AUTONOMIC NERVOUS SYSTEM
ANS effects…
Skeletal muscle, Cardiac output, Vascular tone, Respiration, GI function, Uterine motility, Glandular
secretions, Pain perception, ideation and mood
SNS
↑
Constriction
↑
↓
Constipation
Xerostomia
Mitosis
Ejaculate
Relax
Contract
EFFECT
CO/HR
Vascular tone
Respiration
GI motility
GI
Secretions
Eye
Sex
Uterine SM
Prostate
Neurotransmitters of the PNS
Acetylcholine – released from preganglionic and postganglionic (PSNS) neurons
Norepinephrine – released from post-ganglionic (SNS) neurons
Epinephrine – released from adrenal medulla (anaphylactic shock)
Dopamine – used for shock and hypotension
PSNS (SLUDGE)
↓
Dilate
↓
↑
Diarrhea
Salivating
Miosis
Erection
Contract
Relax
Definitions
Agonist – directly activate receptor (morphine, epi, insulin)
Antagonist – prevent receptor activation (naloxone, antihistamines, beta blockers)
Direct acting – Stimulate receptor
Indirect acting – Stimulate release of NT
Sympathomimetic – adrenergic (SNS)
Sympatholytic – antiadrenergic
Parasympathomimetic – cholinergic (PSNS)
Parasympatholytic – anticholinergic
Cholinesterase – breaks down ACh
Cholinesterase inhibitor – prevents breakdown of ACh and ACh inhibitor
CATECHOLAMINES
Short DOA
Can’t give PO
Can’t cross BBB
Epinephrine, Norepinephrine, Dopamine,
Dobutamine, Isoproterenol
Class
Drug
NON-CATECHOLAMINES
Longer DOA
Can give PO
Crosses BBB
Phenylephrine, ephedrine, terbutaline
MOA
Cholinergic
Parasympathomimetic
Muscarinic agonist
Bethanechol
↑ cholinergic rec. in the smooth
muscle of the urinary bladder & GI
tract:
↑ peristalsis, GI secretions,
bladder muscle contraction
Anti-cholinergic
Parasympatholytic
Muscarinic antagonist
Atropine
Blocks ACh at PSNS receptor:
↑ CO, ↓ secretions, antagonizes
histamine/serotonin
Acetylcholinesterase
inhibitor
Neostigmine
Prevents the breakdown of ACh into
choline and acetic acid (indirectacting cholinergic agonist)
Therapeutic Uses
Adverse Effects
Urinary retention
Treat loss of tone in GI
tract
GERD
Abx cramps, diarrhea, N/V, salivation
Urinary urgency
Lacrimation, miosis, sweating
Bronchial constriction/asthma attacks, ↓ BP,
↑ HR, flushed
Pre-op use
Treat ↓HR
Eye exams
Dry mouth, blurry vision, urinary hesitancy,
constipation, palpitation, anhidrosis, ↑
temp, hallcuinations
Myasthenia Gravis
Additional Info/Contraindications
OD: give Atropine
CI: obstruction of GU/GI, peritonitis,
parkinson’s disease, ↓ HR, asthma
Pregnancy category C drug
DI: cholinesterase inhibitors
OD: give Physostigmine
CI: narrow-angle glaucoma, CAD, obstruct
GU/GI, paralytic ileus, hernia, asthma
NI: ice chips, fluids, assess lung sounds
OD: give Atropine
ANTIBIOTICS
Bactericidal – Bringing death to bacteria; directly lethal to bacteria at clinically achievable concentrations
Bacteriostatic - Restrain the development or production of bacteria; slow bacterial growth but do not cause cell death—that is
For immunocompromised patients: give them a bactericidal drug B/C bacteriostatic drug doesn’t kill the bacteria and their immunocompromised system won’t be strong enough to kill it!!
Kernicterus – bilirubin-induced brain dysfunction from accumulation of bilirubin in CNS tissues (jaundice)
Gram (+) = 2 layers; cytoplasmic membrane has PBPs, Gram (-) = 3 layers; thin cell wall; outer layer difficult to penetrate
Principle of ABX therapy: SELECTIVE TOXICITY - Toxic to microbes—Harmless (or less toxic) to host
7 Major Specific Mechanism of Actions (MOAs) for anti-infectives
Inhibit CW synthesis or activate enzymes that disrupt the CW Penicillins, Cephalosporins, Amphotericin B, Itraconazole
Increase cell wall permeability Amphotericin B
Lethal inhibition of protein synthesis (bactericidal)
Nonlethal inhibition of protein synthesis
Inhibit DNA or RNA synthesis or disrupt DNA function
Aminoglycosides
Tetracyclines, Erythromycins
Rifampin, Fluoroquinolones, Metronidazole
Antimetabolites Sulfonamides & Trimethoprim
Suppress viral replication Antivirals
Acquired Resistance to Antimicrobial Drugs - Over time, organisms develop resistance. May have been highly responsive and then became less susceptible to one or more drugs
**Antibiotics must not be discontinued prematurely
When conditions demand that nurses start therapy before lab data, samples of exudates and body fluids have to be obtained for culture BEFORE treatments
ANTIBACTERIAL DRUGS
Narrow Spectrum
Broad Spectrum
Gram (+) Cocci and Gram (+) Bacilli
Gram (-) Aerobes
Mycobacterium tuberculosis
Gram (+) Cocci and Gram (-) Bacilli
Penicillin G and V
PCN-ase resistant penicillins (NODM)
Vancomycin,
Erythromycin, Clindamycin
Aminoglycosides
Cephalosporins (1st/2nd gen)
Isoniazid
Rifampin
Ethambutol
Pyrazinamide
Broad-spectrum penicillins (AA)
Extended-spectrum penicillins
Cephalosporins (3rd/4th gen), Tetracyclines, Carbapenems, Trimethoprim,
Sulfonamides, Fluoroquinolones
Drug Class
Inhibitors of CW synthesis
Representative
Antibiotic
Penicillins
Cephalosporins
Carbapenem
Vancomycin
Telavancin
Aztreonam
Teicoplanin
Fosfomycin
Drug Class
Representative
Antibiotic
Glucocorticoids Inhaled
Beclomethasone
dipropionate
Budesonide
Fluticasone
Mometasone
furoate
Drugs that disrupt the cell
membrane
Amphotericin B
Daptomycin
Azole drugs
ANTI-INFLAMMATORIES
Glucocorticoids Leukotriene
Oral
modifiers
Prednisolone
Prednisone
Montelukast,
oral
Zafirlukast,
oral
Zileuton, oral
Bactericidal inhibitors of
protein synthesis
Bacteriostatic inhibitors of
protein synthesis
Drugs that interfere with
synthesis or integrity of
bacteria DNA or RNA
Antimetabolites (disrupt
specific biochem rxns)
Aminoglycosides
Tetracyclines
Clindamycin
Macrolides
Chloramphenicol
Linezolid
Telithromycin
Dalfopristin/Quinupristin
Tigecycline
Mupirocin
Fluoroquinolones
Metronidazole
Rifampin
Sulfonamides
Trimethoprim
BRONCHODILATORS
Cromolyn
IgE
Antagonist
SABA,
Inhaled
LABA,
Inhaled
LABA, oral
Methylxanthines
Anticholinergic
Cromolyn,
inhaled
Omalizumah,
subQ
Albuterol
Levalbuterol
Pirbuterol
Arformoterol
Formoterol
Indacaterol
Salmeterol
Albuterol
Terbutaline
Theophylline,
oral
Ipratropium,
inhaled
Tiotropium,
inhaled
ANTI-INFLAMMATORY /
BRONCHODILATOR
COMBINATION
Budesonide/formeterol,
Fluticasone/Salmeterol,
Mometasone/formeterol
ANTIBIOTIC CLASS: PENICILLIN (PCN) → "-cillin" suffix
Penicillin:
Low toxicity
Molecular structures has β-lactam ring (cephalosporins, aztreonam, imipenem, meropenem &
ertapenem have β-lactam ring = same MOA)
Method of Action (MOA):
Weaken cell wall which causes cell wall to take up water & burst (osmotic lysis) = bactericidal
(through activation of autolysins and inhibition of transpeptidases)
Only effective against cells that are undergoing growth and division (vegetative)
Most effective against gram(+) bacteria
Works on g (-) in higher doses; Ampicillin able to cross outer membrane of g (-) bacteria.
Adverse Effects:
Diarrhea
Renal failure or use of Probenecid = delays renal excretion = prolonging antibiotic effects
1-10% of people have allergic reaction (rash → anaphylaxis). Tell pt to report SIGNS.
5-10% will have a cross-sensitivity to Cephalosporins and Carbapenems
Alternatives to PCN: Erythromycin, Clindamycin, or Vancomycin
Resistance to PCN Occurs 2 Ways:
Inability of PCN to reach their targets
Inactivation of PCN by bacterial enzymes
Production of penicillin-binding proteins (PBPs) that have a low affinity for penicillins
Beta-Lactamases (enzymes)
Cleave beta-lactam rings; specific to PCN called "Penicillinase"
G (-) produce PCNase in small amounts, but secrete them into the periplasmic space (more
concentrated)
G (+) produce PCNase in large amounts; goes into surrounding medium (↑ scattered = ↓
effective)
Pharmacokinetics
Renally excreted
Sub-classes
Adverse Effects
Narrow-Spectrum PCN
- PCNase sensitive
Narrow-Spectrum PCN
- PCNase resistant
- Anti-staphylococcal
Individual Drugs
Penicillin G
Potassium,
Procaine (IM),
Benzathine
(IM)
Penicillin V
Nafcillin
Dicloxacillin
Oxacillin
Methicillin
(no longer
available)
Effective Against
Route/Dosage
Additional Information
Gram (+) bacteria
Streptococcus species,
anaerobes
Potassium Pen G – IV
Procaine/Benzathine
Pen G – IM only
PCN V - PO
Staphylococcus aureus
Staphylococcus epidermis
Nafcillin - IV
Dicloxacillin - PO
Oxacillin- IV, PO
Methicillin causes interstitial
nephritis
HIGHLY resistant to β-lactamase
MRSA resistant to PCN b/c β-lactam ring is major
reason for development/evolution of MRSA
(Methicillin-Resistant Staphylococcus Aureus).
Distribution to most tissues/body fluids usually
Distribution ↑ during inflammation (blood flow ↑)
to CSF, joints, and eyes.
Broad-spectrum PCN
- Aminopenicillins
-PCNase sensitive
Ampicillin
Amoxicillin
Gram (-) bacteria:
E. coli, H. influenzae,
H.pylori, Salmonella,
Shigella
Ampicillin - PO, IV
Amoxicillin - PO
Rash & Diarrhea (most w/
Ampicillin)
Suprainfection
Active against some gram (-) bacteria
Refrigerate oral suspensions
Extended Spectrum
PCN
- Penicillinase sensitive
- Anti-pseudomonas
Ticarcillin
Piperacillin
E. coli
Pseudomonas eruginosa
Ticarcillin - IV
Piperacillin - IV
Disrupts PLT formation  bleeding
2+
Ticarcillin: causes Na overload.
MONITOR pts w/ CHF
At risk to β-lactamases = ineffective to S. aureus
Can be paired w/ Aminoglycoside to ↑ toxicity
against pseudomonas, but DO NOT mix w/ PCN in
the same IV solution b/c it can inactivate AG
PCN w/ β-lactamase
inhibitor
Nursing implications
Broad:
Ampicillin/sulbactam (Unasyn)
Amoxicillin/clavulanic acid (Augmentin)
Clavulanic acid ↑risk for diarrhea,
Combo w/ PCN
Extended:
especially in children
Ticarcillin/clavulanic acid (Timentin)
Piperacillin/tazobactam (Zosyn)
Interview patient for history of PCN allergy. NOTE: Skin test can lead to anaphylaxis.
MONITOR INTAKE AND OUTPUT FOR SIGNS OF KIDNEY DYSFUNCTION. Avoid toxic build-up of PCN.
IV PCN used? Monitor patient for at least 30 minutes
IM PCN? Aspirate to avoid injection into artery or peripheral nerves. Also, monitor for at least 30 minutes
PO PCN? Take with full glass of water 1 hour before meals or 2 hours after meals (PCN V and Amoxicillin can be taken with meals)
ALWAYS INFORM THEM TO FINISH COMPLETE COURSE OR ANTIBIOTICS
ANTIBIOTIC CLASS: CEPHALOSPORIN → "ceph-" or "cef-" prefix
Cephalosporin:
Very similar to PCN b/c molecular structures are very similar
Molecular structures also has β-lactam ring = same MOA as PCN
Method of Action (MOA):
Binds to PBPs; disrupts CW synthesis; causes CW lysis = bactericidal
Only effective against cells that are undergoing growth and division (vegetative)
1st gen
2nd gen
3rd gen
4th gen
Gram (-) activity
Low
Higher
Higher
highest
β-lactamase resistance
Low
Higher
Higher
Highest
CSF distribution
Poor
Poor
Good
Good
Pharmacokinetics
Poor GI absorption; therefore many must be given parenterally
Renally excreted except Ceftriaxone (liver)
Sub-classes
Individual Drugs
Effective Against
Route
First Generation
- Cep-nase Sensitive
(VERY)
Cephalexin
Cefazolin
Staphylococci
Streptococci
PO, IM, IV
Second Generation
- Cep-nase Sensitive
Cefaclor
Cefoxitin
Cefuroxime
Pneumonia: H. influenza
Klebsiella & Pneumococci,
Staph.
Third Generation
- Cep-nase Resistant
(HIGHLY)
Fourth Generation
- Cep-nase Resistant
(HIGHEST)
Nursing Implications
Cefotaxime
Ceftriaxone
*liver excretion*
Cefoperzone
Cefditoren
Cefepime
Meningitis &
Pseudomanas aeruginosa
Meningitis &
Pseudomanas aeruginosa
Adverse Effects:
Well-tolerated; low toxicity
Thrombophlebitis
Hemolytic anemia
Hypersensitivity reactions
Drug Interactions:
5-10% will have a cross-sensitivity to penicillins (b/c similar molecular structure)
Probenecid – delays renal excretion = prolonging antibacterial effects
Bleeding caused by: cefmetazole, cefoperazone, cefotetan, ceftriazone
Alcohol reacts w/: cephazolin, cefmetazole, cefoperazone, cefotetan
2+
Ca + Ceftriaxone for neonates= precipitant in lungs and kidneys
Resistance to Cephalosporin:
Cleave beta-lactam rings; specific to Cephalosporins called "Cephalosporinases"
Gram (-) produce Cephalosporinases in small amounts, but secrete them into the
periplasmic space (more concentrated)
Gram (+) produce Cephalosporinases in large amounts and export it into the
surrounding medium (more scattered so less effective)
Additional Information
Used most often b/c inexpensive, often just as effective as newer drugs, & narrow
antimicrobial spectrum
PO, IM, IV
Cefuroxime - the
only one that can be
given both IM & PO
Cefotetan causes bleeding tendencies and alcohol intolerance (check PTT)
2+
PO, IM, IV
PO, IM, IV
Ceftriaxone + Ca : Only give through different IV lines & w/ 48 hours between the two
Cefditoren – excreted w/ carnitine. Don’t give to pts w/ carnitine deficiency
Most activity against gram (-)
Most resistance against β-lactamases
Deepest penetration into CSF
Monitor allergic reactions
o Cefditoren tablets contain milk-protein ∴ don’t give to patients w/ milk-protein allergy
Check PTT before giving cefmetazole, cefoperazone, cefotetan, ceftriazone
Alcohol interacts w/ Cefazolin, cefmetazole, cefoperazone, and cefotetan. Warn patients not to take with alcohol
Monitor for Thrombophlebitis—rotate injection site, inject Cephalosporins slowly & dilute solutions
Monitor for C. diff infection – notify HCP if diarrhea occurs! If CDI is diagnosed, cephalosporin will be discontinued
Advise patients to take with food, refrigerate oral suspensions
ALWAYS INFORM THEM TO FINISH COMPLETE COURCE OR ANTIBIOTICS
ANTIBIOTIC CLASS: CARBAPENEMS (used with Cephalosporins) → "-penem" suffix
Carbapenems:
Molecular structures has β-lactam ring, but resistant to almost all β-lactamases
Extremely broad antimicrobial spectrum (more than almost any other drug), but low toxicity
Has ability to penetrate gram(-) bacteria
Method of Action (MOA):
Binds to PBP1 & PBP2  weakening of wall, lysis & death = bactericidal
Elimination:
Primarily renal
Adverse Effects:
Well tolerated; low toxicity
Can have a cross-sensitivity to other β-lactam antibiotics (b/c similar molecular structure)
Interacts with Valproate – reduces blood level of Valproate (necessary to control seizures)
Individual Drugs
Effective Against (+/-)
Imipenem (broadest)
Gram(+) = High for cocci
Gram(-) = High for most cocci & bacilli
Meropenem
Anaerobes, Staphylococcus aureus, Pseudomanas
aeruginosa
Gram(+) = High
Gram(-) = High for aerobes & anaerobes
Route
Additional Information
IM, IV
Dipeptidase inactivates Imipenem ∴ combine w/ an inhibitor (cilastine)
Must be combined with other antibiotic (like Cephalosporins) when treating
Pseudomanas aeruginosa
IV
Also used in complicated intra-abdominal infections in children & adults
Skin infections
Nosocomial infections where other antibiotics will not work
Bacterial Meningitis (children must be >3 mos)
Ertapenem
Gram(+) = Less than others
Most anaerobes
IM, IV
Is used for acute pelvic inflammation, UTI’s, skin & community-acquired pneumonia
Doripenem
Pseudomanas aeruginosa
IV
Complicated intra-abdominal infections and complicated UTIs
Reserve for seriously ill people
ANTIOBIOTIC CLASS: MONOBACTAM
Method of Action
β-lactam antibiotic, but safe for pts w/ β-lactam allergy
Binds to PBP3
Sub-classes
Individual Drugs
Effective Against (+/-)
Route
Narrow-Spectrum
Aztreonam (Azactam)
P. aeruginosa, Neisseria
Gram(-) aerobic bacteria
IV, IM, inhaled
Adverse effects
Similar to other β-lactam antibiotics
Individual Drug
MOA
Effective Against (+/-)
Route
Adverse effects
Fosfomycin
(single-dose therapy)
Disrupts synthesis of
peptidoglycan strands
that composes cell wall
UTI caused by E. coli and Enterococcus faecalis
PO – water-soluble
powder in packets
Diarrhea, headache, vaginitis, nausea
ANTIBIOTIC: VANCOMYCIN → "vanco-" prefix
Vancomycin:
Elimination
No β-lactam ring (can be used on patients allergic to PCN)
Renal elimination
Use for pts allergic to PCN and Cephalosporin (last resort b/c toxic!)
Adverse Effects – dose related:
DOC for MRSA
Red Man Syndrome (if IV too rapid)

E.g. flushing, rash, pruritus, uticaria, tachycardia,
Use for severe infections only
Method of Action (MOA):
hypotension
Nephrotoxicity
Binds to molecules that are precursors to cell wall synthesis. This weakens cell wall which causes cell
Ototoxicity (may be permanent if exceed 30mcg/mL)
wall to take up water & burst (osmotic lysis) = bactericidal
Thrombophlebitis (change infusion site & dilute)
Only effective against gram(+) bacteria
Individual Drugs
Effective Against
Additional Information
Route Pharmacokinetics
Nursing Implications
Vancocin
Vancoled
Telavancin
Synthetic Vanc
Teicoplanin
(Targocid)
Similar structure &
actions to Vanc
Pseudomembranous
colitis  C. difficile
S. aureus, & S.
epidermidis
MRSA
Gram(+) bacteria
MRSA
C. difficile
PO, IV
Slow IV over 60 min +
Give PO only if infection in GI
Intrathecal administration IV
if meningeal infection
Monitor serum drug levels (peak/trough)
o Check blood drug levels 1.5-2.5 hours after infusion is
complete (peak levels at 30-40 mcg/mL, trough 15-20
mcg/mL)
Monitor serum Creatinine level (50% increase)
Try Flagyl for C. difficile first.
Only use Vanc if Flagyl fails.
IV
Adverse effects of Televancin:
Taste disturbance, nausea, vomiting, foamy urine
Prolong QT interval
Red man syndrome (give slow IV)
Kidney damage (measure function at baseline, every 72 hours during treatment, and at end of treatment)
IV
Additional Information of Teicoplanin:
No Red Man Syndrome
No ototoxicity
ANTIBIOTIC CLASS: TETRACYCLINE → "-cycline" suffix
Tetracyclines:
nd
st
These are mostly 2 line agents when infections resistant to 1 line agents (due to
overuse and resistance factors)
All are broad-spectrum; main differences are pharmacokinetics
Method of Action (MOA):
Inhibit bacterial growth & replication by inhibiting protein synthesis, but are only
bacteriostatic
Gram(+) and gram(-)
Distribution:
Poor distribution to CSF, so not effective against meningitis
Crosses placenta & can enter fetal circulation, so try to avoid in pregnant women
Sub-classes
Individual Drugs
Short-acting
- Low-lipid solubility
Tetracycline
Oxytetracycline
Intermediate-acting
- Moderate lipid solubility
Demeclocycline
Long-acting
- High lipid solubility
Doxycycline
Minocycline
Nursing Implication:
Adverse Effects:
Renal toxicity
Hepatotoxicity
Phototoxicity
GI:
GI irritation: burning, cramps, N/V, diarrhea & cramps
Bones/Teeth – bind to Ca+2 in developing teeth causing brown/yellow discoloration.

Avoid in children less than 8 y/o when tooth enamel is being formed.
Suprainfection:
Causes C. difficile  severe diarrhea
Also fungi in mouth pharynx, vagina & bowel (Candida albicans) stop tetracycline
Effective Against
1. H. pylori, Rickettsia, Spirochetes, Brucella, Chlamydia,
2.
3.
Mycoplasm, Borrelia burgodorfer, Bacillus antracis, Vibrio
cholerae, Lyme disease
Acne vulgaris
Peptic Ulcer Disease (PUD) (use in combo with
metronidazole/Flagyl)
Route
PO preferred, IV, IM
Absorption reduced by food
PO
Elimination
Renally eliminated.
Do not give to pts. with renal failure (Renal
toxicity in pts. with renal disease)
PO, IV
Hepatically eliminated
Absorption NOT reduced
Therefore, can give to pts. with renal failure
by food
Should be taken on an empty stomach: give 2 hours before or 2 hours after chelating agents. Chelation  canceling absorption of drug
Council pts to avoid calcium (milk, antacids), iron, magnesium (laxatives), aluminum & zinc for 2 hours before/after taking Tetracyclines.
ANTIBIOTIC CLASS: MACROLIDES → "-mycin" suffix
Macrolides:
These are mostly 2nd line agents when infections resistant to 1st line agents (due to
overuse and resistance factors)
All are broad-spectrum; main differences are pharmacokinetics
Use if allergic to PCN (same action, but not same molecular structure)
Method of Action (MOA):
Inhibition of protein synthesis, but are only bacteriostatic
Works on most gram (+) and some gram (-) bacteria
Distribution:
Wildly distributed; poor CSF distribution
Crosses placenta & can enter fetal circulation = avoid in pregnant women
Elimination:
Hepatically metabolized P450
Renally excreted
Individual Drugs
Drug interactions:
Inhibits P450: ↑ Theophylline (asthma), Warfarin (anti-coagulant), Carbamazepine (seizures/bipolar)
Prevents binding of Chloramphenicol & Clindamycin to bacterial ribosomes
Inhibit Erythromycin Metabolism by: Verapamil, Diltiazem, HIV protease inhibitors & “Azole” antifungal
Adverse Effects:
Generally very safe
QT prolongation; small risk of sudden cardiac death
Gastrointestinal Suprainfection: Pseudomembranous colitis
Thrombophlebitis
Transient hearing loss w/ high-doses
Hypertrophic pyloric stenosis in infants < 2 wks
Suprainfection:
Causes C. difficile (severe diarrhea) a.k.a. antibiotic-associated Pseudomembranous colitis (give
Metronidazole/Flagyl or Vancomycin)
Effective Against
Route
Azithromycin (Doesn’t inhibit
metabolism of other drugs)
Respiratory tract infections, acute otitis media, GI infections
Bordetella pertussis (Whooping cough), acute diphtheria, Legionella pneumophila,
chlamydial infections, M. pneuonia, Streptococcus pneumoniae & Streptococcus
pyogenes
Mycobacterium avium complex (MAC) infections in pts. with advance HIV
infection
Clarithromycin
Additionally: H. pylori
Erythromycin
Additional Info
PO, IV
NOTE: Take with food
PO, IV
PO
NOTE: ER tabs - take with food
Additional adverse reaction: Metallic taste
ANTIBIOTIC CLASS: LINCOSAMIDE → "-mycin" suffix (NOT a Macrolide)
Lincosamide:
Use if allergic to PCN (same action, but not same molecular structure)
Only indicated for certain anaerobic infections located outside the CNS
Method of Action (MOA):
Inhibiting protein synthesis = bacteriostatic (can be bactericidal against susceptible
organisms or in high concentration)
Drug interactions:
Overlap binding sites with Erythromycin & Chloramphenicol
Individual Drug
Clindamycin
(Cleocin)
Effective Against
Adverse Effects:
Hypersensitive reactions  frequent rashes
Rapid IV can cause electrocardiographic changes
Suprainfection:
Causes C. difficile  severe diarrhea; can develop during 1st week of treatment but may develop 4-6
weeks after treatment ends. Can be fatal!
Route
Anaerobic gram(+/-) & most gram(+) aerobes
Streptococcal infections
Gas gangrene  Clostridium perfringens)
Abdominal & pelvic infx  Bacteroides fragilis
IV, IM, PO, Vaginal suppositories
NOTE: Good GI absorption, can take
with food
Elimination
Additional Information
Hepatically metabolized
Renally eliminated)
½ life = 3 hours
Reduce in dose in pts w/ liver and
kidney problems
NEW CLASSES OF ANTIBIOTICS – also inhibit bacterial protein synthesis
Individual Drugs
Linezolid (Zyvox)
Class: Oxazolidinones
Telithromycin (Ketek)
Class: Ketolide
Method of Action
Binds to 23S part of 50S
ribosome subunit (only
ABX that does this)
Cross-resistance with
other agents unlikely
Close relative to
Macrolides
Effective Against
Adverse effects
Drug interactions
Interacts with MAOIs – causes severe HTN
if combined with ephedrine,
pseudoephedrine, cocaine, or foods with
tyramine
Interacts with SSRIs – risk of serotonin
syndrome
Multi-drug resistant gram(+)
pathogens
Reserved for infections
caused by VRE and MRSA
Diarrhea, N/V, HA
May cause myelosuppression
(anemia, leukopenia,
thrombocytopenia pancytopenia)
NI: Monitor CBCs weekly
Streptococcus pneumoniae
Severe liver injury, GI effects, Visual disturbances
Additional Uses
Nosocomial pneumonia caused by
S. Aureus
CAP – S. pneumoniae
Complicated skin and skin
structure infection by S.aureus
Dalfopristin/Quinupristin
Class: Streptogramins
Inhibit protein synthesis
VRE
CYP3A4 – many drugs including cyclosporine, tacrolimus, cisapride
Hepatotoxicity
ANTIBIOTIC: CHLORAMPHINICOL → "chloro-" prefix
Chloramphenicol:
Broad spectrum antibiotic with NARROW therapeutic index
Pts. w/ serious & life-threatening infections (last resort b/c toxic!)
