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Phase 2a Sam > ICS - PATHOLOGY > Flashcards

ICS - PATHOLOGY Flashcards

1
Q

Define inflammation

TEst

A

It’s hard to define, but its a reaction to a tissue injury or infection.
Involves cells such as neutrophils and macrophages
It is not a disease but instead usually a manifestation of the disease

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2
Q

How is inflammation classified?

A

Acute or chronic.

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3
Q

Outline qualities of acute inflammation. give an example

A

Sudden onset
Short duration
Usually resolves

It is the intial and short lived tissue reactions that occur due to injury
Appendicitis is an example

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4
Q

Outline qualities of chronic inflammation.

A

Slow onset or comes after acute inflammation
Long duration
May never resolve

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5
Q

When is inflammation good?

A

It is able to destroy invading microorganisms
Walling off of an abscess cavity can prevent the spread of infection.

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6
Q

When is inflammation bad?

A

Bad in autoimmunity
Also bad when it over-reacts to the stimulus.
Can cause diesase - eg an abscess in the brain will act as a space pccupying lesion and COMPRESS VITAL STRUCTURES

Fibrosis from chronic inflammation may disort tissues and permanently alter function

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7
Q

Name some cells that are involved in inflammation.

A

Neurtophils Polymorphs
Macrophages
Endothelial Cells
Lymphocytes
Fibrolasts

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8
Q

Outline what Neutrophils Polymorphs are.

THEY ARE GRANUOLCYTES!!!!

A

Short lived cells, that are FIRST ON THE SCENE OF ACUTE INFLAMMATION
They contain cytoplasmic granules that are full of enzymes that kill bacteria
They normally die at the scene of inflammation
They RELEASE CHEMICALS that attract other inflammatory cells eg Macrophages.

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9
Q

Outline what Macrophages are

A

LONG LIVED CELLS, (weeks to months)
They have PHAGOCYTIC PROPERITES
They INGEST bacteria and debris, and may carry them away

present antigen to lymphocytes

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10
Q

How long to Lymphocytes live for? What do they do? What is special about them?

A

They are long lived cells (YEARS)
They produce chemicals which attract in other inflammatory cells
They have an IMMUNOLOGICAL MEMORY for past infections and anitgens

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11
Q

What are endothelial cells?

A

They line the capillary blood vessels in areas of inflammation

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12
Q

What do endothelial cells do in inflammation? How do they help inflammatory cells? 3

A

They BECOME STICKY in areas of inflammation so inflammatory cells can adhere to them
They BECOME POROUS to allow for inflammatory cells to pass into tissues
The GROW into areas of damage to form new capillary vessels

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13
Q

Are fibrobalsts long or short lived? What do they do?

A

They are long lived. They form collagen in areas of chronic inflammation

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14
Q

What are the 5 main features of Acute Inflammation?

A
  • Rubor (Redness)
  • Tumour (Swelling
  • Calor (Heat)
  • Dolar (Pain)
  • Functio Laesa (Loss of function)
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15
Q

What happens to vessel walls in acute inflammation?

A

Precapillary sphincters open (which are regulated by arteriolar walls)
thereby increasing the blood flow
thorough the capillaries contributing to redness and heat

Endothelial cell walls separate, as a response to mediators.

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16
Q

Inflammation can be triggered by internal or external factors- give examples of external factors

A

External are either
Non microbial (eg Allergens, Irritants, Toxic Compounds)
Or Microbial Factors

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17
Q

Outline two main microbial factors

What are PAMPs?

A

Virulence Factors - Help pathogens colonise tissues and cause infections
Pathogenic associated molecular Patterns (PAMPs) = General molecular features common to many types of pathogen - the body recognises to trigger inflammaroty response

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18
Q

Outline what DAMPs Are

A

DAMPs are Damage Associated Molecular Patterns, and are INTRACELLULAR PROTEINS that get released when a cells plasma membrane is injured, or when the cell dies - THEY TRIGGER INFLAMMATION, AN INTERNAL FACTOR

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19
Q

the inflammatory process: Name 3 things Macrophages and Mast Cells release, and what does it do to blood vessels?

A

1 Macrophage and Mast cells release inflammatory mediators like Histamine, Serotonin, Cytokines, and Eicosanoids like prostaglandins.

  1. These mediators act on the endothelial cell wall, causing the cells to separate.
  2. These mediators cause the capillaries to swell/dilate, and the separation of the cells lead to INCREASED VASCULAR PERMEABILITY

Nitric oxide also makes the capillaries more permeable.
Macrophages will start to eat pathogens

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20
Q

What happens to the hydrostatic pressure in capillaries during acute inflammation? why is this? What happens as a consequence?

A

Capillary hydrostatic pressure increased. As mediators cause blood vessels to SWELL/VASODILATE and the cells in the capillary endothelium separate, increasing VASCULAR PERMEABILITY

As a consequence, plasma proteins leave the capillary.

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21
Q

Define Exudation. What is fluid exudate

A

The net escape of protein rich fluid into the exravascular space.
This protein rich fluid is called Fluid exudate.

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22
Q

What are the 5 main causes of acute inflammation?

