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Definitions and concepts covered on the 2nd exam

Post mortem autolysis

Refers to the autolysis of cells occurring after somatic death; total diffuse hypoxia; varies greatly in onset and rate; PM change includes: autolysis and putrefaction

Somatic death

death of the entire body---essentially heart stoppage

Rigor mortis

contraction of muscles after death; average onset is 2-4 hrs; ATP is depleted; irreversible except by autolysis; may not occur efficiently if animal is wasted

Algor mortis

gradual cooling of the body after death; dependent on the temperature of the body at death (wool, insulation, ambient temp, ruminal gas, outside temps, hyperthermia, other factors)

Livor mortis

hypostatic congestion; gravitational pooling of blood to the side that is down after death; separation of serum from cells begins within one hour after death; blood clots within minutes

Post mortem clotting

within 1 hr after death; separation of cells from clot may give a chicken fat appearance; unattached to the BV walls distinguishing them from thrombi

Clots vs. Thrombus

Clots: coagulation after death
Thrombus: coagulation prior to death

Hemoglobin imbibition

red staining of tissue due to leaching of Hg from autolyzed RBCs and BV after death

Bile imbibition

staining of tissues with bile due to leaching from the bile ducts and GB after death


blue-green discoloration of tissue caused by the formation of FeS by bacteria (formed by the Fe released by Hg and H2S) *black to dark brown


results from autolysis of cells and CT; aided by putrefactive bacteria (proteolytic breakdown by anaerobic bacteria)


post mortem bacterial gas formation in the lumen of the GIT; can be difficult to distinguish between post-and-antemortem bloat; feed in rumen at time of death = postmortem bloating
Diagnose: displacing of blood, and shoving it towards the shoulders leaving the Superficial cervical LN full of blood due gaseous distention of GIT

Pale foci

in different organs (kidney, liver) can be due to pressure from the distended viscera expressing blood from the vessels; also by bacterial putrefaction of tissue

Mucosal sloughing

occurs in many tissues, but usually rapidly in the GIT; sloughing of enterocytes from the tips of villi within minutes after death

Lens opacity

frozen or cold carcasses; reverse to normal transparency on warming; often confused with cataracts; change in aqueous humor

PM of Intestinal Mucosa

Sloughing of enterocytes into lumen, dense chromatin (part of necrosis), pyknotic nuclei (very condensed); variability of bowl features possible and likely--may be portions of severe necrosis, and some where cells are still intact


self digestion or degradation of cells and tissues by the hydrolytic enzymes normally present within those tissues; occurs in all cells/tissues that die (and even before they die); can occur before or after death

Causes of Cell Injury

Extrinsic: trauma, thermal, electrical energy, ionizing radiation, infx agents, toxins

Intrinsic: spontaneous genetic mutations, by-products of metabolism (ROI), and hypoxia

Extrinsic and Intrinsic: workload imbalance, nutritional abnormalities, immunologic dysfunction

Cell and Biochemical Sites of Damage in Cell Injury

Decreased ATP: multiple downstream effects
Mitochondrial damage: leakage of proapoptotic proteins
Entry of Ca2+: increased mitochondrial permeability, activation of multiple cellular enzymes
Increased ROS: damage to lipids, proteins, DNA
Membrane damage: PM = loss of cellular components and Lysosomal mem = enzymatic digestion of cellular components
Protein misfolding/DNA damage: activation of proapoptotic proteins

Type of Responses to Injury

dependent on many factors: type of agent, extent of injury, duration of injury, and cell type affected

Maintaining homeostasis

cells respond to stressors in a variety of ways to maintain homeostasis; injury takes place when a cell can no longer maintain a steady state; can be reversible until it reaches limits to which irreversible change and death occur
Respond: 1)adaptation 2)degeneration 3)death


loss of 02 due to inadequate blood flow; most common cause of cell death


NOT necrosis! It is present in reversible situations of cell injury, but at some point may become irreversible

Reversible cell injury

injury from which the cell can adapt or recover and thus return to a normal or almost normal function

Irreversible cell injury

dead cell; the cut between reversible and irreversible is not always clear cut but some cytomorphologic changes include:
-PM damage
-Ca entry into cell
-Mitochondrial swelling/vacuolization
-Amorphous densities (likely Ca) in the mitochondria (impending doom for cell)
-lysosomal swelling

