Module 4: Autoimmune, Steroids, NSAIDs

Which three stages make up the General Adaptation Syndrome (GAS)?

Alarm, Resistance, Exhaustion.

What releases corticotropin-releasing hormone (CRH) and why?

The hypothalamus releases CRH to initiate the stress response.

What does adrenocorticotropic hormone (ACTH) stimulate?

Adrenal cortex to secrete cortisol.

Which hormones are released from the adrenal medulla during acute stress, and what do they do?

Epinephrine and norepinephrine increase heart rate, blood pressure, and redirect blood flow to vital organs and muscle; epinephrine also promotes bronchodilation and raises blood glucose.

What is the primary metabolic role of cortisol in stress?

Maintain blood glucose through gluconeogenesis.

What defines the Exhaustion stage of the General Adaptation Syndrome (GAS)?

Depletion of physiologic reserves with failure of compensatory mechanisms and increased risk of illness.

What is the hypothalamic–pituitary–adrenal (HPA) axis?

A coordinated pathway—hypothalamus (CRH) → anterior pituitary (ACTH) → adrenal cortex (cortisol)—that regulates the stress response.

Define allostasis and allostatic load.

Allostasis is “stability through change”; allostatic load is the cumulative “wear and tear” from repeated or chronic stress responses.

How does chronic stress typically affect adaptive immunity?

It suppresses T-cell and B-cell function (reduced production and activation).

What happens to natural killer (NK) cell activity with chronic stress, and why is that important?

NK cell activity decreases, reducing surveillance against virally infected and malignant cells.

What is meant by cytokine dysregulation in chronic stress?

An imbalance of pro- and anti-inflammatory signaling that leads to either excessive inflammation or inadequate responses.

Name two clinical red flags of stress-related immune impairment.

Frequent infections and poor wound healing.

What is central tolerance in the immune system?

Deletion of self-reactive T and B lymphocytes during development in the thymus and bone marrow.

What is peripheral tolerance in the immune system?

Suppression or anergy of self-reactive lymphocytes that escaped central deletion, preventing autoimmune responses.

Define autoimmunity in one sentence.

Loss of self-tolerance causes an immune attack on the body’s own tissues.

Give one example of a disease with autoantibodies and name the autoantibody.

Systemic lupus erythematosus (SLE) with anti–double-stranded DNA (anti-dsDNA) antibodies.

What is rheumatoid arthritis (RA) and a hallmark symptom pattern?

An autoimmune synovitis; hallmark is symmetric small-joint pain and morning stiffness.

What is multiple sclerosis (MS) and a common presenting feature?

Autoimmune demyelination in the central nervous system; common features include optic neuritis or sensory changes.

What is type 1 diabetes mellitus (T1DM) at the immune level?

Autoimmune destruction of pancreatic beta (β) cells leading to insulin deficiency.

What is severe combined immunodeficiency (SCID)?

A primary (congenital) immunodeficiency with profound T-cell and B-cell dysfunction leading to severe, recurrent infections.

What is the difference between primary and secondary immunodeficiency?

Primary is congenital (e.g., SCID); secondary is acquired (e.g., human immunodeficiency virus (HIV), chemotherapy, glucocorticoids).

What is acquired immunodeficiency syndrome (AIDS) and how is it defined?

Advanced HIV infection defined by a CD4+ T-cell count <200 cells/mm³ or an AIDS-defining illness.

What does a CD4+ T-cell count indicate in human immunodeficiency virus (HIV) care?

The degree of immune function and risk for opportunistic infections.

What does an HIV viral load measure and why is it important?

The amount of circulating HIV RNA; it monitors response to antiretroviral therapy (ART).

Name one opportunistic infection strongly associated with AIDS and its affected organ.

Pneumocystis jiroveci pneumonia (PJP/PCP) affects the lungs.

What immune mechanism mediates Type I hypersensitivity?

Immunoglobulin E (IgE)

What is the priority nursing action in anaphylaxis (Type I hypersensitivity)?

Administer intramuscular epinephrine and secure the airway.

What is the immune mechanism in Type II hypersensitivity?

Immunoglobulin G (IgG) or immunoglobulin M (IgM) binding to host cell antigens with complement or antibody-dependent cellular cytotoxicity (ADCC).

Give one classic example of Type II hypersensitivity.

Acute hemolytic transfusion reaction.

Which process underlies Type III hypersensitivity?

Deposition of circulating antigen–antibody immune complexes with complement activation (e.g., SLE, post-streptococcal glomerulonephritis).

