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Principles > Pathology 2.0 > Flashcards

Pathology 2.0 Flashcards

1
Q

define pathology

A

identification and science of types of diseases

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2
Q

VINDICATEM (mechanisms of disease)

A 
vascular
infection/ inflammation
neoplasia
drugs
intervention (doctor)
congenital
autoimmune
trauma
endocrine
metabolic
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3
Q

vascular changes in acute inflammation

A
  • vasodilation (mediated by histamine and nitric oxide)
  • white cell margination
  • expression of proteins
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4
Q

two types of proteins expressed on white cell surface

A
  1. selectin (endothelial)

2. integrins

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5
Q

two types of cell adhesion molecules expressed on the endothelial cell surface

A
  1. VCAMS

2. ICAMS

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6
Q

do VCAMS and ICAMS have high affinity interactions?

A

no

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7
Q

which substances increase selectin expression?

A

histamine and thrombin

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8
Q

define increased avidity

A

increased strength of binding between VCAMS and ICAMS to integrins

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9
Q

vascular leakage is caused by?

A
  1. endothelial contraction
  2. direct injury
  3. white cells
  4. transcytosis
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10
Q

three stages of phagocytosis

A
  1. recognition and attachment
  2. engulfment
  3. killing
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11
Q

five physical changes during acute inflammation

A
  1. heat
  2. redness
  3. swelling
  4. pain
  5. loss of function
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12
Q

what can be the result of acute inflammation

A
  1. resolution
  2. suppuration
  3. organisation and fibrosis
  4. chronic inflammation
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13
Q

what is the result of acute inflammation dependent on?

A
  • site of injury
  • type of injury
  • duration of injury
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14
Q

describe organisation

A

injury produces lots of necrosis or fibrin or has poor blood supply therefore the dead cells are organised because they cannot be removed.

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15
Q

chronic inflammation is favoured if

A
  • suppuration scarring
  • persistence of injury
  • infectious agent
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16
Q

characteristics of chronic inflammation

A

presence of lymphocytes and macrophages (granulomas)

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17
Q

define infarction

A

cell death after loss of oxygen

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18
Q

define hypoxia

A

no oxygen equals no ATP

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19
Q

what does no ATP cause?

A
  • Na/K ATPase fails and an increase in K causes swelling

- calcium pump fails

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20
Q

what does increased calcium cause?

A
  • ATPase
  • phospholipase and proteases (membrane damage)
  • endonuclease (DNA damage)
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21
Q

first physical signs that cells are dying

A
  • cells shrink (pyknotic)
  • red
  • nucleus shrinks and becomes dark
  • contraction bands appear
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22
Q

three types of necrosis

A
  1. caseous
  2. liquefactive
  3. coagulative
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23
Q

describe caseous necrosis

A

cell death with a cheese-like appearance

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24
Q

describe liquefactive necrosis

A

tissue changed into a liquid mass

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25
Q

describe coagulative necrosis

A

cell death with a ghost outline left

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26
Q

function of fibroblasts

A

attempt to maintain structural integrity

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27
Q

two ways cells respond to increase demand

A
  1. hyperplasia: more cells

2. hypertrophy: increase in cell size

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28
Q

process cells undergo when there is a decrease in demand

A

atrophy: decrease in cell size

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29
Q

what happens to cells if there is an altered stimulus

A

metaplasia: abnormal change in the nature of the tissue

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30
Q

three types of growth receptors

A
  1. receptors with intrinsic tyrosine kinase
  2. transmembrane G protein-coupled receptors
  3. receptors without intrinsic tyrosine kinase
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31
Q

four stages of the cell cycle

A
  • G1
  • S
  • G2
  • mitosis
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32
Q

describe what happens in G1

A

CDK4 is activated by cyclin D activates retinoblastoma protein that is not bound to E2F= cell division

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33
Q

describe what happens in the S phase

A

E2F initiates DNA replication

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34
Q

describe the G2 phase

A

cells growth, P53 checks for mistakes

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35
Q

what happens at the end of the cell cycle?

A

chromosomes are capped to stop degradation. TTAGGG repeats.

