I3 TEST 1 - PHARMACOLOGY

Drug
Aspirin
(acetylsalicylic
acid)

Therapeutic Use
Low dose: protection against
cardiovascular disease
Platelet aggregation
protection (MIs, strokes, etc.)

Mechanism of Action
Non-selective irreversible
inhibitor of COX-1/2.
For COX-1, alters active
binding site to prevent
substrate entry.

Drug/Drug
Interactions
Probenecid blocks
elimination.

Inflammatory bowel disease

See also NSAID uses.

Salicylate

Cogener for aspirin.

See aspirin.

Ibuprofen (Advil)

NSAID

Naproxen (Aleve)

Low dose: analgesia (pain

relief), antipyretic (fever
reducer)

Reversible competitive
inhibitor of COX-1/2.
Inhibition of prostaglandin
synthesis.

Indomethacin
(Idocin)

High dose: antiinflammation, closure of

patent ductus arteriosus for
newborns circulation

Interacts with lithium

and fluconazole drugs.
Compete against the
protective effects of
low-dose aspirin.
Adverse effects with
ACE inhibitor (HT
drug)

Adverse Effects

Phys. Disposition
(ADME)
- Contraindicated in
Aspirin hydrolyzed in
children with fever due
plasma to salicylate.
to virus (may cause
Conjugated by
Reyes syndrome).
glutathione, glucoronic
- GI bleeding/uclers
acid, and sulfate
- Analgesic nephropathy, eliminated renally.
progressive renal failure
- Hepatic injury
- Respiratory and
metabolic acidosis if at
toxic levels.
More adverse effects
Metabolized by CYP
than aspirin.
GI discomfort and stress Acidic so well absorbed.
hemorrhage and
perforation.
Renal excretion,
extensively metabolized,
Analgesic nephropathy
undergo EH circulation.
Postpartum hemorrhage
for pregnant users (also
prolonged gestation and
inhibition of labor)

May reduce risk for colon

cancer.

Found in synovial fluid

(useful for joint pain)
Naproxen has longer
half-life than ibuprofen.

Celecoxib

NSAID
(anti-inflammation)

Inhibits COX-2

Misoprostol

Prevents peptic ulcers that

result from NSAIDs

Heparin

Anti-coagulant

PGE1analog (replaces lost

PGs in GI from
NSAIDs/COX inhibition)
Catalysts for antithrombin
III inhibition of both
thrombin and FXa.

Prevent PE, DVT; acute MI,

Highly protein bound

Cardiovascular disease
(uncontrolled platelet
aggregation).
Black box warning.

Protamine sulfate
antagonist.

- Bleeding
- Hypersensitivity
(sometimes)

Not easily absorbed

because large IV or
subcutaneous injection.

Drug

Therapeutic Use
unstable angina; prevent
thrombosis in extracorporeal
devices

Enoxaparin
(Lovenox)

Anti-coagulant
Prevent DVT,
thromboembolism, Pts with
HIT

Fondaparinux
(Arixtra)

Anti-coagulant
Prevent PE, DVT;
thromboprophylaxis for Pts
undergoing hip/knee surgery,
Pts with HIT

Dabigatran
(PRADAXA)

Anti-coagulant

Rivaroxaban
(Xarelto)
Apixaban
(Eliquis)
Warfarin
(Coumadin)

Anti-coagulant
Anti-coagulant
Anti-coagulant

Mechanism of Action

Drug/Drug
Interactions

- Transient
thrombocytopenia
- Heparin-induced
thrombocytopenia
- Contraindications:
history of
hypersensitivity to
heparins, active
bleeding, threatened
abortion, surgical
procedures in general,
infective endocarditis
- Bleeding
- Hypersensitivity
(sometimes)
- Transient
thrombocytopenia
See above for
contraindications.
- Bleeding
- Hypersensitivity
(sometimes)
- Transient
thrombocytopenia
See above for
contraindications.

