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CELL INJURY Flashcards

1
Q

definition of cell injury

A

occurs when cells are stressed so severely that they are no longer able to adapt OR exposed to damaging agents OR suffer from intrinsic abnormalities

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2
Q

REVERSIBLE CELL INJURY

A 
• The functional and morphologic changes are reversible if the 
damaging stimulus is removed
• Hallmarks of reversible cell injury:
• Reduced oxidative phosphorylation
• Cellular swelling
• Alterations in organelles
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3
Q

2 morphological features of reversal injury on

light microscopy:

A

• Cellular swelling (hydropic
change)
• Fatty change

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4
Q

Cellular Swelling (hydropic change):

A

• First manifestation of cell injury.
• Caused by changes in ion concentrations and water influx.
• Appears whenever cells are incapable of maintaining ionic and fluid
homeostasis.
• Result of failure of energy dependant pumps in the plasma membrane.

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5
Q

Macroscopic and microscopic features of reversible cell injury

A 
Macroscopic Features: If many cells in an organ are affected, the following 
features can be seen:
• Increased weight
• Increased turgor
• Pallor
  • Microscopic Features:
  • Small, clear vacuoles within cytoplasm
  • Increased eosinophilia of the cytoplasm
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6
Q

Fatty Change (steatosis):

A

• Refers to the abnormal accumulation of lipid droplets (triglycerides) in the
parenchymal cells of organs.

  • Causes:
  • Toxins
  • Protein malnutrition
  • Diabetes mellitus
  • Obesity
  • Hypoxia
  • Alcohol
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7
Q

EXAMPLE OF REVERSIBLE CELL INJURYOF FATTY CHANGE

A

• Example: FATTY LIVER
• In developed countries, alcohol abuse is the primary cause of fatty
liver.
• Main causes of non-alcoholic fatty liver include diabetes and obesity.
• Macroscopic Findings:
• May not see anything if mild.
• If more severe the liver may appear enlarged, yellow or greasy.

  • Microscopic Findings:
  • Small vacuoles in the cytoplasm and around the nucleus of hepatocytes.
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8
Q

IRREVERSIBLE CELL INJURY

A

• With continuing damage the injury becomes irreversible, at which
time the cell cannot recover and it dies
• It is difficult to pinpoint the exact time where reversible becomes
irreversible
• Two phenomena consistently characterize irreversibility:
• Inability to reverse mitochondrial dysfunction
• Profound disturbances in membrane function

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9
Q

MECHANISMS OF CELL INJURY

A
  • Depletion of ATP
  • Mitochondrial damage
  • Calcium influx
  • Oxidative stress (accumulation of ROS)
  • Defects in membrane permeability
  • Damage to DNA & proteins
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10
Q

CAUSES OF CELL INJURY

A
  • Oxygen deprivation
  • Physical agents
  • Chemical agents & drugs
  • Infectious agents
  • Immunologic reactions
  • Genetic derangements
  • Nutritional imbalances
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11
Q

OXYGEN DEPRIVATION

A

• Hypoxia is a deficiency of oxygen, which causes cell injury by reducing aerobic
oxidative respiration.
• Causes of hypoxia:
• Reduced blood flow (ischemia).
• Inadequate oxygenation of the blood (cardiorespiratory failure).
• Decreased oxygen-carrying capacity of the blood (anemia,
carbon monoxide poisoning

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12
Q

physical agents

A
  • Mechanical trauma
  • Extremes of temperature (burns and deep cold)
  • Sudden changes in atmospheric pressure
  • Radiation
  • Electric shock
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13
Q

Chemical Agents and Drugs(causes of cell injury)

A

• Simple chemicals such as glucose or salt in abnormal concentrations (high or
low) may injure cells directly or by deranging electrolyte balance in cells.
• Trace amounts of poisons (arsenic, cyanide, or mercuric salts) may damage
sufficient numbers of cells within minutes or hours to cause death.
• Other:
• Environmental and air pollutants, insecticides, and herbicides
• Industrial occupational hazards (carbon monoxide and asbestos)
• Recreational drugs
• Therapeutic drugs

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14
Q

infectious agents

A

• Includes viruses, rickettsiae, bacteria, fungi, parasites.

