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43 Cards in this Set
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- Back
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Somatotropin
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Synthetic Growth Hormone derived from recombinant DNA.
USE * Tx of children with GH deficiency ---> must take at night before bed ---> 50% will reach normal heights ---> Somatotropin MUST be received before epiphisial bone closure to work. * Increase lean muscle/ adipose tissue ratio. SE * Hyperglycemia (from broken down fat). * Edema (Na and H2O retention) * Muscle and joint pain |
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Octreotide Acetate
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Synthetic Somatostatin Analogue
* Inhibits GH Release * Inhibits Serotonin (5-HT) release * Vasoconstrictor!! USE * DRUG OF CHOICE IN THE TX OF ACROMEGALY. * Carcinoid Syndrome -(neoplasia of ECL cells that store serotonin) * Alcoholic Cirrhosis: VC makes it the DRUG OF CHOICE for treating bleeding esophageal varices. |
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Bromocriptine
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Semi-synthetic Ergot Alkaloid Compound
* DOPAMINE AGONIST USE: * Acromegaly - inhibits GH release ---> Normally it stimulates GH release but in acromegaly the cells that are producing the GH are more like lactotrophs and can be inhibited by dopamine.) ---> However, OCTREOTIDE is the DOC!!! * Prolactinomas -> inhibits prolactin release by the ant pit. * Parkinson's Disease (dopamine agonist) SE (ergot alkaloid side effects) * N/V * Dizziness |
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Human Chorionic Gonadotropin (HCG)
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A hormone produced by the placenta by the implanted egg in early pregnancy. It stimulate the corpus luteum to produce Progesterone so it won't die out. It is the hormone detected in early pregnancy tests.
* This hormone has LH-like properties...so it can be used to stimulate ovulation when given as an oral medication. |
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Menotropins
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Human Menopausal Gonadotropins
* Contain FSH and sometimes also LH. * Menopausal women have low estrogen levels...so their FSH and LH levels will be high...you can get this drug from their urine. USE * Induction of ovulation in hypogonadotropic women. (in combo w/ HCG). ---> 1st: Leuprolide (GnRH analogue) is given to stop pit LH and FSH release. (so it doesn't interfere) ---> 2nd: Menotropin given for 10 DAYS to stimulate ovarian follicular development (via FSH). ---> 3rd: After 10 days, HCG given to cause ovulation at the perfect time. SE * Increased incidence of mx births (twins). * Hyperstimulation Syndrome - Microvascular changes cause fluid accumulation in the ovaries, enlarging them. This can lead to LIFE THREATENING HYPOVOLEMIA!! Stop the drug ASAP. |
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Leuprolide
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GnRH Analogue/ Agonist
* Inhibits LH and FSH release when continuously present. USE * Tx of PROSTATE CA (an androgen dependent CA). * Tx of ENDOMETRIOSIS (stops the growth and inflammation of this tissue.) * Pituitary down-regulation prior to menotropin tx for assisted reproduction. (Proves for a controlled ovarian stimulation COS, with menotropon and HCG for in vitro fertilization. This saves $ via less menotropin needed. ). SE * Suppression of gonadol hormones, causing HOT FLASHES, LOSS OF LIBIDO, BONE LOSS * Initial "flare-up" of prostate CA can occur due to increased LH release initially. (kind of like the way succs works). PNEUMONIC * Sounds like Leu-pro-lysis....you are going to the PROfessonal to have your LEUtinizie hormone LYSIS-ed so that you have have in vitro fertilization, tx prostate CA, or endometriosis. |
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Oxytocin/ Pitocin
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Posterior Anterior Pituitary Hormone/ Drug
EFFECTS * Contracts myoepithelial cells causing milk ejection. * Produces sustained contractions * Oxytocin-induced contractions inhibited by Beta2-Adenergic Agonists (terbutaline). USE * Induction and reinforcement of labor at term. * Control of postpartum uterine hemorrhage (d/t contraction of uterine smooth muscle.) SE * Uterine hypercontractility * HOTN - Pitocin IV Push can cause HOTN and STROKE!!! IV infusion only!! |
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Vasopressin
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* Vasopressin (ADH) is a V1 and V2 receptor agonist, causing vasoconstriction and water retention in the kidneys (antidiuretic).
