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624 Cards in this Set
- Front
- Back
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From what embryologic layer is the adrenal cortex derived?
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mesoderm
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From what embryologic layer is the adrenal medulla derived?
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the neural crest of the ectoderm (neuroectoderm)
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What is the secretory product of the zona glomerulosa of the adrenal gland?
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aldosterone
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What are the secretory products of the zona fasciculata of the adrenal gland?
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glucocorticoids (cortisol) and small amount of sex hormones
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What are the secretory products of the zona reticularis of the adrenal gland?
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sex hormones (androgens)
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What are the secretory products of the adrenal medulla?
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catecholamines (epinepherine and norepinepherine)
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What is the primary regulatory control for the zona glomerulosa of the adrenal gland?
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Renin-Angiotensin
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What substances are the primary regulatory controls for the zona fasciculata of the adrenal gland?
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ACTH from pituitary and CRH (corticotropin releasing hormone) from the hypothalamus
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What substances are the primary regulatory controls for the zona reticularis of the adrenal gland?
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ACTH from pituitary and CRH (corticotropin releasing hormone) from the hypothalamus
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True or False: The adrenal medulla is primarily regulated by preganglionic sympathetic fibers.
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True
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Name the five layers of the adrenal gland.
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Capsule, zona glomerulosa, zona fasciculata, zona reticularis, medulla
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What type of cells are found in the adrenal medulla?
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chromaffin cells
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What is the most common tumor of the adrenal medulla in adults?
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pheochromocytoma (associated with MEN IIA and IIB)
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What is the most common tumor of the adrenal medulla in children?
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neuroblastoma
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True or False: A neuroblastoma causes episodic hypertension.
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False; a pheochromocytoma causes episodic hypertension
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What is the effect of a pheochromocytoma on blood pressure?
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increased BP (episodic hypertension)
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What are the three layers of the adrenal cortex and their corresponding products?
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zona glomerulosa (Salt-aldosterone), zona fasciculata (Sugar-glucocorticoids-cortisol), zona reticularis (sex hormones- androgens. Remember GFR and "As you go deeper it gets sweeter- salt, sugar, sex"
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Trace 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.
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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 IVC ("the right adrenal vein drains right into the IVC")
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Which gonadal vein drains directly into the IVC: the right or the left?
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right gonadal vein (just as the right adrenal vein drains right into the IVC)
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From what embryonic layer is the posterior pituitary derived?
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neuroectoderm
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From what embryonic layer is the anterior pituitary derived?
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oral ectoderm
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What does the posterior pituitary gland secrete?
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ADH- Anti Diuretic Hormone (vasopressin) and Oxytocin
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Where are vasopressin (antidiuretic hormone) and oxytocin made?
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made in the hypothalamus
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Where are vasopressin (antidiuretic hormone) and oxytocin secreted from?
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secreted from posterior pituitary (neurohypophysis)
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What is secreted from the anterior pituitary?
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Follicle Stimulating Hormone (FSH)
Lutenizing Hormone (LH) Adrencorticotropic Hormone (ACTH) Thyroid Simulating Hormone (TSH) Prolactin Growth Hormone (GH) and Melanocyte Stimulating Hormone (MSH) (ACTH and MSH both derived from common precursor- POMC) Remember "FLAT PiG" |
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What hormones have an alpha subunit?
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TSH, LH, FSH and hCG (Thyroid-stimulating hormone, luteinizing hormone, follicle-stimulating hormone, and human chorionic gonadotropin)
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What is the clinical significance of the shared α subunit of TSH, LH, FSH, HCG?
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At high enough concentrations, a given hormone can partially activate the receptor of another hormone with the same α subunit
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What is the function of the beta subunit in endocrine pituitary hormones?
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it determines hormone specificity in TSH, LH, FSH, and hCG
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Which hormones are secreted from the acidophilic cells?
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Prolactin and Growth Hormone
(PiGs are Pink--- acidophilic) |
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Which hormones are secreted from the basophilic cells?
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Basophils secrete FSH, LH, ACTH, TSH (remember: B-FLAT)
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What cell types are found in the islets of Langerhans?
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Alpha, beta, and delta endocrine cells
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What do alpha endocrine cells secrete?
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glucagon
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What do beta endocrine cells secrete?
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insulin
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What do delta endocrine cells secrete?
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somatostatin
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Where are islets of Langerhans most numerous?
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pancreatic tail
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From what embryonic structures do the islets of Langerhans arise?
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pancreatic buds
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Where are alpha cells usually located within the islets of Langerhans?
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periphery
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Where are beta cells usually located in the islets of Langerhans?
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central (INSulin secreting beta cells are INSide)
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Where are the delta cells located in the islets of Langerhans?
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Interspersed
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What tissues are dependent on insulin for glucose uptake?
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adipose tissue and skeletal muscle
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What glucose transporter is insulin-dependent and where is it found?
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GLUT-4 on skeletal muscle and adipose tissue
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What cells are not dependent on insulin for glucose uptake?
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Brain, RBCs, Intestine, Cornea, Kidney, and Liver (BRICK L) do need insulin
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What glucose transporters are not insulin-dependent and where are they found?
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GLUT-1- RBCs and brain
GLUT-2 (bidirectional)- beta islet cells, kidney and liver |
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What does the brain use for metabolism under normal circumstances?
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glucose
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What does the brain use for metabolism under starvation states?
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ketone bodies made by the liver
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What do RBCs use for metabolism under normal circumstances?
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glucose
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What do RBCs use for metabolism under starvation states?
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Glucose; RBCs only have the glycolysis pathway to make ATP; thus, it cannot use ketone bodies like the brain in starvation states
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What is always released along with endogenous insulin?
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C-peptide
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if you see high insulin levels without corresponding high C-peptide levels, what does this indicate?
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exogenous insulin
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Where is insulin made and how is it released?
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beta islet cells- glucose enters beta cells via GLUT-2 transporter (non-insulin dependent)-- ATP is produced from aerobic resp leading to closure of ATP sensitive K+ channels-- this leads to depolarization of the cell--> calcium entry--> calcium causes insulin exocytosis from veiscles
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how does insulin act on glucagon release?
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insulin inhibits release of glucagon from alpha cells
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what are the 6 anabolic effects of insulin?
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1. inc glycogen synthesis and formation
2. inc triglyceride synthesis and storage 3. inc glucose uptake/transport 4. inc protein synthesis (muscles) 5. inc Na+ retention (kidneys) 6. inc uptake of K+ into cells |
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What is the effect of prolactin on the hypothalamus?
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Prolactin increases dopamine synthesis and secretion by the hypothalamus (thereby inhibiting its own release- feedback inhibition)
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What is the effect of dopamine on prolactin secretion?
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dopamine inhibits prolactin release from the anterior pituitary
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What is the effect of bromocriptine on prolactin secretion?
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bromocriptine is a dopamine agonist that increases dopamine and thereby inhibits the release of prolactin
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What is the effect of dopamine antagonists (eg, most antipsychotics) on prolactin secretion?
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dopamine antagonists release the inhibitory brake of dopamine on prolactin release-- thus increased prolactin secretion (galactorrhea in women or gynecomastia in men)
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What is the effect of prolactin on ovulation in women?
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prolactin inhibits GnRH and thus inhibits ovulation in women
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What is a common effect of a prolactinoma on a woman's menstrual cycle?
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amenorrhea (may be the first sign in women, dec libido may be the first sign in men)
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What hormone from the hypothalamus stimulates prolactin synthesis and release?
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Thyrotropin Releasing Hormone (TRH)
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Why might a patient with hypothyroidism caused by pituitary dysfunction have amenorrhea?
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Hypothyroidism (low T4) can cause high TRH from hypothalamus and thus prolactinemia which inhibits GnRH--> amenorrhea
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Thyrotropin-releasing hormone _____ (inhibits/stimulates) thyroid-stimulating hormone secretion.
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stimulates
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Thyrotropin-releasing hormone _____ (inhibits/stimulates) prolactin secretion.
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stimulates
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Dopamine _____ (inhibits/stimulates) prolactin secretion.
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inhibits
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Corticotropin-releasing hormone _____ (inhibits/stimulates) adrenocorticotropic hormone secretion.
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stimulates
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Growth-hormone-releasing hormone _____ (inhibits/stimulates) growth hormone secretion.
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stimulates
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Somatostatin _____ (inhibits/stimulates) growth hormone secretion.
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inhibits
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Somatostatin _____ (inhibits/stimulates) thyroid-stimulating hormone secretion.
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inhibits
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Gonadotropin-releasing hormone stimulates secretion of?
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FSH and LH (follicle stimulating hormone and lutenizing hormone)
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Prolactin _____ (inhibits/stimulates) GnRH secretion.
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inhibits
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Which enzyme is responsible for converting cholesterol to pregnenolone?
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desmolase
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Which enzyme catalyzes conversion of testosterone to dihydrotestosterone?
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5α-Reductase
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ACTH has a(n) _______ (inhibitory/stimulatory) effect on desmolase while ketoconazole has a(n) __________ (inhibitory/stimulating) effect on desmolase.
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stimulatory; inhibitory
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What enzyme is responsible for the conversion of pregnenolone to progesterone?
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3β-Hydroxysteroid dehydrogenase
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Why do congenital adrenal enzyme deficiencies cause adrenal enlargement?
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There is increased ACTH stimulation due to decreased cortisol production; negative feedback is diminished
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Do congenital adrenal enzyme deficiencies cause unilateral or bilateral enlargement?
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Bilateral; ACTH stimulation is not specific to either adrenal gland
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Which enzyme catalyzes the conversion of testosterone to estradiol?
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aromatase
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What is testosterone an immediate precursor of?
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estradiol and Dihyrotestosterone (DHT)
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What are the relative levels of adrenal steroids you'd expect to find in a patient with 17α-hydroxylase deficiency?
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Decreased sex hormones and cortisol; increased mineralocorticoids
(aldosterone) |
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What are the systemic symptoms associated with 17α-hydroxylase deficiency?
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HYPERtension, hypokalemia due to increased aldosterone/mineralocorticoids,
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In XY males, what are the symptoms associated with 17α-hydroxylase deficiency?
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XY: pseudohermaphroditism- testis and thus MIF so no internal female genitalia, but no testosterone or DHT so female external genitalia,
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In XX females, what are the symptoms associated with 17α-hydroxylase deficiency?
