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EXAM 1
BASIC PRINCIPLES OF PHARMACOLOGY:
-When asked about a drug or want to know about a drug, focus on these things: Name of Drug, Why is this pt taking this
drug?, Efficacy & toxicity?, What will be given instead of this drug if it doesn’t work?

PHARMACOLOGY: The study or science of drugs. It encompasses a variety of topics & has several subspecialty areas.
Drug: any chemical that affects the physiologic processes of a living organism. These are used to
- Prevent, dx, or treat signs, & disease processes & relieve sxs to improve quality of life & ability to perform ADLs.
There are difference subspecialty areas: pharmaceutics, pharmacokinetics, pharmacodynamics, Pharmacogenetics,
pharmacoeconomics, pharmacotherapeutics, pharmacognosy, & toxicology.

Classifications:
- Effects on body systems
- Therapeutic uses (heart disease, angina, HTN, etc)
- Chemical characteristics
Drug Prototype:
- Individual drug that represents a gp of drugs.
- The standard by which newer, similar drugs are compared.
- Some prototypes replaced over time by newer, more commonly used drugs.
Drug Names:
- Generic name: related to chemical or official name & independent of manufacturer.
- Trade/brand name: aka proprietary name; drug’s registered trademark. It indicates that its commercial use is
restricted to the owner of the patent (manufacturer) for the drug.
- Generic drugs must meet the same standards, same mg & pharmacokinetics, etc. Some brand companies
actually make their own generic meds. Generic drugs are the same or sometimes even better than the brand
drug. However, we do have to watch out for the therapeutic range because it might be smaller.
Access to Drugs: ALL DRUGS CARRY A RISK
- Prescription- physician, dentist, NP, etc. All rx drugs are dangerous & controlled.
- OTC: available w/o prescription outside hospital (in hospital, every med requires an order!). Some meds in some
states are ‘pharmacist dispense”, such as pseudoephedrine.
- CDS- controlled dangerous substances- abuse & risk potential
Controlled Substances: There are schedules I-V categorized according to therapeutic usefulness & potential for drug
abuse. The HIGHER the RISK, the LOWER the number.

SCHEDULE ABUSE MEDICAL DEPENDENCY POTENTIAL DISPENSING EXAMPLES

POTENTIAL USE RESTRICTIONS

CI High None Severe Only with Heroin, LSD, marijuana,

physical/psychological approved protocol peyote, etc

C II High Accepted Severe RX ONLY, warning Codeine, cocaine,

physical/psychological label, & no refills hydromorphone, etc

CIII Less than C II Accepted Moderate RX expires in 6 Codeine w/ others meds

physical/psychological mts. No more (acetaminophen),
than 5 refills hydrocodone, etc
within 6 mts.
Warning label

CIV Less than C III Accepted Limited RX expires in 6 Phenobarbital, chloral

physical/psychological mts. No more hydrate, meprobamate, etc
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than 5 refills
within 6 mts.
Warning label

CV Less than C IV Accepted Limited RX or OTC Meds for relief of coughs or

physical/psychological diarrhea containing limited
quantities of certain opioid
CS

Nurse’s responsible for: Storing CS’s in locked boxes/draws/machines, administering them only to pts for whom they
were prescribed, recording each dose given on narcotic sheets & pt’s MAR, maintaining accurate inventory, reporting
discrepancies to proper authorities.

3 AREAS OF PHARMACOLOGY: PHARMACEUTICS, PHARMACOKINETICS, & PHARMACODYNAMICS

1. PHARMACEUTICS: the study of how various dosage forms influence the way in which the drug affects the body;
How dosage forms influence the way in which the body metabolizes a drug & the way in which the drug affects
the body.
a. Liquids- absorbed faster
b. Suspensions- particles suspended in liquid; MUST shake well!
i. Ex. Pt w/ seizure took meds & was doing well. Then seizures started again & doses were ↑.
Then pt came in w/ toxicity issues. The problem was that the suspension wasn’t being shaken
well. All med was going to the bottom, so top didn’t have enough med & bottom had way more
than needed.
c. Solids - convenient
- If it cannot be crushed, what alternatives exist? *IV can actually be given via NGT!*
- Even if pill was made with a unit of pressure higher than usual that can affect how long it takes the medication
to be absorbed (it will take longer!)
- Fastest TO Slowest: Oral disintegration, buccal tablets, & orals soluble wafers, liquids , elixirs, & syrups,
suspensions solutions, powders, capsules, tablets, coated tablets, enteric-coated tablets.
- Dosage Forms:
a. Enteral: tablets, capsules, oral soluble wafers, pills, timed-release capsules/tablets, elixirs, suspensions,
syrups, emulsions, slns, lozenges/troches, rectal suppositories, sublingual/buccal tablets.
b. Parenteral: Injectable forms, slns, suspensions, emulsions, powders for reconstructions
c. Topical: aerosol, ointments, creams, pastes, powders, slns, foams, gels, transdermal patches, inhalers,
rectal & vagina suppositories.
- Oral meds- Extended Release formulations: Designed to release drug molecules in the pt’s GI tract over a
prolonged period of time. It requires fewer daily doses & promotes pt compliance. THESE SHOULD NOT BE
CRUSHED because it can case accelerated release of drug & possible toxicity.
a. SR- slow/sustained release
b. SA- sustained action
c. CR- controlled release
d. XL- extended length
e. XT- extended time
2. PHARMACOKINETICS: What the body does to the drug molecules. Movement of drug through the body to reach
sites of action, metabolism, & excretion.
a. ABSORPTION: movement of a drug from its site of administration into bloodstream, for distribution to
the tissues.
- Rate of med absorption: how soon the med takes effect
- Amount of medication absorbed: determines intensity
- Route: affects rate & amount of absorption
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1. Bioavailabity: term used to express the extent of drug absorption for a given drug &
route. It is the amount of drug that reaches the systemic circulation.
2. First pass effect: Initial metabolism in the liver of a drug absorbed from the
gastrointestinal tract before the drug reaches systemic circulation through bloodstream.
This reduces a drug’s bioavailability. Occurs with many PO meds.
a. Liver chemically processes a large proportion of a drug into inactive metabolites
so a much smaller amount of drug actually passes into circulation.
b. NTG is given SL to avoid this issue.
3. Extra Notes:
a. Use oral meds if possible because they have fewer side effects.
b. DO NOT do IM if pt’s on anticoagulants
b. DISTRIBUTION: refers to the transport of a drug by the bloodstream to its site of action. Drugs are
usually distributed to areas w/ extensive blood supply.
- Altering Distribution
1. Blood Brain Barrier is composed of capillaries with tight walls & that limits the
movement of drug molecules into brain tissue. BBB protects the CNS. You can have the
best med that can kill a virus but if it can’t get to the site of action IT DOES NOT matter.
It’s a big issue w/ antibiotics
a. Meds need to be lipid soluble OR have a transport system that can cross BBB &
reach therapeutic concentrations in brain tissue
- Unbound drugs are pharmacologically active whereas bound drug (to a plasma protein) is
pharmacologically inactive.
1. Most drugs form a compound w/ plasma proteins, mostly albumin, which act as carriers.
2. Only the FREE UNBOUND drugs freely distribute to tissue to reach site of action, be
metabolized in liver, & be cleared by kidney.
3. The more protein bound, the less active; the more free, the more active
- Extra Notes: Distribution is the reason why weed may be positive in some tests even after not
smoking after a few days. It distributes well in fat & leaves very slowly.
c. METABOLISM: biotransformation- involves the biochemical alteration of a drug into an inactive
metabolite (a more soluble cpd, a more potent active metabolite), a more potent active metabolite
(conversion of a prodrug into its active form), or a less active metabolite
- LIVER is the most imp organ in this step but also occurs in the skeletal muscle, kidneys, lungs,
plasma, & intestinal mucosa also play a role.
1. Those w/ liver dysfxn have ↓ ability to metabolize medication & are at risk of
accumulation of med & possible toxicity.
- Hepatic Metabolism: involves the activity of cytochrome P-450 enzymes aka microsomal
enzymes. These control a variety of rxns that aid in the metabolism of medications. Largely
targeted at lipid-soluble- non polar meds (lipophilic).
1. P450 is a family of metabolic enzymes, which may induce or inhibit. Watch out with
these meds because there are many drug interactions. They need to be checked 3x,
clear w/ MD & document what is told. PREVENT the Swiss cheese effect.
a. ↑ metabolism= less drug
b. ↓ metabolism= more drug levels in blood Toxicity
2. P450 is one of the most important systems that influence drug-drug interactions.
a. Drug metabolizing groups: CYP1, CYP2, CYP3
b. Chronic use of some drugs stimulate liver to produce larger amounts of these
enzymes- ENZYME INDUCTION
i. Accelerate drug metabolism which may lead to needing larger doses of
drugs to reach therapeutic levels
ii. Enzyme induction does not occur for 1-4 wks after an inducing drug is
started since new enzyme proteins must be synthesized
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c. Enzyme Inhibition: can ↓or delay metabolism.

