Pathophysiology Unit 2 | Chapter 3 (Porth 5th Edition)

Question 1

Atrophy

Answer 1

Decrease in cell size due to reduced workload, adverse conditions, or nutrient deprivation. Causes include disuse, denervation, loss of endocrine stimulation, inadequate nutrition, or ischemia. Reversible with stimulus removal.

Question 2

Hypertrophy

Answer 2

Increase in cell size and functional components (e.g., actin/myosin in muscle) due to increased workload. Examples: physiologic (exercise) or pathologic (left ventricular hypertrophy from hypertension).

Question 3

Hyperplasia

Answer 3

Increase in cell number in tissues capable of mitosis (e.g., epidermis, liver). Types: hormonal (uterine enlargement during pregnancy) or compensatory (liver regeneration).

Question 4

Metaplasia

Answer 4

Reversible replacement of one adult cell type with another (e.g., stratified squamous replacing ciliated columnar in smokers’ trachea). Adaptive response to chronic irritation.

Question 5

Dysplasia

Answer 5

Abnormal cell growth with variation in size, shape, and organization. Often precursor to cancer (e.g., cervical dysplasia detected via Pap smear). Potentially reversible.

Question 6

Intracellular Accumulations

Answer 6

Buildup of substances (lipids, proteins, pigments) due to metabolic errors, excess production, or exogenous agents. Examples: fatty liver, Tay-Sachs disease, lipofuscin.

Question 7

Dystrophic Calcification

Answer 7

Calcium deposition in dead/dying tissues (e.g., atherosclerotic plaques, damaged heart valves). Occurs despite normal serum calcium levels.

Question 8

Metastatic Calcification

Answer 8

Calcium deposition in normal tissues due to hypercalcemia (e.g., renal failure, hyperparathyroidism, vitamin D toxicity). Affects lungs, kidneys, blood vessels.

Question 9

Free Radical Injury

Answer 9

Cell damage via reactive oxygen species (ROS) with unpaired electrons. Causes lipid peroxidation, enzyme inactivation, DNA damage. Counteracted by antioxidants (vitamins A, C, E).

Question 10

Hypoxic Cell Injury

Answer 10

ATP depletion from oxygen deficiency, leading to anaerobic metabolism, lactic acidosis, Na+/K+ pump failure, cellular swelling. Irreversible if prolonged (e.g., brain cells after 4-6 minutes).

Question 11

Impaired Calcium Homeostasis

Answer 11

Excess intracellular Ca²+ activates destructive enzymes (proteases, phospholipases). Linked to ischemia, toxins, and mitochondrial damage.

Question 12

Reversible Cell Injury

Answer 12

Cellular swelling or fatty change due to ATP depletion. Fatty liver is an example. Reversible if cause is addressed.

Question 13

Apoptosis

Answer 13

Programmed cell death via caspase activation. Features: cell shrinkage, chromatin condensation, apoptotic bodies. Roles: embryogenesis, immune regulation, tumor suppression.

Question 14

Necrosis

Answer 14

Unprogrammed cell death with membrane rupture and inflammation. Types: coagulative (ischemic infarcts), liquefactive (abscesses), caseous (tuberculosis).

Question 15

Gangrene

Answer 15

Necrosis with tissue decay. Dry gangrene (coagulative, arterial obstruction) vs. wet gangrene (liquefactive, bacterial infection) vs. gas gangrene (Clostridium infection).

Question 16

Ionizing Radiation Injury

Answer 16

Damages DNA via free radicals or direct ionization. Targets rapidly dividing cells (bone marrow, gut). Causes mutations, cancer, tissue fibrosis.

Question 17

Nonionizing Radiation

Answer 17

UV radiation causes DNA pyrimidine dimers (e.g., xeroderma pigmentosum). Infrared/microwaves induce thermal injury.

Question 18

Lead Toxicity

Answer 18

Affects nervous system (neurobehavioral deficits), blood (anemia), kidneys. Sources: paint, soil. Chelation therapy for high blood levels (>45 µg/dL).

Question 19

Oxidative Stress

Answer 19

Imbalance between ROS production and antioxidant defenses. Linked to aging, cancer, cardiovascular diseases, and neurodegenerative disorders.

Question 20

Telomere Shortening

Answer 20

Progressive loss of chromosome-end DNA with cell division. Limits replicative capacity (Hayflick limit). Telomerase in cancer cells prevents senescence.

Question 21

Coagulative Necrosis

Answer 21

Tissue death with preserved architecture (e.g., myocardial infarction). Acidosis denatures proteins, maintaining cell outlines.

Question 22

Liquefactive Necrosis

Answer 22

Tissue liquefaction by enzymatic digestion (e.g., brain infarcts, abscesses).

Question 23

Caseous Necrosis

Answer 23

Cheesy, granular debris in granulomas (e.g., tuberculosis). Combines coagulation and liquefaction.

Question 24

Angiogenesis

Answer 24

Formation of new blood vessels stimulated by hypoxia-inducible factors (HIFs). Critical in wound healing and tumor growth.

Question 25

Metaplasia Example

Answer 25

Squamous metaplasia in smokers’ trachea replaces ciliated epithelium, reducing mucus clearance. Reversible if smoking ceases.

