Term
| Increased amount of calcitonin is indicative of what? |
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Definition
| Medullary carcinoma or C-cell hyperplasia |
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Term
| HLA subtype associated w graves disease |
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Definition
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Term
| Histiologic changes associated with graves disease |
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Definition
| prominent papillary infolding in the follicles, with tall columnar epithelium, scalloped colloid, and lymphocytic infiltrates between the follicles |
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Term
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Definition
| describes a specific form of cutaneous and dermal edema secondary to increased deposition of connective tissues (like glycosaminoglycans, hyaluronic acid, and other mucopolysaccharides) as seen in various forms of hypothyroidism and Graves' disease |
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Term
| Hashimoto’s / Autoimmune thyroiditis |
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Definition
Autoimmune etiology with increased TGI and TSI antibodies (the action of the TGI predominates over the TSI) that stimulate enlargement of the gland. Additional blocking antibodies may mitigate the effect of TSIs. Predilection in persons with HLA-DR5.
Microscopically, there is initially an abundant mononuclear cell infiltrate and lymphoid follicles with large pink “Hürthle cells.” Later, collagenous fibrosis, follicular atrophy, and some residual lymphoid infiltrates are seen.
Patients are at increased risk of developing lymphoma of the thyroid. |
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Term
| Subacute granulomatous thyroiditis (De Quervain’s disease) |
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Definition
Probably viral origin, follows infection i.e. flu. Painful enlarged thyroid, destruction of follicles, granulomatous inflammation and giant cells. hyperthyroid, then hypothyroid, then normal.
This is usually a self-limited disease with a course over weeks to months. |
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Term
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Definition
| Most are small solitary nodules (may be mimicked both clinically and pathologically by a nodular goiter). Most are cold on scintograph, All have a follicular pattern; there are no papillary adenomas. encapsulated tumor with smooth edges. Histologically, there are monotonous, small follicles with little or no colloid, and a fibrous capsule which the adenoma does not invade through |
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Term
|
Definition
all papillary thyroid neoplasms are considered malignant); about 2/3 of all primary thyroid malignancies. Histologically, they may be papillary, solid, or follicular.
Cytologically they typically have cells with clear (“ground glass”) nuclei. Psammoma bodies (laminated circular calcified concretions) may be present.
Tend to metastasize to regional lymph nodes; some papillary carcinomas may even initially present as an enlarged node from metastasis.
Long-term survival is common: >95% ten-year survival |
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Term
|
Definition
about 1/4 of thyroid malignancies, Grossly often difficult to distinguish from an adenoma (must look for capsular or vascular invasion).
Histologically, diagnosed by the absence of the features of papillary carcinoma.
Tend to metastasize hematogenously (lung and bone).
90% five-year survival for minimally invasive tumors; prognosis is far worse for tumors with extensive invasion. |
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Term
|
Definition
comprise about 10% of thyroid malignancies. Derived from “C cells” and therefore has neuroendocrine features--can secrete calcitonin, ACTH, serotonin, somatostatin, etc.
Grossly presents as single mass when the neoplasm occurs “sporadically” (70% of all cases) or multicentric masses when it is “familial.”
Histologically, has polygonal cells arranged in nests; can have an amyloid stroma
Can be associated with multiple endocrine neoplasia (MEN) syndromes.
Survival rate for familial forms (85% over 10 years) is double that of sporadic forms. |
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Term
|
Definition
rare thyroid malignancy, , aggressive neoplasm that is grossly hard and very invasive of surrounding tissues; occurs in older age range; very poor prognosis.
Histologically is undifferentiated with either small, spindled, or giant cells. |
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Term
An otherwise healthy 45-year-old female has a feeling of fullness in the anterior neck. Physical examination reveals a diffusely enlarged, non-tender thyroid gland. The serum T3, T4, and TSH are all normal. She has a goiter.
If she had been hypothyroid, the most likely etiology would be:
A. Radiation therapy
B. Congenital biochemical enzymatic defect
C. Hypopituitarism
D. Chronic thyroiditis
E. Iodine deficiency |
|
Definition
| radiation, hypopituitarism, and chronic thyroiditis would lead to a small thyroid; it is unlikely that she would be a healthy 45-year-old with a biochemical defect leading to hypothyroidism; iodine deficiency, however, is rare in the modern world. e |
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Term
| 4 types of common adenomas |
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Definition
| prolactinomas (~32%), growth hormone secreting adenomas (20%), null cell adenomas (30%), and corticotrophs (14%). Adenomas can occur over a wide age range, including children, but are most common in patients between 40 and 70 years of age. |
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Term
|
Definition
Most are chromophobes (see to left).
Treated with dopamine agonists.
Remember that prolactin may be increased with any lesion that inhibits PIF (dopamine) such as adenomas, suprasellar tumors, cysts, head trauma etc.
Prolactin may also be elevated by stress, drugs (dopamine antagonists and others), estrogen therapy, and renal failure.
Remember that prolactin is moderately increased by any lesion that inhibits hypothalamic regulatory hormones |
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Term
| Growth hormone secreting adenomas |
|
Definition
Can be chromophobic or acidophilic in routine H&E stains.
Are slow growing and may be large, as symptoms develop insidiously.
Is the most common pituitary adenoma in children. |
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Term
|
Definition
No morphologic or biochemical markers.Produce mass effects (visual field defects & headaches).
Hypopituitarism. Hyperprolactinemia (the so-called “stalk section effect” resulting from absence of PIF). |
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Term
|
Definition
| Are often microadenomas; most appear basophilic with H&E stain. Cause Cushings disease. Diagnostic tests include elevated ACTH, dexamethasone suppression test, ACTH elevation with metyrapone (which blocks cortisol synthesis), and MRI. |
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Term
|
Definition
| appearance of an ACTH-producing adenoma following bilateral adrenalectomy for Cushing’s disease. |
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Term
| Gonadotroph-cell adenomas and Thyrotroph cell adenomas |
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Definition
| Small, slow growing and usually non-functioning clinically. If symptomatic, may cause ovarian hyperstimulation with elevated estradiol causing amenorrhea in premenopausal females, and breast development and vaginal bleeding in prepubertal females |
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Term
|
Definition
Probably derived from remnants of Rathke’s pouch. Most common in children and young adults; usually present with headaches and visual disturbances. Calcifications are present radiographically in 75% of cases; are usually grossly cystic; microscopically the epithelium present may resemble a developing tooth or be squamous.
Produces no hormones but can erode the sella and be locally invasive and difficult to eradicate. |
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Term
|
Definition
| Caused by any destructive lesion, but because the physiologic reserve capacity is great, 80-90% destruction is required. |
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Term
| Most common causes of hypopituitarism |
|
Definition
a. Nonsecretory pituitary adenomas are the most common cause.
b. Pituitary necrosis – with shock, DIC etc. Example: Sheehan’s syndrome (post-partum pituitary necrosis).
Other causes of vascular compromise include: hypotension, DIC, trauma, sickle cell anemia, vasculitis.
c. Craniopharyngioma or other suprasellar lesions that interfere with the hypothalamic-pituitary axis.
d. Empty sella syndrome - a poorly understood condition where radiographic techniques reveal an apparent absence of the pituitary.
e. Lymphocytic hypophysitis - a rare autoimmune condition of obscure etiology. |
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Term
| Physiologic consequences of hypopituitarism |
|
Definition
a. Adults - hypogonadism with loss of secondary sex characteristics and sterility; children - growth retardation.
b. TSH deficiency leading to hypothyroidism; ACTH deficiency resulting in secondary adrenal insufficiency.
c. First to decrease is GH, then FSH/LH, then TSH, and finally ACTH. |
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Term
| Posterior Pituitary Insufficiency |
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Definition
Rare. The usual cause is either idiopathic or a hypothalamic tumor.
1. Deficiency of ADH causes diabetes insipidus with polyuria and secondary polydipsia.
Here, serum sodium and osmolality are often normal or can be increased, and the urine osmolarity and specific gravity are low (specific gravity <1.005), even with water deprivation. The problem corrects with administration of ADH.
2. Differential diagnosis is psychogenic polydipsia where patients can concentrate urine with water deprivation.
3. Inappropriate ADH causes hyponatremia and hemodilution.
Most commonly results from a paraneoplastic syndrome with ADH from an oat cell carcinoma of lung; other causes include pulmonary infections or CNS infection or hemorrhage. |
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Term
| MEN I (Wermer’s syndrome) |
|
Definition
a. Pituitary adenoma, Parathyroid hyperplasia or adenoma, Pancreatic islet cell hyperplasia, adenoma, or carcinoma.
b. Often detected by hypercalcemia; deaths are due to the islet cell lesions.
c. Most of the pancreatic islet cell tumors secrete gastrin which causes multiple peptic and duodenal ulcers. |
|
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Term
| MEN II (IIa or Sipple’s syndrome) |
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Definition
a. Medullary carcinoma of thyroid, Pheochromocytoma of adrenal medulla, and Parathyroid hyperplasia.
b. The thyroid carcinomas tend to be multicentric; the pheochromocytomas tend to be bilateral or extra-adrenal. |
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Term
|
Definition
a. Medullary carcinoma of thyroid, Pheochromocytoma of adrenal medulla, mucocutaneous ganglioneuromas.
b. Parathyroids are not involved. |
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Term
A 22-year-old woman complains of vague abdominal pain along with some pain in her extremities. She has felt terrible and depressed for several months. Physical examination reveals no major findings. A chest x-ray is normal. A serum chemistry panel reveals a calcium of 13.8 mg/dl with a serum albumin of 3.9 g/dl and PO4 of 2.2 mg/dl. At surgery, a 1cm mass in the left side of the neck adjacent to the thyroid gland is removed and sent to the surgical pathology lab for frozen section.
