PHARMACOLOGY

PHARMACODYNAMICS
= drug’s mechanism of action
 Drug Actions maybe through;
1. RECEPTORS
2. ENZYMES and PUMPS
3. ION CHANNELS
4. ALTERING METABOLIC PROCESS

 AGONISTS
= binds to a receptor and stimulates the action

 ANTAGONISTS
1. Competitive Antagonist
= binds to a same RECEPTOR
= potency of an agonist is reduced

2. Non-Competitive Antagonist
= binds to a DIFFERENT RECEPTOR
= prevents potency of an agonist

PHARMACOKINETICS
= body’s response to the drug

 Liberation
- drug enters body and releases the active ingredient
 Absorption
- drug in blood
 Distribution
- drug in tissue and cells
 Metabolism (Biotransformation)
- drug in liver
- drug changed to a form easily excreted
 Excretion (Elimination)
- drug changed into inactive form eliminated by the body

• Dose
 amount of drug to be administered to the patient
• Schedule
 frequency, how many dose/s per day
• Recommended dose
 RIGHT amount + RIGHT schedule
• Critical concentration
 level of drug in the blood which produces a therapeutic
effect
• Therapeutic effect
 favorable response after a treatment of any kind
• Loading dose
 initial dose, immediate response
• Half Life
 time it takes for a drug to become half of its
previously peaked level
Rights of Drug Administration
1. Right DRUG
2. Right PATIENT
3. Right DOSE
4. Right ROUTE
5. Right TIME
Considerations to the 5 rights:
1. Right DOCUMENTATION
2. Right CLIENT EDUCATION
3. Right to REFUSE
4. Right ASSESSMENT
5. Right EVALUATION

TOXICOLOGY:
1. PRIMARY ADVERSE EFFECTS
= simple overdose
2. SECONDARY ADVERSE EFFECTS
= the OTHER effect of the drugs
3. HYPERSENSITIVITY
= exaggerated response of the immune response

DOSAGE FORMS OF DRUG:

A. SOLID
 TABLET
a. Scored
b. Layered
c. Enteric-coated
d. Chewable
e. Sustained-release
 CAPSULE
a. Hard Gel
b. Soft Gel
 LOZENGES
o antiseptic action
o analgesic action
 SUPPOSITORY
B. LIQUID
 Syrup
 Suspension
 Elixir
C. TOPICAL
 Ointment
 Cream
 Lotion
 Patch

AUTONOMIC NERVOUS SYSTEM DRUGS

NEUROTRANSMITTERS
= chemicals in the body acting as “messengers”

 Acetylcholine (ACh)
 Norepinephrine and Epinephrine ( NE / E )
 Dopamine (Dopa)
  Serotonin (5HT)
 Gamma Amino Butyric Acid (GABA)

 Includes two neurotransmitters

 Norepinephrine and acetylcholine
 Two branches:
 Sympathetic
 Adrenergic nervous system
 Parasympathetic
 Cholinergic

Fill out the blanks: Review!!!

ADRENERGIC AGONISTS
1. ADRENERGIC AGONISTS
a. Epinephrine
= CPR, Shock
a. Dobutamine
= CHF
a. Dopamine
= CHF, Cardiogenic Shock
a. Norepinephrine
= cardiac arrest
2. ALPHA 1 ADRENERGIC AGONISTS
a. Phenylephrine
= vasoconstriction  decongestion
= allergy
3. ALPHA 2 ADRENERGIC AGONISTS
a. Clonidine (Catapres)
= found in CNS neurons  dec Epinephrine flow
= Hypertension
4. BETA 1 ADRENERGIC AGONIST
a. Dobutamine
= CHF
5. BETA 2 ADRENERGIC AGONISTS
a. Albuterol / Salbutamol
b. Isoproterenol
c. Terbutaline
d. Isosuxprine

Nursing Considerations:
1. Avoid sudden withdrawal of the drug
2. Monitor vital signs
 3. Provide comfort measures
4. Provide adequate health teaching on the name of drug, prescribed
dosage, effects and adverse effects to increase patient’s knowledge
and subsequent compliance.

