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ESA 2 - MoD > Session 1 - Cell Injury > Flashcards

Session 1 - Cell Injury Flashcards

1
Q

What is hypoxaemic hypoxia?

A

Arterial concentration of oxygen is reduced

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2
Q

What is Anaemic Hypoxia?

A

Decreased ability of Hb to carry oxygen

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3
Q

What is Ischaemic Hypoxia?

A

Interruption of blood supply

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4
Q

What is Histiocytic Hypoxia?

A

Inability to utilise oxygen

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5
Q

Apart from hypoxia, what else can cause cell injury do death? (Long list)

A
  • Physical agents
  • Chemical agents
  • Micro-organisms
  • Immune mechanisms
  • Dietary insufficiency
  • Genetic abnormalities
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6
Q

What are the four main targets for cell injury?

A
  • Cell membranes (both plasma and organeller)
  • Nucleus
  • Proteins
  • Mitochondria
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7
Q

What is the general outline for hypoxia cell injury?

A

Cell is deprived of oxygen - No ATP production - Sodium potassium pump stops working - Sodium and water enter cell - Oncosis - pH decreases due to glycolysis - Calcium enters cell - Attacks on membranes, proteins, DNA and cytoplasmic comments - death

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8
Q

What is Ischaemia-Reperfusion injury?

A

Oxygen returns to Ischaemic tissue, causes damage if cells are not yet necrotic. Increase in free radicals, neutrophils and complement pathway

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9
Q

Name the three importance free radicals

A
  • Superoxide
  • Hydroxyl
  • Hydrogen Peroxide
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10
Q

What are the bodies defences against free radicals?

A
  • Enzymes - SOD, catalases and perioxidases
  • Free radical scavengers - glutathione, Vit A,C and E
  • Storage proteins - sequest transition metals
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11
Q

What are Heat shock proteins?

A

Proteins that recognise and repair mis-folded proteins

E.g Ubiquitin

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12
Q

What cytoplasmic changes can we see with light microscopy?

A
  • decrease in pinkness = accumulation of water

- increase in pinkness = accumulation of denatured proteins and ribosomes

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13
Q

What nuclear changes can we see with light microscopy?

A
  • Clumped chromatin
  • Pyknosis - shrinkage
  • Karryohexis - fragmentation
  • Karryolysis - dissolution
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14
Q

What reversible changes can be seen with electron microscopy?

A
  • Swelling
  • Blebs
  • Clumped chromatin
  • Ribosome separation from ER
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15
Q

What irreversible changes can be seen with electron microscopy?

A
  • Big cell swelling
  • Nuclear changes
  • Membrane defects
  • swollen mitochondria
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16
Q

What is Oncosis?

A

Cell death with swelling

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17
Q

What is Apoptosis?

A

Cell death with shrinkage

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18
Q

What is Necrosis?

A

Morphological changes that occur after a cell has been dead for some time

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19
Q

What are the four types of necrosis?

A
  • Coagulative
  • Liquifactive
  • Caseous
  • Fat
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20
Q

What is Coagulative necrosis?

A
  • More desaturation of proteins that release of proteases
  • Solid consistency
  • Appears white
  • Proteins become less soluble
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21
Q

What is Liquifactive necrosis?

A
  • more enzyme degradation that denaturation
  • neutrophil infiltration
  • seen in bacterial infections
  • seen in brain
  • viscous mass
22
Q

When is Caseous necrosis seen?

A

In tuberculosis; amorphous debris with cheesy appearance

23
Q

What is Fat necrosis?

A
  • destruction of adipose
  • Can be caused by acute pancreatitis = lipase release
  • also from direct trauma
  • in breast tissue can be confused for cancer
24
Q

What are the two types of gangrene and how are they caused?

A

Dry - exposure to air

Wet - infection with bacteria

25
Q

What is Infarction?

A
  • Cause of necrosis, namely ischaemia
  • Caused by thrombosis of embolism
  • can also be through external compression of blood vessels
26
Q

What is a White infarct?