Method of Action (MOA):
Inhibiting protein synthesis = bacteriostatic (can be bactericidal against susceptible organisms or
in high concentration)
Drug Interactions:
Phenytoin, Warfarin, Tolbutamide & Chlorpropamide (PO hypoglycemic)
Adverse Effects:
Gray syndrome – mostly newborns (Dose-dependent)
1st – vomiting, abdominal distention, cyanosis & gray discoloration of the skin
2nd – collapse & death
Reversible if detected early
Use low doses and check serum levels!
Individual Drugs
Effective Against
1.
Chloromycetin
- High lipid solubility
2.
3.
4.
Nursing Implications
Route
Gram (+) & gram (-) aerobic (Salmonella typhi, H.
influenzae, Neisseria meningitis & Strep.
Pneumoniae)
Most anaerobic organisms are also susceptible.
Works well against Rickettsia, Chlamydia
mycoplasmas & treponemes
More resistance among gram(-) bacteria
PO, IV
NOTE: Take on
empty stomach
Adverse Effects:
GI effects
Peripheral neuropathy
Reversible Bone Marrow Suppression – (Dose-dependent = > 25 mcg/mL)
Can cause anemia, leukopenia and thrombocytopenia because of protein synthesis in host
mitochondria
Check CBC’s prior to treatment and every 2 days thereafter.
Symptoms: sore throat, fever, unusual bleeding or bruising.
Usually reversible 1-3 weeks after withdrawal.
Fatal Aplastic Anemia – not dose related (1 in 35,000 pts)
Can develop pancytopenia & bone marrow aphasia
Develops weeks/months after treatment stops
Cannot be predicted with monitoring blood
Pharmacokinetics
Distribution
PO has high availability because
active immediately
IV availability is variable and
incomplete b/c needs to be
hydrolyzed to free chloramphenicol
NOTE: usually the opposite; usually IV
faster & PO slower
Highly lipid soluble so widely
distributed
Enters CSF & crosses BBB (to 9
times plasma level); good for
treatment of brain abscesses and
meningitis
Crosses placenta & enters breast
milk
Elimination
Hepatically
metabolized
Renally eliminated
Take antibiotic on an empty stomach (1 hour AC or 2 hour PC)
Reduce dose in pts w/ liver dysfunction
Usual dose for adults/children: 12.5 – 25 mg/kg q 6 hour bactericidal
Dose for infants 7 days and younger: 25mg/kg
Dose for > 7 days old: 25 mg/kg q 12 hours
ANTIBIOTIC CLASS: AMINOGLYCOSIDE → "-mycin" suffix (NOT a Macrolide or Lincosamide)
Aminoglycoside:
Narrow spectrum
Method of Action (MOA):
Rapid bactericidal action through disruption of protein synthesis (dose
dependent)
Resistance
20+ different Aminoglycoside-inactivating enzymes
Amikacin is least susceptible to inactivation by bacterial enzymes (so use as
a last resort drug)
Selection of “glycoside” is based on community resistance.
Individual Drugs
Gentamicin
Tobramycin
*Amikacin
Kanamycin
Neomycin
Streptomycin
Paromomycin
Nursing Implications
Effective Against
1. Aerobic gram(-) bacteria b/c
require O2 for transport (E. coli,
Klebsiella pneumoniae, Serratia
marcesens, Proteus mirabilis,
enterobacteriaceae, P. aeruginosa)
2. Inactive against most gram(+)
Drug interactions:
Never mix PCN and Aminoglycosides in the same IV solution; Mixing increases bacterial kill capability of
Aminoglycosides (can use together, but do not mix)
Other ototoxic drugs: Ethacrynic acid (loop diuretic with ototoxic actions of its own
Other nephrotoxic drugs: Amphotericin B, Cephalosporin's, Polymyxins, Vancomycin, Cyclosporine, Aspirin
Muscle relaxants
Adverse Effects:
Nephrotoxicity: Binds to renal tissue achieving 50X the dose of that of serum levels. REVERSIBLE
Ototoxicity: Penetrates the inner ear  cellular injury: hearing and balance impairment. IRREVERSIBLE
Hypersensitivity reactions, neuromuscular blockade, blood dyscrasias, dilute urine
Dosing
Post-ABX effect
QD? Monitor trough levels
BID/TID? Monitor peak & trough levels
Peak level @ 30 min after IM or IV infusion
Trough, single dose: @ 1h prior to next dose
Trough, divided dosing: @ prior to next dose
Route
Syst.infx: IV, IM
Topical, PO (rare)
Elimination
Renally eliminated
NOT metabolized
Additional Information
Cannot kill anaerobes because “glycosides”
require O2 for transport across cell membrane
Serum levels impacted by: age, percent body fat,
renal function, fever, edema, dehydration
Dose must be individualized!
Monitor trough levels, Creatinine and BUN levels  especially in elderly pts w/ renal dysfunction, pts w/ other nephrotoxic drugs (Amphotericin B, cephalothin, cyclosporine)
Monitor for ototoxicity, renal toxicity, GI disturbances, bone marrow depression, and suprainfections.
Do not use drug for more than 10 days!
ANTIBIOTIC CLASS: SULFONAMIDES → "sulfa-" prefix
Sulfonamides:
Broad spectrum antibiotic
Structural similarity to para-aminobenzoic acid (PABA) allows them to be
competitive inhibitor
High water solubility, so low renal damage
Method of Action (MOA):
Suppress bacterial growth & replication by inhibiting synthesis of folic acid;
folic acid required by all cells to synthesize DNA, RNA & proteins (-static)
Drug Resistance:
Bacteria ↑ PABA
Reduced binding of sulfonamides
Reduced sulfonamide uptake
Individual Drugs
Sulfadiazine
Sulfamethoxazole
Sulfasoxazole
Sulfacetamide
Effective Against
MSRA, gram(-) bacilli, actinomycetes (Nocardia),
chlamydiae, some protazoa (Toxoplasma,
plasmodia, Isospora belli & P. carinii)
Sulfasalazine is used to treat ulcerative colitis
UTIs due to E. Coli
Drug interactions:
Intensify: Warfarin, Phenytoin, Sulfonylureas (oral hypoglycemics)
Cross-sensitivity if allergic to sulfa drugs to: loop diuretics & PCN
Adverse Effects:
•
Stevens-Johnson syndrome (rare) high mortality rate, lesions, fever, malaise & toxemia. Mostly
occur with long acting sulfonamides
•
Rash, photosensitivity, blood dyscrasias
•
Kernicterus (sulfa displaces Bilirubin from plasma protein; cause deposition in brain of
newborns) do not give to infants < 2 y/o, pregnant women, or if breast feeding
•
Renal damage (crystal formation) - take with a lot of water
•
Hemolytic anemia (esp. African Americans)
Dosing/Pharmacokinetics
Distribution
Short-acting PO: Sulfadiazine,
Sulfasoxazole/erythromycin
Intermediate-acting PO: Sulfamethoxazole
Topical (eyes): Sulfacetamide
Topical (burns): Silver sulfadiazine (pain-free)
& mafenide (painful)
Elimination
Well distributed
Crosses the placenta
Metabolized in liver by
acetylating; renally excreted
Reduce dose in pts. with renal
issues (renally eliminated)
ANTIBIOTIC CLASS: TRIMETHOPRIM (usually always given with Sulfamethoxazole)
Trimethoprim:
Broad spectrum antibiotic
Method of Action (MOA):
Bactericidal or bacteriostatic
Inhibits dihydro-folate reductase which converts dihydrofolic acid to tetrahydrofolic acid.
So, suppresses bacterial synthesis of DNA, RNA & protein synthesis
Drug Resistance:
Bacterial synthesis of dihydrofolate reductase
Altered dihydrofolate reductase
Reduced cellular permeability
Individual Drugs
Effective Against
Trimethoprim
Gram(-) bacilli: E. coli, Proteus mirabilis, K.
pneumoniae, Proteus mirabilis, Serratia
marcescens, Salmonella & Shigella
Gram(+) bacilli: Corynbacterium diphtheriae,
Listeria monocytogenes & some protazoa, P.
carinii, Toxoplasma gondii
TMP/SMX
Aerobic gram(+), S. Pneumoniae, S. aureus
Route
PO (with
full glass
of water)
Trimethoprim with Sulfamethoxazole (Bactrim, Septra):
Widely distributed including CSF
Combo inhibits 2 sequential steps in bacterial folic acid synthesis  more powerful than TMP or
SMZ alone.
Adverse Effects:
Hypersensitivity reactions (Stevens-Johnson syndrome)
Blood dyscrasias (hemolytic anemia, agranulocytosis, leukopenia, thrombocytopenia, aplastic
anemia)
Kernicterus
Renal damage: crystalluria
Megaloblastic anemia (in pts who are folate deficient), hyperkalemia, birth defects
Adverse effects
Well-tolerated
Rash, itching
GI effects: Nausea,
vomiting
Distribution
Elimination
Rapidly absorbed; well
distributed,
Crosses the placenta
Excreted in breast milk
Excreted unchanged in urine
Reduce dose in pts. with liver or renal
issues (Hepatically metabolized/renally
eliminated)
Widely distributed
Metabolized in liver
(Bactrim, Septra)
including CSF
Gram(-), Enterobacteriaceae (Not P.
aeruginosa or Pneumocystis carinii)
Excreted in urine
ANTIBIOTIC CLASS: FLUOROQUINOLONES → "-oxacin" suffix
Fluoroquinolones:
Broad spectrum antibiotic
Method of Action (MOA):
Bactericidal
Inhibits bacterial DNA gyrase—enzyme that converts closed circular DNA into a super
coiled configuration (for DNA replication)
Resistance
Alteration in DNA gyrase and ↓ ability to cross bacterial membranes
Drug Interaction
↑ Theophylline (asthma), Warfarin (anti-coagulant), Tinidazole (anti-fungal)
Adverse Effects:
GI: N/V, diarrhea, abdominal pain – C. difficile
Candida infections (pharynx & vagina)
Possible tendon rupture with systemic use (reversible if diagnosed early)
o Affects Achilles tendon
o Do not use in children < 18 y/o. Risk for all pts though.
o Ciprofloxacin ok for kids over 12
Photosensitivity – even w/ sunscreen. D/C med if pt gets a rash
Avoid in pregnant women or breast feeding women
Individual Drugs
Uses
Effective Against
Route
Distribution
Elimination
Ciprofloxacin
Ofloxacin
Moxifloxacin
Norfloxacin
Gemifloxaxin
Levofloxacin
Gram(+) & gram(-): E. coli, P. aeruginosa,
Klebsiella, Salmonella, Shigella, Campylobacter
jejuni, Bacillus anthracis, , Haemophilus influenzae,
gonococci, meningococci and many streptococci
Not useful for infections caused by anaerobes
Nursing Implications
Avoid Ca2+ (milk, antacids), iron, magnesium (laxatives), aluminum & zinc for 2 hours before or 6 hours after taking Fluoroquinolones
Drug
Metronidazole (Flagyl)
(bactericidal by DNA
synthesis interruption)
PO, IV,
topical
Concentrated in urine,
stool, bile saliva, bone &
prostate tissue
CSF penetration is low
Respiratory tract infection,
UTI, GI, bones, joints, skin,
soft tissue & anthrax
Use
Route
Protozoal infections
Infections by anaerobes (prophylaxis for colorectal surgery, abdominal surgery, vaginal surgery)
– therapy include drug active against aerobic bacteria
C. diff, Giardia, trichomoniasis (“trich” – vaginitis), H. Pylori
Hepatically
metabolized
Renally eliminated
Adverse effects
IV infusion
1. Reconstitution
2. Dilution in IV solution
3. Neutralization (NaHCO3
for pH elevation)
Neurotoxicity
Allergy
Suprainfections
BACTERIA
H. pylori
Tetracycline*
Clarithromycin (Macrolide)*
Amoxicillin*
Flagyl (Metronidazole)*
Bismuth
Tinidazole
C. difficile (treatment)
Flagyl (Metronidazole)
Vancomycin
Teicoplanin
C. difficile (cause)
Tetracyclines
Macrolides
Lincosamides
H. influenzae
Broad Spectrum PCN
nd
2 gen Cephalosporins
Bacterial Meningitis
rd
3 gen
Cephalosporins
Meropenem
Chloramphenicol
Mycobacterium avium
complex (MAC)
Macrolides
*w/ a Proton Pump Inhibitor (PPI), OR a
Histamine2 receptor antagonist
E. coli
Aminoglycosides
Sulfonamides/Trimethoprim
Fosfomycin
Broad Spectrum PCN
Extended Spectrum PCN
Fluoroquinolones
Pseudomonas aeruginosa
Aminoglycosides
Fluoroquinolones
Aztreonam
Imipenem
Extended Spectrum PCN
rd
3 gen Cephalosporins
MRSA
Sulfonamides
Vancomycin
Linezolid (Zyvox)
Candida albicans (cause)
Fluoroquinolones
Tetracyclines
Bacillus antracis
Tetracyclines
Fluoroquinolones
VRE
Linezolid
Dalfopristin/Quinupristin
th
Cefepime (4 gen) - better
ANTI-FUNGALS
Individual Drugs
Amphotericin B
Broad spectrum antifungal
Fungicidal or Fungistatic
Azole antifungals
("-azole" suffix)
Itraconazole 
Fluconazole
Voriconazole
Clotrimazole
Ketoconazole
Miconazole
Flucytosine
Echinocandins:
Caspofungin, Micafungin,
Anidulafungin
MoA
↑ cell permeability;
Binds to
membrane sterol
(we also have
sterols toxic)
Effective Against
Systemic fungal
infections, but
highly toxic
Only use drug for
progressive & fatal
infections
Route
IV only – given
over months
Pharmacokinetics
Resistance is rare.
Not easily absorbed by CSF
Detected in tissues up to a
year after withdrawal
Adverse Effects
*Nephrotoxicity*: in almost all pts. (dose-dependent over tx period) usually
reversible unless dose is over 4 grams.

Check kidney function every 3-4 days.

Infuse 1L of saline on treatment days to minimize damage
Infusion reaction: b/c proinflammatory cytokines release
Fever, chills, nausea, HA 1-3 after infusion (give Benadryl, Tylenol or Aspirin (↑
renal damage)
Phlebitis: change IV sites, give through a large central vein & pretreatment with
heparin
Hypokalemia from kidney damage.
Bone marrow suppression
Adverse Effects
Cardio suppression – ↓ ventricular ejection fraction but return to normal in 12 hours after dosing
Liver injury (Check LFT’s when taking PO
Inhibit liver metabolizing enzymes
GI effects: N/V, diarrhea
Inhibit synthesis of
IV, PO
Drug Interactions
Alternative to
ergosterols which
Amphotericin B
Sulfonylurea-type oral hypoglycemic
NOTE: Take with
↑ cell membrane
(safer and PO, IV)
Phenytoin (CNS toxicity)
food
and
cola
↑
permeability and
absorption
Tacrolimus (↑ nephrotoxicity)
cellular leakage
Lovastatin, simvastatin (rhabdomylolysis)
Inhibits CYP450  ↑ cisapride, pimozide dofetilide & quinidine
Hepatically metabolized by P450. Interaction w/ Warfarin, Cyclosporine, Digoxin, Carbamazepine
H2 antagonist and PPI ↓absorption: give 1 h AC or 2h PC
CLOTRIMAZOLE – TOPICAL - Dermatophytic infections and candidiasis of skin, mouth, vagina
KETOCONAZOLE – PO/TOPICAL – Superficial mycoses
MICONAZOLE – TOPICAL – Dermatophytic infections and cutaneous and vulvovaginal candidiasis
Reserved to serious
Hepatotoxicity
Excreted by the kidneys
infections of
Used in common
Candida &
Bone marrow suppression – reversible thrombocytopenia and neutropenia
Absolutely
monitor
renal
PO,
Topically
w/ Amphotericin B
Cryptococcus
function.
Ventricular dysrhythmias
neoformans
Disrupt fungal cell
wall
Asperigillus
Candida
PO
ANTIVIRALS
Viruses
Herpes simplex virus (HSV):
Mouth, face, other (HSV-1)
Genitalia (HSV-2)
Herpes-zoster: shingles (Dormant in sensory nerve roots)
Varicella-zoster virus (VZV): Chickenpox
Cytomegalovirus (CMV): Occurs person to person (body fluids)
Sites of infection: lungs, eyes (loss of vision) & GI
Immunosuppressed patients at high risk for reactivation of dormant virus
Hepatitis B
Transmission via blood and semen
Chronic infection leads to cirrhosis  hepatic failure  hepatocellular carcinoma  death
Hepatitis C
Transmission: primarily through exchange of blood; controversy over sexual transmission
Slow progression but eventually liver damage  cancer  death
There is no vaccine for hepatitis C
Influenza A&B
Spread through aerosolized droplets (coughing & sneezing)
Virus enters body through mucous membranes of nose, mouth, or eyes; Viral replication begins in the lungs
Symptoms: fever, chills, cough, sore throat, HA, myalgia
Individual Drugs
Effective Against
Route
MOA/Pharmacokinetics
PO - for recurrent infection
Drug of choice for HSV 1& 2, VZV, EpsteinBarr, & Cytomegalovirus
Does not eliminate virus or produce cure
Acyclovir
IV - if genital infection is
severe. Infuse slowly over 1h
Topical – reduces shedding
Prevention of CMV retinitis in
immunocompromised pts or CMV infection
in transplant pt
Ganciclovir
Vaccines/Drugs
Effective Against

Interferon alfa-2b

Peg-interferon alfa-2a

Lamivudine (Epivir-HBV)

Adefovir (Hepsera)

Entecavir (Baraclude)

Telbivudine (Tyzeka)
Interferon alfa combined with
ribavirin
Influenza Vaccine
Amantadine (for
Parkinson's, but found it
worked for flu)
Hepatitis B
PO
NOTE: Take with food
Route
Parenterally
only: usually SQ
Adverse Effects
Inhibits viral replication by suppressing synthesis of
viral DNA
VZV = use HIGH dose EARLY (w/in 24-72 hrs) IV if
possible
Avoid sex if lesions present & use condom if not
Renal elimination, normal half-life 2.5h, anuric 20h
Intravenous therapy
o
Phlebitis
o
Reversible nephrotoxicity
Oral therapy: GI, vertigo
Topical therapy: stinging sensation
Bioavailability is low (9%); take with food.
Adjust dose in pts. with kidney disease
TERATOGENIC (Pregnancy C)
Granulocytopenia (40%) &
thrombocytopenia (20%)
exacerbated with zidovudine
o
Monitor CBC’s
MOA/Pharmacokinetics
Adverse Effects
Blocks viral entry into cells, synthesis of viral messenger RNA, viral
proteins, viral assembly & release
Long acting: dosed once weekly
12 months of treatment, but usually relapse after treatment withdrawal
Flu-like syndrome (50%) diminish with use
can give APAP
Severe depression (suicide) give
antidepressants
Protection begins 1 to 2 weeks after vaccination & can last 6 months or
longer
Season Nov-April
Do not give/recommend for pts with
hypersensitivity to eggs (b/c grown in eggs)
Guillain-barre syndrome (GBS) with
inactivated
Hepatitis C
Influenza A & B (A
more)
IM (inactivated)
Nasal Spray
(live/attenuated)
ANTI-PROTOZOAL DRUGS
Malaria
Parasitic disease caused by protozoan of genus Plasmodium vivax and Plasmodium
falciparum
o P. vivax: most common, symptoms can be treated w/ drugs; regular symptoms
o P. falciparum: less common; more severe, w/o treatment 10% of victims die;
many strains are drug resistant
Individual Drugs
Effective Against
Chloroquine (Aralen)
High activity against erythrocytic forms
Not active against exoerythrocytic forms
Primaquine
Used for hepatic forms of malaria
DOC for preventing relapse of vivax malaria
Quinine (older)
Active against erythrocytic forms of malaria
Quinidine gluconate
DOC for Severe malaria in US
Treatment Objectives
o Treatment of acute attack
o Prevention of relapse
o Prophylaxis
Drug choice based on:
o Goal of treatment
o Drug resistance of the causative strain
Route
Doses required for prophylaxis are low
High doses for treatment are taken
only briefly
Adverse Effects
GI effects, visual distubances, pruritus, HA
Hepatotoxicity
Hemolysis: deficiency of glucose-6-phosphate dehydrogenase (G6PD) in RBCs
Populations affected: Iranians, Sephardic Jews, Greeks, Sardinians
IV route combined with doxycycline,
tetracycline, or clindamycin treatment
of choice for severe malaria
Cinchonism – tinnitus, HA, visual disturbances, nausea & diarrhea
Hemolytic anemia
Pregnancy Category C Drug - damage to auditory nerve
IV and PO (only parental drug
approved)
Requires continuous ECG monitoring and frequent BP monitoring
Both IV quinidine and PO quinine should be accompanied by doxycycline,
tetracycline, or clindamycin
Mefloquine (Lariam)
DOC for prophylaxis of malaria in regions where
chloroquine-resistant P. falciparum or P. vivax is found
Ketoconazole, a strong inhibitor of CYP3A4, can increase levels of mefloquine
Chronic Obstructive Pulmonary Disease
Spirometry measures FEV1 which is a diagnostic tool for diagnosing COPD
Hallmark of COPD is a ↓ in FEV1 and forced vital capacity (FVC) ratio to below 75% on spirometry
Chronic Bronchitis
Inflammation of bronchi (hyperplasia/hypertrophy of mucus glands)  bronchial tube narrowing
Chronic/recurrent productive cough, airway obstruction
↓ O2 Blue Bloater
Acute exacerbations usually due to an infection
Signs: wheezing, chest pain or discomfort, a low fever, shortness of breath
Emphysema
Alveolar damage causing ↓ ability to oxygenate blood; air trapped in lungs
Low C.O  tissue hypoxia and pulmonary cachexia  muscle wasting, weight loss
↓CO2 – pink puffer
Normal inhalation, difficult exhalations.
Lowered cardiac output and hyperventilation
Drugs
Adverse Effects
Anticholinergic
Ipratropium {Atrovent)
Tiotropium (Spiriva)
Atropine
MOA
Dosage/Route
Bronchodilation
First line for chronic COPD
Slow onset of action
Scheduled dosing (not PRN)
Via nebulizer or MDI
Bronchodilation
First line for acute COPD
Quick onset of action
Use β2-agonist 5 min BEFORE using
steroid so it can penetrate deeper
into the lungs.
Additional Information
Maintains effectiveness after years of use
Can be used w/ SABA for rescue
β 2 Agonist
Albuterol(SABA)
Levalbuterol (Xopenex)
Salmeterol (LABA)
Salbutamol (Ventolin) (SABA)
Methylxanthines
Theophylline
Glucocorticoids
Asthma
↑ cAMP  inhibit mast
cell degranulation
Anti-inflammatory effect
and reduces mucus
secretions
Albuterol – tremors, tachycardia
Give Levalbuterol if pt. has heart problems
LABA can’t be used to stop an asthma attack (not 1st
line; must give with GCC
Narrow therapeutic index
Monitor other drugs the pt is on
IV; PO: Methylprednisolone, Hydrocortisone, Cortisone, Dexamethasone
Inhaled: Triamcinolone, Beclomethasone, Flnisolide
Always wash mouth after use of inhalation b/c of thrush
•1st long-term control w/ lowdose ICG and continue using
SABA
•2nd use Cromolyn and
leukotriene receptor
antagonist
Symptoms >2/week;
nocturnal symptoms
about 3-4/month
FEV >80% of predicted
Alternatives: Low-dose IGC,
Theophylline SR, LTRA, PRN
SABA
Symptoms daily; nocturnal
awakenings at least 1/week
(not nightly).
Some limitation of daily
activity
PEF/FEV > 60%, but <80% of
predicted.
High-dose IGC w/ LABA. PRN
PO GC. For breakthrough,
use SABA
Can ↓ treatment if
symptoms are managed
Continuous symptoms
throughout day; frequent
nocturnal
awakenings/exacerbations.
Severe limitations on normal
activity
PEF/FEV <60%
IF PT IS TAKING SABA
DAILY, MOVE TO STEP 4.
Uses SABA several times a
day
Acute Severe Exacerbations
Quick-relief
Medium/Low dose IGC w/
inhaled SABA and PRN SABA
Step 4: Severe Persistent
Asthma
Need SABA < 2/week;
nocturnal symptoms
occur <2/month
Long-term control
Step 3: Moderate Persistent
Asthma
Acute attacks treated
with SABA
Step 2: Persistent Asthma
Step 1: Intermittent Asthma
Treated on a PRN basis.
No daily meds are
needed
Administer O2 to relieve
hypoxia. Hospitalization may
be required
Administer systemic GC (IV
Methylprednisolone or PO
Prednisone) to ↓
inflammation
Nebulized high-dose SABA
to ↓ airflow obstruction
Maintain O2 saturation >
95%
• If unconscious or can’t generate
PEFR, give SQ Epinephrine!!
Symptoms: Wheezing, breathlessness, tight chest, dyspnea, cough
Inhalers
 Metered Dose Inhaler - reaches 10% of lung; can be used with a spacer
 Dry-Powered - delivers to 20% of lung
 Nebulizer – coverts drug solution into a mist
Asthma (cont.)
β2 –
Agonist
Glucocorticoids
Drugs
Use
MOA/Pharmacokinetics
Adverse Effects
Additional Information
Inhaled
Beclomethasone
Mometasone
Fluticasone
Trimacinolone
Very effective (INH, PO, IV)
Used on fixed schedule, not PRN
Moderate-severe asthma
↓ inflammation, ↓ bronchial activity
↓ release of inflammatory mediators
↓ airway mucus production
↓ edema of airway mucosa
↑ level of β2-receptors
Oral
Prednisone
Prednisolone
Fludrocortisone
Severe asthma
Used PRN at high doses
Do not use to stop attack
↓ inflammation by suppression of migration
of leukocytes and reversal of capillary
permeability
Hepatically metabolized
Taper withdrawal
Adrenal suppression & bone loss
↑ BG, BP, weight, fluid retention
↑ Na and ↓ K, Muscle weakness
Bronchodilation
↓ release of histamine
↑ HR & BP, ↑ BG
Tremors, sweats, agitation
Pulmonary edema, MI, dysrhythmia
Salmeterol & Formoterol are inhaled long
acting (these are no longer sold alone)
FIXED schedule doses
Immediate SNS response
↑ HR
Don’t give drug w/ other β agonists
Emergency self-relief
↑ BG *caution diabetic pts
Arrhythmia, coronary insufficiency
HTN, HTM
Generally well tolerated
Tachycardia, angina, tremor
Excessive use  paradoxical
bronchospasm
Inhaled
Albuterol, Levalbuterol,
Bitoterol, Pirbuterol
Oral
Albuterol, Terbutaline
Nonselective Epinephrine
PO, INH, PO are all long-acting
INH are all short-acting
*except: Salmeterol and Formoterol
Best drug for exercise asthma
INH, Subq, IM, IS, IV, IC
Relieve severe asthma sx.
