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3 REVISION > pathology transition > Flashcards

pathology transition Flashcards

1
Q

what does vindicate stand for

A 
vascular 
infection/inflammatory 
neoplastic
drugs/toxins 
intervention/iatrogenic 
congenital/developmental
autoimmune 
trauma 
endocrine/metabolic
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2
Q

cellular changes in response to increased demand

A

hyperplasia

hypertrophy

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3
Q

cellular changes in response to decreased demand

A

atrophy

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4
Q

cellular changes in response to altered stimulus

A

metaplasia

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5
Q

what are the two mechanisms for causing cell growth

A

increased production of growth factors

increased expression of growth factor receptors

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6
Q

what are the three classes of growth factor receptors

A

receptors with intrinsic tyrosine kinases
7 transmembrane G-protein-coupled receptors
receptors without intrinsic tyrosine kinases

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7
Q

what are the four main stages of the cell cycle

A

G1, S, G2, M

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8
Q

how is the cell cycle controlled

A

cyclin dependent kinases (CDKs)

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9
Q

what happens in phase G1 of cell cycle

A

cell gets bigger with increased protein synthesis

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10
Q

which CDK and cyclin are associated with G1

A

during G1, CDK4 is activated by cyclin D

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11
Q

what does CDK4 do in G1

A

phosphorylates the retinoblastoma protein

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12
Q

retinoblastoma protein is normally bound to

A

E2F

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13
Q

what is the function of E2F

A

kicks of cell division

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14
Q

how does retinoblastoma protein affect the action of E2F

A

stops it activating cell division

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15
Q

how does CDK4 activate cell division

A

CDK4 phosphorylates retinoblastoma protein so it can’t bind to E2F
when E2F is free, it is able to activate cell division

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16
Q

what happens in the S phase of cell division

A

synthesis phase

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17
Q

what molecular changes occur in the S phase

A

E2F initiates DNA replication
E2F increases levels of Cyclin A
Cyclin A activates CDK2 which also promotes DNA replication

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18
Q

what happens in G2 phase of cell cycle

A

cell gets bigger and more protein synthesis

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19
Q

what is main the checkpoint at the end of G2

A

p53

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20
Q

what is the function of p53

A

checks the cell for mistakes

if there are any the cell will apoptose

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21
Q

how is p53 important in the development of cancer

A

if p53 can be avoided by mutant cells they can keep dividing despite containing faults in their DNA

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22
Q

how are the number of cell divisions limited

A

chromosomes are capped with TTAGGG repeats

with every division the number of repeats gets smaller

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23
Q

examples of physiological hyperplasia

A

breast tissue during puberty

endometrium during pregnancy

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24
Q

examples of pathological hyperplasia

A

excess oestrogen leading to endometrial hyperplasia and abnormal bleeding
prostatic hyperplasia
lymph nodes in infection

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25
Q

is hyperplasia reversible or irreversible

A

reversible

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26
Q

how can hyperplasia be reversed

A

withdrawal of stimulus

eg hormones, infection

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27
Q

hyperplastic tissue is an at risk site for…

A

development of cancer

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28
Q

what is the difference between hyperplasia and hypertrophy

A 
hyperplasia = more cells
hypertrophy = bigger cells
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29
Q

when does cardiac hypertrophy become pathological

A

when the muscle requires more blood supply than it has so can no longer function properly

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30
Q

what is atrophy

A

reduction in cell size

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31
Q

examples of physiological atrophy

A

embryological structures

uterus after birth

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32
Q

examples of pathological atrophy

A 
muscle atrophy due to decreased workload 
loss of innervation 
blocked blood supply 
loss of hormonal stimulation 
pressure 
ageing
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33
Q

which hormones promote degradation and atrophy

A

glucocorticoids

thyroid hormone

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34
Q

which hormones oppose atrophy and promote growth

A

insulin

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35
Q

what can cause acute inflammation

A 
infection 
trauma 
foreign bodies 
immune reaction 
necrosis
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36
Q

what is the response to injury

A

vascular changes
cellular changes
chemical mediators
morphological patterns

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37
Q

what are vascular changes in response to injury

A

vasodilation of arterioles then capillary beds

mediated by histamine and NO

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38
Q

what does vasodilation result in

A 
increased heat (calories)
redness/erythema (rubor)
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39
Q

what are cellular changes in response to injury

A 
stasis 
white cell margination 
rolling 
adhesions 
migration
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40
Q

how does injury affects the flow of cells within a vessel

A

blood normally flows centrally

vascular dilation slows the rate of flow and allows cells to more peripherally

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41
Q

what is white cell margination

A

movement of white cells from the centre of blood vessels to the periphery

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42
Q

what changes occur in the lumens surface of blood vessels in response to injury

A

express various proteins that allow white cells to bind to them

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43
Q

what are selectins are integrins

A

proteins expressed on endothelial cells and white cells respectively that bind together

