Level II

Pharmacology Outline Review Notes

I.

II.

III.

IV.
V.
VI.

VII.

Chapter I Drug Action:

Drugs that are taken by mouth go through three phases
Pharmaceutics Phase: A PO drug has to become a solution so that it can pass through
biological membrane. This process is called dissolution. If a drug is administered
intravenously, intramuscularly or subcutaneously there is no
Pharmacokinetic Phase : There are four phases to this process
A. Absorption
B. Distribution
C. Metabolism
D. Excretion or Elimination
Pharmacodynamic Phase: Is the study of drug concentration and its effect on
body. Drug response can be primary effect or a secondary physiological effect.
A. Think Onset of action-Is the time it takes the drug to reach minimum effect
concentration
B. Time of Peak effect of the drug -Time that it takes for drug to reach its highest blood or
plasma level
C. Duration- The length of time the drug has a pharmacological effect.
Agonist: Drugs that produce a response
Antagonist: Drugs that inhibit/block a response
Categories : There are four
A. Stimulation/or Depression- either the drug stimulates of depresses a cell or a glands
activity.
B. Replacement- drug replaces an essential body compound like insulin
C. Inhibition or killing of Organism- think antibacterial or anti- fungal agents
D. Irritation-here think of laxatives causing intestinal irritation to stimulate peristalsis.
Side Effects / Adverse Reactions and Toxic EffectsA. Side Effects- physiological effects not related to the desired effect of the drug.
B. Adverse Reaction- Anaphylaxis They must always be reported & documented.
C. Toxic effect/Toxicity- can always be identified by drug plasma levels.

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Chapter 2: Nursing Process and Client Teaching

I.

Nursing Process has four phases

A. Assessment/Diagnosis- Data collection involves both Subjective and Objective. Should be
focused on symptoms & organs most likely to be affected by clients drug therapy
1. Subjective- Current Healthy history, client verbalized symptoms, current medications
(dosage, route, frequency, & prescribing physician), clients knowledge of their
medications, drug allergies, clients compliance of drug regimen, over the counter
supplements, past medical history, clients environment, and their support system.
2. Objective Gross and fine motor movement, ROM, laboratory results, diagnostic
studies, clients height weight and other physical assessment values temperature, pulse,
blood pressure and respirations.
B. Planning- Setting of the goals for the patient and developing interventions to help patient
to accomplish them.
1. Goals should always follow SAME:
2. Specific for this patient
3. Action oriented
4. Measurable ( and in a specific time frame)
5. Evaluation- is able to continually be evaluated and revised as necessary.
C. Implementation- this would be our Nursing actions
REMEMBER OUR NURSING RESPONSIBILITY IS TEACHING !

Chapter 20 Central Nervous System Depressants

I.

II.

III.

Sedatives/Hypnotics: Often are prescribed for treatment of insomnia

Remember that dreams occur during Rapid Eye Movement stage of sleep.
A. They are the mildest form of CNS depressants are our sedative drugs.
B. They do not affect the consciousness.
Barbiturates 1900s were introduced as a sedative.
A. Long acting - Phenobarbital
B. Intermediate Acting- Butabarbital (Butisol)
C. Short- Acting Secobarbital ( Seconal) & Pentobarbital (Nembutal) {Prototype}
D. Ultra Short Acting- Barbiturate, Thiopental (Na Pentothal)
Benzodiazepines minor tranquilizer or anxiolytic. Class IV according to Controlled
Substances Act. They the action of the inhibitory neurotransmitter gamma-aminobutyric
acid (GABA) to the GABA receptors. Neuron excitability is . Also of the
Benzodiazepines except temezepam can cause vivid dreams/nightmares. Should not be
used for longer than 3 to 4 weeks. Remember that it is recommended that with renal or
hepatic dysfunction smaller doses should be used.

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IV.

V.

VI.

A. Chlordiazepoxide (Librium) class IV. Used also for treatment of alcohol withdrawl
syndrome DTs, anxiety and tension. For anxiety usual PO dose is 5-25mg t.i.d. or
q.i.d. For alcohol withdrawl PO/IM/IV 50-100mg max. 300mg/d
B. Flurazepam (Dalmane) {Prototype}
C. Temazepam (Restoril)
D. Triazolam ( Halicon)
E. Lorazepam (Ativan)
{Prototype} used for treatment of mild to moderate
anxiety. PB 85-95%, t 3.5- 21 hr.
F. Diazepam (Valium) used to manage anxiety, muscle spasms status post
epilepticus. PO/IM/IV 2-10mg b.i.d.- q.i.d. For Post epilepticus IV 5-10mg q 10-20
min. max. 30mg
Non benzodiazepines Used for short term insomonia (< 10 days duration)
a. Zolpidem (Ambien) .Duration is 6-8 hrs. with a short t1/2 of 2 to 2.5 hrs. M
a. Metabolized in the liver to 3 inactive metabolites and excreted in bile, urine, and
feces.
Chloral Hydrate- It is used to induce sleep and decrease nocturnal awakenings. Fewer
occurrences of hang-over, resp. depression, and tolerance. Effective in older clients. It can
be given to patients with mild hepatic dysfunction, but should be avoided if liver or renal
failure is severe.
Anesthetics - Two classifications
1. General Anesthetic depresses the CNS, alleviates pain, and causes loss of
consciousness. One of the first ones used was Nitrous Oxide (laughing gas)
1. Four Stages of Anesthesia1st stage is Analgesia (induction stage) (consciousness and goes to loss of
consciousness. Loss of sensation of smell and pain occur.
2. 2nd stage is Excitement Or Delirium produces loss of consciousness caused
by depression of the cerebral cortex. Confusion, excitement or delirium occurs.
3. 3rd stage Surgical Surgical procedure is performed during this stage.
4. 4th stage Medullary Paralysis Toxic stage of anesthesia Resp. are lost &
circulatory collapse occurs. Must be on Ventilator.
2. Inhalation Anesthetics- used during the 3rd stage, inhalation gases are used. Some
like Nitrous Oxide are absorbed quickly, have rapid action but also eliminated
quickly. Some examples in the 1950s and later are Halothane, Methoxyflurane,
Enflurane ,Isoflurane, Desflurane, and in 1995 Seroflurane.
Inhalation agents are usually combined with a barbiturate, a strong analgesic like
morphine, and a muscle relaxant like pancuronium.
Potential adverse effects are respiratory depression, hypotension, dysrhythmias,&
hepatic dysfunction.

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3. Intravenous Anesthetics May be used for induction with addition of inhalation

anesthesia or in an outpatient setting for procedures with an anticipated short
surgical time.
a. Midazolam (Versed)
b. Propofol (Diprivan)- this drug supports microbial growth & may risk for
infections. Open vials should be discarded after 6 hours to prevent sepsis.
4. Topical Anesthetics- Available in many different forms. Decrease the sensitivity of
the nerve endings to the affected/injured area.
5. Local Anesthetics These drugs block pain at the site where the drug is
administered, allowing for consciousness to be maintained. Beneficial in many
minor procedures. Consist of two main groups Esters and Amides.
a. Esters Short Acting - Chloroprocaine (Nesacaine), Procaine HCl (Novacain)
which both is effective for (1/2-1hr.).
Long Acting -Tetracaine (Pontocaine), which is effective for (3-10 hr.)
b. Amides Low incident of allergic reactions. Lidocaine Hydrochloride
(Xylocaine) has a rapid onset and long duration of action. Labeled as Moderate
acting (1-3 hr.) Another example would be Prilocaine (Citanest).
Long Acting Bupivacaine (Marcaine & Sensorcaine)
6. Spinal Anesthesia use of local anesthetics injected in the subarachnoid space at
L3-4. Potential complications could be respiratory distress if anesthetic is injected
or travels to high in the spinal column, headaches due to leak of cerebral spinal
fluid.
a. Spinal Nerve Block local anesthetics is injected into the 2nd layer of the
spinal column subarachnoid membrane
b. Epidural Block- local anesthetic is injected into the outer covering of the
spinal column the dura mater.
c. Caudal Block- anesthetic is placed near the sacral area. A
d. Saddle Block anesthetic placed near the lower end of the spinal column to
numb the perineal area.

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Chapter 24 Anti-inflammatory Drugs

Inflammation -is our bodys normal protective response to neutralize and destroy harmful
agents at the site of tissue injury.
Infection- is caused by the presence of microorganisms and results in inflammation, but NOT
all inflammations are infections
I.
Five Cardinal signs of Inflammation - because cardinals are red!
A. Erythema - Redness occurs in the 1st phase of inflammation. Blood
accumulates to the injury site d/t ( kinins, prostaglandins,& histamines)
B. Edema - swelling 2nd phase of inflammation. Plasma leaks into interstitial tissue
at injury. Kinins dilate arterioles cap. Permeability.
C. Heat - can be caused by the inflammation at the site d/t blood accumulation
and may result from pyrogens
D. Pain- Caused by the chemical mediators that were released by injured tissues
and the tissue swelling
E. Loss of Function Loss of function accurse d/t fluid accumulations and d/t
pain which decrease mobility.
b. Chemical Mediator that are released during the Inflammatory processA. Prostaglandins- have many effects vasodilation, relaxation of smooth muscle,
capillary permeability and sensitization of nerve cells to pain.
B. Cyclooxygenase (COX) - enzyme responsible for converting arachidonic acid
into prostaglandins & their products. 2 forms of the cyclooxgenase
COX-1 - protects the stomach lining and regulates blood platelet, promoting
clotting
COX-2 - triggers the inflammation and pain responses.
c. Anti-Inflammatory Agents Group of drugs that inhibit the synthesis of
prostaglandin they are called prostaglandin inhibitors, but are most commonly
called anti-inflammatory agents. They have potent anti-inflammatory effects that
mimic the corticosteroids they are also known as NSAIDS (Nonsteriodal AntiInflammatory Drugs. Some of the newer NSAIDS block only the COX-2.
A. Acetylsalicylic Acid (Aspirin) was developed in 1899 by Adolph Bayer. It is a
prostaglandin inhibitor in the inflammatory process. It is also an Anti
Platelet. Remember that ASA should not be used with other NSAIDS.
{Prototype}. Common symptom of sensitivity to Salicylate is
Tinnitus (ringing in the ears) ,vertigo, bronchospasm. Many foods have
salicylates in them such as wine, prunes, curry, and licorice.
B. Para- Chlorbenzioc Acid- Used to treat Rheumatoid ,Gout and OsteoArthritis. Potent prostaglandin inhibitor, 90% protein bound and displaces other
protein bound drugs drug toxicity. Half life is 4-11hrs.
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1. Examples Indomethacin (Indocin) which is very irritating to the stomach

and should be taken with food. Sulindac (Clinoril), Tolmetin (Tolectin)
these drugs produce less severe reactions then Indocin and may cause
retention of Na and H2O
C. Phenlacetic Acid Derivatives effects are similar to aspirin, but minimal antipyretic properties. Used for same arthritic conditions as para-chlorbenzoic acid
but also for anklosing spondylitis.
1. Examples Diclofenac sodium (Voltaren) and Ketorolac (Toradol). Toradol
was the first injectable NSAID that has high analgesic properties which are
to that of opiods. Intramuscular dose is 30-60mg q 6 hrs.

D. Propionic Acid New group of NSAIDs but are stronger than ASA but have less
GI irritation.
1. Examples Ibuprofen (Motrin Advil) {Prototype}, Fenoprofen Calcium
(Nalfon), Naproxen (Naprosyn), Ketoprofen (Orudis), Flurbiprofen (Ansaid) and
Oxaprozin ( Daypro).
E. Fenarnates and Oxicams are the last two classification of 1st generation of
NSAIDs.
F. Only one true COX2 inhibitor is Celecoxib (Celebrax){Prototype}. Remember
biggest Cautious use listed was Heart Failure and Bleeding tendencies.
G. Corticosteriods Have a long half life of > 24 hrs. When drugs are D/C the dose
should be tapered over a period of 5-10 days before it is just stopped.
I.Examples Prednsone, Prednisolone and Dexamethazone.
H. Disease Modifying Antirheumatic Drugs these therapies include such elements
as Gold {Prototype}, Immunosuppressive Agents, Immunodulators , &
Antimalaries.
I. Antigout Drug - Gout inflammatory condition that affects the joints, tendons, and
other tissues. Characterized by a buildup of urates (uric acid salts) uric acid
levels(hypouricemia) d/t kidneys being unable to excrete. Also uric acid my
buildup in the kidneys causing uric acid calculi. When patient are on anti-gout
medication make sure that fluid intake is .Patients should be instructed to avoid
alcohol. They should also take Tylenol for discomfort instead of aspirin d/t
aspirin would the acid levels even more.
1. Examples of anti-gout medications are Uric acid inhibitors like
Allopurinol (Zyloprin) {Prototype}.
2. Uricosurics increase the rate of uric acid excretion by inhibiting its
reabsorption. They are used for the chronic condition not an acute attack.
Potential side effects flushed skin, sore gums, and headache. Also might

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cause a metallic taste. Instruct patients to avoid alcohol and caffeine because
they can uric acid levels.
Examples - Probenecid (Benemid)- this drug may cause gastric irritation and
when this occurs should be taken with food.
Sulfinpyrazone ( Anturane)- is even more potent the Benemid and should
be taken with food or with and antacid to prevent gastric irritation.

Chapter 25 Nonopioid and Opioid Analagesics

I.

II.
III.

IV.

V.

Pain is defined as an unpleasant sensory and emotional experience related to tissue

injury. The nurse must be knowledgeable and skillful in the assessment and treatment
of pain (it is a subjective type of assessment based on the patients perception of the
level of pain they are experiencing).
Pain Threshold reflects the level of stimulus needed to create a painful sensation.
Analgesics class of drug that reduces the sensation/perception of pain may be
nonopioids (like NSAIDs) or opioids (like narcotics).
A. Nonopioids- like Aspirin, Acetaminopen (tyenol), ibuprofen (motrin/advil) are
used to treat mild pain and are available as OTC. They are especial effective for
dull, throbbing pain of headaches, dysmenorrheal, inflammations, minor
abrasions, and mild arthritic pains.
Types of Pain
A. Duration
Acute - ( sudden onset & responds to treatment verses
Chronic - (pain that persists for > 6 months and is difficult to treat or control).
Cancer pain from pressure on the nerves and organs, blockage to blood supply
or metastasis to the bone.
B. Origin
1. Somatic Pain of the skeletal muscle, ligaments, and joints
2. Visceral Pain from smooth muscle and organs.
Opioid Analgesic (Opioid Agonists) Most Opioids have an antitussive and antidiarrheal effects. Demerol does not have antitussive effect. Opioids taken with kava
kava , St. Johns wart , or valerian may sedation.
A. Morphine- a derivative from Opium.{Prototype} It affects two type of receptors
1. Primarily affects the receptors (responsible for Analgesia, respiratory
depression, euphoria and sedation) when they are activated.
2. It has a weak activating affect on the k receptors (Analgesia, sedation but no
effect on causing respiratory depression or euphoria).
*** Antidote for Respiratory depression is Naxolone (NARCAN).