A

Microbial Infections
Irritant and corrosive chemicals
Physical agents
Tissue necrosis
Hypersensitivity reactions

MIPTH

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23
Q

Briefly outline how microbial infections cause acute inflammation

A

Bacteria release exotoxins, which are chemicals that specifically iniate inflammation,
or ENDOTOXINS, associated with their cell walls

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24
Q

What are the 3 key things that accumulate in extracellular spaces in acute inflammation?

A

oedema fluid (exudate), fibrin and neutrophil polymorphs
accumulate in the extracellular spaces

Fibrin is deposited on the extravascular tissues, hence they are said to be covered in fibrinous exudate

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25
Q

What is said to be the key diagnostic histological feature of acute inflammation?

A

The accumulation of neutrophil polymorphs with the extracellular space

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26
Q

Define pavementing. Why does this not happen in healthy states?

A

pavementing is the adhesion of neutrophils to the vascular endothelium.
In healthy states, leukocytes only flow in the central/axial part of the vessel - not near the edges. They also wouldn’t usually adhere to the vessels.

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27
Q

Where does pavementing occur

A

only in venules. Hence leucocytes will leave/migrate form the walls of venules and small veins, but not normally from capillaries

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28
Q

What are the 4 outcomes of inflammation?

A
  1. Resolution.
  2. Suppuration.
  3. Organisation (scar tissue formation).
  4. Progression onto chronic inflammation.
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29
Q

Give 3 endogenous chemical mediators of acute inflammation. Where do they come from?

A
  1. Bradykinin.
  2. Histamine.
  3. Nitric Oxide.

They are released from the injured tissue, and spread outwards to uninjured areas

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30
Q

What do histamine and thrombin do early on in acute inflammation?

A

Histamine and thrombin cause up regulation of adhesions molecules to endothelial walls - so leukocytes can adhere to it.

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31
Q

Outline some of the broader things that endogenous chemical mediators lead to

A

They lead to vasodilation,
Emigration of neutophils
Increased vascular permemability
itiching and pain
chemotaxis

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32
Q

Define chemotaxis

A

(the attraction of neutrophil polymorphs towards certain
chemicals e.g at the site of inflammation)

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33
Q

What do macrophages release in acute inflammation and what does this do?

A

They release the cytokines That attracts Neutrophil Polymorphs

interleukin-1 (IL-1) and tumour necrosis factor alpha (TNF-alpha)

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34
Q

When do macrophages appear, and when do they predominate?

A

start to appear within a few hours of the commencement of
inflammation, but do not predominate until the later stages when the
neutrophils have diminished

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35
Q

What are macrophages responsible for?

A

clearing away tissue debris and damaged
cells

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36
Q

How is exudate cleared?

A

By lysosomal enzymes, released by both neutrophils and macrophages

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37
Q

What are the outcomes of acute inflammation?

A

Resolution (everythings ok)
Suppuration (formation of pus)
Organisation of tissue
Progression to chronic inflammation

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38
Q

In organisation, what replaces old tissue?

A

Granulation tissue, contains new blood vessels and lots of fibroblasts = can lead to scar formation

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39
Q

When will chronic inflammation happen?

A

If the agent causing acute inflammation is not removed

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40
Q

What cell can form when several macrophages try to ingest the same particle?

A

Multinucleate giant cell.

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41
Q

What cells are involved in chronic inflammation?

A

Macrophages and plasma cells (B and T lymphocytes)

These replace the neutrophils

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42
Q

What are 4 systemic effects of acute inflammation?

A
  1. Fever.
  2. Feeling unwell.
  3. Weight loss. (negative nitrgoen balance due to immune response)
  4. Reactive hyperplasia of the reticuloendothelial system.
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43
Q

Give 4 causes of chronic inflammation.

What is the most common?

A
  1. Primary chronic inflammation. - most common
  2. Transplant rejection.
  3. Recurrent acute inflammation.
  4. Progression from acute inflammation.
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44
Q

Give examples of primary chronic inflammation.

A
  1. Infective substances having resistance to phagocytosis e.g. TB, leprosy.
  2. Endogenous materials e.g. uric acid crystals.
  3. Exogenous materials e.g. asbestos.
  4. Autoimmune diseases e.g. chronic gastritis, rheumatoid arthritis etc.
  5. Other chronic inflammatory diseases e.g. chronic inflammatory bowel disease.
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45
Q

What are some macroscopic features of chronic inflammation?

A
  1. Chronic ulcer.
  2. Chronic abscess cavity.
  3. Granulomatous inflammation.
  4. Fibrosis.
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46
Q

What is granulation tissue?

A

Granulation tissue is new connective tissue and microscopic blood vessels that form on the surfaces of a wound during the healing process

Is composed of small blood vessels in a connective tissue matrix with myofibroblasts. It is important in healing and repair.

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47
Q

What is the difference between a granuloma and granulation tissue?

A

granulation tissue = new connective tissue and tiny blood vessels that form on the surface of a wound, during healing process

granuloma is an organized collection of macrophages that forms in response to persistent inflammation.

