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Endocrine Pharm
Pharmacology: Endocrine
| Term | Definition |
|---|---|
| Surrogate for insulin? | C peptide |
| 2 things insulin does | 1) Inhibits hepatic glucose production 2) Stimulates hepatic, muscle, adipose tissue glucose uptake |
| 3 types of people who need insulin | 1) All w/ type 1. 2) type 2 for initial therapy, uncontrolled, or during acute illness 3) gestational DM |
| Lispro and Aspart (Rapid Acting) | Analog, most used insulin onset w/in 10-20 min (premeal) lasting 3-5 hours. Rx only. |
| Short acting (regular) | 30 min onset (premeal) lasting up to 8 hours. No Rx required. Don't regularly use anymore. |
| Type of insulin used for patients on high doses of insulin. | U-500 |
| Isophane (Intermediate) | NPH, onset 1-2 hours, lasts 10-20 hours. Cloudy. No Rx. |
| Long acting (Lantus) | Onset 1-2 hours, insulin Glargine with pH 4.0 or insulin Detemir (long flat curve, no sharp uptake). Lasts 24 hours. Rx only |
| Initial fluctuating levels of glucose due to increased sensitivity insulin as the body adjusts | Honeymoon period |
| TTD (Total Daily Dose) for insulin about: How does that divide up in a 60 kg pt? | .5 units per kg Ex: If you had 60 kg pt, you would have 30 units to give. Divide it up by half so 2 15 unit doses. 15 Basal at the beginning of the day and 15/3 for each meal. |
| Simplest insulin regimen: | Isophane basally and one of the rapid actings to cover meals |
| Shortest duration of insulin stability at room temperature | 10 days |
| 4 side effects of insulin | 1) Wt gain 2) Nodules 3) Lipohypertrophy 4) Lipoatrophy |
| T/F: Continuous pump > Long acting insulin (glargine)? | True, A1c drops about 1 |
| Glucagon | for hypoglycemic emergency; helps the liver release of glucose store in bloodstream. Injectable good for the unconscious pts. Also good for BB overdose |
| Well managed diabetic that feels bad in the morning due to inadequate intake of food to carry them through the night. Episodes of (profound) hypoglycemia releasing epinephrine and glucagon. Preventable! Adjust dose or diet. | Dawn Phenomenon |
| Sulfonylureas: What it does, MOA, Adverse | Working beta cells are required. MOA: stimulates release by blocking K+ resulting in depolarization of Ca2+ influx promotes insulin secretion; effective for 24 hours (O/D requires 24 hour glucose support). A: hepatic/renal insufficiency ->hypoglycemia |
| Pramlintide | amylin agonist; delays gastric emptying, inhibits secretion of glucagon, wt loss, N/V |
| Meglitinides | MOA: like sulfonylreas, but onset/duration shorter. Combo therapy best. 10-30 min before meals. |
| Biguanides (Metformin): What does it do? Adverse? | insulin sensitizer (increases glucose uptake and use), inhibits hepatic gluconeogenesis, decreases appetite. Adverse: lactic acidosis esp w/ CHF, renal pts. Metallic taste, D/N |
| TZDs (Thiazolidinediones): MOA, Action, Adverse | MOA: increased insulin sensitivity in target tissues; Liver: âglucose output. Muscle: âglucose uptake. Adipose: âglucose uptake, âFA release. A: wt gain, fatal hepatotoxicity |
| Alpha-Glucosidase Inhibitors (AGIs): MOA, Adverse | Inhibits AG in intestinal brush border that delays carb digestion. Adverse: flatulence, GI, metformin bioavailability decreased. Tx overdoses w/ pure glucose as sucrase also inhibited. |
| Incretin therapy: MOA and what is inhibited, adverse | exogenous incretins: stimulate insulin release, decrease glucagon production, reduce hepatic glucose production, slows gastric emptying. Limited by DPP-4 so we inhibit. |
| GLP-1 agonist: MOA, Adverse | MOA: mimic prolonged action of GLP-1, slows gastric emptyhing, enhances insulin, reduces glucagon, reduces appetite A: N/V/wt loss, pancreatitis |
| DPP-4 Inhibitors: MOA, Adverse | stops metabolism of GLP-1 which has the same actions as GLP-1 agonists. Adverse: HAs, vasculitis, pancreatitis, risk for viral infection. |