i. Often occurs w/ concurrent use of 2 or more drugs that compete for the
same metabolizing enzymes
ii. Occurs within hrs or days of starting an inhibiting drug
iii. Smaller doses of the slowly metabolized drug may be needed to avoid
adverse effects & toxicity from drug accumulation
d. Pharmacogenetics affect inh/induction- i.e. Asians & alcohol
- Consequences of medication metabolism:
1. Increased renal excretion of meds
2. Inactivation of meds
3. Increased therapeutic action- enalapril (see below-prodrug!)
4. ↓ toxicity when active forms of meds are converted into inactive form
5. ↑ toxicity when inactive forms of meds are converted to active forms
- Prodrugs: medication is metabolized to a more active form- i.e. enalapril
1. These drugs are initially inactive, exert NO pharmacological effects until they are
metabolized, increase the selectivity of the drug to its target organ, & are frequently
used in chemotherapy agents.
- Metabolism is affected by 1st pass effect & age.
1. Infants have limited medication-metabolizing capacity
2. Metabolism tends to decline w/ age, less drugs are cleared
- Nutritional status: malnourished pt may be deficient in factors that are necessary to produce
specific medication-metabolizing enzymes & that may impair medication metabolism
d. EXCRETION: elimination of drugs from the body. KIDNEY is the main organ in this process but liver &
bowel play a role as well. Drugs can be active or inactive when excreted
- Pts w/ renal dysfxn need to be monitored for ↑ in duration & intensity of medication responses-
monitor serum creatinine
- SERUM DRUG LEVEL: Laboratory measurement of amount of drug in the blood at a particular
time. It can help predict efficacy & serum level related side effects (NOT ALL SIDE EFFECTS ARE
RELATED TO DRUG LEVELS, some are idiosyncratic- like allergies)
1. Serum Drug Level Monitoring: plasma medication levels can be regulated to control med
responses. It is rare when they ask to check blood levels of drugs. If a drug is used for
BP, then BP will be checked not blood levels.
2. THERAPEUTIC RANGE: level at which most experience efficacy & toxicity is minimized.
You want to make sure you’re not above (toxicity) or below
e. HALF-LIFE: the time required for ½ of a given drug to be removed from the body. It is a measure of the
rate at which the drug is eliminated from body. Determined by drug’s rate of metabolism & excretion.
Most drugs are considered to be removed from body after 5 half-lives. It reflects how often you have to
give drugs
- Steady State: The physiologic state in which the amount of drug removed via elimination is
equal to the amount of drug absorbed with each dose. When this state is reached consistent
levels of drug in the body that correlate w/ max therapeutic benefits
- Short Half Life: meds leave quickly 4-8 hrs. Short dosing interval of minimum effective
concentration will drop between doses.
- Long Half Life: Meds leave body more slowly (24hrs). There’s a greater risk for medication
accumulation & toxicity. Meds can be given at longer intervals w/o the loss of therapeutic
effects. Meds take long to reach steady state.
f. ONSET, PEAK, & DURATION: these are DRUG EFFECTS, the physiologic rxns of the body to the drug.
- Onset of action: time required for the drug to elicit a therapeutic response.
- Peak Effect: time required for a drug to reach its maximum therapeutic response
- Duration of action: length of time the drug concentration is sufficient (w/o more doses) to elicit
a therapeutic effect.
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- Peak Level: highest blood level; if too high drug toxicity can occur.
- Trough Level: lowest blood level.
- Therapeutic Drug Monitoring: process of measuring drug levels to identify a pt’s drug exposure
1. allow adjustment of dosages w/ the goals of maximizing therapeutic effects &
minimizing toxicity.
3. PHARMACODYNAMICS: What the drug does to the body. Describes the clinical effects resulting from
interactions between medications & target cells, body systems, & organs to produce effects. I.e. NSAIDs- alter
inflammation, renal fxn, platelet fxn
a. Lock & Key Theory: Drugs act by forming a chemical bond w/ specific receptor sites, similar to a key &
lock. The better the fit, the better the response.
i. Drugs w/ complete attachment & response are called AGONISTS.
ii. Drugs that attach but do not elicit a response are called ANTAGONISTS.
iii. Drugs that attach, elicit some response, & also block other responses are called PARTIAL
AGONISTS or AGONIST-ANTAGONIST

