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231 Cards in this Set
- Front
- Back
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What is GERD?
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gastroentestinal reflux disease
50% people have it 1/month 7% once/day |
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how does sodium bicarbonate work as an antacid?
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potent
short DOA fast acting irreversible not for chronic use- can cause systemic alkalosis reacts with stomach acid to create salt, water, and CO2. can cause milk alkali syndrome causes burping and farting |
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how does aluminum work as an antacid
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absorbs pepsin
causes constipation, especially in dehydrated and immobile patients chronic use can cause a blockade. increases bone concentration of aluminum can also bind dietary phosphate |
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how does calcium work as an antacid?
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has the most effect on the lower esophageal sphincter.
rapid, prolonged, reversible, potent increases fecal bulk, and excretion of fatty acids no effect on bowel movements can cause pancrease hyperactivity can cause systemic alkalosis |
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how does magnesium work as an antacid
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they form insoluble salts, usually not absorbed
causing osmotic diarrhea, but doesn't change bowel motility. can be absorbed and can show up in renal disease in the kidneys and become a CNS depressant |
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how does algenic acid work as an antacid?
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not an actual antacid, but creates a barrier at the top of the stomach and stops the contents from re-entering the esophagus
does not change pH of stomach |
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what are the 4 acid modifier H2-Receptor antagonists?
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Cimetadine
Ranitadine- 4X stronger Famotadine-40-60X stronger Nazitadine- 2-3X stronger all are OTC |
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how do they work?
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reversibly compete with histamine at the H2 binding site.
Very selective- does not effect H1 receptors. decreases acid secretion, but not much effect on the smooth muscles in the GI tract |
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what are the side effects of them?
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famotidine- decrease CO
nazitadine- decrease CO & HR cimetadine- decrease histamine action on heart and vessels, and inhibit CYP450- |
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what are they used for?
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for peptic duodenal or benign gastric ulcers
for erosive esophagus for hypersecretion (Zollinger Ellison syndrome) |
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what else is cimetadine used for?
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immunomodulary effects (to treat warts)
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what are the toxicity effects of them?
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CNS dysfx- slurred speech, delirium, confusion
Endocrine- gynecomastia, galactorrhea Blood problems Liver toxicity- cholecstasis, hepatitis(R) rest are all caused by C. not for pregnant mothers |
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what is the difference between the H2 antagonists and the proton pump inhibitors?
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proton pump inhibitors stop the acid production sooner in the mechanism.
Proton pumps are also non-competitive and irreversible. |
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what suffix is associated with proton pump inhibitors?
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-prazole
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what are the proton pump inhibitors used to treat?
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reflux esophagitus
acid peptic disorders |
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what are the 5 PPI's?
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omeprazole - prodrug
lansoprazole - prodrug pantoprazole rabeprazole esoprazole- s-isomer of omeprazole |
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what do they do?
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stop acid production both day and night.
antimicrobial for H. pylori. |
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what are their side effects?
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headache
diarrhea CYP interactions with warfarin and phenytoin increases concentrations to digoxin, nifedipime, ASA, midazolam, DDI, & methadone. decreases concentrations of keto and itroconazole. because of pH changes |
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how long does it take once stopping the PPI's does it take for stomach acid levels to return to normal
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7 days
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what is sucralfate?
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a mucosal protective agent used to protect ulcers from perforation.
AlOH sulfated sucrose complex. |
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what side effects can sucralfate have
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cause constipation
binds phosphorus reduces bioavailability of other drugs |
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what is Bismuth?
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another mucosal protective agent.
promotes ulcer healing by covering. also is antimicrobial for H. Pylori not readily absorbed, must be taken for a while |
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side effects?
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can cause encephalopathy
causes black stool |
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what is misoprostol
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used for NSIAD caused ulcers
can also be used as an abortive agent. prodrug |
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what is bethanechol
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another mucosal protective agent. used before PPI and H2 antagonists came along.
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what is Metoclopramide?
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used as a antiemetic
used in GERD promotility - improves gastric emptying. dopamine antagonist can be sedating |
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what do anticholinergics do?
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prevent bradycardia and excess fluid secretion
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what do antihistamines do?
