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407 Cards in this Set
- Front
- Back
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What are the effects of pheochromocytomas and neuroblastomas on blood pressure?
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Pheochromocytomas cause episodic hypertension whereas neuroblastomas do not.
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The zona fasciculata of the adrenal gland is regulated by _____ and secretes _____.
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Adrenocorticotropic hormone and hypothalamic corticotropin-releasing hormone; cortisol and sex hormones
2010-284 |
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The zona reticularis of the adrenal gland is regulated by _____ and secretes _____.
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Adrenocorticotropic hormone and hypothalamic corticotropin-releasing hormone; sex hormones (eg, androgens)
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What mnemonic helps you remember the three layers of the adrenal cortex and their corresponding products?
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Zona Glomerulosa (salt), Zona Fasciculata (glucocorticoids), Zona Reticularis (sex hormones): GFR corresponds to salt, sugar, and sex ("the deeper you go, the sweeter it gets")
2010-284 |
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The most common tumor of the adrenal medulla in adults is _____, whereas in children it is _____.
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Pheochromocytoma; neuroblastoma
2010-284 |
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The adrenal medulla is primarily regulated by (parasympathetic/sympathetic) fibers and is composed of (chromaffin/chromophobe) cells.
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Sympathetic; chromaffin
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The zona glomerulosa of the adrenal gland is regulated by _____ and secretes _____.
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Renin-angiotensin; aldosterone
2010-284 |
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Trace blood flow from the right adrenal gland to the inferior vena cava.
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Right adrenal gland to the right adrenal vein to the inferior vena cava
2010-284 |
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Which gonadal vein drains directly into the inferior vena cava: the right or the left?
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Right gonadal vein
2010-284 |
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Trace the blood flow from the left adrenal gland to the inferior vena cava.
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Left adrenal gland to the left adrenal vein to the left renal vein to the inferior vena cava
2010-284 |
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What are the secretory products of the anterior pituitary?
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Follicle-stimulating hormone (FSH), luteinizing hormone (LH), adrenocorticotropic hormone (ACTH), thyroid-stimulating hormone (TSH), Prolactin, growth hormone (GH), and melanotropin (remember: FLAT PiG)
2010-284 |
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Which hormones are secreted from basophilic cells?
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Basophils secrete follicle-stimulating hormone (FSH), luteinizing hormone (LH), adrenocorticotropic hormone (ACTH), and thyroid-stimulating hormone (TSH) (remember: B-FLAT)
2010-284 |
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What is the significance of the β subunit of pituitary hormones?
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It determines the hormone specificity of thyroid-stimulating hormone, luteinizing hormone, follicle-stimulating hormone, and human chorionic gonadotropin
2010-284 |
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Which pituitary hormones have a common alpha subunit?
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Thyroid-stimulating hormone, luteinizing hormone, follicle-stimulating hormone, and human chorionic gonadotropin
2010-284 |
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Which hormones are secreted from acidophilic cells?
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Growth hormone, prolactin
2010-284 |
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Where are the secretory products of the posterior pituitary formed?
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In the hypothalamus
2010-284 |
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What does the posterior pituitary gland secrete?
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Vasopressin (antidiuretic hormone) and oxytocin
2010-284 |
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What is the clinical significance of the shared α subunit of thyroid-stimulating hormone, luteinizing hormone, follicle-stimulating hormone, human chorionic gonadotropin?
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At high enough concentrations, a given hormone can partially activate the receptor of another hormone with the same a subunit
2010-284 |
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Embryologically, the posterior pituitary is derived from the _____, whereas the anterior pituitary is derived from the _____.
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Neuroectoderm; oral ectoderm
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What cell types are found in the islets of Langerhans?
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α, β, and δ endocrine cells
2010-284 |
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Where are islets of Langerhans most numerous?
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In the tail of the pancreas
2010-284 |
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In the islets of Langerhans, δ endocrine cells are located _____ and secrete _____.
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Throughout; somatostatin
2010-284 |
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From what embryonic structures do the islets of Langerhans arise?
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Pancreatic buds
2010-284 |
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In the islets of Langerhans, α endocrine cells are located _____ and secrete _____.
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Peripherally; glucagon
2010-284 |
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In the islets of Langerhans, β endocrine cells are located _____ and secrete _____.
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Centrally; insulin (remember: INSide INSulin)
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What causes the exocytosis of insulin from β-cells?
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The influx of calcium, following depolarization of the cell by potassium channel closure
2010-285 |
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What is the effect of insulin on electrolyte (Na+, K+) handling?
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Insulin increases Na+ retention by the kidneys and shifts K+ into cells
2010-285 |
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What effects does insulin have on glucose, protein, and lipid production and storage?
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Insulin increases glucose transport into cells, increases glycogen and triglyceride synthesis and storage, and increases protein synthesis in muscles
2010-285 |
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Which cells do not need insulin for glucose uptake?
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BRICK L: Brain, RBCs, Intestine, Cornea, Kidney, and Liver
2010-285 |
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What is the effect of insulin on α-cells of the pancreas?
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Insulin inhibits glucagon release
2010-285 |
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What effect would a β-cell potassium channel blocker have on the release of insulin?
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Increased insulin release, because potassium channel closure depolarizes the β-cell
2010-285 |
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β-Cells in the pancreas make insulin in response to what cellular process?
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Increased glucose metabolism increases adenosine triphosphate, which closes potassium channels and depolarizes the cell
2010-285 |
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Which cells require insulin for glucose uptake?
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Skeletal muscle and adipose have glucose transporter type 4 (insulin-responsive) glucose transporters (remember: Insulin moves glucose Into cells)
2010-285 |
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Which cells have glucose transporters type 1?
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Red blood cells and brain cells have glucose transporters type 1, which do not require insulin for glucose uptake
2010-285 |
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Insulin release from β-cells is increased by (opening/closing) potassium channels and (opening/closing) calcium channels.
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Closing; opening
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Which cells have bidirectional glucose transporters?
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Those with glucose transporters type 2 channels: β islet cells, liver, kidney
2010-285 |
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What makes adipose and skeletal muscle dependent on insulin for glucose uptake?
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They have insulin-responsive glucose transporters type 4
2010-285 |
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Why are red blood cells and the brain not dependent on insulin for glucose uptake?
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They have insulin-independent glucose transporters (glucose transporter type 1)
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What does the brain use for metabolism under starvation states?
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Ketones made by the liver
2010-285 |
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What do red blood cells use for metabolism under starvation states?
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Glucose; red blood cells only have the glycolysis pathway to make adenosine triphosphate; thus, they cannot use ketones like the brain in starvation states
2010-285 |
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What is the effect of growth hormone-releasing hormone on pituitary hormone secretion?
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It stimulates growth hormone secretion
2010-286 |
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What is the effect of corticotropin-releasing hormone on pituitary hormone secretion?
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It stimulates adrenocorticotropic hormone secretion
2010-286 |
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What is the effect of prolactin on pituitary hormone secretion?
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It inhibits gonadotropin-releasing hormone, which in turn decreases luteinizing hormone and follicle-stimulating hormone secretion
2010-286 |
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What is the effect of gonadotropin-releasing hormone on pituitary hormone secretion?
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It stimulates luteinizing hormone and follicle-stimulating hormone secretion
2010-286 |
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What is the effect of thyrotropin-releasing hormone on pituitary hormone secretion?
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It stimulates thyroid-stimulating hormone and prolactin secretion
2010-286 |
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What is the effect of dopamine on pituitary hormone secretion?
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Inhibition of prolactin secretion
2010-286 |
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What is the effect of somatostatin on pituitary hormone secretion?
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It inhibits growth hormone and thyroid-stimulating hormone secretion
2010-286 |
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Why might bromocriptine be withheld for a woman who is trying to breast feed?
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Bromocriptine is a dopamine agonist, and so it inhibits prolactin secretion
2010-286 |
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A woman has had her thyroid surgically removed and is not taking thyroid hormone replacement. She now complains of amenorrhea; what is the likely cause?
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She has hypothyroidism, which can cause prolactin release and thus amenorrhea
2010-286 |
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How does prolactin provide negative feedback to its own secretion?
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High prolactin levels cause increased dopamine synthesis and secretion by the hypothalamus
2010-286 |
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How does prolactin affect fertility in men?
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It decreases spermatogenesis by inhibiting gonadotropin-releasing hormone synthesis and release
2010-286 |
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A woman being treated for schizophrenia complains of breast fullness and amenorrhea; what is the likely cause?
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Increased prolactin levels secondary to dopamine antagonists (antipsychotics)
2010-286 |
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Why are women less likely to become pregnant when breastfeeding?
