Immunology Quiz: Immune Response Mechanisms

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Questions and Answers

What is unique about the initial response to an antigen by the immune system?

Interleukins are activated, directly attacking the antigen and preventing its spread.

The initial response relies primarily on plasma cells producing IgM antibodies. (correct)

Memory cells are produced immediately, providing long-term immunity.

Antibodies are produced from pre-existing memory cells, ensuring rapid response.

How do interferons contribute to the body's defense against viral infections?

They suppress viral replication within infected cells, limiting the spread of infection. (correct)

They directly destroy viral particles, preventing them from entering cells.

They stimulate the production of antibodies, targeting and neutralizing the virus.

They enhance the activity of suppressor T cells, regulating the immune response to the virus.

Which type of immunity is most likely to provide long-lasting protection against specific pathogens?

Passive artificial immunity, achieved by administering pre-formed antibodies.

Passive natural immunity, acquired through maternal antibodies.

Active artificial immunity, induced by vaccination.

Active natural immunity, developed after an infection. (correct)

Which of the following BEST describes the role of suppressor T cells in the immune response?

They regulate the immune response, preventing excessive inflammation and tissue damage. (A) Signup and view all the answers

Which of the following is NOT a feature of active artificial immunity?

Immediate, pre-existing immunity against a specific antigen. (B) Signup and view all the answers

What is the primary difference between active and passive immunity?

Active immunity involves the body's own immune system, while passive immunity is externally provided. (C) Signup and view all the answers

Which of these is a common reason for caution when administering vaccines to individuals who are immunosuppressed?

The weakened or inactivated pathogen in the vaccine may actually cause disease. (D) Signup and view all the answers

How does the body's immune system distinguish between self and non-self antigens?

The immune system relies on a complex network of proteins and receptors to identify and target foreign antigens. (C) Signup and view all the answers

Which of the following BEST explains why the human body may experience a more rapid and robust immune response upon subsequent exposure to a previously encountered pathogen?

The initial exposure leads to the development of memory cells specific for that pathogen, enabling a quicker and more effective response. (B) Signup and view all the answers

What is the primary role of tumor necrosis factor (TNF) in the immune response?

It enhances the effectiveness of immune and inflammatory responses, promoting healing and tissue repair. (D) Signup and view all the answers

What is the sequence of activation starting from the exposure of plasma to an injured cell?

Activation of Hageman Factor → Prekallikrein → Active kallikrein → Kininogen (A) Signup and view all the answers

Which option best describes the physiological changes associated with local inflammation?

Increased capillary permeability and exudation of plasma proteins. (B) Signup and view all the answers

Which of the following is a consequence of systemic inflammation?

Hypotension and shock due to loss of fluid in vessels. (B) Signup and view all the answers

What role do pyrogens play in inflammation?

They are released during the cellular phase leading to fever. (A) Signup and view all the answers

What describes nociceptive pain?

Direct stimulus to pain receptors from an injury. (A) Signup and view all the answers

What physiological effect occurs as part of the sympathetic 'fight-or-flight' response?

Increased heart rate (B) Signup and view all the answers

Which neurotransmitter is primarily responsible for vasoconstriction and increasing heart rate in the sympathetic response?

Epinephrine (D) Signup and view all the answers

What is a primary contraindication for administering adrenergic agonists?

Pheochromocytoma (A) Signup and view all the answers

Which of the following adrenergic receptors primarily mediates increased heart rate?

Beta1 (C) Signup and view all the answers

What adverse effect on the cardiovascular system can result from adrenergic agonists?

Hypertension (C) Signup and view all the answers

What is one expected outcome of administering dopamine during a medical emergency?

Preserved renal blood flow (B) Signup and view all the answers

How do adrenergic agonists primarily act on different receptor types?

They respond differently based on neurotransmitter concentrations. (B) Signup and view all the answers

Which function is NOT a role of the skin in the immune response?

Creating mucus to trap pathogens (A) Signup and view all the answers

What is the primary difference between adaptive and innate immunity?

Adaptive immunity involves B and T lymphocytes, while innate immunity includes physical barriers. (A) Signup and view all the answers

What do complement proteins primarily do during an immune response?

Destroy antigens through various mechanisms (C) Signup and view all the answers

Which of the following best describes the function of major histocompatibility complex (MHC)?

Distinguishes self cells from non-self cells (D) Signup and view all the answers

What type of cells primarily respond to non-self cells in the immune response?

Effector/cytotoxic T cells (C) Signup and view all the answers

Which statement regarding lymphoid tissues is incorrect?

They include only the tonsils and spleen. (D) Signup and view all the answers

Which process is NOT associated with the action of innate immunity?

Development of an immune memory (A) Signup and view all the answers

What role do T lymphocytes play in the immune response?

