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Endocrine
Pituitary, Thyroid, Adrenal, Diabetes
| Question | Answer |
|---|---|
| Hypothalamus | master gland, monitor changes in pH, temp, b/p, O2, osmolarity, hemostasis to stimulate hormones in the pituitary gland to release hormones |
| Anterior pituitary | Human growth hormone-bone growth Prolactin-produce milk ACTH-adrenal cortex stimulate glucose MSH-pigmentation TSH-thyroid FSH-follicle stimulating-ovaries, ovulation, progesterone, sperm LH-lutenizing hormone, sex hormones (estrogen, testosterone) |
| Posterior pituitary | Oxytocin, ADH |
| Growth hormone | bone growth, anterior pit, anti-insulin effects, works at longitudinal, epiphyseal plate before puberty (r/t lots of bone cells), powerful |
| What is IGF-1? | mediated by growth hormone, insulin-like/anti-insulin effects: increase BS, decrease glucose uptake by tissues, decrease adiposity |
| Would you use IGF-1 on a child missing growth hormone? | No b/c it will have effects on muscle, bone, adipose, shiftn body mass from fat to more lean muscle = decrease adiposity |
| What would you use for children missing growth hormone? | growth hormone replacement |
| IGF-1 is abused by what group of people? | athletes |
| Decrease in GH result in? | short stature (pre puberty) dwarfism (if severe) |
| GH replacement | expensive, 191 AA peptide so give SQ 6-7x/wk, tolerated in children |
| SE of growth hormone replacement | hyperglycemia, scoliosis (bone issues), growth promoting effects, tumors all at high doses |
| When do you stop using growth hormone replacement? | when child reaches puberty b/c epiphyseal plates are closed so there will be no effects on longitudinal bone |
| What is the cause of hypersecretion of GH? | primary adenomas, depends on age, excess GH levels |
| What is giantism? | excess GH prior to puberty before epiphyseal plate seals |
| What is Acromegaly? | excess GH in the adult |
| Treatment of hypersecretion of GH? | remove tumor - consequences: deficiency in other anterior pituitary hormones, supprss GH levels (drugs) |
| Growth hormone antagonists | used in acromegaly, Octreotide, Pegvisomant |
| Octreotide | GH antagonists used in acromegaly, suppress GH release from anterior pit, seen in GI, helps with esophageal varices, long-acting microsphere formulation (long sustained release over a long period of time), inject into buttocks q.4wks |
| Pegvisomant | GH receptor antagonist used in acromegaly, pegylated GH-like molecule, has polyethylene glycol to reduce clearance, improve efficacy, increase half-life, more stable |
| Where is pegylated also seen with? | interferons |
| What are the two hormones produced by the thyroid gland? | T4 Thyroxine: 4 molecules of iodine T3 Triiodothyronine: 3 molecules of iodine |
| In circulation T4 (active) is converted to? | T3 active |
| Which molecule is the main player in thyroid? | T3 |
| T3 and T4 is produced from where and require what? | produced from tyrosine require iodine (rate limiting enzyme) |
| What is the rate limiting enzyme for thyroid? | iodine |
| Which thyroid hormone is made in the highest quantity? | T4 thyroxine |
| How to suppress thyroid hormone? | block synthesis of T3, T4 block iodine transporters = can't make thyroid hormone = hypothyroidism |
| What are the functions of thyroid hormone? | increase basal metabolic rate, increase use of glucose and O2 for ATP production, stimulate synthesis of Na/K-ATPase, increased Tb (calorigenic effect), stimulates PRO synthesis & tissue growth, stimulates lipolysis, brain development for infants |
| Hashimoto's Thyroiditis | common cause of hypothyroidism, autoimmune which thyroid is destroyed by antibodies, need life-long replacement |
| Thyroid hormone replacement for Hashimoto's | T4 Levothyroxine T3 Liothyronine |