| Sodium-Glucose Cotransporter 2 (SGLT2) Inhibitors: What do they do? Adverse? | Increase insulin sensitivity in muscle and liver, decrease gluconeogenesis, improve beta cell function, INCREASED GLUCOSE EXCRETION; wt loss, minimal hypoglycemia, insulin independence. Adverse: polyuria, bacterial/fungal UTIs, electrolyte disturbances |
| Inadequate insulin to transfer glucose and amino acids into cells where hyperglycemia -> osmotic diuresis, dehydration generates acidotic state, amino acid concentrations in blood decrease -> ^FFA, FFA-> ketone bodies | Diabetic Ketoacidosis (DKA) |
| DKA Tx (4) | 1) Intubate if CNS depression 2) Normal saline 3) regular insulin 4) add glucose when sugar is less than 250 5) Monitor potassium |
| Marked hyperglycemia, azotemia, profound dehydration with NO acidosis or ketotic usually in unattended elderly, alcohol abusers, acute infection. Very high glucose, serum ketones not present, usually in type 2 diabetics. | Hyperglycemic Hyperosmolar Syndrome (HHS) |
| HHS Tx | Similar to DKA (Saline, insulin, glucose when levels drop below 250) |
| Increases stability of hormone, no activity when thyroxine is bound | Thyroxine Binding Globulin (TBG) |
| Inactive thyroid hormone | T4 |
| Active thyroid hormone | T3 |
| SLUGGISH acronym; for hyper or hypothyroidism? | Sleepiness Loss of memory Unusually dry Goiter Gradual personality change Increase in wt Sensitivity to cold Hair loss |
| What is Levothyroxine? | Pure T4 (obviously a med for hypothyroidism) |
| T/F: With thyroid hormone therapy: dosage specific to individual and determined by TSH, T3, T4 levels. What is the typical dose? | True; typical dose is 1.5μg T4 per kg body weight |
| What is the principal effect of thyroid hormone effects? | increase of metabolic rate of body tissues |
| T4 given to older/younger patients and T3 given to older/younger patients? | T4: Older; T3: younger |
| What is Liothyronine? | only pure T3 replacement...fast acting. |
| What is Liotrix? | T4:T3 4:1 ratio is stable, predictable, expensive with immediate burst of T3 followed by T4 conversion giving continuation. |
| Transient use of anti-thyroid drugs? How do they work? Examples of drugs? | Inhibit thyroid hormone synthesis inhibiting its ability to break down iodine and attach it to tyrosine. Propylthiouracil (PTU), Methimazole |
| Main two options for hyperthyroidism? | 1) Radioactive iodine: ablation of grandular cells, emits gamma rays and beta particles upon radioactive decay. 2) Thyroidectomy: cases refractory to medical Tx, cosmetic, or malignant. |
| Transient solution for reducing hyperthyroidism? | Exogenous excessive iodides will decrease serum T4/T3 by negative feedback. Paradoxical increase in hormone release when iodides are used for prolonged time. Effective for thyroid storm. |
| T/F: Anti-thyroid drugs push synthesis of coagulation factors | False, they inhibit synthesis of coagulation factors |
| Inhibits incorporation of iodine into thyroid hormones, but doesn't interfere w/ exogenous thyroid supplementation (conversion). CONTRA in pregnancy: cutis aplasia in fetus. Adverse: insulin autoimmune syndrome (which can result in hypoglycemic coma) | Methimazole |
| DOC in pregnant women with hyperthyroidism? MOA? Adverse? | Propylthiouracil; despite being category D...interferes w/ iodine incorporation into thyroid hormone AND in large doses can prevent conversion of T4->T3. A: bitter taste, RPGN rash |
| T/F: Relapse is a problem with antithyroid drugs. | True, 29% of pts relapse. |
| Most common procedure other than those discussed earlier in study stack? | Subtotal thyroidectomy |
| Dose when you double distance of radiation from source? | 1/4 of the dose |
| Two main drugs that REDUCE thyroid hormone production? Not necessarily anti-thyroid drugs | 1) Lithium 2) Amiodarone |
| Two main drugs that increase thyroid amounts in large doses? | 1) Furosemide 2) Salicylates |
