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BI416 > Chapter 4 - Cell Injury, Aging, and Death > Flashcards

Chapter 4 - Cell Injury, Aging, and Death Flashcards

1
Q

What are cells and their function?

A
  • They are active participants in the environment
  • Adjust structure/function to accommodate change/demands/stress to maintain homeostasis
  • Physiologic stress or pathologic stimuli result in ADAPTATION
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2
Q

Explain cellular injury

- Types

A

Occurs when cell cannot maintain homeostasis in the face of injurious stimuli
- Severity of injury determines response

Types

  • Adapted Cell
  • Reversible Injured Cell
  • Irreversible Injured Cell
  • Apoptosis or necrosis
  • Dead Cell
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3
Q

Explain the mechanism of cell injury

A

1) Depletion of ATP
2) Mitochondrial Damage
3) Influx of intracellular Ca and loss of Ca homeostasis
4) Accumulation of oxygen-derived free radical (oxidative stress)
5) defects in membrane permeability

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4
Q

Define reversible cell injury

A

Reversible: Cell swelling develops when cells are incapable of fluid & ion homeostasis; fatty change accumulation of lipid vacuoles in the cytoplasm

1) Hydropic Swelling:
- Accumulation of water due to malfunction of Na/K pump (increase of Na within cell) or loss of ATP
- Dilated ER, swollen MC, large/pale cytoplasm
- Increase in size/weight of organs (megaly)
Hypoxia > ATP production decrease > Na/H2O in & K out; osmotic pressure increase > distended/rupture of organelles > hydropic degeneration

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5
Q

What is are reversible cell injuries?

A

1) Hydropic Swelling (Kidney):
- Accumulation of water due to malfunction of Na/K pump (increase of Na within cell) or loss of ATP
- Dilated ER, swollen MC, large/pale cytoplasm
- Increase in size/weight of organs (megaly)
Hypoxia > ATP production decrease > Na/H2O in & K out; osmotic pressure increase > distended/rupture of organelles > hydropic degeneration

2) Intracellular Accumulations (Fatty Liver)
- Excess accumulation of substances inside the cell leading to toxicity, immune response, and taking up of cellular space
- Pigments/particles appear because the cell is unable to degrade them

3) Limiting Protein Damage
- Increased synthesis of chaperones to correct protein
- Decrease translation of proteins
- Activate ubiquitin-proteasome to degrade unfolded proteins
- Activate caspases = apoptosis

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6
Q

What is cellular adaptation?

A

The cell’s ability to escape and protect itself from injury

- Common in disease states

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7
Q

What are 5 types of cellular adaptation responses?

A
  • Atrophy
  • Hypertrophy
  • Hyperplasia
  • Metaplasia
  • Dysplasia
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8
Q

Define and describe Atrophy

A

Cells shrink and reduce their functions in response to normal and injurious factors (DISUSE)

  • Causes: Disues, denervation, ischemia, nutrient starvation, aging, etc.
  • Results: reduced ER, MC, and myofilaments (results from decreased functional demand or chronic ischemia)
  • Ex. Broken bone - muscles suffers
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9
Q

Define and describe Hypertrophy

A

Increase in cell mass accompanied by augmented functional capacity in response to physiological and pathophysiologic demands

  • Usually result from increased functional demand
  • Cause: increase cellular protein content or workload, and hormonal stimulation
  • Ex. Cells unable to undergo meiosis
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10
Q

Define and describe Hyperplasia

A

Increase in functional capacity related to increase in cell number due to mitotic division

  • Usually result from increased functional demand
  • Often accompanies hypertrophy
  • Cause: increase physiologic demand and hormonal stimulation, persistent cell injury, and chronic irritation of epithelial cells
  • Ex. Endometrial lining
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11
Q

Define and describe metaplasia

A

Replacement of one differentiated cell type with another

  • result from persistent injury
  • Cause: adaptation to persistent injury, with replacement of a cell type that is better suited to tolerate injurious stimulation
  • Fully reversible when injurious stimulation is removed
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12
Q

Define and describe Dysplasia

A

Disorganized appearance of cells because of abnormal variations in size, shape, and arrangement

  • result from persistent injury
  • Atypical hyperplasia: an adaptive effort gone astray
  • Significant potential to transform into cancerous cells
  • Severe and involves thickness of epithelial (carcinoma in situ)
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13
Q

Define Irreversible Cell Injury

A

Two basic processes:

  • Denaturation of protein
  • Enzymatic digestion of cell components
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14
Q

Define Necrosis

A
  • Pathlogic cell death; consequence of schema or toxic injury (severe or prolonged injury)
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15
Q

5 Types of Necrosis

A

1) Heart (Coagulative)
- Most common
- Arises from ischemic injury @ metabolic acidosis in tissues (hypoxia)
- Dead cells - gel-like
- Ex. Heart, kidney, adrenal glands

2) Brain (Liquefactive)
- When dead tissue dissolves into liquid
- Liquification of lysosomal enzymes
- Formation of abscess or cyst

3) Lung (Caseous)
- Damage second to tuberculosis
- Clumpy cheese - cellular details are gone

4) Pancreas (Fat)
- Death of adipose tissue in breath, pancreas, abdominal structures
- Result of trauma
- Chalky soap like
- Triglycerides digested and free fatty acids precipitate as Ca-salts

5) Gangrene
- Cellular death of large area of tissue
- Result from interruption of blood supply (hypoxia injury)
- Abundance of bacteria determines severity
- Dry: black dry skin separated by line of health tissue
- Wet: internal organs due to anaerobic bacteria, liquid/cold/swollen black appearance (liquefactive)
- Gas: infection of necrotic tissue of anaerobic bacteria; gas bubble

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16
Q

Phases of Necrosis

A

Two Phases:

1) Pyknosis: shrinkage of nucleus with marked clumping of chromatin
2) Karyolysis: loss of nuclear membrane followed by rupturing

17
Q

Processes following cell death (necrosis)

A
  • Cellular self-digestion (autolysis)
  • Dense clumped (degeneration of chromatin)
  • Disruption of plasma & organelle membranes
18
Q

Define Apoptosis

A

Programmed cell death - does not cause inflammation; occurs in response to injury that does not directly kill the cell

  • Not always a pathologic process: animals need to get rid of cells and cells need to die in an orderly manner
  • Activates suicide response
  • Main components are caspases
19
Q

What are the 2 pathways of apoptosis?

