LM 2A Protection & Comfort PDF - NUR 370

# Learning Module 2A: Protection & Comfort ## NUR 370 ## Rebecca Young, MS, RN, CCRN ## Learning Objectives - Describe the sequence of events in the immune and inflammatory responses. - Discuss the role of anti-inflammatory agents and immunizations in mitigating the inflammatory response and pre...

# Learning Module 2A: Protection & Comfort ## NUR 370 ## Rebecca Young, MS, RN, CCRN ## Learning Objectives - Describe the sequence of events in the immune and inflammatory responses. - Discuss the role of anti-inflammatory agents and immunizations in mitigating the inflammatory response and prevention of diseases. - Differentiate between normal and abnormal anatomy and physiology of the autonomic nervous system. - Determine the mechanism of action, indication(s) and expected/unexpected outcomes of medications impacting protection and comfort. # Autonomic Nervous System - Regulates homeostasis of the body's normal functions through CNS, PNS, and endocrine responses. - Nerve impulses in PNS are sent to thalamus, medulla, & spinal cord (CNS). - From the CNS, impulses are sent out to stimulate organs, glands, muscles. - Blood pressure, heart rate, respiratory rate, temperature, fluid status, urinary output, digestion. - Parasympathetic vs Sympathetic. # Sympathetic Nervous System - “Fight-or-flight”: response to a stressor. - CNS cells in thoracic and lumbar areas of spinal cord stimulate nerve ganglia. - Neurotransmitters released; primarily norepinephrine and epinephrine. - Because the body is attempting to survive, it picks organ systems that are most beneficial: ↑ heart rate, ↑ blood pressure, ↑ respiratory rate, bronchodilation, pupil dilation, breakdown of glucose. - Elimination, digestion, reproduction all slow. # Adrenergic/Sympathetic Receptors - Alpha and Beta receptors that respond to circulating epinephrine and norepinephrine. - Alpha1, Alpha2, Beta1, Beta2. - Respond differently based on concentrations of neurotransmitters. - Some drugs may be specific to receptor type, others stimulate all receptors. - More specific drugs result in less systemic side effects. # Adrenergic Agonists - Alpha and Beta Adrenergic Agonist; dopamine, epinephrine. ## Mechanism of Action - **Dopamine:** Increased HR, increased BP; preserves blood flow to kidneys; treats shock. - **Epinephrine:** Vasoconstriction, increased HR, increased BP, bronchodilation; treats shock, severe bronchospasm (asthma), anaphylaxis. ## Pharmacokinetics - IV or IM. ## Contraindications - Pheochromocytoma. - Tachyarrhythmias, Ventricular fibrillation. - Hypovolemia (give fluids). ## Adverse Effects - **Effects on the heart/CV:** Arrhythmias, hypertension, palpitations, angina, dyspnea. - **Depressant effects on the GI tract:** Nausea, vomiting, constipation. - **Sympathetic stimulation effects**: Headache, sweating, feelings of tension or anxiety, and piloerection. # Nonselective Adrenergic Blocking Agents - Nonselective adrenergic blocking agents; labetalol ## Mechanism of Action - Blocks the effects of norepinephrine at alpha and beta-receptors throughout the SNS, decreasing BP, HR and improving renal perfusion. - Treats hypertension and tachycardia. ## Pharmacokinetics - Oral or IV. ## Contraindications - Bradycardia, heart block, asthma. - Caution with clients diagnosed with diabetes (masks symptoms of hypo/hyperglycemia). ## Adverse Effects - Bradycardia, hypotension, bronchospasm, cough. ## Client/Therapy Management - Monitor HR, BP, & blood glucose. # Parasympathetic Nervous System - “Rest and digest”: slows metabolism/function to conserve energy. - CNS cells in cranium and sacral areas of spinal cord stimulate nerve ganglia. - Neurotransmitters released; acetylcholine. - Conserve energy, build up proteins and nutrients, increase digestion: ↑ motility/secretions in GI tract, ↓ heart rate, bronchoconstriction, relaxation of sphincters, contraction of urinary bladder, pupil constriction. # Cholinergic/Parasympathetic Receptors - Receptors found in muscle or organs - Muscarinic or nicotinic - Respond differently based on concentrations of neurotransmitters. - Drugs tend to stimulate all cholinergic receptors, so see systemic effects throughout the body. - Some drugs are specific to muscarinic vs. nicotinic receptors. # Direct-Acting Cholinergic Agonists - Direct-Acting Cholinergic Agonists; bethanechol ## Mechanism of Action - Mimics acetylcholine and