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EMS - MOD > week 2 > Flashcards

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

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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

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3
Q

what does hyperplasia mean?

A

increase in number of cells

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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

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5
Q

what is atrophy?

A

the reduction of cell size and number

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6
Q

what is metaplasia?

A

the change in the morphology of a cell

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7
Q

give a example of pathological hypertrophy?

A

The increase in size of left ventricle because of systematic hypertension

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8
Q

Give example of physiological hypertrophy?

A

increase in size of muscle in atheletes

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9
Q

pathological hyperplasia give a example?

A

angiogenesis occuring during wound repair

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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
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11
Q

what is hypoxia?

A

the reduction of oxygen to a tissue

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12
Q

what is anoxia?

A

the absence of oxygen to a tissue

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13
Q

why can Reperfusion of tissue causea problem?

A

Can lead to free radicals which can potentially damage other cells

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14
Q

give example of chemical agents that can damage the cells

A

alcohol, tobacco, drugs, occupation, enviroment, drugs and poison

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15
Q

give example of endotoxin?

A

produced by a bacteria when they die –> negative charged bacteria –> produce the toxin

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16
Q

what causes pseudomembranous colitis ?

A

Clostridium difficile infection

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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

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18
Q

How does radation damage cells?

A

Causes the formation of free radicals that then attack macromolecules and form more free radicals

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19
Q

which organs have a high sensitivity to radation?

A

bone marrow, gonads and intestins -> have a high cell turn over rate

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20
Q

what happens to the level of ATP in ischemic injury in mitochondria?

A

oxidative phosporylation levels decrease and so does ATP

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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

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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

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23
Q

what affect does alcohol have on a cellular level?

A

Cause fatty deposition and cloud cell swelling

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24
Q

what is free radicals?

A

Highly reactive ions or molecules with single unpaired electron in outer orbital

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25
Q

what process occurs when free radicals damage proteins and nucleic acids?
What proccess occurs when free radicals damage molecules in membranes?

A

apoptosis occurs to proteins and nucleic acid

Chain reaction happens to molecules in membranes as more free radicals are formed

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26
Q

what enzyne and antioxidans helps to protect against free radicals

A

superoxide dismutase and antioxidans –> vit A,C,E

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27
Q

What cells use free radicals to kill bacteria?

A

neutrophils and macrophages and depends on the formation of superoxides

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28
Q

what can cause membrane defects?

A

bacterial toxins, viral proteins, complement, cytolytic lymphocytes, and various physical and chemical agents

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29
Q

what is the consequence of membrane defect?

A

Loss of membrane barriers leads to breakdown in metabolite gradients

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30
Q

why do cells die?

A

Occurs when cells are unable to achieve a new steady state following environmental insults

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31
Q

what are the two types of cell death?

A

necrosis and apoptosis

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32
Q

cause of necrosis?

A

caused by lethal cell injury?

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33
Q

is necorsis a energy dependent reaction?

A

no it occurs naturally unless the cells can stop it from happening

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34
Q

what is the most common type of necrosis?

A

coagulative occurs in most cells and causes tissue to be hard and dry –> infarction and ischaemia

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35
Q

what type of necrosis occurs during TB?

A

caseous –> looks like cream cheese –> loose all structure

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36
Q

what type of necrosis occurs in brain and what is the site of injury eventually marked by

A

colliquitive necrosis –> liquidation of the brain where the site of injury is eventually marked as a cyst

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37
Q

what are the two types of gangerene?

A

wet and dry

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38
Q

how can you test of coagulative necrosis?

A

test for the specific proteins that should be in the tissue in the blood. If present then leakage and damge of that tissue

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39
Q

what type of inflamation occurs in caseous?

A

granulomatous inflammation that surrounds the cellular detial that has been destroyed

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40
Q

is infection assoicated with wet or dry gangrene?

A

wet.

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41
Q

Is there a clear demarcation in wet or dry gangrene?

A

Dry –> clearly see the line of the infection

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42
Q

what type of disease can you see dry gangrene?

A

diabetes

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43
Q

what is apoptosis?

A

energy dependent cell programmed death

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44
Q

give example of physiological apoptosis?

A

Embryogenesis
Involution
Elimination of self-reacting
lymphocytes

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45
Q

give example of pathalogical apoptosis?

A

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

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46
Q

what two proteins are sequestered in mitochondria but released when ischemia injury occurs and what do they activate?

A

cytochrome C and Apoptosis initiating factor and they active capses which are effector molecules of apoptosis

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47
Q

What does P53 do?