5. The pathologist’s diagnosis is most likely to be:
A. Parathyroid carcinoma
B. Medullary thyroid carcinoma
C. Parathyroid adenoma
D. Non-Hodgkin’s lymphoma
E. Parathyroid hyperplasia
Further history: She is found to have an increased serum cortisol along with an increased plasma ACTH.
6. Which of the following radiologic findings is most likely to be present?
A. A left adrenal mass
B. A sella turcica that is enlarged
C. A lung nodule
D. A suprasellar mass with calcifications
E. A mass
compressing the trachea
Further history: A year later she develops mid-abdominal pains which are relieved by eating. She develops an iron deficiency anemia. Following an episode of vomiting a small amount of blood, an upper endoscopy is performed and multiple 0.5 to 1 cm benign gastric and duodenal ulcers are found.
7. She was taken to surgery once more. What was the most likely finding?
A. Adrenal medullary pheochromocytoma
B. Aldosterone secreting adenoma of adrenal cortex
C. Multiple gastrinomas of pancreas
D. Medullary carcinoma of thyroid
E. Oat cell carcinoma of lung
Further history: Prior to surgery, serum gastrin levels were found to be markedly elevated. At surgery, there was one larger 3 cm circumscribed mass at the head of the pancreas that completely obstructed the pancreatic duct and several smaller masses from 0.5 to 1 cm adjacent to the splenic artery. The pancreas was replaced by fibrofatty tissue and the pancreatic duct was not found distal to the large tumor. Microscopically, the masses were all consistent with islet cell tumors, and there was no normal remaining pancreatic parenchyma (either acini or islets).
8. The majority of the above findings can be explained by a syndrome that carries an increased risk for:
A. Development of an extra-adrenal pheochromocytoma
B. Diabetes mellitus
C. Appearance of ganglioneuromas
D. Medullary carcinoma of thyroid
E. Similar findings in siblings |
|
Definition
5. C; parathyroid adenomas are typically solitary masses, and they account for most cases of hyperparathyroidism
6. B; she has Cushing’s disease with a pituitary adenoma secreting ACTH. A lung cancer as the source of ectopic ACTH would be rare at her age.
7. C; islet cell tumors may secrete gastrin
8. E; she has MEN I |
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Term
|
Definition
| Pituitary necrosis – with shock, DIC etc. (post-partum pituitary necrosis) |
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Term
Following a precipitous delivery with substantial blood loss from a placenta previa, a 24-year-old primigravida is in stable condition. However, she is unable to breastfeed the baby. Then, over the next few months she notes a failure to return to normal menstrual cycles along with increasing fatigue, cold intolerance, and weight loss. What is the most likely underlying problem in this patient?
A. Chromophobe adenoma of the pituitary secreting prolactin
B. Astrocytoma of the thalamus and hypothalamus
C. Oat cell carcinoma of lung
D. Empty sella syndrome
E. Sheehan’s syndrome |
|
Definition
| post-partum pituitary necrosis led to the loss of pituitary hormones and hypogonadism, hypothyroidism, and finally secondary adrenal insufficiency. e |
|
|
Term
| Adrenal cortex - Glomerulosa |
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Definition
| secretes mineralocorticoids, principally aldosterone, under the control of the renin-angiotensin mechanism along with serum potassium |
|
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Term
| Adrenal Cortex - Fasciculata |
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Definition
| secretes glucocorticoids, principally cortisol, under the control of ACTH from the pituitary |
|
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Term
| Adrenal cortex - reticularis |
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Definition
|
|
Term
|
Definition
| chromaffin cells secrete catecholamines (norepinephrine and epinephrine). |
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Term
| Clinical features of adrenal insufficiency |
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Definition
a. weakness, nausea, vomiting and weight loss are seen in both primary and secondary adrenal cortical failure.
b. hyponatremia, hypovolemia, hypotension, skin pigmentation, and hyperkalemia are seen in primary failure
c. hypoglycemia is seen in secondary failure |
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Term
| Primary Acute Adrenocortical Insufficiency |
|
Definition
1. Crisis: seen in patients with chronic insufficiency or on exogenous steroids with sudden requirement for increased steroid output
2. Lab test is morning serum cortisol and plasma ACTH. ACTH stimulation test for borderline cases & to rule out secondary causes.
3. Massive adrenal hemorrhage
a. seen in newborns, DIC, bacteremia
b. Waterhouse – Friderichsen Syndrome
- results from acute bacterial infection with sepsis and DIC: Neisseria meningitidis (meningococcus) is most often implicated, but can also occur with Haemophilus, Staphylococcus aureus, and pneumococcus
- adrenal is hemorrhagic and necrotic; patient’s skin shows extensive petechiae and/or purpura |
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Term
| Primary Chronic Adrenocortical Insufficiency |
|
Definition
Addison Disease
1. Infiltration of gland by lymphoma, cancer, amyloid, sarcoid, hemochromatosis and infections (TB)
2. Autoimmune adrenalitis
- More common in white women
- 60-70% of cases
- Sporadic or familial (HLA-B8 and DR-3)
- multiple endocrine glands may be involved in 50%
3. Adrenals are small and scarred (1-3 gm)
4. ACTH is increased resulting in high melanotropic hormone and skin hyperpigmentation. It is due to β-lipotropin, which is part of POMC, the ACTH precursor peptide.
5. In boys / young men, consider adrenoleukodystrophy |
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Term
| Secondary Adrenocortical Insufficiency |
|
Definition
1. Any disorder of the hypothalamus or pituitary that decreases ACTH
2. Exogenous steroids suppress ACTH and adrenal function
3. There is no hyperpigmentation
4. Aldosterone is usually normal (normal K+ and Na+ )
5. An ACTH challenge test results in increased cortisol levels, (cosyntropin) |
|
|
Term
|
Definition
A. Pituitary adenoma secreting ACTH - Cushing Disease is the leading cause of spontaneous hypercortisolism
B. W>M 5:1
C. 20 – 30 yo
D. Adrenal hyperplasia, bilateral |
|
|
Term
|
Definition
A. Adrenal cortical neoplasms (adenoma, carcinoma) 15-30%
1. ACTH is low, cortisol is high
2. Act autonomously, opposite gland is atrophic
B. Paraneoplastic syndrome with ectopic ACTH production (tumors such as oat cell carcinoma, medullary carcinoma of thyroid, or pheochromocytoma).
1. Bilateral cortical hyperplasia
C. Iatrogenic from chronic corticosteroid use (most common cause) - the adrenals are atrophic |
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|
Term
| Clinical Presentation of Cushings disease or syndrome |
|
Definition
Caused by elevated glucocorticoids
a. hypertension
b. truncal obesity and “moon facies”, buffalo hump
c. proximal muscular weakness and atrophy of Type II fibers
d. thin skin, capillary fragility, loss of collagen
e. osteoporosis, often with compressed vertebral fractures
f. hyperpigmentation (if Cushing disease)
g. acne, hirsutism, amenorrhea
h. glucose intolerance (diabetes)
i. immune suppression
j. mental status changes, depression |
|
|
Term
| Laboratory tests for cushings. Distinguish syndrome from disease |
|
Definition
A. Screen with either 24 hour urinary free cortisol OR the overnight (low dose) dexamethasone suppression test. The plasma cortisol is not suppressed in Cushing syndrome.
B. Differential diagnostic tests include:
- 2 day dexamethasone suppression test.
- Plasma ACTH, is decreased with adrenal neoplasms.
- ACTH is increased with Cushing disease and ectopic ACTH production
- CT or MRI to find mass in the adrenal |
|
|
Term
| Adrenal cortical hyperfunction, Hyperaldosteronism |
|
Definition
1. Primary hyperaldosteronism
- Secrete aldosterone
- Na+ retention and K+ excretion
- Hypertension and hypokalemia
- Suppression of renin-angiotensin system
- Caused by adenoma or hyperplasia
- Conn Syndrome
is caused by an adenoma
is more common in women
2. “Secondary” hyperaldosteronism results from renal disease, cirrhosis, or congestive heart failure and is distinguished by increased renin. |
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Term
|
Definition
a. Many are hormonally active and may combine Cushing syndrome and virilization in the female and (rarely) feminization in the male
b. Not suppressed by dexamethasone. ACTH is decreased and does not respond to metyrapone.
c. Grossly are yellow with areas of necrosis; invasion and metastases prove that they are malignant; microscopically composed of clear cells that resemble adrenal cortex to highly anaplastic cells. |
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Term
|
Definition
a tumor of chromaffin cells of the adrenal medulla
a. remember 10%: this describes the number of pheos that are malignant, extra-adrenal, part of multiple endocrine neoplasia syndromes, bilateral, and pediatric. |
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Term
|
Definition
(a tumor of sympathetic ganglion cells)
a. mostly seen in children <5 years of age; is the most common solid extracranial malignant childhood neoplasm and accounts for 15% of childhood deaths from cancer
b. they can secrete catecholamines, VMA, and homovanillic acid (HVA), usually in small amounts, so hypertension and other symptoms of catecholamine excess are uncommon
c. often presents as abdominal enlargement with a mass and is metastatic at the time of diagnosis in 90% of patients |
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|
Term
| Congenital adrenal hyperplasia (Adrenogenital syndrome) |
|
Definition
1. A group of autosomal recessive enzymatic defects in the production of cortisol resulting in decreased cortisol, increased ACTH, and adrenal hyperplasia.
2. 21-hydroxylase deficiency is the most common type. The enzyme is needed for cortisol and aldosterone production, but not androgen synthesis.
