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CNUR 803 > Chapter 4 Altered Cellular & Tissue Biology > Flashcards

Chapter 4 Altered Cellular & Tissue Biology Flashcards

1
Q

Why do cells adapt

A

To escape and protect themselves from injury

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2
Q

What is atrophy

A

Decrease in cellular sizeWh

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3
Q

What are the mechancicsm of atrophy

A

Decrease protein synthesis and increase protein metabolism

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4
Q

What is hypetrophy

A

Increase in cellular size

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5
Q

What are the mecahncims of atropjy

A

Increase in protein synthesisWh

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6
Q

What is hyperplasia

A

Increase in number of cells due to cell divisions

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7
Q

What is the mechanics of hyperplasia

A

Release of growth hormones

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8
Q

What is dysplasia (Atypical hyperplasia)

A

Abnormal size, shape, or organization of the cells

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9
Q

What is metaplasia

A

Reversable replacement of one mature cell type by another

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10
Q

Affects of ATP depletion

A

Reduces cells ability to maintain essential functions.
Leads to failure of energy dependent functions resulting in cellular dysfunction and death

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11
Q

Mitochondrial Damage

A

Affects ATP production and triggers apoptosis
Release cytochrome C which activates cell death pathways

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12
Q

Oxygen and free radical damage

A

Free radicals cause lipid per oxidation, protein modification, and DNA damage
Result from hypoxia and reperfusion injury

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13
Q

Protein folding mechanisms

A

Misfiling proteins accumulate disrupting cellular function and disrupting triggering cellular death

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14
Q

DNA Damage defects

A

Mutations or breaks in DNA can lead to malfunction cells or cancer

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15
Q

Calcium level alterations

A

Disrupts cell signalling, leading to activation of enzymes that damage cell components

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16
Q

What is ischemia reperfusion injury

A

This occurs when blood flow and oxygen is restored causing further injury
Mechanisms include increased oxidative stress
Increased intracellular calcium
Inflammation
Complment activation

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17
Q

What is the affect of prolonged hypoxia

A

Valculoation, lysomal swelling

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18
Q

Oxidative stress

A

Occurs when ROS overwhelms the bodies antioxidant defences leading to cellular damage

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19
Q

Free Radicals

A

Unstable molecules with unpaired electrons making them highly reactive and capable of injuring key cellular components
They stabilize by donating or accepting electrons which can turn other molecules into free radicals causing a chain reaction

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20
Q

Sources of free radicals

A

Redox reactions (Normal respirations(
Absorption of extreme energy (Uv light and radiation)
Enzymatic metabolism of chemicals
Transition metals
Nitric oxide

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21
Q

Lipid per oxidation

A

Destruction of polyunsaturated lipids damaging cells and increasing permeability

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22
Q

Protein alterations

A

Causes fragmentation and misfiling proteins impacting cell function

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23
Q

DNA Damage

A

Leads to mutations contributing to cellular function and disease

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24
Q

Implications of oxidative stress

A

plays a role in many pathological conditions including chemical and radiation injuries aging immune responses and schema reperfusion injury
ROS can alter intracellular signalling pathways modulating enzymes and transcription factors involved in cell regulation

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25
Q

What are xenobotics

A

Foreign compounds including toxic mutagenic and carcinogenic chemical

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26
Q

What organ is the most susceptible to xenobiotic induced injury

A

Liver

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27
Q

How does liver process the injected chemicals

A

The liver metabolizes xenobiotics through biotransformation converting lipophilic compounds into hydrophilic forms for excretion
This process can produce toxiphores though which can damage proteins and DNA through concealment binding forming adducts

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28
Q

Electrophiles

A

Attract to electrons, acce[t electrons creating charged centres that can disrupt cellular structures

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29
Q

Nucleophiles

A

Donate electron pairs and can be oxidized to free radicals causing further dmage

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30
Q

Adduct formation

A

Leads to protein dysfunction fibrogeneis and immune activation

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31
Q

Defence mechanisms against xenobiotics

A

Cytochrome p-450 causes oxidation reduction and hydrolysis Conjugation enzymes like glutathione detoxify reactive intermediates making them water soluble, efflux transporter enzymes remove xenobiotics from cells

32
Q

What does antioxidant systems do against xenobiotics

A

Counteract the effects of rot and other active species

33
Q

Refer to box 4.1 on page 83 for more info on free radicals

A
34
Q

Mechancims of chemical injurt

A

Direct damage: Chemicals interact with critical molecular substances such as cyandie inhibiting mitochondrial function
Exaggerated response: Overdose such as birth defects from thalidomide or tumours from industrial chemical
Toxic metabolites: Many chemicals are biologivcally inactive until metabolized by enzymes like cytochrome p45- leading to toxic intermediates that damage cell membranes through free radicals
Hypersensitivity reactions

