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Pharm Final
Final
| Question | Answer |
|---|---|
| What opioid agonist are most to least lipid soluble? | Sufentil, Remifentil, Fentanyl, Alfentil, Morphine, Demoral |
| Define Half life of a drug? | time for drug concentraction to decrease 50% in plasma |
| Define zero order kinetics? | constant amount of drug is eliminated per unit of time irregardless of plasm concentration. Ex: ASA, ETOH, Pheytoin |
| Define first order kinetics? | % of drug eliminated over time * 5 half-lives the drug plasma concentration declines by 96.9% |
| What drug characteristics will affect a drug's half life? | Vd Clearance Larger the Vd=longer the half life larger clearance= short half life |
| What induction agent lowers ICP? | All except Etomidate: Propofol, Etomidate, Benzo, Thiopental |
| What induction agents increase ICP? | Ketamine |
| What induction agents potentiate GABA? | Etomidate, Benzo, Propofol Barbs they effect the Cl channels |
| What induction agents is classified as a alpha 2 agonist? | Precedex |
| What are effects of Kappa receptors? | Butorphanol a kappa receptor agonistantagonist |
| What agents stimulate kappa receptors? | Butorphanol Meperidine:anti-shivering effects stimulate by kappa receptors |
| What induction agent affects NMDA receptors? | Ketamine |
| What induction agent lowers BP and CO the most? | Propofol,, Barbs, Precedex |
| What induction agent has the least effect on BP and CO? | Etomidate |
| What induction agent increases BP and CO | Ketamine |
| What induction agent has analgesic properties? | Ketamine Precedex(Dexmedetomidine) |
| What induction agent has antiemetic and antipruretic properties? | Propofol |
| What are disadvantages of barbs? | Hangover effect, No analgesic, tolerance, high abuse potential, risk with drug interaction, narrow therapeutic index, assisted suicides, lacks specificity, no reversal |
| What is the MOA of ND NMB agents? | competitive antagonist for Ach at the alpha-subunit of the PMJ nicotinic receptors |
| What is the mechanism of action of Depolarizing NMB agents? | Agonist at the nicotinic receptor at the Motor end plate |
| At what receptors do these agents work (depolarizing NMB) | Nicotinic receptors on the alpha sunbunit |
| Can depolarizing NMB be reversed? Y or N What can? | No! Non-depolarizers |
| What is anticholinergic syndrome? S/S? | Too much anticholingeric drugs exhibit CNS:coma, LOC changes, delrium, confusion Dry as a bone, red as a beet, hyperthermia, mad as a hatter, flush skin, blind as a bat Effects are additive and occur mostly in elderly and young |
| How is anticholinergic syndrome treated? | Physostigmine |
| What anticholinergic agents are the most lipid soluble? and crosses the BBB? | Scopolamine tertiary amines are lipid soluble and can cross the BBB |
| What is the significance of anticholinergics crossing the BBB? | Greater risk for central anticholinergic, risk of drowsiness Elderly |
| What are some of the most common causes of delayed recovery from NMB? | Insufficient time given to wear off,hepatic or renal, drug interactions, acid/base, or list of things that potentiate NMB [CALL MD V.G] |
| How is each of the NMB agents cleared from the body? | Dox, Pan, Pipe:Renal Vec, Roc: renal/bile Atracurium:ester hydrolysis and Hoffman) Cistatracurium: Hoffman Sch:plasma cholinesterase |
| What drugs may potentiate the effects of NMB agents? | Cardiac dysrhythmias, amnioglycosides, lidocaine (locals), lithium, magnesium, diuretics, volitale, ganglionic blockers (phenytoin) [CALL MD V.G.] |
| What patient characteristics potentiate the effects of NMB agents? | Acid/Base, renal or hepatic, hypothermia, hypokalemia, hyperkalemia |
| What are the anticholinergic agents? | Atrophine, Scopolamine, Glycopyrrolate |
| What clinical effects do these agents posses? (anticholinergic) | Block muscarinic receptors on the post ganglionic side of the parasympathetic NS Eyes dilate, dry mouth, flush skin, decrease peristalisis, bronchoconstriction, urinary retention, tachycardia, constipation Antivagal, antimuscarinic, anticholinergics |