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no secondary sex characteristics ("sexual infantilism") due to lack of testosterone
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What are the relative levels of adrenal steroids you'd expect to find in a patient with 21α-hydroxylase deficiency?
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decreased mineralocorticoids and cortisol, increased sex hormones
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What symptoms are associated with 21α-hydoxylase deficiency?
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HYPOtension, hyperkalemia, increased salt wasting, increased renin, decreased blood volume, masculinization and female pseudohermaphrodotism
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Explain the effect of increased sex hormones in female patients with 21α-hydroxylase deficiency?
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decreased 21 alpha hydroxylase shunts precursors down the sex hormone production pathway leading to increased testosterone and DHT and masculinization/androgenization of the female external genitalia
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Explain the effect of decreased mineralocorticoids in patients with 21α-hydroxylase deficiency?
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The deficiency causes shunting of precursors away from the mineralocorticoid pathway leading to decreased aldosterone; thus, there is no Na+ reabsorption with a resultant hypotension and hyperkalemia
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Why would one expect to see increased renin activity in 21α-hydroxylase deficiency?
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The absence of aldosterone leads to volume depletion, thereby activating the renin-angiotensin-aldosterone pathway; since aldosterone cannot be formed to increase blood volume, the patient remains hypovolemic and high renin activity is continually stimulated
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What are the relative values of adrenal steroids you'd expect to see in 11β-hydroxylase deficiency?
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Decreased cortisol, aldosterone, and mineralocorticoids, and increased sex hormones
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What are the symptoms associated with 11β-hydoxylase deficiency?
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hypertension and masculinization
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Why would one expect to see hypertension in 11β-hydroxylase deficiency?
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A precursor of aldosterone, 11-deoxycorticosterone is also a mineralocorticoid; with 11β-hydroxylase deficiency, this precursor builds up, leading to hypertension
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How does ketoconazole inhibit steroid synthesis?
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Ketoconazole inhibits desmolase so that cholesterol is not converted to pregnenolone
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Androstenedione is the precursor to which steroid produced in the adrenal zona reticularis?
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testosterone
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True or False: Aldosterone is produced in the adrenal zona glomerulosa.
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True
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Aldosterone synthase converts what precursor to aldosterone?
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corticosterone
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What is the appearance of a 16-year-old child with untreated 17α-hydroxylase deficiency?
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phenotypically female but no maturation
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What is the role of angiotensin II in aldosterone synthesis?
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angiotensin II stimulates aldosterone synthase which converts corticosterone to aldosterone
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True or False: Androgens are converted to estrogens in the adrenal gland.
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False; they are converted to estrogen in the periphery by aromatase
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Which two reactions cannot be carried out in 17α-hydroxylase deficiency?
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pregnenolone--> 17 hydroxypregnenolone and progesterone--> 17 hydroxyprogesterone
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Which two reactions cannot be carried out without 21α-hydroxylase?
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progesterone--> 11 deoxycorticosterone and 17 hydroprogesterone--> 11 deoxycortisol
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Which two reactions cannot be carried out without 11β-hydroxylase?
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11 deoxycorticosterone--> corticosterone and 11 deoxycortisol--> cortisol
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Where is cortisol made?
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zona fasciculata of the adrenal cortex
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What are five functions of cortisol?
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increase blood pressure (up-regulation of alpha 1 receptors)
dec bone formation dec immune function dec inflammation inc gluconeogenesis, lipolysis, and proteolysis |
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What are five functions of cortisol?
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Anti-inflammatory; increases gluconeogenesis, lipolysis, and proteolysis; decreases immune function; maintains blood pressure; decreases bone formation
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What hormones are involved in regulation of cortisol secretion?
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CRH from the hypothalamus stimulates ACTH release from the anterior pituitary; ACTH then stimulates cortisol production by the adrenal gland
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Is cortisol a bound or unbound molecule in circulation?
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bound to corticosteroid binding globulin (CBG)
estrogen increases CBG-- increases total but not free levels |
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What effect does chronic stress have on cortisol secretion?
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prolonged secretion
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What cell type in the parathyroid produces parathyroid hormone?
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chief cells
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What are five functions of cortisol?
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Anti-inflammatory; increases gluconeogenesis, lipolysis, and proteolysis; decreases immune function; maintains blood pressure; decreases bone formation
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What hormones are involved in regulation of cortisol secretion?
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CRH from the hypothalamus stimulates ACTH release from the anterior pituitary; ACTH then stimulates cortisol production by the adrenal gland
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Is cortisol a bound or unbound molecule in circulation?
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bound to corticosteroid binding globulin (CBG)
estrogen increases CBG-- increases total but not free levels |
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What effect does chronic stress have on cortisol secretion?
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prolonged secretion
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What cell type in the parathyroid produces parathyroid hormone?
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chief cells
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What effect does parathyroid hormone have on serum calcium?
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PTH increases the serum calcium level
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What effect does parathyroid hormone have on bone?
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Increased resorption of calcium and phosphate (leading to increases of serum levels of both minerals)
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What effect does parathyroid hormone have on the kidney?
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increased resorption of calcium from DCT, decreased phosphate reabsorption, stimulation of 1α hydroxylase activity (which converts 25 OH vit D--> 1,25 OH vit D
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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 absorption from the intestines
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What enzyme in the kidney is stimulated by parathyroid hormone?
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1α-Hydroxylase which converts 25 OH vit D--> 1,25 OH vit D
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What overall effect does parathyroid hormone have on serum phosphate?
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PTH decreases the levels of serum phosphates
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What overall effect does parathyroid hormone have on serum calcium?
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PTH increases the serum calcium level
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What overall effect does parathyroid hormone have on urine phosphates?
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PTH increases levels of urine phosphates
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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
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Parathyroid hormone acts _____ (directly/indirectly) on osteoclasts.
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indirectly-- PTH stimulates osteoblasts which then stimulate osteoclasts (RANK Ligand-RANK)
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True or False: Parathyroid hormone (PTH) directly stimulates osteoblasts.
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True
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What is the active form of vitamin D?
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1,25-dihydroxy vitamin D
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What is another name for 1,25(OH)2 vitamin D?
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calcitriol
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Does high or low serum calcium stimulate the formation of active vitamin D?
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low
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Does high or low serum phosphate stimulate the formation of active vitamin D?
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low
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Do high or low levels of parathyroid hormone stimulate the formation of active vitamin D?
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high
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What inhibits parathyroid hormone secretion?
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Increased serum calcium level (and very low levels of magnesium)
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What effect does activated vitamin D have on serum phosphates?
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It increases the levels of serum phosphates
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Which two organs are the targets for 1,25(OH)2 vitamin D?
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The gastrointestinal tract (increased absorption of Calcium and Phosphate) and bone (increased resorption of calcium and phosphate)
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What is the effect of serum magnesium on PTH secretion?
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low magnesium leads to decreased PTH secretion
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What are some causes of low magnesium?
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diuretics, alcohol abuse, diarrhea, aminoglycosides (antibiotics)
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What is the source of Vitamin D3?
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sun exposure of the skin
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What is the source of vitamin D2?
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plants
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What are the two sources of the precursors for activated vitamin D?
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sun- D3 and plants- D2
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In which organ is vitamin D converted to 25-hydroxy vitamin D?
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the liver
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Where is 25-hydroxy vitamin D activated?
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in the kidney
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True or False: 24,25-hydroxy vitamin D is active.
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False; 24-25-hyroxy vitamin D has no action
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What form of vitamin D is active?
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1,25(OH)2 vitamin D
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Do high or low levels of parathyroid hormone stimulate the formation of 1,25(OH)2 vitamin D?
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high levels
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Does a high serum calcium level increase or decrease vitamin D production?
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decrease
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Does a low serum phosphate level increase or decrease vitamin D production?
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increase
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True or False: 1,25(OH)2 vitamin D inhibits the further production of itself.
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true
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A deficiency of vitamin D in children results in what condition?
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Rickets
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A deficiency of vitamin D in adults results in what condition?
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osteomalacia
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What effect does vitamin D have on the gut?
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increased gut absorption of dietary calcium and phosphates
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Compare the effects of 1,25-OH2 vitamin D and PTH on absorption of calcium and phosphorus.
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Vitamin D increases absorption of dietary calcium and phosphates, increases resorption of calcium and phosphate from bone; PTH: increases calcium and phosphorus resorption from the bone, activates vitamin D in the kidney; therefore, PTH does not directly incease absorption of either calcium or phosphorus from the gut
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What effect does vitamin D have on bone?
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increases resorption of calcium and phosphate
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Where is calcitonin made?
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parafollicular (C cells) of the thyroid
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What is the effect of calcitonin?
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Decreases calcium resorption from bone (decreases serum calcium levels)
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What stimulates the secretion of calcitonin?
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high serum calcium (calciTONin- TONes down serum calcium)
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How is calcitonin involved in calcium homeostasis?
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It opposes the action of PTH, but has no role in normal calcium homeostasis
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What hormones use the tyrosine kinase signaling pathway?
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Insulin, IGF-1, FGF, PDGF, prolactin, GH
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What hormones use cGMP as a signaling molecule?
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ANP and NO and Endothelin Derived Relaxing Factor-EDRF= VASODILATORS
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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 (use tyrosine kinase receptors)
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Name the endocrine hormones that use steroid receptors in their signaling pathways.
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glucocorticoids, aldosterone, estrogen, progesterone, testosterone, T3/T4, vitamin D
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True or False: Calcitonin uses a cAMP signaling pathway.
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True
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True or False: Glucagon uses a tyrosine kinase signaling pathway.
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False; Glucagon use cAMP signaling pathway
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What hormones use IP3 signaling pathway?
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GHRH, GnRH, TRH, ADH (V1 receptor--Gq) and Oxytocin
(Remember GGOAT)-all releasing hormones except CRH + posterior pituitary hormones |
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True or False: ADH (V2) utilizes the IP3 signaling pathway.
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False; ADH (V2) uses the cAMP pathway (Gs); ADH (V1) uses the IP3 pathway (Gq)
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Insulin activates the enzyme _____ _____ after it binds to its receptor, while glucagon increases the concentration of _____ in the cell after it binds to its receptor.
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tyrosine kinase (receptor); cAMP (second messenger)
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Name the hormones that use the cAMP signaling pathway.
