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Semester 2 Pathological Processes > L2/3: Cell Injury and Cell Death > Flashcards

L2/3: Cell Injury and Cell Death Flashcards

1
Q

How do cells respond to changes in the environment?

A

Maintain homeostasis
Mild changes–> effective mechanisms
Severe changes–> cell adaptation, injury or death

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2
Q

What does the degree of cell injury depend on?

A

Type injury
Severity
Duration
Type of tissue

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3
Q

What can cause injury to a cell?

A 
Hypoxia
Toxins
Physical agents --> trauma, extreme temp change, pressure change, electric currents
Radiation 
Micro-organisms
Immune mechanisms 
Dietary --> insufficiency, deficiencies and excess 
Chemicals 
Genetic factors
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4
Q

What is hypoxia?

A

Cell deprived of O2

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5
Q

What are the different types/causes of hypoxia?

A

Hypoxaemic –> low arterial O2
Anaemic –> Functional heamoglobin level low
Ischaemic –> interuption to blood supply
Histiocytic –> tissue can’t utilise O2

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6
Q

Hypoxia vs ischaemia?

A

Hypoxia–> cells deprived of O2

Ischaemia–> loss of blood supply, lack O2 and other substances in blood

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7
Q

How does the immune system damage cells?

A

Hypersensitivity reactions–> overly vigorous immune reaction –> host cell injured
Autoimmune–> fails to distinguish self from non self, attacks own cells

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8
Q

Which parts of the cell are principal targets/ most susceptible to cell injury?

A

Cell membrane –> PM and organelle
Nucleus –> DNA
Mitochondria –> OP
Proteins –> Enzymes, structural

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9
Q

What are the two types of cell injury that can occur?

A

Reversible and Irreversible

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10
Q

What happens at the molecular level during hypoxia? (reversible)

A

Mitochondria starved–> no OP
No ATP produced
–> Na+/K+ ATPase stops –> Na+ and Ca2+ –> H20 follows –> swelling
–> ↑ glycolysis–> ↑lactic acid –>↓pH and ↓glycogen–> clumping of chromatin
–> detachment of ribosome –> ↓ protein synthesis–> lipid deposition

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11
Q

What happens at the molecular level during hypoxia? (irreversible)

A

↑ cystolic Ca2+

  • -> ATPase–> ↓ ATP
  • -> ↓ phospholipase–> decreased phospholipids
  • -> protease–> disruption of membrane and cytoskeleton proteins
  • -> endonucleases–> Chromatin damage
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12
Q

How do other methods (not hypoxia) cause cell injury?

A

Often have similar outcome
Attack different key proteins/structures
Frostbite and free radical –> damage membrane

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13
Q

What are free radicals?

A

Single unpaired electron in outer orbit

Reacts –> further free radicals

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14
Q

What are the three important free radicals? (ROS)

A

Hydroxyl (OH•)
Superoxide (O2-)
Hydrogen peroxide (H2O2)

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15
Q

When are free radicals produced?

A
  1. Metabolic reactions –> ETC
  2. Inflammation –> Neutrophils NET
  3. Radiation H20 –> OH•
  4. Contact unbound metals in body–> copper and iron
  5. Drugs and chemicals
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16
Q

How does the body deal with oxidative damage?

A

Antioxidants scavenger–> donate electrons Vit E, C and A
Metal carrier and storage proteins –> sequester iron and copper
Enzymes–> neutralise (superoxide dismutase (SOD), Catalase and glutathione (glutathione peroxidase))

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17
Q

How do free radicals cause injury?

A

Oxidative imbalance= free radicals > antioxidant
Target lipids e.g. plasma membrane,
–>Lipid peroxidation –> autocatalytic chain reaction
Proteins, carbs and DNA
–> change shape
–> broken or cross linked
–> mutagenic and carcinogenic

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18
Q

What are heat shock proteins?

A

E.g. ubiquitin
Mend misfolded proteins
Maintain cell viability
Unfoldase and Chaperonins

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19
Q

What do injured and dying cells look like under a light microscope?

A

Injured–> swelling, watery looking cytoplasm
Dead–> cytoplasm = pink, nucleus shrinks, abnormal intracellular accumulations
nucleus –> pyknosis (condensed DNA) –> karyorrhexis (fragmentation) –> karyolysis (nuclear fading)

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20
Q

What do injured and dying cells look like under EM?