3. Produces virilization secondary to increased androgens.
4. Often presents soon after birth with salt wasting (loss of Na) due to lack of mineralocorticoids and glucocorticoids.
5. Adrenal cortex undergoes hyperplasia as ACTH increases with decreased cortisol. |
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|
Term
|
Definition
| Primary aldosteronism, also known as primary hyperaldosteronism, is characterized by the overproduction of the mineralocorticoid hormone aldosterone by the adrenal glands.[1] Aldosterone causes increase in sodium and water retention and potassium excretion in the kidneys, leading to arterial hypertension |
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Term
A 74 year-old female suffers severe back pain while picking up a basket of clothes. An x-ray reveals a fracture of T12 along with multiple compressed fractures of the vertebrae. Her skin is thin with areas of purpura. She has a serum glucose of 145 mg/dl. Her serum cortisol is normal. If her serum ACTH is decreased, the most likely pathologic finding is:
A. Pituitary adenoma
B. Adrenal cortical carcinoma
C. Adrenal adenoma
D. Marked adrenal atrophy
E. Bilateral adrenal hyperplasia |
|
Definition
| she had rheumatoid arthritis and had received corticosteroid therapy for many years; she had severe osteoporosis. D |
|
|
Term
| Composition of parathyroid gland |
|
Definition
a. Chief cells
- Predominant cell type
- Secretes PTH
- Granular pink to clear
b. Oxyphil cells
- Abundant cytoplasm loaded with mitochondria
- Contain no secretory granules
c. Fat cells
- Increase with age, up to 30% of gland. |
|
|
Term
| How does PTH function to increase serum Calcium levels |
|
Definition
PTH acts by binding a transmembrane receptor and activating a transduction pathway in bone, GI and renal cells.
Serum calcium is increased by
Activating osteoclasts and bone resorption
Increasing renal tubular reabsorption
Activating vitamin D in the kidney
Increasing GI absorption
Increasing renal P04 excretion |
|
|
Term
| Differential Diagnosis for hypercalcemia |
|
Definition
a. Primary hyperparathyroidism - most common cause in outpatients
b. Carcinoma
1. Secretion of a PTH-related protein (paraneoplastic syndrome, most often with squamous cell carcinoma of lung and renal cell carcinoma).
2. Carcinoma of breast, lymphoma, and multiple myeloma cause osteolytic metastases with release of TNFą and IL-1 that stimulate osteoclasts.
c. Rare causes of hypercalcemia include:
- Vitamin D toxicity
- Granulomatous diseases (tuberculosis, sarcoidosis)
- Drugs (thiazide diuretics)
- Prolonged immobilization |
|
|
Term
| Primary Hyperparathyroidism |
|
Definition
1. One of most common endocrine disorders (25 per 100,000)
Adenoma 75-80%
Hyperplasia 10-15%
Carcinoma <5% |
|
|
Term
| Clinical symptoms of Primary Hyperparathyroidism |
|
Definition
“Bones, stones, groans and moans”
a. Often there are no symptoms, just an elevated serum calcium or nonspecific weakness, anorexia, nausea, constipation.
b. Bones: Bone pain from osteoporosis, osteitis fibrosa cystica, “brown tumor” of bone and fractures.
- Prominence of osteoclasts and osteoblasts with thin cortex
- Bone marrow cysts
c. Stones: Nephrolithiasis - 20% of cases have renal stones and obstruction leading to CRI.
d. Groans: Peptic ulcer disease (from increased secretion of gastrin), pancreatitis and gallstones
e. Moans: Depression, confusion, coma and seizures
f. Metastatic calcification (lung, kidney, stomach, heart)
g. Arrhythmias - shortened QT and prolonged PR intervals by EKG, which may proceed to first degree heart block and then to asystole |
|
|
Term
| Most common cause of secondary hyperparathyroidism |
|
Definition
The most common cause is chronic renal failure (serum phosphate increased, calcium low normal or decreased, with increased PTH)
Rare causes include:
Intestinal malabsorption of vitamin D and calcium and steatorrhea |
|
|
Term
A 54 year-old woman was found wandering aimlessly in a city park. She was dressed in an expensive business suit, but was disheveled, disoriented, and didn’t know her name. An uncashed paycheck in her purse was issued by a prestigious law firm. She was extremely weak and had an irregular heart rate. In the hospital, she was found to have a serum calcium of 15.8 mg/dl (normal 8.6 to 10.3) with an ionized calcium of 10.8 mg/dl (normal 4.6 to 5.3), total protein 5.8 g/dl, albumin 3.5 g/dl, urea nitrogen 23 mg/dL, and creatinine 1.1 mg/dL. A chest x-ray revealed clear lungs but osteolytic lesions of ribs and vertebrae.
2. What is the most likely cause for her hypercalcemia?
A. Chronic renal failure
B. Metastatic breast carcinoma
C. Parathyroid adenoma
D. Tuberculosis
E. Parathyroid carcinoma |
|
Definition
| the osteolytic lesions suggest metastases to bone, which are most likely from a carcinoma; parathyroid carcinomas are much less common and usually do not have widespread bone metastases B |
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|
Term
A 40 year old female has enlargement of the anterior neck region. Fine needle aspiration of the thyroid yields cells that are consistent with a neoplasm. A chest radiograph is normal. She is euthyroid, but her serum ionized calcium is elevated, and she has a blood pressure of 155/105 mm/Hg. She is taken to surgery, and a thyroidectomy is performed, after frozen sections of several thyroid masses show a malignant neoplasm composed of polygonal cells in nests. Immunoperoxidase staining for calcitonin of the permanent sections is positive, and the neoplasm has an amyloid stroma with Congo red staining. She is most likely to have:
A Thyroglossal duct cysts
B Multiple endocrine neoplasia
C Papillary thyroid carcinoma
D Metastatic renal cell carcinoma
E Parathyroid carcinoma |
|
Definition
| She has MEN IIa, with medullary thyroid carcinomas (often multiple when familial), parathyroid hyperplasia, and pheochromocytoma. b |
|
|
Term
A 58 year old man with a history of diabetes mellitus has noted the presence of bone pain, especially of his hands, for the past 6 months. There is no swelling or redness. His range of motion is slightly decreased, but there is no joint deformity. A serum chemistry panel shows sodium 139 mmol/L, potassium 4.0 mmol/L, chloride 98 mmol/L, C02 22 mmol/L, glucose 153 mg/dL, creatinine 7.8 mg/dL, calcium 7.8 mg/dL, phosphorus 5.7 mg/dL, total protein 6.2 g/dL, and albumin 4.0 g/dL. Which of the following conditions best accounts for these findings:
A Adrenal adenoma
B Medullary carcinoma
C Extra-adrenal pheochromocytoma
D Parathyroid hyperplasia
E Pituitary adenoma |
|
Definition
| He has secondary hyperparathyroidism from chronic renal failure. Retention of phosphorus drives the calcium down and parathormone secretion up, leading to osteitis fibrosa cystica. d |
|
|
Term
Which of the following pathologic processes is LEAST likely to be associated with laboratory evidence for hyperthyroidism as measured by an increased serum thyroxine:
A Subacute granulomatous thyroiditis
B Multinodular goiter
C Medullary carcinoma of thyroid
D Hashimoto's thyroiditis
E Follicular adenoma of thyroid |
|
Definition
| Medullary carcinomas, derived from interstitial 'C' cells, do not secrete thyroid hormone. c |
|
|
Term
A 49 year old female has passed multiple urinary tract stones over the past year. She is found to have a serum calcium of 13.7 mg/dL, phosphorus of 1.9 mg/dL, creatinine of 1.4 mg/dL, and albumin of 4.8 g/dL. There is an established association between her disease process and each of the following findings EXCEPT:
A Osteitis fibrosa cystica of bone
B Metastatic calcification of tissues
C Parathyroid carcinoma
D Acute pancreatitis
E Tetany |
|
Definition
| Tetany is a feature of hypocalcemia, not hypercalcemia with primary hyperparathyroidism |
|
|
Term
A 30-year-old female from Barcelona has noted enlargement of her neck over the past few months. On physical examination, she has a diffusely enlarged thyroid that is not painful to palpation. Her TSH level is 0.2 microU/ml. A subtotal thyroidectomy is performed and histologically the tissue shows follicles with papillary infoldings lined by tall columnar cells. These findings are most consistent with:
A Subacute granulomatous thyroiditis
B Papillary carcinoma
C Multinodular goiter
D Hashimoto's thyroiditis
E Grave's disease |
|
Definition
| CORRECT. Diffuse hyperplasia is typical for Grave's disease. The TSH is low from negative feedback from increased thyroid hormone production. |
|
|
Term
A 57-year-old male is found comatose with a blood glucose of 780 mg/dl. Urinalysis reveals no ketosis or proteinuria, though there is 4+ glucosuria. He is most likely to have:
A An islet cell tumor secreting glucagon
B Type I diabetes mellitus
C Cushing's syndrome
D Ingested a large quantity of sugar
E Obesity |
|
Definition
| CORRECT. Hyperosmolar coma is most typical for type II diabetes mellitus, seen in overweight persons. |
|
|
Term
The rarest diagnosis in endocrine pathology is:
A Pituitary carcinoma
B Extra-adrenal pheochromocytoma
C Congenital adrenal hyperplasia
D Anaplastic carcinoma of thyroid
E Empty sella syndrome |
|
Definition
| Virtually all tumors of the adenohypophysis are adenomas. a |
|
|
Term
Of the following conditions, the one that is the LEAST likely etiology for primary adrenocortical insufficiency is:
A Meningococcemia
B Metastatic carcinoma
C Tuberculosis
D Amyloidosis
E Trauma |
|
Definition
| The adrenals are in a protected location in the retroperitoneum, with plenty of surrounding fat, and they have three blood supplies. e |
|
|
Term
A 1-year-old male child is found to have a right inguinal hernia with incarceration of a loop of small intestine. A laparotomy is performed and the defect is closed. The tissue from the hernia sac is excised. The surgical pathology report indicates the presence of a focus of adrenal cortex in a hernia sac. This is most consistent with:
A Congenital adrenal hyperplasia
B Adrenal cortical carcinoma metastasis
C Incidental ectopia
D Risk for subsequent adrenocortical insufficiency
E Multiple endocrine neoplasia syndrome |
|
Definition
| Small rests of adrenal cortex are not infrequent in hernia sacs, testis, ovary, or kidney capsule. They may undergo the same changes as the adrenal proper. c |
|
|
Term
A 45-year-old previously healthy female has a solitary palpable non-tender right anterior neck mass. Laboratory findings include a serum free thyroxine index of 1.3 ng/dl, TSH of 2.8 microU/ml, sodium 141 mmol/L, potassium 4.2 mmol/L, chloride 106 mmol/L, CO2 25 mmol/L, glucose 86 mg/dL, and creatinine 1.5 mg/dL. The mass is most likely a(an):
A Lymph node metastasis from papillary carcinoma of the thyroid
B Parathyroid carcinoma
C Medullary carcinoma of the thyroid
D Thyroglossal duct cyst
E Parathyroid adenoma |
|
Definition
| About 10 to 20% of papillary carcinomas of thyroid first present as a lymph node metastasis. Papillary carcinomas comprise 60 to 70% of thyroid carcinomas. a |
|
|
Term
75) Years before, an adult patient had an enlarged thyroid gland with high titer of antimicrosomal and antithyroglobulin autoantibodies present. She then became hypothyroid.