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Prolactin inhibits ovulation via the inhibition of gonadotropin-releasing hormone
2010-286 |
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Androstenedione is converted into _____ in the adrenal zona reticularis and into _____ in the periphery.
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Testosterone; estrone
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Which enzyme catalyzes conversion of testosterone to dihydrotestosterone?
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5α-reductase
2010-287 |
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Which enzyme is responsible for converting cholesterol to pregnenolone?
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Desmolase
2010-287 |
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What is the phenotype of XX females who have 17α-hydroxylase deficiency?
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Externally female, but they lack secondary sexual characteristics ("sexual infantilism") due to decreased testosterone
2010-287 |
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What is the effect of congenital adrenal enzyme deficiencies on adrenal size?
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Decreased cortisol production and loss of negative feedback causes increased adrenocorticotropic hormone stimulation leading to bilateral adrenal enlargement
2010-287 |
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What is the effect of ketoconazole on steroid synthesis?
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Ketoconazole inhibits desmolase so that cholesterol is not converted to pregnenolone
2010-287 |
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What are the symptoms associated with 11β-hydoxylase deficiency?
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Masculinization, hypertension
2010-287 |
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What enzyme is responsible for the conversion of pregnenolone to progesterone?
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3β-hydroxysteroid dehydrogenase
2010-287 |
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Do XY males with 17α-hydroxylase deficiency have male or female internal anatomy?
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Male; these patients still make müllerian inhibitory factor, which leads to development of the male internal reproductive tract
2010-287 |
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A patient has decreased sex hormone and cortisol levels and increased mineralocorticoid levels; what is the diagnosis?
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17α-hydroxylase deficiency
2010-287 |
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A patient has increased sex hormones, decreased cortisol and mineralocorticoids, and HYPOtension; what is the diagnosis?
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21-hydroxylase deficiency
2010-287 |
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What is the phenotype of XX females who have 21-hydroxylase deficiency?
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The deficiency shunts precursors to the sex hormone pathway, increasing dihydrotestosterone, which causes masculinization and androgenization of external female genitalia
2010-287 |
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A patient has increased sex hormones, decreased cortisol, aldosterone, and mineralocorticoids, and has HYPERtension; what is the diagnosis?
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11β-hydroxylase deficiency
2010-287 |
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Adrenocorticotropic hormone has a(n) _____ (inhibitory/stimulatory) effect on desmolase whereas ketoconazole has a(n) _____ (inhibitory/stimulatory) effect on desmolase.
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Stimulatory; inhibitory
2010-287 |
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Why do patients with a deficiency in 11β-hydroxylase have hypertension in the presence of hypoaldosteronism?
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11-deoxycorticosterone has mineralocorticoid properties and builds up, causing hypertension
2010-287 |
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What symptoms are associated with 21α-hydoxylase deficiency?
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Masculinization, female pseudohermaphotidism, hypotension, hyperkalemia, salt wasting, increased plasma renin activity, and volume depletion
2010-287 |
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What is the phenotype of XY males who have 17α-hydroxylase deficiency?
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Pseudohermaphroditism; decreased dihydrotestosterone means that male secondary sex characteristics do not develop
2010-287 |
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A female infant is born with ambiguous genitalia and is found to be severely hypotensive; what is the diagnosis?
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21-hydroxylase deficiency causes hyperreninemic hypoaldosteronism and salt wasting, resulting in hypotension and hyperkalemia
2010-287 |
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Which enzyme catalyzes the conversion of testosterone to estradiol?
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Aromatase
2010-287 |
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What stimulates aldosterone synthase to convert corticosterone into aldosterone?
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Angiotensin II stimulates aldosterone synthase
2010-287 |
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What are the symptoms associated with 17α-hydroxylase deficiency?
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Hypertension and hypokalemia (due to increased mineralocorticoids)
2010-287 |
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In what form is cortisol found in the bloodstream?
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It is bound to corticosteroid-binding globulin
2010-287 |
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What hormones are involved in regulation of cortisol secretion?
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Corticotropin-releasing hormone from the hypothalamus stimulates adrenocorticotropic hormone release from the anterior pituitary; adrenocorticotropic hormone then stimulates cortisol production by the adrenal gland
2010-287 |
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Name five functions of cortisol.
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Maintains Blood pressure (by upregulating a-1 receptors on arterioles), decreases Bone formation, antiInflammatory, decreases Immune function, increases Gluconeogenesis, lipolysis, proteinolysis (remember: cortisol is BBIIG)
2010-287 |
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Active vitamin D formation is stimulated under which conditions?
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Low serum calcium and phosphate and high serum parathyroid hormone levels
2010-288 |
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How does parathyroid hormone affect calcium absorption in the gut?
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It stimulates 1α-hydroxylase activity in the kidney leading to increased levels of active vitamin D; active vitamin D leads to calcium resorption from the intestines
2010-288 |
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What effect does parathyroid hormone have on the kidney?
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Increased resorption of calcium from distal convoluted tubule, decreased phosphate reabsorption, stimulation of 1α hydroxylase activity
2010-288 |
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What is the major stimulus for the release of parathyroid hormone from the parathyroid glands?
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Low free serum calcium levels
2010-288 |
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How does parathyroid hormone exert an effect on osteoblasts and osteoclasts?
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It directly stimulates osteoblast activity and indirectly stimulates osteoclast activity, with a net effect of bone resorption
2010-288 |
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What is the active form of vitamin D?
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1,25-dihydroxy vitamin D, also called calcitriol
2010-288 |
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Low serum calcium levels result in increased _____ secretion, whereas low serum phosphate levels result in increased conversion of _____ in the kidney.
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Parathyroid hormone; 25-(OH) vitamin D to 1,25(OH)2 vitamin D
2010-288 |
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What is the effect of serum magnesium on parathyroid hormone secretion?
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Low magnesium leads to decreased parathyroid hormone secretion
2010-288 |
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Which two organs are the targets for 1,25(OH)2 vitamin D?
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The gastrointestinal tract and bone
2010-288 |
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What are some causes of low magnesium?
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Diarrhea, aminoglycosides, diuretics, and alcohol abuse
2010-288 |
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What effect does parathyroid hormone have on bone?
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Increased resorption of calcium and phosphate from bone (leading to increases of serum levels of both minerals)
2010-288 |
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What is the effect of parathyroid hormone on serum calcium and phosphate?
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Parathyroid hormone increases the serum calcium level and decreases the serum phosphate level (remember: PTH = Phosphate Trashing Hormone)
2010-288 |
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Which cells normally produce parathyroid hormone?
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Chief cells of the parathyroid glands
2010-288 |
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Increased levels of parathyroid hormone would result in what urinary findings?
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Higher urine phosphate and cAMP levels and lower urine calcium levels
2010-288 |
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What are the two sources of the precursors for activated vitamin D?
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Plants (D2 and sun exposure (D3)
2010-289 |
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What effect does vitamin D have on bone?
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Increases resorption of calcium and phosphate
2010-289 |
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Where is 25-hydroxy vitamin D activated?
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The kidney
2010-289 |
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In which organ is vitamin D converted to 25-hydroxy vitamin D?
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The liver
2010-289 |
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A deficiency of vitamin D in children results in what condition?
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Rickets
2010-289 |
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What effect does vitamin D have on the gut?
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It increases the absorption of dietary calcium and phosphate
2010-289 |
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A deficiency of vitamin D in adults results in what condition?
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Osteomalacia
2010-289 |
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Compare the effect of parathyroid hormone on serum calcium and phosphate levels to that of 1,25(OH)2 vitamin D.
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Parathyroid hormone increases serum calcium levels and decreases serum phosphate levels, whereas 1,25(OH)2 vitamin D increases both calcium and phosphate levels
2010-289 |
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What stimulates the secretion of calcitonin?
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Increased serum calcium levels
2010-289 |
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Where is calcitonin made?
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Parafollicular cells (C cells) of the thyroid
2010-289 |
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How is calcitonin involved in calcium homeostasis?
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It opposes the action of parathyroid hormone but is not important in normal calcium homeostasis (remember: calciTONin TONes down calcium levels)
2010-289 |
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Where does calcitonin exert its effect?
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Calcitonin decreases calcium resorption from bone
2010-289 |
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What hormones use the tyrosine kinase signaling pathway?
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Insulin, insulin-like growth factor-1, fibroblast growth factor, platelet-derived growth factor, prolactin, growth hormone
2010-289 |
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Which hormones use steroid receptors in their signaling pathways?