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FSH, LH, ACTH, TSH, CRH, HCG, ADH (V2), MSH, PTH, glucagon, calcitonin (remember FLAT CHAMP)
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Why is there a delay in the onset of the action of steroid hormones?
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time is needed for transcription and protein synthesis
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Are steroid hormones hydrophilic or lipophilic?
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lipophilic so they can act on steroid receptors in the cytoplasm or nucleus
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True or False: Steroid hormones are very soluble in plasma.
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False; they are lipophilic and require binding globulins to increase their solubility in the plasma
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Where can receptors for steroid hormones be found?
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cytoplasm and nucleus
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What event leads to the exposure of DNA-binding domains on the receptors of steroid hormones?
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the binding of a hormone to its specific receptor
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Increased levels of sex-hormone binding globulin may produce what in men?
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gynecomastia (decreased serum free/bioavailable testosterone)
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Why do increased levels of steroid hormone binding protein lead to gynecomastia in men?
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binding protein binds the testosterone leading to decreased free serum testosterone
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Decreased levels of sex-hormone binding globulin may produce what in women?
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hirsuitism-- less testosterone is bound--more is free-- increased serum free testosterone
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How are steroid hormones made water-soluble to be able to travel in the plasma?
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by binding to specific binding globulins
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True or False: Cortisol has a receptor that is found in the nucleus or the cytoplasm.
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True because it is a lipophilic steroid hormone
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True or False: Testosterone, estrogen, and progesterone all act by altering the transcription of specific target genes.
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True
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True or False: The aldosterone receptor activates a G protein to produce its effect.
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False; aldosterone is a steroid. Instead of using second messenger G proteins, it binds receptors within cell nuclei or cytoplasm to transcribe genes and synthesize proteins
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What effect does increasing the levels of sex-hormone binding globulin have on the concentration of free testosterone?
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decreased conc of free testosterone
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What effect does decreasing the levels of sex-hormone binding globulin have on the concentration of free testosterone?
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increased conc of free testosterone
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True or False: All hormones that come from the adrenal cortex are steroids.
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True (aldosterone, cortisol, testosterone etc)
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Which hormones in the body incorporate iodine into their structure and control the body's metabolic rate?
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thyroid hormones (T3 and T4)
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What protein in the plasma binds T3 and T4 for transportation?
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Thyroxin binding globulin (TBG)
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What happens to the level of thyroxine-binding globulin during pregnancy?
|
it increases as a result of higher estrogen levels
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What causes increased thyroxine-binding globulin during pregnancy?
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increased estrogen
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What happens to the level of thyroxine-binding globulin during hepatic failure?
|
it is decreased (less protein synthesis)
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What cell type in the thyroid produces T3 and T4?
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follicular cells
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|
|
What is the location of the majority of T3 formation?
|
the blood/periphery
|
|
|
What effect does thyroid hormone have the on basal metabolic rate?
|
increase basal metabolic rate
|
|
|
What cell membrane protein does T3 and T4 act on to produce an increased basal metabolic rate?
|
increased Na+/K+ ATPase activity
|
|
|
What are the four main functions of T3?
|
The four B's: Brain maturation, Bone growth, Basal metabolic rate inc, Beta adrenergic affects (contractility, HR, SV, CO)
|
|
|
Will increased levels of T3 and T4 lead to an increased or decreased respiratory rate?
|
increased (need more oxygen to make more ATP for increased BMR)
|
|
|
True or False: Thyroid hormone is required for brain maturation.
|
True (T3 needed)
|
|
|
True or False: T3 and T4 lead to decreased lipolysis.
|
False; increased T3 and T4 lead to increased lipolysis (everything gets revved up-- lose weight, burn more fat etc)
|
|
|
True or False: Thyroid hormone stimulates gluconeogenesis.
|
True
|
|
|
True or False: Thyroid hormone decreases glycogenolysis.
|
False; thyroid hormone increases glycogenolysis
|
|
|
What effect does thyroid hormone have on body temperature?
|
increase body temp
|
|
|
True or False: Thyroid hormone inhibits bone growth.
|
False; thyroid hormone promotes bone growth
|
|
|
True or False: Thyroid hormone is required for normal brain maturation.
|
true
|
|
|
Does thyroid hormone increase activation of alpha or beta adrenergic receptors?
|
beta
|
|
|
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.
|
thryotropin-releasing hormone; thryoid stimulating hormone
|
|
|
Negative feedback by what substance decreases the sensitivity of the anterior pituitary to thyrotropin-releasing hormone, thereby leading to decreased thyroid hormone production?
|
free T3
|
|
|
What is the mechanism by which Graves' disease causes hyperthyroidism?
|
Thyroid stimulating immunoglobulin (thyroid receptor antibody) stimulates TSH receptor on thyroid to increase thyroid hormone production (independent of TSH)
|
|
|
True or False: T3 and T4 cause the body to increase cardiac output, heart rate, stroke volume, and cardiac contractility.
|
true via the up-regulation of B1-adrenergic receptors in cardiac tissue
|
|
|
Will the rate of oxygen consumption likely be increased or decreased in a patient who does not produce enough T3 and T4?
|
decreased
|
|
|
From which large precursor protein is thyroid hormone derived?
|
thyroglobulin
|
|
|
What is the role of peroxidase in the production of thyroid hormones?
|
I- is converted to I2 at the apical membrane by peroxidase; this step is necessary because I2 is added to tyrosine yielding MIT and DIT, a precursor for thyroid hormones
|
|
|
Is the conversion of I- into I2 before incorporation into thyroglobulin accomplished through oxidation or reduction?
|
oxidation
|
|
|
Does T3 or T4 have greater affinity for thyroid hormone receptors?
|
T3
|
|
|
A patient has Cushing's syndrome and has an increased ACTH level. Name two mechanisms of increased ACTH production.
|
The overproduction of ACTH by the pituitary (hyperfunctioning pituitary adenoma), and the overproduction of ACTH by an ectopic site (such as in small cell lung cancer)
|
|
|
A patient has Cushing's syndrome and has a decreased ACTH level. Name two mechanisms of increased cortisol production with low ACTH levels.
|
exogenous cortisol (#1 cause of cushing's syndrome) and adrenal tumor overproducing cortisol
|
|
|
Does a high ACTH signify Cushing's disease or Cushing's syndrome?
|
cushing's disease (high ACTH from pituitary adenoma)
|
|
|
A patient is diagnosed with small-cell carcinoma of the lung leading to Cushing's syndrome. Will this patient's ACTH level be high or low?
|
high- small cell lung cancer can lead to ectopic production of ACTH
|
|
|
A patient is diagnosed with primary adrenal cortical hyperplasia. Will this patient's ACTH level be high or low?
|
low-- adrenal cortex is overproducing cortisol which is sending feedback inhibition to the pituitary to decrease ACTH release
|
|
|
What is the effect of long-term steroid administration on ACTH?
|
Leads to suppression of the HPA axis and thus low ACTH levels
|
|
|
What is Cushing's disease?
|
An ACTH-hypersecreting primary pituitary adenoma
|
|
|
What are the results of a low dose dexamethasone suppression test in a healthy person?
|
decreased ACTH secretion and thus decreased cortisol levels
|
|
|
What results would you expect after a dexamethasone suppression test in the setting of an ACTH-producing pituitary tumor?
|
low dose: high ACTH and cortisol
high dose: low ACTH and cortisol adenoma retains some responsiveness to feedback inhibition but requires high dex levels to achieve suppression |
|
|
What would an increased cortisol level after both low- and high-dose dexamethasone challenges indicate?
|
an ectopic ACTH producing tumor (as in small cell lung cancer or bronchial carcinoids) or cortisol producing tumor
|
|
|
Would cortisol levels be high or low after a low-dose dexamethasone suppression test in a patient with a cortisol-producing tumor?
|
High; this tumor activity is independent of ACTH regulation
|
|
|
Would cortisol levels be high or low after a high-dose dexamethasone suppression test in a patient with a cortisol-producing tumor?
|
High; this tumor activity is independent of ACTH regulation
|
|
|
What are the symptoms of Cushing's syndrome?
|
Hypertension, weight gain, moon facies, truncal obesity, buffalo hump, hyperglycemia (insulin resistance), skin changes (thinning and wide striae), osteoporosis, amenorrhea, immune suppression, and proximal muscle wasting
|
|
|
True or False: Cushing's syndrome is associated with immune suppression.
|
true
|
|
|
Why are patients who are taking chronic steroids more susceptible to infection?
|
steroids reduce immune function (thus they are taken for autoimmune diseases)
|
|
|
When are cortisol levels drawn for the dexamethasone suppression test and why?
|
In the morning; this is when cortisol levels should be at the highest
(the most accurate is 24 hour free urine cortisol) |
|
|
Which diuretic is used as a treatment for hyperaldosteronism?
|
spironolactone- aldosterone antagonist
|
|
|
Which medication used to treat hyperaldosteronism is a potassium-sparing diuretic that acts as an aldosterone antagonist?
|
spironolactone
|
|
|
What is the cause of Conn's syndrome?
|
aldosterone secreting tumor
|
|
|
What findings are associated with Conn's syndrome?
|
hypertension, hypokalemia, low renin, metabolic alkalosis
|
|
|
Why does Conn's syndrome lead to low plasma renin?
|
High aldosterone leads to volume expansion by increased salt and water resorption; this in turn leads to increased salt delivery to the JGA leading to decreased plasma renin levels
|
|
|
A patient has hypertension, hypokalemia, metabolic alkalosis, and a high plasma renin level. What is the most likely diagnosis?
|
secondary hyperaldosteronism (renal artery stenosis, CHF, chronic renal failure, nephrotic syndrome-loss of albumin in urine, cirrhosis--low albumin production)
|
|
|
What are findings associated with secondary hyperaldosteronism?
|
hypertension, hypokalemia, high plasma renin, metabolic alkalosis
|
|
|
What are some causes of secondary hyperaldosteronism?
|
renal artery stenosis, chronic renal failure, cirrhosis (edema and not making albumin), CHF, nephrotic syndrome (losing albumin in urine)
|
|
|
Why is secondary hyperaldosteronism associated with high plasma renin levels?
|
All the causes of secondary hyperaldosteronism cause the kidney to perceive a low intravascular volume state, causing up-regulation of the renin-angiotensin pathway (RAAS)
|
|
|
Conn's syndrome is also called _____ _____.
