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Nurs 330 - Test #2
Pharmacology for Nursing
| Question | Answer |
|---|---|
| Which opioid receptor is responsible for sedation? | Kappa |
| Which opioid receptor is responsible for dysphoria and hallucinations? | Delta |
| Which opioid receptor is associated with euphoria (some good shit), respiratory depression, and dependence (all the bad shit)? | Mu |
| Which opioid receptor is associated with endocrine and behavioral effects, along w/ somatic pain? | Sigma |
| What are the pharmacological effects (and side effects) of opioids? | Analgesia, euphoria/dysphoria, nausea (stim+depress), cough depression, neuroendocrine, miosis, and increase bile duct pressure |
| What are the drug-interactions of concern with opioids? | Any CNS depressant, will increase depressant effects. |
| T/F Pain is considered a respiratory stimulant? | True |
| What is the risk of respiratory failure in a client taking appropriate dosage(s) of an opioid? | <1% risk for respiratory failure as long as opioid levels are maintained within therapeutic range |
| How common is hypotension in clients receiving opioids? | Postural (orthostatic) hypotension is much more common than if the client were supine and well-hydrated |
| If a client experiences withdrawal symptoms from D/C of opioids, it is considered: A) Tolerance, B) Dependence, C) Addiction | B) Dependence |
| T/F: Risks of addiction to opioids, even when taken in high doses is <1%. | True |
| In terms of nursing implications, which is most important: sedation or respiratory rate? | Sedation |
| What is the name(s) for the narcotic antagonist used in case of drug OD? | **Naloxone (Narcan) |
| T/F: Kids can have MS IV for pain. | Yes, even children (e.g. Jake) can have Morphine Sulfate IV |
| What should one be watching for when administering Morphine Sulfate IV? | Allergy (histamine; caution with asthma), sedation, nausea |
| After administering 2-4mg (adult) MS IV; how long does one wait to re-assess their pain? | 5-10 minutes (I assume this is exclusive for IV, but notes do not say) |
| What is the major contradiction for Meperidine? | Meperidine (Demerol) is contradicted with MAOI anti-deoressants |
| What is the big bummer about Meperidine (Demerol) toxicity? | Cannot be treated with Narcan |
| What is the different between Fentanyl Sublimaze and Duragesic (transdermal)? | Fentanyl Sublimaz is short acting (conscious sedation, IV analgesia, etc) and Fentanyl Duragesic is longer acting (1 patch q.72.h) |
| What is the name of the ultra-short acting Fentanyl? | Remifentanil |
| What is the name of the Fentanyl "lollipop" for breakthrough pain? | Actiq |
| What is Hydromorphone? | Dilaudid--PO, IV, IM; alternative to Demerol; similar to MS |
| What's up w/Codeine? | Opioid analgesic. Available PO (has synergistic effects w/ Tylenol) and as an elixir for kids; has cough suppressant properties |
| What is Hydrocodone (and maybe some other names/additives)? | Opioid analgesic. Forms include: Vicodin (with acetmpn), Norco (same amt of hydrocodone; low dose acetmpn), Lortabs (acetmpn), Lortab ASA (aspirin), Vicoprofen (ibuprofen) |
| What are the names of opioid analgesics containing Oxycodone, and their respective additives? | Percodan (ASA), Percocet (acetampn), Tylox (acetampn), Oxycontin (a sustained release version...people will crush and sniff to by-pass the slow onset) |
| Tramadol (Ultram)...description...anyone? | Selective MU receptor agonist (weak) thus slow onset, some tolerance and dependence, not controlled, low respiratory depression (but it can happen) |
| Describe (ant)agonistic and other effects of Butorphanol (Stadol) | Competitive Mu antagonist/Kappa agonist; increases cardiac work load (avoid in CHD). Bonus: can use nasal for severe migraines |
| Why is Naloxone our friend? | ***Naloxone (Narcan) is an opioid antagonist, and can be used to reverse the effects of narcotics in the case of an OD...game on! |
| What happens when one ODs on Tramadol? | Tramadol (Ultram) toxicity presents a major risk of seizures, especially with MAOIs (contradiction? -check) |
| What is the goal of combination drugs containing both opioid agonist + antagonists? (e.g. Butorphanol [Stadol]) | Analgesia w/o respiratory depression. |