parasympathetic stimulation - Treats urinary retention, atonic bladder; glaucoma. ## Pharmacokinetics - Oral. ## Contraindications - Bradycardia, hypotension, and coronary artery disease. ## Adverse Effects - **Systemic effects of parasympathetic stimulation:** Bradycardia, hypotension, heart block. - **Bladder Spasm:** # Stress Response - Homeostasis: maintenance of stable internal environment. - Threatened during a stress response. - Ideally, stress responses should be acute. If chronic, issues result with a suppressed immune system and increased energy demands; body begins to break down. - Stress response is designed protect the body but if overwhelmed, can cause damage to the body. - Control systems and feedback mechanisms in place to regulate cell function. # Control Systems/Feedback Mechanisms - Control systems integrate the body’s responses to stressors (physical, emotional, behavioral) and create a stress response. - **Sensor:** detects the change — **Integrator**: assesses incoming information and compares it to “normal” — **Effector:** attempts to reverse the change. # Negative Feedback System - Decrease occurs of substance, body stimulated to increase it// increase occurs of substance, body stimulated to decrease it. # General Adaptation Syndrome (GAS) - HPA axis plays a large role in stress response (hypothalamus-pituitary-adrenal). - Regulates ANS and neurotransmitter release. - 3 stages: alarm, resistance, fatigue. ## Alarm - Stimulation of sympathetic nervous system. - HPA axis stimulated; epinephrine, norepinephrine, dopamine, cortisol release. ## Resistance - Most efficient defenses are initiated. - Cortisol decreases. ## Fatigue - Stressor is prolonged or overwhelms the body. - Resources are depleted. - Systemic damage to the body occurs. # Conditioning Factors: How do Different People Respond and Adapt to Stress? - Age, genetics, sex, life experience, nutrition, social support. - Body reserve, health status, circadian rhythm, hardiness (control over environment + purpose in life), psychosocial factors. # Acute Stress - Should be an acute and time-limited trigger. - Fight-or-flight response (SNS): pounding headache, increased vital signs, increased alertness, blood diverted away from less essential organs. - Client with limited coping may develop stress-induced disease processes: anxiety, depression, eating disorders, sleep disorders, high blood pressure (hypertension), pain, infection, migraine. # Chronic Stress - Chronic intermittent; stressor exposed to many times, over time. - Chronic sustained; stressor exposed to constantly, does not dissipate. - HPA axis becomes overactive or underactive: - Failure in neural or hormonal connections. - Stressor stimulus is prolonged. - Stressor stimulus is so great it overwhelms the system. - Impacts cardiac, immune, neurological gastrointestinal, substance use, mental health. # Learning Module 2B: Protection & Comfort ## NUR 370 ## Rebecca Young, MS, RN, CCRN ## Learning Objectives - Describe the sequence of events in the immune and inflammatory responses. - Discuss the role of anti-inflammatory agents and immunizations in mitigating the inflammatory response and prevention of diseases. - Differentiate between normal and abnormal anatomy and physiology of the autonomic nervous system. - Determine the mechanism of action, indication(s) and expected/unexpected outcomes of medications impacting protection and comfort. # Adaptive vs Innate Immunity - **Adaptive**: against specific pathogens or changed body cells. - **Innate**: against foreign bodies, injuries and pathogens. ## Adaptive Immunity - Defense cells in the blood: B lymphocytes. - Antibodies. - Defense cells in the tissue: T lymphocytes. ## Innate Immunity - Bacteria-killing substances. - Protection on the outside: the skin. - Protection on the inside: all mucous membranes. - First attack in the tissue: scavenger cells. # Barrier Defenses - **Skin**: first line of defense to protect tissues and organs. - Glands secrete chemicals to destroy pathogens. - Skin sheds daily to rid of any pathogens. - Normal bacterial flora. - **Mucous membranes**: line the respiratory tract, gastrointestinal tract, genitourinary tract. - Creates mucus to trap pathogens. - Protects GI cells from stomach acid/digestive enzymes. - **Gastric acid**: destroys ingested pathogens. - Normal gastric flora. - **Major histocompatibility complex (MHC)**: histocompatibility antigens