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prevent allergic reactions
decrease stomach acidity |
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what do barbituates do?
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relieve anxiety
facilitiate amnesia |
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what do antiemetics do
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prevent vomiting
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what do benzodiazepines do?
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amnesia
sedation |
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what do opiods do?
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analgesia
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what are the side effects of all the druds just asked about?
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autonomic instability
hypothermia cardiac dysarythmias nausea/vomiting delirium |
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what are the differences between intravenous and inhaled anesthesias?
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intravenous- rapid onset, good for short procedures
inhaled- used for maintenence, quick recovery, used in longer procedures |
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with inhaled drugs what does the rate of induction and recovery depend on?
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the partial pressure of the anesthetic
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what is henry's law?
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conc of gas physically dissolved in a liquid is directly proportional to the partial pressure of the agent and its affinity for the molecules in the liquid.
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how does controlling the partial pressure affect consiousness?
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by controlling it, you can manage how much of the gas is getting to the brain.
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what does wash-in mean?
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replacing the lungs normal gases with the anesthesia
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what affect do drugs with limited solubility have on the body?
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equilibriate quickly with the tissues.
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what affect do drugs with a high solubility have on the body?
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have higher initial intake, but have a delayed equilibrium, or take longer to work.
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the rate of pulmonary perfusion of the anethesia is equal to what?
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Cardiac output - therefore, the faster your heart pumps, the longer it will take for the partial pressure to get to the needed level. A slower CO allows the partial pressure to be achieved faster.
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what are the 4 steps to balanced anesthesia?
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1. attain partial pressure of inhalational agent in the brain
2- Supplemental analgesic provided 3- Neuromuscular blocking agent 4- MAC is additive, use combo agents to maintain cardiovascular stability. |
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what is the mechanism of action for inhaled anesthetics?
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nonselective, they alter the function of receptors for the neurotransmitters GABA and glutamate
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how are the inhaled drugs grouped?
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halogenated- used with a low inspired partial pressure.
non-halogenated - has a high inspired partial pressure (NO) |
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what are the properties of halothane?
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strong anesthetic, but not a good analgesic.
proarythmic hypotension metabolite are toxic (hepatitis) vagomimetic- slows down the heart. hypercapnia agent of choic in children becuase it is not hepatotoxic in children |
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what are the characteristics of enflurane?
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does not block the sypathetics
less potent arrythmias greater potentiation for paralysis can cause CNS excitiation not to be used with patients with kidney disease becuase of toxic flouride metabolites |
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what are the characteristics of isoflurane?
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isomer of enflurane
doesn't synsetize the myocardium low biotransfer popular becasue it can be used in heart problematic patients becuase it does not cause arrythmias |
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methoxyflurane
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most potent
takes longer to kick in.causes flouride toxic metabolites not used much |
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disflurane
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low tissue solubility, so it acts quickly
can irritate the bronchioles causes tachycardia decreases blood pressure |
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sevoflurane?
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low solubility, quicker onset
hypotension decreased CO no tachycardia can use with patients with history of MI not pugnent- good for kids |
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NO?
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produces anesthesia without causing decreasing blood pressure or CO.
unconsiousness reached at 60-80%. deep anesthesia is not attainable with it. 25-40% - CNS depression, analgesic at maximum. |
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what two sensations do local anesthestics block?
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pain from and sympathetic vasoconstriction to specific areas of the body.
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why does infected tissue decrease the efficacy of the local?
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the local works best in it's non-ionized form. infection lowers the pH, making more of the local ionized, making it less efficient.
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what other factors influence the absorption of the local?
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dose
site drug-tissue binding vasoconstricting substances drug properties |
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what metabolizes esters?
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plasma pseudocholinesterase
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what metabolizes amides?
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cytochrome P450
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with the amides, what is the order of quickest metabolism?
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prilocaine>etidocain>lidocaine>mepivicaine>bupivicaine
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what are the the locals MOA?
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threshold for nerve excitations is increased, impulse conduction is slowed, rate of rise of the action potential declines, action potential amplitude decreases, and the abilitiy to create an action potential is abolished.
It binds to Na channels, blocking Na transport. |
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what indicates how fast the local works?