35
Q

Carmon toxic agents

A

Lead and carbon monoxide which binds to o2 more effectively than o2

36
Q

What are asphyxial injuries

A

a failure of cells to receive oxygen

37
Q

what is the pathogenicity (virulence) of an organizm

A

The ability to survive and proliferate in the human body

38
Q

What does the disease producing potential of a microorganism depend on i

A

It depends on its ability to invade and destroy cells, produce toxins and produce damaging hypersensitivity reactions

39
Q

What happens when a membrane is damaged

A

There is rapid leakage of potassium out of the cell and an influx of water
Antibodies bind to membrane receptors blocking their function and destroying cellular junctions (cell communicators)

40
Q

What are infiltrations

A

Acculations result from sustained injury or inefficient normal cell functions and can be toxic or harmless

41
Q

Mechanicsms of abnormal intracellular acccumulaton

A

Insufficient removal (altered packaging and transport)
Abnormal substance accumulation (Defective protein folding or degradation)
Inadequate metabolism
lack of vital lyxsomal enzymes
Accumulation of heavy metal dust or microorganisms

42
Q

What are the signs and symptoms of accumulation

A

Causes tissues to swell as well ad phagocytes try to remove excess substances

43
Q

hemoproteins

A

Include hug and cytochromes responsible for oxygen transport and cellular respiration
Accumulation of iron due to breakdown of hemoprotesin can lead to hemosiderosis

44
Q

What is dystrophic calculations

A

Occurs in dying or dead tissue despite normal calcium levels

45
Q

What is metastatic calciufication

A

Occurs in normal tissues due to hyperglycemia

46
Q

What is urate crystals

A

Result from disorders in purine. metabolism

47
Q

what is oncosis

A

Cellular swelling due to shift of water into cells it is reversible

48
Q

Causes oncosis

A

Hypoic injury
Atp depletion
Ion imbalance (NA in cell K out of cell)

49
Q

What pathophysiological changes occurs with oncosis

A

Sweeping or ER cistern, rupture and formaition of large values

50
Q

Clinical manifestations of oncosis

A

Increase weight pale and distended organ

51
Q

Refer to slide 21 and 22 for manifestations of cellular injury

A
52
Q

What is necrosis

A

Leathal cell injury or accidental cell death and the process of cellular autodigestion

53
Q

Characteristics of necrosis

A

Rapid loss of the plasma membrane structure
Swelling
mitochondrial dysfunction

54
Q

Coagulative necrosis

A

Associated with ischemia or hypoxia commonly seen in solid organs

55
Q

Liquefactive nectosis

A

Usually associated with infections and brain injuries commonly observed in brain due to its high water cnotent

56
Q

Causes necrosis

A

Associated with tuberculosis

57
Q

Programmed necorisis

A

Is a term for regulated or programmed necrosisW

58
Q

What is apoptosis

A

Programmed cellular death (physiological not pathological)

59
Q

Apoptosis process

A

Cells death that involves orderly dismantling of cell components and packing the remainder in vesicles there is no loss of mitochondrial function

60
Q

Aging characteristics

A

Increased damage to cells and reduced repair capacity
accumulation of damage accumulation of Falange in in dividing cells

61
Q

Somatic death

A

Death of the person not cellular death

62
Q

Signs of death

A

No respiration and circulation becomes pale algor mortis (Temp decrease to room temperature)
Occular changes decreased bp in retinal festal cause pupil dilation
Liver mortis blood settles in dependent tissues creating a purple discolouration skin becomes less elasticc and transparent

63
Q

Purtefecation

A

Apparent 24-48 hours after death

64
Q

Signs and symptoms of purtefecation

A

green skin, loosening skin enzymatic breakdown and tissue dissolution

65
Q

What is rigor mortis

A

Muscle stiffening after death

66
Q

What is liquefactive necrosis

A

When cells are digested by their own enzymes and become soft and runny

67
Q

What is autophagy

A

When cells digests its own components

68
Q

What is Caseous necrosis

A

Dead cells disintegrate but debris is not digested completely

69
Q

Coagulative necrosis

A

Cell death in which denatured proteins appear firm and opaqu

70
Q

Liver mortis

A

blood settles in dependent tissues creating a purple discolouration

71
Q

Which cell death causes inflammation

A

Necrosis

72
Q

Dysplasia

A

Refers to abnormal change

73
Q

During schema what ion is involved and what does it do

A

Calcium damages the membrane

74
Q

How does ROS damage cells

A

They attack the membranes of a cell

75
Q

True or false postmortem changes involve the inflammatory response

A

False

76
Q

Gangeren occurs when cells dies of

A

Hypoxia

77
Q
A

CNUR 803 (12 decks)

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