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Principles > Pathology > Flashcards

Pathology Flashcards

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
Q

Caseous Necrosis???

A

TB

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26
Q

What does infarction mean?

A
  • cell death after loss of oxygen
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27
Q

what is the time window for MI cell damage?

A

less than 20 minutes

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28
Q

What is hypoxic injury?

A
  • pathological and results in necrosis
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29
Q

Necrosis requires __no/some___ energy?

A
  • necrosis requires no energy
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30
Q

Necrosis is pathological

true/false?

A
  • true
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31
Q

Coagulative necrosis?

A
  • preservation of cell outline
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32
Q

Colliquative /liquefactive necrosis?

A
  • pus, no cell structure remains

- stroke

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33
Q

Caseous necrosis?

A
  • cheese like

- TB!

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34
Q

As time progresses after cell injury, neutrophils will be replaced by what?

A
  • macrophages

- yellow in colour at autopsy

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35
Q

What are fibroblasts?

A
  • lay down collagen

- complete after 6 weeks post MI

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36
Q

Chronic inflammation results in what?

A
  • restitution
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37
Q

Define hypertrophy

A
  • increase in cell size/volume
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38
Q

Define hyperplasia

A
  • increase in cell number
39
Q

Define atrophy

A
  • reduction in cell size
40
Q

2 mechanisms of cell death?

A
  • necrosis

- apoptosis

41
Q

Define apoptosis

A
  • programmed cell death
42
Q

Is apoptosis pathological or physiological?

43
Q

Apoptosis requires no energy?

true or false

A
  • false

- apoptosis requires enerrgy

44
Q

Explain extrinsic apoptosis pathway

A
  • outwith the cell
  • TNF
  • Fas L –> Fas Receptor
45
Q

Explain intrinsic apotosis pathway

A
  • aka mitochondrial apoptosis

- bax and bas receptors

46
Q

What protein halts the cell cycle?

A
  • p53

- halts cell cycle and can cause apoptosis

47
Q

Too much apoptosis may result in

A
  • neurodegenerative disease
48
Q

Too little apoptosis may result in

A
  • cancer

- autoimmune diseases

49
Q

What can cause cellular aging?

A
  • oxidative stress
  • free radicals
  • build up of by products of metabolism
50
Q

Tyrosine kinase receptors are what?

A
  • transpcription factors
51
Q

What are the 4 stages of the cell cycle?

52
Q

Explain what occurs during G1

A
  • Cyclin D binds to CDK 4
  • Inactivates Rb
  • Rb can no longer bind to E2F
  • E2F gives the green light for next step
53
Q

Explain what occurs during S phase?

A
  • E2F increases levels of cyclin A
  • cyclin A activates CDK 2
  • promotes DNA replication
54
Q

Explain what occurs during G2 phase?

A
  • checkpoint at end

- p53 , can hault cell cycle and induce apoptosis

55
Q

Explain what occurs during M phase?

A
  • chromosome alignement checked
56
Q

How are chromosomes protected?

A
  • capped by telomeres
57
Q

Define cancer

A
  • uncontrolled cell proliferation and growth that can invade other tissues
58
Q

Define tumour

A
  • swelling

- may be malignant, benign, inflammatory

59
Q

Define malignant

A
  • metastatic growth
60
Q

Define metaplasia

A
  • reversible change from one cell type to another

- in response to stimuli

61
Q

Define hyperplasia

A
  • increase in cell number

- requires stimuli but may become autonomus

62
Q

What does autonomous mean?

A
  • required a growth factor at first, but now doesnt
63
Q

Define dysplasia

A
  • disordered growth

- not in response to a stimuli

64
Q

Define carcinoma in-situ

A
  • a group of abnormal cells that are found only in the place where they first formed in the body
65
Q

What are some examples of weinbergs hallmarks of cancer?

A
  • increase growth signals
  • remove growth supression
  • avoid apoptosis
  • achieve immortality
  • avoid immune system
66
Q

Define Angiogenesis

A
  • Formation of new, abnormal blood vessels

- Successfully growing tumours will develop ability to create own blood supply

67
Q

Explain the double hit hypothesis

A
  • one working gene is enough

- 2 faulty genes results in a functional problem

68
Q

Explain the stepwise progression in the double hit hypothesis?

A
  • initation
  • promtion
  • peristance
69
Q

In terms of malignancy what are the 3 growth receptors?

A
  • receptors with intrinsic tyrosine kinase activity
  • 7 transmembrane g-protein coupled receptors
  • receptors without intrinsic tyrosine kinase activity
70
Q

What signal is used in cell death?

A
  • p53

- halts cell cycle and can induce apoptosis

71
Q

How is unlimited replicative potential achieved in malignant cells?

A
  • mutation which reactivates telomerase

- allows futher replication

72
Q

What is an ant-apoptotic molecule?

73
Q

What must occur to become metastatis?

A
  • avoid immune system

- extend through connective tissue

74
Q

Define homogenous in terms of neoplasia?

A
  • tends to be benign

- round and smooth

75
Q

What does it suggest if a tumour is encapsulated?

A
  • slow growing

- benign

76
Q

What does a malignant tumour tend to look like?

A
  • irregular
  • infiltrative
  • destructive
77
Q

Define heterogenous in terms of neoplasia?

A
  • malignant
  • haemorrhage
  • necrosis
  • irregular
78
Q

What would a cancer of the epithelium be called?

79
Q

What would a cancer of glands be called?

A
  • adenoma

- adenocarcinoma

80
Q

What would a cancer of the squamous cell be called?

81
Q

What would a cancer of the bladder be called?

A
  • transitional cell carcinoma
82
Q

What would a cancer of the connective tissue be called?

A
  • mesenchyme
83
Q

What is the staging for cancer?

A
  • TNM
  • Tumour
  • Node
  • Metasis
84
Q

Define cachexia

A
  • wasting of the body due to malignant energy demand
85
Q

Define a blot clot

A
  • extravascular

- fibrin and platelets

86
Q

Define a Thrombosis

A
  • intravascular
  • static
  • coagulation
87
Q

Define coagulation

A
  • aggregation of platelets

- fibrin binds everything together

88
Q

Explain the intrinsic coagulation cascadate in terms of factors

A
  • XII
  • XI
  • IX
  • X
  • X + V
  • II (Thrombin)
  • I (Firbrin)
89
Q

Explain the extrinsic coagulation cascafe in terms of factors

A
  • III
  • VII
  • X + V
  • II (Thrombin)
  • I (Fibrin)
90
Q

What is the commonest pathway in the coagulation cascade?

A
  • X + V
  • II
  • I
91
Q

What factors are activated when factor II is activated?

A
  • I
  • V
  • VII
  • VIII
  • XI
  • XIII
92
Q

What is Virchows triad?

A
  • the mechanisms of my thrombosis occurs
  • endothelial injury
  • blood flow (turbulent / stasis)
  • Coagulability
93
Q

Define Ischaemia?

A
  • insufficient blood flow
94
Q

What factor is the tissue factor?

A
  • factor III

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