* V2 receptors also stimulate the release of von Willebrand factor!!! USE * Control of GI bleeding from ruptured gastric varices d/t liver cirrhosis. (give along with the VCr Octreotide). SE * Hyponatremia (dilutional) * Seizures |
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Desmopressin
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Selective V2 Vasopressin Analogue
* Possesses 3000 to 1 times the antidiuretic activity over VC activity. B/c it is diuretic activity only...is NOT used for esophageal varices like vasopressin. USE * Pituitary neurogenic diabetes insipidus. (nephrogenic would be thiazide diuretics) * Von willebrand's disease (causes factor release at V2 receptors.) * Primary nocturnal enuresis (bed wetting...but controversial d/t seizure risk in kids). SE * Hyponatremia * Seizures |
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Methimazole
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A thioamide.
MOA: * Thyroid Peroxidase Inhibitor: Pvts the SYNTHESIS of thyroid hormone in the thyroid gland. (does not effect T3, T4 that has already been formed in the gland.) ONSET: *SLOW: Inhibit new hormone synthesis...already synthesized hormone is already there. USE * Tx Grave's Disease (hope is that pt will go into remission). * Preparation for thyroidectomy. ( to pvt massive hormone release and thyroid storm with manipulation). SE * Maculopapular pruritic rash (tx w/ topical steroid) * Agranulocytosis (A sore throat or fever with PTU can be a sign of this. Stop the drug). * Caution with pregnancy..(in cases of pregnancy...PTU would be better than Methimazole). (Cross the placenta and can cause hypothyroidism in fetus. PTU is less effective at crossing the placental barrier.) Pneumonic: * Sounds like "Meth in ma" meth in mom's is bad. So contraindicated in pregnancy d/t passage to fetus. Meth makes you stimulated...this drug decreases stimulation...so if mom took meth, she would need this drug to calm her down by inducing hypothyroidism. The name has THIMA in it...this looks almost like THIOAMIDE. |
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Iodide
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Thyroglobulin Proteolysis Inhibitor
* Inhibits the RELEASE of thyroid hormones from the thyroid gland. MOA: * Prevents the cleaving of T3, T4 from the thyroglobulin inside the thyroid gland. This pvts their release. * Also decreases the vascularity, size, and fragility of the thyroid gland. ONSET: Rapid (inhibits thyroid hormone release..that is immediate). DURATION: Short - Inhibition of thyroglobulin proteolysis is TRANSITORY. So this drug is for ST/ emergency use only. USE * Management of Thyroid Storm (use mg doses!!!) * Preparation for thyroid surgery (decr the size, vascularity, and fragility of the thyroid gland). |
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Propothiouracil
(PTU) |
Thioamide:
MOA * Inhibits thyroid peroxidase enzyme, preventing thyroid hormone synthesis. (Does not effect T3,T4 that has already been formed in the gland). * Deiodinase Inhibitor: inhibits conversion of T4 to T3 in the periphery ONSET: * SLOW!!: this drug works by inhibiting NEW thyroid hormone synthesis. Some hormones are already present in the gland and can't be inhibited. USE * Graves Disease Tx. * Preparation for thyroid surgery (to pvt massive hormone release and thyroid storm with manipulation). SE * Maculopapular pruritic rash (tx w/ topical steroid) * Agranulocytosis (A sore throat or fever with PTU can be a sign of this. Stop the drug). * Caution with pregnancy..(in cases of pregnancy...PTU would be better than Methimazole). (Cross the placenta and can cause hypothyroidism in fetus. PTU is less effective at crossing the placental barrier.) PNEUMONIC * Your PT Uniform is dirty....gives you an allergic rash and bacteria inhibit your WBC formation...agranulocytosis. Meth is bad for moms. |
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Propanolol
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Non-selective Beta Blocker
USE * Drug of choice for prophylactic tx of migraines. * THYROID STORM/ HYPERTHYROIDISM: Deiodinase Inhibitor: Blocks the conversion of T4 to T3 in the periphery. |
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Levothyroxine
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Synthroid
Synthetic T4 * converted to T3 in the periphery. More stable than synthetic T3, with a longer halflife. USE * Chronic Replacement in adult hypothyroidism * Prevention of cretinism in children SE * Induction of hyperthyroid state * Nervousness, weight loss, and cardiac arrythmias with OD. |
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Liothyronine
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Synthetic T3
* Potent! Rapid Acting!! (less stable than levothyroxine, shorter halflife). USE * Myxedema coma! (emergency). SE * Induction of hyperthyroid state * Nervousness, weight loss, and cardiac arrythmias with OD. |
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Iodide 131
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Radioactive Sodium Iodide
MOA * Taken up by iodide pump into follicular endothelial cells of thyroid gland. * Emits radiation after being taken up into the thyroid gland, destroying thyroid cells. HALF-LIFE: 5-7 days USE * Tx Grave's Disease refractory to drug tx. (Pt will have to be on levothyroxine after). * Older pts with graves disease. BENEFITS (over sx). * Easy administration * Low expense * Absence of pain SE * Hypothyroidism |
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Hydrocortisone
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Glucocorticoid AND Mineralocorticoid Activity!!
