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Mechanisms of Disease > Cell Injury > Flashcards

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
Q

What is caseous necrosis and when is it seen?

A

Associated with TB and granulomatus infection
Cheesy appearance
No ghost cell outline, amorphous debris

26
Q

What is fat necrosis and when is it seen?

A

Destruction of adipose tissue

Typically seen as consequence of acute pancreatitis –> release of FA –> reaction with Ca2+ –> calcium soaps

27
Q

What is gangrene

A

The clinical term used to describe necrosis that can be seen

28
Q

What is dry gangrene

A

Coagulative necrosis is the underlying process
Modified by exposure to the air
Bacteria cannot grow in dry tissue

29
Q

What is wet gangrene

A

Modified by infection
Bacteria can easily get into the bloodstream –> septicaemia
Liquefactive necrosis is underlying

30
Q

What is gas gangrene

A

Wet gangrene associated where the tissue is infected by anaerobic bacteria that produce visible bubbles of gas

31
Q

What is an infarction

A

An area of tissue death caused by an obstruction of an tissue’s blood supply

32
Q

What is a white infarct?

A

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
Q

What is a red infarct?

A

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
Q

What molecules can be released in cellular injury

A
  • Potassium
  • Enzymes
  • Myoglobin
35
Q

What are the effects of potassium release

A

Heart stops in high conc. of K+

Can happen from severe burns

36
Q

How can enzyme release be useful

A

can indicate the organ involved

the timing of the damage

37
Q

What are the effects of myoglobin release

A

Released from dead myocardium and striated muscles

Rhabdomyolysis can occur if large amounts are released

38
Q

What are some abnormal accumulations that can occur due to tissue damage

A
  • Fluid
  • Lipids
  • Cholesterol
  • Phospholipids
  • Proteins
  • Pigments
39
Q

What is Mallory’s hyaline

A

Damaged protein in hepatocytes in alcoholic liver disease

Accumulation of altered keratin filaments

40
Q

Give an example of an exogenous and an endogenous pigment

A
  • Exogenous = coal dust/soot/carbon/tattoo

- Endogenous = lipofuscin, haemosiderin

41
Q

What is haemosiderosis

A

Deposition of haemosiderin in organs

42
Q

What is haemochromatosis

A

Iron deposited in the skin, liver, pancreas, heart and endocrine organs

43
Q

What is dystrophic calcification

A

Local changes or disturbance in tissue favours hydroxyapatite crystal formation
Can cause organ dysfunction e.g. calcified heart valves

44
Q

What is metastatic calcification

A

Disturbance is wide-spread

Hypercalcaemia - hydroxyapatite crystals deposited throughout the body in normal tissues

45
Q

What are the stages of changes seen in the liver with excessive alcohol consumption

A

Fatty changes
Acute alcoholic hepatitis
Cirrhosis

Mechanisms of Disease (2 decks)

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