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YR 3 - Illness and Wellbeing > Pathology - Cell Injury/Death > Flashcards

Pathology - Cell Injury/Death Flashcards

1
Q

What are the 3 Cellular Responses that can occur as a result of Cellular Stress?

A

Adaption
Reversible Cell Injury
Irreversible Cell Injury/Death

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2
Q

What is Adaption?

A

the cell tries to adapt to changes in the environment by adjusting its phenotype

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3
Q

What is hypertrophy? 2 types

A

no new cells, cells increase in size

occur physiologically
- body building, muscle fibre increases

occur pathologically
- cardiac hypertrophy from the increase of myocyte size
- from stress and high BP

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4
Q

What is Hyperplasia? 2 types.

A

increased numbers of cells usually from hormones or growth factors, organ size increase

occur physiologically
- hormonal e.g. breast in pregnancy

occur pathologically
- benign tumours

NOT NEOPLASIA - NOT UNCONTROLLED CELL GROWTH

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5
Q

What is Atrophy? 2 types.

A

decrease in cell size and number, organ size decreases

physiological
- post partum uterus

pathological
- decrease workload - waste away
- denervation - no nerve supply
- no blood supply
- inadequate nutrition

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6
Q

What is Metaplasia

A

one differentiated cell type is replaced by another - may be able to better withstand the environment

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7
Q

Give examples of Metaplasia for Adaption in the oesophagus, lungs and cervix

A

oesophagus
- GORD
- acid reflux
- squamous cells
- into gastric-like columnar epit. cells
= Barretts Oesophagus

lungs
- cigarettes
- usual columnar cells
- into squamous cells - more resistant

cervix
- vaginal ph drops
- usual columnar cells
- into squamous cells

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8
Q

basic causes of cell injury (8)

A
  • oxygen deprivation HYPOXIA
  • physical/environmental - trauma, heat, cold, radiation
  • chemical agents - drugs
  • infectious agents - virus, bacteria, parasite
  • immunologic reactions
  • genetic derangements
  • nutritional imbalances - excess or deficiencies
  • ageing
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9
Q

what does oxygen deprivation cause a decrease of?

A

less/no production of ATP

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10
Q

what can oxygen deprivation lead to?

A
  • loss of blood supply
  • ischaemia
  • increase in carbon monoxide
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11
Q

What 6 Mechanisms are Responsible for Cell Injury?

A ROS Might Cause Modified DNA

A
  1. ATP Depletion
  2. Increase of ROS
  3. Mitochondrial Damage
  4. Entry of Ca2+
  5. Membrane Damage
  6. Protein Misfiling, DNA Damage
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12
Q
  1. 3 Purposes of ATP
A

membrane transport
maintain chemical gradient
protein, dna and rna synthesis

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13
Q
  1. how can atp production be impaired? (2)
A

mitochondrial damage
hypoxia

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14
Q
  1. What are the 3 Effects of ATP Depletion, expand on them.
A

na pump depletes
more anaerobic respiration
detachment of ribosomes

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15
Q
  1. Mitochondrial Damage can be Direct or Indirect. How?
A

direct - hypoxia, toxins, radiation
indirect - influx of Ca2+, oxidative stress, phospholipid breakdown

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16
Q
  1. Can mitochondrial damage be reversed?
A

early it can

if sustained, it becomes irreversible

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17
Q
  1. How does Mitochondrial Damage become Irreversible?
A

Necrosis or Apoptosis

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18
Q
  1. Describe Necrosis from Mitochondrial Damage (7)
A

DIRECT DAMAGE
- mitochondria gets damaged
- MPTP forms - mitochrondrial permeability transition pore
- impair oxidative phosphorylation
- ATP depletion
- increased production of ROS
- multiple cellular abnormalities
- necrosis

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19
Q
  1. Describe Apoptosis from Mitochondrial Damage/
A

INDIRECT DAMAGE
- increase pro-apoptotic proteins
- decrease anti-apoptotic proteins
- mitochondrial proteins leak
- apoptosis

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20
Q
  1. How do you get a Calcium Pump Failure?
A

from hypoxia/toxins
- lack of ATP

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21
Q
  1. should the levels of regular cystolic calcium be high or low?
A

low

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22
Q
  1. what happens if there is calcium pump failure?
A
  • release of calcium from mitochondria
  • increase of membrane permeability
  • calcium into the systole
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23
Q
  1. why is it bad for there to be increase calcium within the cell?
A

activation of harmful intracellular enzymes

24
Q
  1. give 3 harmful intracellular enzymes and 3 effects
A

ATPases - ATP into ADP

phospholipases - cleave ester bond within phospholipids - lipid products are generated

endonucleases - cleave phosphodiester bond within polynucleotide chain - cut DNA

LESS ATP
DISRUPT CELL MEMBRANE
DNA DAMAGE

25
Q
  1. what are free radicals?
A

single unpaired radical

26
Q
  1. what is a ROS?
A

Reactive Oxygen Species

27
Q
  1. increased ROS lead to..
A

oxidative stress

28
Q
  1. how is oxidative stress caused?
A

increased production of ROS

29
Q
  1. how can ROS come about? (4)
A
  • ionising radiation
  • ischaemia reperfusion injury
  • metals (iron/copper) or chemicals (CCl4)
  • nitric oxide - leads to inflammation
30
Q
  1. what is ischaemia reperfusion injury
A

the death and dysfunction of cells after blood flow is restored to previously ischaemic tissues