| Tx for a precipitating factor inducing a life-threatening exacerbation of thyrotoxicosis. (3) | Thyroid Storm; 1) Acetominophen for fever preferable. 2) IV BB to control adrenergic tone THEN 3) Iodinated radiocontrast agent to inhibit conversion of T4 to T3 and iodine solution to block the release of thyroid hormone |
| Interacts w/ cell surface receptor and exerts an anabolic effect on cells within body, promotes gluconeogenesis in liver, stimulates immune system. | Growth Hormone! |
| Pituitiary adenoma or Tx of said adenoma most common cause of this deficiency. Short stature, kewpie doll appearance. Tx? | Growth Hormone Deficiency. Tx: HGH (Growth hormone; makes energy available for growth) IGF-1 (induces cells to grow). |
| Excess of growth hormone? Enlargement of hands and feet, deepening of voice, coarsening of skin, excess sweating, hypopituitarism, mandible grwoth | Acromegaly |
| Acromegaly comorbidities (5) | 1) HTN/HD 2) Sleep apnea 3) Type 2 DM 4) Irreversible arthritis 5) CVAs and HAs |
| Where is Vasopressin Receptor 2 and what does it do? | Expressed in kidney tubule where it concentrates urine and contains water in the body. |
| Where is Vasopressin Receptor 1A? 1B? | 1A: vascular smooth muscle, hepatocytes; 1B: anterior pituitary and hippocampus (throughout the brain though) |
| Insensitivity of kidney to vasopressin: Receptor 2 does not function properly | Diabetes Insipidus |
| Name of synthetic vasopressin and where is it administered? Adverse? | Pitressin administered by injection or intranasally to increase water absorption of the kidney. Adverse: anaphylaxis, cardiac arrest, N/V, fingertip necrosis |
| Desmopressin: MOA, Adverse, What is special about it? | Binds to V2 receptors in collecting ducts increasing water reabsorption. Stimulates release of factor VIII. More specific to V2 than vasopressin is and concentrates urine without vasoconstricting. A: facial flushing, nausea, hyponatremia |
| Inappropriate release of vasopressin resulting in fluid retention, ECV expansion, hyponatremia. Tx (3)? | SIADH (Syndrome of Anti-Diuretic Hormone). Tx: 1) Fluid restriction* 2) demeclocycline (ABX w/ inhibition of vasopression action) 3) Conivaptan or Tolvaptan (inhibitor of vasopressin 1/2 receptors) |
| Peak bone mass affected by: (4) | 1) Genetics 2) Nutrition 3) Age of menarche 4) exposure to alcohol and tobacco |
| Secondary problem of lack of calcium or vitamin D | loss of muscle performance |
| T/F: Few fractures occur before -2.5 | FALSE, there are many fractures that occur before the -2.5 level |
| 2 risk factors for osteoporosis; 2 therapies of osteoporosis | RF: 1) Bone loss 2) Tendency to fall; Tx: 1) Increase BMD w/ supplementation 2) Fall prevention w/ strength/balance exercises |
| Risk of Harm dose for Vitamin D and Calcium | D: 4,000 IUs; Ca: 2,000mg |
| 69% reduction in vertebral fractures and 45% reduction in non-vertebral fractures. CANNOT combine w/ bisphosphonate. RESERVED for severe bone mineral density (<-3.5). Don't use for longer than 2 years | Parathyroid Hormone |
| Endogenous peptide that partially inhibits osteoclast activity and produces rapid decrease in bone resorption. Not very effective...Risk>Benefit | Calcitonin |
| Approved by European agencies...not by FDA. Stimulates Ca uptake in bone while inhibiting bone resorption. | Strontium Ranelate |
| Useful after fracture but not great as a preventive tool. MOA: attaches to bony surfaces, PREVENTS OSTEOCLAST DIFFERENTIATIONpromotes osteoclast apoptosis. Used in Ca pts with possible metastasis to bone. | Bisphosphonates |
| Bisphosphonates CONTRAs (3) | 1) Hypocalcemia (osteoblasts can't make new bone) 2) Inability to stand or sit upright for 30 minutes. 3) GI disorders |
| 2 uses for hormone replacement therapy | 1) Women w/ significant risk for osteoporosis 2) women where non-estrogen meds have been tried or carefully considered and not due to individual factors. LOWEST effective dose to minimize cancer risk |