Onset: SHORT ACTING Potency: LOW POTENCY USE * DRUG OF CHOICE FOR ADRENAL INSUFFICIENCY --->Addison's disease...an autoimmune disease that attacks the adrenal cortex. You have a deficiency in Aldosterone AND Cortisol. (weakness, fatigue, weight loss, and inability to maintain blood pressure). ---> Come off of chronic glucocorticoid therapy too soon. * DRUG OF CHOICE FOR ADRENAL HYPERPLASIA --> 21 Hydroxylase deficiency...cannot make cortisol OR Aldosterone. ACTH levels are increased (no ned feedback). Weak androgens are made in excess...leads to testosterone in the periphery and viralizing effects. Hydrocortisone decr ACTH release, replaces cortisol and aldosterone. SE * Chronic use of more than 2 weeks at 20 mg can lead to IATROGENIC CUSHINGS DISORDER. w. the following effects: * Hyperglycemia d/t gluconeogenesis in the liver and inhibited glucose uptake on cells. Could potentiate diabetes with longterm use. * Catabolism of protein, bone, CT, and lymphoid tissue leading to osteoporosis and muscle wasting. * Immunosuppression: Decreases synthesis of TNF and IL-1. * Peptic Ulcers d/t decr prostaglandins and mucoprotective effects * Necrosis of the hip * Abrupt withdrawal can cause Adrenal Insufficiency with fever, weakness, fatigue, etc. |
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Prednisone
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HIGH Glucocorticoid Activity
LOW mineralocorticoid activity. PHARMACOLOGY: * Onset: INTERMEDIATE ACTING * Potency: MEDIUM POTENCY * A prodrug for prednisolone that must be converted in the liver. It has a ketone grp at the 11th position that must be converted to a hydroxyl group. USE * Anti-inflammatory actions: produces lipocortins which inhibit Phospholipase A1. Also inhibits movement of inflammatory cells into infected areas. CONTRAINDICATIONS * Do not give prednisone to a pt who has compromised liver function. Give them prednisolone instead. (prednisolone has an l in it which means it is for the liver). SE * Chronic use of more than 2 weeks at 20 mg can lead to IATROGENIC CUSHINGS DISORDER. w. the following effects: * Hyperglycemia d/t gluconeogenesis in the liver and inhibited glucose uptake on cells. Could potentiate diabetes with longterm use. * Catabolism of protein, bone, CT, and lymphoid tissue leading to osteoporosis and muscle wasting. * Immunosuppression: Decreases synthesis of TNF and IL-1. * Peptic Ulcers d/t decr prostaglandins and mucoprotective effects * Necrosis of the hip * Abrupt withdrawal can cause Adrenal Insufficiency with fever, weakness, fatigue, etc. |
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Dexamethasone
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HIGH glucocorticoid activity
NO mineralocorticoid activity. USE * Diagnosis of Cushing's syndrome and differentiation b/n a pituitary or adrenal cause. ---> LOW DOSE: (1 mg overnight) Dx of Cushings!!: Decreased cortisol levels mean normal pt. No effect on cortisol levels mean Cushing's Syndrome. ---> HIGH DOSE: (8 mg for 24 hrs) Dx of Pit or Adrenal Cause!!: No effect on cortisol levels means an adrenal tumor/cause. A 50% decrease in cortisol levels means Pituitary tumor/cause. * Anti-inflammatory effects: Lipocortins inhibit phospholipase2, inhibited movement of inflammatory mediators into infected areas. SE * Chronic use of more than 2 weeks at 20 mg can lead to IATROGENIC CUSHINGS DISORDER. w. the following effects: * Hyperglycemia d/t gluconeogenesis in the liver and inhibited glucose uptake on cells. Could potentiate diabetes with longterm use. * Catabolism of protein, bone, CT, and lymphoid tissue leading to osteoporosis and muscle wasting. * Immunosuppression: Decreases synthesis of TNF and IL-1. * Peptic Ulcers d/t decr prostaglandins and mucoprotective effects * Necrosis of the hip * Abrupt withdrawal can cause Adrenal Insufficiency with fever, weakness, fatigue, etc. |
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Fludrocortisone
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HIGH mineralocorticoid activity
* Effects mimic aldosterone USE * Addison's disease SE * HTN * Hypokalemia * Metabolic alkalosis |
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Cosyntropin
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Synthetic ACTH
USE * As an assay for adrenal responsiveness after long-term steroid use. --> If you give it and blood cortisol levels increase...then the adrenal cortex is ready (can make enzymes) to come off steroids. --> If you give it and blood cortisol levels do not increase..you have adrenal atrophy...and cannot come off steroids. PNEUMONIC * "Sounds like: "COrtial Stimulating Tropin"....stimulates the adrenal cortex. |
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Fluticasone Propionate
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Glucocorticoid Nasal spray for allergic rhinitis.