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44
Q

what are VCAM and ICAM

A

vascular cell adhesion molecule

intercellular adhesion molecule

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45
Q

describe the integrin/selectin interaction

A

low affinity and binding on and off is fast

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46
Q

how do histamine and thrombin affect selectin expression

A

increased expression

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47
Q

what effect do TNF and IL1 have on expression of the endothelial proteins

A

increase expression of VCAM and ICAM

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48
Q

what is the effect of chemokine of the endothelial cell surface

A

bind to proteoglycans on endothelial cell surface to increase the affinity of VCAMs and ICAMs for integrins

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49
Q

how does injury cause swelling

A

leaky vessels leads to loss of protein

change in oncotic pressure means water follows protein into extracellular space

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50
Q

what makes blood vessels leaky

A 
endothelial contraction: histamine, bradykinin, substance P, leukotrienes 
direct injury 
white cells 
transcytosis 
new vessel formation
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51
Q

what is chemotaxis

A

movement of cells along a chemical gradient

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52
Q

what are the three stages of phagocytosis

A

recognition and attachment
engulfment
killing and degradation

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53
Q

what are clinical features of inflammation

A 
rubor
calor 
tumor 
dolor 
loss of function
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54
Q

what causes rubor

A

increased perfusion
slow flow
increased permeability of vessels

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55
Q

what causes calor

A

increased perfusion
slow flow
increased vascular permeability

56
Q

what causes donor

A

mediated by prostaglandins and bradykinin

57
Q

which inflammatory cell characterises acute inflammation

A

neutrophil

58
Q

what are features of neutrophils

A

polymorphic nucleus

granules

59
Q

define resolution

A

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

60
Q

what is needed for resolution

A

tissue needs good capacity for repair

good vascular supply for delivery of white cells and removal or injurious agents

61
Q

what is in pus

A

living, dying and dead cells

neutrophils, bacteria, inflammatory debris

62
Q

in what type of damage is organisation and repair preferred to resolution

A

damage beyond the basement membrane

63
Q

which cells are characteristic of chronic inflammation

A

lymphocytes

64
Q

caseous necrosis is associated with

A

TB

65
Q

what are the effects of no ATP on membrane transport

A

Na/K ATPase fails = increased K (swelling)

calcium pump fails (increased Ca)

66
Q

what is the effect of increased intracellular calcium

A

stimulates;

  • ATPase (further reduces ATP levels)
  • phospholipidase (membrane damage)
  • proteases (membrane and cytoskeleton damage)
  • endonuclease (DNA damage and breakdown)
  • mitochondrial permeability (release pro death factors)
67
Q

what are the first signs of cellular hypoxic injury

A

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

68
Q

what occurs during the first 24 hours after hypoxic injury

A

cell contents leaked
complement cascade initiated
acute inflammation

69
Q

neutrophils are replaced by

A

macrophages

70
Q

macrophages are replaced by

A

fibroblasts

71
Q

what do fibroblasts do following MI

A

gradually lay down collagen

occurs after 2 weeks and completes at 6 weeks

72
Q

what are the two types of cell death

A

necrosis and apoptosis

73
Q

is necrosis pathological or physiological

A

always pathological

74
Q

what is a feature of coagulative necrosis

A

preservation of cell outline

75
Q

what is liquefactive necrosis associated with

A

localised bacterial and fungal infections

necrosis within the brain

76
Q

what is caseous necrosis

A

granulomatous inflammation with central necrosis

77
Q

investigations for TB

A

culture, PCR and ZN stain

78
Q

defined apoptosis

A

programmed cell death in response to specific signals

79
Q

example of physiological apoptosis

A

removal of self-reactive lymphocytes

hormonal dependent invocation (uterine lining)

80
Q

examples of pathological apoptosis

A 
response to injury 
radiation 
chemotherapy 
viral infection 
cancers 
graft vs host disease
81
Q

which factors are associated with the extrinsic pathway of apoptosis

A

TNF

Fas

82
Q

Fas mutations often result in…

A

autoimmune diseases

83
Q

what is the intrinsic pathway of apoptosis

A

mitochondrial pathway

84
Q

how is the intrinsic pathway of apoptosis activated

A

growth signals promote anti-apoptotic molecules in mitochondrial membrane
when growth signals are removed they are replaced with Bax/Bak which increase permeability of releases proteins that stimulate caspases (proteases)

85
Q

reduced apoptosis can result in

A

cancer

autoimmune disease

86
Q

increased apoptosis can cause

A

neurodegernative disorders

87
Q

morphology of apoptosis

A

cells shrink
chromatin condensation
cytoplasmic blebs (Cytoplasm breaks up)
macrophages come to revoke debris

88
Q

define neoplasia

A

new growth not in response to stimulus

89
Q

what is the only body part that has never been reported to undergo neoplastic change

