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Pathology Flashcards

1
Q

What are the main cells associated with acute and chronic inflammation?

A

Acute - Neutrophils

Chronic - Macrophages & lymphocytes

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2
Q

Are local and systemic signs more prominent in acute or chronic inflammation?

A

Acute

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3
Q

Is tissue injury and fibrosis usually milder in acute or chronic inflammation?

A

Acute

*Chronic can be progressive

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4
Q

What are the responses to injury resulting in acute inflammation?

A

Vascular and cellular changes

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5
Q

Which vessel dilates first in acute inflammation? What dilates after that? Which 2 mediators are involved in this?

A

Arterioles –> pre-capillary sphincter –> capillary beds

Histamine and NO.

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6
Q

What happens to the microvasculature during acute inflammation?

A

Becomes more permeable, allowing exudation to occur thus slowing blood flow –> increased viscosity –> stasis, engorgement and white cell margination/ pavementing (redistribution)

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7
Q

What are the 6 processes involved in cellular changes of acute inflammation?

A 
Stasis
White cell margination/ pavementing
Rolling
Adhesion
Migration via diapedesis
Chemotaxi
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8
Q

Histamine and thrombin released from inflammatory cells can activate endothelium, resulting in the expression of?

A

Selectin (adhesion molecules)

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9
Q

How strongly does selectin bind to WBCs? What movement does this result in?

A

Low/ weak affinity causing a rolling movement

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10
Q

What happens when WBCs encounter chemokines?

A

Changes conformation and expresses integrin which binds at high affinity to VCAM ad ICAM at endothelium

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11
Q

What causes endothelium to express ICAM and VCAM?

A

Cytokines (TNF, IL-1)

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12
Q

Where and how do WBCs migrate to the extravascular space? What is this process called?

A

At post-capillary venules (maximal retraction), WBCs migrate by squeezing though intercellular junction.

Transmigration/ extravasation.

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13
Q

Where and how do leukocytes migrate in the extravascular space?
What is this process called?

A

Front wheel motion towards stimulus where chemoattractants were produced.

Chemotaxi.

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14
Q

What causes swelling/ oedema?

A

Decreased vascular permeability causing loss of protein and oncotic pressure –> water leaves

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15
Q

What are the 4 causes of vascular leakiness

A
  1. Endothelial retraction from mediators (short-lived at post-capillary venule)
  2. Endothelial injury resulting in necrosis and detachment
  3. Transcytosis - increased fluid and protein transport
  4. Angiogenesis - via VEGF (initially leaky e.g. granulation tissue)
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16
Q

What are the 3 components of phagocytosis?

A
  1. Recognition and attachment via mannose receptors (microbes), scavenger receptors (OxLDL) and opsonins
  2. Engulfment via pseudopods and phagosome formation
  3. Killing and degradation in lysosome via ROS (NADPH oxidase), RNS (NO synthease) and lysosomal enzymes
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17
Q

Why can phagocyte engulfment cause bystander damage?

A

Due to granule release into extracellular space

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18
Q

What mediates pain felt in inflammation?

A

Prostaglandins and bradykinins

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19
Q

What are the 4 mediators for endothelial retraction?

A

Histamine, Bradykinin, Substance P, Leukotrienes

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20
Q

How long do neutrophils live after leaving the blood before undergoing apoptosis?

A

A few hours to a day (short-lived)

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21
Q

What are the 4 possible outcomes of acute inflammation?

A
  1. Resolution
  2. Suppuration
  3. Repair, organisation and fibrosis
  4. Chronic inflammation

**All 2-4 are not mutually exclusive

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22
Q

What do the outcomes of acute inflammation depend on?

A
  1. Site of injury (E.g. capacity of organ to repair)
  2. Type of injury (E.g. pathogenicity)
  3. Duration of injury
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23
Q

What the term for when there is complete restoration of tissue function to normal after removal of inflammatory components called?
How long do injuries usually last for this?

A

Resolution.

Short-lived injury with minimal tissue destruction.

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24
Q

An example of an injury that leads to resolution

A

Erosions/ abrasions (with intact basement membrane)

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25
Q

What kind of tissues does resolution occur in? (3)

A
  1. With capacity to repair (E.g. GI high turnover, Parenchymal cells)
  2. Good vascular supply for WBC access and rapid removal of injurious agents
  3. Some scaffold left
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26
Q

What kind of cells can be found in pus/ exudate? (5)

A

Living, dying, dead cells, neutrophils, bacteria

+ Inflammatory debris (Fibrin)

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27
Q

What is an empyema?

A

When local space is filled with pus and walled off by fibrous wall

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28
Q

What kind of bacteria causes liquefactive necrosis?