| T/F: Anti-emetics can sometimes help reduce pain when given with narcotics? | False. Anti-emetics (e.g. Zofran, Phenegran) have NO analgesic properties, nor will they increase sedation. |
| Where are the different of cholinergic receptors located? | Nocinitic N-All ganglia, Adrenal Medulla; Nicotinic M- Neuromuscular junction; Muscarinic- parasympathetic target organs (eyes, heart, lungs, etc) |
| What is another term for cholinergic agent? | Parasympathomimetic |
| What is Bethanechol (Urecholine)? | A cholinergic agent (parasympathomimetic) used to speed things (urinary, GI) up post-operatively, or after pregnancy. |
| What are contradictions with Bethanechol (Urecholine)? | Urinary blockage, paralytic ileus are the big two...also asthma, peptic ulcer disease, hyperthyroidism |
| What kind of nursing implications come with Bethanechol (Urecholine)? | Observe for the good: void/defection; Teach: taking between meals to reduce the bad (nausea) |
| What are MIOTICS, and what do they treat? | Muscarinic agonists; constrict pupils, reduce intra-olcular pressure by increasing flow of aqueous humor. Used to tx glaucoma. |
| Describe Acetylcholine (Miochol) and it's uses. | Parasympathomimetic, specially a muscarinic agonists; thus used to reduce intra-ocular pressure in glaucoma. |
| What are other terms for anti-cholinergic agents? | Muscarinic antagonists, antimuscarinics, cholinergic blockers, and parasympatholytics |
| What is the purpose of an anti-cholinergic agent? | Prevention of parasympathetic receptor activation by ACh; usually selective blockade of specific muscarinic receptors |
| What are the effects of anti-cholinergic agents? | *DOSE DEPENDENT: Increased: HR. DECREASED: saliva production, urination, GI mobility, CNS excitation (delirium) |
| What are the adverse effects of anti-cholinergic agents? | Tachycardia, urinary retention, dry mouth, restlessness, sedation, delirium, blurred vision. (Remember: many drugs can have these side effects) |
| What is Atropine, available routes, and what is it used for? | Anti-cholinergic agent, comes IV or inhaled, used to excite the SA node of the heart. |
| What is Scopolamine, and how is it used? | Scopolamine (Transderm Scope)—is a patch used for motion sickness (seen a lot as a prophylactic for post-op motion sickness) |
| What is Tolteradine (Detrol), and what is it prescribed for? | Anti-cholinergic agent; specifically a muscarinic receptor antagonist used to relax smooth muscle in UT; Rx: overactive bladder issues. |
| Why are anti-cholinergic agents used in GI therapy? | Decrease mobility for IBS, abdominal cramping |
| How are anti-cholinergic agents used in opthalmic treatment? | Mydriasis and cycloplegia (paralize ciliary muscle) for retinal exam; keratitis |
| What is the mechanism of action of a nicotinic agent? | Stimulate sympathetic ganglia and adrenal medulla → promote release of Norepinephrine and Epinephrine |
| What are the general effects nicotine agents? | Vasoconstriction; INCREASED: HR/force of contraction, GI secretion/motility (thus N,V-not digestion), CNS stimulation, tolerance and dependence |
| What forms does Nicotine come in, and what does it treat? | Gum, patch, inhaler; used to tx nicotine addiction |
| What is the name for the nicotine agonist that produces unwanted neuropsychiatric effects (including suicide)? | Varenicline (Chantix); blocks access of nicotine to receptors |
| What's the story with Acetylcholinesterase Inhibitors? | They Prevent breakdown of Ach—Nonselective (Muscarinic & Nicotinic), thus are indirect-acting cholinergics |
| What are Acetylcholinesterase Inhibitors used for? | Reversal agents for neuromuscular blockers, Atropine, and other anticholinergic drugs |
| What are the S/S of cholinergic crisis? | Weakness, paralysis, bradycardia, salivation. Tx: atropine, oxygen |
| What is Neostigmine (Prostigmin)? | Reversible acetylcholinesterase inhibitor. It is used to improve muscle tone in MG, and to reverse anticholinergic drugs. |
| What is Physostigmine (Antilirium)? | Acetylcholinesterase inhibitor used to reverse the effects of anticholinergics such as Atropine, Scopolamine, etc. |
| What do neuromuscular blockers do? (Hint: antinicotinic) | Block ACh at neuromuscular junction (Nicotinic-M) |
