Injury of the cell and tissue

Donatas Petroka
Edvardas urauskas
 Clinical
manifestation
Functional
abnormalities

Structural
changes
 Responses to stress

Reversible
(cell edema)

Cell injury
Irreversible
Cellular responses to (cell death)
Stress

Hypertrophy
Hyperplasia
Adaptation
Metaplasia
Atrophy
 Responses to stress
Reversible cell injury
Cellular swelling
Intracellular organeles show alterations
 Responses to stress
Cell death
Apoptosis is the process of programmed
cell death that may occur in multicellular
organisms
not necessarily associated with cell injury
Necrosis is a form of cell injury that
results in death of cells in living tissue
always a pathologic process
Responses to stress
Causes of Cell Injury
 Responses to stress
Causes of Cell Injury
Oxygen Deprivation - Hypoxia
Reduced blood flow (ischemia)
atherosclerosis
Inadequate oxygenation of the blood
cardiorespiratory failure
Decreased oxygen-carrying capacity in
blood
anemia or carbon monoxide poisoning
Severe blood loss
Mechanisms of ischemic cell death
Responses to stress
Causes of Cell Injury
Physical Agents
Mechanical trauma
Temperature
burns or deep cold
Atmospheric pressure changes
Radiation
Electric shock
Responses to stress
Causes of Cell Injury
Chemical Agents and Drugs

Glucose or salt in hypertonic

concentrations (disturb electrolyte
balance)
Poisons (arsenic, cyanide, mercuric salts)
Insecticides and herbicides
Carbon monoxide
Alcohol
Variety of therapeutic drugs
Responses to stress
Causes of Cell Injury
Infectious Agents

Viruses
Rickettsiae
Bacteria
Fungi
Tape worms
Responses to stress
Causes of Cell Injury
Immunologic Reactions

Immune reactions to external agents

microbes and enviromental substances
Immune reactions to endogenous self-
antigens
autoimmune disease (systemic lupus
erythematosus, rheumatoid arthritis..)
Responses to stress
Causes of Cell Injury
Genetic dearengements

Defects in Structural Proteins

Marfan syndrome
Defects in Receptor proteins
Familial Hypercholesterolemia
Defects in Enzymes
Lysosomal Storage Disesases
Defects in Proteins that Regulate Cell Growth
Tumors
Responses to stress
Causes of Cell Injury
Nutritional Imbalances

Malnutrition
Protein-calorie deficiency (marasmus, kwaschiorkor,
cachexia)
Specific vitamins deficiency (B1-beriberi, A-night
blindness)
Excess diet
Obesity (diabetes, cancer)
Exess of cholesterol (atherosclerosis)
Responses to stress
Cell death
Necrosis
Necrosis is a form of cell injury that results in death of
cells (morphologic changes) that follows cell death in
living tissues
Severe damage
Metabolism stop
Structure destroy
Function lose
Responses to stress
Cell death
Apoptosis
Apoptosis is the process of programmed cell death that
may occur in multicellular organisms
Cell death
Comparisions between apoptosis and necrosis
Cell death
Morphology
Cytoplasmic changes
Increased eosinophilia of cytoplasm
Glassy homogeneous appearance
Cytoplasm is vacuolated
Calcification of dead cells
Appearence of myelin figures
Generation of calcium soaps
Cell death
Morphology
Nuclear changes
Pyknosis
Nuclear shrinkage and increased basophilia
Cell death
Morphology
Nuclear changes
Karyorrhexis
Fragmentation of pyknotic nucleus
Cell death
Morphology
Nuclear changes
Karyolysis
Fading of basophilia of chromatin due to DNAase
activity.
Cell death
Morphology

Normal Pyknosis Karyorrhexis Karyolysis

 Types of necrosis
5 morphological types:

Coagulative necrosis
Liquefactive necrosis
Caseous necrosis
Fat necrosis
Fibrinoid necrosis
Morphological aspects of necrosis
Coagulative necrosis (typical necrosis after
myocardium infarct)
 Coagulative necrosis
Preservation of general tissue architecture
Affected tissue is firm
Denaturation of structural proteins and
enzymatic digestion of cells
Example heart, kidney, spleen.
Normal Coagulative
heart necrosis
Normal Coagulative
kidney necrosis
Normal Coagulation
spleen necrosis
 Morphological aspects of necrosis
Liquefactive necrosis (necrosis involving
tissue digestion; common in the brain)

