Principles of pharmacology
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Principles of pharmacology - Marcador
Principles of pharmacology - Detalles
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| Drug metabolism phase I | Phase I: Small chemical changes and functionalise molecule for phase II -Functionalisation – addition of reaction group (oxidation) , unmasking of reactive group (reduction ) and hydrolysis . This leads to low lipophilicity , higher excretion and change in pharmacological effect. Oxidation by Cytochrome p450, non P450 oxidation , reduction and hydrolysis |
| Drug metabolism phase II | Phase II: - Conjugation reactions , increase water solubility , increase excretion Glucuronidation , sulphation , acetylation , amino acid conjugation , glutathione conjugation . Adding of large group often charges caused large decrease in lipophilicity , higher excretion , lower pharmacological effect. |
| Drug Absorption | Definition: Process by which a drug moves from the site of administration into the bloodstream. |
| Factors affecting absorption | Route of administration (oral, IV, IM, etc.). Lipid solubility of the drug. Presence of food in the stomach. pH and ionization of the drug. |
| Drug distribution | Definition: Dispersion of a drug throughout the body fluids and tissues. |
| Factors affecting drug distribution | Key Factors: Blood flow to tissues. Plasma protein binding (e.g., albumin binding limits free drug concentration). Volume of distribution (Vd): Relates the amount of drug in the body to plasma concentration. |
| Drug metabolism | Biotransformation of a drug into more water-soluble compounds for excretion. |
| Summary of phases in metabolism | Phase I (Functionalization): Oxidation, reduction, hydrolysis (e.g., via cytochrome P450 enzymes). Phase II (Conjugation): Addition of hydrophilic groups (e.g., glucuronidation, sulfation). Liver Role: Major site of metabolism due to high enzyme concentration. First-Pass Effect: Significant metabolism in the liver before reaching systemic circulation. |
| Drug excretion | Removal of drugs and metabolites from the body. |
| Routes and processes in drug excretion - Routes - think greys processes - kidney - STEPS | Primary Routes: Renal (urine). Hepatic (bile, feces). Minor routes: Sweat, saliva, breast milk. Renal Processes: Filtration (glomerulus). Reabsorption (tubules). Secretion (active transport mechanisms) |
| Bioavailability - a in availability = administered | Proportion of the administered dose that reaches systemic circulation |
| Factors affecting bioavailability - ADME | Absorption efficiency. First-pass metabolism. Drug solubility. |
| Half life definition and importance | Time required for the plasma concentration of a drug to decrease by half. Importance: Determines dosing frequency and duration of action. |
| Factors overall affecting drug distribution and metabolism - PATIENT AND DRUG | Patient Factors: Age (neonates and elderly have reduced metabolism). Genetic polymorphisms (e.g., variations in CYP enzymes). Liver and kidney function. Drug Interactions: Enzyme inducers (e.g., rifampin) increase metabolism. Enzyme inhibitors (e.g., ketoconazole) decrease metabolism. |
| Mechanisms of absorption ( think of the letters in the word) | Trans cellular such as diffusion and active transport And Paracellular |
| Routes of administration | Oral Sublingual (spray) Rectan Skin Injection Inhalation |
| Topical and systemic administration | Topical - on the skin Systems - in the body |
| Toxic effect of drug metabolism | Phase I and II often has toxic products rather than a parent drug administration |
| Phase 1 metabolism summary - purpose and processes | Purpose: Introduces or exposes a functional group (e.g., hydroxyl, amine) on the drug molecule to make it more reactive for Phase 2 metabolism. THEY ALL REQUIRE NADPH and oxygen Key Processes: Oxidation: Addition of oxygen (e.g., by cytochrome P450 enzymes in the liver). Codeine to morphine - first pass affect - N DEALKALATION CYP2D6 Reduction: Gain of electrons (less common). Hydrolysis: Splitting a molecule with water. Outcome: Produces a slightly modified, often more polar (but sometimes still active) drug. |
| Phase 2 metabolism summary purpose and processes | Purpose: Attach a large, water-soluble molecule to the drug or its Phase 1 product to enhance excretion via urine or bile. Key Processes: Glucuronidation: Addition of glucuronic acid (most common). Sulfation: Addition of a sulfate group. excretion. Phase 2 reactions are catalysed by TRANSFERASE ENZYMES |
