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SA pathological processes > S1) Cell Injury > Flashcards

S1) Cell Injury Flashcards

1
Q

How do cells respond to environmental changes?

A
  • Cells can maintain homeostasis during mild environmental changes
  • During severe changes, cells undergo physiological and morphological adaptations to remain viable
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2
Q

What happens when cells reach the limits of their adaptive response?

A
  • Reversible cell injury
  • Irreversible cell injury and death
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3
Q

Identify 4 factors which affect the extent of cell damage

A
  • Type of injury
  • Duration of injury
  • Severity of injury
  • Type of tissue
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4
Q

Identify 7 agents by which cells can be damaged

A
  • Hypoxia (low 02)
  • Physical agents (change in pressure, electric currents, burns)
  • Chemical agents and drugs
  • Micro-organisms
  • Immune mechanisms
  • Dietary imbalances
  • Genetic abnormalities
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5
Q

What is hypoxia and how does it cause cell injury?

A
  • Hypoxia is oxygen deprivation and if persistent causes cell adaptation, injury or death
  • Very common
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6
Q

Identify 5 physical agents which can cause cell injury

A
  • Direct trauma
  • Extremes of temperature (burns and severe cold)
  • Sudden changes in atmospheric pressure
  • Electric currents
  • Radiation
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7
Q

Identify 5 chemical agents/drugs which can cause cell injury

A
  • Oxygen in high concentrations
  • Poisons
  • Alcohol
  • Illicit drugs
  • Therapeutic drugs
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8
Q

Identify 4 micro-organisms which can cause cell injury

A
  • Viruses
  • Bacteria
  • Fungi
  • Parasites
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9
Q

Identify 3 types dietary imbalances which can cause cell damage

A
  • Dietary insufficiency (just less that deficiency)
  • Dietary deficiencies
  • Dietary excess
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10
Q

Provide and example of a genetic abnormality which can cause cell damage

A

Inborn errors of metabolism

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11
Q

Identify 4 types of hypoxia (oxygen deprivation)

A
  • Hypoxaemic (arterial content is low)
  • Anaemic (decreased heam ability to carry 02)
  • Ischaemic (interruption to blood supply)
  • Histiocytic (tissue cells are posioned)
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12
Q

What are the targets of cell injury?

A
  • Cell membranes
  • Nucleus
  • Proteins (structural proteins & enzymes)
  • Mitochondria
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13
Q

Provide a 10-point summary of reversible hypoxic cell injury

A
  1. Cell is deprived of oxygen
  2. Mitochondria stops ATP production & membrane ionic pumps stop
  3. Na+ and H20 seep into the cell
  4. Cell swells and initiates a heat-shock response (stress)
  5. Glycolysis keeps cell alive but pH drops as lactic acid accumulates
  6. Calcium enters the cell & activates: phospholipases, proteases, ATPase and endonucleases
  7. ER and other organelles swell
  8. Enzymes leak out of lysosomes and attack cell contents
  9. Cell membrane is damaged (show blebbing)
  10. Cell dies – burst of a bleb
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14
Q

Describe the effect of the following enzymes in causing cell injury:

  • Phospholipases
  • Protease
  • ATPases
  • Endonucleases
A
  • Phospholipases – cause cell membranes to lose phospholipids
  • Proteases – damage cytoskeletal structures and attack membrane proteins
  • ATPases – cause more loss of ATP
  • Endonucleases – cause nuclear chromatin to clump
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15
Q

What is Ischaemia-Reperfusion Injury?

A

Ischaemia-reperfusion injury is the injury that occurs when blood flow is returned to a tissue that has undergone ischaemia but not necrosis

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16
Q

What causes Ischamia-Reperfusion injury?

A
  • Increased production of oxygen free radicals with reoxygenation
  • Delivery of complement proteins activates the complement pathway
  • Increased neutrophils with returned blood flow results in inflammation and increased tissue injury
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17
Q

What are free radicals and what do they do?

A
  • Free radicals are reactive oxygen species and have a single unpaired electron in an outer orbit
  • This is an unstable configuration and hence, they react with other molecules often producing more free radicals
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18
Q

What do free radicals do in Ischaemic reperfusion injury?

A
  • Attack lipids in cell membranes and cause lipid peroxidation (break down of lipids as they lose electrons)
  • Damage proteins, carbohydrates and nucleic acids
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19
Q

Identify 3 free radicals of particular biological significance in cells

A
  • OH• (hydroxyl)
  • 02- (superoxide)
  • H202 (hydrogen peroxide)
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20
Q

What causes cell injury, in terms of free radicals?

A
  • Cell injury is caused by an imbalance between free radical production and free radical scavenging
  • Free radicals accumulate and the cell / tissue is said to be in oxidative stress
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21
Q

What is the anti-oxidant system?