A Papillary carcinoma
B Medullary carcinoma
C Malignant lymphoma
D Follicular carcinoma
E Anaplastic carcinoma |
|
Definition
| This is a long-term complication following Hashimoto's thyroiditis. c |
|
|
Term
(79) Corticosteroid therapy has been administered top a 26-year-old female with systemic lupus erythematosus for many months.
(80) Anencephaly is diagnosed by ultrasound at 20 weeks.
A Adrenal hyperplasia
B Adrenal hypoplasia
C Adrenal cortical carcinoma
D Adrenal necrosis
E Adrenal inflammation |
|
Definition
| Match on 79&80. Anencephaly is a congenital form of adrenal hypoplasia, whereas corticosteroid therapy leads to the acquired form of hypoplasia (atrophy). b |
|
|
Term
(81) A 36-year-old female has had episodic hypertension, headache, and cardiac arrhythmias for the past two months.
(82) A 5-year-old girl presents with virilization and hyponatremia.
A Increased homovanillic acid in urine
B Decreased plasma renin
C Increased urinary free catecholamines
D Decreased plasma cortisol
E Increased serum aldosterone |
|
Definition
Match on 81. Catecholamines are increased with pheochromocytoma. Vanillylmandelic acid (VMA) and metanephrins are also increased.C
Match with 82. Cortisol is decreased with congenital adrenal hyperplasia in which there is an enzyme deficiency in the pathway to cortisol production.D |
|
|
Term
|
Definition
hypoglycemia ~ 3:00 AM, followed by substantial hyperglycemia between 5:00 and 9:00 A.M; probably due to actions of counterregulatory hormones (GH, catecholamines, cortisol) in
response to insulin-induced hypoglycemia. |
|
|
Term
|
Definition
| similar early morning hyperglycemia but due to waning of basal insulin effect |
|
|
Term
|
Definition
Pramlintide
1. Amylin is a 37 amino acid protein co-secreted with insulin; major action is to inhibit glucagon secretion in postprandial period; also slows gastric emptying and may exert satiety effect
2. Amylin secretion is absent in type 1 diabetes and reduced in type 2 diabetes |
|
|
Term
|
Definition
Exenatide - GLP-1 analogue.
a. GLP-1 is released from intestinal endocrine cells after a meal, and
contributes to stimulating the postprandial increase in secretion of insulin (“incretin” effect).
b. GLP-1 also suppresses postprandial secretion of glucagon (resulting in
decreased hepatic glucose production), slows gastric emptying and inhibits food intake
c. In type 2 diabetes, release of GLP-1 is reduced, and glucagon is not
suppressed; along with decreased insulin secretion, these deficits contribute to postprandial hyperglycemia.
d. there is also evidence that GLP-1 may help preserve beta cell mass.
**nausea/vomiting and diarrhea in ~ 50%; hypoglycemia in combo with sulfonylurea
b. recent concerns over development of pancreatitis |
|
|
Term
|
Definition
rosiglitazone (falling out of favor due to adverse cardiovascular effects), pioglitazone
Enhance insulin action by multiple actions, with adipocytes as primary target. PPARGamma agonists. Increase FFA uptake, lipogenesis and glucose uptake by adipose. Increase glucose uptake and glycogenesis by skeletal muscle. Increase glucose uptake, decreases glucogenesis and glycogenolysis by the liver. |
|
|
Term
| Blood supply to the thyroid |
|
Definition
superior thyroid arteries (branches of
the common carotid arteries) and inferior thyroid arteries that are branches of the innominate or brachiocephalic arteries. |
|
|
Term
| Which pouches are the thyroid and parathyroid glands formed from? |
|
Definition
Thyroid: 2nd
Parathyroid: Between 3rd and 4th |
|
|
Term
|
Definition
| most abundantly expressed in the liver, kidney and thyroid gland and is responsible for generating approximately 33% of the T3 in the serum in euthyroid and hypothyroid patients, but 67% in hyperthyroid patients. |
|
|
Term
|
Definition
expressed in skeletal muscle, the
brain, pituitary brown adipose tissue and placenta. Skeletal muscle type-2 deiodinase is responsible for generating 67% of the T3 in the serum in euthyroid and hypothyroid patients and 33% of serum T3 in hyperthyroid patients. The type-2 deiodinase is uniquely adapted to increase intracellular concentrations of T3. |
|
|
Term
|
Definition
catalyses the removal of the
inner ring iodine in the 5 position of T4 to generate reverse T3 (rT3). The generation of rT3 is an important initial step in the degradation of T4 by the
liver. |
|
|
Term
|
Definition
| Thyroid hormone receptor splice variant highly expressed in brain, heart and skeletal muscle |
|
|
Term
|
Definition
most highly expressed in liver and
kidney |
|
|
Term
|
Definition
| limited in expression with expression levels being highest in the pituitary and paraventricular neurons of the hypothalamus that produce TRH, in the developing ear and in the developing retina |
|
|
Term
|
Definition
| expressed in the heart, kidney, liver and cerebral cortex, but not in the pituitary. |
|
|
Term
| Resistance to Thyroid Hormone |
|
Definition
| dominant genetic disorders that are associated with point mutations of thyroid hormone receptors. At the level of the pituitary the mutant TR is nonresponsive to thyroid hormone. Thus, TSH is not suppressed and stimulates the thyroid gland to make more T4 and T3. Despite this, patients may show signs of hypothyroidism because the mutant TRs do not bind thyroid hormone or fail to release coprepressors or to bind to coactivators when thyroid hormones bind. |
|
|
Term
|
Definition
| Selective estrogen receptor modulator, blocks estrogen receptor on breast and endometrium which decreases breast cancer and endometriosis, Has activating effects on bone, fat and blood which stabolize bone, lower LDL cholesterol but increase thromboembolism risk by 3X. |
|
|
Term
| Calcitriol’s Effects on Calcium |
|
Definition
| Calcitriol’s Net Effects: ↑↑[Ca++] & ↑↑[PO4=]. Reabsorption of both in the kidneys. Absorption of Ca in GI tract, + effect on PTH stimulating bone resorbtion. |
|
|
Term
| Rx Osteodystrophy due to chronic renal disease |
|
Definition
paricalcitol or doxercalciferol.
Vit D analogues [already covered re: ESRD]
• They don’t require renal activation
• They don’t stimulates GI Ca++ absorption & are unlikely to cause hypercalcemia. |
|
|
Term
| Type I vitamin‐D dependent rickets |
|
Definition
selective deficiency in 1‐α hydroxylation activity in
kidney; Rx: lots of vit. D or a little calcitriol |
|
|
Term
| Type II vitamin‐D dependent rickets |
|
Definition
| point mutations in calcitriol receptor; only possible Rx involves massive calcitriol |
|
|
Term
| RX of Postmenopausal Osteoporosis |
|
Definition
| an estrogen agonist + Ca++ + vitamin D |
|
|
Term
|
Definition
| main problem is low calcitriol because of deficient 1‐α hydroxylation in kidney; lots of vit. D or a little calcitriol or hytakerol |
|
|
Term
|
Definition
teriparatide: • Used for ddx of true & pseudohypoparathyroidism (Orphan drug
status) but not used for Rx of hypoparathyroidism
• Used for osteoporosis in patients at high risk of fracture or in those
refractory to other Rx
– The newly formed bone is strong & closely resembles normal bone.
– Its paradoxical effects are due to its intermittent dose regimen. When
given SC once daily along with calcium and vitamin D, it increases bone
formation by stimulating osteoblast activity.
• Unfortunately,
– It has to be given parenterally.
– It is expensive.
– Its effect isn’t additive with bisphosphonates. |
|
|
Term
| Calcitonin’s Effects on Calcium |
|
Definition
| Calcitonin’s Net Effects: ↓↓[Ca++] & ↓↓[PO4=]. Increased excretion of both in kidney and decreased bone resorbtion. |
|
|
Term
|
Definition
– Treatment of skeletal remodeling diseases (Paget’s Disease; reduces bone turnover by 30‐50%)
– An adjunct for treatment of serious hypercalcemia
– An adjunct for osteoporosis in women >5 yr postmenopause but not as efficacious in preventing fractures & ↑↑ bone density as the bisphonates |
|
|
Term
|
Definition
Bisphosphonate: P‐C‐P
• **Mechanism of BPs:
– Slows hydroxyapatite crystal
formation/dissolution
– Inhibits osteoclast activity & slows bone resorption (serendipitous!) |
|
|
Term
| Agents act by inhibiting osteoclasts |
|
Definition
– Estrogens
– Calcitonin
– Bisphosphonates |
|
|
Term
| Agents act by stimulating osteoblasts |
|
Definition
– Teriparatide (Forteo, PTH)
– Statins (only investigational) |
|
|
Term
| Hyperthyroidism - Rarer Causes |
|
Definition
• Exogenous Iodine - Jod-Basedow phenomenon
• Amiodarone - Mechanisms .. Thyroiditis>> Iodine Excess
• Interferon alpha - Autoimmune thyroiditis
Factitious - Thyroid Hormone, Hamburger!
