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Mechanisms Of Disease > Cell Injury > Flashcards

Cell Injury Flashcards

0
Q

What is hypoxia?

A

Oxygen deprivation resulting in decreased aerobic oxidative respiration

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1
Q

How can cell injury occur?

A

Hypoxia
Physical agents eg trauma, extremes in temperature
Chemical agents
Drugs

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2
Q

What does hypoxaemic mean?

A

Arterial content of oxygen is low

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3
Q

What can cause someone to be hypoxaemic?

A

High altitude

Lung disease

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4
Q

Definition of anaemia?

A

Decreased ability of haemoglobin to carry oxygen

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5
Q

What is ischaemia?

A

Interruption to blood supply causing lack of oxygen and metabolic substrates to tissue

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6
Q

What is oncosis?

A

Cell death with swelling

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7
Q

What is necrosis?

A

The morphological changes that follow cell death in living tissue

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8
Q

What is apoptosis?

A

Cell induced death by a regulated intra-cellular programme where a cell activates enzymes that degrade its own DNA and proteins

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9
Q

What is liquefactive necrosis?

A

Release of active enzymes is the dominant feature and tissue tends to liquefy - common with neutrophils

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10
Q

When does liquefactive necrosis commonly occur?

A

Bacterial infection due to neutrophils releasing proteolytic enzymes.
In the brain

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11
Q

What is coagulative necrosis?

A

When coagulative denaturation is the dominant feature and proteins clump together leading to solidity of the dead cells and tissue

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12
Q

What is fat necrosis?

A

Destruction of adipose tissue. Fatty acids released which react with calcium to form calcium soaps

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13
Q

When does fat necrosis often occur?

A

Trauma to fatty tissue eg in the breast - irregular scar is left which can mimic a nodule of breast cancer
Acute pancreatitis

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14
Q

Causes of infarction?

A

Thrombosis
Embolism
External compression of a vessel
Twisting of vessels

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15
Q

When and where does a white infarct occur?

A

After occlusion of an end artery in a solid organ
Solid nature limits the amount of haemorrhage from adjacent capillaries
Tissue dies and appears white

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16
Q

Which organs is a white infarct common in?

A

Heart
Spleen
Kidneys

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17
Q

When does a red infarct occur

A

Occurs in organs with a dual blood supply
Organs with numerous anastomoses
In loose tissue where there is poor stromal support for capillaries

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18
Q

What reversible changes occur in hypoxic cell injury?

A

Na/K pump failure so cell swells. Due to a lack of oxygen and therefore ATP
Calcium enters and damages cell components
Accumulation of lactic acid which lowers pH, affecting enzymes and chromatin clumping
Ribosomes detach from the ER, disrupting protein synthesis
Intra cellular accumulations of fat and denatured proteins

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19
Q

Effects of high cystolic calcium ion concentration?

A

Activates ATPase
Activates phospholipase which damages membranes
Activates proteases which break down membranes and cytoskeletal proteins
Activates endonucleases which damage DNA

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20
Q

What is ischaemia-reperfusion injury?

A

When blood flow is returned to tissue which has been subject to ischaemia but isn’t yet necrotic. Can cause tissue injury to be worse

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21
Q

Why does ischaemia-reperfusion injury occur?

A

Increased production of oxygen free radicals with reoxygenation
Increased neutrophils ➡️ more inflammation and tissue injury
Delivery of complement proteins and activation of complement pathway

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22
Q

What damage do free radicals cause?

A

Attack lipids in cell membranes
Damage proteins and nucleic acids
Mutagenic

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23
Q

What cells produce free radicals to kill bacteria?

A

Leukocytes

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24
Q

Which enzymes are involved in defence systems against ROS?

A
  • SOD catalyses O2- to H2O2

- catalases and peroxidases convert H2O2 to oxygen and water

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25
Q

What are the free radical scavengers?

A

ACE vitamins

Glutathione

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26
Q

What do heat shock proteins do?

A

Ensure proteins are refolded correctly

Maintains protein viability and maximises cell survival

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27
Q

What are the main causes of cell injury and death?

A 
Hypoxia
Chemical agents
Physical agents
Microorganisms
Immune mechanisms - hypersensitivity and autoimmune
Dietary deficiency
Genetic abnormalities
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28
Q

When are free radicals often produced?

A

Chemical and radiation injury
Cellular ageing
Ischaemia-reperfusion injury
High oxygen concentrations

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29
Q

Name the three important free radicals

A

Superoxide
Hydroxyl
Hydrogen peroxide

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30
Q

When are heat shock proteins important?

A

When the folding step in protein synthesis goes wrong

When proteins become denatured during cell injury

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31
Q

What nuclear changes occur during cell injury?

A

Chromatin clumping
Pyknosis
Karryohexis
Karryolysis

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32
Q

What does pyknosis mean?

A

When the nucleus shrinks and chromatin clumps

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33
Q

What is karryohexis?

A

Fragmentation of the nucleus

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34
Q

What is karryolysis?

