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Level 4 (Senior 2)

Pharmacology
Self-Study
Packet

Note: This packet is not intended to cover all the material you
will be need to know related to drugs on your pharmacology
test. It is intended as a self-study guide only, and is meant to
help you learn to organize drugs by category. It will also help
you to determine what is MOST IMPORTANT about specific drug
categories. The need for other resources will depend on the
individual student. One resource you have is your Kee
Pharmacology book.

Developed by: Gina Thames, MSN, RN
ginathames@texashealth.org
(817) 462-6112
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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 the
sympathetic nervous system). Although pharmacological class or
family is often seen in the literature, nurses need to focus on the
drugs THERAPEUTIC CLASS OR FAMILY, ALSO KNOWN AS
FUNCTIONAL 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 the
functional classes you should know before your pharmacology test.

1. Drugs affecting the cardiac system
a. Drugs for treating hypertension
i. Calcium channel blockers
ii. Beta blockers
iii. Vasodilators used for hypertensive crises
b. Antidysrhythmics
c. Diuretics and potassium supplementation
d. Drugs to treat hyperkalemia
e. Inotropes
f. Antianginal drugs
g. Anticoagulants, antiplatelet, and thrombolytic drugs
h. Adrenergic agents
2. Drugs for pain, fever, and inflammation
a. Aspirin
b. Acetaminophen
c. Glucocorticoids
d. Opioids and nonopiod analgesics
3. Drugs used in the oncology or transplant patient
a. Drugs to treat bone marrow depression
b. Drugs to treat oral candidiasis
c. Drugs to treat hyperuricemia
d. Antirejection agents
4. Endocrine system drugs
a. Antidiabetic medications
b. Drugs used in hypothyroidism
c. Drugs used in hyperthyroidism
d. Vasopressin


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5. Antimicrobial drugs
a. Drugs to treat urinary tract infections
b. Aminoglycosides and vancomycin
c. Macrolides and tetracyclines
d. Topical ointments and antimicrobials

6. Drugs for the upper and lower respiratory tract
a. Antihistamines
b. Anticholinergics
c. Bronchodilators
d. Surfactant

7. Drugs affecting the nervous system
a. Anticonvulsants
b. Barbiturates
c. Benzodiazepines
d. Anticholinesterase drugs
e. Neuromuscular blockers

8. Psychiatric Drugs
a. Antidepressants
b. Antipsychotics (conventional and atypicals)
c. Drugs used to treat side effects of antipsychotics
d. Mood stabilizers

9. Drugs affecting the gastrointestinal system
a. Antidiarrheals
b. Laxatives
c. Lactulose
d. Neomycin sulfate
e. Vitamin K
f. Antiemetics

10. Drugs affecting fluids and electrolytes or the renal system
a. Crystalloids
b. Colloids
c. Magnesium sulfate
d. Phoslo
e. 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 the
cardiac and arterial smooth muscle (calcium channel blockers),
others block enzymes that increase the rennin-angiotensin-aldosterone
response (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 to
tell a medication is a beta blocker because the generic names
end in LOL. PLEASE NOTE: You may not always be able to
tell a drug by looking at the ending, as some drugs to do not
follow this pattern. You must look up all drugs in which you
are 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 1
receptors? 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 heart
from 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 beta
blockers mechanism of action is to decrease the effect of the SNS.
What the drug does because of the action is called the THERAPEUTIC
EFFECT. 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, you
can 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. Another
side effect is hypotension. These both make sense based on how the
drug works, right?

Nursing interventions that should be done before giving a beta blocker
would make sense too, right? What would a good nurse do before
giving this medication? They would take a BP and heart rate. If
the blood pressure is less than 100 systolic, or the heart rate is less
than 60 beats per minute, the nurse should hold the drug and contact
the physician.

Cardioselective versus noncardioselective: Remember, beta 1
receptors are in the heart, beta 2 are in the lungs. If we give a beta
blocker 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 noncardioselective
beta blocker will block beta 1 and 2 (propranolol): this is not good, as
we dont want to block beta 2 receptors and cause
bronchoconstriction. Therefore, noncardioselective beta blockers
are usually older drugs and they cause more side effects (such
as bronchoconstriction). A word of warning: if a cardioselective
beta blocker is used in a very high dose, there may be some spill-over
onto the beta 2 receptors, thus causing bronchoconstriction.
Therefore, in any patient with an asthma or COPD history, we
are 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 the
heart 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, supraventricular
tachycardia) to slow down the heart rate and AV node
conduction.

Diabetic patients should be told that beta blockers can MASK THE
SIGNS OF HYPOGLYCEMIA (THEY CANT TELL WHEN THEIR BLOOD
SUGAR IS GETTING LOW), AND BECAUSE THE LIVERS BETA 1
RECEPTORS ARE BLOCKED, AN ADEQUATE AMOUNT OF GLUCAGON
CANT BE RELEASE TO FIX THE LOW 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 to
decrease conduction in the heart (antidysrhythmics property), but
these work a little bit differently than the beta blockers. These drugs
work by decreasing the influx of calcium into the vascular and cardiac
smooth muscle, thus causing the arteries to dilate, and decreasing the
heart 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 like
beta blockers). Verapamil and diltiazem are the only 2 drugs in this
class right now.

Now, you should notice one important thing..BETA BLOCKERS AND
NONDIHYDROPYRIDINE CALCIUM CHANNEL BLOCKERS WORK
VERY SIMILARLY!!!!! This is very important to take note of for the
following reason. Lets pretend a patient is getting both a beta blocker
and verapamil. What is the potential for a DRUG-DRUG
INTERACTION? 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). In
this case, there is an increased risk of bradycardia, cardiac
dysrhythmias, and hypotension. Makes sense?

So, the interventions are the same too, right? Monitor pulse, blood
pressure, 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 an
enzyme (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 ACE
inhibitor 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 effect related to these drugs.
The cough is caused because we are blocking angiotensin converting
enzyme 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, it
can 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 potassium
3. Before giving medication, check blood pressure. If less than
100 or otherwise specified by physician, hold medication and
contact 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 class
include NITROPRUSSIDE, NITROGLYCERIN, LABETALOL AND
HYDRALAZINE. Another drug you may see utilized is Corlopam
(fenoldopam). In this section we will discuss only the drugs bolded
above.
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A hypertensive emergency exists when the diastolic blood pressure is greater
than or equal to 120 mmHg. Direct acting vasodilators are given as emergent
treatment of this condition, as they are all give IV and they begin to work in a
matter of seconds or minutes. All of the vasodilators work essentially the same,
they result in either arterial and venous dilation or just arterial dilation. When
dilation occurs, it decreases the pressure in the vasculature, thus lowering the
blood pressure.

Nipride (nitroprusside) is a vasodilator given by IV infusion. Because it is so
effective and works very quickly, extreme hypotension can result. As a rule, any
patient on nitroprusside will have CONTINUOUS BLOOD PRESSURE
MONITORING. This means that every 3-5 minutes, we check the blood
pressure. If the blood pressure is still very high, we titrate the drip by
increasing the dose. If too low, we back down on the drip.

Other adverse effects from nitroprusside include: fluid retention and
tachycardia. Lets figure out why this occurs. Venous dilation will decrease the
blood return coming back to the right heart (preload). If this occurs, less
preload 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 lost
volume somewhere; therefore, the renin-angiotensin system will kick in and
cause fluid retention. Therefore, some patients will actually receive a diuretic
such as furosemide along with nitroprusside. The tachycardia from the drug is
related to the drop in cardiac output. When the resistance falls in the
vasculature, this decreased return to the heart, thus dropping cardiac output.
Therefore, a reduced cardiac output will reflexively result in tachycardia (heart
rate is going up to compensate for the drop in cardiac output).

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

Normodyne (labetalol) ends in lol, so it is a beta blocker. In addition to
being a beta blocker, we use it for hypertensive crisis because it is has alpha
blocker properties as well. Alpha receptors are on the blood vessels and
normally will cause vasoconstriction when norepinephrine binds. With
labetalol, we block the alpha receptors from norepinephrine, so the
result is VASODILATION. Because it is a beta blocker, we would monitor
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patients receiving this drug for BRADYCARDIA and HYPOTENTION. Dont forget
that any beta blocker also has the potential to cause cardiac dysrhythmias as
well!

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? Because
these drugs will dilate cerebral blood vessels, thus increase cerebral perfusion
pressure.

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

Antidysrhythmic drugs:
Antidysrhythic drugs fall into 5 groups. The groups relate to how the
medications impact the conduction system. Remember learning about the
conduction system? The AV and SA node are different than the HIS-purkinje
part of the conduction system. AV and SA node action potentials are called
SLOW POTENTIALSthis is because it takes longer to get an impulse through
these areas than in the HIS-purjinke system. The HIS-purkinje system conducts
impulses very rapidly; therefore, these actions potentials are called FAST
POTENTIALS.

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

Lets review the fast channels: while there are 5 phases, 3 phases are
important, as medications affect these 3 phases.
Phase 0: rapid influx of sodium into 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 of
antidysrhythmics affect the fast channels!
Class 1: quinidine, procainamide, lidocaine, phenytoin, mexiletine
Class 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 will
focus on the major ones only!

Quinidine Major adverse reaction is DIARRHEA! Actually, it happens in about
30% of patients taking quinidine. Quinidine is essentially the same as quinine,
the antimalarial drug both drugs come from the South American cinchona tree!
Quinidine has ANTICHOLINERGIC PROPERTIES. Remember acetylcholine? It is
the neurotransmitter in the parasympathetic nervous system (PNS). Too much
acetylcholine can cause PNS symptoms such as bradycardia, increased oral and
GI secretions, and urinary incontinence. Quinidine, having anticholinergic
properties, can result in the opposite effects..such as dry mouth and
TACHYCARDIA! Cardiotoxicity is the most life-threatening side effect of
quinidine. You can recognize when a patient is getting toxic when the QRS
widens! The QRS complex is the tall and spiked portion of the EKG; normally, it
should be very narrow. When it widens, this is a major sign of cardiotoxicity.

Procainamide This drug is very similar to quinidine, except that it has no
anticholinergic properties and does not cause diarrhea. Just like quinidine,
CARDIOTOXICITY is the most life-threatening side effect (see above).

Lidocaine Yes, lidocaine is an intravenous drug used to treat dysrhythmias. It
also has anesthetic properties (numbing agent)! The major side effects with this
drug are related to the effects on the heart and central nervous systems. In a
manner of speaking, lidocaine numbs the CNS, therefore, confusion,
drowsiness, and numbness/tingling in the limbs are often side effects. If the
patient receives very high doses, SEIZURE AND RESPIRATORY ARREST CAN
OCCUR. It is important to know that lidocaine can cause serious
bradycardia and hypotension.

Mexiletine This is essentially an oral drug that works just like lidocaine.
Similar neurological symptoms can occur (see above).

Phenytoin Yes, believe it or not, Dilantin is also used for cardiac
dysrhythmias. It makes senseit works in seizure by decreasing sodium influx
into 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 TOXICITY
causing 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 decrease
contractility. In addition, they will decrease firing from the SA node and reduce
conduction through the AV node.therefore, they can be used to treat
SUPRAVENTRICULAR TACHYCARDIA (or tachycardia that arises from above the
ventricles). It is important to note that not all beta blockers have been approved
to treat dysrhythmias; at this time, only propranolol, esmolol, and acetubolol
have been approved.