Granulation tissue - result of would healing process

Grannuloma - result of inflammation

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48
Q

What is the actual function of a

granuloma
and
Granulation tissue

A

Grannulation tissue - replaces ded/necrotic tissue, fills the wound and protects wound surface from microbes

Granuloma - to surround/destruct antigens

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49
Q

Define chronic inflammation. what things predominate?

A

The subsequent and often prolonged tissue reactions to injury following the initial
response

lymphocytes, plasma cells and
macrophages predominate

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50
Q

What is the most common way acute inflammation becomes chronic?

A

The Supparitive type - the pus forms an abscess that is deep seated or doesn’t drain properly, so the walls of the abscess cavity fail to come together, leading to scaring

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51
Q

Give some microscopic features of chronic inflammation.

A

of lymphocytes, plasma cells &
macrophages
- A few eosinophil polymorphs may be present but neutrophil polymorphs are
scarce
- Some of the macrophages may form multinucleate giant cells

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52
Q

Define granuloma.

A

An aggregate of epithelioid histocytes.

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53
Q

Give an example of a granulomatous disease

A

TB, leprosy, Crohn’s disease and sarcoidosis.

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54
Q

Outline what epithelioid histocytes are. What is their function?

A

Appear vaguely histologically similar to epithelial cells
* Have large vesicular nuclei

Appear in clusters

Have little phagocytic activity, but secrete angiotensin converting enzyme

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55
Q

The activity of what enzyme in the blood can act as a marker for granulomatous disease?

A

Angiotensin converting enzyme.

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56
Q

Name 5 types of cells capable of regeneration.

A
  1. Hepatocytes.
  2. Osteocytes.
  3. Pneumocytes.
  4. Blood cells.
  5. Gut and skin epithelial cells.
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57
Q

Name 2 types of cells that are incapable of regeneration.

A
  1. Myocardial cells.
  2. Neuronal cells.
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58
Q

Define abscess.

A

Acute inflammation WITH A FIBROTIC WALL (CONTAINS INFLAMMATORY RESPONSE) but can compress

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59
Q

Define thrombosis.

A

Formation of a solid mass from blood constituents WITHIN AN intact vessel in the living.

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60
Q

How is a thrombosis different to a clot?

A

A clot is blood coagulated OUTSIDE OF THE VASCULAR SYSTEM, or after death

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61
Q

Give 2 reasons why thrombosis formation is uncommon.

A
  1. Laminar flow. (Cells flow down the centre of vessels)
  2. Non sticky endothelial cells. (when heatlhy)
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62
Q

What are the 3 factors that can lead to thrombosis formation?

A
  1. Change in vessel wall.
  2. Change in blood constituents.
  3. Change in blood flow.
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63
Q

What are platelets derived from?

A

Megakaryocytes, cells from the bone marrow. They have no nucleus

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64
Q

When are platelets activated? What do they release?

A

They they come into contact with COLLAGEN
Release ALPHA GRANULES (help paltelets adhere to damaged vessel walls eg fibrinogen)
and DENSE GRANULES (Help platelets aggregate eg ADP)

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65
Q

What are the different types of thrombosis and what causes them?

A

Arterial thrombosis - atherogenesis
Venous thrombosis - venous stasis

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66
Q

How do Arterial Thrombus form?

A
  1. starts with Vasospasm, and is Most commonly superimposed on an atheroma
    1. Platelets bind to collagen via VWF factor, activating them
    2. Releasing granules which lead to lead to postive feedback platelet plug
      a. Then after a cascade of reactions fibrinogen becomes activated to fibrin, binding platelets together
    3. ===> so RBCs become entrapped.
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67
Q

How do venous thrombosis commonly form?

A

VENOUS THROMBOSIS - MOST LIKELY TO OCCUR AROUND VALVES, DURING SURGURY OR PERIODS OF POOR MOBILISATION. ===> BLOOD SITS IN VEINS, LEADING TO CLOT FORAMTION. ===> STASIS
Made up mainly of coagulation factors

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68
Q

How do you treat venous thrombosis?

A

known as a RED THROMBUS
treat with ANTI COAGULANTS
eg Warafin, Heparin

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69
Q

How do you treat an arterial thrombosis?

A

Think - White Thrombus, made of platelets
So give ANTIPLATELETS , eg Aspirin, Clopidogerel

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70
Q

Define embolus.

A

A mass of material ( blood clot, air bubble, piece of fatty deposit, or thrombus or other object) which has been carried in the bloodstream to lodge in and block a vessel and cause an embolism.

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71
Q

Define ischaemia.

A

Decreased blood flow.

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72
Q

Define infarction.

A

Decreased blood flow with subsequent cell death.

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73
Q

Why are tissues with an end arterial supply more susceptible to infarction?

A

They only have a single arterial supply and so if this vessel is interrupted infarction is likely.

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74
Q

Give 3 examples of organs with a dual arterial supply.

A
  1. Lungs (bronchial arteries and pulmonary veins).
  2. Liver (hepatic arteries and portal veins).
  3. Some areas of the brain around the circle of willis.
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75
Q

What things make up Virchow’s triad?