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how small and how lipophilic the local is. The smaller it is, the quicker it works. The more water soluble the better too.
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will locals block pain sensation only?
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no, they can block motor too.
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how does fiber diameter and presence of myelination affect the outcome?
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shorter diameter of the nerve, better the local works.
myelinated nerves require at least 3 consecutive nerves to be blocked to stop the action potential. |
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in mixed nerve trunks, what usually is affected first?
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motor is usually more superficial in the nerve trunk, so motor first, then sensory.
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what role do epinephrine and phenylepinephirne play in a local block?
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vasoconstriction, allows local to stay in the area of injection longer.
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which two tend to have the worst side effects on the peripheral nerves?
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chloroprocaine
lidocaine |
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how do locals affect the heart
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decreased strength of contraction (except cocaine)
hypotension arterial dilation |
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what does cocaine do to the heart?
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blocks NOR uptake, causing vasoconstriction and hypertension
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what are the most cardiotoxic drugs?
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bupivicaine
etidocaine ropivicaine- S isomer of bupivicaine is less cardiotoxic, but costs a lot more. |
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what happens if too much of it gets into the blood?
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(>10mg/kg of prilocaine) methemoglobinemia - because of 0-toluidine.
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what two drugs are used to reverse it?
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IV methylene blue and IV vit C
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which locals can cause an allergic reaction and due to what?
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esters
PABA |
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what is TAC?
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topical anasthesia (tetracaine, epinephrine, cocaine, but cocaine isn't used much anymore). Used for lacerations.
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when should you not use TAC?
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patients on TCA's or MAOI's
skin flaps digits, nose, cock, ear hypertension cardiac disorders mucous membranes due to vasoconstriction |
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what is EMLA?
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eutectic mixture of local anesthetics. onset of at least 1 hours. prilocaine and lidocaine.
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Synera?
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another topical made from lidocaine and tetracaine
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what is Zingo?
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lidocaine powder given without a needle. It is blown into the pores. onset of 1-3 minutes. Most expensive.
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what is iontophoresis?
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using an electrical charge to move the drug through the skin.
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what qualifies a person with acute renal failure?
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creatinine level increase in 0.5 mg/dL, or doubling of the Cr.
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what qualifies a person with chronic renal failure?
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GFR < 60 for at least 3 months. end stage renal failure is GR < 15.
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what problems can patients with renal failure develop?
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increased BUN and Cr
drug accumulation Ph and K accumulation acidic blood volume overload HTN anemia |
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what is usually the first sign of renal problems?
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changes in urine output (decline) urine output usually recovers before the creatinine recovers
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when does kidney function start to decline?
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age 30. 1ml/min/yr.
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what is GFR?
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a measure of how wastes are being eliminated from the kidney. Normal is around 120ml/min. Estimated by CrCl.
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what is CrCl?
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comes from skeletal muscle metabolism. Freely filtered and not metabolized or reabsorbed.It overestimates renal function in chronic renal failure
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what is the best way to do a CrCl?
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24 hours of collection. Not always relaible if patient is body building or has muscle wasting.
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what is the cockroft-gault CrCl?
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(140-age x ideal body weight) / 72 x serum Cr
ideal body weight = 50 + 2.3 per inch over 5 foot in males, 45.5 in females Round Cr up to 1 in patients over 65. Use caution in patients with amputations and paralyzed. |
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what pain medications do you need to avoid in renal disease?
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mepiridine
propoxyphene NSAIDs |
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what antidepressant do you need to avoid in renal failure?
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duloxetine
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what anti-epileptics need to be avoided in renal failure?
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gabapentin
pregabalin leveltiractem valproic acid phenytoin |
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what anti-diabetics need to be avoided with renal failure?
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Metformin (CrCl higher than 1.5 in guys, 1.4 in girls)
glyburide insulin effect is also prolonged |
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what things are considered absolute indications for dialysis therapy?
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pericarditis
fluid overload pulmonary edema uremic conditions accelerated HTN persistent N/V creatinine >12 Bun > 100 |
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what are considered relative indications for dialysis?
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anorexia
hypoalbuminemia decreased cognitive tasking depression severe anemia persistent pruritis |
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In hemodialyis what are the two mechanisms used to clear the drugs?
