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PRINCIPLES > PATHOLOGY > Flashcards

PATHOLOGY Flashcards

1
Q

what vascular change can occur due to acute inflammation?

A

changes in flow and vessel calibre such as vasodilation

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2
Q

what can acute inflammation be caused by? (6)

A 
infection 
injury 
trauma 
foreign bodies 
immune reaction 
necrosis of any cause
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3
Q

describe vasodilation as an inflammatory response (3)

A

first involves arterioles then capillary beds

mediated by histamine and nitric oxide

results in increased heat and redness

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4
Q

what does metaplasia commonly occur in response to?

A

a noxious stimulus

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5
Q

what can cause a change in signals to stem cells that will cause metaplasia?

A

cytokines
growth factors
other chemicals in the cells microenvironment

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6
Q

what does metaplasia represent?

A

a change in signals delivered to stem cells causing them to differentiate down a different line

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7
Q

what is metaplasia?

A

the reversible change from one mature cell type to another mature cell type due to stress on the cell

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8
Q

what are the precursor stages to neoplasia?

A

dysplasia
metaplasia
hyperplasia

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9
Q

what occurs in epithelial malignancy?

A

malignancy goes beyond the basement membrane

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10
Q

what does malignant mean?

A

neoplasm has metastatic potential which means it has the ability to spread to other sites

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11
Q

where can neoplasms be found?

A

anywhere in the body

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12
Q

what can a neoplasm be?

A

benign
premalignant
malignant

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13
Q

is neoplasia in response to a stimulus?

A

no

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14
Q

what does neoplasia mean?

A

new growth

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15
Q

what can a tumour be?

A

benign
malignant
inflammatory
foreign body

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16
Q

what is cancer?

A

uncontrolled cell proliferation and growth that can invade other tissues

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17
Q

what are two causes of cellular necrosis?

A

oxidative stress

accumulation of toxic metabolic by products

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18
Q

does apoptosis or necrosis cause a significant inflammatory response?

A

necrosis

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19
Q

what cell clears up debris after apoptosis?

A

macrophages

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20
Q

what happens to cells during apoptosis?

A

pyknosis
chromatin condenses and the nucleus breaks up
cytoplasm breaks up

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21
Q

what is caused by too much apoptosis?

A

neurodegenerative diseases

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22
Q

what is caused by too little apoptosis?

A

cancers

autoimmune diseases

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23
Q

what does p53 do if DNA cant be repaired?

A

stimulates caspases and induces apoptosis

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24
Q

name one protein that stimulates the caspase cascade that can be released from the mitochondria

A

cytochrome C

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25
Q

describe the intrinsic pathway in apoptosis

A

growth signals promote anti-apoptotic molecules in the mitochondrial membrane

when these are removed they are replaced by bak and bax

they increase the permeability of the mitochondria which leads to the release of proteins that stimulate the caspase cascade

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26
Q

what type of pathway is the intrinsic pathway?

A

mitochondrial

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27
Q

what do people with Fas mutations often get and why?

A

autoimmune diseases - Fas is involved in the recognition of self cells and can lead to apoptosis in lymphocytes

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28
Q

name two death receptors

A

tumour necrosis factor

Fas

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29
Q

describe the activation of the extrinsic pathway for apoptosis

A

FasL binds to Fas receptor
activates Fas activated death domain
activates caspase cascade

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30
Q

what is a death receptor?

A

a cell membrane receptor with a death domain

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31
Q

what initiates the extrinsic pathway?

A

death receptors

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32
Q

what are the two mechanisms for apoptosis?

A

extrinsic pathway

intrinsic pathway

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33
Q

what needs to be activated for apoptosis to occur?

A

the caspase cascade

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34
Q

what is pathological apoptosis in response to? (6)

A 
injury 
radiation 
chemotherapy 
viral infections 
cancers 
graft versus host disease
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35
Q

when is apoptosis physiological? (3)

A

part of normal growth - fingers and toes
removes self reactive lymphocytes
hormonal dependant involution - removes cells produced by hormones when not needed anymore

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36
Q

does apoptosis require energy?