A

lens of the eye

90
Q

what is metaplasia

A

reversible change from one mature cell type of another mature cell type

91
Q

what type of metaplasia is often found in response to injury or exposure to noxious stimuli

A

squamous metaplasia

92
Q

example of metaplasia in the lung

A

pseudo stratified ciliated epithelium is exposed thermal/chemical injury (smoking) resulting in squamous metaplasia

93
Q

example of metaplasia in the bladder

A

transitional epithelium is exposed to inflammation (catheter) resulting in squamous metaplasia

94
Q

metaplastic tissue is at risk of

A

development of cancer

95
Q

what is autonomous hyperplasia

A

no longer needs stimulus to occur

96
Q

what is dysplasia

A

abnormal growth not in response to a stimulus

97
Q

define invasion

A

growth beyond the basement membrane

98
Q

what is carcinoma in situ

A

dysplasia affecting the whole of the epithelium but does not go beyond the basement membrane

99
Q

what is. the commonest cancer in men

A

prostate

100
Q

what is the commonest cancer in women

A

breast

101
Q

what are the hallmarks of cancer

A 
increase growth signals 
remove growth suppression 
avoid apoptosis 
achieve immortality 
become invasive 
make your own blood supply 
loss of DNA checks 
avoid the immune system
102
Q

which mutation is diagnostic in burkitt lymphoma

A

t(8:14)

103
Q

how does Bcl-2 prevent apoptosis

A

binds to bax/bak to stop mitchondria become permeable (doesn’t release capsases)

104
Q

what is VEGF

A

vascular endothelial growth factor

105
Q

an encapsulated lesion implies that it is slow/fast growing

A

slow

106
Q

carcinomas arise from

A

epithelium

107
Q

adenoma/adenocarcinoma arise from

A

glandular tissue

108
Q

squamous epithelium can produce what types of tumour

A

papilloma

SCC

109
Q

tumours of connective tissues are called

A

sarcomas

110
Q

benign tumour of fat

A

lipoma

111
Q

benign tumour of bone

A

osteoma

112
Q

malignant cancer of bone

A

osteosarcoma

113
Q

benign cartilage tumour

A

enchondroma

114
Q

malignant cartilage tumour

A

chondrosarcoma

115
Q

define ephelis, naevus, and melanoma

A

freckle
mole
malignant melanocytic tumour

116
Q

stage vs grade

A

stage - how much its grown

grade - how differentiated it is

117
Q

which cancers often present early

A 
vocal cords (voice change)
skin cancers (if you can see them)
breast cancer (self-examine)
testicular cancer (self-examine)
118
Q

weight loss in cancer is known as

A

cachexia

119
Q

risk factors for atheroma

A 
smoking 
HTN
hyperlipidaemia 
DM
age 
sex (males)
genetics
120
Q

where does atheroma occur

A

sites of turbulent blood flow

normally branching sites

121
Q

HDL and LDL: good or bad

A

HDL good

LDL bad

122
Q

how does atheroma occur

A

primary endothelial injury
accumulation of lipids and macrophages
digestion of smooth muscle cells over ‘foamy’ macrophages
increase in size

123
Q

deposition of smooth muscle changes lesion from fatty streak to

A

fibrofatty plaque

124
Q

when is atheromatous narrowing of an artery likely to produce critical disease

A

it is the only artery supplying an organ or tissue
the artery diameter is small (coronary artery vs common iliac artery)
overall blood flow is reduced

125
Q

what are complications of atheroma

A

stenosis
aneurysm
dissection
thrombosis and embolism

126
Q

what is arterial stenosis

A

narrowing of the arterial lumen

reduced elasticity and flow

127
Q

arterial stenosis can cause

A

tissue ischaemia

128
Q

clinical effects of cardiac ischaemia

A 
reduced exercise tolerance 
angina 
unstable angina 
MI
cardiac failure
129
Q

what is cardiac fibrosis

A

loss of cardiac myocytes and replacement by fibrous tissue

130
Q

what are the consequences of cardiac fibrosis

A

loss of contractility

reduced elasticity and filling

131
Q

arterial stenosis affecting the carotid arteries may cause

A

TIA
stroke
vascular dementia

132
Q

arterial stenosis affecting the renal arteries might cause

A

hypertension and renal failure

133
Q

arterial stenosis affecting the peripheral arteries may cause

A

claudication

foot/leg ischaemia

134
Q

define aneurysm

A

abnormal and persistent dilatation of an artery due to a weakness in its wall

135
Q

where is the commonest site of aneurysm formation

A

abdominal aorta

136
Q

what are complications or aneurysm

A 
rupture 
thrombosis 
embolism 
pressure erosion of adjacent structures 
infection
137
Q

what is an arterial dissection

A

splitting within the media by flowing blood resulting in false lumen filled with blood within the media

3 REVISION (7 decks)

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