DRUG-DRUG INTERACTIONS: Occur when the presence of one drug decreases or increases the actions of another drug
that is given at the same time. When 2 medications are highly protein-bound medications may compete for the binding
sites on the protein. Leading to more free, unbound drug. A basic cause of many drug-drug interactions is altered
metabolism.
1. Interactions: alteration of the action of one drug by another, which could be beneficial or harmful. These can
increase the therapeutic or adverse effects of drugs.
a. Additive Effects: (1+1=2) when 2 drugs with similar actions are given together. PHARMACODYNAMIC
EFFECT. Ex, alcohol & sedative drug
b. Synergistic Effects: when 2 drugs administered together interact in such way that their combined effects
are greater than the sum of the effects for each drug given alone. Ex, acetaminophen & codeine.
c. Antagonistic effects: when the combination of 2 drugs results in drug effects that are less than the sum
of the effects for each drug given separately. Ex, naloxone & opioid
d. Incompatibility: most commonly used to describe parenteral drugs. This occurs when 2 parenteral drugs
or slns are mixed together & the result is a chemical deterioration of one or both of the drugs or the
formation of a physical precipitate. Ex, parenteral furosemide & heparin.
- Any IV sln w/ drugs that appear cloudy of visible particulates should be discarded. IV’s are
usually clear except for a few (TPN)
2. Drug-Diet interactions- some drugs reduce food absorption, some foods can decrease or increase drug
absorption, some foods contain substances that react w/ certain drugs (ex. Grapefruit juice inhibits the
metabolism of drugs normally metabolized by CYP3A4)
a. It’s important to check the foods visitors may bring
3. ADVERSE EFFECTS OF DRUGS: any undesirable occurrence involving medication administration. Adverse effects
may produce any sx or disease process & may involve any body system or tissue. May be common or rare, mild
or severe, localized or widespread.
a. FDA Black Box Warning: BBW- drugs that have caused serious or life-threatening adverse effects. FDA
requires manufacturer to place warning on label.
b. Adverse Drug Rxns: ADR is any rxn to a drug that’s unexpected & undesirable & occurs at therapeutic
drug dosages.
- Pharmacologic Rxn: an extension of the drug’s normal effects in the body
- Allergic Rxn: aka hypersensitivity rxn, involves the pt’s immune system. Immunoglobulins
recognize the drug molecules, its metabolites, or other ingredients as a dangerous foreign
substance. An immune response may occur. NOT RELATED TO AMOUNT OF DRUG
- Idiosyncratic rxn: occurs unexpectedly & is determined abnormal response to normal dosages of
a drug.
4. Contraindication: any pt condition that makes the use of the given medication dangerous for the pt. Ex,
penicillin is not given to a pt who is allergic to it.
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5. Precautions: should be taken for a pt who is more likely to have an adverse rxn than another pt.
a. Morphine depresses resp fxn, it should be use w/ caution for pts who have asthma or impaired
respiratory fxn
6. Variables that affect drug responses:
a. Body Wt: meds absorbed & distributed in body tissue. Pt w/ greater body mass may require larger doses
b. Age
c. Gender: females may respond differently to meds than males due to a higher proportion of body fat &
the effects of female hormones
d. Genetics: genetic factors such as missing enzymes can alter metabolism of certain medications can
enhance or reduce medication actions.
e. Children: doses based on wt, BSA, maturation of organs. Certain meds are based on age due to greater
risk for ↓ skeletal bone growth, acute cardiorespiratory failure, or hepatic toxicity.
a. Older adults:
i. Absorption: Gastric pH is less acidic due to ↓ in HCl production, gastric emptying & gastric
movement is slowed because of a decline in smooth muscle tone & motor activity, blood flow to
GI tract ↓ because CO & perfusion is ↓.
ii. Distribution: There is a reduction in the total body water content w/ aging, fat content increases
because of ↓ lean body mass, protein binding sites are ↓ because of ↓ production of proteins
by the aging liver & reduced protein intake
iii. Metabolism: Levels of microsomal enzymes ↓ because the capacity of the aging liver too
produce them is reduced & liver blood flow is reduced which decreases hepatic metabolism.
iv. Excretion: GFR ↓ due to ↓ blood flow & the # of intact nephrons ↓
7. PREGNANCY: Almost every med given to pregnant women will be distributed to fetus as well. Teratogenesis
(structural damage to fetus) most likely to occur in 1st trimester
a. Meds are classified according to potential harm to fetus:

CATEGORY DESCRIPTION
A No risk to the human fetus
B Studies indicate no risk to animal fetus; no human info available
C Studies report effects to animal fetus; no human info available
D Possible risk to human fetus has been reported; however in selected cases consideration
of the potential benefit vs risk may warrant use of these drugs during pregnancy
X Fetal abnormalities have been reported. These are not to be used in pregnant women

8. DRUG THERAPY DURING BREAST FEEDING: Drug properties including fat solubility, low molecular wt,
nonionization, & high concentration increase the likelihood of drug transfer via breastfeeding. However,
medication concentration is usually too low to have an effect on the breastfeeding infant. Giving the med right
after breastfeeding will minimize medication concentration in the next feeding.

Administering Medications:
1. SIX RIGHTS OF MEDICATION ADMINISTRATION:
a. RIGHT DRUG: check specific order against medication label/profile 3x before giving meds:
1. When nurse reaches for the container or unit dose package
2. After retrieval from the drawer & compared w/ CMAR, or compared w/ CMAR
immediately before pouring from a multidose container
3. When replacing the container to the drawer/shelf, or before giving unit dose med to pt
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ii. Verbal orders: prescriber must sign order within 24 hrs. These are often used in emergencies &
time-sensitive pt care situations.
b. RIGHT DOSE: always confirm if it’s appropriate age & size & also check if it’s a normal dosage range.
c. RIGHT TIME: give meds within 30 mins before or after prescribed time. STAT meds need to be given
immediately within 30 mins. Military time is written.
d. RIGHT ROUTE: Never assume the route.
e. RIGHT PATIENT: check pt’s identity (name, DOB, check band).
f. RIGHT DOCUMENTATION: always assess pt’s chart for date & time of med administration, med name,
dose, route, and site of administration; may also be made in the regularly scheduled assessments for
changes in sxs pt’s experiencing; may reflect improvements. These also need to be reported to
prescriber. Other things that need to be documented include if a drug was not administered & why,
refusal of medication w/ reason of refusal, actual time of drug administration, data regarding clinical
observations & treatment of a pt if med error has occurred.
2. Common Med errors: wrong med, IV fluid, wrong pt, route or time, administration of known allergic medication,
omission of dose, incorrect discontinuation of med or IV fluid.
a. High alert meds are potentially toxic therefore require special care when prescribing, dispensing, &
administering.
i. Ex.: adrenergic agonists, adrenergic antagonists, anesthetic agents, antidysrhythmics,
cardioplegic slns, insulin, oxytocin, etc.
EXTRA NOTES:
- Herbal products are not drugs! Ads will never say a herb ‘treats’ or ‘prevents’ something. It is important for a
nurse to ask about what herbs, dietary supplements, or OTC a pt is using!