A

Pyogenic bacteria (Staphylococci)

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29
Q

Why is IV antibiotics not very effective to treat abscess? What should the treatment be then?

A

No blood vessel access.

Drain.

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30
Q

When does scarring and fibrosis occur? (3)

A
  1. Injury with substantial necrosis/ destruction
  2. Injury with a lot of fibrin exudate
  3. Poor vascular supply - difficult to remove debris
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31
Q

What is the term for when fibrosis develops in a tissue space occupied by inflammatory exudate?

A

Organisation

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32
Q

How does healing occur in scarring/ fibrosis?

A

Via connective tissue/ collagen replacement becoming a mass of fibrous tissue

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33
Q

What are the 3 outcomes of scar tissue formation?

A

Loss of function (e.g. muscle, no oil/ sweat secretion, no sensation)
Contracted/ taut
Patches up tissue

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34
Q

What kind of injury will favour scarring/ fibrosis?

A

When injury goes beyond basement membrane (thus no scaffold)

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35
Q

What is the replacement of lost tissue with fibrotic connective tissue and maturation of tissue stem cells?

A

Healing

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36
Q

What is process of granulation tissue formation?

A

Capillaries infiltration (thin-walled and leaky) –> myofibroblasts –> collagen deposition + smooth muscle cells

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37
Q

When a liver is scarred and fibrosed, what is this known as? What would the liver feel like?

A

Cirrhosis.

Hard.

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38
Q

What does cirrhosis cause?

A

Loss of liver function and reduced/ no blood supply to hepatocytes due to fibrous tissue

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39
Q

What are the 2 co-existing processes in chronic inflammation?

A

Inflammation and repair

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40
Q

Must acute inflammation precede a chronic inflammation?

A

Not necessarily

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41
Q

What are the 5 factors that favour chronic inflammation?

A
  1. Suppuration and scarring
  2. Prolonged exposure to injurious agent (endo- or exogenous)
  3. Infectious agent (Hep B, C)
  4. Persistent infection (Mycobacterium - granulomatous inflammation)
  5. Type of injury (Transplant rejection (Ab involvement), Hypersensivitity as in autoimmune, asthma)
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42
Q

What is the morphology that characterizes chronic inflammation?

A

Primarily lymphocytes THEN macrophages

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43
Q

How do macrophages sustain a chronic inflammatory response?

A

Present antigens and co-mediators that activate T cells –> recruit and activates more macrophages

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44
Q

What are granulomas? (3+1)

A

Aggregate of epithelioid histiocytes (Stationary phagocytes in connective tissue) which can fuse to form Langhans giant cell (multi-nucleated)
Central zone of necrosis
Collar of surrounding lymphocytes

**Older granulomas - rim of fibroblasts + connective tissue

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45
Q

Are granulomas and granulation tissue the same?

A

No

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46
Q

What colour are epithelioid histiocytes?

A

Pink due to abundant granular cytoplasm

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47
Q

When do granulomas appear? (3 examples)

What is healing usually accompanied by?

A

Containing an agent that is difficult to eradicate (FB, endo-, exogenous)

Extensive fibrosis

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48
Q

What does caseous necrosis + granulomas under ZN stain suggest?

A

TB

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49
Q

As the calcium pump fails in hypoxic injury, there will be increased intracellular calcium. What does this lead to? (5)

A 
Release of:
ATPase
Phospholipase
Protease
Endonuclease
Pro-death factors (due to mitochondrial permeability)
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50
Q

What is the window period where no macroscopic and microscopic changes are seen in an MI?

A

20min

**Only ECG changes

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51
Q

What happens to cells 30mins post-MI? (3)

A

Pyknosis (shrink), becomes red
Nucleus shrinks and darkens
Marginal contraction bands appear

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52
Q

What happens in the first 24h post-MI? (2)

A 
Acute inflammation from complement cascade due to leakage of cell contents
Vascular changes (Vasodilation, Extravasation of WBCs)
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53
Q

When is risk of cardiac rupture the greatest post-MI?

A

3-7 days

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54
Q

Abundant macrophages give off what appearance?

A

Yellow

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55
Q

Suppuration implies what about the injury?

A

Persistence of injury

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56
Q

When are macrophages replaced by fibroblasts post-MI?

A

After 2 weeks

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57
Q

After 6 weeks is it still possible to date when the MI has occured?

A

No, only scarring from collagen deposition by fibroblasts seen

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58
Q

What can occur if nerve bundles in the heart are damaged/ scarred?

A

Arrhythmia (Fibrillation)

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59
Q

What is the term for increase in cell number in response to external stimuli?

A

Hyperplasia

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60
Q

When does hyperplasia regress?