Isoproterenol
Non-selective β – Agonist
IH, SL, IV
Bronchial asthma, bronchitis,
emphysema
Metabolized by liver and lungs
Excreted by kidneys
SNS response on heart and lungs
Albuterol (Proventil, Ventolin,
Proair (HFA)) (SABA!!)
INH, PO
For exercise induced asthma
For severe acute attack, use a
nebulizer
Relaxes bronchi, uterus, blood vessels
Hepatically metabolized
Kidney/Feces excreted
Adrenal suppression & bone loss
May slow growth in children
Gargle after use to avoid thrush
Hyperglycemia
Can cause glaucoma/cataracts
Use β2 5 min before to open up lungs
Take in morning w/ food
Monitor glucose, insulin coverage
Spray away from nasal septum
Take in morning w/ food
Drug interactions:
↓ drug effect w/: rifampin, barbiturate,
phenobarbital
↑ PUD risk: salicylate, NSAIDs
Rinse mouth after use
Do not use if precipitate or discoloration
occurs
Avoid caffeine & smoking
Rinse after use
Drug Interaction:
MOAI, Epi, other INH SNS-drugs, TCAs
Anticholinergic
Cromolyn
Nasalcrom nasal spray
Nedocromil
Short-acting
Ipratropium Bromide
(Atrovent, Combivent,
DuoNeb)
Long-acting
Tiotropium (Spiriva)
Blocks the muscarinic ACh receptors in the
smooth muscles of the bronchi
Bronchodilation
Blocks phosphodiesterase which ↑ tissue
concentrations of cAMP  induces release of
epinephrine
Hepatically metabolized to caffeine
Renally excreted
Asthma
Chronic bronchitis
Emphysema
Methylzanthines
Theophylline
Aminophylline (slow IV)
Leukotriene Modifiers
↓ release of inflammatory mediators
Mast cell stabilizer
Not a bronchodilator
Prophylactic use (not for acute
attack)
Takes 2-4 weeks for full effect
Prophylactic treatment
Use w/ IGC or β2 – Agonist
↓ bronchoconstriction (less effective
than beclomethasone)
Maintenance Rx for children 5+
Zileuton (Zyflo)
Zafirlukast (Accolate)
Montelukast (Singulair)
Blocks leukotriene synthesis
Hepatically metabolized
Anti-inflammatory leukotriene receptor
antagonist
Hepatically metabolized
Approved for pts 1+
Not for quick relief
Miscellaneous Drugs
Caution w/ impaired renal/hepatic
function
DO NOT USE IN ACUTE ATTACK
↑ fluid intake
Scheduled dosing
Use with steroid inhaler
Cough, nervousness, dry mouth,
hoarseness
Contraindications:
Pts w/ hypersensitivity to atropine or
peanuts
Glaucoma pts
Bladder neck obstruction
Respiratory arrest, ventricular
tachycardia
Tachypnea, palpitations, sinus
tachycardia, nervousness, restlessness,
insomnia, anorexia
Theophylline: narrow index, given orally
↑ fluid intake (↓ viscosity)
Avoid caffeine while on drug
↑ therapeutic
↓ therapeutic
Age, Erythromycin,
Adolescence
cimetidine, ciprofloxacin
Phenobarbital,
Cirrhosis, pulmonary
phenytoin,
edema, CHF, severe COPD
tobacco
Liver damage
↑ levels of ALT activity
↑ levels of Theophylline, Warfarin,
Propranolol
Monitor LFTs and ALTs
Does not cause liver damage
No serious DIs
Take at bedtime
Less effective than IGC
Potential for Neuropsychiatric effects
MOA
Uses
Guaifenesin
Irritates the gastric mucosa & stimulates respiratory tract secretions
↓ coughing
PO; Take with lots of water
Beware of sugar and ETOH content
Dextromethorphan, Codeine, Benzonatate
↓ coughing
Beware of sugar and ETOH content
Pseudoephedrine, Phenylephrine, Afrin
Decongestants
Caution in pts w/ HTN, HTN, CVA, dysrhythmias
Use for 3+ days can cause rebound congestion
Loratadine, Certirizine, Fexofenadine,
Diphenhydramine, Chlorpheneramine
Antihistamines
H1 receptor antagonist
Can cause drowsiness, sedation, dry mouth, constipation, urinary retention
Tuberculosis
Tuberculin Skin Test (TST)
Intradermal injection of Purified Protein Derivative (PPD)
If pt was exposed to TB, the immune system elicits a response in 48-72 hours
Hardness around injection site and size will determine how aggressive treatment should be
Treatment drugs
Isoniazid
MOA/Pharmacokinetics
Bactericidal to active mycobacterium
Bacteriostatic to resting mycobacterium
Hepatically metabolized
Renally excreted
Treatment Regimen
Series of 4 drugs: Isoniazid (INH), Rifampin, Pyrazinamide (PZA), Ethambutol or Streptomycin
Follow closely to ensure compliance and monitor for efficacy and toxicity
Report severe GI problems, yellow sclera, dark urine, clay-colored stool, vision, hearing changes,
numbness or tingling
Uses
Preferred for latent/prophylaxis TB
Duration: 6-9 months, 1-2/weekly
PO, IM
Adverse Effects
↓ B6  peripheral neuropathy
Hepatotoxicity (monthly AST/ALT)
Burning dark urine, jaundice, tingling
Additional Information
Take on empty stomach
ETOH ↑ risk of hepatotoxicity
Antacids ↓ absorption
Disulfiram (Antabuse)
Rifampin
Pyrazinamide
Ethambutol
Streptomycin
Broad spectrum against TB
Bacteriocidal; blocks RNA transcription
Hepatically metabolized
Excreted in feces
Hepatically metabolized
Renally excreted
Bacteriostatic; ↓ RNA synthesis
Only effective to dividing mycobacterium
Hepatically metabolized
Renally excreted
Aminoglycoside
Duration: 6 months-2 years
PO, pedi serum
Give w/ 240 ml H20 w/ no food
Anorexia, discoloration of body fluids,
pruritus, rash, chills, fever, HA, bone
pain, respiratory difficulty
PO, pedi serum
Urination difficulties, pruritus, rash,
photosensitivity, joint pain, jaundice
PO
Take with food
Optic neuritis: blurred vision, loss of
red/green
Renal impairment
Chills, joint pain/swelling
Deep IM, rotate sites
Tinnitus, nephrotoxicity, hepatotoxicity
ETOH ↑ hepatotoxicity risk
Corticosteroids ↓effectiveness
INH ↑ hepatotoxicity risk.
ANTI-ULCER DRUGS
Peptic Ulcer Disease (Gastric erosive disease)
o Cause: Imbalance between mucosal and aggressive factors
o Primary cause of PUD is Helicobacter pylori
o Aggressive factors: H.pylori, NSAIDS, gastric acid, pepsin, smoking
Non-drug therapy: Diet, eat smaller meals (↓ fluctuation of pH), stop smoking (↑ ulcers
and retards recovery), avoid NSAIDS, alcohol, stress & anxiety
Drugs
Antibiotics
Amoxicillin [Amoxil]
Bismuth [Pepto-Bismol]
Clarithromycin [Biaxin]
Metronidazole [Flagyl]
Tetracycline [Achromycin V]
Tinidazole [Tindamax]
Anti-secretory Agents
Class
H2 receptor antagonists
“-tidine”
Proton Pump Inhibitors
“-prazole”
Cimetidine [Tagamet]
Famotidine [Pepcid]
Nizatidine [Axid]
Ranitidine [Zantac]
Dexlansoprazole [Dexilant]
Esomeprazole [Nexium]
Lansoprazole [Prevacid]
Omeprazole [Prilosec, Zegerid, Losec]
Pantoprazole [Protonix]
Goals of Peptic Ulcer (PUD) treatment
1. Eradicate H. pylori
2. Reduce gastric activity
3. Enhance mucosal defenses
Mechanism of Action
Eradicate H. Pylori
Use 2-3 antibiotics in combo with PPI or H2 antagonist given for 10-14 days
Don’t take with alcohol
GI: Nausea and Diarrhea
Suppress acid secretion by blocking H2 receptors on parietal cells
+
+
Suppress acid secretion by irreversible inhibiting H /K -ATPase, the enzyme
that makes gastric acid aka: BLOCKS final step of acid production
Most effective drugs for suppressing secretion of gastric acid
Selection of PPI based on cost and prescriber preference
Mucosal Protectant
Sucralfate [Carafate, Sulcrate]
Forms a barrier over the ulcer crater that protects against acid and pepsin
Anti-secretory Agent that
Enhances Mucosal Defenses
Misoprostol [Cytotec]
Protects against NSAID-induced ulcers by stimulating secretion of mucus and
bicarbonate, maintain submucosal blood flow, and suppressing secretion of
gastric acid
Antacids
Aluminum hydroxide
Calcium carbonate
Magnesium hydroxide
React with gastric acid to form neutral salts aka.
Gastroesophageal Reflux Disease (GERD) Drugs
Drugs
Cimetidine
Uses
Ranitidine
Famotidine
Nizatidine
PPI
Misoprostol
Antisecretory
Prostaglandin
Sucralfate
Cytoprotective
Antacids
Pirenzepine
(Gastrozepin)
Anticholinergic
MOA
Block H2 receptor sites of parietal
cells = ↓ gastric acid secretion and
↑ pH of secretion
↑potency, ↓AE, ↓ DI vs cimetidine b/c ↓ CNS permeability
Does not bind to androgenic receptors; does not inhibit P450
Use: short-term trmt of gastric/duodenal ulcers, prophylactic for recurrent
duodenal ulcers, trmt of Zollinger-Ellison Syndrome & hypersecretory states
and GERD
PUD
GERD
↑ cervical ripening
↑ uterine contraction
Short term trt of ulcers
Prophylaxis
PO
Rapid absorption in GI
Hepatically metabolized
PO
Rapidly absorbed
PO, Suspension
Low absorption
Nonreversible inhibition of
H+/K+ATPase pump (3-5 days for
partial recovery)
Blocks final step of acid production
Analog of prostaglandin E1
Aspirin & NSAID inhibit
prostaglandin, misoprostol serves
as replacement
↑ HCO3 & mucus production
↓ gastric acid secretion
Paste-like material binds to ulcer
crater
↓ pepsin activity and bile salts
Low ANC, long DOA
Binds to pepsin  ↑
ulcer healing
PUD
GERD
High ANC, long DOA
Rapid acting
High ANC, long DOA
Rapid acting
CaOH
NaOH
Excreted by kidneys
Short-term (4-8 wks)
PUD
GERD
Hypersecretory
disorders
Duodenal ulcer
AlOH
MgOH
*DOC
PO - 30 min onset
IV - 10 min onset
PUD
GERD
Hypersecretory
disorders
H2 Receptor
Antagonist
Omeprazole
Route/Kinetics
Acidosis
Short DOA
Rapid acting
Duodenal ulcers
PO
Neutralizes stomach acid = ↓ gut
wall destruction
pH > 5 = ↓ pepsin activity
↑ production of prostaglandins
Selective blockade of muscarinic
receptors that regulate gastric acid
secretion
Adverse Effects
Diarrhea/constipation
Anti-androgenic effects: Gynecomastia, impotence, ↓ libido,
↓ sperm count
CNS S/E in old pts w/ hepatic/liver dysfunction: confusion,
hallucination, lethargy
Pneumonia: ↑ gastric acid pH = ↑ bacteria growth in stomach
 ↑risk of infection of respiratory tract
IV bolus: risk of hypotension and dysrhythmias
Drug Interactions
Inhibits P450: ↑ levels of Phenytoin, Diazepam, Theophylline,
Warfarin, ETOH, Digoxin
Antacids ↓ absorption of cimetidine – GIVE 1 HR APART
Additional Information
Assess pain, renal/hepatic fxn
Maintenance therapy @ HS
Avoid late PM meals
Slow IV
Take w/ food
Avoid ETOH, caffeine, large
meals
Smoking cessation
↑ risk of pneumonia, fractures, rebound acid hypersecretion,
C. diff infection, hypomagnesaemia
Drug Interactions
↓ pH = reduce absorption of HIV antivirals
Plavix = reduce adverse and beneficial effects
Pregnancy category X
Diarrhea, Abdominal pain
N/V, Flatulence, HA, Dyspepsia (indigestion
Toxicity: sedation, tremor, convulsions, dyspnea, fever,
abdominal pain, bradycardia
Constipation
Drug Interactions
Antacids raises pH > 4, interfering w/ Sucralfate
↓ absorption of Warfarin, Digoxin, Fluoroquinolones,
Theophylline, Phenytoin
Constipation
Binding of Warfarin, Digoxin, Tetracyclines ↓ AlOH effects
↓ phosphate absorption (hypophosphatemia)
High Na+ content so be careful with pts. that have HTN
Take 30 min before AM meals
Interacts w/ antacids
Check pt for pregnancy
Assess bowel function
Give 1 hour q ACHS
↑ fiber and fluids
4-8 weeks therapy
Give in combo w/ MgOH to
neutralize S/E
Diarrhea
Renal impairment (Mg toxicity  CNS depression)
DOC for antacids trmt
Don’t give to pts w/
intestinal pain??
Constipation
Acid rebound
Eructation and Flatulence
Tastes bad
Eructation and Flatulence
Don’t give to pts w/ HTN or
renal impairment
Dry mouth, diarrhea, N/V, & visual disturbances
Constipation
Drugs
Dose Response
MOA
Taking
Additional Information
Delayed (1-3 days)
Acts like normal dietary fiber (most gentle)
Softens stool by pulling water into small intestine and ↑
of colonic bacteria  ↑ fecal volume  promotes
peristalsis
Also used for diverticulitis and IBS
Take w/ full glass of
water
Stool formed in 1-3 days
DOC for temporary trmt of constipation
AE: esophageal obstruction
Surfactant
Docusate sodium/calcium
Delayed (1-3 days)
↓ surface tension  water penetrates SI & colon 
softening stool
↑ secretion of water & electrolytes into lumen
↑ intestinal motility
Can take frequently
Take w/ full glass of
water
Most often given with opioids
Stimulant
Bisacodyl (colon)
Senna (colon)
Castor Oil (SI)
Semi-Quick (6-12 hrs)
Castor oil – quick resp.
Suppository – 15-60 min
↑ intestinal motility, peristalsis
↑ secretion of H20 & electrolytes into the intestine
↓ intestinal absorption of fluids
Uses: opioid induced constipation, trmt of slow intestinal
transit
Not for long-term use
Take 1 hr after taking
milk/antacid; swallow
whole
Highly abused
Senna  yellow-brown or pink urine
Do not give castor oil HS!
Poorly absorbed salts  ↑ water in lumen
Fecal mass softens/swells, wall stretches, ↑ peristalsis
↑ fluid intake
NaPO4 is also BC
AE: dehydration, renal decline (Mg toxicity),
Na retention (exacerbates HF, HTN, edema,
acute renal failure)
↑water in lumen, softens feces
Also used as a bowel cleanser
Ingest large volumes
(bad tasting)
Osmotic
Bulk Forming
Methylcellulose
Psyllium
Polycarbophil
Magnesium (OH, SO4, citrate)
Sodium phosphate
Quick (high dose 2-6 hrs)
Semi-quick (low dose 6-12)
PEG (+ELS for bowel cleanser)
Mineral Oil (colon)
Immediate - enema
5-30 minutes
Lubricates & ↓ water absorption
Enema for impaction
Glycerin Supp. (colon)
Immediate
5-30 minutes
Osmotic agent: soften/lubricate feces & causes reflex
rectal contraction
PO or suppository
Lactulose
Delayed (1-3 days)
↓ water absorption, ↑ water in lumen
Only use if no response to bulk-forming laxatives ($$, S/E)
Enema
Lubiprostone (Amitiza)
Delayed (1-3 days)
Opens Cl- channels in intestinal epithelium  ↑intestinal
motility & ↑ secretion of fluid into the lumen of SI/colon
No electrolyte imbalance/dehydration
Safer for pts w/ HF, kidney/liver disease
Aspiration of oil droplets can cause lipid
pneumonia
Systemic absorption can produce deposition
of mineral oil in the liver
Excessive dosing can ↓ absorption of fatsoluble vitamins
Stool in 30 min (use to obtain quick sample)
Used to re-establish normal bowel function
AE: flatulence, cramping
↑ excretion of NH3  helps pts w/ hepatic
disease
Little side effects b/c not absorbed
Used for idiopathic constipation in adults and
IBS in women > 18y.o.
Diarrhea
Opioids are the most effective antidiarrheal agent- ↓ intestinal motility, allowing more time for body to take up fluid, ↑ fluid secretion into SI, ↑ absorption of salts
Drugs
MOA
Diphenoxylate HCL [Lomotil]
Opioid
Increase absorption back into
tissues
Atropine
Anticholinergic
Relieves cramping but does not
alter fecal consistency
Loperamide [Immodium]
Opioid Antagonist
↓ bowel motility & ↓ fluid
secretion into intestinal lumen
Contraindications
Acute bowel infections
Glaucoma
Prostatic hypertrophy
Adverse Effects
CNS- depression, euphoria,
confusion, sedation,
restlessness
Blurred vision, dry mouth,
urinary retention,
tachycardia
Additional Information
Given with atropine to prevent
abuse (schedule V)
For acute self-limiting diarrhea
OTC
Poorly absorbed, doesn’t cross BBB
Disease/Use
Irritable bowel syndrome
Drug therapy is not curative
Inflammatory bowel disease
Drugs
Additional Information
Alosetron [Lotronex]
GI toxicities can cause complicated constipation, leading to perforation and ischemic colitis
Potentially dangerous drug; approved for women only
Lubriprostone [Amitiza]
Only for women older than 18
Tegaserod [Zelnom]
Only for short-term therapy
Aminosalicytes (sulfa)
Glucocorticoids (hydrocortisone)
Immunosuppressants
Immunomodulators (infliximab)
Antibiotics (metronidazole)
Check CBC periodically
Prolonged use can cause osteoporosis, increased risk of infection, adrenal suppression
Risk of infection and pancreatitis
Increase risk of infection
Metoclopramide [Reglan]
Blocks receptors for dopamine and serotonin in the CTZ
Cisapride [Propulsid]
Increases upper GI motility and suppresses emesis
GERD, CINV, Diabetic gastroparesis
↑ tone/motility of GI tract
↓ oral mucositis
Palifermin [Kepivance]
Deficiency of enzymes  ↓ digestion
Pancrelipase
Chenodiol (chenodeoxycholic acid)
Gallstones
Ursodiol (ursodeoxycholic acid)
Anorectal
For hemorrhoids
Stimulates proliferation, differentiation, and migration of epithelial cells
Current only for pts w/ hematologic malignancies (b/c it can stimulate its growth)
Enteric-coated microspheres designed to dissolved in duodenum & upper jejunum
Advise pts to not chew, crush or hold in mouth
Useful for radiolucent stones (not calcium)
Increases production of bile acids
Most successful in women with low cholesterol level
Does not increase bile acids
Reduces the cholesterol content of bile
Gradual dissolution of stone
Local anesthetics (benzocaine)
↓ itching and pain
Hydrocortisone
↓ inflammation, itching, swelling
Emollients
Lubricants ↓ irritation
↓ irritation and inflammation
Astringents (ZnO)
Anti-Emetics  suppress N/V
3 Types of Emesis
Anticipatory – occurs before drugs are given
Acute – begins minutes to hours from initiating drugs
Delayed – a day or more after receiving drugs
Sub-classes
Drugs
Uses
Rules
Anti-emetics are better at preventing than suppressing
Better to administer before other meds given
PO and IV are equally effective
MOA
Adverse Effects
Serotonin Rec
Antagonist
“-tron”
Ondansetron [Zofran]
Granisetron
Dolasetron
Palonosetron
Chemotherapy
Radiation
Postoperative
Pregnancy
Blocks 5HT3 receptor on vagal
afferents in the CTZ
Glucocorticoids
Methylprednisolone
Dexamethasone
Chemotherapy
Unknown
Aprepitant (PO)
Fosaprepitant
Chemotherapy
CINV
Postop N&V
Antagonist of substance
P/neurokinin1 in the brain
Long DOA ∴ prevents
acute/delayed emesis
Hepatic metabolism
Dronabinol
Nabilone
Chemotherapy,
Sickle-Cell Anemia
Appetite
stimulant
Phenothiazine:
Promethazine
[Phenergan]
Butyrophenones:
Halperidol, Droperidol
Other:
Metoclopramide
Domperiodone
Chemotherapy
Post-op N/V
General
Lorazepam [Ativan]
Treats: CINV
Used in combination regimens
Substance P
Cannabinoids
Dopamine Antagonist
Anticholinergic
Benzodiazepine
Antihistamines
Other
Diphenhydramine
(Benadryl)
Hydroxyzine (Vistaril)
Meclizine (Antivert)
Scopolamine patch
[Transderm-Scop]
*DOC
Constipation, HA, rash
Transient ↑ of AST, ALT
Rare: bronchospasm, ↑
HR, CP, ECG changes, tonic
clonic seizures
Additional Information
Most effective drug to combat N/V
Prevents acute emesis
Monitor bowel fxn and liver
enzymes
Contraindications
Impaired hepatic/renal function
Caution pregnancy/lactation
IV for emesis (NOT PO!)
Effective alone or w/ serotonin
antagonist
Enhances when given in combo
Prevents acute & delayed emesis
Absorbed w/ or w/o food
Unknown
Dissociation,
depersonalization,
dysphoria
Tachycardia, hypotension –
caution pts w/ CV disease
Schedule III
Blocks dopamine receptor in the
CTZ
Extrapyramidal effects hand shaking
Anticholinergic effects
Hypotension, sedation
Promethazine causes drowsiness &
dry mouth, ↑ effects of other CNS
depressants
3 primary benefits:
Sedation
Suppression of anticipatory emesis
Production of anterograde anemia
Antihistamines block H1 rec in
pathway from inner ear to vomiting
center
Sedation (H1 blocked)
Dry mouth, blurred vision,
urinary retention,
constipation
Suppresses nerve traffic in the
neuronal pathway connecting the
vestibular apparatus of the inner
ear to the vomiting center
Dry mouth, blurred vision,
drowsiness
Motion sickness
CONDITIONS & ADVERSE EFFECTS
P450 INHIBITORS
P450 METABOLIZES/INTERACTS W/
THEOPHYLLINE, WARFARIN &
CARBAMAZEPINE:
Sulfonamides
Macrolides
Chloramphenicol
Zileuton (Zyflo) (increase levels)
Montelukast (not increase levels)
Cimetidine "tidine"
Omeprazole
Misoprostol
Sucralfate (take this alone)
Substance P/ Neurokinin1 antagonists
Ondansetron (Zofran)
Warfarin
Dilantin
Carbomesapin
Digoxin
Diafalin
HYPERKALEMIA
PCN G
Amphotericin B
MONITOR RENAL
FUNCTION
Ganciclovir
Flucytosine
Trimethoprim
Cimetidine
OTOTOXICITY
Itraconazole
Fluoroquinolores
Zafirlukast (accolate)
Cromolyn
HEPATOTOXICITY
Aminoglycosides
Flucytosine
Cimetidine "tidine"
Ondansetron (Zofran)
Theophylline
Rifampin
Isoniazid (INH)
Pyrazinamide
Cromolyn (renal)
Ethambutol
Glucocorticoids (oral)
HYPERGLYCEMIA
Glucocorticoid Inhalers
Beta 2 Agonists
Isoproterenol
Guaifenesin
NO ALCOHOL (ETOH)
Imipenem
Lincosamides
Isoniazid (INH)
No antabuse
Rifampin
Guaifenesin
Cimetidine "tidine"
Cephalosporins
PHOTOTOXICITY
Aminoglycosides
(irreversible)
Vancomycin
(reversible)
Teicoplanin (rare)
Macrolide
(transient)
Ethacrynic acid
BONE MARROW
SUPPRESSION
CHELATION
Chloramphenicol
Flucytosine
Amphotericin B
NOTE:
Tetracycline (bone
growth)
JAUNDICE
Sulfonamides
Isoniazid
Pyrazinamide
USE SLOW IV
Cimetidine
Lincosamide
Vancomycin - Red Man
syndrome
Acyclovir
IV rxn: Amphotericin B
NEPHROTOXICITY
Sulfonamides
Tetracycline
Fluoroquinolones
Pyrazinamide
NO PREGOS
Fluoroquinolones
Tetracycline
EMPTY STOMACH
Chloramphenicol
Erythromycin
Azithromycin
Tetracycline (short-acting)
Isoniazid
Rifampin
Proton pump inhibitors
“-prazole”
NEUROTOXICITY
Aminoglycosides (reversible)
Amphotericin B (reversible)
Vancomycin (reversible)
Televancin (reversible)
NSAIDS
Aspirin
Tetracycline
Ethambutol (renal)
Sucralfate (renal)
√ PEAK & TROUGHS
Ganciclovir (C)
Misoprostol (X)
Sulfonamides/Trimethoprim
Tetracycline
Chloramphenicol
Fluoroquinolones
Ondansetron
TAKE WITH FOOD
Cephalosporin
Clarithromycin ER
Azole antifungals
Trimethoprim (Full glass of
water)
Ganciclovir
Ethambutol
Prednisone
Cimetidine
PCN G
INH w/o B6
Aminoglycosides
Vancomycin
Chloramphenicol
Theophylline
NARROW THEURAPEUTIC INDEX
Chloramphenicol
Theophylline
HTN CONTRAINDICATION
Ticarcillin
Aluminum hydroxide
Sodium bicarbonate (DO
NOT GIVE)
BLACK - Antibiotics/Antifungals/Antivirals
RED - Respiratory
GREEN - GI
ADRENAL GLAND & GLUCOCORTICOIDS (GCCS) → “-sone” & “-lone"
Adrenal gland: located at the top of each kidney, has 2 parts
Medulla – secretes catecholamines (EPI, NE)
Cortex – secretes corticosteroids (glucocorticoids & mineralcorticoids)
Adrenal cortex produces 3 classes of hormones:
1. Glucocorticoids (cortisone, prednisone) - Influences carbs &
glucose metabolism
2. Mineralcorticoids (aldosterone) - Na+ & H2O balance
3. Androgens - Sex characteristics (Acne)
Cushing’s syndrome – adrenal hormone EXCESS
Addison’s disease – adrenal hormone DEFICIENCY
Adrenogenital syndome – adrenocortical hyperplasia  abnormal secretion
of hormone  manly women, feminine men, precocious sex develop in kids
Sub-classes
Short Acting
Intermediate
Acting*
Long Acting
Nursing
Implications
Individual Drugs
Treats
PO GCCs ↓ CRH & ACTH from hypo/AP → ↓ endogenous GCCs from adrenals
Long-term GCC → ↓ ACTH production  ↓ cortisol synthesis (self corrects 5 day – 1 year)
↓ immune response & inflammation by ↓ chemical mediators (e.g. prostaglandins, histamine,
leukotrienes, lymphocytes, phagocytic cells, neutrophils & macrophages)
Long-term ONLY when treating of life/permanent disability
GCC binds to DNA/codes for RNA protein synthesis (greater anti-inflammatory effect)
NSAIDS inhibit prostaglandin synthesis (non-steroidal anti-inflammatory)
Adverse Effects
Interactions
*high doses & brief w/ tapered dose
↓ adrenal function
RA
Cortisone
Osteoporosis
SLE
Hydrocortisone
↑ risk of infection
IBD
Myopathy
Crohn’s/UC
Prednisone
Fluid/electrolyte imbalance
Allergic RX
Prednisolone
↓ growth (alt day trmt)
Asthma
Methylprednisolone
Psychologic disturbances
Dermatologic conditions
Triamcinolone
Cataracts & glaucoma
Neoplasms
PUD (take with food)
Transplant pts
Betamethasone
Cushing’s syndrome
Infant respiratory syndrome
Dexamethasone
↑ GCCs = hypERglycemia
MUST TAPER DOSE (7 days). Monitor endogenous production of cortisol.