| What are neuromuscular blockers used for? | Conjunct w/anesthesia and/or mechanical ventilation |
| T/F?: Neuromuscular blockers do NOT alter conscious. | True: patient is awake and paralyzed, thus sedation and analgesics are required. |
| How do non-depolarizing neuromuscular blockers work? | Compete with ACh at nicotinic receptors causing skeletal muscle relaxation |
| How do depolarizing neuromuscular blockers work? | Attach to receptor causing sustain depolarization --> paralysis |
| What is Vecuronium (Norcuron)? | A non-depolarizing neuromuscular blocker |
| What is Succinylcholine (Anectine)? | A depolarizing neuromuscular blocker |
| Are are the adverse effects of neuromuscular blockers? | Hypotension, bradycardia. Others: prolonged paralysis, malignant hyperthermia (children), muscle pain --> fasciculations, muscle rigidity (emergent) |
| What is an important consideration when administering reversal agents (e.g. Neostigmine, Physostigmine) to tx paralysis caused by neuromuscular blockers? | These reversal agents do not last as long, thus if a client does not maintain therapeutic levels, they may have re-occuring paralysis |
| How does one assess recovery from paralysis r/t NM blocker toxicity? | Ptosis—Hold eyes open for 5 seconds; Hand Grip—Sustain for 5 seconds; Raise Head—Hold 5 seconds |
| What is pre-load? | End diastolic stretch of muscle fiber (diastolic pressure-ish); venous return to the heart. |
| What is after-load? | Tension in ventricular wall during systole (pretty much arterial pressure) |
| What do ACE Inhibitors do? | Prevent conversion of Angiotensin I to Angiotensin II, and increase activation of bradykinin (vasodilator); thus inhibiting Aldosterone and high BP |
| What is Angiotensin II? | Potent vasoconstrictor & stimulant of Aldosterone release |
| T/F?: ACE inhibitors effect both pulse, and BP. | False. ACE inhibitors do NOT affect pulse |
| T/F?: ACE inhibitors have a slow onset? | True, unless Na+ or H20 depleted |
| How do ACE inhibitors affect the kidneys? | Nephro-protective, also cause renal retention of potassium. |
| What happens to Na+ and H20 when taking ACE inhibitors? | Increased secretion (no net change in electrolytes) |
| What are ACE inhibitors used for? | Pretty much hypertension, sometimes CHF (w/diuretics), and in diabetes to reduce renal failure (contradicted, however with CKD/ESRD). |
| What are some adverse effects of ACE inhibitors? | Renal failure (decrease dose in CKD/ESRD), hypotension (1st dose effect) |
| How are ACE inhibitors named? | Ending in -pril- e.g. ***Lisinopril (Prinivil, Zestril) |
| What are important nursing implications with administration of ACE inhibitors? | Must monitor BP, kidney function (BUN, creatinine, electrolytes...K+!!) Must use caution with K+ sparing diuretics; contraindicated in pregnancy |
| What are angiotensin II receptor blockers? | Selectively blocks binding of Angiotensin II at the receptor, blocks vasoconstriction and aldosterone secretion; similar effects as ACE inhibitors |
| How are ARB's named? | Ending in -arton- e.g. **Losartan (Cozaar) |
| How do renin inhibitors work? | Direct renin inhibitor→ decreasing plasma renin activity (PRA) and inhibiting the conversion of angiotensinogen to Angiotensin I |
| Name a central acting agent used as an anti-hypertensive. | **Clonidine (Catapres): Can be used PO for hypertensive crisis, or transdermal patch—7 days (may see contact dermatitis) |
| What is Clonidine used for besides hypertension? | Tx of addiction to ETOH, cocaine, narcotics, nicotine |
| What are beta adrenergic blockers method of action? | Reduce sympathetic activity in brain vasomotor center, reduce sympathetic stimulation of beta receptors on arterioles reduce renin→ reduce angiotensin II |
| What are the goals of beta blocker administration? | Reduces blood pressure, pulse, cardiac output→ reduces myocardial contractility |
| What are beta blockers used to treat? | Hypertension, chest pain |
| What are the side-effects of beta blockers? | Bradycardia, CHF, bronchospasm, mask hypoglycemia in diabetics, depression, impotence, lowers HDL, increase cholesterol & triglycerides |
