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105 Cards in this Set
- Front
- Back
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Rapid acting insulins
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Lispro
Aspart Glulisine |
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Lispro insulin
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rapid acting insulin (0.25 hr)
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Aspart inslulin
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rapid acting insulin (0.25 hr)
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Glulisine inslulin
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rapid acting insulin (0.25 hr)
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Regular insulin is ______
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short acting (0.50 hr)
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intermediate acting insulins
(2-4 hrs onset) (10-12 hr duration) |
NPH
Lente |
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Long acting insulins
(~16-24 hrs duration) |
Ultralente Insulin
Glargine Insulin Detemir Insulin |
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NPH
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intermediate insulin (2-4 hrs onset)
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Lente
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intermediate insulin (2-4 hrs onset)
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Ultralente
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Long acting insulin (16-20 hrs duratino)
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Glargine
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Long acting insulin (18-24 hrs duration)
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Detemir
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Long acting insulin (18-24 hrs duration)
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Mechanism of action of Sulfonylureas?
What are the drugs? When do they have to be given? SE? |
-stimulates B-cells to secrete insulin by promoting closure of ATP K+ channel
-Tolbutamide, Chlorpropamide, Glyburide, Glipizide, Glimepiride -have to be given 30 min before meals -Disulfiram rxn, hypoglycemia |
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What is the mechanism of action of the Meglitinides/Glinides?
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They act on their own receptor of the K/ATP dependent channel to deoplarize the cell to promote insulin secretion.
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glyburide, glipizide, and glimepiride
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second generation sulfonylurea that is 100x more potent and has less SE
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Biguanides and metformin mechanism of action
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-reduce glucose production by decreasing gluconeogenisis.
-Not hypoglycemic but rather antihyperglycemic -allows the body to use sugar from the blood instead of making it from other substrates |
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Thiazolidinediones mechanism of action?
Drug names? |
Increase insulin sensitivity by two mechanisms:
1) increase synthesis of GLUT4 and GLUT2 in muscle, adipose and liver 2) PPARgamma receptor agonist to upregulate insulin responsive genes -require insulin for action -Rosiglitazone and Pioglitazone |
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What is the mechanism of action of the alpha-glucosidase inhibitors?
What are the drugs? |
-prevent carb absoprtion by inhibiting the hydrolyzing of carbohydrates to monosacchrides
-Acarbose and Miglitol -GI SE, take with meals |
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Rosiglitazone
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thiazolidinedione
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Pioglitazone
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thiazolidinedione
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Acarbose
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alpha-glucosidase inhibitor
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Miglitol
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alpha-glucosidase inhibitor
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What is the mechanism of amylonomimetics?
What is the drug? |
1) inhibit glucagon synthesis
2) delays gastric emptying 3) increases satiety (glucagon stimulates gluconeogenisis) Pramlintide |
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Pramlintide
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amylinomimetic
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GIP
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-AKA glucose dependent insulinotropic peptide
-in type II diabetes response to this is impaired -rapid metabolism (minutes) |
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GLP-1
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-produced in lower SI and colon
-product of alternative splicing of proglucagon gene -stimulates insulin and inhibits glucagon secretion -also delays gastric emptying and induces satiety -secretion is impaired in type II but response is normal |
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Exenatide
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GLP-1 analog
-Increases insulin and decreases glucagon secretion -Delays gastric emptying -Increases satiety |
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What is the mechanism of DDP-IV inhibitors?
What is the drug? |
-dipeptidyl peptidase 4 is responsible for degrading GLP1 and GIP
-these drugs inhibit this -sitagliptin |
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What are the incretins?
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GIP and GLP-1
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Orlistat
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-pancreatic lipase inhibitor to prevent the absorption of fats
-reduces LDL -should give vitamin supplements |
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Sibutramine
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-NE, serotonin, and dopaine reuptake inhibitor
-originally an antidepressant -targets hypothalamus to enhance satiation -do not use in patients with CV diseases |
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Where is TRH synthesized and what is it?
What kind of receptor does it act on? What does it stimulate the release of? |
-3 AA peptide synthesized in the arcuate nucleus of the hypothalamus
-GPCR on the anterior pituitary to activate phospholipase C to increase intracellular Ca -results in the release of TSH |
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What decreases TRH stimulated TSH release?
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somatostatin
dopamine glucocorticoids |
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What type of receptors are for TSH?
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GsPCR to increase cAMP
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What is another name for T3?
What is another name for T4? |
triiodothyroxine
thyroxine |
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Thyroid hormones target the nucleus but how do they get there?
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They are hydrophobic so they require protein carriers
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What is in the thyroid follicle?
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colloid mostly composed of thyroglobin, the building block for thyroid hormone production
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What is contained in the parafollicular cells?
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calcitonin - regulates calcium levels
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What is the enzyme that catalyzes the iodide oxidation?