A

1) Mitochondrial (Intrinsic) Pathway
- cell injury > Mitochondrial pathway becomes dysfunctional > produces cytochrome c and proteins that initiate cascades > executioner caspases > endonuclease activation = membrane bleb = apoptotic body = phagocyte

2) Death Receptor (Extrinsic) Pathway
- Receptor-ligane interactions > adaptor proteins > initiator caspases > executioner caspases > breakdown of cytoskeleton > membrane bleb = apoptotic body = phagocyte

20
Q

Aetiology of schema and hypoxic injury

A
  • Hypoxia often caused by ischema which is the most common cause of cell injury
  • Combination of disruption of oxygen supply with accumulation of metabolic waste
21
Q

Define and explain hypoxia

A
  • Inadequate oxygenation
  • Most common cause of cell injury
  • Usually due to schema
  • Chemical & acid-base imbalances
  • May be reversible if O2 restored
  • Death if not
22
Q

Define and explain ischemia

A
  • restriction of blood supply causing shortage of O2 and glucose needed for cellular metabolism
  • leads to lactic acidosis
  • ## death occurs when plasma, MC, and Lysosomal membranes are damaged
23
Q

What is ischemia-reperfusion injury

A
  • Ca-overlead
  • formation of free radicals
  • subsequent inflammation
24
Q

Hypoxic Injury Induced by Ischemia

A

Best example

  • Reversible change in response to injury
  • Still have chance to rescue cell
  • See that organelles (ER) become distended = effects protein synthesis = deposition of lipids (Intra-cell-accumulations)
25
Q

What is nutritional deficiency?

A

Results from:

  • Poor intake
  • Altered absorption
  • Impaired circulatory system

Causes:

  • Poverty
  • Chronic alcoholism
  • Acute/chronic illness
26
Q

What is nutritional excesses

A

Results from:

  • Excessive intake
  • BMI greater than 27kg/m2 (health risk)
  • BMI greater than 30kg/m2 (obesity)
27
Q

Infectious and immunologic injury…

A
  • Bacteria and viruses can injure cells in a variety of ways depending on their virulence
  • Added injury may occur indirectly by triggering body’s immune response
  • Bacteria rarely gets direct access to the cell
  • Release toxins:
  • Exotoxins – constantly released as long as bacteria is alive
  • Endotoxins – contains in bacteria and are released after death of bacteria (most detrimental)
  • These toxins might actually have generally effect on the body or may trigger a particular type of organ

Viruses are notorious for entering the cell and mingling/reprograming the DNA (cell) for their own proliferation

  • May live for a while within cell or destroy immediately
  • We can use long duration virus for treatments (benefit)

Parasites – fit profile of both protozoa and metazoa

  • Might actually have access inside the cell or might live among cells in various tissues
  • May be destructive and cause death
  • Ex. Malaria

Fungi – symbiotic relationship

  • Both partners benefit esp. in individuals with low immunology
  • Ex. Yeasts
28
Q

Chemical Injury

A

Toxic chemicals or poisons cause injury directly or by being metabolized into reactive chemicals to the body
- Dose related

29
Q

Physical and mechanical injury

A

Factors

  • Extremes in temperature
  • Abrupt changes in atmospheric pressure
  • Mechanical deformation
  • Electricity
  • Ionizing radiation
30
Q

Radiation induced injury

A

Ionizes H2O into H+ & OH-

  • OH- attaches to DNA & prevents cell reproduction
  • DNA mutations
  • Splits into free radicals = destroys cell via necrosis
31
Q

Radiation sicknesses…

A
  • Dermatitis

- Sterility

32
Q

Cellular Basis of Again

A

Cumulative result from two factors cause cellular and molecular damage:

  • Progressive decline in proliferation and reparative capacity of cells
  • Exposure to environmental factors

Responsible mechanisms

  • DNA damage
  • Reduced proliferative capacity of stem cells
  • Accumulation of metabolic damage
33
Q

Cellular Theories

A

1) Free radical theory
- if a cell produces too much excessive amounts of free radical ions = become detrimental = damages organelles and cell itself

2) Programmed senescence theory
- Cells undergo only so many proliferations
- Cancer cells are able to over come shortening of telomeres (via telomerase)
- Repairs caps = proliferate indefinitely

34
Q

Physiologic Changes of Aging

A
  • Age-related decrease in functional reserve

- Inability to adapt to environmental demand

35
Q

Somatic Death

A
  • Death of the entire organism
  • No inflammation or immunologic response occurs prior to death
  • General features: cessation of respirations and heartbeat
  • Presence of stiffened muscles throughout body after death (rigor mortis); then flaccid
  • Release of lytic enzymes in body tissues: postmortem autolysis
  • Determination of “brain death” as proof of somatic death

BI416 (5 decks)

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