ADRENERGIC ANTAGONISTS

1. ALPHA and BETA ADRENERGIC ANTAGONISTS

a. Carvediol
b. Labetalol
2. ALPHA ADRENERGIC ANTAGONISTS
a. Phentolamine
3. ALPHA 1 ADRENERGIC ANTAGONISTS
a. Prazosin
b. Doxazosin
c. Terazosin
d. Alfuzosin
e. Tamsulosin
4. BETA ADRENERGIC ANTAGONISTS “olol “
a. Propranolol
b. Pindolol
5. BETA 1 SPECIFIC ADRENERGIC ANTAGONISTS
a. Betaxolol. Bisoprolol
b. Esmolol
c. Atenolol Acebutolol
d. Metoprolol

MYASTHENIA GRAVIS

• in Women, 20 – 40 y/o, unknown cause or idiopathic

• Autoimmune
• Descending muscle weakness

CHOLINERGIC AGONISTS
1. NEOSTIGMINE
= treatment
2. PYRIDOSTIGMINE
= treatment
3. PHYSOSTIGMINE
= treatment
4. EDROPHONIUM CHLORIDE
= diagnostic

Diagnostic Test: Tensilon Test

Myasthenic Crisis:
 Signs and symptoms: Weakness, paralysis
 Cause: underdose
 Treatment: Cholinergic drugs
Cholinergic Crisis:
 Signs and symptoms: Weakness, paralysis
 Cause: overdose
 Treatment: Anticholinergic drugs:
 ALZHEIMER’S DISEASE

DESCRIPTION:
= degeneration of cholinergic nerves

• Signs & Symptoms:

• A – amnesia
• A - agnosiak
• A – apraxia
• A – aphasia
- Expressive
– brocca’s aphasia
- Receptive
– wernickes aphasia

CHOLINERGIC DRUGS:
1. RIVASTIGMINE
2. TACRINE
3. DONEPEZIL

PARKINSON’S DISEASE

Classes of Anti-Parkinson Agents

I. Anticholinergic DRugs
a. Benztropine (Cogentin)
b. Biperiden (Akineton)
c. Diphenhydramine (Benadryl)
d. Trihexyphenidyl (Artane)

II. Dopaminergic Drugs

a. Dopamine precursors
b. Dopamine receptor agonists
c. MAO Inhibitors
d. Catechol-O-methyltransferase inhibitors
 DRUGS AFFECTING THE RESPIRATORY SYSTEM

I. BRONCHODILATORS:
A. SYMPATHOMIMETICS (Beta 2 Adrenergic Agonist)
o Albuterol
o Ephedrine
o Epinephrine
B. PARASYMPATHOLYTICS
o Ipratropium
C. METHYLXANTHINES
o Caffeine
o Aminophylline
 o Theophylline

II. ANTIINFLAMMATORY DRUGS:

A. INHALED STEROIDS
o Budesonide
o Fluticasone
o Triamcinolone

ANGINA
“chest pain”

DRUGS AFFECTING BLOOD COAGULATION

• Antiplatelets
= blocks the formation of platelet plug
• Aspirin
• Clopidogrel

• Anticoagulants
= blocks thrombin production
• Warfarin
= blocks the Vit. K dependent clotting factors
= Route: oral
= Therapeutic test: PT/INR
= Therapeutic margin: 1.5 – 2.0 times the normal
= Side effect: bleeding
 • Heparin
= blocks the formation of thrombin
= Route: IV / SQ
= Therapeutic test: aPTT
= Therapeutic margin: 1.5 – 2.5 times the normal
= Side effect: bleeding

• Thrombolytics
= dissolve the clot by activating the plasminogen  plasmin
= goal: restore the blood flow
• Alteplase
• Streptokinase
• Reteplase
• Urokinase
= Side effect: bleeding

• Antifibrinolytic
• Aminocaproic acid
• Tranexamic acid

HYPERTENSION

 Mean Arterial Pressure (MAP)

 Average pressure throughout each cycle of the heartbeat
 Normal: 70-100 mmHg
 MAP = SBP + 2 (DBP)
3
 Clinical significance
 perfusion pressure seen by organs in the body

ANTIHYPERTENSIVE DRUGS AFFECTING THE RAAS:

• ACE Inhibitors “pril”

• Angiotensin 2 Receptor Blockers (ARB) “sartan “
• Renin Antagonists
• Selective Aldosterone Antagonist

ANTIHYPERTENSIVE DRUGS AFFECTING THE ANS RECEPTORS:

• Alpha 1 Adrenergic Antagonists “zosin”

