1039203
| Question | Answer |
| The coagualtion system is what type of system | Cascade |
| What are the pathways of the coagulation system | intrinsic pathway & extrinsic pathway |
| what is the result of the coagulation pathway | fibrin, clot-forming substance |
| what is the extrinsic pathway and to what does it respond | It responds to trauma to outside of blood vessel and then certain factors respond |
| what are the factors that respond to the extrinsic pathway? | VII, X, XIII, fibrin, fibrinogen, Prothrombin |
| what is the intrinsic pathway and to what does it respond | It responds to internal damage to blood vessel and then certain factors respond |
| what are the factors that respond to the intrinsic pathway? | X, IX, XII, XIII, prothrombin, fibrin, & fibrinogen w/ the help of calcium |
| what are the settings where clot formation is likly and anticouagulats may be used | MI, unstable angina, atrial fib, indwelling devices (mech. heart valve), major orthopedic surgery (joint replacement) |
| Prevention of further clot formation is useful in | Stroke, MI, DVT, PE |
| Do anticoagulants have direct effect on a blood clot that is already formed | NO |
| Do anticoagulants lyse existing clots? | NO |
| What class of drugs are used to prophylactically used to prevent clot formation (thrombus) and/or air embolus (dislodged clot) | anticoagulants |
| Which group of anticoagulants turn off coagulation pathway and prevent clot formation | Heparin & low molecular weight heparins (LMWT) |
| Adverse effects of anticoagulants | Bleeding (risk inc. with inc. dose, localized or systemic, hep. induced thrombocytpenia HIT) N/V, abdominal cramps |
| What is heparin induced thrombocytopenia (HIT) | Its a reduction in th enumber of platelets; type I is not as severe as type II |
| What is the tx for heparin induced thrombocytopenia (HIT) | direct thromin inhibitors: lepirudin & argatroban |
| What lab needs to be monitored when a pt is on heparin therapy | activated partial thromboplastin times (aPTTs) |
| What is the reversal agent for heparin | protamine sulfate |
| What should aPTT be for a pt on heparin therapy | 1 1/2 - 2 1/2 times the normal |
| T or F: SQ heparin should be given in areas of deep subq fat | False |
| How often should aPTTs be drawn on a pt recieving heparin therapy? | daily |
| Do not giev SQ doses of heparin with in 2 inches of ? | the umbilicus, abd. incisions or open wounds, scars, drainage tubes, stomas |
| T or F You should not aspirate SQ injections of heparin or massage the site | True: may cause hematoma formation |
| what are the advatages of low molecular wt. heparins over traditional heparin | more predictable anticoagulant response & don't require lab. monitoring |
| What are the LMWH drugs | anoxaparin (Lovenox) & dalteparin (Fragmin) |
| Antidote for LMWHs | protamine sulfate |
| What is the Route of administration, site(s) of administration, and why this site(s) for LMWHs? | SQ in the abdomen; b/c other sites do not have enough tissue for adequate absorption and will result in excessive bleeding |
| What labs need to be monitored during warfarin (Coumadin) therapy | prothrombin time (PT) and INR (PT-INR) |
| Route of administration for warfarin (coumadin) | Oral |
| Antidote for warfarin (Coumadin) | Vit. K |
| What is the range for INR in pts taking warfarin (coumadin) | 2-3.5 |
| Can Warfarin (Coumadin) be started while pt is still on heparin | Yes until PT-INR levels reach adequate levels |
| HOw long could it take for warfarin(Coumadin) to reach full therapeutic effect | several days |
| What are some of the herbal supplements that interact with warfarin (Coumadin) | Capsicum; Garlic; Ginger; Gingko; Ginseng; Feverfew |
| What are the Xa inhibitor drugs | dabigatran (pradaxa) rivaroxaban (Xarelto) apixaban (Ellquis) |
| is dabigatran (Pradaxa) a pro drug | Yes |
| dabigatran (Pradaxa) dosing rate | bid |
| % of renal clearence for dabigatran (Pradaxa) | 80% |
| dabigatran (Pradaxa) indications | stroke prophylaxis & atrial fib |
| Is rivaroxaban (Xarelto) a pro drug | no |
| Dosing for rivaroxaban (Xarelto) | Daily |
| % of renal clearance for rivaroxaban (Xarelto) | 66% (1/2 inactive drug) |
| is apixaban (Ellquis) a pro drug | No |
| Dosing for apixaban (Ellquis) | bid dosing |
| % of renal clearance for apixaban (Ellquis) | 25% |
| dabigatran (Pradaxa) drug interactions | Rifampin, Amioderone, Quindine, verapamil, ketoconazole/drondarone |
| Can dabigatran (Pradaxa) capsules be broken open | No |
| Is there and lab values to be monitored for dabigatran (Pradaxa) | no |
| Tx of overdose of dabigatran (Pradaxa) | no antidote but may be dialyzed |
| What foods should be avoided while taking anticoagulants | foods high in vit K (tomatoes, dark leafy greens) |
| anticoagulant pt ed: | importance of regular lab testing; signs of abnormal bleeding; measures to prevent bruising, bleeding, or tissue injury |
| Goal of antiplatelet drugs | inhibit platelet aggregation; prevent platelet adhesion; prevent platelet pulgs |
