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Pharmacology for Nursing - Topic 3: Physiology Concepts
Jun 1, 2024
Pharmacology for Nursing - Topic 3: Physiology Concepts
Introduction
Lecturer:
Professor Jim Hoffman
Topic:
Physiology Concepts for Nursing Pharmacology
Learning Objectives:
Autonomic nervous system, Renin-angiotensin-aldosterone system, and Inflammatory process
Resources:
Online text with hyperlinks to 4.2, 6.2, 10.2 sections
Importance of Basic Anatomy and Physiology
Essential for understanding medications and pharmacodynamics
Definition: Pharmacodynamics - effects of drugs on the body
Key drug responses:
Mimic/Stabilize normal functions
Inhibit/Block normal activities
Autonomic Nervous System (ANS)
Overview
Divisions: Central Nervous System (CNS) and Peripheral Nervous System (PNS)
Components of the PNS:
Motor (outgoing messages)
Sensory (incoming messages) to CNS
Motor Division: Somatic (voluntary) and Autonomic (involuntary)
Autonomic Nervous System Details
Sympathetic Nervous System (SNS):
Fight or Flight
Chemicals: Norepinephrine, Epinephrine, Dopamine, Serotonin (Catecholamines)
Receptor Sites: Alpha-1, Alpha-2, Beta-1, Beta-2
Parasympathetic Nervous System (PNS):
Rest and Digest
Chemical: Acetylcholine
Receptor Sites: Nicotinic, Muscarinic
Drug Actions in the ANS
Agonists:
Drugs that stimulate/mimic normal physiological functions
Antagonists:
Drugs that block normal physiological functions
Key Concepts
Sympathetic (Adrenergic) vs. Parasympathetic (Cholinergic)
Stimulating SNS: Pupil dilation, Inhibited secretions, Accelerated heart rate, Bronchodilation, Increased glucose production, Secretion of adrenaline, Urinary retention
Stimulating PNS: Pupil constriction, Facilitated secretions, Slowed heart rate, Bronchoconstriction, Stimulated bile release, Increased urination
Receptor Site Impacts:
Parasympathetic: Less selectivity (Muscarinic)
Sympathetic: Higher selectivity (Alpha and Beta receptors)
Renin-Angiotensin-Aldosterone System (RAAS)
Basic Components
Maintains fluid and blood pressure homeostasis
Key Players: Renin, Angiotensinogen, Angiotensin 1, Angiotensin 2, Aldosterone
Process:
Kidneys release renin in response to low fluid/Sodium
Renin + Angiotensinogen → Angiotensin 1
Angiotensin 1 + ACE (from pulmonary circulation) → Angiotensin 2
Angiotensin 2 Effects:
Widespread vasoconstriction, Stimulates adrenal cortex to release aldosterone
Aldosterone → Retains sodium and water, increasing blood volume and pressure
Key Concepts
Neural Response:
Sympathetic activation, release of epinephrine/norepinephrine, rapid vasoconstriction, and rise in heart rate
Hormonal Response:
RAAS activation, angiotensin 2 effects, and aldosterone-mediated fluid retention
Integration:
Sympathetic nervous system's short-term response works with RAAS for prolonged responses
Inflammatory Response
Overview
Role:
Body’s response to tissue injury
Components:
Increased permeability, blood flow, mediator chemicals (e.g., prostaglandin), sensitivity of pain receptors
Drugs:
Anti-inflammatories (NSAIDs, Steroids), Immunosuppressants
Key Concepts:
Anti-inflammatory drugs manage pain by blocking or inhibiting parts of the natural inflammatory response
Importance of understanding potential ramifications of interrupting normal physiological responses
Final Notes
Importance of integrating pharmacology with anatomy, physiology, and pathophysiology
Review key systems and their drug interactions:
Autonomic Nervous System
Renin-Angiotensin-Aldosterone System
Inflammatory Response
Understanding physiology concepts aids in comprehending pharmacodynamics of medications
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