They enhance the inflammatory response through cytokine release. (A) Signup and view all the answers

Which statement about adaptive immunity is accurate?

It is specific to particular pathogens or altered body cells. (B) Signup and view all the answers

What is the main function of scavenger cells in the immune response?

To engulf and destroy pathogens in tissues (D) Signup and view all the answers

A client is receiving labetalol for hypertension. Which of the following would be a priority nursing assessment?

Monitor urine output for signs of renal impairment (D) Signup and view all the answers

Which of the following is a contraindication for the use of bethanechol?

Coronary artery disease (D) Signup and view all the answers

A client is receiving bethanechol for urinary retention. The nurse understands that which of the following adverse effects is most likely to occur?

Hypotension (D) Signup and view all the answers

Which of the following is an expected effect of sympathetic stimulation?

Increased sweating (C) Signup and view all the answers

A nurse is caring for a client who is experiencing stress. Which of the following physiological responses is most likely to occur?

Pupil dilation (A) Signup and view all the answers

A client is receiving labetalol for hypertension. Which of the following nursing interventions would be appropriate?

Monitor the client's blood sugar levels closely (D) Signup and view all the answers

Which of the following is a direct-acting cholinergic agonist?

Bethanechol (B) Signup and view all the answers

A client is receiving bethanechol for urinary retention. The nurse should monitor the client for which of the following?

Decreased urine output (D) Signup and view all the answers

A client is experiencing stress. The nurse understands that which of the following is a result of prolonged stress?

Increased risk for chronic disease (C) Signup and view all the answers

Study Notes

Learning Module 2A: Protection & Comfort

NUR 370 is the course number
Rebecca Young, MS, RN, CCRN is the presenter
The module covers immune and inflammatory responses
It discusses anti-inflammatory agents and immunizations' role in mitigating inflammation and disease prevention
It differentiates normal and abnormal autonomic nervous system anatomy and physiology
It determines the mechanism of action, indications, and expected/unexpected outcomes of medications affecting protection and comfort

Autonomic Nervous System

The ANS regulates homeostasis through CNS, PNS, and endocrine responses
Nerve impulses in the PNS travel to the thalamus, medulla, and spinal cord (CNS)
From the CNS, impulses stimulate organs, glands, and muscles
The ANS controls blood pressure, heart rate, respiration rate, temperature, fluid status, urinary output, and digestion

Sympathetic Nervous System

The SNS is the "fight-or-flight" response to stressors
CNS cells stimulate nerve ganglia in the thoracic and lumbar areas of the spinal cord
Neurotransmitters released are primarily norepinephrine and epinephrine
The body prioritizes systems beneficial for survival: heart rate, blood pressure, respiration rate, bronchodilation, pupil dilation, glucose breakdown
Elimination, digestion, and reproduction slow down

Parasympathetic vs. Sympathetic Nerves

Parasympathetic: constricts pupils, stimulates saliva, slows heartbeat, constricts airways, stimulates stomach activity, stimulates gallbladder, stimulates intestines, and contracts bladder
Sympathetic: dilates pupils, inhibits salivation, increases heartbeat, relaxes airways, inhibits stomach activity, inhibits gallbladder, inhibits intestines, and relaxes bladder

Adrenergic/Sympathetic Receptors

Alpha and Beta receptors respond to circulating epinephrine and norepinephrine (Alpha1, Alpha2, Beta1, Beta2)
Receptor response varies based on neurotransmitter concentrations
Some drugs target specific receptors, others stimulate all receptors, resulting in fewer systemic side effects

Adrenergic Agonists (Dopamine, Epinephrine)

Mechanism of Action: Dopamine increases heart rate, blood pressure, and maintains kidney blood flow (treats shock). Epinephrine causes vasoconstriction, increased heart rate, blood pressure, and bronchodilation (treats shock and severe bronchospasm like asthma)
Contraindications: Pheochromocytoma, tachyarrhythmias, ventricular fibrillation, and hypovolemia
Adverse Effects: Effects on the heart (arrhythmias, hypertension, palpitations, angina, dyspnea); GI tract depression (nausea, vomiting, constipation); sympathetic stimulation (headache, sweating, feelings of tension or anxiety, piloerection)
Pharmacokinetics: Generally administered intravenously (IV) or intramuscularly (IM)

Physiological Effects of Adrenergic Stimulation

Specific physiological effects occur in response to stimulation of adrenergic receptors: pupils dilate, loss of lens accommodation, decreased salivation and secretions, bronchodilation, increased respiratory rate/depth, increased blood pressure, increased conduction/heart rate, vasoconstriction, and increased blood flow to muscles
Effects on the GI tract involve decreased pancreatic and gastric secretions, decreased GI motility, and decreased perfusion/spincter contraction. Effects on urinary include decreased renal blood flow, minimal to no uterine activity, and bladder relaxation/sphincter contraction.
Effects on the reproductive system are minimal to no uterine activity. Genital stimulation is a potential effect of the simulation. The effect on skin is vasoconstriction. Pilo-erection and sweating are also effects that could be a result of stimulation.

