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Phase 2a > Pathology > Flashcards

Pathology Flashcards

1
Q

What is a thrombus?

A

The solidification of blood contents that forms within the vascular system during life

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2
Q

What are platelets derived from?

A

Megakaryotes

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3
Q

What granules do platelets contain and what do they do?

A

Alpha granules- platelet adhesion
Dense granules- platelet aggregation

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4
Q

What activates platelets?

A

Contact with collagen

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5
Q

What causes a thrombus to occur?

A

When platelet aggregation occurs in an intact vessel

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6
Q

Why is platelet aggregation difficult to stop?

A

Causes the clotting cascade to begin which is a positive feedback loop

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7
Q

What ideology do we use to discuss causes of thrombosis?

A

Virchow’s Triad

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8
Q

What are the 3 groups in Virchow’s Triad? Give examples for each.

A
  1. Reduced blood flow: AF, long travel, immobility, ventricular insufficiency
  2. Increased coagulability: sepsis, smoking, malignancy, coagulation disorder
  3. Blood vessel injury: trauma, surgery, hypertension
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9
Q

What prevents blood clotting in normal circumstances?

A

Laminar blood flow
Endothelium cells are not sticky when healthy

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10
Q

What are the constituents of a thrombus?

A

Platelets, RBCs, Fibrin

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11
Q

What is the inactive form of fibrin?

A

Fibrinogen

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12
Q

What causes arterial thrombosis vs venous thrombosis?

A

Arterial thrombosis: caused by atheromatous plaque
Venous thrombosis: caused by stasis of blood flow

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13
Q

Describe how an arterial thrombus forms.

A
  1. Atheromatous plaque may have fatty streak
  2. Plaque grows and protrudes into the lumen causing turbulence to blood flow
  3. Turbulence causes loss of intimal cells
  4. Fibrin deposition and platelet clumping occurs
  5. This is self-perpetuating and leads to formation of platelet layer (first later of thrombus)
  6. Fibrin precipitates and RBCs get trapped
  7. Structure protrudes further into lumen causing more turbulence and more platelet deposition
  8. Thrombi grow in direction of blood flow- propagation
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14
Q

Describe how a venous thrombus forms.

A
  1. Valves produce a degree of turbulence and can be damaged
  2. When blood pressure falls, flow through the vein slows which allows thrombus to form
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15
Q

Where in the vein does a thrombus typically form and why?

A

At the value due to turbulence to blood flow

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16
Q

Why does atheroma not occur in veins?

A

Blood pressure is too low

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17
Q

How does an arterial thrombus display clinically?

A

Loss of pulse due to distal thrombus
Area is cold, painful and pale
Possible gangrene

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18
Q

How does a venous thrombus display clinically?

A

Area is tender
Reddened and swollen

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19
Q

What can be prescribed to inhibit platelet aggregation?

A

Aspirin

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20
Q

Describe the 4 possible outcomes of thrombosis.

A
  1. RESOLVE
    - Best case scenario
    - Body dissolves thrombus and clears it
  2. ORGANISED
    - Becomes a scar
    - Slight narrowing of vessel lumen
  3. RECANALISATION
    - Intimal cells may proliferate
    - Capillaries may grown into the thrombus and fuse to form larger vessels
  4. EMBOLUS
    - Fragments of thrombus break off into circulation
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20
Q

Describe the 4 possible outcomes of thrombosis.

A
  1. RESOLVE
    - Best case scenario
    - Body dissolves thrombus and clears it
  2. ORGANISED
    - Becomes a scar
    - Slight narrowing of vessel lumen
  3. RECANALISATION
    - Intimal cells may proliferate
    - Capillaries may grown into the thrombus and fuse to form larger vessels
  4. EMBOLUS
    - Fragments of thrombus break off into circulation
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21
Q

What is the difference in composition of an arterial and venous thrombus?

A

Arterial- mainly platelets
Venous- mainly RBCs

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22
Q

What can arterial thrombosis lead to if untreated?

A

Myocardial Infarction
Stroke

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23
Q

What can venous thrombosis lead to if untreated?