| What class of drug alters platelet function w/o compromising their blood clotting properties | Antiplatelets |
| Antiplatelet drugs | aspirin; dipyridamle (Persantine); clopidogrel (Plavix); ticlopidine (Ticlid); tirofiban(Aggreastat); eptifibatide (Integrilin); abciximab(ReoPro) |
| Does the platelet reaction occur b4 or after the clotting cascade?? | b4 |
| Vasoconstriction leads to dec. blood flow & that will decrease blood loss, what class of drugs stops this action | antiplatelets |
| What class of drugs inhibit prostaglandins so TXA2 cannot be manufactured | antiplatelets |
| Life span of a platelet | 7 days |
| GP llb/llla inhibitor drug indications | unstable angina, MI, percutaneous coronary procedures |
| antiplatelet drug indications | antithrombotic effects (reduce risk of fatal & nonfatal strokes; acute MI, & unstable angina) |
| T or F: dipyridamloe (Persantine) should be taken on an empty stomach | true |
| antifibrionolytic drugs goal | promote blood coagulation; prevent lysis of fibrin; promot clot formation |
| what are the antifibrionlytic drugs | aminocaproic (Amicar) & desmopressin (DDAVP) |
| aminocaproic (Amicar) indications | prevent excessive bleeding from surgery |
| desmopressin (DDAVP) indications | prevent excessive bleeding from surgery; tx of diabetes insipidus; dose dependent increase in plasma factor VIII (Von Willebrand factor) |
| anitifibrionolytic adverse effects | rare reports of thrombotic events; dysrhythmia, orthostatic hypotension; bradycardia; HA; dizzy; fatigue; N/V/D; abdominal cramps |
| thrombolytic drugs purpose | breakdown, or lyse preformed clots; reestablish blood flow to the heart via coronary arteries, preventing tissue distruction |
| What class of drugs activate plasminogen & convert it to plasmin, which can digest fibrin | thrombolytics |
| thrombolytic drugs | streptokinase; urokinase; anistreplase (Eminase); alteplase (Activase); reteplase (Retavase); tenecteplase (TNKase) |
| How is tenecteplase (TNKase) dosed | weight |
| thrombolytic MOA | activate the fibrinolytic system to break down clot; activate plasminogen & convert to plasmin which digests fibrin; reestablish blood flow to heart |
| Thrombolytic drug indications | acute MI; arterial thrombolysis; DVT; occlusion of shunts or catheters; pulmonary embolus; acute ischemic stroke |
| thrombolytic drug adverse effects | bleeding (internal, intracranial, superficial); N/V, hypotension, anaphylactoid reactions; cardiac dysrhythmias |
| two primary forms of lipids in the blood | triglycerides & cholesterol |
| What is a lipoprotien | the combo of triglyceride or cholesterol with apolipoprotien |
| What are the different lipoprotiens | very-low-density lipoprotein (VLDL); low-density lipoprotein(LDL); high-density lipoprotein (HDL) |
| What are very-low-density lipoprotein (VLDL) | produced by the liver, transports endogenous lipids to the cells (the most dense of lipids) |
| Why would you not want many VLDLs | many of these would indicate an increased amount of bad cholesterol (Lg amt of fat) |
| what are LDL | Transport less dense lipoproteins than VLDL but are still the bad cholesterol |
| Why do you want the LDLs low | because they will take the cholesterol to the periphery |
| What are HDLs | they transport the least dense lipoproteins; u want a lot of these they are "good" cholesterol |
| Why do we want a large amt of HDLs | they promote the removal of cholesterol |
| the risk of CHD in pts w/cholesterol levels of 300mg/dL are how many more times greater than those w/levels < 200mg/dL | 3-4 times greater risk |
| what is a negative (beneficial) risk factor for CHD | high HDL: 60mg/dL or higher |
| positive (bad things) risk factors for CHD | Age (M:45 or >; F:55 or >); family history of CHD; smoker; hypertension or on hypertension meds; low HDLs: <40mg/dL; diabetes |
| Antilipemics: HMG-CoA reductase inhibitors (statins) drugs | lovastatin(Mevacor); pravastatin(Pravachol); simvastatin(Zocor); atorvastatin(Lipitor); fluvastatin(Lescol); rosuvastatin(Crestor); pitavastatin(Livalo) |
| What class of drugs are the most potent LDL reducers | Antilipemics: HMG-CoA reductase inhibitors (statins) drugs |
| What must be monitored when taking Antilipemics: HMG-CoA reductase inhibitors (statins) drugs | liver enzymes |
| Which Antilipemics: HMG-CoA reductase inhibitors (statins) drug may actually decrease the size of a plaque that is already formed | rosuvastatin (Crestor) |
| What is HMG-CoA reductase used for | by the liver to produce cholesterol |
| Antilipemics: HMG-CoA reductase inhibitors (statins) drugs indications | 1st line for hypercholesterolemia & tx of types IIa & IIb hyperlipidemias |
| by how much do Antilipemics: HMG-CoA reductase inhibitors (statins) drugs lower LDLs | 30-40% |
| by how much do Antilipemics: HMG-CoA reductase inhibitors (statins) drugs lower triglycerides | 10-30% |
| by how much do Antilipemics: HMG-CoA reductase inhibitors (statins) drugs increased HDLs | 2-15% |
| Antilipemics: HMG-CoA reductase inhibitors (statins) drugs adverse effects | GI disturbance; rash; HA; myopathy (muscle pain) possibly leading to rhabdomyolysis (breakdown of muscle tissue{grapefruit juice interaction}); elevation of liver enzymes; liver disease |