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Vitamin D and PET CAT: Progesterone, Estrogen, Testosterone, Cortisol, Aldosterone, T3, and T4
2010-289 |
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What hormones use the inositol triphosphate signaling pathway?
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Gonadotropin-releasing hormone (GnRH), growth hormone-releasing hormone (GHRH), Oxytocin, antidiuretic hormone (ADH) (V1 receptor), thyrotropin-releasing hormone (TRH); (remember: GGOAT)
2010-289 |
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Name the hormones that use the cAMP signaling pathway.
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Follicle-stimulating hormone (FSH), luteinizing hormone (LH), adrenocorticotropic hormone (ACTH), thyroid-stimulating hormone (TSH), corticotropin-releasing hormone (CRH), human chorionic gonadotropin (hCG), antidiuretic hormone (ADH) (V2 receptor), melanocyte-stimulating hormone (MSH), parathyroid hormone (PTH), calcitonin, glucagon (remember: FLAT CHAMP)
2010-289 |
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What hormones use cyclic guanosine monophosphate as a signaling molecule?
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Atrial natriuretic peptide, nitric oxide/endothelium-derived relaxing factor (think vasodilators)
2010-289 |
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Except for _____ _____ and _____, all the hormones of the anterior pituitary utilize the cAMP signaling pathway.
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Growth hormone and prolactin
2010-289 |
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Insulin utilizes the _____ signaling pathway, whereas glucagon increases the concentration of _____ in the cell after binding its receptor.
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Tyrosine kinase, cAMP
2010-289 |
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What physical finding in a woman could suggest decreased levels of sex-hormone-binding globulin?
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Hirsutism may result from increased serum free testosterone
2010-290 |
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True or False: All hormones that come from the adrenal cortex are steroids.
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True
2010-290 |
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Steroid hormones have an (immediate/delayed) onset of action upon binding to a cell.
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Delayed; time is required for gene transcription and protein synthesis
2010-290 |
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How does the steroid hormone/receptor complex affect cellular physiology?
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By binding enhancer-like elements of the DNA, it alters gene expression and protein synthesis
2010-290 |
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Why do steroid hormones circulate bound to specific binding globulins?
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Steroid hormones are lipophilic and specific binding globulins increase their solubility
2010-290 |
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What physical finding in a man could suggest increased levels of sex-hormone-binding globulin?
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Gynecomastia, due to lower serum free testosterone
2010-290 |
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Do steroid hormones bind receptors found on the cell surface or within the cell?
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Steroids bind their receptors within the cell, in the nucleus or the cytoplasm
2010-290 |
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From which large precursor protein is thyroid hormone derived?
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Thyroglobulin
2010-290 |
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What happens to the level of thyroxine-binding globulin during hepatic failure?
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It is decreased
2010-290 |
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What are the effects of the increased Na+/K+ adenosine triphosphatase activity stimulated by thyroid hormone?
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Increased O2 consumption, respiratory rate, and body temperature
2010-290 |
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What is the mechanism by which Graves' disease causes hyperthyroidism?
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Graves' disease is an autoimmune disorder in which antibodies toward the thyroid-stimulating hormone receptor in the thyroid stimulate the production of thyroid hormones, independent of regulation by thyroid-stimulating hormone
2010-290 |
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What are the four main functions of T3?
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The 4 B's: Brain maturation, Bone growth, Beta-adrenergic effects, BMR increase
2010-290 |
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What protein in the plasma binds T3 and T4 for transportation?
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Thyroxine-binding globulin
2010-290 |
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The major hormone product of the thyroid is _____, and _____ has greater affinity for thyroid hormone receptors.
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T4; T3
2010-290 |
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Which iodine-containing hormones in the body control the body's metabolic rate?
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T3 and T4
2010-290 |
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What happens to the level of thyroxine-binding globulin during pregnancy and oral contraceptive use?
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It is increased as a result of higher estrogen levels
2010-290 |
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By what mechanism do T3 and T4 affect the basal metabolic rate?
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They increase the basal metabolic rate by increasing Na+/K+-adenosine triphosphatase activity
2010-290 |
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How does free T3 exert negative feedback on the hypothalamic-pituitary axis?
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Free T3 decreases the sensitivity of the anterior pituitary to thyrotropin-releasing hormone, leading to decreased thyroid hormone production
2010-290 |
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How do the antithyroid drugs propylthiouracil and methimazole affect thyroid hormone production?
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They decrease the formation of monoiodotyrosine and diiodotyrosine
2010-290 |
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What cell type in the thyroid produces T3 and T4?
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Follicular cells
2010-290 |
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What are the effects of T3 and T4 on the heart?
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Upregulation of the number of β1 receptors causes increased cardiac output, heart rate, stroke volume, and cardiac contractility
2010-290 |
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The hypothalamus releases _____, which stimulates the pituitary to release _____, which in turn stimulates the production of T3 and T4 from follicular cells in the thyroid.
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Thyrotropin-releasing hormone; thyroid-stimulating hormone
2010-290 |
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Which effects of thyroid hormone are similar to those of glucagon?
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Increased glycogenolysis, gluconeogenesis, and lipolysis
2010-290 |
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Newborn screening of an infant shows low thyroid hormone levels; what major organ system should you be concerned about?
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Central nervous system; thyroid hormones are needed for central nervous system maturation, and a congenital deficiency may cause cretinism
2010-290 |
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What is the role of peroxidase in the production of thyroid hormones?
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I- is oxidized to I2 by peroxidase then combines with thyroglobulin to make monoiodotyrosine and diiodotyrosine; peroxidase couples monoiodotyrosine and diiodotyrosine to make T4 and T3
2010-290 |
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What are the results of a low dose dexamethasone suppression test in a healthy person?
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Decreased cortisol level; dexamethasone decreases adrenocorticotropic hormone secretion by negative feedback leading to decreased cortisol levels
2010-291 |
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When are cortisol levels drawn for the dexamethasone suppression test and why?
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In the morning; this is when cortisol levels should be at the highest
2010-291 |
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A patient with Cushing's syndrome has a decreased adrenocorticotropic hormone level; what are two mechanisms of increased cortisol production with low adrenocorticotropic hormone levels?
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Overproduction of cortisol by the adrenal cortex or administration of exogenous cortisol
2010-291 |
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What findings are indicative of Cushing's syndrome?
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Hypertension, weight gain, moon facies, truncal obesity, buffalo hump, hyperglycemia (insulin resistance), skin changes, osteoporosis, amenorrhea, and immune suppression
2010-291 |
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A patient is diagnosed with small-cell carcinoma of the lung leading to Cushing's syndrome. Will this patient's adrenocorticotropic hormone level be high or low?
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High
2010-291 |
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Would cortisol levels be high or low after a high-dose dexamethasone suppression test in a patient with an ectopic adrenocorticotropic hormone-producing tumor?
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High; the secretory activity of this tumor is independent of negative feedback
2010-291 |
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Why are patients who are taking chronic steroids more susceptible to infection?
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Associated immune suppression
2010-291 |
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What is the effect of long-term steroid administration on adrenocorticotropic hormone?
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Suppression of the hypothalamic-pituitary-adrenal axis causing low adrenocorticotropic hormone levels
2010-291 |
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What results would you expect after a dexamethasone suppression test in the setting of an adrenocorticotropic hormone-producing pituitary tumor?
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With low-dose dexamethasone, we would expect high cortisol levels (no suppression); with high doses of dexamethasone, we would expect suppression and thus low adrenocorticotropic hormone and cortisol levels
2010-291 |
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A patient with Cushing's syndrome has an increased adrenocorticotropic hormone level; what are two mechanisms of increased adrenocorticotropic hormone production?
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Overproduction of adrenocorticotropic hormone by the pituitary and overproduction of adrenocorticotropic hormone by an ectopic site (such as in small-cell lung cancer)
2010-291 |
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Would cortisol levels be high or low after a high-dose dexamethasone suppression test in a patient with a cortisol-producing tumor?
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High; the secretory activity of this tumor is independent of negative feedback
2010-291 |
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What is Cushing's disease?
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An adrenocorticotropic hormone-hypersecreting primary pituitary adenoma
2010-291 |
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A patient is diagnosed with primary adrenal cortical hyperplasia. Will this patient's adrenocorticotropic hormone level be high or low?
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Low
2010-291 |
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Name five causes of secondary hyperaldosteronism.
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Renal artery stenosis, chronic renal failure, congestive heart failure, cirrhosis, and nephrotic syndrome
2010-291 |
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A patient has hypertension, hypokalemia, metabolic alkalosis, and a low plasma renin level; what is the likely diagnosis?
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Conn's syndrome
2010-291 |
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What is the cause of Conn's syndrome?