A

Deep vein thrombosis
Pulmonary embolism

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24
Q

What is prescribed for arterial and venous thrombosis?

A

Arterial- antiplatelets (e.g. aspirin)
Venous- anticoagulants (e.g. warfarin)

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25
Q

What are the 2 types of inflammation?

A

Acute & chronic

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26
Q

What is acute inflammation?

A

Initial response of a tissue to injury
Early onset
Short duration
Involved neutrophils and monocytes

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27
Q

What are the 3 main steps of acute inflammation?

A
  1. VASCULAR component: dilation of vessels
  2. EXUDATIVE component: vascular leakage of protein rich fluid
  3. NEUTROPHIL polymorph: cell type recruited to tissue
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28
Q

What are the 6 causes of acute inflammation?

A

Microbial infections
Hypersensitivity reactions
Physical agents (trauma, heat, etc.)
Chemicals (corrosives etc.)
Bacterial toxins
Tissue necrosis

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29
Q

Describe the appearance of acute inflammation.

A

Rubor- redness
Calor- heat
Tumor- swelling
Dolor- pain
Loss of function

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30
Q

What causes rubor in acute inflammation?

A

Dilation of small vessels

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31
Q

Describe neutrophil polymorph emigration in acute inflammation.

A
  1. Migration of neutrophils:
    Due to increase plasma viscosity and slowing of flow due to injury, neutrophils migrate to plasmatic zone
  2. Adhesion of neutrophils:
    Adhesion to the vascular endothelial cells occurs in venules- this is called pavementing
  3. Neutrophil emigration:
    Neutrophils pass through endothelial cells, onto basal lamina and then the vessel wall
  4. Diapedesis:
    Neutrophils pass through blood vessel. RBCs may also escape from vessels. This is a passive process and indicates severe vascular injury
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32
Q

Describe the outcomes of acute inflammation.

A
  1. RESOLUTION:
    - complete restoration of tissues to normal
    - minimal cell death and rapid destruction of the causal agent
  2. SUPPORATION:
    - formation of pus
    - this becomes surrounded by a pyogenic membrane, which is the start of healing
  3. ORGANISATION:
    - replacement by granulation tissue
    - new capillaries grow into inflammatory exudate, macrophages migrate and fibrosis occurs
  4. PROGRESSION
    - causative agent is not removed so there is progression to chronic inflammation
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33
Q

What is the difference between how bacteria and viruses cause harm?

A

bacteria- release of exotoxins/ endotoxins
virus- call death due to intracellular multiplication

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34
Q

What are the systemic affects of acute inflammation?

A

pyrexia
weight loss
reactive hyperplasia of reticuloendothelial system
haematological changes
amyloidosis

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35
Q

What are the endogenous chemical mediators of acute inflammation and what do they do?

A

Bradykinin, histamine, nitric oxide

They lead to vasodilation, recruitment of neutrophils, chemotaxis, increased vascular permeability, itching, pain

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36
Q

List the cell types involved in acute inflammation and whether they are short or long lived.

A

Neutrophil polymorph- short
Macrophage- long
Lymphocyte- long
Fibroblasts- long
Endothelial cells- long

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37
Q

What is the general function of neutrophil polymorphs in acute inflammation?

A
  • first at scene
  • dies at scene
  • releases chemicals that attract macrophages
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38
Q

What is the general function of macrophages in acute inflammation?

A
  • phagocytic properties
  • ingests bacteria and debris (prevent infection)
  • may present antigens and lymphocytes
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39
Q

What is the general function of lymphocytes in acute inflammation?

A
  • produce chemicals that attract inflammatory cells
  • immunological memory for past infections and antigens
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40
Q

What is the general function of fibroblasts in acute inflammation?

A
  • forms collagen in areas of chronic inflammation to aid repair
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41
Q

What is the general function of endothelial cells in acute inflammation?

A
  • sticky so inflammatory cells adhere
  • porous to allow inflammatory cells to pass into tissues
  • grow in areas of damage to form new capillaries
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42
Q

What is chronic inflammation?