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

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

Amiodarone This drug, when given IV, is approved for first line treatment of
ventricular dysrhythmias. Oral amiodarone can result in may long-term
problems, including lung injury and visual abnormalities. The IV form of this
drug is much safer, as it is only used in the short run. Adverse effects from IV
amiodarone include hypotension, widening QRS, and bradycardia. The
bradycardia occurs because the drug will decrease conduction through the AV
and 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 heart
rate. 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 supraventricular
dysrhythmias. 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 than
a 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 the
loop 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 means
essentially 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 in
the body, and lowering blood pressure. Make sense? Another
reason for giving Lasix is in oncology patients..as they can
develop 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 potassium
with Lasix)

Nursing interventions:
1. Check blood pressure before giving drug.
2. Monitor intake and output: if Lasix increases renal flow
and output, then we must watch how much urine the patient
puts out and compare that to what they are taking into the
body by oral or IV means.
3. Check serum potassium.
4. Check for improvement in edema: sometimes we use Lasix
to treat patients with heart failure. These patients can be
very 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, or
hydrochlorothiazide. 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 SPARING
DIURETIC. What this means is that the drug will decrease sodium
and reabsorption (like other diuretics), but potassium will be retained
and not lost. While this drug is not used first line for hypertension, it
is used a great deal in both LIVER FAILURE AND CONGESTIVE
HEART 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. An
important nursing intervention is to check the serum
potassium. 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 OSMOTIC
DIURETIC, 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 the
drug is given, it is always given IV (cant be given PO). It essentially
goes into the cerebral circulation, pulling water from the brain into the
vasculature, then carries the drug and water to the nephron to be
excreted. This is how it relieves cerebral edema. Because mannitol
pulls so much water out of the vasculature, it can very often result in
HYPERNATREMIA (too much sodium because too much water has been
pulled 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 the
body, causing fluid to accumulate in the tissue. This can lead to
pulmonary edema!

Potassium is the most common electrolyte given in hospitalized
patients. 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 of
fluid 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 complain
of nausea. If you give it IV, it BURNS!!!!!!
3. If nauseated, give with crackers or a meal. If burning with IV
infusion 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 their
CREATININE before giving potassium. Also, you want to
know that patients are urinating before you give them
potassium, 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 the
diuretic.

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 swallow
the whole extended release pill, you can either break in half, or
drop in water and let the capsule come apart. The patient can
then drink it.
2. For effervescent tablets, these are in either orange or lime
flavor. Dissolve the pill in 8 ounces of water and have patient
drink it slowly.
3. Give with some sort of food.a meal or crackersremember it is
very 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 that
potassium is irritating to the GI mucosa.



Drugs to treat hyperkalemia: Kayexelate (sodium polystyrene
sulfonate).
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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 the
intestine. In this case, more potassium will move from the blood to
the intestine, and the hyperkalemia will decrease. If given as an
enema, the potassium will fall much quicker than if given orally. If
given orally, DO NOT MIX WITH ORANGE JUICE! The major side
effects are of course, HYPOKALEMIA, constipation, fecal impaction, and
nausea and vomiting (it tastes terrible).

Cancer patients may develop acute hyperkalemia when chemotherapy
rapidly 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-threatening
situation.

Inotropes: An inotropic drug is one that increases cardiac
contractility. Think about conditions that would requires these
drugsdoes congestive heart failure come to mind? It should! If
cardiac contractility increases, so does stroke volume, and
subsequently cardiac output!

Keys:
1. Lanoxin (digoxin) is also known as a cardiac glycoside (this just
is 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 increases
contractility! Isnt that easy?
3. Digoxins mechanism of action is that it keeps sodium and
calcium inside the myocardial cell and the calcium buildup allows
for better contraction. Meanwhile, potassium gets trapped
outside of the myocardial cell and potassium struggles with
digoxin to get back inside the cell. Therefore, digoxin
competes 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 (its
antidysrhythmics 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 than
60. 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 be
signs 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 cause
potassium 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 the
potassium were low, you would either use the potassium sliding
scale (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 mild
digoxin toxicity, as it cost a great deal!
10. Checking the digoxin level is an intervention that can be done
for toxicity, but we usually dont have one readily available, and
it takes hours to get the level back; therefore, CHECKING THE
POTASSIUM IS THE MOST SENSIBLE NURSING
INTERVENTION!

Primacor (milrinone) is also an inotrope, but in addition, it is also a
VASODILATOR. Therefore, we call this drug an INODILATOR. In
congestive heart failure, we need the increase in contractility to
augment cardiac output, but we also need the vasodilation to decrease
the work the heart has to do (afterload). This drug is given as an IV
infusion 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 is
NITROGLYCERIN. 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) the
heart has to do, thus decreasing angina.

17
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 only
nitroglycerin we use to treat chest pain is either sublingual or IV.
Intravenous nitrates, such as nitroglycerin, are obviously given at a
higher dose than PO or sublingual nitrates. Therefore, only IV
nitrates can cause coronary artery vasodilation and increase supply
of 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 in
inches (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 erectile
dysfunction drugs such as Viagra, Cialis, or Levitra. THESE
DRUGS, WITH NITROGLYCERIN, CAN LEAD TO PROFOUND
HYPOTENSION IF GIVEN WITHIN 24-48 HOURS OF ONE
ANOTHER.
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 chest
pain 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 higher
dose and will also increase blood supply to the myocardium!
18
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: These
drug classes work differently; however, they all affect the coagulation
system 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, THEY
WILL 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 is
given 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 artery
thrombi. 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 ventricle
and 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). The
INR is basically the patients PT result and the labs
control 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 SQ
is 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 times
a normal PT).
10. HEMORRHAGE IS THE MAJOR SIDE EFFECT OF
ANTICOAGULANTS: Bleeding can be either minor (gum
bleeding, nose bleed, oozing from IV site) or major (blood in
19
urine, bleeding into brain or GI tract). NURSES MUST MONITOR
FOR BLOOD LOSS IN THESE AREAS WHILE PATIENTS TAKE
THESE DRUGS.
11. If a patients PTT is very high and they have bleeding, a reversal
or 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 for
Coumadin. Hint: Coumadin inhibits vitamin K derived clotting
factors, 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, as
they 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 Coumadins
effect).
15. Pregnant women should never receive COUMADIN. Heparin is
the drug of choice in these women.
16. Many over-the-counter drugs contain aspirin, so be sure to
teach patients this point.
17. Low molecular weight heparin: (Lovenox or Fragmin). These
drugs are given SQ only. The major advantage is that they are
smaller than heparin in molecular size, so there are less drug
interactions. 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 are
not like anticoagulants, as these drugs actually are the only
drugs 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, THE
RISK 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 thrombolytic
drugs today are TPA and Retevase (both given IV).
4. The most important nursing assessments to make after
administration of this drug and for 24 hours after this
drug are the NEUROLOGICAL AND GI TRACT assessments.
20
5. Neurological checks should be done every hour for the
first 12 hours at least to ensure the patient does not have
a cerebral bleed.
6. The stool and/or emesis should be assessed for the first 24
hours 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 bleed
patients will develop. Usually, most patients are also put on GI
drugs such as H2 blockers and proton pump inhibitors to
prevent 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 (or
stick 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 or
clopidogrel.
4. Even low-dose aspirin used to prevent coronary artery disease
can 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 reactions
causing 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, think
about 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 has
supplemental oxygen.

21
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 a
maximum dosage (20 micrograms per kilogram per minute). If the
blood pressure does not increase at this dose, we usually go to
levarterenol (Levophed). Levophed is a pure vasoconstrictor.
Because it can cause very powerful vasoconstriction, the peripheral
arteries are very clamped down, which can result in decreased
perfusion to the distal extremities (which can lead to tissue damage to
fingers 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 by
decreasing prostaglandins which cause pain and inflammation. They work only
in 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 popular
NSAIDs on the market. These drugs decrease inflammation, but not like the
glucocorticoids (like prednisone or dexamethasone). Glucocorticoids suppress
inflammation by decreasing the action of the white blood cells and by decreasing
prostaglandins. NSAIDS only work on the prostaglandins, not the white blood
cells; 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 the
first generation NSAIDs.
2. NSAIDS suppress platelet function..remember, we give aspirin
to patients have a heart attack to prevent the platelets from sticking
22
together. This is also one reason why many patient taking NSAIDS
chronically can develop a GI bleed.they are irritating to the stomach
and 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 resulting
in an elevated serum creatinine. Monitor for this on lab data.
5. Gastrointestinal bleeding is a potentially life-threatening problem from
these drugs. The drugs block prostaglandins which are considered to
be protective in the GI tract; blocking these prostaglandins increases
the potential for GI bleeding. Assess for GI bleeding by looking at
the stool: upper GI bleeding results in black and tarry stools.
Also, a stool that is positive for occult blood could mean a GI
bleed.
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 Reyes
syndrome, a condition that can be fatal (fatty liver, encephalitis).
8. Increased doses of aspirin (over several grams per day) can result in
SALICYLISM, a condition resulting in too much salicylic acid (aspirin
is acetylsalicylic acid). The condition causes ringing in the ears
(tinnitus), dizziness, and headache. This is more likely to happen in
the elderly, but can also happen in patients taking over 2-4 grams per
day of aspirin.
9. If taken with anticoagulants, aspirin and the other NSAIDs can
increase the risk of bleeding. Why? Rememberaspirin suppresses
platelet function and NSAIDS can cause GI bleeds.

Corticosteroids:
Glucocorticoids (such as prednisone) or Solu-Cortef (hydrocortisone)
are adrenal-like drugs, as they act like cortisol in the body; thus they
are called corticosteroids. Cortisol is a glucocorticoid, and it increases
the 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 will
get glucocorticoids, like prednisone, to suppress inflammation.
REMEMBER.LOW DOSES ARE FOR REPLACEMENT OF HORMONES
THEY DONT HAVEHIGHER DOSES ARE TO SUPPRESS
INFLAMMATION. They suppress inflammation by decreasing the
function of the white blood cell and by decreasing the inflammatory
prostaglandins.
23

Drug names:
1. prednisolone or prednisone
2. methylprednisolone
3. hydrocortisone
4. dexamethasone

While there are others, these are the most common IV, PO, IM forms
of 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 the
skin) they are not systemically absorbed, thus less side
adverse drug reactions tend to occur.

Key points to remember:
1. Side effects with chronic glucocorticoid administration (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.
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 will
see many patients who are taking glucocorticoids in the hospital
on 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. If
this is the case, 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
calcium deposition into the bone. If your patient begins
complaining of severe back pain, think about the possibility of a
vertebral compression fracture.
24
5. Adrenal insufficiency: THIS IS CRITICAL TO KNOW. If a
patient who has been taking chronic glucocorticoids suddenly
stops 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 or
just not getting adequate doses. They will become very
hypotensive and hypoglycemic from the lack of cortisol. They
can 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 remember
when you decide to give this drug over an NSAID which does decrease
inflammation.

Acetaminophen reduces fever and pain by decreasing prostaglandins in
the 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 OR
TAKING MORE THAN 4 GRAMS PER DAY will
cause major shifts in metabolism. When we
metabolize this much Tylenol, we can end up with
toxic metabolites (toxic byproducts). These
byproducts can cause HEPATIC NECROSIS AND
FULMINANT LIVER FAILURE in just 3 days if
not treated! Even then, death can still occur
if the blood level of acetaminophen remains
elevated despite treatment.
2. The antidote to Tylenol overdose or toxicity
is MUCOMYST (acetylcysteine). It is given
PO (liquid) mixed in juice, cola, or water. It
has an extremely noxious odor and it is difficult
for the nurse to even give it much less the
patient drink it. They will need to take it every 4
hours for 72 hours (a total of about 17 doses).
25
3. Alcohol can also shift the metabolism of
acetaminophen; therefore, if patients drink
regularly, 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 is
getting every 24 hours..it should not be over
4 grams/24 hours. If so, the physician needs to
be contacted to find an alternative for fever/pain.
5. Remember that acetaminophen is hidden in
many OTC drugs, so you must warn patients
about this when discharging them (especially if
they drink regularly or are taking home a
prescription containing acetaminophen like oral
pain 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.) are
the most addictive, schedule V drugs (cough syrup) are the least addictive.