| Levothyroxine T4 | stable, cheap, 7 day half-life, PO/IV/SQ |
| Liothyronine T3 | more potent, shorter half-life 24hrs, PO/IV/SQ, high levels can cause cardiotoxicity b/c it sensitize catecholamines: tachycardia; heart is very sensitive to thyroxine, most active seen in circulation, better than T4 |
| Side effects of thyroid hormone replacement | hyperthyroidism in excess hypothyroidism in insufficient amounts |
| Which thyroid hormone replacement would you use to prevent cardio SE? | T4 Levothyroxine |
| What is the cause of hypothyroidism? | Hashimoto's Thyroiditis |
| What is the cause of hyperthyroidism? | Graves disease |
| Graves Disease | common cause of hyperthyroidism, autoimmune, thyroid stimulating antibodies (look and act like TSH receptors), need life long replacement after tumor/thyroid is removed |
| Treatment for Hyperthyroidism | Thioamines: Methimazole, Propylthiouracil: inhibits synthesis of thyroid hormone, inhibits synthesis of T3, T4 radioactive iodine (131I): destroys thyroid thyroidectomy beta blockers (short term use) |
| Propylthiouracil | inhibits conversion of T4 to T3, treats hyperthyroidism, thioamine, BLACK BOX WARNING FOR SEVERE HEPATITIS |
| Drugs used to treat hyperthyroidism | Thioamines: Methimazole, Propylthiouracil good PO absorption,bioavailability, short half-life, but accumulate in thyroid = GOOD THING |
| Side effects of Thioamines: Methimazole, Propylthiouracil | NVD, rash (most common), rare, but faal agranulocytosis |
| Which drug for treatment of hyperthyroidism has a black box warning sign? | Propylthiouracil |
| Adrenal cortex has the following hormones? | cortisol (glucocorticoids) and a little bit of male sex hormones: testosterone |
| Adrenal medulla has the following hormones? | aldosterone (mineralocorticoids) |
| Cortisol corticosteroid produced by adrenal gland (cortex) | acts via intracellular receptors in numerous steroid responsive tissues,steroid hormone, lipophilic,doesn't dissolve in blood so it gets picked up by cortisol binding globulin taken to nucleus to binds to DNA activating gene transcription |
| Steroid hormones testosterone, aldosterone, cortisol, estrogen, progesterone | all are lipophilic, doesn't dissolve in blood/water, need a globulin to carry them to target tissues |
| What other hormone act on gene transcription and need a globulin for transport? | aldosterone (steroid hormone) in the renal tubules to increase expression of ATPase and sodium channels |
| Where do globulins come from? | liver |
| If blood sugar decrease (DM) it triggers what? | release of catecholamines, glucagon, cortisol |
| Cortisol is used for? | energy to increase BS so it is released during periods of stress |
| Side effects of corticosteriods | if used more >2 weeks: hyperglycemia, edema, HTN, hypokalemia (mineralcorticoid effect), redistribution of fat, osteoporosis: inhibit vit. D, infection, impair wound healing, insomnia, behavioral changes (steroid rage), iatrogenic Cushing syndrome |
| Who receives long term corticosteroids? | RA, organ transplants, severe autoimmune disease; used for treatment not an replacement |
| Inhibit osteoblasts and stimulate osteoclasts? | corticosteroids leading to osteoporosis |
| Insulin replacement is used for what type of diabetes? | type 1 |
| Insulin is a peptide (PRO) so it is given by? | SQ as a depot injection: bolus injection from tissue to circulation/IV |
| Side effects of Insulin | hypoglycemia, insulin allergy: histamine release, anaphylaxis; IgG formation against insulin |
| Hypoglycemia can trigger what by activating what? | triggers reflex hyperglycemia activates glucagon, catecholamines, cortisol |
| Somogyi effect | hypoglycemia then pt. eats = increase BS excessively r/t activation of glucagon, cortisol, catecholamines |