| Antilipemics: HMG-CoA reductase inhibitors (statins) drugs interactions | oral anticoagulants; drug metabolized by CYP3A4; erythromycin; azole antifungals; verapamil; diltazem; HIV protease inhibitors; amiodarone; grapefruit juice |
| Bile Acid Sequestrant drugs | cholestyramine (Questran); colestipol hydrochloride (Colestid); colesevelam (Welchol) |
| Bile Acid Sequestrant are also called | bile acid-binding resins & ion-exchange resins |
| Bile Acid Sequestrant MOA | prevent resorption of bile acids from SI; bile acids are necessary for absorption of cholesterol |
| Bile Acid Sequestrant can be mixed in but never mixed in what | juice, kool aid, punch, ect.; but never mixed in carbonated beverages |
| Bile Acid Sequestrant indications | type II hyperlipoproteinemia; relief of pruritis asst. with partial biliary obs.; chronic diarrhea (d/t they cause constipation) |
| Bile Acid Sequestrant adverse effects | constipation; heartburn, nausea, belching, bloating (these tend to disappear over time) |
| Niacin (Nicotinic Acid) is | Vitamin B3 |
| niacin (Vit B3) dose lower or higher when used as a lipid lowering tx vs. a vitamin | higher |
| niacin (Vit B3) MOA | thought to increase activity of lipase, which breaks down lipids; reduces the metabolisim or catabolisim of cholesterol & triglycerides |
| niacin (Vit B3) indications | types IIa, IIb, III, IV, & V hyperlipidemias |
| niacin (Vit B3) are effective at? | lowering triglyceride, total serum cholesterol, & LDL levels and increasing HDL levels |
| niacin (Vit B3) adverse effects | flushing & itching(caused by histamine release); Pruritus; GI distress |
| niacin (Vit B3) adverse effects can be lessened by what | taking aspirin 30 min prior to dose |
| Fibric Acid Derivatives (fibrates) drugs | gemfibrozil (Lopid); fenofibrate (Tricor) |
| Fibric Acid Derivatives (fibrates) MOA | believed to work by activating lipase, which breaks down cholesterol; suppresses the release of free fatty acid from adipose; inhibit the synthesis of triglycerides; increase secretion of cholesterol in bile |
| Fibric Acid Derivatives (fibrates) indications | types III, IV, & V hyperlipidemias |
| Fibric Acid Derivatives (fibrates) effects | decrease triglyceride levels & increase HDL by up to 25% |
| Fibric Acid Derivatives (fibrates) adverse effects | GI disturbances; blurred vision; HA; increased risk of gallstones; prolonged prothrombin time; liver studies my show increased function |
| Fibric Acid Derivatives (fibrates) interactions | oral anticoagulants; statins(risk for myositis, myalgais, rhabdomyolysis) |
| Fibric Acid Derivatives (fibrates) lab test reactions | decreased Hgb, HCT, and WBC count; & increased activated clotting time, lactate dehydrogenase level, & bilirubin |
| Cholesterol Absorption Inhibitor drug | ezetimibe (Zetia) |
| Cholesterol Absorption Inhibitor: ezetimibe (Zetia) MOA | inhibits absorption of cholesterol & related sterols from SI |
| Cholesterol Absorption Inhibitor: ezetimibe (Zetia) drug effects | reduce total cholesterol, LDL, & triglycerides |
| Cholesterol Absorption Inhibitor: ezetimibe (Zetia) is only recommended when | pts have not responded to other therapies |
| Herbal antilipemics | garlic flax omega-3 fatty acids |
| Garlic uses | used as an antispasmodic; antihypertensive; antiplatelet; lipid reducer |
| Garlic adverse effects | dermatitis; V/D; flatulence; antiplatelet activity |
| Garlic interactions | warfarin, diazepam, my enhance bleeding when taken with NSAIDs |
| Flax uses | atherosclerosis, hypercholesterolemia; GI distress; menopausal symptoms |
| Flax interactions | diarrhea & allergic reactions; antidiabetic drugs; anticoagulants |
| Omega-3 fatty acid uses | to reduce cholesterol |
| Omega-3 fatty acid adverse effects | rash, belching, allergic reactions |
| Omega-3 fatty acid interactions | anticoagulants |
| Antilipemic contraindications | bililary obstruction, liver dysfunction; active liver disease |
| Pts on long term therapy with Antilipemic may need what supplement | fat-soluble vitamins (A,D,K) |
| Antilipemic should be taken how long before or after meals | 1 hr b4 or 4-6 hrs after |
| two main uses for diuretics | tx of CHF & tx for hypertension |
| where are the greatest amts of sodium reabsorbed in the body | proximal tubules; the farther away from the glomerulus the less amt of Na absorption |
| Types of diuretic drugs | Carbonic anhydrase inhibitors; loop diuretics; osmotic diuretics, K-sparring diuretics; Thiazide & |
| what are Carbonic Anhydrase Inhibitors (CAIs) drugs | acetazolamide (Diamox) & methazolamide (Neptazane) |
| most commonly used CAI | acetazolamides (Diamox) |
| Should CAIs be used in diabetic pts or pts taking Digoxin | CAIs cause increased blood sugars & may cause dig. toxicity d/t lowering the K+ level |
| Carbonic Anhydrase Inhibitors (CAIs) MOA | the enzyme carbonic anhydrase helps to make H+ ions available for exchange w/Na and H2O in proximal tubules, CAIs block this action & reduces H+ conc., causing inc. excretion of bicab, Na, H20, K, urine vol increased |