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B. Other Opioid derivatives are

1. Meperidine (Demerol) preferred drug to be given during pregnancy because it
does not diminish uterine contractions, and it causes less neonatal respiratory
depression. It also causes less constipation and urinary retention than
morphine. It is metabolized in the liver to an active metabolite therefore
decrease the dose with any patient with
hepatic or renal insufficiency. A major side effect is decrease in blood
pressure.
2. Hydromorphone (Dilaudid) is a semisynthetic Opioid similar to morphine.
The analgesic effect is approx. 6 times more potent than morphine with few
hypnotic effects and less GI distress. It has a faster onset and shorter duration
time than morphine. Use of opioids is contraindicated in patients with head
injuries.
Chapter 28 Antibacterial Agents Penicillins and Cephalosporins
I. Types of Bacteria according to their shape and the use of Gram staining
A. Gram Positive If the bacteria after using Crystal violet or methalyne blue
stain keep a purple stain. Examples: Staphylococcus aureus, Streptococcus
pneumoniae, Group B streptococcus, and Closteridium perfingens.
B. Gram Negative Bacteria- doesnt stain. Examples would be: Neisseria
meningitides, Escherichia Coli, Haemophilus Influenzae.
C. Antibacterials/Antimicrobial substances that inhibit bacterial growth or kill
bacterial and other microorganisms including fungus viruses, protozoa.
D. Antibiotic refers to the chemical produced by one kind of microorganism that
inhibits the growth of or kills another. Remember that antibacterial drugs dont
work alone we use other treatment modalities to assist such as natural body
defenses, surgical procedures to excise infected tissue and dressing changes.
They are either obtained for natural sources or manufactured. Five mechanisms
of action:
1. Inhibition of bacterial cell- wall synthesis
2. Alteration of membrane permeability
3. Inhibition of protein synthesis
4. Inhibition of the synthesis of bacterial ribonucleic acid (RNA) and
Deoxyribonucleic acid (DNA)
5. Interference with the metabolism with the cell.
E. Bacteriostatic verses Bactericidal drugs :
1. Bacteriostatic drugs - inhibit the growth of bacteria. Example drugs are
tetracycline and sulfonamides
2. Bactericidal drugs - kill the bacteria. Example of drugs Penicillin and
cephalosporin.
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II.

Penicillins and Cephalosporins Pencillin is a natural antibacterial agent obtained

from the mold genus Penicillium. Was introduced to the military in 1945 during
World War II. Pencillins can be both Bactericidal and Bacteriostatic. Penicillin G is
primarily bactericidal. When Penicillin G is given orally only about 1/3 of the dose
is absorbed that is why it is primarily given by injection. The aqueous form has a
short duration of action time and the IM is very painful.
A. A Longer acting form of Penicillin is Pencillin V (V-Cillin K) although 2/3 of
the oral dose is absorbed by the G.I. tract, it is a less potent than Penicillin
G.Penicillin V is affective against mild to moderate infections including
Anthrax. Initially penicillin was overused. It was used to treat staphylococcal
infections but after a few years mutant strains of staphyloccus developed that
were resistant to both forms G & V penicillin. NOT RECOMMENDED IN
RENAL FAILURE.
Take drug after meals.
B. Board Spectrum Penicillins (Aminopenicilins)- they are not as board
spectrum as was originally thought. This group of drugs is more expensive
than other penicillins. They are effective against some gram-negative organisms
like Eschericha colia, Haemophilus Influenzae, Shigella dysenteriae, Proteus
mirabilis and Salmonella.
C. Examples are- Ampicillin (Omnipen) , Amoxicillin ( Amoxil) , Bacampicillin
(Spectrobid). Amocillin is the most prescribed for adults and children. They can
interfere with the effectiveness of oral contraceptives. Potassium levels can
increase when taking with Penicillin G of V. Used in the treatment of lower
respiratory infections, ottis media, sinusitis, skin infections & UTIs.
D. Penicillnase- Resistant Penicillins (antistaphlylococcal pencillins) are used to
treat penicllinase producing S. aureus.

III. Cephalosporins In 1960s were used with clinical success however there chemical
molecules had to be altered and a semi synthetic cephalosporin was developed.
Active against gram-positive and gram- negative bacteria. They are effective by
inhibiting the bacterial enzyme necessary for cell wall synthesis. Lysis of the cell
occurs and thus the bacterial cell dies.
A. First generation Examples are Cefazolin Sodium ( Ancef, Kefzol )
B. 2nd generation Cefaclor ( Ceclor)
IV.
2nd, 3rd, and 4th Generation Cephalosporins. These drugs are bactericidal with
actions similar to penicillin. It is the 3rd & 4th generations that are effective in
treating sepsis and many strains of gram-negative bacilli.
A. Examples- Aztreonam, Imipenem- cilastain. There is a 10% chance that a
patient who is allergic to Penicillin will also be allergic to cephalosporins
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Pen is effective against Pseudomonas Aeruginosa.

e. Side Effects and Adverse Reactions GI disturbances (N/V, diarrhea), alterations
in blood clotting time (bleeding potential), and when large dosages are
administered Nephrotoxicity
f. Interactions with other substances & other drugs Alcohol may cause flushing,
dizziness, H/A, N/V, and muscular cramps.
A. Drug Interactions If taking Uricosuric there will be a in the excretion of the
cephalosporin drug, which will then increase the serum blood level of the drug.
Chapter 29 Macrolides, Tetracyclines, Aminoglycosides and Fluoroquinolones
I. Macrolides , Lincosamides, and Tetracycline are primarily bacteriostatic & may be
bactericidal depending upon the drug dose or the pathogen.
A. Macrolides- are called Board spectrum antibiotics reflecting their large size.
At low doses Macrolides have a bacteriostatic effect, and with a high dose they
are bactericidal. They can only be administered IV, and must be given slowly to
avoid pain (Phlebitis), and they are not given Intramuscular because it is too
painful. Active agents against most gram- positive bacteria and moderately
active against some gram- negative bacteria. Resistant strains may emerge
during treatment. Used to treat mild to moderate infections of sinuses, GI tract,
soft tissue, diphtheria, impetigo contagiosda, and sexually transmitted diseases.
These drug suppress the bacterial protein synthesis. Onset is for an oral dose is 1
hour, peak is 4 hrs. and duration is 6 hrs. The newer forms have a longer half
life and are administered less frequently
2. Examples - Azithromycin (Zithromax), clarithromycin (Biaxicn) and
erythromycin (E-mycin).
B. Erythromycin {Prototype} gastric acid destroys erythromycin in the stomach
so acid resistance salts are added to erythromycin to dissolution in the
stomach. This will allow the drug to be absorbed in the intestine. It is the drug
of choice for treatment of mycoplasma pneumonia and Legionnaires disease.
C. Clarithomycin- (Biaxcin) is a taken twice /day for 7 days.
D. Azithromycin Zithromax {Prototype} has a longer half life and is only taken
one/day for a total of 7 days. Prescribed frequently used for upper and lower
respiratory infections, gonerrhea and skin infections. Remember to monitor liver
enzymes (alkaline phosphatase, alanine aminotransferase, & bilirubin.
Administer 1 h before or 2 hrs. after meals.Give with a full glass of water not
fruit juice.
1. Pharmocokinetics- 37% is absorbed and 51% is PB. Metabolism is t1/2 68
hrs. Excretion in bile and small amt. in urine.
2. Pharmacodynamics Onset 1 hr. Peak 2.5 hrs. Duration- 24 hr
E. Side Effects- GI disturbance, Hepatic toxicity. Tinnitus
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F. Adverse Reactions- Superinfections, vaginitis, urticaria, stomatitis and hearing

loss.
II. Lincosamides like erythromycin inhibit bacterial protein synthesis and have both
bacteriostatic and bactericidal actions depending upon the dosage of the drug.
A. Examples Clindamycin(Cleocin) widely prescribed d/t active against most
gram-positive organisms like Staphylococcus aureus and other anaerobic
organisms. It is also absorbed better in the GI tract than lincomycin (Lincocin), and
has fewer side effects than lincocin.
B. Side Effects- Both can cause GI irritation, rash.
C. Severe Adverse Colitis and anaphylactic shock.
D. Drug interactions Both are incompatible with aminophyline, phenytoin
(Dilantin), barbiturates and ampicillin.
III. Vancomycin (Vancocin) a glycopeptides bactericidal antibiotic was used widely to
treat staphylococcal infections. Vancomycin is also used against drug- resistant
Staphylococcus aureus, and in cardiac surgical prophylaxis for patients whom are
allergic to penicillin. It is ineffective for treating enterococci.
A. Pharmokinetics given orally to treat staphylococcal entercolitis & antibiotic
associated pseudomembranous colitis d/t Clostridium difficile. When it is given
orally it is not aborbed systemically & is excreted in the feces. Vancomycin given
IV is effective to treat severe infections d/t MRSA, septicemia, bone, skin and
lower respiratory tract. It must be diluted in 250 ml of D5 W, NS or LR. and
administered at of a rate of 10mg/min, when given IV it is excreted in the urine and
30% is PB. Half life is 6 hrs.
B. Pharmacodynamics inhibits the bacterial cell wall synthesis and is active
against several gram-postitive microorganisms.
1. Peak is 30 minutes after the end of the infusion
C. Side Effects Vancomycin may cause nephrotoxicity and ototoxicity. May also
cause chills, dizziness, fever, rashes, N/V , and thrombophelbitis at the injection
site. Redman Syndrome if the IV infusion is given too rapidly which is more a
toxic effect rather than an allergic reaction
D. Adverse Reactions Severe hypotension, tachycardia, generalized tingling,
rarely cardiac arrest, eosinophilia, neutropenia, and Stevens- Johnson syndrome
E. Drug Interactions Dimenhydrinate(Dramamine) if taken with vancomycin may
mask ototoxicity. The risk of nephrotoxicity may be potentiated when taken with
Furosemide, aminoglycosides, amphotericin B, colistin, cisplatin, and cyclosporine.
IV. Ketolides Newer classification of antibiotics structurally related to macrolides.
Telithromycin (Ketek) used for adults and those older than 18 to treat acute chronic
bronchitis, acute bacterial sinusitis and community acquired pneumonia. These
disorders are usually caused by Strptococcus pneumonia and Haemophilis influzena.
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A. Pharmacokinetics- Ketek is given orally and is well absorbed from GI tract and
is not affect by food intake. It is excreted in the feces and urine. It is 60-70% PB.
Half life is 10 hrs.
B. Pharmacodynamics Blocks protein synthesis in microorganisms.
1. Peak is 1 hr.
2. Side Effects visual disturbances, stomatitis glossitis, gastritis, N/V, abdominal
distention, flatulence, oral and vaginal candidiasis, constipation, and watery stools.
3. Adverse Reactions Ketek may also lead to an exacerbation of myasthesis
gravis.
4. Drug Interactions if taken concurrently with anti-lipidemics (simvastatin,
lovastatin, atorvastatin), class 1A or class antidysrhythmics. Ketek blood levels are
decreased when taken with rifamin, phenytoin, carbamazepine, phenbarbital,
producing a sub-therapeutic level.
V. Tetracyclines were the first broad-spectrum antibiotics effective against grampositive and negative bacteria, mycobacteria, rickettsiae, spirochetes, and chlamydiae.
Tetracyclines act by inhibiting bacterial protein synthesis and have a bacteriostatic
effect. They are not effective against Staphylococcus aureus(except for the newer
forms of tetracycline),Pseudomonas, or Proteus. Tetracycline in combination with
metronidazole and bismuth subsalicylate is useful in treating Helicobacter
pylori(bacterium in the stomach that can cause peptic ulcer).It can be given orally,
intramuscular, or intravenously. IM is very painful and is seldom used. Newer oral
forms are : Doxycycline {Prototype}, minocycline and methacycline these
preparations should not be taken with aluminum and magnesium antacids, milk
products containing calcium, or iron- containing drugs d/t substances binding with
tetracycline and prevent absorption.
Doxycycline & Minocycline- there absorption is improved with food ingestion.
A. Side Effects GI disturbances such as N/V, diarrhea. Photosensitivity may
occur especially when taking Demclocycline(Declomycin).Pregnant women should
not take tetracycline during the 1st trimester d/t possible teratogenic effects. Women
in their last trimester and children older than 8 yrs. should not take tetracycline d/t
irreversibly discoloration of the permanent teeth. Minocycline(Minocin)can
cause damage to the vestibular part of the inner ear which leads to difficulty
maintaining balance.
B. Adverse Reactions Nephrotoxicity results when higher doses of tetracycline
have been given. It can also disrupt microflora in the body and lead to
Superinfection.
C. Drug Interactions Antacids (Maalox and others) and iron-containing drugs can
prevent absorption of tetracycline from the GI tract. Milk and other drugs high in
calcium can do the same, so to avoid decrease absorption of tetracycline while those
drugs they should be taken 2 hrs,apart from the tetracycline.The desired effect of
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oral contraceptives can be lessened when taking with tetracyclines. Administering

tetracycline with an aminoglycoside may increase the risk of nephrotoxicity.
VI. Aminoglycosides They act by inhibiting bacterial protein synthesis. They are used
against gram- negative bacteria such as E. coli, Proteus spp , and Pseudomonas.
Streptomycin was the 1st aminoglycoside available for clinical use to treat
tuberculosis. D/t its ototoxicity it is infrequently used today. It is however the drug
of choice for tularemia & bubonic pneumonic forms of the plague.
Aminoglycosides are used for serious infections. They cannot be absorbed from GI
tract and cannot cross into the cerebrospinal fluid. They do cross the blood brain
barrier in children but not in adults. They are primarly given IV or IM. Neomycin,
or paramomycin are 2 types of aminoglycoside that can be given orally . Neomycin
is given for a pre-op bowel antiseptic and paramomycin is useful for treating
intestinal amebiasis and tapeworm infections. Tobramycin, Amikacin , and
Netilmicin are newer aminoglycoside. Gentamycin(Garamycin) {Prototype} is
currently used to treat Pseudomonas Aeruginosa .
A. Pharmacokinetics of Gentamycin has a short half life and the drug can be
given 3-4 times/day. It is primarily excreted unchanged in the urine.
B. Pharmacodynamics- Inhibit bacterial protein synthesis and have a bactericidal
effect.
1. Onset- is rapid or immediate
2. Peak is 1 hr
3. Duration 6-8 hrs.
C. Side Effects/ Adverse Reactions Ototoxicity and nephrotoxicity.
D. Drug Interactions- When aminoglycoside are given with penicillins the desired
effects are greatly decreased. Actions of warfarin can be increased if taken at
the same time as an aminoglycoside.
VII. Fluoroquinolones(Quinolones) - The mechanism of action is to interfere with the
enzyme DNA gyrase, which is needed to synthesize bacterial DNA. Their
antibacterial spectrum includes both gram- positive & negative organisms. They
are bactericidal. The fluoroquinolones that is effective against some grampositive organisms such as Haemophilus influenza, Proteus aeruginosa,
Salmonella and Shigella. Effective for treatment of urinary tract infections;
bronchitis; pneumonia; gastroenteritis; and gonorrhea.
A. Examples: Ciprofloxacin (Cipro)and Norfloxacin (Noroxin) are synthetic
antibacterials related to nalidixic acid and are broad spectrum on both grampositive and negative organisms. Both are indicated for urinary tract infections;
lower respiratory infections; skin; soft tissue; and bone and joint infections. In
the past few years the number of fluoroquinolones has increased. Levofloxacin
(Levaquin) {Prototype} used for community pneumonia, chronic bronchitis,
acute sinusitis.
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B. Pharmacokinetics approximately 70% of Levaquin is absorbed from the GI