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36
Q

two mechanisms of cell death

A
  1. necrosis

2. apoptosis

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37
Q

define apoptosis

A

programmed cell death in response to specific signals

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38
Q

two pathways for apoptosis

A
  1. intrinsic

2. extrinsic

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39
Q

describe the intrinsic pathway of apoptosis

A

growth signals promote anti-apoptotic molecules that are replaced by BAX/BAK. this increases permeability of the mitochondria so cytochrome C can enter the cytosol. this activates caspases that enter the nucleus

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40
Q

describe the extrinsic pathway of apoptosis

A

the receptor FAS activates caspases that enter the nucleus

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41
Q

causes of cellular ageing

A
  1. oxidative stress- free radical damage
  2. accumulation of by-products
  3. lipofuscin (granules involved in lysosomal digestion)
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42
Q

define cancer

A

uncontrolled cell proliferation and growth that can invade other tissues

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43
Q

define neoplasia

A

new growth, not in response to a stimulus

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44
Q

define malignant

A

metastatic potential

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45
Q

define dysplasia

A

abnormal growth in response to a stimulus

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46
Q

define metaplasia

A

change in the differentiation of cells (change in nature)

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47
Q

define hyperplasia

A

increase in the number of cells

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48
Q

describe the double hit hypothesis

A

one faulty gene acquired by inheritance and other by the environment

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49
Q

two genetic sequence mutations that can cause cancer

A
  1. initiators

2. promoters

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50
Q

what can E2F without Rb cause?

A

transcription of DNA polymerase

51
Q

define Myc

A

nuclear transcription factor that promotes growth

52
Q

which is the most commonly mutated kinase in cancer?

A

PI3K

53
Q

describe tumour suppressors

A

stop growth

54
Q

what does PTEN do

A

increases transcription of p27

55
Q

describe Bcl-2

A

anti apoptotic material, stops BAX/BAK

56
Q

define angiogenesis

A

development of new blood vessels

57
Q

describe how cells become metastatic

A
  • avoid immune system
  • chew basement membrane
  • break through vessel wall
58
Q

define encapsulation

A

growing lesion stimulates the formation of a capsule to prevent metastasis

59
Q

define mesenchymal

A

connective tissue tumours

60
Q

define haematopoietic

A

white cells

61
Q

epithelium tumour

A

carcinomas

62
Q

glandular tumour

A

adenoma or adenocarcinoma

63
Q

squamous tumour

A

papilloma

64
Q

bladder tumour

A

transitional cell carcinoma

65
Q

malignant mesenchyme tumours

A

sacromas

66
Q

benign fat tumour

A

lipoma

67
Q

malignant fat tumour

A

liposarcoma

68
Q

benign bone tumour

A

osteoma

69
Q

malignant bone tumour

A

osteosarcoma

70
Q

benign cartilage tumour

A

enchondroma

71
Q

malignant cartilage tumour

A

chondrosarcoma

72
Q

skeletal muscle tumour

A

rhabdo-

73
Q

benign smooth muscle tumour

A

leiomyoma

74
Q

malignant smooth muscle tumour

A

leiomyosarcoma

75
Q

benign nerve tumour

A

neurofibroma/ schwannoma

76
Q

benign blood vessel tumour

A

haemangioma

77
Q

malignant blood vessel tumour

A

angiosarcoma

78
Q

CNS tumours

A

gliomas

79
Q

are all blood growths cancerous

A

yes

80
Q

name of blood cancers

A

leukaemia and lymphomas

81
Q

define stages of cancer

A

how far

82
Q

define grade of cancer

A

how bad, differentiation

83
Q

define a blood clot

A

blood hardens from liquid to solid (extravascular)

84
Q

what does a blood clot consist of?

A
  • red blood cells
  • fibrin (holds it all together)
  • platelets
85
Q

define thrombosis

A

trigger of coagulation/ clotting within a blood vessel (intravascular)

86
Q

define exsanguinate

A

loss of blood sufficient enough to cause death (important to coagulate the blood)

87
Q

cause of thrombosis

A

excess of coagulation

88
Q

what does the end point of thrombosis consist of?

A
  • platelets
  • red blood cells
  • fibrin
89
Q

define the coagulation cascade

A

steps in either the intrinsic or extrinsic pathway to activate coagulation

90
Q

describe the intrinsic pathway of the coagulation cascade

A

activation of factor XII. this can be measured with prothrombin time (PT)

91
Q

describe the extrinsic pathway of the coagulation cascade

A

starts with tissue factors. it can be measured with activated partial thromboplastin time (APTT)

92
Q

describe the end point of the coagulation cascade

A
  • prothrombin to thrombin

- thrombin activates fibrinogen to fibrin

93
Q

explain Virchow’s Triad

A
  1. site of endothelial injury
  2. sites of turbulence
  3. hypercoagulability
94
Q

how can hypertension cause endothelial injury which causes thrombosis?

