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2 Pathological Processes > 2 Cell Injury > Flashcards

2 Cell Injury Flashcards

1
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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2
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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3
Q

What is hypoxia and how does it cause cell injury?

A
  • Hypoxia is oxygen deprivation
  • if persistent causes cell adaptation, injury or death
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4
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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5
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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6
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(bulge in plasma membrane)
  10. Cell dies – burst of a bleb
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7
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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8
Q

What is Ischaemia-Reperfusion Injury?

A

Ischaemia-reperfusion injury:

Tissue = damaged not yet necrotic

Cell=damaged as a result of blood flow return

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9
Q

What causes Ischamia-Reperfusion injury? (3)

A
  1. Reoxygenation- increase in free radicals
  2. Increased neutrophil number- increase inflammation
  3. Complement proteins delivered- activate inflammatory pathway
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10
Q

What are free radicals and what do they do?

A
  • Free radicals are reactive oxygen species
  • have a single unpaired electron
  • This is an _unstable configuratio_n- v reactive
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11
Q

How do free radicals injure cells?

A

Oxidative imbalance- overwhelm anti-oxidant system

    • Attack lipids in cell membranes and cause lipid peroxidation- generate more free radicals
    • Damage (oxidise) proteins, carbohydrates and nucleic acids= mutagenic, carcinogenic
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12
Q

Identify 3 free radicals of particular biological significance in cells

A
  • OH• (hydroxyl)
  • 02- (superoxide)
  • H202 (hydrogen peroxide)
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13
Q

What causes cell injury, in terms of free radicals?

A
  • Imbalance between free radical production and free radical scavenging
  • Free radicals accumulate- oxidative stress
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14
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 (eg vitamins a,c, and e)
  • Storage proteins (eg transferrin) that sequester transition metals in the extracellular matrix
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15
Q

Identify some free radical scavengers

A
  • Vitamin A
  • Vitamin C
  • Vitamin E
  • Glutathione
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16
Q

Identify two storage proteins involved in the antioxidant system

A
  • Transferrin
  • Ceruloplasmin
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17
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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18
Q

Provide 3 examples of heat shock proteins

A
  • Stress proteins
  • Unfoldases
  • Chaperonins
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19
Q

How do cells respond to the heat shock response?

A
  • Decrease usual protein synthesis
  • Increase synthesis of HSPs
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20
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
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21
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
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22
Q

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

A
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23
Q

Define oncosis

A

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

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24
Q

Define necrosis

A

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

  • Not a type of cell death, i.e. it is an appearance and not a process
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25
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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26
Q

What is caseous necrosis?

A
  • Contains amorphous (structureless) debris
  • Associated with infections e.g. TB
  • (inbetween coagulative and liquefactive)*
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27
Q

What is fat necrosis?

A
  • Lipase releases fatty acids from triglycerides
  • Fatty acids complex with calcium to form soaps
  • Soaps appear as white chalky deposits
  • Associated with pancreas (pancreatitis), breast and the salivary glands
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28
Q

What is gangrene?

A

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

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29
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)
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30
Q

Define apoptosis

A
  • Apoptosis is cell death with shrinkage
  • Induced by a regulated intracellular program
    • –>cell activates enzymes that degrade its own nuclear DNA and proteins
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31
Q

What is gas gangrene?

A
  • Gas gangrene:

–> wet gangrene where the tissue has become infected with anaerobic bacteria

- It produces visible and palpable bubbles of gas within the tissues

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32
Q

What is infarction?

A

Infarction= cause of necrosis, namely ischaemia (reduced blood supply)

(Infarct= area of necrotic tissue)

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33
Q

Identify the 2 most common causes of infarction

A
  • Thrombosis
  • Embolism

(could be eg twisted bowel)

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34
Q

Explain how infarcts can be described by their colour and what this indicates?

A
  • Infarcts can be white / red
  • It indicates how much haemorrhage there is into the infarct
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35
Q

Where are white infarcts found?

A

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

36
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
    • Re-perfusion
37
Q

Identify 3 consequences of infarction

A
  • Local irritation
  • Local inflammation
  • General toxic effects on the body
38
Q

Identify 3 types of molecules released from an infarction (high conc in blood).

A
  • Potassium
  • Enzymes e.g. Creatine Kinase, AST, troponin
  • Myoglobin
39
Q

Why does apoptosis not induce inflammation?

A
  • Apoptotic bodies are removed by macrophage phagocytosis
  • No leakage of cell contents occurs
40
Q

What does apoptosis look like under a light microscope?

A
  • Apoptotic cells are shrunken and appear intensely eosinophilic
  • Pyknosis and karyorrhexis are seen
41
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
42
Q

Why are apoptotic bodies phagocytosed?

A

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

43
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
  • Physiological/pathological role
A
44
Q

What are the five main groups of intracellular accumulations?

A
  • Carbohydrates
  • Water and electrolytes
  • Lipids (triglycerides and cholesterol)
  • Proteins
  • Pigments (exogenous and endogenous)
45
Q

Hydropic swelling is a type of abnormal cellular accumulation.

What occurs?

A

Fluid accumulating in cells- due to hypoxia- indicates severe cellular distress. Na+ and water flood into cell

46
Q

When and where does hydropic swelling occur?

A
  • Occurs when energy supplies are cut off e.g. hypoxia
  • Particularly occurs in the brain
47
Q

What is steatosis?

A
  • Steatosis is the accumulation of triglycerides
  • If mild, it is asymptomatic
48
Q

What is the most common site of steatosis?

A

Liver (major organ of fat metabolism)

49
Q

Identify 4 causes of steatosis

A
  • Alcohol
  • Diabetes mellitus
  • Obesity
  • Toxins
50
Q

What might cause choletserol to accumulate in cells?