tract. It has a low PB effect. Moderately short half life of 6.5-7.5 hrs. More than
75% is excreted unchanged in the urine.
C. Pharmacodynamics- This drug has a high tissue distribution. If possible should
be taken before meals, d/t food slowing down absorption rate. Antiacids also
decrease absorption. Levaquin increases the effect of oral hypoglycemic,
theophylline and caffeine.
1. Onset 30 minutes to 1hr
2. Peak 1-2 hrs.
3. Duration- is unknown
Chapter 36 Anticancer Drugs- Chemotherapy, Alkylating & Antimetabolites
I. Pharmaceuticals often used to destroy cancer cells and are called by different
names such as: Anticancer, Cancer Chemotherapeutic agents, Antineoplastic drugs
and Cyotoxic therapy. In the 1970s a combination of two antineoplastic drugs was
used together to battle the growth of the cancer cells with increased success.
Chemotherapy may be used as the sole treatment or in conjunction with other
treatment modalities such as radiation, surgery, biological response modifiers. The
most common route of chemotherapy is IV. Some types of cancer can be cured with
chemotherapy such as Hodgkins, Burkitts lymphoma. Wilms tumor, testicular
cancer.
A. A djunctive therapy - when surgery is performed first and then chemotherapy is
administered to eliminate any residual cells that may have remained.
B. Neoadjuvant Chemotherapy - Chemotherapy is given first to reduce the size of
the tumor then surgery is performed to remove the smaller tumor.
C. Palliative Chemotherapy is used to relieve the symptoms associated with
progressing disease and to improve the quality of life.
D. Chemotherapy Administration administration guided by specific protocols.
The length of treatment determined by the type and extent of the malignancy.
E. Multidrug Resistance malignant tumors often develop resistance to
chemotherapeutic agents. This can occur for several reasons:
1. Anticancer drugs may not kill all neoplastic cells, and these cells may mutate
and become resistant to the chemotherapeutic agent.
2. Some tumor cells have a natural resistance to certain chemotherapy agents.
3. Tumor resistance can occur as a result of gene amplification in which a gene
produces many copies of itself.
F. Combination Chemotherapy - Single drug therapy is not usually effective.
Combination of chemotherapy drugs are used to achieve tumoricidal effect.
They attack the cancer cells at different phases of the cell cycle.
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1. Side Effects These drugs exert adverse effects on rapidly growing normal
cells such as skin, hair blood cells. They also affect the GI tract, mucous
membranes, bone marrow and the reproductive systems.
II. Alkylating Drugs cause cross- linking of DNA strands, abnormal pairing, or
DNA strand breaks. Drugs in this category are effective against many types of
cancer including acute and chronic leukemias, lymphomas multiple myeloma, and
solid tumors of the breast, ovary, uterus, lung, bladder, and stomach.
A. Examples Mustard gas derivatives Cyclophosphamide (Cytoxan)- used to treat
Hodgkins disease. Vesicant can cause tissue necrosis if it infiltrates into the
tissue. Patients should be well hydrated while taking this drug. Drug
Interactions occur when taking aspirin, allopurinol, Phenobarbital, warfarin,
Thiazides and some psychiatric medications.
B. Ethylenimines Thiotepa (Thiopex),
Alkylsulfonates- Busulfan (Myleran)
Metal Salts- Cisplatin (Platinol)
C. Side Effects- N/V, hemorrhagic cystitis, alopecia, anemia, leucopenia,
thrombocytopenia, bone marrow suppression, 2nd malignancy and sterility.
III. Antimetabolites resemble natural metabolites which synthesize, recycle, &
breakdown organic compounds for use by the body. They are used to treat acute
leukemia, breast cancer, head& neck cancer, lung cancer, osteosacroma and nonHodgkins lymphoma This group is classified by the substances with which they
interfere;
A. Folic Acid( folate) antagonists- examples
Methotrexate (Rheumatrex, Trexall) numerous drugs interactions occur with
Methotrexate (MTX ). Leucovorin is needed to rescue normal cells from the
adverse effects of the drug. Protein bound drugs like aspirin, phenytoin
increase the toxicity of MTX. Clients who are taking penicillins,
cyclooxygenase 2 inhibitors and OTC herbs interact with MTX.
The side effects of antimetabolites include bone marrow suppression (anemia,
leucopenia, thrombocytopenia), stomatitis, N/V, alopecia and hepatic and renal
dysfunction.
B. Pyrimidine antagonist- (Fluorouracil, Adrucil) (5 FU, {Prototype} used for
the treatment of colorectal cancer. Also can treat breast, stomach, liver,
pancreas, and skin cancers. Given IV for solid tumors and topically for
superficial basal cell cancer. IV half life is 10-20 minutes. Small amount is
excreted in urine and 80% is excreted by the lungs as CO2.
C. Purine antagonist- (6-mercaptopurine Purinethol
D. Adenosine deaminase inhibitors- (Fludarabine Fludara)

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IV.

VI.

Antitumor Antibiotics - inhibit protein & RNA synthesis and bind DNA, causing
fragmentation. All of these drugs are CCNS except for Bleomycin which has its
major effect on G2. Adverse reactions to antitumor antibiotics include alopecia, N/V,
stomatitis, leucopenia, and thrombocytopenia.
A. Anthracyclines - Doxorubicin (Adriamycin) {Prototype}, Daunorubicin (
Cerubidine), Mitomycin ( Mutamycin), Bleomycin (Blenoxane)
B. Doxorubicin ( Adriamycin) {Prototype} lead to the development of many
analogs Epirubicin (Ellence), Idarubicin (Idamycin). They have severe
cardiotoxic side effects must be given with caution. Maxium lifetime dose
is 550mg/m2 d/t cardiotoxicity.
1. Pharmacokinetics Administered IV and metabolized in the liver to active
and inactive metabolites. The initial phase is 12 minutes, intermediate
phase is 3 to 5 hrs., and final phase is 30 hrs.
2. Pharmacodynamics Prescribed in combination with other anticancer
agents for the treatment of breast, ovarian, lung, bladder, lymphomas and
leukemias. Has maxium lifetime dose of 550 mg/m2. This dose may be
lowered for patients with pre-existing cardiac conditions or those
whom are using other cardiac toxic medications, are older patients, or
have received chest radiation. Prior to administration cardiac function
must be assessed. Pts may be given Dexrazoxane (Zinecard) to help
prevent cardiac toxicities from occurring. It is a cytoprotective agent.
Remember that Green Tea might enhance the antitumor effect.
Use cautiously with Grape Seed(inhibits effects of Doxorubicin)
Garlic (anti- clotting properties may effectiveness of chemotherapy.
3. Side Effects and Adverse Reactions can cause organ toxicity. Patients
receiving Bleomycin may develop pneumonitis which progresses to
pulmonary fibrosis. Assessment of CBC, RBC, WBC, and Platelet counts
should be done. Drugs may be with held if RBCs, WBCs or Platelet
counts below predetermined levels.
Mitotic Inhibitors Plant Alkaloids and other compounds derived from natural
products that are CCS and block cell division at the M phase of the cell cycle.
A. Vinca Alkaloids Vinblastine (Velban),Vincristine (Oncovin) {Prototype},
Vinorelbine ( Navelbine ) are obtained from periwinkle plant.
B. The Docetaxel- ( Taxotere), Paclitaxel (Taxol), were originally procured from
the needles and bark of the Yew tree which only grows in the Pacific northwest;
d/t the scarcity of the natural resources semi-synthetic form of Paclitaxel was
developed Docetaxel ( Taxotere) .
1. Adverse Reactions include : leucopenia, allergic reactions, N/V , diarrhea,
and phlebitis. The plant alkaloids damage peripheral nerve fibers and may
cause reversible and irreversible neurotoxicity (muscle strength, tingling,

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numbness of the fingers and toes (Think Stocking/glove syndrome). May

also cause loss of deep tendon reflexes, joint pain, and bone marrow
depression.
C. Vincristine (Oncovin) {Prototype} Used to treat Wilms tumor in children.
1. Pharmacokinetics Only given IV. Half life between 5 minutes and 85
hours. Primarily PB. Extensively metabolized by the liver.
2. Pharmacodynamics Used to treat leukemia, Hodgkins disease and nonHodgkin Lymphoma , neuroblastoma , rhabdomyosarcoma, Ewings
sarcoma, Wilms tumor, multiple myeloma, chronic leukemia, thyroid cancer
and brain tumors.
3. Onset may be in minutes however therapeutic effect may take several
days.
4. Side Effects and Adverse Reactions Severe drug interactions can occur
with Vincristine such as L- Asparaginase ( Elpar), digoxin ,Phenobarbital
(Sofoton), calcium channel blockers, mitomycin( mutamycin). Some side
effects are sensory loss, hyperuricemia, severe local reactions with
extravasations. Monitor Bilirubin levels dose may be if level > 1.5mg.
Check bowel function Autonomic Neuropathy ileus.
5. Life threatening - Intestinal necrosis, seizures, coma, and acute
bronchospasms.
g. Liposomal Chemotherapy Use of anticancer drugs packaged inside synthetic
fat globules called liposomes. Fatty coating helps the drugs stay in the system
longer and the duration of therapeutic effects while decreasing the side effects (
alopecia, N/V, and cardiac toxicity) . Encapsulated forms are :
Doxorubicin (Doxil, Caelyx, Myocet), Daunorubicin (DaunoXome) and
Vincristine (ONCO- TCS, Marqibo).
I. Hormonal Agents Not considered true chemotherapy. There are several classes:
Corticosteroids, hormones, antitestrogen, aromatase inhibitors, gonadrotropinrelease hormone analogues, and anti androgens.
A. Corticosteriods glucocorticoids, anti inflammatory agents that suppress the
inflammatory process that occurs as a result of tumor growth. These agents
block the inflammatory receptors on the surface of cells. This blocking action
slows the growth of the tumor cells. Examples :
Prednisone ( Cordrol, Deltasone), Dexamethasone ( Cortastat, Dalalone), and
Hydrocortisone ( Hydrocortone, Solu- Cortef) can help to cerebral edema
caused by malignant brain tumor.
B. Side Effects and Adverse Reactions Fluid retention, potassium loss, risk for
infection, in blood sugar, in fat distribution, and bleeding tendencies.
C. Sex Hormones - Estrogen, Androgen used to slow growth of hormone
dependent tumors (prostate & breast cancers).
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1. Estrogen- used as a palliative treatment for men with prostate cancer and
women with hormonal responsive breast tumors to slow the growth of the
tumor down.
Examples: Diethlstibestrol (DES), EthinylEstradiol (Estinyl), Chlorotrianase
(TACE), and conjugated estrogen Premarin.
2. Progestrins may be used to treat breast, endometrial and renal cancers.
There drugs hydroxyprogesterone acetate (Depro- Provera), Megestrol
Acetate ( Megace) , act by shrinking cancer tissures.
3. Side Effects and Adverse Reactions include fluid retention and
thromboitic disorders.
4. Androgens given to treat advanced breast cancer in pre-menopausal
women. Male hormone promotes regression of tumor if taken for prolong
period of time it leads to secondary sexual characteristics like growth of
body hair, lowering of voice, and muscle growth.
5. Anti Estrogens- such as Tamoxifen (Nolvadex) & Fulvestrant (Faslodex)
Are used to treat breast cancer tumors that are estrogen- receptor
positive(ER+). Tamoxifen has shown efficacy in preventing tumor
reoccurrence in both pre- & post menopausal women.
a .Side Effects hot flashes, irregular menses, fatigue, H/A, impotence, and
libdo.
Chapter 41 Cardiac Glycosides, Antianginals, and Antidysrythmics
I. Cardiac Glycosides They are a group of drugs that inhibit the sodium- potassium
pump, resulting in in intracellular Na Ca which causes cardiac muscle fibers
to contract more efficiently. Three effects on the heart muscle are :
1. Positive Inotropic action- ( on mycocardial contraction& stroke volume).
2. Negative Chronotropic action- ( the heart rate)
3. Negative Dromotrophic action- (conduction of the heart cell)
The in myocardial contractility increases cardiac, peripheral and kidney
function by CO, preload, improving blood flow to the periphery and
kidneys, edema, and increasing fluid excretion.
II. Glycosides Used for the Treatment - Atrial Fibrillation and Atrial Flutter with rapid
Ventricular response with rates 200-300 beats/min. REMEMBER DIGOXIN DOES
NOT CONVERT A- FIBRILLATION TO NORMAL SINUS RYTHYM
A. Drugs used for Treatment of Heart FailureFirst drugs of choice is Inotropic medication like Dopamine and Dobutamin,
Phosphodiaesterase inhibitors like ( Inamrinone, & Milrinone -Primacor),

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Diuretics, Beta blockers, ACE inhibitors, Angiotension Receptor

Blockers(ARBs), Calcium Channel Blockers and Vasodilators.
1. Lab Values to consider to confirm diagnosis of Heart Failure in patients
with other Lung Pathophysiological disordera. ANP- Atrial Natriuretic Hormone Peptide 20- 77 ng/l (An elevation may
confirm Heart Failure. It is secreted from the atria of the heart and acts as an
antagonist to the renin and aldersterone. It is released during the expansion
to the atrium, produces vasodilation , and glomerular filtration rate.
b. BNP- Brain Natruiretic Peptide- Desired level < 100 pg/l. A positive result
is recorded as > 100 pg/l and aides in diagnosing Heart failure. It is a more
sensitive test than ANP . Today there is an emergency bedside test available
for measuring BNP.

B.

Other drugs used to treat Heart Failure- Digoxin (Lanoxin) {Prototype}1. Pharmacokinetics - Absorption is 90-100% in the capsule form. The
protein bounding power for Digoxin is low(25%).
t = 30- 45hrs. (remember that because of the longer half life that the
drug accumulation should be monitored very carefully).
Excretion is 70% in the urine and 30 % by liver metabolism.
2. Pharmacodynamics used in treatment of heart failure. They myocardial
contraction and cardiac output and improves circulation through the Atrial
Ventricular node the heart rate .
Therapeutic Serum level 0.5 2.0 ng/ml
3. Digitalis Toxicity Signs & Symptoms Anorexia, diarrhea, N/V, H/A,
Bradycardia, PVCs, blurred vision, (white & green halos), confusion, and
Delirium. Digitalis toxicity can lead to first degree hear t block then to 2nd
degree A V block and finally to a third or complete heart block. The antidote
for Digitalis Toxicity is (Ovine, Digibind) this agent binds with digoxin to
form complex molecules that can be excreted in the urine.
4. Herb Interactions Ginseng may falsely digoxin levels.
St. Johnss wart- absorption of digoxin.
Psyllium (Metamucil) digoxin absorption
Hawthorn - may the effect of digoxin
Licorice- promotes K+ loss digoxin toxicity.

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III. Other Drugs used to Treat Heart Failure- Vasodilators, Angiotension Converting
Enzyme Inhibitors, Angiotension II Receptor Antagonist Blockers, Diuretics,
Aldactone, & some Beta Aderenergic Blockers.
I. Vasodilators- venous blood return which decreases cardiac filling, ventricular
stretching (pre-load) and O2 demand on the heart. Arteriolar dilators act in 3 ways
1. Reduce cardiac after load which cardiac output.
2. Dilate the arterioles of the kidneys which improves renal profusion and
fluid loss
3. prefusion to the skeletal muscle
II.ACE inhibitors - usually prescribed for Heart failure to dilate venules and arterioles
improving renal blood flow(profusion) and blood fluid volume also moderately
Aldesterone which can K+ levels.
III.Angiotension II Receptor Blockers- Valsartan(Doivan) and Cardesartan(Atacand)
have been approved for Heart Failure for those clients whom cant tolerate ACE
inhibitors.
IV.Diuretics First line of drugs for Heart Failure when you are trying to fluid volume
used with Digoxin or other agents.
1. Spirolactone (Aldactone) K+ sparing , used for moderate to severe Heart
Failure. It blocks the production of Aldesterone. (Normally with Heart Failure
the Aldesterone production goes up Na and Water retention K+ and
Magnesium loss ( both electrolytes are need for the hearts contracts.
Usually dose is 12.5mg 25 mg/ day.
E. Beta Blockers usually contraindicated for clients with Heart Failure. Reduces
contractility .
1. Carvedilol- (Coreg) and Metopropolol( Toprolol)- have been shown to
improve cardiac performance.
F. Nesiritide (Natrecor)- an atrial Natuiretic Peptide hormone that inhibits AntiDiuretic hormone by Na loss (causes vasodilation, natriuresis, And diuresis.
G. Bi- Dilators combination of Hydralizine (which B/P) and Isosorbide dinatrate (
a dilator to relieve heart pain) in 2005 FDA approved it for the treatment of Heart
Failure especially in African Americans(who are 2 times more likely to have Heart
Failure than are Caucasians.