• HCG Induced - Hyperemesis gravidarum,
Hydatidiform mole, Choriocarcinoma, Ovarian hyperstimulation
• Ectopic - Struma Ovarii, Metastatic thyroid carcinoma
• Central - TSH adenoma, RTH |
|
|
Term
|
Definition
|
|
Term
|
Definition
| Secondary hyperthyroidism |
|
|
Term
| RX of Hyperthyroidism due to Toxic Adenomas |
|
Definition
|
|
Term
| RX of Hyperthyroidism due to Thyroiditis |
|
Definition
Treatment is symptomatic
• ß-Blockers
• Analgesics
• Occasionally Steroids |
|
|
Term
| RX of Hyperthyroidism due to Amiodarone |
|
Definition
• Antithyroidals ±Perchlorate
• Steroids
• Occ. Surgery |
|
|
Term
| RX of Hyperthyroidism due to Grave’s/Toxic MNG |
|
Definition
• I131 Ablation
• Antithyroidals - Methimazole, PTU
• Surgery |
|
|
Term
| Drug-Induced Hypothyroidism |
|
Definition
• Antithyroidals- Methimazole, PTU
• Amiodarone-autoimmune vs. impaired iodination
• Lithium-impaired T4/T3 synthesis, goiter in ~ 50%
• Cytokines-Risks higher if TPO-ab +ve
• SSRIs e.g. Sertraline (Zoloft), and some Tricyclics, Mechanism ? Increased clearance of T4
• Retinoids (used to treat certain leukemias), Mechanism - Central suppression of TSH |
|
|
Term
| Evaluation of Euthyroid patient with Thyroid Nodules!!! Important |
|
Definition
fine needle aspiration biopsy is the
diagnostic procedure of choice. In most cases cytology will allow categorization of a thyroid nodule as benign 28 or malignant. The majority of all thyroid nodules are benign. Indeterminate aspirates will require additional evaluation such as radioisotope scanning. Hyperfunctional
nodules are usually benign, cold
indeterminate nodules are surgically removed because there is a 30% chance of malignancy. |
|
|
Term
| Evaluation of hyperthyroid patient with Thyroid Nodules!!! Important |
|
Definition
| radioisotope scanning is done initially because hyperactive nodules are invariably benign. If nodules are hypoactive in a hyperthyroid patient, then fine needle aspiration biopsy should be performed. Most malignant thyroid neoplasms are tumors that arise from thyroid follicular cells. The most common thyroid malignancy is papillary carcinoma, followed by follicular carcinoma. The mainstay of treatment for thyroid malignancies is surgery, I131 ablation of remnant thyroid tissue and TSH suppression with thyroid hormone. |
|
|
Term
|
Definition
| In individuals who are acutely ill, numerous abnormalities in thyroid levels can occur that do not necessarily mean that patients are hypo or hyperthyroid. For example increased glucocorticoids can suppress TSH production, and reduce the peripheral conversion of T4 to T3. Therefore reduced TSH and increased free T4 in this situation could be confused with indicating primary hyperthyroidism. The bottom line is that thyroid testing should be avoided in acutely ill patients unless there is a strong suspicion for the existence of underlying thyroid disease. |
|
|
Term
|
Definition
| Patients can be hyperthyroid for a couple of months and then hypothyroid for a couple of months before returning to normal. |
|
|
Term
| When might you measure T3? |
|
Definition
• T3 toxicosis
• F/U of some Graves pts who may have nl. FT4 but persistently T3
• Increased FT4 with nl. TSH as occurs 2º to unusual binding abnormalities such as FDH, or decreased T4-T3 conversion e.g. amiodarone, propranolol. T3 would be
normal
• In non-thyroidal illness T3 is invariably very low 2º to
marked inhibition of peripheral de-iodinases that convert T4-T3 |
|
|
Term
| What does a high T3 resin uptake (T3RU) mean |
|
Definition
| It means that a lot of the binding sites are occupied by T4 and so more of the radioactive T3 added to the assay will bind to the resin. This happens in hyperthyroidism or when total TBG is decreased. |
|
|
Term
|
Definition
• Hereditary (X-linked)
• *Estrogen Induced e.g. Oral Contraceptives, HRT, Tamoxifen
• Estrogen secreting tumors
• *Hepatitis (acute, chronic-active)
• *HIV Infection
• Drugs (clofibrate, 5-fluorouracil, phenothiazines)
• Myxedema (small increase) |
|
|
Term
|
Definition
• Hereditary TBG deficiency
• *Severe hypoproteinemia e.g. nephrotic syndrome, hepatic cirrhosis
• *Severe malnutrition
• Severe Illness
• Drugs (androgens,phenytoin, Lasparaginase, nicotinic acid, phenylbutazone)
• Thyrotoxicosis (small decrease |
|
|
Term
| Feedback hormones for FSH, LH and GH |
|
Definition
FSH: inhibin
LH: Sex steroids
GH: IGF-1 |
|
|
Term
| TRH causes the release of what hormones from the anterior pituitary |
|
Definition
|
|
Term
| Somatostatin has what effect on hormone release from the ant. pituitary |
|
Definition
| Inhibits GH and TSH Release |
|
|
Term
|
Definition
• Screening:
– Random GH levels (may be normal)
– IGF-1
– IGFBP-3
• Definitive:
– GH suppression following oral glucose loading |
|
|
Term
|
Definition
production is stimulated by GH
• Provides another dimension of regulation
– IGFBPs both augment IGF activity and retard the metabolic clearance of IGFs |
|
|
Term
| IGFs are structurally similar to what hormone |
|
Definition
|
|
Term
|
Definition
Sleep
exercise
physiologic stress
fasting/hypoglycemia
sex steroids
Alpha-agonists (Norepinephrine)
Beta-blockers |
|
|
Term
|
Definition
Glucose Loading
Beta-agonists (Epinephrine)
Alpha-blockers (Phentolamine)
Emotiomal/psychogenic stress
Nutrition deficiency
Insulin deficiency
Thyroxine deficiency |
|
|
Term
|
Definition
• Transsphenoidal adenomectomy
– Debulking
• XRT or other forms of ionizing irradiation
• Somatostatin analogs
– Octreotide
• Dopaminergic agonists
– Bromocriptine, cabergoline
• GH receptor antagonists
– Pegvisomant |
|
|
Term
|
Definition
|
|
Term
| TESTS FOR GROWTH HORMONE SECRETION |
|
Definition
• Basal levels:
– GH, IGF-1, IGFBP-3
• Stimulated:
– Arginine
– Insulin
– GHRH
– Estrogen/beta-blockers; L-DOPA
• Suppression:
– OGTT |
|
|
Term
|
Definition
| By augmenting endogenous amylin, pramlintide aids in the absorption of glucose by slowing gastric emptying, promoting satiety via hypothalamic receptors (different receptors than for GLP-1), and inhibiting inappropriate secretion of glucagon, a catabolic hormone that opposes the effects of insulin and amylin. |
|
|
Term
| In the resting state, which organ utilizes the most glucose |
|
Definition
|
|
Term
| Pancreatic polypeptide (PP) |
|
Definition
release is largely neurally mediated.
Sensing of food in the CNS causes vagal nerve-mediated secretion, and presence of food in the proximal GI tract also stimulates release. PP affects GI motility, secretory activity of the stomach, intestine, and pancreas, and in some species affects the release of other hormones such as somatostatin. |
|
|
Term
|
Definition
enhances insulin secretion,
decreases gastric motility (with resulting satiety and weight loss), and
increases B-cell mass. |
|
|
Term
| What stimulates glucagone release |
|
Definition
| Amino acids, exercise, and catecholamines. |
|
|
Term
| Effects of an all protein on insulin and glucose production |
|
Definition
will stimulate both
glucagon and insulin; the insulin will result in enhanced glucose disposal but
in this case glucagon will increase hepatic glucose production to prevent
hypoglycemia. |
|
|
Term
| Role of glucagon in the fasting state |
|
Definition
• Glucagon is the primary hormone determining the blood glucose concentration in the postabsorptive state through its stimulation of hepatic glycogenolysis and, after more prolonged fasting, gluconeogenesis
• Basal glucagon secretion accounts for approximately 75% of hepatic glucose output, with most of the rest dependent on catecholamines.
• With prolonged fasting, glucagon also facilitates the utilization of fatty acids for oxidation by the liver |
|
|
Term
| What is responsible for GLUT4 translocation to the plasma membrane during exercise? |
|
Definition
|
|
Term
| Which glucose transporter acts as a sensor? Which cells express this transporter? |
|
Definition
| The liver and beta cells’ GLUT2 has a low affinity for glucose, allowing those tissues to sense and respond to graded levels of serum glucose. |
|
|
Term
| Insulin receptor isoforms |
|
Definition
| There is an alternately spliced isoform of the IR that has a lower affinity for insulin. It is expressed in the liver and acts as a sensor that allows a graded response to higher portal insulin concentrations. |
|
|
Term
| Insulin pathway leading to GLUT4 translocation |
|
Definition
insulin receptor phosphorylates
docking proteins, Insulin Receptor Substrates (4 family members with tissue specific expression, IRS-1 to -4), that then associate with the insulin receptor. IRS proteins, in turn, bind to the srchomology 2 (SH2) domains of signaling molecules
such as phosphatidylinositol 3'-kinase (PI3K), recruiting them to the membrane where they are phosphorylated and activated. |
|
|
Term
| Shc, PI3kinase and CAP/cbl |
|
Definition
Shc mediates mitogenic signaling of
insulin. PI3kinase and CAP/Cbl promote translocation and activity of the glucose tranporter-4 (GLUT-4), which is expressed primarily in skeletal and cardiac muscle and adipocytes. |
|
|
Term
| Glucokinase vs Hexokinase |
|
Definition
| Glucokinase is found in Beta cells and increases glucose phosphorylation in a more gradual manner allowing for a similarly graded insulin response. |
|
|
Term
|
Definition
• Fasting blood sugar on two occasions of 126 mg/dl (7 mM) or greater; or
• A blood sugar of greater than 200 mg/dl 2 hours after a 75 g oral glucose load (glucose tolerance test); or
• Any random (postprandial) sugar of greater than 200, in association with the typical symptoms of polyuria, polyphagia, and weight loss. |
|
|
Term
| Treatment Principles for DKA |
|
Definition
• Hydration (normal saline initially) with monitoring
• Insulin (parenteral): gradual correction (100mg/dl/hr), adding glucose when level
approaches 200-250.