A
  • occurs in solid organs after occlusion of end artery

- Limits to amount of haemorraging that occurs

27
Q

What is a red infarct?

A

Extensive haemorrhage into dead tissue, occurs when:

  • Dual blood supply eg lungs
  • Numerous anastomoses eg intestine
  • loose tissue eg lung
  • where previous congestion has occurred
  • where there is raised venous pressure
28
Q

What affects the consequences of the infarct?

A
  • Whether tissue has an alternative blood supply
  • How quickly ischaemia developed
  • how vulnerable tissue is to hypoxia
29
Q

What three molecules are released after cell injury?

A

Potassium, Enzymes and Myoglobin

30
Q

What is special about DNA breakdown in apoptosis?

A

It is not random, it is cut in specific places

31
Q

When does apoptosis occur?

A
  • Can be a normal physiological process
  • Can be hormone controllers
  • cytosol T-cells killing virally infected cells
  • cell damage especially if to DNA
32
Q

Which organelle is the central player for intrinsic apoptosis?

A

The mitochondria

33
Q

What is external apoptosis triggered by?

A

External Ligands such as TRAIL and Fas

34
Q

What can we see in electron microscopy in apoptosis?

A
  • Cytoplasmic budding
  • Fragmentation
  • No league of cellular contents
35
Q

What can we see under a light microscope in apoptosis?

A
  • Shrunken cells
  • Chromatin condensation
  • Pyknosis and Karryorrhexis
  • Affects on only single cells or small clusters
36
Q

Name some important apoptotic molecules (long list)

A
  • p53; mediates response to DNA damage
  • Cytochrome c, APAF 1 + cascade 9
  • Bel-2 - prevents cytochrome c release
  • TRAIL - death ligand
  • TRAIL-R - death receptor
  • Caspases
37
Q

Name the 5 main groups of intra cellular accumulations

A
  • Water and electrolytes
  • Lipids
  • Proteins
  • Pigments
  • Carbs
38
Q

How can fluid accumulation appear in cells?

A

Either as small vacuoles or as Hydropic swelling

39
Q

Where is Hydropic swelling most dangerous?

A

The brain; it does not have room to expand and can cause pressure on the blood vessels

40
Q

What are the two types of lipid accumulation?

A

Steatosis and Cholesterol

41
Q

What are two main types of protein accumulation?

A

Mallory’s Hyaline - damaged protein in hepatocytes due to alcohol liver disease
Alpha-1-antitrypsin - Mis-folded protein accumulates in ER and means no regulation of proteases in lung so can cause emphysema

42
Q

Where are exogenous pigment residues found?

A

Lung and Lymph Nodes

43
Q

Name three endogenous pigments

A

Lipofuscin, Haemosiderin, and Bilirubin

44
Q

What is Lipofuscin?

A

Brown pigment found in ageing cells, found in long-living cells

45
Q

What is Haemosiderin?

A

An iron storage molecule, most commonly found in bruising. Also very common in Hereditary Haemochromatosis where Iron absorption in the intestine is increased. (Treated with regular bleeding)

46
Q

What is Bilirubin?

A

Bright yellow bile pigment
If levels too high = Jaundice
Transported to liver to be excreted

47
Q

Name the two types of Pathological Calcification?

A

Dystrophic and Metastatic

48
Q

What are the two main causes of Metastatic Calcification?

A
  • Increased PTH release

- Destruction of bone

49
Q

Why can cells not divide indefinitely?

A
  • Accumulative damage of cell comments and DNA

- Shortened telomeres

50
Q

What enzyme do stem cells and cancer cells have enabling them divide continually?

A

Telomerase

51
Q

What are the three main effects on the liver as a result of chronic excess alcohol intake?

A
  • Fatty change
  • Acute alcohol hepatitis
  • Cirrhosis
52
Q

What is hypoxia?

A

Deficiency of oxygen reaching the tissues

ESA 2 - MoD (7 decks)

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