ALI, JANNA-IZZA B.

BATCH 2023
NEURO 1 MODULE

DRUG COMPENDIUM

ASPIRIN
Generic name: Aspirin
Drug class: Salicylates, Anticoagulants & Fibrinolytics (Thrombolytics)
General Chemistry:

DESCRIPTION

-It is a selective and irreversible inhibitor of cyclooxygenase-1 (COX-1) enzyme

resulting in direct inhibition of the biosynthesis of prostaglandins and
MECHANISM OF ACTION
thromboxanes from arachidonic acid.

It exhibits analgesic, anti-inflammatory, and antipyretic activities.

CLINICAL EFFECTS It also inhibits platelet aggregation.

Fever, Rheumatic disorders, MI, Angina pectoris, Acute ischemic stroke,

CLINICAL INDICATIONS prophylaxis of cardiovascular events in high-risk patients

Absoprtion: Rapidly absorbed from the GI tract. Partially hydrolysed by esterases

to salicylate during absorption in the GI tract.
Bioavailability: 50-75%
Peak plasma levels: Approx 1-2 hours (nonenteric-coated); 3-4 hours (enteric-
coated); Approx 2 hours (extended-release cap)
Distribution: Crosses the placenta and enters breast milk.
PHARMACOKINETICS Volume distribution: 170 mL/kg
Plasma protein binding: 80-90%
Metabolism: Metabolized in the liver into salicyluric acid, salicyl phenolic
glucuronide, salicylic acyl glucuronide, gentisic acid, and gentisuric acid.
Undergoes first-pass metabolism.
Excretion: Via urine (75% as salicyluric acid, 10% as salicylic acid)
Elimination half-lives: 15-20 minutes

Antiplatelet: 40-80 mg/d

Pain/Fever: 325-650 mg/4-6 h

For nonviral etiologies fever: 50-70 mg/kg/day in 4-6 divided doses, max of 3.6 g.
DOSAGE
Rheumatic Fever: 1g/4-6 h

Children: 10 mg/kg/4-6 h
 -Hypersensitivity to aspirin or other NSAIDs, Peptic ulcer, Hemorrhagic disease,
Coagulation disorder (e.g. hemophilia, thrombocytopenia), Gout, Severe
CONTRAINDICATIONS
hepatic and renal impairment, Children <16 years and recovering from viral
infection
Salicylate sensitivity, tinnitus, Anemia, hypoprothrombinemia,
thrombocytopenia, Dyspepsia, gastric irritation, nausea, vomiting, Dizziness,
confusion, Asthma, bronchospasm, dyspnea, rhinitis, Rash, urticarial
ADVERSE REACTION

CLOPIDOGREL
Generic name: Clopidogrel
Drug class: Antiplatelet drug
General Chemistry:

DESCRIPTION

- inhibit the binding of ADP to its receptors on platelets and, thereby, inhibit the
MECHANISM OF ACTION activation of the GP IIb/IIIa receptors required for platelets to bind to fibrinogen
and to each other

- reduce the rate of stroke, myocardial infarction,and death in patients with

CLINICAL INDICATIONS recent myocardial infarction or stroke,established peripheral arterial disease, or
acute coronary syndrome.

Absorption: Rapidly but incompletely absorbed from the gastrointestinal tract

(approx 50%).
Time to peak plasma concentration: Approx 45 minutes.
Plasma protein binding: 98% (parent drug); 94% (carboxylic acid derivative).
Metabolism: They undergo hepatic metabolism by the cytochrome P450 (CYP)
PHARMACOKINETICS system to active metabolites.
Excretion: Elimination of the drugs and metabolites occurs by both the renal
and fecal routes
Half-life: Approx 6 hours (parent drug); approx 0.5 hours (thiol derivative);
approx 8 hours (carboxylic acid derivative).

The usual dose is 75 mg/day with or without an initial loading dose of 300 or 600
DOSAGE
mg

Active pathological bleeding (e.g. peptic ulcer or intracranial haemorrhage).

CONTRAINDICATIONS
Severe hepatic impairment.

ADVERSE REACTION prolonged bleeding

Thrombotic thrombocytopenic purpura
 WARFARIN
Generic name: Warfarin
Drug class: Anticoagulant (Vitamin K Antagonist)
General Chemistry:

DESCRIPTION

- Inhibit the production of vitamin K by vitamin K epoxide reductase.

