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Cell Injury > L1 > Flashcards

L1 Flashcards

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
Q

How does ATP depletion cause cellular membrane damage?

A

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
Q

Examples of reversible cellular changes

A
  • cloudy swelling
  • hydropic change
  • fatty change
  • Hepatic lipidosis
27
Q

Examples of irreversible cellular changes

A
  • Apoptosis (programmed cell death)

- Necrosis (death of cells due to lethal injury)

28
Q

Why does apoptosis not elicit an immune response?

A

Cells don’t release cellular constituents so do not evoke an inflammatory response

29
Q

Discuss microscopic changes of cells due to cell necrosis

A
  • cytoplasmic swelling (autolysis/vacuolation)

- histologically this can be seen as clumped chromatin/ pyknosis/ karyolysis

30
Q

Define Pyknosis

A

-irreversible condensation of chromatin in the nucleus of a cell undergoing necrosis or apoptosis.
Followed by fragmentation of the nucleus (Karyorrhexis).

31
Q

Define karyolysis

A

Dissipation of a cell nucleus, especially during mitosis.

32
Q

Define Karyorrhexis

A

the destructive fragmentation of the nucleus of a dying cell whereby its chromatin is distributed irregularly throughout the cytoplasm.

33
Q

Describe what a cell undergoing pyknosis would look like

A
  • nuclear shrinkage

- DNA condenses into shrunken basophilic mass

34
Q

Describe what a cell undergoing Karyolysis would look like

A
  • nuclear fading

- chromatin dissolution due to action of DNAases & RNAases

35
Q

Describe what a cell undergoing Karyorrhexis would look like

A
  • nuclear fragmentation

- already pyknotic nuclei membrane ruptures and nucleus undergoing fragmentation

36
Q

What is the usual precursor to karyorrhexis?

A

pyknosis

37
Q

discuss macroscopic cellular changes due to cell injury

A
  • reduced blood flow
  • haemorrhage
  • swelling
  • inflammation
  • malacia
38
Q

What is the primary contributor of coagulative necrosis

A

eosinophils

39
Q

What is the primary contributor of liquefaction

A

malacia due to numerous neutrophils

40
Q

What is caseous necrosis

A

cheesy, soft and pasty tissue mm

41
Q

What is the primary cause of gangrene

A

ischaemia

42
Q

Discuss aspects involved in an inflammatory response

A
  • vascular engorgement
  • +/- haemorrhage
  • red zone of infarction
  • infiltration of neutrophils and macrophages
43
Q

define “degree of damage”

A

lethal vs. sublethal

44
Q

define “extent of damage”

A

number injured cells

45
Q

How do the consequences of cell injury vary between particular tissues?

A

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
Q

5 pathological processes are…

A
  1. degeneration & necrosis
  2. tissue deposits and pigmentation
  3. circulatory changes
  4. disorders of growth
  5. inflammation and repair
47
Q

example of metaplasia in mesenchymal tissue (e.g. CT)

A

connective tissue –> bone/ cartilage

48
Q

example of metaplasia in epithelial tissue

A

e. g. columnar –> squamous in bronchi

e. g. squamous –> columnar in oesophagus

Cell Injury (3 decks)

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