| Carbonic Anhydrase Inhibitors (CAIs) indications | adjunct for long term mgm't of open angle glaucoma; used w/miotics to lower intraocular pressure b4 surgery; edema; epilepsy, high altitude sickness |
| acetazolamide (Diamox) indications | mgm't of edema secondary to HF when other diuretics are not effective |
| why are Carbonic Anhydrase Inhibitors (CAIs) less potent than loop or thiazide diuretics? | the metabolic acidosis they induce reduces their diuretic effect in 2-4 days |
| Carbonic Anhydrase Inhibitors (CAIs) adverse effects | metabolic acidosis; anorexia; hematuria; photosensitivity; melena; hypokalemia; drowsy; parethesias; urticaria |
| Loop diuretic drugs | bumetainde (Bumex); ethacrynic (Edecrin); furosemide (Lasix); torsemide (Demedex) |
| Where to loop diuretics work in the body | loop of Henle |
| A fatal skin problem associated with loop diuretics | Steven Johnson |
| Because of their potent diuretic effect what safety issue would need to be considered for a patient being started on a loop diuretic | orthostatic hypotension |
| what electrolyte is at risk of being depleted once a is placed on a loop diuretic | potassium |
| Loop diuretic MOA | possess renal, CV, & metabolic effects; act directly on loop of henele to inhibit chloride & Na resorption; inc. renal prostaglandins (dilation of vessels & dec. peripheral vas. resist.) tx edema |
| loop diuretics drug effects | potent diuresis & subsequent loss of fluid; dec. fluid vol. causes a reduction in: BP, pulmonary vascular resist., systemic vas. resist., central venous press., left ventricular end-diastolic press.); K & Na depletion |
| loop diuretic indications | edema ass. w/HF or hepatic or renal disease; hypertension; inc. renal excretion of Ca in pts with hypercalcemia; HF resulting from diastolic dysfunction |
| CNS adverse effects from loop diuretics | dizzy, HA, tinnitus, blurred vision |
| GI adverse effects from loop diuretics | N/V/D |
| Hematologic adverse effects from loop diuretics | agranulocytosis; neutropenia; thrombocytopenia |
| Metabolic adverse effects from loop diuretics | hypokalemia; hyperglycemia; hyperuricemia |
| what is an osmotic diuretic drug | mannitol (Osmitrol) |
| what special precaution needs to be taken admin mannitol (Osmitrol)? | always given through a filter and is always by IV |
| Can we absorb osmotic diuretic | no |
| Where do osmotic diuretic mainly act in the body | work along the entire nephron; most pronounced in the proximal tubule |
| osmotic diuretic MOA | pull H20 into renal tubules from the surrounding tissues; inhibit tubular resorption of H20 and solutes, thus producing rapid diuresis |
| osmotic diuretic drug effects | increases GFR and renal plasma flow (helps prevent kidney damage during acute failure); reduces excessive intraocular pressure; reduces intracranial pressure or cerebral edema ass. w/head trauma |
| osmotic diuretic indications | pts in the early oliguric phase of ARF; promote excretion of toxic substances; reduce intracranial pressure; tx of cerebral edema; NOT for peripheral edema |
| osmotic diuretic adverse effects | convulsions; thrombophlebitis; pulmonary congestion; HA; chest pains; tachycardia; blurred vision; chills; fever |
| Potassium-Sparing Diuretics drugs | amiloride (Midamor); spironolactone (Aldactone); triamterene (Dyrenium) |
| Potassium-Sparing Diuretics are also known as | aldosterone-inhibiting diuretics |
| why are these drugs useful in hepatic failure with ascites? | b/c the body senses that the intravascular space is depleted & keeps secreting aldosterone. these drugs block the aldosterone |
| Can Potassium-Sparing Diuretics be used in children | Yes |
| Why should amiloride (Midamor) b used with caution in the elderly | e-lyte imbalance |
| Which Potassium-Sparing Diuretic is a synthetic steroid used to tx ascites | spironolactone (Aldactone) |
| Potassium-Sparing Diuretic MOA | works in collecting ducts & distal convoluted tubules; interfere w/Na-K exchange; competitively bind to aldosterone receptors; block reaorption of Na & H20 induced by aldosterone |
| Potassium-Sparing Diuretics drug effects | prevent K from being pumped into the tubule, preventing its secretion; competitively block aldosterone receptors & inhibit their actions; promote the excretion of Na & H20 |
| Potassium-Sparing Diuretic indications for spironolactone (Aldactone); triamterene (Dyrenium) | hyperaldosteronism; hypertension; reversing K loss caused by K-losing drugs; certain cases of HF |
| Potassium-Sparing Diuretic indications for amiloride (Midamor) | HF |
| CNS adverse effects for Potassium-Sparing Diuretic | dizzy; HA |
| GI adverse effects for Potassium-Sparing Diuretic | Cramps; N/V/D |
| other adverse effects for Potassium-Sparing Diuretic | urinary frequency; weakness; hyperkalemia |
| adverse effects for spironolactone (Aldactone) | gynecomastia; amenorrhea; irregular menses; postmenopausal bleeding |