|
primary hyperaldosteronism
|
|
|
Is a patient with Conn's syndrome likely to have a high or a low plasma renin level?
|
low plasma renin
|
|
|
What hormones are deficient in patients with Addison's disease as a result of adrenal atrophy?
|
cortisol and aldosterone
|
|
|
True or False: The adrenal cortex is markedly hypertrophied in patients with Addison's disease.
|
False; there is atrophy and decreased hormone production from all three layers of the adrenal cortex in Addison's disease
|
|
|
True or False: Addison's disease involves all three layers of the adrenal cortex.
|
true
|
|
|
What are the findings associated with Addison's disease?
|
hypotension, hyperkalemia, high ACTH, skin pigmentation
|
|
|
Is primary or secondary hypoaldosteronism associated with skin hyperpigmentation?
|
primary hyperaldosteronism
|
|
|
Is low ACTH production associated with primary or secondary hypoaldosteronism?
|
secondary
|
|
|
A patient is diagnosed with secondary hypoaldosteronism. Will this patient's ACTH levels be high or low?
|
low ACTH
|
|
|
Why is skin pigmentation a finding of Addison's?
|
In Addison's, there is increased ACTH; POMC is the precursor of ACTH and MSH; MSH (melanocyte stimulating hormone) is the product that leads to skin hyperpigmentation
|
|
|
Would the adrenal glands of a patients with Addison's disease appear to be atrophic or hypertrophic?
|
atrophic
|
|
|
What are the findings associated with secondary adrenal insufficiency?
|
decreased ACTH, NO hyperkalemia, NO skin pigmentation
|
|
|
A patient is diagnosed with meningococcal septicemia. What acute endocrine problem would be most concerning?
|
Waterhouse-Friderichsen syndrome, or acute adrenocortical insufficiency caused by adrenal hemorrhage
|
|
|
Waterhouse-Friderichsen syndrome is a hemorrhagic syndrome of which organ?
|
adrenal glands, causing acute adrenocorticol insufficiency
|
|
|
What is Waterhouse-Friderichsen syndrome associated with?
|
Neisseria meningitidis septicemia, epticemia, endotoxic shock, and DIC
|
|
|
What causes Sheehan's syndrome?
|
Enlargement of the anterior pituitary (Due to increased Prolactin production) during pregnancy without corresponding increase in blood supply increases risk of infarction if severe bleeding and hemorrhage occur during pregnancy or delivery
|
|
|
What causes pituitary enlargement during pregnancy?
|
Increased number of lactotrophs (prolactin producing cells)
|
|
|
What is the name of the syndrome associated with postpartum hypopituitarism?
|
Sheehan's syndrome
|
|
|
What symptoms are associated with Sheehan's syndrome?
|
poor lactation (trouble breastfeeding), fatigue, loss of pubic and axillary hair, anorexia
|
|
|
True or False: Increased growth of pubic and axillary hair is characteristic of Sheehan's syndrome.
|
False; associated with loss of pubic and axillary hair (lack of ACTH from pituitary to stimulate androgen production in adrenal cortex)
|
|
|
List three substances that are commonly secreted by pheochromocytoma tumors.
|
dopamine, norepinepherine, epinepherine
|
|
|
The urinary level of what substance is elevated in patients with pheochromocytoma?
|
vanillyl mandelic acid (VMA-breakdown product of norepi)
maybe also metanepherines (breakdown product of epi) |
|
|
The plasma level of what group of substances is elevated in patients with pheochromocytoma?
|
catecholamines (dopamine, norepi, epi)
|
|
|
List three genetic syndromes that are associated with pheochromocytoma.
|
neurofibromatosis, Multiple Endocrine Neoplasia IIA and IIB (MEN IIA and IIB)
|
|
|
What category of drugs is often used to treat pheochromocytoma?
|
alpha- antagonists (like phenoxybenzamine-non-selective, irreversible alpha blocker)
|
|
|
Which α-antagonist in particular is used to treat pheochromocytoma?
|
phenoxybenzamine
|
|
|
True or False: Phenoxybenzamine is a selective α-antagonist.
|
False; it's non-selective
|
|
|
True or False: Phenoxybenzamine is a reversible α-antagonist.
|
False; it is irreversible
|
|
|
List five episodic hyperadrenergic symptoms of pheochromocytoma.
|
Pain (headache), Pallor, Pressure (high blood pressure), Palpitations (tachycardia), Perspiration (5Ps)
|
|
|
List the six components of "the pheochromocytoma rule of tens."
|
10% are maligant
10% are bilateral 10% occur in kids 10% are outside the adrenal medulla 10% are familial (as with MEN 2A & B) 10% calcify |
|
|
Do the symptoms of pheochromocytoma tend to occur with a chronic progressive course or a relapsing and remitting course?
|
relapsing and remitting-- episodic- symptoms occur in "spells"
|
|
|
From what cells does pheochromocytoma develop?
|
enterochromaffin cells of the adrenal medulla (derived from neural crest= neuroectoderm)
|
|
|
Vanillylmandelic acid is a breakdown product of what?
|
norepinepherine
|
|
|
What is the precursor of the cathecholamines?
|
tyrosine
|
|
|
What is the breakdown product of epinephrine?
|
metanepherines
|
|
|
What is the breakdown product of dopamine?
|
homovanillic acid (HVA)
|
|
|
Why is phenoxybenzamine used as a pre-op treatment for pheochromocytoma removal?
|
It is used to counter the hypertensive effects of the catecholamines that may be released during the tumor removal
|
|
|
Neuroblastoma is the most common adrenal tumor in what age group?
|
children
|
|
|
Where does neuroblastoma develop?
|
anywhere along the sympathetic chain
|
|
|
What product is increased in the urine of children with neuroblastoma?
|
homovanillic acid (HVA) a breakdown product of dopamine
|
|
|
What product is increased in the urine of children with neuroblastoma?
|
N-myc oncogene
|
|
|
What effect does neuroblastoma have on blood pressure?
|
Minimal; less likely to cause hypertension, unlike pheochromocytoma
|
|
|
How do hypo- and hyperthyroidism each affect temperature tolerance?
|
Hypothyroidism causes cold intolerance; hyperthyroidism causes heat intolerance
|
|
|
How do hypo- and hyperthyroidism each affect body weight?
|
hypothyroidism causes weight gain despite decreased appetite, hyperthyroidism causes weight loss despite increased appetite
|
|
|
How do hypo- and hyperthyroidism each affect activity levels?
|
hypothyroidism- decreased activity
hyperthyroidism- increased activity |
|
|
Which causes decreased appetite: hypothyroidism or hyperthyroidism?
|
hypothyroidism
|
|
|
How do hypo- and hyperthyroidism each affect bowel movements?
|
hypothyroidism- constipation
hyperthyroidism- diarrhea |
|
|
Which causes fatigue and lethargy: hypothyroidism or hyperthyroidism?
|
hypothyroidism
|
|
|
What cardiac symptoms can hyperthyroidism cause?
|
chest pain, palpitations and arrhythmias
|
|
|
Which causes weakness: hypothyroidism or hyperthyroidism?
|
hypothyroidism
|
|
|
What parameter is a sensitive test for primary hypothyroidism?
|
TSH -thyroid stimulating hormone (should be elevated)
|
|
|
Which causes periorbital myxedema: hypothyroidism or hyperthyroidism?
|
hypothyroidism
|
|
|
Hypothyroidism often causes myxedema in what region?
|
periorbital/facial region
myxedema= non-pitting edema |
|
|
How do hypo- and hyperthyroidism each affect the skin?
|
hypothyroidism- cool, dry skin
hyperthryoidism- warm, moist skin |
|
|
How do hypo- and hyperthyroidism each affect the hair?
|
hypothyroidism- coarse, brittle hair
hyperthyroidism- fine hair |
|
|
What pathologic cardiac process is hyperthyroidism known to induce?
|
arrhytmias like atrial fibrillation
|
|
|
What happens to the thyroid-stimulating hormone level in patients with hypothyroidism?
|
TSH is elevated
|
|
|
What happens to the level of total T4 in patients with hypothyroidism?
|
decreased
|
|
|
What happens to the level of free T4 in patients with hypothyroidism?
|
decreased
|
|
|
What happens to the T3 uptake level in patients with hypothyroidism?
|
decreased
|
|
|
What happens to the thyroid-stimulating hormone level in patients with primary hyperthyroidism?
|
TSH level is decreased
|
|
|
What happens to the level of total T4 in patients with hyperthyroidism?
|
increased
|
|
|
What happens to the level of free T4 in patients with hyperthyroidism?
|
increased
|
|
|
What happens to the T3 uptake level in patients with hyperthyroidism?
|
increased
|
|
|
Hashimoto's thyroiditis falls within what category of diseases: congenital, neoplastic, or autoimmune?
|
autoimmune
|
|
|
Does Hashimoto's thyroiditis result in a hyperthyroid, euthyroid, or hypothyroid state?
|
hypothyroid state
|
|
|
True or False: In Hashimoto's thyroiditis, the thyroid is generally tender.
|
False; False; Hashimoto's thyroiditis involves slow lymphocytic infiltration of the thyroid and produces a moderately enlarged, nontender thyroid
(the thyroid is tender in subacute thyroiditis (de Quervain's) ) |
|
|
Describe the course of Hashimoto's thyroiditis.
|
Slow course, can have an initial period of thyrotoxicosis before hypothyroidism due to release of stored thyroid hormones
|
|
|
True or False: A monocytic infiltrate is seen in patients with Hashimoto's thyroiditis.
|
False; a lymphocytic infiltrate with germinal centers is seen with Hashimoto's thyroiditis
|
|
|
True or False: Germinal centers can be observed in patients with Hashimoto's thyroiditis.
|
True
|
|
|
What would the thyroid feel like on physical exam of a patient with Hashimoto's thyroiditis?
|
diffusely moderately enlarged and non-tender
|
|
|
List two types of antibodies that are sometimes used in the diagnosis of Hashimoto's thyroiditis.
|
antimicrosomal antibodies and antithyroglobulin antibodies
|
|
|
True or False: Thyroid hormone levels can be elevated during Hashimoto's thyroiditis.
|
True; thyroid hormone can be spilled during follicle rupture initially leading to thyrotoxicosis
|
|
|
What are histological findings of Hashimoto's thyroiditis?
