 Erroneous Prescriptions (Click Here for Samples)

https://rxistsource.blogspot.com/2013/02/erroneous-violative-and-impossible.html

 Where the brand name precedes the generic name

 Where the generic name is the one in parenthesis
 Where the brand name is not in parentheses
 Where more than one drug product is prescribed on one prescription form.
 What to do with erroneous prescriptions
Erroneous prescriptions shall be filed. Such prescription shall also be kept
and reported by the pharmacist of the drug outlet or any other interested
party to the nearest DOH office for appropriate action.
Violative Prescriptions (Click Here for Samples)
 https://rxistsource.blogspot.com/2013/02/erroneous-violative-and-impossible.html

 Where generic name is not written

 Where the generic name is not legible and a
brand name which is legible is written
 When the brand name is indicated and
instructions added (such as the phrase " no
substitution") which tend to obstruct, hinder
or prevent proper generic dispensing.
Impossible Prescriptions (Click Here for Samples)
 When only the generic name is written but it is not legible.
 When the generic name does not correspond to the brand name
 When both the generic name and the brand name are not legible
 When the drug product prescribed is not registered with FDA
 What to do with impossible prescriptions
 Impossible prescription shall not be filed. They shall be and reported by
the pharmacist of drug outlet or any other interested party to the nearest
DOH office for appropriate action. The pharmacist shall advise the
prescriber of the problem and/or instruct the customer to get the proper
prescription.
Absorption/Distribution overview
 Drug administered  Drug in circulation
 Not dissolved, lost in feces  Broken down in tissues
 Drug dissolved in GI fluids  Bound to plasma proteins
 Lost in acid  Drug distributed throughout the
 Dissolved drug reaches body
intestine  Reaches reactive tissue
 Lost in food, acid, digestion  Excreted by kidneys, lungs,
skin
 Drug absorbed
 Bound to fat tissue
 Drug in liver
 Drug produces therapeutic effect
 Lost due to biotransformation
to noneffective state
 Bound to plasma proteins

Ref: Roach S. Pharmacology for Health Professionals, 2005)

 Half-life = time taken for drug plasma
concentrations to fall to half of original values

 Bioavailability = the fraction of the drug that

enters the systemic circulation.
Factors Affecting Bioavailability
 Solubility of the Drug
◼ Hydrophobic (Lipophilic)
◼ Hydrophilic
 Instability if the Environment
◼ Stomach & Intestinal Metabolism
◼ Enzymatic Metabolism
 First Pass Metabolism of Liver
Metabolism (biotransformation)
 Before excretion, drugs are metabolised either into
an inactive metabolite, a more soluble compound or
a more potent agent
 Liver is mainly responsible for this, but muscles,
kidneys, lungs, plasma and intestinal mucosa
 Hepatic biotransformation involves the cytochrome
P-450 enzymatic system
 Oral administered drugs are usually absorbed by the
small intestine may be extensively metabolised (first
pass) leading to decrease distribution levels
Phase 1 metabolic reactions
 Oxidation (presence of oxygen):
◼ Most common, Smooth endoplasmic reticulum, Cytochromes P-450
involved
◼ Usually result in the production of inactive drugs but the metabolite
may be active
 Reductions:
◼ the reverse of oxidation, i.e. the formal oxidation state of an atom
(independent or within a molecule) is reduced by the addition of
electrons
 Hydrolysis:
◼ a chemical process in which a molecule is split into two parts by the
addition of a molecule of water

 Purpose = increase polarity of drug (pharmacodynamics)

Phase 2 metabolic reactions
 Phase 1 can prepare a molecule for phase 2
 Involves conjugation:
◼ Attachment of a large chemical group to a drug
◼ Make the drug more hydrophilic (affects
absorption)
◼ Mainly occurs in the liver
◼ Almost always results in the inactivation of the
drug
Excretion
 Elimination of drugs (inactive or active)
 Primary organ = kidney (others liver – via
biliary excretion - and bowel).
 As a result of metabolism, drug agents have
become more polar and water soluble (helps
with drug actions but makes elimination
easier).
 Excretion via urine or feces
Kidney overview
 Filtration: glomerular capilleries allow
passage of molecule with wts <20000.
Drugs bound to plasma proteins will
not be filtered.

Re-absorption: can allow some drugs to

re-enter the circulatory system.

