level 4 pharm packet

8/11/2019 LEVEL 4 Pharm Packet

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DRUGS TO KNOW FOR LEVEL 4

Drugs are easiest to learn when you study by their CLASSIFICATION.

There are 2 different classifications used commonly in pharmacology.The first is the PHARMACOLOGIC FAMILY. This class pretty much

tells you how the drug works (ie: sympathomimetics acts like thesympathetic nervous system). Although pharmacological class or

family is often seen in the literature, nurses need to focus on thedrugs THERAPEUTIC CLASS OR FAMILY, ALSO KNOWN ASFUNCTIONAL CLASS. This tells the nurse what the drug is used for(ie: antihypertensives, antianxiety medications).

I will break down medications into functional classes. Lets look at thefunctional classes you should know before your pharmacology test.

1.

Drugs affecting the cardiac systema.

Drugs for treating hypertensioni. Calcium channel blockersii. Beta blockersiii. Vasodilators used for hypertensive crises

b.Antidysrhythmicsc. Diuretics and potassium supplementationd. Drugs to treat hyperkalemiae. Inotropesf. Antianginal drugsg.Anticoagulants, antiplatelet, and thrombolytic drugs

h.

Adrenergic agents2. Drugs for pain, fever, and inflammation

a.Aspirinb.Acetaminophenc. Glucocorticoidsd. Opioids and nonopiod analgesics

3. Drugs used in the oncology or transplant patienta. Drugs to treat bone marrow depressionb.

Drugs to treat oral candidiasis

c. Drugs to treat hyperuricemiad.Antirejection agents

4.

Endocrine system drugsa.Antidiabetic medicationsb. Drugs used in hypothyroidismc. Drugs used in hyperthyroidismd.Vasopressin


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5. Antimicrobial drugsa. Drugs to treat urinary tract infectionsb.Aminoglycosides and vancomycinc. Macrolides and tetracyclinesd. Topical ointments and antimicrobials

6.

Drugs for the upper and lower respiratory tracta.

Antihistaminesb.

Anticholinergicsc. Bronchodilatorsd. Surfactant

7. Drugs affecting the nervous systema.Anticonvulsantsb. Barbituratesc. Benzodiazepinesd.

Anticholinesterase drugse. Neuromuscular blockers

8. Psychiatric Drugsa.Antidepressantsb.Antipsychotics (conventional and atypicals)c. Drugs used to treat side effects of antipsychoticsd. Mood stabilizers

9.

Drugs affecting the gastrointestinal system

a.

Antidiarrhealsb. Laxativesc. Lactulosed. Neomycin sulfatee.Vitamin Kf. Antiemetics

10. Drugs affecting fluids and electrolytes or the renal systema. Crystalloidsb. Colloidsc. Magnesium sulfate

d.

Phosloe. Buffers (sodium bicarbonate)

Now, lets look at the most important information for each class.


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Drugs affecting the cardiac system

Drugs for treating hypertension:In this section, we will look at BETA BLOCKERS, CALCIUM CHANNEL BLOCKERS,

AND VASODILATORS.

Some antihypertensive medications block the sympathetic nervous

system (beta blockers), some block the calcium influx in to thecardiac and arterial smooth muscle (calcium channel blockers),

others block enzymes that increase the rennin-angiotensin-aldosteroneresponse (ACE inhibitors and ACE receptor blockers), and others

will decrease fluid volume by ridding the body of extra water and

sodium (diuretics).

A. Tenormin (atenolol) is a beta blocker. You might be able totell a medication is a beta blocker because the generic namesend in LOL. PLEASE NOTE: You may not always be able totell a drug by looking at the ending, as some drugs to do not

follow this pattern. You must look up all drugs in which youare unfamiliar.

Tenormin or atenolol, the beta blocker, works to decrease the blood

pressure by blocking the effect of the sympathetic nervous system(SNS) in the heart. The drug essentially prevents norepinephrine from

activating the beta 1 receptors in the heart. Remember beta 1receptors? These are the receptors that increase contractility and

conduction. Therefore, if we block these receptors with a beta blocker,we will decrease contractility and heart rate, thus keeping the heartfrom working too hard, and decreasing the demand on the heart. This

lowers the BP!

How a drug works is called the MECHANISM OF ACTION. So, a betablockers mechanism of action is to decrease the effect of the SNS.

What the drug does because of the action is called the THERAPEUTICEFFECT. Thus, a beta blocker reduces blood pressure.

When you study drugs, UNDERSTAND, BUT DONT MEMORIZE. If

you understand both mechanisms of action and therapeutic effect, youcan predict everything else. Lets see how this works:

If you know that beta blockers reduce heart rate and blood pressure,

and they depress myocardial contractility, you can predict side effects

and nursing interventions rather well.


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One side effect of beta blockers that you should know is

BRADYCARDIA, or a pulse rate less than 60 in an adult. Anotherside effect is hypotension. These both make sense based on how the

drug works, right?

Nursing interventions that should be done before giving a beta blockerwould make sense too, right? What would a good nurse do before

giving this medication? They would take a BP and heart rate. Ifthe blood pressure is less than 100 systolic, or the heart rate is lessthan 60 beats per minute, the nurse should hold the drug and contactthe physician.

Cardioselective versus noncardioselective: Remember, beta 1receptors are in the heart, beta 2 are in the lungs. If we give a betablocker to block the effect of the sympathetic nervous system on the

beta 1 receptors, we impact the heart. A cardioselective beta blocker

will only block beta 1 receptors (metoprolol). A noncardioselectivebeta blocker will block beta 1 and 2 (propranolol): this is not good, as

we dont want to block beta 2 receptors and causebronchoconstriction. Therefore, noncardioselective beta blockers

are usually older drugs and they cause more side effects (suchas bronchoconstriction). A word of warning: if a cardioselective

beta blocker is used in a very high dose, there may be some spill-overonto the beta 2 receptors, thus causing bronchoconstriction.

Therefore, in any patient with an asthma or COPD history, weare very cautious when using any beta blocker!

In addition to using beta blockers for hypertension, we use

them after myocardial infarction to decrease the work of theheart and stabilize the conduction system (beta 1 receptors are

also in the conduction system). We also use them in patients

with very fast heart rates (atrial fibrillation, supraventriculartachycardia) to slow down the heart rate and AV nodeconduction.

Diabetic patients should be told that beta blockers can MASK THE

SIGNS OF HYPOGLYCEMIA (THEY CANT TELL WHEN THEIR BLOODSUGAR IS GETTING LOW), AND BECAUSE THE LIVERS BETA 1RECEPTORS ARE BLOCKED, AN ADEQUATE AMOUNT OF GLUCAGON

CANT BE RELEASE TO FIX THELOW BLOOD SUGAR. Therefore,diabetic patients are at risk for injury related to low blood

sugars!


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B. Calcium channel blockers (CCBs)

CCBs also lower the blood pressure and some can even be used todecrease conduction in the heart (antidysrhythmics property), but

these work a little bit differently than the beta blockers. These drugswork by decreasing the influx of calcium into the vascular and cardiac

smooth muscle, thus causing the arteries to dilate, and decreasing theheart rate and contractility.

There are 2 types of calcium channel blockers: the DIHYDROPYRIDINE

GROUP AND THE NONDIHYDROPYRIDINES. You can remember that

DIHYDROS simply dilate blood vessels, that is all they do. Therefore,if they dilate the vessels, they cause a reduction in blood pressure.

Nondihydropyridines not only dilate blood vessels, but also work

similarly to beta blockers, as they also cause a decrease in heart rate,and decreased conduction through the AV and SA nodes. This means

that the nondihydropyridines have greater uses than the other group.They can be used to lower the heart rate, decrease blood pressure,

and can also be used for certain fast cardiac dysrthymias (just likebeta blockers). Verapamil and diltiazem are the only 2 drugs in this

class right now.

Now, you should notice one important thing..BETA BLOCKERS ANDNONDIHYDROPYRIDINE CALCIUM CHANNEL BLOCKERS WORK

VERY SIMILARLY!!!!! This is very important to take note of for thefollowing reason. Lets pretend a patient is getting both a beta blocker

and verapamil. What is the potential for a DRUG-DRUGINTERACTION? Huge! They can have an additive drug

interaction; this type of interaction occurs when the action of

one drug is similar to the action of the second drug. Therefore,we might see more adverse drug reactions (side effects). Inthis case, there is an increased risk of bradycardia, cardiacdysrhythmias, and hypotension. Makes sense?

So, the interventions are the same too, right? Monitor pulse, bloodpressure, and cardiac rhythm during calcium channel blocker therapy.

Some names of calcium channel blockers you might see are:a. verapamil (generic)

b. nifedipine (generic)c. diltiazem (generic)


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C. Angiotensin converting enzyme inhibitors (ACE

inhibitors).

ACE inhibitors are also used for hypertension. These drugs block anenzyme (angiotensin converting enzyme) that is responsible for

boosting the blood pressure by means of the renin-angiotensin-aldosterone system. Therefore, if you block this enzyme, the blood

pressure falls.

Common drugs names: You may be able to tell a drug is an ACEinhibitor by looking at the generic drug ending. They tend to end in

PRIL. Again, be careful using this method, as not all drugs follow this

rule.

a.

lisinopril

b.

ramipril

Side effects: Cough is the major side effectrelated to these drugs.

The cough is caused because we are blocking angiotensin convertingenzyme and this causes a prostaglandin to increase. This

prostaglandin irritates the lungs, essentially, and causes a dry,irritating, and chronic cough. The cough is so bad that some people

come off of the medication! We also know that since it lowers BP, itcan lower it too much, so another side effect can be hypertension.

Another side effect of these drugs is HYPERKALEMIA, or increased

serum potassium. This is because we are blocking the rennin-angiotensin-aldosterone system and retaining potassium.