A

The anti-oxidant system is the body’s defence system to prevent injury caused by free radicals

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22
Q

Identify and describe the components of the antioxidant system

A
  • Superoxide dismutase catalyse the reaction production of H2O2 (less toxic) from O2-
  • Catalases and peroxidases catalyse the production of H2O and O2 from H2O2
  • Free radical scavengers neutralise free radicals
  • Storage proteins that sequester (hide) transition metals in the extracellular matrix
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23
Q

Identify some free radical scavengers

A
  • Vitamin A
  • Vitamin C
  • Vitamin E
  • Glutathione
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24
Q

Identify two storage proteins involved in the antioxidant system

A
  • Transferrin
  • Ceruloplasmin
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25
Q

What are heat shock proteins?

A

Heat shock proteins are proteins triggered by any form of cell injury to protect the body in the stress response

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26
Q

Provide 3 examples of heat shock proteins

A
  • Stress proteins
  • Unfoldases
  • Chaperonins
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27
Q

How do cells respond to the heat shock response?

A
  • Decrease usual protein synthesis
  • Increase synthesis of HSPs
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28
Q

What are the main cell alterations that can be seen under a light microscope when a cell starts to die/gets injured?

A
  • Cytoplasmic changes - more blue due to more water
  • Nuclear changes - clump
  • Abnormal intracellular accumulations
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29
Q

Identify 4 reversible changes involved in cell injury as seen in electron microscopy

A
  • Swelling of cell & organelles
  • Cytoplasmic blebs
  • Clumped chromatin
  • Ribosome separation from the rER

cytoplasmic blebs

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30
Q

Identify 5 irreversible changes involved in cell injury as seen in electron microscopy.

A
  • Nuclear changes
  • Swelling and rupture of lysosomes
  • Membrane defects
  • The appearance of myelin figures
  • Lysis of the ER

myelin figures, clumps of cell membrane

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31
Q

Identify and describe the three types of nuclear changes that can occur in cell injury

A
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32
Q

Define apoptosis

A

Apoptosis is cell death with shrinkage, induced by a regulated intracellular program where a cell activates enzymes that degrade its own nuclear DNA and proteins

stages

  1. initiation
  2. execution
  3. degradation and phagocytosis
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33
Q

Define oncosis

A

Oncosis is cell death with swelling and the spectrum of changes that occur prior to death in injured cells

  • contigous groups of cells
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34
Q

Define necrosis

A

- Necrosis is the morphologic changes that occur after a cell has been dead some time e.g. 4-24 hours

  • It is not a type of cell death, i.e. it is an appearance and not a process
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35
Q

Why is inflammation often accompanied with necrosis?

A
  • Cell membranes are damaged (plasma and organelle)
  • Lysosomal enzymes are released into the cytoplasm and digest the cell
  • Cell contents leak out of the cell and cause inflammation
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36
Q

How is necrotic tissue removed?

A
  • Necrotic tissue is removed by enzymatic degradation and phagocytosis by white cells
  • If some remains it may calcify (dystrophic calcification)
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37
Q

Coagulative necrosis is a type of necrosis.

Outline this process

A
  • Proteins of dying cells denature and tend to coagulate
  • Denaturation dominates over release of active proteases
  • Cellular architecture is preserved (ghost outline)
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38
Q

Liquefactive necrosis is a type of necrosis.

Outline this process

A
  • Proteins of dying cells undergo autolysis where they are dissolved by the cell’s own enzymes
  • Enzyme degradation dominates over denaturation
  • Leads to liquefaction of tissues
  • mainly found in the brain
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39
Q

Caseous necrosis is a type of necrosis.

Outline this process

A
  • Contains amorphous (structureless) debris
  • Associated with infections e.g. TB
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40
Q

Fat necrosis is a type of necrosis.

Outline this process

A
  • Lipase releases fatty acids from triglycerides which then complex with calcium to form soaps
  • Soaps appear as white chalky deposits
  • Associated with pancreas, breast and the salivary glands
41
Q

What is gangrene?

A

Gangrene is not a type of necrosis, it is a clinical term used to describe necrosis that is visible to the naked eye

42
Q

Classify the different types of gangrene

A
  • Dry gangrene – necrosis is modified by exposure to air (coagulative necrosis)
  • Wet gangrene – necrosis is modified by infection with a mixed bacterial culture (liquefactive necrosis)
43
Q

What is gas gangrene?

A
  • Gas gangrene is wet gangrene where the tissue has become infected with anaerobic bacteria
  • It produces visible and palpable bubbles of gas within the tissues
44
Q

What is infarction?