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duffusion - high to low conc
convection- move by bulk water flow |
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what is adsorption?
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adhesion of the solute to the filter membrane
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what can hemodialysis control?
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acid-base status
electrolytes volume overload drug removal |
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what is dialysate?
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electrolyte solution with different concentration of solutes, used to normalize the plasma.It is not sterile so it should not mix with the blood.
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with hemodialysis, what is the clerance dependant on?
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blood flow rate
dialysate flow rate filter choice length of therapy days of therapy drug characteristics |
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what are the problems seen with hemodialysis?
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cramps - 2-50%
headaches- 5% hypotension - 15-50% itching - 50-90% N/V - 5-15% |
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what are the pros and cons of hemodialysis?
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pros- effective with short time span, can be done in most patients,
cons- hemodynamic instability, may worsen renal function, lifestyle issues |
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what is an ateriovenous fistula?
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anastamosis of artery and vein.
preffered method low infection and thrombus rates may take up to 4 months to mature life span of up to 20 years may not be suitable in elderly and diabetics |
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what is an AV graft?
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plastic tube between the artery and graft
2-3 weeks to reach maturity higher rates of infection and thrombus usually needs to be replaced within 2 years. |
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what are intravenous catheters
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often used while the fistula or graft is maturing, so used in acute situations.
highest rate of infection and thrombus not ideal for permanent use. |
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what is peritoneal dialysis?
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utilizes patietns peritoneal membrane to act as a filter. Clean fluid is put into the belly, let it sit for a couple hours, and then remove the fluid and replace with clean fluid. Is high in glucose to pull the water out of the body. Very high failure rate.
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what are the two differnt types of peritoneal dialysis?
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continuous ambulatory peritoneal dialysis- patient manually fills and drains 4-6 times/day
continuous cyclic peritoneal dialysis- machine does it at night 5-6 times, patient does it 1-2 times during the day. |
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what are the pros and cons of peritoneal dialysis?
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pros- portable, fewer dietary restrictions, patient controlled, hemodynamic stability, maintains residual renal function, suitable for elderly and children.
cons- protein malnutrition, body image issues, therapy fatigue, infection, not sufficient in large patients. |
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what are the indications for acute dialysis?
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A- acidosis
E- electrolytes-potassium I- intoxications - antifreeze O- overload - volume U- uremia |
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what is SCUF?
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slow filtration ultrafiltration
send blood through filter with no other fluid. It pulls off water |
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what is CVVH?
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continuous vena venous hemofiltration. Convective filtration. Requires replacement fluid, but no dialysate.
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What is CVVHD?
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continuous vena venous hemodialysis. No replacement solution. You do use diasylate. Solute removal is determined by diasylate flow.
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CVVHDF?
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both of them going on at once.
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what kind of drugs have good dialysis clearance?
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small molecular weight
low protein binding small volume of distribution ex: gentamicin |
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what kind of drugs have poor dialysis clearance?
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opposite
ex: digoxin, vanco |
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what are three drugs that should be given after dialysis instead of before?
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aminoglycosides
cephalosporins ampicillin |
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when doing a peritoneal dialysis, how can drugs be administered?
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IV or into the peritoneal cavity
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what are the 4 different ways that arachadonic acid is produced?
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cyclooxygenase
lipoxygenase P450 epoxygenase Isoprostane |
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if arachadonic acid is acted upon by cyclooxygenas, what does it become?
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prostiglandins and thromboxanes
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if arachadonic acid is acted upon by lipoxygenase, what does it become?
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leukotrienes
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what do NSAIDs tend to mostly act on?
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cyclooxygenase
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which type of cyclooxygenase is always present in the body?
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COX 1
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which cyclooxygenase is inducible and is the one responisble for prostiglandin production by cells involved in inflammation?
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COX 2
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what are the three products made and what do they do?
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prostacyclin- vasodilator, inhibits platelet aggregation
prostaglandins- imporant processes not involved in inflammation thromboxane- vasoconstrictor, promotes platelet aggregation, smooth muscle mitogen |
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which prostaglandins relax the airway?
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PGE, E2, I2
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which prostiglandins constrict the airway?
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PGF2a, TXA
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which prostaglandins induce the GI tract to move more quickly?
