Pathology Flashcards

(92 cards)

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
liquefactive necrosis?
liquid viscous necrosis with no structure
26
caseous necrosis?
cheesy looking | TB until proven otherwise
27
physiological need for apoptosis
``` normal growth (hand/foot) removal of self lymphocytes ```
28
pathological need for apoptosis
``` injury response radiation chemotherapy infection cancer ```
29
describe extrinsic pathway apoptosis
fas binds to fas death ligand | causes caspase release
30
describe intrinsic pathway apoptosis
growth signals promote anti-apoptotic molecules in mitochondrial membrane Bax/Bac release to increase mitochondrial permeability causing release of cytochrome C and other caspases
31
3 things that happen to cell in apoptosis
pyknosis chromatic condensation cytoplasmic blebs
32
define hypertrophy
cells get bigger
33
define hyperplasia
cell number increases
34
what happens in G1 phase of cell cycle and which cyclin is activated
growth
35
what cyclin activates CDK4?
cyclin D
36
how does activated CDK4 allow the cell to progress to the next cell cycle stage
binds to Rb protein to prevent binding to E2F | E2F allows progression to next stage
37
E2F initiates DNA replication and increases cyclin __ levels
A
38
what does cyclin A do?
propagates DNA replication and binds to CDK2 to move cell to G2
39
what happens in G2
second growth phase
40
what is the G2 checkpoint
p53, checks for mistakes or halts cell cycle | if repair unsuccessful then cell will be apoptosed
41
what is the M phase checkpoint
all chromosomes on metaphase plate and attached to spindle
42
what is the hayflick limit and what are the exceptions
cells can only divide so many times - 50-70 | stem cells and potentially cancer cells are exception
43
true/false - hyperplasia will continue in absence of a stimulus
false
44
example of hyperplasia
lymph nodes in infection | endometrial cell lining at pregnancy
45
example of hypertrophy
physiological or pathological hypertrophy of the heart
46
define atrophy
decrease in cell number
47
reasons for atrophy
``` lost innervation lost blood supply lost hormonal status ageing malnutrition ```
48
true/false - insulin promotes atrophy
false - it opposes it
49
what two hormones promote atrophy and degradation?
glucocotricoids and thyroid hormone
50
what is cancer
uncontrolled cell proliferation and growth that can invade other tissues
51
what is a tumour
swelling
52
what is neoplasia
new growth, not in response to a stimulus
53
what is malignancy
metastatic potential of a neoplastic growth
54
what is dysplasia
disordered growth that is non invasive | rated low to high grade
55
what is carcinoma in situ
dysplasia affecting whole epithelium, last stage before malignancy
56
what is metaplasia
reversible change from one mature cell type to another
57
how are obese patients more likely to have certain cancers
cholesterol mimicks steroid hormones and so can promote growth
58
cancer is identified by the ____
weinberg hallmarks
59
autosomal dominant genes predisposing to cancer
Retinoblastoma | FAP
60
how does chronic inflammation lead to cancer
causes lymphomas - constant lymphocyte production leads to production error
61
3 types of infection that may cause cancer
HPV Epstein-barr Schistosomiasis
62
how does HPV cause cancer
E6 - destroys p53 | E7 - binds to Rb to prevent it binding to E2F
63
how does UVB radiation cause damage to DNA
causes pyrimidine dimers in DNA, can be repaired if minimal
64
chemical causes of cancer
``` smoking - aromatic polycyclic hydrocarbons arsenic aflatoxin beta-naphthylamine nitrosamines ```
65
what test establishes if a chemical may cause cancer?
ames' test
66
what is the double hit hypothesis
those with one dysfunctional gene are predisposed to an issue two dysfunctional genes is a functional problem
67
what is an oncogene
gene promoting cancer growth
68
what is a tumour suppressor
gene discouraging cancer growth
69
most common mutation accounting for carcinoma
EGFR
70
common EGFR mutations
Braf Myc PI3K
71
what is Bcl-2
anti-apoptotic molecule | binds Bax/Bac to stop holes getting punched in mitochondria
72
drug target to prevent angiogenesis in cancer
VEGF | vascular endothelial growth factor
73
what cancers does BRCA cause
breast, ovarian, pancreatic
74
true/false - cancer daughter cells are identical to their cancer parent cells
false
75
how would a benign tumour appear?
smooth, homogenous, encapsulated
76
how would a malignant tumour appear
nasty, heterogenous, irregular, destructive
77
cancer cells are well/poorly differentiated
poorly
78
N:C ratio is raised/lowered in cancer
raised
79
epithelial neoplasm
carcinoma
80
glandular neoplams
adenoma - benign | adenocarcinoma
81
squamous neoplasms
papilloma | SCC
82
bladder neoplasm
transitional cell sarcoma
83
what is immunohistochemistry
binding of antibodies to probe and then to specimen. if it goes brown expected chemical is present
84
how is cancer progression/advance recorded
TNM staging
85
what is cahexia
malignancy related weight loss
86
what is paraneoplastic symptoms
hormone production by tumour to result in electrolyte disturbance
87
what is virchow's triad
site of endothelial injury turbulent blood flow hypercoagulable blood secondary causes
88
what may cause endothelial injury
``` toxins infection smoking hypertension autoimmunity ```
89
4 inherited diaorders causing hypercoagulable blood
factor V leiden Antithrombin III deficiency protein C deficiency Protein S deficiency
90
secondary causes of thrombosis
``` immobility MI AF cancer contraceptives smoking cardiomyopathy tissue injury ```
91
causes of air embolus
decompression sickness | IV injection
92
types of embolism
``` thrombotic septic tumour fat air amniotic fluid ```