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Chapter 41 Cardiovascular Anti Anginal Drugs cont.

I. Anti Anginal Drugs- Acute Cardiac pain caused by inadequate blood flow to the
myocardium due to plaque, occlusion within or spasms of coronary arteries. There are
three types:
A. Stable (Classic) occurs with stress or exertion
B. Unstable (Pre-Infarction) occurs frequently over the course of a day with proseverity.
C. Variant (Printz Metal or Vasospasic)- occurs during rest often wakes pt. from a
sleep.
II. Non- Pharmacological Measures- Avoid eating a heavy meals, smoking, extremes
in weather changes, strenuous exercise , emotional upsets, proper nutrition and rest,
moderate exercise.
III. Pharmacological Agents- Anti- Anginals work one of 2 ways :
Either it O2 supply or by O 2 demand by the myocardium. Three types of
medications are: 1. Nitrates 2. Bate- Blockers 3. Calcium Channel Blockers
A. Nitrates- major systemic effect is they venous tone, which workload of the
heart and promotes vasodilatation. Beta Adrenergic & Calcium Channel Blockers
the workload of the heart by O 2 demands. Nitrates and Calcium blockers are
helpful in the treatment of Variant Angina because they actively preload and
afterload both of which O2 demand.
1. Sublingual NTG 0.4 mg or 1/150 gr can be repeated every 5 minutes for a total
of 3 doses. Effect last for 10 minutes. Must be protected from light and heat.
2. Isosorbide Dinatrate ( Isordil Sorbtrate)- available sublingual, chewable tablets,
immediate release tablets, and sustained released.
3. Nitroglycerine ( Nitrostat, Nitro-Bid, Transderm Nitro Patch, Nitrogard
SR){Prototype} used to control angina pectoris (angina pain).
a. Pharmacokinetics: Approximately 40-50% GI tract inactivated by
the liver.
SL > 75% absorbed rapidly directly into the internal Jugular Vein Right
Atrium.
Topical Transderm Nitro Patch- slow absorption by the skin acts on the smooth
muscle, blood vessel, causing relaxation & dilatation cardiac preload and after
load( Peripheral vascular resistance) myocardial O 2 demand.

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Distribution Protein Bound 60%

Metabolism- t 1 4 minutes
Excreted Liver & in the urine
Pregnancy - C
b. PharmacodynamicsSLOnset- 1- 3 minutes, Peak- 4 min.
Slow Released Onset 20-45 min.
Onset 20 -60 min Peak 1-2 hrs.
Ointment Patch - Onset 30- 60 min
Peak 1-2 hrs.
I.V. - Onset 1-3 min.

Duration- 20-30 min

Duration- 3-8 hrs.
Duration 6-8hrs.
Duration20-24hrs.
Duration 3-5 min.

c. Side Effects nausea, vomiting, H/A, dizziness, syncope, weakness,

flush, confusion, pallor, rash, dry mouth.
d. Adverse Reactions: Hypotension, reflex tachycardia, paradoxical
bradycardia.
e. Drug-Lab-Food Interactions - effect with alcohol, beta-blockers,
calcium channel blockers, anti-hypertensives, effects of heparin.
B. Beta Adrenergic Blockers Beta I and Beta II the effects of the Sympathetic
nervous Systems by blocking catecholamines Epinepherine and Norepinepherine
which heart rate and blood pressure. Used as an anti-anginal, anti-dysrhythmic, and
antihypertensive. Patients should be told that they should NOT abruptly stop these
medications.
1. Beta1- Atenolol ( Tenorium) - PO dose is 25-100 mg/d with max. dose of
200mg/day. It can be used with asthmatic patients. Protein bound 5-15%
t = 6-7 hrs.
a) Metoprolol( Lopressor)- Beta1 50-100mg/ B.I.D. High dose can effect
Beta2 Bronchoconstriction Protein Bound 12%
t = 3-7 hrs.
2. Beta1 and Beta2 - used to treat Angina Pectoris and hypertension
a) Nadolol (Corgard) - PO 40 mg/day Protein B. 28% t = 10-24 hrs.
b) Propanolol (Inderal) - PO initial dose 10-20 mg B.I.D. or T.I.D.
Maintenance 20-60 T.I.D. or Q.I.D. if using SR 80-160mg /day
Risk for Bronchospasms Protein B.- 90% t = 3-6 hrs.
C. Calium Channel Blockers - myocardial contractions O2 demand by
myocardial tissue. Relax coronary artery spasms and peripheral arterioles, cardiac
oxygen demand.
1. Amilodipine (Norvasc) PO initial dose 10 mg maintenance dose 2.5-10mg/day
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Preganancy - C
Protein B. 95% , t = 30-50 hrs., Angina and Hypertension
1. Diltiazem ( Cardizem) - PO 30-60 mg Q.I.D. SR 60mg every 12 hrs.
Used for treatment of Angina Pectoris, its hypotensive effect is not as severe as with
procardia. Kidney function should be monitored, Pregnancy = C Protein B. = 7085%
t = 3.5- 9 hrs.
2. Nifedipine ( Procardia) - PO 10-30 mg every 6-8 hrs. max. dose = 180 mg/day. It is
used for to treat angina pectoris and hypertension. Suppresses contraction of cardiac
and vascular smooth muscle. Increases heart rate and cardiac output. Decreases
blood pressure. Pregnancy = C Protein B. > 99% t = 7-12 hrs.
3. Three of the Calcium Channel Blockers are used for the long term treatment of
Angina Verapamil( Calan), Nifedipine (Procardia), and Diltiazem (Cardizem).
Procardia is the most potent.
4. Side Effects H/A, hypotension ( more common with procardia) and less common
with Diltiazem.
D. Antidysrhythmia - A dysrhythmia is any deviation from a normal rate or pattern of a
heartbeat.
1. Dysrhythmia- disturbance of a heart rhythm.
2. Arrhythmia- absence of a heart rhythm
3. Aterial Dysrhythmia- prevents ventricular filling and.
4. Arrhythmia- absence of a heart rhythm
5. Aterial Dysrhythmia- prevents ventricular filling and cardiac output by 1/3
6. Ventricular Dysrhythmia- are life threatening because of ineffective filling of the
ventricle resulting in or absence of cardiac output.
7. Cardiac Dysrhythmias commonly occur after a M.I.(myocardial infarct) or
hypoxia or hypercapnia (level of CO 2 in the blood) , thyroid disease, C.A.D.,
Cardiac Surgery, Excessive catecholamines, or electrolyte imbalances.
8. Action Potential- Remember when Na+ and Ca+ enter the mycocardial cells muscle
contraction and depolarization occurs.
E. Anti-dysrhythmia drugs- there are four class of anti-arrhythmic drug which effect the
different phases of the action potential.
F. Class I: Sodium Chanel Blockers:
1A Slow condition which prolongs Repolarization (Atrial and Ventricular such as
PAT- Paroxysmal Atrial Tachycardia and SVT Supra Ventricular
Tachycardia)
1B Slow conduction that shortens Repolarization(Acute Ventricular Dysrhythmias)
1C Prolong condition with little effect on Repolarization (Life threatening
Ventricular dysrhythmias).
G. Class II: Beta Blockers: Reduce Ca+ entry, conduction velocity ,automaticity and
recovery time (refractory period) Used to treat (Atrial flutter & Fibrillation,
tachydysrhythmias and Ventricular and Supraventricular dysryhthmias).
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H. Class III: Drugs that prolong Repolarization: Prolong repolarization during

ventricular dysrhythmias, and prolong action potential duration. Used to treat (Life
threatening Atrial & Ventricular dysrhythmias resistant to other drugs).
I. Class IV: Calcium Channel Blockers: Block influx of Ca+, Slow conduction
velocity, myocardial contractility (Negative Inotropic), and refraction in the AV
node. Used to treat (Supraventricular tachdysrhythmias, prevention of Paroxysmal
supraventricular tachycardia PSVT).
J. Examples:
1. Na+ Channel Blockers: Class IA
a. Napamide (Norpace) Adult dose PO: 100-200mg every 6 hrs. or if CR is used
then PO 300mg every 12 hrs.
b. Procainamide (Procanbid or Pronestyl)- Adult PO 250-500mg q 3-4 hrs.,
or if SR is used dose is 250mg 1 Gm. q 6 or q 12 hrs.
2. Na+ Class IB :
a. Lidocaine (Xylocaine)- USE cautiously with patients who have Liver
Failure or an AV Block. Given I.V. Bolus dose: 50-100mg over 2-3min.:
then Continuous infusion at dose 20-50mcg/kg/min.
b. Mexiletine (Mexitil)- Adult dose PO 200-400mg q 8hrs.
c. Tocainide (Tonocard)- Adult loading dose is 600mg then 400mg q 8hrs. with
a maximum dose of 2.4 Gm/day.
3. Na+ Class IC :
a.

Flecainide (Tambor) Adult PO initial dose 50-100mg q 12hrs, then dose

by 50mg q 12hrs every 4 days; Maintenance dose of 150mg q 12hrs. Maximum
dose of 300mg/day.

b.

Propafenone (Rythmol) Adult PO dose 150-300mg q 8hrs. Maximum dose

is 900mg /day.

4. Class II Beta-Adrenergic Blockers- (more frequently used prescription for

dysrhythmias than Na+ channel blockers.
A. Acetbutolol (Sectral)-Beta1 blocker - {Prototype} Adult dose PO 200mg
B.I.D.
1. Pharmocokinetics- Well absorbed from the GI tract.
Metabolized in Liver to active metabolites- 50-60% is eliminated in bile
via feces. 30-40 is excreted in urine. Pregnancy class is B. Protein
Bound: UK .
Metabolism: t : 3-4 hrs. Metabolites: 8-13 hrs.
2.Pharmocodynamics: Ventricular dysrhythmia: PO: Onset: 1 hr.
3.Peak: 4-6 hrs.
4.Duration: 10 hrs. For treatment of HTN duration = 20-24 hrs.
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5. Therapuetic : to help in treatment of recurrent stable ventricular

dsyrhythmias.
6. Side Effects: Dizziness, H/A , B//P, diaphoresis, fatigue, constipation,
contraindicated in 2 or 3rd degree heart blocks, and severe bradycardia,
severe HF, or in cardiogenic shock.
7. Adverse Reactions: Palpitations with abrupt withdrawal . Life
Threatening: agranulocytosis, bronchospasm with high doses.
8. Teach patients that they should avoid alcohol, smoking and caffeine.
B. Esmolol (Brevibloc Beta1)- Adult IV dose 500mg/kg over 1 min.
Maintenance dose is 50-100mcg/kg/min. Maximum dose of
200mcg/kg/min.
C. Propanolol ( Inderal Beta1&2 Blockers- Adult dose PO 10-30mg T.I.D. ,
IV bolus 0.5-3mg at a rate of 1mg/min. Used for treatment of Ventricular
dysrhythmia, angina, and hypertension.
D. Sotalol (Betapace) Beta1&2 Blockers {Prototype} - Adult PO 80 mg B.I.D.
with a Maximum dose of 240mg-320mg/day
1. Pharmocokinetics- Well absorbed from the GI tract.
2. Metabolized in Liver to active metabolites- 50-60% is eliminated in bile
via feces. 30-40 is excreted in urine. Pregnancy class is B.
5. Class III- Drugs that prolong Repolarizationa. Adenosine (Adenocard)- Adult IV initial dose is 6mg rapid bolus
May repeat the dose at 12 mg IV x 2 more doses.
b. Amiodarone (Cordarone) Adult loading dose is 400mg-1600mg/day.
Be-aware of the photosensitivity it causes.
c. Bretylium Tosylate (Bretylol)- Adult IM 5-10mg/kg q 6-8hr. or IV 5-10 mg/kg
may repeat in 15-30 min, IV bolus or drip.
d. Sotalol (Betapace)- {Prototype} Adult PO dose is same as Class II .
6. Calcium Channel Blockers- Contraindicated in 2nd & 3rd degree heart blocks
a.
Verapamil (Calan Isoptin)- Adult dose 240-480 mg/day in 3 to 4 divided
doses. IV 5- 10 mg IV push.
b. Diltiazem (Cardizem)- Adult IV 0.25mg/kg IV bolus over 2min. or 510mg/hrs in IV infusion.
7. Other
a. Phenytoin (Dilantin)-Adult IV 100mg q 5-10 min until dysrhythmia ceases.
Maximum dose 1000mg. Used for digitalis induced dysrhythmia.
b. Digoxin (Lanoxin) - Adult IV loading dose 0.6-1mg/d in 24hrs.

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IV. Diuretics- Two main purposes A). Blood Pressure; & B). Edema
(peripheral/pulmonary). Diuretics work by inhibiting Na+ and H2O re-absorption
from the kidneys in the tubules thus promoting their loss through excretion in the
form of urine.
Renal Tubule Components- Proximal tubules, Loop of Henle descending and
ascending loops, and the collecting tubule. Every 1.5 hrs the total volume of the
bodys extracellular fluid goes through the kidneys glomeruli. Our glomeruli filter
electrolytes, drugs, glucose, and the waste products of protein metabolism. Large
particles such as protein & blood cells are not filtered from the blood & they remain
in the circulation. Na+ and H2O are the largest filtrate substances. Normally 99% of
Na+ is reabsorbed (50-55% is reabsorbed in the proximal tubules, 33-40% in the
Loop of Henle, 5-10% in the distal tubules and <3% in the collecting tubules.).
Diuretics that act on the tubules closest to the glomeruli have the > effect in causing
Natriuresis (Na+ loss in the urine). An example is Mannitol an osmotic Diuretic.
A. Five Categories of Diuretics:
1. * Thiazide and Thiazide like
2. * Loop or high ceiling diuretics
3. Osmotic
4. Carbonic anhydrase inhibitor
5. * Potassium sparing
(* Most frequently prescribed for HTN, edema associated with Heart failure)
6. Combination Diuretics- (Both K+ sparing and K+ wasting) used for the
treatment of HTN
Thiazide- Diuretics used primarily in patients with normal renal functions. If creatinine
clearance is < 3oml/min the effectiveness of thiazide is greatly decreased. Thiazide drugs cause
not only loss of Na+, K+, and magnesium they also cause calcium re-absorption, which may
lead to Hypercalcemia, another consideration that it cause glucose intolerance or possible
Hyperglycemia so it should be used with caution in patients with diabetes mellitus.1st drugs
used are in the Short Acting Chlorothaizide then Hydrochlorathiazide- HydroDIURIL,
HCTZ, Esidex, Oretic, Urozide{Prototype}- PO dose for HTN 12.5-50 mg/d
Edema PO dose: 25- 200mg in divided doses; maintenance dose 25100mg/day
Drug -Lab/Food Interactions: Drugs: digitalis toxicity with digitalis and
hypokalemia; K+ loss with steroids; antidiabetic effect; thiazide effect
with cholestramine and colestipol.
Lab: serum calcium, glucose, uric acid, serum potassium, sodium &
magnesium.
A. Pharmacokinetics- Readily absorbed from the GI tract
1. 65% Protein bound
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2. Metabolism: t = 6-15 hrs.