| Selective toxicity | Selective toxicity refers to the ability of a drug to target specific microorganisms or cancer cells without damaging the host's cells. |
| On what basis is selective toxicity achieved | Selective toxicity is based on differences between the biology of the target and the host, such as: Unique structures (e.g., bacterial cell walls). Specific metabolic pathways (e.g., folic acid synthesis in bacteria). Genetic or molecular differences. |
| Examples of selective targets | Bacterial cell walls: Targeted by penicillins and cephalosporins. Bacterial ribosomes: Targeted by tetracyclines and macrolides. Viral enzymes: Targeted by reverse transcriptase inhibitors. Cancer cell DNA replication: Targeted by antimetabolites like methotrexate. |
| How do selective drug targets work | Inhibition of cell wall synthesis (e.g., β-lactams). Inhibition of protein synthesis (e.g., aminoglycosides bind to 30S ribosome). Disruption of membranes (e.g., amphotericin B targets ergosterol in fungi). Inhibition of nucleic acid synthesis (e.g., fluoroquinolones). Metabolic antagonism (e.g., sulfonamides inhibit folate synthesis). =S= SYNTHESIS |
| Therapeutic index = t for toxic | The therapeutic index is the ratio of a drug's toxic dose to its effective dose. A high therapeutic index indicates better selective toxicity. |
| : How do antibiotics achieve selective toxicity? | Antibiotics exploit unique bacterial features, such as: Peptidoglycan in cell walls (e.g., penicillin). Bacterial-specific DNA gyrase (e.g., ciprofloxacin). Prokaryotic ribosome differences (e.g., erythromycin). |
| Why is ST harder in antiviral drugs - antiviral - more risk | Viruses use host cell machinery for replication, so targeting the virus often risks harming host cells. Selective toxicity is achieved by targeting: Viral-specific enzymes (e.g., protease, reverse transcriptase). Viral entry or uncoating mechanisms. |
| 4 challenges to selective toxicity - SRDS | Similarity between host and pathogen/cell. Emergence of drug resistance. Collateral damage to host microbiota. Off-target effects leading to side effects. |
| Provide an example of selective toxicity in antimicrobials. | Penicillin targets bacterial cell wall synthesis, which is absent in human cells. |
| How do antifungals achieve selective toxicity? | Target unique fungal cell components, such as ergosterol in the cell membrane. |
| Why are some drugs more toxic than antimicrobials | Such antifungals , fungi has similairites with humans cells |
| How do antivirals achieve selective toxicity? | Target viral proteins and processes essential for replication that are absent in host cells. |
| What is the basis of selective toxicity for anticancer drugs? | Exploit differences in the growth rate of cancer cells versus normal cells. |
| What are common targets for anticancer drugs? Mum had cancer - M= Microtubule functions to be stablised | DNA synthesis: Methotrexate inhibits dihydrofolate reductase. Microtubule function: Paclitaxel stabilizes microtubules. Topoisomerase: Doxorubicin inhibits topoisomerase II. |
| Why do anticancer drugs often have significant side effects? | Normal rapidly dividing cells (e.g., in the GI tract, hair follicles) are also affected. |
| What is pharmacogenetics? | The study of genetic variations that influence individual responses to drugs. |
| What is the clinical relevance of pharmacogenetics? | Optimizes drug dosing. Minimizes adverse drug reactions. Improves therapeutic efficacy. |
| What are the two divisions of the peripheral nervous system (PNS)? | Somatic Nervous System: Controls voluntary muscles. Autonomic Nervous System (ANS): Regulates involuntary functions (divided into sympathetic and parasympathetic). |
| What neurotransmitters are primarily involved in the PNS? | Acetylcholine (ACh) and noradrenaline (NA). |
| What are the two types of cholinergic receptors? | Nicotinic receptors: Ionotropic, found in ganglia and skeletal muscles. Muscarinic receptors: G-protein-coupled, found in parasympathetic target organs. |
| What activates cholinergic receptors - agonists activate receptors | Cholinomimetics, e.g., bethanechol (muscarinic agonist), nicotine (nicotinic agonist). |
| What are the two main types of adrenergic receptors? Think a= alpha | Alpha receptors: α1 (vascular smooth muscle), α2 (presynaptic terminals). Beta receptors: β1 (heart), β2 (lungs, smooth muscle), β3 (adipose tissue). |
| What drugs stimulate adrenergic receptors? a= alpha receptors so adnergic receptors such as a.... | Adrenergic agonists, e.g., adrenaline, salbutamol (β2 agonist). |
