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Pathology Flashcards

1
Q

What are the 2 types of autopsy? Describe them.

A

hospital: audit, research, teaching, governance

medico-legal: 90% of autopsies, either coronial or forensic

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2
Q

What are the 3 types of death?

A

presumed natural: unknown/not seen by doctor in last 14 days
presumed iatrogenic: because of their care eg postoperative, anaesthetic, abortion
presumed unnatural: accidents, unlawful, suicide

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3
Q

What happens in an autopsy?

A

history -> external exam -> evisceration -> internal exam -> reconstruction

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4
Q

How does inflammation appear? (5 things)

A
  1. redness: vessel dilation
  2. heat: increased blood flow = vessel dilation/systemic fever
  3. swelling: oedema/mass of infl cells/formation of new connective tissue
  4. pain: stretching of tissue due to pus + oedema/chem mediators eg bradykinin
  5. loss of function
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5
Q

When is inflammation good?

A

infection

injury

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6
Q

When is inflammation bad?

A

autoimmunity

over-reaction to stimulus

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7
Q

What are the features of acute inflammation?

A

sudden onset
short
usually resolves
involves neutrophil polymorphs

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8
Q

What are the features of chronic inflammation?

A

slow onset/sequel to acute
long
may never resolve
involves lymphocytes and macrophages

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9
Q

How are neutrophil polymorphs involved in inflammation?

A 
short lived
first on scene
die at scene + produce pus
release chemicals to attract other infl cells
phagocytosis
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10
Q

How are macrophages involved in inflammation?

A

last weeks to months
phagocytic: ingets debris
don’t always die: carry debris away or present antigens to lymphocytes
eg Kupffer cells (name depends on location)

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11
Q

How are lymphocytes involved in inflammation?

A

last years
produces chemicals to attract other infl cells
immunological memory

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12
Q

How are fibroblasts involved in inflammation?

A

long lived

form collagen = scarring

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13
Q

How are endothelial cells involved in inflammation?

A

line capillary vessels
become sticky so infl cells adhere to them
become porous so infl cells can pass to tissues
grow into areas of damage = new capillaries

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14
Q

What are granulomas?

A

type of chronic inflammation

epitheliod = group of pale macrophages surrounded by lymphocytes

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15
Q

What is the treatment for inflammation?

A

NSAIDs eg aspiring, ibuprofen

steroid cream for skin rash eg betnovate

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16
Q

How do corticosteroids work?

A

bind to DNA
up regulate inflammatory inhibitors
down regulate chemical mediators of inflammation

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17
Q

How does inflammatory treatment work?

A

inhibit prostaglandin synthetase

prostaglandin is a chemical mediator of inflammation

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18
Q

What are the 5 causes of acute inflammation?

A 
microbial infections
hypersensitivity
physical agents eg UV, cold
chemicals
tissue necrosis
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19
Q

What is cellulitis?

A

skin infection due to vascular dilation in acute inflammation = red, hot skin

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20
Q

What are the 3 main stages of acute inflammation?

A
  1. changes in vessel calibre + flow
  2. increase in vascular permeability + formation of fluid exudate
  3. formation of cellular exudate: neutrophil polymorphs move into EVS
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21
Q

What chemical mediators are released in acute inflammation?

A

histamine + thrombin: create very firm neutrophil adhesion to endothelial surface

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22
Q

What do chemical mediators cause in the acute inflammation process?

A 
vasodilation
emigration of neutrophils
chemotaxis
increased vascular permeability
itching and pain
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23
Q

What are the harmful effects of acute inflammation?

A

digestion of normal tissue
swelling
inappropriate response

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24
Q

What are the 4 outcomes of acute inflammation?

A

resolution
suppuration
organisation
chronic inflammation

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25
Q

What is resolution in acute inflammation?

A

usual process: restoration back to normal
happens in: minimal cell death, an organ able to regenerate, rapid destruction of cause, rapid removal of fluid by vascular drainage
eg acute lobar pneumonia

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26
Q

What is suppuration in acute inflammation?

A

occurs due to excessive exudate
formation of pus, neutrophils + bacteria, cellular debris and liquid globules
persistent and usually infective agent
abscess will heal, form granulation and then scar = organisation

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27
Q

What is a collection of pus called?

A

abcess

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28
Q

What is organisation in acute inflammation?

A

due to excessive necrosis
replacement of tissues by granulation tissue
happens when: lots of fibrin which can’t be removed, lots of necrotic tissue, exudate/debris can’t be digested

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29
Q

What is the process of organisation in acute inflammation?

A 
new capillaries grow into exudate 
macrophages migrate
fibroblasts proliferare
fibrosis
scar
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30
Q

Why does acute inflammation lead to chronic?

A

persistent cause

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31
Q

Which 2 outcomes of acute inflammation lead to fibrosis?

A

chronic inflammation

organisation

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32
Q

What are the systemic effects of acute inflammation?

A 
pyrexia
weight loss
amyloidosis
hyperplasia of reticuloendothelial system
haematological changes
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33
Q

Which cells predominate in chronic inflammation?

A 
lymphocytes
plasma cells
macrophages
giant cells
fibroblasts
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34
Q

What are the main causes of chronic inflammation?

A

primary cause
transplant rejection
progression from acute inflammation
recurrent episodes of acute inflammation

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35
Q

What is the main complication of chronic inflammation?

A

amyloidosis

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36
Q

Give some examples of a cause of chronic inflammation?

A

infective agent: TB, leprosy
exogenous materials: sutures
primary granulomatous diseases: Crohn’s

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37
Q

What are the stages of connective tissue proliferation?

