Cell Injury Flashcards

1
Q

What is hypoxia?

A

oxygen deprivation

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2
Q

Which cells are most quickly affected by hypoxia?

A

Neurones

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3
Q

Name 4 types of hypoxia

A
  • Hypoxaemic hypoxia
  • Anaemic hypoxia
  • Ischaemic hypoxia
  • Histiocytic hypoxia
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4
Q

What is hypoxaemic hypoxia and what might be the cause

A

The arterial content of O2 is low

Due to decreased pO2 at high altitude or decreased absorption due to lung disease

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5
Q

What is anaemic hypoxia and what might be the cause

A

Decreased ability of Hb to carry O2

Due to anaemia or cardon monoxide poisoning

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6
Q

What is ischaemic hypoxia and what might be the cause

A

An interruption interruption in blood supply

Due to blockage of vessel/heart failure

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7
Q

What is histiocytic hypoxia and what might be the cause

A

Inability of the cells to use O2 due to disabled oxidative phosphorylation
Due to cyanide poisoning

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8
Q

Name 7 mechanisms of cellular injury

A
  • Hypoxia
  • Physical agent
  • Chemical agents and drugs
  • Microorganisms
  • Immune mechanisms
  • Dietary insufficiency
  • Genetic abnormalities
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9
Q

Describe the process of reversible hypoxic injury

A
  • Decrease in oxidative phosphorylation –> decrease in the production ATP
  • Lipid deposition due to detachment of ribosomes and therefore decreased protein synthesis and therefore lipid deposition
  • Clumping of nuclear chromatin due to increase in glycolysis –> decrease pH, decrease in glycogen
  • Oncosis due to decrease in Na+ pump therefore cellular influx of Ca2+, Na+, H2O and efflux of K+ –> cellular swelling, blebbing, ER swelling
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10
Q

What two things occur in irreversible hypoxic injury

A

-Influx of Ca2+ into the cytoplasm –> also release from stores in mitochondria and ER
-Activation of enzymes e.g. ATPases, phospholipases, proteases, endonucleases
Lysosomal membranes also become damaged and leak their enzymes into the cytoplasm

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11
Q

What is ischaemia reperfusion injury?

A

The damage caused by blood flow returning to an ischaemic area which isn’t yet necrotic
Damage caused by:
- increased production of free radicals
- increased no. of neutrophils –> inflammation and tissue injury
- delivery of complement proteins and activation of complement

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12
Q

What are free radicals? Give the 3 main free radicals

A

Reactive oxygen species

OH. O-2 H2O2

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13
Q

What use do we use free radicals for?

A

Oxidative bursts by leukocytes

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14
Q

What are two reactions that produce free radicals

A
  • Fenton reaction uses Fe2+

- Haber-Weiss reaction

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15
Q

What anti-oxidants do we have?

A
  • Enzymes e.g. catalases, peroxidases
  • Scavengers which neutralise free radicals e.g. glutathione, vitamins A,C and E
  • Storage proteins - sequester transition metals in ECM (transferrin)
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16
Q

When are heat shock proteins produced?

A

In response to stress there production is increased

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17
Q

What is the function of heat shock proteins?

A

Recognised incorrectly folded proteins and repair them by ensuring they are folded correctly and if not then destroying them

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18
Q

What do you see under a light microscope when cellular injury occurs?

A
  • decreased pink staining due to accumulation of H2O
  • followed by increased pink staining due to detachment and loss of ribosomes from ER accumulation of denatured proteins
  • Nuclear changes
  • Abnormal intracellular accumulations
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19
Q

Describe the pattern of nuclear changes that occur with cell injury

A

Chromatin clumped (reversible)
Pyknosis (shrinkage)
Karryohexis (fragmentation)
Karrolysis (dissolution)

20
Q

What is oncosis?

A

Cell death with swelling

The spectrum of changes that occur in injured cells prior to death

21
Q

What is necrosis?

A

In living organisms the morphological changes that occur after a cell has been dead some time (4-24 hours)

22
Q

What is apoptosis?

A

Cell death with shrinkage induced by regulated intracellular program where cell activates enzymes that degrade its own nuclear DNA and proteins
Uses energy

23
Q

What is coagulative necrosis and when is it seen?

A

Denaturation of proteins predominates
‘Ghost outline remains’
White
Solid consistency of tissue

24
Q

What is liquefactive necrosis and when is it seen

A

Enzymatic degradation of tissues
Seen in massive neutrophil infiltration due to release of proteases –> seen in bacterial infection
Pus can be present
Occurs in fragile tissues such as brain

25
What is caseous necrosis and when is it seen?
Associated with TB and granulomatus infection Cheesy appearance No ghost cell outline, amorphous debris
26
What is fat necrosis and when is it seen?
Destruction of adipose tissue | Typically seen as consequence of acute pancreatitis --> release of FA --> reaction with Ca2+ --> calcium soaps
27
What is gangrene
The clinical term used to describe necrosis that can be seen
28
What is dry gangrene
Coagulative necrosis is the underlying process Modified by exposure to the air Bacteria cannot grow in dry tissue
29
What is wet gangrene
Modified by infection Bacteria can easily get into the bloodstream --> septicaemia Liquefactive necrosis is underlying
30
What is gas gangrene
Wet gangrene associated where the tissue is infected by anaerobic bacteria that produce visible bubbles of gas
31
What is an infarction
An area of tissue death caused by an obstruction of an tissue's blood supply
32
What is a white infarct?
Infarct that occurs in a solid organ after occlusion of an end artery If solid then limits the amount of haemorrhage from adjacent capillaries e.g. in heart, spleen and kidneys Coagulative necrosis occurs
33
What is a red infarct?
Infarct that occurs in a loose tissue e.g. lungs due to dual blood supply or also in tissues with numerous anastomoses such as intestines
34
What molecules can be released in cellular injury
- Potassium - Enzymes - Myoglobin
35
What are the effects of potassium release
Heart stops in high conc. of K+ | Can happen from severe burns
36
How can enzyme release be useful
can indicate the organ involved | the timing of the damage
37
What are the effects of myoglobin release
Released from dead myocardium and striated muscles | Rhabdomyolysis can occur if large amounts are released
38
What are some abnormal accumulations that can occur due to tissue damage
- Fluid - Lipids - Cholesterol - Phospholipids - Proteins - Pigments
39
What is Mallory's hyaline
Damaged protein in hepatocytes in alcoholic liver disease | Accumulation of altered keratin filaments
40
Give an example of an exogenous and an endogenous pigment
- Exogenous = coal dust/soot/carbon/tattoo | - Endogenous = lipofuscin, haemosiderin
41
What is haemosiderosis
Deposition of haemosiderin in organs
42
What is haemochromatosis
Iron deposited in the skin, liver, pancreas, heart and endocrine organs
43
What is dystrophic calcification
Local changes or disturbance in tissue favours hydroxyapatite crystal formation Can cause organ dysfunction e.g. calcified heart valves
44
What is metastatic calcification
Disturbance is wide-spread | Hypercalcaemia - hydroxyapatite crystals deposited throughout the body in normal tissues
45
What are the stages of changes seen in the liver with excessive alcohol consumption
Fatty changes Acute alcoholic hepatitis Cirrhosis