Cell Injury And Death Flashcards

1
Q

What 4 things does the degree of injury depend on

A
  • Type of injury
  • Severity of injury
  • Duration of injury
  • Type of tissue
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2
Q

What 7 things can cause cell injury

A
Hypoxia
Chemical agents 
Physical agents 
Micro-organisms
Immune mechanisms 
Dietary deficiencies/ excesses
Genetic abnormalities
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3
Q

Name 5 physical agents that can cause cell injury

A
Direct trauma 
Extreme temperatures 
Pressure changes 
Electric currents
Radiation
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4
Q

Compare Hypoxia and Ischaemia

A

Hypoxia- Low O2

Ischaemia- Low O2 AND other substances

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5
Q

Compare the 4 types of Hypoxia

Give one example of each

A

Hypoaxemic Hypoxia: Low O2 in arteries
High altitude

Anaemic Hypoxia: Decreased ability of Hb to carry O2
Anaemia or CO poisoning

Ischaemic Hypoxia: Interruption to blood supply
Vessel blockage

Histiocytic Hypoxia: Unable to use O2, due to disabled Oxidative phosphorylation enzymes
Cyanide poisoning

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6
Q

Explain 2 ways in which immune system can damage the body

A
  • Hypersensitivity reactions: Overly vigorous immune reaction damages tissue
  • Autoimmune reactions: Immune system fails to distinguish self from non-self
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7
Q

Which 4 cell components are most susceptible to injury

A
  1. Membranes (Plasma + Organellar)
  2. Nucleus (DNA)
  3. Proteins (Structural)
  4. Mitochondria (Oxidative phosphorylation)
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8
Q

In reversible Hypoxia, explain;

  1. Cellular swelling
  2. Decreased pH
  3. Decreased protein synthesis
A

Reduced Oxidative phosphorylation-> Reduced ATP

  1. Reduced ATP= Reduced Na Pump activity-> Influx of Ca, H2O, Na-> Swelling of cell
  2. Reduced ATP= Increased anaerobic glycolysis-> Increased [lactic acid]—> Reduced pH
  3. Reduced ATP= Ribosomes detachment-> Reduced protein synthesis
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9
Q

In irreversible hypoxia,

  1. How does cytosolic Ca increase
  2. Which 4 enzymes are stimulated and what is their effect
A
  1. Enters from Extracellular space, mitochondria, ER
  2. ATPase- Reduced ATP

Phospholipase- Less Phospholipids

Protease- Disrupted membrane

Endonuclease- Damages chromatin

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10
Q

Give 5 ways free radicals can be made in the body

A
  1. Normal metabolic reactions
  2. Inflammation
  3. Radiation
  4. Reaction with unbound metals
  5. Drugs/ chemicals
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11
Q

How do heat shock proteins protect the cell

Give on example of one of these

A

When damaged, these proteins ‘mend’ mis-folded proteins and maintain cell viability

Ubiquitin

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12
Q

What is Ischaemia-Reperfusion injury

Explain 3 causes

A

If blood flow is returned to a damaged, but not necrotic, damage can be worse than if blood flow wasn’t retuned

Possible causes;

  • Increased production of free radicals with reoxygenation
  • Increased neutrophil number-> More inflammation and tissue injury
  • Delivery of complement proteins
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13
Q

In injured/ dying cells appear under a light microscope in hypoxia, explain the visible changes

A
  1. Cytoplasm swells, becomes more pink and watery
2. 
Nucleus shrinks ( Pyknosis)
Nucleus fragments (Karyorrhexis)
Nucleus dissolves (Karyolysis)
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14
Q

In hypoxia, what are the 3 cellular changes in order

A
  1. Cytoplasmic changes
  2. Nuclear changes
  3. Abnormal cellular accumulations
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15
Q

When looking through an electron microscope, Compare Reversible and Irreversible injury in terms of;

  1. Cell membrane
  2. ER
  3. Ribosomes
  4. Mitochondria
  5. Nucleus
A
  1. Reversible-Blebs. Irreversible- Myelin figures, defects
  2. Reversible- ER Swells. Irreversible- ER Lysis
  3. Reversible- Dispersion. Irreversible- Rupture
  4. Reversible- Swelling, small densities. Irreversible- Swelling, Large densities
  5. Reversible- Chromatin clumping. Irreversible- Shrinking, Fragmenting, Dissolving
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16
Q

Define Oncosis
Define Necrosis
When is necrosis seen

A

Oncosis: Cell death with swelling, changes prior to death

Necrosis: Morphologic changes in a living organism, after a cell has been dead some tome

  • seen after 12 to 24 hours
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17
Q

Name the 4 types of Necrosis

Where do the main 2 types occur, Give 2 examples

A

Coagulative Necrosis: In solid organs (Heart, Liver)

Liquefactive/ colliquitive Necrosis: In loose tissues (Brain, lungs)

Caseous Necrosis

Fat Necrosis

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18
Q

Define Liquefaction

Compare Coagulative and Liquefactive

A

Liquefaction= enzymatic digestion

Coagulative: Protein denaturation, Ghost outline of cells remains
Liquefactive: Tissue digestion by enzymes