Liquefactive necrosis of the brain demonstrates many

As this infarct in the brain is organizing and being
macrophages at the right which are cleaning up the
resolved, the liquefactive necrosis leads to resolution
necrotic cellular debris.
with cystic spaces.
Normal Liquefactive
brain necrosis
Liquefactive necrosis
Morphological aspects of necrosis
Fat necrosis (necrosis involving release of
enzymes in tissue containing or surrounded
by fat cells, such as the pancreas)

This is fat necrosis of the pancreas. Cellular injury to the

pancreatic acini leads to release of powerful enzymes which
damage fat by the production of soaps, and these appear
grossly as the soft, chalky white areas seen here on the cut
surfaces.
 Fat necrosis
Seen in pancreas, breast
In acute pancreatitis, activated lipase
causes fat necrosis
Grossly visible chalky white areas
Presence of shadowy outlines of necrotic
cells
Fat necrosis
Fat necrosis
Morphological aspects of necrosis
Caseous necrosis (typical necrosis for
tuberculosis)

Microscopically, caseous necrosis is

characterized by acellular pink areas of
necrosis, as seen here at the upper
right, surrounded by a granulomatous
inflammatory process.

This is the gross appearance of caseous necrosis in a hilar lymph

node infected with tuberculosis. The node has a cheesy tan to
white appearance.
 Caseous necrosis
Type of coagulative necrosis
Seen in tuberculous infections
Tisseue is cheesy white in appearance
Caseous necrosis
Caseous necrosis
Caseous necrosis lymph node
Caseous necrosis lymph node
Caseus necrosis
 Morphological aspects of necrosis
Gangrene (dry gangrene; ischemic injury in
fingers, toes)
This is gangrene, or necrosis of many tissues in a body part. In
this case, the toes were involved in a frostbite injury. This is an
example of "dry" gangrene in which there is mainly coagulative
necrosis from the anoxic injury.
Gangrenous necrosis involves the tissues of a
body part. The inflammation seen here is
extending beneath the skin of a toe to involve
soft tissue (fat and connective tissue) and bone.
Because multiple tissues are non-viable,
amputation of such areas is necessary.
 Gangrenous necrosis
Wet gangrene
Dry gangrene
Gas gangrene
 Wet gangrene
Occurs in moist tissues like mouth, bowel,
lung, cervic
Diabetic foot
Bed sores
Wet gangrene Intestine
 Wet gangrene

This is gangrene of the lower extremity. In this case the term "wet" gangrene is
more applicable because of the liquefactive component from superimposed
infection in addition to the coagulative necrosis from loss of blood supply. This
patient had diabetes mellitus.
 Dry gangrene
Toes and feet due to arteriosclerosis
Thrombangitis obliterans
Raynauld disease
Trauma
Wet gangrene Dry gangrene

Bowel Limb
Venous obstruction Artery obstruction
Moist, swolwen, dark Dry, shrunken, black
No clear line of Presence of line of
demarcation demarcation
Bacteria present No bacteria
Prognosis poor Prognosis better
 Gas gangrene
Wet gangrene caused by gram positive
anaerobic bacteria
Seen in muscule and in colon
Gas gangrene
 Fibrinoid necrosis
Deposition of fibrin like material
Seen in immunologic cell injury,
hypertension.
 Fibrinoid necrosis

Micrograph showing (intensely pink) fibrinoid necrosis (large

blood vessel - right of image) in a case of vasculitis (Churg-
Strauss syndrome). H&E stain.
 Consequences of necrosis
Acute or chronic inflammation
Immunological reactions to sub-cellular
components
Lysis and absorption
Isolation and discharge: ulceration and cavity
formation
Organization
Encapsulation, calcification.
Injury of the cell and tissue

Responses Conseq. of
Cell injury Cell death
to stress necrosis

Apoptosis 1. Inflammation
2. Immunological
reactions
3. Lysis and
Necrosis: absorption
4. Isolation and
Cell death Coag discharge:
ulceration and
Liq cavity formation
Cell injury Cas 5. Organization
Reversible Fat 6. Encapsulation,
calcification.
Fibr