Pt may require ↑ GCCs in times of stress
Withdrawal sx: hypotension, hypoglycemia, myalgia, arthralgia & fatigue
Dosing: Alt day or tapering dose  body can produce own ACTH.
Take before 0900
Digoxin, Thiazides, Loop diuretics
(↓K=  cardiotoxicity)
NSAIDs
Insulin & oral hypoglycemic
Vaccines (↓ Ab rxn)
Additional Information
Contraindications:
DON’T give to pts w/ systemic fungal
infections or if giving live vaccines
Precautions:
Kids, pregnant/lactating, HTN, HF, renal
impairment, esophagitis, gastritis, PUD,
myasthenia gravis, DM, osteoporosis,
diuretics, digoxin, insulin, hypOglycemics
and NSAIDs
MINERALOCORTICOIDS (MCCs) → “-sone”
Aldosterone – regulates K+, Na+ & H2O balance
Promotes reabsorption of Na+ into the blood in exchange for K+ secretion
↑ aldosterone = ↑ Na+ & H2O retention & ↓ K+
Control of aldosterone levels
1. ↓ serum Na+ levels or ↑ K+ levels  aldosterone levels ↑
2. ↓ renal blood flow ↑ aldosterone levels by the RAAS
a.
↑ aldosterone → ↑ renin → ↑ Na+, H2O follows → ↑ volume mediated expansion → ↑ blood to the heart ↑ workload on the heart → issues
b. Na+/K+ pump; 3/2; ↑ to ↓ concentration
3. GCCs produced in adrenal cortex have MCC effects
Individual Drugs
MOA
Fludrocortisone
(Florinef Acetate)
Acts on distal renal tubule to
enhance reabsorption of Na+ and
to increase urine output of K+
↑ dose: MCC activity
↓ dose: GCC activity
Nursing Implications
Treats
Adrenocortical insufficiency
(Addison’s disease)
Salt-losing adrenogenital syndrome
Adverse Effects
↑ dose:
Inhibits endogenous adrenal cortical secretion &
pituitary corticotropin excretion
Promotes deposition of liver glycogen
↓ dose:
Na+ retention & K+ excretion leading to increase BP
Additional Information
Contraindications: systemic fungal infections
Precautions: pregnant/lactating
Use cautiously in pts. with cardiovascular disease due to Na+ & fluid levels
Addison’s: Teach pt to take entire dose upon waking or divide into 2 doses-1 upon waking & second at noon. Need dose increase during high stress (infection, surgery, trauma).
Teach about S&S of fluid retention (unusual weight gain, edema), hypokalemia (muscle weakness, irregular heartbeat) & call provider ASAP w/ S&S
They need the med lifelong. Need medical alert bracelet
DIABETES (DM), INSULIN & HYPOGLYCEMICS
Type 1 Diabetes – NO INSULIN PRODUCED BY PANCREAS (DIFFICIENT/DEPENDENT)
5-10% of all cases (~ 1 million)
Starts young, usually from destruction of pancreatic β cells (autoimmune disease)
Type 2 Diabetes – INSULIN RESISTANT/DECREASE SECRETION (can still make insulin)
Starts middle age & progresses gradually
Usually obese
Same long-term risks/complications as type 1 diabetes
Diagnosis
Fasting Plasma Glucose: > 8 hours since last meal; normal is < 100, diabetes is > 126
Casual Plasma Glucose: test anytime; normal is < 200, diabetes is >200
o Must also have the s/s polyuria, polydipsia, ketonuria & rapid weight loss
o Test on 2+ days; both must be positive
Oral Glucose Tolerance Test: first two test not definitive. Glucose load of 75g &
measure 2 hours later; normal is <140, diabetes is > 200
HgA1c: reflects average BS past 2-3 months; 5.7-6.4 is prediab; diabetes is > 6.5%
Sustained hypERglycemia causes: polyuria, polydipsia, ketonuria & weight loss. Overtime
causes HTN, heart disease, renal failure, blindness, neuropathy, amputations, impotence &
stroke.
Long-term complications are a result of decreased blood flow.
Microvascular
o Small blood vessels and capillaries; retinopathy, nephropathy, sensory/motor
neuropathy, autonomic neuropathy, amputations, erectile dysfunction.
Macrovascular
o Heart dz, HTN, CVA (usually due to artherosclerosis; hypERglycmia & lipid
metabolism)
Treatment Targets
Premeal BS: 70-130
Postmeal BS: <180
HbA1c (3 month period): < 7%
BP: 130/80
Albumin/Creatinine: <30 mcg/mg
Preventing Complications
Type 1
o Diet – spread caloric intake throughout the day
o Exercise – ↑ response to insulin & ↑ glucose tolerance
o Insulin replacement – pancreas is essentially dead
o ACE/ARB – helps prevent diabetic neuropathy & HTN (130/80)
o “-statins” – ↓ high LDL levels to prevent stroke
Type 2
o Diet & exercise – ↓ obesity, normalize insulin release, ↓ insulin resistance
o Medications (???)
 1 oral (metformin HCl)
 2 orals (metformin + sulfonylurea or basal insulin)
 3 orals & insulin
 Insulin
Ketoacidosis – hyperglycemia, production of ketoacids, hemoconcentrations, acidosis & coma
Insulin
Synthesized in the pancreas by β-cells and secreted by sympathetic activation of β-receptors
o Activation of α-cells in the pancreas inhibit the release of insulin
o GLUCOSE is the main stimulus for insulin release
Insulin is anabolic (stores & build-up energy)
o Stimulates cellular transport of glucose, AA, nucleotides & K+
Insulin deficiency promotes hyperglycemia in 3 ways:
1. ↑ glycogenolysis (breakdown of glycogen to glucose)
2. ↑ gluconeogenesis (breakdown of protein & fats to AAs & fatty acids)
3. Reduces glucose utilization (↓ cellular uptake & ↓ conversion from glucose to glycogen)
Drugs that ↓ blood glucose:
1. Sulfonylureas
2. Meglitinides
3. Beta-Blockers (masks s/s of hyperglycemia (↑ HR & palpitations) & blocks glycogenolysis)
4. ETOH
Drugs that counteract insulin:
1. Thiazide diuretics
2. Glucocorticoids
3. Sympathomimetics (speeds ↑)
Changing insulin doses:
st
↑ insulin for: infection, stress, obesity, growth spurt, pregnancy > 1 trimester
st
↓ insulin for: exercise & pregnancy (1 trimester)
Insulin Info:
1. Mix short & long; clear → cloudy
2. Only NPH can be mixed with short
3. Good for 1 month
4. Sub-Q because GI enzymes would inactivate insulin
5. ↑ arm & thigh = slow
6. Tummy = fast
7. Rotate injection site monthly (lipohypertrophy)
Dosing
Needles
o 5 mm = kids
o 8 mm = adults
o 12.7 mm = obese
Units
o 1 cc = 100 units
o 1/2 cc = 50 units
o 1/3 cc = 30 units
Insulin pumps
Pen injectors
INSULINS → NO PO MEDS
Duration
Individual Drugs
Onset
Duration
Route
Appearance
Short Duration/
Rapid Acting
Insulin lispro (Humalog)
Insulin aspart (NovoLog)
Insulin glulisine (Apidra)
15-30
10-20
10-15
3-6
3-5
3-5
SQ AC or PC
SQ 5-10m AC
SQ >15m AC <20m PC
Clear
Short Duration/
Slower Acting
Intermediate
Duration
Regular insulin
(Humulin R, Novolin R)
(Exubera)
30-60
15-30
NPH insulin
(Humulin N, Novolin N)
Insulin detemir (Levemir)
60-120
6-10
6.5
16-24
12-24
SQ, IM, Oral, IV
*Exubera = INH
SQ
Adverse Reaction
Prescription
Additional Info
Humalog: Faster than R but slower DOA
Yes
Apidra: Do not give IV
No: Humulin R
& Novolin R
Clear
NPH: Cloudy
(roll in hands
before admin)
HypOglycemia
Edema
↑ weight
Yes: Exubera
No: NPH (N)
Yes: Detemir
Detemir: Clear
Long Duration
Insulin glargine (Lantus)
70
24
Clear
Yes
Only regular insulin can be given via IV
o Given for ketoacidosis or hyperkalemia
Give AC to control postprandial hyperglycemia
Only LA that can be mixed with a SA
Administer BID btw meals & HS (w/o food)
Detemir: DO NOT GIVE IV or w/ other insulins.
Slow onset.
DO NOT GIVE IV or w/ other insulins
↓ risk of hypOglycemia b/c of long DOA w/
stable steady state
Discard insulin that has any precipitate (Except for NPH).
Mix SA and LA instead of injecting them separately??
ONLY NPH can be mixed with SA. Draw SA into syringe first to avoid contamination of NPH vial.
Mixtures are stable for 28 days at room temp and 1 month in fridge
Insulin left out of the refrigerator is good for 1 month, MUST NOT be EXPOSED to HEAT
SMBG before meals & hs.
Store UNOPENED insulin in refrigerator to maintain med integrity until expiration date
Pre-filled syringes store in vertical position in refrigerator. Stable x1 week-max 2 wks
All insulins can be given SQ because digestive enzymes would inactivate insulin
SQ injection sites are in the upper arm, thigh (slowest) & abdomen (fastest)
Rotate sites of injection q month to reduce incidence of lipohypertrophy
Must check within 15-30 minutes after giving fast-acting insulin for: tachycardia, palpitations, sweating, headache, drowsiness, confusion, fatigue.
If you miss these S&S, can lead to convulsions, coma & eventual DEATH
Nursing
Implications
HYPOGLYCEMICS
Hypoglycemia = BG < 50
S/S of slowly falling BG: HA, confusion, drowsiness & fatigue
S/S of rapidly falling BG: Activation of sympathetic nervous system
o
Tachycardia, palpitations, sweating & nervousness
HypOglycemia worse than hyperglycemia
Tx: fast-acting sugar: glucose tabs, OJ, sugar cubes, honey, corn syrup, diet soda
Glucagon
o
Produced by α-cells in the pancreas (↑BG)
o
Elevates BG levels following insulin overdose

↑glycogenolysis, ↓glycogen synthesis, ↑biosynthesis of glucose
o
Produces arousal within 20 minutes
**Insulin stores glucose; B-cells
**Glucagon ↑ glucose; A-cells
Glucagon: IM, Sub-Q & IV (for severe hypoglycemic)
Classification
Adverse Effects
st
1 Generation
Sulfonylureas
“-ide”
2nd Generation
Sulfonylureas
“-ide”
Meglitinides
“-linide”
Drugs
Tolbutamide
Acetohexamide
Tolazamide
Chlorpropamide
Glipizide
Glyburide
Glimepiride
Repanglinide
Nateglinide
MOA
Glucose dependent: ↑ insulin release from pancreas
dependent on glucose concentration
Only for type 2
(Stimulates Beta-Cells)
Meglitinide has a shorter DOA and needs more BG to
activate insulin release
Contraindications
Additional Information
Weight gain
Hypoglycemia (fatigue,
excessive hunger, profuse
sweating & palpitations)
Pregnancy
Breastfeeding
Alcohol = antabuse
Can be used alone or in combo
Drugs that intensify ↓BG: NSAIDs,
sulfonamide antibiotics, ranitidine &
cimetidine
Β-blockers mask s/s of ↓BG
Weight gain
Hypoglycemia (less than
sulfonylurea)
Eat in 30 minutes
after drug intake
Gemfibizol ( ↓BG)
No response w/ sulfonylureas = no
response w/ metglitinides
Mono/combo treatment; metformin
& glitazones
DO NOT MIX with sulfonylureas
HYPOGLYCEMICS, CONT’D
Classification
Drugs
MOA
Adverse Effects
Weight loss
↓ appetite
↓ B12 & folic absorption
Lactic acidosis (rare)
Nausea/diarrhea
Biguanide
“-formin”
Metformin
↓ glucose production by liver
↑ glucose uptake by muscle
DOES NOT ↑ insulin release
Type 1 or Type 2
Thiazolidinediones
“-glitazone”
Rosiglitazone
Pioglitazone
↓ insulin resistance by ↑ insulin sensitivity of
skeletal muscles, liver & tissues
*Insulin must be present*
Only use with type 2
HypOglycemia
Fluid retention
(wt↑, edema)
↑ HDL/LDL/TGs
Acarbose
Miglitol
↓ absorption of carbs, by preventing their
breakdown into monosaccharides in the small
intestine → lack of postprandial BG rise
Flatulence (beano)
Cramps
Abdominal distention
Borborygmus
Diarrhea
↓ iron absorp  anemia
Alpha-Glucosidase
Inhibitors
“-bose” & “-litol
Contraindications
Additional Information
Heart failure
Liver disease
Severe infx, alcohol excess,
pt w/ shock (hypoxemia)
≥ 1.4 creatinine clearance
Class III or IV heart failure
Hepatoxicity
Strong CYP2C8 inhibitor and
inducers(??)
Severe CHF, bladder cancer
Can be used w/ sulfonylureas or Exenatide
Absorbed slowly from SI & excreted
unchanged in kidneys (check renal fxn,
creatinine cl)
Take w/ food
Avoid giving with metformin
→ GI effects
Combo w/ insulin, sulfonylureas or
metformin
Combo w/ metformin, sulfonylureas &
insulin
Careful w/ insulin b/c both causes edema
HYPOGLYCEMICS, INJECTIBLES
Classification
Amylin Mimetics
(Big lizard)
Incretin Mimetics/
Glucagon-like
Peptide-1 Agonist
Nursing
Implications
Drugs
MOA
Adverse Effects
Contraindications
Pramlintide
Delays gastric emptying & suppresses
glucagon secretion
Acts to↑ sense of satiety → ↓ caloric intake
Type 1 or type 2
HypOglycemia (esp w/ insulin trmt)
Nausea
Injection site reactions
Anorexia
Weight-loss
DO NOT give with drugs that
slow intestinal motility or
slow absorption of nutrients
Exenatide (Byetta)
Delays gastric emptying
Glucose dependent: ↑ insulin release
Inhibits postprandial release of glucagon
Suppresses appetite (satiety effect of GLP-1)
HypOglycemia (w/sulfon’s)
GI effects
Pancreatitis
Weight-loss
DO NOT give to pts w/ ESRD
Oral contraceptives and ABX
Liraglutide (Victoza)
Glucose dependent: ↑ insulin release
More convenient than Byetta
Dose-related GI effects
HypOglycemia (w/sulfon’s)
Take PO meds 1 h before administering Pramlintide and Byetta
Eat w/i minutes of taking Pramlintide
Ask if pt is taking oral contraceptives or antibiotics b/c of reduced absorption
Monitor BG if taking 1+ hypoglycemics
Patient teaching:
Nature of disease
Importance of glucose control
Treatment components: SBGM, diet, exercise, A1C test, medications, foot care
Insulin-storing, administration, injection site rotation, S&S hypo & hyperglycemia
Additional Information
Combo w/ insulin in type 1 & 2
Combo w/ metformin &
sulfonylureas in type 2
PO drugs should be taken 1 hr
before injection
Eat in 20 minutes
Combo w/ sulfonylureas or
metformin
PO drugs should be taken 1 hr
before injection
Combo w/ sulfonylureas or
metformin
Adminster QD regardless of
meals
THYROID
Thyroid effects: metabolism, cardiac function, growth & development
Produces 2 hormones:
Triiodothronine (T3) (most potent)
Thyroxine (T4)
Thyroid hormones are mediated by T3; T4 serves as a source for T3
Half-life: 1 day for T3, and 7 days for T4
T4 is released greater than T3 → T4 becomes T3
Only a small amount of thyroid is free; not bound to protein (99.5% bound)
All thyroid hormones are bound to TBG (thyroxin-binding globulin)
Lack of iodine  ↓ thyroid fxn, ↑ TSH  goiter
Actions of thyroid hormones
1. Stimulation of energy use: ↑BMR  ↑O2, ↑HR, ↑metabolism of fats/carbs/proteins
2. Stimulation of the heart: ↑ HR, ↑ force of contraction  ↑ CO and ↑O2 demand
3. Promotion of growth & development during fetal stages
4. Increases production & release of other hormones (estrogen, test, cats, gccs)
5. Stimulates appetite
Thyroid function tests:
Serum TSH – high TSH is dx for hypothyroidism. Good diagnostic because small changes in serum T3 &
T4 cause a dramatic rise if TSH
Serum T4 Test – measures either total T4 (bound & free) or free T4, measurement of T4 is preferred
Serum T3 Test – measures either total T3 (bound & free) or free T3. Measurement of free T3 is
preferred. Good for hyperthyroidism. T3 rises sooner & to a greater extent than T4
Metabolized in liver & secreted in urine
Contraindicated in patients with recent MI
Overdose: irritability, insomnia, ↑HR, arrhythmias, ↑ BP, anxiety & ↓ weight
Hyperthyroid
Hypothyroid
Eyes
Prominent
Ptosis, edematous
Integumentary
Fine, thin hair, hot, moist skin
Dry, brittle hair, cold, dry skin
Temperature
Heat intolerant
Cold intolerant
Weight
↑ appetite, ↓weight
↓appetite, ↑weight
Emotional
Nervous, irritable, insomnia
Lethargic, depressed, ↑sleep
GI
diarrhea
Constipation
HYPOTHYROIDISM ↑ TSH LEVELS
Classification
Individual
Drugs
Natural Thyroid Extract,
T 3 & T4
Armour
Thyroid
Levothyroxin
e Na+, Lthyroxine
(Synthroid,
Levoxyl,
Levothroid)
Liothyronine
(Cytomel,
Triostat)
Liotrix
(Thyrolar)
Synthetic T4
Synthetic T3
Mixed T3 & T4
Nursing Implications
MoA
Identical to natural
hormone
T4 rapidly converted to T3
Binds to receptors
throughout body to ↑
metabolic rate, ↑ protein
synthesis, ↑ cell growth
Adverse Reactions
Excessive dosing  Thyrotoxicosis
↓ weight, tachycardia, angina,
CHF, tremors, nervousness, HA,
insomnia, menstrual irregulatities,
impotence, ↑ bowel motility,
hyperthermia, heat intolerance &
sweating
Interactions
Additional Information
Drugs that ↓ absorption: Cholestyramine,
Colestipol, Ca+ supplements, Sucralfate, Al
antacids
Drugs that ↑ absorption:
Phentyonin, Carbamazepine, Rifampine,
Sertraline, Phenobarbital
Better absorbed & more potent than Levo
DOA is 3 days shorter than Levothyroxine
Not recommended for maintenance
Available T3 & does NOT
require conversion of T4 so
has faster onset of action
4:1 ratio of T3 & T4
Low cost & long DOA
Minimal allergic reaction
Narrow therapeutic range (√ TSH 6-8 wk)
Give 30 min before breakfast
Levo ↑ Vit K  may need to reduce Warfarin
dose
Thyroid ↑cardiac resp to catecholamines
Stinky!
Minimal allergic reaction
Take Levothyroxine on empty stomach in the morning, at least 30 minutes before breakfast
Educate to take only as directed & that replacement therapy is for life & never discontinue without talking with provider first!
HYPERTHYROIDISM ↓ TSH LEVELS
Individual Drugs
MOA/Tx
Adverse Effects
Agranulocytosis (rare, develops quickly during first 2
Propylthiouracil (PTU)
Preventing oxidation of iodide by blocking peroxidase thus
inhibiting iodine into tyrosine (thyroid gland)
Blocks conversion of T4 into T3 (peripheral tissue)
Therapeutic uses: Grave’s disease, adjunct to radiation tx,
suppresses thyroid hormone synthesis in preparation for thyroid
surgery, thyrotoxic crisis
Methimazole (Tapazole)
Not protein bound
Lactating women
Beta Blockers
(propranolol)
Does NOT correct HTM. ONLY controls the adrenergic effects of excessive thyroid hormone until slower-acting antithyroid medications can take effect.
Nursing implications
Take at same time of day daily
Inform patient of agranulocytosis (report fever, sore throat)
months; sore throat, fever, ulcers in mouth, rectum, vag)
Hypothyroidism
Rashes, Urticaria, N/V
Thrombocytopenia, Hepatoxicity, Hepatic
necrosis
Additional Information
Does NOT destroy pre-existing hormone
(takes 3-12 wks to reach euthyroid effect)
PTU is NOT as likely to cross placenta as Methimazole. So PREFERRED
drug to use during pregnancy.
Take w/ food. If missed, take dose ASAP
Store in light resistant container
Report wt ↑, cold intolerance, depression, bruising, bleeding, fever,
and sore throat
↑ potent ↓ toxic than PTU
Long DOA, provides better control of hyperthyroidism
Emergency use. QD – QID dosing, Rapid onset of action 1 h
Treats thyrotoxic crisis
OSTEOPOROSIS
Low bone mass (bone mass declines after age 50).
Prevention:
Adequate Calcium
Vitamin D for calcium absorption
Weight-bearing exercise important to ↑ tensile strength of bone (not swimming)
Vitamin D alone treats Vitamin D deficiency
Calcium alone treats indigestion, acid reflux
Calcium needs to be given together with Vitamin D to be absorbed to treat bone deterioration
Drug
Adverse Reactions
Biphosphonate
Vitamin D
Calcium
Vitamin D2
Vitamin D3
(cholecalciferol,
calcifediol, calcitriol)
Doxercalciferol
Paricalcitol
Alendronate: qd, qw
Risedronate: qd, qw,
qm
Ibandronate, qd, qm,
q3m
Zoledronate: qy, q2y
Teriparatide (Forteo)
Rankl Inhibit
SERMs
Calcitonin-salmon
(Miacalcin, Fortical)
Raloxifene
Tamoxifen
Toremifene
Denosumba
(Prolia, Xgeva)
Hypercalcemia:
N/V, constipation, polyuria, nephrolithiasis
(kidney stones develop), lethargy, depression,
cardiac dysrhythmias
Hypervitaminosis D:
Early Response: Weakness, fatigue,
nausea, vomiting, and constipation
Later Presentation: polyuria, nocturia,
and proteinuria
Vitamin D supplementation should never
be >1000 IU/day in children or >50,000
IU/day in adults
Antiresorptive therapy: Estrogen, Raloxifene, Bisphosphates, Calcitonin, Denosumab
Biphosphonate: Prevents and treat osteoporosis in males and in postmenopausal females to
help maintain bone strength and prevent bone loss.
Interactions
↓ absorption of thyroid hormone - must give 1 hour apart
Prednione ↓ Ca absorption
Calcium ↓ tetracycline & thyroid hormone absorption
Thiazide diuretics ↓ renal calcium excretion  hypercalcemia
Additional Information
Never consume >600 mg at one time to
ensure proper absorption.
Vitamin D2 - requires Rx, dosed 50,000 units once weekly, produced through PLANTS.
Vitamin D3 - dosed 5.000 units once daily, produced naturally through skin exposure to SUNLIGHT.
Esophagitis – if pt lie down/eat w/i 30 min
Atypical femoral fractures (with long-term
bisphosphonate therapy), esophageal cancer,
musculoskeletal pain, ocular problems (scleritis,
conjunctivitis), osteonecrosis of jaw, renal
toxicity
TAKE in AM on empty stomach w/ full glass of
water.
Do NOT lie down OR take any other food or
beverages for 30 minutes after taking med
Only drug used for osteoporosis that actually increases bone formation
A form of Parathyroid Hormone (PTH) produced by recombinant DNA technology. Used to treat osteoporosis in postmenopausal women, in men and in glucocorticoid-induced osteoporosis
Must be kept in refrigerator and is only good for 28 days after first dose is used
Treatment of post-menopausal osteoporosis NOT prevention!
Can lower plasma calcium level in hypercalcemia; Also used to treat Paget’s disease
Should be taken with vitamin D
Refrigeration is required
Protect against osteoporosis and decrease in LDL
Gives protection against breast cancer, uterine cancer and thromboembolism
Adverse effects: Hot flashes, ↑risk of endometrial cancer
Raloxifene is a Pregnancy Category X drug
Raloxifene treats both osteoporosis and breast cancer (Tamoxifen and Toremifene only treats osteoporosis)
Inhibition of RANKL receptor ↓ formation and function of osteoclasts
Prolia is used for osteoporosis patients at high risk for fracture
Xgeva is used to prevent skeletal events in patient with bone metastasis from solid tumors
Adverse effects: hypocalcemia, infections, skin reactions and osteonecrosis of jaw (ONJ)
CYCLOOXYGENASE INHIBITORS: NSAIDS AND ACETAMINOPHEN
Cyclooxygenase: enzyme responsible for synthesis of prostanoids (prostaglandins, prostacyclins, and
Benefit
Protection against MI and stroke
(reduced platelet aggregation)
COX-2
↓inflammation, pain, fever
colorectal cancer protection
Adverse effect
Gastric erosion
Bleeding tendencies
Renal impairment
Renal impairment
↑MI risk (vasodilation suppression)
AE
Inhibition of…
COX-1
Uses
thromboxanes)
Classification
NSAIDS
Aspirin
1st gen
Drugs
MOA
Aspirin
(acetylsalicylic
acid)
COX-2 Inhibitors
2nd gen
Acetaminophen
(Tylenol)
Nursing Implications
Ibuprofen
Naproxene
Diclofenac
Meloxicam
Celecoxib
Rofecoxib
Valdecoxib
Adverse Effects
Nonselective and irreversible
COX inhibitor
↓ renal function ↓ COX-1,
thereby depriving the kidneys
of PGE needed for normal fxn
(acute, reversible)
↓ mild-moderate pain
DOC: ↓fever in adults
Thrombotic disorders
↓ risk of MI/stroke
DOC: RA, OA, Juvi arthritis
Rheumatic fever, tendinitis,
bursitis
↑ bleeding by inhibiting plt
aggregation (lasts 8 days)
GI distress, heartburn, nausea,
edema
Longterm use: GI ulcer,
perforation, bleeding
Salicylism: ASA > theurapeutic
Tinnitus, sweating, headache,
dizziness
Renal impairment  Na & H20
retention and edema.
