
|
Term
| What would cause thyrotoxicosis without hyperthyroidism? |
|
Definition
| Excess thyroid hormone ingestion and thyroiditis. |
|
|
Term
| What is the most common cause of hyperthyroidism? |
|
Definition
|
|
Term
| What are the S&S and Graves' Disease? What causes Graves' Disease? |
|
Definition
| Diffuse goiter, exopthalmos and pretibial myxedema. It is caused by an autoantibody, TSI (Thyroid stimulating immunoglobulin), against the thyroid TSH receptor that is stimulatory. |
|
|
Term
| Does Graves' Disease affect women or men more often? |
|
Definition
|
|
Term
| What is the most common etiology of a Toxic Nodular Goiter? How is it differentiated from Graves' Disease? What is the initial presentation? |
|
Definition
| It develops most common in older patients with chronic nontoxic nodular goiter. The goiter is multinodular rather than diffuse in Graves' Disease. The initial presentation may be dysrhthymia and heart failure. |
|
|
Term
| What is the major cause of primary and secondary hypothyroidism? |
|
Definition
| Primary is damage to the thyroid gland. Secondary is deficiency of TSH secretion from the pituitary. |
|
|
Term
| What are the 5 main etiologies of Primary hypothyroidism? |
|
Definition
| Congenital (Cretinism), Hashimoto's thyroiditis, Iodine deficiency, Thyroidectomy and drugs (amiodarone). |
|
|
Term
| What are the 2 common causes of secondary hypothyroidism? |
|
Definition
| Hypopituitarism and Hypothalamic disease |
|
|
Term
| What are the typical clinical manifestations of congenital hypothyroidism? What will result if this condition is not recognized and treated? |
|
Definition
| (Cretinism) Clinical manifestations include: jaundice, hoarse cry, constipation, somnolence, and feeding problems and delay in development milestones. If unrecognized and untreated, will lead to mental retardation. |
|
|
Term
| What are some common adult clinical manifestations of hypothyroidism? |
|
Definition
| Goiter, hoarseness, cold intolerance, decreased sweating, cool/dry skin, facial puffiness, slowed intellectual and motor activity, slowed deep tendon reflexes, hypermenorrhea and weight gain. |
|
|
Term
| What is the most common cause of primary hypothyroidism in the US? |
|
Definition
|
|
Term
| What is the etiology of Hashimoto's Thyroiditis? |
|
Definition
| It is an autoimmune disorder in which T-cells and autoantibodies prevent normal thyroid function. |
|
|
Term
| How is Hashimoto's Disease typically diagnosed and distinguished from other forms of thyroiditis? |
|
Definition
| It is differentiated by the presence of very high levels of thyroid antibodies (antiperoxidase and antithyroglobulin). |
|
|
Term
| How does Hashimoto's Thyroiditis present on PE? |
|
Definition
| Painless, enlargement of the thyroid galnd that feels firm and rubbery. |
|
|
Term
| What kind of temperature intolerance is seen with hypo- and hyperthyroidism? |
|
Definition
Hypo = Cold intolerance.