CARDIOVASCULAR PHARMACOLOGY

HYPERTENSION

- Common disease affecting many ppl; CHRONIC disorder; ↑ risk for developing MO, HF, Kidney disease, & stroke.
a. JNC 8:
▪ 60yo who do not have DM or CKD, the goal blood pressure is now <150/90 mmHg
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▪ 18 to 59 yo w/o major comorbidities, & in pts 60 yo who have DM, CKD, or both, the new goal
BP is <140/90 mmHg OR 130/80
b. American Society of HTN & International Society of HTN:
▪ Adults older than 18- SBP over or equal to 140 mmHg or DBP over or equal to 90 mmHg, or
both, on repeated examination.
▪ Aged 80 or older- SBP up to 150 mmHG is now acceptable
- There is pre-hypertension: 120 mmHg-139 mmHg, or diastolic pressures between 80-89 mmHg. It’s not treated
w/ BP meds, lifestyle changes are encouraged instead in hope to delay or prevent progression to HTN
- Stage 1: 140-159 mmHg or DBP 90-99 mmHG
- Stage 2: SBP over or equal to 160 mmHg or DBP over or equal to 100 mmHg.
- PRIMARY: most pts have this one; idiopathic or essential, may be asymptomatic for years- UK CAUSE
- SECONDARY: resulting from specific disorder- tumors, renal disease, etc.
- BP: important to evaluate pt with the right size cuff, position pt properly, may need to take BP in different
positions to evaluate effects of medications, & multiple readings over several week are needed to dx HTN.
a. Blood Pressure (BP)= Cardiac Output (CO) x Systemic Vascular Resistance (SVR)
▪ CO: amount of blood that is ejected from LV; measured in L/m
▪ SVR: resistance to blood flow that is determined by diameter of vessel & vascular musculature
▪ Renin system also works on BP:
● Aldosterone causes Kidneys to retain Na & water, which ↑blood volume & CO = ↑ BP.
Meds take several weeks to see max benefits; initial effects are seen within hrs. May cause orthostatic hypotension or
first dose hypotension. Also often used to treat other cardiac disease states or may worsen other cardiac disease states.
1st Line HTN meds: Thiazide diuretics, Calcium Channel blockers, ACE Inhibitors, Angiotensin Receptor blockers
2nd Line HTN meds: Beta Blockers, Alpha blockers, alpha 1/beta-blockers, central alpha 2-adrenergic agonists, direct
vasodilators, loop diuretics, aldosterone antagonists
- Common receptors involved in the pharmacologic control of HTN:
a. Beta-1: myocardium; stimulation of this receptor will increase the force & rate of contraction (positive
chronotropic [heart rate] & inotropic [force of contraction] response)= CONSTRICTION- blocking this
receptor causes ↓ of force/rate of contraction of heart= DILATION
b. Beta-2: in body- bronchi & uterus. Stimulation causes relaxation while blocking it will cause constriction
c. Alpha-1: stimulation of this receptor causes vasoconstriction in peripheral blood vessels. Blocking this
receptor will result in vasodilation.
d. Presynaptic alpha 2: stimulation decreases catecholamines output
e. Renin: stimulation of this causes an increase in production of vasoactive substances

A. DIURETICS: decrease plasma & ECF volumes, thus ↓ preload, CO, & total peripheral resistance, with overall effect of
↓ workload of heart & ↓ BP. There are 3 types thiazide, loop, & potassium sparing.
1. THIAZIDE: HYDROCHLOROTHIAZIDE & CLORTHALIDONE- primary for HTN
a. Mechanism of action:
i. Work by impairing active reabsorption of Na + Cl at the distal tubule.
ii. Cause direct relaxation of the arterioles decreasing peripheral resistance. HOWEVER, it is NOT
considered a vasodilator, they just have that effect
iii. Na is excreted & water follows
iv. Ability to promote diuresis depends on kidney fxn (so w/o for pts w/ renal issues). CrCl
(creatinine clearance) must be >25-30 ml/min in order to rx Thiazide diuretics
b. Pharmacokinetics:
i. These are only available in PO form-tablets & oral slns.
ii. Diuresis occurs 2 hrs after administration- if a pt on diuretics rings bell, do not make them wait
iii. Peaks 4 to 6 hrs
iv. Lasts 6-24 hrs
c. Monitoring Parameters:
i. BP, HR- if HR ↑ too fast, pt is dehydrated or BP is going ↓ too fast
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ii. Potassium (↓), Mg (↓) , Calcium (↑), glucose (↑, w/o w/ diabetics), lipids, electrolytes.
iii. Watch out with these pts in the summer because pts sweat & if they sweat too much & are on
diuretics, there is a risk of losing too much fluid.
d. Drug interactions:
i. Digoxin: hypokalemia; ↑ digoxin toxicity
ii. Lithium (used in depression meds): decreased clearance; ↑ lithium toxicity
iii. SULFONAMIDE based diuretic-watch out for pts w/ allergies

2. LOOP DIURETICS: FUROSEMIDE, BUMETANIDE, TORSEMIDE

a. Mechanism of action: Generally used for HF instead of HTN
i. Inhibits passive resorption of Na at the descending limb of the loop of Henle causing an increase
in the excretion of sodium. It is more potent than thiazide since it ↓ BP quicker a thiazide
however, it is for less time & causes loss of more fluid
b. Pharmacokinetics: Oral & IV formulations available. Speed of IV needs to be slow. It can cause
ototoxicity.
c. Monitoring parameters:
i. BP, HR, urine output
ii. Potassium (↓), Mg (↓), calcium (↓), glucose (↑), lipids (↑)
iii. Fluid in/out, wt (if dropping quickly=dehydrated)
iv. HYPOKALEMIA: <3.5 mEq/L; muscle weakness, constipation, cardiac arrhythmias, cramping,
tingling, numbness, nausea, confusion, drowsiness, alkalosis, shallow respirations, lethargy
1. Decision needs to be made regarding K+ supplements.
2. w/o for IV K+ because it burns- rate needs to be slow
d. Drug interactions:
i. Digoxin: hypokalemia; ↑ digoxin toxicity
ii. Lithium (used in depression meds): decreased clearance; ↑ lithium toxicity
iii. it is a SULFONAMIDE based diuretic-watch out for pts w/ allergies

3. POTASSIUM SPARING DIURETICS: cannot be used alone for HTN because they do not cause enough
diuresis/fluid loss. Most often used in combination w/ a thiazide diuretic to decrease the risk of hypokalemia.
- Spirinolactone, Eplerenone, Triamterine
a. Aldosterone receptor blockers: these also block actions of aldosterone  Na excretion
b. Caution with ACE inhibitors, ARB’s, & if taking K supplements- these ↑ K+ levels
i. W/O for new salt, it contains K+ instead of Na
NURSING ACTIONS:
- Monitor pt’s I/O & serum electrolyte levels regularly
- Daily wt to evaluate pt’s response to diuretic therapy
- Give diuretic in AM to ensure that major diuresis occurs before bedtime
- Keep urinal/bedpan within reach of pt or ensure that bathroom is easily accessible
- Be alert for potential drug interactions
- Be alert for potential Hyperkalemia with potassium sparing diuretics
- Monitor lab results for electrolyte imbalance
- Monitor for adverse effects
- Pt education

B. BETA ADRENERGIC BLOCKING AGENTS= BETA BLOCKERS: Used for HTN, angina, etc.
- Beta 1 Blockade: act on myocardium to ↓ conduction, contraction, & workload- relaxation= ↓ HR + force-
decreases force & rate. (Remember stimulation of Beta1 causes constriction/ blockage  dilation)
- Beta 2 Blockade: act on to produce bronchoconstriction of the smooth muscle of the respiratory tract by
blocking beta 2 receptors (Stimulation causes relaxation)
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a. Relatively B1 selective: these prefer to only block B1 and not B2 as well- given to people w/ asthma since
these have less risk of causing bronchial constriction
▪ Atenolol (Tenormin)
▪ Metoprolol (Lopressor, Toprol XL)
b. Non selective: these block both b1 & b2. Have to watch out w/ asthmatic because these meds can cause
an acute asthma attack since blocking b2 receptors on bronchi causes bronchoconstriction.
▪ Carvedilol (Coreg)- (alpha & beta blocker as well)
▪ Labetalol (alpha & beta blocker as well)
▪ Nadolol (Corgard)
▪ Propranolol (Inderal)
These are not used first line for HTN but are used first line based upon comorbid disease states or in other disease states
such as angina, CHF, arrhythmias, stage fright, essential tremor.
- BBs were never used for HF pts because these would worsen it (heart is already not working at its max capacity
why would you want it to slow down even more?) but now it is used because it can also be beneficial
Adverse effects/monitoring parameters:
- Onset/duration- you’ll see effects right away BUT max benefits are seen in 1-2 wks
- BP/HR
- Issues relating to the diabetics*- when body notices there is ↓ glucose, liver will break down glycogen into
glucose. This requires a beta adrenergic effect- catecholamines. When a pt is taking a BB, the meds will also
block the catecholamines therefore a pt may not experience tremors, shaking, as they would normally do when
experiencing hypoglycemia when not taking BBs.
- Sedation exacerbation of CHF, sexual difficulties*, bradycardia, bronchospasm, pt may feel tired & sluggish
- Need to taper the dose up & down
- Often used w/ other meds
Extra notes: for pts experiencing glaucoma there are BBs in eye drop form since oral forms won’t treat this. These eye
drop BB can also worsen HF like regular BBs. – Timilol