• Electrolytes (particularly K+)
• Search for precipitating event. |
|
|
Term
| How HDL is destroyed in diabetes |
|
Definition
CETP stimulates the transfer of
triglycerides from VLDL to HDL in exchange for cholesterol esters from HDL. The resulting triglyceride-enriched HDL becomes an excellent substrate for another enzyme, hepatic lipase (HL). As HL hydrolyzes the triglycerides from HDL, HDL becomes smaller and begins to shed a portion of its surface including apo-A1 which is essential for reverse cholesterol transport. End result is atherosclerosis |
|
|
Term
| The genesis of small, dense LDL |
|
Definition
| CETP exchanges cholesterol esters from LDL for triglycerides from VLDL. The resulting triglyceride-enriched LDL becomes a substrate for HL, and as the triglycerides are hydrolyzed, the LDL particle becomes smaller and denser. |
|
|
Term
|
Definition
• Vastly more atherogenic than “normal”
LDL particles
– Lower affinity for the LDL receptor
– Prolonged circulating T½ in comparison (5 days
vs 2 days)
– Interacts more strongly with arterial wall
– Readily oxidized |
|
|
Term
|
Definition
Function: Activate LCAT; ABCA-1.
Production site: Intestine; Liver
Lipoprotein location: HDL
Gets pushed of and cleared by kidney when triglycerides get too high. Loss of A-1 Makes HDL unable to participate in reverse cholesterol transfer |
|
|
Term
|
Definition
| Located in the liver, functions to assemble VLDL amd LDLr recogntion, and is located on VLDL and LDL |
|
|
Term
|
Definition
| Removes triglycerides and phospholipids from CM and VLDL remnants |
|
|
Term
| Cholesterol ester transfer protein (CETP) |
|
Definition
| Exchanges triglycerides in VLDL and CM (plus remnants) for cholesterol esters in HDL and LDL |
|
|
Term
|
Definition
| refers to the inhibitory effects of chronic elevations of FFA (free fatty acids) (commonly found in obese DM 2s) on insulin action in liver and muscle by inhibiting the entry of fructose-6-phosphate into the glycolytic pathway with shunting toward the formation of hexosamine-6-phosphate into the HBP as with glucose toxicity. Also, elevated FFA’s increase PEPCK (phospho-enolpyruvate carboxykinase) gene expression stimulating hepatic gluconeogenesis. |
|
|
Term
|
Definition
| refers to the inhibitory effects of chronic hyperglycemia on insulin secretion and action. Increased flux of glucose through the hexosamine biosynthetic pathway (HBP) inhibits multiple sites in the insulin signaling cascade. |
|
|
Term
What part of the brain is involved in
reg-ulation of food intake and thermogenesis |
|
Definition
ventromedial hypothalamus is involved in
reg-ulation of food intake and thermogenesis. This control is subject to multiple inputs: vagal, hormonal and nutrient. |
|
|
Term
|
Definition
| Fasting or any other drive to feeding causes NPY to increase, and refeeding causes it to fall back down again. At least part of the latter is signaled by insulin in the CNS. However, NPY knockout mice have nearly normal feeding behavior, so there must be other parallel and/or dominant pathways as well. |
|
|
Term
| Melanocyte Stimulating Hormone (MSH) |
|
Definition
| acts as a negative control on appetite to balance the positive effects of NPY. Binds to the melanocortin 4 receptor. |
|
|
Term
|
Definition
leptin acts in the CNS to reduce appetite, at least partly by decreasing NPY levels.
4. Leptin also has peripheral effects to
increase lipolysis and lipid oxidation and reverse hyper-insulinemia that work in parallel with the decreased food intake to prevent further weight gain.
5. Finally, leptin has interactions with other endocrine systems that allow a coordinated response to the availability (or lack thereof) of food. For example, the decrease in fertility seen in starvation can be explained, at least in part, by the interaction of leptin with the gonadotrophin system. |
|
|
Term
| DEFINITION OF HYPOGLYCEMIA |
|
Definition
WHIPPLE’S TRIAD
• 1. Low blood sugar--no absolute level at which a low sugar is or is not pathologic. In general, levels below 50 are abnormal is men, below 45 in women. In infants, levels below 50 are watched, below 40 are treated and investigated.
• 2. Symptoms--adrenergic and neuroglycopenic although beware that over time, some systems accommodate to low blood sugar and the symptoms can become more and more subtle
• 3. Prompt resolution of symptoms with glucose administration |
|
|
Term
| Adrenergic Response to Hypoglycemia |
|
Definition
1. Epinephrine stimulates hepatic glucose production, activates production
of alternate fuels (lipolysis, free fatty acid production) and limits glucose utilization.
• 2. Symptomatically, the subject notices anxiety, palpitations, tremor,
hunger, and sweating.
• 3. Threshold is usually at glucose of 60-70, but can change |
|
|
Term
|
Definition
| At glucose levels below 30-40, however, brain function slows and the subject experiences headache, confusion, fatigue, eventually strange behavior, coma, convulsions, and death. |
|
|
Term
|
Definition
• Decreased glucose production
– Liver damage
– Inborn errors
– Drugs and toxins
• Increased utilization
– Too much insulin--fasting hypoglycemia
– Inappropriate matching of insulin to food absorption--reactive hypoglycemia |
|
|
Term
| Practical Approach to Hypoglycemia, ill nondiabetic patient, post prandial, or only during fasting. |
|
Definition
• In an acutely ill, nondiabetic person
– Usually due to decreased glucose production
• In a healthy person, always after meals
– Usually benign and/or physiologic
• In a healthy person, in the fasted state
– Almost always pathologic and worth investigating; consider insulinoma |
|
|
Term
Hypoglycemia in Diabetes
• If a previously well-controlled diabetic starts having hypoglycemia, |
|
Definition
consider a second intervening problem.
– Renal failure--decreased insulin clearance and decreased gluconeogenesis
– Hypothyroidism--decreased insulin requirement
– Adrenal failure--lack of cortisol
• In type 1 diabetes there is a higher incidence of other autoimmune endocrinopathies including primary adrenal failure and hypothyroidism.
– Weight loss--increased insulin sensitivity--can be either a good
thing (finally getting with the program) or a bad thing (e.g. cancer
or HIV or TB) |
|
|
Term
Hypoglycemia in Diabetes
• If someone with diabetes recently diagnosed and treated starts having hypoglycemia |
|
Definition
consider resolution of “glucose toxicity.”
– Hyperglycemia in and of itself causes insulin resistance and "poisons" the beta cell in terms of its ability to secrete insulin. |
|
|
Term
|
Definition
| synthesized by the liver and is found in chylomicrons, VLDL, IDL, and HDL lipoproteins. Its main function is to activate capillary lipoprotein lipase. |
|
|
Term
|
Definition
| synthesized by the liver and is necessary for the hepatic assembly and secretion of VLDL. It is the major structural protein of VLDL (30%), IDL (60%), LDL (90%) and acts as a ligand for the LDL receptor |
|
|
Term
|
Definition
| produced in the small intestine and is the key structural protein for chylomicrons and is a product of the same gene that encodes apo B-100. It is found exclusively in chylomicrons and their remnants. |
|
|
Term
|
Definition
| ligand for binding of several lipoproteins to the LDL receptor and to the LDL receptor-related receptor. This apolipoprotein is found in chylomicrons, VLDL, IDL and HDL lipoproteins. The gene for apo E has three major alleles that differ in DNA sequence and in amino acid composition. Apo E- 3 is associated with normal VLDL and LDL metabolism. Apo E-2 cannot bind well to the LDL receptor and its presence, particularly in the homozygous state, can be associated with the accumulation of cholesteryl ester-enriched VLDL. Interestingly, Apo E-4 is associated with high risk of Alzheimer’s disease. |
|
|
Term
|
Definition
| synthesized in both the liver and small intestines. It is the major structural complement of HDL (75% of protein mass). It works together with LCAT to esterify free cholesterol on the surface of HDL particles. The cholesteryl esters can then be packed into the HDL core. It plays a critical role in reverse cholesterol transport. |
|
|
Term
|
Definition
High levels of lipoprotein(a) are an
independent risk factor for premature cardiovascular disease. Lipoprotein (a) occurs when apo(a) is covalently bonded to apo B100 of an LDL particle. The amino acid sequence of apo(A) is similar to the sequence of plasminogen. |
|
|
Term
| Lecithin-Cholesterol Acyltransferase (LCAT) |
|
Definition
| requires apoA-I as a cofactor. It converts free cholesterol on the surface of HDL particles into cholesteryl ester. The newly formed cholesteryl esters sink to the core, allowing the HDL particle to sponge up more free cholesterol on its surface. The esterified cholesterol can be transferred to VLDL and LDL particles. |
|
|
Term
| Cholesteryl Ester Transfer Protein (CETP) |
|
Definition
| mediates the exchange of triglycerides from VLDL and chylomicrons particles with cholesteryl esters from HDL. This is important in reverse cholesterol transport. |
|
|
Term
Low Density Lipoprotein Receptor-Related
Protein (LRP) |
|
Definition
Like the LDL receptor, LRP is a cell
surface receptor that is internalized once it is occupied. It is expressed primarily in liver, neurons and placenta and is involved in the clearance of apo E-enriched chylomicron remnants and VLDL remnants. LRP does not bind LDL. |
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Term
|
Definition
| HDL deficiency. Orange tonsils (secondary to deposition of cholesterol in reticuloendothelial tissues), cloudy corneas, lymphadenopathy and occasionally, peripheral neuropathy are seen with patients with this condition. This condition should be suspected when total plasma cholesterol is below 120 mg/dL. HDL levels are 2-5% of normal. The defect has been linked to a mutation in the ABC1 transporter. ApoA-I interacts with the ABC1 transporter on macrophages (and other cells) to facilitate the efflux of cholesterol. If the transporter is defective, nascent HDL particles are poorly lipidated. Poorly lipidated HDL particles are rapidly metabolized, thus leading to low HDL levels and a slight increase in CAD |
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Term
| Primary adrenal insufficiency |
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Definition
– Defect in adrenal gland
– Dx: ↓cortisol ↑ ACTH
– Treat: glucocorticoids, mineralcorticoids, ± androgens |
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Term
| Secondary/tertiary adrenal insufficiency |
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Definition
– Defect centrally
– DX: ↓ cortisol ↓ ACTH
– Treat: glucocorticoids |
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Term
| Drugs that Inhibit cortisol synthesis |
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Definition
| ketoconazole, metyrapone, etomidate |
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Term
| Drugs that lead to Accelerated cortisol metabolism |
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Definition
| phenytoin, barbiturates, rifampin |
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Term
| Gold standard for hypercortisolism |
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Definition
|
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Term
| The clinical features listed below should provoke biochemical screening for hypercortisolism |
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Definition
• Abnormal fat distribution – Mid abdominal with thin limbs, supraclavicular and temporal region. “Lemon on Match Sticks”
• Proximal muscle weakness.