Hyper = Heat intolerance. |
|
|
Term
| If a patient has a thyroid nodule, how is it distinguished if the nodule is benign or malignant? |
|
Definition
| Fine Needle Aspiration (FNA) biopsy. |
|
|
Term
| What is the most common benign lesion forming a single thyroid nodule? |
|
Definition
|
|
Term
| How will a toxic and nontoxic thyroid adenoma appear on an RAI (Radioactive iodine) scan? |
|
Definition
| Toxic will be "hot" because they produce excess hormones and nontoxic will be "cold" because they do not produce excess hormones. |
|
|
Term
| How do most carcinomas appear on RAI (Radioactive iodine)? What are the 4 types of Thyroid carcinomas? |
|
Definition
| Most are "cold" because they do not produce excess hormones. They 4 types of thyroid carcinomas include: Papillary (80%), Follicular (15%), Medullary (4%) and Anaplastic (1%). |
|
|
Term
| What is the most common type of thyroid carcinoma? Which thyroid carcinoma has the poorest prognosis? |
|
Definition
| Papillary is the most common at 80% of the cases. Anaplastic has the poorest prognosis. |
|
|
Term
| What is a thyroid storm? How is it treated? |
|
Definition
| Exceedingly high levels of thyroid hormone that is usually preceded by stress, infection, surgery or RAI ablation that is a potentially fatal complication of hyperthyroidism. It is treated with IV steroids, PTU (propylthiouracil), propanolol and ice baths. |
|
|
Term
| What volume of steroid is secreted daily by the fetal cortices of the adrenal glands? |
|
Definition
| 100-200 mg of steroids daily. |
|
|
Term
| Which hormones are secreted from each of the 3 zones of the Adrenal cortex? (zona glomerulosa, zona fasciculata, zona reticularis) |
|
Definition
Glomerulosa = Aldosterone.
Fasciculata = Glucocorticoids.
Reticularis = Androgens and estrogens. |
|
|
Term
| What hormones are produced and secreted by the Medullary layer of the Adrenal glands? |
|
Definition
| Catecholamines (Epinephrine and Norepinephrine). |
|
|
Term
| What is an example of a glucocorticoid? Mineralocorticoid? |
|
Definition
Glucocorticoid = Cortisol.
Mineralocorticoid = Aldosterone. |
|
|
Term
| What is the effect of excessive glucocorticoids (Cortisol) on gluconeogenesis, the effects of insulin, bodily protein, bone mass? |
|
Definition
| It stimulates gluconeogenesis, it decreases the effects of insulin causing hyperglycemia and it causes protein loss in muscle and bone leading to atrophy and osteoporosis. |
|
|
Term
| What is the effect of excessive glucocorticoids (Cortisol) on immune responses and PUD? |
|
Definition
| It inhibits the immune response and can increase the risk of PUD by stimulating pepsin and HCl. |
|
|
Term
| Describe how cortisol secretion is regulated. |
|
Definition
| Hypothalamic-pituitary-adrenal axis. Hypothalamic CRH (Corticotropin-releasing hormone) causes the release of ACTH from the pituitary which binds with receptors on the adrenal cortex and causes the release of cortisol. |
|
|
Term
| What will result from excess adrenal androgens in females? Males? |
|
Definition
| Hirsutism and virilization (becoming more manly). It will cause early sexual development in males. |
|
|
Term
| What is the most common cause of Cushing's Syndrome? |
|
Definition
| Excessive administration of corticosteroids for chronic medical problems such as RA, asthma and supression of organ rejection. |
|
|
Term
| Will Cushing's Syndrome have a oversecretion of glucocorticoids, mineralocorticoids and androgens? |
|
Definition
|
|
Term
| What 3 tests can be used to diagnose Cushing's Syndrome? |
|
Definition
| Dexamethasone supression test, 24-hour urinary free cortisol level and ACTH measurement. |
|
|
Term
| What is the treatment for Cushing's Syndrome due to a pituitary tumor? Tx for primary adrenal hypertrophy? |
|
Definition
| Pituitary tumor Tx would be transphenoidal hypophysectomy or radiation. Adrenal hypertrophy Tx would be Adrenalectomy. |
|
|
Term
| What is the active form of thyroid hormone? |
|
Definition
| T3 is the active form, there is more T4 but when it is needed T4 is deiodinated into T3. |
|
|
Term
| What serologic markers are the most diagnostic for diagnosis of Hashimoto's Thyroiditis? |
|
Definition
| TPO (Anti-tyrosine peroxidase) antibodies and antithyroglobulin |
|
|
Term
| What is the ionic effect of the mineralocorticoid Aldosterone? |
|
Definition
| It increases sodium absorption in exchange for excretion of potassium or hydrogen ions. |
|
|
Term
| What protein is responsible for the secretion of aldosterone? |
|
Definition
|
|
Term
|
Definition
| It is primary hyperaldosteronism, due to a tumor or adrenal hyperplasia of the zona glomerulosa. |
|
|
Term
| What is secondary hyperaldosteronism? What conditions is it commonly associated with? |
|
Definition
| It is hyperaldosteronism that occurs in response to the Renin-Angiotensin-System when arteriolar pressure in the renal glomerulus decreases. Common with CHF, cirrhosis of the liver and nephrotic syndrome. |
|
|
Term
| What is the chief clinical sign of Hyperaldosteronism? |
|
Definition
| HTN due to sodium retention |
|
|
Term
| How will plasma renin activity change with primary and secondary Hyperaldosteronism? |
|
Definition
