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MB1: Principles > Pathology > Flashcards

Pathology Flashcards

1
Q

VINDICATE?

A 
Vascular disease 
infection/inflammation
neoplasia 
drugs 
iatrogenic 
congenital 
autoimmune 
trauma 
endocrine/metabolic
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2
Q

what is stasis

A

slowing of blood due to vasodilation

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3
Q

what is margination

A

blood cells moving to periphery of vessels

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4
Q

thrombin and histamine increase expression of which adhesion molecules

A

integrin and selectin

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5
Q

increased TNF and IL-1 increase expression of which adhesion molecules

A

ICAM and VCAM

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6
Q

what is rolling

A

low affinity binding of adhesion molecules along vascular wall until they become higher affinity closer to infection site to allow for white cells to bind

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7
Q

what is chemotaxis

A

exiting of vascular system to follow concn gradient to reach infection site

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8
Q

3 stages of phagocytosis

A

recognition/attachment
engulfment
killing and degradation

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9
Q

how do phagocytes recognise bacteria

A

mannose receptors

opsonins

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10
Q

how do phagocytes engulf pathogens

A

pseudopods trap bacteria
trapped in phagosome
joins with lysosome to form phagolysosome

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11
Q

what is resolution and in what conditions is it favoured?

A 
fully healed tissue 
minimal cell death
capacity to repair 
good vascular supply 
removing injurious agent
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12
Q

what is suppuration

A

pus formation

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13
Q

what is organisation

A

formation of scar tissue

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14
Q

when is organisation indicated

A

no tissue capacity to repair
poor blood supply
damage beyond basal lamina

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15
Q

how does organisation occur

A

deposition of granulation tissue (smooth muscle and collagen)
resolution attempted, when impossible myofibroblasts produce collagen to scar

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16
Q

what is chronic inflammation characterised by?

A

presence of lymphocytes and sometimes monocytes

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17
Q

causes of chronic inflammation

A

exogenous/endogenous material

infection

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18
Q

when may resolution occur after MI

A

within 20 min window

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19
Q

what happens in first 24 hours post MI without treatment

A

cell contents leak into ECF

inflammation occurs due to necrosis

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20
Q

when is cardiac perforation most likely to occur

A

3-7 days

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21
Q

how long does it take cardiac muscle to fully scar

A

6 weeks

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22
Q

complications of scarring to the heart

A

structural impairment

arrhythmia

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23
Q

true/false - necrosis requires energy input

A

false

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24
Q

coagulative necrosis?

A

cell outline preservation

most common

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25
Q

liquefactive necrosis?

A

liquid viscous necrosis with no structure

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26
Q

caseous necrosis?

A

cheesy looking

TB until proven otherwise

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27
Q

physiological need for apoptosis

A 
normal growth (hand/foot)
removal of self lymphocytes
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28
Q

pathological need for apoptosis

A 
injury response 
radiation 
chemotherapy 
infection
cancer
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29
Q

describe extrinsic pathway apoptosis

A

fas binds to fas death ligand

causes caspase release

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30
Q

describe intrinsic pathway apoptosis

A

growth signals promote anti-apoptotic molecules in mitochondrial membrane
Bax/Bac release to increase mitochondrial permeability causing release of cytochrome C and other caspases

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31
Q

3 things that happen to cell in apoptosis

A

pyknosis
chromatic condensation
cytoplasmic blebs

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32
Q

define hypertrophy

A

cells get bigger

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33
Q

define hyperplasia

A

cell number increases

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34
Q

what happens in G1 phase of cell cycle and which cyclin is activated

A

growth

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35
Q

what cyclin activates CDK4?

A

cyclin D

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36
Q

how does activated CDK4 allow the cell to progress to the next cell cycle stage

A

binds to Rb protein to prevent binding to E2F

E2F allows progression to next stage

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37
Q

E2F initiates DNA replication and increases cyclin __ levels

A

A

38
Q

what does cyclin A do?

A

propagates DNA replication and binds to CDK2 to move cell to G2

39
Q

what happens in G2

A

second growth phase

40
Q

what is the G2 checkpoint

A

p53, checks for mistakes or halts cell cycle

if repair unsuccessful then cell will be apoptosed

41
Q

what is the M phase checkpoint

A

all chromosomes on metaphase plate and attached to spindle

42
Q

what is the hayflick limit and what are the exceptions

A

cells can only divide so many times - 50-70

stem cells and potentially cancer cells are exception

43
Q

true/false - hyperplasia will continue in absence of a stimulus

A

false

44
Q

example of hyperplasia

A

lymph nodes in infection

endometrial cell lining at pregnancy

45
Q

example of hypertrophy

A

physiological or pathological hypertrophy of the heart

46
Q

define atrophy

A

decrease in cell number

47
Q

reasons for atrophy

A 
lost innervation
lost blood supply 
lost hormonal status 
ageing 
malnutrition
48
Q

true/false - insulin promotes atrophy

A

false - it opposes it

49
Q

what two hormones promote atrophy and degradation?

