Final patho terms for mod. 1

Rubor

Redness — one of the 5 cardinal signs of acute inflammation; caused by vasodilation

Calor

Heat — cardinal sign of inflammation caused by increased blood flow

Tumor (inflammation)

Swelling — cardinal sign of inflammation from fluid leaking into tissue (edema)

Dolor

Pain — cardinal sign of inflammation caused by bradykinin/prostaglandins plus pressure from swelling

Functio laesa

Loss of function — the 5th cardinal sign of inflammation

RICE

Rest, Ice, Compression, Elevation — intervention to reduce local signs of inflammation

Left shift (WBC)

An increase in immature neutrophils on a CBC, indicating an active/severe infection

Leukocytosis

An increase in circulating white blood cells; a systemic sign of inflammation

CRP

C-reactive protein — an acute-phase reactant biomarker of inflammation

ESR

Erythrocyte sedimentation rate — indirectly increases with inflammation

Serous exudate

Watery, low-protein fluid leaked during inflammation (e.g., a blister)

Fibrinous exudate

Thick, sticky, high-fibrin exudate seen in more severe inflammation

Purulent exudate

Pus — exudate containing leukocytes, cell debris, and microorganisms

Hemorrhagic exudate

Exudate containing RBCs, indicating significant vascular damage

Vascular phase of inflammation

Vasodilation and increased capillary permeability that follows the trigger of injury

Cellular phase of inflammation

Neutrophils/WBCs migrate into tissue and release cytokines to recruit more immune cells

Mast cell degranulation

Immediate (seconds) release of preformed granules — histamine, chemotactic factors, cytokines

Mast cell synthesis (mediators)

Production of new mediators (prostaglandins, leukotrienes, PAF) over minutes to hours

Histamine H1 receptor

Pro-inflammatory receptor — causes vasodilation and increased permeability

Histamine H2 receptor

Anti-inflammatory receptor — limits the inflammatory response

PRRs

Pattern Recognition Receptors — on mast cells, macrophages, dendritic cells; detect danger signals

PAMPs

Pathogen-Associated Molecular Patterns — molecular patterns found on the pathogen itself

DAMPs

Damage-Associated Molecular Patterns — signals released by the body's own damaged cells

Phagocytosis steps (in order)

Recognition/adherence (opsonization) → Engulfment (phagosome) → Fusion with lysosome (phagolysosome) → Destruction

Opsonization

Coating a pathogen (e.g., with C3b or antibodies) to make it easier for phagocytes to engulf

Granuloma

A walled-off collection of activated macrophages around material the body can't clear (e.g., TB)

Complement system

Plasma protein cascade with 3 activation pathways (classical, lectin, alternative) that produces C3a/C5a, C3b, and MAC

C3a and C5a

Complement products that trigger mast cell degranulation and increased capillary permeability

C3b

Complement product that opsonizes (coats) pathogens

MAC

Membrane Attack Complex — complement product that pokes holes in bacterial membranes, causing lysis

Clotting system (plasma protein)

Cascade where intrinsic (damaged vessel) and extrinsic (tissue factor) pathways converge at factor X → thrombin → fibrin, forming a clot that traps microbes and stops bleeding

Kinin system

Cascade: Factor XII → prekallikrein → kallikrein → kininogen → bradykinin

Bradykinin

Kinin system product causing redness, warmth, vasodilation, increased permeability, and pain

TNF-alpha

Pro-inflammatory cytokine that induces fever

IL-1

Pro-inflammatory cytokine that enhances innate immunity and acts as a growth factor

IL-6

Pro-inflammatory cytokine that promotes liver production of acute-phase proteins

IL-10

Potent anti-inflammatory cytokine

TGF-beta

Anti-inflammatory cytokine that promotes wound healing and scar formation

Cytokine storm

Massive, rapid release of pro-inflammatory cytokines (e.g., in COVID-19, sepsis) that can lead to ARDS and multi-organ failure

Acute inflammation

Fast onset (minutes-hours), self-limiting (~8-10 days), dominated by neutrophils, forms an abscess

Chronic inflammation

Slow onset (days), lasts weeks to years, dominated by monocytes/macrophages and lymphocytes, forms a granuloma, usually shows necrosis

First line of defense

Physical barriers (skin, epithelial linings) + biochemical barriers (mucus, saliva, tears) + the normal microbiome

Second line of defense

Inflammation — vascular and cellular response, non-specific

Third line of defense

Adaptive immunity — specificity, memory, diversity; key cells are T cells and B cells

Dysbiosis

Disruption of the normal microbiome

Atrophy

Decrease in cell size (sometimes number); example: disuse muscle atrophy, Alzheimer's brain atrophy

Hypertrophy

Increase in cell size in non-dividing cells (cardiac/skeletal muscle); example: athlete's heart or hypertensive enlarged left ventricle

Hyperplasia

Increase in cell number in dividing cells; example: liver regeneration, BPH

Metaplasia

Reversible replacement of one mature cell type with another better suited to a chronic irritant; example: smoker's airway (ciliated columnar to stratified squamous)