A

Endothelial injury (Trauma Surgery, MI)
change in blood constituents (Sepsis
Change in blood flow (laminar to turbulent) (AF)

Not all three factors are needed for
thrombosis to occur; any one of them
may result in thrombosis
- However, most usually its a combination of two or three of these,

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76
Q

What are the two types of thrombosis?

A

Arterial and venous

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77
Q

How do arterial thrombosis form?

A

Through ARTHEROGENESIS - CLOT FORMATION:
- Leads to turbulence
- Turbulence exposes collagen
- Platelets bind to collagen, fibrin mesh

Turbulence is greatest down stream of the aterial thrombosis, as blood passes over the thrombus, disrupting laminar flow

Propagation - Thrombi growing in the direction of blood flow

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78
Q

Name some conditions assocociated with arterial thrombosis

A

MI , Ischaemic heart disease, stroke, periperhal vascular disease

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79
Q

Where does the greatest degree of tubulence happen in arterial thrombosis?

A

Downstream of an arterial thrombosis, as
the blood passes over the thrombus, disrputing laminar flow

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80
Q

Platelet plug: what do e dense granules do? Give an example of a substance found in them

A

Helps platelets adhere to one another. A substance released is ADP

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81
Q

Platelet plug: what do alpha granules do? Give an example of a substance found in them

A

Alpha granules help platelets adhere to the damaged vessel wall
Fibrinogen is found here, which when activated becomes fibrin via enzyme Thrombin

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82
Q

Define Propagation

A

Thrombi growing in the direction of blood flow

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83
Q

Name some system specific complications of atherosclerosis.

A

Obstruction/ occlusion of arteries in the head and neck = cerebral infarction
Obstruction/ occlusion of coronary artery = myocardial infarction
Obstruction/ occlusion of artery in the limbs = peripheral vascular disease or gangrene
Obstruction/ occlusion og renal arteries = increased renin release → increased blood pressure
Atherosclerosis in the aorta can cause an aortic aneurysm, a result of excessive dilation of the aorta to the point that it rupture. Results in sudden death

84
Q

Where do most venous thrombi occur?

A

Around the valves, as they can cause turbulence, as its easier for clots to accumulate. Good blood pressure can prevent this

85
Q

When are venous thrombosis likely?

A

If blood pressure is allowed to fall during surgery, or after an MI. If elderly people have poor calf muscle contraction, as this can help aid venous return

86
Q

What are the consequences of a venous embolus?

A

An embolus in the venous system will go onto the vena cava and then through the pulmonary arteries and become lodged in the lungs causing a pulmonary embolism. This means there is decreased perfusion to the lungs.

87
Q

What does it mean if a thrombi is resolved?

A

In the best case scenario the thrombus may resolve as a result of the
body dissolving it and clearing it away

88
Q

What does it mean if a thrombi becomes organised?

A

may become organised INTO A SCAR

Macrophages clear away thrombus and fibroblasts REPLACE IT WITH COLLAGEN

Resulting in the slight narrowing of the vessel lumen

89
Q

What does it mean if a thrombi proliferates?

A

intimal cells of the vessel in which the thrombus lies may
proliferate, and small sprouts of capillaries may grow into the thrombus and later fuse to from larger vessels.
Vessel can become functional again

90
Q

What are the four fates of thrombi?

A

Resolution
Organisation
Proliferation
Embolism

91
Q

What does Aspirin do in respect to thrombosis?

A

it INHIBITS PLATELET AGGREGATION (get far less positive feedback)

Inhibits thromboxane A2

92
Q

What does Warafin do in respect to thrombosis?

A

it INHIBITS VITAMIN K (CLOTTING FACTOR) so prevents clotting

93
Q

where does atrial thrombi normally originate? What are the two main causes of arterial thrombi here?

A

from the heart or from an atheromatous plaque

thrombi may form on areas of cardiac muscle that have died as a result of a myocardial infarction, these have lost their normal endothelial lining and will expose the underlying collagen to the circulating platelets

atrial fibrillation - this ineffectual movement of the atria cause blood to stagnate in the atrial appendages and thrombosis to occur

94
Q

What are the effects of ischaemia dependant on? 2 things

A
  • the duration of the ischaemic period: brief ischaemic periods may be recoverable
  • the metabolic demands of the tissue
95
Q

What tissue is most susceptible to ischaemia?

A

: cardiac myocytes and cerebral
neurones are most vulnerable, due to high metabolic demand

96
Q

What can happen if ischaemia is rectified?

A

Re-perfusion injury can occur due to the release of waste products, which can activate free radical systems (ROS) that begin the clearing away of dead cells

97
Q

how can smoking cuase thrombosis ?

A

can damage endothelial cell walls, and also causes a change in blood flow (stasis)

98
Q

Define diapedesis. When would you see it?

A

RBCs escaping from vessels, due to severe vascular injury. this is a passive process - seen in acute inflammation.

99
Q

What are the 4 stages of Neutrophil polymorph emigration?

A
  1. Migration of neutrophils - neutrophils migrate to the plasma zone of the vessels (each side) due to increased plasma viscosity and slower blood flow
  2. Adhesions of neutrophils - Neutorhpils stick to vascular endothelium (pavementing)
    • Neutrophil emigration - Neutrophils pass through endothelial cells and basal lamina, then through vessel wall

4 - Diapedesis - RBCs may also escape from vessels - passive process - severe vascular injury.

