Pathology Flashcards

(94 cards)

1
Q

What are the 4 responses to injury?

A
  • vascular changes
  • cellular changes
  • chemical mediators
  • morphologic patterns
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2
Q

Explain the vascular changes in response to injury?

A
  • vasodilation

- mediated by histamine and nitric oxide

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3
Q

Explain the cellular changes in response to injury?

A
  • stasis
  • white cell margination
  • rolling
  • adhesion
  • migration
  • chemotaxis
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4
Q

What happens to the vessels during acute inflammation?

A
  • become leaky
  • loss of proteins
  • can cause ‘tumour’ –> swelling
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5
Q

What is chemotaxis?

A
  • cells follow a chemical gradient and move along it
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6
Q

Explain the 3 steps involved in phagocytosis

A
  • recognition and attachment
  • engulfment
  • killing and degradation
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7
Q

what causes recognition and attachment in phagocytosis

A
  • mannose binding

- opsonisation

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8
Q

What is formed during engulfment in phagocytosis?

A
  • phagosome
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9
Q

What is involved in killing and degradation in phagocytosis?

A
  • reactive oxygen species

- NO is oxidised

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10
Q

Rubor?

A
  • redness
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11
Q

Calor?

A
  • heat
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12
Q

Tumour? and what causes it?

A
  • swelling

- fluid in extracellular space

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13
Q

Dolor? and what causes it?

A
  • painful

- prostaglandins and bradykinin

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14
Q

“Mediators of inflammation are long lived” true/false

A

FALSE

mediators of inflammation are short lived

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15
Q

What is the process of resolution

A
  • good as new
  • complete restoration
  • minimal cell death
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16
Q

What is the process of suppuration

A
  • pus (contains living, dead and dying cells)
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17
Q

What is an empyema?

A
  • pus filled cavity
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18
Q

What is organisation?

A
  • injury produces lots of necrosis and fibrin

- when damage goes beyond the basement membrane

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19
Q

What is granulation tissue?

A
  • undergoes organisation to form fibrous scar
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20
Q

Scarring leads to____

A
  • loss of function
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21
Q

The term given to fibrosis of the liver is____

A
  • cirrhosis
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22
Q

Chronic inflammation is characterised by what cell?

A
  • lymphocytes
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23
Q

What is chronic inflammation dependent on?

A
  • persisent injury

- suppuration etc

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24
Q

What is a granuloma

A

localised collection of cells usually produced in response to an infectious agent