Nursing interventions:

1. Assess for a cough.

2. Check serum potassium3. Before giving medication, check blood pressure. If less than

100 or otherwise specified by physician, hold medication andcontact physician.

4. Avoid salt substitutes (they have potassium in them and can

raise potassium even more).

D.

Vasodilators for hypertensive crisis: The major drugs in this classinclude NITROPRUSSIDE, NITROGLYCERIN, LABETALOL ANDHYDRALAZINE. Another drug you may see utilized is Corlopam(fenoldopam). In this section we will discuss only the drugs boldedabove.


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A hypertensive emergency exists when the diastolic blood pressure is greaterthan or equal to 120 mmHg. Direct acting vasodilators are given as emergenttreatment of this condition, as they are all give IV and they begin to work in amatter of seconds or minutes. All of the vasodilators work essentially the same,

they result in either arterial and venous dilation or just arterial dilation. Whendilation occurs, it decreases the pressure in the vasculature, thus lowering theblood pressure.

Nipride (nitroprusside) is a vasodilator given by IV infusion. Because it is soeffective and works very quickly, extreme hypotension can result. As a rule, anypatient on nitroprusside will have CONTINUOUS BLOOD PRESSUREMONITORING. This means that every 3-5 minutes, we check the bloodpressure. If the blood pressure is still very high, we titratethe drip byincreasing the dose. If too low, we back down on the drip.

Other adverse effects from nitroprusside include: fluid retention andtachycardia. Lets figure out why this occurs. Venous dilation will decrease theblood return coming back to the right heart (preload). If this occurs, lesspreload gets to the left heart, thus reducing the work of the heart. However,when the preload to the left heart falls, the kidney then believes we have lostvolume somewhere; therefore, the renin-angiotensin system will kick in andcause fluid retention. Therefore, some patients will actually receive a diureticsuch as furosemide along with nitroprusside. The tachycardia from the drug isrelated to the drop in cardiac output. When the resistance falls in thevasculature, this decreased return to the heart, thus dropping cardiac output.

Therefore, a reduced cardiac output will reflexively result in tachycardia (heartrate is going up to compensate for the drop in cardiac output).

What is important for you to remember for the pharm test is that thenurse should assess for tachycardia and edema in any patient receivingnitroprusside. In addition, nitroprusside must be SLOWLY titrated. Thismeans that when we go up even a fraction on the dose, the blood pressure candrop significantly. Therefore, careful blood pressure monitoring is required forany patient receiving this drug; the nurse should plan to assess the BP at leastevery 2-3 minutes for the first 15 minutes or so, and at least every 5-10 minutesuntil the BP is stable.

Normodyne (labetalol) ends inlol, so it is a beta blocker. In addition tobeing a beta blocker, we use it for hypertensive crisis because it is has alphablockerproperties as well. Alpha receptors are on the blood vessels andnormally will cause vasoconstriction when norepinephrine binds. Withlabetalol, we block the alpha receptors from norepinephrine, so theresult is VASODILATION. Because it is a beta blocker, we would monitor


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patients receiving this drug for BRADYCARDIA and HYPOTENTION. Dont forgetthat any beta blocker also has the potential to cause cardiac dysrhythmias aswell!

Apresoline (hydralazine) is a vasodilator that causes arterial dilation only.

When given IV push for hypertensive crisis, effects are seen within 10 minutes.The adverse effects are similar to nitroprusside.so fluid retention, hypotension,and tachycardia.

Headache can also occur with all of the vasodilators..why? Becausethese drugs will dilate cerebral blood vessels, thus increase cerebral perfusionpressure.

When vasodilators are used that are known to cause tachycardia, beta blockerscan be given to reduce the tachycardia. A prudent nurse should anticipatethat tachycardia is a side effect of many antihypertensive drugs, especially whengiven IV; therefore, beta blockers are often given to treat this side effect andfurther reduce blood pressure.

Antidysrhythmic drugs:Antidysrhythic drugs fall into 5 groups. The groups relate to how themedications impact the conduction system. Remember learning about theconduction system? The AV and SA node are different than the HIS-purkinjepart of the conduction system. AV and SA node action potentials are calledSLOW POTENTIALSthis is because it takes longer to get an impulse throughthese areas than in the HIS-purjinke system. The HIS-purkinje system conducts

impulses very rapidly; therefore, these actions potentials are called FASTPOTENTIALS.

Remember learning about the movement of sodium, potassium, and calcium inthe conduction system? You should recall that IT IS THE MOVEMENT OFTHESE IONS THAT RESULTS IN A CARDIAC ACTION POTENTIAL.

Lets review the fast channels: while there are 5 phases, 3 phases areimportant, as medications affect these 3 phases.

Phase 0: rapid influx of sodiuminto the cell (also called depolarization).Phase 2: Calcium enters cell and causes contraction of atria/ventricles.

Phase 3: Potassium leaves the cell (repolarization)

Antidysrhythmic drugs affecting the fast channels: The first 4 classes ofantidysrhythmics affect the fast channels!

Class 1: quinidine, procainamide, lidocaine, phenytoin, mexiletineClass 2: Beta blockers (propranolol)Class 3: amiodarone, bretylium


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Class 4: calcium channel blockers (verapamil and diltiazem)

Class 1: These are drugs that block the sodium influx (so they impair phase 0);therefore, they slow down impulse conduction, thus suppressing

VENTRICULAR DYSRHYTHMIAS SUCH AS VENTRICULAR

TACHYCARDIA/VENTRICULAR FIBRILLATION.

Unfortunately, not all of these drugs have the same side effects, but we willfocus on the major ones only!

QuinidineMajor adverse reaction is DIARRHEA! Actually, it happens in about30% of patients taking quinidine. Quinidine is essentially the same as quinine,the antimalarial drugboth drugs come from the South American cinchona tree!Quinidine has ANTICHOLINERGIC PROPERTIES. Remember acetylcholine? It isthe neurotransmitter in the parasympathetic nervous system (PNS). Too muchacetylcholine can cause PNS symptoms such as bradycardia, increased oral andGI secretions, and urinary incontinence. Quinidine, having anticholinergicproperties, can result in the opposite effects..such as dry mouth andTACHYCARDIA! Cardiotoxicity is the most life-threatening side effect ofquinidine. You can recognize when a patient is getting toxic when the QRSwidens! The QRS complex is the tall and spiked portion of the EKG; normally, itshould be very narrow. When it widens, this is a major sign of cardiotoxicity.

ProcainamideThis drug is very similar to quinidine, except that it has noanticholinergic properties and does not cause diarrhea. Just like quinidine,CARDIOTOXICITY is the most life-threatening side effect (see above).

LidocaineYes, lidocaine is an intravenous drug used to treat dysrhythmias. Italso has anesthetic properties (numbing agent)! The major side effects with thisdrug are related to the effects on the heart and central nervous systems. In amanner of speaking, lidocaine numbs the CNS, therefore, confusion,drowsiness, and numbness/tingling in the limbs are often side effects. If thepatient receives very high doses, SEIZURE AND RESPIRATORY ARREST CANOCCUR. It is important to know that lidocaine can cause seriousbradycardia and hypotension.

MexiletineThis is essentially an oral drug that works just like lidocaine.

Similar neurological symptoms can occur (see above).

PhenytoinYes, believe it or not, Dilantin is also used for cardiacdysrhythmias. It makes senseit works in seizure by decreasing sodium influxinto the brain cells, and it works by doing the same thing in the cardiac cell!Typically, when used as an antidysrhythmic, it is for DIGOXIN TOXICITYcausing ventricular dysrhythmias. This is the reason it appears in the crash carts


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in most hospitals! If given too rapidly IV push (greater than 50 mg/min),hypotension and cardiac arrest can result.

Class II drugs: beta blockers. Recall that beta blockers will decreasecontractility. In addition, they will decrease firing from the SA node and reduce

conduction through the AV node.therefore, they can be used to treatSUPRAVENTRICULAR TACHYCARDIA (or tachycardia that arises from above theventricles). It is important to note that not all beta blockers have been approvedto treat dysrhythmias; at this time, only propranolol, esmolol, and acetubololhave been approved.

Class III: Potassium channel blockers. When potassium exits the conductionsystem cell, this marks the stage of repolarization (when the cell is attempting toreturn to resting state). Drugs that affect this stage are called potassiumchannel blockers (bretylium and amiodarone).

BretyliumThis drug is never used first line; it is used if an only if other drugssuch as lidocaine ARE NOT EFFECTIVE against the ventricular dysrhythmias.One of the reasons it is not used first is the problem of HYPOTENSION (this canoccur in 60% of patients receiving it). The hypotension may be so severe thanthey need drugs to increase their blood pressure (dopamine).

AmiodaroneThis drug, when given IV, is approved for first line treatment ofventricular dysrhythmias. Oral amiodarone can result in may long-termproblems, including lung injury and visual abnormalities. The IV form of thisdrug is much safer, as it is only used in the short run. Adverse effects from IV

amiodarone include hypotension, widening QRS, and bradycardia. Thebradycardia occurs because the drug will decrease conduction through the AVand SA nodes.

Class IV: Calcium channel blockers. Recall that calcium channel blockers(verapamil and diltiazem only) and beta blockers work essentially the same?They both decrease conduction through the SA and AV nodes, decreasing heartrate. So.the major side effects include hypotension and bradycardia!

Other antidysrhythmics: In this classification are adenosine and digoxin.Remember that digoxin works not only or heart failure, but it also decreases

conduction through the AV node and decreases SA node firing!

Adenosine is a unique drug. It is given very fast IV push for supraventriculardysrhythmias. The drug is actually cleared from the body within just seconds!Because the drug works so quickly and is gone, side effects last literally less thana minute and include intense flushing, chest pain, hypotension, and dyspnea.They may even have up to a 3 second period of asystole (flat line) on the EKG.


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Remember.by the time you push the drug and hold your breath 30 seconds,

the side effects are gone

Diuretics and potassium supplementation:We know that diuretics rid the body of excess sodium and water!