100
Q

What happens in the first stage of neutrophil movement, migration?

A
  1. Migration of neutrophils - neutrophils migrate to the plasma zone of the vessels (each side) due to increased plasma viscosity and slower blood flow
101
Q

Chronic inflammation - what do Granulomas and eosinophil presence indicate?

A

parasites

102
Q

Chronic inflammation - what are B lymphocytes responsible for?

A

Transform into plasma cells and produce antibodies

103
Q

Chronic inflammation - what are T lymphocytes responsible for?

A

Cytotoxic T cells
Cytotoxic T lymphocytes kill their target cells primarily by releasing cytotoxic granules into the target cell. CD8+

T-Helper Lymphocytes
CD4+ T cell functions include activating other immune cells, releasing cytokines, and helping B cells to produce antibodies

Memory T cells
They provide the immune system with memory against previously encountered antigens. Memory T lymphocytes may either be CD4+ or CD8+.

104
Q

Define atherosclerosis

A

Inflammatory process characterised by hardened atherosclerotic plaques in the intima of a vessel wall.

105
Q

Name some conditions that atherosclorosis can lead to

A

Cerebral infraction
Carotid atheroma, leading to TIAs
MI
Aortic aneurysm (can cause sudden death)
Peripheral vascular disease
Gangrene

106
Q

Is atherosclerosis more common in the systemic or pulmonary circulation?

A

It is more common in the systemic circulation because this is a higher pressure system.

You barely see any atherosclerosis at all in the pulmonary system

107
Q

name 4 main constituents of an atheromatous plaque

A
  • Lipids
    • Cholesterol
    • Lymphocytes
      Fibrous tissue
108
Q

Give 5 risk factors for atherosclerosis.

A
  1. Cigarette smoking.
  2. Hypertension.
  3. Hyperlipidaemia.
  4. Uncontrolled diabetes mellitus.
  5. Lower socioeconomic status.
    Being Male
109
Q

What is the primary cause of atherosclerosis?

A

Endothelial cell damage.

110
Q

Why can hypertension lead to atherosclerosis?

A

A higher blood pressure means there is a greater force exerted onto the endothelial cells and this can lead to damage.

111
Q

Outline the progression of athersclorosis.

A
  1. High levels of cholesterol damages endothelium.
  2. LDLs and inflammatory cells like monocytes and macrophages and T-cells begin to accumulate in arterial wall
  3. Macrophages try to break down LDLs, turning into foam cells, which produce a LIPID CORE/FATTY STREAK
  4. This inflammatory reaction leads to tissue repair, so the smooth muscle proliferates forming a fibrous cap that encloses the lipid core.
112
Q

What can fully formed atherosclorotic plauqes do? Why is this bad?

A

They can “HAEMORRHAGE”, through the leaking of microvessels in the plaque. this can lead to a rapid expansion of plaques, producing clinical symptoms.

113
Q

How can hypertension damage endothelial cells?
Where in aterial vessels are particualy prone to high BP damage?

A

becuase it sheers/damage the vessel walls, thorugh more force, particularly where they bifurcate

114
Q

How can smoking damage endothelial cells?

A

free radicals , nicotine and carbon monoxide all damage Endothelial cell wall

115
Q

How can uncontrolled diabetes damage endothelial cells?

A

Endothelial cells taking in more glucose causing them to form more glycosylation products (eg Superoxide anions) that reduce release of NO and cause the Basement membrane to thicken and weaken

116
Q

Name some measures to prevent atherosclorosis.

A
  • Smoking cessation
  • Control of blood pressure
  • Weigh reduction
  • Low dose aspirin - inhibits the aggregation of platelets, advised for people
    with clinical evidence of atheromatous disease
  • Statins - cholesterol reducing drug
117
Q

Define apoptosis

A

Programmed cell death of a single cell. No harmful products are released to the surrounding cells.

118
Q

Name 3 things that Inhibit apoptosis

A
  • Growth factors
    -Extracellular cell matrix
  • Sex steroids
119
Q

outline some characteristics of Apoptosis

A

It is non inflammatory cell death

Cells shrink, and organelles are retained and cell surface membrane is intact

Chromatin is unaltered, just fragmented for easy phagocytosis

120
Q

outline some characteristics of necrosis

A

Inflammatory and traumatic

Cells burst, the cell surface membrane is damaged

chromatin is altered,

cell is fucked

121
Q

name things that induce apoptosis

A

Withdrawal of Growth factor
- Glucocorticoids
- Some viruses
- Free radicals
- Ionising radiation
- DNA damage
- Ligand binding at death receptors

122
Q

What does the intrinsic pathway respond to? What is it also known as?