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An aldosterone-secreting tumor
2010-291 |
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Why is secondary hyperaldosteronism associated with high plasma renin levels?
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All the causes of secondary hyperaldosteronism cause the kidney to perceive a low intravascular volume state, causing up-regulation of the renin-angiotensin pathway
2010-291 |
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A patient has hypertension, hypokalemia, metabolic alkalosis, and a high plasma renin level; what is the likely diagnosis?
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Secondary hyperaldosteronism
2010-291 |
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Which diuretic is used as a treatment for hyperaldosteronism?
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Spironolactone, a K+-sparing diuretic that works as an aldosterone antagonist
2010-291 |
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Which hormones are deficient in patients with Addison's disease?
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Cortisol and aldosterone
2010-291 |
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What pathologic findings would be expected in the adrenal glands of a patient with Addison's disease?
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Adrenal Atrophy affecting All three cortical divisions and Absence of hormone production
2010-291 |
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Why is skin pigmentation a finding of Addison's?
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In Addison's, there is increased adrenocorticotropic hormone; proopiomelanocortin is the precursor of adrenocorticotropic hormone and melanocyte-stimulating hormone; melanocyte-stimulating hormone leads to skin hyperpigmentation
2010-291 |
|
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Is low adrenocorticotropic hormone production associated with primary or secondary hypoaldosteronism?
|
Secondary
2010-291 |
|
|
How is primary adrenal insufficiency distinguished from secondary adrenal insufficiency?
|
Secondary adrenal insufficiency has decreased adrenocorticotropic hormone, no skin hyperpigmentation, and no hyperkalemia
2010-291 |
|
|
Name three findings associated with Addison's disease (primary adrenal insufficiency).
|
Hypotension, skin hyperpigmentation, hyperkalemia
2010-291 |
|
|
What processes can cause primary adrenal insufficiency?
|
Atrophy or destruction by autoimmune disease, tuberculosis infection, or metastatic malignancy
2010-291 |
|
|
Is primary or secondary hypoaldosteronism associated with skin hyperpigmentation?
|
Primary
2010-291 |
|
|
A patient with meningococcal septicemia suddenly becomes severely hypotensive, with disseminated intravascular coagulation and endotoxic shock; what is the likely diagnosis?
|
Waterhouse-Friderichsen syndrome, or acute adrenocortical insufficiency caused by adrenal hemorrhage
2010-291 |
|
|
Based on a history suggestive of pheochromocytoma, you order serum and urine tests for confirmation; what would be consistent with this diagnosis?
|
Increased plasma catecholamines and urinary vanillylmandelic acid
2010-292 |
|
|
List three genetic syndromes that are associated with pheochromocytoma.
|
Multiple endocrine neoplasia types IIA and IIB, neurofibromatosis
2010-292 |
|
|
What are five common symptoms associated with pheochromocytoma?
|
Pressure (elevated blood pressure), Pain (headache), Perspiration, Palpitations (tachycardia), Pallor (remember: the 5 P's)
2010-292 |
|
|
List the six components of "the pheochromocytoma rule of tens."
|
10% malignant, 10% bilateral, 10% extra-adrenal, 10% calcify, 10% kids, 10% familial
2010-292 |
|
|
What category of drugs is often used to treat pheochromocytoma?
|
α-Antagonists
2010-292 |
|
|
From what cells does a pheochromocytoma develop?
|
Chromaffin cells of the adrenal medulla, which are of neural crest origin
2010-292 |
|
|
What characteristic of pheochromocytoma distinguishes it from chronic, poorly controlled hypertension?
|
Symptoms occur in "spells" and are thus relapsing and remitting
2010-292 |
|
|
From which two amino acids are catecholamines synthesized?
|
Phenylalanine and tyrosine
2010-292 |
|
|
Why is phenoxybenzamine a good choice in the treatment of pheochromocytoma?
|
It is a nonselective, irreversible α-blocker
2010-292 |
|
|
Where in the body can a neuroblastoma develop?
|
Anywhere along the sympathetic chain
2010-292 |
|
|
What oncogene is associated with neuroblastoma?
|
N-myc
2010-292 |
|
|
The most common adrenal tumor is _____ in adults and _____ in children.
|
Pheochromocytoma; neuroblastoma
2010-292 |
|
|
What product is increased in the urine of children with neuroblastoma?
|
Homovanillic acid (a breakdown product of dopamine)
2010-292 |
|
|
How do hypo- and hyperthyroidism each affect bowel movements?
|
Hypothyroidism causes constipation; hyperthyroidism causes diarrhea
2010-292 |
|
|
How do hypo- and hyperthyroidism each affect the skin?
|
Hypothyroidism causes dry, cool skin; hyperthyroidism causes warm, moist skin
2010-292 |
|
|
What cardiac symptoms can hyperthyroidism cause?
|
Chest pain and palpitations
2010-292 |
|
|
How do hypo- and hyperthyroidism each affect body weight?
|
Hypothyroidism causes weight gain; hyperthyroidism causes weight loss
2010-292 |
|
|
A patient is lethargic and has swelling in the face and periorbital region; you diagnose myxedema resulting from what condition?
|
Hypothyroidism
2010-292 |
|
|
What are the lab findings in hypothyroidism?
|
Elevated thyroid-stimulating hormone with a low total T4, free T4, and T3 uptake
2010-292 |
|
|
Which serologic marker is a sensitive test for primary hypothyroidism?
|
Elevated thyroid-stimulating hormone
2010-292 |
|
|
How do hypo- and hyperthyroidism each affect temperature tolerance?
|
Hypothyroidism causes cold intolerance; hyperthyroidism causes heat intolerance
2010-292 |
|
|
What are the lab findings in hyperthyroidism?
|
Decreased thyroid-stimulating hormone with elevated total T4, free T4, and T3 uptake
2010-292 |
|
|
How do hypo- and hyperthyroidism each affect the hair?
|
Hypothyroidism causes coarse, brittle hair; hyperthyroidism causes fine hair
2010-292 |
|
|
What potentially fatal cardiac process is hyperthyroidism known to induce?
|
Arrhythmia
2010-292 |
|
|
Describe the course of Hashimoto's thyroiditis.
|
A slow course; it can have an initial period of hyperthyroidism before hypothyroidism due to follicular rupture causing thyrotoxicosis
2010-293 |
|
|
What are histological findings of subacute (de Quervain's) thyroiditis?
|
Granulomatous inflammation
2010-293 |
|
|
What is the most common cause of hypothyroidism?
|
Hashimoto's thyroiditis, an autoimmune disorder
2010-293 |
|
|
What condition is a result of severe fetal hypothyroidism?
|
Cretinism (meaning "Christlike," these children were considered so mentally retarded as to be incapable of sinning)
2010-293 |
|
|
While traveling in China, you learn that there is a high prevalence of cretinism; what intervention would decrease the prevalence of this disease?
|
This is likely endemic cretinism, found wherever endemic goiter occurs; it could be treated by dietary iodine supplementation
2010-293 |
|
|
Which two autoantibodies are associated with Hashimoto's thyroiditis?
|
Antimicrosomal antibodies and antithyroglobulin antibodies
2010-293 |
|
|
What is the pathophysiology of Reidel's thyroiditis?
|
Thyroid tissue is replaced by fibrous tissue
2010-293 |
|
|
What histologic findings are suggestive of Hashimoto's thyroiditis?
|
A lymphocytic infiltrate with germinal centers and Hürthle cells
2010-293 |
|
|
What physical exam findings would suggest congenital hypothyroidism in an infant?
|
Pot belly, protruding umbilicus, pale skin, and a puffy face with protuberant tongue
2010-293 |
|
|
What are causes of sporadic congenital hypothyroidism?
|
Defect in T4 formation or developmental failure in thyroid formation (congenital hypothyroidism)
2010-293 |
|
|
In the presence of hypothyroidism, what historical and physical exam findings would be consistent with Hashimoto's thyroiditis?
|
Hashimoto's thyroiditis follows a slow course and produces a moderately enlarged, nontender thyroid
2010-293 |
|
|
Name four findings, other than hypothyroidism, associated with subacute (de Quervain's) thyroiditis.
|
Elevated erythrocyte sedimentation rate, jaw pain, early inflammation, and a tender thyroid gland
2010-293 |
|
|
A patient with hypothyroidism has a fixed, hard (rock-like), painless goiter; what is the likely diagnosis?
|
Riedel's thyroiditis
2010-293 |
|
|
Following a flu-like illness, a patient is found to be hypothyroid and to have a tender thyroid gland; what is the prognosis?
