L1 Flashcards

(48 cards)

1
Q

If a cell’s adaptive capacity is surpassed..

A

They lose ability to respond to functional demands –> cell injury/ death

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2
Q

How to clinical signs (generally) present

A

they lag behind biochemical changes

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3
Q

General factors influencing Cell injury

A
  • cell type
  • physiological state
  • intensity and duration of exposure to aetiological agent
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4
Q

Define Hypertrophy

A

Inc cell size

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5
Q

Examples of cells influenced by Hypertophy

A

Physiological= muscle cells due to inc workload/ cells of uterus due to hormone induced changes

Pathological= chronic overload of cardiac cells

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6
Q

Define Hyperplasia

A

Inc cell proliferation

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7
Q

Examples of cells undergoing hyperplasia

A

Physiological= pregnant uterus and breast tissue undergoing hormonal changes

Pathological= excessive hormonal stimulation

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8
Q

Define Atrophy

A

Dec cell size

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9
Q

Examples of atrophied cells

A

Physiological= disuse of muscle cell

Pathological= Aging/ inadequate blood supply and nutrition

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10
Q

Define Metaplasia

A

Change in differentiation of cells.

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11
Q

Is Metaplasia reversible?

A

Yes

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12
Q

Define Displasia

A

Disordered growth mostly seen in squamous epithelial cells following chronic injury

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13
Q

Example of Metaplasia

A

E.g. pathological irritation by cigarette smoke causing ciliated pseudostratified columnar respiratory epithelial cells in airways to be replaced by stratified squamous epithelium

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14
Q

Generalised examples of Dysplasia

A
  • nuclear changes
  • variation in size / shape
  • disorderly arrangement
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15
Q

Describe the cell injury continuum

A

Normal cell homeostasis&raquo_space; Adaptive cell homeostasis (Hypertrophy, Atrophy)&raquo_space; Reversible cell injury (cloudy changes, fatty change)&raquo_space; Irreversible cell injury (oncosis, apoptosis)

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16
Q

Discuss Hypoxia

A
  • occurs in tissue due to circulatory disturbance
  • reduced O2 carrying capacity
  • disturbances of cell respiratory chain
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17
Q

Discuss physical agents causing cell injury

A

e. g. heat/ trauma/ radiation

- often exacerbated by subsequent hypoxia due to local vascular damage

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18
Q

Discuss chemical agents causing cell injury

A

e. g. toxins/ metabolites/ drugs/ poisons

- ***Free radicals

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19
Q

Discuss genetic factors causing cell injury

A

e.g.

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20
Q

Causes of cell injury

A
  • hypoxia
  • physical agents
  • chemical agents
  • genetic factors
  • infectious agents
  • inflammation
21
Q

What are the two major cellular processes/disturbances contributing to cell injury?

A
  1. Membrane damage

2. Energy (ATP) depletion

22
Q

What can cause cellular membrane damage?

A

*** Free radicals
(highly reactive 02 species with short 1/2 life)

*** ATP depletion

23
Q

Consequences of cellular membrane damage?

A
  • disruption of membrane permeability characteristics
  • disruption of protein synthesis (rER)
  • disruption of mitochondrial energy production

e.g. white muscle disease caused by necrosis of certain cell poplns due to oxidative damage

24
Q

How do free radicals cause cellular membrane damage?

A
  • from radiation/ complement/ Vit E deficiency/ Se deficiency/ ischaemia
  • lack of antioxidants (endogenous FR’s usually “mopped up” by antioxidants)
25
How does ATP depletion cause cellular membrane damage?
e.g. from hypoxia/ ischaemia which stimulates anaerobic ATP production via glycolysis 1. inhibits ATP production usually produced via oxidative phosphorylation 2. Slows TCA cycle 3. Pyruvate --> lactic acid 4. pH lowers 5. Further reduces ATP production
26
Examples of reversible cellular changes
- cloudy swelling - hydropic change - fatty change - Hepatic lipidosis
27
Examples of irreversible cellular changes
- Apoptosis (programmed cell death) | - Necrosis (death of cells due to lethal injury)
28
Why does apoptosis not elicit an immune response?
Cells don't release cellular constituents so do not evoke an inflammatory response
29
Discuss microscopic changes of cells due to cell necrosis
- cytoplasmic swelling (autolysis/vacuolation) | - histologically this can be seen as clumped chromatin/ pyknosis/ karyolysis
30
Define Pyknosis
-irreversible condensation of chromatin in the nucleus of a cell undergoing necrosis or apoptosis. Followed by fragmentation of the nucleus (Karyorrhexis).
31
Define karyolysis
Dissipation of a cell nucleus, especially during mitosis.
32
Define Karyorrhexis
the destructive fragmentation of the nucleus of a dying cell whereby its chromatin is distributed irregularly throughout the cytoplasm.
33
Describe what a cell undergoing pyknosis would look like
- nuclear shrinkage | - DNA condenses into shrunken basophilic mass
34
Describe what a cell undergoing Karyolysis would look like
- nuclear fading | - chromatin dissolution due to action of DNAases & RNAases
35
Describe what a cell undergoing Karyorrhexis would look like
- nuclear fragmentation | - already pyknotic nuclei membrane ruptures and nucleus undergoing fragmentation
36
What is the usual precursor to karyorrhexis?
pyknosis
37
discuss macroscopic cellular changes due to cell injury
- reduced blood flow - haemorrhage - swelling - inflammation - malacia
38
What is the primary contributor of coagulative necrosis
eosinophils
39
What is the primary contributor of liquefaction
malacia due to numerous neutrophils
40
What is caseous necrosis
cheesy, soft and pasty tissue mm
41
What is the primary cause of gangrene
ischaemia
42
Discuss aspects involved in an inflammatory response
- vascular engorgement - +/- haemorrhage - red zone of infarction - infiltration of neutrophils and macrophages
43
define "degree of damage"
lethal vs. sublethal
44
define "extent of damage"
number injured cells
45
How do the consequences of cell injury vary between particular tissues?
e.g. small amounts of disfunctional cells in the myocardium can drastically affect function whereas large numbers of cells need to be affected to adverse affect skeletal muscle
46
5 pathological processes are...
1. degeneration & necrosis 2. tissue deposits and pigmentation 3. circulatory changes 4. disorders of growth 5. inflammation and repair
47
example of metaplasia in mesenchymal tissue (e.g. CT)
connective tissue --> bone/ cartilage
48
example of metaplasia in epithelial tissue
e. g. columnar --> squamous in bronchi | e. g. squamous --> columnar in oesophagus