A

Intrinsic pathway happens when cells are exposed to stress - from when things that can occur within the cell

Eg
Radiation
Hypoxia
Oxidative stress from free radicals stealing electrons

Known as the mitochondrial pathway

123
Q

Types of Apoptosis: Outline the intrinsic (mitochondrial ) pathway

A
  1. stress causes 2 intracellular proteins, BAX and BAK to move from the cytoplasm to the mitochondria
  2. BAX and BAK pierce the mitochondrial membrane, making it porous and leaky
  3. Cause the release from the mitochondria of Cytochrome C
  4. Cytochrome C leads to the activation of caspases, triggering apoptosis
124
Q

What does the extrinsic pathway respond to? What is it also known as?

A

receives Signals for apoptosis coming from outside the cell

Known as the death receptor pathway

125
Q

Outline the extrinsic (death receptor ) pathway

A

Instigated by two things: Macrophages and Cytoxic T cells

  • Macrophages and Cytotoxic T cells detect old or diseased cells, and hence go on to release

Tumour Necrosis factor alpha (TNF-a) (macrophage) or FAS Ligand (Cytoxic T cell)

===> This Binds to death receptors on the cell surface membrane

This leads to activation of caspases within the cell, once again triggering apoptosis

126
Q

What decides whether a cell apoptoses?

A

One of the mechanisms is detecting amount of DNA damage within the cell.

127
Q

What can detect DNA damage?

A

p53 is a protein in cells which can detect DNA damage
and can then trigger apoptosis

128
Q

What protein can inhibit apoptosis in the intrinsic pathway?

A

the BcL2 protein

129
Q

When can we see apoptosis, in healthy states
(give Examples)

A

villi in the gut
formation of foeus’ hands and feet in the womb

130
Q

In regard to apoptosis, how does cancer damage cells?

A

Often this is due to mutations in the P53
gene so the p53 protein can no longer detect DNA damage, and instigate apoptosis

So tumours don’t apoptose when they should

131
Q

Define necrosis

A

It is the wholesale destruction of large numbers of cells by some external factor.

The only thing it shares with apoptosis is that it is a form of cell death

132
Q

Name some of the different types of necrosis, and where in the body/when you could see them

What is most common?

A

Coagulative - most common, due to organ ischaemia - see in heart/kidney

Liquefactive - seen in brain

Caseous - cheesy, see infections like TB

Gangrenous - seen in distal limbs eg Finger

133
Q

give some clinical examples of necrosis

A

Infarction due to loss of blood supply e.g. myocardial
infarction, cerebral infarction

  • Frostbite
  • Toxic venom from reptiles and insects
  • Pancreatitis
134
Q

What is the body’s response to necrosis?

A

all the body can do is try to clear up the
mess by macrophages phagocytosing dead cells

And then replacing the necrotic tissue with fibrous scar tissue (unless the tissue can regenerate).

135
Q

Give 3 differences between apoptosis and necrosis.

A
  1. Apoptosis is programmed cell death whereas necrosis is unprogrammed.
  2. Apoptosis tends to effect only a single cell whereas necrosis effects a large number of cells.
  3. Apoptosis is often in response to DNA damage. Necrosis is triggered by an adverse event e.g. frost bite.
136
Q

Define hypertrophy.

A

Increase in the size of a tissue due to an increase in the size of constituent cells.

137
Q

Define hyperplasia.

A

Increase in the size of a tissue due to an increase in the number of constituent cells.

138
Q

Define atrophy.

A

Decrease in the size of a tissue due to a decrease in the size of the constituent cells OR due to a decrease in the number of constituent cells.

139
Q

Define metaplasia.

A

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

140
Q

Give an example of a disease that demonstrates metaplasia.

A

Barrett’s oesophagus - the cells at the lower end of the oesophagus change from stratified squamous cells to columnar.

141
Q

Define dysplasia.

A

Morphological changes seen in cells in the progression to becoming cancer. The cells become more ‘jumbled up’.

  • Disorderly growth
142
Q

Define neoplasm.

A

An autonomous, abnormal, persistent new growth.

143
Q

Define carcinoma.

A

Malignant tumour of epithelial tissue.
Forms on the skin/tissues that line the body’s internal organs such as kidney and liver

144
Q

Define Carcinogenesis

A

The transformation of healthy cells to NEOPLASTIC cells through permanent genetic alterations or mutations

145
Q

What does a neoplasm release in order to initiate angiogenesis?

A

Vascular endothelial growth factors.

146
Q

Why does necrosis often occur in the centre of a neoplasm?

A

The neoplasm grows quickly and outgrows its vascular supply.

147
Q

What are the two ways in which neoplasms can be classified?

A
  1. Behavioural classification.
  2. Histogenetic classification.
148
Q

What is the behavioural classification of neoplasms?

A

Neoplasms can be classified as benign, malignant or borderline. Borderline tumours (e.g. some ovarian lesions) defy precise classification.

149
Q

What is the histogenetic classification of neoplasms?

A

Histogenetic classification is based on the specific cell or origin of the tumour, with their likeness to the original cell graded 1-3

150
Q

What is essential for neoplasm growth?

A

Angiogenesis.

151
Q

Why wont a ductal carcinoma spread to the rest of the body?