| What meds to use to treat Type 2 DM | inhibit glucose absorption increase insulin secretion (secretagogues) decrease hepatic glucose output insulin sensitizers amylin analogs, GLP-1 agonists, DPP-4 inhibitors |
| What are the targets of type 2 DM and where glucose comes from? | liver, spleen, intestines (GUT), muscles |
| Alpha Glucosidase inhibitors Acarbose, Miglitol | bind to intestinal brush border glucosidase (maltase, sucrose) enzymes, treat type 2 DM, slows carb absorption=decrease postpreandial spike in BG, prevents cleavage of complex carbs which facilitates glucose absorption |
| bind to intestinal brush border glucosidase (maltase, sucrose) enzymes, treat type 2 DM, slows carb absorption=decrease postpreandial spike in BG, prevents cleavage of complex carbs which facilitates glucose absorption | Alpha Glucosidase inhibitors Acarbose, Miglitol |
| Side effects of Alpha Glucosidase inhibitors: Acarbose, Miglitol | gas, bloating, diarrhea, abdominal discomfort, contraindicated with IBD (Crohns, UC), PUD, GERD, irritable bowel disease |
| Insulin secretagogues Sulfonylureas Meglitinides | treat type 2 DM, inhibit K/ATP channels in beta cells leading to increase insulin release/secretion |
| Sulfonylureas first generation | tolazamide, tolbutamide; bind K+ channels with lower affinity, higher doses required, PO, liver metabolized, safe, inexpensive |
| Sulfonylureas second generation | glipizide, glyburide; higher affinity binding to K+ channels than 1st generation, PO, liver metabolized, safe, inexpensive |
| tolazamide, tolbutamide; bind K+ channels with lower affinity, higher doses required, PO, liver metabolized, safe, inexpensive | Sulfonylureas first generation |
| glipizide, glyburide; higher affinity binding to K+ channels than 1st generation, PO, liver metabolized, safe, inexpensive | Sulfonylureas second generation |
| treat type 2 DM, inhibit K/ATP channels in beta cells leading to increase insulin release/secretion | Insulin secretagogues Sulfonylureas Meglitinides |
| What are the side effects of sulfonylureas? | weight gain due to increased activity in adipose tissues, hypoglycemia due to oversecretion of insulin |
| Meglitinides Noteglinide (Starlix), Repaglinide (Prandin) | treat type 2 DM, bind to same K+ channel subunit as sulfonylureas but at different site, short duration 4-7 hrs, absorption, metabolism & safety similar to sulfonylureas |
| treat type 2 DM, bind to same K+ channel subunit as sulfonylureas but at different site, short duration 4-7 hrs, absorption, metabolism & safety similar to sulfonylureas | Meglitinides Noteglinide (Starlix), Repaglinide (Prandin) |
| What are Noteglinide (Starlix), Repaglinide (Prandin)? | Meglitinides,treat type 2 DM, bind to same K+ channel subunit as sulfonylureas but at different site, short duration 4-7 hrs, absorption, metabolism & safety similar to sulfonylureas |
| Biguanides-Metformin | treats type 2 DM, reduce hepatic glucose production by targeting activation of AMP-Dependent Protein Kinase (AMPPK) to inhibit hepatic gluconeogenesis & glycogenolysis; action does not depend on working Beta cells; only work on hepatocytes (liver cells) |
| treats type 2 DM, reduce hepatic glucose production by targeting activation of AMP-Dependent Protein Kinase (AMPPK) to inhibit hepatic gluconeogenesis & glycogenolysis; action does not depend on working Beta cells; only work on hepatocytes (liver cells) | Biguanides-Metformin |
| Side effects of Biguanides-Metformin | GI distress, impair vitamin B-12 absorption (annual screening), lactic acidosis: block the flow of metabolic acids into gluconeogenic cycles (avoid in pts w/liver disease, CHF, resp.disease, hypoxemia, severe infection, alcoholism) |
| Benefits of Metformin | no hypoglycemia, no weight gain, lowers serum lipids, half-life 1.5-3hrs, not metabolized but excreted unchanged by kidneys, block gluconeogenesis in liver cells |