| What risks do anticholinergics possess? | Increase risk of aspiration, central anticholinergic syndrome, additive effects |
| What effects does ASA have on thromboxane/prostacycline? | Thromboxane inhibited by low dose ASA Prostacycline inhibited by high dose ASA |
| How long should we hold ASA prior to elective surgery? | at least 1 week |
| Does ASA cause a higher or lower risk of renal toxicity compared to NSAIDs | ASA is less of a risk All NSAIDs can lead to toxicity |
| What is the MOA of NSAIDs? | inhibition of cyclooxygenase activity and synthesis of prostagladins (responsible for pain) |
| What is the MOA of steroids? | inhibit the synthesis of prostaglandins |
| What effect do ASA/NSAISs have on leukotrienes? | both increase production of leukotrienes which can lead to bronchoconstriction and asthma and hyperactive airway disease pts are at rist |
| What is the result of increasing leukotrienes? | increased bronchial smooth muscle vasoconstriction |
| What are the common adverse reactions associated with the use of NSAIDs? | Post-op bleeding, ulcers, GIBs, decreased bld flow to kidneys, worsen heart failure by inhibiting prostaglandins, inhibit PLT agg, CNS effects |
| How is acetaminophen classified? | Central-acting prostagladin inhibitors not a NSAIDs |
| What are the clinical effects of acetaminophen? | analgesic, antipyretic, doesn't inhibit PLT, no affects on GI system, no anti-inflammatory effects. |
| What is the risk associated with acetaminophen use? | long term use can destroy kidneys |
| what are adverse effects associated with acetaminophen? | long term use can destroy kidneys, overdose can cause liver damamge |
| what is ketorolac? | potent NSAIDs, only NSAID that comes in IV form |
| What are the recommended doses for ketorolac in adults and in pts > 60 years old? | no more than 30 mg bolus at once 15 mg q 6 hrs |
| What pts are at greatest risk from adverse reactions from ketorolac? | underlying kidney problems, heart failure, hypovolemic pts, IDDM pts. |
| What is ASA related asthma? | caused by ASA worsening asthma, not immune reaction, causes bronchoconstriction, increased bronchial smooth muscle vasoconstriction |
| What pts are at risk for ASA related asthma? | Asthma, nasal polyps, rhinosinusitis, NSAIDs and ASA share cross reactivity |
| what role do NSAID have in the management of post op pain? What are the benefits of combining NSAID with opioids? How should agents be used? | Combination with local anesthetic or opioids, an cause increase post-op bleeding, they have a ceiling effect |
| What agents are used to prevent gout attacks? | Allopurninol:prevents the formation of uric acid Colchicine: inhibits the migration of the granulocytes Probenacid: get rid of uric acid |
| Which of these agents can be used to treat an acute attack of gout? | Colchicine NSAIDs |
| Describe the effects of thromboxane and prostacycline? | Prostacycline:vasodilator, inhibits PLT agg. by high dose ASA Thromboxane: vasoconstrictor, inhibits PLT agg. by low dose ASA |
| Describe the risk of associated with an imbalance b/n thromboxane and prostacycline? | Too much Thromoboxane and not enough Prostacycline the pts will be at risk for clotting and organ infarction Too much Prostacycline and not enough Thromboxane the pts at risk for bleeding |
| What is epoprostenol? | Flolan |
| What are indications for this drug? | Pulm. HTN assoc. with Lupus, heart failure an valvular do |
| What is alprostadil? What are indications for this drug? What are adverse reactions assoc, with alprostadil? | Prostaglandin Used to control HTN, keep ductus arterious open for a short period of time, erectile dysfuntion |
| What are adverse reactions assoc. with alprostadil? | Bronchoconstriction, HTN, Hyopvolemia, N/V, flushing |
| What is carbopost? What are indications for this drug? | Prostaglandin Uterine bleeding post-op Pregnancy termination |
| What are adverse reactions assoc, with carboprost? | Heart failure, DM, bronchoconstrictions |
