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

Chapter 4 Altered Cellular & Tissue Biology Flashcards

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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
What are xenobotics
Foreign compounds including toxic mutagenic and carcinogenic chemical
26
What organ is the most susceptible to xenobiotic induced injury
Liver
27
How does liver process the injected chemicals
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
28
Electrophiles
Attract to electrons, acce[t electrons creating charged centres that can disrupt cellular structures
29
Nucleophiles
Donate electron pairs and can be oxidized to free radicals causing further dmage
30
Adduct formation
Leads to protein dysfunction fibrogeneis and immune activation
31
Defence mechanisms against xenobiotics
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
What does antioxidant systems do against xenobiotics
Counteract the effects of rot and other active species
33
Refer to box 4.1 on page 83 for more info on free radicals
34
Mechancims of chemical injurt
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
Carmon toxic agents
Lead and carbon monoxide which binds to o2 more effectively than o2
36
What are asphyxial injuries
a failure of cells to receive oxygen
37
what is the pathogenicity (virulence) of an organizm
The ability to survive and proliferate in the human body
38
What does the disease producing potential of a microorganism depend on i
It depends on its ability to invade and destroy cells, produce toxins and produce damaging hypersensitivity reactions
39
What happens when a membrane is damaged
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
What are infiltrations
Acculations result from sustained injury or inefficient normal cell functions and can be toxic or harmless
41
Mechanicsms of abnormal intracellular acccumulaton
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
What are the signs and symptoms of accumulation
Causes tissues to swell as well ad phagocytes try to remove excess substances
43
hemoproteins
Include hug and cytochromes responsible for oxygen transport and cellular respiration Accumulation of iron due to breakdown of hemoprotesin can lead to hemosiderosis
44
What is dystrophic calculations
Occurs in dying or dead tissue despite normal calcium levels
45
What is metastatic calciufication
Occurs in normal tissues due to hyperglycemia
46
What is urate crystals
Result from disorders in purine. metabolism
47
what is oncosis
Cellular swelling due to shift of water into cells it is reversible
48
Causes oncosis
Hypoic injury Atp depletion Ion imbalance (NA in cell K out of cell)
49
What pathophysiological changes occurs with oncosis
Sweeping or ER cistern, rupture and formaition of large values
50
Clinical manifestations of oncosis
Increase weight pale and distended organ
51
Refer to slide 21 and 22 for manifestations of cellular injury
52
What is necrosis
Leathal cell injury or accidental cell death and the process of cellular autodigestion
53
Characteristics of necrosis
Rapid loss of the plasma membrane structure Swelling mitochondrial dysfunction
54
Coagulative necrosis
Associated with ischemia or hypoxia commonly seen in solid organs
55
Liquefactive nectosis
Usually associated with infections and brain injuries commonly observed in brain due to its high water cnotent
56
Causes necrosis
Associated with tuberculosis
57
Programmed necorisis
Is a term for regulated or programmed necrosisW
58
What is apoptosis
Programmed cellular death (physiological not pathological)
59
Apoptosis process
Cells death that involves orderly dismantling of cell components and packing the remainder in vesicles there is no loss of mitochondrial function
60
Aging characteristics
Increased damage to cells and reduced repair capacity accumulation of damage accumulation of Falange in in dividing cells
61
Somatic death
Death of the person not cellular death
62
Signs of death
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
Purtefecation
Apparent 24-48 hours after death
64
Signs and symptoms of purtefecation
green skin, loosening skin enzymatic breakdown and tissue dissolution
65
What is rigor mortis
Muscle stiffening after death
66
What is liquefactive necrosis
When cells are digested by their own enzymes and become soft and runny
67
What is autophagy
When cells digests its own components
68
What is Caseous necrosis
Dead cells disintegrate but debris is not digested completely
69
Coagulative necrosis
Cell death in which denatured proteins appear firm and opaqu
70
Liver mortis
blood settles in dependent tissues creating a purple discolouration
71
Which cell death causes inflammation
Necrosis
72
Dysplasia
Refers to abnormal change
73
During schema what ion is involved and what does it do
Calcium damages the membrane
74
How does ROS damage cells
They attack the membranes of a cell
75
True or false postmortem changes involve the inflammatory response
False
76
Gangeren occurs when cells dies of
Hypoxia
77

CNUR 803 (12 decks)

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