| Thiazide & Thiazide-like diuretic drugs | hydrochlorothiazide (Esidrix, HydroDIURIL); chlorothiazide (Diuril); trichlormethiazide (Metahydrin); metolazone (Mykrox, Zaroxolyn) |
| Thiazide & Thiazide-like diuretic MOA | inhibit tubular resorption of Na, chloride, & K ions; action primarily in distal convoluted tubule (H20, Na, Ch are excreated, K excresed lesser extent); dilate arteriles by direct relaxation |
| Thiazide & Thiazide-like diuretic drug effects | lowered peripheral vascular resistance; depletion of Na & H20 (& K) |
| T or F: Thiazide & Thiazide-like diuretic should not be used if creatinine clearance in < 30-50 mL/min (normal is 125mL/min) | true |
| Does metolazone remain effective to a creatinine clearance of 10 mL/min | yes |
| Thiazide & Thiazide-like diuretic indications | HTN (most prescribed drug for this); edematous states; idiopathic hypercalciuria; diabetes insipidus; HF d/t diastolic dysfunction; adjunct in tx of edema d/t HF, hepatic cirrhosis or steroid/estrogen therapy |
| CNS adverse effects for Thiazide & Thiazide-like diuretic | dizzy, HA, blurred vision, paresthesias, decreased libido |
| GI adverse effects for Thiazide & Thiazide-like diuretic | anorexia, N/V/D |
| GU adverse effects for Thiazide & Thiazide-like diuretic | impotance |
| integumentary adverse effects for Thiazide & Thiazide-like diuretic | urticaria; photosensitivity |
| Metabolic adverse effects for Thiazide & Thiazide-like diuretic | Hypokalemia; glycosuria; hyperglycemia; hyperuricemia |
| Why should pts be instructed to take diuretics in the morning | to avoid interference with sleep patterns |
| What lab needs to be monitored during diuretic therapy | serum K |
| What should be monitored in pts taking Thiazide & Thiazide-like diuretic | blood glucose; these drugs will increased blood sugar and inactivates oral hypoglycemic agents |
| Hypothalamus is part of what system and is thought to control what | CNS; pituitary gland |
| the hypothalamus and pituitary gland work together in what system | neuroendocrine system |
| what are the two glands that make up the pituitary gland | anterior pituitary (adenohypophysus) & posterior pituitary (neurohypophysis) |
| Most hormone secretion is regulated by what | negative feedback loop |
| What hormones are secreted by the posterior lobe of pituitary gland | antidiuretic hormone (makes u "pee") & Oxytocin (causes uterine contraction "Pregnancy) |
| anterior pituitary agents | cosyntropin (Cortrosyn, Solu Cortef); somatropin (Humatrope); comatrem (Protropin); octreotide (Sandostatin) |
| posterior pituitary drugs | vasopressin (Pitressin); desmopressin (DDAVP) |
| cosyntropin (Cortrosyn, Solu Cortef) MOA | stimulates adrenal cortex which causes an increased secretion of cortisol (anti-inflammatory, reduced leukocyte functions, dec. edema, reduce scar formation) |
| cosyntropin (Cortrosyn, Solu Cortef) indications | to diagnose adrenal insufficiency; exacerbation of MS by inhibiting the immune response which is overly active in MS |
| cosyntropin (Cortrosyn, Solu Cortef) route of admin. | IV, SQ, IM, gel |
| Somatropin (Genotropin) & Somatrem (Protropin) MOA | stimulate growth |
| Somatropin (Genotropin) & Somatrem (Protropin) indications | for tx of growth failure; AIDS related wasting or cachexia |
| Somatropin (Genotropin) & Somatrem (Protropin) mimic what | growth horomone=linear growth |
| octreotide (Sandostantin) MOA | inhibits growth hormone |
| octreotide (Sandostantin) indications | Acromegaly (excessive GH production); intestinal tumors (VIPomas, carcinoid tumors); dumping syndrome; esophageal varices |
| octreotide (Sandostantin) route of admin | SQ, IV, IM (depot monthly) |
| octreotide (Sandostantin) adverse effects | use with caution with diabetes, can cause hypo &/or hyperglycemia depending on type of diabetes |
| vasopressin (Pitressin) MOA | mimics action of ADH which increases resorption of H20 casueing fluid retention; its also a vasoconstrictor which can raise BP |
| vasopressin (Pitressin) indications | diabetes insipidus (deficiency of ADH); septic shock (vasodilation); pulseless cardiac arrest (ACLS guidelines) |
| vasopressin (Pitressin) therapeutic effect | decreased urine output |
| vasopressin (Pitressin) route of admin | parenterally |
| Demopressin (DDAVP) indications | diabetes inspidus; nocturnal enuresis (bed wetting); bleeding disorders (vasoconstricting properties) |
| Demopressin (DDAVP) route of admin | nasal spray; PO, SQ, IV |
| RN indications for Cosyntropin (Cortrosyn, Solu Cortef) | fluid intake at 2000mL; watch e-lytes (low K & Ca); avoid vaccinations during therapy; watch for mood changes & insomnia |
| RN implications for desmopressin (DDAVP) | don't take OTCs, don't stop abruptly |
| RN implications: monitoring for therapeutic responses for cosyntropin (Cortrosyn, Solu cortef) | eliminate pain ass. with inflammation & produce inc. comfort & muscle strength in MS pts |
| RN implications: monitoring for therapeutic responses for somatropin (Protropin) | should increase growth in children |
