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ESA 2 Mech Of Disease > Cell Injury > Flashcards

Cell Injury Flashcards

0
Q

With a severe change in environment what are the 3 main outcomes for cells?

A
  • Cell adaption
  • Cell injury
  • Cell death
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1
Q

What is the definition of disease?

A
  • Consequence of failed homeostasis with consequent morphological and functional disturbances
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2
Q

What does the degree of injury depend on?

A
  • Type
  • Severity
  • Type of tissue
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3
Q

What is hypoxiaemic hypoxia?

A
  • Arterial O2 content is low
  • Reduced inspired PO2 at altitude
  • Decreased absorption
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4
Q

What is anaemic hypoxia and what are the possible causes?

A
  • Decreased ability of Hb to carry O2
  • Anaemia
  • Co poisoning
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5
Q

What is Ischaemia what are the possible causes and consequences?

A
  • Interruption of blood supply
  • Blockage of a vessel
  • Heart failure
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6
Q

What is histiocytic hypoxia and the possible causes?

A
  • Inability to utilise O2 in cells due to disabled oxidative phosphorylation enzymes
  • Cyanide poisoning
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7
Q

Give examples of possible toxins to cells.

A
  • Poisons
  • Alcohol
  • Increased concentration of O2
  • Pollutants
  • Medicines
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8
Q

What is a hypersensitivity reaction?

A
  • Host’s tissues are injured due to an overly vigorous immune reaction
  • e.g urticaria
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9
Q

What is autoimmune damage?

A
  • When immune system fails to distinguish self from non-self
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10
Q

What are the biochemical results of ischaemia and why?

A
  • Decreased ox. phosphorylation of mitochondria -> decreased ATP
  • Decreased Na/K pump -> Increased Ca/Na/H2O, decreased K -> cellular swelling/loss of microvilli/ER swelling/myelin figures
  • Increased glycolysis -> decreased pH/glycogen -> clumping of nuclear chromatin
  • Detachment of ribosomes -> decreased protein syn. -> lipid deposition
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11
Q

What is the main free radical injury and what can this go on to do?

A
  • Lipid peroxidation -> more free radicals -> autocatalytic chain reaction
  • Attacks other proteins/carbs/DNA -> mutagenic
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12
Q

What are the cellular defences to free radicals?

A
  • Enzymes
  • Vit A/C/E are free radical scavengers
  • Storage proteins
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13
Q

What is the link between ischaemia and free radical damage?

A
  • Reperfusion injury: blood flow returned to damaged cell

- Increased O2 free radicals with re-oxygenation

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14
Q

Heart shock proteins are a defence against cell injury, what do they do?

A
  • Mends misfolded proteins and maintains cell viability

- Via unfoldases/chaperones

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15
Q

What is oncosis?

A
  • Process of cell death with swelling.

- Spectrum of changes that occurred in injured cells prior to death

16
Q

What is necrosis?

A
  • Morphological changes in a living organism
17
Q

What is apoptosis?

A
  • Shrinkage
  • Induced by a regulated intracellular programme where a cell activates enzymes that degrades it’s own nuclear DNA and proteins
18
Q

What is coagulative necrosis?

A
  • Denaturation of proteins dominates over release of active proteases
  • Ghost outline of cells
19
Q

What is Liquefactive necrosis?

A
  • Enzyme degradation’s substantially greater than denaturation
  • Leads to enzymatic digestion (liquefaction) of tissues
20
Q

What is caseous necrosis and what does it look like?

A
  • Structureless debris

- Cheese

21
Q

What are the causes of the following:

  • Dry gangrene
  • Wet gangrene
  • Gas gangrene
A
  • Dry: dehydrated necrosis
  • Wet: liquefactive necrosis
  • Gas: anaerobic bacteria
22
Q

What is an infarction?

A
  • Tissue death caused by obstruction of tissue’s blood supply
  • Ischaemia necrosis
23
Q

What is a white infarct?

A
  • Solid tissue

- End arteries affected so no blood supply.

24
Q

What is a red infarct?

A
  • Haemorrhage
  • Dual blood supply
  • Obstruction of venous pressure builds up hence red colour.
25
Q

What does the consequences of infarct depend on?

A
  • Alternative blood supply
  • Speed of ischaemia
  • Tissues involved
  • O2 content of blood.
26
Q

During cell death potassium can leak from cells what effect can it have on the body?

A
  • Toxic to the heart
  • Can damage heart if damaged heart cells or massive necrosis
  • Tumour lysis syndrome
27
Q

How can enzymes be used for diagnosis?

A
  • Enzymes with smallest molecular weight are released first so can be used to pinpoint the damage area.
28
Q

How does physiological apoptosis work and what’s its use in embryonic development?

A
  • Kills individual cells if infected
  • Apoptotic cells are in inter-digital web space so need to break down otherwise -> webbed digits
  • Helps to sculpt during embryonic development
29
Q

What is pathological apoptosis?

A
  • Destruction of cell due to faulty DNA
30
Q

Draw a condensation, fragmentation cell and apoptotic bodies

A
  • Condensation: very curvy
  • Fragmentation: almost spikey
  • Apoptotic bodies: droplets
31
Q

What needs to be activated before apoptosis will occur?

A
  • Capsases
32
Q

What is intrinsic apoptosis?

A
  • Mainly when DNA damage has occurred
  • Mitochondria become more permeable
  • Cytochrome C is released
  • Caspases activated
33
Q

What is extrinsic apoptosis?

A
  • TRAIL and FAS ligands bind to ‘death receptors’ this activates caspases mediating apoptosis
34
Q

Why may abnormal accumulations occur?

A
  • Cell’s own metabolism
  • Extracellular space e.g spilled blood
  • Outer environment e.g dust
35
Q

What are the 5 main groups of Intracellular accumulations?

A
  • Water & electrolytes
  • Lipids
  • Carbohydrates
  • Proteins
  • Pigments
36
Q

What happens in aspirin overdose?

A
  • Arachidonic acid -> COX 1 -> Protective prostaglandins -> stomach mucosa / Platelet stickiness
  • Arachidonic acid -> COX 2 -> Inflammatory prostaglandins -> pain/inflam/fever

ESA 2 Mech Of Disease (11 decks)

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