A

because its Surrounded by a band of collagen, so wont spread into the rest of the body. No access to blood vessels/lympathcts

once a tumour leaves the duct, then its bad, as it can get through the extracellular matrix and then vessels

152
Q

What do cancer cells in a duct need to do in order to spread through the body

A

get through the basement membrane - by producing enzymes that will break down the collagen (collagenases)

153
Q

what does a tumour bigger than one 1mm need in order to survive?

A

its own blood suppply

154
Q

huow do cancer cells evade host immune defense

A

*aggregation with platelets
*shedding of surface antigens
*adhesion to other tumour cells

155
Q

Give an example of 5 carcinoma’s that can spread to bone.

A
  • Breast
  • Lung
  • Thyroid
  • Kidney
  • Prostate

BLT for KP

156
Q

Give 3 inhibitors of tumour angiogenesis. HOw can this be used

A

. Angiostatin.
2. Endostatin.
3. Vasculostatin.

Use medications like these to stop angiogenesis so tumours cannot make their own blood supply, so they cant exceed more than 1mm in size

157
Q

Give an example of carcinomas that can spread to the liver.

A

Colon, stomach and pancreatic carcinomas can spread to the liver via the portal vein

158
Q

Give an example of a malignant tumour that often spreads to the lung

A

Sarcoma (via venae cavae -> heart -> pulmonary arteries)

Alot of common cancers can spread to lung, as they travel through the venous system and heart, only to get stuck in the pulmonary circulation

159
Q

Tumours from where commonly metastasise to bone?

A

Prostate, breast, thyroid, lung and kidney

160
Q

define cell motility

A

Cellular motility is the spontaneous movement of a cell from one location to another by consumption of energy.

Cancer cells need this in order to spread (obvs)

161
Q

What are 2 types of genes that if have mutations in them, can lead to cancer?

A

Either DNA mutation in
Proto-oncogenes - Promote/accelerate cell division

Tumour suppressor genes - lead to a loss of inhibition of cell division

162
Q

what is an invasive carcinoma?

A

Invasive carcinoma means the cancer cells have broken out of the lobule where they began and have the potential to spread to the lymph nodes and other areas of the body.

163
Q

Name some things that cancer cells that are in situ need in order to spread through the body

A

Proteases
Collagenases
Cell motility
Adhesion receptors, so it can leave the blood stream

164
Q

What percentage of cancer risk is due to environmental factors?

A

85% environmental, 15% genetic

165
Q

Give an advantage and a disadvantage of conventional chemotherapy.

A

Advantage: works well for treatment against fast dividing tumours e.g. lymphomas.
- Disadvantage: it is non selective for tumour cells, normal cells are hit too; this results in bad side effects such as diarrhoea and hair loss.

166
Q

What is the theory behind targeted chemotherapy?

A

It exploits the differences between cancer cells and normal cells; this means it is more effective and has less side effects.

167
Q

in what cell can neoplasm not occur? why is this?

A

Red blood cells
Neoplasm cannot arise in erythrocytes as they do not have nuclei)

168
Q

Define tumour

A

any abnormal swelling

169
Q

define carcinogen.

A

An ENVIRONMENTAL AGENT that can particpate in the causation of tumour

170
Q

briefly outline the process of metastasis.

A
  1. Tumour cells detach from neighbouring cells
  2. Tumour invades surrounding connective tissue to reach blood/Lymph vessels etc
  3. Intravasation into the lumen of vessels
  4. Tumour adheres to endothelium at remote location
  5. Extravasation of the cells from the vessel lumen into the surrounding tissue

Tumour cells proliferate in the new environment

all this while evading host defence mechanisms

CD44

171
Q

define sarcoma.

A

A type of cancer that begins in bone or in the soft tissues of the body, including cartilage, fat, muscle, blood vessels, fibrous tissue, or other connective or supportive tissue.

172
Q

In the behavioural classification - give some features of benign tumours

A

Benign -
Localised (no invasion of basement membrane)
Slow growing
Well circumscribed ( at least 75% of contour of the tumour is well defined)
Exophytic (outward growth)
Rarely ulcerate or necrose
Closely resemble normal tissue

173
Q

behavioural classification - give some features of malignant tumours

A

Invades basement membrane
fast growing
Poorly circumscribed (tumour has poorly defined contours)
Endophytic (inward growing)
Commonly necrose and ulcerate
Do not resemble normal tissue

174
Q

Give 2 examples where a benign tumour is pathological

A

Prolactinoma - presses on pituitary gland, so too much prolactin is produced
tumours on pituitary gland causing a lesion at the optic chasm, leading to a bitemporal hemianopia

Benign can also transform into malignant tumours - big risk

175
Q

Outline what Histogenic classification is

A

Based on the specific cell or origin of the tumour
Determined by histopathological examination and specifies the tumour
type

176
Q

What are the major Histogenic classifcations?

A

Epithelial cells (forming carcinomas)
Connective tissues (forming sarcomas)
Lymphoid (ONLY GIVE RISE TO MALIGNANT NEOPLASMS)

177
Q

What are non glandular epithelial benign tumours called?

A

Papilloma

178
Q

What are non glandular epithelial malignant tumours called?

A

carcinoma

179
Q

What is a glandular epithelial benign tumour known as?