| What are important nursing implications for clients taking beta blockers? | Monitor BP (>100), P (>60), S/S of CHF (edema), BG (diabetics) |
| How are beta blockers named? | Ending in -olol- e.g. **Propranolol (Inderal) |
| Name a non-selective (b1 +b2) beta blocker. | **Propranolol (Inderal) |
| What class of drug is **Metoprolol (Lopressor, Toprol)? (hint: be specific) | Cardioselective Beta-1 blocker; anti-hypertensive; better for lungs, lipid panels, and possibly insulin sensitivity in type I diabetes. |
| What sort of effects to alpha-1 blockers have? | relax vascular smooth muscle, no effect on cholesterol, cardiac output or heart rate, reduces afterload, increases plasma volume→edema, ***requires diuretic, 1st-dose effect--dose at night |
| How are alpha-1 blockers named? | Ending in -azosin- e.g. **Prazosin (Minipress) |
| How do calcium channel blockers work? | Block Ca+ exchange across cell membrane, decrease afterload (vasodilation) |
| What are the two types of calcium channel blockers? | 1) Cardioselective (nondihydropyridine) 2) Dihydropyridine |
| What class of drugs end in -pine-? | Dihydropyridine (calcium channel blockers) e.g. Amlodipine (Norvasc) NOT CARDIOSELECTIVE CHANNEL BLOCKERS |
| Give an example of a cardioselective (nondihydropyridine) calcium channel blocker. | **Diltiazem (Cardizem, Tiazac), also Verapamil (Calan, Isoptin) |
| What are calcium channel blockers used for? | Hypertension, angina, supraventricular dysrhythmias, a-fib |
| Which calcium channel blocker slows contractility AND can worsen CHF? | Cardioselective agents,e.g. Diltiazem, Verapamil |
| What are important nursing implications of calcium channel blockers? | Observe for s/s CHF, monitor edema; monitor BP—frequently if IV administration; hold for pulse < 60; BP < 90 systolic |
| What is **Hydralazine (Apresoline)? | A vasodilator that directly relaxes arterial and venous smooth muscle |
| What can happen as a result of taking Hydralazine? | Reflex tachycardia (stimulation of renin, Na+ H20 retention, etc). |
| Hydralazine is most effective when given with ____ ________, and _________. | Beta blockers and diuretics (can otherwise cause reflex tachycardia) |
| What are the target levels of antilipemic drugs? | Lower total cholesterol <200mg/dl; LDL < 130 mg/dl |
| How do bile-acid binding resins work? | All work is done in the gut (not absorbed into blood; oldest/safest way); bind with bile acids in intestine → excreted in stools; increase in cholesterol oxidated to bile acids --> excretion |
| What are the end-results of bile-acid binding resins? | LDL & cholesterol decrease secondary to Increased clearance of LDL from plasma |
| What are bile-acid binding resins used to treat? | Rx: primary type II hyperlipoproteinemia |
| What are some side effects of bile-acid binding resins? | DOSE DEPENDENT... Constipation (common); others: abd bloating, flatulence, nausea, vomiting, diarrhea, indigestion |
| What class of drugs is contraindicated with the use of fat-soluble vitamins? | Bile-acid binding resins |
| What are some contraindications of bile-acid binding resins? | Use of fat-soluble vitamins, digoxin, thiazides, lasix, warfarin, STATINS |
| What class of drug is **Cholestyramine (Questran)? | An anti-lipemic (specifically, a bile-acid binding resin) |
| What do Hmg-CoA deductase inhibitors do? (Hint, also referred to as “The Statins”) | Lower total and LDL cholesterol—up to 20-50% depending on agent and dose; lower TG’s, especially with very high TG’s |
| What are important nursing implications for clients taking Hmg-CoA deductase inhibitors? | Monitor cholesterol, and liver enzymes (AST, ALT for 1st three months if healthy). Know that muscle aches, and weakness are BAD; so is pregnancy. |
| What is the classification of Atorvastatin (Lipitor)? | Antilipemic; specifically a Hmg-CoA deductase inhibitor |
| What are the therapeutic effects of Niacin (Nicotinic acid)? | Lowers serum LDL and VLDL & increases HDL, decreases triglycerides 20-50%; higher than vitamin B3 doses; mechanism not clear |
| What drug is thought to affect cyclic AMP (control activity of lipase), and thus lipolysis? | Niacin (Vitamin B3) |
| What are some adverse effects of taking prescription strength Niacin? | GI upset--N/V, bloating, gas, hunger, elevate hepatic function tests, flushing--face and neck (transient; goes away), pruritis, and INSULIN RESISTANCE |
