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Principles > Pathology > Flashcards

Pathology Flashcards

1
Q

vindicate V

A

vascular

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2
Q

vindicate I

A

infection/inflammatory

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3
Q

vindicate N

A

neoplastic

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4
Q

vindicate D

A

drugs/toxins

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5
Q

vindicate I

A

Interventions/iatrogenic

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6
Q

vendicate c

A

congenital

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7
Q

vindicate A

A

autoimmune

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8
Q

vindicate T

A

trauma

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9
Q

vindicate E

A

endocrine/metabolic

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10
Q

what would neoplasia include

A

new growth

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11
Q

what does Iatrogenic mean

A

something caused by a doctor

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12
Q

what five things can cause inflammation?

A

trauma, injury, foreign bodies, immune reaction, necrosis of any cause

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13
Q

what are vascular changes mediated by?

A

histamine and nitric oxide

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14
Q

what are the four main changes to injury

A

vascular changes, cellular changes, chemical changes, chemical mediators and morphologic patterns

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15
Q

what are the vascular changes in response to injury?

A

vasodilation, increased heat (calor) and increased redness (rubor)

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16
Q

what are the five phases of cellular changes as a response to injury?

A

stasis, white cell margination, rolling, adhesions, migrations

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17
Q

what is the change in flow during dilation?

A

the flow slows down

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18
Q

why do blood cells start to stick to vessel walls during inflammation?

A

the vessels express various proteins on the lumen surface

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19
Q

why do you want the blood vessels to be sticky?

A

so that WBC stick to the vessel wall and get to the tissue (lock and key ligands)

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20
Q

what is margination?

A

the white blood cell moving to the vessel walls

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21
Q

what do histamine and thrombin cells do from inflammatory cells?

A

they increase selection expression

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22
Q

what do tumour necrosis factor and interleukin-1 do??

A

increase endothelial cell expression of VCAM and ICAM

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23
Q

result of leaky vessels

A

loss of proteins, change in osmotic pressure, water follows protein and then swelling

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24
Q

what is chemotaxis?

A

cells follow a chemical gradient and move along it

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25
Q

what are the three phases of phagocytosis?

A

recognition and attachment, engulfment and killing and degradation

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26
Q

what do bacterial surface glycoproteins and glycolipids contain?

A

terminal mannose residues. mammalian ones don’t

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27
Q

what do opsonins do?

A

coat bacteria which makes them stand out from the crowd

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28
Q

what is the vesicle formation structure called?

A

phagosome

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29
Q

what is it called when the phagosome joins with a lysosome?

A

phagolysosome

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30
Q

what is the main cell of acute inflammation?

A

the neutrophil

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31
Q

what three things are the result of acute inflammation?

A

injury, vascular changes and cellular changes

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32
Q

briefly describe the vascular phase of acute inflammation?

A

vasodilation, increased permeability, stasis (slowing down of laminar flow)

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33
Q

wether tissues go through resolution, suppuration, repair organisation and fibrosis or chronic inflammation depends on what three things?

A
  • site of injury. Different organs have different capacity for repair and vascular supplies
  • type of injury. Severity, pathogenicity of organism
  • duration of injury - can it be removed or is it sustained
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34
Q

what are the conditions for full repair (resolution)?

A
  • minimal damage
  • tissue/organ type. GI tract good but brain bad
  • good vascular;ar supply for the delivery of WBC and removal of injurious agents
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35
Q

what is suppuration?

A

the production of pus

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36
Q

what does pus consist of?

A

living, dying and dead cells, neutrophils, bacteria, inflammatory debris (fibrin)

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37
Q

what is an empyema?

A

a space filled with pus and walled off

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38
Q

what is necrosis?

A

cell death

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39
Q

when will organisation of tissue happen?

A

when injury produces lots of necrosis (cell death) and lots of fibrin that isn’t easily cleared. Also if there is a poor blood supply and debris can’t be removed

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40
Q

conditions that favour suppuration?

A

persistence and virulence of causative agent

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41
Q

what is organisation?

A

replacement of damaged tissue by granulation tissue

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42
Q

common response to damage beyond the mucosae?

A

granulation tissue formation

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43
Q

what does granulation tissue do?