| Why did hormone replacement fall out of favor and why are they coming back into it? | Study showed more CHD, CVA, PEs and invasive breast cancers than expected. Women who get it who have had a hysterectomy actually have a LOWER chance of developing breast cancer |
| decreases risk of vertebral fracture by 40 percent. Ideal for those with a history of breast cancer (lowers risk w/o stimulating endometrial hyperplasia | SERMS or Raloxifene |
| What does Denosumab do? | Antibody to RANKL that prevents osteoclast precursor differentiation |
| What is the absolute best for osteoporosis? What should you start out with? | Synthetic PTH best. Bisphosphonate (alendronate) is first. |
| Worthwhile combos for osteoporosis? | Bisphosphonate and HRT (hormone replacement), Bisphosphonate and Raloxifen. NOT Bisphosphonate and PTH. |
| A necessary follow up test (initial and follow up) | Bone alkaline phosphatase |
| T/F: Don't stop taking bisphosphonate during dental surgery | FALSE, can't close bone trauma w/ bisphosphonates. Can lead to osteonecrosis of the jaw |
| T/F: Androgens anabolic effects (steroids) will not work unless you work out | True |
| How does testosterone affect women? | Enhances libido, energy, immune function and protects against osteoporosis |
| What are testosterone analogs used for in adult males? | Hypogonadism and delayed onset of male puberty |
| Normal ratio for epimers in urine for testosterone? (testosterone: epitestosterone) | 1:1, much more than that can get you banned from sports (>6:1) |
| Steroid used by veterinarians on livestock? | Trenbolone |
| Adverse effects of anabolic steroids? In general? In males? In adolescents? | Gen: Increase LDL/decreases HDL, increases BP. Males: reduced sperm count/shrunken testicles, gyneocomastia. Adolescents: premature skeletal maturation and precocious puberty leaving them w/short stature. |
| What is ovulation triggered by? | Spike in Follicle-Stimulation Hormone (FSH) and Luteinizing Hormone (LH) |
| What hormone stabilizes endometrium and will increase in pregnant women? | Progesterone |
| What do oral contraceptives do? | Suppress release of FSH and LH. Increase the amount and viscosity of cervical mucus. |
| Absolute CONTRAs of contraception (10, don't memorize all) | 1) Breastfeeding 2) 15+ cigs/day 3) >160/100 mm Hg 4) venous thromboembolism 5) Ischemic HD 6) valvular HD 7) migraine w/focal neuro Sx 8) Breast Ca 9) DM w/Sx 10) significant liver disease |
| Relative CONTRAs of contraception (7, don't memorize all) | 1) <15 cigs 2) controlled HTN 3) any migraines 4) Sx gallbladder disease 5) mild cirrhosis 6) cholestasis 7) anti-seizures and other meds |
| Do antibiotics interfere with contraceptives? If so, which ones? What other drugs interfere? | Rifampin and anti-seizures |
| Major non-contraception benefits of oral contraceptive (OCPs) (4) | 1) Menstrual cycle regulation/decreased flow 2) increased bone mineral density 3) decreased acne, hirsutism, endometrial cancer 4) decreased moliminal/PMS Sx |
| OCP Adverse: | Breakthrough bleeding (amenorrhea), decreased libido, THROMBOEMBOLIC events, may trigger vascular HAs, wt gain |
| T/F: Regular smoker w/o contraceptives >risk than non-smoking oral contraceptives. | True: <15 cigs: 3x and >15 cigs: 21x average risk |
| Missed one or 2 pills? | Take missed pills as soon as remembered. |
| 2 options when missing 3 or more active pills? What should you consider for both methods? | 1) less than 7: finish active pack and discard inactive pills starting new pack immediately. 2) more than 7 pills: finish active pills and take hormone-free break. For both: CONSIDER EMERGENCY CONTRACPTION |
| Formulation for majority of today's oral contraceptives | Triphasic formulation |
| Too much estrogen? | N, bloating, breast tenderness, ^BP, HA, melasma |
| Too little estrogen? | Early/mid-cycle breakthrough bleeding |
| Too much progestin? | Breast tenderness, HA, fatigue, depression |