A

glucocotricoids and thyroid hormone

50
Q

what is cancer

A

uncontrolled cell proliferation and growth that can invade other tissues

51
Q

what is a tumour

A

swelling

52
Q

what is neoplasia

A

new growth, not in response to a stimulus

53
Q

what is malignancy

A

metastatic potential of a neoplastic growth

54
Q

what is dysplasia

A

disordered growth that is non invasive

rated low to high grade

55
Q

what is carcinoma in situ

A

dysplasia affecting whole epithelium, last stage before malignancy

56
Q

what is metaplasia

A

reversible change from one mature cell type to another

57
Q

how are obese patients more likely to have certain cancers

A

cholesterol mimicks steroid hormones and so can promote growth

58
Q

cancer is identified by the ____

A

weinberg hallmarks

59
Q

autosomal dominant genes predisposing to cancer

A

Retinoblastoma

FAP

60
Q

how does chronic inflammation lead to cancer

A

causes lymphomas - constant lymphocyte production leads to production error

61
Q

3 types of infection that may cause cancer

A

HPV
Epstein-barr
Schistosomiasis

62
Q

how does HPV cause cancer

A

E6 - destroys p53

E7 - binds to Rb to prevent it binding to E2F

63
Q

how does UVB radiation cause damage to DNA

A

causes pyrimidine dimers in DNA, can be repaired if minimal

64
Q

chemical causes of cancer

A 
smoking - aromatic polycyclic hydrocarbons 
arsenic
aflatoxin 
beta-naphthylamine 
nitrosamines
65
Q

what test establishes if a chemical may cause cancer?

A

ames’ test

66
Q

what is the double hit hypothesis

A

those with one dysfunctional gene are predisposed to an issue
two dysfunctional genes is a functional problem

67
Q

what is an oncogene

A

gene promoting cancer growth

68
Q

what is a tumour suppressor

A

gene discouraging cancer growth

69
Q

most common mutation accounting for carcinoma

A

EGFR

70
Q

common EGFR mutations

A

Braf
Myc
PI3K

71
Q

what is Bcl-2

A

anti-apoptotic molecule

binds Bax/Bac to stop holes getting punched in mitochondria

72
Q

drug target to prevent angiogenesis in cancer

A

VEGF

vascular endothelial growth factor

73
Q

what cancers does BRCA cause

A

breast, ovarian, pancreatic

74
Q

true/false - cancer daughter cells are identical to their cancer parent cells

A

false

75
Q

how would a benign tumour appear?

A

smooth, homogenous, encapsulated

76
Q

how would a malignant tumour appear

A

nasty, heterogenous, irregular, destructive

77
Q

cancer cells are well/poorly differentiated

A

poorly

78
Q

N:C ratio is raised/lowered in cancer

A

raised

79
Q

epithelial neoplasm

A

carcinoma

80
Q

glandular neoplams

A

adenoma - benign

adenocarcinoma

81
Q

squamous neoplasms

A

papilloma

SCC

82
Q

bladder neoplasm

A

transitional cell sarcoma

83
Q

what is immunohistochemistry

A

binding of antibodies to probe and then to specimen. if it goes brown expected chemical is present

84
Q

how is cancer progression/advance recorded

A

TNM staging

85
Q

what is cahexia

A

malignancy related weight loss

86
Q

what is paraneoplastic symptoms

A

hormone production by tumour to result in electrolyte disturbance

87
Q

what is virchow’s triad

A

site of endothelial injury
turbulent blood flow
hypercoagulable blood
secondary causes

88
Q

what may cause endothelial injury

A 
toxins 
infection 
smoking 
hypertension 
autoimmunity
89
Q

4 inherited diaorders causing hypercoagulable blood

A

factor V leiden
Antithrombin III deficiency
protein C deficiency
Protein S deficiency

90
Q

secondary causes of thrombosis

A 
immobility 
MI
AF
cancer 
contraceptives
smoking 
cardiomyopathy 
tissue injury
91
Q

causes of air embolus

A

decompression sickness

IV injection

92
Q

types of embolism

A 
thrombotic 
septic 
tumour 
fat 
air 
amniotic fluid

MB1: Principles (10 decks)

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