| RN implications: monitoring for therapeutic responses for desmopressin (DDAVP) & vasopressin (Pitressin) | reduce severe thirst & decrease urinary output |
| RN implications: monitoring for therapeutic responses for octreotide (Sandostatin) | should reduce symptoms of watery diarrhea |
| Thyroid is responsible for secretion of | T3, T4, and calcitonin |
| T3 (triodothyronine), T4 (Thyroxine), & Calcitonin regulate what | metabolisim |
| T3 (triodothyronine), T4 (Thyroxine), & Calcitonin are needed for what | normal growth and development; control of the heart regulating system in brain; effects on heart, endocrine, & neuromuscular systems |
| 3 types of hypothyroidism | Primary, Secondary, & Tertiary |
| what is cretinism | hypothyroidism in kids |
| what is myxedema | hypothyroidism in adults |
| S & S of hypothyroidism | decreased metabolic rate (wt gain); hair loss; lethargy, dec. stamina; anorexia, constipation; cold intolerance; bradycardia |
| what is primary hypothyroidism | when thyroid glad is not able to perform one of its functions (most common) |
| what is secondary hypothyroidism | is at level of pituitary gland and means there is reduced secretion of TSH to T3 & T4 are not released properly form thyroid gland |
| what is tertiary hypothyroidism | reduction of hormone from hypothalamus, which also reduces TSH and thyroid hormone levels |
| what is a goiter | enlargement of thyroid gland resulting from overstimulation by elevated TSH levels |
| thyroid drugs natural form | thyroid (Armour) |
| thyroid replacement drug for T4 | levothyroxine (Stnthroid, Levoxyl, Levothyroid) |
| what is the most prescribed thyroid hormone replacement agent | levothyroxine (Stnthroid, Levoxyl, Levothyroid) |
| what is the hormone replacement for T3 | liothyronine (Cytomel) |
| what is the combo drug that is replacement for T3/T4 | liotrix (Thyrolar) |
| RN implications: thyroid replacement | admin. in a.m. to reduce insomnia; S & S of toxicity (nervous, irritable, insomnia, angina, palpitations, tachy, wt. loss, HTN) |
| does thyroid replacement therapy need to be taken on empty stomach | yes |
| why should thyroid replacement brands not be switched during therapy | course of tx can be destabalized |
| What is hyperthyroidism | increased secretion of thyroid hormones |
| hyperthyroidism disorders | graves disease; thyroid storm |
| what is thyroid storm | life-threatening exacerbation of the S/S of hyperthyroidism triggered by stress or infection |
| what is the most common form of hyperthyroidism | graves disease |
| what is graves disease | autoimmune disease where antibodies bind to TSH receptor cites causing hyperplasia of thyroid gland, causing increase in hormones |
| S & S of hyperthyroidism | inc. metabolic rate (wt. loss); altered menstral flow; irritability; nervous, sleep disorders, muscle weakness, fatigue; inc. appetite, diarrhea, tachy, palpitations, heat intol. |
| Antithyroid drugs indications | palliate hyperthyroidism |
| antithyroid drugs adverse effects | liver and bone marrow toxicity |
| antithyroid drugs | methimazole (Tapazole) & propylthiouracil (PTU) |
| how long for propylthiouracil (PTU) therapy for results | couple of weeks |
| RN implications: antithyroid drugs | better tol. w/food; give at same time ea. day; don't stop abruptly; avoid eating high iodine foods (seafood, soy sauce, tofu, iodized salt) |
| What is euthyroid | normal thyroid hormone levels are achieved |
| Glucagon is released form | released from alpha cells (increased glucose levels) |
| Insulin is released from | beta cells (decrease glucose levels) |
| Glucagon causes: | glycogenolysis (breakdown of glycogen) & gluconeogenesis |
| what is the stimulus for the pancreas to release insulin | carbohydrates |
| insulin causes glucose to | be transported across cellular membranes for energy & insulin also converts glucose to glycogen which is stored in liver |
| optimal blood glucose levels | 70-100 mg/dL |
| Diabetes Mellitus is a reading of | Fasting plasma glucose >126mg/dL or HgA1C level >= 6.5% |
| What is a disorder of carb metabolisim involving either a deficiency of insulin, resistance or tissue to insulin or both | diabetes mellitus |
| S & S of diabetes mellitus | elevated blood glucose; polyuria; polydipsia; polyphagia; glucosuria; wt. loss; blurred vision; fatigue |
| Type I diabetes mellitus | lack of insulin production or insulin is defective |
| Type I diabetes mellitus usual onset | <20yrs of age |
| treatment for type I diabetes | exogenous insulin |
| Etiology of type I diabetes | auto immune destruction of beta cells |
| what is type II diabetes | a decreased production of insulin (not a absolute def.), insulin receptors are decreased or become resistant to insulin |
| general onset of type II diabetes | >40 years of age |
| tx for type II diabetes | lifestyle changes first (diet, exercise, wt. loss) if these don't work start oral antidiabetic meds |
| % of pt that had gestational diabetes develop type II DM w/in 10-15 yrs | 30% |
| Insulin measurements | 100units/mL now also U-500 |
| What type of insulin mimics insulin release with a meal | Rapid acting |