|
This is most consistent with subacute thyroiditis, which has a self-limited course
2010-293 |
|
|
What physical exam findings would suggest that Grave's disease is the cause of a case of hyperthyroidism?
|
Exophthalmos, pretibial myxedema, diffuse goiter
2010-293 |
|
|
A patient with hyperthyroidism has a thyroid scan that shows several highly active nodules; what is the diagnosis?
|
Toxic multinodular goiter, in which patches of follicular cells work independently of thyroid-stimulating hormone
2010-293 |
|
|
What is the Jod-Basedow phenomenon?
|
Thyrotoxicosis when a patient with endemic goiter moves to an iodine-replete area
2010-293 |
|
|
What is the risk of the nodules in a toxic multinodular goiter becoming malignant?
|
None; the nodules in a toxic multinodular goiter are not malignant
2010-293 |
|
|
When does Graves' disease most often present?
|
During stress (eg, childbirth)
2010-293 |
|
|
What mutation is responsible for the activity of the follicles in a toxic multinodular goiter?
|
A mutation in the thyroid-stimulating hormone receptor makes these cells function independently of thyroid-stimulating hormone
2010-293 |
|
|
What is the pathophysiology of Graves' disease?
|
It is an autoimmune disorder associated with thyroid-stimulating hormone receptor antibodies that stimulate thyroid hormone release
2010-293 |
|
|
What is a potentially fatal complication of hyperthyroidism?
|
A stress-induced catecholamine surge, which can lead to death by cardiac arrhythmia
2010-293 |
|
|
What type of hypersensitivity reaction is Graves' disease?
|
Type II hypersensitivity
2010-293 |
|
|
Which thyroid cancer is the most common?
|
Papillary carcinoma
2010-293 |
|
|
Undifferentiated/anaplastic carcinoma of the thyroid is most commonly found in what population?
|
Older patients
2010-293 |
|
|
What are the histological findings of medullary carcinoma of the thyroid?
|
Sheets of cells in amyloid stroma
2010-293 |
|
|
Medullary carcinoma of the thyroid originates from which cells?
|
Parafollicular C cells
2010-293 |
|
|
What are the histological findings of papillary carcinoma of the thyroid?
|
Psammoma bodies, "ground-glass" nuclei (Orphan Annie), nuclear grooves
2010-293 |
|
|
Medullary carcinoma of the thyroid is associated with what two genetic syndromes?
|
Multiple endocrine neoplasia types 2A and 2B
2010-293 |
|
|
Place the following thyroid cancers in order from best to worst prognosis: follicular, undifferentiated/anaplastic, and papillary.
|
Papillary, follicular, and undifferentiated/anaplastic
2010-293 |
|
|
What risk factor is associated with papillary carcinoma of the thyroid?
|
Childhood irradiation
2010-293 |
|
|
Which thyroid cancer has the best prognosis?
|
Papillary carcinoma
2010-293 |
|
|
Medullary carcinoma of the thyroid produces what substance?
|
Calcitonin
2010-293 |
|
|
What type of cancer is associated with Hashimoto's thyroiditis?
|
Lymphoma of the thyroid
2010-293 |
|
|
What mnemonic illustrates the causes of hypercalcemia?
|
Calcium ingestion, Hyperparathyroidism, Hyperthyroidism, Iatrogenic (thiazides), Multiple myeloma, Paget's disease, Addison's disease, Neoplasms, Zollinger-Ellison syndrome, Excess vitamin D, Excess vitamin A, Sarcoidosis (remember: CHIMPANZEES)
2010-294 |
|
|
How does chronic renal disease contribute to secondary hyperparathyroidism?
|
Renal failure leads to decreased activation of vitamin D which, in turn, leads to decreased absorption of calcium from the gut
2010-294 |
|
|
What is the mechanism by which a patient develops secondary hyperparathyroidism?
|
Decreased calcium absorption from the gut and increased levels of phosphate lead to secondary hyperplasia of the parathyroid gland
2010-294 |
|
|
What are the relative levels of parathyroid hormone, calcium, phosphate, and alkaline phosphatase in secondary hyperparathyroidism?
|
Increased parathyroid hormone, phosphate, and alkaline phosphatase, and decreased serum calcium
2010-294 |
|
|
What is the classic triad of symptoms in primary hyperparathyroidism?
|
When present, symptoms include weakness, constipation, and renal stones (remember: stones, bones, and groans)
2010-294 |
|
|
What is the most common cause of primary hyperparathyroidism?
|
A parathyroid adenoma
2010-294 |
|
|
What is the most common cause of secondary hyperparathyroidism?
|
Chronic renal disease
2010-294 |
|
|
What is the bone pathology associated with osteitis fibrosa cystica?
|
Cystic bone spaces filled with brown fibrous tissue causing pain; due to elevated levels of parathyroid hormone
2010-294 |
|
|
What are the relative levels of parathyroid hormone, calcium, phosphate, and alkaline phosphatase in primary hyperparathyroidism?
|
Increased parathyroid hormone, calcium, and alkaline phosphatase and decreased phosphate
2010-294 |
|
|
What bone pathology might you see in a dialysis patient?
|
Renal osteodystrophy, caused by secondarily elevated parathyroid hormone levels
2010-294 |
|
|
What neuromuscular finding is common among patients with hypoparathyroidism?
|
Tetany, secondary to hypocalcemia
2010-294 |
|
|
Would parathyroid hormone be increased or decreased in pseudohypoparathyroidism?
|
Increased; since the end-organ targets are resistant to the hormone, serum calcium levels will remain low, causing increased secretion of parathyroid hormone.
2010-294 |
|
|
Upon tapping the facial nerve, a patient has twitching in the ipisilateral facial muscles; what is the sign?
|
Chvostek's sign, indicating hypocalcemia
2010-294 |
|
|
A patient with hypocalcemia is of short stature and has shortened fourth/fifth digits. What genetic condition should be considered?
|
Pseudohypoparathyroidism, also known as Albright hereditary osteodystrophy
2010-294 |
|
|
List three causes of hypoparathyroidism.
|
Accidental surgical excision (thyroid surgery), autoimmune destruction and DiGeorge's syndrome
2010-294 |
|
|
In what manner is pseudohypoparathyroidism inherited?
|
Autosomal dominant
2010-294 |
|
|
Following thyroid surgery, a patient presents with muscle spasms; what electrolyte abnormality is likely present?
|
Hypoparathyroidism and resultant hypocalcemia
2010-294 |
|
|
After occluding the brachial artery with a blood pressure cuff, your patient has spasms in the wrist; what is the name of the sign?
|
Trousseau's sign, indicating hypocalcemia
2010-294 |
|
|
What is the name of the condition in which the kidneys are unresponsive to parathyroid hormone?
|
Pseudohypoparathyroidism, a genetic condition
2010-294 |
|
|
A 40-year-old patient presents with a headache and cannot see on the temporal sides of his visual fields; what should you look for?
|
Brain imaging may reveal a pituitary adenoma, which can impinge on the optic chiasm and cause bitemporal hemianopsia
2010-294 |
|
|
What is the medical treatment for a prolactinoma?
|
Bromocriptine or cabergoline (dopamine agonists)
2010-294 |
|
|
A patient complains of amenorrhea, galactorrhea, and low libido. She has been trying to get pregnant for 3 years. What tumor should be considered?
|
Prolactinoma
2010-294 |
|
|
What is the most common type of pituitary adenoma?
|
Prolactinoma
2010-294 |
|
|
Excess growth hormone in children causes what disease?
|
Gigantism (increased linear bone growth)
2010-294 |
|
|
A patient has an elevated growth hormone level; what are three situations in which this increase in growth hormone production is normal?
|
Stress, exercise, and hypoglycemia
2010-294 |
|
|
A 50-year-old patient has a large tongue with deep furrows, a deep voice, large hands and feet, and coarse facial features; what is the likely diagnosis?
|
Acromegaly
2010-294 |
|
|
How is acromegaly diagnosed with lab tests?
|
Increased insulin-like growth factor-1 or failure to suppress serum growth hormone following oral glucose tolerance test
2010-294 |
|
|
Acromegaly is the result of an excess of what hormone?
|
Growth hormone
2010-294 |
|
|
What is the treatment of acromegaly?
|
Pituitary adenoma resection followed by octreotide administration
2010-294 |
|
|
Why are pregnant women more susceptible to pituitary infarction?
|
An increased number of lactotrophs without an increase in the blood supply to the anterior pituitary
2010-294 |
|
|
A postpartum patient has fatigue, anorexia, difficulty lactating, and thin sparse pubic and axillary hair; what is the likely diagnosis?