Long chains wrap

thrombin and antithrombin together.

Catalysts for antithrombin

III inhibition of FXa (cant
wrap around thrombin).

Catalysts for antithrombin

III inhibition of FXa:
synthesized
pentasaccharide mimics
the binding site on
antithrombin III,
enhancing FXa binding
and inhibition.
Inhibits FII (thrombin) via
blocking active site

Inhibits FXa via blocking

active site
Indirect inhibition of FXa
active site
Vitamin K analog
inhibits VKOR prevents

Adverse Effects

Transported by Pglyocoprotein (drugs

that inhibit PGP will
enhance dabigatran,
drugs that induce will
inhibit)

Phys. Disposition
(ADME)
Does not cross into
placenta.
Must routinely monitor
Pt. because drug is
mixture of
unfractionated peptides.

Subcutaneous injection

Oral dose

Bleeding

Administered as
dabigatran etexilate
(prodrug).

Bleeding

Metabolized by CYP3A4

Bleeding
MANY. See last page.

Bleeding

100% bioavailable;
highly bound to plasma

Drug

Therapeutic Use

Mechanism of Action

Drug/Drug
Interactions

Gla modifications in
clotting factors factors
inactive

Adverse Effects
Pro-cogulative states
(inhibition of protein C
and S)

Can be overcome by
excess Vitamin K.

Phys. Disposition
(ADME)
protein; long half-life.
Extensively metabolized
(CYP-2C9), excreted in
urine.
Crosses placenta can
be teratogen.

Desirudin

Anti-coagulant

Bivalrudin

Anti-coagulant

Agratroban

Anti-coagulant

Clopidogrel
(Plavix)

Anti-coagulant (anti-platelet)
Use with Pt who are allergic
to aspirin or need synergic
effect with aspirin.

Aspirin

Anti-coagulant (anti-platelet)

Abciximab

NSAID
Anti-coagulant (anti-platelet)

Cortisol

Anti-inflammatory steroid;
immuno-suppressant

Direct acting inhibitor of

thrombin
Direct acting inhibitor of
thrombin
Direct acting inhibitor of
thrombin (blocks catalytic
active site)
Irreversibly binds to
P2Y12 receptor no
ADP activation of platelet
aggregation

No TXA2 formation.
No hemostasis (platelet
change initiation).
Ig that inhibits GP2b/3a
receptor on platelets no
fibrinogen binding no
aggregation
- Inhibit phospholipase A2
(AA mobilization) via
increased synthesis of
annexin-1
- Decrease production of
PG and LT
- Inhibit COX-2 upregulation/synthesis
- Decrease TNF-
production by inhibiting

Rash, diarrhea,
abdominal pain,
dyspepsia, bleeding,
thrombotic
thrombocytopenia

Well absorbed;
extensive metabolism by
liver; 8 hr half life; urine
and fecal elimination

See above.

See above.

Needs to get
metabolized to be active.
See above.

May cause
hypertension because
also interacts with
mineralcorticoid
receptor with high
affinity.
(Licorice has
glycyrrhizic acid
which inhibits 11HSD 2 from

Abrupt cessation of
therapy acute adrenal
insufficiency (fever,
myalgia, arthralgia,
malaise).

Fat soluble, go through

membranes. Prepared as
nasal sprays, inhalers,
topical, injectable,
sprays well absorbed.

High doses: HPA

suppression,
hypertension,
hyperglycemia,

Inactivated by liver
conjugation into inactive
metabolites, excreted in
liver

Drug

Therapeutic Use

Mechanism of Action
NFB (TNF-
transcription factor)

Prednisolone

Dexamethasone

Aldosterone
Flurocortisone

Chlorpheniramine
(Chlortrimeton)
Diphenhydramine
(Benadryl)
Dimenhydrinate
(Dramamine)

Anti-inflammatory steroid;
immuno-suppressant

Anti-inflammatory steroid;
immuno-suppressant
Diagnose causes of
hypercorticism
Mineralcorticoid (low blood
pressure)
Replacement therapy of
mineralcorticoid (low blood
pressure, aldosterone
deficiency)

Anti-histamine (1
generation)

st

Allergic rhinitis,
conjunctivitis, itching, atopic
& contact dermatitis,
urticaria, drug reactions,
motion sickness, local

Cortisol analog with

intermediate half life (4x
more potent)

Drug/Drug
Interactions
regulating high
cortisol levels.)

