Dental Therapeutics Flashcards
(34 cards)
What is pharmacodynamics and what do pharmacodynamic mechanisms of drug actions describe?
Pharmacodynamic refers to is what the drug does to the body. - is the study of how drugs affect the body by interacting with biological systems to produce therapeutic or toxic effects. Pharmacodynamic mechanisms describe the specific ways drugs exert these effects at the molecular or cellular level, primarily by binding to receptors, enzymes, ion channels, or transport proteins, thereby altering normal physiological functions.
How do drugs interact with receptors to produce effects, and what is the difference between agonists and antagonists?
Drugs often produce effects by binding to receptors—specialized proteins on or inside cells that mediate biological responses. Agonists bind to receptors and activate them, mimicking the body’s natural ligands to trigger a response, such as morphine activating opioid receptors for pain relief. Antagonists bind to receptors but do not activate them; instead, they block the receptor and prevent natural ligands from eliciting their effect, like propranolol blocking beta-adrenergic receptors to reduce heart rate and blood pressure.
What is pharmacokinetics and what do pharmacokinetic factors describe?
Pharmacokinetics is the study of how a drug moves through the body overtime, including absorption, distribution and where its taken, metabolism(through liver) (how long it takes to achieve the peak effect at site of action), and excretion (how the body makes the drug inactive through the kidney). Pharmacokinetic factors are the biological and physiological variables that influence these processes, ultimately determining the drug’s onset, intensity, and duration of effect.
What factors influence drug absorption and why is absorption important?
The transfer of a drug from its site of administration into the bloodstream. It is influenced by the drug’s formulation, route of administration, solubility, pH, blood flow at the site, and presence of food or other drugs. Absorption determines how much and how quickly a drug becomes available for action; for example, oral drugs can be affected by stomach acidity or first-pass metabolism in the liver.
What are the main enteral routes of drug administration?
Enteral routes involve the gastrointestinal tract and include:
Oral : Swallowed, absorbed mainly in the small intestine; most common method.
Sublingual: Placed under the tongue for rapid absorption, bypassing stomach and liver metabolism.
Rectal: Inserted into the rectum; useful when oral administration isn’t possible, but absorption can be variable.
What factors influence the absorption of orally administered drugs, and how does sublingual administration differ?
Most oral drugs are absorbed in the small intestine due to its large surface area and neutral pH. Absorption is influenced by several factors:
Gastrointestinal motility: Affects drug contact with absorptive surfaces.
Food intake: Slows absorption.
Mesenteric blood flow: More blood flow enhances absorption.
Drug interactions: Other substances can slow, enhance, or block absorption.
Dosage form: Controlled-release or enteric coatings affect the rate and site of absorption (e.g. extended-release tramadol).
In contrast, sublingual administration involves placing the drug under the tongue, where it is rapidly absorbed through blood vessels. This route bypasses the digestive system and liver, offering a faster onset of action—ideal in emergencies (e.g. glyceryl trinitrate for chest pain).
How do pH and pKa affect the absorption of orally administered drugs?
Oral drugs must cross cell membranes made of phospholipid bilayers, which allow lipophilic (fat-soluble), non-ionized drugs to pass through more easily.
Most drugs are weak acids or weak bases. Their ionization (charged or uncharged state) depends on the drug’s pKa (the pH at which 50% is ionized) and the pH of the environment (e.g., stomach vs. intestine).
Non-ionized drugs are better absorbed.
In the small intestine (pH ~7–8), many drugs become non-ionized and are well absorbed.
For weak bases (like local anesthetics), low pH (e.g., in infected tissue) causes more ionization, reducing absorption and effectiveness.
What are the main parenteral routes of drug administration?
Parenteral routes bypass the GI tract and include:
- Intravenous (IV): Direct injection into a vein; immediate effect and 100% bioavailability.
- Intramuscular (IM): Injection into muscle tissue; slower absorption than IV but faster than oral.
- Subcutaneous (SC): Injection under the skin; slow, sustained absorption.
- Intradermal: Injection into the skin’s dermis, used mainly for allergy tests or vaccines.
when to use parental administration?
Parenteral administration is used when:
The oral route isn’t possible (e.g. vomiting, unconsciousness, difficulty swallowing).
- A rapid onset of drug action is required (e.g. in emergencies).
- Precise blood concentrations are needed (e.g. in hospital or ICU settings).
- Also, since the drug bypasses the stomach and intestines, it avoids: Acidic degradation, Delays from food, First-pass metabolism by the liver
What is the time to peak concentration?
This refers to how long it takes for a drug to reach its highest concentration in the blood after being given:
- IV: Immediate (goes straight into the blood).
- IM: Quick but slightly slower than IV.
- SC: Slower and more gradual.
- Oral: Slower due to digestion, stomach acid, food interactions, and liver metabolism.
- Rectal: Can be effective but absorption is less predictable.
what are the main topical (applied to body parts) routes of drug adminstration?