A

Dissolution of the nucleus

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35
Q

What cytoplasmic changes occur under the light microscope during cell injury?

A
  1. Reduced pink staining due to increase in water in cytoplasm
  2. Increased pink staining due to increase in denatured proteins and detachment of ribosomes from the ER
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36
Q

When does coagulative necrosis commonly occur?

A

In most solid organs, where the cause of death is ischaemia

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37
Q

How does caseous necrosis appear?

A

Amorphous debris

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38
Q

What is caseous necrosis often seen with?

A

Granulatomous inflammation

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39
Q

What is gangrene?

A

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

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40
Q

What type of necrosis is it if the gangrene is dry?

A

Coagulative necrosis

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41
Q

What can wet gangrene lead to?

A

Septicaemia

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42
Q

What is wet gangrene often due to?

A

Infection

43
Q

Is an MI normally liquefactive or coagulative?

A

Coagulative

44
Q

Is a cerebral infarction normally coagulative or liquefactive?

A

Liquefactive

45
Q

What does the outcome of ischaemia depend on?

A

If there is an alternate blood supply
How quickly ischaemia has occurred - may be time for other perfusion pathways to develop
How vulnerable a tissue is to hypoxia
Oxygen content of the blood - in anaemic patients may be more serious

46
Q

Examples of when physiological apoptosis might occur

A

Embryogenesis
Body needs to remove cells to maintain a steady state
Cells infected by a virus
Cancerous cells

47
Q

During apoptosis, what changes occur which can be seen under the light microscope?

A 
Shrunken
Appear very pink (intensely eosinophilic)
Chromatin condensation
Pyknosis
Fragmentation of nucleus
48
Q

What changes occur that can be seen under the electron microscope during apoptosis?

A

Cytoplasmic blebbing which progresses to fragmentation into membrane-bound apoptotic bodies - contain cytoplasm, organelles and often nuclear fragments
Apoptotic bodies are removed by macrophages in phagocytosis

49
Q

Why does apoptosis not induce inflammation?

A

No leakage of cell contents

50
Q

What are the three phases of apoptosis?

A

Initiation
Execution
Degradation

51
Q

What are caspases?

A

Proteases that mediate the cellular effects of apoptosis

52
Q

How do caspases work?

A

Cleave proteins to break up the cytoskeleton

Initiate the degradation of DNA

53
Q

Why is the intrinsic pathway called intrinsic?

A

All of the apoptotic machinery is inside the cell

54
Q

What are some triggers for intrinsic apoptosis?

A

DNA damage

Withdrawal of growth factors or hormones

55
Q

Which protein is important in triggering intrinsic apoptosis?

A

p53

56
Q

After being triggered, what happens in intrinsic apoptosis?

A

Membrane permeability of mitochondria increases
Release of cytochrome C from mitochondria
Interacts with APAF1 and caspase 9 to form an apoptosome that activates various downstream caspases

57
Q

What are triggers of extrinsic apoptosis?

A

External ligands such as TRAIL and Fas

They bind to ‘death receptors’ which activate caspases

58
Q

What does p53 do?

A

‘Guardian of the genome’

Mediates apoptosis in response to DNA damage

59
Q

Which three proteins make up the apoptosome?

A

Cytochrome C
APAF 1
Caspase 9

60
Q

What does bcl-2 do?

A

Inhibits apoptosis by preventing cytochrome c from being released from mitochondria

61
Q

Name a death ligand and a death receptor

A

TRAIL

TRAIL-R

62
Q

What is pathological calcification

A

The abnormal deposition of calcium salts within tissues

63
Q

What is steatosis?

A

Accumulation of triglycerides in cells

64
Q

What are common causes of liver steatosis?

A

Alcohol abuse
Diabetes mellitus
Obesity
Toxins

65
Q

What type of cells can cholesterol accumulate in? What are these cells known as?

A

Smooth muscle cells and macrophages in atherosclerotic plaques
Foam cells

66
Q

What is it called when cholesterol is deposited in the skin of people with hyperlipidaemia?

A

Xanthomas

67
Q

What is Mallory’s hyaline seen in?

A

Alcoholic liver disease

68
Q

What is Mallory’s hyaline caused by?

A

Accumulation of altered keratin filaments

69
Q

What is the pathology of α1-antitrypsin deficiency

A

Liver produces a version of α1-antitrypsin that is incorrectly folded. Cannot be packaged by the ER so accumulates within it. Therefore not secreted by the liver.

70
Q

How does α1-antitrypsin defence affect the lungs?

A

Proteases within the lung can act unchecked and patients develop emphysema as lung tissue is broken down.

71
Q

What happens of someone has a high exposure to urban pollutants such as coal/coal dust?

A

Lungs can become fibrotic or emphysematous.

72
Q

What happens to coal dust when it is inhaled?

A

Phagocytosed by macrophages within lung tissue and is seen as blackened tissue or blackened peribronchial lymph nodes.

73
Q

Give some examples of endogenous pigments

A

Bilirubin
Lipofusin
Haemosiderin

74
Q

How is lipofusin produced?