A

Upon withdrawal of stimulus

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61
Q

Is hyperplastic tissue at risk of cancer?

A

Yes, can start to grow in absence of stimuli

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62
Q

What are 3 examples of physiological causes of hyperplasia?

A
  1. Hormonal (breast tissue in puberty)
  2. Pregnancy (endometrial lining)
  3. Compensatory (after loss of bone marrow/ tissue tissue)
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63
Q

What are 2 examples of pathological causes of hyperplasia?

A
  1. Hormonal (Excess oestrogen causing endometrial hyperplasia and abnormal menstrual bleeding; excess andogens causing prostatic hyperplasia)
  2. Infection (LNs; and Skin warts and mucosal lesiosn due to HPV)
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64
Q

What is the term used to describe an increase in cell size in response to a stimulus?

A

Hypertrophy

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65
Q

Is hypertrophy reversible?

A

Yes, upon withdrawal of stimulus

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66
Q

What kind of cells do hypertrophy occur in?

A

Those with limited dividing capacity (Skeletal and cardiac muscle cells)

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67
Q

When does hypertrophy occur?

A

In response to mechanical stress

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68
Q

What does hypertrophy of myocytes result in?

A

Increases requirement of blood supply (mismatch)

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69
Q

What is the term used to describe shrinkage in cell size by loss of cell substance?

A

Atrophy

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70
Q

What are 2 examples of physiological atrophy?

A
  1. Uterus after parturition

2. Endometrium after loss of hormonal stimulation (menopause)

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71
Q

What are 7 examples of pathological atrophy?

A
  1. Remains of congenital structures
  2. Decreased workload
  3. Loss of nerve innervation –> loss of function
  4. Atherosclerosis and brain atrophy (decreased blood supply)
  5. Inadequate nutrition
  6. Senile atrophy/ ageing in cells with no replicative ability
  7. Pressure atrophy (normal tissues adjacent to tumours/ upstream to obstruction)
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72
Q

What are the 2 hormones that promote degradation and atrophy?
What is the hormone antagonistic to this?

A

Glucocorticoids and Thyroid hormones

Insulin (growth-promoting)

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73
Q

Reduced metabolism decreases synthesis of?

A

Protein

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74
Q

Which pathway does protein degradation undergo due to nutrition deficiency/ disuse?

A

Ubiquitin proteasome pathway (Autophagy)

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75
Q

What does activation of MAPK/ ERK pathway via intrinsic tyrosine kinase receptors result in? (4)

A

Protein synthesis
Cell growth
Cell proliferation
Decreased apoptosis

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76
Q

What is the outcome of the Wnt canonical pathway (GPCR)?

A

Increase transcription

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77
Q

Cyclin and CDKs.

Which controls which?

A

Cyclins control/ activates CDKs

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78
Q

Which cyclin activates which CDK in G1 and what is the downstream outcome?

A

Cyclin D activates CDK4.

Rb phosphorylated thus releasing E2F, allowing cell cycle to progress to S phase

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79
Q

What is the role of E2F and what inhibits it?

A

E2F promotes DNA replication (S phase)

Rb inhibits it by binding to it

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80
Q

What CDK is able to phosphorylate Rb other than CDK4?

A

CDK2 (activated by Cyclin E)

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81
Q

Which cyclin is involved in the S phase? What CDK does it activate?

A

Cyclin A activates CDK2 (also promotes DNA replication)

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82
Q

Where does the MAIN checkpoint of mitosis occur? By which protein?

A

END of G1.

By p53.

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83
Q

What is the role of p53?

A

Pauses cell cycle when mistake is found to attempt repair.

If repair fails, cell is signaled for apoptosis (intrinsic)

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84
Q

Which structure caused replicative senescence?

A

Telomeres

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85
Q

Where are telomeres found on a chromosome? Which is its role?

A

End of chromosomes (caps),

Protection and prevent ends from degradation and fusion

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86
Q

What is the sequence found in telomeres?

A

TTAGGG repeats

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87
Q

What is Hayflick limit?

A

50-70 divisions

**Dividing capacity in a normal cell

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88
Q

How are telomeres like in stem cells?

A

Can switch on and off

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89
Q

With every division, what happens to the telomere repeats?

A

Gets smaller

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90
Q

How much energy is required for necrosis to occur?

A

None

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91
Q

When is necrosis physiological?

A

Never

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92
Q

What happens to the nuclei and mitochondria in necrosis?

A 
Mitochondria dilates
Nuclei disappears (fragmented)
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93
Q

Loss of basophillic cytosol RNA in necrosis gives it a ___ picture

A

Eosinophillic (red)

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94
Q

What are the 3 types of necrosis?