Topical routes involve application to body surfaces:
- Transdermal: Absorbed through the skin into systemic circulation (e.g., nicotine patch).
- Local topical: Applied on skin or mucous membranes for localized effect (e.g., creams, eye drops).
- Inhalation: Absorbed through lung tissues; fast action, commonly used for respiratory drugs.
What are some other less common routes of drug administration?
Other routes include:
Intrathecal/epidural: Injection into spinal fluid or epidural space for anesthesia or pain relief.
Intranasal: Sprayed into the nose for rapid absorption through nasal mucosa.
Buccal: Placed between gums and cheek for absorption through oral mucosa.
How does drug distribution occur and what factors affect it?
the movement of drugs throughout the body fluids and tissues to reach its action site. it depends on:
- Drug properties (size, water- or fat-solubility)
- Plasma protein binding (less binding in liver disease increases free drug and toxicity)
- Body fluid compartments (blood plasma, interstitial fluid, intracellular fluid)
- Barriers like the placenta limit drug transfer to the fetus
What is drug metabolism and what factors influence it?
Drug metabolism is the process by which the body chemically modifies a drug, usually in the liver, to make it more water-soluble (hydrophilic) so it can be more easily eliminated from the body. This often reduces the drug’s activity and helps prepare it for excretion.
- if the enzyme/ liver function is inadequate, the metabolic affect in the liver can be compromised, so to excrete the drug, the drug needs to become more hydrophilic and lipophilic, it can excrete and be soluble in the urine.
How is drug excretion carried out and what affects it?
Drug excretion is mainly carried out by the kidneys, where drugs or their metabolites are eliminated through urine. Factors that affect drug excretion include:
- Kidney function: Impaired kidney function slows excretion, causing drugs to accumulate.
- Drug properties: Drugs must be sufficiently hydrophilic to be excreted in urine.
- Metabolism: Metabolism usually converts drugs into more water-soluble forms to aid excretion.
- pH of urine: Can influence the ionisation of drugs, affecting their reabsorption or elimination.
what is the difference between half life of drugs and steady state?
half life is the time it takes for the amount of drug in the body to reduce by half.
steady state when the amount of drug taken equals the amount removed, so the drug level in the body stays stable.
Outline the difference between type A and type B adverse drug reactions, and list examples of the clinical signs and symptoms of each.
Type A is predictable reactions related to the known pharmacological effects of the drug. it is dose dependent (more drug= more reaction.
e.g. bleeding from anticoagulants like warfarin
- explained by the pharmacology of the drug
Type B- bizarre reactions- unpredictable, not related to the drug’s normal action
- can happen at any dose, often immune- mediated/ allergic reactions, can be severe/ life threatening
e.g. anaphylaxis/ allergic rash from penicillin
What are the main types of drug receptors?
- Ion channels
- ligand gated: activated by a ligand or substrate which can be a drug on your transmitter
- voltage-gated: activated by a change in the voltage of the cell (action potential) and may prevent the action potential from firing. - G protein-coupled receptors (GPCRs)-
- Ligand-regulated transmembrane enzymes (e.g., receptor tyrosine kinases)- activation of cell signalling.
- Intracellular receptors (e.g., steroid hormone receptors)- receptors that regulate gene transcription and translation.
Define agonists and antagonists.
Agonists bind receptors and activate them to produce a physiological response (have affinity and efficacy).
Antagonists bind receptors but block activation, preventing a response (have affinity but no efficacy).
what is inverse agonist and partial agonist
- inverse agonist: any drug that binds to a receptor and produces an opposite effect as that of an agonist
- partial agonist has affinity for the receptor, binds to it, but has lower efficacy than a full agonist and doesnt produce the maximal resonse.
Explain drug synergism and antagonism.
Synergism: Two drugs together produce a greater effect than the sum of their individual effects.
Antagonism: One drug reduces or blocks the effect of another, which can be physical, chemical, physiological, or receptor-based.
Describe competitive vs non-competitive antagonism.
Competitive: Antagonist competes with agonist at the same receptor site; effect can be overcome by increasing agonist concentration.
Non-competitive: Antagonist binds a different site, reducing agonist efficacy; effect cannot be overcome by more agonist.
What is the therapeutic window and why is it important?
The therapeutic window is the dosage range between the minimum effective dose and the minimum toxic dose. Drugs with narrow windows require careful monitoring to avoid toxicity.
- with increasing doses of a drug, we see a particular percentage of people exhibiting a therapeutic effect, further increasing doses, we receive percentage of people exhibiting a toxic effect.
what is therapeutic index?
The therapeutic index is a measure of a drug’s safety. It compares the amount of drug that causes a therapeutic effect to the amount that causes toxicity.
A high TI = wide safety margin (safe drug)
e.g. Paracetamol, Penicillin
A low TI = narrow safety margin (requires close monitoring)
e.g. Warfarin, Digoxin, Lithium