| What is SAR in pharmacology? (structure activity relationship) | The relationship between the chemical structure of a drug and its biological activity. |
| What are the structural requirements for muscarinic agonists? | Positively charged nitrogen (usually a quaternary ammonium group). An ester or ether group to mimic acetylcholine. Correct stereochemistry for receptor binding. |
| What are key SAR points for nicotinic agonists? | A positively charged nitrogen. A proper distance between the nitrogen and the carbonyl group to fit the receptor |
| What are anticholinesterases? | Drugs that inhibit acetylcholinesterase, increasing ACh levels in the synapse. |
| What are the two main types of anticholinesterases?,think inhibitors | Reversible inhibitors: E.g., neostigmine, donepezil. Irreversible inhibitors: E.g., organophosphates like sarin. |
| How do irreversible anticholinesterases bind? irrevirsible to permantly inactivates | Covalently bind to the serine residue in the enzyme's active site, permanently inactivating it. |
| What structural modifications affect potency and selectivity? | Alkyl groups increase lipophilicity and CNS penetration (e.g., physostigmine). Larger substituents reduce enzyme degradation. |
| Who developed the idea of selective toxicity | Paul Ehrlich - from staning dyes - the term was magic bullet |
| What is chemotherapy | A chemical bonds to and kills a microbe or tumour cell |
| What are B-lactams | They target cell wall synthesis in bacteria used in antibiotics such as penicillin is a type of B-lactam |
| What is antimicrobial resistance | The inability to kill or inhibit the organism with clinically achievable drug concentrations - mutations or innate |
| Types of bacterial resistance | Intrinsic and acquired ( gene transfer) |
| Differences between fungi and bacteria | Fungi is eukaryotic , organelles , contain sterols , cell wall is chittin. Bacteria is prokaryotic , no organelles , no sterols , cell wall is peptidoglycocans |
| What are viruses | Not living , No organelles No cell wall or membrane Dependent on the host |
| What is cancer | Unregulated cell growth |
| Differences between normal cells and cancer cells | Cancer cell nucleus has mutated genes and has high metabolic demands |
| Ways of treating cancer | Surgery Radiation and immunotherapy |
| Cancer therapies | If the cancer is due to hormones then hormonal anti cancer agents would be used etc |
| What is immunotherapy | Activating the host immune response to target tumour cell antigens |
| What is personalised medicine | Tailored to that person based on genetics , life style and environment |
| Priciples of personalised medicine | Individualisation Targeted therapy Predictive and preventive |
| Benefits of personalised medicine | Reduce side affects And more drug efficacy |
| Function of the PNS | Sensory Input: Gathers information from the external and internal environment (via sensory receptors). Example: Feeling heat on your skin. Motor Output: Sends signals to muscles and glands for action. Example: Moving your hand away from heat. Homeostasis: Maintains balance in bodily functions through the ANS. |
| Muscarinic receptors have 2 types | Excitatory and inhibitory |
| Drugs acting on the cholinergic system | Agonists (enhance cholinergic activity) Antagonists (inhibit cholinergic activity) Acetylcholinesterase Inhibitors (prolong ACh action) |
| Analogy of the cholinergic system | ACh is the "mail." Nicotinic and muscarinic receptors are "mailboxes." Enzymes like AChE are the "cleanup crew" to clear old mail. |
| Antibiotics - | Bactericidal - irrevirsable lethal action on bacteria bacteriostatic - reversibly inhibit growth |
| Test the susceptibility of anttimicrobial | Determine which pathogen the bacteria is susceptible to |
| Types of bacteria resistance | Intrinsic - gram negative bacteria harder to penetrate Acquired - resistance by gene transfer |
| Antifungal exam answer | Explain selective T example terbinafine makes hole in the cell membrane of the fungi , by breaking down ergosterol in the cell membrane it causes the fungi to lose its structural integrity, leading to leakage of essential cellular contents and ultimately causing the fungi to die. |
| Antiviral answer | Explain selective T Remdesivir. Remdesivir inhibits the activity of the RNA-dependent RNA polymerase which is a type of viral protein so INHIBITS VIRAL PROLIFERATION |
| Anticancer answer | Explain Selective T Vinca alkoid - anti cancer drug - more effective as only targets rapidly dividing cells - via targeting microtubules leads to a disruption in the cell cycle so programmed cell death |