A

Coagulative, Liquefactive, Caseous

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95
Q

What kind of necrosis is cheesy and what is this associated with?

A

Caseous necrosis.

TB.

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96
Q

What is the microscopic picture of caseous necrosis? (5)

A

Granulomatous inflammation with central zone of necrosis
Structureless/ Amorphous
No cellular outline
Eosinophilic and granular debris

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97
Q

What kind of necrosis does stroke cause?

A

Liquefactive

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98
Q

How does ischaemic and haemorrhagic stroke appear on CT?

A

Ischaemic - dark region

Haemorrhagic - bright region

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99
Q

What are the features of liquefactive necrosis? (3)

A

Pus
Localised bacterial and fungal infections
Liquid viscous mass (no cell structure left)

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100
Q

What is the tissue architecture like in coagulative necrosis?

A

Preserved for days after death

Firm texture

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101
Q

How do dead cells look like in coagulative necrosis?

A

Cell outline preserved

Ghost outline before complete phagocytosis

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102
Q

Why is proteolysis not favoured in coagulative necrosis?

A

Microenvironment too toxic

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103
Q

What is colour and nuclei picture in coagulative necrosis?

A

Eosinophilic

Anucleate

104
Q

Where is coagulative necrosis commonly seen?

A

Infarcts of solid organs (e.g. MI) except brain

105
Q

What is needed for apoptosis to occur?

A

Energy/ ATP

106
Q

What is the term for ‘programmed cell death in response to specific signals’?

A

Apoptosis

107
Q

When is apoptosis physiological? (4)

A
  1. Development as part of normal growth (finger, toes during embryogenesis)
  2. Remove self-reactive lymphocytes
  3. Decline of WBCs at end of immune response (stimulus gone)
  4. Hormonal-dependent involution (removal of hormonal stimuli for growth of endometrium)
108
Q

Which apoptosis pathway does recognizing self-antigens induce?

A

Extrinsic and Intrinsic

109
Q

When is apoptosis pathological? (7)

A
  1. Injury
  2. Radiation (UV, sunburn, DNA strand breaks)
  3. Chemotherapy
  4. Accumulation of misfolded proteins (ER stress)
  5. Viral infected cells
  6. Cancer
  7. Graft vs Host disease (signals from WBC from transplanted tissue)
110
Q

What do viral proteins activate to cause apoptosis? (2)

A

Mitochondrial pathways

Killed by CTLs

111
Q

WBCs from where is responsible for GVHD?

A

From the transplanted tissue

112
Q

What are the 2 ligands that are involved in extrinsic/ death receptor-initiated pathway?

A

FasL

TNF

113
Q

What does FasL interact with to induce intrinsic apoptosis?

A

Crosslinks with Fas protein with cytosolic conserved death domain –> activates caspase 8

114
Q

What can occur if Fas proteins of CTLs recognises self-T cells?

A

Apoptosis of lymphocytes (Autoimmune)

115
Q

What are 2 anti-apoptotic molecules found in the mitochondrial membrane?

A

Bcl-2

Bcl-xL

116
Q

What is the role of Bcl-2? (2)

A

Hold Bax and Bak in check

Controls mitochondrial membrane permeability

117
Q

What happens to the BH3 sensors when cell is exposed to injurious agents?

A

BH3 sensors are released –> Bax and Bak released –> Dimerize and form channel at membrane –> release cytochrome C –> stimulates caspases

**Absence of Bcl-2 facilitates release of proteins from mitochondria (reduced permeability)

118
Q

What are the 2 pro-apoptotic proteins?

A

Bax and Bak

119
Q

What is the common endpoint in the instrinsic and extrinsic apoptotic pathway?

A

Activates caspase 3

120
Q

What is the result of caspase 3?

A

Acts on nucleus to cause DNA fragmentation by endonuclease –> formation of apoptotic bodies, phospholipid flip

121
Q

Are cellular contents released in apoptosis?

A

No, they are phagocytosed

122
Q

Where does the intrinsic apoptotic pathway mainly occur/ regulated at?

A

Mitochondria

123
Q

p53 is a mitotic checkpoint protein.

If the damage is too great for repair, what does it stimulate? Apoptosis will be via which pathway?

A

Stimulates BH3 sensor.

Instrinsic/ mitochondrial pathway

124
Q

What are the morphological features of apoptosis? (5)

A

Pkynosis (shrinkage)
Chromatin condensation (nucleus clumps and breaks up)
Cytoplasmic blebs
Macrophages (antigen presentation and clears debris)
More organization and architecture

125
Q

What is the marker of past free radical injury called? What colour is it?

A

Lipofuscin.

Brownish-yellow intracellular material

126
Q

What does reduced IGF-1 signalling do to cell growth and metabolism?