3. Excretion in the urine
B. Pharmacodynamics- PO Onset : 2 hr
1. Peak: 3-6 hrs
2. Duration: 6- 12 hrs
3. Therapeutic Effects: to urine output, to treat: HTN, edema from HF, hepatic
cirrhosis, renal dysfunction. Mode of action to Na+, K+, and H2O excretion and
preload and cardiac output.
4. Side Effects: dizziness, vertigo, weakness, N/V, diarrhea, hyperglycemia,
constipation, rash, and photosensitivity.
5. Adverse Reaction: Severe dehydration, hypotension, severe hypokalemia,
uremia, aplastic anemia, hemolytic anemia, thrombocytopenia, &
agranulocytosis.
2. Loop (High Ceiling) Diuretics: act in the thick ascending Loop of Henle to inhibit
chloride transport of Na+ into the circulation.They inhibit passive re-absorption of Na+
which leads to loss of Na+ , water, K+, Ca+, Mg+ . They can also effect blood sugar
levels and uric acid levels. These groups of drugs are extremely potent causing a
marked electrolyte and water depletion. Less effective as anti hypertensive agents than
the Thiazides. They can renal blood flow up to 40%. Frequently prescribed when pt.s
creatinine clearance is < 30ml/min. & for end stage renal disease. This group of
diuretics cause Ca+ excretion where as the Thiazides inhibit Ca+ loss.
Example: Furosemide (Lasix) {Prototype} Both Lasix and Bumex are
sulfonamide derivatives for patients who are allergic to Sulfa (use Ethancrynic
Acid) Lasix should never be prescribed with another loop diuretic. It should be
administered in the AM when taken orally or administered IV when the clients
condition warrants immediate removal of body fluid.
a.

Pharmacokinetics: PO readily absorbed from the GI tract. Adult PO dose 20-80mg in a

single dose/day may increase in 6-8 hrs. 20-40mg; maximum dose 600mg/day.
1.Distribution : Protein bound 95%
2. Metabolism: t = 30-50 min
3. Excretion: In urine, some in feces: crosses the placenta.
4. Drug-Lab/Food Interactions : Drug- orthostatic hypotension with alcohol;
ototoxicity with aminoglycosides; bleeding with anticoagulants; K+ loss with steroids;
digitalis toxicity with digoxin and hypokalemia; lithium toxicity;amphotericin B
ototoxicity and nephrotoxicity.
Lab: BUN, blood/urine glucose, serum uric acid, ammonia, potassium, sodium,
calcium, magnesium, & chloride serum levels.
b. Pharmacodynamics:
1. Onset: < 60 min. PO
IV Onset: 5 min
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2. Peak: 1-4 hrs.

3. Duration: UK

PO
PO

IV Peak: 20-30 min

IV
2 hrs.

c.

Side Effects: dizziness, electrolyte imbalances, vertigo, cramping, rash, headache,

weakness, ECG changes, blurred vision, photosensitivity.
d. Adverse Reactions: Severe dehydration; marked hypotension.
e. Life threatening: Renal failure, thrombocytopenia, and agranulocytosis. Transient
deafness. Prolonged use could cause Thiamine deficiency.
f. Aloe K+ level especially when taken with K+ wasting diuretics and licorice can K+
loss.
3. Osmotic Diuretics: osmolality & Na+ re-absorption in proximal tubules and in Loop of
Henle. This group of drugs are used to prevent kidney failure, Intracranial pressure,
Intraocular pressure (glaucoma). Mannitol potent osmotic K+ wasting diuretic frequently used
in Emergency situations. It can also be used with Chemotherapy drugs Crisplatin and
Caboplatin to induce diuresis( common side effect of these drugs fluid retention). Diuresis
with Mannitol occurs in 1-3 hrs. for IV route.
a. Side Effects: Fluid and Electrolyte Imbalances, pulmonary edema from rapid fluid shift,
N/V, tachycardia, acidosis, crystallization of Mannitol may occur in the vial due to exposure
to lower temperatures. Vial may be warmed to dissolve the crystals. CRYSTALS MUST BE
DISOLVED BEFORE DRUG CAN BE GIVEN IV.
MUST BE GIVEN WITH EXTREME CAUTION in Patients with Heart Disease & Heart
Failure.
4. Carbonic Anhydrase Inhibitors: Acetazolamide, Dichlorphenamide, Ethoxzolamide,
Methazolamide block the action of the enzyme carbonic anhydrase (needed to maintain
acid/base). Inhibition of this enzyme causes Na+, K+, HCO3 excretion. These groups of
drugs are used to intraocular pressure in patients with open angle (chronic) glaucoma. Other
uses are for diuresis, treatment of Epilepsy, and treatment of high altitude or acute mountain
sickness.
a. Side Effects: Acetazolamide can cause fluid and electrolyte imbalance, metabolic
acidosis, N/V, anorexia, confusion, orthostatic hypotension, hemolytic anemia,& renal
calculi.
5. Potassium Sparing Diuretics: Weaker drugs than the Thiazides and Loop Diuretics( daily
K+ supplements are not used when patients is taking K+ sparing diuretics).
Monitor : K+ levels if > 5.3 Meq/L while on these drugs, stop drugs and restrict diet of foods
K+. Area of action is in the collecting ducts and distal tubules to promote Na+ and H2O
excretion and K+ retention.
a. Spironolactone ( Aldactone)- An Aldosterone antagonist. First K+ sparing diuretic.
Remember Aldosterone is a mineralocorticoid secreted by Adrenal Cortex. Other
examples are : Amiloride(Midamor), Triamterene(Dyrenium){Prototype},
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6.

Eplerenone(Inspra). They are used in treatment of edema caused by HF or cirrhosis of the

liver.None of the K+ sparing drugs should be taken with ACE inhibitors & Angio II
Recptor Blockers (ARBs) because they also can K+ levels. The commons combinations
of diuretics contain Spironolactone & Hydrochlorothiazide (Aldactazide), Amiloide and
HCTZ( Moduretic), and Triamterene & HCTZ (Dyazide & Maxzide).
b. Side Effects- K+ especially with patient with poor renal function. Urine output should
be @ least 600ml/day. GI disturbances like N/V, diarrhea, numbness & tingling of hands
and feet.
Triameterene ( Dyrenium)- Adult dose for edema 100mg/day in 2 divided doses p.c., not to
exceed 300mg/day. Contraindications severe kidney or hepatic disease severe K+.
Use with Caution : In patients with renal ,hepatic dysfunction and those who have diabetes
mellitus.
a. Pharmacokinetics: PO rapidly absorbed from GI tract
1. Distribution : 67 % Protein Bound
2. Metabolism: t = 1.5 2.5 hrs
3. Excretion: in urine; mostly as metabolites and bile
b. Pharmacodynamics: PO Onset : 2-4 hr
1. Peak: 6-8 hrs
2. Duration: 12-16 hrs
c. Drug-Lab/Food Interactions: Drug- Serum K+ level with K+ supplements; effects
of antihypertensive and lithium; Life threatening: Hyperkalemia if given with ACE
inhibitor. Lab- Increase serum K+ level; may BUN, AST, alkaline phosphatase levels;
serum sodium chloride.
d. Side Effects: N/V, diarrhea, rash, dizziness, H/A, weakness, dry mouth, photosensitivity.
e. Adverse reactions: - Life threatening severity hyperkalemia, thrombocytopenia,
megaloblastic anemia. Monitor signs and symptoms of K+ - peaked T wave,
Bradycardia, oliguria. Teach patient to avoid exposure to direct sunlight.
Chapter 43 Anti-Hypertensives

I. Hypertension is defined as an increase in systolic B/P > 140 and the diastolic > 90 mmHg.
Essential HTN: affecting 90 % of persons with HTN exact origin of essential HTN is unknown.
A. Contributing Factors- Family Hx of HTN
Hyperlipidemia
African American backgroundDiabetes
Obesity
Aging
Stress
Excessive smoking and alcohol
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II. Secondary HTN- it is the other 10% of HTN cases are related to Renal & Endocrine disorders
Kindeys regulate the Reni- Angiotension I to Angiotension II-(causes release of Aldosterone
from the Adrenal glands). Baro-receptors in the Aorta and Carotid Sinus and the vasomotor in
center of the medulla assist in regulating B/P.
Catecholamines Norepinepherine released from sympathetic nerve terminals and Epinepherine
released from the Adrenal Medulla B/P through vasoconstriction activity on the blood vessels.
Anti- Diuretic Hormone (produced by hypothalamus by stored and ANP (atrial naturetic peptide
and Brain Naturetic Peptide) released by the posterior pituitary gland.
III. Non- Pharmacologic Control for HTN : If systolic is > 140 anti hypertension drugs are
generally necessary.
A. Stress reduction techniques
B. Exercise
C. Salt restriction
D. Alcohol ingestion
E. Weight reduction
IV. Most Clients may need two or more Anti - hypertensive drugs to achieve a goal Blood
pressure reading:
1. Six Categories of drugs to treat HTN:
1. Diuretics- ** see chapter 41
2. Sympatholytics-(Beta Adrenergic Blockers)
3. Direct- acting Arteriolar Vasodilators4. Angiotension Convert Enzyme inhibitors5. Angiotension II receptor Blockers
6. Calcium Channel Blockers
2. Beta Adrenergic Blocker : Beta ( 1 & 2) Adrenergic Blockers reduce cardiac output by
diminishing the sympathetic nervous system response to basal sympathetic tone. They
reduce heart rate, contractility, and Renin release. African Americans with HTN do NOT
respond as well to Beta blockers for HTN control so they are given beta blockers combined
with diuretics.
1. Metroprolol (Lopressor, Toprol SR)- Beta1 {Prototype}PO Adult dose for HTN 50-100mg/d in 1-2 divided doses Maintenance dose is 450mg/day
in divided doses.
Elderly- PO 25mg/day Maintenance dose of 25-300mg/day
Myocardial Infarction-

PO:

100mg B.I.D.

IV: 5mg q 2 min X 3 doses.

Drug- Lab/Food Interactions: Drug- bradycardia with digitalis: Hypotensive effect with
other anti-hypertensive, alcohol, anesthetics.
a. Pharmacokinetics :
1. Absorption: PO 95%
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2. Distribution: Protein Bound is 12%

3. Metabolism: t1/2= 3-7 hrs.
4. Excretion : in urine
b. Pharmacodynamics: PO : Onset 15 min

IV Onset: Immediate

Peak: 1.5 hrs

IV Peak : 20 min

Duration: 10-19 hrs.

IV Duration: 5-10 hrs.

c. Side Effects: Fatigue, weakness, dizziness, nausea, vomiting, diarrhea, mental

changes, nasal stuffiness, impotence, libido, depression.
d. Adverse Reaction: Bradycardia, thrombocytopenia
e. Life Threatening: Complete heart block, bronchospasm, and agranulocytosis.
1. Cardioselective Beta-blockers- are preferred Beta Blockers because they act mainly on
the cardiac Beta1 receptors rather than Beta2 so bronchoconstriction is less likely to occur.
Medications in this group are: Acebutolol ( Sectral), Atenolol ( Tenormin), Betaxolol(
Kerlone), Bisoprolol (Zebeta).
2. Centrally Acting Alpha2- Centrally acting alpha2 agonists the sympathetic response
from the brainstem to the peripheral vessels. By stimulating the alpha2 receptors which in
turn sympathetic activity: vagus activity, cardiac output and serum epinephrine,
norepinepherine, & renin release. All actions result in reducing peripheral vascular
resistance and vasodilation. This group of drugs has minimal effect on cardiac output
and kidney perfusion. Beta Blockers are NOT given with centrally acting
sympatholytics, because of bradycardia during therapy and rebound hypertension on
discontinuing therapy that can occur. Example: Of these types of drugs is Methyldopa
(Aldomet). In higher doses Methyldopa & clonidine can cause water retention therefore
they should be used with a diuretic. Potential side effects: drowsiness, dry mouth,
dizziness, and slow heart rate(bradycardia). Methyldopa should NOT be used in clients
with impaired liver functions & serum liver enzymes should be monitored periodically.
These drugs must not be stopped abruptly d/t rebound hypertensive crisis.
3. Alpha-Adrenergic Blockers: - These drugs block the alpha receptor sites resulting in
vasodilation B/P. Useful in treat of HTN in patients with Hyperlipidemia. They the
very low density lipoproteins (VLDL) and the low density lipoproteins (LDL) which
cause plaque buildup leads to artherosclerosis, they also build up the good lipoproteins
High density ones (HDL). They are also good for diabetic patients because they do not
effect Glucose metabolism.
4. Examples of Alpha Adrenergic Blockers: Prazosin (Minipres) {Prototype}, Terazosin(
Hytrin), Doxazosin( Cardura) are mainly used for HTN but can also be used for treatment
of Benign Prostatic Hypertrophy. Terazosin & Doxazosin have longer half lives so they
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usually are given once/day. They do cause NA+ & water retention therefore a diuretic is
also given concomitantly to fluid accumulation.
More potent medications like Phenoxybenzamine and Tolazoline are used to treat HTN
Crisis & vere HTN resulting from catecholamine secreting tumors of the adrenal medulla
like (phenochromocytomas).
A. Prazosin HCL (Minipres) Alpha Adrenergic Blocker PO Adult dose 1mg B.I.D. or
T.I.D. With a maintenance dose of 3-15mg/day. Drug- lab/ Food Interactions:
Hypotension effect with other anti-hypertensives, nitrates and alcohol.
a.
Pharmacokinetics : Absorption in G.I. 60%, 5% in circulation
1. Distribution: Protein Bond 95%
2. Metabolism: 3 Hours
3.
Excretion: in bile & Feces 10% in urine.
4. Mode of Action: Dilation of peripheral blood vessels via blocking Alpha
Adrenergic receptors.
2. Pharmacodynamics: P.O. Onset o.5 2 hrs. Peak: 2-4 hrs. Duration: 10 hrs.
a. Adverse Reactions: Orthostatic Hypotension, palpitations, Tachycardia,
pancreatitis
b.
Side Effects: Drowsiness, H/A, N/V, diarrhea, impotence, vertigo, urinary
frequency, tinnitus.
c. Drug Interactions: when Alpha Adrenergics Blockers are taken with Antiinflammatory drugs and nitrates Fluid Retention peripheral edema
Nitrates - Lower B/P as do Alpha-Adrenergic which leads to syncope/fainting.
II. Adrenergic Neuron Blockers are potent antihypertensive drugs that block Norepinepherine
Release from the Sympathetic nerve endings, causing a decrease in B/P, & decrease in
Cardiac output & in peripheral vascular resistance.
A. Reserpine, Guanethidine, Guanadrel (are 3 very potent drugs) that are used to treat severe
HTN. Adrenergic Neuron Blockers are the LAST drugs considered for treatment of HTN
because of the orthostatic hypotension.
Reserpine can cause nightmares and suicidal tendencies.
III. Alpha1, Beta1, Adrenergic Blockers : Labetalol( Normodyne) & Carteolol(Cartrol) are
examples of Alpha/Beta blockers. When the Alpha1 receptor sites are blocked it causes
Vasodilation. , which decreases the resistance of the blood flow. The blocking of effect on
the Alpha receptor site is stronger than that on the Beta receptor therefore B/P is lowered
and pulse rate is moderately decreased.
A. Common side Effects: Orthostatic Hypotension, GIdistrubances, nervousness, dry
mouth, fatigue.
*** Large doses of Labetalol may cause Atrial Ventricular Heart Block. (Property of
Beta blockers that slows Atrial Ventricular conduction which in turn slows heart rate).
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IV. Direct Acting Arteriolar Vasodilators: This group of drugs act by relaxing the smooth
muscle of mainly the arterioles. Vasodilatation leads to blood flow to the Brain and
kidneys, with a decrease in B/P Na and water are retained leading to edema. This is why a
diuretic would be given with these drugs. Examples would be Hydralazine and Minoxidil
both can be used to treat mild to moderate HTN. Also because of the vasodilatation that
these drugs cause Reflex Tachycardia and Renin is released. Beta Blockers are frequently
prescribed with D.A.A. V. to decrease the Heart rate (counter act the Reflex Tachycardia).
A. Nitroprusside & Diazoxide : These are 2 very potent vasodilators used for acute
HTN emergency. Nitroprusside acts on both arterial & venous blood vessels, whereas
Diazoxide acts on only arteries. Common side effects: Hydralazine side effects are
tachycardia, palpitations, edema, nasal congestion, H/A, dizziness, bleeding, and
Lupus like symptoms.
Minoxidil & Diazoxide : Refex Tachycardia, palpitation, restlessness, agitation,
nausea, and confusion.
Diazoxide: hyperglycemia due to its action of inhibiting release of insulin from the
Pancreatic Beta cells.
V. Angiotension Converting Enzyme Inhibitors: They inhibit the formation of Angiotension II
and blocks the release of Aldesterone. When aldesterone is blocked Na and water are not
retained but are excerted. K + is retained. ACE inhibitors cause little change in Cardiac
Output or HR but do peripheral vascular resistance. These drugs can be used in patients
with renin levels. They are primarily used to treat HTN , some are effective in treatment of
Heart Failure. There are 10 drugs in this category:
1. First one discovered in 1970s is Captopril (Capoten)
7. Moexipril(Univasc)
2. Benzepril (Lotension)
8. Perindopril (Aceon)
3. Enalapril (Vasotec)
9. Fosinopril (Monopril)
4. Ramipril(Altace)
10. Quinapril (Accupril)
5. Trandolapril(Mavik)
6. Lisinopril(Prinavil Zestril)
These drugs can be used as the first line Anti Hypertensive agents but the use of Thiazide
diuretics are also recommended.
****** African Americans and Older Adults DO NOT RESPOND TO ACE inhibitors until
diuretics are added. SHOULD NOT PRESCRIPED/ADMINISTERED DURING
PREGNANCY (D/T the effect they have of reducing Placental blood flow).
A. Side Effects: Constant irritating cough; Nausea/Vomiting, diarrhea, H/A, dizziness,
fatigue, insomnia, Hyperkalemia, and tachycardia.
B. Contraindications: Should not be administered while pregnant will cause fetal harm
d/t decrease placental blood flow. Should not be taken with K+ sparing diuretics or salt
substitutes (those that use K instead of Na).
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VI. Angiotension II Receptor Blockers (ARBs): They are similar to the ACE drugs except
ARBs block Angiotension II from Angiotension receptors found in many tissues. ARBs
cause vasodilatation and peripheral resistance. They do not cause the constant irritating
cough. ARBs should not be taken during pregnancy either.
A. Examples: Losartan (Cozaar), Valsartan (Diovan) Irbesartan (Atacand), Olmesaran
Medoxomil (Benecar)- these agents block the vasoconstrictor effects of Angiotension II
at the receptor sites. ARBs can be used as a first line Treatment for HTN.
B. Pharmacokinestics: Cozaar is used primarily to manage HTN and to form active
metabolites.
1. Distribution: They are Highly Protein Bond
2. Metabolism: t - 1.2- 2 hours & metabolite half life is 6- 9 hrs.
3. Excretion: In the Urine and Feces
C. Pharmacodynamics: Losartan (Cozaar) is a potent vasodilator which blocks the binding of
Angiotension II to the Angiotension receptors found in many tissues. PATIENTS WITH
MILD HEPATIC INSUFFICENCY CAN TAKE THESE DRUGS. The Peak time is 6
hrs., Duration is 24 hrs. THEY ARE LESS EFFECTIVE IN AFRICAN AMERICAN and
may cause Angioedema
VII. Direct Renin Inhibitors: Aliskiren ( Tekturna) 1st FDA approved Renin inhibitor.
Aliskiren binds with Renin causing a in Angiotension, Angiotension II and Aldesterone
levels. Effective for the treatment of mild to moderate HTN. Can be used alone or with
another antihypertensive agent. Has an added effect in B/P when combined with Thiazide
diuretics or ARBs.
A. Prototype: Losartan ( Cozaar) Angiotension II receptor Blockers . Pregnancy C ( First
Trimester), D (2nd or 3rd Trimester can use Hyzaar). PO: For HTN- 25- 50 mg/day in single
or divided doses. Maxium dose is 100mg/ day.
Contraindicated: During Pregnancy and while Breastfeeding
Caution: Renal & Hepatic Impairment.
B. Pharmacokinestic:
1. Absorption: Rapidly absorbed in blood in 25-30 minutes.
2. Distribution: Protein bond 90-95%
3. Metabolism: t 1.2- 2 hrs. metabolites in 6-9hrs.
4. Excretion: 35% in the urine.
5. Side Effects: Dizziness, diarrhea, insomnia, & occ. Cough
6. Drug & Lab Interactions: Phenobarbital effect of Cozaar & its metabolites
May increase ALT, AST, ALP ,Bilirubin , Creatinine , Hbg. and Hct.
7. Adverse: Upper Respiratory Infections.
C. Pharmacodynamic: Onset: < 1 hr.
Peak : 6 hrs.
Duration: 24 hrs.