| Too little progestin? | late breakthrough bleeding |
| ACHES acronym | Abdominal pain Chest pain Headache Eye:blurred vision Sharp leg pain; oral contraceptive complications |
| Depo-Provera: BLACK BOX WARNING; other Adverse: | loss of bone mineral density...significant loss in bone mineral density possible. Other adverse: significant wt gain |
| How does the implanon rod work? Main active ingredient? | Suppresses LH (LH and FSH both required for ovulation) which drops cervical mucous viscosity; Etonogestrel |
| Anti-estrogens/SERMS Benefits and Adverse | Benefits: anti-tumor and bone preservation. Adverse: vaginal bleeding, hypercalcemia, thromboembolism |
| Mifepristone: What is it? Combined with what makes it most effective? MOA: | competitive progesterone receptor antagonist. Combined with prostaglandin is most effective abortifacient less than 7 weeks. MOA: leads to high likelihood of trophoblast detachment and facilitates uterine contractions. (prostaglandin dump ->menstration) |
| Methotrexate: MOA and Use | blocks DNA synthesis inhibiting growth of placental trophoblast cells. Used in ectopic pregnancy. |
| Misoprostol: Use | in combo w/ mifepristone and methotrexate: causes uterine contractions in large doses |
| How long do you have to use emergency contraception? Best method? | 72 hours; Plan B: 2 doses of progestin separated by 12 hours. If no menses in 3 days: perform preg test |
| Intrauterine devices (IUDs): what do they contain? | can contain progestin or copper , safest that have been made in past 50 years. Fertilization still occurs, implantation does not. |
| What happens to estrogen and progesterone levels in menopause? | lower to a level where pregnancy is no longer possible |
| Lowest possible dose for shortest time for Hormone Replacement Therapy (HRT). Why? | Risk of thromboembolic disease and breast cancer |
| What is the role of estrogen? Why is it a problem? | Role: cell proliferation around lactation and pregnancy. Can lead to cancer...why we use tamoxifen (anti-estrogens) |
| High levels of PCBs, phthlates resulted in lowest: | semen quality in men |
| Environmental compounds that interfere w/ normal function of endogenous hormones...stimulate or block actions | Endocrine disruptors |
| DNA modifications that do not involve changes in sequence of DNA | Epigenetic |
| T/F: Because children have more future years of life than most adults, they have more time to develop chronic diseases that may be triggered by early exposures | True |
| What is DDT? Risks: | Anti-androgen. Larger risk of breast cancer among women with highest blood levels |
| PFC | Perfluorinated compounds: found in non-stick cookware (Teflon) and insecticides |
| What was DES (diethylstilbestrol) initially prescribed for? What were the complications? | Pregnant women to prevent miscarriages. Ended up inducing them and interfered with normal development of reproductive tract and fertility of sons/daughters and adenocarcinoma of vagina. |
| What do PCBs or Polychlorinated Biphenyls do to thyroid levels? | Reduce serum T4 and T3 |
| What happened to offspring of veterans exposed to agent orange or dioxin? | ^ miscarriages, cleft lip, spina bifida, hydrocephalus, childhood cancers |
| What chemical is in hospital equipment like IV bags and tubing and long-term exposure increases risk? | Phthalates |
| Impedes sexual maturation in boys, accelerates in girls | Phytoestrogens from soybeans and legumes (isoflavones) |
| T/F: in USGS studies, many contaminants were found from samples. As many as 40 contaminants in 1 sample found. | True :( and these were just the targeted contaminants |
| Where are endocrine disruptors being found? | Vet livestock and waste, human waste, all leading to municipal sewage Tx facilities where they are escaping degradation. |
| # 1 compound found in drinking water: | Atenolol |
Created by:
crward88
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