Cell Injury Flashcards Preview

Year 2 EMS MoD > Cell Injury > Flashcards

Flashcards in Cell Injury Deck (79):
1

Who was the 'father of cellular pathology', and what did he discover?

Virchow.
-cell injury is the basis of all disease

2

What happens to normal cells when they are put under stress?

They adapt.
-inability to adapt >> cell injury

3

What happens if cell injury is irreversible?

Necrosis / apoptosis.

4

What is necrosis?

Cell death caused by enzymatic degradation.
-passive/unprogrammed, due to lethal cell injury

5

What is apoptosis?

Programmed cell death in multicellular organisms.
-active
-physiological and pathological

6

What is the difference between hyperplasia and hypertrophy?

HYPERPLASIA = increased cell reproduction rate.
HYPERTROPHY = increased cell size.

7

What do hyperplasia and hypertrophy both lead to?

Enlargement of an organ or tissue.

8

What is atrophy?

Wasting away of an organ or tissue due to cell degradation.

9

What is metaplasia?

Change in cell type to an abnormal type for that tissue.
-reversible and non-cancerous

10

What is dysplasia?

Proliferation of cells of an abnormal type.
-early stage of cancer and irreversible

11

What happens to the cell type in the exocervix at puberty?

Changes from columnar epithelium to squamous epithelium.

12

What is Barrett's oesophagus an example of?

Metaplasia.
-replacement of normal squamous epithelium with columnar glandular epithelium due to gastric reflux.

13

Give an example of physiological atrophy?
-NB not always pathological

Organ formation in embryology.

14

What is an increase in bone marrow cells at high altitude an example of?

Physiological hyperplasia.

15

What is an increased size of skeletal and heart muscle an example of?

Physiological hypertrophy.
-increased cell size

16

What are the main causes of cell injury? (6)

-O2 availability
-Physical trauma
-Chemical agents
-Infectious organisms
-Irradiation
-Genetic disorders

17

What is the difference between hypoxia and anoxia?

HYPOXIA = lack of oxygen.
ANOXIA = absence of oxygen.

18

What is a common cause of hypoxia/anoxia?

Ischaemia.
-lack of blood flow

19

What is generated when ischaemic tissues are reperfused?

Oxygen free radicals.

20

How does cyanide work on cells?

Inhibits cytochrome c oxidase, meaning cells are unable to use oxygen.
>> hypoxia

21

What are the main types of physical trauma? (2)

-Mechanical trauma (e.g. thrombosis)
-Temperature extremes (e.g. heat denaturation)

22

How can chemical agents lead to cell injury?

-Denaturation
-Breakdown of macromolecules
-Interference with cellular metabolism

23

What toxic metabolite forms if someone takes a paracetamol overdose?

N-acetyl-p-benzoquinone imine (NAPQI).

24

How is paracetamol overdose treated?

N-acetylcysteine (NAC).
-precursor for glutathione; promotes normal conjugation of any remaining paracetamol

25

What are the 2 types of toxins produced by bacteria?

Endotoxins and exotoxins.

26

What is the difference between endotoxins and exotoxins?

ENDOTOXINS - secreted by bacterial cells.
EXOTOXINS - contained within bacterial cells, and released when it degenerate.

27

How does C. difficile cause cell injury?

Bacteria that produces exotoxins.

28

What is molluscum contagiosum?

Skin lesions produced by a pox virus infection.
-virions accumulate in cells

29

How does ionisation cause cell injury?

Generation of free radicals
>> damage to macromolecules, proteins and nucleic acids.

30

Which organs have high sensitivity for ionisation? (3)

-Bone marrow
-Gonads
-Intestines

NB. high cell poliferation rate

31

Which organs have low sensitivity for ionisation? (3)

-Uterus
-Adrenals
-Pancreas

32

What are the main targets of cell injury? (5)

-Mitochondrial function
-Membrane integrity
-Protein synthesis
-Cytoskeleton
-Genetic apparatus

33

What does mitochondrial damage cause?

Decreased oxidative phosphorylation >> decreased ATP.

34

What are the main consequences of mitochondrial damage? (5)

-Cellular and ER swelling
-Loss of microvilli
-Decreased glycogen
-Clumping of nuclear chromatin
-Lipid deposition

35

How does mitochondrial damage lead to cellular swelling and loss of microvilli?

Decreased ATP
>> decreased Na pump activity
>>influx of Ca, H2O and Na, and efflux of K
>> cellular swelling and loss of microvilli

36

How does mitochondrial damage lead to decreased glycogen?

Decreased ATP
>> increased glycolysis
>>decreased glycogen

37

How does mitochondrial damage lead to clumping of nuclear chromatin?

Decreased ATP
>> increased glycolysis
>> decreased pH (lactic acid)
>> clumping of nuclear chromatin

38

How does mitochondrial damage lead to lipid deposition?