Nonselective Adrenergic Blocking Agents (Labetalol)

Mechanism of Action: Blocks norepinephrine effects on alpha and beta receptors, decreasing heart rate and improving renal perfusion and blood pressure
Contraindications: Bradycardia, Heart block, Asthma, and caution with diabetic clients (masks hypo/hyperglycemia symptoms)
Adverse Effects: Bradycardia, hypotension, bronchospasm, and cough
Client/Therapy Management: Monitor heart rate, blood pressure, and blood glucose levels

Effects of Nonselective Adrenergic Blockers

Block the effects of the sympathetic nervous system
Adverse effects include decreased glucose regulation, loss of bronchodilation, decreased venous return, lowered blood pressure, and increased gastrointestinal activity.

Parasympathetic Nervous System

The parasympathetic nervous system is responsible for the "rest and digest" response.
Promotes conservation of energy by slowing metabolism and function
CNS cells in the cranium and sacral areas stimulate nerve ganglia, releasing acetylcholine
Effects include increased motility and secretions in the GI tract, decreased heart rate, bronchoconstriction, relaxation of sphincters, and pupil constriction.

Cholinergic/Parasympathetic Receptors

Receptors found in muscle and organs – muscarinic or nicotinic
Varying response based on neurotransmitter concentrations
Drugs tend to stimulate all cholinergic receptors.

Direct-Acting Cholinergic Agonists (Bethanechol)

Mechanism of Action: Mimics acetylcholine to stimulate parasympathetic function, used for urinary retention and atonic bladder
Contraindications: Bradycardia, hypotension, coronary artery disease
Adverse Effects: Systemic effects of parasympathetic stimulation, including bradycardia, hypotension, heart block, and bladder spasm
Pharmacokinetics: Usually administered orally

Effects of Direct-Acting Cholinergic Agonists

The effects of direct-acting cholinergic agonists include pupil constriction, lens accommodation, lacrimal and salivary secretions, increased secretions, and increased heart rate/contractility/conduction, muscle/sphincter contraction, and vasodilation
Cholinergic effects can increase secretions (salivation, bronchial secretions, etc.), increase gastrointestinal motility, contract sphincters (GI, urinary), and cause vasodilation.

Anticholinergic Agents (Atropine)

Mechanism of Action: Blocks acetylcholine receptors, diminishing parasympathetic stimulation
Contraindications: Glaucoma, paralytic ileus, GI obstruction, benign prostatic hypertrophy, bladder obstruction, cardiac impairments (arrhythmias, tachycardia), and myocardial infarction.
Adverse Effects: Increased sympathetic responsiveness, blurred vision, photophobia, dizziness, and insomnia; Cardiovascular (tachycardia); Gastrointestinal (dry mouth, altered taste, and constipation); Genitourinary (hesitancy and urinary retention); and decreased sweating/heat tolerance
Client/Therapy Management: Monitor heart rate and blood pressure, monitor neuro status.

Stress Response

Homeostasis: Maintaining stable internal environment
Stress responses should ideally be acute
Chronic stress leads to immune suppression and increased energy demands.
Body breaks down; may cause damage.
Control systems and feedback mechanisms maintain cell function.

General Adaptation Syndrome (GAS)

The HPA axis plays a large role in the stress response
Alarm: sympathetic nervous system stimulation—increased heart rate, blood pressure, and epinephrine/norepinephrine/dopamine release
Resistance: Body's most efficient defenses initiated, and cortisol decreases
Fatigue: Prolonged or overwhelming stress depletes resources, with systemic damage occurring.

Acute Stress

Acute and time-limited trigger
Fight-or-flight response (SNS response)
Symptoms include pounding headache, increased vital signs, and increased alertness.
Blood is diverted from less essential organs
Clients with limited coping may develop stress-related illnesses (anxiety, depression, eating disorders, sleep disorders, high blood pressure (hypertension), and migraine)

Chronic Stress

Chronic intermittent: repeated exposure of stressors, not dissipated
Chronic sustained: prolonged exposure to consistent stressors
Overactive or underactive HPA axis due to neural or hormonal impairments
Prolonged/overwhelming stressor
Impacts include cardiac, immune, neurological, gastrointestinal, substance use, and mental health issues.

