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1.
Citicoline is the precursor of phosphatidylcholine, an essential phospholipid component of all cell membranes in the CNS
and the PNS
2.
Citicoline stabilizes the membranes of neuronal cells and inhibits formation of FFAs
3.
4.
5.
2.
Citicoline is easily absorbed and broken down into uridine and choline and is used as raw material for phosphatidylcholine
synthesis
2.
Neurons convert uridine into cytidine, which reacts with choline to produce citicoline
3.
Category:
Antihypertensive
Indications
Accepted
Hypertension (treatment)The combination of candesartan and hydrochlorothiazide is indicated for the treatment
of hypertension {01}. The fixed dose combination is not indicated for initial therapy. {01}
For additional information on initial therapeutic guidelines related to the treatment of hypertension, see Appendix
III.
Pharmacology/Pharmacokinetics
Physicochemical characteristics:
Molecular weight
Candesartan cilexetil: 610.67{01}
Hydrochlorothiazide: 297.72{01}
Mechanism of action/Effect:
Candesartan is a nonpeptide angiotensin II antagonist that selectively blocks the binding of angiotensin II to the
AT 1 receptors in tissues such as vascular smooth muscle and the adrenal gland {01}. In the renin-angiotensin
system, angiotensin I is converted by angiotensin-converting enzyme (ACE) to form angiotensin II {01}. Angiotensin II
stimulates the adrenal cortex to synthesize and secrete aldosterone, which decreases the excretion of sodium and
increases the excretion of potassium {01}. Angiotensin II also acts as a vasoconstrictor in vascular smooth
muscle {01}. By blocking the binding of angiotensin II to the AT 1 receptors, candesartan causes vasodilation and
decreases the effects of aldosterone {01}. The negative feedback regulation of angiotensin II on renin secretion also
is inhibited, resulting in a rise in plasma renin concentrations and a consequent rise in angiotensin II plasma
concentrations; however, these effects do not counteract the blood pressurelowering effect that occurs {01}.
Hydrochlorothiazide is a diuretic that directly increases excretion of sodium and chloride and indirectly reduces
plasma volume. The mechanism of its antihypertiensive effect is not known {01}.
The administration of candesartan, an angiotensin II receptor antagonist, in combination with hydrochlorothiazide, a
diuretic, reduces the potassium loss associated with diuretics {01
The following may be especially important in patient monitoring (other tests may be warranted in some patients,
depending on condition; = major clinical significance):
Blood glucose determinations
oral hypoglycemic agents{01})
Cardiac glycoside,
Cardiotonic
Pregnancy Category C
Therapeutic actions
Digoxin is a cardiac glycoside which has positive inotropic activity characterized by an increase in the force of
myocardial contraction. It also reduces the conductivity of the heart through the atrioventricular (AV) node. Digoxin
also exerts direct action on vascular smooth muscle and indirect effects mediated primarily by the autonomic
nervous system and an increase in vagal activity.
Indications
CHF
Atrial fibrillation
Adverse Effects
Diarrhea in elderly, confusion, dizziness, drowsiness, restlessness, nervousness, agitation and amnesia,
visual disturbances, gynecomastia, local irritation (IM/SC inj), rapid IV admin may lead to vasoconstriction
and transient hypertension.
History: Allergy to digitalis preparations, ventricular tachycardia, ventricular fibrillation, heart block, sick
sinus syndrome, IHSS, acute MI, renal insufficiency, decreased K+, decreased Mg2+ increased Ca2+,
pregnancy, lactation
Physical: Weight; orientation, affect, reflexes, vision; P, BP, baseline ECG, cardiac auscultation, peripheral
pulses, peripheral perfusion, edema; R, adventitious sounds; abdominal percussion, bowel sounds, liver
evaluation; urinary output; electrolyte levels, LFTs, renal function tests
Interventions
[box type="note"]WARNING: Monitor apical pulse for 1 min before administering; hold dose if pulse < 60 in adult or
< 90 in infant; retake pulse in 1 hr. If adult pulse remains < 60 or infant < 90, hold drug and notify prescriber. Note
any change from baseline rhythm or rate.[/box]
Have emergency equipment ready; have K+ salts, lidocaine, phenytoin, atropine, and cardiac monitor
readily available in case toxicity develops.
[box type="note"]WARNING: Monitor for therapeutic drug levels: 0.52 ng/mL.[/box]
Digoxin Mechanism of Action
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May be used as primary prevention in individuals with multiple risk factors for coronary heart disease (CHD) and as secondary prevent
angina, and revascularization procedures. May be used to reduce the risk of cardiovascular events in patients with acute coronary syn
dyslipidemia, homozygous familial hypercholesterolemia, primary dysbetalipoproteinemia, and/or hypertriglyeridemia as an adjunct to
C), apolipoprotein B (apoB), and triglyceride concentrations, while increasing high-density lipoprotein cholesterol (HDL-C) levels.
Pharmacodynamics
Atorvastatin, a sele
cholesterol, apoB, a
TG concentrations
disease. The total c
are associated with
cardiovascular risk.
cardiovascular mor
selectivity, explaini
Mechanism of action
Atorvastatin selecti
reductase is respon
this results in a sub
stimulates upregula
serum LDL-C conce
DRUG CLASS AND MECHANISM: Atorvastatin is an oral drug that lowers the level of cholesterol in the blood. It
belongs to a class of drugs referred to as statins, which includes lovastatin (Mevacor), simvastatin,
(Zocor),fluvastatin (Lescol), and pravastatin (Pravachol) and rosuvastatin (Crestor). All statins, including
atorvastatin, prevent the production of cholesterol in theliver by blocking HMG-CoA reductase, an enzyme that
makes cholesterol. Statins reduce total cholesterol as well as LDL cholesterol in blood. LDL cholesterol is believed to
be the "bad" cholesterol that is primarily responsible for the development of coronary artery disease. Reducing LDL
cholesterol levels retards progression and may even reverse coronary artery disease. Atorvastatin also raises the
concentrations of HDL ("good") cholesterol that protects against coronary artery disease and reduces the
concentration oftriglycerides in the blood. (High blood concentrations of triglycerides also have been associated
with coronary artery disease.) The FDA approved atorvastatin in December 1996.
Omeprazole
Omeprazole is indicated for the treatment of duodenal ulcers, benign gastric ulcers, gastroesophageal reflux disease (GERD), heartbur
treatment of pathological hypersecretory conditions like Zollinger-Ellison syndrome, multiple endocrine adenomas, and systemic mast
Pharmacodynamics
Mechanism of action
Mechanism of action/Effect:
Omeprazole is a selective and irreversible {47} proton pump inhibitor. {48} Omeprazole suppresses gastric acid
secretion by specific inhibition of the hydrogenpotassium adenosinetriphosphatase (H +, K +-ATPase) enzyme
system found at the secretory surface of parietal cells {46}. It inhibits the final transport of hydrogen ions (via
exchange with potassium ions) into the gastric lumen. {03} {04}Since the H +, K +-ATPase enzyme system is regarded
as the acid (proton) pump of the gastric mucosa, omeprazole is known as a gastric acid pump inhibitor. {46} {01} The
inhibitory effect is dose-related. {46} Omeprazole inhibits both basal and stimulated acid secretion irrespective of the
stimulus. {01} {46}
Omeprazole does not have anticholinergic or histamine H 2-receptor antagonist