Goljan: Cell Injury

Front 1

Hypoxia

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inadequate oxygenation of tissue


Inadequate oxygen (O2) decreases synthesis of adenosine triphosphate (ATP).

ATP synthesis occurs in the inner mitochondrial membrane by the process of oxidative phosphorylation (see later).

O2 is an electron acceptor located at the end of the electron transport chain (ETC) in the oxidative pathway.

A lack of O2 or a defect in oxidative phosphorylation culminates in a decrease in ATP synthesis.

Front 2

Clinical findings of hypoxia

Back 2

1) cyanosis
2) confusion
3) cognitive impairment
4) lethargy

Front 3

Ischemia

Back 3

Decreased arterial blood flow or venous outflow of blood


Examples-coronary artery atherosclerosis, decreased cardiac output, thrombosis of splenic vein


Consequences of ischemia
(1) Atrophy (reduction in cell/tissue mass)
(2) Infarction of tissue (localized area of tissue necrosis)
(3) Organ dysfunction (e.g., heart failure)

Front 4

Consequences of ischemia

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Consequences of ischemia
(1) Atrophy (reduction in cell/tissue mass)
(2) Infarction of tissue (localized area of tissue necrosis)
(3) Organ dysfunction (e.g., heart failure)

Front 5

Hypoxemia

Back 5

1) Decrease in Pao2 (<40 mm Hg)
2) Normal ventilation and perfusion

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Causes hypoxemia

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(1) Decreased inspired Po2 (Pio2)
Examples-high altitude, breathing reduced %O2 mist
(2) Respiratory acidosis (hypoventilation)
(a) Carbon dioxide (CO2) retention in the lungs always produces a corresponding decrease in Pao2.
↑Alveolar Pco2 = ↓ alveolar Po2 = ↓ Pao2 = ↓ Sao2
(b) Examples-depression of the medullary respiratory center (e.g., barbiturates), paralysis of the diaphragm, chronic bronchitis
(3) Ventilation defect (Fig. 1-1B)
(a) Impaired O2 delivery to alveoli
Example-respiratory distress syndrome (RDS) with collapse of the distal airways due to lack of surfactant
(b) No O2 exchange in lungs that are perfused but not ventilated
Ventilation defect: perfused but not ventilated; intrapulmonary shunt
(c) Diffuse disease (RDS) produces intrapulmonary shunting of blood
Pulmonary capillary blood has the same Po2 and Pco2 as venous blood returning from tissue (i.e., a large fraction of pulmonary blood flow has not been arterialized).
(d) Inspired %O2 from 24% to 28% or greater does not significantly increase the Pao2.
This only applies to a diffuse ventilation defect involving both lungs; smaller defects are compensated for in normally ventilated lung.
(4) Perfusion defect (Fig. 1-1C)
(a) Absence of blood flow to alveoli (e.g., pulmonary embolus)
(b) No O2 exchange in lungs that are ventilated but not perfused
Perfusion defect: ventilated but not perfused; ↑ dead space
(c) Produces an increase in dead space
Exchange of O2 and CO2 does not occur.
(d) Inspired %O2 from 24% to 28% or greater increases the Pao2.
Other parts of ventilated and perfused lung have normal gas exchange.
(5) Diffusion defect
Diffusion defect: interstitial fibrosis, pulmonary edema
(a) Decreased O2 diffusion through the alveolar-capillary interface
(b) Examples-interstitial fibrosis, pulmonary edema
(6) Ventilation, perfusion, and diffusion defects increase the difference in O2 concentration between alveolar Po2 (Pao2) and arterial Po2 (Pao2).
This difference is called the alveolar-arterial (a-a) gradient

Front 7

Anemia

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Anemia
(1) Decreased Hb concentration (<7 g/dL)
(2) Causes
(a) Decreased production of Hb (e.g., iron deficiency)
(b) Increased destruction of RBCs (e.g., hereditary spherocytosis)
(c) Decreased production of RBCs (e.g., aplastic anemia)
(d) Increased sequestration of RBCs (e.g., splenomegaly)
Anemia: normal Pao2 and Sao2
(3) Normal Pao2 and Sao2