There are different classes of diuretics, including the loops, thiazide,and potassium sparing diuretics. Lasix (furosemide) is what we call a

LOOP DIURETIC. That means it works in the ascending limb of theloop of Henle. If you dont remember this structure in the renal

tubule, please go back to youre anatomy books!

Lasix will inhibit sodium reabsorption in the loop. This meansessentially that Lasix will prevent sodium from getting back into the

blood. Well..what follows sodium? WATER! Where sodium goes,water flows! This was my little memory trick in nursing school .

So, Lasix gets rid of sodium and water, thus getting rid of extra fluid inthe body, and lowering blood pressure. Make sense? Another

reason for giving Lasix is in oncology patients..as they candevelop hypercalcemia. Lasix will help to rid the body of the

extra calcium.

Side effects:1. Hypotension. This should make sense nowyou have

gotten rid of extra preload (volume).2. Dizziness/lightheadedness: related to the lower BP.

3.

Low serum potassium (along with sodium goes potassiumwith Lasix)

Nursing interventions:1. Check blood pressure before giving drug.

2. Monitor intake and output: if Lasix increases renal flowand output, then we must watch how much urine the patient

puts out and compare that to what they are taking into thebody by oral or IV means.

3. Check serum potassium.

4.

Check for improvement in edema: sometimes we use Lasixto treat patients with heart failure. These patients can bevery edematous before Lasix, and after Lasix, we want to

check that the edema has improved.

Another diuretic you will give a great deal is HCTZ, orhydrochlorothiazide. HCTZ works in the distal tubule, not in the

loop of Henle, so it is not as powerful of a diuretic as furosemide. It is


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usually given for hypertension, but is not very effective if you are

trying to get rid of a great deal of fluid! There is no IV form of HCTZ;it is only available as a pill.

Aldactone (spironolactone) is yet another diuretic. It is very different

than the loops and HCTZ, as it is a POTASSIUM SPARINGDIURETIC. What this means is that the drug will decrease sodium

and reabsorption (like other diuretics), but potassium will be retainedand not lost. While this drug is not used first line for hypertension, itis used a great deal in both LIVER FAILURE AND CONGESTIVEHEART FAILURE. For these patients, it will actually help to prevent

the fluid accumulation associated with the liver and heart failure

because it inhibits sodium (and yeswater) from being retained. Animportant nursing intervention is to check the serumpotassium. If elevated, the drugs should be held and the prescribed

informed.

Osmotic diuretics: A drug you will hear about this semester is

Osmitrol (mannitol). This type of diuretic is called an OSMOTICDIURETIC, as it is essentially a sugar that pulls water with it as it goes

into the nephron. It also keeps water from going back to the blood(being reabsorbed). Typically, you will see mannitol used mostly for

severe head injured patients who have cerebral edema. When thedrug is given, it is always given IV (cant be given PO). It essentially

goes into the cerebral circulation, pulling water from the brain into thevasculature, then carries the drug and water to the nephron to be

excreted. This is how it relieves cerebral edema. Because mannitolpulls so much water out of the vasculature, it can very often result in

HYPERNATREMIA (too much sodium because too much water has beenpulled out). Before we give mannitol, we always check the serum

sodium to be sure it within a normal range.

Mannitol should be used very cautiously to patients with heart failure,as it can exit the vasculature in the lungs and the periphery of thebody, causing fluid to accumulate in the tissue. This can lead to

pulmonary edema!

Potassium is the most common electrolyte given in hospitalizedpatients. You must know the following about giving potassium.

1. Give PO (orally) or IV. When given IV, 10 mEq of potassium

(a normal dose) must be mixed in at least 100-250 mL offluid and given via an IV pump, over at least 1 hour.


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2. Remember that oral and IV potassium is IRRITATING TO

THE BODY. This means that if you give it orally, they complainof nausea. If you give it IV, it BURNS!!!!!!

3. If nauseated, give with crackers or a meal. If burning with IVinfusion occurs, contact physician to see if you can give the

potassium over 2 hours instead of 1 hour.4. If a patient has severely impaired renal function, they cannot

excrete potassium; therefore,you must monitor theirCREATININE before giving potassium. Also, you want toknow that patients are urinating before you give thempotassium,as you need to make sure they can excrete it.

5.

Commonly, we give potassium along with certain diuretics (like

Lasix) to prevent the patient from losing potassium with thediuretic.

Common potassium names:

a. K-Dur (extended release pills).

b. Micro K Extencaps (extended release)c. Klor-Con (extended release)

d. K-Tab (extended release)e. K-Lyte (effervescent tabletdrop in water and it fizzes)

f. Potassium chloride (IV)

Administration tips:1. NEVER CRUSH EXTENDED RELEASE MEDICATIONS! If you are

giving a large potassium pill to a patient and they cant swallowthe whole extended release pill, you can either break in half, or

drop in water and let the capsule come apart. The patient canthen drink it.

2. For effervescent tablets, these are in either orange or lime

flavor. Dissolve the pill in 8 ounces of water and have patientdrink it slowly.

3.

Give with some sort of food.a meal or crackersremember it isvery irritating to the stomach! Make sure that with any oral

potassium, you should always give it with at least 1 cup or 8

ounces of water. Again, this is related to the fact thatpotassium is irritating to the GI mucosa.

Drugs to treat hyperkalemia: Kayexelate (sodium polystyrenesulfonate).


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The drug is given orally or rectally in patients with high potassium

levels. The drug essentially exchanges sodium for potassium in theintestine. In this case, more potassium will move from the blood to

the intestine, and the hyperkalemia will decrease. If given as anenema, the potassium will fall much quicker than if given orally. If

given orally, DO NOT MIX WITH ORANGE JUICE! The major sideeffects are of course, HYPOKALEMIA, constipation, fecal impaction, and

nausea and vomiting (it tastes terrible).

Cancer patients may develop acute hyperkalemia when chemotherapyrapidly kills cells. The contents of these cells then leaks into the

circulation; one major component is POTASSIUM. Therefore,

Kayexelate may be used rectally in this acute and life-threateningsituation.

Inotropes: An inotropic drug is one that increases cardiac

contractility. Think about conditions that would requires thesedrugsdoes congestive heart failure come to mind? It should! If

cardiac contractility increases, so does stroke volume, andsubsequently cardiac output!

Keys:

1. Lanoxin (digoxin) is also known as a cardiac glycoside (this justis a fancy name for sugary cardiac drug) Dont let that name

trip you up on an exam.

2. Digoxin, in addition to being an antidysrhythmics drug, is also a

positive inotropic agent. This means that is positively increasescontractility! Isnt that easy?

3. Digoxins mechanism of action is that it keeps sodium and

calcium inside the myocardial cell and the calcium buildup allowsfor better contraction. Meanwhile, potassium gets trapped

outside of the myocardial cell and potassium struggles withdigoxin to get back inside the cell. Therefore, digoxincompetes with potassium.

4.

Because digoxin competes with potassium, low levels of

potassium in the blood means that digoxin will be

unopposed, and toxicity from digoxin can result!!!!!!5.

Because digoxin also slows the heart rate and conduction (itsantidysrhythmics property), we must also monitor the heart rate

before giving the medications (even if giving it orally). Digoxin

should not be given to anyone with a heart rate less than60. Nurses should check the apical heart rate (more

accurate than radial) before giving digoxin. It should be


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held if the rate is less than 60, and the prescriber should

be contacted for further orders.6. Signs of toxicity can be early or late:

a. Early: Nausea, vomiting, anorexia (these can also besigns of low potassium, hint, hint).

b.

Later: Halos around lights, green-yellow vision changes,AND CARDIAC DYSRHYTHMIAS!

7. Digoxin toxicity is more likely when the serum potassium is low;therefore, drugs such as loop or thiazide diuretics, which causepotassium loss, can increase the risk of toxicity.

8.

Treatment of toxicity: Usually most cases of toxicity are caused

by hypokalemia; therefore, the nursing intervention that would

be first line would be to check the potassium! If thepotassium were low, you would either use the potassium slidingscale (if ordered), or you would contact the physician for orders.

9.

Digibind is a drug that can be used for serious digoxin toxicity

(such as from an overdose; but it is usually not used for milddigoxin toxicity, as it cost a great deal!

10.Checking the digoxin level is an intervention that can be donefor toxicity, but we usually dont have one readily available, and

it takes hours to get the level back; therefore, CHECKING THEPOTASSIUM IS THE MOST SENSIBLE NURSING

INTERVENTION!

Primacor (milrinone) is also an inotrope, but in addition, it is also aVASODILATOR. Therefore, we call this drug an INODILATOR. In

congestive heart failure, we need the increase in contractility toaugment cardiac output, but we also need the vasodilation to decrease

the work the heart has to do (afterload). This drug is given as an IVinfusion only. It is only given in the presence of congestive symptoms

of heart failure (pulmonary edema, shortness of breath, peripheral

edema).

Antianginals: The drug you will need to know for S2 isNITROGLYCERIN. Most of you have already heard of this drug, as it

is used both preventatively for cardiac patients, and also is used as

treatment for acute chest pain.

This drug works by DILATING THE VEINS and reducing the blood

return to the heart, thus lowering the work (cardiac output) theheart has to do, thus decreasing angina.


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nitroglycerin is a generic name. There are several formulations of

nitroglycerin, including oral, sublingual, transdermal (patch), topical(paste) and IV. We will focus on oral and topical nitroglycerin.

Oral, transdermal, and topical nitroglycerin are all used for

PREVENTION OF ANGINA, not treatment. The onlynitroglycerin we use to treat chest pain is either sublingual or IV.

Intravenous nitrates, such as nitroglycerin, are obviously given at ahigher dose than PO or sublingual nitrates. Therefore, only IVnitrates can cause coronary artery vasodilation and increase supplyof blood and oxygen to the heart muscle. The other nitrates (PO,

topical, or sublingual) will simply decrease demand on the heart,

not increase supply.