Question 26

Hyperplasia vs. Hypertrophy

Answer 26

Hyperplasia increases cell number; hypertrophy increases cell size. Both may coexist (e.g., pregnant uterus).

Question 27

Programmed Cell Death

Answer 27

Includes apoptosis (controlled) and autophagy. Contrasts with necrosis (inflammatory).

Question 28

Caloric Restriction

Answer 28

Extends lifespan by reducing mitochondrial free radical production. Linked to insulin/IGF-1 signaling pathways.

Question 29

Xeroderma Pigmentosum

Answer 29

Genetic defect in DNA repair enzymes. Causes UV sensitivity, skin cancer. Demonstrates importance of DNA repair mechanisms.

Question 30

Endothelial Dysfunction

Answer 30

Caused by oxidative stress, contributing to atherosclerosis. Impaired vasodilation and increased inflammation.

Question 31

Lipofuscin

Answer 31

Wear-and-tear' pigment from lysosomal digestion of organelles. Accumulates with age in heart, liver, nerve cells.

Question 32

Metastatic Calcification Cause

Answer 32

Hypercalcemia from hyperparathyroidism, bone metastases, or vitamin D excess. Deposits in lungs, kidneys, gastric mucosa.

Question 33

Free Radical Sources

Answer 33

Endogenous (mitochondrial respiration, phagocytosis) or exogenous (radiation, toxins). ROS include superoxide, hydroxyl radical, H₂O₂.

Question 34

Hypoxia-Inducible Factors (HIFs)

Answer 34

Activate genes for erythropoiesis, glycolysis, angiogenesis. Critical in adapting to low oxygen conditions.

Question 35

Apoptosis Pathways

Answer 35

Extrinsic (death receptors like Fas) and intrinsic (mitochondrial cytochrome c release). Both activate caspases for cell dismantling.

Question 36

Necrosis vs. Apoptosis

Answer 36

Necrosis: accidental, inflammatory, cell swelling. Apoptosis: regulated, non-inflammatory, cell shrinkage.

Question 37

Disuse Atrophy Example

Answer 37

Muscle wasting after cast immobilization. Reversed with resumed activity via IGF-1 and insulin signaling.

Question 38

Neurohumoral Factors in Hypertrophy

Answer 38

Biomechanical stress (e.g., hypertension) and hormones (e.g., IGF-1) drive cardiac hypertrophy via gene activation.

Question 39

Chemotherapy Injury

Answer 39

Antineoplastic drugs cause direct cell damage (e.g., liver necrosis from acetaminophen overdose due to glutathione depletion).

Question 40

Mercury Toxicity

Answer 40

Affects CNS (neurodegeneration) and kidneys. Forms: vapor, inorganic, methyl/ethyl. Sources: fish (methyl), vaccines (thimerosal, rare).

Question 41

Reperfusion Injury

Answer 41

Oxidative damage after restoring blood flow (e.g., post-heart attack). Free radicals overwhelm antioxidant defenses.

Question 42

Ubiquitin-Proteasome System

Answer 42

Degrades cytosolic proteins (e.g., in atrophy). Tagged proteins are broken down in proteasomes.

Question 43

Denervation Atrophy

Answer 43

Muscle wasting from loss of nerve supply (e.g., paralysis). Irreversible if prolonged.

Question 44

Endometrial Hyperplasia

Answer 44

Excessive estrogen stimulation causes thickened endometrium, increasing cancer risk. Treated with progestins or surgery.

Question 45

Papanicolaou (Pap) Smear

Answer 45

Detects cervical dysplasia (pre-cancerous changes). Early intervention prevents progression to invasive cancer.

Question 46

IGF-1 Role

Answer 46

Stimulates muscle growth, inhibits protein degradation. Low levels contribute to atrophy (e.g., aging, malnutrition).

Question 47

Antioxidant Enzymes

Answer 47

Include catalase, superoxide dismutase, glutathione peroxidase. Neutralize ROS to prevent oxidative damage.

Question 48

Line of Demarcation

Answer 48

In dry gangrene, separates necrotic tissue from viable tissue. Indicates inflammatory response to dead cells.

Question 49

Clostridium perfringens

Answer 49

Anaerobic bacterium causing gas gangrene via toxin production. Treatment includes debridement, antibiotics, hyperbaric oxygen.

Question 50

Senescence

Answer 50

Aging-related cell cycle arrest due to telomere shortening or DNA damage. Evaded in cancer via telomerase activation.

Question 51

Wet Gangrene Features

Answer 51

Swollen, foul-smelling tissue with bacterial infection. No clear demarcation. Requires urgent intervention to prevent sepsis.

Question 52

FAS Receptor

Answer 52

Death receptor in apoptosis extrinsic pathway. Binding triggers caspase cascade (e.g., cytotoxic T cell-induced apoptosis).

Question 53

Hypoxia in ATP Depletion

Answer 53

Loss of oxidative phosphorylation reduces ATP. Anaerobic glycolysis causes lactic acidosis, worsening cell injury.

Question 54

Rubin’s Pathology Reference

Answer 54

Key textbook cited for mechanisms of cellular adaptation, injury, and death (e.g., metaplasia, necrosis).