A
  • Cannot be broken down and is insoluble
  • Can only be eliminated through the liver
  • Excess stored in cell in vesicles
51
Q

How are foam cells formed?

A

Foam cells formed from:

cholesterol accumulating in the smooth muscle cells + macrophages of atherosclerotic plaques

52
Q

Where are xanthomas found?

A

Xanthomas:

  • present in macrophages in skin and tendons
    • -people with hereditary hyperlipidaemias
53
Q

How do protein accumulations appear in tissues?

A
  • Look like eosinophilic droplets
  • Look like aggregations in the cytoplasm
54
Q

How would an α1-antitrypsin deficiencyn cause abnormal protein accumulation in cells?

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

–>(emphysema) (proteases in lungs act unchecked)

55
Q

When might endogenous pigments accumulate in cells?

A
  • Tatoos:
      • Phagocytosed by macrophages in dermis and remains there
      • Some pigment will reach draining lymph nodes
  • Haemosiderosis:
    • ​-deposition haemosiderin in many organs (caused by blood transfusions/haemolytic anaemias
    • HAEMOSIDERIN=iron storage molecule- derived from haemoglobin. If in excess=bruise
56
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)
57
Q

What is pathological calcification?

A

Pathological calcification is the abnormal deposition of calcium salts within tissues

58
Q

What are the 2 types of pathological calcification?

A
  • Dystrophic calcification (local – more common)
  • Metastatic calcification (general)
59
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

60
Q

Identify 4 locations where dystrophic calcification occurs

A
  • An area of dying tissue
  • Atherosclerotic plaques
  • Aging or damaged heart valves
  • Tuberculous lymph nodes
61
Q

What is metastatic calcification?

A

Metastatic calcification :

  • hydroxyapatite crystals are deposited in normal tissues throughout the body
  • due to hypercalcaemia secondary to disturbances in calcium metabolism

(can regress if cause corrected)

62
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
63
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

64
Q

What causes jaundice?

A

Accumulation of bilirubin

65
Q

What is bilirubin?

A

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

66
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
67
Q

What is chronic hepatitis?

A

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

68
Q

Identify 5 laboratory features of hepatitis

A
  • Raised serum ALT, AST and LDH
  • Raised bilirubin
  • Decreased albumin
  • Raised PT (prothrombin)
  • Raised ammonia
69
Q

Identify 3 laboratory features of alcoholic liver disease

A
  • Raised bilirubin
  • Raised alkaline phosphatase
  • Raised gamma GT (glutamyl transpeptidase)
70
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
71
Q

How do we take measurements to identify myocardial infarctions?

A

Measure blood levels:

  • intracellular macromolecules that leak out of injured myocardial cells
72
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
73
Q

What are the 4 different types of hypoxia and how are they caused?

A
  1. Hypoxaemic hypoxia: O2 arterial content=low eg high altitude
  2. Anaemic hypoxia: Oxygen carrying capacity of blood=reduced eg CO poisoning
  3. Ischaemic hypoxia: blood supply interuption
  4. Histiocytic hypoxia: disabled oxidative phosphorylation, inability to use oxygen eg cyanide poisoning
74
Q

When and what causes free radicals to be produced? (5)

A
  1. Normal metabolic rxns eg oxidative phosphorylation
  2. Radiation
  3. Inflammation: oxidative burst of neutrophils
  4. Contact with unbound metals in body eg iron
  5. Drugs and chemicals
75
Q

What are the types of necrosis? (4)

A
  1. Coagulative -most cases
  2. Liquefactive (colliquitive) -brain
  3. Caseous
  4. Fat necrosis
76
Q

Differentiate between the 2 main types of necrosis.

A
77
Q

What are the consequences of potassium levels in the blood getting to high?

A

Arythmia, ventricular fibrillation, tachycardia

78
Q

How does apoptosis occur?

A
  1. Equal and opposite force to mitosis
  2. Enzymes activated
  3. Membrane integrity maintained
  4. NOT using lysosomal enzymes
  5. Quick- few hours
79
Q

What causes abnormal cellular accumulations?

A
  • Metabolism of cell=deranged.
  • Sublethal/chronic injury
80
Q

What is a xanthoma?

A

Abnormal accumulation of cholestrol/ lipid in skin

81
Q

What accumulation in the liver cells might we see with alchoholic liver disease?

A

Mallory’s hyaline

82
Q

What is hereditary haematochromatosis?

A
  1. Increased intestinal absorption-dietary iron
  2. Iron= deposited in skin, liver, pancreas etc
  3. (Associated w./ liver and pancreas cirrhosis)
  4. Causes:
    1. Liver damage
    2. Heart dysfunction
  5. =bronze diabetes

Treatment= repeated bleeding to expel iron

83
Q

Whar are the 2 main causes of hypercalcaemia?

A

1) Increase secretion- PTH (stimulates osteoclast activity)
2) Destruction of bone tissue

84
Q

What are the 3 different causes of increased PTH secretion?

A
  1. Primary-tumour/parathyroid hyperplasia
  2. Secondary- renal failure&retention of phosphate
  3. Ectopic- malignant tumours
85
Q

What may cause destruction of bone tissue?

A
  1. Primary tumours of bone marrow eg leukaemia
  2. Paget’s disease of bone (acclerated bone turnover)
  3. Immobilisation
86
Q

Why can’t cells live forever?

A

Cells age, accumulate damage

Telomeres shorten- eventually length=critical

87
Q

What is the function of telomerase?

A

Maintain original length to telomere- present in germ cells

(many cancer cells have telomerase)

2 Pathological Processes (12 decks)

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