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TXA, PG
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which prostaglandins cause colicky cramps in the GI?
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PGE2, and PGF2a
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what type of thromboxane inhbits platelet aggregation
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TXA2
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what prostiglandins inhibit platelet aggregation?
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E1, I2
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what are the 2 goals for treating patients with inflammation?
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releive the pain,
stop the tissue damage |
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which NSAId is not given to relieve inflammation?
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Acetaminophen
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what does salyciate bind to in the serum?
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albumin, but the higher the conc, the higher free salyciate is found.
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what is aspirin metabolized to and what will help you excrete it?
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acetic acid and salicylate. Excretion is increase when you alkinalize the urine.
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what does aspirin not have an effect on?
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leukotrienes
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what is aspirin used for?
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muscular, dental, vascular, post partum, arthritis, bursitis.
NOT visceral |
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what are the antipyretic effects of aspirin?
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temp fall due to vasodilation of superficial vascualture, and it blocks the CNS response to interluekin 1, and stops PG
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how long before surgery do you need to stop taking aspirin?
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7 days, becuase it irreversibly stops pletelet aggregation, especially in mutli dosers
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what are some imporrtant therapeutic uses for aspirin?
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decreases ischemic attacks and unstable angima
lowers incidence levels for artery bypass grafts. good for preventing or decreasing the severity of MIs |
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what dose of aspirin will decrease the chance of an MI by 40%?
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325 mg every other day
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what is the difference between dosing aspirin when dosing for antipyretic/analgesic effect compared to anti-inflammatory effect
|
650 mg/4-6 hours
3.2-4 g/day |
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what can you do to aspirin to avoid gastritis?
|
use the kind that has an enteric-coating, it allows it to stop dissolution in the stomach
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what are the adverse effects with aspirin?
|
upset stomach
erosive gastritis, ulcers, bleeding vomiting salicylism- tinnitus, hearing loss, vertigo (reversible) hyperpnea <2g increases UA, >4g dereases UA mild hepatitis with AU disease decrease of GFR hypersensitivity with asthma bronchoconstriction can effect glucose tolerance in diabetics |
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who needs to avoid using aspirin?
|
hemophiliacs
pregnant women kids- can cause Reye's syndrome (fatty liver and brain) patients with ckickenpox |
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what dose is considered an overdose with aspirin?
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150-175mg/kilogram
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what happens if you mix acohol with aspirin?
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increases GI bleeding
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what effect can aspirin have on protein binding of other drugs in the serum?
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can displace them:
methotrexate probenacid phenytoin NSAIDs chloroporpamide tolbutamide |
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what affect does coticosteroid have on ASA?
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decreases it.
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what affect does ASA have on spironolactone?
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decreases it
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what does penecillin G do when taken with aspirin?
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competes with it for excretion in the renal tubules
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what is the NSAID that is the most selective and is still on the market?
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Celecoxib
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what are the non-acylated salicylates and what are they used for?
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Mg, Na, and salicylsalicylates.
Good anti-inflammatory, less analgesic effect than ASA. Better for asthmatics and people with bleeding problems |
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what is diflunisal?
|
derived from salicylic acid
used for OA, RA and pain similar side effects to NSAIDs |
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describe what happens with NSAIDs with joints.
|
it gets into the synovial fluid, and even NSAIDS with shorter half lives tend to stay in the synovial fluid longer than in the rest of the body.
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what is the NSAID MOA?
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similar to ASA.
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what is the NSAID selectivity?
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varies for each drug between COX 1 and COX2.
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what are NSAIDs with shorter half lives used for in comparision to longer half lives
|
short- acute musculoskelatal pain
long- RA |
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if a particular NSAID doesn't work for you, are you screwed?
|
no, you can try another and it is very possible it will work instead.
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what is the order for amount of GI upset for NSAIDs?
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piroxicam>indomethacin> Naproxen> sulindac > diclofenac > ketoprofen > ibuprofen
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what is the most common reason for stopping NSAID therapy?
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GI adverse effects, not a risk for ulceration.
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what can reduce the dyspepsea effect done by NSAIDs?
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H2 antagonists
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when is nephrotoxicity more likely to be seen in patients taking NSAIDs?