| What is the big idea behind ***Extended Release Niacin (Niaspan)? | Less flushing, not really sure what else. |
| What are fibric acids (fibrates) all about? | Used for lowering triglycerides (VLDL), some lowering of LDL, increased HDL |
| What are the side effects of fibric acids (fibrates)? | GI: N, D, abd pain, Increased risk of gallstones, myopathy—report muscle pain, weakness, DON'T COMBINE w/ STATINS, hepatotoxicity—monitor liver enzymes, potentiate oral anticoagulants (monitor INR levels) |
| Given an example of a fibric acid (fibrate). | **Fenofibrate (Tricor) |
| What are diuretics used for? | Increase in: rate of urine formation, and urine volume; net loss of solute (electrolytes) and water |
| What's an indication for diuretics? | Mobilization of edema |
| What are the mechanisms for osmotic diuretics? | Increase osmotic pressure of tubular filtrate, fluid moves from ICF→ECF, inhibits renin release (decrease ICP), increases renal blood flow (prevents nephrotoxicity) excretion of electrolytes—Na, K, Ca, Mg, Cl, HCO3, phosphate |
| What is Mannitol (Osmitrol) used for? | Reduce CSF pressure (pre/post neuro surgery), Reduce intraocular pressure (glaucoma/post-op), nephrotoxicity prevention (diluting urine) |
| What are the adverse effects of Mannitol (Osmitrol)? | (osmotic diuretic) H/A, N, V; contraindicated w/ CHF (too much ECF!!!!) can cause renal failure, liver failure...BAD, BAD, BAD |
| Important nursing implications r/t osmotic diuretics? | "Give IV via filter" (WTF that is), monitor output (looking for diuretic effect), BP, lung sounds (fluid overload), serum osmolality (electrolytes; not too high), ICP (couple of ways= LOC, catheters, etc.) |
| What is the mechanism of action in carbonic anhydrase inhibitors? | MAKE YOU PEE BiCARB; Inhibit secretion of H+ (retains H+), Increase excretion of Na+ and bicarbonate --> urine alkalinizes, metabolic acidosis a risk, marked potassium excretion, reduce aqueous humor production |
| What is **Acetazolamide (Diamox) used for? | Carbonic anhydrase inhibitor (pee bicarb, K+); alkalinize urine for drug excretion (of acidic drugs) altitude sickness (prevention; inhibits hyperventilation, thus metabolic alkalosis) |
| What special precautions does **Acetazolamide (Diamox) have? | It's a sulfanamide (check allergies), can cause hypokalemia, and renal calculi, ➢ Metabolic acidosis → contraindicated with COPD (retain CO2; Resp. Acidosis), ALSO IT MAKES BEER TAST LIKE METAL! |
| What are some precautions with thiazide diuretics? | Sulfa-derivative; electrolyte loss (spec. K+), hyperglycemia (in diabetics), and hyper-lipidemia |
| What is **Hydrochlorothiazide (HCTZ, Hydrodiuril)? | Thiazide diuretic --> sulfa-derivitive causing loss of water, potassium, BG, and other electrolytes |
| What are the affects of loop diuretics | Inhibit electrolyte reabsorption in ascending loop of Henle, weak carbonic anhydrase effects, Increase renal blood flow (to improve excretion), Increase loss of K+, Mg, acid, ammonia |
| What are loop diuretics used for? | Edema (heart, liver, kidney), acute pulmonary edema, nephrotic syndrome (stage 1 CKD), and HTN |
| What are the precautions for loop diuretics? | Sulfa allergy (except Ethacrynic acid), Ototoxicity (esp. E. acid), hypotension (give slow IV), loss of Na+, and K+ |
| When should Furosemide (Lasix)*** be given? | Early in the day... has long half life, given PO q.8.h |
| What are aldosterone agonists used for? | They are potassium sparing diuretics (e.g.**Spironalactone); Hypertension, edema, drug of choice for edema and ascites with hepatic disease (blocks the very cause for acites |
| What are adversed effects of **Spironalactone? | Potassium sparing diuretics; hyperkalemia; problems with girls and boys parts |
| What are some precautions of aldosterone agonists? | Caution when combined with other diuretics, ACE inhibitors or in renal disease, no potassium supplements; teach—do not use salt substitutes--(most contain KCl) |
| What are some effects of Nitrates? |
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scottheadrick
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