C. ANGIOTENSIN-CONVERTING ENZYME INHIBITORS & ANGIOTENSIN II RECEPTOR BLOCKERS

- ACE inh block the angiotensin converting enzyme from
converting Angiotensin I to Angiotensin II therefore inhibiting
vasoconstriction + Na & H2O retention which lead to ↑ BP.
- ARB’s compete w/ Angiotensin II for receptor sites blunting
the effects of angiotensin II.
- These are NOT diuretics (they do not ↑ urine output)
although they ↓ volume.
- They are vasodilators. DO NOT USE together to their
synergistic effects. Can use w/ diuretics CCCs, or BBs though

1. ACE INHIBITORS: block the enzyme that converts AI to AII in turn causing vasodilation & ↓ aldosterone
production resulting in vasodilation, excretion of Na, & retention of K.
a. Has beneficial effects on heart (↓ remodeling) & kidneys (↓ proteinuria). Also has beneficial effects in
diabetic kidney disease.
i. REMEMBER: BBs mask hypoglycemia & thiazide & loop diuretics ↑ glucose. ACE inh are safe to
give to DM pts.
b. ‘PRILS’- captopril (capoten), enalapril, lisinopril, fosinopril
i. Often used in combo w/ a thiazide
ii. Used once or 2x/d
iii. Used for HTN but it’s also beneficial in diabetes & CHF.
c. Monitoring parameters of efficacy & toxicity:
i. BP
ii. Hypotension w/ initial dosing (have pt take medication at bed time)
 11

1. Always start w/ low dose then increase

iii. Disease dependent
d. CANNOT be used during pregnancy
e. May cause:
i. Hyperkalemia- Monitor carefully
ii. Cough- dry & non productive
iii. Angioneurotic edema- mouth, tongue, throat swell up- MEDICAL EMERGENCY- rare; AA have
higher risk than Caucasians
iv. Reversible acute renal failure in pts w/ renal artery stenosis-major ppl at risk
v. Dehydrated ppl are at risk as well.
vi. ATI notes: Neutropenia can be caused as well; can ↑ lithium levels as well
- Extra notes:
a. How much K+ is in a banana? Approx 422mg.
b. How much in orange juice? Approx 470-493 mg
▪ To convert mg to mEq Formula= mEq=mg/atomic wt x valence
▪ AW of K+ is 39 and valence is 1

2. ARB’S: compete with AII for receptor sites, ↓ AII effects causing vasodilation & ↓ aldosterone production
resulting in vasodilation, excretion of Na, & retention of K. Used for HTN, not used in pregnancy
a. Monitoring for efficacy & toxicity: many pts go straight to using these instead of ACEIs
i. Use specific BP vs CHF
ii. Hyperkalemia, reversible acute renal failure in pts w/ renal artery stenosis, dehydration pts are
at risk as well, do not use in pregnancy. (ATI: lithium levels can increase as well)
iii. Rare to cough- so some pts are going straight to using ARBs & not using ACE inhibitors
iv. Rare angioedema
b. ‘SARTAN’: losartan, valsartan, irbesartan, candesartan, olmesartan.
c. Losartan:
i. Metabolized in liver by cytochrome p450 system, max effects may not be seen until 3 weeks
from starting, less likely to cause cough than ACE inhibitors, contraindicated in pregnancy

D. CALCIUM CHANNEL BLOCKING AGENTS: used for HTN, angina, arrhythmias. These prevent calcium from entering
cells.
- CCB’s have different effects on CV system. Some act to promote vasodilation, some ↓ vascular resistance, some
have effect of heart & blood vessels, some have effect on rate & contractility. There are the dihydropyridines &
the non-dihydropyridines.
- ALL CCB’s cause CONSTIPATION since these decrease action on the smooth muscle of the intestines.
1. NON-DIHYDROPYRIDINE: VERAPAMIL & DILTIAZEM
a. Decrease BP by decreasing force & rate of contraction & also cause vasodilation. HOWEVER they are
NOT considered BBs. These can be used in pts w/ asthma & DM. Not used in pts w/ HF.
b. CCB at arteries & arterioles of heart causes ↑ coronary perfusion.
c. CCB at SA node ↓ HR
d. CCB at AV node ↓ AV nodal conduction (that’s why they are used for prevention/treatment of Afib)
e. First line treatment of HTN due to their effectiveness & safety
- Monitoring efficacy & toxicity:
a. BP, HR
b. Pedal edema (CHF)- since it also affects force & rate it can worsen CHF & cause pedal edema
c. Constipation
d. Rash
e. Pedal edema due to vasodilation- leakage syndrome: when fluid falls out of vessel
f. Verapamil may ↑ digoxin levels- 60%
g. BBs are generally not used in combo because they may ↓ HR too much
 12

h. Grapefruit interaction: it increases the amount of medicine that enters your blood stream. As a result,
your blood pressure can drop very suddenly.
i. PR intervals: AV node conduction; you can see heart block
2. DIHYDROPYRIDINES: AMLODIPINE (Norvasc) & NIFEDIPINE (Procardia)
a. Vasodilators
b. DO NOT DECREASE FORCE & RATE OF CONTRACTILITY – so do not worsen HF
c. Also used to treat angina
- Monitoring efficacy & toxicity:
a. BO, HR
b. CV: hypotension, palpitations, tachycardia
c. GI- constipation
d. Other: rash, flushing, peripheral edema (pedal edema), dermatitis

E. ANTI-ADRENERGICS:
a. Alpha-1 Receptor blockers: Stimulation= constriction; Blockage=relaxation/dilation. These act by blocking
the alpha 1 receptors. Lowering BP by dilating blood vessels & ↓ peripheral vascular resistance. Second line
for HTN.
i. First dose effect of hypotension. To counteract this give first dose at bedtime. There is risk of falling
if pt gets up fast.
ii. May also lead to sodium & fluid retention.
- Prazocin (Minipress): also used in PTSD
- Doxazosin (Cardura): used in BPH pts to shrink prostate even if they do not have HTN
- Terazosin (hytrin): also used in BPH pts

b. Centrally acting alpha agonist- alpha 2 blockers: these inhibit the release of norepinephrine in the brain
hereby decreasing sympathetic NS stimulation. 2nd to 3rd line for HTN.
i. Clonidine (catapress): ↓ HR & vascular stimulation
1. May be given transdermal (wkly)- therapeutic levels in 2-3 days. They also have it oral form
2. Also used in :
a. Drug addicts who are experiencing withdrawal- since the sxs include ↑HR, agitation,
etc. This med can help calm those sxs
b. Also used in kids w/ ADHD: given at night because it may cause sedation
i. GUANFACINE (TENEX)
3. Monitoring parameters:
a. BP, HR
b. Sedation
c. Depression
d. Dry mouth
e. REBOUNG HTN*- do not stop abruptly
ii. METHYLDOPA: used in pregnant pts with HTN or in females w/ HTN who are trying to get prego

