Inflammation, Fever, and Tissue Repair

100 vocabulary flashcards covering concepts related to inflammation, fever, tissue repair, and relevant pharmacology from the lecture notes.

Inflammation

The body’s protective response to injury or infection.

Inflammatory Reaction

A rapid, non-specific defense against injury.

Immune Response

A specific defense mechanism recognizing and targeting pathogens.

Tissue Repair/Wound Healing

The process of restoring tissue structure and function.

Neutralize Harmful Agents

A function of inflammation to render injurious substances inactive.

Remove Damaged Tissue

A function of inflammation to clear away necrotic cells and debris.

Initiate Tissue Repair

A function of inflammation to begin the restoration process.

Causes of Inflammation

Infection, physical injury, chemical injury, and ischemic damage.

Rubor (Redness)

A cardinal sign of inflammation caused by vasodilation.

Calor (Heat)

A cardinal sign of inflammation caused by vasodilation.

Tumor (Swelling)

A cardinal sign of inflammation caused by increased vascular permeability.

Dolor (Pain)

A cardinal sign of inflammation caused by fluid/protein leakage and mediators.

Functio Laesa (Loss of Function)

A cardinal sign of inflammation.

Local Vascular Response

Initial vascular changes like vasodilation and increased permeability.

Vasodilation

Widening of blood vessels, leading to redness and heat.

Increased Vascular Permeability

Allows fluid and proteins to leak from vessels, causing swelling and pain.

Exudate Formation

The leakage of fluid and proteins from blood vessels into tissues.

Cellular Response (Inflammation)

The movement and action of white blood cells at the injury site.

Neutrophils

Early responder white blood cells in acute inflammation, involved in phagocytosis.

Monocytes

White blood cells that differentiate into macrophages at the site of inflammation.

Macrophages

Cells that perform cleanup, phagocytosis, and orchestrate tissue repair.

Lymphocytes

White blood cells prominent in chronic inflammation and immune regulation.

Histamine

An inflammatory mediator causing vasodilation and increased vascular permeability.

Prostaglandins

Inflammatory mediators involved in pain, fever, and vascular tone.

Leukotrienes

Inflammatory mediators involved in pain, fever, vascular tone, and bronchoconstriction.

Cytokines (ILs, TNF)

Inflammatory mediators that recruit white blood cells and cause systemic effects.

Complement System

A mediator system involved in opsonization, chemotaxis, and cell lysis.

Acute Inflammation

Inflammation characterized by rapid onset, neutrophils, and exudate, lasting hours-days.

Chronic Inflammation

Inflammation lasting weeks-years, characterized by macrophages, lymphocytes, and fibrosis.

Granulomatous Inflammation

A pattern of chronic inflammation with localized collections of macrophages and giant cells.

Resolution (Acute Inflammation)

Outcome where injury clears and full healing occurs.

Abscess Formation

Outcome of acute inflammation involving a localized collection of pus.

Fibrosis/Scarring (Inflammation)

Outcome where normal tissue is replaced by fibrous connective tissue.

Systemic Effects of Inflammation

Body-wide manifestations like fever, WBC changes, and acute-phase proteins.

Fever

A systemic effect caused by pyrogens resetting the hypothalamic set-point.

Pyrogens

Substances that induce fever by affecting the hypothalamus.

Leukocytosis

An increase in the total number of white blood cells.

Leukopenia

A decrease in the total number of white blood cells.

Acute-Phase Proteins

Plasma proteins like CRP and fibrinogen that increase during systemic inflammation.

Sepsis

A severe, life-threatening systemic inflammatory response to infection.

Septic Shock

A life-threatening condition of widespread inflammation leading to hypotension and organ failure.

Immediate Transient Response (Vascular)

Brief vasodilation and increased permeability due to minor injury.

Immediate Sustained Response (Vascular)

Prolonged vascular leakage and endothelial damage from more serious injury.

Delayed Hemodynamic Response (Vascular)

Gradual onset of increased capillary permeability seen in mild burns or UV injury.

Margination

The process where leukocytes move to the vessel walls.

Adhesion

White blood cells sticking to the endothelium via adhesion molecules like selectins and integrins.

Diapedesis/Transmigration

The process of white blood cells squeezing through blood vessel walls.

Chemotaxis

The chemical attraction of white blood cells to an injury site.

Phagocytosis

The engulfment and destruction of pathogens or cellular debris by white blood cells.

Selectins/Integrins

Adhesion molecules involved in leukocyte binding to endothelial cells.

Serous Exudate

A watery, low-protein inflammatory exudate (e.g., in blisters).

Hemorrhagic Exudate

An exudate rich in red blood cells, indicating vascular injury.

Purulent Exudate (Pus)

A thick, yellow-white exudate containing white blood cells and cellular debris, characteristic of infection.

Fibrinous Exudate

An exudate containing large amounts of fibrin, forming a mesh-like consistency (e.g., in pericarditis).

Regeneration (Tissue Repair)

Replacement of damaged tissue with the same cell type, restoring original function.

Fibrous Repair (Tissue Repair)

Scar formation; replacement of damaged tissue with connective tissue when regeneration is not possible.