A

hypertension causes increased banging on the vessel walls. this gives increased exposure to tissue factors which weakens the vessel walls resulting in atheroma and aneurysms.

95
Q

other things that can cause endothelial injury

A
  • toxins
  • infectious agents
  • smoking
  • autoimmune diseases
96
Q

define the site of turbulence

A

swirling of blood in stasis. blood flow is normally laminar (central), however there is increased margination (increased contact of platelets and less washing out).

97
Q

define hypercoagulability

A

anything that causes increased viscosity of the blood

98
Q

primary causes of hypercoagulability

A

inherited disorders including:

  • factor V leiden
  • protein C deficiency
  • protein S deficiency
  • antithrombin III deficiency
99
Q

high risk secondary causes of hypercoagulability

A
  • prolonged immobility
  • significant tissue injury (burns,RTA)
  • antiphospholipid syndrome (autoimmune)
  • myocardial infarction
  • atrial fibrillation
  • cancer
100
Q

low risk secondary causes of hypercoagulability

A
  • pill
  • smoking
  • renal disease
  • cardiomyopathy
101
Q

describe how cancer causes hypercoagulability

A

activation of coagulation cascade as the tumour produces TF, mucin and inflammatory cytokines. therapy agents can injure the endothelium too.

102
Q

define an embolism

A

referring to a thrombus that has been transported through the vasculature to a point where it gets stuck

103
Q

where does an embolism stick?

A

it circulates in the blood until it reaches a vessel small enough to stick

104
Q

define ischaemia

A

insufficient blood supply

105
Q

define infarction

A

death of tissue as a result of ischaemia

106
Q

define a hypoxic injury

A

no oxygen equals no ATP

107
Q

examples of embolism no linked to blood constituents

A
  • air
  • amniotic fluid
  • fat
  • tumour
  • septic
108
Q

describe air embolism

A
  • injection of air
  • high pressure results in more dissolved gas
  • reduction in pressure causes nitrogen to leave
  • multiple bubbles causes decopression sickness
109
Q

describe amniotic embolism

A

tear in placenta or uterine vessels

110
Q

describe tumour emboli

A

tumours invade vasculature

111
Q

describe septic emboli

A

in association with infectious agents

112
Q

define haemostasis

A

stops bleeding and maintenance of vascular patency

113
Q

primary haemostasis

A

platelet plug (phospholipid)

114
Q

secondary haemostasis

A

fibrin blood clot (prothrombin to thrombin activates fibrinogen to fibrin).

115
Q

which system does an atheroma occur in?

A

arterial

116
Q

which system does a thrombosis occur in?

A

venous

117
Q

causes of atheroma

A
  • haemodynamic injuries
  • pathogenesis
  • smoking
  • hyperlipidaemia (HDLs and LDLs)
  • diabetes
  • age
  • males
  • genetics
118
Q

describe haemodynamic injuries

A

sites of turbulent blood flow can cause damage

119
Q

describe pathogenesis

A

it is when endothelial injury causes increased vessel permeability and increased white cell adhesion (VCAMs).

120
Q

describe the steps in pathogenesis

A
  • monocytes migrate out of the vessel
  • turn into macrophages and take in cholesterol
  • they are over-run and the cells get stuck
  • accumulation of lipids and macrophages
  • migration of smooth muscle from the media to the initima
  • extracellular matrix is produced
  • fatty streak becomes a fibrofatty plaque
  • increase in size can lead to thrombosis.
121
Q

describe poiseuille’s law

A

small change in diameter of the vessel greatly affects the flow rate

122
Q

what can happen when plaques rupture?

A

release tissue factors that cause injury

123
Q

complications of atheroma’s

A
  • stenosis (narrowing reducing elasticity)
  • aneurysm (dilation of artery due to swelling)
  • dissection (splitting of media)
  • thrombosis and embolism
124
Q

define atheroma

A

degeneration in the walls of the arteries caused by accumulation of fatty deposits and scar tissue leading to restriction.

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