embedded in cell membranes. - Distinguishes self cells vs. non-self cells. - Cells that do not have histocompatibility antigens are destroyed by the body. # Protein Defenses - **Complement proteins**: destroy antigen through many processes. - Alter cell membrane: fluid moves into pathogen and pathogen bursts and is destroyed. - Chemotaxis: attracts phagocytes to the site of the pathogen. - Increases phagocytosis by neutrophils. - Stimulates inflammatory response: histamine release, vasodilation, increased blood flow and blood cells to area. # Cellular Defenses - Stem cells in bone marrow produce leukocytes (white blood cells). - **Lymphocytes**: T cells, B cells, natural killer cells. - **Myelocytes**: neutrophils, basophils, eosinophils, monocytes/macrophages. # Lymphoid Tissues - Lymph nodes, thymus, bone marrow, portions of respiratory and GI tract. - Play a role in creation and regulation of immune cells. # Immune Response - Specific pathogen invasion can stimulate a specific immune response through lymphocytes. - **T cells**: made in bone marrow, migrate to the thymus to be matured and activated. - **Effector/cytotoxic**: respond to non-self cells; release cytokines to destroy cell or mark it for destruction by phagocytes during inflammatory response. - **Helper**: stimulate B cells to be more aggressive and responsive. - **Suppressor**: slows immune response to allow body to conserve energy and prevent further cellular destruction. - Helper and Suppressor T cells balance each other to allow for quick initial reaction to destroy pathogens, yet preserve further cell destruction. - **B cells:** programmed to identify specific antigens. - B cell reacts with antigen and forms an antigen-antibody complex which activates complement proteins. - **Plasma cell (IgM)**: antibodies produced at first exposure. - **Memory cell (IgG)**: antibodies made for later exposure to same pathogen — quick release. # Other Immune Mediators - **Interferons**: cytokines (chemicals) that are secreted by cells invaded by a virus. - Prevent viral replication, suppress malignant cell replication, suppress tumor growth. - **Interleukins**: cytokines secreted by active leukocytes. - Stimulate T and B cells to mount immune response. - **Tumor necrosis factor (TNF)**: secreted by macrophages to inhibit tumor growth and increases effectiveness of immune and inflammatory responses. # Question - The body is exposed to injected antibodies, referred to as immunoglobulins. What form of immunity is this? - Active natural immunity. - Passive natural immunity. - **Passive artificial immunity.** - Active artificial immunity. # Active immunity - Host mounts an immune response to an antigen and produces antibodies. - Immune system develops memory of the antigen. - T cells and Memory B cells will respond on future exposures. ## Active Artificial Immunity - Antigen is administered similar to a pathogen antigen - vaccination. ## Active Natural Immunity - Antigen enters the body through environmental exposure - infection. # Passive Immunity - Antibodies are transferred from another source; lasts weeks to months. ## Passive Artificial Immunity - Administer antibodies intravenously (immunoglobulins). ## Passive Natural Immunity - IgG antibodies from mother to fetus through the placenta or breast milk. # Vaccination/Immunization - Artificial active immunity: body is exposed to weakened proteins associated with specific disease. - Bacterial cell membrane, protein coat of virus, weakened virus, chemically inactivated organisms, weakened toxins. - Caution used for those with immunosuppression: vaccine could cause actual disease. - Caution with acute infection, immunosuppressant drugs, stress on the body. # Inflammatory Response Overview - Injury to cells or tissue causes chemical reactions and a cascade of events. - Goal to remove the invader, limit tissue damage, and restore homeostasis. - Two stages: - Vascular stage: increased blood flow to injured tissues. - Cellular stage: leukocytes (WBCs) move into tissues - Can be acute (minutes to hours) or chronic (days to years). # Inflammatory Response Cells - **Endothelial cells**: line the blood vessels and allow selective permeability; vasoconstrict and vasodilate. - **Platelets**: release inflammatory mediators which increase vessel permeability. - **Neutrophils**: phagocytic - destroy invaders in the tissues - **Leukocytosis**: increase in number of