Oral nitroglycerin (like Imdur or Cardilate) is taken on a daily basis.

Topical nitroglycerin (nitroglycerin paste) is applied to the chest

wall using a small paper guide. Nitroglycerin paste is ordered ininches (ie: inch, 1 inch, 1 inches, 2 inches). Usually, the

paste is administered to the chest wall up to 4 times per day.Nitroglycerin medicated disks (Nitro-Disk) can be applied to the

chest wall once the backing of the disk is removed.

Side effects:1. Hypotension (due to vasodilation)

2.Headache (due to cerebral vasodilation)

Nursing interventions:1. Assess blood pressure prior to administering the medication.

2. Ensure the patient has not taken any of the erectiledysfunction drugs such as Viagra, Cialis, or Levitra. THESE

DRUGS, WITH NITROGLYCERIN, CAN LEAD TO PROFOUND

HYPOTENSION IF GIVEN WITHIN 24-48 HOURS OF ONEANOTHER.

3.

Assess for response: Is the patient having less chest pain?4.

Assess for headache.

5. For acute chest pain in ER or hospital patients: Give 1

sublingual Nitro-Stat (0.4 mg) every 5 minutes x3 maximum.After each dose, check blood pressure, heart rate, and chestpain on 1 to 10 scale. If no relief after 3 SL nitroglycerin, call

physician.6. IV nitroglycerin is reserved for patients with acute chest pain

(unstable angina or myocardial infarction). It is much higherdose and will also increase blood supply to the myocardium!


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7. When giving IV nitroglycerin, glass bottles and special tubing

are used to prevent the drug from sticking to the surfaces.8. Alcohol increases the potential for hypotension when

nitroglycerin is used.9. Other vasodilators will increase the hypotensive effect (Ace

inhibitors, calcium channel blockers, etc).

Anticoagulants, thrombolytics, and antiplatelet agents: Thesedrug classes work differently; however, they all affect the coagulationsystem in one way or another.

Anticoagulant Key Points:

1. The major drugs used are heparin and Coumadin (warfarin).2.

THESE DRUGS WILL NOT LYSE EXISTING CLOTS, THEYWILL ONLY PREVENT FORMATION OF NEW ONES!

3.

They both work because they INHIBIT CLOTTING FACTORS,

therefore, reducing the formation of a fibrin clot.4. Coumadin is given orally and is taken by most patients for life;

however, heparin is only given for a short period of time. It isgiven either IV or SQ, as heparin cannot be absorbed in the GI

tract.5. Heparin: IV heparin is used for treatment of DVTs, pulmonary

embolism prevention, or in patients with coronary arterythrombi. SQ heparin is NOT GIVEN TO TREAT A CLOTTING

PROBLEM, IT IS GIVEN USUALLY TO PREVENT CLOTS!6. Coumadin: Used mostly for patients with atrial fibrillation (a

cardiac dysrhythmia) to prevent clots from entering the ventricleand thus systemic circulation, which can lead to stroke and/or

myocardial infarction.7. Lab monitoring: For heparin, check the PTT (partial

thromboplastin time). For Coumadin, check the PT/INR

(prothrombin time/international normalized ratio). TheINR is basically the patients PT result and the labscontrol PT result put together in ratio format.

8.

A GOAL PTT for patients on INTRAVENOUS heparin is about

60-80 seconds, or 2x the normal result. Usually for SQ heparin,

PTT is monitored once and then periodically, as the dose of SQis lower than IV.9.

A GOAL PT/INR for patients on Coumadin is based on the INR;

the goal INR should be between 2-3 (basically, this is 2-3 timesa normal PT).

10.HEMORRHAGE IS THE MAJOR SIDE EFFECT OFANTICOAGULANTS: Bleeding can be either minor (gum

bleeding, nose bleed, oozing from IV site) or major (blood in


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urine, bleeding into brain or GI tract). NURSES MUST MONITOR

FOR BLOOD LOSS IN THESE AREAS WHILE PATIENTS TAKETHESE DRUGS.

11.If a patients PTT is very high and they have bleeding, a reversalor antidote may be given. This antidote is PROTAMINE

SULFATE.12.If a patients PT/INR is elevated and they have signs of

bleeding, VITAMIN K WILL BE GIVEN, as it is the antidote forCoumadin. Hint: Coumadin inhibits vitamin K derived clottingfactors, this is why vitamin K is used to reverse Coumadin.

13.

Patients may be taking aspirin and other drugs that affect

coagulation while on heparin or Coumadin. If so, these

patients are at high risk for bleeding!14.

There are many teaching points for patients on Coumadin, asthey will be taking this drug outside of the hospital. One major

point is to make sure their diet stays stable in vitamin K. They

should not suddenly increase their intake of green leafy veggies,fish, eggs, meats, cheeses while taking Coumadin, as the effect

will be reduced (remember, vitamin K reversed Coumadinseffect).

15.Pregnant women should never receive COUMADIN. Heparin isthe drug of choice in these women.

16.Many over-the-counter drugs contain aspirin, so be sure toteach patients this point.

17.Low molecular weight heparin: (Lovenox or Fragmin). Thesedrugs are given SQ only. The major advantage is that they are

smaller than heparin in molecular size, so there are less druginteractions. Also, PTT does not need to be monitored on

these drugs.

Thrombolytic Keys to Know:

1. These drugs are also referred to as CLOT BUSTERS. They arenot like anticoagulants, as these drugs actually are the onlydrugs that will LYSE EXISTING CLOTS.

2.

They are usually given with anticoagulants and antiplatelet

agents for patient with unstable angina and/or myocardial

infarction. WHEN GIVEN WITH THESE OTHER DRUGS, THERISK OF BLEEDING CAN BE HIGH.3.

Streptokinase was used a long time ago, but because of

allergies, it is usually not used. The most common thrombolyticdrugs today are TPA and Retevase (both given IV).

4. The most important nursing assessments to make afteradministration of this drug and for 24 hours after this

drug are the NEUROLOGICAL AND GI TRACT assessments.


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5. Neurological checks should be done every hour for the

first 12 hours at least to ensure the patient does not havea cerebral bleed.

6. The stool and/or emesis should be assessed for the first 24hours to rule out a bleed in the GI tract. An upper GI bleed will

cause black and tarry stool. This is usually the type of bleedpatients will develop. Usually, most patients are also put on GI

drugs such as H2 blockers and proton pump inhibitors toprevent GI bleeding.

Antiplatelet Key Points:

1.

Aspirin is the major antiplatelet drug used today. Plavix

(clopidogrel) is also used.2.

These drugs impair the ability of the platelet to aggregate (orstick together); therefore, they reduce the risk of expansion of

clots (remember, platelets come to the site of clots to help out).

3.

Bleeding is the major side effect from aspirin orclopidogrel.

4. Even low-dose aspirin used to prevent coronary artery diseasecan cause GI bleeding.

Adrenergic agonists: Adrenergic is the same as saying like the

sympathetic nervous system (SNS)it sounds like adrenaline, right?An agonist will increase an effect.

Drug names: dopamine, dobutamine, epinephrine, levarterenol, and

isoproterenol.

Keys:1. These drugs will act just like the SNS, they will cause

vasoconstriction, increased contractility, and/or increased heart

rate.2. Epinephrine is the major drug in this class.3.

It is used in anaphylactic reactions (severe allergic reactionscausing vasodilation and bronchoconstriction), as it will dilate

the bronchi and constrict the blood vessels.

4.

It is also used in severe shock states or in cardiac arrest.5.

When you try to remember side effects for this drug, thinkabout what you would see if the SNS were overactive:

tachycardia, hypertension, dilated pupils, increased blood sugar.6. Because this drug increases the heart rate and contractility, the

heart will need more oxygen! Be sure that your patient hassupplemental oxygen.


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When a patient is hypotensive, we usually use these IV infusions in a

stepwise manner. The first drug we use is typically DOPAMINE.Dopamine will increase contractility at moderate doses and will cause

vasoconstriction at higher doses. Like all drugs, dopamine has amaximum dosage (20 micrograms per kilogram per minute). If the

blood pressure does not increase at this dose, we usually go tolevarterenol (Levophed). Levophed is a pure vasoconstrictor.

Because it can cause very powerful vasoconstriction, the peripheralarteries are very clamped down, which can result in decreasedperfusion to the distal extremities (which can lead to tissue damage tofingers and toes). If Levophed does not increase the blood pressure,

the last resort is EPINEPHRINE. Epinephrine will not only cause

vasoconstriction, but it will increase the HR and contractility.

Drugs for Pain, Fever, and Inflammation

NSAIDs:Stands for nonsteroidal anti-inflammatory drugs. These drugs work bydecreasing prostaglandins which cause pain and inflammation. They work onlyin the periphery of the body, not in the central nervous system, so there are no

CNS side effects.

Everyone has heard of ibuprofen or Motrin, as this is one of the most popularNSAIDs on the market. These drugs decrease inflammation, but not like theglucocorticoids (like prednisone or dexamethasone). Glucocorticoids suppress

inflammation by decreasing the action of the white blood cells and by decreasingprostaglandins. NSAIDS only work on the prostaglandins, not the white bloodcells; this is the reason they are called NONSTEROIDAL.

Common drug names:1. Aspirin (yes, aspirin is an NSAID)2. Motrin or Advil (ibuprofen)3. Toradol (ketorolac)4. Celebrex (celecoxib), Vioxx (rofecoxib), and Bextra (valdecoxib)

(second generation NSAIDs)5.

Indocin (indomethacin)

Key points to know:1.

Not all NSAIDS are alike. The second generation NSAIDs (see above)are suppose to cause less GI bleeding and renal dysfunction than thefirst generation NSAIDs.

