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Path Pro > Cell Injury And Death > Flashcards

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
Q

Name the 3 PHASES in apoptosis

A

Initiation
Execution
Degradation and Phagocytosis

26
Q

Compare the 2 mechanisms for apoptosis and which phases they trigger

What do they both result in

A

Intrinsic- Initiating signal from within cell
Extrinisc- Extracellular initiating signals
Initiation and execution

Activation of caspases (enzymes than mediate apoptosis)

27
Q

Define Gangrene

Compare Dry and Wet gangrene
What type of necrosis are these

What is Gas gangrene

A

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
Q

Define an Infarction

Define Infarct

A

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
Q

What are the 2 most common causes of infarction

A

Thrombosis

Embolism

30
Q

What is a white Infarct called
Where does it happen
What shape are they

A

Anaemic Infarct
In solid organs, at end artery
Wedge shaped

31
Q

What is a red Infarct called

Where does one occur

A

Haemorrhagic Infarct

Loose tissue

32
Q

What is the range of consequences of an infarction

What 4 factors does this depend on?

A

None to death

Alternative blood supply
Ischaemia speed
Tissue involved
Oxygen content of blood

33
Q

What 3 molecules are released by injured cells

A

Potassium
Myoglobin
Enzymes

34
Q

What 5 types of molecules can accumulate in injured cells

A
  1. Water and electrolytes
  2. Lipids
  3. Carbs
  4. Proteins
  5. Pigments
35
Q

When fluid accumulates in cells,

  1. What the type of swelling
  2. When does it occur
  3. What enters cell
A
  1. Hydropic swelling
  2. When Energy supplies cut off
  3. Na and H2O flood into cell
36
Q

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

A

Hepatic Steatosis

Alcohol (Reversible)
Diabetes Mellitus
Obesity
Toxins

None

37
Q

In what 2 conditions do proteins accumulate in a cell

Explain these

A
  • Alcoholic liver disease, Mallory’s hyaline accumulates

- Alpha1 anitrypsin deficiency. Incorrectly folded “” protein (A protease inhibitor)

38
Q

Name 2 exogenous pigments that accumulate in cells

How do phagocytes play a role

A

Carbon/ coal dust/ soot- Phagocytosed by alveolar macrophages

Tattoos- Phagocytosed by macrophages in dermis and remains

39
Q

Inhalation of carbon leads to which 2 conditions

A

Anthracosis

Pneumoconiosis

40
Q

Name 2 endogenous pigments that accumulate in cells

A

Haemosiderin (Iron storage molecule)

Bilirubin (breakdown product of heme)

41
Q

When does Haemosiderin accumulate in a cell
Give one way this can occur

What is Haemosiderosis

A

When there is systemic or local excess of Iron
Bruising

Systemic Iron overload, so Fe deposited in organs

42
Q

What is hereditary Haemochromatosis

Name 2 organs other than endocrine organs where Fe is deposited

Name 3 symptoms

A

A genetic disorder caused increased Fe absorption in intestine

Skin, Heart

Liver damage, Heart dysfunction, endocrine failures

43
Q

Compare Dystrophic/ Metastatic calcification

Which is more common

A

Dystrophic: Abnormal localised deposition of Ca salts in tissues

Metastatic: Abormal systemic deposition of Ca salts in tissues

More common- Dystrophic

44
Q

Where does Dystrophic calcification occur, give 3 examples?

A

Area of dying tissue, aging/ damaged valves, TB Lymph nodes

45
Q

Why does Dystrophic calcification occur

A

No abnormality in Ca metabolism

Local change favours nucleation of hydroxyapatite crystals

46
Q

Why does Metastatic calcification occur

Compare normal symptoms and lethality

A

Due to hypercalcaemia, secondary to disturbances In Ca metabolism

usually no symptoms, can be lethal

47
Q

What are 2 causes of hypercalcaemia

A
  • Increased secretion of PTH causing Bon resporption

- Destruction of bone tissue

48
Q

Why can cells not keep diving forever

A

Telomere is shortened each division

When telomere is at critical length, cell can’t divide anymore

49
Q

How do germ cells have the capability to keep dividing

Name 2 other cell types which can do this

A

Contain telomerase, which maintains original length of telomeres

Stem cells, Cancer cells

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