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D. Calicum Channel Blockers: These are a group of drugs that are slow channels found only in
myocardium & vascular smooth muscle. Free Ca+ muscle contractility, peripheral
resistance, & B/P. Ca+ channel blockers also called Calcium anti-agonist promote
vasodilation. Large central arteries are not as sensitive to Ca+ as the coronary, Cerebral and
peripheral arteries are. They are highly protein bond but have a short half- life. 3 groups of
Ca+ blockers. Calcium Channel Blockers lower B/P better in African Americans than
drugs in other categories.
1. Verapamil (Calan): is used for treatment of chronic HTN, angina pectoris & cardiac
dysrhythmias. Verapamil and Diltiazem act on the arterioles & the heart. Nifedopine is
used to prevent ischemic brain injury due to vasospasm that often accompanies
subarachnoid hemorrhage. Also used as treatment of choice in Variant angina (Prentz
Metal ) also thought to be caused by vasospasm of the coronary arteries.
2. Nifedipine (Procardia): Decreases B/P in older adults & in those with low serum Renin
values. In the immediate released capsules (10-20mg) it has been associated with
increased incident of sudden Cardiac Death especially when prescribed for outpatient at
high doses d/t the fact that Ca+ channel blockers cause reflex tachycardia. This tachycardia
is more prevalent with Procardia.
3. Prototype: Amlodipine (Norvasc) : It is used to treat mild to mod. HTN, and Angina
Pectoris.
Mode of action: Decreases peripheral vascular resistance (vasodilation), promoting in
B/P. PO 5- 10mg/day or for Elderly 2.5- 5mg/day.
Lotrel is a combination of Amlodipine with Benzepril.
Contra-Indications: Severe hypotension.
Cautious Use: Liver Disease, Heart Failure, Aortic Stenosis, pregnancy & lactation.
Drug- Lab Interactions: Drugs bradycardia with Adenosine
Labs: May Amlodipine
with Grapefruit juice.
1. Pharmacokinetics:
a. Absorption: > 90% is absorbed; gradually absorbed from the G.I. tract.
b. Distribution: Highly Protein Bond > 95%
c. Metabolism: t 30- 50 hrs. Elderly: t : 50- 100 hrs.
d. Excretion: in urine & feces as inactive metabolites.
2. Pharmacodynamics: Onset is gradual
only prescribed once a day.

Peak: 6-9 hrs.

Duration 24 hrs. Usually

4. Side Effects : Peripheral edema may occur because of its vasodilator effect, flushing,
dizziness and nausea.
5. Adverse: Reflex Tachycardia
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Chapter 44 Anti-Coagulants/Anti- Platelets & Thrombolytics

Thrombosis - Formation of a clot in an arterial or venous vessel.
Arterial clots could be caused by stasis of blood, platelet aggregation (clumping) on vessel
wall. They are usually made up of white & red clots.
White clots: - (Platelets) initiating the process followed by fibrin formation trapping red
blood cells into fibrin. Blood clots of the veins are from platelet aggregation with fibrin that
attaches to red blood cells. Both kinds of thrombosis formation can become dislodged from
the wall of the vessel and lead to embolus.
Platelets dont usually stick together unless there is a break in the endothelial lining of the
blood vessel. When platelets do stick to the lining they synthesize Thromboxane A2 (product
of prostaglandins and protein synthesis). Platelet receptor protein glycoprotein IIb & IIIa.
Thromboxane A2, and adenosine diphosphate (ADP) the activation of this receptor. As
thrombus inhibits blood flow, fibrin, platelets and red blood cells surround the clot building
the clots size and structure. As clots occludes the vessel, tissue ischemia occurs. The
venous thrombus usually develops because of slow blood flow. Venous clots can occur
rapidly.
Heparin & Warfrin: Act primarily to prevent venous thrombosis whereas Anti-platelet
drugs act to prevent ARTERIAL thrombosis. Both groups of drugs suppress thrombosis in
general.
I. Anticoagulants: Used to inhibit clot formation. They DO NOT dissolve clots like
Thrombolytics. They are used in clients with venous & arterial vessel disorders that put
them at high risk for clot formation. They can be administered Orally, Intravenously, or
Subcutaneous.
Venous- deep vein thrombosis, Pulmonary Emboli
Arterial Coronary artery thrombosis (MI) presence of artificial valves, CVA/Strokes
A. Heparin: Introduced in 1938, it is a natural substance found in the liver. It was used
with blood transfusions to prevent clotting. Is indicated for a rapid anti-coagulant effect
when thrombus occurs d/t DVT, Pulmonary Emboli, or an evolving stroke and for open
heart surgery to prevent blood from clotting & in Disseminated Intravascular
Coagulopathy. Heparin works with anti-thrombin III to inactivate Xa thus preventing
thrombus formation. Poorly absorbed through the GI tract and much is destroyed by
Heparinase (a Liver enzyme). IV bolus and or IV fluid for continuous drip Heparin
prolongs clotting time.
Heparin affects Partial Thromboplastin Time - (PTT). Heparin can platelet count
causing Thrombocytopenia.
ANTIDOTE: PROTAMINE SULFATE.
B. Low Molecular Weight Heparin( LMWH) - Lowers the risk for DVT, Pulmonary
Emboli after abdominal or orthopedic surgeries. Commonly used to prevent Pulmonary
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Emboli. LMWHs produce more stable responses at recommended doses, therefore frequent
monitoring of PTT is not required. LMWH inactivates factor Xa , but it is less able to
inactivate thrombin like Heparin is able to.
1. 4 Types of LMWH are: All can be given subcutaneously and do not require
monitoring of aPTT. Treatment is injection in the abdomen for 7-14 days. It is
usually started in the hospital 24 hrs. post-operatively. The half life of LMWH are
2 to 4 times longer than that of heparin. Instruct clients not to take aspirin or other
anti-platelet drugs while on LMWH. Bleeding with these drugs is less likely to
occur than with Heparin. If bleeding dose occur Protamine Sulfate is the antidote.(dose would be 1mg of Protamine S. for every 1mg of LMWH given.)
Contra-Indications: Pt. whom have had a stroke, peptic ulcers, or other blood
anomolies
a. Enoxaparin Sodium: (Lovenox)
b. Dalteparin Sodium: (Fragmin)
c. Danaparoid : ( Orgaran) - **It is considered LMWH but actually does not
have Heparin in its structure.
d. Tinzaparin Sodium: (Innohelp)
2. Direct Thrombin Inhibitors: Anticoagulants II There are 4 new parental anti-coagulants
that directly inhibit thrombin from converting fibrinogen to fibrin. Three are given
Intravenously and are very costly!
a. Argotroban ( Acova)
b. Bivalirudin (Angiomax) binds with inhibitors free flowing thrombin
c. Lepirudin (Refludan)
d. The 4th Drug is given Subcutaneously Desirudin (Iprivask)
C. Oral Anti-Coagulants- Examples would be Warfrin/Coumadin before it was used on humans it
was used on rodenticides to kill rats by causing them to hemorrhage. Oral anti-coagulants inhibit
hepatic synthesis of Vitamin K thus affecting clotting factors II, VIII, IX, and X. Warfrin is used
mainly to prevent thromboembolic conditions such as:
1. Thrombophlebitis
2. Pulmonary Embolism
3. Embolisms formation caused by Aterial Fibrillation which can lead to CVA
Prolong clotting time and monitoring of Prothrombin Time . INR = International Normalized
Ratio is used to account for the varibilities in reported levels from different labatories. Normal
INR is 1.3 to 2 however patients on Warfrin therapeutic range is 2-3 INR and for patients with
Mechanical Heart Valves INR is maintained at 2.5-3.5 and could go as high as 4 on the INR.
Coumadin has a long t and a very long duration. Drug accumulation can occur and lead to
external and internal bleeding. Teach patients to watch for signs of bleeding(petechiae,
ecchymosis, tarry stools, & hematemsis.

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ANTIDOTE FOR COUMADIN IS VITAMIN K or Aquamephyton-but it takes 24-48

hrs to be effective.
Usually a low dose of oral Vitamin K is recommended for patient with INR of 5.5.
** If excessive Vitamin K is given it may take Warfrin 1- 2 weeks before it can be effective
again. If patient with acute bleeding give Fresh Frozen Plasma.
D. Anti- Platelet Drugs: are used to prevent thrombosis in the arteries by suppressing platelet
aggregation. (Heparin and Warfrin are used to prevent thrombosis in the veins).
Anti- platelet drug therapy is mainly for prophylactic use in :
1. Prevention of myocardial infarction or stroke for patients who have a family history.
2. Prevention of a repeat M.I.
3. Prevention of a stroke in patients who have had a transient ischemic attack.
Long term therapy of a low dose aspirin has been found to be both an effective and cheap
treatment for suppressing platelet aggregation. Aspirin works by inhibiting cyclooxyganase,
an enzyme needed by the platelets to synthesize thromboxane (A2). Because aspirin has a
prolonged anti-platelet activity it should be stopped/discontinued for at least 7 days
prior to surgery.
1. Other Examples of anti-platelets:
a. Dypridamole (Persantine)
b. Ticlopidine (Ticlid)
c. Clopidogrel (Plavix) Prototype It may be prescribed by itself or in combination
with Aspirin.
d. Tirofiban (Aggrastat)
Clopidogrel, dypridamole and ticlopidine have similar effects as aspirin but they are known
as Adenosine Diphosphate antagonists affecting platelet aggregation.
2. Clopidogrel (Plavix) Anti- Platelet Used to prevent recurrence of MI, CVA, vascular
death.
Pregnancy Category: B
Usual PO dose is a loading dose of 3oomg then 75 mg.
A. Pharmacokinetics:
1. Absorption: Rapid
2. Distribution: (Protein Bond) 94%-98%
3. Metabolism: t : 8 hours
4. Excretion : 50% in urine and 50% in feces
B. Pharmacodynamics: PO: Onset- 1-2 hrs. Peak- 2 -3 Duration: 3 days or
longer.
C. Side Effects- Upper Resp. Tract Infection, flu-like symptoms, dizziness,
headaches, fatigue, chest pain, diarrhea
D. Adverse Reactions: None of significance May cause hypertension, bronchitis.
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E. Thrombolytic: Remember that normally it takes about 1-2 weeks for a blood
clot to disintegrate by natural fibrinolytic mechanisms. Our goal with
thrombolytic therapy is for this to occur much quicker thus preventing ischemia
& then tissue necrosis. These drugs work by promoting the mechanism of
converting plasminogen to plasmin, which destroys the fibrin in blood clot. The
thrombosis will disintegrate within 4 hours after the administration of a
thrombolytic drug. These drugs should be administered within 3 hours of a
thrombolytic stroke. They are also used in treatment of Pulmonary Emboli, &
Deep Vein thrombosis.
1. Five Types of Thrombolytics:
a. Steptokinase- enzyme
b. Urokinase- enzyme
c. Alteplase- alos know as a tissue plasminogen activator(tPA) Prototype)
d. Reteplase (Retavase)
e. Tenecteplase(TNKase)
*** all five of these drugs induce Fibrinolysis (fibrin breakdown)
** Anticoagulants and Anti-platelets increase the risk of hemorrhage
F. Alteplase: promotes the conversion of plasminogen to plasmin. Thrombolytic
agent. It Initiates fibrinolysis. Pregnancy Category :C
Trade name: tPA, Activase Adult Dose: IV Bolus 15mg, then 50mg infused
over 30 minutes, then 35mg infused over 60min. Maximum; 100 mg
Drug- Lab Food Interactions:
Drug: Increase bleeding when taken with oral anticoagulants, NSAIDS,
cefotetan, plicamycin
Lab; Decreases in plasminogen, fibrinogen, hematocrit, and hemogloblin
1. Pharmacokinetics:
a. Absorption: IV
b. Distribution: Protein Bind Unknown
c. Metabolism: t1/2- 5min
d. Excretion: Urine
2. Pharmacodynamics: PO Onset: immediate Peak: 5-10 min. Duration: 3hrs
3. Side Effects: Bleeding
4. Adverse Reactions: Life-threatening: Intracerebral hemorrhage, stroke,
atrial or ventricular dysrhythmias.
5. The Antithrombolytic drug Aminocaproic Acid(Amicar) is used to stop
bleeding by inhibiting plasminogen activation, which inhibits
thrombolysis.