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19
Q

In caseous necrosis,

  1. What is seen under a microscope
  2. What it is associated with
  3. Appearance by the eye
A
  1. Amorphous debris
  2. Infections, especially TB
  3. Cheesy
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20
Q

In fat necrosis;

  1. Describe the appearance
  2. When and how does it occur
A
  1. Melted candle-like

2. Often, acute pancreatitis causes pancreatic lipase release

21
Q

Define Apoptosis
Does it use ATP
What are the 2 types

A

Cell death with shrinkage, induced by a regulated intracellular program

Yes
Pathological and Physiological

22
Q

When does Physiological Apoptosis occur

Give 3 examples

A
  1. To maintain a steady-state
  2. Hormone controlled involution
  3. Embryogenesis
23
Q

when does pathological Apoptosis occur

A
  1. Graft VS Host disease
  2. Damaged cells (Especially DNA)
  3. Virus-infected OR Neoplastic cells
24
Q

Name the 4 visible stages in apoptosis

A

Normal cell
Shrinkage, chromatin Condensation
Fragmentation/ budding
Apoptic bodies

25
Name the 3 PHASES in apoptosis
Initiation Execution Degradation and Phagocytosis
26
Compare the 2 mechanisms for apoptosis and which phases they trigger What do they both result in
Intrinsic- Initiating signal from within cell Extrinisc- Extracellular initiating signals Initiation and execution Activation of caspases (enzymes than mediate apoptosis)
27
# Define Gangrene Compare Dry and Wet gangrene What type of necrosis are these What is Gas gangrene
Necrosis visible to the naked eye Dry: Necrosis modified by exposure to air- Coagulative Necrosis Wet: Necrosis modified by infection- Liquefactive Necrosis Gas: Wet gangrene where the infection is with anaerobic bacteria that produce gas
28
Define an Infarction | Define Infarct
Infarction: Necrosis caused by reduction in arterial blood flow Infarct: An area of necrotic tissue which is the result of loss of an arterial blood supply
29
What are the 2 most common causes of infarction
Thrombosis | Embolism
30
What is a white Infarct called Where does it happen What shape are they
Anaemic Infarct In solid organs, at end artery Wedge shaped
31
What is a red Infarct called | Where does one occur
Haemorrhagic Infarct | Loose tissue
32
What is the range of consequences of an infarction | What 4 factors does this depend on?
None to death Alternative blood supply Ischaemia speed Tissue involved Oxygen content of blood
33
What 3 molecules are released by injured cells
Potassium Myoglobin Enzymes
34
What 5 types of molecules can accumulate in injured cells
1. Water and electrolytes 2. Lipids 3. Carbs 4. Proteins 5. Pigments
35
When fluid accumulates in cells, 1. What the type of swelling 2. When does it occur 3. What enters cell
1. Hydropic swelling 2. When Energy supplies cut off 3. Na and H2O flood into cell
36
What is triglyceride accumulation called, where is it most often What are 4 causes of lipid accumulation in cells If mild, what are the symptoms
Hepatic Steatosis Alcohol (Reversible) Diabetes Mellitus Obesity Toxins None
37
In what 2 conditions do proteins accumulate in a cell | Explain these
- Alcoholic liver disease, Mallory’s hyaline accumulates | - Alpha1 anitrypsin deficiency. Incorrectly folded “” protein (A protease inhibitor)
38
Name 2 exogenous pigments that accumulate in cells How do phagocytes play a role
Carbon/ coal dust/ soot- Phagocytosed by alveolar macrophages Tattoos- Phagocytosed by macrophages in dermis and remains
39
Inhalation of carbon leads to which 2 conditions
Anthracosis Pneumoconiosis
40
Name 2 endogenous pigments that accumulate in cells
Haemosiderin (Iron storage molecule) Bilirubin (breakdown product of heme)
41
When does Haemosiderin accumulate in a cell Give one way this can occur What is Haemosiderosis
When there is systemic or local excess of Iron Bruising Systemic Iron overload, so Fe deposited in organs
42
What is hereditary Haemochromatosis Name 2 organs other than endocrine organs where Fe is deposited Name 3 symptoms
A genetic disorder caused increased Fe absorption in intestine Skin, Heart Liver damage, Heart dysfunction, endocrine failures
43
Compare Dystrophic/ Metastatic calcification | Which is more common
Dystrophic: Abnormal localised deposition of Ca salts in tissues Metastatic: Abormal systemic deposition of Ca salts in tissues More common- Dystrophic
44
Where does Dystrophic calcification occur, give 3 examples?
Area of dying tissue, aging/ damaged valves, TB Lymph nodes
45
Why does Dystrophic calcification occur
No abnormality in Ca metabolism Local change favours nucleation of hydroxyapatite crystals
46
Why does Metastatic calcification occur | Compare normal symptoms and lethality
Due to hypercalcaemia, secondary to disturbances In Ca metabolism usually no symptoms, can be lethal
47
What are 2 causes of hypercalcaemia
- Increased secretion of PTH causing Bon resporption | - Destruction of bone tissue
48
Why can cells not keep diving forever
Telomere is shortened each division | When telomere is at critical length, cell can’t divide anymore
49
How do germ cells have the capability to keep dividing Name 2 other cell types which can do this
Contain telomerase, which maintains original length of telomeres Stem cells, Cancer cells