Inflammatory Response Overview

Injury to cells or tissues triggers chemical reactions and events.
The body's goal is to remove the invader, limit tissue damage, and restore homeostasis, occurring in two stages • Vascular Stage: Increased blood flow to injured tissues

• Cellular Stage: Leukocytes (WBCs) move into tissues

Inflammatory Response Cells

Endothelial Cells: Line blood vessels, permitting selective permeability; vasoconstrict and vasodilate to regulate flow.
Platelets: Release inflammatory mediators; increase vascular permeability
Neutrophils: Phagocytic cells that destroy invaders in tissues; leukocytosis is an increased number in the blood during inflammation; lifespan of 10 hours
Monocytes/Macrophages: Phagocytic cells that destroy invaders in tissues; produce inflammatory mediators

Inflammatory Response (Vascular Stage)

Initial injury activates the Hageman factor (Factor XII) which triggers the kinin system and the beginning of the vascular stage
Quick vasoconstriction, followed by vasodilation, occurs from increased blood flow, which causes redness, warmth, fluid leakage, and swelling.
Bradykinin release causes local vasodilation, increased blood vessel permeability, and pain sensation.
Cell membrane release arachidonic acid activates chemicals increasing inflammatory responses (prostaglandins, leukotrienes, cyclooxygenase, thromboxanes).

Inflammatory Response (Cellular Stage)

Vessel lining changes to allow leukocytes to stop and adhere
Leukocytes migrate from the blood vessel to the injured tissues.
Leukocytes are drawn to the site of inflammation through chemotaxis.

Pain Summary

Unpleasant sensation + emotional experience related to actual or potential tissue damage
When tissues are damaged, cells release chemicals (kinins, prostaglandins) stimulating sensory nerves.
Classifications:
Acute pain: surgery, injury, infection
Chronic pain: constant/intermittent
Nociceptive pain: direct stimulus to pain receptor
Neuropathic pain: nerve injury or dysfunction
Psychogenic pain: emotional, behavioral, psychological factors

Patho of Pain

Nociception: transmission of unpleasant stimuli to the brain.
Sensory nerves (a-delta and c-fibers):
A-delta fibers: fast, myelinated, respond quickly to acute pain
C fibers: slow, unmyelinated, transmit persistent pain (chronic pain)
Pain impulses from tissues/organs to the spinal cord
Larger fibers (large fibers) carry pain information faster; conduct pressure, stretch, and vibration signals quickly. Smaller fibers are less fast.

Gate Control Theory

Interneurons in the spinal cord can block pain impulse transmission to the brain
A-fibers (touch fibers) compete with smaller fibers for spinal cord pathways, regulating pain transmission
Descending impulses from the brain (e.g., cerebral cortex, limbic system, reticular activating system) contribute to modulating pain signals, along with serotonin and norepinephrine.

Pain Pathway

Tissue injury releases inflammatory mediators, activating nerve fibers.
Pain signals travel through the dorsal horn of the spinal cord and spinothalamic tracts.
Reaching the reticular activating system (RAS), signals cause the brain to integrate pain information to contribute to the subjective sensation of pain

Pain Receptors

Some receptors are specific to stimuli.
Thermal receptors are sensitive to temperature extremes. Inflammatory mediators perpetuate a loop where the inflammatory mediators from injured tissues stimulate pain receptors, leading to more pain.

Pain Receptors (Opioid Receptors)

Found in the central nervous system (CNS) and peripheral nerves, also found in GI cells.
Influence pain signaling, pain modulation, and emotional responses. (modulation of pain responses to endorphins and enkephalins)

Types of Pain

Acute Pain: Results from tissue injury; resolves once treated. Short duration.
Chronic Pain: Persistent pain; often musculoskeletal, visceral, or vascular related; caused by stressors (emotional, mental, physical). Lacks typical sympathetic nervous system responses (e.g., decreased appetite, loss of sleep, depression).

Acute vs. Chronic Pain

Differentiates aspects of acute and chronic pain including the onset, duration, autonomic and psychological response, and other responses

Nonpharmacologic Pain Management

Question: Examples of nonpharmacological pain management techniques

Opioid Agonist (Morphine)

Mechanism of Action: Binds to opioid receptors, causing analgesia, sedation, and euphoria.
Adverse Effects: Respiratory depression, hypotension, constipation, sedation, cough suppression.
Client/Therapy Management: Monitor sedation, respirations/oxygen saturation, constipation, and dependence.

Opioid Agonist-Antagonist (Buprenorphine)

Mechanism of Action: Partial opioid agonist action. Stimulates opioid receptors while blocking others.
Adverse Effects: Respiratory depression, sedation, impaired mentation; withdrawal syndrome possible with switching therapies.
Client/Therapy Management: Monitor for respiratory rate, oxygen saturation, sedation, and dependence. Avoid sudden switching of pain management regimens.

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Description

Test your knowledge on the immune system's response to antigens, including the roles of T cells, interferons, and various types of immunity. This quiz covers key concepts like active and passive immunity, vaccine administration, and the distinction between self and non-self antigens. Perfect for anyone studying immunology or related fields.