Citicoline Mode of Action

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.

Citicoline has a targeted action for increasing brain phospholipid synthesis

4.

Citicoline is also converted to the neurotransmitter acetylcholine

5.

Acetylcholine functions both in the PNS and in the CNS as a neuromodulator

Citicoline in the PNS

1.

Acetylcholine activates muscles

2.

Acetylcholine is a major neurotransmitter in the autonomic nervous system

Citicoline in the CNS

1.

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.

Citicoline enters the metabolic pathway of phosphatidylcholine production in the CNS

How Citicoline Works:

The primary mechanism of action for Citicoline is as a source of Choline. Choline is a nutrient similar to the B Vitamins that is
necessary for the brain to be able to make the acetylcholine neurotransmitter. However, the vast majority of the population does not
get the recommended amount of choline form their diet which can lead to mental impairment even with minor deficiencies. Citicoline
can help to supplement the amount of choline in your bloodstream which them promotes greater acetylcholine production. What is
most interested about Citicoline is that it has proven more effective at increasing brainpower than taking equivalent amounts of
choline supplements. This is because Citicoline is actually more bioavailable and a closer precursor to acetylcholine.
After taking a Citicoline dosage, this compound is absorbed into the bloodstream fairly quickly and then crosses the blood-brain
barrier, reaching the brain. The two main components of the supplement, cytidine and choline, are broken down and then widely
distributed. As it becomes incorporated into phospholipids it helps to activate their continued biosynthesis.
A number of different neurotransmitters and brain chemicals are also affected by Citicoline. It acts as a precursor to Acetylcholine
and helps to influence a number of cognitive processes through this action. Dopamine and Norepinephrine levels are also increased
throughout the central nervous system. This may also be why many users report their overall stress levels decrease and a
feeling of general well-being to be improved while using this supplement.
Citicoline may also help to protect the brain. This includes the possible activation of a number of anti-oxidants. This helps to rid the
brain of a number of poisons and toxins, improving overall health. The increase in phospholipid metabolism is also thought to help
aid in this brain protection effect, keep the individual cell membranes better able to communicate with one another.
- See more at: http://nootriment.com/citicoline/#sthash.uibwzmEX.dpuf

Candesartan and Hydrochlorothiazide (Systemic)

VA CLASSIFICATION
Primary: CV408
Secondary: CV805/CV701
Commonly used brand name(s): Atacand HCT 16-12.5; Atacand HCT 32-12.5.
Note: For a listing of dosage forms and brand names by country availability, see Dosage Forms section(s).

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})

(recommended at periodic intervals for necessary dosage adjustment of insulin or

Blood pressure measurements

response{01})

(periodic monitoring is necessary for titration of dose according to the patient's

Electrolyte concentrations, serum

imbalance{01})
Renal function determinations

(determinations recommended periodically to detect possible electrolyte

(recommended at periodic intervals{01})

Clonidine: Mechanisms of Action

Mechanism of action
Clonidine is a centrally-acting Alpha adrenergic receptor agonist with more affinity for alpha 2 than alpha 1. It
selectively stimulates presynaptic alpha2 receptors in the brain that monitor Catecholamine levels in the blood.
These receptors close a negative feedback loop that begins with descending sympathetic nerves from the brain that
control the production of catecholamines (adrenaline and norardenaline) in the adrenal medulla.
By fooling the brain into believing that catecholamine levels are higher than they really are, clonidine causes the
brain to reduce its signals to the adrenal medulla, which in turn lowers catecholamine production and blood levels.
The result is a lowered heart rate and blood pressure.
It has also been proposed that the antihypertensive effect of clonidine is due to agonism on the I 1-receptor or
Imidazoline receptor, which mediates the sympatho-inhibitory actions of imidazolines to lower blood pressure.
INTRODUCTION
Aspirin, an acetylated salicylate (acetylsalicylic acid), is classified among the nonsteroidal antiinflammatory drugs
(NSAIDs). These agents reduce the signs and symptoms of inflammation and exhibit a broad range of
pharmacological activities, including analgesic, antipyretic, and antiplatelet properties. Aspirin was first introduced
by the drug and dye firm Bayer in 1899. Aspirin and the other NSAIDs do not generally change the course of the
disease process in those conditions where they are used for symptomatic relief.
The mechanism of action, efficacy, and toxicity of aspirin in rheumatic and other inflammatory disorders are
reviewed here. The nonsalicylate NSAIDs, including nonspecific NSAIDs and cyclooxygenase (COX)-2 selective
agents; the use of aspirin for primary and secondary prevention of cardiovascular disease; and the prevention of
gastroduodenal and other toxicities from aspirin are discussed in detail elsewhere.
MECHANISM OF ACTION
Effect of dose Aspirin's effects and respective mechanisms of action vary with dose:
Low doses (typically 75 to 81 mg/day) are sufficient to irreversibly acetylate serine 530 of cyclooxygenase (COX)1. This effect inhibits platelet generation of thromboxane A2, resulting in an antithrombotic effect.
Intermediate doses (650 mg to 4 g/day) inhibit COX-1 and COX-2, blocking prostaglandin (PG) production, and
have analgesic and antipyretic effects.
Digoxin (Lanoxin) is a cardiac glycoside that is usually used for patients with heart failure. Digoxin has a positive
inotropic activity characterized by an increase in the force of myocardial contraction.
Classification

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

Extra beats, anorexia, nausea and vomiting.

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.

Potentially Fatal: Cardiac arrhythmias in combination with heart block.

Contraindications

Digitalis toxicity, ventricular tachycardia/fibrillation, obstructive cardiomyopathy.

Arrhythmias due to accessory pathways (e.g. Wolff-Parkinson-White syndrome).

Nursing considerations
Assessment

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]

Take care to differentiate Lanoxicaps from Lanoxin; dosage is very different

Check dosage and preparation carefully.

Avoid IM injections, which may be very painful.

Follow diluting instructions carefully, and use diluted solution promptly.

Avoid giving with meals; this will delay absorption.

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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from eMedTV.com
Available by prescription only, digoxin (Lanoxin) is used to treatcongestive heart failure (CHF) and a type of
irregular heart rhythm known as atrial fibrillation. Many people wonder about the actions of digoxin in the body,
specifically how it works to treat these heart conditions.
This medication works by blocking a specific enzyme in the body (known as sodium-potassium ATPase). This
enzyme controls the amount of sodium and potassium that enters the cells. Blocking this enzyme increases the
amount of calcium and potassium inside heart
cells. This helps the heart contract more forcefully with each heartbeat, making it more efficient at pumping blood
throughout the body. It also slows down the rate at which the heart beats.
Atorvastatin

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

After oral administration, the onset

occurring within two hours. At 24 ho
lasts up to 72 hours. Although omep
due to prolonged binding to parieta
return to baseline over 3-5 days. Th
dosing, reaching a plateau after fou
during the first 1 to 2 weeks of once
acid secretion. Systemic effects of o
date.

Mechanism of action

Omeprazole is a proton pump inhibi

the gastric parietal cell. By acting sp
reducing gastric acidity.

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