A

Sign of previous damage by free radicals and lipid peroxidation.
Seen in ageing cells
Brown pigment

75
Q

When does haemosiderin form?

A

When there is localised or systemic excess of iron.

Eg bruises

76
Q

What is haemosiderin derived from?

A

Haemoglobin

77
Q

What colour is haemosiderin

A

Yellow/brown

78
Q

What is haemosiderosis and what damage can it cause?

A

When haemosiderin is deposited in many organs.

Can damage the liver, pancreas and heart.

79
Q

What conditions is haemosiderosis seen in?

A

Hereditary haemochromatosis
Haemolytic anaemias
Blood transfusions

80
Q

What does dystrophic calcification occur in?

A 
Dying tissues
Atherosclerotic plaques
Ageing
Damaged heart valves
Tuberculus lymph nodes
81
Q

When does metastatic calcification occur?

A

As a consequence of hypercalcaemia secondary to disturbances in calcium metabolism.

82
Q

Four main causes of hypercalcaemia?

A

Increased PTH secretion due to parathyroid tumours or ectopic secretion of PTH-related protein by malignant tumours
Vitamin D related disorders
Destruction of bone secondary to primary tumours of bone
Renal failure

83
Q

List some things that accumulate in cells as they age

A

Damage to DNA
Abnormally folded proteins
Lipofuscin

84
Q

What is telomerase and which cells have it?

A

An enzyme which prevents the shortening of telomeres so cells can divide many times
Stem and germ cells

85
Q

What is ethanol broken down into and by which enzymes?

A

Ethanol ➡️ acetaldehyde dehydrogenase

Alcohol dehydrogenase
a cytochrome P450 enzyme - CYP2E1
catalase

86
Q

What happens to acetaldehyde?

A

Acetaldehyde ➡️ acetic acid

Acetaldehyde dehydrogenase

87
Q

Which enzyme involved in alcohol metabolism do women have a lower concentration of than men

A

Alcohol dehydrogenase

88
Q

Which enzyme do about half of oriental people have reduced activity of? What does this result in?

A

Aldehyde dehydrogenase
Build up of acetaldehyde
Facial flushing

89
Q

Toxicity of alcohol affects the liver by causing a fatty change. What is this?

A

Steatosis which can cause hepatomegaly.

It is reversible and generally asymptomatic.

90
Q

What happens in acute alcoholic hepatitis?

A

Focal hepatocytes necrosis
Mallory body formation
Neutrophilic infiltrate

91
Q

Symptoms of acute alcoholic hepatitis?

A

Fever

Liver tenderness and jaundice

92
Q

What changes occur to the liver in cirrhosis?

A

Hard and shrunken liver

Micronodules of regenerating hepatocytes form surrounded by bands of collagen.

93
Q

How is paracetamol detoxified?

A

Glucaronidation and sulphonation

94
Q

Which enzyme in metabolism of paracetamol leads to the production of the toxic metabolite? What is it called?

A

When cytochrome P450 is used

NAPQI

95
Q

How is NAPQI detoxified?

A

Interaction with glutathione

96
Q

What does NAPQI do?

A

Binds sulphydryl groups on hepatocytes membranes, causing necrosis and liver failure

97
Q

What can cause people to have lower reserves of glutathione?

A 
If they drank alcohol with the paracetamol overdose
If they are alcohol dependent
If they are malnourished
On enzyme inducing drugs
HIV positive/AIDS
98
Q

What is the antidote to paracetamol overdose?

A

N-acetylcysteine

99
Q

What is measured to decide whether or not to give NAC

A

Serum conc of paracetamol

4 hours after over dose

100
Q

What is used to assess liver damage by paracetamol overdose?

A

The pro-thrombin time 24hrs after overdose

101
Q

What does aspirin do?

A

Acetylates platelet cyclooxygenase

Blocks platelet ability to form thromboxane A2, a substance which activates platelet aggregation

102
Q

What are the consequences of an aspirin overdose?

A

Stimulates respiratory centre ➡️ respiratory alkalosis
Causes metabolic acidosis to compensate

Interferes with carbohydrate, fat and protein metabolism and oxidative phosphorylation ➡️ production of lactate, pyruvate and ketone bodies ➡️ acidosis

Deceased platelet aggregation

Acute erosive gastritis and GI bleeding

103
Q

What damage can free radicals cause?

A

Cross link proteins

Oxidise membrane lipids

104
Q

Describe what is seen in fatty change of the liver after alcohol

A

Steatosis from toxicity of alcohol
Hepatomegaly
Acute, reversible and asymptomatic

105
Q

Explain what is seen in acute alcoholic hepatitis

A 
Alcohol and acetaldehyde are directly toxic
Acute hepatitis
Focal hepatic necrosis
Mallory body formation
Neutrophils infiltrate
Fever, liver tenderness and jaundice
106
Q

Explain changes seen in cirrhosis

A

Shrunken, hard liver
Micro nodules of regenerating hepatocytes surrounded by bands of collagen
Irreversible, serious, sometimes fatal

Mechanisms Of Disease (11 decks)

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