Opioids work by activating pain receptors (called mu and kappa) in the
central nervous system. These receptors normally respond to endorphins in the
body, the feel-good hormones. When we give pain medications such as the
opioids, 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, oxycodone
3. 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 strong
opioids are usually given PO.
2. The major life-threatening side effect related to the strong
and the moderate to strong opioids is RESPIRATORY
DEPRESSION. This occurs because we are activating the mu
receptors, which can depress the respiratory center.
3. Also, by activating mu receptors, euphoria occurs (which can lead to
addiction in patients not using it for pain control), and sedation occur.
26
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 been
getting these drugs for a while, they will develop TOLERANCE, this is
not the same as addiction. Tolerance means they need more to get
the 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. This
is a common problem, especially in patients who take them for longer
periods of time. Prevention is the keyincrease fluids and fiber and
get patient to move around! They may ever need Colace, a stool
softener 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 CONTAIN
ACETAMINOPHEN (Tylenol) IN ADDITION TO THE OPIOID!
This means you should know how much acetaminophen the
patient is getting in 24 hours. Patients cannot have more than 4
grams per day of acetaminophen (if they drink regularly, they cant
have more than 2 grams per day). More than the recommended dose
of Tylenol can cause serious liver dysfunction!

Drugs Used in the Oncology or Transplant Patient
Note: While this packet will not cover chemotherapeutic drugs, it is
important to know for the pharm test that DRUGS USED TO KILL
CANCER CELLS ALSO KILL MANY OTHER CELLS IN THE BODY.
Cells damaged by chemotherapy are those of the bone marrow, the
mucosa, hair, and GI tract. The most significant damage is obviously
when the bone marrow cells are destroyed, resulting in potentially
fatal anemia, thrombocytopenia, and/or neutropenia.

Drugs to treat bone marrow depression:

1. Anemia can be caused by several different problems. The most
common cause of anemia in our country is iron deficiency; however,
B12 deficiency and folate deficiency can also cause anemia. In the
oncology patient, the anemia is usually caused by chemotherapeutic
drugs 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
27
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 also
used 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 NOT
LONG ACTING; however, darbepoetin is long acting.
Procrit/Epogen is generally given 3x weekly by
subcutaneous injection. Aranesp is only given once
weekly.
2. In patients who are severely anemic and require a
transfusion, it is important to remember that THESE
DRUGS WORK VERY SLOWLY; THEREFORE, IT MAY
TAKE 2-4 WEEKS BEFORE THE HEMOGLOBIN WILL
GO UP. If we cant wait that long for these drugs
to work, we must transfuse!
3. How do we monitor patients on this medication? We
check the CBC (complete blood count); we should
expect to see a rise in hemoglobin in 2-4 weeks. We
can also assess the patients symptoms: are they less
fatigued? Less short of breath? More able to carry out
ADLs?
4. The major side effect of these medications is
HYPERTENSION. This occurs because the drugs
increase the volume of red cells in the blood, increasing
the 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 iron
deficiency, iron replacement will be needed. Iron is given in the form
of 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 patients
taking iron in your career.

28
2. Neutropenia (decreased white blood cells) is a common side
effect of chemotherapy. There are several drugs that will
increase 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 the
increased 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). In
addition, these oral lesions/sores can become infected because of the
reduced white blood cells. When an oral fungal infection occurs, this is
called oral candidiasis (also known as thrush). Typically, the drug
most often used in this situation is nystatin. While nystatin is
available 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 swish
and spit.

Drugs to treat hyperuricemia:
When large numbers of cancer cells are destroyed by chemotherapy,
the intracellular contents can leak out and cause severe metabolic
derangements. One such problem is HYPERURICEMIA; this condition
is 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
29
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 can
reduce the metabolism of warfarin, leading to WARFARIN
TOXICITY.
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 done
so that the uric acid crystals will not crystallize in the renal
tubules.
An important nurse intervention associated with Diamox is to
monitor glucose in diabetic patients, as it can substantially
increase glucose (think Diamox and Diabetes).

Antirejection drugs:
Glucocorticoids (such as prednisone) or Solu-Cortef (hydrocortisone)
are adrenal-like drugs, as they act like cortisol in the body; thus they
are called corticosteroids. Cortisol is a glucocorticoid, and it increases
the 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 will
get glucocorticoids, like prednisone, to suppress inflammation.
REMEMBER.LOW DOSES ARE FOR REPLACEMENT OF HORMONES
THEY DONT HAVEHIGHER DOSES ARE TO SUPPRESS
INFLAMMATION. They suppress inflammation by decreasing the
function of the white blood cell and by decreasing the inflammatory
prostaglandins.

Drug names:
prednisolone or prednisone
methylprednisolone
hydrocortisone
dexamethasone

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
30
transplant rejection, we would typically use 500-1500 mg of
methylprednisolone IV.

While there are others, these are the most common IV, PO, IM forms
of 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 the
skin) they are not systemically absorbed, thus less side
adverse drug reactions tend to occur.

Key points to remember:
Side effects with chronic glucocorticoid administration (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 by
maintaining the mucus-bicarb layer. Because of this, you will
see many patients who are taking glucocorticoids in the hospital
on 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 the
case, 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 calcium
deposition into the bone. If your patient begins complaining of
severe 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 suddenly
stops taking the drug, or if they are physiologically stressed
(trauma, surgery, illness), they may develop ADRENAL CRISIS
31
(AKA acute adrenal insufficiency). In this case, they have a
need for the glucocorticoids, but they are not getting it at all or
just not getting adequate doses. They will become very
hypotensive and hypoglycemic from the lack of cortisol. They
can 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 organ
transplant rejection, but have other uses as well. Because each of these drugs
decreases the ability of the body to fight the immune system, NEUTROPENIA
IS 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 and
glucocorticoids to suppress transplant rejection. In addition to
neutropenia, this drug can decrease the platelet count
(thrombocytopenia).
Cytoxan: This drug is a cancer drug that is also used to treat inflammatory
conditions such as rheumatoid, lupus, and multiple sclerosis. It is not
often used for organ transplant rejection. In addition to causing
neutropenia, it can cause HEMORRHAGIC CYSTITIS.
Sandimmune: This drug is really the most effective of the
immunosuppressants. It is the drug of choice for preventing organ
transplant 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 up
to 75% of patients. We need to be looking at the BUN and creatinine to
see if this is developing; however, in a patient who has had a kidney
transplant, an elevated BUN and creatinine can be a sign of rejection, so
this 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 a
DISEASE MODIFYING ANTIRHEUMATOID DRUG (DMARD). DMARDs
reduce joint destruction and slow down the disease progression.
There are more side effects and potential toxicity associated with these drugs
than NSAIDs (as discussed above). Methotrexate (a first-line DMARD) is
the most rapid acting and will begin working within about a month to a
month and a half. It can cause liver problems, GI ulcers, and bone marrow
depression (decreased WBC function). The drug is given once weekly for
RA.

32

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 accomplishes
the task differently. Insulin is a hormone normally produced by the body, which
enable glucose to be actively transported into the cells. Oral diabetes
medications vary in their action.

Insulin key 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 15
minutes 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), and
the glitazones (Actos, Avandia).
Sulfonylureas: know that these drugs increase insulin secretion from the
pancreas, so it just makes sense that the side effect seen most often
would 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 THIS
MEDICATION.
One of the more common and dangerous side effects of metformin is LACTIC
ACIDOSIS. If a patient has renal failure, or they are in a state of
physiologic shock, or they are dehydrated, lactate can accumulate. If
33
this drug is given on top of these conditions, lactate is not effectively
cleared from the body, and lactic acidosis can result. Therefore, these
patients should not receive metformin. Also, if the serum
creatinine is above 1.5, metformin should be held and the
physician called.
Metformin and contrast dye: if you have a question that asks you what to do
when a patient has had IV contract dye, you always want to make
sure you HOLD THE METFORMIN FOR 48 HOURS AFTER CONTRAST
DYE IS GIVEN. The reason why is this: contrast, if not adequately
cleared by the kidneys, can be nephrotoxic. If metformin is given
before the contrast is excreted fully, renal insult can occur and lactic
acidosis can result.
Glitazones: What is most important to remember is that these drugs allow
the cells to respond to insulin, therefore, INSULIN MUST BE PRESENT
FOR THESE DRUGS TO WORK. Remember that type 2 diabetes is the
inability of the cell to response to insulin. Many diabetics who have
had the disease for years may not produce enough insulin, and may
eventually need to inject insulin every day after being on years of oral
medications. In this case, glitazones may be used along with insulin to
help the cells respond better to the insulin. Glitazones are taken PO
and are also often combined with sulfonylureas or metformin.
Two major adverse drug reactions with glitazones: fluid retention (which
can lead to heart failure in certain patients) and liver injury.
Therefore, weight and symptoms of shortness of breath and/or edema
should be assessed. In addition, liver function (ALT and AST) should
be 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 usually
discontinued. Typically, the ALT falls back to normal once the drug is
stopped.

Glucagon: remember that glucagon is a counter regulatory hormone.THE
OPPOSITE OF INSULIN! Therefore, if a patient outside the hospital were
hypoglycemic, glucagon could be given IM; however, it requires 5-20 minutes to
work when given via this route. In nursing home patients glucagon is the usual
treatment for hypoglycemia. In hospitalized patients we simply use
intravenous dextrose 50% for hypoglycemia, as D50% works immediately
once 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 in
thyroid hormone; therefore, replacement is the way to treat these patients.
Keys to know:
34
1. Synthroid (levothyroxine) stays in the body for a very
long time (it has a long half-life). Therefore, PATIENTS
MUST BE INFORMED THAT WHEN THEY FIRST
STAY TREATMENT WITH THIS DRUG, THEY MAY
NOT HAVE SYMPTOM REDUCTION FOR A MONTH!
Remember, the longer the half-life of a drug, the longer
it will take to get a therapeutic effect.
2. Side effects usually dont occur unless the DOSE IS TOO
HIGH FOR THE PATIENT. This is why this drug is
started at a very low dose and gradually increased if the
patient 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 the
patinets metabolism has increased (remember thyroid
hormone has a great deal to do with the metabolic rate)!

While there are other drugs to treat hypothyroidism, by far levothyroxine is the
most 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. Memory
trick: 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 the
case of hyperthyroidism, the excess thyroid hormone creates extra work for the
heart, which can lead to cardiac dysrhythmias, tachycardia, and palpitations.