| Primary will have decreased plasma renin activity and secondary will have an increase in plasma renin activity. |
|
|
Term
| What is the treatment for adrenal hyperplasia leading to over secretion of Aldosterone? |
|
Definition
| Spironolactone (K-sparing diuretics) |
|
|
Term
| What is the most potent androgen? |
|
Definition
|
|
Term
| What is the most common cause of excess androgen production? |
|
Definition
| Polycystic ovarian syndrome |
|
|
Term
| What is the etiology of Classic Congenital Adrenal Hyperplasia? |
|
Definition
| It is caused by an enzyme deficiency that leads to a cortisol and aldosterone deficiency in which their precursors are shunted towards the formation of androgens, and with a deficiency in cortisol and aldosterone there is no negative feedback so excess CRH from the hypothalamus and ACTH from the anterior pituitary accumulates. |
|
|
Term
| Is hirsutism and virilization common with polycystic ovarian syndrome? |
|
Definition
| Hirsutism is very common but virilization is not. |
|
|
Term
| How is polycystic ovarian syndrome treated? |
|
Definition
| It is treated with androgen supression with oral contraceptives, synthetic corticosteroids, spironolactone or metformin. |
|
|
Term
| What is the hallmark of a Pheochromocytoma? |
|
Definition
|
|
Term
| How is a pheochromocytoma diagnosed? |
|
Definition
| 24 hours urine catecholamine and VMA test and an adrenal CT/MRI. |
|
|
Term
| Describe what primary and secondary adrenal insufficiency are caused by. |
|
Definition
Primary is a disease of the adrenal cortex such as Addison's disease.
Secondary is due to a deficiency of the secretion of ACTH from the pituitary or by sudden withdrawal of corticosteroid medication. |
|
|
Term
| Describe the levels of ACTH seen with primary and secondary adrenal insufficiency. |
|
Definition
| Primary will have high leves of ACTH and secondary will have low levels of ACTH. |
|
|
Term
| What is the most common cause of Addison's disease? |
|
Definition
| Autoimmune destruction of the adrenal glands. |
|
|
Term
| What do the manifestations of Addison's disease result from? |
|
Definition
| Deficiency of cortisol, aldosterone and androgen deficiency. |
|
|
Term
| What are the symptoms of Addison's disease? |
|
Definition
| Symptoms include weakness, anorexia, weight loss, low blood pressure, orthostatic hypotension, hypoglycemia, hyperpigmentation and reproductive disturbances. |
|
|
Term
| Describe the fluid and electrolyte disturbances seen with Addison's disease. |
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Definition
| Hyperkalemia, hyponatremia, hypovolemia, and metabolic acidosis. |
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Term
| What causes the hyperpigmentation seen with Addison's disease? |
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Definition
| It is caused by the increased secretion of melanocyte stimulating hormone (MSH). |
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Term
| What ionic disturbances are due to the aldosterone deficiency seen with Addison's disease? |
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Definition
| Aldosterone deficiency leads to hyponatremia, hypovolemia, hyperkalemia and metabolic acidosis. |
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Term
| How will acute adrenal insufficiency (Addisonian crisis) present? Is it an emergency? |
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Definition
| It will present with vomiting, dehydration, hypotension and hypoglycemia. It is a medical emergency. |
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Term
| How is Addison's Disease diagnosed in response to cortisol, aldosterone, ACTH, serum sodium content, serum potassium content and serum renin content? |
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Definition
| Cortisol and aldosterone will be decreased. ACTH will be increased. Hyponatremia and hyperkalemia and a high serum renin level. |
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Term
| Can the brain use any substance other than glucose for energy? |
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Definition
|
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Term
| What is the function of insulin and what cells require it? |
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Definition
| Its function is to transport glucose across the cell membrane of fat and muscle cells. |
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Term
| What is the effect of high and low blood glucose on the pancreas? |
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Definition
| Low blood glucose will stimulate the pancreas to release glucagon by the alpha cells which tells the liver to release glucose into the blood. High blood glucose will stimulate the pancreas to release insulin by the beta cells and glucose is taken up by the body from the blood stream. |
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Term
| Describe the two functional states involved in metabolism (absorptive and postabsorptive)? Describe what the main source of energy is in each stage. |
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Definition