A

undergo organisation to form fibrous scar

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44
Q

what things are repaired with scar tissue?

A

severe, deep injury
cells that don’t heal well
tissues with poor blood supply

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45
Q

disadvantage to scar tissue

A

it has no function

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46
Q

name for scarring and fibrosis in the liver

A

cirrhosis

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47
Q

result of liver cirrhosis

A

liver failure as there is a loss of liver function

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48
Q

what is chronic inflammation the result of?

A
  • acute inflammation
  • persistence of injury
  • autoimmune (transplant rejection)
  • viral infection
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49
Q

which type of phagocyte is better, neutrophil or macrophage?

A

macrophage

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50
Q

what is a granuloma

A

epitheliod macrophages and are surrounded by lymphocytes. They are giant

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51
Q

what can granulomas react to?

A

specific infections, parasites, worms, eggs, syphilis, mycobacterium (TB) and foreign bodies

52
Q

does necrosis require energy?

A

no

53
Q

what is tuberculous granulomas (TB) an example of?

A

caseous necrosis

54
Q

what is the time limit for myocardium infarction that allows for a reversible change?

A

20 minutes

55
Q

what are pyknotic cells?

A

cells that shrink

56
Q

what do cells do first when they are damaged in MI?

A

shrink, become red, nucleus shrinks and becomes dark, marginal contraction bands appear

57
Q

what vascular changes happen in the first 24 hours after MI?

A

vasodilation, slowing of flow, white cell margination, rolling, pavementing, diapedesis, chemotaxis and phagocytosis

58
Q

what are neutrophils associated with? they accumulate at the site of?

A

acute inflammation

59
Q

what two properties do neutrophils have?

A

phagocytic and cytokine production

60
Q

what are the three types of necrosis?

A

caseous, liquefactive and coagulative

61
Q

when is the greatest risk of cardiac rupture after myocardium infarction?

A

after 3-7 days

62
Q

what are neutrophils replaced with during restitution?

A

macrophages

63
Q

what happens when there is no atp?

A

the sodium potassium pump fails so there is a build up of K which leads to swelling
The calcium pump also fails. Increased calcium in the cell is bad

64
Q

what does cardiac rupture look like?

A

a big hole in the heart

65
Q

what happens after cardiac rupture? resolution? restitution?

A

restitution

66
Q

what replaces macrophages during restitution?

A

fibroblasts

67
Q

what do fibroblasts do?

A

lay down collagen and occur progressively after two weeks. Scar tissue is complete at 6 weeks

68
Q

when you see restitution, think of….

A

fibroblasts laying down collagen and forming scar tissue

69
Q

why does necrosis and apoptosis have to take over from hyperplasia and hypertrophy?

A

hypertrophy and hyperplasia only cope so far and they take time to happen

70
Q

does necrosis require energy?

A

no, no ATP required

71
Q

does necrosis happen normally?

A

no, always pathological

72
Q

what is coagulative necrosis?

A

cell outline is preserved and dead cells are consumed by various enzymatic processes and cells

73
Q

where is cogaulative necrosis often seen?

A

in cardiac muscle in myocardial infarction

74
Q

what happens in liquefactive necrosis?

A

there is a liquid viscous mass that turns to liquid and then there is nothing left

75
Q

what is caseous necrosis?

A

granulomatous inflammation with central necrosis

76
Q

how to diagnose caseous necrosis?

A

ask for a culture, PCR, and look for the result of the Ziehl Neelson stain

77
Q

does apoptosis require energy?

A

yes, in the form of ATP

78
Q

examples of situations when pathological apoptosis is needed?

A
  • in response to injury
  • radiation (including UV light)
  • chemotherapy
  • viral infection
  • cancers
  • graft versus host disease
79
Q

example of an extrinsic pathway death receptor?

A

tumour necrosis factor (TNF), Fas

80
Q

what is Fas important in?

A

recognition of self antigens

81
Q

what do people with Fas mutations often get?

A

Autoimmune diseases

82
Q

what does p53 do if it senses cell damage that can’t be repaired?

A

it halts the cell cycle, stimulates caspases and induces apoptosis

83
Q

too little apoptosis leads to?

A

cancers and autoimmune diseases

84
Q

too much apoptosis leads to?