| What insulin type should have dietary try b4 admin. | rapid acitng |
| Rapid acting insulin should not be given more than how many min b4 a meal | 15min |
| rapid acting insulin onset | 5-15min |
| Rapid acting insulin peak | 1-2 hrs |
| rapid acting insulin duration | 3-5 hrs |
| what are the short acting insulins | Humulin R & Novolin R |
| What are the rapid acting insulins | insulin aspart (Novolog); insulin lispro (Humalog); insulin glulisine (Apidra) |
| What is the only insulin suitable for IV admin | Short acting |
| Short acting insulins can be mixed with all other insulins except | Lantus |
| short acting insulin onset | 30-60 min |
| short acting insulin peak | 2.5 hrs |
| short acting insulin duration | 6-10 hrs |
| Intermediate acting insulin | Insulin isophane suspension: NPH Humulin N & Novolin N |
| Why are intermediate acting insulins cloudy | has particles suspended in the solution making them cloudy in appearance; if they settle roll vial to mix |
| Onset of intermediate acting insulin | 1-2 hrs |
| intermediate acting insulin peak | 4-8 hrs |
| intermediate acting insulin duration | 10-18hrs |
| Long acting insulins | insulin glargine (Lantus) & insulin detemir (Levimir) |
| insulin glargine (Lantus) onset | 3-4 hrs |
| insulin glargine (Lantus) peak | 8-14hrs |
| insulin glargine (Lantus) duration | 10-24 hrs |
| When should insulin glargine (Lantus) be given | at bedtime once daily |
| Insulin detemir (Levimir) should be given how much | once or twice daily: if two doses they should be 12hrs apart; if 1 dose then with evening meal or bedtime |
| Can Insulin detemir (Levimir) be mixed with other insulins in same syringe | no |
| Insulin detemir (Levimir) peak | 6-8hrs |
| Insulin detemir (Levimir) onset | 1-2 hrs |
| Insulin detemir (Levimir) duration | 24hrs |
| Insulin adverse effects: | hypoglycemia d/t too much insulin, inadequate food intake & exercise (glucose < 70) |
| Mgmt of hypoglycemia | Rule of 15: 15g of carbs, recheck in 15min, if still below 70, repeat 15g carbs, if linger than 1hr b4 meal follow w/protein; if pt unconscious IV dextrose or glucagon |
| Insulin drug interactions | Lasix, Dilantin, thiazides, & thyroid hormones dec. effect of insulin; Alcohol, MAOI, Inderal, & Aspirin inc. effect of insulin |
| Insulin: Pt ed | open vials can be stored @ room temp or 1mth; don't freeze; unopened vials good refrig. for 3yrs; |
| SQ insulin injection sites | abdomen; post. aspect of upper arms; thighs |
| A biguanide oral antidiabetic drug | Metformin (Glucophage) |
| metformin (Glucophage) MOA | dec. conversion of glycogen to glucose in liver, dec. absorption of glucose from the intestine & improves sensitivity of receptor sites to insulin |
| What is the biggest concern when taking metformin (Glucophage) | is person is having a test involving IV dye; should be held 48hrs b4 and after test (don't resume until we know kidney function is ok) |
| metformin (Glucophage) side effects | lactic acidosis(hyperventilation, cold/clammy skin, muscle pain, abd. pain, dizzy, irregular HR); bloating; diarrhea; metallic taste in mouth |
| Sulfonylureas MOA | stimulate insulin secretion from beta cells; improve sensitivity to insulin in tissues |
| Sulfonylureas side effects | hypoglycemia; agranulocytosis; sore throat; fever; infection; anemia; thrombocytopenia |
| Sulfonylureas drugs | glipizide (Glucotrol); glyburide (DiaBeta, Micronase, Glynase); glimepiride (Amaryl) |
| is glipizide (Glucotrol) contraindicated in renal failure | no |
| is glipizide (Glucotrol) short or long duration | short; give 30 b4 meal |
| glyburide (DiaBeta, Micronase, Glynase) long or short acting | long acting, slow onset |
| Decreased enzymes & BF in geriatrics effect what | decreased metabolism |
| Glinides drugs | repaglinide (Prandin) & nateglinde (Starlix) |
| repaglinide (Prandin) & nateglinde (Starlix) | Glinides |
| Glinides dosing | given w/each meal; shorter duration |
| Glitazone type/Thiazolidinediones drugs | rosiglitazone (Avandia) & pioglitazone (Actos) |
| Glitazone type/Thiazolidinediones drugs MOA | decrease insulin resistance by improving sensitivity of tissues; decrease glucose production in liver |
| Glitazone type/Thiazolidinediones drugs monitoring needs | monitor liver enzymes every 2 mths for 1st year |
| Glitazone type/Thiazolidinediones drugs contraindications | HF |
| alpha-glucosidase inhibitor drugs | acarbose (Precose) & miglitol (Glyset) |
| alpha-glucosidase inhibitors MOA | lower postprandial blood sugar; block enzyme that assists w/glucose absorption- thereby dec. glucose absorption from intestine |
| alpha-glucosidase inhibitor side effects | flatulence, diarrhea, abd. pain |
| alpha-glucosidase inhibitor must be taken when | with 1st bite of meal |
| dipeptydyl peptidase IV inhibitors (DPP-IV) MOA | inc. secretion of insulin from pancreas; slow absorption of glucose from gut; reduces action of glucagon; reduces appeitie |
| dipeptydyl peptidase IV inhibitors (DPP-IV) side effects | nausea; hypoglycemia |
| Don't give dipeptydyl peptidase IV inhibitors (DPP-IV) with what | insulin |