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

1. Antithyroid medications: PTU (propylthiouracil) and Tapazole
(methimazole) are both drugs that inhibit the synthesis of
thyroid hormone. It is important to know that it DOES NOTHING TO
STOP EXISTING HORMONE, IT ONLY PREVENTS THE FORMATION OF
NEW HORMONE; THEREFORE, IT CAN TAKE 3-12 WEEKS TO SEE THE
EFFECT OF THESE DRUGS.
a. The most serious side effect of these drugs is AGRANULOCYTOSIS
(decrease granulocytesthe first line white blood cells). If this
does occur, it will happen in the first 2 months of therapy. Serious
35
infection can result; therefore, weekly CBCs are usually done for
the first 2 months of therapy.
b. Usually, if agranulocytosis does occur, the patient will complain of
FEVER AND SORE THROAT. This is a signal to the nurse to
check 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 make
the gland less active before surgery. How? BY GIVING IODINE
SOLUTIONS SUCH AS LUGOLS SOLUTION.
a. When high doses of iodine are given, this will suppress the function
of the thyroid gland, and less hormone will be produced.
b. Usually Lugols solution is given 7-10 days preoperatively. It is
prescribed in drops. The drops (2 to 6) are mixed in water or juice
and the mixture is drank up to 3 times daily.
c. Lugols is not pleasant to drink; therefore, mixing with juice or cola
is usually helpful.
d. The most common side effect of Lugols is IODISM: a metal taste,
burning of the mouth, soreness of mouth and gums, increased
saliva, and even skin eruptions. These symptoms occur because of
the high iodine content.
3. Radioactive iodine: In Graves disease (a type of hyperthyroidism),
radioactive iodine can actually be given to destroy thyroid tissue. The
goal is to destroy enough of the gland to treat the hyperthyroidism, but
not completely destroy all of the gland. However, typically patients
undergoing this treatment can end up with hypothyroidism afterwards.

Vasopressin:
Antidiuretic hormone (ADH) occurs naturally in the body and allows us to
conserve water (think about the name and you have what it does). Certain
conditions 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 and
EXTREME AND LIFE-THREATENING DEHYDRATION CAN OCCUR. In this case,
patients will require VASOPRESSIN, 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.
36
The major reason for water intoxication in patients taking vasopressin is
FAILURE TO STOP DRINKING A LOT OF WATER. Therefore, patients
should be instructed to reduce their fluid intake.
Vasopressin can cause vasoconstriction..because it is a powerful
vasoconstriction, 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 decreased
perfusion to the extremities. The nurse should ASSESS DISTAL
CAPILLARY REFILL AND SKIN COLOR/TEMPERATURE to prevent tissue
ischemia 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 tract
infections, prostate infections, respiratory infections, and maybe even some bone
or soft tissue infections. By far, respiratory and GU infections will be the
more common reasons you use them. Everyone has probably at least heard
of Cipro (ciprofloxacin). This is an older quinolone, but is still widely used today.

Keys to know about quinolones:
Drugs names tend to end in oxacin (ciprofloxacin, ofloxacin/Floxin,
sparfloxacin/Zagam, lomefloxacin/Maxaquin,
levofloxacin/Levaquin).
The quinolones cover mostly gram negative bacteria (like E. colithis is why
they work great for UTIs).
The most common side effect is nausea and vomiting. This can be reduced
by giving the oral medication with food; however, food can decrease
absorption of oral quinolones by up to 20%.
Drug interactions are not really common to the group, unfortunately, they are
related more to the individual drug.
Cipro: MAJOR DRUG INTERACTION PROBLEMS WITH WARFARIN,
THEOPHYLLINE. The CIPRO REDUCES METABOLISM OF THESE
DRUGS, THEREFORE, INCREASING THEIR LEVEL AND
POTENTIALLY 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 decreased
abosorption and effect.
Tendon rupture: Most of the quinolones, but not all, can cause tendon
rupture in any age group. This caused extreme pain and limited
mobility. The major drugs are Cipro, Avelox (moxifloxacin), Floxin.
37
Quinolones can increase sensitivity to the sun.

Sulfonamides: This group of drugs are used for UTIs caused by E. coli. They
have other uses as well, but primarily are used for UTIs. You may also find
them used in AIDS patients, as this drug is effective against
Pneumocystis carinii, an opportunistic organism that is known to cause
pneumonia 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 this
fixed combination as Bactrim or Septra.
2. Many patients are allergic to this group of drugs. It is critical to assess for
allergies 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 avoid
prolonged 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-JOHNSON
SYNDROME, a rare but potentially dangerous skin and mucous membrane
reaction. The patient will develop lesions that almost resemble a burn all
over the skin and mucous membranes, they will also develop fever. THE
NURSE CARING FOR THIS PATIENT MUST DO A SKIN ASSESSMENT
EVERY DAY TO ENSURE THE PATIENT IS NOT DEVELOPING THIS
REACTION.
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 GLASSES
OF WATER PER DAY. Therefore, it is very important to monitor
urine output in these patients; you want to see at least 1,200 mL
of 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 proteins
in the bacteria, thus cause the cell to die (cidal effect). THE ONLY ORGANISMS
38
THAT ARE KILLED BY THESE DRUGS ARE THE GRAM NEGATIVE ONES (LIKE
PSEUDOMONAS).

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 have
the patient take it orally, but the drugs does not get systemically
absorbed.
2. These drugs are RENALLY ELIMINATED; therefore, careful monitoring of
the patients renal function is required. Daily assessment of the creatinine
should be done and if moderately elevated, the physician should be
notified 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 is
drawn 30 minutes after the infusion ends. TROUGH TELLS YOU
IF THE PATIENT IS TOXIC! This is drawn immediately before the
drug is to be given. If trough is elevated, the dose is held and
the prescriber called.
4. If renal function is impaired and/or the trough is elevated,
SERIOUS TOXICITY can occur to the kidney and the ear (nephrotoxicity
and ototoxicity). Therefore, patients who are not excreting the drug
normally will require smaller and less frequent doses.
5. Ototoxicity: these drugs can accumulate in the ear and cause both
cochlear damage (hearing loss) and vestibular damage (dizziness and
vertigo). 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 IS
ELEVATED.
6. Nephrotoxicity: These drugs can injure the delicate cells of the tubules.
THE RISK IS HIGHER WHEN THE SERUM TROUGH LEVEL IS
ELEVATED. The risk is highest in the elderly or those with
preexisting renal disease. BUN and creatinine should be closely
monitoring during therapy.

Vancomycin: This drug is given mostly for MRSA (methicillin resistant
Staphylococcus aureus). MRSA is a common hospital organism that costs our
healthcare 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 work
the same way or cover the same organisms (remember that gentamicin
covers gram negatives and vanco covers gram positives, but mostly
used for the gram positive MRSA).



39
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 this
causes a massive histamine reaction, which can cause serious flushing
and 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 Strep
endocarditis).
The most serious adverse reaction is OTOTOXICITY. If you remember,
gentamicin can cause this too. IF the patient is getting both vancomycin
and gentamicin, the risk is even higher. The risk is high as well if the
patient receiving vancomycin has reduced kidney function.
Vancomycin is mixed in at least 250 mL of solution before giving it IV
because it can be extremely painful to the patient while it is infusing. The
more fluid it is diluted in, the more comfortable the patient is, and the less
damage to the veins.

Macrolides and tetracyclines:

Macrolides: This group of antibiotics are also broad spectrum and are also
cidal (at higher doses). The oldest drug in this group is ERYTHROMYCIN. The
newest 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, liver
injury is caused by high doses of erythromycin. Therefore, LFT
monitoring will be needed for those patients.
2. The newer drugs have few side effects. Erythromycin causes diarrhea
because it stimulates the motolin receptors in the bowel and increases
peristalsis. Sometimes, we can give this drug to patients for this very
reason!
3. Erythromycin can increase the levels of other drugs (theophylline,
Tegretol, and Coumadin) because erythromycin will decrease the
liver 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 patients
taking the oral Zithromax packets (Z-Pak) that the MEDICATION WILL
CONTINUE TO WORK FOR 14 DAYS AFTER THEY FINISH THE
MEDICATION.
40
5. Biaxin (clarithromycin) tends to decrease metabolism of many drugs,
especially digoxin. Digoxin doses should be reduced in any patient
receiving Biaxin.

Tetracyclines: These are very old drugs and include both tetracycline and
doxycycline. They are broad spectrum and useful in many infections, including
acne, sexually transmitted diseases (STDs), periodontal infections, and peptic
ulcer 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 A
NON-ABSORBABLE COMPLEX WITH CALCIUM, MAGNESIUM,
IRON, AND ZINC; therefore, it should not be given with calcium
supplements, milk products, and most antacids (because they
contain either calcium or magnesium).
2. Doxycycline is a longer acting drug and is not renally eliminated. It does
not have the same issues with forming complexes. Doxycycline is used a
great deal for STDs.
3. Most tetracyclines can cause GI upset, causing burning, cramping,
nausea, and vomiting. Because these drugs can also cause
esophageal irritation, DO NOT GIVE AT BEDTIME!
4. Staining of the teeth can develop with tetracycline, again due to the
complexes formed with calcium. Therefore, we dont give tetracyclines to
children 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 major
one. If this bowel infection occurs, it is caused by Clostridium difficile (C.
diff). Severe dehydration and electrolyte depletion can occur, so the
patient must be monitored carefully if it develops.
6. Tetracyclines can cause fat to infiltrate in the liver and hepatotoxicity can
result. This is rare, but patients with abdominal pain and jaundice should
be suspected of having this condition.
7. There are conflicting reports as to whether tetracycline actually reduces
the effect of estrogen contraceptives. For most antibiotics, we simply
warn patients anyway to use backup birth control while on antibiotics, but
scientific evidence does not seem to show that tetracyclines reduce the
effect of oral contraceptives.

Macrobid/Macrodantin (nitrofurantoin)
This antibiotic is most commonly used for urinary tract infection treatment, but
an also be used for chronic prevention of recurrent UTIs. Because absorption is
increased with food, this drug should always be given with food.

41
Side effects include: The most common problem is GI-related, nausea,
vomiting, diarrhea. If taken every day for UTI prevention, the drug can cause
pulmonary problems, such as chronic cough and dyspnea, which may be signs of
a more serious side effects, fibrosis.

A drug that may be utilized for a urinary tract infection is Pyridium
(phenazyridine). This drug is used only to decrease pain associated with
UTIs; it is not an antiinfective and it is not an anticholinergic. It will discolor the
urine yellow/orange, and patients; should be warned of this side effect. They
should also be told it can stain fabric. In patients with renal insufficiency, the
blood level can accumulate and worsen renal status.

Topical ointments and antimicrobials:
Burn patients will require a topical antimicrobial to prevent bacterial growth and
infection of the burned tissue. One very commonly used drug is Silvadene
(silver sulfadiazine). This is a white thick cream applied to burned tissue at
least once daily. The way the drug works is not because of the sulfa group in
the drug, but by the release of silver, which has antibacterial properties. It is
important to remember that this drug, although topically applied, can
result in systemic absorption. The biggest problem with systemic absorption
is due to the sulfa component of the group.ALLERGIES. In addition, rash and
severe skin reactions can occur. In patients with extensive burns, anemia
and agranulocytosis can occur.therefore, these patients will need
daily or at least 3x weekly CBCs.

Another topical antimicrobial is neomycin. This drug has many different topical
indications. One way this drug is delivered is by an ointment applied to the skin
(typically it is mixed with other antibiotics and/or hydrocortisone) to prevent
infection caused by lacerations and abrasions. Other ways we can use this drug
is to treat ear infections (ear drops), and to clean out the bowel before surgery
(by having the patient drink the medication). When used to cleanse the bowel, it
is not systemically absorbed from the GI tract; therefore, it acts only topically or
locally.

Another reason we use neomycin is for patients with liver failure. In liver
failure, the excess proteins in the GI tract are broken down and converted to
ammonia. The ammonia is not eliminated by the body, the serum ammonia level
increases, and hepatic encephalopathy can occur. Therefore, NEOMYCIN is
used to rid the GI tract of the bacteria breaking down the protein, thus lowering
ammonia.