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Chapter 46 Anti-Lipidemics And Peripheral Vasodilators

I.

There are 4 major categories of lipoproteins:

1. High Density Lipoproteins= HDL AKA Friendly or Good lipoproteins. It is
responsible for removing cholesterol from the blood stream and sending it to the liver
for excretion in the bile.
2. Low Density Lipoproteins= LDL= Bad Cholesterol contains 50- 60% of the
cholesterol in the blood stream. With an elevated LDL there is a greater risk for
developing atherosclerotic plaques and heart disease.
3. Very Low- Density Lipoprotein= VLDL- they carry mostly triglycerides & less
cholesterol.
4. The first treatment for hyperlipodemia should be a reducing the intake of saturated fats
and cholesterol in the patients diet. The plan is to reduce total intake of fats to 30-40%
of intake and reduce cholesterol intake to 300mg/day.
**Remember that 75-80% of our total cholesterol is produced Endogenously. **
Diet modification will only reduce cholesterol levels by 10%- 30%.
Exercise is another important non-pharmacuetical way to work on for lowering
cholesterol levels. Exercise will increase the HDL and lower cholesterol levels.
Smoking increase the LDL, cholesterol and decreases the HDL.

Antilipidemics: Drugs that lower lipoproteins. Lipids (Cholesterol, triglycerides, and

phospholipids) are bound in the inner shell of protein, which is a carrier that transports lipids into
the blood stream. Hyperlipidemia is defined as an excess amount of one or more lipids in the blood
stream. Drugs that lower lipid levels include bile-acid sequestrants, fibrates (fibric acid), nicotinic
acid, cholesterol absorption inhibitors and hepatic 3 hydroxy-3methylglutary-coenzyme A
reductase inhibitors (statins). The statins have fewer adverse effects and are tolerated well.
Clients need to be educated that if they stop Antilipidemic therapy that their cholesterol levels will
go back to pretreatment levels.
A. Questran One of the first bile sequestrants, which reduces LDL. It binds with bile salts
in the intestines. It can be used with Statin drugs .It is a gritty powder that must be dilated in
liquid like water or juice.
B. Clofibtate (Atromid- S) & Gemfibrizol( Lopid)- are fibratic acid derivatives that are
more effective in lowering triglcerides and VLDL. They are highly protein bond and should
not be taken with anticoagulants. It is not suggested for long term use d/t many side effects
like cardiac dysrhythmias, angina, thromboembolism, and gall stones.
C. Nictotinic Acid-(Niacin)or (Vitamin B2)- reduces VLDL& LDL. Because of its
numerous side effects and need for larger doses ( al low as 20% of clients can tolerate it.
It can be used and tolerated by some whom concomitant use of Aspirin.

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D. Ezetimibe (Zetia)- is a cholesterol absorption inhibitor that acts on the cells in the small
intestine to inhibit cholesterol absorption. It lowers levels of cholesterol and lipids from the
foods that are ingested. It lowers LDL, triglycerides, and ApoB levels. It also causes small
increase to the HDL. It MUST be combined with statins for optimum effect.
E. Statins- first introduced in 1987, inhibits the enzyme HMG CoA reuctase in cholesterol
synthesis in the liver. These drugs decrease the concentration of cholesterol, decreases the
LDL, and slightly increased HDL. May see a decrease in LDL in as early as 2 weeks. All
statins should be monitoring Liver enzymes and yearly eye examinations because of risk of
cataract formation and rhabdomyolysis.
1. Atorvastitin Calcium (Lipitor) Prototype
2. Fluvastain (Lescol)
3. Lovastatin (Mevacor)- 1st statin to be used . Side effects: GI disturbances, H/A, muscle
cramps, and tiredness .
4. Pravastatin Sodium ( Pravachol)
5. Simvastatin (Zocor)
6. RosuvastatinCalcium (Crestor)
F. Prototype Atrovastatin( Lipitor)- Decreases LDL by 25% with lower doses and 55% with
higher doses. It inhibits HMG-CoAreductase, the enzyme necessary for hepatic production of
cholesterol. Adult PO : 10mg/day may increase up to 80mg/day.
Drug Lab-Food Interactions:
Drug: Decrease effect with antiacids, propanolol. May increase digoxin level, oral contraceptives.
Increases effects with macrolide antiobiotics, and antifungals.
1. Pharmacokinetics;
a. Absorption: rapid
b. Distribution: Protein bond 98%
c. Metabolism: t1/2 14 hours: metabolites 20-30 hrs.
d. Excretion: to primarily in bile; some in urine
2. Pharmacodynamics: PO onset: 2 week for decreasing cholesterol
Peak: 1-2 h. 2-4 weeks to be effective
Duration: 24 hrs.
3. Side effects: Rare H/A, rash/pruitus, constipation/diarrhea, sinusitis, pharyngitis
4. Adverse Reactions: Rhabdomyolysis, myalgia, photosensitivity, cataracts

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Chapter 50 Endocrine

The endocrine System consists of ductless glands that secrete hormones in the blood stream.
Endocrine glands include: Pituitary (Hypophysis), Thyroid, Parathyroid, Adrenal , gonads, and
the Pancreas.

I.
II.

Hormones are chemicals synthesized from amino acids & cholesterol that act on body
tissue, organs & affect cellular activity.
GlandsA. Pituitary Gland- Located at the base of the brain. Divided into 2 lobes Anterior and
Posterior.
1. Anterior Lobe: (Adenohypophysis) Often called the Master Gland D/T its function of
secretions of hormones that stimulate the release of other hormones from target glands like
the thyroid. Parathyroid, adrenals, and gonads. It secretes a total of 6 hormones
a. Thyroid Stimulating Hormone (TSH) also called Thyrotropic Hormone - is
secreted in response to the Hypothalmus releasing Thyroid Releasing Hormone. When
this hormone is over secreted (hypersecretion) can cause Hyperthyroidism.
b. Adrenocorticotropic Hormone ( ACTH)- Hormone secreted to stimulate Adrenal
Cortex to release Glucocorticoid (cortisol), Mineralcorticoid hormone( Aldesterone).
More ACTH is secreted in the AM then in the PM
c. Gondtropins- Follicle stimulating hormone (FSH), & Luteinizing Hormone (LH) these
hormones control the release of hormones from the Thyroid and Adrenal, and
ovaries. Regulate hormone secretion from the ovaries & testes.
d. Growth Hormone (GH)or the Somatotrophic Hormone acts on body tissues,
particularly the bones & skeletal muscles. Regulated by the amount of Growth
Hormone Releasing Hormone & Growth Hormone Inhibiting Hormone (Somatostatin)
that is released from the Hypothalamus. Sympathomimetics drugs, Serotinin,
glucocorticoids can inhibit the secretion of Growth Hormone.
e. Prolactin (PL)- stimulates milk formation in the glandular breast tissue after childbirth
f. Melanocyte Stimulating Hormone (MSH)
Remember the amount of each hormone is regulated by negative feedback system to
the Anterior Pituitary Gland.

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2. Posterior Lobe: (Neurohypophysis) secretes 2 Neurohormones:

A. Antidiuretic Hormone- Increases the reabsorbtion of water in the tubules, returning it
to the systemic circulation. Secretion of ADH is regulated by serum Osmolality .If
serum osmolality is increased so is the production of ADH. (Vasopressin).
B. Oxytocin- Stimulates the contraction of the smooth muscles of the Uterus.
III.

Thyroid Gland- It also has 2 lobes and is located on either side of the anterior Trachea. It
secretes two hormones:
A. Thyroxine (T4)
B. Triiodothyronine( T3)
These hormones affect nearly every tissue & organ by controlling their metabolic rate.
Stimulation by the Thyroid hormone results in cardiac output, O2 consumption,
carbohydrate use, protein synthesis, & the breakdown of fats (Lipolysis). These hormones
also affect body heat regulation and womens menstrual cycles.\
IV. Parathyroid Gland: There are 4 parathyroid glands 2 pairs that lie on the dorsal surface of
the thyroid gland. It secretes 2 hormones
A. Parathyroid Hormone/PTH - this hormone regulates serum Ca+ levels. When there is a
in serum Ca+ (Hypocalcemia)the PTH is release from the parathyroid gland. PTH will
serum Ca+ levels by: 1) Mobilizing Ca+ from the bone. Remember PTH P for PTH pulls
Ca+ from the bone and puts it back into the blood stream; 2).Promotes Ca+ absorption from
the intestines; 3) Promotes Ca+ re-absorption from the renal tubules.
B. Calicitonin- Hormone that primarily is produced by Thyroid (and to a lesser extent the
Parathyroid & Thymus Glands). Its purpose is to inhibits Ca+ re-absorption by the bone &
renal excretion of Ca+ . Think Calcitonin Keeps Calcium in the bone, which is the
opposite effect of P.T.H.
V. Adrenal Glands: Located at the top of each Kidney. There are two separate sections:
A. Medulla or Center secretes catechlomanines Epinephrine and Norepinephrine.
B. Cortex- or known as the outer portion of the gland. Secretes 2 major hormones:
1. Glucocorticoids- Principal hormone is Cortisol
2. Mineralcorticoid- Aldersterone which acts in the kidney telling the kidney to
reabsorb Na+ and then water back in the systemic circulation. Some other
hormones to a smaller extent would be Androgen, Estrogen, and Progestin.
VI. Pancreas: Located to the left and behind the stomach is both an Exocrine and Endocrine
gland.
A. Exocrine property would be the secretion of digestive enzymes into the duodenum of
the small intestines.
B. Endocrine- hormones are secreted by cluster of cells called Islets of Langerhans
There are 2 types of cells the Alpha islet cells produce glucagon(which breaks glycogen
down into glucose in the liver). The Beta islet cells secrete Insulin (Regulates glucose
metabolism).
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VII. Growth Hormones: There are 2 which are secreted from the Hypothalamic Hormones:
A. Growth Hormone- releasing Hormone and Growth Hormone Inhibiting Hormone
(Somatostatin). Growth Hormone doesnt have a specific target gland but it does affect body
tissues and bones. Synthetic Growth Hormone Drugs cannot be given orally due to them
being inactivated by gastric enzymes. They are given subcutaneously or intramuscularly.
G.H. replacement therapy is very expensive. G.H. acts on newly forming bone and it must
be administered before the epiphyses are fused. Prolonged G. H. therapy can antagonize
Insulin secretion and eventually cause Diabetes Mellitus.
A. G. H. Deficiencies Drug Therapy: Drugs used to treat growth failure in children are :
1. Somatrem (Protropin)- Has identical amino acid plus an additional amino acid.
2. Somatropin (Humatrope) has identical amino acid sequences as Human G Hormone
(contraindicated in children with Prader Willi Syndrome and those children who are
severely obese or who have Respiratory impairment.
B. Growth Hormone Excess- Gigantism- excessive growth during childhood or
Acromegaly (excessive growth after puberty) can occur with Hypersecretion of G.H.
and is associated with Pituitary tumors. If the treatment with radiation is ineffective
the Prolactin- Release Inhibitor: Bromocriptine can inhibit the release of G. H.
C. Octreotide(Sandostatin) : is a potent synthetic Somatostatin used to suppress G.H.
release. It can be used alone or with Surgery and or Radiation. This drug is expensive.
G.I. side effects are common. This drug can also be used for severe diarrhea resulting
from carcinoid tumors.
VIII. Thyroid Stimulating Hormone: Adenohypophysis secretes T.S.H. in response to ThyroidReleasing Hormone from the Hypothalamus. TSH stimulates the thyroid to secrete:
Thyroxine (T4) & Triiodothyronine(T3).
A.

Excessive or Deficiency in production of TSH:

1. Excessive Production of TSH causes Hyperthyroidism:
2. Deficiency of TSH causes Hypothyroidism: Primary Hypothyroidism caused by
Thyroid gland disorder. Secondary Hypothyroidism caused by decrease amount of TSH.
B. Thyrotropin(Thytropur): is a purified extract of TSH used as a diagnostic agent to
differentiate between primary and secondary hypothyroidism.
IX.

Adrenocorticotrophic Hormone: Corticotropin Releasing Factor (CRF) stimulates the

Pituitary corticotrophs to secrete (ACTH) secretion stimulates the release o
Glucocorticoids(Cortisol) and Mineral Corticoids (Aldesterone) and Androgens from the
Adrenal cortex. Usually ACTH & Cortisol secretions are in the morning versus lower in
the evening , also stressors like Surgery , Sepsis, and trauma override diurnal rhythm.
A. ACTH Corticotropin (Acthar) {Pro totype}- Is used to diagnosis Adrenal
disorders; treat Adrenal Insufficiency and as an anti-inflammatory drug in treatment of
allergic response, if it is administered I.V. Should see in serum cortisol levels in 30-60
min. ACTH the symptoms of Multiple Sclerosis during its exacerbation phase.

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Pregnancy- C. Dosage: As a diagnostic test 10- 25 Units IV in 500 ml of D5W q 8 Hr.

Acute MS: - Sub Q/IM 80-120 Units/day for 2-3 weeks
1. Pharmacokinestics: Absorbed well Protein Bond - Unknown
a. Metabolism: t - 5-20 min.
b. Excretion: Excreted in the urine.
2. Pharmacodynamics: IM Onset: 6hr. Peak: 6- 18 hrs. Duration: 12- 24 hrs.
IV Onset: UK
Peak: 1 hr.
Duration: UK
a. Side Effects: Nausea/vomiting, appetite, mood swing, Euphoria to depression,
petechiae, water and Na+ retention, hypokalemia and hypocalcemia
b. Adverse: Edema, ecchymosis, osteoporosis, muscle atrophy, growth retardation,
depressed wound healing, cataracts, glaucoma, menstrual irregularities.
c. Life Threatening: Ulcer perforation, pancreatitis.
d. Drug;Food and Lab: Drug- Increase in ulcer formation with aspirin; may increase effect
of potassium- wasting diuretics; decrease effects of oral antidiabetics or insulin
(hypoglycemia).
X.

Posterior Pituitary Gland: Secrets Antidiuretic Hormone (Vasopressin) and Oxytocin.