MECHANISM OF ACTION

- Prophylaxis and treatment of venous thromboembolism and related

CLINICAL INDICATIONS pulmonary embolism; atrial fibrillation; cardiac valve replacement; Secondary
prevention of stroke.
Absorption: Completely absorbed from the GI tract. The mean Tmax for warfarin
sodium tablets is 4 hours.
Distribution: Volume of distribution 0.14 L/kg; Protein binding: 99%.
Metabolism: Major metabolic pathway is oxidation to various hydroxywarfarins,
comprising 80-85% of the total metabolites; minor pathway of metabolism is the
reduction of the ketone group to warfarin alcohols, comprising 20% of the
PHARMACOKINETICS
metabolites.
Excretion: Almost entirely by metabolism with a small amount excreted
unchanged; 80% of the total dose is excreted in the urine with the remaining
20% appearing in the feces; Half-life for R-warfarin is 37-89 hours. Half-life for S-
warfarin is 21-43 hours.

DOSAGE 5-10 mg QD as starting dose.

Severe bleeding
Hemoptysis
ADVERSE REACTION black or bloody stool
joint pain

DABIGATRAN
Generic name: Dabigatran
Drug class: Direct Oral Thrombin Inhibitor
General Chemistry:

DESCRIPTION
 - Dabigatran competitively and reversibly blocks the active site of free and clot-
bound thrombin. In turn, this blocks thrombin-mediated conversion of fibrinogen
MECHANISM OF ACTION
to fibrin, feedback activation of coagulation, and platelet activation.

-Treatment of acute venous thromboembolism after at least 5 days of

parenteral anticoagulation with heparin, LMWH, or fondaparinux
- Secondary prevention of venous thromboembolism
CLINICAL INDICATIONS - Stroke prevention in patients with nonvalvular atrial fibrillation
- Thromboprophylaxis after knee or hip arthroplasty (lower-dose regimens of
once-daily dabigatran)

Administration: Taken orally twice a day in capsule

form
Bioavailability: 6% (altered if capsules are chewed or
broken prior to ingestion)
PHARMACOKINETICS Peak onset of action: 2 h
Half-life: 12-14 h
Plasma protein binding: 35%
Excretion: 80% excreted unchanged by kidneys

- Dosage reduction is required when administered to patients with severe renal

impairment (creatinine clearance 15-30 mL/min).
- Dosage recommendations are not available for patients with a creatinine
DOSAGE
clearance <15 mL/min.

- Patients with mechanical heart valves

CONTRAINDICATIONS
- Bleeding
ADVERSE REACTION

BETAHISTINE
Generic name: Betahistine
Drug class: Antivertigo drugs
General Chemistry:

DESCRIPTION

- Betahistine is a histamine analogue. The exact mechanism is not yet fully

determined; however, it is known to act as both partial histamine H1-receptor
MECHANISM OF ACTION agonist and histamine H3-receptor antagonist in neuronal tissue, with negligible
histamine H2-receptor activity.

- For vertigo, tinnitus and hearing loss associated in patients with Meniere’s
CLINICAL INDICATIONS disease

Absorption:When given orally, betahistine is rapidly and almost completely

absorbed from the gastrointestinal tract.In the fasted state, Cmax is achieved
within 1 hour of administration; in the fed state, Cmax is delayed, but the total
drug absorption is similar. Food, therefore, has little effect on the absorption of
betahistine
PHARMACOKINETICS Plasma protein binding: less than 5%.
Metabolism: metabolized primarily into the inactive metabolite 2-pyridylacetic
acid.
Excretion: Betahistine is mainly excreted in the urine; with approximately 85-91%
being detected in urine samples within 24 hours of administration
Half-life: 3-4 hours
 As betahistine dihydrochloride: Initially, 8-16 mg tid or 24 mg bid, adjusted
DOSAGE according to individual response. Maintenance: 24-48 mg daily. Max: 48 mg
daily.
As betahistine mesilate: 6-12 mg tid.
Salicylate sensitivity, tinnitus, Anemia, hypoprothrombinemia,
thrombocytopenia, Dyspepsia, gastric irritation, nausea, vomiting, Dizziness,
CONTRAINDICATIONS
confusion, Asthma, bronchospasm, dyspnea, rhinitis, Rash.

- nausea, upset stomach, vomiting, diarrhea and stomach cramping.

ADVERSE REACTION

CINNARIZINE
Generic name: Cinnarizine
Drug class: Antivertigo drugs, Peripheral Vasodilators & Cerebral Activators
General Chemistry:

DESCRIPTION

- inhibits contractions of vascular smooth muscle cells by blocking L-type and T-

type voltage gated calcium channels, thereby reducing free Ca ions available
MECHANISM OF ACTION
for the induction and maintenance of contraction.