|
Postpartum hypopituitarism, or Sheehan's syndrome
2010-294 |
|
|
What causes Sheehan's syndrome?
|
Postpartum infarction of the anterior pituitary gland following severe bleeding during delivery
2010-294 |
|
|
What treatment is specifically used for central diabetes insipidus?
|
Intranasal desmopressin, an antidiuretic hormone analog
2010-295 |
|
|
What are some causes of nephrogenic diabetes insipidus?
|
Hereditary or secondary to hypercalcemia, lithium, demeclocycline
2010-295 |
|
|
How does the serum osmolality help diagnose patients with diabetes insipidus?
|
It is high, often above 290 mOsm/L
2010-295 |
|
|
What is the primary defect in central diabetes insipidus?
|
Lack of antidiuretic hormone production
2010-295 |
|
|
A patients comes to the emergency room with intense thirst, polyuria, and very dilute urine; what endocrine disorder should be on your differential?
|
Diabetes insipidus
2010-295 |
|
|
How can one distinguish between central and nephrogenic DI?
|
Administration of desmopressin. In central diabetes insipidus symptoms will improve with exogenous antidiuretic hormone; in nephrogenic diabetes insipidus the kidneys are resistant to antidiuretic hormone and addition of antidiuretic hormone will have no effect
2010-295 |
|
|
What test is used to diagnose diabetes insipidus?
|
Water deprivation test (urine osmolality does not increase even with low fluid intake)
2010-295 |
|
|
What lifestyle change can be used to manage both central and nephrogenic diabetes insipidus?
|
Adequate fluid intake
2010-295 |
|
|
What is the primary defect in nephrogenic diabetes?
|
Lack of renal response to antidiuretic hormone
2010-295 |
|
|
What are some causes of central diabetes insipidus?
|
Pituitary tumor, trauma, surgery, histocytosis X
2010-295 |
|
|
Name three drugs used in the treatment of nephrogenic diabetes insipidus.
|
Hydrochlorothiazide, indomethacin, and amiloride
2010-295 |
|
|
How does the urine-specific gravity help diagnose patients with diabetes insipidus?
|
It is low, often below 1.006 g/mL
2010-295 |
|
|
In patients with syndrome of inappropriate antidiuretic hormone secretion, there is excessive retention of what substance in the kidneys?
|
Water
2010-295 |
|
|
Give an example of an ectopic source of antidiuretic hormone.
|
Small cell lung cancer (paraneoplastic syndrome)
2010-295 |
|
|
What serum electrolyte abnormality is characteristic of syndrome of inappropriate antidiuretic hormone secretion?
|
Hyponatremia
2010-295 |
|
|
How do you treat a patient with syndrome of inappropriate antidiuretic hormone secretion?
|
Water restriction or demeclocycline are the treatments for syndrome of inappropriate antidiuretic hormone secretion
2010-295 |
|
|
What neurologic condition is associated with severe hyponatremia?
|
Seizures; hyponatremia must be corrected slowly to avoid central pontine myelinolysis
2010-295 |
|
|
Name four causes of syndrome of inappropriate antidiuretic hormone secretion.
|
Ectopic antidiuretic hormone (small cell lung cancer), central nervous system disorders/head trauma, pulmonary diseases, drugs (eg, cyclophosphamide)
2010-295 |
|
|
A patient with pneumonia is found to be hyponatremic with high urine osmolarity and low serum osmolarity; what is the likely diagnosis?
|
Syndrome of inappropriate antidiuretic hormone secretion
2010-295 |
|
|
What might you see on fundoscopic exam of a patient with longstanding diabetes mellitus?
|
Hemorrhages, exudates, microaneurysms, and vessel proliferation
2010-295 |
|
|
You are looking at histological samples from a patient with longstanding diabetes mellitus; what do you expect to see in the small vessels?
|
A diffuse thickening of basement membrane
2010-295 |
|
|
________ ________ is an acute manifestation of type 1 diabetes; it is not generally seen in type 2 diabetes.
|
Diabetic ketoacidosis
2010-295 |
|
|
Why are patients with uncontrolled diabetes often acidemic?
|
Ketone bodies are acids, and osmotic diuresis causes lactic acidosis by decreased intravascular volume and decreased perfusion of the vital organs
2010-295 |
|
|
What three direct effects on cellular metabolism can a diabetic insulin deficiency create?
|
Decreased glucose uptake, increased protein catabolism, and increased lipolysis
2010-295 |
|
|
List three pathologic processes caused by small-vessel disease in patients with diabetes.
|
Retinopathy, glaucoma, and nephropathy
2010-295 |
|
|
What are the effects of decreased cellular glucose uptake?
|
Hyperglycemia, glycosuria, osmotic diuresis, and electrolyte depletion
2010-295 |
|
|
In diabetic patients, what is the underlying mechanism of dehydration?
|
Hyperglycemia overwhelms the ability of the renal tubules to reabsorb glucose leading to increased glucose in the urine; this, in turn, leads to osmotic diuresis and dehydration
2010-295 |
|
|
In patients with chronic diabetes, osmotic damage can cause what two disease states?
|
Neuropathy and cataracts
2010-295 |
|
|
What accumulates in the lens to cause cataracts in patients with diabetes mellitus?
|
Sorbitol, due to high circulating glucose levels
2010-295 |
|
|
List two direct effects of increased protein catabolism in diabetes.
|
Increased plasma amino acids and nitrogen loss in urine
2010-295 |
|
|
Failure to treat a diabetic patient who is severely volume depleted and has a low serum pH may result in what?
|
Coma and death
2010-295 |
|
|
In diabetes, what process directly causes ketogenesis and increased plasma free fatty acids?
|
Increased lipolysis
2010-295 |
|
|
What three glucose-related tests are diagnostically useful for diabetes?
|
Fasting serum glucose, glucose tolerance, and glycosylated hemoglobin (HbA1c)
2010-295 |
|
|
List four acute manifestations that can be seen in both type 1 and 2 diabetes mellitus.
|
Polydipsia, polyuria, polyphagia, and weight loss
2010-295 |
|
|
Which blood test is used to monitor long-term diabetic control?
|
Glycosylated hemoglobin (HbA1c)
2010-295 |
|
|
List four forms of renal disease that can occur as a result of diabetic nephropathy.
|
Nodular sclerosis, progressive proteinuria, chronic renal failure, and arteriosclerosis leading to hypertension
2010-295 |
|
|
_____ _____ is an acute manifestation of type 2 diabetes; it is not generally seen in type 1 diabetes.
|
Hyperosmolar coma
2010-295 |
|
|
The chronic manifestations of diabetes can be broken down into what two categories on the basis of pathogenesis?
|
Nonenzymatic glycosylation and osmotic damage
2010-295 |
|
|
In patients with diabetes, the chronic manifestations of nonenzymatic glycosylation can be broken down into what two categories?
|
Small-vessel disease and large-vessel disease
2010-295 |
|
|
Does diabetic neuropathy affect the motor, sensory, or autonomic nervous systems?
|
Diabetic neuropathy can affect motor, sensory, and autonomic nerves
2010-295 |
|
|
Name three specific vascular diseases that can result from large vessel atherosclerosis as a result of diabetes.
|
Coronary artery disease, peripheral vascular occlusive disease and gangrene, and cerebrovascular disease
2010-295 |
|
|
Whereas diabetes mellitus always has a polygenic inheritance, familial history is a strong predictor in type _____ and weak in type _____ diabetes.
|
Type 2; type 1
2010-296 |
|
|
What age group is most commonly affected by type 1 diabetes mellitus?
|
Individuals who are less than 30 years old
2010-296 |
|
|
What age group is most commonly affected by type 2 diabetes mellitus?
|
Individuals who are greater than 40 years old
2010-296 |
|
|
What happens to the serum insulin level in patients with type 1 diabetes mellitus?
|
The serum insulin level is decreased
2010-296 |
|
|
Ketoacidosis is common in patients with what form of diabetes mellitus?
|
Type 1; ketoacidosis is rare in type 2 diabetes mellitus
2010-296 |
|
|
What happens to the serum insulin level in patients with type 2 diabetes mellitus?
|
The serum insulin level is elevated initially and is variable during disease progression, often low late in the course
2010-296 |
|
|
Which form of diabetes mellitus has an association with obesity?
|
Type 2 diabetes is associated with obesity
2010-296 |
|
|
What is the underlying etiology of type 2 diabetes mellitus?
|
Increased resistance to insulin
2010-296 |
|
|
Which human leukocyte antigen types are associated with diabetes mellitus?
