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Pathological Processes > Cell Injury Lecture 1 > Flashcards

Cell Injury Lecture 1 Flashcards

1
Q

What a few things that cause cell injury ?

A

1) hypoxia
2) toxins eg illicit drugs
3) physical agents eg direct trauma
4) radiation
5) microorganisms
6) immune mechanisms
7) dietary insufficiencies or dietary excess

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2
Q

Define hypoxia

A

Deprivation of oxygen

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3
Q

Define ischaemia

A

Inadequate blood supply To a particular organ

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4
Q

What are the 4 causes of hypoxia ?

A

1) hypoxaemic hypoxia
2) anaemia hypoxia
3) ischaemic hypoxia
4) histiocytic hypoxia

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5
Q

What is hypoxaemic hypoxia ?

A
  • arterial content of oxygen is low this is often caused by reduced p02 at altitidue
  • reduced absorption of oxygen due to lung disease
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6
Q

What is anaemia hypoxia ?

A
  • decreasd ability for. haemoglobin to carry oxygen because of anaemia or carbon monoxide poisoning
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7
Q

What is ischaemic hypoxia ?

A

Interruption to blood supply often caused by a blockage of a vessel or heart failure

  • this is the most dangerous form of hypoxia
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8
Q

What is histiocytic hypoxia

A

Inability to utilise oxygen in cells due to disabled oxidative phosphorylation enzymes for example cyanide poisoning which inhibits cytochrome C oxidase on a carrier protein which prevents oxygen from acting as a final electron acceptor

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9
Q

Why is hypoxia generally considered to be dangerous ?

A

1) neurones only last a few minutes without oxygen so the brains blood supply would be cut off very quickly
2) fibroblasts last a few hours

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10
Q

How does the immune system damage the body cells ?

A

1) autoimmune diseases for example Graves’ disease of thyroid
2) hypersensitivity reactions - host tissue is injured due to overly vigorous immune reaction

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11
Q

What cell components are most susceptible to injury ?

A

1) cell membrane ( plasma membrane and organelles membranes )
2) nucleus

3( proteins

4) mitochondria

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12
Q

What is happening at the molecular level in hypoxia in reversible injury ?

A

1) for example , blood supply towards the heart stops ( ischaemia).
2) mitochondrial production of ATP stops due to the lack of oxygen.
3) because Na+/K+ pump is ATP dependant , this disrupts this pump. This leads to an influx of Na+ and water into cells. This causes oncosis.
4) due to the lack of ATP being produced by oxidative phosphorylation , glucose would enter the glycolysis more. This causes and increase in lactic acid due to anaerobic respiration. This causes a decrease in pH. This leads to clumping of nuclear chromatin

5)

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13
Q

What is occurring at the molecular level of irreversible hypoxia ?

A
  • there will be an increase in cytosolic Ca2+. This causes the activation of ATPase which causes decreased ATP,
  • this also activates phospholipase which decreases phospholipids
  • this activates Protease which causes a disruption of membrane cytoskeleton and proteins
  • this activates endonuclease which causes damage to chromatin.
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14
Q

What are free radicals ?

A
  • reactive oxygen species that have a single unpaired electron in their outer orbit
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15
Q

What are the 3 free radicals that are of biological significance in cells ?

A

1) Oh**
2) o2-*
3) h202

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16
Q

When are free radicals produced ?

A

1) normal metabolic reactions : oxidative phosphorylation
2) inflammation : oxidative burst of neutrophils
3) radiation : H20 = OH*
4) contact with unbound metals within the body : iron and copper

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17
Q

How does the body control free radicals ?

A

1) Anti-oxidant scavengers : donate electrons to free radicals for example vitamin A , C and E
2) enzymes that neutralise free radicals : catalase , superoxide dismutase , glutathione peroxidase
3) metal carrier and storage proteins

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18
Q

Define oxidative stress

A

An imbalance between free radicals and antioxidants in the body

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19
Q

How do free radicals injure cells ?

A
  • most important targets are lipids in cell membranes : free radicals cause lipid peroxidation which leads to further free radicals - autolytic chain reaction
  • oxidise proteins , carbs and DNA
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20
Q

What are heat shock proteins ?

A
  • during periods of stress , usual protein synthesis decreases and synthesis of heat shock proteins increases
  • heat shock response aims to mend mis folded proteins and maintain cell viability
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21
Q

What is one important example of a heat shock protein ?

A

Ubiquitin

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22
Q

What do injured and dying cells look like under a microscope ? ( irreversible )

A

1) pyknosis: nuclear shrinkage
2) karyorrehexis : nuclear fragmentation
3) karyolysis : nuclear fading

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23
Q

Define oncosis

A

Cell death with swelling - the spectrum of changes that occur in injured cells prior to death

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24
Q

Define. Necrosis

A

In a living organism , the morphological changes that occur after a cell has been dead some time. This is seen after 12-24 hours post death

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25
Q

What are the two main types of necrosis ?