The nurse should remember that neomycin is AN AMINOGLYCOSIDE. Even
though it is used topically, the drug can be systemically absorbed.
RememberAminoglycosides can cause ototoxicity and nephrotoxicity!
42


Drugs for the Upper and Lower Respiratory Tracts

Antihistamines:
There are 2 major ways histamine is released in the body, nonallergenic release
and allergenic release. Histamine, when released, affects one of two different
receptors, the H1 receptors and the H2 receptors. We will talk about H2
blockers when we discuss GI drugs below. For now, just know that histamine 2
receptors produce gastric acid when stimulated. H1 receptor blockers are
given for ALLERGIC REACTIONS and a few other reasons. Everyone is
probably familiar with Benadryl (diphenhydramine), the most well-known of the
H1 receptor blockers. Histamine is released when there is an antigen-antibody
response. This drug and all the other H1 blockers work by blocking the
histamine on cells in the blood vessels, lungs, skin, CNS, and mucous
membranes. If histamine cannot bind to those cells receptors, then
allergic symptoms cannot occur.

Keys:
1. H1 blockers do not stop histamine from being produced, they only
block the receptors on the cells and stop the symptoms of allergy.
2. Mild allergic reactions can cause skin eruptions, itching, and increased
capillary permeability resulting in local edema. H1 blockers will decrease
these symptoms.
3. Severe allergic reactions can result in vasodilation (causing a drop in blood
pressure) and bronchoconstriction (causing respiratory distress). For a
severe allergic reaction, antihistamines are given only after
epinephrine (which reverses these symptoms) has been given!
How does epi reverse the symptoms? It causes vasoconstriction and
bronchodilation. Make sense?
4. There are 2 generations of the H1 blockers, first and second. The first
generation drugs include Benadryl and others. FIRST GENERATION
DRUGS CAUSE SEDATION. The second generation drugs include
Claritin, Zyrtec, and Allegra. THESE DRUGS DO NOT CAUSE
SEDATION.
5. First generation drugs can cause more side effects than second generation
(as they are older drugs). These include ANTICHOLINERGIC SIDE
EFFECTS. Blocking acetylcholine (cholinergic neurotransmitter)
means you get drying of secretions. Therefore, dry mouth,
constipation, urinary retention are all common side effects.
6. Nursing interventions for anticholinergic side effects include giving the
patient frequent sips of water (for dry mouth), performing mouth care,
increasing fluid intake (constipation), and monitoring urine output (urinary
retention).
43
7. When mixing first generation H1 blockers with alcohol or pain
medications, PLEASE BE AWARE THAT THE PATIENT IS AT RISK
FOR INCREASED CNS DEPRESSION. Therefore, patient safety is
of utmost concern. You must assess the respiratory, neurological, and
cardiac system for adverse effects. You must protect these patients from
injury by ensuring the side rails are up, bed is locked, and call light is in
reach.
8. Antivert (meclizine) and Dramamine (dimenhydrinate) are 2 drugs
you will study this semester. Both of these drugs, although they are
antihistamines, they are primarily used as an antiemetic. You have
probably heard of Dramamine for motion sickness (motion sickness). You
will learn, in the GI section, that histamine and other neurohormones are
causes of nausea and vomiting; blocking histamine in the CNS reduces
nausea and vomiting. Benadryl is also considered an antiemetic as well as
an antihistamine; however, it is not commonly used as an antiemetic.

Anticholinergics:
Remember from anatomy and physiology that acetylcholine (ACH) is the major
neurotransmitter of the PARASYMPATHETIC NERVOUS SYSTEM. When the PNS
is stimulated by ACH, gastric and oral secretions increase, heart rate and cardiac
conduction slows down, and urine output is increased. In essence, it allows us
to REST AND DIGEST. When we stimulate the PNS with drugs, we call these
drugs CHOLINERGIC DRUGS. When we block the ANS, we call these drugs
ANTICHOLINERGIC DRUGS.

For preoperative use, most of the time you will see two drugs used: atropine
sulfate and Robinul (glycopyrrolate).

For patients with COPD and asthma, Atrovent (ipratroprium bromide) is
available to promote bronchodilation. It works by blocking the cholinergic
receptors in the lung, thus blocking small airway constriction (bronchioles). It is
given as either an inhaled or nebulized drug. It is not as effective as the
bronchodilator drugs below (such as albuterol); however, it is very helpful for
COPD and allergen-induced asthma.

Anticholinergic drugs:
1. We have already discussed the major anticholinergic drug, atropine!
2. Atropine is used for symptomatic bradycardia (why? Because it blocks
the cholinergic receptors in the SA node and increases heart rate).
Atropine is one of the drug used in cardiac arrest; it is used to decrease
any vagal (parasympathetic nervous system) response that might be
occurring, as it blocks cholinergic receptors in the conduction system.

Key points to remember:
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1. Anticholinergic drugs block ACH, therefore, you get DRYING OF
SECRETIONS. This is helpful to do preoperatively, as you want to limit
the amount of secretions in the upper airway when the patient is given
general anesthesia (prevent aspiration).
2. The most common side effect with Atrovent is dry mouth. Now you know
why
3. Atropine may also be used preoperatively to stabilize the heart rate,
as some general anesthetics can cause bradycardia. Atropine will keep
the heart rate up and prevent the bradycardia.
4. Side effects of these drugs are most commonly: TACHYCARDIA, dry
mouth, urinary retention.

Bronchodilators:
Do you recall the beta 2 receptors from your anatomy/physiology classes? There
are beta 2 receptors in the lung, on the bronchial smooth muscle. When these
receptors are stimulated, bronchodilation occurs. For asthma, it would just make
sense that we would want to give a beta 2 agonist (agonist is another word for
stimulant). A beta 2 agonist would bind to these receptors and cause
bronchodilation.

Common drug names:
1. albuterol (Proventil/Ventolin)
2. levalbuterol (Xopenex)
3. salmeterol (Serevent)
4. formoterol (Foradil)

Keys to know:
In the hospital, albuterol and levalbuterol are the most commonly used
bronchodilators for asthma. They are also used to bronchodilate patients
with pneumonia, retained secretions, patients on ventilators, and COPD
patients.
There are 2 types of bronchodilators short acting (also called rescue
drugs) and long acting (also called maintenance drugs).
Short acting drugs included albuterol by nebulizer or by MDI (metered dose
inhaler). MDI simply means that every time the patient takes a puff from
their inhaler, a preset dose is inhaled.
Short acting bronchodilators are used to THWART OFF AN ACUTE ASTHMA
BY PROVIDE QUICK BRONCHODILATION. Again, you will see these short
term nebulizer treatments used in the hospital in patients who do not
have asthma; we are simply using them to cause quick bronchodilation in
hopes of removing secretions and improving airflow.
Long acting formulations are salmeterol and formoterol. These drugs are
taken every day by certain asthma patients to provide long lasting
bronchodilation throughout the day. The patient takes these medications
45
by inhaler (Diskus or Aerolizer) every day, whether they have symptoms
or not.
When inhaled medications are given, this is considered a topical treatment;
therefore, side effects are usually minimal. However, administering back
to back nebulizer treatments (which you will see in the ER a great deal)
can lead to angina, tachycardia, and muscle tremors.

Theophylline: this is reserved for patients who are experiencing status
asthmaticus (the most severe asthma exacerbation). This drug is an IV
bronchodilator which works differently than albuterol. While it is a great drug,
it has some major side effects. It is structurally similar to caffeine; therefore,
theophylline/aminophylline can cause tachycardia, CNS excitability,
insomnia, cardiac dysrhythmias.
1. Due to the side effects (toxicity) from theophylline, blood levels
are usually checked. The normal blood level should be between
10-20 mcg/mL.
2. You may find patients on oral theophylline for chronic obstructive
pulmonary disease, chronic severe asthma, or other pulmonary reasons.
These patients need to have their theophylline level checked periodically
as well.
3. Many drug interactions can occur with this drug: caffeine will
increase the effect of the theophylline, making the risk of toxicity
higher.
4. Patients who smoke will need more theophylline, as nicotine increases the
metabolism of the drug.

Other drugs you will commonly see used for patients with colds/cough include
the EXPECTORANTS, MUCOLYTICS, DECONGESTANTS, AND ANTITUSSIVES. An
expectorant that is found in may OTC and prescription medications is
guaifenesin. This drug works by increasing the flow of respiratory tract
secretions. A mucolytic is a drug that makes mucus more water. These are not
very often used first line, as they require inhalation to be administered. Usually,
we would try an expectorant first; however, if the pulmonary secretions were still
thick, a bronchodilator might then be used.

Decongestants are all used to reduce nasal congestion. They are taken either
orally or nasally. Common drug names are pseudoephedrine and phenylephrine.
Because they stimulate the sympathetic nervous system, common side effects
include tachycardia, dysrhythmias, and hypertension.
Antitussives are cough suppressants. The most effective drug on the market is
CODEINE, an opioid; however, it is not often prescribed because of the abuse
potential. The nurse should pay particular attention to use pattern with this
medication. In addition, the patient should be monitored for signs of opioid
toxicity. Nonopioid antitussives include DEXTROMETHORPHAN (known to many
46
as Robitussin and many other brand names). This is a common ingredient found
in OTC medications.

Drugs affecting the Nervous System

Anticonvulsant Drugs:
While there are many types of seizure disorders, we will focus our discussion on
the drugs used to treat generalized seizures. Generalized seizures include the
classic tonic-clonic seizure (used to be called grand mal) and absence seizure
(used to be called petit mal).

Dilantin (phenytoin): Keys to know
1. Used for generalized and other types of seizures. WIDELY USED!
2. It works by decreasing the influx of sodium into the brain cells, thus
decreasing activation of cells and seizure activity.
3. A therapeutic phenytoin blood level is 10-20 mcg/ml.REMEMBER
THOUGH THAT A PATIENT MAY BE TOXIC AND STILL HAVE A NORMAL
LEVELASSESS THE PATIENT, LOOK AT THE LEVEL AND THEN DECIDE
IF TOXIC.
4. Toxicity looks like they have been drinking: they have impaired
gait, may have slurred speech, double vision (diplopia),
nystagmus (jerking of the eyes), and sedation.
5. The nurse should monitor the patients blood sugar. When the
blood level of phenytoin is increased, the blood sugar is more
likely to rise.
6. For the first 2 weeks of drug therapy, they are very sedation. After 2
weeks, this goes away.
7. Chronic phenytoin use can cause gingival hyperplasiaovergrowth of
the gums. This can not only be disfiguring, but painful and cause many
oral health problems. Good oral hygiene and regular dental visits are keys
to prevention.
8. Dilantin should not be taken if there is a concern of pregnancy. If a
pregnant woman has seizures and needs to take Dilantin, this should be
thoroughly discussed with the neurologist, the OB doctor, and the patient.
Fetal hydantoin (phenytoin) syndrome can cause motor and growth
problems after birth, cognitive problems, and deformities of the limbs and
head.
9. Phenytoin can lead to many drug interactions, as it alter metabolism of
some drugs and can compete for albumin binding sites with other drugs.
Always be aware of what medications your patients takes. Be especially
careful with warfarin, cimetidine (Tagamet), and alcohol (acute ingestion).
Toxicity can often result from drug-drug interactions.
10. Noncompliance and drug-drug interactions that can reduce phenytoin
levels are the 2 biggest reason for seizures in patients taking this drug.
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11. WHEN GIVING DILANTIN IV, IT IS CRITICAL THAT YOU KNOW IT
IS ALWAYS MIXED IN NORMAL SALINE (NEVER ANYTHING
ELSE), AND IT IS GIVEN VERY SLOWLY (ABOUT 50 MG/MINUTE
BUT NO FASTER). If pushed fast, the patient can experience
cardiac arrest!!!!!!