Dysplasia

Abnormal, disordered cell growth ("atypical hyperplasia"), not protective, can precede cancer; example: cervical dysplasia from HPV

Cellular adaptation order of events

Normal cell → stress → adapts (reversible) → if stress too severe/prolonged → injury → cell death

Paracrine signaling

Cell signals nearby cells over a short distance

Endocrine signaling

Hormone travels via the bloodstream to a distant target

Autocrine signaling

Cell signals itself (e.g., cancer cells stimulating their own growth)

Gap junction signaling

Contact-dependent, direct cell-to-cell coordination via protein channels

GPCR

G-protein coupled receptor — uses cAMP/Ca2+ signaling cascades

Diffusion

Passive transport: movement from high to low concentration

Osmosis

Passive transport: water moves toward higher solute concentration across a semipermeable membrane

Filtration

Passive transport driven by hydrostatic pressure

Na+/K+ pump

Active transport: 3 Na+ pumped out, 2 K+ pumped in per cycle; uses ~60-70% of cellular ATP in muscle/nerve cells; makes cell interior more negative (electrogenic)

Pinocytosis

Endocytosis of fluid/solutes ("cell drinking")

Phagocytosis (transport)

Endocytosis of large particles ("cell eating")

Exocytosis

Active transport of substances out of the cell (e.g., secretion of lysosome contents)

Osmolality

Concentration measured in milliosmoles per kilogram of water (mOsm/kg)

Osmolarity

Concentration measured in milliosmoles per liter of solution (mOsm/L)

Isotonic solution

Same osmolality as ICF/ECF, about 285 mOsm

Hypotonic solution

Lower solute concentration than the cell, less than 285 mOsm

Hypertonic solution

Higher solute concentration than the cell, greater than 294 mOsm

Oncotic pressure

Pressure exerted by plasma proteins that pulls water into the vascular system

Resting membrane potential

The electrical charge difference across a cell membrane at rest, about -70 to -85 mV

Depolarization

Movement of membrane potential from negative toward zero (more positive)

Repolarization

Return of the membrane potential to its resting state

Hyperpolarized state

Cell interior more negative than normal; requires a stronger stimulus to reach threshold

Anabolism

Metabolic process that builds molecules and uses ATP

Catabolism

Metabolic process that breaks down molecules and releases ATP

3 phases of catabolism (in order)

Digestion → Glycolysis and oxidation → Citric acid (Krebs) cycle

Glycolysis

Splitting of glucose; produces 2 ATP molecules per glucose molecule

Krebs cycle (citric acid cycle)

Final phase of catabolism where most ATP is generated; begins with pyruvate oxidation, ends with oxidative phosphorylation

Oxidative phosphorylation

Mitochondrial process that transfers energy from nutrients to ATP via the electron-transport chain

Aerobic catabolism pathway

Glycolysis → pyruvic acid → Krebs cycle → CO2 + H2O + lots of ATP

Anaerobic catabolism pathway

Glycolysis → pyruvic acid → lactic acid, with little ATP produced (reversible once O2 is restored)

Interphase

Longest phase of the cell cycle; consists of G1 (pre-DNA synthesis), S (DNA synthesis), and G2 (RNA/protein synthesis, pre-mitosis)

Prophase

Mitosis phase where chromosomes appear, sister chromatids attach at the centromere, nuclear membrane disappears

Metaphase

Mitosis phase where spindle fibers align the chromosomes

Anaphase

Mitosis phase where centromeres split and sister chromatids are pulled to opposite poles

Telophase

Mitosis phase where new nuclear membranes form and spindle fibers disappear

Cytokinesis

Division of the cytoplasm into two identical daughter cells, completing cell division

Meiosis

Cell division of gametes; one cell becomes four non-identical cells

Cell cycle arrest

Halting of cell cycle progression triggered by the DNA damage response

Cellular accumulation

Buildup of a substance inside a cell because it can't be properly removed or metabolized

Hydropic (cellular) swelling

Water accumulation in a cell; first sign of reversible cell injury, caused by Na+/K+ pump failure

Fatty liver (steatosis)

Lipid accumulation in liver cells, commonly from alcohol use, obesity, or diabetes

Mallory bodies

Abnormal protein accumulation seen in alcoholic liver disease

Dystrophic calcification

Calcium deposits in already-damaged tissue, with normal blood calcium levels

Metastatic calcification

Calcium deposits in normal tissue due to high blood calcium (hypercalcemia)

Gout

Accumulation of uric acid (urate) crystals in and around joints, causing painful inflammation

8 chief cellular functions

Movement, conductivity, metabolic absorption, secretion, excretion, respiration, reproduction, communication

Nucleus (function)

Controls genetic information; site of cell division, DNA replication and transcription

Ribosomes (function)

Protein synthesis ("protein factories")

Rough ER

Endoplasmic reticulum studded with ribosomes; site of protein production