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thyroid perioxidase (TPO) target of thioamides
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What is thyroid bound to in circulation?
When is it increased? When is it decreased? |
TBG (thyroid binding globulin)
-increase in pregnancy, estrogen treatment and hypothyroidism -decreased by androgens, hyperthyroidism, malnutitrion and nephritic syndrome |
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T4 or T3
Which is more bound to TBG? Which has a higher affinity for THR? |
-T4 (99.98% compared to 99.5%)
-T3 |
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Deiodinase I
Deiodinase II Deiodinase III Which iodines do they remove? |
-any iodine
-outer iodination (T4 -> T3) or (rT3 -> T2) (for intracellular) -inner iodination (T4 -> rT3) or (T3 -> T2) (for deactivation) (if you remove the inner iodine frmo T4 you get rT3) |
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how does thyroid hormone act to increase HR?
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1) increases Beta receptor sensitivity
2) increases rate of depolarization and repolarization of SA node |
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What affects does thyroid hormone have on the liver?
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it increases hepatic gluconeogenisis and glyconeolysis. This increases glucose absorption and leads to loss of control in diabetes.
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What effects does thyroid hormone have on RBC's?
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the demand for O2 increases so erythropoiesis is increased to increase the number of RBC's.
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What is the congenital lack of thyroid hormone?
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Cretinism
-mother with hashimoto's -iodine deficiency in mother -drugs or radioactive iodine |
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What is it called with too much thyroid hormone?
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thyroid storm (thyroid toxicosis)
-give corticosteroids, beta blockers and antithyroids |
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How can goiter result from iodine deficiency?
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-iodine deficiency will result in decreased thyroide hormone and the hypothalamus will try to produce more by increasing TRH and TSH. No negative feedback.
(increased TSH and TRH) |
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How can goiter result from grave's disease?
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-the thyroid is constantly being stimulated by antibodies to produce thyroid hormone.
(low TSH and TRH) |
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Thyroid replacement drugs?
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Levothyroxine (T4)
Liothyroxine (T3) |
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Levothyroxine info
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-narrow therapeutic index
-long duration of action -incomplete absorption -CYP450 sensitive |
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Liothyroxine info
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shorter half life (4-6 hours)
more potent |
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What are the thioamides?
What is their mechanism of action? |
-propylthiouracil (PTU) and methimazole
-inhibit thyroid peroxidase -PTU also inhibits deiodinase I -use these as little as possible during pregnancy |
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What is the enzyme responsible for oxidation of iodide and conjugation DIT and MIT?
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thyroid peroxidase
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What is the mechanism of actionof PTU?
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thyroid peroxidase inhibitor and deiodinase I inhibitor
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What does giving iodide do?
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-Prep for thyroidectomy, to treat thyroid storm, and protect from radioactive iodine
-high concentrations inhibit iodine metabolism |
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iodination occurs on what residues?
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tyrosine residues
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Mature thyroglobulin is endocytosed into vesicles but what has to happen before it is turned into thyroide hormone?
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proteolytic cleavage
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What family do thyroid hormone receptors belong to?
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steroid receptor super family
-bind intracellularly -regulate transcription |
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What does the zona glomerulosa synthesize?
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mineralocorticoids (aldosterone)
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What does the zona reticularis synthesize?
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glococorticoid (cortisol), androgens (DHEA) and androstenedione
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What part of the kidney is derived from neural crest?
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the medulla, it is a modified sympathetic ganglion that releases catecholamines (epinephrine)
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Where does the rate limiting step occur for steroid production?
What is this step? What regulates this step? |
-side chain cleavage of cholesterol by CYP11A1 to pregnenolone
-ACTH |
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What enzymes do the zona glomerulosa cells lack and express?
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-they lack 17alpha-hydroxylase
-but have aldosterone synthase |
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What does the zone fasciculata produce?
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cortisol and androgens
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What does the z. reticulars and the z. fasciculata have that allows it to make cortisol and androgens?
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17alpha-hydroxylase?
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What is the result of 21 beta hydroxylase deficiency?
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-cortisol and aldosterone are no longer able to be made
-more androgens will be made leading to virilization -increased ACTH -hypotension |
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What is the result of 11 beta hydroxylase deficiency?
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-this happens downstream of the 21 beta hydroxylase deficiency
-decreased cortisol and aldosterone so more androgens will be made -increased virilization from more androgens -increase ACTH -HYPERTENSION bc 11-deoxycortisol has mineralcorticoid activity |
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How is aldosterone controlled?
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1) RAS and increased plasma potassium
2) ACTH 3) excreted quickly |
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Where does aldosterone act primarily?
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-in the distal tubule and collecting duct of the kidney, also colon, and salivary glands, on MR receptors
-MR is a member of the steroid-hormone receptor super family to regulate gene expression |
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What does aldosterone do?