| Absorptive is eating, glucose rises above the baseline and is the main source of energy. Postabsorptive is after eating or during fasting, fat stores provide energy. |
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Term
| What are the possible fates of excess glucose? |
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Definition
| Glycogen in the liver and muscles or converted into fat. |
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Term
| Which organ is primarily responsible for the physiologic regulation of glucose? |
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Definition
|
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Term
| Which cells produce insulin? |
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Definition
| Beta cells of the islets of Langerhans in the pancreas. |
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Term
| What are 4 common hormones that can raise blood glucose? |
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Definition
| Glucagon, epinephrine, glucocorticoids and growth hormone. |
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Term
| What are the normal fasting blood glucose levels? |
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Definition
|
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Term
| At what threshold will the kidneys begin to excrete glucose and not reuptake all of the filtered glucose? |
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Definition
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Term
| What conditions are commonly associated with diabetic excretion of glucose and why? |
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Definition
| Diabetic ketoacidosis or coma because the excretion of glucose is accompanied by increased excretion of water and electrolytes. |
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Term
| :a chronic disorder of absolute or relative deficiency of insulin or insulin resistance |
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Definition
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Term
| Describe Type I Diabetes. |
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Definition
| autoimmune disease that leads to a lack of endogenous insulin. |
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Term
| What percentage of the beta cells much by destroyed in Type I DM to get clinical manifestations? |
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Definition
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Term
| Describe Type II Diabetes. |
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Definition
| Insulin resistance, impaired insulin secretion, and excessive hepatic glucose production with no evidence of autoimmune disease and is often associated with obesity. |
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Term
| What is primarily responsible for the resistance to insulin in Type II Diabetes? |
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Definition
| Defective insulin receptors. |
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Term
| What is gestational diabetes? |
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Definition
| Diabetes that occurs during pregnancy and they have an increased risk of developing type II diabetes later in life. |
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Term
| What fasting glucose levels are considered normal, impaired and diabetes? |
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Definition
| Less than 110 is considered normal. 111-125 is considered impaired. Over 126 on 2 occasions is considered diabetes. |
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Term
| What is primarily responsible for a Type I Diabetic that is in a diabetic coma? |
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Definition
| volume depletion due to hyperglycemia and ketoacidosis effects on the kidney. |
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Term
| What glucose tolerance test results at 2 hours are indicative of normal and diabetic levels? |
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Definition
| Normal is less than 140 mg/dl. Diabetes is over 200 mg/dl. |
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Term
| Which type of Diabetes is HLA linked? |
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Definition
|
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Term
| What are the 3 ways to diagnose diabetes according to ADA criteria? |
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Definition
| 2 hour GTT blood glucose over 200 mg/dl at 2 hours, fasting blood glucose over 126 mg/dl, and random glucose over 200 mg/dl + classic symptoms. |
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Term
| Acromegaly is diagnosed by? |
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Definition
|
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Term
| What is a common triggering event for Type I DM? |
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Definition
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Term
| What 3 factors are responsible for maintaining normal fasting glucose levels? |
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Definition