Cerebyx (fosphenytoin): this is a prodrug (a drug that gets converted to
phenytoin). It is usually a better choice than Dilantin, as we can give Cerebyx in
other types of IV fluids besides just normal saline, and we can give it faster than
50 mg/min.

Tegretol (carbamazepine) key point to know:
Effectively treats both partial and tonic-clonic seizures. It is now even being
used in bipolar disorder.
It essentially works the same was Dilantin does.
One of the major problems with this drug is the adverse drug reaction of
BONE MARROW DEPRESSION. When this occurs, the white and red blood
cells and the platelets can be reduced, leading to anemia, bleeding,
and infection. This is the reason we check the complete blood
cell count (CBC) on patients during therapy.
This drug, like Dilantin, is involved in many types of drug interactions. One
common interaction is because this drug can increase metabolism of other
drugs in the body, thereby decreasing their levels. Therefore, if a
patient taking other medications has a decreased effect from
those meds, it may be the Tegretol causing it!

Valproic acid (Depakote/Depakene) Keys to Know:
1. This is a commonly used drug for all types of seizure disorders.
2. The major problem with this drug is severe hepatotoxicity, which can
be fatal. Therefore, liver function testing should be done regularly while
patients take this medication.
3. This drug works the same way as Tegretol and Dilantin; however, it also
works by suppressing calcium influx into the brain. Think of valproic acid
as being more broad spectrum in its action than the other drugs.
4. Normal therapeutic level is between 6-12. Toxicity looks much
like phenytoin toxicity.

Management of status epilepticus: It is important that you know about this
condition! It is a medical emergency, as it is a state of continuous seizure and
brain cell death can occur if not treated. We treat this drug BY FIRST
STOPPING THE SEIZURE ACTIVITY.WE USE BENZODIAZEPINES
(ATIVAN MOSTLY) TO DO THIS. Benzos stop the seizure activity very
quickly. After this, an anticonvulsant is given (such as the ones above)this is
48
to keep the patient from seizing again, not to stop the seizure. Once the seizing
starts, only the benzos can stop it!

Benzodiazepines and benzo-like drugs:
These drugs DEPRESS THE CENTRAL NERVOUS SYTEM, therefore, sedation is
the major important side effect to monitor. These drugs work by increasing
GABA, a neuroinhibitory neurotransmitter in the brain.

Common drug names: Xanax (alprazolam), Valium (diazepam), Ativan
(lorazepam), Versed (midazolam), Restoril (temazepam). A trick to remembering
these generic names is that they all end in azolam.

Key points to remember:
Valium, Ativan, and Versed can be used IV to induce anesthesia (this means
they are given before anesthetics to reduce anxiety and cause
preoperative amnesia). Versed is used very often for minor surgical
procedures that allow a semiconscious state. In this way, Versed is used
for CONSCIOUS SEDATION. Procedures using conscious sedation may
include endoscopic GI procedures or GU procedures.
Some patients have been taking benzodiazepines for years and have become
dependent on them. The major drug we see today that has been abused
for years is Xanax! SUDDEN DISCONTINUATION OF THIS DRUG
(AND ALL CHRONICALLY INGESTED BENZOS) CAN LEAD TO
SEIZURE, SO PLEASE DONT STOP THEM SUDDENLY!
The major side effect with these drugs, especially when given IV, is
respiratory depression.
When Restoril or other benzos are used for sleep, a daytime hangover feeling
may occur, as it interrupts the sleep cycle.
These drugs are often used for other conditions such as anxiety, seizures,
drug withdrawal, alcohol withdrawal, and in critically ill patients along with
analgesics.
In patients who have a seizure disorder, rectal Valium can be given at home
for continuous seizures!
Benzodiazepine-like drugs are sleep-inducing drugs such as Ambien
(zolpidem) and Sonata (zaleplon). Again, these drugs depress the
CNS and can cause dizziness and drowsiness.
Drugs such as Klonopin (clonazepam) and Tranxene (clorazepate) are
also used for chronic seizure disorders; however, these are much older
drugs and are not commonly used today.

Barbiturates are similar, yet very different, to benzodiazepines. The main
differences are: 1) Barbs are more addicting, cause more side effects, and more
drug interactions than benzos, and 2) barbs are more fatal if overdosed.

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Keys to know about barbiturates:
1. We dont often use these drugs today; we replaced them with better
drugs that are better tolerated. You might however see a patient on
phenobarbital. This drug might be used in a patient who has had a
seizure disorder for a very long time and they cant be taken off of it.
2. Adverse drug reactions: CNS depression (from sedation to actual
anesthesia), hypotension, and bradycardia (cardiac toxicity).
3. When these drugs are combined with any other CNS depressant (alcohol,
opioids, benzodiazepines), the risk of respiratory depression is very high!


Anticholinesterase drugs:
Understand first that anticholinesterase is NOT ANTICHOLINERGIC. They are 2
entirely different classes of drugs. An anticholinesterase drug works against
cholinesterase, the enzyme that chews up acetylcholine. Therefore, if something
works against this enzyme, we went up with MORE ACETYLCHOLINE, NOT LESS.
I hope that makes sense

We use anticholinesterase drugs to increase acetylcholine in 2 well-known
conditions: MYASTHENIA GRAVIS AND ALZHEIMERS DISEASE.

Myasthenia gravis: This is a neuromuscular condition characterized by
skeletal muscle weakness. There are 2 anticholinesterase drugs used to TREAT
myasthenia gravis, including Prostigmin (neostigmine) and Mestinon
(pyridostigmine).

Keys to know about Prostigmin and Mestinon:
1. They are both used to TREAT myasthenia gravis. This will be important to
remember when we talk about drugs used to DIAGNOSE the condition.
2. When these drugs are used in THERAPEUTIC (normal) oral doses, the
drug will mainly improve NEUROMUSCULAR ACETYLCHOLINE
TRANSMISSION, resulting in improved skeletal muscle contraction.
3. If used in higher than average doses, too much acetylcholine in the
neuromuscular junction will result in loss of contraction.
4. If the dose is too high (acute toxicity), paralysis of the muscles
(including the diaphragm) can occur. If the diaphragm is
paralyzed, the patient cannot ventilate, the CNS is depressed
(the breathing center), and death will result. THIS IS CALLED
CHOLINERGIC CRISIS.
5. In the event of acute toxicity, IV ATROPINE IS THE ANTIDOTE!
Why? Because atropine will block the excess acetylcholine.
6. Because the drug increases acetylcholine, secretions can increase in the
GI tract and in the oral cavity (drooling, diarrhea, nausea), the GU tract
(urinary urgency), and bradycardia can result.
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We also have a drug that allows us to diagnosis myasthenia gravis: Tensilon
(edrophonium). This drug is also an anticholinesterase. It is given to
determine whether a patient is having a cholinergic crisis (too much medication
is causing decreased muscle strength) or if they are having a myasthenic crisis
(the disease is causing decreased muscle strength). If the patient improves after
Tensilon is given, then we know it was a myasthenic crisis.therefore, they need
more daily medications. If the crisis gets worse, we know that this is a
cholinergic crisistherefore, what drug do you think we should give to block all
that acetycholine? If you said atropine, you were 100% right

Note: Antilirium (physostigmine) is another drug you may see. It is the
same as the other anticholinesterase drug above; however, the only use for the
drug is ATROPINE TOXICITY OR TREATMENT OF ANTICHOLINERGIC
DRUG OVERDOSE). So, if a patient comes into the ED with a Benadryl,
Lomotil, or Elavil overdose (these drugs all have anticholinergic side effects), we
give Antilirium to treat the atropine toxicity! Make sense?

Alzheimers disease: In patients with Alzheimers, cholinergic neurons in the
CNS degenerate, reducing the transmission of acetylcholine in the brain.
Therefore, drugs that increase the amount of acetylcholine are used to treat the
condition.

Common drug names:
1. Cognex (Tacrine)
2. Aricept (donepezil)
3. Exalon (rivastigmine)
4. Reminyl (galantamine)

This semester, you will be learning about Cognex, but all of the above drugs
have been approved for Alzheimers disease. Aricept, Exalon, and Reminyl are
much newer drugs.

Keys to know about Tacrine:
1. It has to be taken 4 times per day (short half-life).
2. Food decreases absorptiontake on empty stomach.
3. Serious hepatotoxicity (liver injury) can occur with this drug;
therefore, liver function testing (AST and ALT) is done every 2 weeks for
the first 3-4 months of therapy. If ALT increased to 5x normal, the drug
should be discontinued.

Neuromuscular blockers:
These drugs work by blocking acetylcholine receptors in the SKELETAL MUSCLE,
not in the autonomic nervous system (GI, GU, etc). Recall that in order for
51
skeletal muscle to contract, acetylcholine is mandatory. Without ACH, the
respiratory muscle and the skeletal muscles are nonfunctional. These drugs
work by blocking skeletal and respiratory muscle contraction.

Keys to know:
1. Common drug names:
a. Very short acting drugs: succinylcholine (Anectine). This drug is
usually only given when we need to intubate the patient very
quickly, as the drug will only cause paralysis for about 5 minutes.
b. Intermediate acting (usually given by IV infusion) vecuroniuim,
atracurium, and pancuronium. These drugs are used in anesthesia
and in the ICU to maintain chemical paralysis.
2. Why do we use them: In the ICU or in anesthesia, if we want to
chemically paralyze the patient, we give these drugs. Why would we want
to chemically paralyze a patient? To relax the muscles during surgery, to
reduce the metabolic rate in severe brain injury or critical illness, and/or
to facilitate mechanical ventilation/intubation.
3. Once the patient is given an IV paralytic (neuromuscular
blocker), the WILL NOT BE ABLE TO BREATHE ON THEIR OWN!
This is critical to remember. The patient will need to be ventilated in
order for oxygenation to occur.
4. It is also very important to remember that the patient is PARALYZED, NOT
IN A COMA. They can hear everything going on around them, but they
just cant respond. It is cruel to give paralytics and not to provide
sedation and/or pain relief. Diprivan (a sedative) or Versed are
excellent agents to use along with neuromuscular blocker
infusions.


Psychiatric Drugs

Antidepressants:
There are several classes of antidepressants on the market, including the oldest
ones (tricyclics and MAO inhibitors); however, the SSRI antidepressants and the
atypicals are by far, the most utilized today. Antidepressants will work either by
increasing dopamine, norepinephrine, and/or serotonin in the brain. It is
important to point out that, in general, antidepressants will not begin
to work for at least 4-6 weeks.