Nonselective and reversible
inhibition of COX (1&2)
Anti-inflammatory
Analgesic
Antipyretic
RA and OA
GI ulceration
Bleeding
Renal impairment
↑ risk of thrombolytic event
Selective inhibition of COX-2
↓COX2 vasoconstriction
w/o ↓ of COX1  ↑ MI risk
↓ inflammation/pain
OA, RA, ankylosing
spondylitis, acute pain,
dysmennorrhea
Renal impairment  HTN, edema
↑ risk of thrombolytic event
Dyspepsia, abdominal pain
Mg Salicylate
Non-Aspirin
1st gen
Uses
Inflammation
Pain
Fever
Prevent MI/stroke
GI ulcers
Renal impair
Bleeding
MI/stroke
Liver damage w/ OD
1st gen NSAID
Aspirin
Yes
Yes
Yes
Yes
Yes
Yes
Yes
No
No
↓PGE synthesis in CNS
Minimal effects in PNS
Analgesic
Antipyretic
Overdose  severe liver injury
Hepatic necrosis
Never exceed recommended APAP (Tylenol) dose. Maximum dose: 4000 mg/24 hours
Need to count for the acetaminophen in the combination drugs (Vicodin, Percocet)
Inform of potential liver damage/toxicity
Malnourished patients should not take >3000 mg/24 hr.
NO ALCOHOL while taking APAP
If alcohol consumption: maximum <2000 mg/24h
1st gen NSAID
All others
Yes
Yes
Yes
No
Yes
Yes
Yes
Yes
No
2nd gen NSAID
Coxibs
Yes
Yes
No
No
Yes*
Yes
No
Yes
No
Contraindications
DO NOT use for febrile kids 
risk of Reye’s syndrome
DO NOT give to pt’s with bleeding
disorders, hx of ulcers/GI bleed
Daily use w/ HTN pts  ↑ risk of
brain bleed
↑ effect of Warfarin, Heparin,
other A-Cs
ACE and ARBs
Acetaminophen
No
Yes
Yes
No
No
No
No
No
Yes
Additional Information
Pregnancy Category D
Do not take with alcohol  ↑ risk
of gastric bleeding
Give with food
DOES NOT ↓ risk MI and stroke
CABG, heart disease pts
CAUTIOUS use for pt w/ CV risk
factors: HTN, DM, Dyslipidemia
Can cause allergic RXN in pt w/
sulfonamide allergy
↑ effect of Warfarin
LAST CHOICE drug for long-term
management of pain
↑ risk of warfarin bleeding by ↓
warfarin metabolism in body
Alcohol use w/ excessive APAP
Percocet, Vicodin has APAP!
Watch out for overdose
NOT anti-inflammatory, anti-RA
DOES not ↓ plt clot, ↑ GI ulcer,
↓ renal blood flow/impairment
Minimize liver damage: give
Acetylcysteine (Mucomyst,
Acetadote)
HYPERTENSION “THE SILENT KILLER”
CONGESTIVE HEART FAILURE
UNTREATED  HEART DISEASE, KIDNEY DISEASE, STROKE!!! 
Risk factors: smoking, obesity, inadequate exercise, dyslipidemia, diabetes, age (> 55 men & > 65 women),
family hx or premature CV disease, salty foods
Primary HTN = no identifiable cause
Secondary HTN = identifiable cause; other disease process
Systole
Diastole
Treatment
Normal
120
80
Nothing
Pre-HTN
120-139
80-89
Diet, exercise
Stage 1 HTN
140-159
90-99
Thiazide diuretics
Stage 2 HTN
>160
>100
Thiazide diuretics + β-blocker, ACE inhibitor, CCB/ARB
If systolic > 140 & diastolic < 90 = Isolated systolic HTN (ISH)
Consequences of HTN
Degree of pressure is directly related to degree of injury
Risk of CV dz is doubled by systolic increase of 20 and diastolic increase of 10 (+20/+10)
Interventions
1. Weight loss & exercise
2. Na+ restriction < 2.4 g/day
3. DASH
4. No alcohol, smoking
5. Maintenance of K+ & Cl- intake (K+ can
↓ BP so maintain K+ intake)
Treatment Goals
BP < 140/< 90
Pts w/ DM or kidney dz target BP is
130/80
Treatment Drugs
Diuretics
Thiazide, Loop, Potassium-sparing
RAAS inhibitors
ACEI, ARB, AA, DRI
Sympatholytics (antiandrenergic drugs)
β-blockers, α1 – blockers, α/β
blockers, CNS α1 agonists,
Adrenergic neuron blockers
Direct-acting vasodilators
Calcium channel blocker
Promote Compliance!
Educate pt (lifelong trmt!)
Monitor BP daily
↓ SEs, ↓ dose when possible
Schedule regular check-ups
Hypertensive crisis (Diastole >120)
Sodium nitroprusside
Fenoldopam
Labetalol
Diazoxide
Clevidipine
Hypertensive & Pregnant
Methylodopa
Can’t use ACEI, ARBs, and DRIs
Preclampsia BP >140/90 + proteinuria
 Mg sulfate and Hydralazine
Characterized by:
↓ CO
Inadequate tissue perfusion (fatigue, SOB, exercise intolerance)
Volume overload (venous distention, peripheral & pulmonary edema)
Treatment drugs:
Diuretics
RAAS inhibitors
Beta-blockers
Digoxin and other cardiac glycosides
Inotropic agents (other than cardiac glycosides)
Vasodilators (other than ACEI/ARBS)
Functional
Management Goal Treatment
limitations
No structural heart
Reducing risk
Control underlying cause
Stage
disease
(smoking, ETOH)
ACEI/ARB
A
Stage
B
Stage
C
Stage
D
No symptoms of HF
High risk for HF
Structural heart
disease
No symptoms of HF
Structural heart
disease
Prior or current
symptoms of HF
Obvious sign of
heart failure
present here
Advanced
structural heart
disease
Symptoms at rest
despite meds
Special therapy
required
Repeat
hospitalizations
Preventing
symptomatic HF
ACEI/ARB + β-blocker
↓ pulmonary and
peripheral edema
↑ quality of life
Slow cardiac
remodeling and
progression of LV
dysfunction
Prolong life
1st line:
ACEI/ARB
β-blocker
Diuretic
Control fluid
retention
2nd line:
Digoxin
Aldosterone
antagonist
ISDN/hydralazine
Device therapy
ICD
Pacemaker
AVOID:
Antidysrhythmics – cardiosuppressant
& prodysrthythmic
Calcium channel blockers
NSAIDs – Na+ retention & peripheral
vasoconstriction
Stage C treatments AND…
IV dopamine/dobutamine to ↑ renal
perfusion  ↑ diuresis
HEART TRANSPLANT
LVAD until heart available
DIURETICS
Osmotic
(-itol)
Furosemide (Lasix)
Torsemide (Demadex)
Bumetanide (Bumex)
Ethacrynic acid (Edecrin)
Hydrochlorothiazide
(6-12 hrs)
Aldosterone
antagonist
Chlorthalidone
(24-72 hrs)
Non-Aldosterone
antagonist
Potassium Sparing
Thiazides
(-thiazide)
High ceiling/Loops
(-semide)
Individual Drugs
Mannitol
Nursing
Implications
Spironolactone
Triamterene
Amiloride
MOA
Compete for the Cl site on the
Na-K-2Cl co-transporter on the
ascending loop
Block NaCl reabsorption 
blocks potassium recycling
Vasodilation
Loss of volume
Therapeutic Uses
Pulmonary edema r/t CHF
Edema r/t hepatic, cardiac, or renal
Uncontrolled HTN by other meds (only
Furosemide & Torsemide approved for
this)
Interactions/Considerations
Digoxin (↓K+ = ↑ ventricle dysrhythmia)
Ototoxic drugs
Lithium (decreased renal clearance)
HTN drugs + ↓ FV + vasodilation = BAD
NSAIDs – blunts furosemide effect
Add K+ supplement to tx.
Adverse Reactions
Hypokalemia: K < 3.5, give K or use Ksparing diuretics - monitor electrolytes
Hypochloremia, Dehydration
(↑thrombus)
Hypocalcemia, hypomagnesemia
Hypotension – pt rise slowly
Ototoxicity
Reversible w/ Lasix, Irreversible w/
Edecrin
Hyperglycemia: ↓ insulin release, ↑
glycogenolysis, ↓ glycogen synthesis
Hyperuricemia – watch out for gout
↓ HDL, ↑ LDL and TGs
Blocking reabsorption in the
early segment of DCTs
 ↑ excretion of Na, Cl, K H2O
Promote calcium retention
Does NOT work well if low GFR
*can’t have low urine flow*
Essential HTN – 1st line
Edema r/t mild/moderate CHF, hepatic,
renal
Diabetes insipidus
Post-menopausal osteoporosis
Best for African American
Digoxin
HTN drugs + ↓ FV + vasodilation = BAD
Lithium (decreased renal clearance)
NSAIDs – blunts furosemide effect
Combo w/ β-blocker ↑ incidence onset
of diabetes
NO OTOTOXICITY! (can use w/ ototoxic rx)
Hyponatremia, hypochloremia,
dehydration
Hyperglycemia: ↓ insulin release, ↑
glycogenolysis, ↓ glycogen synthesis
Hyperuricemia – watch out for gout
↓ HDL, ↑ LDL and TGs
Blocks actions of aldosterone in
distal nephron
 keep K; lose Na
ALSO PART OF RAAS SYSTEM
**Used in combo w/ LOOP or THIAZIDES
to REDUCE LOSING K
Primary hyperaldosteronism
HTN, edema r/t CHF
Avoid HYPERKALEMIA
K+ supplements
ACEI/ARBs
Direct renin inhibitors
Hyperkalemia
Benign/malignant tumors
Binds to androgen receptors
(gynecomastia, menstrual irregularities,
impotence, hirsutism, & deeper voice)
Disrupts Na+/K+ exchange in
distal nephron
 keep K; lose Na
Alone or in combo to treat
Counteracts the K-wasting efx of more
powerful diuretics – most common use
HTN, edema r/t CHF
↑ osmotic pressure in tubule
↓H2O reabsorption
Prophylaxis of renal failure
↓ICP
↓IOP
Never use with:
Another K-sparing diuretic
K supplements
Salt substitutes (KCl)
ACEI/ARBs
Direct renin inhibitors
Caution in pts w/ CHF & edema
Greatest amt of diuresis (good for ICP)
IV only
Hyperkalemia
Leg cramps, N/V, vertigo
Blood dyscrasias (rare)
Can leave vascularedema
N/V, HA, fluid/electrolyte imbalance
Can crystallized in low temp (use filter
position & in-line filter)
CHECK electrolyte levels and weigh the patients; check sites for edema; measure abdominal girth (ascites)
Severe CHF – assess lung sounds
Monitor and teach about: ototoxicity, hypovolemia, hypotension, hypokalemia, hyperuricemia, hyperglycemia, and disruption of lipid metabolism
PO Loops: take in AM for QD. take w/ food if GI upset
Monitor BP – teach about postural hypotension and to sit/lie down if this occurs – dangle legs before standing & rise slowly
Hypokalemia - irregular heartbeat, muscle weakness, cramping, flaccid paralysis, leg discomfort, extreme thirst, confusion; and stress importance of having regular blood tests
Teach patients about high urine volume & frequency of voiding – frequency will subside in 6-8 hrs
RAAS (RENIN ANGIOTENSIN ALDOSTERONE SYSTEM)
Aldosterone Antagonist
Direct Renin Inhibitor
Angiotensin II receptor blocker
-sartan
ACE Inhibitors
-pril
Individual Drugs
Lisinopril
Captopril
Losartan
Ibersartan
MOA
Blocks conversion of angiotensin I to II
Prevents vasoconstriction, aldosterone
release, and alteration of
cardiac/vascular structure
↓SNS, K-retention, ↓afterload, ↓ADH
Blocks angiotensin II receptor
Prevents vasoconstriction, aldosterone
release, and alteration of
cardiac/vascular structure
Therapeutic Uses
TX: HTN, CHF
PREVENT: MI, DM/non-DM nephropathy/retinopathy
PROLONGS LIFE
Best for Whites
NO COUGHING!! 
TX: HTN, CHF
PREVENT: MI, DM/non-DM nephropathy/retinopathy
USE FOR PTs who can’t tolerate ACEI!!!
Prophylactic for migraine HA
Interactions/Consideration
Do not use in pregnancy
Diuretics, other anti-HTN
↑ K drugs
Lithium
NSAIDs
Do not use in pregnancy
Diuretics, other anti-HTN
Adverse Reactions
Persistent cough (give ARBs instead?)
1st dose hypotension (vascular dilation)
Angioedema (bradykinin)
Hyperkalemia (aldosterone blocking)
RF (↓GFR) pts
Disgeusia, rash, neutropenia
Angioedema (less than ACEI though)
RF (↓GFR) pts
Research shown: ↑ LV EF, ↓HF symptoms, ↑ exercise
tolerance, ↑ quality of life, ↓ mortality, doesn’t ↑ kinin
Aliskiren
(Tekturna)
Binds w/ Renin; stops
angiotensinogenangiotensin II
Reduces influence of entire RAAS
ONLY HTN
Spironolactone
Blocks actions of aldosterone in distal
nephron
 keep K; lose Na
ALSO PART OF RAAS SYSTEM
**Used in combo w/ LOOP or THIAZIDES to REDUCE
LOSING K
Primary hyperaldosteronism
↓ myocardial remodeling & fibrosis, ↓SNS
HTN, edema r/t CHF
Eplerenone
Selective ARB
Blocks aldosterone receptor w/o
androgen blocking effects
HTN and CHF
↓ myocardial remodeling & fibrosis, ↓SNS
Nursing Implications
Avoid K+ supplements, K+ sparing diuretics
Check WBCs and differentials q2weeks during 1st 3months of therapy for ACE inhibitors
HOLD Diuretics 1 week before starting ACEI
Captopril and moexipril must be given 1 hr A.C. (other ACEI no regard to meals)
Do not use in pregnancy
Avoid HYPERKALEMIA
K+ supplements
ACEI/ARBs
Direct renin inhibitors
Inhibitors of P450 ↑ *Eplerenone+
Angioedema (less than ACEI)
Cough (less than ACEI)
GI effects  dose-dependent diarrhea
Hyperkalemia when combo w/ ACE, Kspare diuretic, K-supples, KCl subs
Fetal injury and death
Hyperkalemia
Benign/malignant tumors
Binds to androgen receptors
(gynecomastia, menstrual irregularities,
impotence, hirsutism, & deeper voice)
Hyperkalemia
SYMPATHOLYTICS
Therapeutic Uses
Interactions/Considerations
Adverse Reactions
1st non-selective: Propanolol
2nd β1-selective: Metoprolol
3rd non-selective:
Carvedilol, Labetelol
3rd selective: Nebviolol
↓ HR, ↓ PVR, ↓ SV, ↓ FOC
↓ renin release (↓RAAS)
Carvedilol
Labetalol
α blockade  dilate vascular
β1 blockade on heart
β blockade at kidneys
Alpha + Beta uses
Best for African Americans
Alpha and Beta adverse reactions
α2 inhibits α1 receptor
 blocks vasoconstriction
HTN
Dry mouth sedation
Severe rebound HTN
Methyldopa: hemolytic anemia, liver dz
CNS α2agonist
Clonidine
Methyldopa
(only used during pregnancy)
Adrenergic
neuron blockers
Reserpine
Sympathic
ganglia
α/βblockers
α1-blocker
-osin
MOA
Prazosin
Terazosin
Doxazosin
Tamslosin (BPH only)
Alfuzosin (BPH only)
Sildosin (BPH only)
Phentolamine (pheochromycytoma)
Phenoxybenzamine (pheo irrever)
β-blocker
-lol
Individual Drugs
Mecamylamine
Nursing Implications
Blocks α1-receptor
Vasoconstriction  ↓PVR
Depletes NE @ post-ganglionic
terminal
 ↓ sympathetic stimulation of
heart & blood vessels  ↓ CO, BP
Interrupts transmission through
ganglia
 no SNS to the nerve
Primary HTN (vasodilation)
Reversal α1 toxicity
BPH
Pheochromcytoma
Raynaud’s disease
HTN, CHF, Glaucoma
Angina, dysrhythmia, MI
Migraine, Stage fright
Pheochromocytoma
Hyperthyroidism
Best for whites
Orthostatic HTN (take 1st dose HS)
Reflex tachycardia
Na retention, ↓ blood volume
Nasal congestion
Inhibition of ejaculation
Β1:
Less effective in blacks
Bradycardia, ↓ CO
Can mask s/s of hypoglycemia
Reflex tachycardia
Arrhythmia meds can cause arrhythmia
AV heart block
CNS effects (rare)  depression
Β2:
LARGE DOSE  ↓FOC  ↑fluids,
Bronchoconstriction
worsening heart failure
Inhibition of glycogenolysis
HTN
Orthostatic hypotension
Deep depression
Hypertensive emergency
Access HR and BP before giving med
Teach pts to carry enough meds on away trips
Teach s/s of HF: SOB, night coughs, edema at extremities
CHECK for ↑RR, BP, HR, crackles
Caution w/ respiratory pts
DON’T discontinue BB abruptly (rebound cardiac excitation)
BB can mask risk of hypoglycemia b/c of ↓glycogenolysis
Teach s/s of ↓BG: sweating, hunger, fatigue, poor concentration
DIRECT ACTING VASODILATORS
Individual Drugs
MOA
Therapeutic Uses
Interactions/Considerations
Adverse Reactions
Selective dilation of arterioles
Hydralazine
Minoxodil (for severe HTN)
Dilate arterioles = ↓cardiac afterload
= ↓cardiac work = ↑CO/perfusion
Primary HTN
Hypertensive crisis
Heart failure
Combine w/ ISDN for CHF
Reflex tachycardia (combo w/ βblocker to counter)
Na retention: ↑ BV (combo w/ diuretic to counter)
SLE-like syndrome: muscle/joint pain, fever
HA, Dizziness, weakness, fatigue (from orthostatic HTN (take
1st dose HS)
Monoxidil: hypertrichosis (Rogaine), N/HA, pericardial
effusion, thrombocytopenia, skin rxns, breast tender
Selective dilation of veins
Nitroglycerin
Dilate veins = ↓cardiac preload
= ↓blood return = ↓ventricular filling
= ↓cardiac work = ↓CO/perfusion
↓ severe pulm edema
(HF)
Nitroglycerin can be given SL or TOP
(1st pass effect)
Stored in dark container
Hypotension
Reflex tachycardia
Dilation of arterioles/veins
Prazosin
Sodium nitroprusside (IV)
Nitroprusside: Immediate onset
HTNsive emergencies
Diastolic > 120
Heart failure (↑CO, ↓
pulm. edema)
Don’t infuse > 72 hours
Excessive ↓ BP
Cyanide poisoning (rare): give thiosulfate to counter
Thiocyanate toxicity; monitor CNS for efx (disorient,
psychotic behavior), monitor plasma thiocyante levels
Isosorbide dinitrate
Synthetic BNP
↓RAAS, ↓SNS, dilates veins/arterioles
Nesiritide (Natrecor)
Symptomatic hypotension
CALCIUM CHANNEL BLOCKERS (CCBS) (2)
Individual drugs
MOA
Dihydropyridines
Nifedipine (fast-acting)
Amlodipine, Isradipine,
Felodipine, Nimodipine,
Nisoldipine, Clevidipine
↑ arteriole dilation
Acts on the heart
Blocks Ca+ channels in peripheral arterioles
vascular smooth muscle (little blockage in heart)
↓BP  baroreceptor reflex
Non-dihydropyridines
Verapamil
Diltiazem
Acts on arterioles and the heart
Block at peripheral arterioles: ↓ arterial pressure
Block at artery/arterioles of heart: ↑coronary
perfusion
Block at SA node: ↑HR
Block at AV node: ↓ AV nodal conduction
Block in myocardium: ↓force of contraction
↓BP  baroreceptor reflex
Therapeutic uses
Interactions/considerations
Primary HTN
Angina
Migraine, ↓ preterm labor
CANNOT BE USED FOR DYSRHYTHMIAS
Less likely than verapamil to exacerbate
pre-existing heart problems
Best for African Americans
NET EFFECT: ↓BP, ↑HR, ↑FOC
HTN
Angina
Cardiac dysrhythmias (↓ AV node cont)
Migraine
NET EFFECT: Little or no net effect on cardiac
performance. Overall effect is just ↓AP,
↑coronary perfusion
Digoxin (↑ risk of AV block)
β-blockers (excess cardiosuppression)
Grapefruit juice (verapamil toxicity)
Monitor BP and ECG with resuscitation
equipment immediately available
Adverse reactions
Reflex tachycardia 
use βblock to ↓ (opposite Verapamil)
Vasodilation  Dizziness, Facial
flushing, HA, Edema in ankles/feet
Chronic eczematous eruptions (old pts)
Gingival hyperplasia
Very little constipation
Reflex tachycardia
Constipation (block SM in GI) (less w/
Diltiazem)
Vasodilation  Dizziness, Facial
flushing, HA, Edema in ankles/feet
Cardiac effects of blocking
Chronic eczematous eruptions (old pts)
Gingival hyperplasia
INOTROPIC AGENTS
+ iontropic action: ↑ myocardial contractile force which ↑ CO by inhibiting Na+/K+ ATPase which promotes
Ca++ build up in myocyes (actin/mysin)
Neurohormonal systems: altered due to alteration of electrical activity of the heart
Reduces s/sx; does not prolong life, may shorten lives of women
Digoxin Toxicity S/sx:
Dysrhythmias
GI (anorexia, N/V)
CNS (fatigue, visual disturbances; blurred vision, yellow tings, halos around dark objects)
Treatment of digoxin toxicity:
Stop digoxin & K+ wasting diuretics
Monitor K+ serum level
Give atropine if pt develops AV block
Give phenytonin & lidocaine for dysrhythmias
Give activated charcoal to bind to digoxin & prevent absorption
Individual drugs
Sympathomimeti
Digoxin (2nd line agent)
MOA
Through direct & indirect mechanism to help with s/sx of HF:
1. ↑ CO
2. ↓ HR; sympathetic tone decreases
3. ↓ heart size; decrease stretch d/t increase CO
4. ↓ constriction of arterioles & veins; decrease venous return
5. Reverses H2O retention; increase urine output
6. ↓ blood volume; increase urine output
7. ↓ peripheral & pulmonary edema; increase CO
8. ↓ weight; due to increase H2O loss
9. ↑ exercise tolerance; increased O2 to lungs
10. ↓ fatigue; increased O2 to lungs
Therapeutic uses
Interactions/considerations
↑ FOC and ↑ CO:
 ↓ baroreceptor reflex 
↓HR: more time to vent fill
↓afterload: more time to empty
↓venous pressure: ↓edema/congestion
↑urine prod: ↑renal perfusion, ↓BV
↓renin: ↓aldosterone/angiotensin2
Alters electrical properties of heart
↑ firing rate of vagal fibers: ↓ firing rate at SA
↑ SA response to acetylcholine: ↓ conduction
to AV node
NARROW THERAPEUTIC INDEX: 0.5-0.8 ng/mL
(not a DOC)
NOT BEEN SHOWN TO PROLONG LIFE
May shorten life in women
Hypokalemia ↑ DIG
Diuretics - ↓ K
ACEI/ARB - ↑ K  ↓ DIG effect
Sympathomimetics - ↑HR
Quinidine - ↑DIG toxicity
Verapamil - ↑ DIG toxicity, ↓FOC
Adverse reactions
Severe dysrhythmias (oxymoronic efx)
Anorexia, N/V, fatigue, visual
distubances (precedes dysrhythmia)
Assess for orthopnea, dyspnea, JVD,
edema, rales, sleep
β1
Dopamine
Dobutamine (preferred)
Phosphodiesterase inhib
Inamrinone (Amrinone)
Milrinone
Nursing Implications
Activates β1 receptors
Activates α1 receptors (ONLY DOPAMINE)
↑ HR, ↑ heart contractility,
↑ renal blood flow, urine output
α1: ↑ vascular resistance, ↓ CO
Risk of tachycardia
↑ CO while ↓ filling of left ventricle and
↓ resistance of peripheral vasculature
TEACH pts to take Digoxin as instructed, with K+ supplements as instructed. MONITOR K+ levels (3.5-5)
Teach pts to look out for symptoms of toxicity: altered HR/rhythm, visual/GI disturbances
Obtain HR and rhythm before administering DIG. Check Apical HR for full minute! <60bpm or changes in rhythm, hold med/call HCP
IV Dig: monitor cardiac status closely for 1-2 hrs after IV injection
Don’t double up, take as prescribed, limit salt intake to 2gm/d, avoid excess fluids, reduce calories, regular exercise
ANGINA PECTORIS
1. Chronic stable
a. Triggered by physical activity & large meals. Cause is plaque (coronary artery disease)
b. Treatment: ↑ O2 supply & ↓ O2 demand
2. Variant
a. Coronary artery spasm restricts O2 to the heart causing pain; can happen ANYTIME
b. Treatment: ↑ O2 supply
i. Drugs: CCBs, organic nitrates
ii. Only treat S/sx not underlying disease
3. Unstable
a. MEDICAL EMERGENCY
b. Severe CAD complicated by vasospasm, platelet aggregation & transient coronary thrombi/emboli, s/sx
my present at rest or exertion but intensify of existing angina
c. Treatment:
i. sublingual nitrates then IV nitrates
ii.
iii.
iv.
v.
beta-blockers then non-dihydropyridine CCBs
ACE inhibitor only if presistant HTN or L ventricular dysfunction/CHF
Aspirin, clopidogrel, aciximab only if angioplasty is planned
Eptibibatide only if high risk pt w/ ischemia and angioplasty is not planned
Sub-Q ↓ molecular weight Heparin
Preload: “stretch” volume, R atria
Afterload: “pressure/resistance” the heart has to overcome to eject blood (force)
O2 Demand: HR, contractility & intramycardial wall tension (pre/afterload)
O2 Supply: determined by myocardial blood flow. Need to ↑ blood flow to supply demand. When O2
demand ↑ coronary arterioles dilate and blood flow ↑. Mocardial infusion only takes places during
diastole (heart relaxes).