31
Q
  1. what does ROS do in the cell? (3)
A
  • damage cell membrane
  • break nucleic acid
  • protein oxidation and fragmentation
32
Q
  1. which three ways can membrane be damaged?
A

direct - bacteria, virus, immune proteins

indirect - increase calcium, ros, decrease ATP

lysosomal membrane damage - auto-digestion

33
Q
  1. what can protein misfolding lead to?
A

ER stress

34
Q
  1. what does ER stress end in?
A

apoptosis

35
Q

What 2 Microscopic Features do you see in REVERSIBLE CELL INJURY?

A
  • cellular swelling
  • fatty change
36
Q

what does ultrastructural mean?

A

the biological structure not visible through ordinary microscope

37
Q

What 4 Ultrastructural Features do you see in REVERSIBLE CELL INJURY?

A
  • plasma membrane bulge
  • mitochondria swells
  • ER dilates
  • chromatin clumps
38
Q

what are the two main forms of cell death?

A

apoptosis
necrosis

39
Q

describe apoptosis - contents and inflammation

A

programmed cell death
cell contents contained
no surrounding inflammation

40
Q

5 Instances of Physiological Apoptosis’ and what happens

A

Embryogensis - removal of unwanted cells during development

Hormone Withdrawal

Cell Turnover

Harmful self-reactive lymphocytes

death of host cells after immune response

41
Q

4 Instances of Pathological Apoptosis

A

from DNA damage - radiation/drugs/free radicals

accumulation of misfolded proteins

Infections - direct or indirect

Pathological Atrophy

42
Q

Give 2 Pathways for Apoptosis.

A

mitochondrial intrinsic pathway
death receptor extrinsic pathway

43
Q

Describe Mitochondrial Instrinsic Pathway - Apoptosis

A
  • DNA damage
  • pro-apoptotic proteins leak
  • caspases activate
  • fragmentation of contents
    = apoptotic bodies
  • engulfed by phagocytes
  • broken down
44
Q

Describe Death Receptor Extrinsic Pathway - Apoptosis

A
  • extrinsic ligand binds to cell surface receptor
  • activates caspases
  • fragmentation of contents
    = apoptotic bodies
  • engulf by phagocytes
  • break down
45
Q

Under a microscope, how does apoptosis appear?

A
  • cell shrinks
  • chromatin condenses
  • cytoplasm blebs - blisters
  • no surrounding damage
46
Q

describe necrosis - contents and inflammation

A

membrane breakdown
- contents leak
- inflammation

47
Q

compare necrosis to apoptosis in terms of: cell size, nucleus, plasma membrane, nearby inflammation, physiological or pathological

A
48
Q

Give 6 Types of Necrosis
CCCGFF

A

Coagulative
Colliquative
Caseous
Gangrene
Fat
Fibrinoid

49
Q

Where does Coagulative Necrosis Occur, how does it appear?

A

tissues with connective tissue e.g. heart
- the shape/structure is still preserved

50
Q

Where does Colliquitive Necrosis Occur, how does it appear?

A

tissues with minimal connective tissue e.g. brain
- the shape liquefies

51
Q

Where does Caseous Necrosis Occur, how does it appear?

A

usually see in an abscess or granulomatous inflammation
- cheese-like necrotic debris in a defined border

52
Q

Where does Gangrene Occur, what are the 3 types and how they arise?

A

it is coagulative necrosis but of a limb
dry gangrene - coagulative necrosis sterile
wet gangrene - with infection
gas gangrene

53
Q

Where does Fat Necrosis Occur and why does it appear?

A

specific pattern necrosis in fat
- due to action of lipases or traumatic injury to the fat

54
Q

Where does Fibrinoid Necrosis Occur, how does it appear?

A

specific necrosis when damage to vessel walls
- get a pink material deposited in the vessel wall

55
Q

How Clinical Diagnosis’ be Reached from Necrosis or Apoptosis e.g. myocardial infarction, pancreatitis

A

Myocardial Infarction
- myocardial enzymes released into blood e.g. Troponin
- this then acts as a biomarker for diagnostic tests

pancreatitis
- necrosis
- enzymes released into blood
= more amylase
= more lipase
- leads to saponification = less Ca2+ in the blood

Apoptosis can be seen microscopically

YR 3 - Illness and Wellbeing (31 decks)

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