A

Infarction refers to a cause of necrosis, namely ischaemia (reduced blood supply)

45
Q

Identify the 2 most common causes of infarction

A
  • Thrombosis
  • Embolism
46
Q

Explain how infarcts can be described by their colour

A
  • Infarcts can be white / red
  • It indicates how much haemorrhage there is into the infarct
47
Q

Where are white infarcts found?

A

A white (anaemic) infarct occurs in ‘solid’ organs (kidney) after occlusion of an “end” artery

white as it dies and no blood

48
Q

Where are red infarcts found?

A

A red (haemorrhagic) infarct occurs where there is extensive haemorrhage into dead tissue due to:

  • Loose tissue
  • A dual blood supply
  • Numerous anastomoses
49
Q

Identify 4 consequences of infarction

A
  • Local irritation
  • Local inflammation
  • General toxic effects on the body
  • Substances appear in high concentrations in the blood
50
Q

Identify 3 types of molecules released from an infarction

A
  • Potassium
  • Enzymes e.g. Creatine Kinase, AST, troponin
  • Myoglobin
51
Q

Why does apoptosis not induce inflammation?

A
  • Apoptotic bodies are removed by macrophage phagocytosis
  • No leakage of cell contents occurs
52
Q

What does apoptosis look like under a light microscope?

A
  • Apoptotic cells are shrunken and appear intensely eosinophilic
  • Pyknosis and karyorrhexis are seen
53
Q

What does apoptosis look like under an electron microscope?

A
  • Cells show cytoplasmic budding (not blebbing as is seen in oncosis)
  • This progresses to fragmentation into membrane-bound apoptotic bodies
54
Q

Why are apoptotic bodies phagocytosed?

A

The apoptotic bodies express proteins on their surface which are recognised by phagocytes or neighbouring cells

55
Q

Compare and contrast the structural changes in oncosis/necrosis and apoptosis in terms of:

  • Pattern
  • Cell size
  • Nucleus
  • Plasma membrane
  • Cellular contents
  • Adjacent inflammation
A
56
Q

When and why do abnormal cell accumulations occur?

A
  • Occurs when cell cannot metabolise something
  • Occurs with sub-lethal or chronic injury
  • Can be reversible / harmless / toxic
57
Q

Where are abnormal cell accumulations derived from?

A
  • Cell’s own metabolism
  • The extracellular space e.g. spilled blood
  • The outer environment e.g. dust
58
Q

What are the five main groups of intracellular accumulations?

A
  • Carbohydrates
  • Water and electrolytes
  • Lipids (triglycerides and cholesterol)
  • Proteins
  • Pigments (exogenous and endogenous)
59
Q

Hydropic swelling is a type of abnormal cellular accumulation.

What occurs?

A
  • Indicates severe cellular distress
  • Na+ and H2O flood into the cell
60
Q

When and where does hydropic swelling occur?

A
  • Occurs when energy supplies are cut off e.g. hypoxia
  • Particularly occurs in the brain
61
Q

What is steatosis?

A
  • Steatosis is the accumulation of triglycerides
  • If mild, it is asymptomatic
62
Q

What is the most common site of steatosis?

A

Liver (major organ of fat metabolism)

63
Q

Identify 4 causes of steatosis

A
  • Alcohol
  • Diabetes mellitus
  • Obesity
  • Toxins
64
Q

Outline the metabolism of cholesterol

A
  • Cannot be broken down and is insoluble

- travel in blood via chylomicrons

  • Can only be eliminated through the liver
  • Excess stored in cell in vesicles

diseases:

atherosclerosis (thickening of inside of arteries)

xanthoma (yellow bumps around eyelids)

65
Q

How are foam cells formed?

A

Foam cells are formed from cholesterol accumulating in the smooth muscle cells and macrophages of atherosclerotic plaques

66
Q

Where are xanthomas found?

A

Xanthomas are present in macrophages in skin and tendons of people with hereditary hyperlipidaemias

67
Q

How do protein accumulations appear?

A
  • Look like eosinophilic droplets
  • Look like aggregations in the cytoplasm
68
Q

Outline abnormal protein accumulations as seen in α1-antitrypsin deficiency

A
  • Liver produces incorrectly folded α1-antitrypsin protein
  • Protein cannot be packaged by ER, accumulates and is not secreted
  • Systemic deficiency results (emphysema)
69
Q

Describe the effect of accumulations of exogenous pigments (tattoos)

A
  • Phagocytosed by macrophages in dermis and remains there
  • Some pigment will reach draining lymph nodes
70
Q

Explain how coal, dust or soot (endogenous pigments) accumulate in the body

A
  • Pigment inhaled and phagocytosed by alveolar macrophages
  • Anthracosis and blackened peribronchial lymph nodes
  • Harmless unless in large amounts (fibrosis/emphysema)
71
Q

What is pathological calcification?