F. DIRECT ACTING VASODILATORS: HYDRALAZINE (APRESOLINE) & MINOXIDIL- LAST LINE MEDS FOR HTN
a. Side Effects: headaches, tachycardia, hypotension, syncope, sodium-water retention
b. Minoxidil: hypertrichosis- increased hair growth
c. CONTRAINDICATIONS: severe coronary artery disease, cerebral edema
________________________________________________________

ANGINA:
Angina Pectoris: Clinical syndrome characterize by episodes of chest pain caused by deficit in oxygen supply→ ischemia
- Patho: arteriosclerotic plaque develops & narrows the lumen of the blood vessel
1. Stable Angina: classic effort induced angina
 13

2. Unstable Angina- aka pre-infarction or crescendo angina; occurs w/ plaque rupture that partially occludes the
artery. It causes intermittent pain that can take place even at rest & during sleep
3. Vasospastic angina- aka Prinzmetal’s or variant angina; occurs at rest or w/ any precipitating cause
Therapeutic Objectives:
- ↓ morbidity & mortality
- Minimize the frequency of attacks & ↓ the duration & intensity of pain
- Improve pt’s functional capacity with as few adverse effects as possible
- Prevent or delay the worst outcome: MI
MEDICATIONS: NITRATES/NITRITES, BB’S, & CCB’S.
A. NITRATES/NITRITES: vasodilators; relaxes smooth muscle promoting vasodilation.
a. Decreases preload (primary mech) & causes coronary vasodilation- primarily peripheral vessels
i. ↓ fluid load back to heart
b. Lowers BP- decreases cardiac workload.
i. Think of the heart as a rubber band, the more it’s stretched the more work (O2) it’ll need. So
nitrates prevent that & decrease preload.
c. Indications: relieves acute angina pain & prevents exercise induced pain (prophylactic)
d. Route of administration:
i. SL, buccal, transdermal-
1. TO AVOID FIRST PASS EFFECT; when given oral it is metabolized & only small amounts
make it to circulation
2. Patient Education: store in glass bottle, do not store in fridge (moisture messes with the
meds), remove cotton & do not put back
3. Side Effects: headache, hypotension, drug interactions, flushing
ii. SL works within 1-3 mins & lasts 60 mins- NOT USED AROUND THE CLOCK, IT’S FOR ACUTE PAIN
1. There is also a spray that can go SL for pts with dry mouth
iii. Transdermal patches are effective 4-8 hrs- put on in am because that’s when ppl move around
therefore start getting pain. Take off at night to prevent tolerance (good for 12-16 hrs)- hairless
part of body; this is to prevent pain & it is maintenance therapy
iv. There is a paste as well, that can be put on, but has to be removed. It is messy.
e. Side Effects of Nitrates: hypotension, dizziness, lightheadedness, tachycardia, palpitations, headache
f. Contraindications: severe anemia, closed angle glaucoma, hypotension, severe head injury, use of
erectile dysfxn (SHOULD NOT BE USED IF PT IS TAKIN VIAGRA DUE TO RISK OF HYPOTENSION & MI)
g. NTG RELATED MEDS:
▪ Isosorbide dinitrate (isordil)- generic version used SL as well instead of NTG
▪ Isorsoride mononitrate: used for prevention (around the clock), used instead of cream or patch

B. BETA BLOCKERS: act to block stimulation of the B receptors of the heart. They ↓ the workload of the heart
thereby ↓ pain. Used in long term management, NOT for acute episodes. Prescribed when nitrates alone are
not effective. These DO NOT work on Prinzmetal’s angina.
a. Contraindications:
i. Second or third degree heart block
ii. Severe bradycardia
iii. Cardiogenic shock- remove patch!
C. CALCIUM CHANNEL BLOCKERS: As a gp they stop coronary artery spasm & cause vasodilation. Used for
prevention not acute. These treat prinzmetal angina.
a. VERAPAMIL & DILTIAZEM: ↓ coronary artery spasm, force & rate of contraction, & cause vasodilation
b. & AMLODIPINE & NIFEDIPINE: ↓ coronary artery spasm & cause vasodilation

Nursing Considerations:
- Monitor HR, BP before administration of each drug
- Monitor number & severity of angina episodes
 14

- Use with cautions in pts with hepatic or renal dysfxn

- Educate pt to avoid alcohol & grapefruit juice
- If using transdermal patch rotate sites
CHF
HF: heart is unable to pump enough blood to meet metabolic demands of body. Characterized by inadequate
tissue perfusion. Sxs of this are: SOB, fatigue, & exercise intolerance. Plus signs of fluid overload: venous
distention, edema, pulmonary edema.
Classification:
a. Mild: no limitations on physical activity or sxs of disease
b. Severe- sxs occur at rest & there’s structural damage of the heart
MEDS: Diuretics, ARBs, ACEIs, BBs, Cardiac Glycosides

A. DIURETICS: act by reducing blood volume↓ preload, CO, total peripheral resistance ↓ venous & arterial
pressure, pulmonary & peripheral edema, & causing cardiac dilatation- heart works more efficiently
a. LOOP- SEE ABOVE***
b. POTASSIUM SPARING: for CHF used to prevent long term deterioration. May lessen K+ ↓ but it’s not
used for this in CHF pts, these prevent long term deterioration
i. Aldosterone receptor blockers: Spirinolactone, Eplerenone
1. Block aldosterone receptors therefore its effect
2. Reduce retention of sodium & water
3. Major side effect:
a. Hyperkalemia-potentiated by ACEI or ARB
b. Spironolactone may cause gynecomastia
c. Extra Note: HF causes RAAS to ↑ aldosterone levels

B. ACEI: block the angiotensin converting enzyme from converting Angiotensin I to Angiotensin II therefore
inhibiting vasoconstriction + sodium & water retention which lead to increased BP.
a. LOOK ABOVE FOR MORE INFO

C. ARBS: compete w/ Angiotensin II for receptor sites blunting the effects of angiotensin II.
a. LOOK ABOVE FOR MORE INFO

D. BBS: action is by blocking SNS stimulation to the heart & cardiac conduction system. ↓ Excessive stimulation &
↓ chances of dysrhythmias. Protect heart from catecholamines from hitting & destroying it. Used to prevent
deterioration, no acute benefit in CHF
i. Side Effects: fluid retention, HF worsening sxs, fatigue, hypotension, bradycardia, heart block
b. Carvedilol (Coreg)- non selective
c. Metoprolol (Lopressor): B1 selective

E. CARDIAC GLYCOSIDES: oldest gp of cardiac drugs- DIGOXIN (Lanoxin, Lanoxicaps, Digitek)

a. Foxglove plant- Digitalis purpurea or Digitalis Lanata
b. Positive inotropic rxns: increases the force of ventricular contractions ↑ CO- reducing sxs
c. This increases renal flow, ↓ renin release
- Digoxin: decreases SA node firing & AV node conduction and affects Purkinje fibers
a. Given orally or IV
▪ Oral onset- 30 mons to 2 hrs
▪ IV- 10-30 mins, peak effects 1-5 hrs
▪ Loading dose (or digitalizing dose) may be given for Afib. This has ↑ toxicity
b. Pharmacokinetics:
▪ Very narrow therapeutic range- .8-2ng/ml
▪ Absorption can vary depending if it’s tablet (60-80%) or capsule (90-100% but more expensive)
 15