What is the timeline and mediator for Type IV hypersensitivity?

Delayed (24–72 hours), T-cell–mediated (no antibodies).

What is the mechanism of nonsteroidal anti-inflammatory drugs (NSAIDs)?

Inhibition of cyclooxygenase (COX) enzymes, reducing prostaglandin synthesis (analgesic, antipyretic, anti-inflammatory effects).

What is a key difference between COX-1 and COX-2 inhibition?

COX-1 inhibition increases gastrointestinal bleeding/ulcer risk; COX-2–selective inhibition reduces GI risk but may increase cardiovascular risk.

Name a common indication and a major risk for ibuprofen (an NSAID).

Indication: pain/inflammation/fever; risk: gastrointestinal irritation/ulcer and renal impairment.

What is the core anti-inflammatory mechanism of glucocorticoids?

Suppression of pro-inflammatory cytokines (e.g., interleukin-1 (IL-1), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α)) and eicosanoid pathways via gene regulation.

Why must long-term glucocorticoid therapy be tapered?

To avoid adrenal insufficiency due to suppression of the hypothalamic–pituitary–adrenal (HPA) axis.

List two high-yield adverse effects of chronic glucocorticoid use.

Hyperglycemia and increased infection risk (others: osteoporosis, mood/sleep changes, skin thinning).

How does acetaminophen relieve pain and fever, and what is a key safety limit?

Central cyclooxygenase (COX) inhibition (no peripheral anti-inflammatory effect); maximum daily dose is 4 grams (lower with liver disease or alcohol use).

Define the Alarm stage of the General Adaptation Syndrome (GAS) in one line.

Sympathetic surge and adrenal hormone release that rapidly mobilize energy and perfusion.

What two simple bedside findings can suggest stress-related immune suppression?

Recurrent infections and delayed wound healing.

Which stress hormone primarily causes bronchodilation and increased blood glucose?

Epinephrine (adrenaline)

Which stress hormone primarily drives vasoconstriction to maintain blood pressure?

Norepinephrine (noradrenaline)

Acetaminophen (Tylenol) drug class

Non-opioid analgesic and antipyretic; not an NSAID.

Acetaminophen (Tylenol) mechanism of action

Inhibits prostaglandin synthesis; decreases pain and fever. Has minimal to no anti-inflammatory activity

Ibuprofen drug class

Ibuprofen: NSAID (Nonsteroidal Anti-inflammatory Drug)

Naproxen drug class

Naproxen: NSAID (Nonsteroidal Anti-inflammatory Drug)

Diclofenac drug class

Diclofenac: NSAID (Nonsteroidal Anti-inflammatory Drug)

Ketorolac drug class

Ketorolac: NSAID (Nonsteroidal Anti-inflammatory Drug)

Meloxicam drug class

Meloxicam: NSAID (Nonsteroidal Anti-inflammatory Drug)

Celecoxib drug class

Celecoxib: NSAID (Nonsteroidal Anti-inflammatory Drug)

Ibuprofen mechanism of action

Ibuprofen: Inhibits both COX-1 and COX-2 enzymes, decreasing prostaglandin production; results in reduced pain, inflammation, and fever.

Naproxen mechanism of action

Naproxen: Inhibits both COX-1 and COX-2 enzymes, decreasing prostaglandin production; results in decreased pain, inflammation, and fever.

Diclofenac mechanism of action

Diclofenac: Inhibits both COX-1 and COX-2 enzymes, decreasing prostaglandin production; results in decreased pain, inflammation, and fever.

Ketorolac mechanism of action

Ketorolac: Inhibits both COX-1 and COX-2 enzymes, decreasing prostaglandin production; results in decreased pain, inflammation, and fever.

Meloxicam mechanism of action

Meloxicam: Inhibits both COX-1 and COX-2 enzymes, decreasing prostaglandin production; results in decreased pain, inflammation, and fever.

Celecoxib mechanism of action

Selectively inhibits COX-2 enzymes, decreases pain and inflammation. Has lower risk of GI toxicity because of less COX-1 inhibition. Increased risk for MI and stroke!!

Aspirin drug class

Aspirin: NSAID (Nonsteroidal Anti-Inflammatory Drug)

Aspirin mechanism of action

Non-selective COX-1 and COX-2 inhibitor; irreversibly inhibits platelet aggregation. An adverse effect of the drug, Tinnitus, may indicate toxicity!