Front 8

Methemoglobinemia

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Methemoglobinemia
(1) Methemoglobin (metHb) is Hb with oxidized heme groups (Fe3+).
(2) Causes
(a) Oxidant stresses
Examples-nitrite- and sulfur-containing drugs, sepsis, local anesthetics (e.g., benzocaine)
(b) Congenital deficiency of cytochrome b5 reductase
(3) Pathogenesis of hypoxia
(a) Fe3+ cannot bind O2
MetHb: heme Fe3+; ↓ Sao2
Normal Pao2, decreased Sao2
(b) Ferric heme groups impair unloading of O2 by oxygenated ferrous heme.
This causes a left-shifted O2-binding curve (see later).
MetHb: Rx with IV methylene blue

Front 9

Carbon monoxide (CO) poisoning

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1) Leading cause of death due to poisoning
(2) Produced by incomplete combustion of carbon-containing compounds
(3) Causes include automobile exhaust, smoke inhalation, wood stoves, methylene chloride (paint thinner).
(4) Pathogenesis of hypoxia
(a) CO competes with O2 for binding sites on Hb.
Decreases Sao2 without affecting Pao2
CO poisoning: normal Pao2, ↓Sao2
(b) CO inhibits cytochrome oxidase in the electron transport chain (ETC).
(c) CO causes a left-shifted O2-binding curve (OBC)

Treatment: Treatment is O2 via nonbreather mask or endotracheal tube (100% O2)

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Clinical findings of CO poisoning

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1) Cherry-red discoloration of skin and blood
2) Headache (first symptom at levels of 10-20%)
3) Dyspnea, dizziness (levels of 20-30%)
3) Seizures, coma (levels of 50-60%)
4) Lactic acidosis due to hypoxia
(Rx CO poisoning: O2 via nonbreather mask)

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Consequences of hypoxic cell injury

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Decreased synthesis of ATP
Anaerobic glycolysis is used for ATP synthesis and is accompanied by several changes-
Activation of phosphofructokinase
Caused by low citrate levels and increased adenosine monophosphate
Net gain of 2 ATP
Anaerobic glycolysis: primary source ATP in hypoxia; lactic acidosis
Decrease in intracellular pH caused by an excess of lactate
(1) Also accumulates in blood producing lactic acidosis
(2) Denatures structural and enzymic proteins
Impaired Na+/K+-ATPase pump
(1) Diffusion of Na+ and H2O into cells causes cellular swelling.
(2) Potentially reversible with restoration of O2
Decreased protein synthesis
Due to detachment of ribosomes (potentially reversible)
Irreversible cell changes
↑Ca2+ in cytosol: "point of no return"; activates enzymes
Impaired calcium (Ca2+)-ATPase pump
Normal function of the pump is to keep Ca2+ out of the cytosol.
Increased cytosolic Ca2+ has two lethal effects.
(1) Enzyme activation
(a) Phospholipase increases cell and organelle membrane permeability.
(b) Proteases damage the cytoskeleton.
(c) Endonucleases cause fading of nuclear chromatin (karyolysis).
(2) Reentry of Ca2+ into mitochondria
(a) Increases mitochondrial membrane permeability
Cytochrome c in cytosol: activates apoptosis (cell death)
(b) Release of cytochrome c into the cytosol activates apoptosis (see later)

Front 12

free radicals

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Unstable chemical compounds with a single unpaired electron in their outer orbital

Front 13

FRs attack a molecule and "steal" its electron.

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The attacked molecule becomes an FR that begins a chain reaction leading to cell death.

FRs primarily target nucleic acids and membrane molecules.

Free radicals: damage membranes and DNA
(1) FRs produce DNA fragmentation and dissolution.
(2) FRs initiate lipid peroxidation of polyunsaturated lipids in cell and mitochondrial membranes.
(a) Lipid FRs combine with molecular O2.
(b) Increases membrane permeability leading to increased cytosol Ca2+ concentration (see section ID).