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25
Caseous Necrosis???
TB
26
What does infarction mean?
- cell death after loss of oxygen
27
what is the time window for MI cell damage?
less than 20 minutes
28
What is hypoxic injury?
- pathological and results in necrosis
29
Necrosis requires __no/some___ energy?
- necrosis requires no energy
30
Necrosis is pathological | true/false?
- true
31
Coagulative necrosis?
- preservation of cell outline
32
Colliquative /liquefactive necrosis?
- pus, no cell structure remains | - stroke
33
Caseous necrosis?
- cheese like | - TB!
34
As time progresses after cell injury, neutrophils will be replaced by what?
- macrophages | - yellow in colour at autopsy
35
What are fibroblasts?
- lay down collagen | - complete after 6 weeks post MI
36
Chronic inflammation results in what?
- restitution
37
Define hypertrophy
- increase in cell size/volume
38
Define hyperplasia
- increase in cell number
39
Define atrophy
- reduction in cell size
40
2 mechanisms of cell death?
- necrosis | - apoptosis
41
Define apoptosis
- programmed cell death
42
Is apoptosis pathological or physiological?
- both
43
Apoptosis requires no energy? | true or false
- false | - apoptosis requires enerrgy
44
Explain extrinsic apoptosis pathway
- outwith the cell - TNF - Fas L --> Fas Receptor
45
Explain intrinsic apotosis pathway
- aka mitochondrial apoptosis | - bax and bas receptors
46
What protein halts the cell cycle?
- p53 | - halts cell cycle and can cause apoptosis
47
Too much apoptosis may result in
- neurodegenerative disease
48
Too little apoptosis may result in
- cancer | - autoimmune diseases
49
What can cause cellular aging?
- oxidative stress - free radicals - build up of by products of metabolism
50
Tyrosine kinase receptors are what?
- transpcription factors
51
What are the 4 stages of the cell cycle?
- G1 - S - G2 - M
52
Explain what occurs during G1
- Cyclin D binds to CDK 4 - Inactivates Rb - Rb can no longer bind to E2F - E2F gives the green light for next step
53
Explain what occurs during S phase?
- E2F increases levels of cyclin A - cyclin A activates CDK 2 - promotes DNA replication
54
Explain what occurs during G2 phase?
- checkpoint at end | - p53 , can hault cell cycle and induce apoptosis
55
Explain what occurs during M phase?
- chromosome alignement checked
56
How are chromosomes protected?
- capped by telomeres
57
Define cancer
- uncontrolled cell proliferation and growth that can invade other tissues
58
Define tumour
- swelling | - may be malignant, benign, inflammatory
59
Define malignant
- metastatic growth
60
Define metaplasia
- reversible change from one cell type to another | - in response to stimuli
61
Define hyperplasia
- increase in cell number | - requires stimuli but may become autonomus
62
What does autonomous mean?
- required a growth factor at first, but now doesnt
63
Define dysplasia
- disordered growth | - not in response to a stimuli
64
Define carcinoma in-situ
- a group of abnormal cells that are found only in the place where they first formed in the body
65
What are some examples of weinbergs hallmarks of cancer?
- increase growth signals - remove growth supression - avoid apoptosis - achieve immortality - avoid immune system
66
Define Angiogenesis
- Formation of new, abnormal blood vessels | - Successfully growing tumours will develop ability to create own blood supply
67
Explain the double hit hypothesis
- one working gene is enough | - 2 faulty genes results in a functional problem
68
Explain the stepwise progression in the double hit hypothesis?
- initation - promtion - peristance
69
In terms of malignancy what are the 3 growth receptors?
- receptors with intrinsic tyrosine kinase activity - 7 transmembrane g-protein coupled receptors - receptors without intrinsic tyrosine kinase activity
70
What signal is used in cell death?
- p53 | - halts cell cycle and can induce apoptosis
71
How is unlimited replicative potential achieved in malignant cells?
- mutation which reactivates telomerase | - allows futher replication
72
What is an ant-apoptotic molecule?
- Bcl-2
73
What must occur to become metastatis?
- avoid immune system | - extend through connective tissue
74
Define homogenous in terms of neoplasia?
- tends to be benign | - round and smooth
75
What does it suggest if a tumour is encapsulated?
- slow growing | - benign
76
What does a malignant tumour tend to look like?
- irregular - infiltrative - destructive
77
Define heterogenous in terms of neoplasia?
- malignant - haemorrhage - necrosis - irregular
78
What would a cancer of the epithelium be called?
- carcinoma
79
What would a cancer of glands be called?
- adenoma | - adenocarcinoma
80
What would a cancer of the squamous cell be called?
- papilloma
81
What would a cancer of the bladder be called?
- transitional cell carcinoma
82
What would a cancer of the connective tissue be called?
- mesenchyme
83
What is the staging for cancer?
- TNM - Tumour - Node - Metasis
84
Define cachexia
- wasting of the body due to malignant energy demand
85
Define a blot clot
- extravascular | - fibrin and platelets
86
Define a Thrombosis
- intravascular - static - coagulation
87
Define coagulation
- aggregation of platelets | - fibrin binds everything together
88
Explain the intrinsic coagulation cascadate in terms of factors
- XII - XI - IX - X - X + V - II (Thrombin) - I (Firbrin)
89
Explain the extrinsic coagulation cascafe in terms of factors
- III - VII - X + V - II (Thrombin) - I (Fibrin)
90
What is the commonest pathway in the coagulation cascade?
- X + V - II - I
91
What factors are activated when factor II is activated?
- I - V - VII - VIII - XI - XIII
92
What is Virchows triad?
- the mechanisms of my thrombosis occurs - endothelial injury - blood flow (turbulent / stasis) - Coagulability
93
Define Ischaemia?
- insufficient blood flow
94
What factor is the tissue factor?
- factor III