2. NSAIDS suppress platelet function..remember, we give aspirinto patients have a heart attack to prevent the platelets from sticking


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together. This is also one reason why many patient taking NSAIDSchronically can develop a GI bleed.they are irritating to the stomachand they suppress platelet function.

3. A small percentage of asthmatics may be allergic to aspirin;therefore, if allergic to aspirin, they cannot have any of these

other drugs.4.

Chronic ingestion of these drugs can cause renal dysfunction resultingin an elevated serum creatinine. Monitor for this on lab data.

5.

Gastrointestinal bleeding is a potentially life-threatening problem fromthese drugs. The drugs block prostaglandins which are considered tobe protective in the GI tract; blocking these prostaglandins increasesthe potential for GI bleeding. Assess for GI bleeding by looking atthe stool: upper GI bleeding results in black and tarry stools.

Also, a stool that is positive for occult blood could mean a GIbleed.

6. Toradol is used instead of morphine in many situations, as the pain-relieving capacity of Toradol is that of morphine! Toradol, however,has very little anti-inflammatory properties.

7. Aspirin is never given to children because of the risk of Reyessyndrome, a condition that can be fatal (fatty liver, encephalitis).

8. Increased doses of aspirin (over several grams per day) can result inSALICYLISM, a condition resulting in too much salicylic acid (aspirinis acetylsalicylic acid). The condition causes ringing in the ears(tinnitus), dizziness, and headache. This is more likely to happen inthe elderly, but can also happen in patients taking over 2-4 grams perday of aspirin.

9.

If taken with anticoagulants, aspirin and the other NSAIDs canincrease the risk of bleeding. Why? Rememberaspirin suppressesplatelet function and NSAIDS can cause GI bleeds.

Corticosteroids:Glucocorticoids (such as prednisone) or Solu-Cortef (hydrocortisone)

areadrenal-like drugs, as they act like cortisolin the body; thus theyare called corticosteroids. Cortisol is a glucocorticoid, and it increasesthe amount of glucose to the brain. Some patients will need to take

corticosteroids because they have a pituitary disorder or adrenal

disorder and cant produce them. Most of the other patients will takethese drugs in higher doses than just replacement. These patients willget glucocorticoids, like prednisone, to suppress inflammation.REMEMBER.LOW DOSES ARE FOR REPLACEMENT OF HORMONES

THEY DONT HAVEHIGHER DOSES ARE TO SUPPRESSINFLAMMATION. They suppress inflammation by decreasing the

function of the white blood cell and by decreasing the inflammatoryprostaglandins.


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Drug names:1. prednisolone or prednisone

2. methylprednisolone3. hydrocortisone

4.

dexamethasone

While there are others, these are the most common IV, PO, IM formsof glucocorticoids that you will see!

Important to remember: When these drugs are given orally,

IM, or IV, they are SYSTEMICALLY ABSORBED. If they are

given locally (into a joint, inhaled for asthma, applied to theskin) they are not systemically absorbed, thus less sideadverse drug reactions tend to occur.

Key points to remember:1. Side effects with chronic glucocorticoidadministration (more

than several weeks or months) include weight gain, puffiness offace (moon face), protuberance of abdomen (pot belly),

elevated glucose, fractures (due to decreased effect on bone-building cells), depression or mood swings, muscle wasting

(extremities), and increased risk of infections.2. Nursing interventions:

a. Monitor serum glucose levels, especially if diabetic.b. Safety: due to increased risk of fractures, protect patient

from injury.c. Monitor for signs of infection, as they are immune

suppressed.3. Remember that glucocorticoids will also alter the normal

prostaglandins in the GI tract.the ones that protect us by

maintaining the mucus-bicarb layer. Because of this, you willsee many patients who are taking glucocorticoids in the hospitalon H2 blockers or proton pump inhibitors!

4.

Often times glucocorticoids are used on an acute basis. This

means that they come into the hospital having not been on these

drugs, but are placed on them (usually IV) in the hospital. Ifthis is the case, adverse drug reactions can include GIdisturbances (remember, they decrease the function of the

mucus-bicarb layer) such as abdominal pain, nausea. They canalso cause vertebral compression fractures, as they impair

calcium deposition into the bone. If your patient beginscomplaining of severe back pain, think about the possibility of a

vertebral compression fracture.


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5. Adrenal insufficiency: THIS IS CRITICAL TO KNOW. If a

patient who has been taking chronic glucocorticoids suddenlystops taking the drug, or if they are physiologically stressed

(trauma, surgery, illness), they may develop ADRENAL CRISIS(AKA acute adrenal insufficiency). In this case, they have a

need for the glucocorticoids, but they are not getting it at all orjust not getting adequate doses. They will become very

hypotensive and hypoglycemic from the lack of cortisol. Theycan die if we dont replace cortisol with a glucocorticoid.

Acetaminophen:

Most lay people dont believe that acetaminophen can cause serious

problems; however, in this section, you will see that it can and does!

Tylenol (acetaminophen) is very similar to aspirin, in that it is an

excellent pain reliever and fever reducer; however, it has NO

ANTIINFLAMMATORY PROPERTIES. This is important to rememberwhen you decide to give this drug over an NSAID which does decrease

inflammation.

Acetaminophen reduces fever and pain by decreasing prostaglandins inthe CNS. By now must be thinking that all prostaglandins are

bad.some are, but some are not!

Key Points:1. Metabolism of acetaminophen is usually normal;

however, TAKING TYLENOL IN OVERDOSE ORTAKING MORE THAN 4 GRAMS PER DAY will

cause major shifts in metabolism. When wemetabolize this much Tylenol, we can end up with

toxic metabolites (toxic byproducts). These

byproducts can cause HEPATIC NECROSIS ANDFULMINANT LIVER FAILURE in just 3 days ifnot treated! Even then, death can still occurif the blood level of acetaminophen remains

elevated despite treatment.2.

The antidote to Tylenol overdose or toxicityis MUCOMYST (acetylcysteine). It is givenPO (liquid) mixed in juice, cola, or water. It

has an extremely noxious odor and it is difficultfor the nurse to even give it much less the

patient drink it. They will need to take it every 4hours for 72 hours (a total of about 17 doses).


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3. Alcohol can also shift the metabolism of

acetaminophen; therefore, if patients drinkregularly, they should not consume any more

than 2 grams per day of Tylenol.4. Nursing actions: Make sure to add up the total

amount of acetaminophen your patient isgetting every 24 hours..it should not be over

4 grams/24 hours. If so, the physician needs tobe contacted to find an alternative for fever/pain.

5.

Remember that acetaminophen is hidden inmany OTC drugs, so you must warn patients

about this when discharging them (especially if

they drink regularly or are taking home aprescription containing acetaminophen like oralpain medications).

Opioids and opioid antagonists:These are drugs that relieve pain. Opioids are considered controlled substances,as they have the potential for addiction. Schedule II drugs (morphine, etc.) arethe most addictive, schedule V drugs (cough syrup) are the least addictive.

Opioids work by activating pain receptors(called mu and kappa) in thecentral nervous system. These receptors normally respond to endorphins in thebody, the feel-good hormones. When we give pain medications such as theopioids, we are stimulating the receptors artificially with drugs.

Common drugs names:1. Strong opioids: morphine: given PO, topically, or IV (many formulations

available), fentanyl, Demerol (meperidine) are the most common.2. Moderate to strong: codeine, hydrocodone, oxycodone3.Agonists-antagonist opioids: Stadol (butorphanol), Talwin (pentazocine),

and Nubain (nalbuphine).4. Narcotic antagonist: Narcan (naloxone)

Key points to remember:1.

Strong opioids are usually given IV in the hospital. Moderate to strongopioids are usually given PO.

2.

The major life-threatening side effect related to the strongand the moderate to strong opioids is RESPIRATORYDEPRESSION. This occurs because we are activating the mureceptors, which can depress the respiratory center.

3. Also, by activating mu receptors, euphoria occurs (which can lead toaddiction in patients not using it for pain control), and sedation occur.


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This euphoria is the reason for addiction.the false sense of well -being.

4. We always start patients off with small doses of these medications,and then we increase as needed for pain. If patients have beengetting these drugs for a while, they will develop TOLERANCE, this is

not the same as addiction. Tolerance means they need more to getthe same pain relief.

5.

All of the strong opioids can be given as patient-controlled analgesia(PCA) while in the hospital.

6. Other less serious side effects of opioids include CONSTIPATION. Thisis a common problem, especially in patients who take them for longerperiods of time. Prevention is the keyincrease fluids and fiber andget patient to move around! They may ever need Colace, a stoolsoftener to prevent constipation.

7. In the event of respiratory depression, the antidote is NARCAN.This will reverse respiratory depression quickly, as it is given IV.

8.

PLEASE REMEMBER THAT THE ORAL OPIOIDS ALL CONTAINACETAMINOPHEN (Tylenol) IN ADDITION TO THE OPIOID!This means you should know how much acetaminophen thepatient is getting in 24 hours. Patients cannot have more than 4grams per day of acetaminophen (if they drink regularly, they canthave more than 2 grams per day). More than the recommended doseof Tylenol can cause serious liver dysfunction!

Drugs Used in the Oncology or Transplant PatientNote: While this packet will not cover chemotherapeutic drugs, it is

important to know for the pharm test that DRUGS USED TO KILLCANCER CELLS ALSO KILL MANY OTHER CELLS IN THE BODY.

Cells damaged by chemotherapy are those of the bone marrow, themucosa, hair, and GI tract. The most significant damage is obviously

when the bone marrow cells are destroyed, resulting in potentiallyfatal anemia, thrombocytopenia, and/or neutropenia.

