SIMVASTATIN (GN)

C: anti hyperlipidemic
I: To treat hyperlipidemia; To treat homozygous familial hypercholesterolemia; To
treat adolescent heterozygous familial hypercholesterolemia
MOA: Interferes with the hepatic enzyme hydroxymethylglutaryl-coenzyme A
reductase. This action reduces the formation of mevalonic acid, a cholesterol
precursor, thus interrupting the pathway necessary for cholesterol synthesis.When the
cholesterol
level declines in hepatic cells, LDLs are consumed, which in turn reduces the levels of
circulating total cholesterol and serum triglycerides.
HMG-CoA reductase (or 3-hydroxy-3-methyl-glutaryl-CoA reductase orHMGCR) is the
rate controlling enzyme (EC 1.1.1.88& EC 1.1.1.34) of the mevalonate pathway,
the metabolic pathway that produces cholesterol and otherisoprenoids.
SE: Nausea (eat frequent small meals); headache, muscle and joint aches and pains
(may lessen); sensitivity to light (use a sunscreen and wear protective clothing).
AE: severe GI upset, changes in vision, unusual bleeding or bruising, dark urine or lightcolored stools, fever, muscle pain, or soreness.
NSG I:
1. Assess
2. Take drug in the evening. Do not drink grapefruit juice while using this drug.
3. Give in the evening; highest rates of cholesterol synthesis are between
midnight and 5 AM.

CARVEDILOL (GN)
C: Antihypertensive, heart failure treatment adjunct
I: To control hypertension; As adjunct to treat mild to severe heart
failure of ischemic or cardiomyopathic origin
MOA: Reduces cardiac output and tachycardia, causes vasodilation, and decreases
peripheral vascular resistance, which reduces bloodpressure and cardiac
workload.When given for at least 4 weeks, carvedilol reduces plasma renin activity.
Competitively blocks alpha-, beta-, and beta2-adrenergic receptors and has
some sympathomimetic activity at beta2-receptors. Both alpha and beta blocking
actions contribute to the BP-lowering effect; beta blockade prevents the reflex
tachycardia seen with most alpha-blocking drugs and decreases plasma renin activity.
Significantly reduces plasma renin activity.
Carvedilol is used for treating high blood pressure and congestive heart failure.
It is related to labetalol (Normodyne, Trandate). Carvedilol blocks receptors of
the adrenergic nervous system, the system of nerves in which adrenalin
(epinephrine) is active. Nerves from the adrenergic system enter the heart and
release an adrenergic chemical (norepinephrine) that attaches to receptors on
the heart's muscle and stimulates the muscle to beat more rapidly and
forcefully. By blocking the receptors, carvedilol reduces the heart's rate and
force of contraction and thereby reduces the work of the heart. Carvedilol also
blocks adrenergic receptors on arteries and causes the arteries to relax and the
blood pressure to fall. The drop in blood pressure further reduces the work of
the heart since it is easier to pump blood against a lower pressure. The FDA
first approved carvedilol in 1995.
AE: difficulty breathing, swelling of extremities, changes in color of stool or urine, very
slow heart rate, continued dizziness.
SE: Depression, dizziness, light-headedness (avoid driving or performing dangerous
activities; getting up and changing positions slowly may help ease dizziness).
NSG I:

1. Monitor for orthostatic hypotension and provide safety precautions

2. Give with food to decrease orthostatic hypotension and adverse effects
Do not discontinue drug abruptly after chronic therapy (hypersensitivity
to catecholamines may have developed, causing exacerbation of angina, MI,
and ventricular arrhythmias); taper drug gradually over 2 wk with
monitoring.