• Wide (>1 cm) purple striae.
• Failure of a child to grow in the height chart, with normal (or excess) weight gain.
• Atraumatic or low trauma fractures in
individuals with little or no risk for thin bones.
• Hypertension in young individuals.
• Cutaneous atrophy in young individuals.
• Inexplicable bone loss in males. |
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Term
| Inferior Petrosal Venous Sinus Sampling |
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Definition
| MRI scans detect corticotroph adenomas in about 50 – 60% of the time. If the adenoma is invisible on sellar MRI, the next step in the detection of the site of over production is by inferior petrosal venous sinus sampling. |
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Term
| Endocrine causes of hypertension |
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Definition
Pheochromocytoma and paraganglionomas
Primary hyperaldosteronism
Cushing’s disease and syndrome
2) Apparent Mineralocorticoid Excess:
Genetic: Type 1 AME and Type 2 AME
Acquired: Licorice and Carbenoxalone
3) Thyroid disease: Hyperthyroidism (systolic hypertension)
and Hypothyroidism (diastolic hypertension)
4) Parathyroid: Primary hyperparathyroidism.
5) Pituitary disease: Acromegaly and Cushing’s. |
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Term
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Definition
| Can be Similar in manifestation to pheochromocytoma but they only are able to produce NE |
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Term
| Etiology of primary hyperaldosteronism |
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Definition
1) Aldosterone producing adenoma:
Approximately 30 – 60 % of patients
have solitary adenomas. Surgical
excision is the treatment of choice.
2) Bilateral adrenal hyperplasia: Generally causes milder disease and is treated with medications.
3) Familial hyperaldosteronism
a. type I – ACTH dependent production of aldosterone from the zona fasiculata due to CYP11B2 mutation resulting in a fusion gene between the aldosterone synthase and ACTH response element. Due to ACTH mediated hypersecretion,
hypertension in this subset of
patients is ameliorated by the use
of dexamethasone.
b. type II – ACTH independent
familial type and therefore not
dexamethasone responsive. |
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Term
| Apparent mineralocorticoid excess (AME) |
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Definition
| Mutations of 11 β HSD type 2 result in hypertension and AME syndrome. There is a mutation specific severity of the enzymatic defect and the severity of inhibition of cortisol to cortisone conversion and the manifestation of the clinical syndromes. Can be caused by licorice. |
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Term
| Caveats regarding adrenal incidentalomas |
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Definition
1) Rule out pheochromocytoma even if you
choose not to operate.
2) If cortisol is secreted even in a subclinical manner, replace cortisol orally following resection of the adrenal incidentaloma. The adrenal axis (hypothalamus, pituitary and the contralateral adrenal gland will be suppressed by the excess cortisol).
3) Never attempt needle biopsy of adrenal masses without ruling out pheochromocytoma. |
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Term
| Adrenal incidentaloma evaluation |
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Definition
| if it's > 6 cm or secreting always remove. if it;s 4-6 cm <10 HU consider removing. Anything smaller just observe and recheck for secretion/increase in size. |
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Term
| Vast majority of Hyperaldosteronism is due to |
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Definition
|
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Term
| Glucocorticoid responsive hypertension |
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Definition
| %5 of primary aldosteronism, due to a Fusion gene between ACTH response element And aldosterone synthase gene. ACTH = increased aldosterone. |
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Term
|
Definition
| Osteoclasts express RANK are activated by RANKL and blocked by OPG (secreted by osteoblasts) |
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Term
| Effects of Vit D in the gut |
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Definition
Vitamin D mediates GI calcium &
phosphate absorption |
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Term
|
Definition
Activates PLC, PLD, PLA2
Stimulation of PLC leads to activation of PKC and ITP, which releases intracellular calcium
CSR is found in parathyroid, renal tubules, bone, GI and c-cells
Cell membrane G protein receptor (intra, extra and cell membrane domains
Calcium binds to the extracellular domain |
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Term
|
Definition
Hydroxyproline
N telopeptides
C telopeptides
Cross links
TRAP |
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Term
|
Definition
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Term
| Osteoblasts, osteoclast and their receptors |
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Definition
Osteoblasts:
PTH receptor
Active Vit D receptor
Estrogen receptor
Alkaline phosphatase
Secrete OPG and RANK L
Osteoclasts:
4-20 nuclei
RANK (receptor for RANKL)
Calcitonin receptor
Not thought to have PTH or vit D receptor
PTH acts on blasts and the blasts communicate to the osteoclasts. |
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Term
| Stimulates bone resorption |
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Definition
PTH
PTHrP
1,25(OH)2D
Prostaglandins
Interleukins
Cytokines
Paracrine factors (RANKL) |
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Term
|
Definition
Estrogen
Androgens
Bisphosphonates
Calcitonin
Osteoprotegerin |
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Term
| Stimulates bone formation |
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Definition
IGF-1
IGF-2
Bone-derived growth
factors
Sex steroids
PTH
Mechanical stress |
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Term
|
Definition
|
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Term
| Calciopenic rickets: Vit D dependent type 1 |
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Definition
AR inheritance, presents before 2nd year of life. High PTH
a. Defect in renal hydroxylation to 1,25(OH)2D
b. Findings: normal 25(OH)D, low 1,25(OH)2D levels
c. Controlled with very high
dose 1,25(OH)2D supplementation |
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Term
| Calciopenic rickets: Vit D dependent type 2 |
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Definition
a. Findings: low calcium, very high 1,25(OH)2D levels; alopecia. high PTH
b. Don’t respond to 1,25(OH)2D
c. Treat with increased dietary calcium |
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Term
| Hypophosphatemic (“vitamin D resistant”) Rickets |
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Definition
Pretty much all the subtypes (except HHRH) lead to increase in FGF23 activity which inhibits a NaPO4 cotransporter and leads to lack of reabsorption in the kidneys.
HHRH is a defect in the cotransporter itself.
Proximal tubular defect causing renal
phosphate wasting
Multiple forms, vary by point where defect in regulation of renal phosphate reabsorption occurs
Common findings: HTN, bone pain, growth stunting, low phosphate
Tx: phosphate, 1,25(OH)2D |
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Term
| X-linked hypophosphotemia rickets |
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Definition
PHEX (Phosphate regulating Endopeptidase on the Xchromosome) mutation
a. See dentin defects leading to
abscesses and tooth decay |
|
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Term
| ADHR - Autosomal dominant hypophosphotemia rickets |
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Definition
FGF23 (Fibroblast growth factor 23) gain
of function mutation |
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Term
|
Definition
| Autosomal recessive: inactivating mutations in DMP1 (Dentin matrix protein 1) resulting in defective osteocyte maturation and increased FGF23 |
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Term
| Treatment of any hypophosphotemia rickets |
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Definition
|
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Term
|
Definition
Paraneoplastic syndrome causing renal
phosphate wasting
Mixed connective tissue tumors most common |
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Term
|
Definition
Abnormal activity of alkaline phosphatase
Clinical findings: osteomalacia/rickets, premature loss of teeth, metatarsal fractures
Biochemical findings: low alk phos levels |
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Term
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Definition
Large, highly active osteoclasts
Excessive resorption → intense ↑ in osteoblastic activity
Formation of chaotically patterned collagen fibers
“ woven bone”
Elevated alk phos & urinary hydroxyproline |
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Term
| Treatment of Paget's disease |
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Definition
Bisphosphonates
To normalization of alkaline phosphatase
To control pain
To prevent fracture/deformity at high-risk sites |
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Term
| Who should be screened for osteoperosis |
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Definition
Women ≥65 y/o
Women 60-65 + multiple RFs
Height loss, prior fragility fracture, etc.