A

neurodegenerative disorders, heart attacks and viral infections (hepatitis)

85
Q

what are some causes for cellular ageing?

A

oxidative stress (free radical damage) and accumulation of metabolism by-products (lipofuscin)

86
Q

if cells want to grow, one of two things can happen. what are the two things?

A

cells can produce more growth factors or produce more growth receptors

87
Q

what is hyperplasia

A

an increase in the number of cells

88
Q

what process happens for hyperplasia?

A

the cell cycle

89
Q

four stages of the cell cycle

A

G1, S, G2, S

90
Q

what are the three types of growth receptors?

A
  • receptors with intrinsic tyrosine kinase activity
  • 7 transmembrane G protein-coupled receptors
  • receptors without intrinsic tyrosine kinase activity
91
Q

what activates each CDK?

A

a specific cyclin

92
Q

what happens during G1?

A

cell growth and protein synthesis

93
Q

during G1, which cyclin activates CDK4

A

cyclin D

94
Q

What does active CDK4 phosphorylate?

A

Rb Protein

95
Q

normally, Rb is bound to…

A

E2F

96
Q

when Rb has been activated by CDK4, it can no longer…

A

bind to Rb protein

97
Q

what activates (phosphorylates) Rb protein?

A

CDK4

98
Q

what will an unbound Rb protein do?

A

kick off cell division

99
Q

what happens during S phase?

A

DNA replication

100
Q

what does E2F do during s phase?

A

initiate DNA replication and increase levels of cyclin A

101
Q

what does cyclin A do during s phase?

A

activate CDK2

102
Q

What does activated CDK2 do during s phase?

A

promote DNA replication

103
Q

what should the cell contain by the end of s phase?

A

two copies of its genome

104
Q

what happens during G2?

A

more cell growth and protein synthesis

105
Q

what do telomeres provide to chromosomes?

A

protection and stops chromosome fusion and degradation

106
Q

what do telomeres consist of?

A

TTAGGG repeats

107
Q

with every division, the number of repeats in telomeres gets…

A

smaller

108
Q

what is the hay flick limit

A

50-70 divisions

109
Q

when does compensatory hyperplasia happen and in which organs?

A

after loss of tissue, in the liver and bone marrow

110
Q

when will lymph nodes undergo hyperplasia?

A

in response to infection

111
Q

how can hyperplasia be reversed?

A

withdrawal of stimulus

112
Q

what is hypertrophy?

A

increase in cell size and not cell number, often in response to mechanical stress

113
Q

what is cell atrophy?

A

decrease in cell size

114
Q

when might tissue undergo atrophy?

A

decreased work load, loss of function after nerve supply is removed, blocked blood supply, atherosclerosis, post menopausal uterus, inadequate nutrition, ageing, pressure due to endogenous or exogenous structures

115
Q

what does stress on cells result in?

A

cellular adaptation

116
Q

mechanisms of atrophy?

A

reduced cellular components, protein degradation and lysosome digestion

117
Q

define cancer

A

uncontrolled proliferation and growth that can invade other tissues

118
Q

what is neoplasia?

A

new growth not in response to a stimulus. Growth can be benign, premalignant or malignant

119
Q

what is a malignant tumour?

A

a tumour with metastatic potential

120
Q

what is a metastases tumour?

A

a tumour that has spread to other sites

121
Q

what precursors can lead to tumours becoming malignant?

A

dysplasia (disordered growth), metaplasia (change from one mature cell type to another) and even hyperplasia

122
Q

define metaplasia

A

reversible change form one mature cell type to another mature cell type

123
Q

what can metaplasia be in response to?

A

cytokines, growth factors and other chemicals in cells microenvironment

124
Q

what is dysplasia?

A

disordered growth, cells growing in an abnormal way beyond the basement membrane

125
Q

what does CIS stand for?

A

carcinoma in-situ

126
Q

what does carcinoma in-situ look like?

A

dysplasia affecting the whole of the epithelium

127
Q

rank in order which is most likely to be maligant and which is least likely to be malignant? dysplasia, CIS, hyperplasia, metaplasia

A 
MOST
-CIS
-dysplasia
- metaplasia
- hyperplasia
LEAST

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