A

very important in recognising DNA damage and inducing apoptosis

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48
Q

Why is mutation in p53 key for tumor growth?

A

allowing cells to accumulate genetic abnormalities and become malignant

49
Q

what does BCL-2 do?

A

sequesters cytochrome C and thus inhibits apoptosis

50
Q

what does mutation in BCL-2 do?

A

over activation and allows tumors to grow as apoptosis is further inhibited

51
Q

what is intrisic pathway?

A

where apoptosis is triggered from within the cell

52
Q

what is extrinisic pathway?

A

when apoptosis is triggered outside the cell due to a protein binding to a cell receptor on the surface of the cell

53
Q

what are the number of cells invovled in necrosis and apoptosis ?

A

multiple in necorsis and single in apoptosis

54
Q

what is the cell size after necoriss and apoptosis?

A

necrosis –> swelling –> enarlages before it dies

apoptosis the cell reduce in size

55
Q

what happens to the nucles during necrosis?

A

Pyknosis → karyorrhexis → karyolysis

56
Q

What is Pyknosis ?

A

is the irreversible condensation of chromatin in the nucleus of a cell undergoing necrosis or apoptosis

57
Q

what is karyorrhexis ?

A

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

58
Q

what is karyolysis?

A

dissolution of a cell nucleus, especially during mitosis.

59
Q

what is a chromatin ?

A

the material of which the chromosomes of organisms other than bacteria are composed, consisting of protein, RNA, and DNA

60
Q

what happens to the nucleus of a apoptic cell?

A

Fragmentation → apoptotic bodies

61
Q

what happens to cellular content during necrosis and apoptosis?

A

necrosis –> Enzymatic digestion; may leak out of cell

apoptosis –> Intact; may be released in apoptotic bodies

62
Q

is there adjecent inflamation during necrosis?

A

frequently?

63
Q

is there adjecent inflamation during apoptosis?

A

no

64
Q

what are the different causes of tissue death?

A

Ischaemia, Trauma, Toxins

Chemical insults , Thermal injury. Radiation

65
Q

what is the most common type of infenction for accute inflammation?

A

‘pyogenic’ bacterial formation

66
Q

what does pyogenic mean?

A

formation of pus

67
Q

what are the two ways in which healing can occur after accute inflammation?

A

regeneration and growth of cells

healing is done by the cells being repaired

68
Q

what are the purposes of acute inflammatory response ?

A

clear away dead tissue
allow access of immune system components
localise the infection

69
Q

what are the 4 cardinal signs of inflammation?

A 
calor --> heat
tumor --> swelling
rubor -->redness
dolor --> pain
also functio laesa --> disturbance of function
70
Q

what are the different types of acute inflammation?

A

serous –> the outpouring of serous fluid
fibrinous –> precipitation
purulent
Pseudomembranous

71
Q

in order give the components of the acute inflammatorty response

A

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
Q

what is pyrexia?

A

increased body temperature

73
Q

what are acute phase reactions and give a example

A

roteins produced by the liver and c reactive proteins

74
Q

what are the non mediated causes of vascular reaction?

A

direct damage to endothelium –> trauma and physical agent

75
Q

what are the mediated causes of vascular reaction?

A 
Histamine
Bradykinin
NO
Leukotriene B4
Complement components
76
Q

in normal blood vessel is the hydrostatic pressure or oncotic pressure of macromolceulces greater at the artery end?

A

hydrostatic pressure –> macrolecules move out

77
Q

in normal blood vessel is the hydrostatic pressure or oncotic pressure of macromolceulces greater at the venous end?

A

oncotic pressure –> causes the moleceules to move back into the blood vessel

78
Q

in the exudative reaction of acute inflammation what is in the protein rich substance produced?:

A

fribinogen and immunoglobins

79
Q

what are the outcome of turn over during exudative reaction?

A 
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
Q

what WBC is involved in the cellular reaction of acute inflammatory response?

A

Accumulation of neutrophils in extracellular space

In severe cases, accumulation of neutrophils, cellular debris and bacteria forms pus

81
Q

Where is neutrophil produced and how common is it?

What is there life span

A

Produced in bone marrow
Commonest white cell in blood

Short life span –> few hours in tissue

82
Q

what enzyme is invovled in the 02 dependent reaction of phagocytosis of a neutrophil and what is produced?

A

Myeloperoxidase

H2O2, Cl-, O2-, OH- –> free radicals that damage the substance being engulfed

83
Q

what is pavementing?