Excreted Urine

Secretion back into

tubules. Loop of
Henle

 Kidney excretion:
 Achieved by glomerular filtration, re-absorption and tubular secretion
Pharmacodynamics
 How the drug effects the body!
 The study of the mechanism of action at sites
of need
 Drugs have to alter physiological function to
produce therapeutic effect
◼ Cellular level interactions
 How do drugs enter the cell/tissue and interact
with cellular components
Pharmacodynamics
 Mechanism by which drugs produce changes
in body tissue.
 Desired Effect: Intended action of drugs
 Adverse Effect: Harmful unintended reactions
 Side Effects: Consequence reaction
 Toxicity: The degree which something is
poisonous
 Digoxin: 0.5-2.0 ng/mL
 Lithium: 0.5-1.5 mEq/L
Molecular Basis – How drugs work?
 Exertion of a chemical influence on cells or cellular
components
 Drug molecules most get up ‘close and personal’
 Can not have a randomised distribution of drugs in the human
body
 Drugs must be ‘bound’ to produce effect (increase or
decrease physiological processes)
◼ How they do this is a major component of pharmacological research.
 Majority of agents produce their binding effects to protein
molecules.
◼ General anaesthetics – interact with membrane lipids
◼ Antitumor and antimicrobial – target DNA
Protein targets
 Ion channels

 Carrier molecules

 Enzymes

 Receptors
Ion channels
 Pores in the cell membrane that allow for
selective transport of ions in and out of a cell.
 Opening and closing = gating; by either a
transmitter substance or a voltage change in
the membrane.
 Some drugs target these directly by binding to
the channel protein (eg. Blocking of sodium
channels by local anaesthetics)
Ion Channels
Carrier molecules
 Transportation of ions and small molecules into the
cell across the membrane
 2 main types:
◼ ATP-powered ion pumps:
 Sodium; calcium
◼ Active Transportors:
 Symporters: use electrochemical gradient of one ion (usually
sodium) to carry another molecule
 Antiporters: use the electrochemical gradient of one ion to drive
another ion or molecule across the membrane
Enzymes
 Protein catalysts that increase the rate of specific
chemical reactions without undergoing any net
change

 Drugs act as a false substrate (amphetamine) or as

inhibitors

 Certain drugs need an enzyme to degrade it in order

for the active agents to be created.
Enzymes

Enzyme NORMAL FUNCTION

Substrate Products

Enzyme
DRUG INTERACTION

Inhibitor Substrate

?
Source: http://www.fleshandbones.com/readingroom/
Examples
Substrate Enzyme Products Inhibitor Uses

Acetylcholine A. Esterase Choline; acetate Neostigmine Reverse

neurological
block
Arachidonate Cyclooxygenase Prostaniods Asprin Heart diesase and
inflammation
Angiotensin I AT converting AT II Captopril Hypertension,
enzyme heart failure,
Post-infact
Hypoxanthine Xanthine oxidase Uric acid Allopurinol Gout

Source: http://www.fleshandbones.com/readingroom/
Receptors
 Are protein molecules that receives and responds to a specific
neurotransmitter, hormone, or other substance.
 Therefore, to have a drug-receptor reaction the structure of
the drug is vital
 Drugs that resemble endogenous substances are highly
effective
 Substances that will either do:
◼ Active receptors and produce a response (agonists)
◼ Associate with receptors but not cause activation (antagonists)
 Electrostatic forces (polarity) initially attract a drug to a
receptor.
4 main types of receptors
 G-protein coupled receptors (GPCR)
 Receptors linked to ion channels (ligand-
gated)
 Receptors that affect gene transcription
 Receptors linked to enzymes that mostly
initiate a kinase cascade within the cell
Gene expression receptors
Drug Reactions
 You want a therapeutic effect without side effects.
 You can have:
◼ Adverse drug reactions
◼ Allergic drug reactions (hypersensitivity, anaphylactic
shock)
◼ Drug idiosyncrasy (abnormal/unusual response)
◼ Drug tolerance (decrease response)
◼ Cumulative drug effect (kidney, liver; Paracetamol)
◼ Toxic reactions
◼ Pharmacogenetic reactions (genetically caused abnormal
reaction)
Drug Interactions
 Drug-Drug:
◼ Interaction between drugs (interference)
◼ Additive (combination), synergistic (greater effect) or antagonistic
(neutralisation)
◼ Absorption, distribution, metabolisn and excretion competition
◼ Interfere at site of action (agonist or antagonist reactions)

 Drug-Food:
◼ Food may enhance or inhibit absorption
◼ Empty stomach might increase absorption into bloodstream
◼ Drugs that are irritable (nausea, vomiting) take with food.
Factors influencing drug response
 Age (metabolism rates decrease with age)
 Weight (perfusion rates increase with size)
 Gender (woman have a different body fat to water ratio – may
require smaller dosages)
 Physiological (acid-base balance, hydration, electrolyte
balance)
 Pathological (disease alters cellular function)
 Immunological (hypersensitivity)
 Pyschological (Placebo?)
 Environmental (sedation drugs)
 Tolerance (over time may need to increase dose)
Pharmacology and health care
 Assessment – recording and understanding a pts
drug history (subjective and objective)
 Diagnosis – judgements about risk for problems and
pt needs
 Planning – informed clinical decisions; outcome
goals; multidimensional Rx plans
 Implementation – Know the drugs; Right drug,
right dose, right time, right route and right Pt.
 Evaluation – monitoring pt response (adverse
effects)