Pharmacokinetics
1. Definition: Pharmacokinetics (PK) is the study of how drugs are
absorbed, distributed, metabolized, and excreted by the body.
2. Absorption: The process by which a drug enters the bloodstream from
its site of administration (e.g., orally, intravenously, topically).
3. Distribution: Once in the bloodstream, drugs are carried to various
tissues and organs throughout the body via the circulatory system.
4. Metabolism: Also known as biotransformation, metabolism is the
process by which drugs are chemically altered in the body, usually in
the liver, to facilitate their elimination.
5. Liver Enzymes: Many drugs are metabolized by enzymes in the liver,
such as the cytochrome P450 enzymes.
6. Metabolites: The products of drug metabolism, which may be
pharmacologically active or inactive.
7. Half-Life: The time it takes for the concentration of a drug in the
bloodstream to decrease by half. It is an important measure of how
long a drug remains in the body.
8. Clearance: The rate at which a drug is removed from the bloodstream,
often measured in units of volume per time (e.g., liters per hour).
9. Bioavailability: The fraction of a drug dose that reaches systemic
circulation unchanged after administration, typically expressed as a
percentage.
10. First-pass Metabolism: Some drugs undergo extensive
metabolism in the liver before reaching systemic circulation, leading to
reduced bioavailability.
11. Factors Affecting Absorption: Factors such as drug
formulation, route of administration, gastric emptying time, and
gastrointestinal pH can affect drug absorption.
12. Factors Affecting Distribution: Drug distribution is influenced
by factors such as blood flow to tissues, plasma protein binding, and
tissue permeability.
13. Factors Affecting Metabolism: Genetic variations in drug-
metabolizing enzymes, drug interactions, and disease states can affect
drug metabolism.
14. Renal Excretion: Many drugs and their metabolites are
eliminated from the body via the kidneys through urine.
15. Drug-Drug Interactions: Pharmacokinetic interactions occur
when one drug affects the absorption, distribution, metabolism, or
excretion of another drug, altering its concentration and effects in the
body.
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Pharmacodynamics :
1. Drug Binding: The drug binds to its target, typically a
receptor or enzyme, forming a drug-receptor complex.
2. Receptor Activation/Inhibition: This binding triggers a
series of biochemical events, leading to either activation or
inhibition of the receptor.
3. Signal Transduction: Activation of the receptor initiates
signal transduction pathways within the cell.
4. Cellular Response: The signal transduction pathways lead
to specific cellular responses, which can include changes in
gene expression, ion channel activity, enzyme activity, or
other cellular functions.
5. Physiological Effect: The cellular responses ultimately
produce a physiological effect, such as muscle contraction,
hormone secretion, or neurotransmitter release.
6. Dose-Response Relationship: The intensity of the
physiological effect is often related to the dose of the drug
administered.
7. Potency: Potency refers to the amount of drug required to
produce a certain effect. Drugs with higher potency require
lower doses to produce the same effect compared to drugs
with lower potency.
8. Efficacy: Efficacy refers to the maximum effect that a drug
can produce, regardless of dose. Drugs with higher efficacy
produce a greater maximal response.
9. Affinity: Affinity refers to the strength of the binding
between a drug and its receptor. Drugs with higher affinity
bind more tightly to their receptors.
10. Specificity: Drugs often exhibit specificity for certain
receptors or enzyme subtypes, which can influence their
effects and side effects.
11. Duration of Action: The duration of action of a drug
depends on factors such as its half-life, rate of metabolism,
and rate of elimination from the body.
12. Tolerance: Prolonged exposure to certain drugs can
lead to tolerance, where higher doses are required to
produce the same effect.
13. Desensitization/Downregulation: Continued
exposure to certain drugs can lead to desensitization or
downregulation of receptors, reducing the cellular response
to the drug.
14. Drug Interactions: Drug-drug interactions can occur
when
Protein synthesis inhibitors:
Protein synthesis inhibitors are a class of antibiotics that
target bacterial ribosomes, preventing them from
synthesizing proteins essential for their survival. Here are
ten points about them:
1.Mechanism of Action: Protein synthesis inhibitors
interfere with various stages of protein synthesis in
bacteria, including initiation, elongation, and termination.
2.Ribosome Targeting: They primarily target bacterial
ribosomes, which are structurally different from
eukaryotic ribosomes, thus reducing the risk of toxicity to
human cells.