Acute cell swelling

Sequence of events:
1. hypoxia
2. decrease in ox. phos and ATP
3. increased glycolysis, increased IC lactate, and depletion of glycogen stores
4. failure of Na/K pump (no ATP)
5. Net influx of Na, Ca, and H20 (loss of IC K and Mg)
6. swelling of mitochondria and cytocavitary network (RER, SER, etc)
7. detachment of ribosomes, clumping of nuclear chromatin, loss of microvilli, vesiculation of ER, formation of membrane whorls (myelin figures)
8. severe disruption of CM, influx of Ca into mitochondria and cytosol, overall cell enlargement, and clearing of cytosol
9. Irreversible cell injury, necrosis


partial reduction in the 02 concentration supplied to cells or tissue; common cause of cell death


complete loss of 02 supplied to cells or tissue

Causes of 02 deficiency

-heart failure
-respiratory failure
-CO toxicity (reduced transport of 02)
-HCN toxicosis (blockage of cell resp. enzymes)
*Cells of increased susceptibility due to high energy demands: neurons, cardiac monocytes, hepatocytes, renal tubules

Physical agents: extrinsic factors of cell death

trauma-direct cell rupture and death of large numbers of cells, or damage to BV

thermal-ice crystalization(impairs blood flow and ruptures CM), CM damage, denaturation of enzymes and structural proteins, increased rate of enzymatic rxns with accum. of metabolic end products and pH changes

electrical-heat generation, ionic changes, altered conduction of nerves and muscles

ionizing radiation-ionization of cellular water with prod. of highly ROI injuring cell comp, DNA damage

Viral effects on cell changes

viruses are obligate IC parasites that redirect host cell enzymes toward synthesis of viral proteins and genetic materials to the detriment of host cells; vary from little effect to cell death or neoplastic transformation

Bacterial effects on cell changes

Bacteria are EC, facultative, or obligate IC who can be either opportunistic or the primary pathogen. Cell changes/injury also vary but can be the result of potent toxins or overwhelming/ineffective inflammatory response to bacteria

Fungal effects on cell changes

EC or IC, eukaryotic but not protists that resist destruction by the body that can lead to progressive, chronic inflammatory disease with the loss of normal host tissues; protozoal agents replicate in specific host cells resulting in destruction of infected cells; metazoal parasites cause inflammation, distort tissue, and use host nutrients


single-cell, eukaryotes w/o cell walls; protists non-fungi pathogens; Ic or EC; similar to other infx agents: cause host cell inflammation, death; coccidia are one example


protists, uni/multicellular, phototropic and contain cell walls; some may infect animals and cause disease

Helminthic parasites

nematodes (roundworms), cestodes (tapeworms), and trematodes (flukes); diverse life cycles; metazoans; cause nutritional deficiencies, tissue destruction, inflammation, create opportunities for secondary infection with other agents

Protein-Calorie Deficiencies

known as kwashiorkor in humans; caloric deficiency forces glycogenolysis, lipolysis, and proteolysis to meet energy demands; sporadically seen ; require metabolic adaptation by a large population of cells

Caloric and other nutrient excesses

result of obesity; excess fat soluble vit = toxicity; mineral imbalances (Ca and P); implicative of cardio disease and others

Genetic Derangment diseases

-Enzyme deficiencies(clotting factor, lysosomal storage disease, maldigestion)
-anatomical defects (poor collagen synthesis)
-physiological (hormone def/excess)
-many others

Hormone imbalance or workload

overworked cells may adapt or become exhausted and die; cells that are no longer stimulated atrophy and ultimately disappear

Chemicals, Drugs, and Toxins

can influence cells by a multitude of mechanisms
-modify function and morphology of specific cells
-most drugs cause cells to adapt within a tolerable range of homeostasis
-block or stimulate CM receptors
-alter specific enzymes
-produce toxic free radicals
-alter cell permeability
-damage chromosomes
-modify metabolic pathways
-damage structural components of cells


having the immune system attenuated; from immunisuppressive drugs, irradiation, malnutrition, or disease process


deficiency of immune response or a disorder characterized by a deficient immune response; classified as inherited or acquired disorders in which some aspect of the host defense are absent or functionally defective


prevention or dimunition of the immune response, by irradiation or by administration of anti-metabolites, anti-lymphocyte serum, or specifc Ab (immunosuppressive drugs-treatment of graft rejection and autoimmune disease)