| dipeptydyl peptidase IV inhibitors (DPP-IV) drug | sitagliptin (Januvia) |
| pramlintide (Symlin) MOA | mimics natural hormone amylin; slows gastric emptying; suppressed glucagon secretion, reducing hepatic glucose output; centally modulates appetite & satiety |
| drug that mimics hormones from intestines that cause an inc. in insulin secretion from the pancreas, dec. abs. of glucose, & dec. production of glucose in liver & suppressed appetite . Not insulin | exenatide (Byetta) |
| Glucose elevating drugs | concentrated glucose; D50; glucagon; diazoxide |
| diazoxide MOA | inhibits release of insulin from the pancreas; not for quick use but for long term tx for pancreatic problems |
| Glucagon as a drug indications | used to tx hypoglycemia when pt is not awake to take oral carbs |
| Glucagon as a drug dosing | IM 1mg/mL, can repeat in 15-20 min but no more than 2 doses |
| When drawing up 2 types of insulin in same syringe which one should be drawn up first | regular or rapid-acting insulin first |
| adrenal glands two parts | adrenal cortex & adrenal medulla |
| adrenal cortex & adrenal medulla | 80-90% of adrenal gland (outer part) |
| adrenal medulla make up | 10-20% (most internal layers) |
| which part of the adrenal gland secretes the corticosteroids | adrenal cortex |
| adrenal cortex secretes what corticosteroids | glucocorticoid & mineralcorticoids |
| How do mineralcorticoids regulate e-lytes | use of aldosterone which causes Na+ to be resorbed from the urine block into the blood exchange for k+ & H+ ions. |
| what does "moon face" result from | when adrenal supplements are given in increased amts |
| Glucocorticosteroids do what for us | protect us from stress and affect protein & carb metabolism |
| Glucocorticosteroids effects | anti-inflammatory; maintain BP; carb/protein metabolism; fat metabolism; salt & H20 retention variable |
| mineralcorticoid effects | help regulate e-lytes, aldosterone; maintains levels of Na+; BP control; K and pH balance |
| Increased aldosterone leads to | H20 retention |
| what is Addison's disease | under secretion of adrenal hormones; dec. blood Na & glucose; inc. K, dehydration & wt. loss |
| What is Cushing's disease | over secretion of adrenal hormone; is a redistribution of body fat from arms and legs to face, shoulders, trunk, and abdomen "moon face" |
| corticosteroids are preg. cat. what | Category C: cross placenta and breast milk |
| Adrenal agents need to be taken with? | food to aid in GI |
| what class of drugs decrease WBC (leukopenia) by increasing the life & stimulation of growth of the RBCs | adrenal agents |
| adrenal agent indications | cerebral edema; collagen dx; dermatologic prob.; endocrine prob.; inflammatory bowel; organ transplant; leukemia; lymphoma; spinal cord injury |
| adrenal agent adverse effects | ulcer; fragile skin; osteoporosis; wt. gain; increase in blood glucose |
| adrenal agents contraindications | allergy; cataracts; glaucoma; peptic ulcer; mental health issues; DM; infection (septicemia, systemic fungal, varicella) |
| use adrenal agents cautiously with: | gastritis; reflux disease; ulcer disease; cardiac, renal, liver dysfunction |
| long acting synthetic glucocorticosteroids could cause development of | hypoadrenal shock |
| long acting synthetic glucocorticosteroid drugs | dexamethasone(decadron, Hexadrol); fludrocortisone(Florinef); Methylprednisolone(Solu-Medrol); predinisone (Orasone, Deltasone) |
| what drug is a mineralocorticoid exclusive | fludocortisone (Florinef) |
| fludrocortisone (Florinef) indications | Addison's dx; postural hypotension |
| dexamethasone (decadron, Hexadrol) indications | anti inflammatory; immunosuppressant; cerebral edema |
| what is the preferred long acting synthetic glucocorticosteroids for anti inflammation and immunosuppressant | predinisone (Orasone, Deltasone) |
| short acting natural glucocorticosteroid drugs | hydrocortisone sodium succinate(SoluCortef) & hydrocortisone cypionate (Cortef) |
| Adrenal steroid inhibitors MOA | obstruct the normal action of the adrenal cortex |
| antiadrenal drug | aminoglutethimide (cytadren) |
| antiadrenal aminoglutethimide (cytadren) indication | Cushing's (want to stop production of hormones); metastatic breast cancer; adrenal cancer |
| Adrenals are naturally suppressed when | at night |
| adrenals should be taken when | during the day |
| what is sometimes given with adrenals to prevent ulcer formation | H2-receptor agonist or PPI |
| Inhaled glucocorticoids can lead to what | fungal infections of oral cavity (Rinse out) |
| IV push adrenals should be given fast or slow | slow |
| IM adrenals should be given where | Lg muscle |
| T or F: oral adrenals should be given with milk or food | true |
| antiadrenal side effects | rash; jaundice; fever; skin lesions |
| Adrenals: pt ed | avoid sick people d/t immune suppression d/t drugs; monitor wt. gain; do not stop abruptly could cause adrenal crisis (N/V, fatigue, hypoTN, hyponatremia, Hyperkalemia |
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