A
  • subsequent and prolonged response to tissue injury
  • involves lymphocytes, macrophages and plasma cells
  • longer onset
  • longer lasting effects
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43
Q

What is the name for several macrophages joined together?

A

multinucleated giant cell

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44
Q

What are the causes of chronic inflammation?

A
  • endogenous/ exogenous materials (necrosis, asbestos)
  • autoimmune conditions
  • transplant rejection
  • recurrent acute inflammation
  • progression from acute inflammation
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45
Q

How does chronic inflammation present macroscopically and microscopically?

A

MACROSCOPIC:
- chronic ulcer
- chronic abscess cavity
- granulomatous inflammation
- fibrosis

MICROSCOPIC:
- lymphocytes, plasma cells, macrophages
- possible tissue necrosis
- continuing destruction

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46
Q

Which cell is present in chronic inflammation but not acute?

A

Plasma cells

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47
Q

Describe the role of lymphocytes and macrophages in chronic inflammation.

A

B lymphocyte:
- transforms into plasma cells
- produce antibodies

T lymphocytes:
- cell-mediated immunity

Macrophages:
- respond to chemotactic stimuli
- produce cytokines

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48
Q

Which cytokines are produced in chronic inflammation?

A

interferons:
alpha
beta
IL6, IL7, IL8
TNF-alpha

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49
Q

What is granuloma?

A

aggregate of epithelioid

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50
Q

In what type of inflammation can granuloma occur?

A

chronic

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51
Q

What is an embolism?

A

A mass of material in the vascular system able to lodge in a vessel and block it’s lumen

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52
Q

What can form an embolus?

A
  • thrombus
  • air
  • cholesterol crystals
  • tumour
  • amniotic fluid
  • fat
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53
Q

Where can arterial embolisms travel? Are there any exceptions to this?

A

Anywhere downstream of its entry point

Mural thrombi in left ventricle can go anywhere
Cholesterol crystals from atheromatous plaque in descending aorta can go anywhere

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54
Q

What is another name for an arterial embolism?

A

Systemic embolism

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55
Q

Where do emboli in the venous system travel?

A

Travel to the vena cava and lodge in pulmonary arteries = pulmonary embolism

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56
Q

Describe the different sizes of emboli.

A
  1. Small emboli:
    - may occur unnoticed
    - can cause idiopathic pulmonary hypertension
  2. Large emboli:
    - can result in acute respiratory or cardiac problems
    - resolve slowly
    - result in chest pain and shortness of breath
  3. Massive emboli:
    - sudden death
    - arise from long thrombi derived from leg veins
    - often impacted across the bifurcation of one of the pulmonary arteries
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57
Q

What does idiopathic mean?

A

Any disease or condition which arises spontaneously or for which the cause is unknown

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58
Q

What is ischaemia?

A

reduction of blood flow to a tissue or part of the body caused by constriction or blockage of the blood vessels supplying it

does not result in any further complications by itself

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59
Q

How long are ischaemic attacks?

A

brief (usually 1 hr, max 24 hrs)

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60
Q

Which cells are most vulnerable to ischaemia?

A

cardiomyocytes
cerebral neurons

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61
Q

Is ischaemia reversible?

A

yes

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62
Q

What is infarction?

A

reduction in blood flow that leads to cell death due to an inadequate oxygen supply to sustain metabolic demand

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63
Q

What usually causes infarction?

A

arterial thrombosis

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64
Q

Which organs are least susceptible to infarction and why?

A

Liver, brain and lungs

They are the only organs with a dual blood supply

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65
Q

What is a reperfusion injury?

A

damage to tissue during deoxygenation after an infarct

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66
Q

What causes retinoblastoma?

A

A gene inherited on chromosome 13

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67
Q

What is the meaning of resolution in terms of healing?

A
  • tissue restored to normal, pre-injury state
  • tissue architecture undamaged (able to regenerate)
  • initiating factor (cause of injury) is removed
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68
Q

What is the meaning of repair in terms of healing?

A
  • tissue is repaired, but unable to regenerate to pre-injury state- replaced with scar/ fibrotic tissue
  • tissue architecture is damaged- unable to regenerate
  • initiating factor still present
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69
Q

Which cells can regenerate?