Autoimmune disease

body directs its adaptive immune response against its own tissues


immune responses to innocuous Ags that lead to symptomatic reactions upon re-exposure


involves a collection of different processes and events; altered control of cell growth; many processes lead back to the accum. of damage to DNA; slowed metabolic processes; lifetime damage to DNA or accumulation of cellular debris interfering with normal cell functions

Hydropic degeneration

cell swelling; increased cell size and volume due to overload of water in the cell; occurs due to loss of cell homeostasis
-damage to CM
-failure of cellular energy production
-injury to enzymes regulating ion channels of membranes

Process of Cell Swelling

1. Injury
2. hypoxia-induced failure of ATP formation or CM damage
3. decreased ATP
4. Na and water into cell, K out of cell
5. Increased osmotic pressure
6. Moves water into cell
7. Cisternae of ER rupture forming vacuoles
8. Extensive vacuolization
9.Hydropic degeneration

CCL4 Toxicity

can induce fatty change and cell necrosis by lipid peroxidation; direct damage to membranes by radicals; disrupts double bonds in FA and inserts 02 (peroxidation); radicals have unpaired electros that are highly reactive and pull H2 off of other compounds creating more radicals

-OH radical

Most toxic radical

CCL4 toxicity leading to fatty liver

CCL4->SER->CCL3- =>lipid radicals-> 02->lipid peroxidation-> membrane damage to RER->polysome detachment-> decreased apoprotein synthesis->fatty liver

CCL4 toxicity leading to Inactivation of Mitochondria, Cell Enzymes, and Denaturation of Proteins

CCL4->SER->CCL3-=>lipid radicals-> 02-> Lipid peroxidation->release of products of lipid peroxidation->damage to PM->decreased permeability to Na+, H20, Ca2+->Cell swelling->massive influx of Ca2+-> inactivation of mitochindria, cell enzymes, and denaturation of proteins

Hydropic degeneration

microscopic appearance of acute cell swelling; it occurs in endothelium, epithelium, alveolar pneumocytes, hepatocytes, renal tubular epithelial cells, neurons, and glial cells of the brain

Ballooning degeneration

severe hydropic degeneration; cells become very large due to swelling, and may rupture. Some may even include viral inclusion bodies; cytoplasm = clear space; typically seen in epidermal cells infected by epitheliotropic viruses (poxviruses) progressing to blisters

Significance and Fate of Acute Cell Swelling

- loss of function
- necrosis
- secondary lesions may develop from swollen cells casuing obstructions or thrombosis/ischemic necrosis of tissue
- reversion of the cell back to a normal state may occur if the injurious state is corrected before the damage becomes irreversible

Reversible cell injury

characterized by: generalized swelling of the cell and its organelles, blebbing of the PM, detachment of ribosomes from the ER, and clumping of nuclear chromatin

Irreversible cell injury

characterized by: increasing swelling of the cell, swelling and disruption of lysosomes, presence of large amorphous densities in swollen mitochondria, disruption of cellular membranes, and profound nuclear changes


nuclear condensation; shrunken, dark, homogenous, and round due to chromatin clumping


fragmentation of nucleus; NE ruptures, dark nuclear fragments are released into cytoplasm


dissolution of the nucleus; nucleus is extremely pale or absent due to the dissolution of chromatin by RNAses and DNAses

Laminated (myelin) figures

derived from damaged membranes of organelles and the PM; first appear during the reversible stage and become more pronounced in irreversibly damaged cells

Necrosis or Oncotic necrosis or oncosis

death of cells in the LIVING animal following irreversible cell injury that initially results in cellular swelling; lack or loss of ATP; causes inflammation


death of cells in the LIVING animal that occurs following cellular shrinkage; may be PCD or type 1 cell death; it may also be physiologic or pathologic; energy dependent; does not elicit inflammation; PCD is often used to describe physiologic and apoptosis to pathologic

Postmortem autolysis

death and degradation of cells that occurs after somatic death; no ATP; tissues and cells dying; cell swelling can be difficult to differentiate from necrosis