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more than 2 weeks
patients with CHF, cirrhosis, intrinsic renal disease |
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which NSAID can cause clinical hepatitis?
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diclofenac
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which NSAID is more likely to cause an acute liver injury?
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sulindac
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whe is liver dysfucntion more likely to be seen when using Naproxen?
|
more common in OA than RA
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what sideeffect can be seen with NSAIDs involving the CNS?
|
aseptic meningitis
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how soon do you need to stop taking NSAIDs before surgery?
|
5 half lives
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how can NSAIDs affect the eyes?
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deposits in the cornea
corneal edema |
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what happens to methotrexate, lithium, cyclosporine, and phenytoin when given with an NSAID?
|
it increases
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what are the two NSAIDs that do not require a prescription?
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ibuprofen
naporxen |
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what happens if you use aspirin and ibuprofen together?
|
decreases the anti-inflammatory effect
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what NSAID is said to be good for bone pain due to cancer?
|
ibuprofen
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which NSAID ismost likely to cause interstitial nephritis?
|
Fenoprofen
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which NSAID is also available as an Opthlamic formuation?
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flurbiprofen
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which NSAID acts on both cyclo and lipooxygenase, and does not alter warfarin or digoxin levels?
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Ketoprofen
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which NSAID is considered to be uricosuric
|
oxaprozin
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which NSAID can be used for RA and OA and dysmenorrhea?
|
Diclofenac
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which NSAID is used for OA,RA, and Gout and is a prodrug but has been known for serious side effects like Stevens/Johnsons epidermal necrolysis syndrome, and blood and kidney disorders
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sulindac
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what NSAID is approved for kids and is used in juvinile arthritis?
|
tolmetin
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which drug is a selctive cox 2 inhibitor and is used as a post op analgesic?
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etodolac
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which NSAID is a selective cox 2 inhibitor, but only has once a day dosing and is a prodrug so it has less GI toxicity?
|
Nabumetone
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which NSAID is a worse anti-inflammatory than ASA, and you can't ake it for more than a week because it can cause hemolytic anemia?
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meclofenamate, and mefenamic acid
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which NSAID is a very good anti-inflammatory and is only once a day dosing so only 5% discontinue due to side effects?
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Piroxicam
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which NSAID is considered to be slightly more toxic but more effective than ASA, and is a very potent inhibitor of PG synthesis, but is more likely to cause GI bleeding, and don't want to give to a patient on furosimide. It is often used in gout. It has complications with asthma and peptic ulcers. It can also decrease the pain with pericarditis and pluersy.
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indomethacin
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what can indomethacin do to premature infants with heart problems?
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it can inhibit the Cox 1 depedendent PG that is holding the ductus arteriosus open and allow it to close without surgery
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what disease cna indomethacin cause in the kidney?
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hyperkalemia
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which is the only NSAID that can used both orally and parentally for pain
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ketorolac
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which NSAID is selcetive COX 2 and can be used to prevent colon cancer and is used to treat RA and OA? It does not have affect on bleeding time, or warfarin, but does cause Na and K retention.
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celecoxib
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what is the major endogenous gluccocoritcoid?
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cortisol
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what is the major mineralocorticoid?
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aldosterone
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what are small doses of synthetic corticosteroids used for?
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to diagnose and treat adrenal dysfunction
large dose is used to treat inflammatory and immunologic disorders |
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when are peaks of cortisol seen?
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early morning and afterm meals bound to corticosteroid-binding globulin.
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which classes of drugs are said to work specifically during the S phase of the cell cycle for chemotherapy?
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Antibiotics and antimetabolites
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what drugs are specific for the G1 phase?
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L-asparaginase
peg-asparaginase erwinia-asparaginase |
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what drugs are specific for the G2 phase?
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Etoposide
Teniposide Bleomycin |
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What drugs are specific for the M phase?
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Vinca alkaloids
Taxanes |
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what is the MOA for asparaginase?
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breaks down asparagine into ammonia and aspartic acid
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what type of cancer is asparaginase used for?
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leukemia.
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what are the side effects of using asaparaginase?
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myelosuppression- anemia and leukopenia
pancreatitis coagulopathy |
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what is the antimetabolite MOA?
