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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
What does hyperlipidaemias cause?
Xanthomas--> lipid in tendons and skin macrophages
26
Under what conditions do proteins accumulate in cells?
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
When do pigments accumulated inside cells?
``` 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
What is hereditary haemochromatosis?
``` Genetic Increased intestinal absorption of iron Deposited--> skin, liver, pancreas, heart, endocrine organs--> scaring (cirrhosis) Bronze diabetes Treatment: repeated bleeding ```
29
What is jaundice?
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
What are the four main mechanisms of intracellular accumulations?
1. abonormal metabolism 2. alterations in protein folding and transport 3. deficiency of critical enzymes 4. inability to degrade phagocytosed particles
31
What causes calcification of tissues?
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
Why does dystrophic calcification occur?
No abnormalities in calcium metabolism etc... Local change/ disturbance favours nucleation of hydroxyapeptite crystals, causes organ dysfunction
33
What cause hypercalcaemia?
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
Define oncosis?
Cell death with swelling | Changes that occur in injured cells prior to death
35
Define necrosis?
Morphologic changes that occur after a cell has been dead sometime seen 12-24 hrs later
36
What are the two types of necorosis? What are the two special types?
Main: Coagulative and Liquefactive | Special types: Caseous and fat necrosis
37
What is coagulative necrosis?
Dying cells--> proteins denature--> coagulate Cell architecture preserved Normally ischaemia of solid organs (heart, kidneys, spleen)
38
What is liquefactive necrosis?
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
What is caseous necrosis?
Structureless debris Cells split up Associated with infections
40
What is fat necrosis?
Destruction of adipose tissue --> release fatty acids | Accumulates --> like candle wax???????
41
Define gangrene?
Necrosis visible to the eye
42
Define infarction?
Necrosis caused by reduction in arterial blood flow
43
Define infarct?
Area of necrotic tissue, result of loss of arterial blood supply
44
What is the difference between dry and wet gangrene?
Dry--> necrosis --> exposure to air | Wet--> necrosis --> infection
45
What is gas gangrene?
Infection caused by anaerobic bacteria that produce gas
46
What causes infarction?
Blockage to blood supply Heart--> thrombosis (thrombus) Brain--> embolism (small bit of thrombus broken off)
47
What is the difference between red and white infarction?
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
What determines outcome after infarction?
Whether there is - alternative blood supply - speed of ischaemia - tissue involved - O2 content of blood
49
What is ischaemia-reperfusion injury?
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
What happens when membrane integrity is lost?
``` Molecules leak out as well as in Consequences: - local inflammation and irritation - general toxic effects - Used for diagnosis as ↑ levels in blood ```
51
What can leak out?
Potassium- hyperkalemia (cardiac problems) Enzymes - Useful for diagnosis (tropoinin, creatin kinase) Myoglobin- dead myocardium released
52
What is apoptosis?
``` Programmed cell death with shrinkage Activates own enzymes --> degrade own DNA and proteins Active process Quick No inflammatory response ```
53
What are the characteristic of apoptosis?
Membrane integrity maintained Non random internucleosomal cleavage of DNA Lysosomes not involved
54
When does apoptosis occur physiologically?
Embryogenesis Hormone controlled involution Maintain steady state
55
When does apoptosis occur pathologically?
Damaged cells Cytotoxic T cells kill neoplastic or virus infected cells Graft vs host disease
56
What is the process of apoptosis?
Three phases: - Initiation - Execution - Degradation and phagocytosis
57
What happens during initiation and execution?
Intrinsic and extrinsic mechanisms | Activation of caspases --> cleavage of DNA and cytoskeletal proteins
58
Initiation of the intrinsic pathway of apoptosis is caused by what?
Irreparable DNA damage, withdrawal of GF hormones Activate p53 --> mitochondrial membrane leaky Cytochrome C --> released activates caspases
59
Initiation of the extrinsic pathway is caused by what?
Cells in danger | T killer cells --> TNF alpha --> bind to death receptor --> activated caspases
60
What causes apoptotic bodies to be phagocytosed?
Inititation and execution result in shrinkage Proteins expressed on surface Phagocytes or neighbouring cells uptake and degrade
61
Compare and contrast oncosis/necrosis and apoptosis?
Slide 60
62
Can cells live forever?
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
How have cancer cells adapted to replicate many times?
Produce telomerase enzyme maintain length of telomeres.

Semester 2 Pathological Processes (16 decks)

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