▪ Different foods or brands or drugs can affect absorption

▪ Eliminated by renal system
▪ Decreased urine output= ↑ digoxin levels
▪ Half-life is 1.5 days:
● Takes about 6 days to reach plateau & about 6 days to be completely eliminated; renal
insufficiency is a problem.
▪ Therapeutic Range: monitor closely since it is only slightly lower than the toxic does. Toxicity
may occur at any level- depends on renal fxn
● Draw levels 6-8 hrs after does, just prior to next dose is preferred.
o Distribution takes a while. If drawn right after giving dose then the levels will be
toxic because those are the levels in plasma- has not reached heart yet. Toxicity
occurs on the heart not plasma. It is better to be measured at trough level
c. Interactions:
▪ Decreased absorption in cardiac glycosides may be caused by medications such as: antacids,
antidiarrheal, sucralfate & others. It may also be caused by frequent consumption of bran
▪ The following slow down digitalis excretion: amiodarone, quinidine, nifedipine, verapamil.
● Dosage of digitalis may be lowered to account for this decrease in excretion
▪ Some herbs such as Siberian Ginseng may ↑ digitalis levels
d. Digoxin Toxicity:
▪ GI effects: anorexia, nausea & vomiting*
▪ CNS: fatigue, visual disturbances (halos; Van Gogh may have had too. Toxicity of digoxin include
seeing yellow & green halos), blurred vision, yellow tinge to vision
▪ ECG changes: AV block/PR prolongation, arrhythmias (may be lethal)
▪ Hypokalemia: increases risk of digoxin toxicity
▪ Bradycardia
e. Conditions that may increase this risk of toxicity:
▪ Hypokalemia-monitor K & other e- levels closely (makes myocardium more sensitive to dig)
▪ Decreased renal fxn
▪ Advanced Age: due to ↓ body mass & ↓ renal fxn
▪ Hypomagnesemia
▪ Liver disease
f. Digoxin Immune Fab: Used for life threating digitalis toxicity (toxicity of dig occurs in myocardium)
▪ Antibody that recognizes digoxin as antigen & forms an antigen antibody rxn w/ drug thus
inactivating it
▪ This binds to digoxin in the plasma digoxin leaves heart cells to go into plasma to maintain an
equilibrium more fab binds to digoxin
▪ Once given, digoxin levels can up or down depending if level drawn is free or total
● Free dig will ↓ because DIB is binging to it. However, TOTAL (includes the bound med)
will ↑ (not active unless it’s free)
g. Nursing management of suspected Digoxin toxicity:
▪ Hold the dose
▪ Notify provider
▪ Plan to being cardiac monitoring
▪ Expect serum digoxin levels & serum electrolytes to be ordered
▪ Expect digoxin fab to be ordered
▪ Ask provider to call poison center & get them involved

Miscellaneous Meds Used for HF:

1. HYDRALAZINE/ISOSORBIDE (BIDIL):
o Combination of 2 meds
o First drug approved for a specific group, African Americans
 16

o Important to monitor BP
o Evaluate for syncope esp. with initial dosing
2. DOBUTAMINE (DOBUTREX):
o Beta-1 elective vasoactive adrenergic drug
o Stimulates the beta-1 receptors in the heart
o ↑ cardiac contractility & output
o Given by IV ONLY
o Indicated in severe HF
3. B-TYPE NATRIURETIC PEPTIDE:
o Newest class of meds for HF
o Prototype drug: Nesiritide (Natrecor)
o Synthetic hormone (recombinant version of the human) that has vasodilating effects
o Given by IV ONLY
o Indicated for life threatening HF in the intensive care setting
4. PHOSPHODIESTERASE INHIBITORS:
o Have an inotropic & a vasodilation effect referred as INODILATORS
o 2 Drugs: Milrinone (primacor)
o Used primarily in the intensive care unit for short term management of HF
o Given by IV ONLY
o Adverse effects are ventricular dysrhythmias, hypotension
o Make sure to monitor HR, RR, I&O, Hypokalemia
HYPERLIPIDEMIA DRUGS
- Risk of developing CHD is directly related to ↑ levels of low-density lipoproteins (LDL’s)- the higher the levels,
the higher the risk
Cholesterol: component of all cell membranes; required for the synthesis of certain hormones (estrogen, progesterone,
testosterone, adrenal corticosteroids) & bile salts
- Sources: dietary sources, manufactured by cells, primarily in liver (body makes it!), hydroxymethylglutaryl
coenzyme A (HMG-CoA) reductase (enzyme necessary for the synthesis of cholesterol).
Dyslipidemia- Hypercholesterolemia
- Elevated serum cholesterol levels
- Primary dyslipidemia: genetic or familial disorder of lipid metabolism
- Secondary dyslipidemia:
a. ↑ serum cholesterol related to dietary intake of saturated fat
b. Disease process- DM, alcoholism, hypothyroidism, obesity, obstructive liver disorder
c. Medications: (not a significant change if these meds are stopped though) beta blockers, cyclosporine,
oral estrogens, glucocorticoids, sertraline, thiazide diuretics, AIDS protease inhibitors
- Dietary Measures:
a. ↑ in dietary cholesterol: small ↑ in serum cholesterol; also inhibits endogenous cholesterol synthesis
b. ↑ circulating cholesterol; saturated fats are a substrate for cholesterol production by liver
c. Dietary changes will NOT ↓ cholesterol greatly
- Lipoproteins: There are 6 major classes
a. VLDL: TGs
b. LDL: mostly cholesterol; bad cholesterol; greatest contributor to CHD
c. HDL: good cholesterol
d. Triglycerides: levels above 200mg/dL is an independent risk factor for CHD
▪ High levels are associated w/ metabolic syndrome, DMII, obesity, sedentary levels, high carb
intake, smoking, excessive alcohol consumption, pancreatitis
Hyperlipidemia: elevation of blood lipid levels. Risk for atherosclerosis, CAD,
production of thromboses
 17

- Total Cholesterol levels are not used to determine treatment, LDL levels are
- HDL & LDL are treated independently
- There are new guidelines have: depending on how much LDL needs to be ↓
- The higher the LDL, the more aggressive the treatment

Therapeutic Lifestyles Changes: diet, wt control, exercise, smoking cessation; important things to discuss w/ pt
Drug Therapy: drugs used should also ↓ morbidity & mortality
- HMG-CoA reductase inhibitors- statins
- Bile-acid sequestrants
- Nicotinic Acid (Niacin)
- Fibrates
- Omega 3 FA (fish oil)