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15
Q

infectious agents

A

• Includes viruses, rickettsiae, bacteria, fungi, parasites.

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16
Q

Immunological Reactions

A

• Serves an essential function in defense against infectious pathogens.
• Immune reactions may also cause cell injury (e.g. autoimmune diseases and
responses to pathogens).

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17
Q

Genetic Derangements( causes of cell injury)

A

• Different mechanisms:
• Deficiency of functional proteins, such as enzyme defects in
inborn errors of metabolism.
• Accumulation of damaged DNA or misfolded proteins.

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18
Q

• Nutritional Imbalances (causes of cell injury)

A

• e.g. Deficiencies of specific vitamins, self-imposed (anorexia nervosa), nutritional
excesses (cholesterol predisposes to atherosclerosis)

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19
Q

necrosis

A

Definition: the death of tissues following bioenergetic failure & loss of plasma membrane integrity

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20
Q

NECROSIS - MORPHOLOGY of cytoplasm

A
  • Increased eosinophilia
  • Glassy & homogenous
  • Vacuolated, moth-eaten
21
Q

ECROSIS - MORPHOLOGY of nucleus

A

• Karyolysis- which reflects loss of DNA by the action of endonucleases, in which case the basophilia (very dark purple appearance) of chromatin fades.

Pyknosis – which reflects nuclear shrinkage and increased basophilia. In this scenario, the chromatin condenses into a solid, shrunken chromatin mass

Karyorrhexis – which reflects a scenario where a pyknotic cell undergoes fragmentation into several clumped chromatin strands, after which it disappears.

22
Q

Types of necrosis

A
  • Coagulative
  • Liquefactive
  • Caseous
  • Fibrinoid
  • Fat necrosis
  • Gangrene
23
Q

COAGULATIVE NECROSIS

A
  • Architecture preserved for days
  • Anucleate eosinophilic cells
  • Enzymes are denatured preventing proteolysis of dead cells
  • Localised area of coagulative necrosis = infarct
24
Q