When there is a deficiency of ADH large amounts of water is excreted by the Kidneys
Diabetes Insipidus severe fluid volume defecit. Head injuries, Brain tumors can be some
of the major causes of Sudden Inappropiate Appropiate Antidiuretic Hormone secretion.
ADH prepartion Vasopressin (Pitressin), Desmopressin Acetate (DDAVP) can both be
administered Intravascularly or by injections.
XI. Thyroid Gland: Hormones that it secretes are Thyroxine(T4) and Triiodothyronine(T3) both
are to regulate protein synthesis & energy activity . 20% of circulating T3 is secreted from
the Thyroid gland and the other 80% comes from the degradation of about 40% oof the T4 .
Both are carried by the blood by the Thyroxine binding globulin(TBG) and Albumin. T3 is
more potent than T4 and only free unbound T3 & T4 are active and produce a hormonal
response.
A. Hypothyroidism: Synthetic T4 & T3 may be prescribed and can have either primary cause
(gland disorder) or 2nd cause (lack of TSH secretion). Primary occurs more frequently T 4 &
TSH = Primary HypoThyroidism. The causes can be either acute or chronic inflammation
of the Thyroid gland, radioiodine therapy, excessive intake of antithyroid drug or surgery.
Myxedema is a severe Hypothyroidism- symptoms are lethargy, apathy, memory
impairement, emotional changes, slow speech, deep coarse voice, edema of eyelids and face,
thick dry skin, cold intolerance, slow pulse, constipation, weight gain, and abnormal menses.
In children Hypothyroidism can be congenital (Cretinism).

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B. Levothyroxine Sodium( Levothyroid, Synthyroid){Prototype} - If levels of T3 and T4 ;

also used to treat a simple goiter and chronic Lymphocytic Thyroiditis (Hoshimoto). To treat
Hypothyroidism,Myxedema and Crentinism. Mode of action is to metabolic rate, oxygen
consumption and body growth. Highly Protein Bound . Pregnancy Catergory A.
Dosages- PO intially 25-50mcg/day; maintance Dose: 50-200 mcg/day.
IV 0.2- 0.5 mg initially then 0.1- 0.2 mg/day until stable then go to PO doses
1. Pharmacokinesticsa. Absorption- PO 50-75%
b. Distribution- PB 99%
c. Metabolism- t 1/2 : 6-7 days
d. Excretion- in bile and feces
2. Pharmacodynamics- PO Onset: UK
Peak : 24 hr.-1 week Duration: 1- 3 weeks
IV Onset: 6-8 hrs. Peak: 24-48hrs.
Duration: UK
a.Side Effects- Nausea, vomiting,diarrhea, cramps, tremors, nervousness, insomnia, H/A,
and weight loss.
b. Adverse- Tachycardia, hypertension, palpitations
c.Life Threatening- Thyroid crisis, angina pectoris, cardiac dysrhythmias, and
cardiovascular collapse.
d. Drug;Food; Labs- cardiac insufficiency with epinepherine; effects of
anticoagulants, tricyclic antidepressants, vasopressors, decongestants.
effects of antidiabetics (oral and insulin), digitalis, and decrease absorption with
cholestyramine, colestipol.
2.Lithyronine (Cytonel)- Synthetic T3 short t life and duration of action; not recommended
for maintain therapy. It is better absorbed from GI then Levothyroid. It is used for the
initial treatment of myxedema.
3. Liotrix( Euthroid, Thyrolar)- is a mixture of Levothyroxine & Liothyronine (4:1 ratio).
No advantage to using this drug over Levothyroxine alone.
XII.

Hyperthyroidism: in circulating T4 & T3 which results from an overactive thyroid gland. It

may be mild or severe as in Thyroid Storm.
Graves Disease or Thyrotoxicosis- most common type of Hyperthyroidism caused by
Hyperfunction of thyroid gland. Characterized by Tachycardia, palpitations, excessive
perspiration, heat intolerance, nervousness, irritability, Exophthaalmos(bulging eyes), and
weight loss. Can be treated surgically where a portion of the thyroid gland is
removed(subtotal thyroidectomy) , by administering radioactive Iodine therapy, or
antithyroid medications. Any of these treatments can cause Hypothyroidism. Propanolol

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XIII.

(Beta- Adrenergic Blocker) is used to control cardiac symptoms like the tachycardia and
palpitations.
A. Drugs- the purpose is to reduce excessive secretion of thyroid hormones T4 & T3 by
inhibiting their secretions.
1. Thiourea Derivatives (Thioamides) - are the drugs of choice. These drugs interfere
with the synthesis of thyroid hormones. They DO NOT destroy the thyroid tissue.
2. Propylthiouracil (PTU) and Methimazole(Tapazole)- are effective thiamide
antithyroid drugs. Useful for treatment for Thyrotoxic Crisis. PTU does inhibit peripheral
conversions of T4 & T3. Methimazole also doesnt inhibit peripheral conversion T4 & T3 but
is 10 times more potent and has a longer half life then PTU. Prolong use of thioamides may
cause a goiter to form. Stron Iodine solutions Lugols solution has been used to suppress
thyroid function. Sodium Iodine administered IV is useful for the management of thyrotoxic
crisis.
Drug Interaction Digoxin and Lithium can the action of thyroid drugs.
Dilantin serum T3 levels.
Parathyroid Gland- Parathyroid Hormone is secreted from this gland and is important in
serum Ca+ levels. The other hormone that is important in Ca+ levels is Calcitonin this
hormone serum Ca+ levels. The treatment for Hypoparathyroidism is the administration of
Parathyroid Hormone. The treatment of Hyperparathyroidism is with a synthetic form of
Calcitonin.
A. Calcitriol (Rocaltrol) is a Vitamin D analogue that promotes Ca+ absorption from the
GI tract & secretion of Ca+ from the bone into the blood stream. Mode of action enhancement of Calcium deposits in the bone.
Pregnancy Category: C
Dosage: PO 0.25 mcg/day
Contraindication: Hypersensitivity, hypercalcemia, hyperphosphatemia,
Hypervitaminosis D, malabsorption syndrome.
Caution: Cardiovascular diseases, renal calculi
1.Pharmacokinestics:
a. Absorption: PO well absorbed
b. Distribution: PB UK, crosses the placenta
c. Metabolism: t : 3-8 hrs.
d. Excretion: mostly in the feces
2. Pharmacodynamics: PO Onset: 2-6hrs. Peak: 10-12 hrs. Duration: 3-5 days
Side Effects- Anorexia, nausea, vomiting, diarrhea, cramps, drowsiness, H/A,
dizziness, lethargy, and photophobia.
Adverse Effects- Hypercalciuria, hyperphosphatemia, and hematuria
Drug; Food; Labs- Increase cardiac dysrhythmias with Digoxin and Verapamil.

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Decreases calcitriol absorption with cholestyramine.

Lab- Increases serum Ca+ with thiazide diuretics and calcium supplements.
XIV. Adrenal Glands- 2 types of Hormones produced in the cortex : Glucocorticoids and the
Mineral Corticotoids.
A. Glucocorticoids(Cortisol)- is secreted from the Adrenal gland in response to the
hypothalamus pituitary adrenal axis as a result of feedback. They are influenced by
ATCH(Adrenalocorticoid Hormone) which is released by the anterior Pituitary gland. They
affect carbohydrate, protein, and fat metabolism. Cortisol is the main Glucocorticoid is has
an anti-inflamatory, anti- allergic, and anti stress effect. Indications for their use are;
trauma, surgery, infections, emotional stress and anxiety. Drugs in this class are mostly a
synthetic form. Conditions that they would be used for are : Mutiple Sclerosis, Rheumatiod
arthritis, Myasthesia Gravis, Ulcerative Cololitis, Glomerulonephritis, shock, ocular and
vascular inflammations, cerebral edema, polyarteries nosa, Hepatitis, allergic conditions,
drug reactions, contact dermatitis, and anaphylaxis. Maybe used to treat organ rejections by
the reciepant.
1. Dexamethasone(Decadron)- drug used to treat severe inflammatory response resulting
from head injuries or allergic reactions.
2. Prednisone(Deltasone, Orasone, Meticorten) {Prototype} Class is Glucocorticoid.
Mode of action is to suppress inflammation and adrenal function. Also used as an
immunosuppressant. Pregnancy Category- C. Adult Dose- PO 5-60 mg/day in divided doses.
Contraindications- Hypersensitivity, psychosis, fungal infections. Caution- Diabetes
Mellitus.
Pharmacokinetics a. Absorption - absorbed from the GI tract
b. Distribution- PB 65-91% crosses the placenta
c. Metabolism- t - 3-4 hr.
d. Excretion- In urine
Pharmacodynamics- PO Onset- UK Peak- 1-2 hr. Duration- 24-36 hrs.
Side Effects- Nausea, diarrhea, abdominal distention, appetite, sweating, H/A, depression,
flush, and mood changes.
Adverse Effects/ Reactions- Petechiae, ecchymosis, hypertension, tachycardia, osteoporosis,
and muscle weakness.
Life Threatening- GI hemorrhage, pancreatitis, circulatory collapse, thrombophlebitis, and
embolism.
Drug; Food; Labs Interactions- Drugs- effect with barbiturates, phenytoin, rifampin, ephedrine,
theophylline,
effects of aspirin, anticonvulsants, Ioniazid (INH), antidiabetics, and vaccines.

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B. Mineral Corticosteriods- promote Na+ retention/reabsorption and K+ excretion . They

influence electrolytes, carbohydrate, protein, and fat metabolism a deficiency in them can
result in a serious illness or death. A decrease in their secretion is called Adrenal
Hyposecretion or Addisons disease.

Chapter 51 Ant Diabetics Medications

Complications from Diabetes are the 3rd leading cause of death. Ethnical groups more
suspectable to Diabetes are Native Americans, Hispanics, African- Americans (2 to 3 times
higher incidence) than Caucasians.
Diabetes Mellitus is a disorder of the Pancreas
Diabetes Insipidus- is a disorder of the Posterior Pituitary gland & Anti-Diuretic Hormone.
I.

There are 4 Forms of Diabetes:

Type I Insulin- Dependent Diabetes Mellitus(Previously known as Juvenile onset
Diabetes
2) Non- Insulin Dependent Diabetes Mellitus(previously known as Adult onset
Diabetes)Most common occurrence of 85-90% of all diabetic cases.
3) Secondary Diabetes( due to medications such as Glucocorticoid cortisol or
prednisone, thiazide diuretics like hydrochlothiazide, and epinepherine or hormonal
changes)
4) Gestational Diabetes Mellitus (GDM)- during 2nd and 3rd trimesters levels of
progesterone , cortisol and Human Placental Hormone increase and they can inhibit
insulin usuage.
There are 2 groups of Drug Therapies to treat Diabetes
A Insulin it is a protein hormone secreted by the Beta cells in the Pancreas. They are
needed for metabolism of carbohydrates, and play a role in protein and fat metabolism
too.
B. Oral Hypoglycemic agents

Insulin Is released from the Pancreatic Beta cells when there is an increase in serum glucose
level. Normal serum glucose levels are from 70-11-mg/dl. When serum levels go above 180mg/dl
then glucosuria (glucose in the urine) can occur. glucose in the blood acts as an osmotic
diuretic polyuria, when blood serum glucose levels are > 200mg/dl Diabetes Mellitus occurs.
Normally our bodies produce 0.2 to 0.5 units/kg/day of Insulin. Example pt weighs 154lbs which
is approx. 70 kg he would produce 14-35 units of Insulin/day.
Commercially prepared InsulinParental Insulin is obtained from either Pork or Beef . Pork Insulin is closely related to the Human
Insulin, it has only one different amino acid than Humans. Therefore Pork Insulin is a weaker
allergen then Beef. Beef Insulin has 4 different amino acids.
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Since 1983 Humulin Insulin was introduced. It has a very low incidence of causing an allergic
reaction and an Insulin resistance. Subcutaneous Human (humulin) insulin is absorbed much
faster and has a shorter duration than the animal insulins. This type of insulin is usually prescribed
for newly diagnosed clients that are insulin dependent diabetics or in a pregnant clients whom
develop hyperglycemia and those women who are diabetics and who become pregnant.
The usual dose concentration of Insulin is 100 Units/ml and is packaged in a 10 ml vial. Syringes
are also calibrated to match 100Units/ml to be used for the 100U/ml Insulin type. Before using a
vial of Insulin the nurse and or client must be taught not to shake the vial but to roll the vial
between their palms to mix contents.
Remember that Insulin is a protein and can NOT be given orally because GI secretions destroy
the insulin structure! Please also remember that REGULAR Insulin is the only type of insulin that
can be administered INTRAVENOUSLY! Clients should be taught a site rotation pattern to
help avoid Lipodystrophy (tissue atrophy or hypertrophy) which can interfere with insulin
absorption.
Insulin Absorption- > when given in the Deltoid & Abdominal areas. ( the use of heat and
massage will absorption). Of course illness and stress increase the need for insulin.
Types of Insulins- Go Back and Review your Onset Peak and Durations
Rapid Acting- clear Include Lispro Humalog, Novolog. Onset: 5-15min Peak 30-60 min D: 3-4h
Short Acting- Regular Humulin R. Onset:30-60min. Peak:2-3h D: 4-8 h
Intermediate Acting- cloudy. Humulin N. Onset:1-2h Peak:4-12h D: 18-24h
It may contain protamine (protein that prolongs action of or zinc that slow the onset of action and
prolongs the duration of action.
Long Acting- Glargine Lantus. Onset:1h Peak: None D: 24h
Combination-Humulin 70/30, Novolin 70/30, Humulin 50/50.
Review
Insulin Resistance- antibodies develop overtime in clients taking animals insulins which slows
down the onset and extends the duration of the insulin.
Insulin Pump
Somogyi Effect
Pre Dawn Syndrome

A. Oral Anti Diabetic Medications Used mostly for Type II diabetics because these clients
do produce some amounts of Insulin. First group of oral diabetics were Sulfonylureas.
These drugs stimulate beta cells to secrete more insulin. In the first generation of this
group :
Short Acting Tolbetamide Orinase
Intermediate Acting- Acetohexamide (Dymelor), Tolazamide(Tolinase)
Long Acting- Chlorpropamide (Diabinese)
2nd generation of Sulfonylureas- the tissue response to insulin& glucose production
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from the liver. They have greater hypoglycemic potency, longer duration and cause fewer
side effects. They should not be used in clients with liver or kidney dysfunction is present.
Glimepiride (Amaryl)
Glipizide (Glucotrol, Glucotrol XL) {Prototype} side effects Nausea/vomiting, diarrhea
and abdominal pain. Hypoglycemia is a major side effect.
Adverse: Hematological disorders aplastic anemia, leucopenia, thrombocytopenia,
seizures, coma
DosePharmacokinetics
Pharmacodynamics
Biguanides (Metformin, Glucophage) acts by hepatic production of glucose from the
stored glycogen, and absorption of glucose in the small intestine & it insulin receptor
sensitivity. It does not cause Hypoglycemia or Hyperglycemia. It is not recommended for
clients with Renal impairment. Hold for 48 hrs. before and after the client has IV contrast
d/t lactic acid build up or possible development of acute renal failure.
Other Anti- Diabetic Agents- Exenatide (Byetta) from amylin .Improves Betta Cell
responsivenessimproves glucose control in clients with Diabetes Type II. Action is to
enhance insulin secretion ; beta cell responsiveness , suppress glucagon secretion, slows
gastric emptying & food intake. It is not a substitute for Insulin & should be given to
patient whom have Type I Diabetes, Diabetic Ketoacidosis, some renal dysfunction, or
severe GI disease. Available in injectable pens.
Promlintide Acetate(Symlin) used to improve post prandial glucose control in diabetic clients
who are using Insulin but are

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