A. HMG-COA REDUCTASE INHIBITORS- STATINS- most effective for ↓LDL, morbidity & mortality, therapeutic goals
a. Fewer side effects
b. Six statins available: these reduce LDL & slightly increase HDL
i. ATORVASTATIN (LIPITOR)- mostly used
ii. LOVASTATIN (MEVACOR)
iii. FLUVASTATIN (LESCOL)
iv. ROSUVASTATIN (CRESTOR)
v. PRAVASTATIN (PRAVACHOL)- not as potent
vi. SIMVASTATIN (ZOCOR)
c. MECHANISM OF ACTION: inhibits HMG-CoA reductase, the enzyme that catalyzes the early rate-limiting
step in cholesterol biosynthesis
d. Effects: ↓ if LDL significant within 2 wks w/ max benefits within 6-8 weeks. Best taken at night because
theoretically lipids are made at night. Plus these pts are probably on other meds, so why not give this
separately
e. Pharmacokinetics: absorption 30-90% dependent of the drug. Potency varies for each statin. Most of the
absorbed drug is extracted from the blood on its first pass through liver-main site where statins work
f. STATIN METABOLISM: Big fear of the P450 metabolized drugs is if these drugs being ind/inh metabolism
by other drugs. Since pravastatin is not metabolized by P450, there is less risk of its metabolism being
inhibited or induced.
i. If another drug is given (besides the statin) that is an INDUCER to a CYP, then the statin will be
metabolized more leading to ↓ levels in plasma & cholesterol will. If the other drug is a CYP
inhibitor then the levels of the statin will ↑ & can lead to toxicity
ATORVASTATIN (LUPITOR) CYP3A4
FLUVASTATIN (LESCOL) CYP2C9
LOVASTATIN (MEVACOR) CYP3A4
PRAVASTATIN (PRAVACHOL) Not metabolized by p450 system
SIMVASTATIN (ZOCOR) CYP3A4
ROSUVASTATIN Minimal CYP2cp & 2C19
PITAVASTATIN Minimal CYP2c8 & 2C9

g. Adverse effects:
i. Mild & usually transient: headache, rash, GI disturbances
ii. Serious side effects: myopathy/rhabdomyolysis & hepatotoxicity
1. Get LFT’s before starting statins then repeat when clinically needed
a. ↑ ALT & AST= liver damage
 18

2. Keep an eye out for CPK for severe muscle breakdown, the ↑ dose the ↑ the risk
a. This can lead to renal failure because muscle breakdown leads to myoglobin in
urine. High levels of myoglobin are associated w/ renal failure
h. Contraindications: acute liver disease, unexplained persistently elevated LFTs, pregnancy (category X),
breastfeeding
i. Drug Interactions: RISK VS BENEFIT*
i. Fibrates & Ezetimbe: these also cause myopathy
ii. Agents that inhibit p450 enzymes
1. Statin specific: cyclosporine, macrolide antibiotics, azole antifungal drugs, HIV protease
inhibitors, grapefruit juice, combining drugs could also potentiate dosage of statin drug

B. BILE-ACID SEQUESTRANTS- second line drugs great alternative to pts who cannot take statins
- Sequestrants bind to bile acids in the intestine & are eliminated in stool. The liver then produces more bile to
replace lost bile. Because the body needs cholesterol to make bile, the liver uses up the cholesterol in the
blood ↓circulating LDL. Also ↑ HDL & TG’s circulating in blood; ↓USED IN GI not absorbed by body
a. CHOLESTYRAMINE (QUESTRAN), COLESTIPOL- older agents- powdered form, messy to use, taste nasty
b. COLESEVELAM- newer, better tolerated- tablet form
c. Allowed in pregnant women; can be used in conjunction with a statin or niacin
d. Adverse effects: constipation, GI effects (abd discomfort, bloating), ↓ uptake of fat-soluble vitamins
e. Drug interactions: forms complexes w/ other drugs in GI so prevents the absorption of those (thiazide
diuretics, digoxin, warfarin, some antibiotics).Take other drug 1 hr before or 4 hrs after bile-sequestrant
f. Nursing Actions:
▪ Monitor Pt: Adverse rxn & drug interactions; Fat-soluble vitamin deficiency (A, D, K, E, folic acid)
▪ Pt education: knowledge of drug therapy, s/s of adverse rxns, encourage lifestyle changes

C. FIBRATES: most effective drug for ↓ TG’s

a. GEMFIBROZIL (LOPID), GENOFIBRATE (TRICOR)
b. Occasionally used alone, most frequent used in combo with a statin
c. Effects: ↓ TG’s & VLDL levels, ↑HDL cholesterol, little to no effect on LDL levels
d. MOA: ↑ the oxidation of FAs in liver & muscle tissue ↓ hepatic production of TGs
e. Therapeutic Use: main indication for use is TG levels of >500mg/dL
f. Adverse effects: rashes, GI, gallstones (don’t see this in other drugs), myopathy & liver injury (risk would
be greater when used w/ a statin)
g. Drug Interaction: displaces warfarin from plasma albumin & ↑ anticoagulant effects
h. Administration: oral meds, 30 mins before breakfast & dinner

D. NICOTINIC ACID (NIACIN): NIACOR, NIASPAN, VIT B3; ↓reduce LDL & TG levels,↑ HDL more than any other drug
a. MOA: ↓ VLDL (TG) production which leads to ↓ in LDL
b. Therapeutic Use: usually used in combination w/ another dyslipidemic drug (BAS or fibrate)
c. Adverse Effects:
i. Skin (flushing, itching)- when started or when dose ↑
1. Intense flushing of face, neck, ears in mostly ALL pts
2. Can be reduced by taking small doses & gradually ↑, take with meals, take 325 mg
aspirin @ 30 mins before taking niacin
ii. GI, Hepatotoxicity, Hyperglycemia, affect platelets, hyperuricemia

E. CHOLESTEROL ABSORPTION INHIBITOR: EZETIMBE (ZETIA)

a. Used as an adjunct to diet modification, ↓ TC & TG, small ↑ in HDL
b. MOA: acts on cells in small intestine to inhibit cholesterol absorption & blocks absorption of dietary
cholesterol & cholesterol secreted in bile
 19

c. Adverse Effects: hypersensitivity (rash)-most common, myopathy/rhabdomyolysis (watch out with

statins), hepatitis, pancreatitis, thrombocytopenia

HIGH CHOLESTEROL TREATMENT

- Drug selection is based on type of dyslipidemia & its severity
- LDL levels will return to pretreatment values if drugs are withdrawn- treatment is lifelong
- Just because these ↓ cholesterol, it does not mean it also ↓ morbidity & mortality
- MONOTHERAPY:
a. To ↓ cholesterol- statin is preferred
b. To ↓ cholesterol & TGs: statin, cholesterol absorption inhibitor, gemfibrozil, or niacin
c. To ↓ TGs: gemfibrozil, CAI, or niacin
▪ Gemfibrozil, rather than niacin, preferred in diabetics because niacin causes hyperglycemia
- COMBINATION DRUG THERAPY: when monotherapy is not effective
a. To ↓ total & LDL cholesterol:
▪ Statin combined w/ CAI or BAS
▪ Niacin with BAS
- To ↓ total & LDL & ↑ HDL: statin combined w/ fibrate, CAI, niacin
- WATCH OUT*:
a. Fibrate + Statin- ↑ risk of severe myopathy
b. Niacin & statin: ↑ risk of hepatotoxicity

Nursing Actions:
- Assess pt’s cholesterol level before therapy
- Monitor Blood cholesterol & lipid levels
- Monitor drug’s effectiveness by checking cholesterol & TG levels every 4 wks
- Monitor pt for adverse rxn & drug interactions
- Monitor for fat soluble vitamin deficiency A, D, E, K
- Pt education:
a. Therapy Knowledge
b. S/S of adverse rxns
c. Encourage lifestyles changes