|
lymphocytic infiltrate with germinal centers and Hurthle cells
|
|
|
Overall, does subacute thyroiditis result in hypothyroidism, euthyroidism, or hyperthyroidism?
|
Hypothyroidism, although these patients may show early hyperthyroidism
|
|
|
True or False: The course of subacute thyroiditis is self-limited.
|
True (start beta blocker only to prevent afib/arrhythmia)
|
|
|
What often precedes subacute thyroiditis?
|
a flu-like illness
|
|
|
True or False: Erythrocyte sedimentation rate is often elevated in patients with subacute thyroiditis.
|
true
|
|
|
List two places where pain and tenderness often occur in patients with subacute thyroiditis.
|
the jaw and the thyroid
|
|
|
True or False: In patients with subacute thyroiditis, the thyroid gland is found to be very tender.
|
true
|
|
|
When during the course of subacute thyroiditis can patients be hyperthyroid?
|
Early during the course of disease (release of stored thyroid from colloid)
|
|
|
What are histological findings of subacute thyroiditis?
|
granulomatous inflammation
|
|
|
Can subacute thyroiditis be painless?
|
yes-- lymphocytic subacute thyroiditis is painless
|
|
|
What is the pathophysiology of Reidel's thyroiditis?
|
Thyroid tissue replaced by fibrous tissue
|
|
|
Does Reidel's thyroiditis cause hyper- or hypothyrodism?
|
hypothyroidism
|
|
|
What are physical exam findings of Reidel's thyroiditis?
|
Fixed, hard (rock-like), painless goiter
|
|
|
What is the pathophysiology of Graves' disease?
|
It is an autoimmune disorder associated with TSH receptor antibodies that stimulate thyroid hormone release
|
|
|
What are physical exam findings associated with Graves' disease?
|
Exophthalmos (proptosis), pretibial myxedema, diffuse goiter
|
|
|
When does Graves' disease most often present?
|
During stress (eg, childbirth)
|
|
|
What is a potentially fatal complication of Graves' disease?
|
stress-induced catecholamine surge leading to arrhythmia and possible death
|
|
|
What type of hypersensitivity reaction is Graves' disease?
|
type II hypersensitivity- antibody mediated
|
|
|
What causes toxic multinodular goiter?
|
focal patches of hyperfunctioning follicular cells working independently of TSH due to mutation in TSH receptor (may also be caused by making an person with iodine deficiency goiter iodine replete)
|
|
|
Which thyroid hormone(s) are produced in toxic multinodular goiter?
|
T3 and T4
|
|
|
What is the Jod-Basedow phenomenon?
|
thyrotoxicosis resulting from making a person with an iodine deficiency hypothyroidism goiter iodine replenished/replete
|
|
|
True or False: The nodules in toxic multinodular goiter are malignant.
|
False; these "hot nodules" are benign
|
|
|
Which thyroid cancer is the most common?
|
papillary thyroid carcinoma
|
|
|
Which thyroid cancer has the best prognosis?
|
papillary thyroid carcinoma
|
|
|
What are the histological findings of papillary carcinoma of the thyroid?
|
Psammoma bodies, "ground-glass" nuclei (Orphan Annie)-clear in the center, nuclear grooves
|
|
|
Place the following thyroid cancers in order from best to worst prognosis: follicular, undifferentiated/anaplastic, and papillary.
|
(best) papillary, follicular, undifferentiated/anaplastic (worst)
|
|
|
Is the prognosis of follicular carcinoma of the thyroid considered excellent, good, or poor?
|
good
|
|
|
Histologically, follicular carcinoma of the thyroid can be described as _____ _____.
|
uniform follicles
|
|
|
Medullary carcinoma of the thyroid originates from which cells?
|
parafollicular C-cells--produce calcitonin
|
|
|
Medullary carcinoma of the thyroid produces what substance?
|
calcitonin
|
|
|
What are the histological findings of medullary carcinoma of the thyroid?
|
sheets of cells in amyloid stroma
|
|
|
Medullary carcinoma of the thyroid is associated with what two genetic syndromes?
|
MEN IIA and IIB (multiple endocrine neoplasia)
|
|
|
Undifferentiated/anaplastic carcinoma of the thyroid is most commonly found in what population?
|
elderly
|
|
|
Is the prognosis of anaplastic thyroid cancer considered excellent, good, poor, or very poor?
|
very poor
|
|
|
What type of cancer is associated with Hashimoto's thyroiditis?
|
lymphoma
|
|
|
What risk factor is associated with papillary carcinoma of the thyroid?
|
prior/childhood neck radiation
|
|
|
Endemic goiter is usually the result of what?
|
lack of dietary iodine
|
|
|
What are causes of sporadic cretinism?
|
Defect in T4 formation or developmental failure in thyroid formation (congenital hypothyroidism)
|
|
|
Give an example of an abdominal finding in cretinism.
|
protruding belly (pot belly) plus protruding umbilicus
|
|
|
Give an example of a skin finding in cretinism.
|
pale skin
|
|
|
Give an example of a facial finding in cretinism.
|
puffy face with protuberant tongue
|
|
|
Give an example of a country where cretinism is still common.
|
China
|
|
|
What is the etymology of the term cretinism?
|
It is french for Christ-like; children were considered so mentally retarded that they were incapable of sinning
|
|
|
True or False: Endemic cretinism occurs wherever endemic goiter is prevalent.
|
True; severe fetal hypothyroidism due to lack of dietary iodine causes cretinism
|
|
|
Acromegaly is the result of an excess of what hormone?
|
growth hormone in adults
|
|
|
Excess growth hormone in adults causes what disease?
|
acromegaly
|
|
|
Excess growth hormone in children causes what disease?
|
gigantism
|
|
|
What are physical exam findings are associated with acromegaly?
|
large tongue, deep voice, large hands and feet, deep furrows (wrinkles on the face), coarse facial features
|
|
|
Give an example of a metabolic defect that is commonly found in patients with acromegaly.
|
impaired glucose tolerance (insulin resistance) may lead to DM2
|
|
|
What is the treatment of acromegaly?
|
surgical resection of pituitary adenoma plus tx with octreotide (synthetic somatostatin inhibits GH)
|
|
|
List three situations in which an increase in growth hormone production is normal.
|
stress, exercise, hypogylcemia
|
|
|
How do you diagnose acromegaly with lab tests?
|
increased IGF-1 (GH is too pulsatile to measure) and glucose tolerance test-- oral glucose load should suppress GH release
|
|
|
Primary hyperparathyroidism is usually a result of what?
|
parathyroid adenoma
|
|
|
What serum electrolyte abnormalities are seen in patients with primary hyperparathyroidism?
|
hypercalcemia and hypophosphatemia
|
|
|
What urine electrolyte abnormality is seen in patients with primary hyperparathyroidism?
|
hypercalciuria and increased urinary cAMP (PTH uses cAMP receptor)
|
|
|
The urine electrolyte abnormalities of primary hyperparathyroidism often contribute to the development of what pathologic process? The urine electrolyte abnormalities of primary hyperparathyroidism often contribute to the development of what pathologic process?
|
renal stones-- high urine calcium plus high urine phosphate--> precipitation
|
|
|
What happens to the level of parathyroid hormone in patients with primary hypoparathyroidism?
|
it is decreased
|
|
|
What are symptoms of primary hyperparathyroidism?
|
weakeness, renal stones, constipation, osteoporosis
(stones, bones, groans--constipation) |
|
|
Secondary hyperparathyroidism is the result of hyperplasia, which is caused by a decrease in the serum ________ level.
|
calcium
|
|
|
Secondary hyperparathyroidism most often occurs in the setting of what chronic disease?
|
chronic renal disease-- cannot convert 25 OH vit D to the active form so there is less calcium absorption from the gut--chronic hypocalcemia--> hyperplasia of PTH
|
|
|
Secondary hyperparathyroidism most often occurs in the setting of what chronic disease?
|
hypocalcemia, hyperphospatemia (enhanced bone turn over-- but little dietary absorption of calcium and inability to excrete phosphate in urine)
|
|
|
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--> hyperplasia of the parathyroid glands
|
|
|
Osteitis fibrosa cystica is also known as what syndrome?
|
von Recklinghausen's syndrome
|
|
|
What is the bone pathology associated with osteitis fibrosa cystica?
|
Cystic bone spaces filled with brown fibrous tissue (bone pain)
|
|
|
True or False: Tetany is a common finding in patients with hypoparathyroidism.
|
True - tetany due to hypocalcemia
|
|
|
True or False: Hypercalcemia is a common finding in patients with hypoparathyroidism.
|
False; hypocalcemia is seen because PTH normally increases serum calcium levels
|
|
|
List three causes of hypoparathyroidism.
|
Accidental surgical excision (thyroid surgery), autoimmune destruction and DiGeorge's syndrome
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|
What is Chvostek's sign and how is it elicited?
|
Twitching of the facial muscles caused by tapping the skin above the facial nerve caused by hypocalcemia
|
|
|
What is Trousseau's sign and how is it elicited?
|
The brachial artery is occluded with a blood pressure cuff caused by hypocalcemia
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|
What is seen when the brachial artery is occluded in patients with hypocalcemia?
|
Carpal spasm (Trousseau's sign)
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|
|
List two signs of hypocalcemia.
|
Trosseau's sign (BP cuff) and Chvostek's sign (cheek tap)
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|
What is the name of the condition in which the kidneys are unresponsive to parathyroid hormone?
|
pseudohypoparathyroidism- Albright's hereditary osteodystrophy
|
|
|
In what manner is pseudohypoparathyroidism inherited?
|
autosomal dominant
|
|
|
List three findings of pseudohypoparathyroidism.
|
hypocalcemia, shortened 4th/5th digits, and short stature
|
|
|
A patient with hypocalcemia is of short stature and has shortened fourth/fifth digits. What genetic condition should be considered?
|
Albright's hereditary osteodystrophy- pseudohypoparathyroidism
|
|
|
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 PTH
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|
|
What is the name for the condition in which hypercalcemia occurs as a result of calcium ingestion?
|
milk-alkali syndrome
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|
|
List three endocrine conditions that can cause hypercalcemia.
|
hyperparathyroidism, hyperthyroidism, Addison's disease
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|
|
Give an example of a common iatrogenic cause of hypercalcemia.
|
tx with thiazide diuretics
|
|
|
List two bone diseases that can cause hypercalcemia.