|
Human leukocyte antigens DR3 and DR4 are associated with type 1 diabetes mellitus; there is no association between human leukocyte antigen and type 2 diabetes mellitus
2010-296 |
|
|
What happens to the number of beta cells in the islets of patients with type 1 diabetes mellitus?
|
They are decreased
2010-296 |
|
|
Insulin is always necessary for the treatment of which type of diabetes mellitus?
|
Type 1 diabetes mellitus; it is sometimes necessary to treat type 2 diabetes mellitus
2010-296 |
|
|
Glucose intolerance is severe in patients with type _____ diabetes mellitus but is mild to moderate in patients with type _____ diabetes mellitus
|
Type 1; type 2
2010-296 |
|
|
What is the underlying etiology of type 1 diabetes mellitus?
|
The viral or immune destruction of β-cells
2010-296 |
|
|
What happens to the number of β-cells in the islets of patients with type 2 diabetes mellitus?
|
Their numbers are variable; amyloidosis is seen
2010-296 |
|
|
The classic symptoms of polyuria, polydipsia, thirst, and weight loss are common with what form of diabetes mellitus?
|
Type 1
2010-296 |
|
|
When would it make sense to give glucose to patients with diabetic ketoacidosis?
|
When they are becoming hypoglycemic from continuing insulin treatment (so that they can continue to be given insulin)
2010-296 |
|
|
What causes intracellular potassium depletion in diabetic ketoacidosis?
|
Increased hydrogen ions and decreased insulin cause a shift of potassium out of the cells
2010-296 |
|
|
You suspect diabetic ketoacidosis in an emergency room patient; what would the glucose, pH, and bicarbonate levels be?
|
Increased glucose, low pH (increased H+ levels), and decreased bicarbonate
2010-296 |
|
|
Describe Kussmaul's respirations.
|
Deep respirations and air-hunger characteristic of diabetic ketoacidosis
2010-296 |
|
|
What acid-base disturbance is found in patients with diabetic ketoacidosis?
|
Anion gap metabolic acidosis
2010-296 |
|
|
The chemistry panel on a patient with diabetic ketoacidosis shows a high potassium level. Why?
|
Although the extracellular potassium is elevated, the intracellular and total potassium levels are depleted because of the body's excess of hydrogen ions
2010-296 |
|
|
A diabetic patient has high circulating levels of ketone bodies and is determined to be in diabetic ketoacidosis; how were the ketone bodies formed?
|
Increased fat breakdown and free fatty acids increase the ketogenesis pathway, converting free fatty acids into ketone bodies
2010-296 |
|
|
The fruity breath sometimes encountered in patients with diabetic ketoacidosis is the result of what?
|
Exhaled acetone
2010-296 |
|
|
A diabetic patient presents with Kussmaul's respirations, nausea and vomiting, abdominal pain, and delirium; what is the diagnosis and volume status?
|
This patient is likely in diabetic ketoacidosis and is dehydrated
2010-296 |
|
|
What are the two types of ketone bodies made during diabetic ketoacidosis?
|
β-hydroxybutyrate, acetoacetate
2010-296 |
|
|
Name an infectious complication of diabetic ketoacidosis that can prove fatal if not treated
|
Mucormycosis, or Rhizopus, infection
2010-296 |
|
|
Give two examples of common cardiovascular complications of diabetic ketoacidosis.
|
Arrhythmias and heart failure
2010-296 |
|
|
What is the pathogenesis of diabetic ketoacidosis?
|
Diabetic ketoacidosis is usually caused by an increase in insulin requirements as a result of an increase in stress (eg, infection)
2010-296 |
|
|
Give an example of a common neurologic complication of diabetic ketoacidosis.
|
Cerebral edema
2010-296 |
|
|
List the three core components of the treatment of diabetic ketoacidosis.
|
Fluids, insulin, and potassium
2010-296 |
|
|
What is the most common tumor of the appendix?
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Carcinoid tumor
2010-296 |
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What urinary finding might assist in the diagnosis of carcinoid syndrome?
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An elevated urine 5-hydroxyindoleacetic acid
2010-296 |
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Carcinoid syndrome can be treated with what drug?
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Octreotide, a somatostatin analogue
2010-296 |
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What causes carcinoid syndrome?
|
Neuroendocrine tumors that secrete high levels of serotonin
2010-296 |
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A patient with a known carcinoid tumor in the small intestine presents with wheezing and flushing; do you expect liver metastases on imaging? Why or why not?
|
Carcinoid syndrome occurs only with metastasis; this patient likely has liver metastases because serotonin secreted by tumors that have not metastasized undergo first-pass metabolism in the liver
2010-296 |
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A patient has diarrhea, flushing, and asthmatic wheezing, and you suspect carcinoid syndrome; what might the cardiac exam reveal?
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Tricuspid regurgitation due to right-sided valvular disease
2010-296 |
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Gastrinomas causing Zollinger-Ellison syndrome are usually found in which two sites?
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The pancreas and the duodenum
2010-296 |
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A patient has failed several proton pump inhibitors and is noted to have many ulcers on endoscopy, including several in the jejunum; what malignancy should you consider?
|
Zollinger-Ellison syndrome caused by a gastrin-secreting tumor
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Zollinger-Ellison syndrome may be associated with what genetic syndrome?
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Multiple endocrine neoplasia type I
2010-296 |
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Zollinger-Ellison syndrome is the result of a tumor that secretes what substance?
|
Gastrin
2010-296 |
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What three tumors are associated with multiple endocrine neoplasia 2B?
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Medullary thyroid carcinoma, Pheochromocytoma, oral or intestinal ganglioneuromas (remember: multiple endocrine neoplasia 2B = 1 P)
2010-297 |
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What gene mutation is seen in multiple endocrine neoplasia 2A and multiple endocrine neoplasia 2B?
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A mutation in the ret gene
2010-297 |
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What three tumors are associated with multiple endocrine neoplasia 1, or Wermer's syndrome?
|
Multiple endocrine neoplasia 1 = 3 P's: Pancreas, Pituitary, and Parathyroid
2010-297 |
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An elevation in which serum marker may indicate medullary thyroid cancer?
|
Calcitonin
2010-297 |
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Which multiple endocrine neoplasia syndrome is associated with a marfanoid body habitus?
|
Multiple endocrine neoplasia 2B
2010-297 |
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What three tumors are associated with multiple endocrine neoplasia 2A, or Sipple's syndrome?
|
Medullary thyroid carcinoma, Pheochromocytoma, Parathyroid tumors (remember: multiple endocrine neoplasia 2A = 2 P's)
2010-297 |
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Which of the multiple endocrine neoplasia syndromes commonly presents as nephrolithiasis and ulcer disease?
|
Multiple endocrine neoplasia 1, or Wermer's syndrome; elevated parathyroid hormone can cause renal stones, and ulcers may be associated with a gastrinoma
2010-297 |
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What is the likelihood that a child of a parent who has any of the multiple endocrine neoplasia syndromes will also have the disease?
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50%; all multiple endocrine neoplasia syndromes have autosomal-dominant inheritance
2010-297 |
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Name four pancreatic endocrine tumors seen in multiple endocrine neoplasia 1.
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Zollinger-Ellison syndrome (gastrinomas), insulinomas, vasoactive intestinal peptide tumors, and rarely glucagonomas
2010-297 |
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Describe the mechanism of action of sulfonylureas.
|
Sulfonylureas close the K+ channel on the β-cell membrane leading to cell depolarization and causing insulin release by increased calcium influx
2010-298 |
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What are toxicities of exenatide use?
|
Nausea, vomiting and possibly pancreatitis
2010-298 |
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Name three short-acting insulins.
|
Lispro, aspart, regular
2010-298 |
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To which class of diabetes drugs does metformin belong?
|
Biguanides
2010-298 |
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Name three second generation sulfonylureas.
|
Glyburide, glimepiride, glipizide
2010-298 |
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|
What is the basis of treatment of diabetes mellitus type 1?
|
Low-sugar diet and insulin replacement
2010-298 |
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|
What is the most common adverse effect of insulin treatment?
|
Hypoglycemia; very rarely, one may see a hypersensitivity reaction
2010-298 |
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Insulin binds insulin receptors which have ______ _____ signaling pathways.
|
Tyrosine kinase
2010-298 |
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To which class of diabetes drugs do pioglitazone and rosiglitazone belong?
|
Glitazones
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|
Name two long-acting insulins.
|
Glargine, detemir
2010-298 |
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How do glitazones work?
|
They increase target cell response to insulin via the peroxisome proliferator-activated receptor-γ pathway
2010-298 |
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A patient is in the intensive care unit and noted to have a blood glucose of 225 mg/dL; what medication is appropriate for this condition?
