week 2 Flashcards
1
Q
what factors are needed to mainatin a stable cell
A
preserve genetic integrity
normal cell enzyme activity
intact membrane and transmembrane proteins
adequate supply of oxygen and nutrients
2
Q
what is the affect of stress on cells?
A
To a certain extent cells can deal with stress by celullar adaption. However if there is to much stress then the cells become injured. Can have either reversible or irrerversible injury to the cells
3
Q
what does hyperplasia mean?
A
increase in number of cells
4
Q
What is hypertrophy? Give a example
A
The enlargement of an organ or tissue from the increase in size of its cells.
muscle cells undergo hypertrophy –> cannot increase in cell number and therefore increase in cell size to increase activity
5
Q
what is atrophy?
A
the reduction of cell size and number
6
Q
what is metaplasia?
A
the change in the morphology of a cell
7
Q
give a example of pathological hypertrophy?
A
The increase in size of left ventricle because of systematic hypertension
8
Q
Give example of physiological hypertrophy?
A
increase in size of muscle in atheletes
9
Q
pathological hyperplasia give a example?
A
angiogenesis occuring during wound repair
10
Q
what factors can cause cell injury?
A
lack of o2 and nutrients physical trauma chemical agens infectious agens radation genetic disorder ageing lack of essential vitamins and minerals immunological
11
Q
what is hypoxia?
A
the reduction of oxygen to a tissue
12
Q
what is anoxia?
A
the absence of oxygen to a tissue
13
Q
why can Reperfusion of tissue causea problem?
A
Can lead to free radicals which can potentially damage other cells
14
Q
give example of chemical agents that can damage the cells
A
alcohol, tobacco, drugs, occupation, enviroment, drugs and poison
15
Q
give example of endotoxin?
A
produced by a bacteria when they die –> negative charged bacteria –> produce the toxin
16
Q
what causes pseudomembranous colitis ?
A
Clostridium difficile infection
17
Q
why is Clostridium difficile infection problem in hosptials?
A
Broad antibiotics are given which disrupt normal bowel flora and allow organisms to overgrow –> exotoxin is produced
18
Q
How does radation damage cells?
A
Causes the formation of free radicals that then attack macromolecules and form more free radicals
19
Q
which organs have a high sensitivity to radation?
A
bone marrow, gonads and intestins -> have a high cell turn over rate
20
Q
what happens to the level of ATP in ischemic injury in mitochondria?
A
oxidative phosporylation levels decrease and so does ATP
21
Q
what is the consequence of reduction of Activity of plasma membrane ATP-driven “sodium pumpin because of ischemic injury
A
influx of both sodium and calcium into the cells and isosmotic gain of water and acute cellular swelling
22
Q
what are the end effects of ischemic injury to mitochondria ?
A
cellular swelling, ER swelling, lipid deposition, loss of microvilli –> hypoxia is associated with cellular swelling
Reduction of ATP and protein synthesis
23
Q
what affect does alcohol have on a cellular level?
A
Cause fatty deposition and cloud cell swelling
24
Q
what is free radicals?
A
Highly reactive ions or molecules with single unpaired electron in outer orbital
25
what process occurs when free radicals damage proteins and nucleic acids?
What proccess occurs when free radicals damage molecules in membranes?
apoptosis occurs to proteins and nucleic acid
Chain reaction happens to molecules in membranes as more free radicals are formed
26
what enzyne and antioxidans helps to protect against free radicals
superoxide dismutase and antioxidans --> vit A,C,E
27
What cells use free radicals to kill bacteria?
neutrophils and macrophages and depends on the formation of superoxides
28
what can cause membrane defects?
bacterial toxins, viral proteins, complement, cytolytic lymphocytes, and various physical and chemical agents
29
what is the consequence of membrane defect?
Loss of membrane barriers leads to breakdown in metabolite gradients
30
why do cells die?
Occurs when cells are unable to achieve a new steady state following environmental insults
31
what are the two types of cell death?
necrosis and apoptosis
32
cause of necrosis?
caused by lethal cell injury?
33
is necorsis a energy dependent reaction?
no it occurs naturally unless the cells can stop it from happening
34
what is the most common type of necrosis?
coagulative occurs in most cells and causes tissue to be hard and dry --> infarction and ischaemia
35
what type of necrosis occurs during TB?
caseous --> looks like cream cheese --> loose all structure
36
what type of necrosis occurs in brain and what is the site of injury eventually marked by
colliquitive necrosis --> liquidation of the brain where the site of injury is eventually marked as a cyst
37
what are the two types of gangerene?
wet and dry
38
how can you test of coagulative necrosis?
test for the specific proteins that should be in the tissue in the blood. If present then leakage and damge of that tissue
39
what type of inflamation occurs in caseous?
granulomatous inflammation that surrounds the cellular detial that has been destroyed
40
is infection assoicated with wet or dry gangrene?
wet.
41
Is there a clear demarcation in wet or dry gangrene?
Dry --> clearly see the line of the infection
42
what type of disease can you see dry gangrene?
diabetes
43
what is apoptosis?
energy dependent cell programmed death
44
give example of physiological apoptosis?