FR damage accumulates with age; important in the aging process

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Neutralization of Free radicals

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Superoxide dismutase (SOD)
Converts superoxide free radicals to peroxide and O2

Glutathione peroxidase (enhances glutathione, GSH)
Located in the pentose phosphate pathway
Neutralizes H2O2, hydroxyl, and acetaminophen FRs

Catalase (present in peroxisomes)
Degrades peroxide into O2 and water

Vitamins as antioxidants
Antioxidants neutralize FRs by donating one of their own electrons.
(1) Stops the "electron stealing" of FRs
(2) Antioxidants remain stable and do not become an FR.
Vitamin E (fat-soluble vitamin)
(1) Prevents lipid peroxidation in cell membranes
(2) Neutralizes oxidized LDL
Vitamin C (water-soluble vitamin)
Vitamin C: best neutralizer of hydroxyl FRs
(1) Neutralizes FRs produced by pollutants and cigarette smoke
Smokers have decreased levels of vitamin C because they are used up in neutralizing FRs derived from cigarette smoke.
(2) Best neutralizer of hydroxyl FRs

Selenium
Neutralizes FRs in the cytosol

Front 15

Lysosome formation

Back 15

Hydrolytic enzymes synthesized by the rough endoplasmic reticulum (RER) are transported to the Golgi apparatus for post-translational modification.

Modification involves attaching phosphate (via phosphotransferase) to mannose residues on hydrolytic enzymes to produce mannose 6-phosphate.

The marked lysosomal enzymes attach to specific mannose 6-phosphate receptors on the Golgi membrane.

Primary lysosomes: derive from Golgi apparatus
Vesicles containing the receptor-bound lysosomal enzymes pinch off the Golgi membrane to form primary lysosomes in the cytosol.

Fusion of additional vesicles to the primary lysosome further increases their content of hydrolytic enzymes.

Small vesicles containing only the receptors pinch off the primary lysosomes and return to the Golgi apparatus to bind more marked lysosomal enzymes so the cycle can repeat itself.

Front 16

Lysosomal functions

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Phagolysosome: contain lysosomal enzymes
(1) Fusion with phagocytic vacuoles containing bacteria
These lysosomes are designated secondary or phagolysosomes.
(2) Destruction of cell organelles (autophagy)
(3) Degradation of complex substrates (e.g., sphingolipids, glycosaminoglycans)

Front 17

Dystrophic calcification

Back 17

Deposition of calcium phosphate in necrotic tissue

Dystrophic calcification:
calcification of necrotic tissue

Normal serum calcium and phosphate

Examples
(1) Calcification in chronic pancreatitis
(2) Calcified atherosclerotic plaque
(3) Periventricular calcification in congenital cytomegalovirus infection

Front 18

Metastatic calcification

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Metastatic calcification: calcification of normal tissue

Deposition of calcium phosphate in normal tissue

Due to increased serum calcium and/or phosphate

(1) Causes of hypercalcemia-primary hyperparathyroidism, malignancy-induced hypercalcemia
(2) Causes of hyperphosphatemia-renal failure, primary hypoparathyroidism
Excess phosphate drives calcium into normal tissue.
Examples of metastatic calcification
(1) Calcification of renal tubular basement membranes in the collecting ducts (nephrocalcinosis) This can produce nephrogenic diabetes insipidus and renal failure.
(2) Basal ganglia calcification in hypoparathyroidism

Front 19

Atrophy

Back 19

Decrease in size and weight of a tissue or organ
Atrophy: ↓ size/weight of tissue or organ

Front 20

Causes of atrophy

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Decreased hormone stimulation
Example-hypopituitarism causing atrophy of target organs, such as the thyroid and adrenal cortex
Decreased innervation
Example-skeletal muscle atrophy following loss of lower motor neurons in amyotrophic lateral sclerosis
Decreased blood flow
Example-cerebral atrophy due to atherosclerosis of the carotid artery (Fig. 1-10A)
Decreased nutrients
Example-total calorie deprivation in marasmus (see Fig. 7-1)
Increased pressure
(1) Example-atrophy of the renal cortex and medulla in hydronephrosis (see Fig. 19-14)
(2) Example-thick pancreatic duct secretions in cystic fibrosis occlude the lumens causing increased luminal back-pressure and compression atrophy of the exocrine glands and tubular epithelium (Fig. 1-10B).

