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Anatomical pathology > CELL INJURY > Flashcards

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
Q

CASEOUS NECROSIS

A

• Most often in TB
• Refers to gross appearance
• Microscopically: amorphous
eosinophilic granular debris

26
Q

FIBRINOID NECROSIS

A 
• Seen in immune reactions 
involving blood vessels & 
malignant hypertension
• Circumferential, deeply 
eosinophilic, amorphous 
appearance of blood vessel 
wall
27
Q

EXAMPLE OF FIBRINOID NECROSIS

A

• 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
Q

FAT NECROSIS

A
  • May occur with direct trauma eg. Fat necrosis of the breast
  • Or with the release of lipases eg. pancreatitis
29
Q

GANGRENOUS NECROSIS

A

• 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
Q

DEFINE OPTOSIS

A

: 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
Q

PHYSIOLOGIC CAUSE OF APOPTOSIS

A
  • 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
Q

PATHOLOGIC CAUSE OF APOPTOSIS

A
  • DNA damage
  • Accumulation of misfolded proteins
  • Cell death in certain infections
  • Pathologic atrophy in parenchymal organs after duct obstruction
33
Q

APOPTOSIS – MORPHOLOGY

A 
• 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
Q

MECHANISM OF APOPTO

A
  • 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
Q

APOPTOSIS CLINICAL CORRELATIONS

A

• Decreased apoptosis

  • Malignancy
  • Autoimmune diseases

• Increased apoptosis

  • Neurodegenerative diseases
  • Death of virus-infected cells
36
Q

NECROSIS FEATURES

A

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
Q

APOPTOSIS FEATURE

A

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
Q

A process in
which a cell eats its own
contents

A

AUTOPHAGY

39
Q

AUTOPHAGY

A

• Can be physiologic or pathologic
• Aging, exercise, atrophy
• Maintains cellular integrity
under stress conditions

examples 
• Cancer
• Neurodegenerative 
diseases
• Infectious diseases
• Inflammatory bowel 
diseases
40
Q

INTRACELLULAR ACCUMULATIONS

A 
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
Q

NTRACELLULAR ACCUMULATIONS

• Lipids

A

• Steatosis (fatty change)
• Cholesterol & cholesterol
esters (atherosclerosis

42
Q

INTRACELLULAR ACCUMULATIONS

• Proteins

A

appear as rounded eosinophilic droplets, vacuoles or aggregates within the cytoplasm
• Eg. amyloid

43
Q

INTRACELLULAR ACCUMULATIONS

• Glycogen

A

appears as clear vacuoles within the cytoplasm

• Diabetes mellitus, glycogen storage diseases

44
Q

PIGMENTS

A 
PIGMENTS
• Coloured substances 
• Some are normal constituents of cells
• Others are abnormal 
• May be exogenous or endogenous
45
Q

EXOGENOUS PIGMENT

A
  • Exogenous
  • Carbon (coal dust): anthracosis
  • Tattooing
46
Q

ENDOGENOUS PIGMENT

A
  • Endogenous
  • Lipofuscin
  • Melanin
  • Haemosiderin
47
Q

PATHOLOGIC CALCIFICATION

A 
• The abnormal tissue 
deposition of calcium salts, 
together with smaller 
amounts of other mineral 
salts
•
 Two types:
  • Dystrophic
  • Metastatic
48
Q

PATHOLOGIC CALCIFICATION - DYSTROPHIC

A

• Occurs locally in diseased or necrotic tissue
• Advanced atherosclerosis, aging/damaged heart
valves
• Normal serum calcium; normal calcium metabolism

49
Q

PATHOLOGIC CALCIFICATION - METASTATIC

A
  • 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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