A

hepatocytes
pneumocytes
blood cells
gut epithelium
skin epithelium
osteocytes

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70
Q

Which cells can’t regenerate?

A

myocardial cells
neurones

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71
Q

Give some examples of repair

A
  • myocardial cell after MI
  • neurones in brain after cerebral infarct
  • neurones in spinal chord after trauma
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72
Q

How does the liver heal? What if damage is repeated? e.g. chronic alcoholism

A
  • hepatocytes can fully regenerate (resolution) is damage is not repeatedly occurring
  • if damage is repeated (patient keeps drinking) repair will occur instead of resolution leading to fibrous scarring, regenerative nodules and eventually cirrhosis
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73
Q

What is fibrosis?

A

scarring

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74
Q

How is fibrosis classified?

A

Staging system ranging from 1 to 4

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75
Q

What is cirrhosis?

A

Stage 4 fibrosis

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76
Q

How does fibrosis affect tissues?

A

As fibrosis progresses, normal functional tissue is replaced by scar tissue (not functional)

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77
Q

How does cirrhosis affect the liver?

A
  • alteration of blood flow
  • inability to synthesise proteins
  • inability to process drugs and toxins
  • decreased immune function
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78
Q

What is lobar pneumonia?

A

bacterial infections in one lobe of the lungs caused by strep pneumonia

one lobe of lungs fills with pus
alveoli fill with neutrophil polymorphs

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79
Q

Can alveoli regenerate after global pneumonia?

A

pneumocystis of alveoli can regenerate as long as infection/pus has cleared

resolution can occur in walls of alveoli if architecture is intact

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80
Q

How does COVID-19 affect the lungs?

A
  • interstitial pneumonia affecting more than one lobe
  • interstitium and connective tissue of lungs fill with fluid- patchy appearance on chest x-ray
  • severe COVID can destruct alveoli architecture, leading to fibrosis- presents as honeycomb lung
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81
Q

How do skin abrasions heal?

A

repair- as long as skin has been scraped and no hole has been made

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82
Q

Describe the process of skin repair.

A
  • top stratified layer of squamous epithelial cells are scraped off to expose stem cells underneath
  • these stem cells regenerate the skin underneath the scab
  • initially a thin confluent epidermis forms before being replaced by final epidermal growth
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83
Q

How does skin heal if the stem cells are removed in the abrasion?

A

The skin will regenerate via the stem cells associated with hair follicles

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84
Q

What is the difference between healing by first and second intention?

A

Healing by first intention occurs in surgical incisions or wounds with close edges whereas healing by second intention occurs when you cannot bring the edges together due to a gap or hole in the skin

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85
Q

Describe the process of healing by first intention

A
  1. edges are brought together using stitches
  2. incision would fills with blood and a thrombus forms
  3. exudation of fibrinogen causes formation of weak fibrin
  4. epidermal growth and collagen synthesis leads to a strong collagenous join
  5. epidermis grows over top
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86
Q

Why is a scar initially red? What colour does it turn after time has passed?

A

initially red as there is still blood present in the collagen

eventually turns white (colour of collagen)

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87
Q

Describe the process of healing by second intention

A
  1. small blood vessels move in from the edges of the gap
  2. fibroblasts enter the site of trauma and make collagen- granulation of tissue
  3. fibroblasts organise tissue to form organised collagen fibrils
  4. early thrombus scar forms before skin contracts
  5. epidermis grows over the top leaving a white scar
88
Q

What is atherosclerosis?

A

a disease characterised by the formation of atherosclerotic plaques the intima of large and medium sized arteries

it is often asymptomatic

89
Q

What is an atheroma?

A

focal thickening of the tunica intimal of arteries, produced through the movement of LDLs from the lumen

90
Q

What is an atherosclerotic plaque made up of?