Sources and Consequences of Increased Cytosolic Calcium in Cell Injury

activates many different enzymatic processes and essentially starts chewing everything up; induces the release of mitochondrial contents; some enzymes activated are: phospholipases, proteases, endonucleases, and ATPases

ROS in Cell Injury

This is a normal process that can cause problems for the cell; 02 free radicals are always forming as a normal phys process; cellular components at risk: proteins, membrane lipids, and nucleic acids

Major antioxidant enzymes

superoxide dismutase, catalase, and glutathione peroxidase (Vit E is a precursor for glutathione peroxidase)

Fenton (Haber-Weiss) Reaction

normal reaction where Fe2+ is oxidized by H202 to Fe3+ => OH radical and OH anion; it is then reduced back to Fe2+, a OOH radical, and a proton by the same H202

Cytochrome P450 enzymes

primarily located in the SER of hepatocytes, but may be found in other cells also.
-main role: metabolize lipid-soluble chemicals into water soluble compounds for excretion from their body in bile or urine; occurs in 3 phases; require a wavelength of 450 and have red pigmentation => why they are called P450 enzymes

3 phases of lipid metabolism by Cyt P450

Phase 1: biotransformation: chemicals are bioactivated to a high energy reactive intermediate molecule (involve oxidation, reduction, and hydrolysis); enzymes: centrolobular region of liver; require 02 and NADPH (how liver detoxifies drugs)

Phase 2: involves formation of covalent bonds with polar molecules (glucuronic acid); forms water soluble metabolite that can be excreted

Phase 3: transport of molecules across the cell membrane into the lumen of the canniculus by molecular pumps

*These functions in the centrolobular area make it more susceptible to toxic damage b/c it contains the most P450, and it also has less 02


reactive aldehyde and forms covalent protein adducts; referred to as advanced lipoxidation end products; also reacts with deoxyadenosine and deoxyguanosine forming mutagenic DNA adducts

Cytoplasmic changes in cellular necrosis

- increased acidophilia due to loss of rRNA
- increased paleness, due to preceding water loading, and loss of proteins
- detachment of cells from the BM and neighboring cells
- shrinkage of cells after they have ruptured and lose their contents (may give a darker staining intensity)
- fragmentation and loss of structure once the cell has ruptured

Coagulative necrosis

1st type of oncotic necrosis: preservation of the basic cell outlines of necrotic cells, cytoplasm homogenous and eosinophilic due to coagulation of proteins, nuclei are pyknotic, karyorrhetic, karyolytic or absent; due to reduced blood flow usually infection in cattle (thrombi from g- bacterial infection)

Infarct vs. Infarction

Infarct: necrotic lesion caused by ischemia
Infarction: process by which an infarct occurs
*Infarcts are typically manifested by coagulative necrosis of affected tissues (kidney, liver, heart, skeletal muscle)
*Those in the brain and SC = liquefactive necrosis

Caseous necrosis

2 type of oncotic necrosis: continual breakdown of necrotic cells into granular fragments (grossly resembles cottage cheese); occur in any tissue and most of the debris is dead leukocytes; older lesion; found within sites of granulomas or chronic inflammation---(Mycobacterium TB); frequently calcified (dystrophic calcification) called tubercles because macrophages cannot breakdown/kill bacteria

Liquefactive necrosis

3rd type of oncotic necrosis: conversion of the necrotic tissue into liquid that varies from clear to cloudy to opaque; occurs in brain due to small % of CT and high lipid content (dissolution of neutropil); other tissues seen as purulent (suppurative) inflammation with neutrophiles having infiltrated the causing formation of pus (necrotic tissue + neutrophils); contain macrophages called "gitter cells"

Gangrenous necrosis

initially characterized by coagulative necrosis then complication by saprophytic bacterial infection(bacteria that live in dead, organic matter) and subsequently suppuration and putrefaction (decomposition of organic matter by these microbes); clinically referred to as gangrene


clinical condition characterized by lesions of gangrenous necrosis; 3 types: moist, dry, and gas gangrene

Moist gangrene

an area of necrotic tissue (usually coagulation necrosis) which is further degraded by the liquefactive action of saprophytic bacteria that usually cause putrefaction; grossly tissues become soft, moist, and reddish-brown to black; if saprophytic produce gas with putrid odor (Moist and nutrient rich environment = happy bacteria)