| hepatic glucose production, peripheral tissue glucose uptake and hormonal regulation of glucose metabolism. |
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Term
| If hyperglycemia due to diabetes exceeds the renal threshold and glucosuria results, what are the typical S&S? |
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Definition
| They typically have weight loss and fatigue due to the negative caloric balance. |
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Term
| Explain how hemoglobin A1c is the single best marker for evaluating the risk for glycemic damage to tissues. |
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Definition
| Glucose is normally incorporated into hemoglobin over the lifespan of the RBC, if the blood glucose levels are higher over the 120 day lifespan then they will also be higher within the RBC and that can be measured as hemoglobin A1c. |
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Term
| What are the normal values for hemoglobin A1c? |
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Definition
|
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Term
| Which type of diabetes always requires insulin? |
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Definition
|
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Term
| Which insulin is short acting? Intermediate acting? Long acting? |
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Definition
Short = Regular insulin.
Intermediate = NPH.
Long = Ultralente. |
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Term
| How long does Regular insulin typically last? NPH? |
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Definition
Regular = 6-10 hours.
NPH = 12-20 hours.
Ultralente = 18-24 hours. |
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Term
| Explain the MOA for the 4 main types of oral hypoglycemic agents that are the cornerstone of Type II DM treatment (Sulfonylureas, Biguanides, Thiasolidinediones, and Acarbose) |
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Definition
Sulfonylureas (glipizide or glyburide) - stimulate the release of endogenous insulin.
Biguanides (Metformin) - supress hepatic glucose release and enhance insulin sensitivity.
Thiazolidinediones (rosiglitazone and pioglitazone) - lessen insulin resistance.
Acarbose - delays the absorption of ingested carbohydrates. |
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Term
| What are the factors seen with DM Type I that lead to diabetic ketoacidosis? |
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Definition
| marked hyperglycemia (300-600 mg/dl) with glucosuria and increased lipolysis (ketone bodies). |
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Term
| Describe Hyperosmolar Hyperglycemic state or (Nonketotic Acidotic State). |
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Definition
| It is seen with Type II DM and it has a more severe hyperglycemia (600-1200 mg/dl) and a more severe hyperosmolality but no ketosis or metabolic acidosis. |
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Term
| What blood glucose level is considered hypoglycemia? |
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Definition
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Term
| What are the common symptoms of hypoglycemia due to excessive epinephrine release? |
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Definition
| sweating, shaking, palpitations and headache. |
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Term
| What are the treatments for a conscious and unconscious hypoglycemic patient? |
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Definition
Conscious = oral sugar containing drink.
Unconscious = IM glucagon or an ampule of 50% IV glucose. |
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Term
| What macrovascular problems are individuals with DM more susceptible to? |
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Definition
| They commonly get atherosclerosis leading to coronary artery disease, stroke, peripheral vascular disease and increased risk of infection. |
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Term
| What is the leading cause of blindness in the US? |
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Definition
|
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Term
| What is the leading cause of end-stage renal disease (ESRD) in the US? |
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Definition
| Diabetic glomerulosclerosis |
|
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Term
| Describe how Diabetes leads to end stage renal disease. |
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Definition
| It causes renal hypertrophy which decreases the GFR and leads to microalbuminuria and HTN which leads to nephropathy with proteinuria and then a rapid decline of the GFR leading to ESRD. |
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Term
| What are the components of Syndrome X or Metabolic Syndrome? |
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Definition
3 or more of the following:
Blood pressure equal to or higher than 130/85 mmHg.