A

fibrous tissue
lipid component (cholesterol)
lymphocytes

91
Q

Describe the process of atheroma formation

A
  1. endothelial cell dysfunction (e.g. lots of cholesterol damages wall)
  2. high density of LDLs in blood begin to accumulate in artery wall
  3. macrophages are attracted to site of damage and take up lipid to form foam cells (inflammatory response)
  4. formation of fatty streak
  5. activated macrophages will release lots of their own products- cytokines and growth factors
  6. smooth muscle proliferation to intimal around lipid core and formation of fibrous cap (collagen)
  7. plaque may rupture leading to thrombosis and complete occlusion of vessel lumen
92
Q

What kind of systems do you find atherosclerosis in?

A

high pressure systems - never low pressure

93
Q

What can happen if a thrombus forms on a disrupted atherosclerotic plaque?

A

cerebral infarct
carotid atheroma, leading to TIA
MI
aortic aneurism
peripheral vascular disease
gangreen

94
Q

What happens in an aortic aneurism ruptures?

A

sudden death

95
Q

What are the risk factors of atherosclerosis?

A

hypercholestrolaemia (most important)
smoking
hypertension
diabetes
male sex
increasing age

96
Q

What are the preventative measures for atherosclerosis?

A

smoking cessation
blood pressure control
weight reduction
low dose aspirin
statins

97
Q

What is the standard drug for reducing cholesterol?

A

statins

98
Q

What is apoptosis?

A

programmed cell death

99
Q

What inhibits apoptosis?

A

growth factors
extracellular cell matrix
sex steroids

100
Q

What induces apoptosis?

A

glucocorticoids
free radicals
ionising radiation
DNA damage

101
Q

When does apoptosis occur?

A

in fully differentiated cells
in development
in normal function
in disease processes

102
Q

How is apoptosis mediated?

A

via capase enzymes

103
Q

Describe the extrinsic pathway of apoptosis.

A
  • Fas ligand binds to Fas receptor on cell surface
  • ligand binding results in clustering of receptor molecules on the cell surface and initiation of signal transduction cascade
  • capases are activated which triggers apoptosis
104
Q

What are the 2 types of Fas receptor?

A

TNFR1
CD95

105
Q

What is the extrinsic pathway for apoptosis used for?

A

used by immune system to eliminate lymphocytes

106
Q

Describe the intrinsic pathway of apoptosis

A
  • involves inducers and inhibitors
  • inducer or p53 gene acts on Bax receptor inside cell which activates capase enzymes and stimulates apoptosis
  • inhibitors act on Bcl-2 receptor inside cell and inhibit capase enzymes which inhibits apoptosis
107
Q

What does the Bcl-2:Bax ratio of a cell determine?

A

the cell’s susceptibility to apoptotic stimuli

108
Q

What is necrosis?

A

traumatic cell death which induces inflammation and repair

characterised by bioenergetic failure and loss of plasma membrane integrity

109
Q

What is coagulative necrosis?

A
  • most common type
  • can occur in most organs
  • caused by ischaemia
110
Q

What is liquefactive necrosis?

A

occurs in brain due to its lack of substantial supporting stroma

111
Q

What is caseous necrosis?

A
  • causes a “cheese” pattern
  • TB is characterised by this form of necrosis
112
Q

What is gangrene?

A

necrosis with rotting of the tissue

113
Q

Why does gangrene appear black?

A

affected tissue appears black due to deposition of iron sulphide from degraded haemoglobin

114
Q

What is genetic disease?

A

disease that occurs primarily from a genetic abnormality

115
Q

What is congenital disease?

A

disease that has symptoms present at birth

116
Q

What is inherited disease?

A

disease caused by an inherited genetic abnormality, may not manifest itself until later in life

117
Q

What is acquired disease?

A

caused by non-genetic environmental factors usually occurring after birth

118
Q

Give an example of a disease which is both acquired and congenital.

A

fetal alcohol syndrome

119
Q

Define hypertrophy

A

increase in tissue size due to increase in size of constituent cells

120
Q

Give examples of hypertrophy

A
  • muscle hypertrophy in body builders
  • uterine hypertrophy in pregnancy
  • cardiac muscle hypertrophy due to hypertension
121
Q

Define hyperplasia

A

increase in tissue size due to increase in number of constituent cells

122
Q

What cells are susceptible to hyperplasia?