A

Reversible –> Swelling (Na+/K+pump failure)

  • -> Cytoplasmic blebs
  • -> Clumped chromatin (reduced pH)
  • -> Ribosome separates from ER–> require ATP
  • -> Autophagosomes

Irreversible –> Increased cell swelling

  • -> Nuclear changes pyknosis (condensed DNA) –> karyorrhexis (fragmentation) –> karyolysis (nuclear fading)
  • -> Lysosomes swelling and rupture
  • -> Membrane defects
  • -> Myelin figures –> damaged membranes
  • -> ER lysis –> membrane defects
  • -> Swollen mitochondria –> amorphous densities
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21
Q

Where do abnormal cellular accumulations come from?

A

Derranged metabolic processes (Na+/K+ ATPase dysfunction)
Can be reversible
Sublethal or chronic
Harmless or toxic
Obtain from –> cell metabolism, EC space (spilled blood), outer environment (dust)

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22
Q

What are the 5 main intracellular accumulations?

A
  1. Water and electrolytes
  2. Lipids
  3. Carbohydrates
  4. Proteins
  5. Pigments (endo and exogenous)
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23
Q

What causes lipids to accumulate in cells? What is it called?

A

Alcohol, diabetes mellitus, obesity, toxins

Steatosis–> often in liver

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24
Q

What happens when cholesterol accumulates in cells?

A

Can’t be broken down, excess stored in liver vesicles

Stored SMC and macrophages –> foam cells

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25
Q

What does hyperlipidaemias cause?

A

Xanthomas–> lipid in tendons and skin macrophages

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26
Q

Under what conditions do proteins accumulate in cells?

A

Forms eosinophilic droplets or aggregations in cytoplams
Alcoholic liver disease (Mallory’s hyaline)
alpha1- antitrypsin deficiency
–> incorrectly folded alpha1 (protease inhibitor)
–> not packages or secreted
–> systemic deficiency–> proteases in lung act unchecked resulting in emphysema

27
Q

When do pigments accumulated inside cells?

A 
Exogensous 
Urban air pollution 
--> inhaled and phagocytoses
--> lungs--> disease --> anthracosis and blacked peribronchial lymph nodes
--> can causes fibrosis--> emphysema
Tatooing
--> phagocytosed--> remains in dermis

Endogenous
Haemosidernin –> bruise (local) and haemosiderosis (systemic)
–> iron storage molecule
–> yellow brown

28
Q

What is hereditary haemochromatosis?

A 
Genetic
Increased intestinal absorption of iron
Deposited--> skin, liver, pancreas, heart, endocrine organs--> scaring (cirrhosis)
Bronze diabetes
Treatment: repeated bleeding
29
Q

What is jaundice?

A

Accumulation of bilirubin (yellow)
Product of heme (porphyrin rings)
Albumin takes to liver conjugated with bilirubin –> bile
Bile flow obstructed or overwhelmed –> jaundice
Bilirubin stored extracellularly in tissues or macrophages

30
Q

What are the four main mechanisms of intracellular accumulations?

A
  1. abonormal metabolism
  2. alterations in protein folding and transport
  3. deficiency of critical enzymes
  4. inability to degrade phagocytosed particles
31
Q

What causes calcification of tissues?

A

Abnormal deposit of calcium salts in tissues.
Localised (dystrophic) or generalised (metastatic)
Dystrophic –> more common –> dying tissue, atherosclerotic plaques, againg or damaged heart valves, tuberculus lymph nodes and some malignancies

32
Q

Why does dystrophic calcification occur?

A

No abnormalities in calcium metabolism etc…
Local change/ disturbance favours nucleation of hydroxyapeptite crystals,
causes organ dysfunction

33
Q

What cause hypercalcaemia?

A

Hypercalcaemia–> distribance in metabolism
Cause by
–> ↑ PTH secretion –> ↑bone resorption
–> primary = parathyroid hyperplasia or tumour
–> secondary = renal failure and retention of phosphate
–> ectopic –> PTH secreted from elsewhere malignant tumours
–> Destruction of bone tissue
–> Primary tumours or bone marrow
–> Diffuse skeletal metastases
–> Paget’s disease of bone –> accelerated bone turnover
–> Immobilisation

34
Q

Define oncosis?

A

Cell death with swelling

Changes that occur in injured cells prior to death

35
Q

Define necrosis?

A

Morphologic changes that occur after a cell has been dead sometime
seen 12-24 hrs later

36
Q

What are the two types of necorosis? What are the two special types?

A

Main: Coagulative and Liquefactive

Special types: Caseous and fat necrosis

37
Q

What is coagulative necrosis?