Keys to know:
1. Tricyclic antidepressants: Elavil (amitriptyline) is still used today, but
not so much for depression; it is used a great deal for pain, insomnia,
panic disorder, OCD, and ADD.
52
a. Side effects result because this drug class has a chemical structure
that is similar to the phenothiazines (you will study these in a few
minutes when we study antiemetics). THE MAJOR SIDE EFFECTS
ARE SEDATION, ORTHOSTATIC HYPOTENSION
(POSITIONAL HYPOTENSION), AND ANTICHOLINERGIC
EFFECTS (oopshere is acetylcholine again )
b. If taken in overdose, DEATH CAN RESULT RELATED TO
CARDIOTOXICITY AND SEIZURE. The cardiotoxicity is due to the
drugs impact on the cardiac conduction system; therefore,
dysrhythmias can occur.
c. Inform patients that dry mouth, constipation, urinary retention are
all related to the anticholinergic side effects. What nursing
interventions do you think you would perform? Mouth care,
teaching about fluids and fiber.
2. SSRIs This stands for SELECTIVE SEROTONIN REUPTAKE INHIBITORS.
There are so many of these drugs on the market right now, including
Prozac (fluoxetine), Lexapro (escitalopram), Paxil (paroxitine), and Zoloft
(sertraline)just to name a few
a. SSRIs are used for obsessive-compulsive disorder, addiction, and
anxiety, in addition to depression.
b. These drugs inhibit the uptake of serotonin, so more is available in
the synapse, and more gets to the next neuron.
c. Adverse reactions with SSRIs are mainly NAUSEA, HEADACHE,
WEIGHT GAIN, AND SEXUAL DYSFUNCTION.
d. A condition known as SEROTONIN SYNDROME can occur in
patients taking too high of a dose, or in patients combining SSRIs
together (or taking St Johns Wort in addition). This syndrome
includes CONFUSION, DISORIENTATION, HALLUCINATION,
SWEATING, TREMOR, FEVER.
e. Abrupt discontinuation of SSRIs can make a person feel as if they
have the flu.this is called WITHDRAWAL SYNDROME. It will
result in dizziness, headache, nausea, tremor, and anxiety. It can
happen in just days after the SSRI is suddenly stopped.
3. MAO inhibitors: Monoamine oxidase is an enzyme in the brain that
destroys dopamine, norepinephrine, and serotonin. Therefore, the brain
is depleted of these important hormones, and depression can occur. MAO
inhibitors block this process.
a. While they are not first line therapy for patients with typical
depression, they may be initial therapy for patients with atypical
depression, or patients who have not responded to other safe
medications.
b. MAO inhibitors STIMULATE THE CNS; remember that tricyclics
DEPRESSED THE CNS.
53
c. Hypotension is a major side effect of this drug; therefore, when
changing positions, patients should be told to move slowly and not
get up rapidly.
d. Diet restrictions and MAO inhibitors: Patient taking these drugs will
be told to avoid foods high in tyramine (an amino acid that
essentially increased norepinephrine). If these foods are ingested,
norepinephrine increases, and this means that HYPERTENSIVE
CRISIS CAN OCCUR. Foods high in tyramine include aged cheeses,
smoked meats or fish, avocados, figs, pepperoni, salami, imported
beer, Chianti, DIETARY PROTEIN SUPPLEMENTS. Think of foods
you would serve at a party
4. Atypical antidepressants: They are called atypical because they do not
work like other classes of antidepressants.
a. Wellbutrin (buproprion) This drug is similar to amphetamines,
and therefore will suppress appetite, so there is no weight gain
associated with this drug (in fact, patients lose weight). It may
even increase sexual desire and pleasure. The major problem with
the drug is SEIZURE if taken in high doses.
b. Effexor (venlafaxine) Used for both depression and anxiety
disorders. This drug is MORE EFFECTIVE THAN SSRI drugs!!!!
c. Desyrel (trazodone) This drug has very strong sedative effects;
therefore, it is usually used for patients who have depression-
related insomnia. It is not that great of an antidepressant, so it
would not be used alone.

Antipsychotics:
This group of drugs is used for hallucinations, delusions, acute mania, and other
psychoses. Schizophrenia, a chronic psychotic illness, is one of the major
conditions for which patients take these drugs. Schizophrenia results in both
positive (exaggeration of normal function) and negative (loss of normal function)
symptoms. Positive symptoms are mostly the delusions and hallucinations.
Negative symptoms include the social and emotional withdrawal and flat affect.

Medications used for schizophrenia will more than likely be required for life, as
the disease is not curable and can result in psychotic episodes followed by
intervals of partial remission.

There are 2 classifications of antipsychotics: THE CONVENTIONALS AND THE
ATYPICALS. The conventionals are older and can produce serious and
debilitating side effects. On the other hand, the atypical antipsychotics are a
relief for patients with this disease, as they cause few debilitating side effects;
therefore, patients will usually be more compliant.

Keys to know:
54
1. Conventionals: The first antipsychotic ever developed was Thorazine
(chlorpromazine). Haldol (haloperidol) and Prolixin (fluphenazixne) are
other names you will hear a great deal. Haldol and Prolixin can even be
given as a DEPOT INJECTION; this is a long-acting IM injection that lasts
up to 4 weeks. It has been shown to decrease periods of psychotic
relapse.
2. Haldol can be given IM in the event of an acute psychosis or
agitated state. It is beneficial because it is not as sedating as other
antipsychotics.
3. The major adverse drug reactions with CONVENTIONALS INCLUDE:
ANTICHOLINERGIC EFFECTS, SEDATION, AND ORTHOSTATIC
HYPOTENSION. If you recall, many other of the psychiatric medications
we looked at did this as well
4. The most debilitating and sad adverse effects are the EXTRAPYRAMIDAL
SIDE EFFECTS. These side effects consist of different movement
disorders that are caused by blockage of dopamine in the brain (this is
how the psychosis is decreased). Lets look at the disorders:
a. Acute dystonia: Spasm of the tongue, face, neck, back,
extremities. This is dangerous, as it can lead to LARYNGOSPASM
AND AIRWAY COMPROMISE.
b. Parkinsonism: While the drugs dont cause Parkinsons disease,
they can cause a Parkinsons like effect because of the dopamine
blockade. The symptoms look just like Parkinsons, and include
resting tremor, drooling, bradykinesis (slow movement), shuffling
gait, rigidity, and forward posture.
c. Tardive dyskinesia: Perhaps the worst of them all, and certainly
the most debilitating for the patient! It occurs in up to 25% of
patients who take these conventional antipsychotics chronically. It
results in involuntary movements of the lips and tongue, lip
smacking, and protrusion of the tongue intermittently. It can result
in serious nutritional problems, as it interferes with chewing and
swallowing.
5. Atypical antipsychotics: These drugs, as mentioned, have far less
debilitating side effects; however, they are not wonder drugs, they still
have their problems: WEIGHT GAIN AND DYSRHYTHMIAS.
a. Clozaril (clozapine) was the first atypical we had. The major side
effect of this drug IS agranulocytosis, which can lead to life-
threatening infection!
b. Because of the side effect above, Clozaril requires that the patient
have weekly CBCs drawn to check white blood cells. It is not a
drug that is often used today, as we have several newer atypicals.
c. Zyprexa (olanzapine) is a newer atypical that works just like
Clozapine, but no agranulocytosis!
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d. Geodon (ziprasidone) is the newest drug; it can be given orally for
maintenance therapy, or can be given IM for acute psychosis. It
does however have a higher risk of dysrhythmias than the others.
It does not cause weight gain.

Drugs to treat side effects of antipsychotics:
As mentioned, the older (conventional) antipsychotics are well-known to cause
EPS (extrapyramidal symptoms). So, when these occur, how do we treat them?
We treat them with ANTICHOLINERGIC DRUGS. Are you sick of hearing about
acetylcholine yet?

Remember from anatomy/physiology that movement is controlled by both
DOPAMINE AND ACETYLCHOLINE. Recall that EPS are caused by BLOCKAGE OF
DOPAMINE. If dopamine is blocked, then what is the result? Too much
acetylcholine! That was not too painful right . Okay.so we would use an
anticholinergic drug to block the excess acetylcholine. Lets look at some drugs
we have:
1. Benadryl (diphenhydramine) not just for allergies! Recall that is has
anticholinergic properties, so it will work to block excess ACH.
2. Artane (trihexyphenidil)
3. Cogentin (benztropine)

For a patient experiencing acute dystonia (it can be life-threatening),
DIPHENHYDRAMINE IS THE DRUG OF CHOICE!

Mood stabilizers:
Lithium is the most well-known of the mood stabilizers. It is considered a salt,
as it sits right between sodium and potassium on the periodic table of elements
(remember that fun chemistry chart?) Mostly, you will see this drug in bipolar
patients. It is called a mood stabilizer because it relieves symptoms of mania
and depression (the features of bipolar). Also, the medication helps to prevent
recurrences of mania and depression.

Keys to know:
1. Lithium is removed rather quickly from the body; therefore, divided doses
need to be given instead of one large daily dose.
2. If renal function is impaired, lithium toxicity can occur. Also, a blood level
greater than 1.5 mEq/L can result in toxicity.
3. Early toxicity results in HAND TREMORS and EXTREME NAUSEA.
4. Later, toxicity can progress to sedation, hypotension, cardiac
dysrhythmias, and seizure.
5. Death can occur at levels 2.5 or greater.
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6. At therapeutic levels, side effects can be troublesome for the patient, and
include a GREAT DEAL OF NAUSEA, headache, AND THIRST. Thirst and
headache can occur in up to 50% of patients.
7. A troublesome side effect may be a fine tremor of the fingers, which can
interfere with writing, cooking, typing, etc.
8. Since lithium antagonizes ANTIDIURETIC HORMONE, increased urine
output can occur, sometimes even up to 3 L per day. RememberADH
will hold water in. Antagonizing it will let water out.
9. This drug should absolutely not be used during pregnancy (first 3 months)
and lactation. The drug is Category D, the benefits must outweigh the
risks before it is considered.
10. Diuretics promote sodium loss; thereby increasing the loss of
sodium. When sodium is depleted, then lithium thinks it should
stick around (because it acts like sodium). Therefore, lithium
retention occurs and toxicity results.
11. Other mood stabilizers include Tegretol (carbamazepine) and Depakote
(valproic acid), antiseizure medications). Valproic acid can cause
hepatotoxicity, so liver function tests should be monitored.

Drugs affecting the Gastrointestinal System

Stool softeners and laxatives:
There are several categories of laxatives/stool softeners, including the BULK
FORMING LAXATIVES, THE SURFACTANT LAXATIVES, AND THE STIMULANT
LAXATIVES. The osmotic laxatives are ones used to prep the bowel for surgical
procedures, and will not be discussed here.

Common drug names:
1. Bulk forming laxatives: Citrucel (methylcellulose), Metamucil
(psyllium).
2. Surfactant laxatives: Colace (docusate sodium)
3. Stimulant laxatives: Dulcolax or Correctol (bisacodyl), Ex-Lax
(senna).

Keys points to know:
1. You need to know when you would see results (stool) with these
laxatives: remember that the stimulant laxatives work the fastest (6-
12 hours), and the surfactant and bulk-forming laxatives work the
slowest (1-3 days). Therefore, if a patient were uncomfortable due to
retained stool, the stimulant laxative would be the one needed. If you
only wanted to make the stool softer for patients, then the surfactant
laxative would be used.
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2. In the hospital, we dont use a great deal of bulk-forming laxatives, as
drug interactions can occur from the laxative binding the drug and
decreasing absorption.
3. Dulcolax can be given either PO or suppository. PO Dulcolax works in
6-12 hours; however, Dulcolax suppositories act in 15-60 minutes!
4. If you were asked a question about bulk-forming laxatives, know that
you must tell patients to mix with a great deal of water, as these drugs
can cause esophageal obstruction if they are not mixed well. ALSO,
when you mix the bulk-forming laxative with water or juice, it, it must
be administered PO immediately.
5. The most widely abused laxatives are the stimulant laxatives (bisacodyl
and senna), as they stimulate the bowel. The other laxatives do not
stimulate intestinal motility.
6. Laxatives should not be given to patients with ULCERATIVE COLITIS
OR DIVERTICULITIS.


Antidiarrheals:
These drugs will only treat the symptoms of diarrhea, not the underlying cause.
These drugs are considered opioid-related drugs, as you will see in just a minute.