| What does Amylin analog Pramlintide (symlin) do? | treats type 2 DM, injectable synthetic; SQ before meals, may cause hypoglycemia, N/V, appetite suppression-good b/c type 2 pts are obese and works w/hypothalamus to promote satiety (fullness) |
| What is amylin? | a protein produced by beta cells along with insulin after a meal, suppress glucagon secretion, and delays gastric emptying |
| Benefits of Pramlintide (Symlin) | suppress postprandial glucagon secretion from pancreas to decrease hepatic glucose output, slow gastric emptying of the stomach to allow for timely glucose absorption, enhances the felling of fullness at meals to decrease food intake |
| What is the amylin analog? | Pramlintide (Symlin) |
| GLP-1 agonist Exenatide, Liraglutide | synthetic analog of glucagon-like peptide-1 (first incretin hormones used therapeutically), SQ (PRO/peptide), dependent on food intake, mediated by CNS, short-lived, used in combo to improve glycemic control |
| What are the GLP-1 agonists? | Exenatide, Liraglutide |
| What are incretin hormones? | incretin hormones are released by GI tract in response to food intake: enhance glucose-dependent insulin release, suppress glucagon levels (glucagon raise BG) |
| Exenatide | GLP-1 agonist, treats type 2 DM, SQ given 60 min before meals |
| Liraglutide | GLP-1 agonist, treats type 2 DM, SQ given before meals, long half-life, once a day dosing |
| Benefits of GLP-1 agonists | stimulates glucose-dependent insulin secretion, improves first-phase insulin response, suppress postprandial glucagon secretion, which decreases hepatic glucose production, slows gastric emptying, reduce food intake |
| Adverse effects of GLP-1 agonists | NVD, severe pancreatitis, antibody formation |
| DDP-4 inhibitors: Dipeptidyl Peptidase-4 Sitagliptin, Saxagliptin, Linagliptin | treat type 2 DM, inhibits DDP-4 the enzyme that degrades incretin hormones increasing levels of incretin hormone (GLP-1 and GIP); increase insulin secretion, decrease glucagon release, suppress appetite, weight loss |
| Benefits of DDP-4 | used PO (major advantage) rare hypoglycemia approved for monotherapy can work at beta and liver cells |
| Adverse effects of DDP-4 | increase URTI pancreatitis (sitagliptin) |
| What are Sitagliptin, Saxagliptin, Linagliptin? | DDP-4 inhibitors |
| What are DDP-4 inhibitors? | Sitagliptin, Saxagliptin, Linagliptin |
| Which DDP-4 inhibitor has an adverse effect of pancreatitis? | sitagliptin |
| Insulin sensitizers thiazolidinediones: rosiglitazone, pioglitazone | treats type 2 DM, activate PPAR-y (peroxisome proliferator-activated receptor gamma), do not affect insulin release but romote glucose and fatty acid uptake by adipocytes, increase cellular responsiveness to insulin |
| PPAR-y are found where? | everywhere (tissues) |
| What are the insulin sensitizers? | thiazolidinediones: rosiglitazone, pioglitazone |
| What are thiazolidinediones: rosiglitazone, pioglitazone? | insulin sensitizers |
| Insulin sensitizers side effects thiazolidinediones: rosiglitazone, pioglitazone | weight gain, fluid retention, MI, bone fractures |
| Rosiglitazone insulin sensitizer | increase risk of MI, only use when all agents fail |
| Pioglitazone insulin sensitizer | PO daily, approved for mono and combo therapy, dose-dependent risk for bladder cancer b/c PPAR-y is found everywhere |
| Troglitazone | insulin sensitizer, removed from market r/t hepatotoxicity |
| Meglitinides: Repalinide (Prandin) | half-life 1 hr and duration 4-7 hours |
| Meglitinides: Nateglinide (Starlix) | half-life 1 hr and duration 4 hrs |
| GLP-1, DPP-4, Amylin all do what to decrease BG in type 2 DM? | block glucagon that produces gluconeogenesis |
Created by:
cburrows
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