| What drug characteristics has the greatest effect on a local anesthetics | Lipid solubility (potency) Protein binding (DOA) Ionization (onset) |
| What local anesthetics are most potent? | Bupivicaine, Ropivicaine |
| What local anesthetics have longest DOA? | Bupi, Tetra, Ropiv, Etido |
| What local anesthetics have the fastest onset of action? | Lido, Mipiv, Cholor, Etido |
| How are nerve fibers classified? What is the function of each nerve fiber? | alpha fibers: most myelinate, fastest conduction,motor fx, last blocked beta-motor fx, touch and pressure sensation gamma-reflexes delta fibers-pain and temp sensation B:preganglioin ANS(BP)1st blocked c:unmyelinated, 2nd blocked, pain temp |
| What are the first nerve fibers to be blocked by local? | B-fibers |
| What are the last nerve fibers to be blocked? | A-alpha are the last to be blocked |
| What is cocaine | ester of benzioic acid |
| is cocaine an amide or an ester? | ester |
| what effects does cocaine have on vasculature? | vasoconstriction |
| How is cocaine metabolized? | liver; the only ester that is metabolized |
| What agents are effective when appiled topically | lido, procaine, cocaine, benzo |
| What are differences b/n ester and amide local anesthetics? | how there metabolized |
| How are ester and amides metabolized? | amides: liver ester: hydrolysis |
| What class is assoc. with a higher risk of allergic reactions? | esters due to byproduct of PABA amides only with perservatives |
| What local anesthetic is assoc. with methemeglobinemia? | Prilocaine |
| Why is epi added to local solutions? | keep drug at site of action allowing a better block and decrease systemic absorption |
| Why is sodium bicarbonate added to local anesthetic solutions? | increase the onset of action by changing the ionization, greater lipid solubility |
| What durgs increase the risk of systemic toxicity from locals? | Anything that decreases hepatic bld flow: Beta-blockers volatile ca channel blockers Anything that decreases C.O. cimetidine |
| What H2 antagonist has highest risk of drug interactions? | Cimetidine |
| what is the mechanism for cimetidine? | inhibits CP450-3A |
| what are indications for the use of ca containing antacids? | used to decrease gastric pH, phosphate binding, |
| What are the side effects for ca containing antacids? | Rebound, milk-alkalizing syndrome |
| what are the used of magnesium containing antacids? | laxative antacid |
| what are the side effects of magnesium antacids? | diarrhea |
| what are uses for aluminum containing antacids? | antacid, phosphate binding |
| what are the side effects of aluminum? | constipation dementia in renal insuff. pts |
| what are non-particulate antacids? | Bicitra, Polycitra, Na Citrate |
| What are the benefits of non-particulate antacids? | If aspirated they have a less risk of causing PNA |
| What are risk factors for aspiration PNA? | Obesity, Hiatal hernia, Pregnancy, CVA, Parkinson's, Huntington's, Anticholinergics, Narcotics, Trauma/pain, scleroderma |
| what is the risk of using H2 antagonist alone when giving drugs that are know to release histamine? | will cause exaggerated release of histamine, H2 and H3 blockers |
| What are the clinical effects of histamine? | bronchoconstriction, tachycardia, vasodilation, decreased CO, |
| What are the major differences b/n 1st and 2nd generation H1 antagonist? | 1st generation: more anticholinergenic side effects, greater side effects, sedation Diphenhydramine 2nd generation: less sedation, prolonged QT interval, additive effect Loratadine(claritin) Fexofenadine (allergra) |
| What are PPI? What are there indications? | Block final step of gastric acid, more effective for GERD than H2 blockers, all end in -azole |
| What are common side effects of PPI? | Diarrhea, H/A |
| compare onset of action of PPI and H2 antagonist? | PPI have slower onsets at least 2 hrs prior |
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melbacs
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