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-stimulates sodium reabsorption and K+ and H+ excretion in kidneys, colon, and salivary glands
-this results in volume expansion - K+ diuresis and urine acidity |
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How is aldosterone stimulated?
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-ACTH, increased K+ on the adrenals
-RAS from low volume causes vasoconstriction in the adrenal glands |
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How does stress (physical and psychological) play a role in producing cortisol?
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-it stimulates the hypothalamus to release CRF (or CRH) to act on the AP to release ACTH
-cytokines augment the release of CRF |
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What is ACTH derived from?
Where does it bind? What does it do? |
-it is derived from the POMC
-it binds to melanocortin-2-receptors (Gs, inc cAMP) -rapidly stimulates side chain cleavage (CYP11A) |
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Where does ACTh have little effect?
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-on the glomerulosa cells, so it doesn't do much to increase aldosterone levels
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Principle glucocorticoid?
What is it bound to? |
cortisol
60% to CBG (transcortin) 30% to albumin 10% free |
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What do hyperthyroidism and hypothyroidism have on CBG (transcortin)?
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hyper: decrease CBG
hypo: increase CBG |
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How is cortisol excreted?
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-converted to cortisone
-in the liver it is conjugates or sulfated so that they can dissolve and be excreted in the kidneys |
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What does cortisol do?
What are its receptors? |
-GR intracellular steroid hormone receptor
-alpha portion has physiological affects -beta has negative regulation -increases carb, fat and protein metabolism to put them into circulation |
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What do excess glucocorticoids do?
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-obesity, HTN, skin thinning, muscular atrophy, decreased bone mass and osteoporosis, immunosuppression
-Cushing Syndrome |
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What is addison's disease?
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primary (autoimmune) destruction of adrenal cortex
(decreased cortisol, increased aldosterone and ACTH) |
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What are the signs of hypoadrenalism?
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Pigmentation (from increased ACTH)
loss of weight hypotension muscular weakness |
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What rhythms do ACTH and cortisol follow in the body?
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ACTH is pulsatile
cortisol is circadian |
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What are the short term signals for control of body weight?
What are they responsible for? |
CCK, PYY, ghrelin (Ghr)
-they regulate onset and termination of individual meals |
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What are the long term signals for control of body weight?
What do they do? |
leptin
-monitor body energy stores |
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Neurons that label with and release ____and _____ are _____ promoting food intake and slowing metabolism.
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AgRP
NPY orexigenic |
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Neurons that label with _____ and release the neurotransmitters _____ and _____ are ______ promoting reduced food intake and increasing metabolism.
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POMC
alpha MSH CART anorexigenic |
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Satiety is regulated by the balance of stimulation vs. inhibition of neurons in _____ nucleus of the hypothalamus. These signals are interpreted by the “Satiety Center” of the nuclear _____ _____.
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Arcuate
tractus solitarus |
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NPY release is inhibited by _____ and stimulated by _____.
What does NPY do? |
leptin
ghrelin -it increases before mealtime and stimulates food intake. |
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AgRP inhibits the action of the anorexigenic agonist _____, which is the neurotransmitter released from POMC/CART neurons.
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a-MSH
AgRP is orexigenic |
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_____ is the product of POMC cleavage and is an agonist for MC4.
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alpha or beta MSH
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_____ mutations account for 5% of severe childhood obesity.
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MC4 receptors
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alpha or beta MSH release is stimulated by _____ and inhibited by _____.
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leptin
ghrelin |
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alpha or beta MSH is anorexigenic or orexigenic
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anorexigenic
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_____ may explain the anorexigenic effect of cocaine and amphetamine, but a deficiency in this does not affect energy balance.
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CART
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What are the hormones in the stomach that have short term regulation of appetite?
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Ghrelin increases appetite
CCK decreases appetite |
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What are the hormones in the GI have short term regulation of appetite?
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GLP-1 and PPY decreases appetite
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What are the endocrine organs that control appetite?
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T4, cortisol increase appetite
insulin decreases appetite |
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What does CCK stimulate?
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-the vagus in response to fatty acid
-anorexigenic |
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What does PYY stimulate?
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-influences motility, inhibits orexia
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What does Ghrelin do?
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the only mediator that stimulates appetite.
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Leptin is a long term control of appetite, an (anorexigenic or orexigenic) mediator from adipose.
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anorexic
-inhibits NPY/AgRP -stimulates POMC/CART -increases energy expenditure -deficiency leads to obesity in mice |
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Leptin secretion is based on _____.
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Circadian rhythms
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Drug for peripheral regulation of food intake, lipase inhibitor and reduces serum LDL?
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Orlistat
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Drug for central regulation of appetite, NE, Serotonin and some dopamine reuptake inhibitor?
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Sibutramine
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