Dry gangrene

is coagulative necrosis secondary to infarction followed by mummification (lower portions of extremities--terminal blood supply); usually due to ingested toxins--ergot and fescue cause vasoconstriction leading to thrombosis and infarction or cold---direct freezing and disruption of cells by IC and EC ice crystal formation and vascular damage; mummification due tot loss of water from dead tissue b/c of lack of blood supply

Gas Gangrene

coagulative necrosis with other changes, particularly by gas build up from bacterial fermentation in the necrotic tissue; caused by toxigenic promary pathogen (Clostridium spp.); usually induced by wound; thoroughbred mare case

Fat necrosis

3 types:
enzymatic: pancreatic necrosis of fat; most important (dogs primarily); activation of pancreatic lipases that have escaped the duct system of the pancreas

traumatic: trauma involved; thermal injury (heating pad case); adipose tissue is crushed (subcutaneous tissues and fat adjacent to pelvic canal in dystoic heifers)

necrosis of abdominal fat in cattle: cause unknown

*All appear grossly as white, chalky lesions; histologically see basophilic fluid representing saponification (Na, Ca, and K salts of FA)


any fragment of necrotic material, especially bone, that resists degradation; may cause irritation and delay repair

Healing of an abcess

occurs after sequestered pus is phagocytosed and/or carried off by lymphatics; greatly hastened by drainage (rupture to outside or surgical drainage)

Purpose of inflammation of necrotic tissue

to allow digestion by heterolytic enzymes of WBCs and liquefaction of necrotic tissue so that it can be removed by macrophages to promote regeneration of normal tissue


dilated blood vessels engorged with blood


degradation of cytoplasmic proteins and organelles by their enclosure in double membrane bound cytoplasmic vesicles that fuse with lysosomes (in living animal); considered alternative form of PCD or type 2 cell death that does not require caspases and characterized by lysosome accumulation


chromatin in nuclei of cells undergoing apoptosis often is condensed into a pattern that resembles a torus (ring-shape); chromatin condensation in apoptotic cells may also be crescent-shaped (crescentic caps)

Histopathologic characteristics of apopotosis

-individual cells are shrunken
-chromatin is condensed
-cytoplasm is fragmented
-cytoplasmic buds often contain a fragment of nucleus from on the surface, separate, and are phagocytosed by adjacent cells as apoptotic bodies
-inflammation is absent

Some Cell Uses for Apoptosis

- normal embryonic/fetal development
- normal tissue makeover
- metamorphosis
-atrophy: pancreatic duct obstruction
- Hormone-independent atrophy: endometrium cyclic proliferation and deletion in females
- GF-dependent survival

Mechanisms of Apoptosis

Major inducers of apoptosis: withdrawal of GFs/hormones, receptor-ligand interactions (Fas, TNF), CTLs, Injury (radiation, toxins, free radicals)

Control and Regulation: Bcl-2 family

Executioner caspases-> endonuclease activation, breakdown of cytoskeleton

Apoptotic body formation


one of the signals recognized by phagocytes (normally it is expressed on the inner leaflet of the PM, but for apoptosis it is flipped and expressed on the outer leaflet)---an "Eat Me" signal for the cell to be phagocytosed


an important executioner caspase leading to PCD


member of a family of proteases that can bring about PCD; enzymes that have cysteine residues and cleave after aspartate ; nuclear lamins are one target of caspases

Other targets: ICAD (inhibitor of DNAse), cytoskeletal proteins, golgi matrix proteins

Caspase activation

Caspase-9 is activated as a complex with Apaf-1 and cyt C in the apoptosome -> activated Caspase-9 cleaves caspase-3 causing its activation->effector caspase->apoptosis

Bcl-2 family

a member of a family of proteins that regulate PCD; closely related to Ced-9 in C. elegans that activates Ced-3 for PCD
Antiapoptotic: Bcl-2
Pro-apoptotic: Bax and Bak
Pro-apoptotic BH3-only: Bid, Bad, Noxa, Puma, Bim

Mitochondrial pathway of apoptosis

Death signal->Bak, Bax form oligomers in the outer membrane of the mitochondria->cyt c from intermembrane space->formation of apoptosome containing Apaf-1 and caspase-9->caspase-9 activated further activating other caspases (caspase-3) by proteolytic cleavage->apoptosis