NICORANDIL
C: anti anginal
I: angina *chest pain
MOA: Nicorandil relaxes coronary vascular smooth muscle by stimulating guanylyl
cyclase and increasing cyclic GMP (cGMP) levels (as shown first in our laboratory) as
well as by a second mechanism resulting in activation of K+ channels and
hyperpolarization Nitrate: Nicorandil stimulates guanylate cyclase to increase
formation of cyclic GMP (cGMP).[6] cGMP activates protein kinase G (PKG) which
phosphorylates and inhibits GTPase RhoA and decreases Rho-kinase activity.[6]
Reduced Rho-kinase activity permits an increase in myosin phosphatase activity,
decreasing the calcium sensitivity of the smooth muscle.[6] PKG also activates the
sarcolemma calcium pump to remove activating calcium.[7] PKG acts on K+ channels
to promote K+ efflux and the ensuing hyperpolarization inhibits voltage-gated calcium
channels.[5] Overall, this leads to relaxation of the smooth muscle and coronary
vasodilation.
K+ATP channel opener: Nicorandil activates K+ATP channel, causing K+ efflux. This
hyperpolarizes the cell, which inactivates voltage-gated calcium channels and reduces
free intracellular Ca2+.[5]
The effect of nicorandil as a vasodilator is mainly attributed to its nitrate property.[5]
Yet, nicorandil is effective in cases where nitrates, such as nitroglycerine, are not
effective.[5] Studies show that this is due to its K+ATP channel agonist action which
causes pharmacological preconditioning and provides cardioprotective effects against
ischemia.[5] Nicorandil activates K+ATP channels in the mitochondria of the
myocardium, which appears to relay the cardioprotective effects, although the
mechanism is still unclear.
AE: mouth sores; sore throat, fever, chills; swelling of the hands or feet; irregular
heartbeat, chest pains; swelling of the face, eyes, lips or tongue; difficulty breathing.
SE: flushing, palpitations, weakness and vomiting.
Most Common- Headache, dizziness, drowsiness, nausea, vomiting, flushing, weakness
and rectal bleeding.
Heart- Fast heart rate and low blood pressure.
Miscellaneous- Rash, abnormal liver function, mouth ulcer and muscle pain.
NSG I:
1.
2.
3.

Monitor blood pressure causes hypotension ,

Maybe taken with/out food
Ensure safety

METIMAZOLE
C: Antithyroid
I: hyperthyroidism
MOA: Grave's disease is the most common cause of hyperthyroidism. Grave's
disease is an autoimmune disease resulting from antibodies that attach to
receptors on thyroid hormone-producing cells in the thyroid gland and trigger
overproduction of thyroid hormone. An enzyme (peroxidase) produces thyroid
hormones, i.e., thyroxine (T4) and triiodothyronine (T3), by combining iodine
with a protein called thyroglobulin. Methimazole prevents iodine and peroxidase
from their normal interactions with thyroglobulin to form T4 and T3. This action
decreases thyroid hormone production. Methimazole also interferes with the
conversion of T4 to T3. Since T3 is more potent than T4, this also reduces the
activity of thyroid hormones.
Directly interferes with thyroid hormone synthesis in the thyroid gland by
inhibiting iodide incorporation into thyroglobulin. iodination of thyroglobulin is an
important step in synthesizing the thyroid hormones thyroxine and
triiodothyronine. Eventually, thyroglobulin is depleted and the circulating
thyroid hormone level drops.
AE: CNS: Drowsiness, headache, paresthesia,
vertigo
CV: Edema
EENT: Loss of taste
ENDO: Hypothyroidism
GI: Diarrhea, indigestion, nausea, vomiting
HEME: Agranulocytosis, aplastic anemia,
leukopenia, thrombocytopenia
MS: Arthralgia, myalgia
SKIN: Alopecia, jaundice, pruritus, rash, skin discoloration, urticaria
Other: Lupus-like symptoms, lymphadenopathy
NSG I:
Closely monitor thyroid function test results during methimazole therapy.
Check CBC results to detect abnormalities caused by inhibition of myelopoiesis.
Watch for signs and symptoms of hypothyroidism, such as cold intolerance,
depression, and edema.
Instruct patient to take drug with meals to avoid adverse GI reactions.
Explain about possible hair loss or thinning during and for months after therapy.
Instruct patient to notify prescriber immediately about cold intolerance, fever,
sore throat, tiredness, and unusual bleeding or bruising

