PK- effect of body to drug

PD- effect of drug to body

Pharmacon-drug
Dynamis-power
Kinesis-movement

1. Replace or act as subs?tutes;

2. S?mulate cellular ac?vi?es;
3. Slow down cellular func?ons;
4. Interfere with the func?oning of foreign cells;

ODA- star?ng effect of the drug; ?me it takes to reach MEC.

POA-drugs effects at its highest.
DDA- length of ?me the drug exerts its effects.
MEC/cri?cal concentra?on- plasma drug concentra?on (PDC) to cause therapeu?c effect.
MTC- lowest PDC that can cause adverse effects.
TR- PDC between MEC and MTC to achieve the desire Tx effect.

<MEC-drug exerts no therapeu?c effect.

>MTC- causes undesirable effects.

Dose response curve

- Low drug dose corresponds to typical cellular response.
- Increasing the dose would cause drama?c rise in cellular response.
- When the drug has reached its maximum effec?veness, increasing the dose would only
produce minimal to no response.

Proper ?ming of drug administra?on is essen?al to maintain therapeu?c level and prevent the
toxic level of the drug.

The trough level is the lowest drug concentra?on (DC) in the Px bloodstream; collected just
before the administra?on of the next drug dose.

The peak level is the highest dc in the Px bloodstream. PO drugs – 1-3 hours; IV 10 mins.

TL- measures the rate of drug excre?on.

PL- indicates rate of drug absorp?on.

TI- indicates the margin of safety between the Tx dose (ED) and Lethal Dose (LD). Rela?onship is
LD50:ED50.
LD50- median lethal dose in 50% of sample popula?on.
ED50-median effec?ve dose in 50% of sample popula?on.
The more significant the differences, the greater the TI, and the safe the medica?on.
Drug-receptor interaction- The receptor theory of drug action explains that drug molecule
usually acts on receptor sites within the body, resulting in increased or decreased cellular
activity, change in the permeability of cell membranes, or modification of cellular metabolism.

intrinsic theory of drug action- The initiation of a response after the drug and the receptor
binds.

occupational theory of drug action- Likewise, the intensity of drug action is influenced by the
amount of occupied receptor sites. More receptors are filled- the intensity of the drug action is
stronger.

the rate theory - considers the time when drug-receptor interaction occurs. This means that
when the drug interacts with the receptor faster, the cellular response will also be faster.

This is known as the law of mass action- This law implies that drug effects depend on drug
concentration (or dose) that interacts with receptors; thus, the greater the drug dose, the
greater the percentage of occupied receptors, and the greater the cellular response.

the induced-fit theory proposes that a receptor does not necessarily need to be in an exact
shape or configuration to bind with the active substrate (drug). As the substrate binds with the
receptor, the latter changes its shape in conformation with the substrate’s shape (induced fit
mechanism) to permeate a better fit and cause a cellular response.

An agonist drug binds with the receptor to stimulate a response. (insulin)

An antagonist is a drug that attaches to the receptor but does not cause a response.
(Monoamine oxidase -relief of depression)

- Competitive antagonists compete with agonists for receptor sites.

- While non-competitive antagonists bind on other sites of the receptor or cell and
inactivate it.
- partial agonist is a drug that interacts with the receptor but produces only a slight
chemical action and response. (buprenorphine-partially binds with opiate receptors in
the CNS)

the cellular system theory explains that drugs can cause biological effects by interacting with
the body’s enzyme systems, either by inhibiting or enhancing the action of the enzyme.

Nonselective and nonspecific interactions. Selectivity refers to a drug’s ability to preferentially

bind or attach to specific receptors in a particular organ or system. The specificity of drug action
relates to the number of different mechanisms involved. Ideally, all pharmacologic agents would
act only on the target receptor sites or enzyme systems to cause therapeutic effects on human
cells.

Most drugs are nonselective and nonspecific, causing alteration of many cellular processes.
These nonselective and nonspecific interactions explain the secondary effects that patients
experience while on drug therapy.

Libera?on-drug is released from its pharmaceu?cal or dosage form.

Excipients- Most drugs have mixtures with one or more inac?ve substances.

- to serve as fillers that give the product its shape and size
- to enhance drug absorption
- to lessen the strength of very potent drugs
- to enable a more convenient and accurate measurement of drug dosage
- to control the release of the active drug over a period of time

Libera?on: (3D)
- Disintegra?on – breakdown of the drugs dosage into smaller granules
- Disaggrega?on-further breakdown of granules to smaller fine par?cles
- Dissolu?on- drugs molecules are dispersed in gastric fluid, body cavi?es, or ?ssues
before absorp?on.

Immediate release- release of Tx drug without delay. (analgesics, an?bacterial, an?HTN)

Delayed- Tx drug is released some?me aaer it is taken. (Enteric-coated aspirin, NSAIDs)
Extended- formulated to make the drug available over extended period; steadier PDC.
(nevirapine, methylphenidate, felodipine, carbidopa levodopa)

Absorp?on- movement of the drug par?cle from the source of entry to the bloodstream.

a. passive diffusion – the drug moves from an area of higher concentration to an area of lower
concentration. This mechanism does not require energy or a carrier protein to move the drug
across biological membranes.

b. facilitated diffusion – this mechanism does not use energy. However, it needs a
transmembrane carrier protein (such as an enzyme) to facilitate the movement of a large drug
molecule from an area of higher concentration to an area of lower concentration.

c. active transport – carrier proteins are needed to facilitate drug absorption across
membranes. Drug molecules must closely resemble the structure of the carrier protein to
facilitate absorption. Also, energy (ATP) is required to facilitate movement against a pressure
gradient (from an area of lower concentration to an area of higher concentration)
d. endocytosis – this mechanism involves the absorption of large-sized drug particles through
engulfment by the cell membrane. The drug is transported into the cell by pinching the drug-
filled vesicle. Vitamin B12 in the gut is absorbed through this mechanism

Factors affec?ng drug absorp?on

a. Drug from, dosage, and solubility
b. Route of administra?on
c. pH of body fluids
d. blood circula?on
e. surface area
f. food and other drugs
g. exercise
h. pain and stress
i. first-pass effect

Distribution - occurs when the drug particle is delivered from the site of absorption to its site of
action.

Factors affec?ng distribu?on

a. volume of distribu?on
b. obesity
c. drug solubility
d. plasma protein binding
e. natural barriers of the system

Metabolism- process of chemically altering the drug within the body by enzyma?c ac?ons.
Takes place in the liver.

Occurs through:
- Detoxifica?on-modified and converted into inac?ve, water-soluble form, excreted
through the kidneys.
- Ac?va?on- inac?ve drugs are transformed into a more ac?ve metabolite.
- Forma?on of toxic metabolites- some drugs may be converted into a more dangerous
from when acted by the liver.

Factors that influence Metabolism

a. Age
b. Malnutri?on
c. Diseases
d. Drugs
e. Gene?cs
Excre?on- drugs and their metabolites are removed from the body via excretory organs.

Factors that influence excre?on:

a. Renal excre?on
b. Drugs
c. Blood concentra?on
d. Half-life (t1/2)
e.