Mechanism - decreases inflammation of mucosa. Low potential for peripheral side effects (pituitary suppression). d/t NOT PERIPHERAL INHIBITION OF ACTH!! (no adrenocorticosuppression). |
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Beclomethasone
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) Nasal sprays for allergic rhinitis.
2) Mechanism - decreases inflammation of mucosa. 3) Low potential for peripheral side effects (pituitary suppression) d/t NO PERIPHERAL INHIBITION OF ACTH! |
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Metyrapone
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Corticosteroid Inhibitor
MOA: * Inhibits conversion of 11-deoxycortisol to cortisol. USE * Tx of Cushings Syndrome until corrective sx can be performed. * Pituitary Response Assay SE * Increased ACTH levels * Hypokalemia and Metabolic Alkalosis (d/t buildup of 11-Deoxycortisol and deoxycorticosterone (a mineralocorticoid). ) * Dizziness and HTN (d/t salt and water retention). |
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Spironolactone
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Aldosterone Antagonist (K-sparing diuretic)
* Blocks aldosterone receptors on the BASOLATERAL MEMBRANE of the principal cells of the CD, preventing induction of Aldosterone Induced Proteins (AIP). * Natriuresis is limited since only 2-3% of filtered load is reabsorbed in the CD. Their real effect is preventing K and H secretion. MOA: Decreased Na reabsorption means no neg lumen potential, no K secretion and no stimulation of the proton pump...H+ is not secreted. USE: * Main use is to pvt Hypokalemia when used in combo with loop or thiazides. * CHF (counteracts stim of RAAS and Aldos and REDUCES FIBROSIS.) * Female Hirsutism (has antiandrogen activity) * Primary or secondary Hyperaldosteronism. SE: * Hyperkalemia (esp in renal pts, DM) * Metabolic Acidosis (especially with cirrhosis). * Anti-androgen effects: Impotence, menstrual irregularities, Gynecomastia, galactorrhea (d/t no androgens and decrease prolactin inhibition). INTERACTIONS: * Interacts with ACEI's, and ARBs. ...too much!! |
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Humulin R
Novolin R |
Regular Insulin
PEAK: 2-4 hours |
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Lispro (Humalog)
Aspart (Novolog) |
Rapid Acting Insulins (analogues)
PEAK: 0.5-1.5 hours |
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Humilin N.
Novolin N. Humilin L. Novolin L. |
Intermediate Acting Insulins
NPH and Lente ONSET: 1-3 hours PEAK: 6-12 hour |
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Humulin U.
Lantus |
Slow-Acting Insulins
Humilin Ultralente ONSET: 6-8 hours PEAK: 16-20 hrs Insulin Glargine (lantus): This is an analogue of Insulin PEAK: 20-24 hrs |
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Lispro
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Regular insulin analogue
ONSET: RAPID PEAK .5-1.5 hours. |
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Exanatide
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Oral Hypoglycemia Agent
ISOLATED FROM THE GILA MONSTER. An incretin mimetic similiar to GLP-1 MOA: * (GLP-1 is normally stimulated by a meal and causes incr insulin release w/ oral glucose. It is rapidly degraded by DIPEPTIDYL-PEPTIDASE enzyme. ) * Enhances GLUCOSE-DEPENDENT insulin release * Suppresses Glucagon secretion PNEUMONIC * Sounds like "Exam I tied"....got the same score on an exam as someone else because you copied (mimicked) someone's test. Incretin mimetic. Glucose dependent insulin release because you are DEPENDENT on someone else for your grade. Inhibits Glucagon because you are inhibiting your own brain (glucagon incr's glucose to feed the brain) when you cheat. Come from the Gila monster because you teacher got so mad she turned into a Gila monster when she found out you cheated. |
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Acarbose
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Oral Hypoglycemic Agent
MOA * Reduces glucose absorption from the GI tract. * Inhibits the enzyme GLUCOSIDASE, pvting the breakdown of complex sugars. USE * DM II SE * Flatulence and GI distress. PNEUMONIC * Sounds like "A car blow" ...farting in the car. People who eat complex carbs end up farting in the car. |
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Repaglinide
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A "glinide" hypoglycemic agent.