A

1) coagulative

2) liquefactive

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26
Q

What is coagulative necrosis ?

A

The proteins within the dying cell denature where they then coagulate together.

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27
Q

What is liquifactive necrosis ?

A

Dying cells undergo autolysis - this is where the proteins undergo dissolution by the cells own enzymes
.

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28
Q

What is another two special types of necrosis ?

A

Caseous and fat necrosis

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29
Q

In what organs , does coagulative necrosis. Often occur in ?

A
  • solid organs for example the heart , spleen and kidneys
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30
Q

In what organs does liquefactive necrosis occurs ?

A

Loose tissues for example lungs and the brain

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31
Q

What does coagulative necrosis look like ?

A

Denaturalising of proteins dominates over release of processes

  • cellular architecture is somewhat preserved.
32
Q

What does liquefactive necrosis look like ?

A
  • cells fall apart

- enzymatic digestion of tissues

33
Q

What is caseous necrosis ?

A

Contains amorphous( structreless) debris

  • tissue maintains a cheese like appearance
  • often associated with Tb
34
Q

What is fat necrosis ?

A

The enzyme lipase releases fatty acids .

  • this fatty acids then combine with calcium to form soaps
  • these soaps appear as white , chalky deposits in tissues
35
Q

Is gangrene and infarction types of necrosis ?

A

No ! They are not types of necrosis !

36
Q

Define gangrene

A

A clinical term used to describe necrosis that is visible to the naked eye

37
Q

What can gangrene be further classified into ?

A

Dry and wet gangrene

38
Q

What is dry gangrene

A
  • when necrosis is modified by exposure to air resulting in drying
  • the underlying process is coagulative necrosis
39
Q

Why is wet gangrene

A

When necrosis is modified by mixed bacterial culture

  • the underlying process is liquifactive necrosis
40
Q

What is gasgangrene?

A

Is wet gangrene where the tissue has become infective with anaerobic bacteria that produce visible and palpable bubbles of gas within the tissues

41
Q

What is infarction

A

Necrosis caused by reduction in arterial blood flow (ischaemia)

42
Q

What is an infarct

A

An area of necrotic tissue which is the result of loss of arterial blood supply

43
Q

How can infarcts be described by ?

A

Their colour - either red or white which indicates how much haemorrhage there is into the infarct

44
Q

What does a white infarct indicate and where does it often occur ?

A
  • it often occurs in solid organs for example the heart , spleen and kidneys after the blockage of an end artery.
  • underlying process is coagulative necrosis
45
Q

What does a red infarct indicate and where does it often occur ?

A
  • often occurs in organs such as the lungs or the brain.
  • occurs in organs that have loose tissue and dual blood supply ( no end arteries)
  • so a haemorrhage occurs in extensive dead tissue.
46
Q

What are the two main causes of infarction ?

A

1) thrombosis

2) embolism ( blockage of a vessel either by blood , gas bubble or fat gobule )

47
Q

What does the severity of infraction depend on ?

A

1) alternative blood supply
2) speed of ischaemia
3) tissue involved

4( oxygen content of the blood

48
Q

What is ischaemia reperfusion injury ?

A
  • tissue damage caused when blood supply is returned to tissue where there was ischaemia
  • this is because increased production of oxygen free radicals can occur with re-oxygenation
  • increased number of neutrophils when more blood is supplied which could cause inflammation and increase tissue injury
  • delivery of complement proteins and activation of the complement pathway
49
Q

When membranes are leaky , what molecules can leak out as well as in ?

A

1) potassium
2) enzymes such as troponin and creatine kinase
3) myoglobin following rhabdomyolysis which is often caused by prolonged intense exercise or marathon runners.

50
Q

Define apoptosis

A

Cell death with shrinkage induced by a regulated intracellular programme where a cell activate enzymes that degrade its own nuclear DNA and proteins

51
Q

Is apoptosis an activate or inactive process ?

A

Active process because it requires energy

52
Q

Is apoptosis a good or bad thing ?

A

It can be both pathological and physiological

53
Q

When does apoptosisnoccur physiologically?

A

1) embryogenesis: Hox genes regulates apoptosis of cells between webbed hands
2) in order to maintain a steady state

54
Q

What are the three phases of apoptosis ?

A

1) initiation
2) execution
3) degradation and phagocytosis

55
Q

What two mechanisms is initation and execution triggered by ?

A

Intrinsic and extrinsic mechanisms

56
Q

How is the intrinsic pathway initiated and carried out ?

A

1) initiating signal comes from within the cell
2) it is triggered by irreparable DNA damage and withdrawal of growth factors
3) p53 protein is activated and this causes outer mitochondrial membrane to become leaky
4) cytochrome C oxidase is released from the mitochondria and this causes activation of caspases

57
Q

How is the extrinsic pathway initiated and carried out ?