- Motion Sickness
- Nausea and Vertigo caused by Meniere’s disease, Vertigo and vestibular
CLINICAL INDICATIONS disorders
- Cerebrovascular disorders
- Peripheral Circulatory Disorders
Absorption: slowly absorbed
Time to peak plasma concentration: 4 hours
Plasma protein binding: 91%
PHARMACOKINETICS Metabolism: Extensively metabolized mainly by cyp2d6.
Excretion: via feces (mainly as unchanged drug) and urine (as metabolites)
Half-life: 3-6 hours.

Motion Sickness
Adult: Initially, 30mg 2 hours before travel, then 15 mg 8 hourly during the
journey if necessary.
Child (5-12years old): 15 mg 2 hours before travel, then 7.5 mg 8 hourly during
the journey if necessary.
Nausea and Vertigo caused by Meniere’s disease, Vertigo and vestibular
DOSAGE disorders
Adult: 30 mg tid
Child (5-12 years old): 15 mg tid
Cerebrovascular disorders
Adult: 25 mg tid
Peripheral Circulatory Disorders
Adult: 50-75 mg bid to tid with Max: 225 mg daily

Hypersensitivity to Cinnarizine
CONTRAINDICATIONS
Children <5 years of age

- Epigastric discomfort
ADVERSE REACTION
 CITICOLINE
Generic name: Citicoline
Drug class: Nootropics & Neurotonics/Neurotrophics
General Chemistry:

DESCRIPTION

- Citicoline is a naturally occurring endogenous nucleoside involved in the

biosynthesis of lecithin. It increases the synthesis of phosphatidylcholine (main
MECHANISM OF ACTION
neuronal membrane phospholipid) and enhances acetylcholine production.

- Cerebrovascular disorders
- Cognitive disorder
CLINICAL INDICATIONS
- Head Injury
- Parkinson’s disease
Absorption: Rapidly absorbed in the gastrointestinal tract.
Bioavailability: >90%
Time to peak plasma concentration: 1 hour after oral administration followed by
2nd peak at 24 hours post-dosing.
Distribution: Distributed throughout the body, crosses blood-brain barrier.
PHARMACOKINETICS
Metabolism: Metabolised in the liver and gut wall via hydrolysis to choline and
cytidine
Excretion: Mainly via respiratory CO2
Half-life: 71 hours (urine); 56 hours (respiratory CO2)

- IM, IV: 500-1000mg daily given via IM inj or slow inj 3-5 minutes, or infused at a
DOSAGE rate of 40-60 dpm.
- PO: As tab: 500 mg once daily or bid, or 1000 mg once daily. As solution: 100-
200 mg bid or tid.
Hypertonia of the parasympathetic nervous system.
CONTRAINDICATIONS

LOSARTAN
Generic name: Losartan
Drug class: Angiotensin Receptor Blocker (ARB)
General Chemistry:

DESCRIPTION
 - It binds to AT1 receptors with much higher affinity than AT2 receptors. It blocks
MECHANISM OF ACTION Angiotensin in vascular smooth muscle and adrenal cortex.

ARB inhibits most of the biological effects of AngII, which include AngII-induced
(1) contraction of vascular smooth muscle; (2) rapid pressor responses; (3) slow
pressor responses; (4) thirst; (5) vasopressin release; (6) aldosterone secretion; (7)
CLINICAL EFFECTS
release of adrenal catecholamines; (8) enhancement of noradrenergic
neurotransmission; (9) increases in sympathetic tone; (10) changes in renal
function; and (11) cellular hypertrophy and hyperplasia
- Hypertension
CLINICAL INDICATIONS - Diabetic Mellitus nephropathy
- Stroke prophylaxis
Absoprtion: Well absorbed from the GI tract. Decreased absorption with food.
Bioavailability: 33%
Peak plasma levels of losartan and EXP 3174 occur about 1–3 hrs after oral
administration.
Distribution: Volume distribution: 34 L.
PHARMACOKINETICS
Plasma protein binding: >98%
Metabolism: it undergoes extensive hepatic first-pass metabolism and
converted by CYP2C9 and CYP3A4 to 5-carboxylic acid metabolite, EXP 3174
Excretion: Via urine (35%) and feces.
Elimination half-lives: 2.5 hrs and 6–9 h (active metabolite)
DOSAGE 50 – 100 mg daily
- Concommitant use with aliskiren-containing products in patients with diabetes
mellitus or renal impairment.
CONTRAINDICATIONS
- Severe hepatic impairment
- Pregnancy
- Renal failure,
- Symptomatic hypotension,
- Hyperkalemia,
ADVERSE REACTION
- Angioedema