A

any cells that can divide, i.e. not myocytes or neurones

123
Q

Give an example of hyperplasia

A

hyperplasia in bone marrow cells in those living at high altitudes

124
Q

Define atrophy

A

decrease in tissue size caused by either decrease in number of constituent cells or a decrease in their size

125
Q

Which organs are most susceptible to atrophy?

A

skeletal muscle
cardiac muscle
secondary sex organs
brain

126
Q

Give examples of atrophy

A
  • thymus after puberty
  • skeletal muscle atrophy after disuse
127
Q

Define metaplasia

A

the change in differentiation of a cell from one fully-differentiated cell type to another

128
Q

What causes metaplasia?

A

alterations in cellular environment
thought to be caused by stem cell reprogramming

129
Q

Is metaplasia reversible?

A

yes

130
Q

Give an example of metaplasia

A

Barrett’s oesophagus- squamous epithelium of oesophagus becomes columnar due to exposure to stomach acid

131
Q

What happens if metaplasia persists?

A

it can progress to dysplasia and eventually carcinoma

132
Q

What happens is Barrett’s oesophagus persists?

A

metaplasia becomes dysplasia and progresses to adenocarcinoma

133
Q

Define dysplasia

A

morphological changes seen in cells in the progression to becoming cancer

134
Q

What type of epithelium is prone to dysplasia?

A

cervical
respiratory

135
Q

Define carcinogenesis

A

the transformation of normal cells to neoplastic cells via permanent genetic alterations or mutations

136
Q

Define carcinogenic

A

cancer causing

137
Q

Define oncogenic

A

tumour causing

138
Q

Define tumour

A

any abnormal swelling

139
Q

Define neoplasm

A

an abnormal mass of tissue that forms when cells grow and divide more than they should/ not die when they should

can be benign or malignant

140
Q

Define oncogenesis

A

process by which normal cells transform into benign neoplasms

141
Q

What percentage of cancers are environmental vs genetic?

A

85% environmental
15% genetic

142
Q

Define carcinogen

A

mutagenic agent known to cause cancer

143
Q

List the DNA viral carcinogens and the cancer that they cause

A

Human Herpes Virus (HHV8) - Kaposi sarcoma

Epstein Barr Virus (EBV) - Burkitt lymphoma, nasopharyngeal carcinoma

Hep B - Hepatocellular carcinoma

Human Papillomavirus (HPV) - squamous cell carcinomas of the cervix, penis, anus, head and neck

Merkle cell polyomavirus (MCV) - merkle cell carcinoma

144
Q

List the RNA viral carcinogens and the cancer that they cause

A

Human T-lymphotrophic virus (HTLV-1) - adult T-cell leukaemia

Hep C - hepatocellular carcinoma

145
Q

Where does Kaposi sarcoma affect?

A

GI tract

146
Q

What cancer is caused by polycyclic aromatic hydrocarbons?

A

lung cancer
skin cancer

147
Q

What cancer is caused by aromatic amines?

A

bladder cancer

148
Q

What cancer is caused by nitrosamines?

A

gut cancer

149
Q

What cancer is caused by alkylating agents?

A

leukaemia

150
Q

Which non ionising radiation causes cancer? What types of cancer does it cause?

A

increased exposure to UVA or UVB

causes basal cell carcinoma
squamous cell carcinoma
melanoma

151
Q

How does UV radiation cause cancer?

A

causes DNA strand to break down and DNA mutations occur

152
Q

Which patients are more susceptible to cancer caused by UV radiation?

A

patients with xeroderma pigmentosum (extreme sun sensitivity)

153
Q

What cancer are radiographers susceptible to?

A

skin cancer

154
Q

What cancer are uranium miner susceptible to?

A

lung cancer

155
Q

What sort of cancer does granite bedrock cause and why?

A

lung cancer

uranium decays to radon which is ionising radiation

156
Q

What cancer is prevalent in Ukrainian children and why?

A

thyroid cancer

Chernobyl disaster

157
Q

What cancer is caused by increased exposure to oestrogen?