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Mechanisms of atrophy

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1) Shrinkage of cells due to increased catabolism of cell organelles (e.g., mitochondria) and reduction in cytosol
Atrophy: autophagic vacuoles
(1) Organelles and cytosol form autophagic vacuoles.
(2) Autophagic vacuoles fuse with primary lysosomes for enzymatic degradation.
(3) Undigested lipids are stored as residual bodies (lipofuscin).
Atrophy: ↑ lipofuscin in cells

2)Loss of cells by apoptosis

Front 22

Hypertrophy

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Increase in cell size

Front 23

Causes of hypertrophy

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Hypertrophy: ↑ cell size; ↑ workload

Increased workload
(1) Left ventricular hypertrophy in response to an increase in afterload (resistance) or preload (volume) (Fig. 1-10C)
(2) Skeletal muscle hypertrophy in weight training
(3) Smooth muscle hypertrophy in the urinary bladder in response to urethral obstruction (e.g., prostate hyperplasia)
(4) Surgical removal of one kidney with compensatory hypertrophy (and hyperplasia) of the other kidney

Cell enlargement in cytomegalovirus infections

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Mechanisms of cardiac muscle hypertrophy

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1)Induction of genes for synthesis of growth factors, nuclear transcription, and contractile proteins
2)Increase in cytosol, number of cytoplasmic organelles, and DNA content

Front 25

Hypertrophy

Back 25

Increase in cell size
Causes of hypertrophy
Hypertrophy: ↑ cell size; ↑ workload
Increased workload
(1) Left ventricular hypertrophy in response to an increase in afterload (resistance) or preload (volume) (Fig. 1-10C)
(2) Skeletal muscle hypertrophy in weight training
(3) Smooth muscle hypertrophy in the urinary bladder in response to urethral obstruction (e.g., prostate hyperplasia)
(4) Surgical removal of one kidney with compensatory hypertrophy (and hyperplasia) of the other kidney
Cell enlargement in cytomegalovirus infections (see Fig. 16-10B)
Mechanisms of cardiac muscle hypertrophy
Induction of genes for synthesis of growth factors, nuclear transcription, and contractile proteins
Increase in cytosol, number of cytoplasmic organelles, and DNA content

Front 26

Hyperplasia

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Increase in the number of normal cells

Front 27

Causes of hyperplasia

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yperplasia: ↑ number of cells
Hormone stimulation
(1) Acromegaly due to an increase in growth hormone and insulin growth factor-1 (see Fig. 22-3)
(2) Endometrial gland hyperplasia due to hyperestrinism (see Fig. 21-20)
Increased risk for developing dysplasia (see later)
(3) Benign prostatic hyperplasia due to an increase in dihydrotestosterone (Fig. 1-10D)
(4) Gynecomastia (male breast tissue) due to increased estrogen (see Fig. 18-9)
(5) Polycythemia due to an increase in erythropoietin
Chronic irritation
(1) Thickened epidermis from constant scratching
(2) Bronchial mucous gland hyperplasia in smokers and asthmatics
(3) Cirrhosis of the liver due to alcohol excess (see Fig. 18-8)
Chemical imbalance
(1) Hypocalcemia stimulates parathyroid gland hyperplasia
(2) Iodine deficiency produces thyroid enlargement (goiter; see Fig. 22-12)
Combination of hypertrophy and hyperplasia
Stimulating antibodies
Example-Graves' disease due to thyroid-stimulating antibodies (IgG) directed against thyroid-stimulating hormone receptors (see Fig. 22-9)
Viral infections
Example-epidermal hyperplasia (wart) due to human papillomavirus

Front 28

Mechanisms of hyperplasia

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Dependent on the regenerative capacity of different types of cells
Labile/stable cells: can divide
Labile cells (stem cells)
(1) Divide continuously
(2) Examples-stem cells in the bone marrow, stem cells in the crypts of Lieberkühn, and basal cells in the epidermis
(3) May undergo hyperplasia as an adaptation to cell injury
Stable cells (resting cells)
(1) Divide infrequently, because they are normally in the G0 (resting) phase
(2) Must be stimulated (e.g., growth factors, hormones) to enter the cell cycle
(3) Examples-hepatocytes, astrocytes, smooth muscle cells
(4) May undergo hyperplasia or hypertrophy as an adaptation to cell injury
Permanent cells (nonreplicating cells)
Permanent cells: cannot divide
(1) Highly specialized cells that cannot replicate
(2) Examples-neurons and skeletal and cardiac muscle cells
(3) May undergo hypertrophy (only muscle)

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Labile cells (stem cells)

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(1) Divide continuously
(2) Examples-stem cells in the bone marrow, stem cells in the crypts of Lieberkühn, and basal cells in the epidermis
(3) May undergo hyperplasia as an adaptation to cell injury

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Stable cells (resting cells)