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they compete with the nucleotide precursors of DNA. causing DNA strand breakage and cell death
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what drugs target purine specifically?
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cytarabine
mercaptopurine thioguaninecladribine fludarabine pentostatin |
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what drugs target pyrimidines specifically?
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flourouracil
floxuridine gemcitabine capecitabine |
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fluorouracil is used mainly for what?
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colon cancer- the limiting part of it is myelosuppression
IV |
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what doe leucoovorin do?
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it enhances fluorouracil by allowing for tighter binding of the molecules to the enzyme.
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what side effect is often associated with fluorouracil?
What can be used to suppress it? |
hand-foot syndrome
Vit B6 |
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what is cytarabine specifically used for?
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leukemia
lymphoma |
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what is the dose limitation and side effects of cytarabine
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myelosuppression, it can also cause neurotoxicity and N/V and transient hepatic function
pancreatitis Ara-C-syndrome occular toxicity (conjunctivitis) |
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what is the MOA for methotrexate?
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folic acid analog
myelosuppresion is the limiting factor renal failure is the biggest worry worst chemotherapeutic drug. given many fluids and leucovorin rescue. |
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what drugs do you need to avoid 24 hours before and 48 hours after administering methotrexate
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NSAIDs
Aspirin penecillin bactrum |
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what is fludarabine usually used for?
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leukemia, usually as a last resort. dose limitied by myelosuppression.. Cuases N/V and neurotoxicity
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what is the MOA for etoposide, teniposide, and etopiside phosphate?
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topoisomerase II inhibitor in G2 and S phase.
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when is it used?
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leukemias
lymphomas sarcomas in the brain, lungs, and testes. |
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what are the side effects of using these?
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myelosuppression
N/V hypersensitivity secondary leukemias mucositis hyperpigmenttion extravasation |
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what drugs are specific to the mitotic phase?
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vinka alkaloids- vincristine (worst), vinblastine, and vinorelbine.
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what are they used for?
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lymphomas
leukemias lung and breast myelomas |
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what is vinka alkaloids dose limiting effect?
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neurotoxicity- peripheral neuropathy, constipation, myelosuppression, it is a vescicant
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what way do you never give vinka alkaloids?
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intrathecally
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what is the MOA of Taxanes?
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mitotic phase, inhibition if microtubule dysassembly and inhibition of DNA/RNA synthesis
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what are the taxanes used for?
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breast cancer, ovarian cancer, lung and sarcoma.
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what is the dose limiting thing with taxanes?
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myelosuppression
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what do you have to do with all of the taxanes?
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premedicate anaphlactics because it causes neurotoxicity and peripheral neuropathy, alopecia, and edema
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what is the MOA of alkalating agents?
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non-specific cell cycle. causes DNa strand breaks, interferes with DNA replication, transcription of RNA, and nucleic acid function.
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what are wrong with them?
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vescicants
teratogenic carcinogenic mutagenic |
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what is busulfan used for?
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bone marrow transplant
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what is the SLR for it?
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myelosuppression, also causes hyperpigmentation, veno occlusion with transplant patients. will cause sterility and cataracts, seizures, alopecia,
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dacarbazine is used for what?
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melanoma, hodgkins, neuroblastoma.
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what side effects
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severe N/V
hypotension facial flushing photosensitivity alopecia chemical hepatitisivenous irritant |
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what is melphalam used for?
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multiple myeloma and bone marrow transplants.
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what is its DRT?
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myelosuppression
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other side effects?
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alopecia
delayed N/V sterility pulmonary fibrosos dermatitis |
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what is thiotepa used for?
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bladder cncer
lymphomas sarcomas bone marrow transplant |
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DTR?
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myelosuppression, also causes mucositis, severe dermatitis
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what drug is considered the be the last chance drug for refractoryanaplastic astrocytoma gliomas, , melanoma, nad non-hodgkins disease?
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temozolomide - oral
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toxicity withit?
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nauseas
headache fatigue myelosuppression |
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what is cyclophosphamide used for?
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leukemia
lymphoma sarcomas multiple myeloma lung cncer breast ovarian carvical TTP RA multiple sclerosis |