neutrophils in the blood during inflammatory response; only live for 10 hours and must be present to respond to infection injury. - **Monocytes/macrophages**: phagocytic - destroy invaders in tissues. - Produce inflammatory mediators. # Inflammatory Response - Initial injury activates Hageman factor (factor XII): activates the kinin system — vascular stage begins. ## Vascular Stage - Quick vasoconstriction of vessels for seconds, then vasodilate. - **Bradykinin release**: local vasodilation, increased capillary permeability, stimulates nerve endings to cause pain. - Cell membrane releases arachidonic acid which activates chemicals that increase inflammatory response; prostaglandins, leukotrienes, cyclooxygenase, thromboxanes. # Inflammatory Response - **Vascular stage**: - **Histamine release**: vasodilation, increased blood flow, increased capillary permeability, stimulates pain perception. - Vasodilation causes tissue congestion; red, warm, swollen. - Neutrophils are brought to and enter tissues, then eliminate invader or injured cells. ## Cellular Stage - Changes occur on the vessel linings to allow leukocytes to stop and adhere to vessel. - This then allows the leukocyte to move from the vessel into the injured tissue. - Leukocytes are then attracted to site of inflammation through chemotaxis. - Upon arrival at the tissue, monocytes, neutrophils, and macrophages engulf bacteria or injured cell through phagocytosis. # The Inflammatory Response in Relation to the Four Cardinal Signs of Inflammation - **Exposure of plasma to injured cell, etc.** → **Activation of Hageman Factor** → **Prekallikrein** → **Active kallikrein** → **Kininogen** → **Bradykinin** → **Release of arachidonic acid** → **↑ Capillary permeability** → **Vasodilation** → **Leukotrienes (LTs)** → **Prostaglandins (PGs)** → **Exudation of plasma proteins** → **Edema** → **↑ Blood Flow** → **Chemotaxis of leukocytes, Activation of neutrophils** → **Dolor (pain)** → **Tumor (swelling)** → **Rubor (redness)** → **Calor (heat)** → **Phagocytosis** → **Removal of debris and preparation of injured site for healing** # Manifestations of Local Inflammation - Related primarily to vasodilation and increased capillary permeability. - Increased blood flow, fluid leaks into tissues, congestion of tissues occurs. - 5 cardinal signs: pain (dolor), swelling (tumor), redness (rubor), warmth (calor), loss of function. # Pyrogen - Released once cellular phase occurs; can result in fever. # Manifestations of Systemic Inflammation - Inflammatory mediators are released into circulation and cause a widespread response: leukocytes, cytokines, erythrocyte sedimentation rate (ESR). - Vasodilation, large increase in capillary permeability, loss of fluid in vessels (moves into tissues), can lead to hypotension and shock (low BP that causes depressed organ function/damage). # Inflammatory + Immune Response - Both responses work together to maintain homeostasis. - Hageman factor and histamine cause increased capillary permeability that allows for neutrophils to get to damaged tissues and destroy pathogens. - Inflammatory reaction continues to activate leukocytes. - Inflammatory reaction destroys invader cells through phagocytosis that have been marked by T cells. # Pain Summary - An unpleasant sensation + emotional experience related to actual or potential tissue damage. - When tissues are damaged, cells release chemicals such as kinins and prostaglandins which stimulate sensory nerves. - Acute pain; surgery, injury, infection. - Chronic pain; constant or intermittent. - Nociceptive pain: direct stimulus to pain receptor. - Neuropathic pain: nerve injury or nerve dysfunction (sensory axons). - Psychogenic pain: emotional, behavioral, psychological. # Patho of Pain - Nociception: transmission of unpleasant stimuli from area of injury to the brain via sensory nerve fibers. - **A-delta fibers**: respond quickly to acute pain, myelinated. - **C fibers**: slow to conduct, unmyelinated; persistent stimuli (chronic pain). - **Pain impulses sent from tissues/organs to the spinal cord** - **A fibers**: transmit sensations associated with pressure, stretch, vibration. - Large fibers, conduct most quickly. - Can block smaller fibers. # Patho of Pain - **Gate Control Theory**: transmission of the impulses to the brain can be blocked at any point. - Interneurons in spinal cord. - A fibers (touch fibers) compete with smaller fibers. - Descending