A

yes

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37
Q

what do you ask for if someone has TB?

A

culture
PCR
result of Ziehl Neelson stain

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38
Q

what is caseous necrosis associated with?

A

TB

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39
Q

what is caseous necrosis?

A

granulomatous inflammation with central necrosis

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40
Q

what is liquefactive necrosis often the result of?

A

localised bacterial and fungal infections

stroke in the brain

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41
Q

what happens during liquefactive necrosis?

A

no cell structure is left, it is all turned in to liquid

pus is often produced

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42
Q

where is coagulative necrosis often seen?

A

in cardiac muscle after an MI

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43
Q

why cant processes such as proteolysis occur during coagulative necrosis?

A

the microenvironment formed is too toxic

44
Q

what are dead cells consumed by in coagulative necrosis?

A

various enzymatic processes and cells

45
Q

what is the most common form of necrosis?

A

coagulative

46
Q

what is preserved in coagulative necrosis?

A

the outline of the cell

47
Q

what are the three types of necrosis?

A

coagulative
liquefactive
caseous

48
Q

what is necrosis always?

A

pathological

49
Q

does necrosis require energy?

A

no

50
Q

what are the two types of cell death?

A

apoptosis and necrosis

51
Q

what is resolution?

A

complete restoration of the tissue to normal after removal of inflammatory components

52
Q

what is what happens after inflammation dependent on and why?

A

the site of imjury - different capacity for repair and different vascular supplies
the type of injutry - severity
duration of injury - can it be removed, is it being sustained

53
Q

when are mediators of inflammation produced?

A

only as long as the stimulus persists

54
Q

what can progress to fibrosis?

A

suppuration

chronic inflammation

55
Q

what can occur after acute inflammation?

A 
resolution 
suppuration 
repair 
fibrosis 
restitution 
chronic inflammation
56
Q

what cell characterises acute inflammation?

A

neutrophil

57
Q

what is dolor and what is it mediated by?

A

pain

prostaglandins and bradykinin

58
Q

what is tumor and what is it caused by?

A

swelling
vascular changes i.e. leakiness of vessels
tumours, cysts, inflammation

59
Q

what is calor and what is it caused by?

A

heat

caused by increased perfusion, slow flow and increased vascular permeability

60
Q

what is rubor and what is it caused by?

A

redness

increased perfusion, slow flow and increased permeability of vessels

61
Q

what are the clinical features of inflammation?

A 
rubor
calor
tumor
dolor
loss of function
62
Q

what do phagocytes produce that are used to kill and degrade foreign material?

A

reactive oxygen species - NADPH oxidase
reactive nitrogen species - nitric oxide synthase
cytotoxic granules

63
Q

what do phagocytes use to engulf foreign material?

A

extensions of the cytoplasm called pseudopods

64
Q

what are pathogens coated in that make them stand out?

A

proteins called opsonins

- such as components of the complement cascade and imunoglobulin

65
Q

what do phagocytes look for that is found on the surface of bacterial cells?

A

mannose

66
Q

what are the three phases of phagocytosis?

A

recognition and attachment
engulfment
killing and degradation

67
Q

what can make a chemical gradient for chemotaxis?

A

bacterial components
complement
leukotrienes
cytokines - interleukins

68
Q

what is chemotaxis?

A

when white cells have moved out of the bloodstream and follow a chemical gradient and move along it

69
Q

what is VEGF?

A

vascular endothelial growth factor

70
Q

what mediates transcytosis?

A

VEGF

71
Q

what causses endothelial contraction?

A

histamine
bradykinin
substance P
leukotrines

72
Q

why do blood vessels become permeable?

A

endothelial contraction
direct injury
white cells causing harm to the inside of vessels
transcytosis
VEGF makes new vessels but also increases permeability

73
Q

what does vascular permeability cause?