A

the movement of neutrophils next to the endothelium lining and eventually adhering to it

84
Q

What is the normal flow of neutrophils and how does margination change this?

A

Normal flow of neutrophils is axial stream .

Margination causes the movement of macromolecules away from the axial flow and to the periphery

85
Q

what factors in plasma mediate acute inflammation?

A

Kinin system
Clotting pathway
Thrombolytic pathway
Complement pathway

86
Q

what factors in cells mediate acute inflammation?

A

stored in the cell –> histamine
synthesised in cells –> Prostaglandins, Leukotrienes
PAF ,Cytokines (IL1,8; TNFa), NO, Chemokines

87
Q

what is one mechanism in ensuring that acute inflammation does not occur for too long?

A

all substance that mediate acute inflammation have a short half life and are brocken down or scavenging occurs of them

88
Q

what does TNF do?

A

neutrophil adhesion

89
Q

Prefix of “ana” indicates what?

A

Absence–> anemia

90
Q

Prefix of “dys” indicates what?

A

Disorder–> dysplasia

91
Q

Prefix of “meta” indicates what?

A

Change from one state to another –> metaplasia

92
Q

Suffix of “itis” indicates what?

A

Inflammation

93
Q

Suffix of “oma” indicates what?

A

Tumour –> carcinoma

94
Q

Suffix of “penia” indicates what?

A

A lack of something –> Thrombocytopenia

95
Q

Suffix of “cytosis” Indicates what?

A

Increased number of cells –> leukocytosis

96
Q

Suffix of “ectasis” indicates what?

A

Dilation –> bronchiectasis

97
Q

Suffix of “plasia” indicates what?

A

Disorder of growth –> hyperplasia

98
Q

What type of change occurs in barrets oesophagus?

A

Metaplasia
From squamous epithelium to glandular columnar epithelium
Due to gastric reflux

99
Q

what are the Targerts of cell injury?

A 
Cytoskeleton
Membrane integrity and function
Genetic apparatus
Mitochondria
Protein synthesis and function
100
Q

Loss of membrane protection leeds to a break down of membrane gradient. What is the consequence of this?

A

The increaes levels of calcium which causes activation of various enzymes as calcium is coenzyme

101
Q

What enzymes are activated by increase levels of ca2+due to membrane break down?

A

ATPases (thereby hastening ATP depletion),
Phospholipases (which cause membrane damage),
Proteases (break down membrane and cytoskeletal proteins)
Endonucleases (responsible for DNA fragmentation)

102
Q

What are the features of Coagulative necrosis?

A

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
Q

What occurs in fat necrosis?

A

Fat is traumatised and you get break down of lipid chains and see free fatty acid chains
The level of calcium increase

104
Q

What occurs in fibrinoid necrosis?

A

Occuris in arterial walls and it is assoicated with malignant hypertrophy

105
Q

what happens in vascular dilation?

A

Microvascular dilation
Increase in initial blood flow then a decrease
Due to the increase permeability

106
Q

When will the level of neutrophil increase and how do you test for it?

A

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
Q

How to neutrophils move?

A

They are mobile, amoeboid and move through tissue

They move along the concentration gradient

Directional chemotaxis

108
Q

Bradykinin acts as what mediator of acute inflammation?

A

Increase permeability

109
Q

Histamine and NO act as what mediators in acute inflammation?

A

Vascular dilation and increase permeability

110
Q

What mediators are invovled in neutrophil adhesion

A

IL-8 and IL-1

TNF

111
Q

What mediators are invoveld in neutrophil chemotaxis

A

IL-8

Chemokines

112
Q

What is the 3 laboratory assesment of inflammation?

A

Acute phase reaction
Full blood count
Erythrocyte sedimentation rate

113
Q

What are the 4 outcomes of acute inflammation?

A

Resolution
Fibrosis
Suppuration –> abscess
Chronic inflammation

114
Q

What is the result of “resolution” after acute inflammation?

A

There is no tissue damage and the organ/tissue goes back to working normally

115
Q

What is the result of “fibrosis” after acute inflammation?

A

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
Q

What is the result of “suppuration” after acute inflammation?

A

There is absecess and a marked neutrophil reaction.

Tissue is damaged

117
Q

How does chronic inflammation occur?

A

The noxious agent causing the acute inflammation persists and is not dealt with leading to chronic inflammation

118
Q

What are the two ways in which neutrophils engulf bacteria?

A

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
Q

Explain the process in which neutrophils go from the blood vessels and out to the tissues?

A

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)

EMS - MOD (5 decks)

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