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EMS MOD > cell injury and cell death > Flashcards

cell injury and cell death Flashcards

1
Q

what happens in left ventricular hypertrophy?

A

muscle of ventricle thickens

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2
Q

what is necrosis?

A

when there is irreversible cell death - long term cell injury and therefore cannot be repaired

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3
Q

what is oncosis?

A

oncosis is the pre lethal changes to cells that precede death

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4
Q

what are some cellular adaptions?

A

atrophy and hypertrophy

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5
Q

what happens in necrosis?

A

there is severe cell swelling and rupture

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6
Q

what is apoptosis?

A

it is internally controlled cell death

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7
Q

why does CO reduce oxygen transport?

A

it binds to Hb preferentially as it has a higher affinity for Hb than oxygen does - hypoxia

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8
Q

what can cause cell death?

A

CO, physical agents - trauma, radiation, temp, chemical agents - drugs, immunological reaction, infectious agent, genetic derangement and nutritional imbalances

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9
Q

what is the mode of action for trauma, acid, paracetamol OD, bacteria and radiation?

A 
mechanical disruption of tissue 
coagulates tissue proteins 
metabolites will bind to liver cell proteins and lipoproteins 
toxins and enzymes 
damage to DNA
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10
Q

why does ATP depletion result in death?

A

there is not enough energy for the cell so the tissue dies , loss of intercellular calcium hemostasis, oxygen and oxygen free radicals, defects in membrane permeability and irreversible mitochondrial damage

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11
Q

`what are the three types of cell injury?

A

reversible, irreversible or ischaemia/reperfusion

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12
Q

what is the basis of reperfusion?

A

damage on reperfusion mediated by oxygen free radicals

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13
Q

what is reversible?

A

pallor, hydropic change, vacuolar degeneration and cell swelling

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14
Q

what is irreversible?

A

lysosome or mitochondrial swelling, leakage of enzymes or damage to membrane

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15
Q

what happens if damage is left too long?

A

reversible goes to irreversible

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16
Q

how is a cascade of damage caused?

A

sever mitochondrial injury

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17
Q

what is characteristic of reversible?

A

decrease in generation of ATP, loss of cell membrane integrity and defects in protein synthesis, and DNA damage

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18
Q

what does persistent and excessive injury lead to and what are the characteristics of this?

A

irreversible damage
severe mitochondrial damage
extensive damage to plasma membranes
lysosome swelling

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19
Q

what happens in irreversible damage?

A

there is leakage of membranes, therefore leakage of enzymes leading to apoptosis

20
Q

what are three types of cell death?

A

necrosis, oncosis and apoptosis

21
Q

what are some examples of programmed cell death?

A

menstruation and losing webbed digits - individual cell deletion in physiological growth control and in disease

22
Q

how does atrophy result?

A

increased apoptosis in excessive cell loss

23
Q

what are the characteristics of atrophy?

A

cell shrinkage, DNA fragmentation, formation of apoptotic bodies

24
Q

how does reversible cell injury result in cell swelling?

A

decrease in ATP production, decrease in acitivity of Na/K pump, increased sodium in the cell, osmosis and water movement into the cell

25
Q

how does enzymatic degradation and apoptosis occur in irreversible cell damage?

A

there is damage to the lysosome, mitochondrial and plasma membrane resulting in lysosome enzyme release into cytosol, Calcium into the cell and Cyt C leakage. Ca activated proteases and other enzymes and with lysozymes this results in enzymatic degradation. Cyt C and Calcium activate caspaces resulting in apoptosis

26
Q

what is necrosis?

A

cell death that results from failure in bioenergy and loss of plasma membrane integrity - includes inflammation and repair

27
Q

what are the differences between apotosis and necrosis?

A

size: A - cell shrinkage in one cell, N - cell swelling in many cells
uptake: A - cell contents ingested by enighbouring cells with no inflammatory response, N - cell contents is ingested by macrophages and significant inflammation
membrane: A - membrane blebbing but still integrity, apoptotic bodies form and N - loss of membrane integrity and cell lysis occurs
organelles: A - mitochondria release pro-apoptotic proteins, chromatin condensation and non-random DNA degradation, N - organelle swelling and lysosomal leakage, random degradation of DNA

28
Q

does autophagy have an inflammatory response?

A

no - there is increased quantity of autophages formation - Atg proteins participation

29
Q

what can you see under microscope in necrosis?

A

disorganisation - inflammatory responses

30
Q

what types of necrosis are there?

A

fat, fibrinoid, coagulative, caseous, gangrenous or liquefactive

31
Q

what is an example of coagulative necrosis?

A

in MI

32
Q

what are the characteristics of coagulative necrosis?

A

it is the commonest form and happens in most cells, cells retain their outline and architecture is preserved but proteins coagulate, there is no proteolysis, and metabolic activity ceases. Proteins and enzymes are lost.

33
Q

what is liquefactive necrosis?

A

it is seen in the brain and is bacterial or fungal. It results in CNS hypoxia and is due to lack of substantial supporting stroma. It may result in neural tissue liquefying

34
Q

what is an example of gangrenous necrosis?

A

limb ischaemia

35
Q

what is gangrenous necrosis?

A

the types are wet, dry or gangrenous. The causes are infectious or bacterial. It is putrefaction of tissue and will appear black

36
Q

what can TB in lung cause?

A

it is the main cause of caseous necrosis and can cause military, cavitary or primary TB necrosis

37
Q

what is caseous TB?

A

it is structureless dead tissue that macrophages cannot digest

38
Q

how will caseous TB present in histology?

A

amorphous pink material in centre with necrotic debris and granulomas

39
Q

what are the causes of fat necrosis?

A

enzymes, trauma, panreatitis and excessive alcohol

40
Q

how will fat necrosis present?

A

loss of architecture, lots of vacuoles

41
Q

what 2 conditions is fibrinoid necrosis seen in and how does it present on histology?

A

malignant hypertension and autoimmune disease

wall of artery is bright pink with dark neutrophils

42
Q

what happens in mycocyte necrosis after an Mi?

A

enzymes are released - LDH, troponins and CK-MB - biomarkers for diagnosis

43
Q

what enzymes are released in pancreatic cell necrosis?

A

amylase

44
Q

where is troponin released from?

A

complex is released from actin filament

45
Q

how is apoptosis used in immune system?

A

death of post inflammatory neutrophils, virally infected cells and self reactive lymphocytes

EMS MOD (28 decks)

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