|
Paget's disease and multiple myeloma (Paget's is usually normocalcemic though)
|
|
|
What syndrome is a gastrointestinal neoplastic syndrome that can cause hypercalcemia?
|
Zollinger-Ellison syndrome
|
|
|
True or False: Sarcoidosis is an infiltrative disease that can cause hypercalcemia.
|
true
|
|
|
Excess intake of what three substances can cause hypercalcemia?
|
calcium (milk-alkali syndrome), vitamin D, vitamin A
|
|
|
Name all the causes of hypercalcemia.
|
Calcium ingestion (milk-alkali syndrome), Hyperparathyroidism, Hyperthyroidism, Iatrogenic (thiazide diuretics), Multiple myeloma, Paget's disease, Addison's disease, Neoplasms, Zollinger-Ellison syndrome, Excess Vit D, Excess Vit A, Sarcoidosis (CHIMPANZEES)
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|
|
What is the most common type of pituitary adenoma?
|
prolactinoma
|
|
|
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 (Prolactin stimulates lactation and inhibit GnRH--> amenorrhea and lack of fertility/ovulation)
|
|
|
What is the medical treatment for a prolactinoma?
|
bromocriptine and cabergoline (dopamine agonists)
|
|
|
True or False: Prolactinomas can impinge on the optic chiasm, causing seizures
|
False; prolactinomas can impinge on the optic chiasm causing bitemporal hemianopia
|
|
|
True or False: Bromocriptine, a dopamine agonist, shrinks prolactinomas.
|
True--- dopamine provides tonic inhibition of prolactin release from the pituitary
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|
List four acute manifestations that can be seen in both type 1 and 2 diabetes mellitus.
|
polydipsia, polyuria, polyphagia, and weight loss
|
|
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________ ________ is an acute manifestation of type 1 diabetes; it is not generally seen in type 2 diabetes.
|
diabetic ketoacidosis
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|
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_____ _____ is an acute manifestation of type 2 diabetes; it is not generally seen in type 1 diabetes.
|
hyperosmolar coma
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|
Acutely, diabetes mellitus can lead to the unopposed secretion of what two substances?
|
growth hormone and epinepherine
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|
|
The unopposed secretion of growth hormone and epinephrine in patients with diabetes mellitus has what effect on glucose levels?
|
increase glucose, exacerbating hyperglycemia
|
|
|
What is the overall primary defect in patients with diabetes mellitus?
|
Insulin deficiency and glucagon excess
|
|
|
What three direct effects can a diabetic insulin deficiency have?
|
decreased glucose uptake, increased protein catabolism (inc serum [AA]), increased lipolysis (inc serum [FFA])
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|
|
List at least three direct effects of decreased glucose uptake in diabetes.
|
hyperglycemia, glucosuria, osmotic diuresis, electrolyte depletion
|
|
|
List two direct effects of increased protein catabolism in diabetes.
|
increased plasma amino acids + nitrogen loss in urine
|
|
|
In diabetes, what process directly causes ketogenesis and increased plasma free fatty acids?
|
increased lipolysis
|
|
|
In diabetes, increased lipolysis causes increased plasma levels of what two substances?
|
ketones and free fatty acids
|
|
|
Diabetic ketogenesis causes ketone levels to increase in what two body fluids?
|
blood and urine
|
|
|
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
|
|
|
True or False: In patients with diabetes, osmotic diuresis can cause lactic acidosis.
|
True; osmotic diuresis causes lactic acidosis by decreased intravascular volume and hence, hypoperfusion of the vital organs--increased anaerobic respiration of which lactic acid is a byproduct
|
|
|
True or False: In patients with diabetes, increased plasma free fatty acids and ketones cause alkalosis.
|
False; diabetes causes dehydration and acidosis
|
|
|
True or False: In patients with diabetes, increased plasma free fatty acids and ketones cause acidosis.
|
True
|
|
|
In patients with diabetes, dehydration and acidosis can directly cause what two serious adverse effects?
|
coma and death
|
|
|
The chronic manifestations of diabetes can be broken down into what two categories on the basis of pathogenesis?
|
nonenzymatic glycosylation and osmotic damage
|
|
|
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
|
|
|
In patients with diabetes, what pathologic change can be seen as a result of nonenzymatic glycosylation in the small vessels?
|
diffuse basement membrane thickening
|
|
|
List three pathologic processes caused by small-vessel disease in patients with diabetes.
|
retinopathy, glaucoma, and nephropathy
|
|
|
List four findings of diabetic retinopathy.
|
vessel proliferation, microaneurysms, exudate, and hemorrhage
|
|
|
List four forms of renal disease that can occur as a result of diabetic nephropathy.
|
nodular sclerosis, progressive proteinuria, chronic renal failure, arteriosclerosis leading to hypertension, (kimmelsteil wilson nodules may be seen)
|
|
|
List four pathologic processes that are caused by diabetic large-vessel disease.
|
atherosclerosis, coronary artery disease (CAD), peripheral vascular occlusive disease (sometimes with gangrene) and cerebrovascular disease
|
|
|
In patients with chronic diabetes, osmotic damage can cause what two disease states?
|
neuropathy and cataracts
|
|
|
What neuronal systems can degenerate as a result of diabetic neuropathy?
|
sensory, motor, and autonomic systems
|
|
|
In patients with diabetes, the osmotic damage of cataracts is the result of what?
|
sorbitol accumulation
|
|
|
What three glucose-related tests are diagnostically useful for diabetes?
|
fasting blood glucose, glucose tolerance test, and HbA1c (glycosylated hemoglobin--measure of long term control)
|
|
|
What test measures long-term diabetic control?
|
HbA1c--glycosylated hemoglobin--measures control over the lifespan of an RBC
|
|
|
True or False: Type 1 diabetes is also known as noninsulin-dependent diabetes mellitus.
|
False; it is known as insulin dependent DM or juvenille diabetes
|
|
|
True or False: Type 1 diabetes is also known as insulin-dependent or juvenile-onset diabetes mellitus.
|
True
|
|
|
True or False: Type 2 diabetes is also known as noninsulin-dependent or adult-onset diabetes mellitus.
|
True
|
|
|
What is the primary defect of type 1 diabetes mellitus?
|
The viral or immune destruction of beta cells
|
|
|
What is the primary defect of type 2 diabetes mellitus?
|
progressive insulin resistance (leading to beta cell decline)
|
|
|
Insulin is always necessary for the treatment of which type of diabetes mellitus?
|
type 1 DM
|
|
|
Insulin is sometimes necessary for the treatment of which type of diabetes mellitus?
|
type 2 DM
|
|
|
What age group is most commonly affected by type 1 diabetes mellitus?
|
< 30 although there are frequent exceptions
|
|
|
What age group is most commonly affected by type 2 diabetes mellitus?
|
> 40 yo
|
|
|
True or False: Type 1 diabetes mellitus shows an association with obesity.
|
False; type 2 diabetes is associated with obesity
|
|
|
True or False: Type 2 diabetes mellitus shows an association with obesity.
|
True
|
|
|
What are two characteristics of the genetic predisposition of type 1 diabetes mellitus?
|
weak, polygenic
|
|
|
What are two characteristics of the genetic predisposition of type 2 diabetes mellitus?
|
strong, polygenic
|
|
|
True or False: Type 1 diabetes mellitus has an association with a human leukocyte antigen system.
|
True (HLA DR3 and DR4)
|
|
|
True or False: Type 2 diabetes mellitus has an association with a human leukocyte antigen system.
|
False; type 2 diabetes has no association with HLA system, but type 1 is associated with HLA-DR3 and -DR4
|
|
|
What two human leukocyte antigen types are associated with type 1 diabetes mellitus?
|
HLA DR3 and HLA DR4
|
|
|
What is the severity of glucose intolerance in patients with type 1 diabetes mellitus?
|
severe
|
|
|
What is the severity of glucose intolerance in patients with type 2 diabetes mellitus?
|
mild to moderate
|
|
|
Ketoacidosis is common in patients with what form of diabetes mellitus?
|
type 1 DM
|
|
|
Ketoacidosis is rare in patients with what form of diabetes mellitus?
|
type 2 DM
|
|
|
What happens to the number of beta cells in the islets of patients with type 1 diabetes mellitus?
|
markedly decreased
|
|
|
What happens to the number of β cells in the islets of patients with type 2 diabetes mellitus?
|
sometimes decreased (depends on severity/progression in the illness)- variable, amyloidosis may be seen
|
|
|
What happens to the serum insulin level in patients with type 1 diabetes mellitus?
|
markedly decreased
|
|
|
What happens to the serum insulin level in patients with type 2 diabetes mellitus?
|
variable (may be elevated at first in response to insulin resistance and then declining with progressive beta cell dysfunction)
|
|
|
What are the classic symptoms of diabetes?
|
polyuria, poydypsia, thirst, and weight loss
|
|
|
The classic symptoms of polyuria, polydipsia, thirst, and weight loss are common with what form of diabetes mellitus?
|
type 1 DM
|
|
|
Which type of diabetes is associated with diabetic ketoacidosis?
|
type 1 DM
|
|
|
Diabetic ketoacidosis is usually caused by a(n) _____ (increase/decrease) in insulin requirements as a result of a(n) _____ (increase/decrease) in stress (eg, infection).
|
increase; increase
|
|
|
Give a common example of an increase in stress that can cause diabetic ketoacidosis.
|
infection (infarction, ischemia, missed insulin dose also)
|
|
|
What is the cause of ketoacidosis in DKA?
|
There is increased fat breakdown and increased ketogenesis from increased free fatty acids which are then made into ketone bodies (which are acids!!)
|
|
|
Name all the symptoms of DKA.
|
kussmaul respirations (deep/rapid), nausea/vomiting, abdominal pain, psychosis/delirium, and dehydration
|
|
|
Describe Kussmaul's respirations.
|
deep and rapid breathing (although may become slow and labored later in response to acidosis)
|
|
|
Name two neurologic/psychiatric findings in patients with diabetic ketoacidosis.
|
psychosis/delirium
|
|
|
Why do DKA patients present with dehydration?
|
Patients are in a state of metabolic acidosis due to increased ketone bodies and attempt to compensate by developing a compensatory respiratory alkalosis; with an increase in respiration there is increased insensible loss of water; there is also osmotic diuresis that can occur with the hyperglycemic state
|
|
|
The fruity breath sometimes encountered in patients with diabetic ketoacidosis is the result of what?