Drugs to treat bone marrow depression:

1. Anemiacan be caused by several different problems. The mostcommon cause of anemia in our country is iron deficiency; however,

B12 deficiency and folate deficiency can also cause anemia. In theoncology patient, the anemia is usually caused by chemotherapeuticdrugs depressing the cells of the bone marrow (red blood cells).To treat this type of anemia, hematopoietic growth factors are

prescribed. So, what are hematopoietic growth factors?Erythropoietin (a renal hormone) is the growth factor that must be

present to stimulate the production of red blood cells in the bone


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marrow. We have 2 generic drugs which we give certain cancer

patients undergoing chemotherapy to prevent and treat anemia,darbepoetin (Aranesp) and epoetin alfa (Procrit and Epogen).

In addition to treating cancer-related anemia, these drugs are alsoused in anemia caused by HIV medications, and chronic renal failure.

Keys to know:1. All of the drugs work the same way. The only major

difference between them is that epoetin alfa is NOTLONG ACTING; however, darbepoetin is long acting.

Procrit/Epogen is generally given 3x weekly by

subcutaneous injection. Aranesp is only given onceweekly.

2.

In patients who are severely anemic and require a

transfusion, it is important to remember that THESE

DRUGS WORK VERY SLOWLY; THEREFORE, IT MAYTAKE 2-4 WEEKS BEFORE THE HEMOGLOBIN WILL

GO UP. If we cant wait that long for these drugsto work, we must transfuse!

3. How do we monitor patients on this medication? Wecheck the CBC (complete blood count); we should

expect to see a rise in hemoglobin in 2-4 weeks. Wecan also assess the patients symptoms: are they less

fatigued? Less short of breath? More able to carry outADLs?

4.

The major side effect of these medications isHYPERTENSION. This occurs because the drugs

increase the volume of red cells in the blood, increasingthe viscosity. That makes sense, right? Some

patients may require antihypertensive medications

while taking these drugs.5. These drugs should not be given to anyone with

UNCONTROLLED HYPERTENSION.

Recall that anemia has many causes, thus there are many ways to

treat anemia. In non-cancer patients, if anemia is caused by irondeficiency, iron replacement will be needed. Iron is given in the formof ferrous sulfate, ferrous gluconate, or ferrous fumarate. These iron

products all work the same way and cause the same side effects:constipation, black stools, and nausea. It is important to know these

side effects and monitor for them, as you will care for many patientstaking iron in your career.


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2. Neutropenia (decreased white blood cells) is a common side

effect of chemotherapy. There are several drugs that willincrease the production of white cells, including: Neupogen

(filgrastim), Neulasta (pegfilgrastim), and Leukine(sargramostim).

Keys to know:

1. Neupogen is the shorter acting drug; Neulasta LASTS LONGER(you can remember that one by the name).

2.

Most common side effects are BONE PAIN; this is caused by theincreased cell production in the bone marrow, resulting in pain.

3.

We must monitor patients white blood cells on their CBC at least

2x weekly when on this medication.4.

The medications can be given either IV or subcutaneously.

Drugs to treat oral candidiasis:During chemotherapy, cells of the mucous membranes are destroyed,

which can result in very painful sores in the mouth (stomatitis). Inaddition, these oral lesions/sores can become infected because of the

reduced white blood cells. When an oral fungal infection occurs, this iscalled oral candidiasis (also known as thrush). Typically, the drug

most often used in this situation is nystatin. While nystatin isavailable as a cream, ointment, powder, or vaginal tablet, it is used

orally as a suspension for oral candidiasis.

Keys:1. The most common side effects are nausea, vomiting, diarrhea.

2. When we given nystatin for oral thrush, we shake the container,open it, and ask the patient to SWISH AND SWALLOW. This

means they need to swish the medication around in their mouth

and then swallow it. You may also see it prescribed as swishand spit.

Drugs to treat hyperuricemia:

When large numbers of cancer cells are destroyed by chemotherapy,

the intracellular contents can leak out and cause severe metabolicderangements. One such problem is HYPERURICEMIA; this conditionis dangerous because it can lead to the formation of crystals which can

damage the renal tubules.

Two medications can be used to treat hyperuricemia: allopurinol(Zyloprim) and a carbonic anhydrate inhibitor drug called


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acetazolamide (Diamox). The allopurinol will help control the high

uric acid, and the acetazolamide will help control the uric acid crystals.

Keys to know:A hypersensitivity reaction can occur with allopurinol: fever,

rash, liver and kidney damage. If rash is seen,discontinue the drug immediately.

If the patient is also taking warfarin (Coumadin), allopurinol canreduce the metabolism of warfarin, leading to WARFARINTOXICITY.

Diamox is a carbonic anhydrase inhibitor which inhibits the enzyme

that forms carbonic acid. It is used to keep the urinary pH

elevated (alkaline) in the event of hyperuricemia. This is doneso that the uric acid crystals will not crystallize in the renaltubules.

An important nurse intervention associated with Diamox is to

monitor glucose in diabetic patients, as it can substantiallyincrease glucose (think Diamox and Diabetes).

Antirejection drugs:Glucocorticoids (such as prednisone) or Solu-Cortef (hydrocortisone)areadrenal-like drugs, as they act like cortisolin the body; thus they

are called corticosteroids. Cortisol is a glucocorticoid, and it increasesthe amount of glucose to the brain. Some patients will need to take

corticosteroids because they have a pituitary disorder or adrenal

disorder and cant produce them. Most of the other patients will take

these drugs in higher doses than just replacement. These patients willget glucocorticoids, like prednisone, to suppress inflammation.REMEMBER.LOW DOSES ARE FOR REPLACEMENT OF HORMONES

THEY DONT HAVEHIGHER DOSES ARE TO SUPPRESSINFLAMMATION. They suppress inflammation by decreasing the

function of the white blood cell and by decreasing the inflammatoryprostaglandins.

Drug names:

prednisolone or prednisone

methylprednisolonehydrocortisonedexamethasone

Patients who have had organ transplants, such as kidney transplant,

will take immunosuppressants drugs every day for the rest of their

lives to prevent organ rejection. In the event of acute organ


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transplant rejection, we would typically use 500-1500 mg of

methylprednisolone IV.

While there are others, these are the most common IV, PO, IM formsof glucocorticoids that you will see!

Important to remember: When these drugs are given orally,

IM, or IV, they are SYSTEMICALLY ABSORBED. If they aregiven locally (into a joint, inhaled for asthma, applied to theskin) they are not systemically absorbed, thus less sideadverse drug reactions tend to occur.

Key points to remember:Side effects with chronic glucocorticoidadministration (more

than several weeks or months) include weight gain, puffiness of

face (moon face), protuberance of abdomen (pot belly),

elevated glucose, fractures (due to decreased effect on bone-building cells), depression or mood swings, muscle wasting

(extremities), and increased risk of infections.Nursing interventions:

d. Monitor serum glucose levels, especially if diabetic.e. Safety: due to increased risk of fractures, protect patient

from injury.f. Monitor for signs of infection, as they are immune

suppressed.Remember that glucocorticoids will also alter the normal

prostaglandins in the GI tract.the ones that protect us bymaintaining the mucus-bicarb layer. Because of this, you will

see many patients who are taking glucocorticoids in the hospitalon H2 blockers or proton pump inhibitors!

Often times glucocorticoids are used on an acute basis. This means

that they come into the hospital having not been on these drugs,but are placed on them (usually IV) in the hospital. If this is thecase, adverse drug reactions can include GI disturbances(remember, they decrease the function of the mucus-bicarb

layer) such as abdominal pain, nausea. They can also cause

vertebral compression fractures, as they impair calciumdeposition into the bone. If your patient begins complaining ofsevere back pain, think about the possibility of a vertebral

compression fracture.Adrenal insufficiency: THIS IS CRITICAL TO KNOW. If a

patient who has been taking chronic glucocorticoids suddenlystops taking the drug, or if they are physiologically stressed

(trauma, surgery, illness), they may develop ADRENAL CRISIS


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(AKA acute adrenal insufficiency). In this case, they have a

need for the glucocorticoids, but they are not getting it at all orjust not getting adequate doses. They will become very

hypotensive and hypoglycemic from the lack of cortisol. Theycan die if we dont replace cortisol with a glucocorticoid.

Imuran (azathioprine), Cytoxan (cyclophosphamide), and Sandimmune(cyclosporine). These drugs are most often used in prevention of organtransplant rejection, but have other uses as well. Because each of these drugsdecreases the ability of the body to fight the immune system, NEUTROPENIAIS THE MOST SERIOUS CONSEQUENT, RESULTING IN LIFE-THREATENING INFECTION.

Imuran: This drug suppresses the function of both the B and T lymphocytes.Mostly, this drug is used in combination with cyclosporine andglucocorticoids to suppress transplant rejection. In addition toneutropenia, this drug can decrease the platelet count(thrombocytopenia).

Cytoxan: This drug is a cancer drug that is also used to treat inflammatoryconditions such as rheumatoid, lupus, and multiple sclerosis. It is notoften used for organ transplant rejection. In addition to causingneutropenia, it can cause HEMORRHAGIC CYSTITIS.

Sandimmune: This drug is really the most effective of theimmunosuppressants. It is the drug of choice for preventing organtransplant rejection. The major adverse effect is of course,NEUTROPENIA, and infection can occur in up to 80% of patients. Another

major problem with this drug is NEPHROTOXICITY, which can occur in upto 75% of patients. We need to be looking at the BUN and creatinine tosee if this is developing; however, in a patient who has had a kidneytransplant, an elevated BUN and creatinine can be a sign of rejection, sothis is difficult.

A word about methotrexate: This drug has multiple uses,

including RHEUMATOID ARTHRITIS and cancer (it is a

chemotherapy drug). For rheumatoid, methotrexate is considered aDISEASE MODIFYING ANTIRHEUMATOID DRUG (DMARD). DMARDsreduce joint destruction and slow down the disease progression.There are more side effects and potential toxicity associated with these drugsthan NSAIDs (as discussed above). Methotrexate(a first-line DMARD) isthe most rapid acting and will begin working within about a month to amonth and a half. It can cause liver problems, GI ulcers, and bone marrowdepression(decreased WBC function). The drug is given once weekly forRA.