A

Adenoma

180
Q

What is a glandular epithelial malignant tumour known as?

A

Adenocarcinoma

181
Q

Connective tissue tumours - what is the rule for suffixes to classify
a) Benign
b) Malignant
Tumours?

A

Benign - named after cell or tissue of origin suffixed by -oma:
Malignant - always designated sarcoma, prefixed by the name that
describes the cell or tissue of origin:

182
Q

Connective tissue tumours - what is an
a) Benign
b) Malignant
Tumour of fat cells known as?

A

Lipoma: benign tumour of adipocytes
Liposarcoma: malignant tumour of adipocytes

183
Q

Connective tissue tumours - what is an
a) Benign
b) Malignant
Tumour of cartilage known as?

A

Chondroma: benign tumour of cartilage
Chondrosarcoma: malignant tumour of cartilage

184
Q

Connective tissue tumours - what is an
a) Benign
b) Malignant
Tumour of bone known as?

A

Osteoma: benign tumour of bone
Osteosarcoma: malignant tumour of bone

185
Q

Considering that not all malignant tumours are eitther carcinoma or sarcomas, what is
a) malignant neoplasm of melanocytes
b) malignant tumour of mesothelial cells (line body
cavities and outer surface of internal organs, secrete lubricating
fluid)
Known as?

A

a) Melanoma
b) Mesothelioma

186
Q

Histogenic classification - What arises from Lymphoid cancers

A

lymphomas or leukaemias

187
Q

What do we compare tumours to when we grade them 1-3?

A

the histological Similarity to the parent cell

188
Q

Explain the graded 1-3 system for tumours

A

Grade 1 – Well differentiated (most closely resembles parent tissue, 75% or more)
Grade 2 – Moderately differentiated (10-75% resemblance to parent tissue)
Grade 3 – Poorly differentiated (less than 10% resemblance to parent tissue)

189
Q

Outline the 3 main characteristics of the neoplastic cell that allow them to spread and grow rapidly.

A

Autocrine growth stimulation (over expression of growth factors)
Able to Evade apoptosis (over expression of apoptosis inhibiting genes bcl-2)
Telomerase - prevents the telomeres from shortening over lots of cell divisions, making able to replicate much more

190
Q

What are the classes of carcinogens

A
  • Chemical
  • Viruses
  • Ionising & non-ionising radiation
  • Hormones, parasites & mycotoxins
  • Miscellaneous
191
Q

What are the two main methods of spreading of tumours

A

haematogenous - via the bloodstream
Lympathic - via the lymph nodes / lymphatic system

192
Q

Generally, how do
a) Sarcomas
b) Carcinomas
spread?

A

Sarcomas - mostly haematogenous
Carcinomas - mostly lymphatic

193
Q

What is the most common system for staging tumours?

A

The TNM system, standing for
Tumour
Node
Metastasis

194
Q

TNM staging - what does the T stand for

A

Tumour - looks AT THE SIZE of the primary tumour

195
Q

TNM staging - what does the N stand for

A

Node - Refers to the degree of lymph node involvement

Nx for nodes can’t be assessed
N0 - no nodal involvement

N1-3 - number/location of node metastases

196
Q

TNM staging - what does the M stand for

A

Metastatic status - the extent of distant metastases
either

M0 - no distant spread

M1 - Distant metastises

197
Q

What are the two main (higher yield) mutations involved in colorectal cancers?

A

FAP - Familial Adenomatous polyposis,
HNPCC - Hereditary nonpolyposis colorectal cancer, also known as Lynch Syndrome -

(Both are Autosomal dominant)

198
Q

What are the mutations for
FAP, and
HNPCC - Lynch syndrome>?

A

FAP - mutation in APC gene

HNPCC - Mutated MSH Gene

199
Q

With cancer, at what level of prevention does screening look for?

A

Always secondary (detecting early to make management easier)

200
Q

What are the 3 cancers screened for in the UK?

A

Breast
Cervical
Colorectal

201
Q

How do you screen for cervical cancer?

A

A cervical swab

202
Q

How do you screen for breast cancer?

A

Using mammography (an x-ray for the breast tissue)

203
Q

How do you screen for colon cancer?

A

Testing faeces for occult blood

Occult blood is blood you can’t see it with the naked eye

204
Q

Name 3 conditions that the heel prick test screens for, at birth

A

Cystic Fibrosis
Sickel Cell anaemia
Hypothyroidism

205
Q

Define what a cancer tumour in situ is

A

Carcinoma in situ refers to an epithelial neoplasm exhibiting
all the cellular features associated with malignancy, but which
has not yet invaded through the epithelial basement
membrane,

separating it from potential routes of metastasis e.g. blood vessels and lymphatics

206
Q

Do basal cell carcinoma metastise?

A

No

207
Q

Outline a benign and malignant tumour of
a) Striated muscle
b) Smooth muscle

A

Rhabdomyomas = benign tumours of striated muscle
Rhabdomyosarcoma = malignant tumour of striated muscle

Leiomyoma = benign tumours of smooth muscle cell
Leiomyosarcoma = malignant tumour of smooth muscle cells

Phase 2a Sam (18 decks)

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