A

mammary (breast) cancer
endometrial cancer

158
Q

What cancer is caused by anabolic steroids?

A

hepatocellular cancer

159
Q

What cancer is caused by aflatoxin B1?

A

hepatocellular carcinoma

160
Q

What is aflatoxin B1 and how is it produced?

A

mycotoxin

released by fungus aspergillus

161
Q

Name a carcinogenic parasite and the cancer it causes

A

shistoma
bladder cancer

162
Q

What type of cancer is caused by asbestos?

A

mesothelioma (pleural cancer)

163
Q

What type of cancer does arsenic cause?

A

bladder
skin

164
Q

What is classification of a tumour based on?

A

behaviour and histogenesis

165
Q

What is histogenesis?

A

formation of different tissues from undifferentiated cells

166
Q

What are the 2 types of neoplasia?

A

benign
malignant

167
Q

Describe the differences between benign and malignant neoplasms.

A
  1. INVASION: Benign do not invade basement membrane, malignant does
  2. DIRECTION OF GROWTH: benign are exophytic (grow outwards), malignant of endophytic (grow inwards)
  3. RATE OF GROWTH: benign have low mitotic activity (slow growing), malignant have high mitotic activity (fast growing)
  4. CIRCUMSCRIBED: benign are circumscribed, malignant are poorly circumscribed
  5. NECROSIS: necrosis and ulceration rare for benign, common for malignant
168
Q

Why do malignant neoplasms cause necrosis but benign neoplasms do not?

A

malignant neoplasms grow too fast to grow an adequate blood supply hence tissue dies, benign neoplasms grow much slower

169
Q

What are the long term effects of benign neoplasms?

A
  • pressure on adjacent tissues
  • obstruction of ducts/ hollow organs
  • produce hormones
  • can be pre-malignant (can become cancerous)
170
Q

What are the components of a neoplasm?

A

neoplastic cells
stroma

171
Q

Give the features of neoplastic cells

A
  • always derived from nucleated cells
  • usually monoclonal
  • growth pattern related to parent cell
  • synthetic activity related to parent cells (collagen, hormone secretion, etc)
172
Q

What is the stroma of a neoplasm?

A

connective tissue framework providing mechanical and nutritional support

173
Q

What cancer is the exception to the usual structure of a neoplasm?

A

leukaemia/ blood cancer- no stroma

174
Q

What promotes blood vessel growth in neoplasms?

A

VEGF
fibroblast growth factors

175
Q

What is angiogenesis?

A

formation of new blood vessels

176
Q

What is classification of a neoplasm based on?

A

behaviour
histogenesis

177
Q

What are the behaviour categories of a neoplasm?

A

benign
borderline
malignant

178
Q

What are the component of histogenesis of a neoplasm?

A

specific cell/ origin of tumour
histological grading

179
Q

Give 4 possible neoplasm origins

A

epithelial
connective tissue
lymphoid
haemopoetic

180
Q

What is histological grade of a neoplasm based on? Describe the grading system.

A

based on extent to which the tumour resembles it’s original histology

grade 1: well-differentiated (most closely resembles parent tissue)
grade 2: moderately differentiated
grade 3: poorly differentiated

181
Q

What does suffix -oma imply?

A

any neoplasm

182
Q

Describe types of benign and malignant epithelial tumours.

A

BENIGN:
papilloma- benign tumour of non glandular tissue
adenoma- benign tumour of secretory tissue

MALIGNANT:
carcinoma- malignant tumour of epithelial cells
adenocarcinoma- malignant tumour of glandular epithelium

183
Q

What is a lipoma?

A

benign

connective tissue tumour

of adipocytes

184
Q

What is rhabdomyoma?

A

benign

connective tissue tumour

of striated muscle

185
Q

What is leiomyoma?

A

benign

connective tissue tumour

of smooth muscle

186
Q

What is angioma?

A

benign

connective tissue tumour

of vascular system

187
Q

What is chondroma?

A

benign

connective tissue tumour

of cartilage

188
Q

What is osteoma?