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(1) Divide infrequently, because they are normally in the G0 (resting) phase
(2) Must be stimulated (e.g., growth factors, hormones) to enter the cell cycle
(3) Examples-hepatocytes, astrocytes, smooth muscle cells
(4) May undergo hyperplasia or hypertrophy as an adaptation to cell injury

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Permanent cells (nonreplicating cells)

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Permanent cells: cannot divide
(1) Highly specialized cells that cannot replicate
(2) Examples-neurons and skeletal and cardiac muscle cells
(3) May undergo hypertrophy (only muscle)

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Metaplasia

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Replacement of one fully differentiated cell type by another
Substituted cells are less sensitive to a particular stress.
Metaplasia: one cell type replaces another

Front 33

Types of metaplasia

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Metaplasia from squamous to glandular epithelium
(1) Example-distal esophagus epithelium shows an increase in goblet cells and mucus-secreting cells in response to acid reflux (Fig. 1-10E)
(2) This is called Barrett's esophagus.
Barrett's esophagus: glandular metaplasia, gastric reflux
Increased risk for developing dysplasia (see later)
Metaplasia from glandular to other types of glandular epithelium
(1) Example-pylorus and antrum epithelium shows an increase in goblet cells and Paneth cells in response to Helicobacter pylori-induced chronic atrophic gastritis
(2) This is called intestinal metaplasia (see Fig. 17-14).
Increased risk for developing dysplasia (see later)
Metaplasia from glandular to squamous epithelium
(1) Mainstem bronchus epithelium develops squamous metaplasia in response to irritants in cigarette smoke (Fig. 1-10F).
(2) Endocervical epithelium develops squamous metaplasia in response to the acid pH in the vagina.
Metaplasia/hyperplasia: in some cases, may progress to dysplasia
(3) Both of the above alterations have an increased risk for developing dysplasia (see later).
Metaplasia from transitional to squamous epithelium
(1) Schistosoma hematobium infection in the urinary bladder causes transitional epithelium to undergo squamous metaplasia.
(2) Increased risk for developing dysplasia (see later)

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Mechanism of metaplasia

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Stem cells have an array of progeny cells that have different patterns of gene expression.
Under normal physiologic conditions differentiation of these progeny cells is restricted.
Metaplasia may result from reprogramming stem cells to utilize progeny cells with a different pattern of gene expression; the following signals may initiate this change:
(1) Hormones (e.g., estrogen)
(2) Vitamins (e.g., retinoic acid)
(3) Chemical irritants (e.g., cigarette smoke)
Metaplasia is sometimes reversible if the irritant is removed.

Front 35

Dysplasia

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Disordered cell growth
Precursor to cancer
Dysplasia: disordered cell growth
Risk factors for dysplasia
Some types of hyperplasia (see section V)
Some types of metaplasia (see section V)
Infection
Example-human papillomavirus type 16, causing squamous dysplasia of the cervix
Chemicals
Example-irritants in cigarette smoke, causing squamous metaplasia to progress to squamous dysplasia in the mainstem bronchus
Ultraviolet light
Example-solar damage of the skin, causing squamous dysplasia
Chronic irritation of skin
Example-draining sinus tracts in osteomyelitis
Dysplasia may progress to cancer.
Microscopic features of dysplasia (Fig. 1-10G)
Nuclear features
(1) Increased mitotic activity, with normal mitotic spindles
(2) Increased nuclear size and chromatin
Disorderly proliferation of cells with loss of cell maturation as cells progress to the surface
Dysplasia is sometimes reversible if the irritant is removed.

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Cell Death

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cell death occurs when cells or tissues are unable to adapt to injury.

Front 37

Necrosis

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Death of groups of cells, often accompanied by an inflammatory infiltrate

Front 38

Coagulation necrosis

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Preservation of the structural outline of dead cells
Coagulation necrosis: preservation of structural outlines
Mechanism of coagulation necrosis
(1) Denaturation of enzymes and structural proteins
(a) Intracellular accumulation of lactate or heavy metals (e.g., lead, mercury)
(b) Exposure of cells to ionizing radiation
(2) Inactivation of intracellular enzymes prevents dissolution (autolysis) of the cell.
Microscopic features (Fig. 1-11A)
(1) Indistinct outlines of cells within dead tissue
(2) Absent nuclei or karyolysis (fading of nuclear chromatin)