CEFIXIME
rd
C: 3 gen cephalosporin
I: infections of the middle ear (otitis media), tonsillitis, throat infections
(pharyngitis), laryngitis, bronchitis, and pneumonia caused by susceptible
bacteria. It also is used for treating urinary tract infections and gonorrhea as
well as acute bacterial bronchitis in patients with chronic obstructive pulmonary
disease (COPD).
MOA: Interferes with bacterial cell wall synthesis by inhibiting the final step in the
crosslinking of peptidoglycan strands. Peptidoglycan makes cell membranes rigid
and protective. Without it, bacterial cells rupture
and die.
AE: CNS: Chills, fever, headache, seizures
CV: Edema
EENT: Hearing loss
GI: Abdominal cramps, diarrhea, elevated liver function test results, hepatic
failure, hepatitis, hepatomegaly, jaundice, nausea, oral candidiasis,
pseudomembranous colitis, vomiting
GU: Elevated BUN level, nephrotoxicity, renal failure, vaginal candidiasis
HEMEEosinophilia, hemolytic anemia, hypoprothrombinemia, neutropenia,
thrombocytopenia, unusual bleeding
MS: Arthralgia
RESP: Dyspnea
SKIN: Ecchymosis, erythema, erythema multiforme, pruritus, rash, StevensJohnson syndrome, toxic epidermal necrolysis
Other: Anaphylaxis, angioedema, facial edema, superinfection
NSG I:
1. Give drug with food or after meals if GI upset occurs.
2. Assess for signs of superinfection, such as perineal itching, fever, malaise,
redness, pain, swelling, drainage, rash, diarrhea, and cough or sputum
changes.
3. Assess for pharyngitis, ecchymosis, bleeding, and arthralgia; they may
4. Inform patient that yogurt and buttermilk can help maintain intestinal
flora and decrease diarrhea.

ALPRAZOLAM (XANOR)
C: Benzodiazepine, anxiolytic
I: Management of anxiety disorders, short-term relief of symptoms of anxiety; anxiety
associated with depression.
Treatment of panic attacks with or without agoraphobia
Unlabeled uses: Social phobia, premenstrual syndrome, depression
MOA: Alprazolam is an anti-anxiety medication in the benzodiazepine family, the same
family that includes diazepam(Valium), clonazepam (Klonopin), lorazepam (Ativan),
flurazepam (Dalmane), and others. Alprazolam and other benzodiazepines act by
enhancing the effects of gamma-aminobutyric acid (GABA) in the brain. GABA is a
neurotransmitter (a chemical that nerve cells use to communicate with each other)
that inhibits activity in the brain. It is believed that excessive activity in the brain may
cause anxiety or other psychiatric disorders.
SE: : Drowsiness, dizziness (may lessen; avoid driving or engaging in other dangerous
activities); GI upset (take drug with food); dreams, difficulty concentrating, fatigue,
nervousness, crying (reversible).
AE: chest pain, hypotension, diarrhea, irritability, ECG changes, tachycardia,
palpitations, blurred vision, diaphoresis
NSG I:

1. Hypersensitivity
2. Skin color, t, orientation, reflexes, affect, ophthalmic exam, p, bp, abdomen
3.
4.
5.
6.

exam, bowel sounds, cbc ,lfts

Warn stopping drug abruptly>withdrawal symptoms
Avoid alcohol
Avoid activities that require mental alertness
Eat with meals

ROSUVASTATIN (GN)
C: anti hyperlipidemic
I: To treat hyperlipidemia; To treat homozygous familial hypercholesterolemia; To
treat adolescent heterozygous familial hypercholesterolemia
MOA: Interferes with the hepatic enzyme hydroxymethylglutaryl-coenzyme A
reductase. This action reduces the formation of mevalonic acid, a cholesterol
precursor, thus interrupting the pathway necessary for cholesterol synthesis.When the
cholesterol level declines in hepatic cells, LDLs are consumed, which in turn reduces
the levels of circulating total cholesterol and serum triglycerides.
HMG-CoA reductase (or 3-hydroxy-3-methyl-glutaryl-CoA reductase orHMGCR) is the
rate controlling enzyme (EC 1.1.1.88& EC 1.1.1.34) of the mevalonate pathway,
the metabolic pathway that produces cholesterol and otherisoprenoids.
SE: Nausea (eat frequent small meals); headache, muscle and joint aches and pains
(may lessen); sensitivity to light (use a sunscreen and wear protective clothing).
AE: severe GI upset, changes in vision, unusual bleeding or bruising, dark urine or lightcolored stools, fever, muscle pain, or soreness.
NSG I:
1. Assess
2. Take drug in the evening.
3. Do not drink grapefruit juice while using this drug. Give in the evening;
highest rates of cholesterol synthesis are between midnight and 5 AM.