MOA: * Stimulates insulin release from the pancreatic beta cells. PHARM * Fast Onset, Short duration (advantage over Chloropropamide AND Glyburide) USE * DM II SE * Hypoglycemia PNEUMONIC * Sounds like "Re-pack Glee" . Imagine someone who is being released from prison. They are full of Glee and are re-packing their things to go home. RELEASE. When you are full of glee you have high BG. So this stimlates insulin release for hyperglycemia. When you know you are being released from prison...you get out as fast as you can...Fast onset, short duration. When you are happy you get fat...side effect is weight gain. |
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Chloropropamide
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First generation Sulfonylurea
MOA: Stimulates the K channel on pancreatic beta cells...causing it to close. This depolarizes the membrane, activating Ca channel. Incr intracellular Ca causes insulin release. * Also has some mild peripheral actions. PHARM * Longer DOA than 2nd generation but less potent. USE * Tx DM II SE * Hypoglycemia * Weight Gain (d/t insulin release). * GI disturbances * Allergic Skin reactions. * Stim of ADH release (retain water) INTERACTIONS * Incr effectiveness with NSAIDS and Clofibrate d/t displacement from plasma proteins. ...need to decrease the dose with NSAIDS. PNEUMONIC * Sounds like "Chloraprep." Imagine someone being released from prison who is repacking to go home (pneumonic for Repaglinide). Well before you are RELEASED into society, you have to be sanitized so you don't spread nasty prison infections. So you have to wash yourself in chloroprep. You wash for a LONG time so you kill it all (long duration) and because it doesn't work well for some reason (low potency). After you wash with it, it burns, so you get an ALLERGIC SKIN REACTION. The allergic rxn causes 3rd spacing so you have hypovolemia and STIMULATED ADH RELEASE. You decr the inflammation from the rxn with NSAIDS...so INCREASED EFFECTIVENESS WITH NSAIDS. Full of Glee...people who are happy are fat...WEIGHT GAIN d/t insulin release. |
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Rosiglitazone
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Oral Hypoglycemic Agent
**REDUCES THE INSULIN REQUIREMENTS FOR DIABETIC PATIENTS. ** MOA * Reduces Insulin resistance * (Binds to Peroxisome Proliferator-Activated Receptors (PPARs). These are nuclear receptors w/n cells. The result is incr production of proteins that enhance the effects of insulin. * DECR GLYCOSYLATED HGB. USE * DM II SE * Hepatic toxicity (especially with troglitazone) ---> Pt's need to have their liver enzymes checked once a month. * Can cause CV disease (could be pulled from the market). PNEUMONIC * Sounds like "Rosey Glitter Zone". People that are covered in rosey glitter are in the "friend zone." You have REDUCED RESISTANCE to them...you like them. Hgb is also rosey red...so HGB IS DEGLYCOSYLATED. You like them so much that your heart is hurting...can cause CV disease!! The glitter clogs up your liver...can cause hepatoxicity. Reduces insulin resistance means you don't need as much insulin...so reduced insulin requirements for diabetics. |
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Metformin
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Oral Hypoglycemic agent.
MOA * Decreases hepatic glucose production via glycogenolysis and gluconeogenesis. * Does NOT incr insulin release!!! USE * DM II SE * Diarrhea * Anorexia * Lactic Acidosis: Metformin was removed in the 90's b/c it caused lactic acidosis, but not as much as Phenformin. PNEUMONIC * Sounds like "I met 4 men!!" Too many men in your life are toxic. Toxicity destroys your liver. So you cannot have glycogenolysis or gluconeogenesis. Too many men make you anorexic due to the stress. (okay so this one sucks...). |
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Glyburide
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Second generation Sulfonylurea
MOA: Stimulates the K channel on pancreatic beta cells...causing it to close. This depolarizes the membrane, activating Ca channel. Incr intracellular Ca causes insulin release. * Also has some mild peripheral actions. PHARM * Shorter DOA than 1st generation but MORE POTENT. USE * Tx DM II SE * Hypoglycemia * Weight Gain (d/t insulin release). * GI disturbances * Allergic Skin reactions. PNEUMONIC * Sounds like " Glee bus ride. When you are RELEASED from prison and you get on the bus...you are fill of Glee. That means you are POTENT AND SHORT DURATION. Get out of there fast. Yellow bus - sulfur. This is a sulfonurea. Shorter DOA than chloropropamide. You still have an allergic skin reaction due to the yellow sulfur bus. Still have weight gain becasue you are happy. |
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Sitagliptin
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Dipeptidyl Peptidase Inhibitor
Increases the DOA of GLP-1 or Exanatide (drug) so that insulin will work better. PNEUMONIC * Looks like "sit out GLP-1". ...GLP-1 Inhibitor. |