A

Lowers rates.

Less errors in DNA replication, better repair

127
Q

What are the 2 key features of cancer?

A

Uncontrolled cell growth

Ability to invade and survive

128
Q

Is tumour and cancer the same?

A

No, tumour just means a lump

129
Q

What is neoplasm?

A

Irreversible growth not in response to stimulus

130
Q

What are the 3 classes of neoplasia?

A

Benign
Pre-malignant
Malignant

131
Q

Which organ does neoplasia not occur in?

A

Lens of the eye

132
Q

Is neoplasia the same as cancer?

A

No

133
Q

What is the term for the ability of neoplastic cells to spread to other sites? What structure does it have to cross?

A

Metastasis.

Basement membrane

134
Q

What is disordered/ irregular growth?

A

Dysplasia

135
Q

Is there invasion in dysplasia?

A

No, no growth beyond basement membrane

136
Q

What is the last stage before malignancy known as? What does it affect?

A

Carcinoma-in-situ.

Dysplasia affecting whole epithelium (including non-glandular epithelium)

137
Q

What have to precede before cells become malignant?

A

Several precursor stages (accumulate mutations)

138
Q

What is metaplasia?

A

REVERSIBLE change from one MATURE cell type to other MATURE cell type

139
Q

What causes metaplasia?

A

Change in stimulus (noxious) resulting in stem cells differentiating to a different cell line

140
Q

Which metaplasia is common in response to injury?

A

Squamous metaplasia (resistant to injury as in skin)

141
Q

What kind of epithelium is found in the bladder?

A

Transitional

142
Q

What is the pre-malignant change in the oesophagus known as?

A

Barrett’s oesophagus

*Risk of dysplasia

143
Q

What is used to tell if a dysplasia is bad or not?

A

Grading system

144
Q

Why are obese post-menopausal females more at risk of endometrial hyperplasia?

A

Structure of cholesterol mimics steroid hormones –> eventual autonomous hyperplasia

145
Q

What are the risk factors/ causes of cancer? (9)

A 
Smoking
Alcohol
Drugs
Obesity
UV radiation

Chemical
Infections
Genes (Predisposition)
Inflammation (Chronic)

SADOU CIGI

146
Q

What are the Weinberg Hallmarks to denote cancer? (10)

A

Metastasis (Invasion)
Angiogenesis
Mutation (Genome instability)
Avoid cell death and immune destruction

Deregulating cellular energetics
Evade growth suppressors
Sustain proliferative signaling
Tumour-promoting inflammation
Immortality

**MAMAa DESTI

147
Q

Which gene is mutated in Familial Adenomatous Polyposis (FAP)? % chance of colon cancer?

A

APC gene

100% chance before 50yrs old

148
Q

What is the double hit hypothesis?

A

1 working gene is enough to function well
2 faulty copies will result in functional problem

*Inheritance of 1 faulty copy increases risk

149
Q

Mutation in p53 causes?

A

Li Fraumeni

150
Q

Mutation in APC causes?

A

FAP colon cancer

Gardner syndrome

151
Q

Mutation in PTCH causes?

A

Gorlin’s syndrome

152
Q

Mutation in PTEN cauuses?

A

Cowden’s syndrome

153
Q

Mutation in MLH1 causes?

A

HNPCC

Muir Torres

154
Q

Mutation in RET causes?

A

MEN1

155
Q

What are initiators and promoters in cancer?

A

Initiators - cause long lasting genetic damage but not enough to cause cancer; needs to be followed by promoter

Promoters - requires damage to be caused by initiators first

156
Q

How is DNA damaged in chemical carcinogenesis?

A

Direct

157
Q

What test can be used to test if compound is possibly mutagenic/ carcinogenic?

A

Ames Test

158
Q

Which cancer is smoking strongly associated with?

A

Small cell lung cancer (Bad prognosis)

159
Q

What is the worst constituent chemical found in cigarettes?

A

Polycyclic aromatic hydrocarbons

160
Q

A cell may have a lot of genetic damage but why does it not necessarily progress to cancer?

A

DNA repair mechanisms

161
Q

What cancer is aflatoxins associated with?

A

Liver cancer

162
Q

What mutation is aflaxtoxin associated with?

Where is aflatoxins found in?

A

p53 mutation.

Fungus (Eastern/ chinese diet)

163
Q

What cancer is beta-napthalene associated with?

A

Bladder cancer

*Due to glucuronidase in urine turning it back to its toxic state

164
Q

What cancers are associated with background nuclear radiation?

A

Leukemia

Thyroid cancer

165
Q

UVB radiation exposure is associated with which skin cancer?