• Alpha 2 Adrenergic Agonist
• Beta Adrenergic Blockers “olol”

VASODILATORS:

• Indirect-Acting Vasodilator
= Calcium Channel Blocker
• Direct-Acting Vasodilator
= Vasodilators
OTHERS:
 DIURETICS
 ARRHYTHMIA

• CLASS I: blocks the sodium channel

 Class Ia: QUINIDINE, PROCAINAMIDE
 Class Ib: LIDOCAINE, PHENYTOIN
• CLASS II: blocks the beta receptor
 PROPRANOLOL
 ESMOLOL
• CLASS III: blocks the potassium channel
• AMIODARONE
• CLASS IV: blocks the calcium channel
• VERAPAMIL
• DILTIAZEM

ELECTRICAL IMPULSE

CONGESTIVE HEART FAILURE

= “PUMP FAILURE”

DRUGS FOR CONGESTIVE HEART FAILURE:

• CARDIOTONIC DRUGS
 Cardiac Glycosides: Digoxin (Lanoxin)
 Phosphodiesterase Inhibitors: Inamrinone
 Sympathomimetic: Dobutamine
 Diuretics: Furosemide
 Vasodilators
 ACE Inhibitors: Captopril, Enalapril
 Vasodilators: Nitroglycerine
 DRUGS USED FOR PEPTIC ULCER DISEASE (PUD)

PEPTIC ULCER
= an erosion in the mucosal lining

• ANTACIDS
= neutralize the hydrochloric acid in the stomach
 Al (OH)
 Mg (OH)
 Mg + Al (OH)2
• HISTAMINE 2 RECEPTOR BLOCKERS
= blocks the histamine 2 receptors  decreasing the HCl- secretion
 CIMETIDINE
 RANITIDINE
 FAMOTIDINE
• PROTON PUMP INHIBITORS
= blocks the proton pump  decreasing the HCl- secretion
 OMEPRAZOLE
 PANTOPRAZOLE
• CYTOPROTECTIVES
= coats the ulcer
 SUCRALFATE
• PROSTAGLANDIN AGONIST
= stimulates prostaglandin 
 MISOPROSTOL ( CYTOTEC )

DRUGS USED TO CONTROL BLOOD GLUCOSE LEVEL

 INSULIN
 Action: liver, muscle & adipose to facilitate passage of glucose, K+, and Mg
 Indications : DM type 1, DM type 2
 onset, peak & duration
• Storage:
1. avoid extremes of temperature
2. before injection : should be room temp
3. if vial will be used in 1 month: room temp
4. Otherwise : refrigerate

• Dawn phenomenon
• reduced tissue sensitivity to insulin
• develops between 5 – 8 am
• prebreakfast hyperglycemia
• caused by nocturnal release of GH
• tx: inc intermediate-acting insulin at 10 pm
• Somogyi phenomenon
• normal or elevated blood glucose levels at bedtime
• hypoglycemia occurs 2-3 am causing inc of counterregulatory hormones
• 7 am as a response  rebound hyperglycemia
• Tx: dec pm production of glucagon after meals, slows gastric emptying ( w/c
limits the rise in the blood glucose level pc ) reduces fasting and postprandial
blood glucose levels and reduces caloric intake  weight loss

 Glucose-Elevating Agents
- diazoxide
- glucagon

THYROID AGENTS

 AntiThyroid Agents
- Levothyroxine
- Liothyronine
- Liotrix
- thyroid desiccated

 Thyroid Replacement Agents

Antithyroid Agents
Thiomides
- methimazole
- propylthiouracil
Iodine solutions
- sodium iodide L131
- strong iodine solutions
- potassium iodide
-

ANTIMICROBIALS

 BLOCKS CELL WALL SYNTHESIS

 BETA LACTAMS
 PENICILLINS
 CEPHALOSPORINS
 CARBAPENEMS
 MONOBACTAM
 VANCOMYCIN

 BLOCKS PROTEIN SYNTHESIS

 MACROLIDES
 CHLORAMPHENICOL
 LINCOSAMINES
 AMINOGLYCOSIDES
 TETRACYCLINES

 FOLIC ACID SYNTHESIS INHIBITOR

 SULFONAMIDES
 TRIMETHOPRIM

 NUCLEIC ACID SYNTHESIS INHIBITOR

 FLUOROQUINOLONES