Front 39

Infarction

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Gross manifestation of coagulation necrosis secondary to the sudden occlusion of a vessel
Infarctions: pale and hemorrhagic types
(2) Usually wedge-shaped if dichotomously branching vessels (e.g., pulmonary artery) are occluded
(3) Pale (ischemic) type
Increased density of tissue (e.g., heart, kidney, spleen) prevents RBCs from diffusing through necrotic tissue (Fig. 1-11B).
(4) Hemorrhagic (red) type
Loose-textured tissue (e.g., lungs, small bowel) allows RBCs to diffuse through necrotic tissue (Fig. 1-11C).
Dry gangrene: predominantly coagulation necrosis

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Factors influencing whether an infarction will occur in tissue

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(1) Size of the vessel that is occluded
(a) Infarction is unlikely with obstruction of a major branch of a pulmonary artery.
(b) Infarction is likely if a thrombus overlies an atherosclerotic plaque in a coronary artery.
(2) State of development of a collateral circulation
Infarction is less likely if a well-developed collateral circulation is present (e.g., arcade system of the superior and inferior mesenteric arteries).
(3) Presence of a dual blood supply
(a) Infarction is less likely if a dual blood supply is present (e.g., pulmonary and bronchial arteries in the lungs).
(b) Renal and splenic arteries have end-arteries with an inadequate network of anastomosing vessels beyond potential points of obstruction; hence, infarction is likely to occur.
Infarction less likely: dual blood supply, collateral circulation
(4) Sudden onset of ischemia in an organ with preexisting disease will more likely produce an infarction.
Example-a pulmonary embolus will more likely produce an infarction in a patient with preexisting chronic lung or heart disease.
(5) Tissues with a high O2 requirement (e.g., brain, heart) are more likely to infarct than other less sensitive tissues (e.g., muscle, cartilage).
(6) Rapidity with which a vessel is occluded often determines whether an infarction will occur.
(a) Slow occlusion often allows time for development of a collateral circulation.
(b) Abrupt occlusion often results in infarction.

Front 41

Liquefactive necrosis

Back 41

ecrotic degradation of tissue that softens and becomes liquefied
Mechanisms
Lysosomal enzymes released by necrotic cells or neutrophils cause liquefaction of tissue.
Examples
Cerebral infarction: liquefactive not coagulative necrosis
(1) Central nervous system infarction
Autocatalytic effect of hydrolytic enzymes generated by neuroglial cells produces a cystic space (Fig. 1-11E).
(2) Abscess in a bacterial infection
Hydrolytic enzymes generated by neutrophils liquefy dead tissue.
Wet gangrene: predominantly liquefactive necrosis

Front 42

Caseous necrosis

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Variant of coagulation necrosis
Associated with acellular, cheese-like (caseous) material
Mechanism
(1) Caseous material is formed by the release of lipid from the cell walls of Mycobacterium tuberculosis and systemic fungi (e.g., Histoplasma) after immune destruction by macrophages.
(2) Other diseases associated with granuloma formation do not exhibit caseation.
Examples-Crohn disease, sarcoidosis, foreign body giant cell reaction
Tuberculosis: most common cause of caseous necrosis
Microscopic features of a granuloma
Acellular material in the center surrounded by activated macrophages, CD4 helper T cells, and multinucleated giant cells

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Enzymatic fat necrosis

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Peculiar to adipose tissue located around an acutely inflamed pancreas
Enzymatic fat necrosis: acute pancreatitis
Mechanisms
(1) Activation of pancreatic lipase (e.g., alcohol excess) causing hydrolysis of triglyceride in fat cells with release of fatty acids
(2) Conversion of fatty acids into soap (saponification)
Combination of fatty acids and calcium
Gross appearance
Chalky yellow-white deposits are primarily located in peripancreatic and omental adipose tissue (Fig. 1-11H).
Microscopic appearance
Pale outlines of fat cells filled with basophilic-staining calcified areas

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Traumatic fat necrosis

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Traumatic fat necrosis: not enzyme-mediated
Occurs in fatty tissue (e.g., female breast tissue) as a result of trauma
Not enzyme-mediated

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Fibrinoid necrosis

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Limited to small muscular arteries, arterioles, venules, and glomerular capillaries
Fibrinoid necrosis: necrosis of immune-mediated disease
Mechanism
Deposition of pink-staining proteinaceous material in damaged vessel walls due to damaged basement membranes
Associated conditions
Immune vasculitis (e.g., Henoch-Schönlein purpura), malignant hypertension