A

Dying cells–> proteins denature–> coagulate
Cell architecture preserved
Normally ischaemia of solid organs (heart, kidneys, spleen)

38
Q

What is liquefactive necrosis?

A

Dying cells–> enzyme degradation (autolysis) of proteins (greater than denaturation), cells fall apart, enzymatic digestion (liqufaction) of tissues
Cells lost
Mainly loose tissues (Lungs, brain)

39
Q

What is caseous necrosis?

A

Structureless debris
Cells split up
Associated with infections

40
Q

What is fat necrosis?

A

Destruction of adipose tissue –> release fatty acids

Accumulates –> like candle wax???????

41
Q

Define gangrene?

A

Necrosis visible to the eye

42
Q

Define infarction?

A

Necrosis caused by reduction in arterial blood flow

43
Q

Define infarct?

A

Area of necrotic tissue, result of loss of arterial blood supply

44
Q

What is the difference between dry and wet gangrene?

A

Dry–> necrosis –> exposure to air

Wet–> necrosis –> infection

45
Q

What is gas gangrene?

A

Infection caused by anaerobic bacteria that produce gas

46
Q

What causes infarction?

A

Blockage to blood supply
Heart–> thrombosis (thrombus)
Brain–> embolism (small bit of thrombus broken off)

47
Q

What is the difference between red and white infarction?

A

Indicates amount of heamorrhage
White–> anaemic infarct–> solid organs –> occlusion of end artery –> wedge shaped necrosis–> coagulative necrosis
Red–> heamorrhagic infarct–> blood into dead tissue–> loose tissue –> good perfusion

48
Q

What determines outcome after infarction?

A

Whether there is

  • alternative blood supply
  • speed of ischaemia
  • tissue involved
  • O2 content of blood
49
Q

What is ischaemia-reperfusion injury?

A

Blood flow returned to tissue before necrosis
Outcome worse
Possibly because:
- ↑ free radicals = result of burst mitochondrial activity
- ↑ neutrophils = more inflammation
- Delivery of complement proteins and activation of pathway

50
Q

What happens when membrane integrity is lost?

A 
Molecules leak out as well as in
Consequences:
- local inflammation and irritation
- general toxic effects
- Used for diagnosis as ↑ levels in blood
51
Q

What can leak out?

A

Potassium- hyperkalemia (cardiac problems)
Enzymes - Useful for diagnosis (tropoinin, creatin kinase)
Myoglobin- dead myocardium released

52
Q

What is apoptosis?

A 
Programmed cell death with shrinkage
Activates own enzymes --> degrade own DNA and proteins
Active process
Quick
No inflammatory response
53
Q

What are the characteristic of apoptosis?

A

Membrane integrity maintained
Non random internucleosomal cleavage of DNA
Lysosomes not involved

54
Q

When does apoptosis occur physiologically?

A

Embryogenesis
Hormone controlled involution
Maintain steady state

55
Q

When does apoptosis occur pathologically?

A

Damaged cells
Cytotoxic T cells kill neoplastic or virus infected cells
Graft vs host disease

56
Q

What is the process of apoptosis?

A

Three phases:

  • Initiation
  • Execution
  • Degradation and phagocytosis
57
Q

What happens during initiation and execution?

A

Intrinsic and extrinsic mechanisms

Activation of caspases –> cleavage of DNA and cytoskeletal proteins

58
Q

Initiation of the intrinsic pathway of apoptosis is caused by what?

A

Irreparable DNA damage, withdrawal of GF hormones
Activate p53 –> mitochondrial membrane leaky
Cytochrome C –> released activates caspases

59
Q

Initiation of the extrinsic pathway is caused by what?

A

Cells in danger

T killer cells –> TNF alpha –> bind to death receptor –> activated caspases

60
Q

What causes apoptotic bodies to be phagocytosed?

A

Inititation and execution result in shrinkage
Proteins expressed on surface
Phagocytes or neighbouring cells uptake and degrade

61
Q

Compare and contrast oncosis/necrosis and apoptosis?

A

Slide 60

62
Q

Can cells live forever?

A

Only cells protected by telomeres- germ cells and stem cells
Telomerase enzyme maintains original length of telomeres
Rest accumulate DNA damage or reach replicative senesence –> telomere shortened to critical lenght

63
Q

How have cancer cells adapted to replicate many times?

A

Produce telomerase enzyme maintain length of telomeres.

Semester 2 Pathological Processes (16 decks)

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