A

benign

connective tissue tumour

of bone

189
Q

What is neuroma?

A

benign

connective tissue tumour

of nerves

190
Q

What is liposarcoma?

A

malignant

connective tissue tumour

of adipocytes

191
Q

What is rhabdomyosarcoma?

A

malignant

connective tissue tumour

of striated muscle

192
Q

What is leiomyosarcoma

A

malignant

connective tissue tumour

of smooth muscle

193
Q

What is Chondrosarcoma?

A

malignant

connective tissue tumour

of cartilage

194
Q

What is osteosarcoma?

A

malignant

connective tissue tumour

of bone

195
Q

What is angiosarcoma?

A

malignant

connective tissue tumour

of vascular system

196
Q

What is neurosarcoma?

A

malignant

connective tissue tumour

of nerves

197
Q

Define anaplastic

A

a tumour in which the cell-type of origin is unknown, so tumour origin is said to be anaplastic

198
Q

What is granuloma?

A

a type of inflammation

199
Q

What is a mycetoma?

A

NOT A NEOPLASM

ball of fungus in lung cavity

200
Q

What is a tuberculoma?

A

NOT A NEOPLASM

inflammation due to TB

201
Q

What is melanoma?

A

malignant neoplasm (exception to nomenclature)

of melanocytes

202
Q

What is mesothelioma?

A

malignant neoplasm (exception to nomenclature)

of mesothelial cells

203
Q

What is lymphoma?

A

malignant neoplasm (exception to nomenclature)

of lymphoid cells

204
Q

What is blastoma?

A

embryological malignant neoplasm

205
Q

Define neoplasm “in situ”

A

when the neoplasm has proliferated but has not broken through the basement membrane to other tissues

206
Q

What type of neoplasms can you say are “in situ”?

A

epithelial neoplasms only

207
Q

Define metastasis

A

the process whereby malignant tumours spread from their site of origin to form other tumours at distant sites

208
Q

What is the type of malignant neoplasm that does not metastasise?

A

basal cell carcinomas never metastasise

209
Q

Describe the process of metastasis

A
  1. detachment of tumour cells from their neighbours
  2. invasion of surrounding connective tissue to reach conduits of metastases
  3. intravasation into the lumen of vessels
  4. evasion of host defence mechanisms, such as NK cells
  5. adherence to endothelium at a remote location
  6. extravasation of the cells from the vessel lumen to the surrounding tissues
  7. tumour cells proliferate in the new environment
210
Q

What route of metastasis does carcinomas and sarcomas usually take?

A

carcinoma- lymphatic spread
sarcoma- haematogenous spread

211
Q

What is the most common metastasis?

A

metastasis from lymphatic system

212
Q

Give 5 ways in which metastasis physically occurs?

A

via blood vessels (haematogeneous)
via lymphatics
across body cavities (transcoelomic)
along nerves
direct implantation during surgery

213
Q

Describe the process of metastasis to the lung

A
  1. If carcinoma enters venous system, it will travel through the blood vessels to the vena cavae, right atrium, right ventricle and onto pulmonary circultion
  2. From there, as the lung blood vessels act as a sieve, it will get stuck at some point
  3. If this new neoplasm site then grows into venous system of the pulmonary circulation, it can travel anywhere in the body
214
Q

Describe the process of metastasis to the liver

A
  1. liver receives 100% of blood from colorectal
  2. neoplasm may break off from digestive system and travel in the blood stream to the liver through the portal venous system
  3. liver blood vessels act as sieve as they go down to capillary level
  4. neoplasm imbeds at some point in vasculature tree
215
Q

When is cancer considered to be invasive?

A

when it has breached its own tissue type into another area

216
Q

What is the name for a metastatic tumour that has only JUST broken through the basement membrane?

A

micro-invasive carcinoma

217
Q

What is invasion of cancer dependant on?

A

decreased cellular adhesion
increased cellular motility
production of lytic enzymes to break down surrounding tissues

218
Q

What is tumour staging?

A

the extent of tumour spread determined by histopathological examination and clinical examination

Phase 2a (18 decks)

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