Decreased ATP
>> detachment of ribosomes
>> decreased protein synthesis
>> lipis deposition

39

Are the effects of mitochondrial damage reversible?

Yes, with the restoration of normal blood flow.

40

What is sublethal cell injury?

Injury that is insufficient to cause death.

41

What are the sublethal effects of alcohol on liver cells?

-Cell swelling
-Fat accumulation (steatosis)

42

What are free radicals?

Highly reactive, uncharged molecules with an unpaired electron.

43

How does free radical toxicity cause cell injury?

Free radicals
>> chain reaction in membranes to produce more free radicals
>> damage proteins and nucleic acids
>> apoptosis

44

What can detoxify free radicals?

-Superoxide dismutase
-Antioxidants (e.g. vitamins A,C,E)

45

What does killing of bacteria by neutrophils and macrophages depend on?

Formation of superoxide.

46

How can membrane defects cause cell injury?

Increased Ca due to loss of membrane can activate enzymes >> harmful effects.

47

What are the main enzymes that Ca activates following membrane defects? (4)

-ATPases
-Phospholipases
-Proteases
-Endonucleases

48

What is the effect of activating ATPases?

Faster ATP depletion.

49

What is the effect of activating phospholipases?

Causes membrane damage.

50

What is the effect of activating proteases?

Break down membrane and cytoskeleton proteins.

51

What is the effect of activating endonucleases?

DNA fragmentation.

52

What causes cell death?

Irreversible breakdown of interactions between DNA, membranes and enzymes.
-not always pathological

53

Which is passive and unprogrammed; necrosis or apoptosis?

Necrosis.

54

Which is active and programmed; necrosis or apoptosis?

Apoptosis.

55

What causes necrosis and what does it lead to?

-Caused by lethal cell injury
-Leads to an inflammatory reaction

56

What are the main morphological types of necrosis? (5)

-Coagulative
-Colliquative
-Caseous
-Gangrene
-Fat, fibrinoid

57

What is the most common type of necrosis?

Coagulative.
-typical of ischaemic injury

58

Which type of necrosis does TB cause?

Caseous.

59

Which type of necrosis is found in the brain?

Colliquative.

60

Which type of necrosis is described as 'wet and dry'?

Gangrene.

61

What is the process of coagulative necrosis formation?

Denaturation of intracytoplasmic protein
>> dead tissue becomes firm/swollen
>> cellular proteins may leak into blood

62

What type of protein are denatured to form coagulative necrosis?

Intracytoplasmic proteins.

63

How can coagulative necrosis be detected by a blood test?

Detection of cellular protein in blood.
-e.g. myocardial infarction >> creatine kinase (MB subtype) and troponin T and I

64

What is colliquative necrosis?

Necrotic tissue in the brain >> neutrophils release toxins >> total liquefaction to form a cyst.

65

Why does brain injury lead to colliquative necrosis?

It does not have a collagenous tissue framework.

66

What is caseous necrosis?

Cells destroyed and surrounded by granulomatous inflammation, lacking structure.
-'cheese like'
-characteristic of TB

67

What is gangrenous necrosis?

Caused by a critically insufficient blood supply.
-can be wet (e.g. bowel infarct) or dry (e.g. diabetes)
-skin looks black/dead

68

What is fat necrosis?

Damaged cells release lipases >> chalky free fatty acids and calcium deposits.
-e.g. acute pancreatitis

69

What is fibrinoid necrosis?

Immune reactions in vessels >> thickened vessel walls.

70

Give 3 examples of physiological apoptosis.

-Embryogenesis
-Elimination of self-reacting lymphocytes
-Involution

71

Give 3 examples of pathological apoptosis.

-DNA/protein damage
-Viral infections
-Cell death by cytotoxic T-cells

72

Where are apoptosis initiating factor (AIF) and cytochrome C normally located?

In mitochondria.

73

What do apoptosis initiating factor and cytochrome C activate when released into the cytosol?

Capases,
-final effector molecules of apoptosis
-amplify cell signal

74

What are the mechanisms of apoptosis?

Intrinsic and extrinsic pathways.

75

What does apoptosis cause?

Cell becomes fragmented and pieces are phagocytosed.
-no inflammatory reaction

76

What role does P53 play in apoptosis?

Activated by DNA damage and causes the elimination of damaged cells by apoptosis.

77

How can mutation in P53 lead to cancer?

Allows cells to accumulate genetic abnormalities and become malignant.

78

What role does Bcl-2 have in apoptosis?

Bcl-2 isolates cytochrome C >> inhibits apoptosis.

79

How can Bcl-2 lead to cancer?

Bcl-2 overexpression >> tumours gain ability to proliferate in uncontrolled way.