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Endocrine system drugs

Antidiabetic medications:Insulin and oral diabetes medications are used to lower the blood glucose in

diabetic patients. It is important to note that each of these drugs accomplishesthe task differently. Insulin is a hormone normally produced by the body, whichenable glucose to be actively transported into the cells. Oral diabetesmedications vary in their action.

Insulinkey points:1. Draw up regular before NPH.2. Know the peak time of regular and NPH insulin in order to predict when

hypoglycemia is most likely.3. Know that HYPOGLYCEMIA is the most common symptom with insulin.4. Know the early signs of hypoglycemia: hunger and nausea.5.

Know the more serious signs of hypoglycemia: restlessness, sweating,tachycardia, and confusion.

6. Know how to administer insulin subcutaneously.7. Know that the only insulin we give IV is regular!!!!!! All the others are

suspensions, which are never given IV.8. Remember that if regular insulin is injected subcutaneously, it will BEGIN

TO WORK IN 30 MINUTES.9. Lispro is the fastest acting insulin available. It is given subcut and should

be injected 15 minutes before a meal, as it will begin to work in 15minutes and will peak in 1-1.5 hours.

Oral diabetes medications key points:Remember that there are several different categories of this drug class. The

three you need to focus on are the sulfonylureas (glyburide,glipizide), the biguinides (with only one drug, metformin), andthe glitazones (Actos, Avandia).

Sulfonylureas: know that these drugs increase insulin secretion from thepancreas, so it just makes sense that the side effect seen most oftenwould be HYPOGLYCEMIA.

Know that since sulfonylureas have a sulfa group in their chemical structure,persons highly allergic to sulfa may not be able to take this drug.

Glucophage (metformin) is used to decrease glucose production in the liver,and to make the cells more sensitive to the insulin that already exists.Therefore, HYPOGLYCEMIA IS NOT A COMMON SIDE EFFECT OF THISMEDICATION.

One of the more common and dangerous side effects of metformin is LACTICACIDOSIS. If a patient has renal failure, or they are in a state ofphysiologic shock, or they are dehydrated, lactate can accumulate. If


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this drug is given on top of these conditions, lactate is not effectivelycleared from the body, and lactic acidosis can result. Therefore, thesepatients should not receive metformin. Also, if the serumcreatinine is above 1.5, metformin should be held and thephysician called.

Metformin and contrast dye: if you have a question that asks you what to dowhen a patient has had IV contract dye, you always want to makesure you HOLD THE METFORMIN FOR 48 HOURS AFTER CONTRASTDYE IS GIVEN. The reason why is this: contrast, if not adequatelycleared by the kidneys, can be nephrotoxic. If metformin is givenbefore the contrast is excreted fully, renal insult can occur and lacticacidosis can result.

Glitazones: What is most important to remember is that these drugs allowthe cells to respond to insulin, therefore, INSULIN MUST BE PRESENTFOR THESE DRUGS TO WORK. Remember that type 2 diabetes is theinability of the cell to response to insulin. Many diabetics who havehad the disease for years may not produce enough insulin, and mayeventually need to inject insulin every day after being on years of oralmedications. In this case, glitazones may be used along with insulin tohelp the cells respond better to the insulin. Glitazones are taken POand are also often combined with sulfonylureas or metformin.

Two major adverse drug reactions with glitazones: fluid retention (whichcan lead to heart failure in certain patients) and liver injury.Therefore, weight and symptoms of shortness of breath and/or edemashould be assessed. In addition, liver function (ALT and AST) shouldbe assessed every 2 months for the first year to monitor for increased

liver enzymes. If the ALT is 2.5-3x normal limits, the drug is usuallydiscontinued. Typically, the ALT falls back to normal once the drug isstopped.

Glucagon: remember that glucagon is a counter regulatory hormone.THEOPPOSITE OF INSULIN! Therefore, if a patient outside the hospital werehypoglycemic, glucagon could be given IM; however, it requires 5-20 minutes towork when given via this route. In nursing home patients glucagon is the usualtreatment for hypoglycemia. In hospitalized patients we simply useintravenous dextrose 50% for hypoglycemia, as D50% works immediatelyonce injected IV push.

Drugs used in hypothyroidism:The most common mediation to treat hypothyroidism is levothyroxine(Synthroid, Levothroid, etc). This drug essentially mimics the action of T4,one of the thyroid hormones. In hypothyroidism, the patient is deficient inthyroid hormone; therefore, replacement is the way to treat these patients.Keys to know:


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1. Synthroid (levothyroxine) stays in the body for a verylong time (it has a long half-life). Therefore, PATIENTSMUST BE INFORMED THAT WHEN THEY FIRSTSTAY TREATMENT WITH THIS DRUG, THEY MAYNOT HAVE SYMPTOM REDUCTION FOR A MONTH!

Remember, the longer the half-life of a drug, the longerit will take to get a therapeutic effect.

2.

Side effects usually dont occur unless the DOSE IS TOOHIGH FOR THE PATIENT. This is why this drug isstarted at a very low dose and gradually increased if thepatient does not have symptom reduction.

3. If the dose is too high for the patient, THYROTOXICOSIS

CAN OCCUR. Symptoms include: tachycardia,restlessness, insomnia, palpitations, anxiety, tremor,heat intolerance. All of these symptoms tell you thepatinets metabolism has increased (remember thyroidhormone has a great deal to do with the metabolic rate)!

While there are other drugs to treat hypothyroidism, by far levothyroxine is themost common. In the event of acute and life-threatening hypothyroidism(bradycardia, hypotension, coma), a drug by the name of Cytomel(liothyronene)can be used, as it will begin to work very quickly. Memorytrick: think comaneed Cytomel. Can you see why levothyroxine could not

be used in a life-threatening situation?

Drugs to treat hyperthyroidism:

The opposite of decreased thyroid hormone is too much thyroid hormone. In thecase of hyperthyroidism, the excess thyroid hormone creates extra work for theheart, which can lead to cardiac dysrhythmias, tachycardia, and palpitations.

We can treat hyperthyroid by giving medications, doing surgery, or treating withradioactive iodine. We will focus on discussion on medications that relate to allthree of these options.

1.Antithyroid medications: PTU (propylthiouracil) and Tapazole(methimazole) are both drugs that inhibit the synthesis ofthyroid hormone. It is important to know that it DOES NOTHING TO

STOP EXISTING HORMONE, IT ONLY PREVENTS THE FORMATION OFNEW HORMONE; THEREFORE, IT CAN TAKE 3-12 WEEKS TO SEE THEEFFECT OF THESE DRUGS.

a. The most serious side effect of these drugs is AGRANULOCYTOSIS(decrease granulocytesthe first line white blood cells). If thisdoes occur, it will happen in the first 2 months of therapy. Serious


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infection can result; therefore, weekly CBCs are usually done forthe first 2 months of therapy.

b. Usually, if agranulocytosis does occur, the patient will complain ofFEVER AND SORE THROAT. This is a signal to the nurse tocheck the WBC count!

2.

Surgery: Often times, a thyroidectomy is indicated for hyperthyroidism(depending on the patient and the cause). In this case, we must makethe gland less active before surgery. How? BY GIVING IODINESOLUTIONS SUCH AS LUGOLS SOLUTION.

a. When high doses of iodine are given, this will suppress the functionof the thyroid gland, and less hormone will be produced.

b. Usually Lugols solution is given 7-10 days preoperatively. It isprescribed in drops. The drops (2 to 6) are mixed in water or juiceand the mixture is drank up to 3 times daily.

c. Lugols is not pleasant to drink; therefore, mixing with juice or colais usually helpful.

d.

The most common side effect of Lugols is IODISM: a metal taste,burning of the mouth, soreness of mouth and gums, increasedsaliva, and even skin eruptions. These symptoms occur because ofthe high iodine content.

3. Radioactive iodine: In Gravesdisease (a type of hyperthyroidism),radioactive iodine can actually be given to destroy thyroid tissue. Thegoal is to destroy enough of the gland to treat the hyperthyroidism, butnot completely destroy all of the gland. However, typically patientsundergoing this treatment can end up with hypothyroidism afterwards.

Vasopressin:Antidiuretic hormone (ADH) occurs naturally in the body and allows us toconserve water (think about the name and you have what it does). Certainconditions can cause a deficiency of ADH, including head injury (trauma),neurosurgery, cancer, and a condition called diabetes insipidus (not mellitus).

In the event of decreased ADH, the body is unable to conserve water andEXTREME AND LIFE-THREATENING DEHYDRATION CAN OCCUR. In this case,patients will requireVASOPRESSIN, a drug that mimics the action of ADH.

Keys to know:

Vasopressin is given in a variety of routes (IV, IM, SC).Because the drug will cause water retention, if too much retention occurs, the

patient can develop WATER INTOXICATION.Signs of water intoxiciation: headache, drowsiness, listlessness (early on).

Laster, seizure and coma can occur.


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The major reason for water intoxication in patients taking vasopressin isFAILURE TO STOP DRINKING A LOT OF WATER. Therefore, patientsshould be instructed to reduce their fluid intake.

Vasopressin can cause vasoconstriction..because it is a powerfulvasoconstriction, it can lead to constriction of the coronary arteries in

patients with coronary artery disease, which can lead to angina and/or MI.Also, peripheral arteries, when vasoconstricted, can result in decreasedperfusion to the extremities. The nurse should ASSESS DISTALCAPILLARY REFILL AND SKIN COLOR/TEMPERATURE to prevent tissueischemia from this drug.

Antimicrobial Drugs

Drugs to treat urinary tract infections:Fluoroquinolones (aka quinolones)

Primary, in the hospital, you will see this group of drugs used for urinary tractinfections, prostate infections, respiratory infections, and maybe even some boneor soft tissue infections. By far, respiratory and GU infections will be themore common reasons you use them. Everyone has probably at least heardof Cipro (ciprofloxacin). This is an older quinolone, but is still widely used today.