A

1) initiated by extracellular signals
2) it is triggered by cells that are a danger for example rumour cells , virus- infected cel,s
- one of the signals is TNFa which is secreted by T killer cells. This signal binds to cell membrane receptor which results in activation of caspases.

58
Q

How are the apopototic bodies phagocytosed?

A

Both intrinsic and extrinsic pathways cause the cells to shrink and break up into adoptive bodies

  • the apoptic bodies express proteins on their surface
  • they can now be recognised by phagocytes
59
Q

What are a few differences between necrosis/oncosis and apoptosis?

A

1) apoptosis involves shrinkage of cells , whereas oncosis/necrosis involves swelling of a cell so apoptopic cells are smaller than necrotic cells.
2) membrane is intact with apoptosis , whereas in oncosis/necrosis the plasma membrane is disrupted
3) in oncosis / necrosis , the nucleus undergoes pyknosis , karyorrhexis and karyolysis whereas in apoptosis fragmentation of nucleosome forms clumps beneath nuclear membrane
4) in apoptopic cells area , there are NO inflammatory cells whereas in necrotic area there are inflammatory cells
5) apoptosis can be physiological or pathological , whereas necrosis isnALWAYS pathological

60
Q

What kind of things can accumulate in cells ?

A

1) water and electrolytes
2) lipids
3) carbohydrates
4) proteins
5) pigments

61
Q

When does fluid accumulation occur ?

A
  • occurs when energy supplies are cut off eg hypoxia
  • Na+ and water flow into cell
  • this can be a particular problem in the brain
62
Q

When do lipids accumulate in the cells a.

A

1) accumulation of TAGS this is called steatosis
2) fatty liver
3) causes are alcohol , diabetes , obesity , toxins
4) cholesterol builds up to form atherosclerotic plaques

63
Q

In what conditions do proteins accumulate in cells ?

A

1( alcoholic liver disease

2) a1-antitrypsin deficiency : liver produced incorrectly folded a1-antitrypsin protein , which cannot be packaged by the ER and is not secreted from the ER.

64
Q

When do pigments accumulate in cells ?

A

1( urban air pollutants causes carbon /dust / coal to accumulate

2) tattooing - pigments are prickled into the dermis of the skin
3) endogenous pigments eg haemosiderin which is an iron storage molecule that is derived from HB. Forms when there is a bruise ( increase in iron)

65
Q

What is herediatry haemochromatosis?

A
  • genetics,lay inherited disorder which results in increased intestinal absorption of iron.
  • iron is deposited in the skin , liver , pancreas , heart and endocrine organs o
  • symptoms include liver damage , heart dysfunction and endocrine failures
66
Q

What is the cause of jaundice?

A

Accumulation of bilirubin.

Which is a breakdown product of haem

  • when bile flow is obstructed or overwhelmed , bilirubin in blood rises and jaundice results
67
Q

What is calcification

A

Abnormal deposition of calcium salts within tissues

  • can be localised ( dystrophic) or generalised ( metastatic )
68
Q

Where does calcification usually occur ?

A
  • some malignancies ,

Aging or damaged heart valves

In atherosclerotic plaques

Areas of dying tissues

69
Q

How would calcification appear under a microscope ?

A

As a purpose chunk

70
Q

What causes hypercalcaemia?

A

1) increased secretion of parathyroid hormone resulting in bone restoration. This could be due to parathyroid hyperplasia or tumour. Secondary cause could be because of renal failure or retention of phosphate
Ectopic cause - secretion of PTH related protein by malignant tumours

2) destruction of bone tissue by leukaemia , skeletal metastasis , immbolisation

71
Q

Can cells live forever ?

A

No , because after certain number of divisions DNA chromosomes decrease in length. The enzyme telomerase helps to decrease the effects of shortening of the chromosome. However as you age , this enzyme slowly becomes to inactivate.

Whereas in cancer cells , they produce many telomerase so they have the ability to replicate many times

72
Q

In what organs does coagulative necrosis occur ?

A

ALL organs can experience coagulative,necrosis apart from the BRAIN.

73
Q

What does. A secondary haemorragic transformation mean ?

A

Haemorrhage occurs after something else has happened eg an infarct could happen first.

74
Q

What proteins / enzymes are elevated during hepatitis?

A

1) bilirubin
2) lactate dehydrogenase
3) aminotransferase T

3)

75
Q

What proteins / enzymes are elevated during acute pancreatitis?

A

Amylase

Lipase

76
Q

What proteins / enzymes are elevated during MI ?

A
  • troponin I ( main one )
  • troponin C
  • creatine kinase ( CK-MB) - not commonly used because it takes quite a long time for these levels to elevate during MI.
  • myoglobin
77
Q

Why are these enzymes / proteins elevated in blood after these conditions ?

A
  • the integrity of the cell membrane is damaged so they spread out of the cells

Pathological Processes (13 decks)

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