3.Classes: There are different classes of protein
synthesis inhibitors, including aminoglycosides,
tetracyclines, macrolides, chloramphenicol, and
oxazolidinones.
4.Aminoglycosides: These antibiotics bind to the 30S
subunit of bacterial ribosomes, causing misreading of
mRNA and inhibiting protein synthesis.
5.Tetracyclines: Tetracyclines inhibit protein synthesis
by binding to the 30S subunit and preventing the
attachment of aminoacyl-tRNA molecules to the A site.
6.Macrolides: Macrolides bind to the 50S subunit of
bacterial ribosomes, inhibiting the translocation step of
protein synthesis.
Chloramphenicol: Chloramphenicol inhibits protein
synthesis by binding to the 50S subunit and inhibiting
peptidyl transferase activity
7 :Drugs like linezolid inhibit protein synthesis by binding
to the 50S subunit and preventing the formation of the
initiation complex.
8.Broad Spectrum: Protein synthesis inhibitors have a
broad spectrum of activity against various bacterial
species, making them useful in treating a wide range of
infections.
9.Resistance: Bacteria can develop resistance to protein
synthesis inhibitors through mechanisms such as
enzymatic modification of the drug, efflux pumps, or
target site alterations.
Anti-cancer drugs :
Types: Anti-cancer drugs include chemotherapy, targeted
therapy, immunotherapy, and hormone therapy. Each
type works differently to target and kill cancer cells.
Chemotherapy: These drugs work by targeting rapidly
dividing cells, which is a hallmark of cancer cells. They
can affect both cancerous and healthy cells, leading to
side effects like hair loss and nausea.
Targeted Therapy: These drugs target specific
molecules or pathways involved in cancer cell growth.
They can often spare healthy cells, resulting in fewer side
effects compared to chemotherapy.
Immunotherapy: This approach harnesses the body’s
immune system to fight cancer. Immunotherapy drugs
help the immune system recognize and attack cancer
cells.
Hormone :Therapy: Certain cancers, such as breast and
prostate cancer, are driven by hormones. Hormone
therapy works by blocking hormone receptors or reducing
hormone levels in the body to slow or stop cancer growth.
Combination Therapy: Often, multiple anti-cancer
drugs are used together to increase effectiveness or
overcome drug resistance.
Side Effects: While anti-cancer drugs can be life-saving,
they can also cause side effects such as fatigue, nausea,
vomiting, hair loss, and increased risk of infections.
Drug Resistance: Cancer cells can develop resistance to
anti-cancer drugs over time, leading to treatment failure.
Researchers are continually working on strategies to
overcome drug resistance.
5. Human insulin.
Human insulin is a protein hormone crucial for regulating blood
sugar levels in the body. The process of producing human insulin
involves genetic engineering techniques. Here’s a simplified
overview:
1. **Isolation of the Insulin Gene**: The gene that encodes
human insulin is isolated from human DNA.
2. **Insertion into Host Cell**: The isolated gene is then
inserted into a host cell, typically a bacterial cell like
Escherichia coli (E. coli) or yeast. These cells serve as
“factories” for producing insulin.
3. **Gene Expression**: The host cell’s machinery reads the
inserted gene and produces mRNA (messenger RNA) based
on its instructions.
4. **Translation**: The mRNA is translated into a precursor
protein called preproinsulin.
5. **Processing**: Preproinsulin undergoes modifications inside
the cell, including cleavage of signal sequences, to form
proinsulin.
6. **Folding and Disulfide Bond Formation**: Proinsulin folds
into its three-dimensional structure, and disulfide bonds form
between specific amino acids, stabilizing the protein.
7. **Further Processing**: Enzymes within the host cell cleave
proinsulin to yield mature human insulin.
8. **Harvesting and Purification**: The insulin is harvested from
the host cells and purified to remove any impurities.
9. **Formulation**: The purified insulin is formulated into
various forms, such as rapid-acting, short-acting,
intermediate-acting, or long-acting, depending on the needs
of patients.
10. **Packaging and Distribution**: The final insulin product
is packaged and distributed to pharmacies and healthcare
facilities for use by individuals with diabetes.
This process enables the mass production of human insulin,
providing a life-saving treatment for millions of people worldwide
with diabetes.