2 types of dysrhythmias
Tachydysrhythmias (hr ↑)
Bradydysrhythmias (hr ↓)
2 major groups of dysrhythmias
Supraventricular
Above the ventricles
Dangerous when excessive ventrical excitation, diastolic filling
Ventricular
Drugs used to treat dysrhythmias can cause dysrhythmias
Supraventricular
Dysrhythmia
DYSRHYTHMIAS
Atrial fibrillation
Atrial flutter
Ventricular
Dysrhythmia
Sustained supraventricular tachycardia
Supraventricular dysrhythmias
Atrial fibrillation (most common)
Atrial flutter
Sustained ventricular tachycardia
Ventricular dysrhythmias
Ventricular fibrilation
Digoxin-induced ventricular dysrhythmias
Torsade’s de pointes
Sustained ventricular tachycardia
Ventricular fibrillation
Ventricular premature beats
Digoxin-induced ventricular dysrhythmia
Torsade’s de pointes
Improve ventricular pump:
B-blocker: atenolol, metoprolol
CCB: verapamil, diltiazem
Stroke prevention: long-term oral anticoagulants, RF ablation
Cardioconversion, RF ablation
Control ventricular rate
B-blocker: atenolol, metoprolol
CCB: verapamil, diltiazem
↑ vagal tone , Valsalva maneuver
IV Beta-Blocker or CCB
Cardiovert; Implantable cardioverter-defibrillator
Amiodarone, lidocaine, procainamide, sotalol
ICD or drugs
Beta-blocker
Lidocaine; phenytoin
Prolongation of QT interval
IV magnesium, CV, Class IA/III rx
DYSRHYTHMIA DRUG CLASSES
MOA
Therapeutic Uses
Interactions/Considerations
Adverse Reactions
Quinidine
Procainamide
Disopyramide
↓ impulse conduction in atria, vent, His-purkinje, ↓
repolarization
Strong anticholinergic
Widens QRS complex, prolong QT interval
Supraventricular dysrhythmia
Ventricular dysrhythmia
Give w/ Digoxin, Verapamil,
βblocker to ↓ ventricular
rate
Diarrhea, hypotension
Cinchonism (tinnitus, HA, nausea,
vertigo, blurred vision
Cardiotoxicity, Arterial embolism
Lidocaine
Mexiletine, Phenytoin
↑ repolarization, ↓ automaticity in vent/HP
↓ conduction in atria, vent, His-purkinje
Ventricular dysrhythmia only
Lidocaine : NEED
resuscitation equipment
available
CNS (paresthesias, drowsiness)
Convulsion, respiratory arrest
Flecainide
Propafenone
Moricizine
Reduce conduction velocity in atria, vent, HP
↓ vent repolarization
Life-threatening vent dysrhythmia
Propranolol, Acebutolol
(non-selective)
Esmolol (IV)
Sotalol (selective β1, KCB)
↓ automaticity of the SA node, ↓ FOC
↓ velocity of conduction through the AV node which
prolongs PR interval
Dysrhythmias caused by excessive SNS
Vent rate in pts w/ supraventricular
tachydysrhythmias
SOTALOL is given for lifethreatening dysrhythmias
Hypotension
Bronchospasm
Bretylium: short-term trmt of vent
dysrhythmia
Amiodarone: life-threatening vent
dysrhythmia and now for atrial
dysrhythmia
No pregos
P450-CYP3A4; ↑quinidine,
phenytoin, digoxin,
warfarin, statins, diltiazem
Grapefruit ↑ Amiodarone
levels
Cholestyramine, St. John’s
wort, rifampin ↓
Amiodarone levels.
Combo w/ diuretics 
dysrhythmia
Combo w/ BB, CCB  ↓ HR
Profound hypotension
Pulmonary damage
Cardiotoxicity
Blue-gray discoloration
Optic neuropathy
Control vent rate in pts w/
supraventricular dysrhythmia
↑ digoxin
Combo w/ BB  ↓ HR
Bradycardia, AV block, HF
Hypotension, peripheral edema, constip
IV
CCB
Amiodarone
Bretyllium
Sotalol (also a BB)
Verapamil
Diltiazem
Other
III K+-channel blocker
II βblockers
I Na+ channel blockers
Individual Drugs
Adenosine
Digoxin
Delay repolarization of fast action potentials, prolong
duration & prolong QT interval
↓ SA node automaticity
↓ AV node conduction
Reduction of Myocardial contractility
↓ automaticity in SA node
↓ conduction through AV node
Prolongation of PR interval
Supraventricular dysrhythmia
DOC for termination of paroxysmal SVT
½ life: 1.5-10 – GIVE RAPID IV PUSH
ANTITHROMBOEMBOLIC
3 major groups:
1. Antiplatelet drugs (ASA, ADP blockers, etc.) - inhibit platelet aggregation. Prevents arterial thrombosis
2. Anticoagulants (warfarin, heparins, direct thrombin inhibitors, etc.) - suppress production of fibrin. Most effective against venous thrombosis
a.
Inhibit synthesis of clotting factors (warfarin)
b. Inhibit activity of clotting factors
3. Thrombolytic drugs (alteplase, streptokinase, etc.) - promote lysis of fibrin
Antiplatelet
Individual Drugs
Aspirin
Nonselective and irreversible COX inhibitor
TXA2 inhibition  ↓ platelet aggregation
&vasoconstriction
Clopidogrel
Prasugrel
Ticagrelor
Adenosine diphosphate receptor
antagonist
Irreversible blockade of ADP receptors on
plt surface  ↓ aggregation
Stroke
MI
Abciximab
Tirofiban
Eptifibatide
Glycoprotein IIB/IIIA receptor antagonist
Reversible, inhibits final step of
aggregation
Heparin
Anticoagulant
Therapeutic Uses
↓ risk of MI/stroke
Chronic stable/unstable angina
Coronary stenting
Thrombotic disorders
Unfractionated
Low Molecular Weight
Enoxaparin
Dalteparin
Tinzparin
Fondaparinux
Warfarin
Direct thrombin inhibitors
Dabigatran Etexialte
Rivaroxaban
Antithrombin
Thrombolytic
MOA
Fibrinolytics
Alteplase
Tenecteplase
Replase
Urokinase
Highly polar, cannot cross membranes
easily, non-specific binding
↑ effects of anti-thrombin
Short-term: prevent ischemic in
ACS pts and pts undergoing
percutaneous coronary
intervention
Prophylaxis: venous thrombosis,
open heart surgery, pregnancy,
acute MI, DVT
↑ effects of anti-thrombin
Higher bioavailability
1st line tx in DVTs
Only inhibits facter Xa reduces thrombin
Antagonize vitamin K (need for factor VII,
IX, X, & prothrombin
Has no effect factors already in circulation
Long term prophylaxis
PO prodrug
A fib
Direct factor Xa inhibitor
Oral anticoagulant
Thrombus in pts w/ AT defiency
Acts by indirect mechanism – binds to
plasminogen then catalyzes into plasmin
which digests fibrin in clots; degrades other
clotting factors
Dissolve thrombi already formed
Acute MI, DVT, massive PE
Interactions/Considerations
Dose: preventative: 81 mg; ACS: 325 mg
Stop 7-8 days before surgery
Adverse Reactions
GI bleed
Hemorrhagic stroke
Potential fatal hematologic effects
Risk higher w/ ticlopidine
Neutropenia/agranulocytosis
Thrombotic thrombocytopenic pupura
Most effective anti-plt drug on market
VERY EXPENSIVE
Bleeding
IV/SUBq only
Monitor aPTT (1.5-2 fold increases therapeutic)
OD: use protamine sulfate; give slow IV
Monitor for bleeding
HITreduce platelet count
Hypersensitivity (small test dose 1st)
SUBq
Doesn’t need aPTT monitoring (given at home)
OD: use protamine sulfate; give slow IV
SUBq
Can’t reverse w/ protamine sulfate
Several days to peak
Initial response 8-12hrs
Monitor PT & INR (keep between 2 - 4.5)
Monitor levels no sooner than 5 h after IV or
no sooner than 24 h after SQ injection
OD: use vitamin K or whole blood
Heparin, ASA, APAP, non-ASA
↑anticog: miconazole, cimetidine, disulfiram,
sulfonamides
↓anticog: vit k, phenobarbital, carbamazepine,
rifampin
Doesn’t require monitoring anticoag
Little risk of AEs
Same dose be used for all pts despite wt
Start trmt w/i 4-6 hrs of symptom onset
IV infusion or infuse directly into occluded
coronary artery
Rapid activation: 40-80 min
Restore patency in clogged central venous cath
Avoid ASA, other anticoags, Subq/IM inj,
invasive
Hemorrhage
Pregnancy Category X
DO NOT USE during breast feeding
Bleeding (&ICH)
Hypotension
Fever, Ab production
HYPERLIDIPIDEMIA
Classification
HMG-CoA reductase
inhibitor
“-statins”
Bile-acid
sequestrans
Drugs
Atorvastatin
Lovastatin
Rosuvastatin
Simvastatin
Pravastin
Fluvastatin
Colesevelam
Cholestyramine
Colestipol
Niacin (nicotinic acid)
Niacor (IR)
Niaspan (ER)
Fibrates
Gemfibrozil
Fenofibrate
Fenofibric acid
Combination drugs
Ezetimibe
Zetia
Ezetrol
MOA
Inhibit HMG-CoA reductase
(enzyme for CHO synthesis)
 ↓CHO, ↑ LDL receptors
Therapeutic uses: HLD,
Primary/Secondary CV events,
Post-MI therapy, Diabetes
↓bile reabsorption  ↑ LDLreceptors  ↓ LDLs
Uses
↓LDL, TG (most effective)
↑HDL
Nonlipid CV Benefits:
↑ plaque stability
↓ inflammation @ site
Slow CAD calcification
Vasodilation
↓ A.fib risk
↓ thombus risk
↑ bone formation
↓LDL, ↑VLDL (2nd line)
Unknown how it raises HDL
Acts on liver to ↓ TG, VLDL,
LDL
↓LDL, TG
↑HDL (most effective)
Activate PPAR-alpha
↓ TG (most effective)
↑HDL
Little effect on LDL
Acts on cells at SI lining to ↓
dietary CHO absorption and
CHO reabsorption from bile
↓Total CHO
↓LDL, APO B
Small HDL ↑
Adverse Effects
HA
Rashes
GI disturbances
Myopathy/rhabdomylolysis (RARE)
Hepatoxicity (RARE)
GI (constipation)
Skin flushing (take ASA before), itch
GI upset, N/V, diarrhea
↑ uric acid levels (no gout pts!)
Hepatotoxicity
Hyperglycemia
Gouty arthritis
Rashes
GI disturbances
Gallstones
Myopathy
Liver injury
Myopathy
Rhabdomylolysis
Hepatitis
Pancreatitis
Thrombocytopenia
Contraindications
Additional
Information
Other-lipid lower drugs (↑ risk
of AE)
Drugs that inhibit CYP3A4 (↑
statin toxicity)
Grapefruit juice inhibits
too!!
Pregnancy Category X
Pts w/ viral or ETOH hepatitis
Give at bedtime (endogenous
CHOL synthesis occurs PM)
Forms insoluble complexes
with: Warfarin, thiazide
diuretics, digoxin, some ABX
Colesevelam is newer and
better tolerated
Doesn’t ↓ uptake of fatsoluble vitamins
Doesn’t significantly ↓
absorption of statins,
warfarin, digoxin
Helps control
hyperglycemia in DM2
↑ bleeding risk for Warfarin
pts (monitor INR)
↑ rhabdomylolysis in Statin
pts
Statins: ↑liver damage &
myopathy
Fibrates: ↑ CHO in bile, ↑ risk
of gallstone
Monotherapy or use w/
BAS ↓ absorption of
statins
ezetimibe (give 2h b4, or 4h
after)
Cyclosporine ↑ ezetimibe
levels
High doses ↓ TG
↓ platelet formation → prolonged bleeding.
Caution when used with anticoagulants or antiplatelet drugs
↓intestinal absorption of CHO by 10%
↓ LDL by 14%
Lovastatin/Niacin (Advicor)
Statin ↓ LDL
Niacin ↑ HDL & ↓ trigs
Fish oil (Omega 3 Fatty Acid)
Simvastatin/Niacin (Simcor)
Simvastatin/Ezetimibe (Vytorin)
Statin ↓ LDL, niacin ↑ HDL & ↓ trigs;
Ezetimibe ↓ total CHO, LDL, and APO B
Plant stanol, Sterol esters
Pravastatin/Aspirin (Pravigard)
ASA prevents MI, stroke, & death [suppresses plt aggregation],
Statin ↓ LDL
Estrogen
Atorvastatin/Amlodipine
(Caduet)
Atorva (dylipidemia) & CCB (HTN & angina)
Fewer pills to take & lower cost
↓ LDL by 15%, ↑ HDL by 10%
Does not ↓ CV morbidity or mortality in older women
Simvastatin/Sitaglipitin (juvisync)
Statin & Oral antidiabetic
Cholestin
(dietary supplement)
↓TCHOL, LDL
↑ HDL
NEURODEGENERATIVE DISORDERS
ANTI-EPILEPSY AND MUSCLE SPASM/SPASTICITY
Blood Brain barrier – only lipid-soluble; no protein-bound or highly ionized drugs
Parkinson’s Disease – progressive and degenerative
Degeneration of the neurons that supply dopamine to the striatum  ↓ dopamine  acetylcholine
excessively stimulating GABA-releasing neurons.
s/sx: TRAP (tremor, rigidity, akinesia, postural instability)
90% develop: autonomic disturbances, depression, dementia, and psychosis
Can give Amitriptyline to treat depression (but it can exacerbate dementia)
Alzheimer’s Disease – progressive and degenerative
β-amyloid, neuritic plaques, neurofibrillary tangles
Risk factors: Age, family history, TBI, CV disease, female, low education level, estrogen therapy, smoking
Biomarkers: ↑ apoE4, ER-associated binding protein, ↑ homocysteine, ↓ folic acid
s/sx: memory loss (1st), confusion, disorientation, ↓judgment, ↓ADLs, behavior problems, “sundowning”
Multiple Sclerosis
Chronic, inflammatory, autoimmune disorder that damages the myelin sheath of neurons in the CNS
s/sx: paresthesias, muscle/motor problems, visual impairment, bladder/bowel symptoms, sexual
dysfunction, disabling fatigue, emotional lability, depression
Treatments by Subtypes:
Relapsing-remitting
85-90%; trmt ASAP, indefinitely
Immunomodulator
Secondary progressive
RR-MS that has worsened (50%)
Interferon-beta, Mitoxantrone
Primary progressive
Sx are more intense from onset (10%)
No drugs effective
Progressive-relapsing
Acute exacerbations + ↑ symptoms
Mitoxantrone
PARKINSON’S DISEASE
Class
Dopamine
replacement
Individual Drugs
Levodopa
Carbidopa
MOA
Seizures - paroxysmal, uncontrolled, brief event due to excessive neuronal discharge associated with sensory,
motor, and/or behavioral changes
Epilepsy - a chronic syndrome w/ recurring seizures without evidence of reversible metabolic activity
Status Epilepticus - recurrent or continuous seizure activity w/o the return to normal function (>5 min)
Types:
Partial seizures
Simple, Complex, Secondarily; begins focally in
Carbamazepine,
cerebral cortex and spreads
Phenytoin, Valproic acid,
Phenobarbital, Primidone
Tonic-clonic
Tonic – stiffening/rigidity of the muscles, mainly
Carbamazepine,
“grand-mal”
arms/legs; LOC gone
Phenytoin, Valproic acid,
Clonic – rhythmic, jerking of all extremities
Phenobarbital, Primidone
Absence “petit mal”
Brief period of LOC like day dreaming. More
Ethosuximide, Valproic
common in children
acid
Myoclonic
Brief jerking or stiffening of the extremities which
Valproic acid
occur singly or in groups
Atonic
Sudden loss of muscle tone, pt. falls
Valproic acid
Treatment goal: ↓ seizures so pt can live as normal as possible; balance control w/ acceptability of S/Es
Withdrawing AED: withdrawn slowly (over a period of 6 weeks to several months)
Muscle Spasm - involuntary contraction of muscle or muscle group.
Muscle Spasticity – heightened muscle tone, spasms, loss of dexterity
Causes: Epilepsy, Hypocalcemia, Pain syndromes: adult/chronic, trauma: localized skeletal injury
Treatment: immobilization of affected muscle, cold compresses, whirlpool baths, PT, drug therapy, ASA
Therapeutic Uses
Dopamine precursor
1st line PD
Restless leg syndrome
Activate DA receptors
1st line PD
Use w/ Levo in late PD
Restless leg syndrome
Inhibit Levodopa breakdown
↓ DA degradation
↑ effects of Levodopa
↑ DA release
↓ DA reuptake
Cholinergic antagonist (↓ACh)
PD. Combo w/ Levodopa
2nd/3rd line PD. Combo
with Levodopa
Early PD (↓TRA)
Anti-viral
Tremor/Rigid of early PD
Dopaminergic agents
Combo=Sinemet
Dopamine agonist
Pramipexole (Non-Ergot)
Ropinirole (Non-Ergot)
Bromocriptine (Ergot)
Cabergoline (Ergot)
COMT Inhibitor
Entacapone
MAO-B Inhibitor
Selegiline
Dopamine Releaser
Amantadine
Anti-cholinergic
Benztropine
Adverse Effects
N & V – most common
Dyskinesias, Confusion
Loss of balance; ↓ BP
Drowsiness & sudden sleep onset
Acute psychosis, nightmares
Additional Info/Contraindications
CI: narrow-angle glaucoma
DI: 1st gen anti-psychotics, MAOIs,
anticholinergics, pyroxidine,
FI: protein/vitamins w/ pyroxidine
Lev/Carb/Ent (Stalevo) – cheap combo
Need 3-6 months to work
Does not cause dyskinesias when alone
Monotherapy: nausea, dizziness, daytime somnolence, insomnia, constipation, weakness,
and hallucinations
Combo w/ Levodopa: ortho HTN, dyskinesias, hallucination
Pathologic gambling (rare)
Levodopa toxicity
Monotherapy: Insomnia, abd symptoms;
DI: Levodopa
confusion, and hallucination
Dry mouth, Blurred vision
Needs to be withdrawn gradually
Insomnia, hallucinations, delirium
Can be used w/ Sinemet
Trihexyphenidyl
ALZHEIMER’S DISEASE
Class
Individual Drugs
MOA
NMDA receptor blocker
Memantine [Namenda]
Cholinesterase inhibitor
Galantamine
Rivastigmine
Donepezil (advanced AD)
Tacrine (not rec’ed)
MULTIPLE SCLOROSIS
Class
Individual Drugs
Prevent ACh degeneration
Blocks cholinergic receptors
MOA
Adverse Effects
Additional Info/Contraindications
Moderate-severe AD
Confusion, HA, dizziness, hallucinations
Mild-moderate AD
Muscle cramps, bradycardia, ↓appetite/weight
Cholinergic side effects
GI, Dizziness, Headache
Bronchoconstriction
Liver injury (tacrine)
Therapeutic Uses
Adverse Effects
Inteferon-beta
Inhibits migration of proinflammatory
leukocytes across BBB
↓ T-helper cell activity
↓ frequency/severity of attacks
↓ #/size of MRI-detectable lesions
↓ progression of disability
Flu-like reactions (HA, fever, chills, malaise)
Hepatotoxicity
Myelosuppression
Injection-site reactions
Depression
Glatiramer Acetate
↑ TH2 anti-inflammatory, crossing
BBB  block myelin destruction
Long-term therapy of relapsingremitting MS
Well-tolerated
Natalizumab
(Tysabril)
Binds to integrins  prevent
leukocytes from leaving vasculature
MS (not first line)
Crohn’s disease
Mitoxantrone
Binds with DNA and inhibits
topoisomerase II
Cytotoxic drug, suppresses T/B cell
production
Prevents myelin destruction
↓ neurologic disability
↓ clinical relapses of MS
Relapsing-remitting, Secondaryprogressive, Progressive-relapsing
MS pts (not effective for primary)
Immunomodulators
Immunosuppressant
Therapeutic Uses
Blocks glutamate  ↓ Ca influx
 slows neurodegeneration
Better tolerated than cholinesterase
inhibitor
Additional Info/Contraindications
APAP, ibuprofen for flu-like sx
Single-use syringes and vials
Check CBC, LFTs (baseline/before)
Report PML symptoms ASAP: unilateral weakness, clumsiness, disturbed vision/think
Headache, fatigue, abdominal discomfort, arthralgia, depression, diarrhea,
gastroenteritis, UTI, lower respiratory tract infection
Myelosuppression
LFT: baseline & before each dose
Cardiotoxicity
CBC: baseline, before, q10-14 d
after each infusion (do not give if
Fetal harm
neutrophil <1500 cells/mm3)
Reversible hair loss, injury to GI mucosa, N/V,
Pregnancy test before each dose
amenorrhea, allergy symptoms, blue-green
tint to urine, skin, and sclera
Determine LVEF (before the 1st
dose, before all doses once
Bladder/bowel dysfunction, fatigue, spasticity
cumulative dose reached,
depression, sexual dysfunction, neuropathic
whenever signs of CHF develops)
pain, tremor, cognitive dysn, dizziness, vertigo
SEIZURES
Individual Drugs
Phenytoin [Dilantin]
MOA
Inhibit Na+-channels
 suppresses seizure
generating neurons
Therapeutic Uses
Partial seizures
Tonic-Clonic seizures
Adverse Effects
Nystagmus, sedation, ataxia, diplopia,
cognitive impairment, gingival hyperplasia,
skin rash, gastric distress, hirsutism,
anemia
Effects in pregnancy, CV effects
Elevated Blood levels:
20-30: nystagmus
30-40: ataxia
> 40: ↓ LOC
Additional Info/Contraindications
DI: ↓ the effects of oral contraceptives, warfarin, and glucocorticoids
DI: ↑ levels of diazepam, isoniazid, cimetidine, alcohol, and valproic acid
↓ metabolism by warfarin, chloramphenicol, isoniazid, carbamazepine, &
digoxin
NARROW THERAPEUTIC INDEX!!! Therapeutic blood level 10-20 mcg/ml
(CHECK PLASMA DRUG LEVELS!!)
For IV administration, flush IV line with NS before & after. Give slowly, no
more than 50 mg/ml (NO DEXTROSE)
Peaks in brain in 15 minutes, ½ life = 24 hours
Give twice a day  allows for a consistent serum level
Large loading doses are required
Check CBC & Ca++ levels
Phenytoin & dilantin are not exactly the ‘”same.” Can’t interchange
Carbamazepine
[Tegretol]
Delays recovery of
Na+-channels
Epilepsy
Bipolar disorder
Trigeminal and
glossopharyngeal neuralgias
Neuro: nystagmus, ataxia
Heme: leukopenia, anemia, ↓ plts
Birth defects, Hypo-osmolarity
Skin: rash, photosensitivity reactions
Diplopia, blurred vision, N/V, leukopenia
Therapeutic blood level: 8-12 mcg/ml
Give with meals, no grapefruit juice
Can cause SIADH
SJ syndrome (withdraw drug)
Contraindication for pts w/ glaucoma, cardiac, renal, or hepatic disease.
SEIZURES (cont.)
Individual Drugs
MOA
Therapeutic Uses
Inhibit Na-channels
↓ Ca channels
Mimics GABA
Seizure disorders (myoclonic)
Bipolar disorder
Migraine
Ethosuximide
Inhibits low threshold Cachannels
Absence seizures
↑ effects of GABA
↓ anxiety through limbic
system
↑ sleep through the cortical
areas & on the sleepwakefulness-clock.
↑ muscle relaxation through
effects on the supraspinal
motor areas including
cerebellum (MUSCLE SPASM
and MUSCLE SPASTICITY)
↑ effects of GABA
Anxiety
Seizures
Alcohol withdrawal
Anesthesia induction
Benzodiazepine
Valproic Acid
Diazepam
(Valium)
Lorazepam
(Ativan)
Barbiturates
Alprazolam
(Xanax) st
drug
Phenobarbital
Thiopental
(+ anesthesia)
↑ effects of GABA
Mimics GABA
Rapidly crosses the BBB
Adverse Effects
Hepatotoxicity, Pancreatitis
N/V, lethargy, impaired PT/ PTT, hair loss,
leukopenia, & liver toxicity
Drowsiness, blood dyscrasias, ataxia,
nystagmus, GI distress
Drowsiness, dizziness, lethargy
N/V, anorexia, lethargy, blood dyscrasias
CNS depression (sedation)
Respiratory depression/arrest
Less respiratory depression compared to
Barbiturates
Hypotension
Confusion and Anterograde amnesia: impaired
recall of events especially w/ triazolam
Paradoxical effects: insomnia, excitation,
euphoria, heightened anxiety & rage
High abuse potential
Additional Info/Contraindications
NO PREGGOS (use magnesium sulfate instead)
Monitor for CBC & AST
DI: ↑ serum phenobarbital levels, alters serum phenytoin
levels
Therapeutic blood level: 50-100 mcg/ml
Therapeutic blood level: 30-100 mcg/ml
Monitor CBC & LFT q 4-6 months
Contraindicated for pts w/ renal & liver disease
NOT FOR LONG-TERM USE (pt develops sedation/tolerance)
Good for initial management to terminate seizures
PO: No effect on heart & blood vessels
IV: Produce profound hypotension & cardiac arrest.
Administered IV suppresses activity within 10-15 seconds
Peaks in the brain within 8 min
Effectiveness (1/2 life) is approximately 15 min
May not be eliminated for as long as 2-3 days
Dose 10-20 min at a rate 5mg/min
Administer IV
Enters the brain within 2-3 min and peaks within 30
minutes
Duration of effectiveness between 8 - 25hrs
Dose 0.1 mg/kg administered at 2mg a min
Takes longer to enter the brain. Be careful of overdose.
Tonic-clonic seizure
↑ sleep/sedation
Sedation, porphyria, fetal malformations,
respiratory depression, paradoxical excitement,
hyperalgesia
Excess doses: nystagmus, ataxia, hypotension,
shock
Phenobarbital
IV, oral or IM. Enter brain within 5 min and peak brain
levels will occur within 30 min (??)
½ life = 4 days
Dose range: 60-120 mg/day
Plasma range = 15-45 mcg/mL
Epilepsy
CNS depression
Hypotension (MONITOR!!)
Respiratory suppression
Risk for bacterial infection
Risk for abuse: Not a controlled substance. No
“high”, supplies are not closely monitored,
Widely available in operating rooms,
Instantaneous but brief sleep period, pts
awaken “refreshed”, talkative, report elated/
euphoric
Short ½ life of 2-4 min, loading dose 2mg/kg over 10 min
Use EEG monitoring for burst suppression
Continuous infusion may be used to eliminate seizures
Do not stop the infusion abruptly, may precipitate a seizure
Propofol (Diprivan)
General anesthetic
↑ release of GABA
New Generation
AEDs
Gabapentin (Neurotin) = partial complex seizures
Lamotrigine (Lamictal) = partial complex seizures
Levetiracetam (Keppra) = partial complex seizures
NURSING
IMPLICATIONS
Medical management of seizure drugs:
MD will introduce 1 anticonvulsant at a time
Balance must be maintained between therapeutic effects and side-effects. This may take months of trial and error
If chosen drug not effective, then dosage may be increased or another drug added.
Drug dosage adjusted to achieve therapeutic blood levels without causing major S/E.