A

Skin cancer

166
Q

UVB radiation causes?
How is this overcome?
What condition can arise if this mechanism is mutated?

A

Pyrimidine dimers in DNA.
NER.
Xeroderma Pigmentosa (increases risk of skin cancer)

167
Q

What are the 2 oncogenes found in HPV and how do they cause cancer?
How are they involved in mutation?

A

E6 - increases p53 degradation by ubiquitination
E7 - binds to Rb protein; E2F free to promote cell growth

They do not cause mutations thus they INDIRECTLY causes cancer

168
Q

What cancers are associated with EBV (Infectious mononucleosis)? (4)

A

Burkitt-lymphoma
B-cell lymphoma
Hodgkin lymphoma
Nasopharyngeal carcinoma

169
Q

How does chronic inflammation cause cancer?

A

Lymphocytes constantly produced and activated –> tissue instability

170
Q

What 2 cancers are strongly associated with obesity?

A 
Endometrial cancer (Background hyperplasia)
Renal cell carcinoma (Especially centripetal obesity)
171
Q

Which pathway is strongly associated with obesity-causing cancers?

A

mTOR pathway (cell growth and biomolecule synthesis)

172
Q

What does processed meat contain that’s associated with cancer?

A

N6 polyunsaturated fats - angiogenic, anti-apoptotic

*N3 PUFAs (good)

173
Q

Which growth factor is associated with obesity-causing cancers?

A

IGF-1

174
Q

What is the MAPK/ERK pathway?

Defect in this pathway contributes to which Weinberg hallmark?

A

EGRF –> RAS –> RAF –> MEK –> MAPK –> MYC –> Transcription

Sustained growth signalling

175
Q

What drugs target EGRF and BRAF?

A

EGRF - Trastuzumab (Herceptin)

BRAF - Vemurafenib

176
Q

What cancers are associated with RAS mutation (4)?

A

Pancreas
Colorectal
Thyroid undifferentiated papillary
Thyroid follicular

177
Q

What tumour is implicated in c-KIT mutation?

Defect in this pathway contributes to which Weinberg hallmark?

A

GI stromal tumours.

Sustained growth signalling (instrinsic tyrosine kinase activator)

178
Q

What is the most commonly mutated kinase in cancer?

A

PI3K

*Associated with haematological malignancies

179
Q

Which pathway does APC act on?

A

Wnt/APC/B-catenin pathway

180
Q

MYC translocation detected via FISH is diagnostic of?

A

Burkitt lymphoma t(8;14)

181
Q

What does p53 increases the level of and what apoptosis does it induce if irreparable?

A

p21 (CDK inhibitor - not activated by cyclins, Rb not phosphorylated)
Intrinsic apoptosis

182
Q

von-Hippel Lindau syndrome is implicated in which cancer?
Loss of VHL increases?
Which weinberg hallmark does this contribute to?

A

Renal cancer
Increases angiogenic growth factors.

Loss of growth inhibition.

183
Q

Tumour suppressor proteins are usually prefixed with?

A

p

E.g. p21, p53

184
Q

What does pTEN increases the transcription of? What does that lead to?
What pathway does it inhibit?

A

p27 (CDK inhibitor) –> blocks cell cycle progression

PI3K/AKT pathway

185
Q

What do cancer cells express to renew length of telomeres?

A

Telomerase (mutation in gene)

186
Q

What can be used to target replicative immortality in cancer?

A

Telomerase inhibitors

187
Q

What happens in follicular lymphoma?

What is the translocation?

A

Switches on Bcl-2 (anti-apoptotic) –> evades cell death.

t(14;18).

188
Q

What can be used to target cells that evade apoptosis?

A

Pro-apoptotic BH3 mimetics

189
Q

Why does angiogenesis occur in cancer?

Which growth factor is up-regulated?

A

Oxygen demand increases –> must create own blood supply.
VEGF.

**Necrosis commonly seen as malignant tissue dies from hypoxia

190
Q

What can be used to inhibit angiogenesis in cancer?

A

VEGF signal inhibitors

191
Q

What cancers (3) are associated with BRCA mutation?

A

Breast, Ovarian, Pancreatic tumours

192
Q

What is the role of BRCA (2)?

A

DNA repair

Cell arrest at G1/S phase

193
Q

What is the role of mismatch repair proteins (MMR)?

Examples?

A 
Identify faults (spellcheck) in sequence and repair
E.g. MLH1,3; MSH2,3; PMS1,2
194
Q

What kind of cancers are screened for MMR abnormalities in Tayside?

A

All colorectal cancers

195
Q

How can expression of faulty proteins be identified?

A

Via immunohistochemistry

196
Q

What are microsatellites?

What does analysing them tell us?

A

Non-coding segments of DNA specific to an individual.