A

Pathological calcification is the abnormal deposition of calcium salts within tissues

despite this there will still be normal calcium serum levels and serum phosphate levels

72
Q

What are the 2 types of pathological calcification?

A
  • Dystrophic calcification (local – more common)
  • Metastatic calcification (general)
73
Q

What is dystrophic calcification?

A
  • Dystrophic calcification is when a local change or disturbance in the tissue favours the nucleation of hydroxyapatite crystals

- No abnormality in calcium metabolism

74
Q

Identify 4 locations where dystrophic calcification occurs

A
  • An area of dying tissue
  • Atherosclerotic plaques
  • Aging or damaged heart valves
  • Tuberculous lymph nodes
75
Q

What is metastatic calcification?

A

Metastatic calcification is when hydroxyapatite crystals are deposited in normal tissues throughout the body due to hypercalcaemia secondary to disturbances in calcium metabolism

causes:

primary hyperthyroidism - parathyroid hyperplasia

secondary - renal failure

tertiary - ectopic production

76
Q

Distinguish between the acute and chronic liver disease

A
  • Acute liver disease is when damage to the liver develops over a few months
  • Chronic liver disease is when damage to the liver occurs over a number of years
77
Q

Identify 2 effects of chronic excessive alcohol intake on the liver

A
  • Oxidative stress – liver tries to break down alcohol and the resulting chemical reaction damages its cells, leading to inflammation and scarring

- Toxins – alcohol damages our intestine which releases toxins from gut bacteria into the liver, leading to inflammation and scarring

78
Q

What causes jaundice?

A

Accumulation of bilirubin

79
Q

What is bilirubin?

A

Bilirubin is a breakdown product of heme, formed in all cells of body and excreted in bile

80
Q

How does jaundice arise?

A
  • Bile flow is obstructed or overwhelmed
  • Bilirubin in blood rises and is deposited in tissues extracellularly or in macrophages
81
Q

What is chronic hepatitis?

A

Chronic hepatitis is defined as over 6 months history with histology of inflammation and necrosis in the liver

82
Q

Identify 4 laboratory features of hepatitis

A
  • Raised serum ALT, AST and LDH
  • Raised bilirubin
  • Decreased albumin
  • Raised PT
  • Raised ammonia
83
Q

Identify 3 laboratory features of alcoholic liver disease

A
  • Raised bilirubin
  • Raised alkaline phosphatase
  • Raised gamma GT (glutamyl transpeptidase)
84
Q

What are the clinical and laboratory features of acute pancreatitis?

A
  • Raised serum amylase in first 24 hours
  • Raised serum lipase from 72-96 hours
  • Glycosuria (10%)
  • Hypocalcaemia possible
85
Q

How do we take measurements to identify myocardial infarctions?

A

Measure blood levels of intracellular macromolecules that leak out of injured myocardial cells through damaged cell membranes

86
Q

Identify 5 substances which indicate the occurrence of a myocardial infarction

A
  • Troponin T (TnT)
  • Troponin I (TnI)
  • Creatine kinase (CK)
  • Lactate dehydrogenase (LDH)
  • Myoglobin
87
Q

how does an immune system damage bodys cells

A
  • hypersensitivity (host tissue is injured)
  • autoimmune
88
Q

consequence of low ATP

A
  • swelling, influx of NA and Ca and H20
  • clumping of nuclear chromatin
  • low protein synthesis so lipid deposition
89
Q

consequence of increased intracellular calcium

A
  1. low ATP
  2. low phospholipids
  3. disruption of membrane
  4. nuclear chromatin damage
90
Q

intrinsic pathway

A
  • intiating signal comes from within

triggers:

  • DNA damage
  • wothdrawal of growth factors and hormones
  • p53 activated = outermitichondrial membrane leaky
  • activation of capsases
91
Q

extrinsic pathway

A

initiated by extracellular signals

  • triggers are cells in danger
  • activates capsases
92
Q

compare aptoptosis and oncosis

A
93
Q

ischaemia-reperfusion injury

A
  • if blood flow returns to a damaged but not yet necrotic tissue the damage can be much worse than if the blood hadnt had returned

causes:

o2 free radicals

increased neutrophils so more inflamed and more tissue injury

94
Q

steatosis

A
  • accumalation of fat
95
Q

what can enzymes help diagnose

A
  • location of damage
  • troponin I
96
Q

what can be observed in a myocardial infarction

A

influx of Na and Ca

97
Q

what can be seen in an ultrasound of pancreatitis

A

fat nectosis

inflammation

98
Q

what chemical is released as a sign of muscular damage

A

creatine kinase

SA pathological processes (15 decks)

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