Embryogenesis
Involution
Elimination of self-reacting
lymphocytes
45
give example of pathalogical apoptosis?
DNA/protein damage
Viral infections
Cell killing by cytotoxic T-cells
46
what two proteins are sequestered in mitochondria but released when ischemia injury occurs and what do they activate?
cytochrome C and Apoptosis initiating factor and they active capses which are effector molecules of apoptosis
47
What does P53 do?
very important in recognising DNA damage and inducing apoptosis
48
Why is mutation in p53 key for tumor growth?
allowing cells to accumulate genetic abnormalities and become malignant
49
what does BCL-2 do?
sequesters cytochrome C and thus inhibits apoptosis
50
what does mutation in BCL-2 do?
over activation and allows tumors to grow as apoptosis is further inhibited
51
what is intrisic pathway?
where apoptosis is triggered from within the cell
52
what is extrinisic pathway?
when apoptosis is triggered outside the cell due to a protein binding to a cell receptor on the surface of the cell
53
what are the number of cells invovled in necrosis and apoptosis ?
multiple in necorsis and single in apoptosis
54
what is the cell size after necoriss and apoptosis?
necrosis --> swelling --> enarlages before it dies
| apoptosis the cell reduce in size
55
what happens to the nucles during necrosis?
Pyknosis → karyorrhexis → karyolysis
56
What is Pyknosis ?
is the irreversible condensation of chromatin in the nucleus of a cell undergoing necrosis or apoptosis
57
what is karyorrhexis ?
is the destructive fragmentation of the nucleus of a dying cell whereby its chromatin is distributed irregularly throughout the cytoplasm
58
what is karyolysis?
dissolution of a cell nucleus, especially during mitosis.
59
what is a chromatin ?
the material of which the chromosomes of organisms other than bacteria are composed, consisting of protein, RNA, and DNA
60
what happens to the nucleus of a apoptic cell?
Fragmentation → apoptotic bodies
61
what happens to cellular content during necrosis and apoptosis?
necrosis --> Enzymatic digestion; may leak out of cell
| apoptosis --> Intact; may be released in apoptotic bodies
62
is there adjecent inflamation during necrosis?
frequently?
63
is there adjecent inflamation during apoptosis?
no
64
what are the different causes of tissue death?
Ischaemia, Trauma, Toxins
| Chemical insults , Thermal injury. Radiation
65
what is the most common type of infenction for accute inflammation?
‘pyogenic’ bacterial formation
66
what does pyogenic mean?
formation of pus
67
what are the two ways in which healing can occur after accute inflammation?
regeneration and growth of cells
| healing is done by the cells being repaired
68
what are the purposes of acute inflammatory response ?
clear away dead tissue
allow access of immune system components
localise the infection
69
what are the 4 cardinal signs of inflammation?
```
calor --> heat
tumor --> swelling
rubor -->redness
dolor --> pain
also functio laesa --> disturbance of function
```
70
what are the different types of acute inflammation?
serous --> the outpouring of serous fluid
fibrinous --> precipitation
purulent
Pseudomembranous
71
in order give the components of the acute inflammatorty response
vascular reaction --> dilation (rubor) and also change in blood flow
Exudative reaction - formation of inflammatory exudant --> leaky
Cellular reaction - migration of inflammatory cells out of vessels into the tissues
72
what is pyrexia?
increased body temperature
73
what are acute phase reactions and give a example
roteins produced by the liver and c reactive proteins
74
what are the non mediated causes of vascular reaction?
direct damage to endothelium --> trauma and physical agent
75
what are the mediated causes of vascular reaction?
```
Histamine
Bradykinin
NO
Leukotriene B4
Complement components
```
76
in normal blood vessel is the hydrostatic pressure or oncotic pressure of macromolceulces greater at the artery end?
hydrostatic pressure --> macrolecules move out
77
in normal blood vessel is the hydrostatic pressure or oncotic pressure of macromolceulces greater at the venous end?
oncotic pressure --> causes the moleceules to move back into the blood vessel
78
in the exudative reaction of acute inflammation what is in the protein rich substance produced?:
fribinogen and immunoglobins
79
what are the outcome of turn over during exudative reaction?
```
Dilution of noxious agents
Transport to lymph nodes
Supply of nutrients, O2 metabolic requirement
of inflammatory response
Spread of inflammatory mediators
Spread of antibodies
Spread of drugs important at BBB
```
80
what WBC is involved in the cellular reaction of acute inflammatory response?
Accumulation of neutrophils in extracellular space
In severe cases, accumulation of neutrophils, cellular debris and bacteria forms pus
81
Where is neutrophil produced and how common is it?
| What is there life span
Produced in bone marrow
Commonest white cell in blood
Short life span --> few hours in tissue
82
what enzyme is invovled in the 02 dependent reaction of phagocytosis of a neutrophil and what is produced?
Myeloperoxidase
| H2O2, Cl-, O2-, OH- --> free radicals that damage the substance being engulfed
83
what is pavementing?
the movement of neutrophils next to the endothelium lining and eventually adhering to it
84
What is the normal flow of neutrophils and how does margination change this?