|
Insulin is effective in treating stress-induced hyperglycemia
2010-298 |
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Acarbose and miglitol work by inhibiting what enzyme?
|
α-Glucosidase, an intestinal brush border enzyme; this results in decreased postprandial hyperglycemia
2010-298 |
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What is the principal toxicity of α-glucosidase inhibitors?
|
Gastrointestinal disturbances
2010-298 |
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What is the mechanism of action of the GLP-1 mimetics?
|
Increases insulin and decreases glucagon
2010-298 |
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|
Before prescribing metformin, it is important to assess the function of what organ?
|
Kidney; if metformin cannot be excreted it may build up leading to lactic acidosis
2010-298 |
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What is an adverse effect of second-generation sulfonylureas?
|
Hypoglycemia
2010-298 |
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|
What are some toxicities of pramlintide?
|
Hypoglycemia, nausea, diarrhea
2010-298 |
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|
True or False: Metformin can be used in patients without islet function.
|
True
2010-298 |
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|
Name two α-glucosidase inhibitors.
|
Acarbose, miglitol
2010-298 |
|
|
What are the side effects of glitazones?
|
Glitazones can cause weight gain, edema, hepatotoxicity, and cardiovascular toxicity
2010-298 |
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|
Is neutral protamine Hagedorn (NPH) insulin considered a short-, intermediate-, or long-acting insulin?
|
Intermediate-acting insulin
2010-298 |
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|
Will sulfonylureas work in type 1 diabetes mellitus?
|
No; these drugs require islet cell function and the ability to secrete endogenous insulin (defective in type 1 diabetes)
2010-298 |
|
|
Which diabetes drugs can cause a disulfiram-like reaction?
|
First-generation sulfonylureas
2010-298 |
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|
Give an example of a glucagon-like peptide-1 mimetic drug.
|
Exenatide; this drug was discovered in the saliva of the gila monster
2010-298 |
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|
What is the basis of treatment for diabetes mellitus type 2?
|
Dietary modification and exercise for weight loss, oral hypoglycemics, insulin replacement (late)
2010-298 |
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|
What is the mechanism of action of pramlintide?
|
Pramlintide is a mimetic of an endogenous hormone and acts by inhibiting glucagon
2010-298 |
|
|
Name two first generation sulfonylureas.
|
Tolbutamide, chlorpropamide
2010-298 |
|
|
What is the mechanism of action of metformin?
|
Unknown; may decrease gluconeogenesis, increase glycolysis, thereby decreasing serum glucose levels; overall, it acts as an insulin sensitizer
2010-298 |
|
|
For what electrolyte disturbance can insulin be used as a treatment?
|
Hyperkalemia
2010-298 |
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|
Orlistat is properly used for the long-term management of obesity in conjunction with what other therapy?
|
A modified diet (remember: orlistat gets rid of fat)
2010-298 |
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|
Which drug used in the treatment of obesity may result in vitamin A, D, E, and K deficiency?
|
Orlistat, which can reduce the absorption of fat-soluble vitamins
2010-298 |
|
|
What adverse effects are associated with the use of orlistat?
|
Steatorrhea, gastrointestinal discomfort, reduced fat-soluble vitamin absorption, and headache
2010-298 |
|
|
Orlistat works by inhibiting _____ _____.
|
Pancreatic lipases
2010-298 |
|
|
Sibutramine works by inhibiting what processes?
|
The reuptake of serotonin and norepinephrine
2010-299 |
|
|
Sibutramine is used to treat what condition?
|
Sibutramine is used for the short-term and long-term management of obesity
2010-299 |
|
|
What are side effects of sibutramine?
|
Hypertension, tachycardia
2010-299 |
|
|
Methimazole and propylthiouracil inhibit what process?
|
Thyroid hormone synthesis (by inhibiting the organification and coupling of thyroid hormone)
2010-299 |
|
|
What are the known toxicities of methimazole and propylthiouracil?
|
Skin rash, aplastic anemia and agranulocytosis (rare)
2010-299 |
|
|
Propylthiouracil inhibits which biochemical pathway that methimazole does not?
|
Both affect thyroid hormone synthesis, but propylthiouracil also decreases the peripheral conversion of thyroxine to triiodothyronine
2010-299 |
|
|
What laboratory test should be ordered to avoid a rare but devastating adverse effect when starting a patient on methimazole or propylthiouracil?
|
Complete blood count, to monitor for aplastic anemia or agranulocytosis
2010-299 |
|
|
What disorder is treated using methimazole or propylthiouracil?
|
Hyperthyroidism
2010-299 |
|
|
What toxicities are associated with thyroid hormone replacement therapy?
|
Tachycardia, heat intolerance, tremors, arrhythmias (symptoms of hyperthyroidism)
2010-299 |
|
|
What pharmacotherapies are used as thyroxine replacements in hypothyroidism?
|
Levothyroxine and triiodothyronine
2010-299 |
|
|
A patient with hypothyroidism and myxedema is started on thyroid replacement therapy; what should you tell him about the prognosis of his myxedematous changes?
|
Myxedema can be treated by levothyroxine or triiodothyronine therapy
2010-299 |
|
|
List four indications for the use of octreotide.
|
Acromegaly, carcinoid tumor, gastrinoma, and glucagonoma
2010-299 |
|
|
List three processes that can be stimulated with the use of exogenous oxytocin.
|
Labor, uterine contractions, and milk let-down
2010-299 |
|
|
Following delivery, a woman continues to have uterine bleeding; what normally endogenous substance can be given to stop the blood loss?
|
Oxytocin (also known as pitocin)
2010-299 |
|
|
What are two medical indications for use of growth hormone?
|
Growth hormone deficiency, Turner's syndrome
2010-299 |
|
|
Can desmopressin be used in the treatment of nephrogenic diabetes insipidus?
|
No; desmopressin is an antidiuretic hormone analog that requires renal response and thus is effective only in pituitary diabetes insipidus
2010-299 |
|
|
What are the adverse effects of demeclocycline?
|
Photosensitivity, abnormalities of bones and teeth (demeclocycline is in the tetracycline family)
2010-299 |
|
|
A patient has hyponatremia with low serum osmolarity and high urine osmolarity; name a drug that works by antagonizing the defective pathway.
|
This is syndrome of inappropriate antidiuretic hormone secretion and can be treated by demeclocycline, which is an antidiuretic hormone antagonist
2010-299 |
|
|
A patient who is on chronic glucocorticoid therapy becomes ill and is found to have very low blood pressure; how might this be related to the medication history?
|
Long-term glucocorticoid therapy may lead to adrenocortical atrophy and failure to mount a stress response during illness
2010-299 |
|
|
What is the effect of chronic glucocorticoid use on fat distribution?
|
Patients develop truncal obesity, a buffalo hump, and moon facies
2010-299 |
|
|
A patient with a longstanding history of severe asthma, rheumatoid arthritis, and psoriasis has a buffalo hump and a blood glucose of 230 mg/dL; what is the likely cause of the hyperglycemia?
|
This patient has iatrogenic diabetes mellitus secondary to long-term glucocorticoid use
2010-299 |
|
|
What effect does chronic glucocorticoid use have on the musculoskeletal system?
|
It can cause muscle wasting and lead to osteoporosis
2010-299 |
|
|
What medication can be injected into a joint to treat the inflammation associated with degenerative arthritis?
|
Glucocorticoids, which are potent antiinflammatories
2010-299 |
|
|
A patient is found to have peptic ulcer disease. His medications include hydrochlorothiazide, oral prednisone, and atenolol; which is most likely to cause his ulcers?
|
Peptic ulcers are an adverse effect of glucocorticoids
2010-299 |
|
|
List five examples of glucocorticoid drugs.
|
Hydrocortisone, prednisone, triamcinolone, dexamethasone, and beclomethasone
2010-299 |
|
|
What effect can glucocorticoid toxicity have on the skin?
|
Thin skin and easy bruisability
2010-299 |
|
|
Give an example of a common pediatric pulmonary disease that can be treated with glucocorticoids.
|
Asthma
2010-299 |
|
|
What is the mechanism of action of glucocorticoids?
|
Decreases production of leukotrienes and prostaglandins by inhibiting phospholipase A2 and expression of COX-2
2010-299 |
|
|
Glucocorticoids can cause what iatrogenic endocrine disorder?
|
Cushing's syndrome
2010-299 |
|
|
What endocrine disease causes hypotension and skin pigmentation and can be treated with glucocorticoids?
|
Addison's disease
2010-299 |
