Practice Questions Flashcards
(8 cards)
Discuss the factors that affect the bioavailability of orally administered drugs. How does first-pass metabolism influence bioavailability?
• First-Pass Metabolism: Drugs absorbed from the gastrointestinal tract enter the hepatic portal circulation and are metabolized in the liver before reaching systemic circulation, reducing bioavailability.
• Solubility: Hydrophobic, non-polar drugs pass through cell membranes easily, increasing bioavailability, while hydrophilic, polar drugs have lower bioavailability.
• Instability: Some drugs are unstable in the gastrointestinal environment (e.g., Penicillin
G) and are destroyed before absorption.
• Formulation: The physical form of the drug (e.g., liquid vs. tablet) affects the rate and extent of absorption.
• pH: The ionization state of the drug, influenced by the pH of the environment, affects its ability to cross cell membranes.
Explain the concepts of drug affinity, potency, and efficacy. How are these parameters measured.
Affinity: The strength of attraction between a drug and its receptor. High affinity means lower doses are needed.
• Potency: The relationship between drug dose and the magnitude of effect. Measured by EC50 (the concentration that produces 50% of the maximum effect).
• Efficacy: The maximum response achievable from a drug. Measured by Emax (the maximal effect).
Describe the structure and function of the peripheral nervous system (PNS). How do the afferent and efferent neurons contribute to the overall function of the PNS?
• Structure of the PNS: Comprises nerves and sensory receptors that transmit information to and from the CNS.
• Afferent Neurons: Carry sensory information to the CNS (e.g., from skin, muscles, joints, and internal organs).
• Efferent Neurons: Carry motor signals from the CNS to effectors (e.g., muscles and glands).
• Function of the PNS: Facilitates communication between the CNS and the rest of the body.
• Voluntary Actions: Somatic nervous system controls voluntary movements via skeletal muscles.
• Involuntary Actions: Autonomic nervous system controls involuntary functions (e.g., heart rate, digestion).
Explain the pharmacological actions of cholinergic drugs on the autonomic nervous system. Discuss the differences between nicotinic and muscarinic receptors. How do cholinergic agonists and antagonists interact with these receptors?
• Cholinergic Drugs: Act on receptors where acetylcholine binds.
• Nicotinic Receptors: Found at ganglia of the sympathetic and parasympathetic nervous systems, neuromuscular junctions, and CNS. Respond to nicotine.
• Agonists: Mimic acetylcholine, stimulating receptors (e.g., nicotine).
• Antagonists: Block receptors, preventing acetylcholine action (e.g., curare).
• Muscarinic Receptors: Found in the postganglionic parasympathetic nervous system and CNS. Respond to muscarine.
• Agonists: Mimic acetylcholine, stimulating receptors (e.g., pilocarpine).
• Antagonists: Block receptors, preventing acetylcholine action (e.g., atropine).
Describe the four major processes involved in the perception of pain: transduction, transmission, modulation, and perception. How do these processes interact to create the experience of pain?
- Transduction converts noxious stimuli into electrical signals.
- Transmission carries these signals to the brain.
- Modulation influences the strength of the signals along the pathway.
- Perception is the subjective experience of pain, which integrates sensory messages with other factors like attention, expectation, and interpretation
Expected answer:
* Transduction: Activation of primary afferent neurons by noxious stimuli, leading to the generation of action potentials.
* Transmission: Pain impulses travel through A-delta and C fibres to the dorsal horn of the spinal cord, where they synapse with second-order neurons.
* Modulation: Pain signals are modulated at various levels, including the dorsal horn and brainstem, altering neural activity along the pain pathway.
* Perception: Pain signals are projected from the thalamus to the cerebral cortex, where they are perceived and interpreted.
Discuss the management strategies for hypovolemic, cardiogenic, obstructive, and distributive shock. How do the treatments differ based on the underlying pathophysiology?
Include the roles of intravenous fluids, vasopressors, and inotropes in your discussion.
• Hypovolemic Shock:
• Primary Problem: Decreased central venous pressure (CVP) due to volume loss.
• Treatment: Rapid intravenous fluid resuscitation to restore preload and maintain perfusion.
• Vasopressors: May be used temporarily if hypotension is profound.
• Inotropes: Not indicated; may worsen tachycardia.
• Cardiogenic Shock:
• Primary Problem: Decreased cardiac output due to pump failure.
• Treatment: Inotropes to improve contractility and support cardiac output.
• Intravenous Fluids: Not indicated; may worsen pulmonary congestion.
• Vasopressors: Generally contraindicated.
• Obstructive Shock:
• Primary Problem: Mechanical obstruction to circulation.
• Treatment: Relieve the obstruction (e.g., needle thoracostomy for tension pneumothorax).
• Response to Fluids/Vasopressors/Inotropes: Often minimal or short-lived
• Distributive Shock:
Primary Problem: Decreased systemic vascular resistance (SVR).
Treatment: Vasopressors to restore vascular tone and maintain perfusion pressure.
Intravenous Fluids: Required due to concurrent hypovolemia or maldistribution of fluids.
Inotropes: May be helpful in patients with sepsis-induced cardiomyopathy.
Explain the role of oxytocin in the management of labour and postpartum haemorrhage. How does oxytocin exert its effects on the uterus, and what are the potential side effects of its use?
Expected Answer:
• Role in Labour and PPH:
• Induction of Labour: Stimulates uterine contractions to initiate labour.
Management of PPH: Increases uterine tone to reduce bleeding.
• Mechanism of Action:
Receptor Binding: Binds to G-protein coupled receptors on uterine myofibrils.
Intracellular Calcium: Increases intracellular calcium levels, leading to uterine contractions.
Positive Feedback: Uterine contractions stimulate further oxytocin release.
• Potential Side Effects:
• Maternal: Hypotension, tachycardia, water intoxication (due to antidiuretic effect).
• Foetal: Foetal distress due to hyperstimulation of the uterus.
Discuss the pharmacodynamics of beta-agonists and anticholinergics in the treatment of asthma. How do these drugs exert their effects on the respiratory system?
Compare the mechanisms of action of salbutamol and ipratropium, and explain their roles in managing acute asthma exacerbations.
Beta-Agonists (Salbutamol):
• Mechanism of Action: Stimulate beta-2 adrenergic receptors, increasing CAMP levels, leading to bronchial smooth muscle relaxation.
• Effects: Bronchodilation, reduced airway resistance, improved airflow.
• Anticholinergics (Ipratropium):
• Mechanism of Action: Block muscarinic cholinergic receptors, reducing bronchoconstriction and mucus secretion.
• Effects: Bronchodilation, decreased mucus production.
• Comparison:
• Salbutamol: Rapid onset, short duration, primarily used for quick relief of acute symptoms.
• Ipratropium: Slower onset, longer duration, used as an adjunct to beta-agonists in acute exacerbations.