Regulation of caspases by IAPs in Drosophilia

IAPs inhibit both effector and iniator caspases; inhibits apoptosis by interacting with caspases

p53 Role in DNA Damage-Induced Apoptosis

DNA damage leads to activation of ATM and CHK2 protein kinases->CHK2 and activated ATM phosphorylate and stabilize p53->results in increased IC levels of p53->p53 induces cell cycle arrest and allows for an attempt to repair damaged DNA

*Important for preventing the formation of mutations and cancer
*Inhibits p21 halting Cdk1/cyclin and CDK2/cyclin in the cell cycle (arrests in G1)
*targets PUMA and NOXA for PCD

PI 3-Kinase Pathway and Cell Survival

promotes cell survival by keeping apoptosis from occurring; AKT-kinase activated also by mTOR can trigger cell survival; requires growth factors that signal cell survival and activate tyrosine kinases leading to the activation of PI-3->PIP3->protein kinase AKT->phosphorylates a number of proteins that lead to cell survival

mTOR pathway

central regulator of cell growth that couples the control of protein synthesis to the availability of GFs, nutrients, and energy

Cell death receptors

Extrinsic death cell receptors: TNF and other receptors consist of 3 polypeptide chains so their binding to cell death receptors induces receptor trimerization; recruiting caspase 8 by adaptor molecules; activation of caspase 8 cleaves/activates effector caspases->BID->caspase 9->effector capases->apoptosis
(Fas ligand is another example)

Intrinsic mitochrondrial pathway of apoptosis

survival signal->production of antiapoptotic proteins (Bcl2)->no leakage of Cyt C from mitochondria->no cell death
*if there is a lack of survival signals or DNA damage due to irradiation (etc) sensors activate BH3 only proteins->antagonism of Bcl2->Bak/Bax->cyt c leakage->activation of caspases


Poly-ADP ribose polymerase found in the cells nucleus whose main role is to detect any single stranded DNA breaks to the enzymatic machinery in SSB repair; if SSB is detected PARP synthesizes PAR which signals DNA repairing enzymes

*With DNA cleavage by caspases, PARP can deplete cellular ATP and lead to cell necrosis
*PARP can also induce apoptosis via PAR which stimulates AIF

Tunel assay

detecting DNA strand breaks in the tissue; light microscope level a tunel assay is used to detect apoptosis (allows for quantification of apoptosis in cells)

Autophagy and Integrated Stress Response

autophagy is a response of the cell to stress, and many of the same stressors that trigger apoptosis also trigger autophagy
(Stimulated by multiple forms of cell stress: nutrient or GF factor deprivation, hypoxia, ROS, DNA damage, protein aggregates, damaged organelles, or IC pathogens)

Autophagy & Metabolic Stress

generates free aa and fa that can be recycled in a cell-autonomous fashion or delivered systemically to distant sites within the organism (de novo synthesis of proteins are essential for stress adaptation)

Autophagy as Housekeeper

-eliminates defective proteins and organelles
-prevention of abnormal protein aggregate accumulation
-removal of IC pathogens
-can degrade entire organelles and pathogens: unique function separating it from the ubiquitin-proteosome system
*Critical for autophagy-mediated protection against cancer, aging, neurodegenerative diseases, and infection

Autophagy-Guardian of the Genome

can limit DNA damage and chromosomal instability
*Deficient autophagy: failure of checkpoints, repair proteins, insufficient energy for proper DNA replication and repair, deregulated turnover of centrosomes, excess ROS, etc

Autophagy and Neurodegenerative Disease

clearance of aggregate-prone mutant proteins associated with several different neurodegenerative diseases
*similar roles in muscle disease

Autophagy and Cancer

regulation of autophagy overlaps closely with signaling pathways that regulate tumorigenesis
-AKT and PI3 inhibit autophagy (Tor pathways)
-p53 is the most common tumor suppressor gene positively regulating DNA damaged cells

Autophagy and Aging

dietary restriction (intermittent fasting) is a potent inducer of autophagy and increased lifespan in all species
-IGF-1 pathway: fasting decreases insulin and IGF-1 synthesis which increases autophagy through a reduction in Akt pathway