Labile Cells

Cells that continuously divide and regenerate (e.g., skin, gastrointestinal lining).

Stable Cells

Cells that normally have low mitotic activity but can divide when stimulated (e.g., liver, kidney).

Permanent Cells

Cells that cannot regenerate (e.g., neurons, cardiac muscle).

Inflammatory Phase (Wound)

The initial phase (0-4 days) of wound healing involving hemostasis, neutrophils, and macrophages.

Proliferative Phase (Wound)

The second phase (4 days-3 weeks) of healing, characterized by fibroblasts, collagen synthesis, angiogenesis, and epithelialization.

Remodeling Phase (Wound)

The final phase (3 weeks-months) of healing involving collagen reorganization and gaining tensile strength.

Primary Intention Healing

Healing of wounds with approximated edges, resulting in minimal scarring.

Secondary Intention Healing

Healing of open wounds that fill with granulation tissue, leading to larger scars and slower healing.

Tertiary Intention Healing

Delayed wound closure after controlling contamination.

Factors Impairing Healing

Conditions like age, malnutrition, diabetes, infection, ischemia, and steroid use.

NSAIDs (Pharmacology)

Drugs like aspirin and ibuprofen that block prostaglandins to reduce inflammation, pain, and fever.

Aspirin (Acetylsalicylic Acid)

A salicylate NSAID that irreversibly inhibits COX-1 and COX-2; acts as analgesic, anti-inflammatory, antipyretic, and antiplatelet.

Reye’s Syndrome

A severe adverse effect of aspirin in children with viral illnesses.

Cyclooxygenase (COX)

An enzyme that synthesizes prostaglandins and is inhibited by NSAIDs.

Antiplatelet Effect

The ability of aspirin to inhibit platelet aggregation, preventing blood clots.

Salicylism

Aspirin toxicity causing symptoms like tinnitus and hearing loss at high doses.

Ibuprofen (Advil, Motrin)

A non-selective NSAID that reversibly inhibits COX-1 and COX-2; used for pain, inflammation, and fever.

GI Bleeding (NSAID Risk)

A common adverse effect of NSAIDs, particularly with chronic use or high doses.

Cardiovascular Thrombotic Events

Increased risk of heart attack or stroke, a black box warning for some NSAIDs.

Renal Impairment (NSAID Risk)

Potential kidney damage caused by NSAIDs, especially at high doses or in vulnerable patients.

Celecoxib (Celebrex)

A COX-2 selective NSAID indicated for pain and inflammation, with lower GI risk but increased cardiovascular risk.

COX-1 (Enzyme)

Constitutively expressed enzyme involved in physiological functions like gastric protection and platelet aggregation.

COX-2 (Enzyme)

Inducible enzyme primarily involved in inflammation, pain, and fever.

Acetaminophen (Tylenol)

A non-opioid analgesic and antipyretic that inhibits COX in the CNS but lacks significant anti-inflammatory effect.

Hepatotoxicity (Acetaminophen)

Liver damage, the primary severe adverse effect of acetaminophen, especially in overdose or with alcohol.

Para-aminophenol Derivative

The pharmacologic classification for acetaminophen.

Hypothalamus

The brain region where acetaminophen acts to lower fever.

N-acetylcysteine (Acetadote)

The antidote used to treat acetaminophen overdose.

Corticosteroids (Pharmacology)

Potent anti-inflammatory and immunosuppressant hormones used to manage various conditions.

Adrenal Gland

Endocrine gland that secretes corticosteroids.

Glucocorticoids

A class of corticosteroids that increase blood glucose, promote protein/lipid breakdown, and suppress inflammation/immunity.

Mineralocorticoids

A class of corticosteroids that regulate sodium and water balance by the kidneys.

Alternate-Day Dosing (Corticosteroids)

A dosing strategy to minimize adrenal suppression by taking medication every other day.

Adrenal Atrophy

The shrinking of the adrenal glands due to prolonged exogenous corticosteroid use.

Adrenocortical Insufficiency

A condition resulting from insufficient production of adrenal hormones, often from abrupt cessation of corticosteroids.

Adrenal Crisis

A life-threatening acute exacerbation of adrenocortical insufficiency.

Hydrocortisone (Cortef, Solu-Cortef)

A prototype corticosteroid used for replacement therapy and anti-inflammatory effects.

Prednisone

A common oral corticosteroid used for anti-inflammatory, immunosuppressant, and antineoplastic effects.

Cushing's Syndrome (Induced)

A collection of symptoms (e.g., fluid retention, hyperglycemia, osteoporosis) caused by prolonged high-dose corticosteroid use.

Osteoporosis (Corticosteroid-induced)

Bone density loss and increased fracture risk due to long-term corticosteroid therapy.

Hyperglycemia (Corticosteroid-induced)

Elevated blood glucose levels caused by corticosteroid use.

Immunosuppression (Corticosteroid-induced)

Decreased immune response, increasing infection risk with corticosteroid use.

GI Protection (with NSAIDs/Corticosteroids)

Strategies like PPIs or H2 blockers to prevent gastrointestinal adverse effects.

Antidote (Pharmacology)

A substance that counteracts the effects of a poison or overdose.