Flumazenil is the antidote for benzodiazepines
Centrally-acting
relaxant
MUSCLE SPASMS AND MUSCLE SPASTICITY
Individual Drugs
MOA
Tizanidine
Agonist action at presynaptic α2
receptors
Diazepam (Seizure
↑ effect of GABA
meds)
Therapeutic Uses
↓ local muscle spasm
↓ local muscle pain
↑ range of motion
Adverse Effects
Look under Benzodiazepines
Baclofen (Lioresal)
Acts in the spinal cord
↓ hyperactive reflexes
Mechanism unknown
Mimic GABA on spinal neurons
MS, spinal cord injury, cerebral palsy
NOT with stroke
↓ flexor and extensor spasms
↓ resistance to passive movement
No direct effect on skeletal muscle
CNS depressant
GI symptoms (nausea,
constipation)
Urinary retention
Dantrolene (Dantrium)
Acts directly on skeletal muscle
↓ release of Ca from
sarcoplasmic reticulum
MS, spinal cord injury, cerebral palsy
Malignant hyperthermia (potentially fatal
condition caused by succinylcholine and general
anesthetics)
Hepatotoxicity
Muscle weakness
Drowsiness
Diarrhea
Acne-like rash
ANESTHETICS
Additional Info/Contraindications
Generalized CNS depression
Hepatotoxicity
Physical dependence (Abstinence syndrome)
No antidote for overdose
Gradual withdrawal over 1 to 2 weeks
Abrupt intrathecal withdrawal: risk for
rhabdomyolysis
Procaine
Formerly the anesthetic of choice for injection, now replaced by others
Preparations: Available in solution (1%, 2%, and 10%)
Lidocaine
Most widely used local anesthetic
Topical and injectable applications
Effects extended if given with epinephrine
Also used for cardiac dysrhythmias
Preparations: cream, ointment, jelly, solution, aerosol, and patch
Cocaine
First local anesthetic
Central nervous system (CNS) effects
Peripheral nervous system (PNS) effects (sympathetic)
Cardiovascular effects
Preparation and administration: should not be given with vasoconstrictor (NO
EPI)
PAIN MANAGEMENT
Inhalation
Local anesthetics: ↓ pain by blocking Na+-channels, thereby blocking impulse conduction along axons
Adverse effects: ↓ CNS, CV, Allergic reaction, Labor/delivery (prolonged)
Local anesthetics do not reduce consciousness, and they blunt pain only in a limited area
Intravenous
Anesthesia = Loss of pain and loss of all other sensations
Analgesia = Loss of sensibility to pain
General anesthetic: produces unconsciousness and lack of responsiveness to all painful stimuli
AE: respiratory/CV depression, sensitization of heart to CATS, malignant hyperthermia (succinylcholine),
aspiration of gastric contents, hepatotoxicity, toxicity to OR personnel
Adjuncts to Inhalation anesthesia:
Preanesthetic: benzo, opioid, α2-agonist (HTN, ↓pain), anticholinergic (↓ saliva), neuro-block (skeletal
mus relax)
Postanethestic: analgesics, antiemetic, muscarinic agonist (↓ ab distention/urinary retention w/
bethanechol)
Isoflurane
Most widely used inhalation anesthetic
Halothane
Properties much like those of halothane
Isoflurane
Better muscle relaxant, but still requires NMB
Enflurane
Not associated with renal or hepatic toxicity
Desflurane
Nitrous oxide “laughing gas”
Sevoflurane
Very LOW anesthetic potency and very HIGH analgesic potency
Nitrous ox.
Never used as primary anesthetic
Frequently combined with other inhalation agents to enhance analgesia
20% nitrous oxide = Pain relief of morphine
No serious side effects (nausea and vomiting)
Benzodiazepines:
Diazepam (LOOK UNDER SEIZURES)
Induction with intravenous diazepam (Valium)
SA Barbiturates
Unconsciousness within a minute, Very little muscle relaxation
Benzodiazepine
NI: need to repeat instructions b/c of anterograde amnesia S/E
Propofol
Midazolam
Etomidate
Unconsciousness within 80 seconds
Ketamine
Neuroleptic-opioid
Can cause dangerous cardiorespiratory effects
combination:
Propofol: Unconsciousness develops within 60 seconds and lasts 3–5’ Sedativedroperidol/
hypnotic for induction and maintenance of analgesia (LOOK UNDER SEIZURES)
fentanyl
Ketamine: Dissociative anesthesia, sedation, immobility, analgesia, and amnesia
Uses: young children with minor procedures
AE: Hallucinations, disturbing dreams, and delirium, Soothing environment
Nociceptive pain
Results from injury to tissues
Somatic and Visceral pain
Neuropathic pain
Results from injury to peripheral
nerves
Responds poorly to opioids
Pain in cancer patients – pure
opioid agonists preferred
WHO ANALGESIC LADDER
Step 1
mild-moderate pain
Step 2
more severe pain
Step 3
severe pain
Nonopioid analgesic
NSAIDs and APAP
Add opioid analgesic,
oxycodone, hydrocodone
Subsititute powerful opioid—
morphine, fentanyl
Pain Management Strategy
ASK about pain regularly. Assess pain systematically.
BELIEVE the patient and family in their reports of pain and what relieves it. (PAIN = SUBJ)
CHOOSE pain control options appropriate for the patient, family, and setting.
DELIVER interventions in a timely, logical, coordinated fashion.
EMPOWER patients. Enable patients to control their trmt to the greatest extent possible.
Use w/ caution: Methadone, Levorphanol, Codeine
Avoid: Meperidine
Adjuvant analgesic – used to complement the effect of opioids—not used as substitutes (
E.g. TCAs, Anti-seizures, Local anesthetics, CNS stimulants, antihistamines, glucocorticoid,
bisphosphonate
Opioid = any drug, natural or synthetic, that has actions similar to those of morphine
Opiate = applies only to compounds present in opium
Drugs that act at opioid receptors are classified on the basis of how they affect receptor
function
3 main types of opioid receptors
Mu receptor
MOST opioid activation
Receptor activation: analgesia, resp depression, euphoria, sedation, cough
suppression, physical dependence, ↓ GI motility
Kappa receptor
Some opiod activation
Receptor activation: analgesia, sedation, ↓ GI motility
Delta receptor
No opioid activation
Responses to activation of Mu and Kappa receptors
Mu
Analgesia √
Respiratory depression √
Sedation √
Euphoria √
Physical dependence √
↓ GI motility √
Drug Actions at Mu and Kappa receptors
Drugs
Pure Opioid Agonist (strong and moderate-strong agonist)
Morphine, codeine, merperidine, other morphine-like drugs
Agonist-antagonist Opioids
Pentazocine, nalbuphine, butorphanol
Buprenorphine
Pure Opioid Antagonist
Naloxone, naltrexone, others
Kappa
√
√
√
Mu
Kappa
Agonist
Agonist
Antagonist
Partial agonist
Agonist
Antagonist
Antagonist
Antagonist
OPIOIDS
Strong opioid agonist
MOA
Moderate-strong
Pure Opioid Angonist
Drugs
Morphine
Mimic action of endogenous
opioid peptides, at mu
receptor
Does not cross BBB easily
(only small fraction of drug
makes it)
Therapeutic Uses
Mu receptor: pain relief, reduces
anxiety, sense of well-being,
drowsiness, mental clouding
Moderate to severe pain
Pre-operative treatment of anxiety
Adverse Effects
S/E’s of Mu receptor agonist
Respiratory depression
Constipation, emesis
Orthostatic hypotension
Cough suppression,
euphoria/dysphoria
Biliary colic, urinary
retention, sedation
Additional Info/Contraindications
AE: Respiratory depression
Babies/Old ppl especially sensitive
Onset: IV = 7 min; IM = 30 min; SQ = 90 min
Spinal injection-response delayed by hours
↑ depression w/ concurrent use of other drugs w/ CNS depressant
actions (alcohol, barbiturates, benzodiazepines
DI: CNS depressants, anti-cholinergic, hypotensive, MAOIs, agonistantagonist, opioid antagonist,
Toxicity: Coma/Respiratory depression, Miosis
Treatment: Ventilation and Naloxone
Others
Fentanyl: 100x more potent than morphine; 5 formulations in 3 routes
Meperidine: short ½ life; interacts adversely with several other drugs; toxic metabolite accumulation
Methadone: treatment for pain/opioid addicts
Heroin: used legally in Europe to relieve pain, HIGH ABUSE LIABILITY, not more effective than other opioids
Codeine
10% converts to morphine in
liver
Others
Oxycodone: analgesic effect = codeine; Long-acting analgesic; IR or CR (Oxycontin); Abuse: crush/snort/inject med. 2010 OP formulation is much harder to crush and does nto dissolve
into injectable solution
Hydrocodone: Most widely prescribed drug in the United States; combined w/ ASA, APAP, Ibuprofen
Tapentadol: analgesic effect = oxycodone; causes less constipation than traditional medications
Propoxyphene analgesic effect = ASA; combined w/ ASA, APAP; Darvon & Darvocent withdrawn b/c of limited efficacy and potentially fatal dysrhythmias
Pain and cough suppression
Infant intoxication
30 mg codeine = 325 mg APAP
Usually oral (formulated alone or w/ ASA or APAP)
OPIOIDS (cont.)
Individual Drugs
MOA
Therapeutic Uses
Adverse Effects
Additional Info/Contraindications
A-A
Opioids
Pure Opioid
Antagonist
Antagonists at mu receptor
Agonist at kappa receptor
Pentazocine
Relieves pain w/o adverse effects from pure
opioid agonists
Less respiratory depression vs morphine
Limited
respiratory
depression
Caution before giving a pt physically dependent on pure opioid an A-A;
can precipitate withdrawal
Reverse opioid overdose
Relief of opioid-induced constipation
Can precipitate an immediate withdrawal reaction in pts w/ physical
Competitive antagonist
Reversal of postoperative opioid effects
dependence to pure opioid agonists
Management of opioid addiction
Reverse neonatal respiratory depression
Methylnaltrexone – Treatment of opioid-induced constipation in late-stage disease for patients on constant opioids
Morphine:
Tolerance: ↑ doses needed to obtain same response; cross-tolerance to other opioid agonists. No tolerance to miosis or constipation develops
Physical dependence: abstinence syndrome w/ abrupt discontinuation about 10 hrs after last dose. Lasts 7-10 days if untreated. NOT LETHAL, just unpleasant.
Initial rxn (yawning, rhinorrhea, sweating)  violent sneezing, weakness, nausea, vomiting, diarrhea, abdominal cramps, bone and muscle pain, muscle spasm, kicking movements
ABUSE LIABILITY
Take caution when giving to pts with: ↓ respiratory reserve, pregnant, during labor/delivery, head injury
Monitor full vitals before giving Morphine and give on fixed schedule
Naloxone
Others
Nursing Implications
NON-OPIOID CENTRALLY ACTING ANALGESICS
Relieve pain by mechanisms largely or completely unrelated to opioid receptors
Do not cause respiratory depression, physical dependence, or abuse
Not regulated under the Controlled Substances Act
Only 4: tramadol, clonidine, ziconotide, dexmedetomide
Controlled Substances Schedule
Schedule I
High abuse, no medical use
Schedule II
Schedule III
Schedule IV
Schedule V
Individual Drugs
MOA
Therapeutic Uses
Heroin, Ecstasy, LSD
High abuse, accepted uses
Morphine, Cocaine, Codeine, Amphetamine
Less abuse, accepted uses
APAP/codeine, Testosterone
Lower abuse, accepted uses
Phenobarbital, Benzodiazepines
Low abuse
Lomotil
Adverse Effects
Additional Info/Contraindications
Tramadol
Weak agonist activity at Mu
Blocks reuptake of NE/Serotonin 
monoaminergic spinal inhibition of pain
Moderate-moderately severe pain
Less effective than morphine
Vehicle for suicide
Abuse liability
Sedation, dizziness, headache, dry mouth, constipation, seizures
Clonidine
Α2-adrenergic agonist
Relief for severe pain
Hypertension
CV: severe hypotension, rebound hypertension, bradycardia
HEADACHE
Mild HAs can be relieved by OTCs
Characteristics
Migraine
Neurovascular disorder that involves dilation and inflammation
of intracranial blood vessels
Cluster
Tension
Severe, throbbing, unilateral pain near the eye
Attacks: 15 minutes – 2 hrs
Most common
Moderate, nonthrobbing pain
“Head band” distribution; episodic or chronic
Serotonin1B/1D
Receptor
Agonists
Ergot Alkaloid
Individual Drugs
MOA
Symptoms
Treatment
Abortive drugs: ASA, ergot alkaloids, triptans
Preventative drugs: β-blockers, TCAs, anti-epileptic (Divalproex,
Topiramate) – take everyday
Non-drugs: ice-pack, dark room, sleep, exercise, avoid triggers
N/V, photophobia
Throbbing; moderate-severe intensity
Ipsilateral: conjunctival redness, lacrimation, nasal congestion,
rhiniorrhea, ptosis/miosis
Prophylaxis
Uncommon
Nonopioid analgesics
Stress management
Therapeutic Uses
Adverse Effects
Ergotamine
Unknown
Abort migraine
Combo with Caffeine to enhance
vasoconstriction/absorption
Dihydroergotamine
Alters transmission at
serotonergic, dopaminergic, and
α-adrenergic agents
Abort migraine
Cluster headaches
Diarrhea
No physical dependence
Sumatriptan
(Imitrex)
Binds to receptors on
intracranial blood vessels,
causes vasoconstriction
↓ perivascular inflammation
Abort migraine
“heavy arms” “chest pressure”
Coronary vasospasm (rare angina)
Teratogenesis, Pregnancy Class C
Vertigo, malaise, fatigue, tingling sensations
N/V, weakness in the legs, myalgia,
numbness and tingling in fingers or toes,
angina-like pain, tachycardia or bradycardia
Additional Info/Contraindications
OD  Ergotism
DI: Triptans, CYP3A4 inhibitors
CI: Hepatic or renal impairment
DI: CYP3A4 inhibitors, serotonin agonist
CI: Pts with CAD, PVD, sepsis, pregnancy,
hepatic/renal impairment
DI: Ergot alkaloids, other triptans (vasoconstriction)
Can only take 2 doses/day
Monitor for serotonin syndrome sx: AMS,
incoordination, myoclonus, hyperreflexia, excessive
sweating, tremor, fever
ANTIPSYCHOTICS
Psychotic disorders: schizophrenia, delusional disorders, bipolar, depressive psychoses, drug-induced
Anti-psychotics should not be used to treat dementia in the older adult
Three major objectives of drug therapy:
Suppression of acute episodes
Prevention of acute exacerbations
Maintenance of the highest possible level of functioning
Adjunctive drugs: Benzodiazepines, Antidepressants
Class
1st gen
antipsychotics
“conventional”
2nd gen
antipsychotics
“atypical”
Depot
preparations
Lithium
Individual Drugs
MOA
Low potency: Chlorpromazine HCl
Medium potency: Loxapine
High potency: Haloperidol
Block receptors for dopamine
in CNS
Cause serious movement
disorders (extrapyramidal
symptoms [EPS])
Clozapine
Blocks dopamine and
serotonin
Bipolar disorders (aka manic depressive illness)
Cyclic disorder, recurrent fluctuations in mood, persist for months without treatment
Bipolar I disorder: Pure manic episode (euphoric mania) or Mixed episode
Bipolar II disorder: Hypomanic episode (hypomania) or Major depressive episode (depression)
Treatment: Mood stabilizers (Lithium, Valproate, Carbamazepine), Antipsychotics (olanzapine,
risperidone), Antidepressants (buproprion, venlafaxine, SSRI)
Therapeutic Uses
Schizophrenia
Bipolar disorder (manicdepressive illness)
Tourette’s syndrome
Prevention of emesis
Schizophrenia
Levodopa-induced psychosis
Adverse Effects
Additional Info/Contraindications
Extrapyramidal symptoms (EPS)
Acute dystonia
Parkinsonism
Akathisia
Tardive dyskinesia
DI: Anticholingergic drugs, CNS depressants,
Levodopa and direct dopamine receptor agonist
Toxicity: OD  HTN, CNS depression, EPS
Treatment for OD: IV fluids, α-adrenergic agonist,
gastric lavage (no emetics!)
Costs 10x LESS than SGAs
Angranulocytosis
Seizures
Diabetes, wt gain, myocarditis
Risk of metabolic effects
Less side-effects than 1st gen antipsychotics
Effects older pts w/ dementia (2x mortality)
Haloperidol decanoate
Long-acting, injectable formulations used for long-term maintenance therapy of schizophrenia
Fluphenazine decanoate
No evidence that depot preparations pose an increased risk of side effects
Risperidone microspheres
Altered distribution of ions
Bipolar disorder
Lithium toxicity (>1.5)
Altered synthesis of NE, serotonin, dopamine
Alcholism
GI, tremors, polyuria, renal
Mediates intracellular responses to neurotransmitters
Bulimia
toxicity, goiter, hypothyroidism,
Facilitate regeneration of damaged optic nerves
Schizophrenia
teratogenesis
↑ total gray matter in regions known to atrophy in BPD
Glucocorticoid-induced psych
Lithium excretion reduced when sodium level is low
Plasma level: 0.8-1.4 mEq/L
Monitor levels q 2-3 days initial & q 3-6 months
DI: diuretics, NSAIDs, anticholinergics
ANTIDEPRESSANTS
Most common psychiatric disorder
Incidence of depression in women is twice than in men.
Pathogenesis: caused by functional insufficiency of monoamine neurotransmitters
Treatment: Drugs, Depression-specific psychotherapy, Electroconvulsive therapy, Vagus nerve stimulation
Clinical Manifestations: Depressed mood, Loss of pleasure or interest, Insomnia (or sometimes
hypersomnia), Anorexia (or sometimes hyperphagia), Mental slowing and loss of concentration, Feelings
of guilt, worthlessness, helplessness, Thoughts of death and suicide, Overt suicidal behavior
Symptoms must be present most of the day, nearly every day, for at least 2 weeks
NI: ↑ suicide risk w/ drugs early in therapy; watch pts for: suicidality, ↓ mood, changes in behavior
Classes
Tricyclic
Antidepressants
(TCAs)
Individual Drugs
Amitriptyline
MOA
Block neuronal reuptake of NE
and serotonin
NOT IMMEDIATE (takes 6-12
wks for effects to be seen)
Fluoxetine [Prozac]
Selective
Serotonin
Reuptake
Inhibitors (SSRIs)
Sertraline [Zoloft]
Serotonin/NE
Reuptake
Inhibitors (SNRIs)
Monoamine
Oxidase Inhibitors
(MAOIs)
Selective inhibition of serotonin
reuptake
Blocks uptake of serotonin and
dopamine
CNS stimulation (minimal
effects on seizure threshold)
Venlafaxine [Effexor]
Duloxetine
[Cymbalta]
Blocks NE and serotonin uptake
Does not block cholinergic,
histaminergic, or alpha1adrenergic receptors
Isocarboxazid
Phenelzine
Tranylcypromine
Selegiline
Convert monoamine
neurotransmitters (NE,
serotonin, and dopamine) into
inactive products
Inactivate tyramine and other
biogenic amines
Electroconvulsive therapy
Used for pts who have failed to respond to drugs and severely depressed/suicidal pts
Daily 40-minute sessions for 6 weeks
AE: some memory loss of immediate events surrounding treatment, transient headaches and scalp
discomfort. Patients may also experience eye pain, toothache, muscle twitching, and seizures
Vagus nerve
Long-term therapy of treatment-resistant depression (when at least 4 antidepressant drugs failed
AE: hoarseness, voice alteration, cough, dyspnea
Therapeutic Uses
Adverse Effects
Additional Info/Contraindications
DOC for major depression
Bipolar disorder
Neuropathic pain
Chronic insomnia
Attention-deficit/hyperactivity
disorder
Panic disorder
Obsessive-compulsive disorder
Cardiac toxicity, seizures
Sedation
Orthostatic hypotension
Anticholinergic effects
Diaphoresis, sedation
Hypomania
“Yawngasm”
May increase risk of suicide early in treatment
DI: MAOIs, sympathomimetic drugs,
anticholinergics, CNS depressants
Toxicity: dysrhythmias, ↑HR, intraventricular
block, AV block, VT, VF
Treatment: gastric lavage, activated charcoal,
physostigmine (ACh), propranolol, phenytoin,
lidocaine (dysrhythmias)
Major depression
Obsessive-compulsive disorder
Bulimia nervosa
Premenstrual dysphoric
disorder
Serotonin syndrome: 2-72 hrs after trmt
(AMS, incoordination, tremor, fever)
Withdrawal syndrome, wt gain
Teratogenesis, bruxism, nausea, weight
gain, Sexual dysfunction
EPS, bleeding disorders,
Most commonly prescribed antidepressants
As effective as TCA, but no ↓ BP, sedation,
anticholinergic effects
OD does not cause cardiac toxicity
DI: MAOIs, Warfarin, TCAs
Major depression
Panic disorder
Obsessive-compulsive disorder
Post-traumatic stress disorder
Premenstrual dysphoric
disorder
Social anxiety disorder
Major depression
Generalized anxiety disorder
Social anxiety disorder (social
phobia)
2nd-3rd DOC for depression
Atypical depression
Headache, N/V
Tremor, nervousness, diarrhea
Insomnia, weight gain
Agitation, sexual dysfunction
Neonatal abstinence syndrome (NAS)
and persistent pulmonary hypertension
of the newborn (PPHN ) when used late
in pregnancy
Nausea, anorexia, sweating, somnolence
Nervousness, headache, diastolic
hypertension, insomnia
Weight loss/anorexia
Sexual dysfunction
Hyponatremia (in older adult patients)
Neonatal withdrawal syndrome
CNS stimulation
Orthostatic hypotension
Hypertensive crisis from dietary
tyramine
DI: MAOIs, Pimozide
DI: MAOIs
NO ALCOHOL
As effective as TCAs/SSRIs, but more dangerous
Drug Interactions:
Indirect-acting sympathomimetic agents,
Interactions secondary to inhibition of
hepatic MAO
Antidepressants: TCAs and SSRIs
Antihypertensive drugs
Meperidine
SEDATIVE-HYPNOTIC DRUGS
Drugs that depress CNS function
Primarily used to treat anxiety and insomnia
Distinction between antianxiety effects and hypnotic effects is often a matter of dosage
Hypnotics promotes sleep (higher doses)
Anxiety: most common psychiatric illness
Uncontrollable worrying that lasts +6 months
Treatment:
Non-drug (supportive therapy, cognitive, biofeedback, relaxation training)
Benzodiazepines, Buspirone
Barbiturates
(pg 3)
Benzodiazepines
(pg 3)
Drugs
MOA
Diazepam
Lorazepam
Alprazolam
Ultrashort-acting: Thiopental
Short- to intermediate-acting:
Secobarbital
Long-acting: Phenobarbital
Panic disorders
Palpitations, pounding heart, racing heartbeat; chest pain/discomfort, fizziness, lightheadedness,
sensation of SOB, feeling of choking, nausea, abdominal discomfort, derealization/depersonalization,
fear of losing control/dying, flushes, chills, tingling/numbness in hands
Treatment: cognitive behavioral therapy, antidepressants (SSRI, TCA, MAOI), benzodiazepines
Obsessive-compulsive disorder: persistent obsessions/compulsions
Treatment: behavioral therapy, drug therapy: SSRI, Clomipramine
Social anxiety disorder: intense, irrational fear that one might be scrutinized by others
Treatment: Psychotherapy, drug therapy
Therapeutic Uses
Adverse Effects
Additional Info/Contraindications
Block neuronal reuptake
of NE and serotonin
Effects: CNS, CV,
Respiratory
DOC for insomnia and anxiety
DOC for panic disorders
Induce general anesthesia
Seizure disorders, muscle
spasm, withdrawal from
alcohol
CNS depression
Anterograde amnesia
Sleep driving
Paradoxical effects
Respiratory depression
Abuse/use in pregnancy/lactation
Binds to the GABA
receptor–chloride
channel complex
CNS depression
Cardiovascular effects
Induction of hepatic drugmetabolizing enzymes
Seizure disorders
Induction of anesthesia
Respiratory depression, suicide,
abuse, hangover
Use in pregnancy, hyperalgesia,
paradoxical excitement
Exacerbation of intermittent
porphyria
Non-CNS depressant
Does not cause sedation
Dizziness, nausea, HA,
nervousness, lightheadedness,
excitement
Buspirone [Buspar]
DI: CNS depressants
Tolerance/Physical dependence (Low though)
Acute toxicity (treat with flumazenil)
DI: CNS depressants, interactions resulting from induction of
drug-metabolizing enzymes, chloral hydrate, meprobamate
Tolerance/Physical dependence
Rapid onset and brief duration
Acute toxicity: respiratory depression, coma, pinpoint pupils
Treatment: remove barbiturate, give O2
No abuse potential
Does not intensify effects of CNS depressants
Anxiolytic effects develop slowly
DI: Erythromycin, Ketoconazole, grapefruit juice
CNS/ADHD
ADHD in children
CNS stimulants, Atomoxetine (non-stimulant), Anti-depressants (TCA, Buproprion)
S/sx: inattention, hyperactivity, impulsivity, fidgety, unable to concentrate, present before 7yo, for 6 months
ADHD in adults
S/sx: poor concentration, stress intolerance, antisocial behavior, outbursts of anger, can’t maintain routine
CNS stimulants
↑ activity of CNS neurons
Enhance neuronal excitation
Can cause convulsions in sufficient doses
Drugs
Amphetamine -50:50 combo
of: Dextroamphetamine &
Levamphetamine
MOA
Therapeutic Uses
Adverse Effects
Release NE and DA
ADHD
Narcolepsy
CNS stimulation, wt loss
CV effects, psychosis
Tolerance: ↑ mood, ↓ appetite, stimulate heart and blood vessels
Physical dependence: abstinence syndrome w/ abrupt d/c
HIGH ABUSE POTENTIAL due to euphoria
Toxicity: dysrhythmias, HTN, dizziness, confusion, hallucinations,
convulsions, paranoia, coma, palpitations, cerebral hemorrhage
Trmt: Chlorpromazine (hallu), α-blocker (HTN), Diazepam
Reversible blockade of adenosine
receptors
Calcium permeability
Accumulation of cyclic AMP
Low doses: ↓ drowsiness/
fatigue and ↑ intellect use
Neonatal apnea
↑ wakefulness
Increasing doses: nervousness,
insomnia, tremors
Seizures with very large amounts
Readily absorbed from GI, peak w/i 1 hour, hepatic elimination
Toxicity: CNS & respiratory stimulation, ↑HR, sensory phenomena
↑ wakefulness
HA, nausea, nervousness, diarrhea,
rhinitis
DI: oral contraceptives, cyclosporine
ADHD in children
GI, ↓ appetite, dizzy, somnolence,
mood swings, trouble sleeping
No potential for abuse
DI: MAOIs, CYP2D8 (paroxetine, fluoxetine, quinidine)
Methylphenidate [Ritalin]
Methylxanthines:
Caffeine
Theophylline
Theobromine
Modafinil [Provigil, Alertec]
Atomoxetine
Additional Info/Contraindications
Influence hypothalamic areas
involved w/ sleep-wakefulness
cycle
Selective inhibitor of NE reuptake
Non-stimulant
CANCER
Women: Breast (most cases), Lung (most deaths)
Men: Prostate (most cases), Lung (most deaths)
Cancer staging: T(tumor), N(nodes), M(metastasis)
Treatment approaches:
Neoadjuvant – ↓ tumor size; given prior to surgery
Adjuvant – target minimal disease or micrometastases ↓ risk of recurrence; given after surgery
Conditioning – chemo/radiation to prep for marrow transplant
Anticancer drugs classes:
Cytotoxic (chemotherapy)– drugs that kill cells directly
Hormones and hormone antagonists – mimic/block actions of endogenous hormones
Biologic response modifiers - enhance immune attacks against cancer cells
Targeted drugs – drugs bind w/ specific molecular targets on cancer cells  ↓ tumor growth, ↑ cell
death
5 stage reproductive process – 50% cytotoxic drugs are cell-cycle phase (CCP) specific, 50% CCP non-specific
Gap 0: resting or dormant phase; non-proliferative
Gap 1: postmitotic phase; 1st phase of protein/RNA synthesis needed for cell division
Synthesis (S): DNA is replicated
Gap 2: premitotic (postsynthetic) phase; 2nd phase of protein/RNA synthesis. Prep for mitotic spindle
formation; cell is now prepared for division.