Blood glucose higher than 100 mg/dL.
Waist circumference greater than 40 inches in men and 35 in women.
Low HDL cholesterol (under 40 for men and under 50 for women).
Triglycerides equal to or higher than 150 mg/dL |
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Term
| What are the physiologic processes that calcium plays a role in regulating? |
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Definition
| Activation of clotting enzymes, membrane excitation of muscle and nerves, membrane stabilization, milk production and bone/teeth formation. |
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Term
| What is the action of calcitonin? Where is it released from? |
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Definition
| It is secreted by the thyroid and it stimulates the uptake of calcium from the blood into the bone. |
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Term
| What is the action of PTH? |
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Definition
| It causes osteoclasts to degrade bone matrix and deposit calcium into the blood. |
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Term
| What is the normal plasma concentration of total calcium? |
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Definition
|
|
Term
| What is the effect of vitamin D on serum calcium content? |
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Definition
| Vitamin D works to increase serum calcium by being converted into calcidiol in the liver then to calcitriol in the kidney and then calcitriol causes the bone to release calcium and it causes the small intestine to increase dietary absorption of calcium. |
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Term
| What is the active form of vitamin D? Where is it made? |
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Definition
| calcitriol, which is synthesized from D2 or D3 in the kidneys. |
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Term
| What are the effects of PTH in the kidneys? |
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Definition
| It increases the reabsorption of calcium and inhibits the reabsorption of phosphate which increases the formation of calcitriol (active form of vitamin D) which works synergistically with PTH to increase blodo calcium levels. |
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Term
| What are the effects of vitamin D on the bone tissue? |
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Definition
| It leads to the release of calcium from the bone into the blood and it also helps with calcium binding to protein in the bone and has an antirachitic (soft bones) action. |
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|
Term
| What is the most common cause of primary hyperparathyroidism? |
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Definition
|
|
Term
| What is the most common cause of secondary hyperparathyroidism? |
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Definition
| Hypocalcemia due to chronic renal disease. |
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Term
| What are the clinical manifestations of primary hyperparathyroidism? |
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Definition
| Severe bone disease, urinary calculi due to hypercalciuria, hypercalcemia leading to kidney failure, osteoporosis and osteitis fibrosa cystica (severe bone pain, demineralization and fractures with bone cysts and brown tumors) |
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Term
| What is diagnostic of primary hyperparathyroidism? |
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Definition
| CT/MRI showing an adenoma and serum calcium over 11 mg/dl. |
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Term
| What drugs can be used to treat hyperparathyroidism? |
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Definition
| Calcimimetics bc they turn off the secretion of PTH. |
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Term
| Should marked hypercalcemia cases (13-15 mg/dl) be considered an emergency? |
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Definition
|
|
Term
| What is DiGeorge syndrome? |
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Definition
| A condition leading to hypoparathyroidism due to a congenital T cell disorder of thymic hypoplasia and parathyroid hypoplasia. |
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Term
| What is the hallmark of hypoparathyroidism? |
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Definition
|
|
Term
| What are the clinical manifestations of hypoparathyroidism? |
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Definition
| Tetany, twitching of muscles and muscular fatigue. Seizure may occur in severe cases. |
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Term
| What are some consequences of long term hypocalcemia due to hypoparathyroidism? |
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Definition
| Atrophy and brittle skin, calcification of the basal ganglia and calcification of the optic lens which may lead to cataract. |
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Term
| What is the treatment for hypoparathyroidism? |
|
Definition
| calcium supplementation with vitamin D |
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Term
| What is Chvostek's and Trousseau's signs of hypoparathyroidism? |
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Definition
| Positive Chvostek's sign (involuntary facial twitching in response to tapping of the facial nerve) and positive Trousseau's sign (flexion of the thumb and hyperextension of the fingers in response to inflating a BP cuff on that arm for 3 minutes. |
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