|
exhaled acetone
|
|
|
In patients with diabetic ketoacidosis, is the glucose level normal, increased, or decreased?
|
increased (hyperglycemia)
|
|
|
In patients with diabetic ketoacidosis, is the hydrogen level normal, increased, or decreased?
|
increased (acidosis)
|
|
|
In patients with diabetic ketoacidosis, is the bicarbonate level normal, increased, or decreased?
|
decreased (metabolic acidosis)
|
|
|
What acid-base disturbance is found in patients with diabetic ketoacidosis?
|
anion gap metabolic acidosis
|
|
|
What blood count abnormality is often seen in patients with diabetic ketoacidosis?
|
increased leukocytes (leukocytosis)
|
|
|
In patients with diabetic ketoacidosis, is the blood potassium level most commonly normal, increased, or decreased?
|
increased (insulin keeps K+ in cells)-- although the intracellular potassium level is depleted due to transcellular shift from decreased insulin
|
|
|
In patients with diabetic ketoacidosis, is the intracellular potassium level normal, increased, or decreased?
|
decreased
|
|
|
What causes intracellular potassium depletion in DKA?
|
There is an increase in serum hydrogen ions which shift into the cells. Potassium shifts out of the cells to maintain electroneutrality giving the illusion of hyperkalemia
|
|
|
True or False: Mucormycosis can be a life-threatening complication of diabetic ketoacidosis.
|
True
|
|
|
Give an example of a common serious neurologic complication of diabetic ketoacidosis.
|
cerebral edema
|
|
|
Give two examples of common cardiovascular complications of diabetic ketoacidosis.
|
arrhythmias and heart failure
|
|
|
List the three core components of the treatment of diabetic ketoacidosis.
|
insulin, fluid and potassium
|
|
|
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)
|
|
|
What are the two types of ketone bodies made during DKA?
|
β-hydroxybutyrate, acetoacetate
|
|
|
What are the three characteristics of diabetes insipidus?
|
excessive thirst, polyuria, and inability to concentrate urine
|
|
|
What are the two forms of diabetes insipidus?
|
central (lack of ADH) and nephrogenic (kidney does NOT respond to ADH)
|
|
|
What is the primary defect in central diabetes insipidus?
|
Lack of ADH production
|
|
|
What is the primary defect in nephrogenic diabetes?
|
Lack of renal response to ADH
|
|
|
What are some causes of central DI?
|
pituitary tumor, trauma, surgery, histocytosis X
|
|
|
What are some causes of nephrogenic DI?
|
hereditary, lithium, secondary to hypercalcemia, demeclocyline (ADH antagonist)
|
|
|
True or False: Lithium can cause central diabetes insipidus.
|
False; Lithium can cause nephrogenic diabetes insipidus
|
|
|
What test is used to diagnose diabetes insipidus?
|
Water deprivation test (urine osmolality does not increase)
|
|
|
When a water deprivation test is used to diagnose diabetes insipidus, what parameter is measured?
|
urine osmolality (will not be increased in DI)
|
|
|
How does a water deprivation test differentiate people with diabetes insipidus from those without it?
|
In a patient with diabetes insipidus, urine osmolality does not increase with water deprivation (normal people will retain water and concentrate urine--> inc urine osmolality)
|
|
|
In patients with diabetes insipidus, is the urine specific gravity typically high, normal, or low?
|
low (unconc)
|
|
|
The urine specific gravity is typically below what value in patients with diabetes insipidus?
|
1.006 g/mL
|
|
|
In patients with diabetes insipidus, is the serum osmolality typically high, normal, or low?
|
high
|
|
|
In patients with diabetes insipidus, the serum osmolality is typically above what value?
|
290 mOsm/L
|
|
|
How can both central and nephrogenic diabetes insipidus be managed with lifestyle changes?
|
Adequate fluid intake
|
|
|
What treatment is specifically used for central diabetes insipidus?
|
intranasal desmopressin (ADH/vasopressin analogue)
|
|
|
What drug is an ADH analog used to treat central diabetes insipidus?
|
desmopressin
|
|
|
True or False: Hydrochlorothiazide can be used to treat nephrogenic diabetes insipidus.
|
True
|
|
|
True or False: Lithium can be used to treat nephrogenic diabetes insipidus.
|
False; lithium causes nephrogenic diabetes insipidus
|
|
|
True or False: Indomethacin can be used to treat nephrogenic diabetes insipidus.
|
True
|
|
|
True or False: Amiloride can be used to treat nephrogenic diabetes insipidus.
|
True (K+ sparing diuretic)
|
|
|
How can one distinguish between central and nephrogenic DI?
|
Administration of desmopressin; in central DI, the absence of ADH is addressed with desmopressin, and patients should be able to concentrate their urine; with nephrogenic DI, the kidneys are resistant to ADH,so there is no response to desmopressin (ADH analogue)
|
|
|
What does the acronym SIADH stand for?
|
syndrome of inappropriate antidiuretic hormone secretion
|
|
|
In patients with SIADH, there is _____ (excessive/inadequate) secretion of ADH.
|
excessive
|
|
|
In patients with SIADH, there is excessive retention of what substance?
|
water
|
|
|
What serum electrolyte abnormality is characteristic of SIADH?
|
hyponatremia (retaining water dilutes serum sodium)
|
|
|
In patients with SIADH, the _____ (urine/serum) osmolality is greater than the _____ (urine/serum) osmolality.
|
urine; serum
|
|
|
In patients with SIADH, severe hyponatremia can lead to what neurologic complication?
|
seizures
|
|
|
True or False: Hydrochlorothiazide is a treatment for SIADH.
|
False; demeclocycline and water restriction are the treatments for SIADH
|
|
|
Give an example of an ectopic source of ADH.
|
Small cell lung cancer (paraneoplastic syndrome)
|
|
|
Which of the following pharmacologic agents most commonly causes SIADH: hydralazine, carbamazepine, or cyclophosphamide?
|
cyclophosphamide
|
|
|
A patient with small cell lung cancer is found on laboratory studies to have hyponatremia and urine osmolarity greater than serum osmolarity. What are the treatments for this patient's condition?
|
This patient has SIADH, which is treated with demeclocycline or water restriction
|
|
|
A patient is diagnosed with SIADH. Regarding this patient's water intake, which is more appropriate, water restriction or adequate hydration, and why?
|
SIADH is characterized by excessive water retention; hence, it should be treated with water restriction
|
|
|
Name four causes of SIADH.
|
ectopic ADH (eg small cell lung carcinoma), pulmonary disease, drugs (eg. cyclophosphamide), CNS disorders/head trauma
|
|
|
What causes carcinoid syndrome?
|
Caused by tumors from neuroendocrine cells that secrete high levels of serotonin
|
|
|
Carcinoid syndrome is caused by the secretion of high levels of what substance?
|
serotonin (5-HT= 5-hydroxytryptamine)
|
|
|
Carcinoid tumors are made up of what type of cells?
|
neuroendocrine cells
|
|
|
True or False: Carcinoid syndrome results from primary carcinoid tumors in the GI tract.
|
False; carcinoid syndrome occurs only with metastasis; in tumors that have not spread outside the small bowel, the high levels of serotonin secreted by the tumors undergoes first-pass metabolism in the liver
|
|
|
In what location is a carcinoid tumor prevented from causing carcinoid syndrome?
|
liver--first pass metabolism degrades serotonin
|
|
|
Why do carcinoid tumors that are limited to the gastrointestinal tract not cause carcinoid syndrome?
|
Because the secreted serotonin/5-hydroxytryptamine undergoes first-pass metabolism in the liver
|
|
|
What is the characteristic gastrointestinal symptom of carcinoid syndrome?
|
diarrhea
|
|
|
What is the characteristic dermatologic symptom of carcinoid syndrome?
|
flushing
|
|
|
What is the characteristic respiratory symptom of carcinoid syndrome?
|
asthmatic wheezing
|
|
|
What is the characteristic cardiovascular symptom of carcinoid syndrome?
|
right sided valvular disease
|
|
|
What is the most common tumor of the appendix?
|
Carcinoid tumor
|
|
|
What substance is found in increased concentration in the urine of patients with carcinoid syndrome?
|
5-Hydroxyindoleacetic acid (5-HIAA)--metabolite of serotonin
|
|
|
What fraction of carcinoid tumors metastasize?
|
about 1/3
|
|
|
What fraction of carcinoid tumors present with a second malignancy?
|
about 1/3
|
|
|
In patients with carcinoid tumor, in how what fraction of cases are multiple tumors found?
|
about 1/3
|
|
|
Carcinoid syndrome can be treated with what drug?
|
octreotide (somatostatin analogue)
|
|
|
Zollinger-Ellison syndrome is the result of a tumor that secretes what substance?
|
gastrin
|
|
|
The tumors of Zollinger-Ellison syndrome are usually found in what two structures of the gastrointestinal tract?
|
duodenum and pancreas
|
|
|
The ectopic secretion of gastrin in Zollinger-Ellison syndrome cause recurrent _____.
|
ulcers
|
|
|
Zollinger-Ellison syndrome may be associated with what other genetic syndrome?
|
MEN1 (multiple endocrine neoplasia 1)-- parathyroid, pancreas, pituitary
|
|
|
How can one test for Zollinger-Ellison syndrome?
|
Obtain a fasting gastrin level; high levels would indicate ectopic secretion from a tumor
|
|
|
What is the basis of treatment of diabetes mellitus type 1?
|
Low-sugar diet and insulin replacement
|
|
|
What is the basis of treatment for diabetes mellitus type 2?
|
Dietary modification and exercise for weight loss, oral hypoglycemics, insulin replacement (late)
|
|
|
List four classes of drugs (other than insulin) that are used to treat diabetes mellitus.
|
Sulfonylureas, biguanides, glitazones (thiazolidinediones), α-glucosidase inhibitors
|
|
|
Name the short-acting insulins.
|
LiSpro, aSpart, and regular/human insulin
|
|
|
Is neutral protamine Hagedorn (NPH) insulin considered a short-, intermediate-, or long-acting insulin?
|
intermediate (Not Prolonged or Hasty)
|
|
|
Name two long-acting insulins.
|
Glargine (Large and long) and Detemir (determined)
|
|
|
Insulin binds insulin receptors which have ______ _____ activity. (which receptor do they work on?)