impulses from cerebral cortex, limbic system, reticular activating system; serotonin and norepinephrine. - Some truth to this, but not this simple; many other factors contribute to experiencing pain. - Pain receptors, neurotransmitters, learning, culture, tolerance. # Pain Pathway - **Tissue Injury** → **Inflammatory Mediators Released** → **Stimulate Nerve Fibers** → **Dorsal Horn of Spinal Cord** → **Spinothalamic Tracts** → **RAS** → **Cerebral Cortex** - **Nerve Endings:** detect stimuli that cause tissue damage. - **Dorsal Horn of Spinal Cord:** process the sensation of pain. - **Thalamus/Cerebral Cortex:** integrate pain + pain sensation occurs — client’s subjective reaction. # Mechanism of Acute Pain - **Nociceptor** → **Mediator release** → **Inflammation** → **Tissue Injury** → **Substance P, Prostaglandins, Serotonin, Acetylcholine** → **Pain**, → **Somatosensory cortex** → **Thalamus, RAS** → **Spinothalamic Pathway** # Pain Receptors - Some receptors respond to all stimuli, some are specific. - Thermal: temperature extremes. - Mechanical: stretch, pressure, violent contraction. - Chemical: tissue trauma, ischemia, inflammation. - Inflammatory response to painful stimulus becomes a loop: inflammatory mediators released from injured tissues stimulate pain receptors perpetuates the inflammatory response more inflammatory mediators released more pain occurs — # Pain Receptors - Opioid receptors found in CNS, peripheral nerves, GI cells. - Respond to endorphins and enkephalins; modulate pain information coming into the brain. - Brainstem: BP, nausea, vomiting, respiration, cough. - Integrate and communicate current info about pain. - Activate endocrine or neural response to pain. - Emotional response to pain. - Block neurotransmitters related to pain. # Types of Pain ## Acute Pain - Results from tissue injury. - Short duration, resolves once injury is treated or stimulus is removed. - Protective mechanism to alert you of tissue injury. - If untreated, prolonged stimulation of sympathetic nervous system (vital sign changes in HR, BP, RR). ## Chronic Pain - Persistent pain, often musculoskeletal, visceral, vascular. - Causes stressors; emotional, mental, physical. - Lacks sympathetic nervous system response. - Loss of appetite, insomnia, depression. # Acute vs Chronic Pain | Characteristic | Acute Pain | Chronic Pain | | - | - | - | | Onset | Recent | Continuous or intermittent | | Duration | Short (<3 months) | 3 months or more | | Autonomic Response | Consistent with sympathetic fight or flight response: Increased HR, BP, Increased RR, Pupillary dilation, Muscle tension, Decreased gut motility | Absence of autonomic responses | | Psychological Component | Associated anxiety | Increased irritability, associated depression, somatic preoccupation, withdrawal from outside interests, decreased strength of relationships | | Other types of responses | | Decreased sleep, decreased libido, appetite changes | # Question - What are examples of nonpharmacologic pain management? # Opioid Agonist - **Opiod Agonist**: morphine. ## Mechanism of Action - React with opioid receptors causing analgesia, sedation, euphoria. - Treats acute pain, and moderate to severe chronic pain. ## Pharmacokinetics - Oral, PR, SQ, IM, IV ## Contraindications - GI obstruction (paralytic ileus), other medications with CNS depression. ## Adverse Effects - Respiratory depression, hypotension, constipation, sedation, cough suppression. ## Client/Therapy Management - Monitor for sedation: no driving. - Monitor respirations/oxygen saturation: due to decrease respiratory drive. - Monitor for constipation: increase fiber and fluid intake, increase mobility. - Monitor for dependence and tolerance. # Opioid Agonist-Antagonist - **Opioid Agonist-Antagonist**: buprenorphine. ## Mechanism of Action - Stimulate certain opioid receptors, while blocking others. - Treat moderate to severe pain or opioid use disorders; chronic pain. ## Pharmacokinetics - Buccal, IM, IV, SQ implant ## Contraindications - Other medications with CNS depression. ## Adverse Effects - Respiratory depression, sedation, impaired mentation. - **Withdrawal syndrome if switching therapy:** abdominal cramps/pain, hypertension, anxiety, vomiting, fever, severe pain. ## Client/Therapy Management - Monitor for dependence: less risk than with opioid agonists. - Monitor for respiratory rate, oxygen saturation. - Monitor sedation.