Men/premenopausal women with
secondary causes/fragility fracture |
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Term
| Who to treat for osteoperosis |
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Definition
Postmenopausal women and men 50+
T-score -2.5 or worse
Hx of fragility fracture
T-score -1.0 to -2.5 and:
1. ≥3% 10-year probability of hip fracture or
2. ≥20% 10-year probability of major osteoporotic fx
Probability calculated by FRAX |
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Term
| Treatment for osteoperosis |
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Definition
Calcium and vitamin D
Antiresorptives:
Bisphosphonates
SERMS
Anabolic:
teriparatide |
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Term
| Correction for Ca according to protein concentration |
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Definition
Add 0.8 mg per dl to total calcium for every gram of albumin <4.0 and subtract 0.8 mg per dl from measured calcium level for each gram of
albumin >4 grams. |
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Term
| Indications for surgery to treat PHPT |
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Definition
1. Serum calcium levels >11.5 mg per
dl on at least 2 determinations.
2. Urinary calcium level of >400 mg in
24 hours or urine random calcium to
creatinine ration of > or equal to 0.4
on 2 determinations.
3. Creatinine clearance that has dropped >30% (unexplained by 98 other reasons) corrected for age and sex.
4. Loss of bone density >-2.5 standard
deviations below young normal (Tscore)
, cortical bone is preferentially lost in PHPT- e.g.;
wrist and hips)
5. Age <50 years of age. |
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Term
| Important points for Primary Hyperparathyroidism |
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Definition
• Insidious onset and gradual progression
• Kidney stones in 20-30 %
• Bone loss – cortical > trabecular bone
• Surgery is the only definitive
management
• Single gland tumor is common (85%) |
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Term
Familial hypocalciuric hypercalcemia
(FHH) |
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Definition
Due to a genetic defect in the calcium sensing receptor
• Low urine calcium
• No end-organ damage
• Multiple family members are affected
• Mild elevation of magnesium
• No surgery |
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Term
Secondary and Tertiary
hyperparathyroidism (SHPT and THPT): |
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Definition
| Usually due to chronic renal failure. No Vit D + renal failure = High PO4 and low Ca. PTH glands eventually become hyperplastic and autonomous which leads to high Ca and PO4. Treat with Vit D and Cinacalcet(activates Ca receptor to lower PTH levels etc..) |
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Term
| Parathyroid related polypeptide (PTHrp) |
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Definition
| PTHrp is secreted by normal lactation human breast. This can induce hypercalcemia in breast feeding mothers and resolves promptly after cessation of breast feeding. Can also be produced in paraneoplastic syndrome. Doesn't full activate Vit D |
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Term
| Drugs related to hypercalcemia |
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Definition
Hydrocholrothiazide and lithium are
the commonest of drugs inducing
hypercalcemia. HCTZ enhances distal tubular calcium absorption. Lithium affects formation of IP3 there by upsetting the CASR function (similar to that of FHH). Tamoxifen can cause severe hypercalcemia in patients with bony metastasis. |
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Term
| Which end of PTH is active, N or C terminal |
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Definition
|
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Term
|
Definition
impairs PTH secretion and PTH action leading to hypocalcemia, Malabsorption, chronic alcoholism, and cisplatin
therapy are currently the most common causes of hypomagnesemia |
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Term
| CONGENITAL HYPOPARATHYROIDISM |
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Definition
| most common form of genetic hypoparathyroidism is autosomal dominant hypocalcemia. In it, hypocalcemia is mild to moderate, urinary calcium excretion is high and serum PTH is inappropriately low. Activating mutations in the calcium-receptor gene causes it |
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Term
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Definition
| present with hypocalcemia and hyperphosphatemia, and elevated PTH levels from resistance to all the actions of PTH. Two types of pseudohypoparathyroidism have been described. |
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Term
| Type 1 — Pseudohypoparathyroidism |
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Definition
diminished cyclic AMP response to
PTH. Two types have been described (type 1a and 1b) as well as pseudopseudohypoparathyroidism, and the
gene encoding the stimulatory Gs-alpha-one protein of the adenylyl cyclase complex (GNAS1) appears to be involved in all cases. |
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Term
| Type 1a Pseudohypoparathyroidism |
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Definition
mutation in the stimulatory Gsalpha-
one protein of the adenylyl cyclase complex (GNAS1). They often have round facies, short stature, and short metacarpal and metatarsal bones (Albright's hereditary osteodystrophy). The hyperphosphatemia induced by the renal defect causes hypocalcemia and, thereby, secondary hyperparathyroidism and hyperparathyroid bone disease (osteitis fibrosa). |
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Term
| pseudopseudohypoparathyroidism |
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Definition
| With paternal transmission of a mutated GNAS1 gene, Albright's hereditary osteodystrophy occurs without hypocalcemia, since the normal maternal allele results in the maintenance of renal responsiveness to PTH |
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Term
|
Definition
| hypocalcemia but do not have the phenotypic abnormalities described above. The PTH resistance is apparently confined to the kidney in this disorder, leading to hypocalcemia, hyperphosphatemia, and secondary hyperparathyroidism but not Albright's hereditary osteodystrophy. |
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Term
| THERAPEUTIC USES OF ANDROGENS |
|
Definition
• HRT in primary or secondary hypogonadism
• Induction of puberty in delayed
maturation
• Rx of osteoporosis in males |
|
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Term
THERAPEUTIC USES OF ANDROGENS IN
WOMEN |
|
Definition
• Adjunct in HRT in menopause (e.g.,
methyltestosterone)
• Danazol: endometriosis in women |
|
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Term
| THERAPEUTIC USES OF ANABOLIC STEROIDS |
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Definition
• Rx of anemias (nandrolone)
• Rx of hereditary angioedema
(stanozolol)
• Stimulate weight gain after surgery,
infection, AIDs (oxandrolone) |
|
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Term
| CONTRAINDICATIONS TO USE OF ANDROGENS |
|
Definition
• ABSOLUTE:
– known or suspected carcinoma of the prostate or breast
– pregnancy
– age < 13-15 years
– HRT preps are contraindicated in women
• RELATIVE:
– cardiovascular, liver, renal disease
– Rx w/ anticoagulants |
|
|
Term
| Androgen receptor blockers what are they and what uses do they have |
|
Definition
– bicalutamide
– flutamide (concern with hepatotoxicity)
– spironolactone
• Used adjunctively in prostate cancer and to treat acne or hirsutism in women |
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Term
|
Definition
GnRH agonist
• Pro-fertility effects require episodic
administration, mimicking physiology.
• Antifertility effects occur with chronic, nonphysiological regimens.
• Indicated in males for:
– Precocious puberty
– Advanced prostate cancer (w/ bicalutamide or flutamide)
• Adverse effects: impotence, hot flashes |
|
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Term
|
Definition
| Menin gene on Chromosome 10 |
|
|
Term
| What genes are mutated in MENIIa, b, and FMTC |
|
Definition
| RET proto onco gene on chromosome 10q11.2 |
|
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Term
Autoimmune Polyglandular Syndrome Type I
(APS1) |
|
Definition
Never associated with graves disease!APS1 is a rare autosomal recessive
disease that arises due to mutations in the autoimmune regulator (AIRE) gene on
chromosome 21q22.3. The AIRE gene is important in regulating thymic T-cell tolerance to autoantigens and immune system homeostasis.
APS1 manifestations:
Hypoparathyroid.
Oral Candiasis
Addison's disease
primary hypogonadism (45%),
primary hypothyroidism 12%
Nonendocrine – malabsorption syndromes, alopecia, pernicious anemia, chronic
hepatitis, vitiligo. |
|
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Term
| Autoimmune polyglandular Syndrome II (APS II): |
|
Definition
Addison's disease with either Hashimoto’s Thyroiditis, or with Type I diabetes mellitus (T1DM). Develops in adulthood, in 30’s or 40’s.
Genetics: APS II is associated with the DR3/DR4 HLA genotype |
|
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Term
| Excessive production of 1,25-OH Vitamin D is usually seen in what type of cancer |
|
Definition
|
|
Term
| What is his yearly risk of developing diabetes if you have prediabetes |
|
Definition
| Patients with prediabetes have a vastly increased risk of progressing to type 2 diabetes---5-10% per year |
|
|
Term
| What are criteria for parathyroid carcinoma |
|
Definition
| Parathyroid carcinoma is rare (<1% of parathyroid masses). Must see mitotic figures and invasion (adjacent structures or vessels) or metastases. Serum calcium is often extremely high (>14 mg/dL), and the patients often die from uncontrollable hypercalcemia |
|
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Term
| What are the causes of a false positive overnight dexamethasone suppression test (ONDST)? |
|
Definition
| estrogens, depression, rapid metabolism of dexamethasone, poor night’s sleep, forgetting to take the medication. |
|
|
Term
| Secondary (Acquired) Causes of Dyslipidemia |
|
Definition
Work up with blood sugar, TSH and Urine protein.
1. Diabetes (overproduction of VLDL and reduced LPL)
2. Diabetes (atherogenic or dense LDL)
3. Diabetes (reduced HDL)
4. Insulin resistance (see diabetes)
5. Hypothyroidism (impaired LDL clearance)
6. Nephrotic syndrome (increased TG and LDL)
7. Others |
|
|
Term
| A DIFFERENT ATD: PROPRANOLOL |
|
Definition
• 1° ‐ Beta‐adrenergic Receptor Blocker: slows the heart by blocking the beta receptors (= expected drug effect)
• 2° ‐ Decreases Peripheral Deiodination of Thyroxine:
T3 in plasma falls by up to 20%! (a serendipitous drug effect)
• Its Main Use is in Rx of Thyrotoxicosis: It is the most effective drug and is usually used in combination with a thioamide and/or iodide. |
|
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Term
| Which has higher levels of free hormone in circulation T3 or T4 |
|
Definition
| T3 is six times higher. Half life is 1 day in comparison to T4 half life of 7 days for this very reason. |
|
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Term
| ADVERSE REACTIONS TO ATDs, PTU and Methimazole |
|
Definition
Rash is most common, not for nursing/pregnant moms.
*Agranulocytosis can occur Occurs suddenly in first few months mimicing sore throat/fever. |
|
|
Term
| What blocks the absorption of bisphosphonates? |
|
Definition
| Divalent cations, oral calcium! |
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