Cellular Injury Flashcards

1
Q

Cellular injury

A

-Most diseases begin with cell injury
-Cell unable to maintain homeostasis
-Injured cells may recover (reversible injury) or die (irreversible)

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2
Q

Dependent factors of cellular injury

A

-Cell being affected: type, nutritional state, level of differentiation, level of susceptibility, adaptive process of the cell
-Injurious agent: type, severity, duration of the stimulus

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3
Q

Mechanism of cell injury

A

-Hypoxia: lack of oxygen due to ischemia (low blood supply)
1. Vacuoles form in the mitochondria = low ATP
2. Na+/K+ pump of the cell membrane is disturbed: Na+ and Ca2+ into the cell, K+ flows out
3. Water follows = edema
4. Ribosomes detach from E.R. = protein synthesis diminishes
5. Reversible if oxygen is restored; if not = cell death

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4
Q

Free radicals

A

-Electrically uncharged atoms having an unpaired electron; in an attempt to become stable, they form chemical bonds with other molecules

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5
Q

Where do these free radical come from?

A

-Absorption of UV radiation, redox reactions (oxygen is reduced to water), enzymatic metabolism of chemicals/drugs

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6
Q

Damaging effects of free radicals

A

-Lipid peroxidation (H2O2): increases membrane permeability
-Attacks critical proteins (affects ion pumps)
-Fragmenting DNA (affects protein synthesis)
-Damaging mitochondria (increases calcium cytoplasm)
-Certain antioxidants (vitamins s E, C, cysteine, etc) and certain enzymes can combat free radicals

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7
Q

Chemical injury

A

-Biochemical interaction between a poison (toxin) and cell membrane
-General mechanisms of destruction: direct toxicity or formation of free radicals
-Ex: CCl4, arsenic, cyanide, CO, alcohol, lead, social drugs

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8
Q

Injuries (intentional and unintentional)

A

-Blunt force, contusion, abrasion, laceration, bone fractures, stab wounds, puncture wounds, gunshot wounds, asphyxial injuries, drowning

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9
Q

Blunt force

A

-Blows/impact causing tearing, shearing, crushing

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10
Q

Contusion (bruise or hematoma)

A

-Blow that squeezes soft tissue causing bleeding underneath skin/underlying tissue

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11
Q

Abrasion (scrape)

A

-Removal of superficial skin

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12
Q

Laceration

A

-Jagged or irregular tear/rip

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13
Q

Asphyxial injuries

A

-Suffocation, strangulation, chemical asphyxiants (CO, cyanide)

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14
Q

Infectious injuries

A

-Caused by any microbial agent that can survive and thrive in the body (bacteria, virus, protozoan, fungus, helminths)

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15
Q

Pathogenicity or virulence depends on

A
  1. Ability to invade and destroy cells
  2. Toxin production
  3. Production of hypersensitivity reactions in host
  4. Overall health of host (especially the condition of the immune system)
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16
Q

Cellular injuries

A

-Cellular swelling due to water infiltration (affects ion pump)
-Abnormal accumulation of lipids and carbohydrates in cells (spleen, liver, CNS); glycogen (diabetes), proteins, pigments (melanin and hemoproteins), calcium, and urate (uric acid)

17
Q

Clinical manifestations of cellular injury

A

-Fever; acute inflammatory response
-Increased heart rate; increased metabolism due to fever
-Leukocytosis
-Release of cellular enzymes into extracellular fluid (type of enzyme depends)

18
Q

Cellular death

A

-Necrosis: dense clumping of DNA and disruption of plasma and organelle membranes
-Autolysis: cellular self-digestion
-Karyolysis: nuclear dissolution

19
Q

Types of necrosis

A

-Coagulative
-Liquefactive
-Caseous
-Fat
-Gangrenous

20
Q

Coagulative necrosis

A

-Due to hypoxia
-protein denaturation (albumin hardens)
-Occurs in kidneys, heart, and adrenal glands

21
Q

Liquefactive necrosis

A

-Ischemic injury to brain neurons
-Cells become digested by their own enzymes

22
Q

Caseous necrosis

A

-Pulmonary infection (usually tuberculosis)
-Dead cells disintegrate but leave cellular debris

23
Q

Fat necrosis

A

-Lipases destroy cells
-Breast, pancreas, abdomen

24
Q

Gangrenous necrosis

A

-Severe hypoxia
-Bacterial infection

25
Q

Apoptosis

A

-Programmed cell death
-Deletion of individual cells by fragmentation into membrane bound particles which are then phagocytized
-Both normal (needed for tissue turnover) and pathologic

26
Q

Aging

A

-Normal wear and tear due to accumulation of small microinsults caused by UV light, mechanical insults, and metabolic reactions
-Many theories on aging: genetic and environmental factors, degenerative extracellular changes, changes in cellular control mechanisms

27
Q

Somatic death

A

-Death of the entire person
-Postmortem change:
-Complete cessation of breath, circulation
-Falling body temp (algor mortis)
-Gravity causes blood to settle in lowest tissues causing purple color (livor mortis)
-Muscle stiffening starts within 6 hours (rigor mortis); entire body 12-14 hours
-Putrefaction 24-48 hours; then flaccid again
-Postmortem autolysis (microscopic putrefactive changes due to lytic enzymes)