A

loss of proteins
change in osmotic pressure
water follows protein out the vessel = swelling

74
Q

what do proteoglycans do?

A

increase the affinity of VCAM and ICAM for integrins

75
Q

what do chemokines bind to?

A

proteoglycans on the surface of endothelial cells

76
Q

what increases endothelial cell expression of VCAM and ICAM?

A

tumour necrosis factor (TNF)

interleukin 1

77
Q

what increases selectin expression?

A

histamine and thrombin from inflammatory cells

78
Q

what increases the affinity of the ligands binding white cells to the luminal surface of blood vessels?

A

chemokines

79
Q

what proteins are expressed in blood vessels and on white cells that slow flow during an inflammatory response

A

selectins (on endothelial cells and white cells)
integrins (bind to ICAM)
vascular cell adhesion molecule
intercellular adhesion molecule

80
Q

what do vessels express during inflammation?

A

various proteins on the luminal surface that have a matching protein on the surface of the white cells

81
Q

what is white cell margination?

A

larger white blood cells moving peripherally in blood vessels due to vascular dilation

82
Q

what happens in normal blood flow?

A

blood flows centrally within a blood vessel

83
Q

what cellular changes occur in acute inflammation? (5)

A 
stasis
white cell margination
rolling
adhesions 
migration
84
Q

what are the different causes of disease?

A 
vascular 
infectious/inflammatory 
neoplasia 
drugs and toxins 
iatrogenic 
congenital 
autoimmune 
trauma 
endocrine/metabolic 
psychological
85
Q

what is vascular disease?

A

disease in blood vessels including inflammation, clots and blockages

86
Q

what does neoplasia mean?

A

new growth

87
Q

what is iatrogenic disease?

A

caused by a doctor, medical complications

88
Q

what is a congenital disease?

A

conditions someone is born with, not necessarily genetic

89
Q

who is more likely to have a congenital disease?

A

young people

90
Q

when does resolution occur? (4)

A

minimal cell death
tissue has the capacity to repair
good vascular supply
injurious agent easily removed

91
Q

what is suppuration?

A

the production of pus

92
Q

what does pus contain?

A

living, dead and dying cells

93
Q

what is an empyema?

A

a space filled with pus that has been walled off

94
Q

why wont an abscess go away by itself and why cant they be treated with antibiotics?

A

they have no vascular supply

95
Q

what is needed to heal and repair any injury?

A

a good vascular system to deliver white cells and to remove injurious agents

96
Q

what is organisation/restitution?

A

scarring

97
Q

when does restitution occur?

A

when an injury produces lots of necrosis or fibrin
poor blood supply
tissue cant regenerate

98
Q

what type of healing is favoured when the damage goes beyond the basement membrane of the epithelium?

A

restitution, because you need a basic structure to remain for resolution to occur

99
Q

how does restitution occur?

A

defect infiltrated by capillaries and myofibroblasts

deposit collagen and smooth muscle cells for things to be built upon

100
Q

what can scarring and fibrosis cause?

A

loss of function and contraction

101
Q

what is fibrosis in the liver called?

A

cirrhosis

102
Q

what does cirrhosis result in?

A

liver failure, liver cant remove toxins or make proteins, disturbs large volume of blood that needs to flow through the liver

103
Q

what does chronic inflammation not tell you anything about?

A

duration or severity of injury

104
Q

what cell characterises chronic inflammation?

A

the lymphocyte (macrophages also present)

105
Q

when is chronic inflammation favoured?

A 
there is suppuration or scarring 
persistent foreign injury 
persistent infectious agent 
autoimmune disease 
transplant rejection
106
Q

what is a granuloma?

A

aggregate of epithelioid histiocytes caused by an inflammatory response

107
Q

what are granulomas caused by?

A

foreign bodies
endogenous substances
exogenous substances
infections such as parasites, worms, mycobacterium

PRINCIPLES (13 decks)

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