LIQUEFACTIVE NECROSIS

A 
• Transformation of the tissue 
into a liquid viscous mass
• Occurs in the brain because 
of a lack of supporting stroma 
& high lipid content
• Also occurs with infections 
(proteolysis by leukocytes)
25
CASEOUS NECROSIS
• Most often in TB • Refers to gross appearance • Microscopically: amorphous eosinophilic granular debris
26
FIBRINOID NECROSIS
``` • Seen in immune reactions involving blood vessels & malignant hypertension • Circumferential, deeply eosinophilic, amorphous appearance of blood vessel wall ```
27
EXAMPLE OF FIBRINOID NECROSIS
• Example: Malignant hypertension: • Arterioles are under a lot of pressure  necrosis of the smooth muscle wall  seepage of plasma into the media with subsequent deposition of fibrin  fibrinoid necrosis.
28
FAT NECROSIS
* May occur with direct trauma eg. Fat necrosis of the breast * Or with the release of lipases eg. pancreatitis
29
GANGRENOUS NECROSIS
• Coagulative necrosis (ischaemia) with superimposed bacterial infection resulting in putrefaction • Infarction of mixed tissues in bulk • Often occurs in the lower limband bowel • May be wet or dry
30
DEFINE OPTOSIS
: a pathway of cell death induced by a tightly regulated suicide program in which cells destined to die activate intrinsic enzymes that degrade the cells own DNA & proteins
31
PHYSIOLOGIC CAUSE OF APOPTOSIS
* Physiologic * Destruction of cells during embryogenesis * Involution of hormone-dependent tissues upon hormone withdrawal * Cell loss in proliferating cell populations * Elimination of potentially self-reactive lymphocytes * Death of host cells that have served their useful purpose
32
PATHOLOGIC CAUSE OF APOPTOSIS
* DNA damage * Accumulation of misfolded proteins * Cell death in certain infections * Pathologic atrophy in parenchymal organs after duct obstruction
33
APOPTOSIS – MORPHOLOGY
``` • Cell shrinkage • Chromatin condensation • Formation of cytoplasmic blebs & apoptotic bodies • Phagocytosis of apoptotic bodies • Appears as a mass of intensely eosinophilic cytoplasm with fragments of dense nuclear chromatin ```
34
MECHANISM OF APOPTO
* Two pathways: * Intrinsic (mitochondrial) * Extrinsic (death-receptor mediated) * Two phases: * Initiation * Execution * Involves the activation of caspases * Interactions between sensors ,pro-apoptotic & anti-apoptotic molecule
35
APOPTOSIS CLINICAL CORRELATIONS
• Decreased apoptosis * Malignancy * Autoimmune diseases • Increased apoptosis * Neurodegenerative diseases * Death of virus-infected cells
36
NECROSIS FEATURES
Induction: invariably pathologic Extent: Cell groups Biochemical events: Energy failure Cell size: Swelling Plasma membrane: Disrupted Intact Cellular contents: Leakage Nucleus: Karyolysis/karyorrhexis/pyknosis Inflammation :Frequent
37
APOPTOSIS FEATURE
Induction: physiologic/pathologic Extent: single Biochemical events: Energy dependant Cell size: Shrinkage Plasma membrane: Disrupted Intact, altered structure Cellular contents: intact Nucleus: Fragmentation into nucleosome-size fragments Inflammation :None
38
A process in which a cell eats its own contents
AUTOPHAGY
39
AUTOPHAGY
• Can be physiologic or pathologic • Aging, exercise, atrophy • Maintains cellular integrity under stress conditions ``` examples • Cancer • Neurodegenerative diseases • Infectious diseases • Inflammatory bowel diseases ```
40
INTRACELLULAR ACCUMULATIONS
``` Accumulations of abnormal amounts of substances within a cell • May be within the cytoplasm, nucleus, other organelles Can be reversible or progressive leading to cell injury & death ```
41
NTRACELLULAR ACCUMULATIONS | • Lipids
• Steatosis (fatty change) • Cholesterol & cholesterol esters (atherosclerosis
42
INTRACELLULAR ACCUMULATIONS | • Proteins
appear as rounded eosinophilic droplets, vacuoles or aggregates within the cytoplasm • Eg. amyloid
43
INTRACELLULAR ACCUMULATIONS | • Glycogen
appears as clear vacuoles within the cytoplasm | • Diabetes mellitus, glycogen storage diseases
44
PIGMENTS
``` PIGMENTS • Coloured substances • Some are normal constituents of cells • Others are abnormal • May be exogenous or endogenous ```
45
EXOGENOUS PIGMENT
* Exogenous * Carbon (coal dust): anthracosis * Tattooing
46
ENDOGENOUS PIGMENT
* Endogenous * Lipofuscin * Melanin * Haemosiderin
47
PATHOLOGIC CALCIFICATION
``` • The abnormal tissue deposition of calcium salts, together with smaller amounts of other mineral salts • Two types: ``` * Dystrophic * Metastatic
48
PATHOLOGIC CALCIFICATION - DYSTROPHIC
• Occurs locally in diseased or necrotic tissue • Advanced atherosclerosis, aging/damaged heart valves • Normal serum calcium; normal calcium metabolism
49
PATHOLOGIC CALCIFICATION - METASTATIC
* Occurs in normal tissues * Hypercalcaemia * Altered calcium metabolism * Increased PTH secretion * Resorption of bone * Vitamin D-related disorders * Renal failure

Anatomical pathology (13 decks)

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