Pathology - Cell Injury/Death Flashcards

(55 cards)

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
4. what are free radicals?
single unpaired radical
26
4. what is a ROS?
Reactive Oxygen Species
27
4. increased ROS lead to..
oxidative stress
28
4. how is oxidative stress caused?
increased production of ROS
29
4. how can ROS come about? (4)
- ionising radiation - ischaemia reperfusion injury - metals (iron/copper) or chemicals (CCl4) - nitric oxide - leads to inflammation
30
4. what is ischaemia reperfusion injury
the death and dysfunction of cells after blood flow is restored to previously ischaemic tissues
31
4. what does ROS do in the cell? (3)
- damage cell membrane - break nucleic acid - protein oxidation and fragmentation
32
5. which three ways can membrane be damaged?
direct - bacteria, virus, immune proteins indirect - increase calcium, ros, decrease ATP lysosomal membrane damage - auto-digestion
33
6. what can protein misfolding lead to?
ER stress
34
6. what does ER stress end in?
apoptosis
35
What 2 Microscopic Features do you see in REVERSIBLE CELL INJURY?
- cellular swelling - fatty change
36
what does ultrastructural mean?
the biological structure not visible through ordinary microscope
37
What 4 Ultrastructural Features do you see in REVERSIBLE CELL INJURY?
- plasma membrane bulge - mitochondria swells - ER dilates - chromatin clumps
38
what are the two main forms of cell death?
apoptosis necrosis
39
describe apoptosis - contents and inflammation
programmed cell death cell contents contained no surrounding inflammation
40
5 Instances of Physiological Apoptosis' and what happens
Embryogensis - removal of unwanted cells during development Hormone Withdrawal Cell Turnover Harmful self-reactive lymphocytes death of host cells after immune response
41
4 Instances of Pathological Apoptosis
from DNA damage - radiation/drugs/free radicals accumulation of misfolded proteins Infections - direct or indirect Pathological Atrophy
42
Give 2 Pathways for Apoptosis.
mitochondrial intrinsic pathway death receptor extrinsic pathway
43
Describe Mitochondrial Instrinsic Pathway - Apoptosis
- DNA damage - pro-apoptotic proteins leak - caspases activate - fragmentation of contents = apoptotic bodies - engulfed by phagocytes - broken down
44
Describe Death Receptor Extrinsic Pathway - Apoptosis
- extrinsic ligand binds to cell surface receptor - activates caspases - fragmentation of contents = apoptotic bodies - engulf by phagocytes - break down
45
Under a microscope, how does apoptosis appear?
- cell shrinks - chromatin condenses - cytoplasm blebs - blisters - no surrounding damage
46
describe necrosis - contents and inflammation
membrane breakdown - contents leak - inflammation
47
compare necrosis to apoptosis in terms of: cell size, nucleus, plasma membrane, nearby inflammation, physiological or pathological
48
Give 6 Types of Necrosis CCCGFF
Coagulative Colliquative Caseous Gangrene Fat Fibrinoid
49
Where does Coagulative Necrosis Occur, how does it appear?
tissues with connective tissue e.g. heart - the shape/structure is still preserved
50
Where does Colliquitive Necrosis Occur, how does it appear?
tissues with minimal connective tissue e.g. brain - the shape liquefies
51
Where does Caseous Necrosis Occur, how does it appear?
usually see in an abscess or granulomatous inflammation - cheese-like necrotic debris in a defined border
52
Where does Gangrene Occur, what are the 3 types and how they arise?
it is coagulative necrosis but of a limb dry gangrene - coagulative necrosis sterile wet gangrene - with infection gas gangrene
53
Where does Fat Necrosis Occur and why does it appear?
specific pattern necrosis in fat - due to action of lipases or traumatic injury to the fat
54
Where does Fibrinoid Necrosis Occur, how does it appear?
specific necrosis when damage to vessel walls - get a pink material deposited in the vessel wall
55
How Clinical Diagnosis' be Reached from Necrosis or Apoptosis e.g. myocardial infarction, pancreatitis
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