|
tyrosine kinase
|
|
|
What is the primary effect of insulin on the liver?
|
Increases storage of glucose as glycogen
|
|
|
Insulin causes muscle to increase the synthesis of what two substances?
|
glycogen and protein
|
|
|
What effect does insulin have on electrolyte handling by muscle cells?
|
Insulin causes increased potassium uptake
|
|
|
What is the primary effect of insulin on fat?
|
Insulin aids in triglyceride storage
|
|
|
For what electrolyte disturbance can insulin be used as a treatment?
|
Hyperkalemia
|
|
|
Insulin can be used to treat _______-induced hyperglycemia in addition to diabetes mellitus.
|
stress
|
|
|
What is the most common adverse effect of insulin treatment?
|
Hypoglycemia
|
|
|
True or False: Hepatotoxicity is an important toxicity of insulin.
|
False; hepatotoxicity is not a toxicity of insulin, but hypoglycemia and hypersensitivity (very rare) are
|
|
|
Name two first generation sulfonylureas.
|
Tolbutamide, chlorpropamide
|
|
|
Name three second generation sulfonylureas.
|
Glyburide, glimepiride, glipizide
|
|
|
Which diabetes drugs can cause a disulfiram-like reaction?
|
first generation sulfonylureas (Tolbutamide, chlorpropamide)
|
|
|
To which class of diabetes drugs does metformin belong?
|
biguanides
|
|
|
To which class of diabetes drugs does pioglitazone belong?
|
Glitazones/thiazolidinediones
|
|
|
To which class of diabetes drugs does rosiglitazone belong?
|
Glitazones/thiazolidinediones
|
|
|
Name two α-glucosidase inhibitors.
|
Acarbose, Miglitol
|
|
|
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
|
|
|
Sulfonylureas are used to stimulate the release of _____ _____ in patients with type 2 diabetes mellitus.
|
Endogenous insulin
|
|
|
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)
|
|
|
What is a toxicity of first-generation sulfonylureas?
|
Disulfiram-like effects (anatabuse-- sensitivity to EtOH that leads to n/v)
|
|
|
What is a toxicity of second-generation sulfonylureas?
|
hypoglycemia
|
|
|
What is the mechanism of action of metformin?
|
Unknown; overall, it acts as an insulin sensitizer (may decrease gluconeogenesis, increase glycolysis, thereby decreasing serum glucose levels)
|
|
|
How is metformin administered?
|
Orally
|
|
|
True or False: Metformin can be used in patients without islet function.
|
true
|
|
|
What is the most serious adverse effect of metformin treatment?
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lactic acidosis
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How do glitazones work?
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They increase target cell response to insulin
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True or False: Glitazones can be used as monotherapy to treat type 2 diabetes mellitus.
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true
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True or False: Glitazones can be combined with other oral hypoglycemics.
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true
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What are the side effects of glitazones?
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weight gain, hepatotoxicity, CV toxicity, edema
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Acarbose and miglitol work by inhibiting what enzyme?
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α-Glucosidase; an intestinal brush border enzyme
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What is the mechanism of action of the α-glucosidase inhibitors?
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Prevention of sugar hydrolysis and glucose absorption, resulting in lower postprandial serum glucose levels
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True or False: α-glucosidase inhibitors can be used as monotherapy for patients with type 2 diabetes mellitus.
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True
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What is the principal toxicity of α-glucosidase inhibitors?
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Gastrointestinal disturbances (osmotic diarrhea)
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Give an example of a diabetes drug in the mimetic class.
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Pramlinitide
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What is the mechanism of action of pramlinitide?
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Decreases glucagon
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What are some toxicities of pramlinitide?
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Hypoglycemia, nausea, diarrhea
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Give an example of a GLP-1 mimetic drug.
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Exenatide
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What is the mechanism of action of the GLP-1 mimetics?
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Increases insulin and decreases glucagon
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What are toxicities of exenatide use?
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Nausea, vomiting and possibly pancreatitis
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The danger of hypoglycemia is highest with which oral diabetes drug class?
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Second-generation sulfonylureas (glyburide, glibizide, glimepiride)
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Orlistat works by inhibiting _____ _____.
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pancreatic lipases
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Orlistat alters _____ _____ by inhibiting pancreatic lipases.
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fat metabolism/absorption
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True or False: Orlistat is used for the long-term management of obesity?
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true
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True or False: Orlistat is used for the short-term management of obesity.
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False; orlistat is used for long-term obesity management
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Orlistat is properly used in conjunction with what other therapy?
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dietary modifications
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True or False: Lactic acidosis is a toxicity of orlistat.
|
False; lactic acidosis is not a toxicity of orlistat, but steatorrhea, gastrointestinal discomfort, reduced fat-soluble vitamin absorption and headache are
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Orlistat use can result in the reduced absorption of what type of vitamins?
|
fat soluble vitamins (D, A, K, E)
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What is a sympathomimetic drug that is used to treat obesity?
|
Sibutramine
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Sibutramine works by inhibiting what processes?
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serotonin and norepi reuptake
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What are side effects of sibutramine?
|
tachycardia and hypertension (norpi on alpha 1)
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Sibutramine is used to treat what condition?
|
(short and long term) Obesity
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Propylthiouracil and methimazole share the mechanism of inhibiting the _____ and _____ of thyroid hormone synthesis.
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organification; coupling
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Methimazole and propylthiouracil inhibit what process?
|
Thyroid hormone synthesis (by inhibiting the organification and coupling of thyroid hormone)
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What mechanism does propylthiouracil use that methimazole does not?
|
Propylthiouracil decreases the peripheral conversion of thyroxine (T4) to triiodothyronine (T3)
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What disorder is methimazole mainly used to treat?
|
Hyperthyroidism
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What disorder is propylthiouracil mainly used to treat?
|
hyperthyroidism
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What are the known toxicities of methimazole and propylthiouracil?
|
agranulocytosis (low WBC--rare), aplastic anemia, hepatotoxicity, skin rash
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True or False: Agranulocytosis is a relatively common toxicity of propylthiouracil and methimazole.
|
False; it is a rare toxicity
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True or False: Growth hormone can be used to treat acromegaly.
|
False; somatostatin (octreotide) is used to treat acromegaly (acromegaly = growth hormone excess)
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|
What are two pharmaceutical uses of growth hormone?
|
GH deficiency, Turner's syndrome
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|
List four indications for the use of octreotide.
|
GH excess (acromegaly), glucagonoma, gastrinoma, carcinoid
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|
List three processes that can be stimulated with the use of exogenous oxytocin.
|
uterine contractions, labor, milk ejection/let-down
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What hormone can be given pharmaceutically to conrol post-partum hemorrhage?
|
oxytocin
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|
Exogenous ADH is called _____.
|
desmopressin
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|
Desmopressin can be used to treat which disorder?
|
central diabetes insipidus (lack of ADH from posterior pituitary)--NOT for nephrogenic DI
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|
|
What drug is used to treat pituitary diabetes insipidus?
|
desmopressin (ADH analogue)
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|
|
Levothyroxine can be used to replace what endogenous substance?
|
Thyroxine (T4)
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|
|
Triiodothyronine can be used to replace what endogenous substance?
|
Thyroxine
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|
|
True or False: Levothyroxine and Triidothyronine can be used to treat myxedema.
|
True (facial/orbital myxedema is a feature of hypothyroidism)
|
|
|
What toxicities are associated with thyroid hormone replacement therapy?
|
tachycardia, heat intolerance, tremors, arrhythmias (sx of thyrotoxicosis)
|
|
|
What is the mechanism of action of glucocorticoids?
|
Decreases production of leukotrienes and prostglandins by inhibiting phospholipase A2 and expression of COX-2
|
|
|
List five examples of glucocorticoid drugs.
|
prednisone, methylprednisolone, beclomethasone, hydrocortisone, triamcinolone
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|
|
Do the anti-inflammatory mechanisms of glucocorticoids involve an increase, a decrease, or no change in the production of leukotrienes? prostaglandins?
|
decrease; decrease
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|
What endocrine disease causes hypotension and skin pigmentation and can be treated with glucocorticoid drugs?
|
Addison's disease
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|
|
True or False: Glucocorticoids can be used to suppress an immune response.
|
true
|
|
|
Glucocorticoids are often used clinically for their anti-_____ effects.
|
inflammatory
|
|
|
Give an example of a common pediatric pulmonary disease that can be treated with glucocorticoids.
|
asthma
|
|
|
True or False: The treatment of Addison's disease and diabetes are two important clinical uses of glucocorticoids.
|
False; diabetes is a toxicity of glucocorticoid use
|
|
|
True or False: The treatment of inflammation and headache are two important clinical uses for glucocorticoids.
|
False; headache is not a clinical indication for glucocorticoid use (unless from temporal arteritis etc)
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|
|
Glucocorticoids can cause what iatrogenic endocrine disorder?
|
cushing's syndrome
|
|
|
What can sometimes be found on the back of the neck of patients with Cushing's syndrome?
|
buffalo hump (dorsal cervical fat pad)
|
|
|
What effect can glucocorticoid toxicity have on the trunk/abdomen?
|
central/truncal obesity
|
|
|
What effect can glucocorticoid toxicity have on the face?
|
moon facies
|
|
|
What effect can glucocorticoid toxicity have on the muscles?
|
proximal muscle weakness/wasting
|
|
|
What effect can glucocorticoid toxicity have on the skin?
|
Thin skin and easy bruisability- wide striae
|
|
|
What effect can glucocorticoid toxicity have on the bones?
|
osteoporosis
|
|
|
What effect can glucocorticoids have on the adrenal glands?
|
Adrenocortical atrophy-adrenal suppression
|
|
|
Give an example of a gastrointestinal symptom of glucocorticoid toxicity.
|
Peptic ulcers
|
|
|
List common findings of iatrogenic Cushing's syndrome.
|
Buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, easy bruisability, osteoporosis, adrenocortical atrophy, and peptic ulcers (diabetes with chronic use)
|
|
|
Demeclocycline opposes the effects of which hormone?
|
ADH/vasopressin
|
|
|
Demeclocycline can be used to treat hyponatremia caused by which syndrome?
|
SIADH
|
|
|
What are the adverse effects of demeclocycline?
|
nephrogenic Diabetes insipidus, photosensitivity, abnormalities of teeth and bone
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