Keys to know about quinolones:Drugs names tend to end inoxacin (ciprofloxacin, ofloxacin/Floxin,

sparfloxacin/Zagam, lomefloxacin/Maxaquin,levofloxacin/Levaquin).

The quinolones cover mostly gram negative bacteria (like E. colithis is whythey work great for UTIs).

The most common side effect is nausea and vomiting. This can be reducedby giving the oral medication with food; however, food can decreaseabsorption of oral quinolones by up to 20%.

Drug interactions are not really common to the group, unfortunately, they arerelated more to the individual drug.Cipro: MAJOR DRUG INTERACTION PROBLEMS WITH WARFARIN,

THEOPHYLLINE. The CIPRO REDUCES METABOLISM OF THESEDRUGS, THEREFORE, INCREASING THEIR LEVEL ANDPOTENTIALLY LEADING TO TOXICITY.

For some of the other quinolones, like Zagam, Maxaquin, and Floxin,theophylline is not a problem.

All the quinolones, if given with antacids, will result in decreasedabosorption and effect.

Tendon rupture: Most of the quinolones, but not all, can cause tendonrupture in any age group. This caused extreme pain and limitedmobility. The major drugs are Cipro, Avelox (moxifloxacin), Floxin.


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Quinolones can increase sensitivity to the sun.

Sulfonamides: This group of drugs are used for UTIs caused by E. coli. Theyhave other uses as well, but primarily are used for UTIs. You may also findthem used in AIDS patients, as this drug is effective against

Pneumocystis carinii, an opportunistic organism that is known to causepneumonia in HIV+ patients.

Keys:1. The main sulfa drug we give is called Bactrim or Septra. These drugs

contain 2 sulfa drugs in one: trimethoprim and sulfamethoxazole.The 2 drugs work better than just one sulfa drug, and are given in thisfixed combination as Bactrim or Septra.

2. Many patients are allergic to this group of drugs. It is critical to assess forallergies to sulfa-related drugs before administering this medication.

3. These drugs will increase a patients susceptibility to the sun(photosensitivity); therefore, the patient should be instructed to avoidprolonged sun or tanning bed exposure, wear protective clothing outside,and use SPF every day while on this drug.

4. The most severe reaction to this group of drugs is STEVENS-JOHNSONSYNDROME, a rare but potentially dangerous skin and mucous membranereaction. The patient will develop lesions that almost resemble a burn allover the skin and mucous membranes, they will also develop fever. THENURSE CARING FOR THIS PATIENT MUST DO A SKIN ASSESSMENTEVERY DAY TO ENSURE THE PATIENT IS NOT DEVELOPING THISREACTION.

5.

In the HIV/AIDS patient, side effects can be very common. In fact, 55%of these patients will develop toxicity (rash, fever, decreased white cells).

6. This drug IS NEVER USED IN INFANTS UNDER 2 MONTHS OF AGE,as it will increase bilirubin concentration in the brain (kernicterus).

7. Because the drugs can cause renal damage and urinary crystals,PATIENTS MUST BE TOLD TO DRINK AT LEAST 8 TO 10 GLASSESOF WATER PER DAY. Therefore, it is very important to monitorurine output in these patients; you want to see at least 1,200 mLof urine per day.

8. Many other drugs are affected by this drug, including Coumadin, Dilantin,and the oral sulfonylureas (glucose-lowering oral agents). The blood

levels of these drugs may increase, putting the patient at risk for toxicity.

Aminoglycosides and vancomycin:

Aminoglycosides (gentamicin and others): These drugs interrupt proteinsin the bacteria, thus cause the cell to die (cidal effect). THE ONLY ORGANISMS


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THAT ARE KILLED BY THESE DRUGS ARE THE GRAM NEGATIVEONES (LIKEPSEUDOMONAS).

Keys:1.Aminoglycosides are usually only given IV; however, if we need to locally

decontaminate the bowel (prior to surgery on the bowel), we may havethe patient take it orally, but the drugs does not get systemicallyabsorbed.

2.

These drugs are RENALLY ELIMINATED; therefore, careful monitoring ofthe patients renal function isrequired. Daily assessment of the creatinineshould be done and if moderately elevated, the physician should benotified immediately for possible dose or frequency change.

3. Because this drug can cause toxicity, peak and troughs are measured.PEAK TELLS YOU IF THE DOSE IS TOO HIGH OR TOO LOW. It isdrawn 30 minutes after the infusion ends. TROUGH TELLS YOUIF THE PATIENT IS TOXIC! This is drawn immediately before thedrug is to be given. If trough is elevated, the dose is held andthe prescriber called.

4. If renal function is impaired and/or the trough is elevated,SERIOUS TOXICITY can occur to the kidney and the ear (nephrotoxicityand ototoxicity). Therefore, patients who are not excreting the drugnormally will require smaller and less frequent doses.

5. Ototoxicity: these drugs can accumulate in the ear and cause bothcochlear damage (hearing loss) and vestibular damage (dizziness andvertigo). The first sign of cochlear damage is RINGING IN THE EARS.The first sign of vestibular damage is HEADACHE. DAMAGE TO THE

EAR IS MORE LIKELY WHEN THE SERUM TROUGH LEVEL ISELEVATED.

6. Nephrotoxicity: These drugs can injure the delicate cells of the tubules.THE RISK IS HIGHER WHEN THE SERUM TROUGH LEVEL ISELEVATED. The risk is highest in the elderly or those withpreexisting renal disease. BUN and creatinine should be closelymonitoring during therapy.

Vancomycin: This drug is given mostly for MRSA (methicillin resistantStaphylococcus aureus). MRSA is a common hospital organism that costs ourhealthcare system a great deal of money to treat, and can cost patients their

lives. Like gentamicin, it is a potentially toxic drug, but it does not workthe same way or cover the same organisms (remember that gentamicincovers gram negatives and vanco covers gram positives, but mostlyused for the gram positive MRSA).


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Keys to know for vancomycin:Administration is very important to understand: You MUST GIVE THIS DRUG

SLOWLY, OVER AT LEAST 1.5 HOURS. Giving the drug faster than thiscauses a massive histamine reaction, which can cause serious flushingand hypotension. Because the patient flushes and turns red, we also call

this the Red man syndrome.Vancomycin might also be used in patients allergic to penicillins and

cephalosporins to treat severe infections such as Staph or Strependocarditis).

The most serious adverse reaction is OTOTOXICITY. If you remember,gentamicin can cause this too. IF the patient is getting both vancomycinand gentamicin, the risk is even higher. The risk is high as well if thepatient receiving vancomycin has reduced kidney function.

Vancomycin is mixed in at least 250 mL of solution before giving it IVbecause it can be extremely painful to the patient while it is infusing. Themore fluid it is diluted in, the more comfortable the patient is, and the lessdamage to the veins.

Macrolides and tetracyclines:

Macrolides: This group of antibiotics are also broad spectrum and are alsocidal (at higher doses). The oldest drug in this group is ERYTHROMYCIN. Thenewest members of the group are Zithromax (azithromycin) and Biaxin(clarithromycin).

Keys:

1.

Erythromycin causes many more adverse reactions than the newer ones,including DIARRHEA, and can also cause liver injury. Usually, liverinjury is caused by high doses of erythromycin. Therefore, LFTmonitoring will be needed for those patients.

2. The newer drugs have few side effects. Erythromycin causes diarrheabecause it stimulates the motolin receptors in the bowel and increasesperistalsis. Sometimes, we can give this drug to patients for this veryreason!

3. Erythromycin can increase the levels of other drugs (theophylline,Tegretol, and Coumadin) because erythromycin will decrease theliver metabolism of the other drugs.

4.

Zithromax is given as either single dose, 2 days, 3 days or 5 days(outpatient), or is given IV to inpatients. It is important to tell patientstaking the oral Zithromax packets (Z-Pak) that the MEDICATION WILLCONTINUE TO WORK FOR 14 DAYS AFTER THEY FINISH THEMEDICATION.


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5. Biaxin (clarithromycin)tends to decrease metabolism of many drugs,especially digoxin. Digoxin doses should be reduced in any patientreceiving Biaxin.

Tetracyclines: These are very old drugs and include both tetracycline and

doxycycline. They are broad spectrum and useful in many infections, includingacne, sexually transmitted diseases (STDs), periodontal infections, and pepticulcer disease.

Keys to know about tetracyclines:1. Tetracycline is a short-acting drug and is renally excreted. Patients with

renal impairment should be closely monitored. Tetracycline FORMS ANON-ABSORBABLE COMPLEX WITH CALCIUM, MAGNESIUM,IRON, AND ZINC; therefore, it should not be given with calciumsupplements, milk products, and most antacids (because theycontain either calcium or magnesium).

2.

Doxycycline is a longer acting drug and is not renally eliminated. It doesnot have the same issues with forming complexes. Doxycycline is used agreat deal for STDs.

3. Most tetracyclines can cause GI upset, causing burning, cramping,nausea, and vomiting. Because these drugs can also causeesophageal irritation, DO NOT GIVE AT BEDTIME!

4. Staining of the teeth can develop with tetracycline, again due to thecomplexes formed with calcium. Therefore, we dont give tetracyclines tochildren under age 8.

5.

Superinfection (an infection caused by wiping out normal organisms in the

body) can occur with these drugs, infection of the bowel being the majorone. If this bowel infection occurs, it is caused by Clostridium difficile (C.diff). Severe dehydration and electrolyte depletion can occur, so thepatient must be monitored carefully if it develops.

6. Tetracyclines can cause fat to infiltrate in the liver and hepatotoxicity canresult. This is rare, but patients with abdominal pain and jaundice shouldbe suspected of having this condition.

7. There are conflicting reports as to whether tetracycline actually reducesthe effect of estrogen co

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