Heterophagy vs. Autophagy

Heterophagy: source of phagocytosed material is external to the cell (neutrophils, macrophages, and other cells participating in uptake of cell debris)
Autophagy: sources of phagocytosed material is internal to the cell (remove non-functional organelle)

Autophagic vacuoles (autophagosomes)

appearance in the light microscope: eosinophilic inclusions (liver and kidney)
-residual bodies with lipofuscin (golden-brown pigment associated with aging in heart and neurons)
-lamellar debris (myelin figures)
-accumulates: products of ubiquitin-proteosome pathway, misfolded proteins, lipoprotein membranes


increase in size of cells or organs (can be due to an increase in number and/or size of organelles)


increase in number of cells of a tissue or organ


decrease in size or amount of cell, tissue, or organ AFTER normal growth has been reached


potentially reversible change in which one adult cell is replaced by another adult cell of the same germ line (ciliated columnar epithelium->stratified squamous epithelium)


disorderly arrangement of cells within epithelium


a new growth composed of cells, originally derived from normal tissues, that have undergone heritable genetic changes allowing them to become relatively unresponsive to normal growth controls and to expand beyond their normal anatomic boundaries
*Hyperplasia, hypertrophy, Metaplasia, and dysplasia can be predispositions to neoplasia, but only Meta and Dysplasia can persist in neoplastic tissue

Simple cellular hypertrophy

number of cells DOES NOT increase
-can synthesize more organelles, larger organelles or both
-more prominent in cells that undergo little replication (stable or permanent cells)

Physiologic vs Compensatory hypertrophy

Physiologic: occurs as a result of a physio process (increased work load)
Compensatory: occurs b/c compensation is needed (opposite kidney when one is removed)


increase in the number of cells; increased mitotic division is implied; increases the size of tissues and organs; hyperplastic cells themselves can be hypertrophic but is not a requirement

Hyperplastic Cell Types

Only some can be hyperplastic; labile and stable cells (either proliferate normally or can be stimulated to proliferate)
Permanent cells cannot undergo hyperplasia unless you are a neonate, a frog, fish, or bird (these have regenerative capabilities in their cardiac myocytes)

2 types of hyperplasia

Physiologic: hormonal (mammary gland epithelium before lactation) or compensatory (epidermal response to skin abrasion)
Pathologic: hormonal or in response to chronic irritation
*Some physiological processes can progress into pathologic processes (goiter)

Causes of Metaplasia

-chronic irritation from particles and chemicals inhaled into the respiratory tract
-vitamin A deficiency
-Ammonia toxicity in chicken bronchi
-E2 toxicity: urinary and prostatic epithelium
-healing of mammary gland epithelium following mastitis
-blockage of ducts in salivary gland, biliary tract, and pancreas
-conversion of soft tissue to bone following injury (osseous metaplasia--very common)
-extramedullary hematopoiesis in spleens and livers following bone marrow injury or insufficiency (myeloid metaplasia--very common)
-formation of cartilage or bone in mammary gland tumors of dogs (chrondroid or osseous metaplasia)


failure of organs or tissues to obtain full size DURING development


a complete failure of an organ to develop


decrease in size of a tissue caused by reduction in the number of cells, usually by apoptosis (or PCD) and usually refers to physiological processes
-thymus and bursa involute with age
-uterine involution following parturition

Causes of Atrophy

-deficient nutritive supply
-decreased workload
-loss of endocrine stimulation

Serous atrophy

important necropsy finding that indicates starvation; grossly fat deposits are completely or partially depleted and a clear or yellowish gelatinous material remains; most common in epidural and perineal fat but may affect fat depot in bone marrow; common in neonates

3 main substances that accumulate in cells

1. normal cellular constituent: water, lipids, proteins, and CHOs in excess
2. Abnormal substance: either exogenous, such as a mineral or product of infx agents, or endogenous such as a product of normal synthesis or metabolism
3. Pigment accumulates

5 mechanisms leading to Fatty liver

1. Excessive delivery of free FA either to the gut or adipose tissue
2. Decreased B-oxidation of FA to ketones and other substances because of mitochondrial injury (toxins, hypoxia)
3. Impaired synthesis of apoprotein (CCL2 toxicity)
4. Impaired combination of TGs and proteins to form lipoprotein
5. Impaired release of lipoproteins from the hepatocyte

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