Common drug names:
1. Opium tincture (contains 10 mg morphine)not used often
2. Paregoric (4 mg of morphine)not used often anymore
3. Imodium (loperamide)
4. Lomotil (diphenoxylate)

Key points to remember:
1. Imodium is not considered a controlled substance. However, Lomotil
is an opioid; in high doses, it can cause a morphine-like response.
High doses are very unlikely, unless overdosed. The drug is still
considered a scheduled drug, category V (limited potential for abuse).
2. Lomotil also has anticholinergic side effects (this was done to keep
people from overdosing on it). The side effects are anticholinergic-
related: dry mouth, blurred vision, constipation, and urinary retention.
Therefore, in any patient with glaucoma, vision may worsen and
intraocular pressure may increase.
Lactulose:
Lactulose is a essentially a sugar that cannot be digested. In the GI tract, it is
broken down by bacteria to compounds that end up pulling water into the bowel
and decreasing constipation. However, lactulose is more often used in liver
failure, as it will increase excretion of ammonia. How does it increase ammonia
excretion: it works by drawing ammonia into the colon from the blood.
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Remember.ammonia can get very high in liver failure patients. The major side
effect of this drug is DIARRHEA!

Neomycin:
This drug is an aminoglycoside antibiotic; however, it is not absorbed when given
PO. Therefore, it only works against bacteria in the colon! It is typically given
before a major bowel surgery to decontaminate the bowel. In addition,
neomycin can be used to decrease ammonia in liver failure. It essentially
decreases the activity of the bacteria (remember, bacteria break down proteins
in the colon that then lead to accumulation of ammonia). Since it is not
systemically absorbed, there are few issues of toxicity (unlike giving gentamicin,
another aminoglycoside).

Vitamin K:
Remember that vitamin K is needed to make certain clotting factors and to
eventually clot! In liver failure, the liver is unable to make the clotting factors
and bleeding can occur (GI). If we give vitamin K, we can help this process
along, so bleeding is minimized.

Antiemetics:
Nausea and vomiting can be caused by hormones. The most well-known are
dopamine, serotonin, histamine, and acetylcholine. Some antiemetic drugs block
dopamine, others serotonin, histamine, or acetylcholine. Therefore, as you can
see, there are at least 4 different actions of antiemetic drugs. THEY DONT ALL
WORK THE SAME WAY!

Common drug names are broken down into the action:
1. Antihistamine and anticholinergic: Antivert (meclizine)
2. Serotonin antagonists: Zofran (ondansetron) and Kytril
(granisetron)
3. Anticholinergic: Robinul (glycopyrrolate)
4. Dopamine antagonists: Reglan (metoclopramide), Phenergan
(promethazine), Compazine (prochlorperazine), and Inapsine
(droperidol)

The drugs you will give most often will be the serotonin antagonists and the
dopamine antagonists.

Key points to know:
1. Antihistamine and anticholinergics: Sedation is THE MOST COMMON
side effect. These are used mostly for motion sickness and require
that the drug be taken 1 hour before the nausea-provoking event.
Other side effects are because they block acetylcholine (the
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parasympathetic neurotransmitter).dry mouth, urinary retention, and
blurred vision.
2. Serotonin antagonists:
a. These are the most effective drugs for nausea and vomiting.
b. There is NO SEDATION WITH THESE DRUGS.
c. Because they dont block dopamine, there are no associated
abnormal movements of the face or body. Remember, dopamine
is important to motor control. If dopamine is blocked, motor
abnormalities can occur.
d. These drugs were first used for chemotherapy-related nausea, but
now you see them used for many other types of patients.
3. Dopamine antagonists:
a. Remember, motor problems are a major issue with these drugs
because they block dopamine receptors. These motor
abnormalities can occur in the face, tongue, jaw, neck, or
extremities; they are called EPS SYMPTOMS, or extrapyramidal
symptoms. Remember back to anatomy/physiology that the
extrapyramidal system is in the CNS and helps to control
movement.
b. The most alarming side effects (and more common side effects) in
this class are SEDATION AND HYPOTENSION.
c. Reglan (metoclopramide), although not only used for nausea and
vomiting, also blocks dopamine. Reglan also promotes motility of
the intestine, whereas these drugs do not increase motility.
4. Anticholinergics: scopolamine is the only drug to really talk about in
this class; it is used for motion sickness (similar to Antivert). It can
cause symptoms just like those of Antivert.

Drugs affecting Fluid and Electrolytes or the Renal System

Crystalloids:
Intravenous solutions are classified in many ways. Two types of IV fluids we will
study here include free water and calorie-containing solutions and
crystalloids.

Dextrose 5% in water is an example of a free water and calorie-containing
solution. Once the fluid is given, the dextrose is used for calories and the
remainder is the water. This water is meant to hydrate the body; however, it
will not replace fluid loss from bleeding or other sources. D5W is frequently
given to patients in hospitals as MAINTENANCE FLUID. Patients with
tachycardia, fever, excessive sweating, or fast respiratory rates lose more water
from the body. These fluids cannot be measured however, thus they are called
INSENSIBLE FLUID LOSSES. One reason we give IV solutions to these patients
is to replace these insensible losses. So, the next time you care for a patient
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who is febrile, tachycardic, breathing very fast, or sweating, remember they have
higher fluid loss than normal and can become dehydrated without adequate fluid
compensation.

Crystalloids, on the other hand, will replace fluid lost from the body. One very
common source of fluid loss is bleeding. We can use solutions which
contain sodium chloride and electrolytes to replace these losses. Some solutions
include 0.9% NS normal saline (which is the same as the sodium concentration
of the blood, 0.9%), 0.45% or NS (less than sodium concentration in the
blood), or Ringers Lactate (contains very small amounts of potassium, calcium,
and lactate). These solutions are either isotonic (same sodium
concentration as blood), such as NS, while others are hypotonic (lower
sodium than blood), such as NS. Other solutions are hypertonic
(more sodium concentration than the blood); these would include D5LR, 3%
saline, D5NS, D51/2NS, The reason the dextrose mixed in with the sodium
chloride is hypertonic is because of the sugar molecule (dextrose).

Why might we see NS (0.9% sodium chloride) used? Remember, we use
crystalloids to replace fluid losses. NS is isotonic; therefore, it will match the
concentration of sodium in the blood and will stay in the vasculature, replacing
what has been lost.

NS has a lower concentration of sodium than the blood; therefore, it is
isotonic. This solution might be used as a maintenance fluid, but would not be
used to replace lost fluids.

Hypertonic solutions, such as those listed above, would be a good choice for
postoperative patients. Lets see why: When a patient has surgery, they are
usually given a large volume of isotonic fluids during surgery. Then, after
surgery, we usually switch them to a hypertonic solution (as above). This
hypertonic solution will help to keep more fluid in the blood, as fluid will move
from the interstitium to the vessel in attempt to dilute the plasma.

D5W (dextrose 5% in water) is hypotonic

Plasma-Lyte is similar to LR, but it has more electrolytes. It is a replacement
fluid.

Remember that too much of a good thing can result in consequences The
same is true for IV therapy. Too much fluid can result in overhydration. Some
of the adverse effects associated with overhydration with crystalloids include:

1. Edema: Although we cannot measure interstitial fluid, we can often see
excessive accumulation by assessing for edema.
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2. Dilutional hyponatremia: When we increase plasma volume, we can dilute
the serum sodium. It is not that there is a sodium loss, it is due to
dilution.
3. Effects may be short lived: This means that our crystalloid infusion may
correct the problem in the short run, but not the long run. For example:
The blood pressure may go up and then fall back down, requiring more
fluid.
4. Complications associated with IV therapy: Any time we introduce
something into the body, such as an IV catheter, there is a potential for
infection. Inflammation and injury to the vein (phlebitis) can result from
irritating IV medications. Phlebitis can cause pain and the need to restart
the IV in another location.

Colloids:
Remember that plasma proteins in the blood vessel pull fluid into the vasculature
and away from the ECF. Colloids are products that we can give that resemble
our plasma proteins. They are MUCH MORE EXPENSIVE than crystalloids. The
advantage is that you need much less of a colloid than a crystalloid!

COP = colloidal oncotic pressure (remember?) Remember that COP moves fluid
from the 3rd space to the vasculature. There are 3 major colloids you will see
clinically:
1. Dextran: 40 or 70: This is a sugar-based colloid, not protein based. 70
will last a longer time in the body than 40. This product can cause
allergies and even bleeding.
2. Hetastarch: This is not a protein, it is a starch.
3. Albumin: This is a protein, or true colloid, that has been synthesized from
human donors.

Why might we give these products? To move fluid back to the vasculatureso
situations such as burns, low serum proteins (low albumin), capillary leakage
(from sepsis), plasma volume loss.


Usually these products have few adverse effects; however, because they contain
no clotting factors, bleeding can occur. This is major problem when we give
large volumes of these. In addition, they have no oxygen-carrying capacity;
therefore, if a patients condition has resulted in poor tissue oxygenation, these
will not help us to deliver oxygenwe can only increase perfusion with these
solutions.

If too much albumin is given, or it is given too quickly, this results in a very fast
and powerful fluid shift into the vasculature. When this occurs, hydrostatic
pressure increases in the vessels. In the lungs, increased hydrostatic pressure
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results in leakage of fluid from the pulmonary vessels to the interstitium (space
between the alveoli and the vessels). This can result in fine crackles heard on
exam. In addition, fluid can move into the alveoli, resulting in severe pulmonary
edema.

Magnesium sulfate:
In your second semester of nursing school you learned that magnesium sulfate
was used to relax the uterus. Well, it makes sense if you remember the action
of magnesium! MAGNESIUM DECREASES INTRACELLULAR CALCIUM
CONCENTRATION! Remember, calcium increases smooth muscle contraction.
If we block calcium from entering smooth muscle, then guess what? You get
relaxation of smooth muscle. This could be the smooth muscle of the uterus or
the arteriole, right? Pretty easy?

Another reason you may use it in OB is for prevention of seizure in eclampsia! It
is actually the drug of choice in this situation!

So, while magnesium sulfate can be used in OB, it can also be used for cardiac
patients as well. We just saw how this would make sense! In the cardiac
patient, we might use it for patients who are in cardiac arrest and are not
responding to anything else. It may work in arrest situations such as this
because low magnesium levels can actually cause cardiac dysrhythmias;
therefore, giving IV magnesium sulfate can bring the patient out of the
dysrhythmias.

Phoslo:
Remember, in renal failure, patients cannot excrete phosphorus, and therefore,
calcium levels can drop (remember the relationship between calcium and
phosphorus?). Therefore, when phosphorus rises in these patients, we can give
phosphate binders. These work by decreasing absorption of phosphate,
therefore, if little phosphate is getting absorbed, the blood level will eventually
decrease. Remember also that in renal failure, patients should decrease
phosphorus in their diet! This is why!

Buffers:
The major buffer we will cover is SODIUM BICARBONATE. While this drug is
given for lots of different reasons, one major reason is HYPERKALEMIA. This is
how it works: if potassium is high, the sodium bicarbonate will make the blood
pH more alkalotic! In alkalosis, more hydrogen is trying to come into the blood
to buffer the blood, and thus something must be exchanged. Guess what is
exchanged? Potassium. Potassium is taken into the cell as hydrogen leaves the
cells and comes into the blood. This is how we can treat hyperkalemia (know
that there are other ways too such as insulin and glucose). Insulin forces the
potassium into the cell!
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Sodium bicarbonate can also be used to raise the pH of the blood in severe
acidosis. In most cases, we try to fix the problem causing the acidosis before we
actually give the bicarbonate; however, we cant do this all the time. In some
extreme cases, we cant correct certain patients pH levels and we must use
sodium bicarbonate.