Accumulates mutations thus determine frequency of mismatched sequences

*full of errors = microsatellite instability

197
Q

What can be used to target genome instability and mutation in cancer?

A

PARP inhibitors

198
Q

Do cancers that mount or not mount the immune system do better?

A

Those that causes inflammatory response do better.

Not evading immune system

199
Q

What kind of treatment can be used to prime the immune cells to target cancer cells?

A

Immunotherapy

200
Q

What inhibits T-cell proliferation (causes apoptosis)?

What kind of cancer is tested for the expression of this?

A

PD-L1.

All lung cancers.

201
Q

What can be used to target cancer cells avoiding immune destruction?

A

Immune activating anti-CTLA4 monoclonal Ab

202
Q

What happens in G1 and G2 phase?

A

Increase in cell size and synthesis

203
Q

What must cells invade through to metastasize and expression of what enzyme is increased?

A

Basement membrane and stromal network of blood vessels (must survive).
Matrix metalloproteinases.

204
Q

What can be used to inhibit invasion/metastasis?

A

HGF/c-Met inhibitors

205
Q

Is cancer clonal?

A

No.
With new mutations each division, successive sub-clones are formed

**Resistance when tx does not work on all sub-clones; not all sub-clones will become malignant

206
Q

What is the difference between stage and grade?

A

Stage - size/ how far tumour has gone

Grade - degree of differentiation

207
Q

What is used to stage tumours?

A

Tumour (Tis, 1-4)
Metastasis (0, 1)
Node (0 - 2)

208
Q

What can be used to deregulated cellular energetics caused by cancer?

A

Aerobic glycolysis inhibitors

209
Q

What can be used to target tumour-promoting inflammation?

A

Selective anti-inflammatory drugs

210
Q

What is the N:C ratio in functional and malignant cells?

A

Functional - lower (cytoplasm 4-5x bigger)

Malignnat - higher (0.5) + hyperchromasia (darkly stained nuclei)

211
Q

What does it mean for a cell to be poorly differentiated?

A

Difficult to tell cell of origin

212
Q

What are the 10 characteristic of a benign tumour?

A 
Organised
Smooth edges
Repetitive
Rounded
Well-defined
Regular
Symmetrical
Homogenous (uniform)
Slow-growing
Encapsulated (esp. slow growing lesions)
213
Q

What are the 10 characteristic of a malignant tumour?

A 
Unnatural looking
Irregular
Jaggy corners
Destructive 
Infiltrative
Heterogenous (solid + soft)
Haemorrhage
Necrosis
Pleomorphic (different degrees of differentiation)
Increased mitotic activity
214
Q

What are the terms for glandular, squamous and bladder cancers?

A

Glandular - adenoma/ adenocarcinoma
Squamous - papilloma/ squamous cell carcinoma
Bladder - Transitional cell carcinoma, Urothelial cell carcinoma

215
Q

What are the terms for cancer of smooth and striated (skeletal) muscles?

A

Smooth - Leiomyoma/ sarcoma

Striated - Rhadomyoma/ sarcoma

216
Q

What are the terms for cancer of blood vessels, lymph vessels, mesothelium and brain coverings?

A

Blood vessels - hemangioma/ angiosarcoma
Lymph vessels - lymphangioma/ sarcoma
Mesothelium - x/ mesothelioma
Brain covering - meningioma/ invasive meningioma

217
Q

What are the terms of cancer of melanocytes?

A

Nevus/ malignant melanoma

218
Q

What are the terms for cancer from haematopoetic cells and lymphoid tissues?

A

Leukemias
Lymphomas (Hodgkin, Non-hodgkin)

**No benign

219
Q

What are the terms of cancer of the mesenchymal (connective tissue)? (4)

A

Fibroma, Lipoma, Chondroma, Osteoma

**Malignant: -sarcoma

220
Q

What can be used to further confirm the morphology of cancer cells?

A 
Immunohistochemistry
Genetics (karyotyping, FISH, molecular genetics)
221
Q

What is the mass effect of tumour?
Which organ is affected badly by this?
Which blood vessel tend to be affected by this?

A

Compresses adjacent structures.

Brain.
Veins (softer)

222
Q

What are the terms for cancer of primitive nerve cells?

A

Benign: Ganglioneuroma
Malignant: Neuroblastoma, Retinoblastoma

223
Q

What are the terms for cancer of glial cells?

A

Glioma

*Only malignant forms

224
Q

Why are people with lung cancers more susceptible to infection?

A

Secondary to obstruction; cannot clear mucus

225
Q

What emergencies can tumours cause to the colon?

A

Obstruction

Perforation

226
Q

What can tumour obstruction of the bladder and kidney cause?