Normal flow of neutrophils is axial stream .
| Margination causes the movement of macromolecules away from the axial flow and to the periphery
85
what factors in plasma mediate acute inflammation?
Kinin system
Clotting pathway
Thrombolytic pathway
Complement pathway
86
what factors in cells mediate acute inflammation?
stored in the cell --> histamine
synthesised in cells --> Prostaglandins, Leukotrienes
PAF ,Cytokines (IL1,8; TNFa), NO, Chemokines
87
what is one mechanism in ensuring that acute inflammation does not occur for too long?
all substance that mediate acute inflammation have a short half life and are brocken down or scavenging occurs of them
88
what does TNF do?
neutrophil adhesion
89
Prefix of "ana" indicates what?
Absence--> anemia
90
Prefix of "dys" indicates what?
Disorder--> dysplasia
91
Prefix of "meta" indicates what?
Change from one state to another --> metaplasia
92
Suffix of "itis" indicates what?
Inflammation
93
Suffix of "oma" indicates what?
Tumour --> carcinoma
94
Suffix of "penia" indicates what?
A lack of something --> Thrombocytopenia
95
Suffix of "cytosis" Indicates what?
Increased number of cells --> leukocytosis
96
Suffix of "ectasis" indicates what?
Dilation --> bronchiectasis
97
Suffix of "plasia" indicates what?
Disorder of growth --> hyperplasia
98
What type of change occurs in barrets oesophagus?
Metaplasia
From squamous epithelium to glandular columnar epithelium
Due to gastric reflux
99
what are the Targerts of cell injury?
```
Cytoskeleton
Membrane integrity and function
Genetic apparatus
Mitochondria
Protein synthesis and function
```
100
Loss of membrane protection leeds to a break down of membrane gradient. What is the consequence of this?
The increaes levels of calcium which causes activation of various enzymes as calcium is coenzyme
101
What enzymes are activated by increase levels of ca2+due to membrane break down?
ATPases (thereby hastening ATP depletion),
Phospholipases (which cause membrane damage),
Proteases (break down membrane and cytoskeletal proteins)
Endonucleases (responsible for DNA fragmentation)
102
What are the features of Coagulative necrosis?
Denaturation of intracytoplasmic proteins
Dead tissue are firm and slightly swollen
Tissue retains microscopic architecture
Cytoplasmic proteins can seep into blood
Common in ischeamia but not in the brain
103
What occurs in fat necrosis?
Fat is traumatised and you get break down of lipid chains and see free fatty acid chains
The level of calcium increase
104
What occurs in fibrinoid necrosis?
Occuris in arterial walls and it is assoicated with malignant hypertrophy
105
what happens in vascular dilation?
Microvascular dilation
Increase in initial blood flow then a decrease
Due to the increase permeability
106
When will the level of neutrophil increase and how do you test for it?
Increase in blood when there is acute inflammation
Can test neutrophil to see how bad the acute inflammation
Do a blood count
To see if the treatment is working/how the infection is developing
107
How to neutrophils move?
They are mobile, amoeboid and move through tissue
They move along the concentration gradient
Directional chemotaxis
108
Bradykinin acts as what mediator of acute inflammation?
Increase permeability
109
Histamine and NO act as what mediators in acute inflammation?
Vascular dilation and increase permeability
110
What mediators are invovled in neutrophil adhesion
IL-8 and IL-1
| TNF
111
What mediators are invoveld in neutrophil chemotaxis
IL-8
| Chemokines
112
What is the 3 laboratory assesment of inflammation?
Acute phase reaction
Full blood count
Erythrocyte sedimentation rate
113
What are the 4 outcomes of acute inflammation?
Resolution
Fibrosis
Suppuration --> abscess
Chronic inflammation
114
What is the result of "resolution" after acute inflammation?
There is no tissue damage and the organ/tissue goes back to working normally
115
What is the result of "fibrosis" after acute inflammation?
There is so tissue damage and the tissue is not replaced by normal tissue but by collagen so therefore have scar tissue. If this occurs on a organ it will potentially not work as well
116
What is the result of "suppuration" after acute inflammation?
There is absecess and a marked neutrophil reaction.
| Tissue is damaged
117
How does chronic inflammation occur?
The noxious agent causing the acute inflammation persists and is not dealt with leading to chronic inflammation
118
What are the two ways in which neutrophils engulf bacteria?
Engulph them by phagocytosis to form a phagolyzosome Oxygen dependent - Enzyme myeloperoxidase makes free radicals which damage the macromolecules from which the bacteria are formed thus killing them
Oxygen independent - Involves specific enzymes such as lysozyme which break down bacteria cell walls
119
Explain the process in which neutrophils go from the blood vessels and out to the tissues?
Normal flow in the blood vessel is an axial stream so neutrophils dont come into contact with the endothelium When vessels dilate and exudate moves out of the vessles the flow is slowed and neutrophils are no longer adhered to an axial stream, they come into contact with the endothelium and various ligand-receptor reactions take place Have: 1) Margination 2) Rolling - adhesion (pavementing when the neutrophils line up on the endothelium) 3) Migration into the tissues (facilitated by the increased permeability of the vessels)