Mitosis (M): cell division occurs; shortest phase of the cell life cycle  two daughter cells result with exact
copies of the parent cell’s DNA
Growth fraction – proliferating cells/cells in G0
↑ GF = lots of proliferating cells
↓ GF = cells mainly in G0
CYTOTOXIC DRUGS MORE TOXIC TO CANCER W/ HIGH GF!!
EX: Bone marrow, skin, hair follicles, sperm, GI tract
Obstacles to chemo
Toxicity to normal cells (marrow, GI epithelium, hair, testes)
Cure needs 100% kill (1st order kinetics, unhelpful host defenses,
unclear treatment end date)
No truly early detection (metastases by time of discovery)
Solid tumors respond poorly (low GF, large tumors )
Drug resistance
Heterogeneity of tumor cells (drug responsiveness, growth rate, metastatic ability)
Limited drug access to tumor cells (poor vascularization, BBB)
Maximum benefits from chemo?
Intermittent chemo – normal cells repopulate
Combination chemo - ↓ drug resistance, ↑ cell kill, ↓ injury to normal cell
IDEALLY, rx should have different MOAs, minimal overlapping toxicities, good efficacy when used alone
Optimizing dosing schedules (drugs can act on specific phase of cell cycle
Regional drug delivery (intra-arterial, intra-thecal)
Toxicities of Chemotherapy
Myelosuppression  neutropenia (↑ infection), thrombocytopenia (↑bleed), anemia (↓ erythrocytes)
GI: N/V (CTZ), diarrhea, stomatitis (GI lining has high GF)
Alopecia, reproductive toxicity (fetus, testes), hyperuricemia, extravasation of vesicants, carcinogenesis
Breast cancer treatments
Surgery, radiation
Hormonal agents (antiestrogens, aromatase inhibitor)
Cytotoxic drugs – used before or after surgery; Doxorubicin + Cyclophosphamide + Paclitaxel
Bisphosphonates (Zoledronate, Pamidronate) or Denosumab – breast cancer can metastasize to bone
(most common site)  hypercalcemia/fractures
Targeted therapies – adjuvant treatments
Trastuzumab (Herceptin) – monoclonal Ab, binds to HER2 receptor  inhibit cell proliferation;
immune-mediated cell death
Lapatinib (Tykerb)
Prostate cancer treatments
Early stage: surgery, radiation, can be followed by ADT
Advanced stage: androgen deprivation therapy (ADT) – castration and/or drugs
GnRH agonists, GnRH antagonists, androgen receptor blockers, CYP17 inhibitors
S/E: ED, loss of libido, gynecomastia, reduced muscle mass, new-onset diabetes, MI, stroke
Patient-specific immunotherapy: Sipuleucel-T
Cytotoxic drugs – Docetaxel, cabazitaxel, estramustine
Targeted anticancer drugs
Kinase inhibitors – prevent phosphorylation shut down signaling pathway inhibit proliferation;
apoptosis
Others - can bind with specific antigens on tumor cells, inhibit angiogenesis, inhibit proteasomes etc.
Biologic response modifiers – alter host responses to cancer
Stimulates immune response (cytokines)
Selectively destroys cancer cells (monoclonal antibodies)
Purpose: curative, supportive (HGFs), adjunctive (↑ immune response to remaining malignant cells)
Types: Interferon α/β/γ, Interleukins, Hematopoietic growth factors, Monoclonal antibodies
S/E: chills, myalgias, skin changes, fatigue, altered mental status, fever, arthralgias, allergic reaction,
anorexia, hypotension
Indicators of AE: weight changes, intense inflammatory reaction, dyspnea, cardiac symptoms, excessive
fatigue, uncontrolled or unrelated fevers, dizziness, oliguria, allergic reactions
Hematopoietic growth factors
Applications: ↓ chemotherapy induced myelosuppression, stimulate hematopoiesis in marrow failure,
support cellular differentiation, support peripheral stem cell harvesting, enhance antibiotic therapy
EGF: Stimulation of erythrocyte production in patients undergoing myelosuppressive chemotherapy
G-CSF: Accelerate bone marrow recovery after autologous bone marrow transplant
TGF: Accelerate neutrophil and platelet repopulation after cancer chemotherapy
Other non-cytotoxic cancer drugs:
Glucocorticoids – cancer pts require high doses (*but serious S/E!)
Combo w/ other agents to treat lymphoid tissue cancers (direct toxic)
Other uses: ↓CNV, ↓ cerebral edema 2°to irradiation of the cranium, ↓ pain 2° to nerve compression
or edema, ↓ hypercalcemia in steroid-responsive tumors; ↑ appetite, ↑ weight gain
S/E: osteoporosis, adrenal insufficiency, ↑ infection risk, peptic ulcers, diabetes.
Thalidomide
Uses: MM, erythema nodosum leprosum
Cause severe birth defects
Retinoids, Alitretinoin, Bexarotene, Tretinoin, Arsenic trioxide, Denileukin diftitox, Lenalidomide,
Progestins
CYTOTOXIC DRUGS
Class
Alkylating agents
Subclass: drug
Nitrogen mustard:
Cyclophosphamide
Nitrosoureas:
Carmustine
Platinum
compounds
Cisplatin
Hypomethylating
agents
Antitumor ABX
Streptomyces
Mitotic
inhibitors
Topoisomerase
inhibitors
Misc cytotoxic
drugs
Nursing
Implications
Therapeutic Uses
CCP nonspecific
Alkylation of DNA  inhibit replication
Bifunctional > monofunctional agents
CL, Ovarian, breast
Hodgkin’s, NHL
Multiple myeloma
CNS tumor
HL, NHL, MM
CCP nonspecific
Produce cross-links in DNA
Ovarian, testicular, bladder, lung
Adverse Effects
Hemorrhagic cystitis
Sterility, Myelosuppression, N/V
Cardiotoxic in high doses
Additional Info/Contraindications
NI: Give early in the day, hydrate, monitor
for hematuria, void frequently (especially
HS)
Can cross BBB
Nephrotoxicity
Peripheral neuropathy, emesis,
electrolyte imbalance, ototoxicity
NI: Monitor I&O/Cr/BUN, hydrate, give
mannitol, Monitor Mg++, K++, give hearing
tests
Leucovorin rescue: high dose of
methotrexate (for metho-resistant cells) +
leucovorin (to save norms)  failure to
give timely leucovorin = LETHAL
HD, NHL, ALL, CNS, lung, breast,
head/neck tumors, gestational
choriocarcinoma
RA, Crohn’s, psoriasis
Pemetrexed
Combined with cisplatin for malignant pleural mesothelioma. NSCLC initial trmt w/ cisplatin, or single trmt after prior chemo
Cytarabine: All, AML, CML, CNS leukemia
CCP specific S-phase
Fluorouracil: colorectal, breast, pancreatic, & stomach
Pyrimidine analog:
Can be incorporated into DNA/RNA 
Cytarabine
Capecitabine: breast & metastatic colon cancer
disrupt fxn
Fluorouracil
Inhibit biosynthesis of pyrimidines,
Floxuridine: adenocarcinoma of GI tract with metastasis to liver, gallbladder, or bile duct
DNA/RNA
Gemcitabine: pancreatic, breast, ovarian & non-small cell lung-cancer
Purine analog: Mercaptopurine (ALL), Thioguanine (AML), Pentostatin (Hairy cell leukemia) Fludarabine (CLL) Cladribine (HCL), Nelarabine: T-cell ALL & T cell lymphoblastic lymphoma
Azacitidine
CCPS: S-phase. Drug is incorporated into DNA, inhibits DNA methyltransferase  apoptosis, normalizing differentiation/proliferation. Used for myelodysplastic syndrome
Decitabine
Red drug
Breast, prostate, ovarian, stomach,
Poor GI absorption, IV administration
CCP nonspecific
Severe Myelosuppression
bladder, thyroid, small cell lung
Stop infusion if pain, redness, infiltration.
Intercalation – insert drug molecule btw 2
Cardiotoxic (heart failure!)
Anthracyclines:
cancers, MM, HL, NHL, ALL, AML,
Call MD
DNA strands  can’t use DNA as template
Doxorubicin
Wilms tumor, lymphoma, sarcoma &
Vesicant agent
Cumulative lifetime dose <550 mg/m2
Disrupts topoisomerase II  strand
neuroblastoma
Alopecia
breakage (can’t repair)
Give with Dexrazoxane to protect heart
Liposomal: AIDS-related Kaposi
NI: Baseline/periodic ECHO’s
DOES NOT INJURE HEART
Malignant pleural effusion,
NI: Baseline PFTs
Nonanthracycline:
squamous cell cancer of head &
CCP-specific: G2 phase
Pulmonary toxicity
Must give first dose with first
Bleomycin
neck, cervical, vulvar, penile &
administration (anaphylaxis reaction
testicular cancers, HL, NHL
CI: ppl > 70 y.o.
Peripheral neuropathy (ft drop,
Vinca alkaloids:
ALL, HL, NHL, neuroblastoma,
Little myelosuppression  can combine
ileus, paresthesia), N/V
Vincristine
Wilms, rhabdomuosarcoma
with drugs that causes myelosuppression
CCP specific: M phase
Vesicant agent
Block assembly of microtubules
Testicular cancer, HL, Kaposi
Vinblastine
Myelosuppression
Harmless to peripheral nerves
sarcoma, histiocytosis, NHL, breast
Taxanes:
CCP specific: G2, M phase
Severe hypersensitivity
Metastatic breast & ovarian, NSCLC,
Pretreat hypersensitivity rxn w/ GCC,
Paclitaxel
Stabilize microtubules bundles  inhibit
AIDs related Kaposi
H1/H2 receptor antagonist
Alopecia
cell division  apop
Metastatic ovarian cancer, cervical,
CCP specific: S phase
Topetecan
Diarrhea
SCLC
Inhibit Topoisomerase I  DNA can’t
replicate correctly
Irinotecan
Metastatic colorectal cancer
Diarrhea
IV atropine can suppress early diarrhea
Etoposide
CCP specific: S, G2
Testicular cancer, SCLC
Hypotension, bronchospasm
Monitor BP
Converts asparagine into aspartic acid 
Asparaginase
ALL
can’t make proteins
Antineoplastic drugs are often mutagenic, teratogenic, and carcinogenic. AVOID DIRECT CONTACT. Use gloves (∆ q60m), gown, eye/face protection), flush toilet twice
NEVER administer chemo before: knowing pt’s height/weight, calculate pt’s body surface area with another nurse, check physician’s orders to ensure chemo dose is w/i acceptable guidelines with
another nurse, check labs pertinent to drug, review the protocol for drugs to be given, have signed chemo consents, patent IV or CVC, ensure good blood return, extravasation protocols?
Vesicants: IV admin < 1 hr – nurse must be present the whole time; > 1 hr need CVC; blood return must be checked q 2-3 ml of infusion for IV and q 4 hr for CVC; PT ON FLOOR IF INFUSING!
Folic acid analog:
Methotrexate
Antimetabolites
MOA
CCP specific: S-phase
Inhibits dihydrofolate reductase  can’t
activate FA  can’t replicate DNA
HORMONAL AGENTS
Class
Drug
MOA
Therapeutic Uses
Antiestrogens
Tamoxifen
Block estrogen receptors
Prevention and treatment of
breast cancer
Adjuvant therapy after surgery
Aromatase
inhibitor
Anastrozole
Block estrogen synthesis from adrenals
Breast cancer (in postmenopausal
women only)
GnRH agonist
Leuprolide
GnRH antagonist
Abarelix
Androgen
receptor blockers
Flutamide
CYP17 inhibitors
Abiraterone
Block androgen production
Others…
Sipuleucel-T
Patient-specific immunotherapy  cause
immune attack against prostate cancer
cells
Initial phase: ↑ release of interstitial cellstimulating hormone from pituitary  ↑
production of testosterone  “flare” of sx
Cont use: ↓ICSH release ↓testosterone
↓ production of androgens
Prevent cancer cells from undergoing ↑
stimulation during the initial phase of
GnRH therapy
Blocking the effects of adrenal and
prostatic androgens on prostate cells
Prostate cancer
Adverse Effects
Additional Info/Contraindications
Endometrial cancer
Thromboembolism
Hot flushes, fluid retention,
vaginal discharge, N/V,
menstrual irregularities
Musculoskeletal pain
Osteoporosis
Fractures
Thromboembolism (rarely)
Generally well tolerated
Hot flushes
Testosterone loss  bone
pain, urinary obstruction
Prostate cancer
Tumors need to have estrogen receptors to work
DI: fluoxetine, paroxetine, sertraline
SSRIs are strong inhibitors of CYP2D6, can
prevent tamoxifen activation  risk of breast
cancer recurrence
More effective than Tamoxifen
No risk of endometrial cancer
Cotreatment with androgen receptor blocker to
minimize S/E of testosterone loss
Does not produce initial tumor flare
Advanced androgen-sensitive
prostate cancer with castration
Gynecomastia
N/V
Diarrhea
Combo w/ prednisone to treat
metastatic castration-resistant
prostate cancer
Hypokalemia, joint swelling,
muscle discomfort
Hepatotoxicity
Each dose is custom made from the patient’s
own immune cells, collected by leukapheresi
TARGETED THERAPY
Class
EGFR-Tyrosine
Kinase Inhibitors
BCR-ABL Tyrosine
Kinase Inhibitors
Multi-Tyrosine
Kinase Inhibitors
mTOR Kinase
Inhibitor
CD20-drected
antibodies
Angiogenesis
inhibitor
Proteasome
inhibitors
Drug
Cetuximab
Imatinib
MOA
MAb that blocks the receptor portion of
EGFR-TK  ↓ cell growth; ↑ apoptosis
Blocks receptor portion of BCR-ABL-TK
Therapeutic Uses
Adverse Effects
Refractory colorectal cancer (non-KRAS
gene, head & neck
Infusion reactions
Acne-like rash
Interstitial lung disease
DOC for CML
N/V, diarrhea, rash, headache,
fever, musculoskeletal problems
Fluid retention (effuse, ascites)
Sorafenib: unresectable hepatocellular and advanced renal cell
Sunitinib: treatment of GIST after disease progression, advanced renal cell cancer, metastatic pancreatic neuroendocrine tumors
Pazopanib: advanced renal cell cancer
Vandetanib: locally advanced or metastatic multifocal medullary thyroid cancer
Termsirolimus: advanced renal cell cancer
Everolimus: breast cancer (combo w/ Exemestane), neuroendocrine pancreatic tumors, advanced renal cell, subependymal giant cell astrocytoma
Tumor lysis syndrome
MAb that binds to CD20 (membrane Ag)
Reactivation of Hepatitis B
Rituximab
B-cell NHL
 apoptosis, lethal attack on B cells
Severe infusion related
hypersensitivity reactions (SJ)
Impair wound healing
Combo
w/
5-FU:
colorectal
ca
↓ formation of new blood vessels 
Bevacizumab
HTN, hemorrhage, GI perforation,
deprive solid tumors of blood supply
Combo w/ Cisplatinum: NSCLC
thromboembolism, nephrotic syn
Intracellular multienzyme complexes
st
MM: 1 line after other therapies fail?
Weakness, nausea, diarrhea/constip
Bortezomib
that degrade proteins  ↓ cell viability,
Mantle cell lymphoma: 1 y therapy
↓PLT, anemia, neutropenia,
↑apoptosis, ↑ sensitivity XRT, chemo
Additional Info/Contraindications
Highly effective, well-tolerated
Inhibit cytochrome 450 pathway  ↑
warfarin!
DI: ketoconazole ↑ levels of drug
Active against wide variety of tumors
Inhibit growth (doesn’t kill existing cells)
Pregnancy Category C
BIOLOGIC RESPONSE MODIFIERS
Class
Interferon
Drug
Interferon alfa-2a
Interferon alfa-2b
MOA
Therapeutic Uses
↓ DNA & protein synthesis
↑ Ag on cancer cell surface  immune
system recognize the cancer cells
easier
↑ action of other cells in immune
system
Adverse Effects
Additional Info/Contraindications
Cancers: Kaposis, MM, renal
cell carcinoma, bladder, hairy
cell leukemia, CML, MM, NHL
Viruses: rhinovirus, HPV, Hep
C, Retrovirus, condyloma
Multiple sclerosis
Fever/chills, HA, malaise, myalgia, fatigue
GI: N/V, diarrhea, anorexia
CNS: paranoia, dizziness, confusion
CV: tachycardia
Hem: neutropenia, ↓ plt
Renal: ↑. BUN & creatinine
Pysch: depression, suicidal
Monitor CBC, renal function tests
Monitor VS at each visit
May need Tylenol for flu-like symptoms
Teach about fever patterns
Watch for depression, suicidal ideation!!
Assess baseline neuropsychiatric status
Renal cell carcinoma
Malignant melanoma
Colorectal cancer
Capillary leak syndrome (severe toxicity) 
edema
↑ fluid  CHF, arrhythmias, MI,
hypotensive, pulmonary edema
Fever/chills, rash, fatigue, HA, myalgia
Cross BBB  cerebral edema
(hallucinations, anxiety, HA)
Monitor fluid balance, I&O, weight gain, (2030 lbs) edema, breath sounds (rales)
Neurologic assessments!
Treat flu-like symptoms with Tylenol
DO NOT GIVE DIURETICS DESPITE EDEMA
Give basic IVF to ↑ BP, UOP. If that fails, then
give 250-500 ml of NS bolus.
Interleukin
Aldesleukin
↑ NK cell, TNF production 
recognizes cancer cells as non-self,
ignores normal cells  destroys cancer
cell
Increases production of B lymphocytes
GCSF
Filgrastim
↑ WBC production
Cancer, chronic neutropenia
WBC > 15K: bone pain, leukocytosis
Erythropoietin
Epoetin-alfa
↑ RBC production
CRF, Chemo anemia, HIV
Hg >12 mg/dl: ↑ risk of DVT, HTN, CV
Thrombopoiesis
Oprelvekin
↑ PLT production
↓ thrombocytopenia
↓ need for PLT transfusion
Fluid retention, cardiac dysrhythmia
Anaphylaxis, sudden death
Give SQ, IV, intrapleral, intraperitoneal
Can accelerate tumor progression/shorten life
USE WITH CAUTION IN PATIENT’S WITH BONE
MARROW CANCER
TYPE OF CANCERS
TREATMENT DRUGS (e.g…)
Hodgkin’s lymphoma (HL)
Cyclophosphamide, Doxorubicin, Bleomycin, Vincristine, Vinblastine,
Non-hodgkin’s lymphoma (NHL)
Cyclophosphamide, Interferon, Vinblastine, Vincristine
Multiple myeloma
Cyclophosphamide, Carmustine, interferon
CNS tumor
Carmustine (crosses BBB)
Kaposi sarcoma
Doxorubicin (liposomal), Vinblastine, Interferon
Burkitt’s lymphoma
Cyclophosphamide, Vincristine, Methotrexate, Doxorubicin, Prednisone
Choriocarcinoma
Methotrexate, Leucovorin
Non-small cell cancer of lung (NSCLC)
Paclitaxel, Gemcitabine, Pemetrexed
Small cell cancer of lung (SCLC)
Topetecan, Etoposide, Cisplatin, Carboplantin
Wilm’s tumor
Dactinomycin, Vincristine, Doxorubicin, Cyclophosphamide
Eqing’s sarcoma
Cyclophosphamide, Doxorubicine, Vincristine, Etoposide, Ifosfamide
Acute myeloid leukemia
Daunorubicin, Cytarabine, Etoposide
Breast cancer
Fluorouracil, Doxorubicin, Capecitabine, Cyclophosphamide, Paclitaxel, Tamoxifen, Toremifene, Raloxifene, Fulvestrant, Anastrozole, Letrozole, Exemestane
Prostate cancer
Leuprolide, Triptorelin, Goserelin, Abarelix, Degarelix, Flutamide, Bicalutamide, Nilutamide, Abiraterone, Sipuleucel-T, Ethinyl estradiol, Estramustine, Megestrol acetate
Testicular cancer
Cisplatin, Etoposide, Bleomycin, Vinblastine
Ovarian cancer
Cyclophosphamide, Cisplatin
Colorectal cancer
Fluoroouracil, Leucovorin, Oxaliplatin, Interleukin, Irinotecan
Acute lymphocytic leukemia
Vincristine, Prednisone, Asparaginase, Daunorubicin, Doxorubicin, Cyclophosphamide
IMMUNIZATIONS
Adverse Effects of Vaccines
Vaccines are generally very safe; Mild reactions common, Severe reactions rare
Immunocompromised children are at special risk from live vaccines
Immunocompromised pts: congenital immunodeficiency, HIV infection, leukemia, lymphoma, generalized
malignancy, therapy with radiation, cytotoxic anticancer drugs, high-dose glucocorticoids
Vaccine Adverse Event Reporting System (VAERS) & the National Vaccine Injury Compensation Program
Live vaccines: MMR, Varicella, Nasal spray Flu, Rotavirus, oral poliovirus vaccine
Pregnancy CI: MMR, Varicella, HPV
Immune responses
Natural immunity – innate; skin, phagocytic
cells, NK cells
Specific acquired immunity (occur after
exposure)
Cell mediated – cytolytic T cells, macrophages
Antibody-mediated: humoral
Opsonization
Immune system cells
B lymphocytes – make antibodies; made in
bone marrow
Cytolytic T cells (CD8 cells) – attack and kill
target directly; cells mature in thymus
Helper T cells (CD4 cells) – antibody production by B cells; release factors that ↑ delayed-type
hypersensitivity; activate cytolytic T cells; required for effective immune response
Macrophages – phagocytosis; required for activation of T cells (Th and Tc); final mediators of DTH
Cytokine – any mediator, communicator molecule (that isn’t an antibody)
Immunizations – purpose to protect against infectious diseases; create highly immune population.
b/c of vaccines  ↓diphtheria, rubella, mumps, pertussis, tetanus, measles, polio, smallpox
Vaccine: ↑ antibody synthesis against bacteria & viruses; toxoids ↑ Ab synthesis against toxins bacteria
produce (but not against bacteria themselves)
Killed vaccines: composed of whole, killed microbes or isolated microbial components
Live vaccines: composed of live microbes that have been weakened or rendered completely avirulent
Vaccination: administration of any vaccine or toxoid; produces active immunity; antibodies develop over
weeks to months & then persist for years
Passive immunity: conferred by administering preformed antibodies (Ig). Protection is immediate but lasts
only as long at the antibodies remain in the body.
Specific Ig: contain a high [Ab] directed against a specific antigen (e.g. Hep B), made from donated blood
Contraindications (do not administer vaccine if…)
Anaphylactic rxn to a specific vaccine  contraindicates all further doses of that vaccine
Anaphylactic rxn to a vaccine component  contraindicates all vaccines that contain that component
Moderate to severe illnesses with or without a fever
Not a contraindication
Mild to moderate local reaction (soreness, erythema, swelling) following a dose of an injectable vaccine
Mild acute illness with or without low-grade fever
Diarrhea
Current antimicrobial therapy
Convalescent phase of illness
Prematurity (same dosage & indications as for normal full term infants)
Recent exposure to an infectious disease
Personal or family history for either penicillin allergy or nonspecific allergies
Go to: www.cdc.gov/vaccines for information about immunization schedules
Target Diseases
Measles, Mumps, Rubella, Diphtheria, Tetanus (lockjaw), Pertussis (whooping cough), Poliomyelitis (polio or
infantile paralysis), Haemophilus influenzae type B, Varicella (chickenpox), Hepatitis B, Hepatitis A,
Pneumococcal infection, Meningococcal infection, Influenza, Rotavirus gastroenteritis, Genital human
papillomavirus infection
Annual influenza vaccination is recommended for all children age 6 months to 18 years.
All infants should receive Hep B w/i 12 hours of birth
ANEMIA
Iron deficiency - Results from an imbalance in iron uptake and iron demand
Causes: Pregnancy (blood volume expansion), Infancy and early childhood, Chronic blood loss
Consequences: Microcytic, hypochromic anemia
Definition: Decrease in the number, size, or hemoglobin content of erythrocytes
Causes: blood loss, hemolysis, bone marrow dysfunction
Red blood cell development
Begins in the bone marrow, matures in the blood
Needs: healthy bone marrow erythropoietin, iron, and other factors to support DNS synthesis
Class
Oral Iron
Parenteral Iron
Vitamin B12
Individual Drugs
Ferrous sulfate
Ferrous gluconate
Iron Dextran
Sodium ferric gluconate
Iron sucrose (Venofer)
Ferumoxytol
Cyanocobalamin
Vitamin B12 deficiency
Causes: impaired absorption, regional enteritis, celiac disease, absence of intrinsic factor
Consequences: megaloblastic (macrocytic) anemia, neurologic injury, GI disturbances
Folic Acid deficiency – FA is an essential factor for DNA synthesis; absorbed in early segment of small intestine
Causes: poor diet (alchoholics), malabsorption secondary to intestinal disease
Consequence: megaloblastic (macrocytic) anemia, neural tube defects in developing fetus
Expecting moms should take 400-800 mcg of folate daily
Therapeutic Uses
DOC of Iron-deficiency anemia
Prophylactic therapy
For pts who have experienced intolerable/ineffective oral dosing
Iron deficiency anemia in CKD pts
Only pts undergoing chronic hemodialysis
Iron deficiency anemia in CKD pts
Vitamin B12 deficiency (give FA too if deficiency is severe)
Adverse Effects
GI disturbances, Staining of teeth
Toxicity
Anaphylactic reactions, ↓ BP
Low risk of anaphylaxis
Hypotension, cramps
Hypokalemia
Additional Info/Contraindications
DI: Antacids, Tetracycline, Ascorbic acid
Persistent pain with IM injection
All pts must also receive erythropoietin
Requires only 2 doses
IM injections administered monthly