A

Infection
Renal injury (back pressure)
Toxin build-up and electrolye abnormalities

227
Q

What effect does tumour in the brain have?

A

Depend on where the lesion is at

228
Q

Tumour cells are metabolically active, thus consume a lot of energy.
What effect does this have?

A

Cachexia/ weight loss.

229
Q

Is pain in cancer a late or early sign?

A

Late

230
Q

What can tumour cells directly invade (infiltrate)?

What are the effects?

A

Nerves (loss of function), blood vessels (haemorrhage), bone marrow (asplastic/ anaemia)

Can cause fistula (abnormal connections)

231
Q

What are paraneoplastic syndromes?

A

Side effects of cancer

232
Q

What should be considered/ ruled out in Pyrexia of Unknown Origin?

A

Cancer

233
Q

Cancer or cancer drugs can cause leukopenia/ immunosuppression.
Is the bone marrow involved?
What can manifest from this?

A 
Not necessarily.
Unusual infections (E.g. Shingles)
234
Q

What can bone metastases result in?

A

Bone breakdown –> calcium release –> arrhythmia and renal problems

235
Q

What is the growth pattern between benign and malignant cancer?

A

Benign - expansion, remain localised, slow growth

Malignant - local infiltration, metastasize, rapid growth

236
Q

What is the resemblance to tissue of origin between benign and malignant cancer?

A

Benign - resembles

Malignant - less well-differentiated

237
Q

What is the nuclei structure between benign and malignant cancer?

A

Benign - Small, regular, uniform

Malignant - Large, Pleomorphic

238
Q

What is the mitoses between benign and malignant cancer?

A

Benign - few, normal

Malignant - numerous, atypical

239
Q

What is the treatment between benign and malignant cancer?

A

Benign - local excision

Malignant - local excision (+ systemic tx if metastasized)

240
Q

What are the clinical effects between benign and malignant cancer?

A

Benign - Local pressure effects, hormone secretion

Malignant - Local pressure and destruction, inappropriate hormone secretion, distant metastases

241
Q

What cancers are HPV 16/18 associated with? (5)

A

Cervical, anal, penile, vulva, oropharyngeal

242
Q

What cancers are Human T-lymphotropic virus 1 associated with? (2)

A

Tropical spastic paraparesis

Adult T cell leukaemia

243
Q

What cancer is human herpesvirus 8 associated with?

A

Kaposi’s sarcoma

244
Q

When do myofibroblasts appear in wounds?

A

6 weeks - 1 year

245
Q

What are the phases of wound healing (4), cells involved in each phase and timeframe?

A

Haemostasis: RBCs and PLTs (sec/min)
Inflammation: Neutrophils, Fibroblasts, Macrophages (Days)
Regeneration (granulation tissue): Fibroblasts, endothelial cells, macrophages (Weeks)
Remodelling (longest phase; wound contraction; pale scar): Myofibroblasts (6 weeks - 1 yr)

246
Q

Which protein facilitates transmigration of WBCs?

A

PECAM proteins

247
Q

What are 6 potent vasodilators?

A

histamine, prostaglandins, nitric oxide, platelet activating factor, complement C5a (and C3a) and lysosomal compounds

**Serotonin is a vasoconstrictor in damaged tissue and vasodilates healthy, intact tissue

248
Q

What is the difference between dystrophic and metastatic calcification?

A

Dystrophic - tissues that damaged in presence of normal serum calcium
Metastatic - normal tissues in presence of increased serum calcium

249
Q

Does vasodilation or vasoconstriction occur first in acute inflammation?

A

Transient vasoconstriction occurs first due to thromboxane A2 and pain receptor reflex then vasodilation occurs (Histamine and NO)

250
Q

What histological features are seen 0-24hr post-MI? (4)

A

early coagulative necrosis, neutrophils, wavy fibres, hypercontraction of myofibrils

251
Q

What histological features are seen 1-3 days post-MI? (2)

A

Extensive coagulative necrosis, neutrophils (associated with fibrinous pericarditis)

252
Q

What histological features are seen 3-14 days post-MI? (2)

A

macrophages + granulation tissue at margins

253
Q

What histological features are seen 2 weeks to several months post-MI?

A

contracted scar complete

254
Q

What risks are associated with 0-24hr post-MI? (3)

A

ventricular arrhythmia, HF and cardiogenic shock

255
Q

What risks are associated with 3-14 days post-MI? (3)

A

free wall rupture, papillary muscle rupture and LV pseudoaneurysm

256
Q

What diseases are associated with 2 weeks to several months post-MI? (4)

A

Dressler syndrome, HF, arrhythmias, mural thrombus

Principles (14 decks)

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