See Cortisol.

Cortisol analog with longer See Cortisol.

half life (25x more potent)

Adverse Effects
increased susceptibility
to infection, peptic ulcer
disease, osteoporosis,
osteonecrosis,
myopathy,
cataracts,behavior
disturbance, growth
suppression, Cushings
syndrome
See Cortisol.

See Cortisol.

Phys. Disposition
(ADME)
Use the lowest dose
possible to achieve
desired result because
not specific/curative.

See Cortisol.
Active ingredient for
prednisone. If Pt has
hepatic failure,
administer prednisolone
straight.
See Cortisol.

Retains Na+
Retains Na+ (125x
potency)

Inverse agonists to H1
receptor on smooth
muscle, endothelial
vessels, and CNS.

Depression drugs
inhibit MAO more
histamine
accumulation

Sodium and water

retention, high blood
pressure, edema, low
potassium, muscle
weakness, fatigue,
increase susceptibility to
infection, peptic ulcer,
cataracts, hyperglycemia
Impairment of alertness,
cognition, learning,
memory, and
performance. Sinus
tachycardia, reflex
tachycardia,
antimuscurinic effects
(pupil dilation, blurred

Moderate glucocorticoid
potency.
Fat soluble, go through
membranes. Well
absorbed.
Hepatic metabolism.
Liposoluble, well
absorbed. Metabolized
by liver. Renal
excretion.
Crosses placenta and
breast milk.
Penetrates BBB anti-

Drug

Therapeutic Use

Mechanism of Action

Drug/Drug
Interactions

anesthetic, insomnia, some

symptom relief for colds

Loratadine
(Claritin)
Cetirizine
(Zyrtec)
Fexofenadine
(Allegra)

Anti-histamine (2nd
generation)

Adverse Effects
vision, dry eyes, dry
mouth, urinary retention,
constipation, ED),
fatality in young
children

Inverse agonists to H1
receptor on smooth muscle
and endothelial vessels

Allergic rhinitis,
conjunctivitis, itching, atopic
& contact dermatitis,
urticaria, drug reactions

Depression drugs
inhibit MAO more
histamine
accumulation

Contraindicated for
people with glaucoma,
prostatic hypertrophy,
impaired renal function,
elderly (impairs their
cognition), pregnant and
lactating women,
neonates, infants and
young children.
Even 30x overdose has
not seen any adverse
effects or fatality!
Contraindicated for
pregnant and lactating
women.

Phys. Disposition
(ADME)
Ach and sedation.

Liposoluble, well
absorbed. Metabolized
by liver. Renal
excretion.
Crosses placenta and
breast milk.
Differences:
Does not penetrate BBB,
longer lasting, some
metabolized by CYP3A4
Cetirizine is metabolite
of hydroxyzine.
Fexofenadine excreted
by bile and abs is
inhibited by some fruit
juices.

Cromolyn sodium
(Nasalcrom)

Mast cell stabilizer

Blocks ion channels on

mast cells directly
inhibits degranulation
no histamine release

ADVERSE EFFECTS OF WARFARIN.

1.
Phenobarital induces microsomal enzymes that increase warfarin metabolism
2.
Sulfinpyrazone inhibition of CYP-450 will cause inhibition of warfarin metabolism
3.
Decrease of binding to plasma protein-sulfonamides increase in free warfarin
4.
Aspirin interference with normal platelet function intensified anticoagulation function
5.
Cholestyramine binds to warfarin and inhibits absorption in GI