A
  1. angiogenesis
  2. fibroblast proliferation and collagen synthesis
    = granulation tissue
    (regulated by growth factors)
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38
Q

What are the 2 lymphocytes involved in inflammation?

A

B: contact with antigen = form plasma cells = produce antibodies
T: cell-mediated immunity, produce cytokines = recruitment, activation

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39
Q

Where does acute inflammation occur in disease?

A

after an acute MI
complications of an MI
atherosclerosis

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40
Q

Where does chronic inflammation occur in disease?

A

cancer
myocardial fibrosis after MI
neurodegenerative diseases eg MS
atheroclerosis

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41
Q

What is resolution?

A

initiating factor is removed = tissue is undamaged and able to regenerate

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42
Q

What is repair?

A

initiating factor is present = tissue damaged and unable to regenerate

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43
Q

What is organisation?

A

repair of specialised tissue by the formation of a fibrous scar

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44
Q

What happens after hepatocyte loss in the liver?

A

complete restitution

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45
Q

What happens after the hepatic architecture is damaged in the liver?

A

cannot be regenerated

only regenerate on hepatocyte loss

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46
Q

When does cirrhosis occur in the liver?

A

when there is an imbalance between hepatocyte regeneration and failure tor reconstruct the hepatic architecture

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47
Q

When does complete restitution occur?

A

when there is a loss of a labile cell population that can be completely restored eg skin abrasion

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48
Q

What happens when the lungs are damaged?

A

as long as the structure isn’t damaged, pneumocytes will regenerate

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49
Q

Why do skin abrasions heal so quickly?

A

not all the epithelium is removed
hair follicles and sweat glands remain
only the small vessels are occluded by thrombosis

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50
Q

What happens in 1st intention healing of the skin in an incised wound?

A

cut through all layers of the skin
cut fills with fibrin from the blood = weak and rapid fibrin joint
coagulated blood forms a scab
fibroblasts bring collagen forming a white scar = strong collagen joint
capillaries proliferate

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51
Q

What happens in 2nd intention healing of the skin?

A

deep cut with no sutures/tissue loss
fills with capillaries and fibroblasts that produce collagen
phagocytosis occurs to remove debris
granulation tissue forms
epithelial regeneration occurs to cover surface

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52
Q

What is the difference between 1st and 2nd intention repair of the skin?

A

2nd is slower and forms a bigger scar than if sutured

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53
Q

What is the process of repair?

A

damaged tissue is replaced by fibrous tissue
collagen produced by fibroblasts
eg after MI, CI, spinal cord trauma

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54
Q

Which cells do regenerate?

A 
hepatocytes
pneumocytes
all blood cells
gut epithelium
skin epithelium (if in right place)
osteocytes
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55
Q

Which do NOT regenerate?

A

myocardial cells

neurones

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56
Q

What happens in organisation?

A

tissue contracts
accumulates collagen to forma a scar
remodelling occurs

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57
Q

How does granulation tissue form?

A

capillary endothelial cells proliferate into loops and grow into damaged area
fibroblasts stimulated to divide and secrete collagen
(acquire myofibroblasts for collagen and wound contraction)
capillary loops + myofibroblasts = granulation

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58
Q

How does a thrombus form?

A
  1. endothelial cell injury
    - collagen exposed: platelets stick to collagen and each other
    - release platelet aggregating factor = more platelets (positive feedback)
    - triggers clotting cascade
    - disrupted laminar flow means rbc are also trapped
  2. platelet aggregation = thrombus formation
    - chemicals cause fibrinogen to polymerise to fibrin
    - fibrin is deposited forming a mesh which traps rbcs
    - fibrin increases its own polymerisation (positive feedback)
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59
Q

What is a thrombus?

A

solidification of blood contents that forms WITHIN the vascular system during LIFE

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60
Q

What’s the difference between a thrombus and a clot?

A

a clot forms outside the vascular system or after death

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61
Q

What are the 3 main reasons a thrombus forms?

A
  1. change in vessel wall eg endo cell damage
  2. change in blood flow
  3. change in blood constituents
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62
Q

How is a thrombus usually prevented?

A
  1. laminar flow: cells flow in the centre of the artery and don’t touch the sides
  2. endo cells aren’t sticky when they are healthy
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63
Q

How do venous thrombi differ to arterial thrombi?

A

slower due to slower flow and contraction of surrounding muscles

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64
Q

Why are venous thrombi a big problem in hospitals?

A

lying down too often: cells hit the endothelium due to a slow flow = endothelial cell injury

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65
Q

What can a venous thrombi lead to?

A

pulmonary embolism

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66
Q

Where do venous thrombi most commonly form?

A

at valves

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67
Q

What types of granules are platelets made up of?

A

alpha: platelet adhesion to damaged wall, contains fibrin, fibrinogen, PGF
beta: platelet aggregation, contains ADP

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68
Q

How are platelets involved in the formation of a thrombus?

A
  • platelets activated + granule contents released on contact with collagen
  • change shape + extend pseudopodia
  • forms a mass over the damage until the endothelial cells have regenerated
  • if this starts in an intact vessel = thrombus
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69
Q

What are the clinical effects of an arterial thrombus?

A

loss of pulse distal to injury
area is cold, pale + painful
tissue dies + leads to gangrene

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70
Q

What are the clinical effects of a venous thrombus?

A

area tender due to ischaemia
reddened as it can’t be drained by the veins
swollen

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71
Q

What are the 4 possible outcomes of a thrombus?

A
  1. lysis + resolution (body dissolves it away)
  2. organisation (invasion of macrophages and fibroblasts - can cause narrowing)
  3. recanalisation (intimal cells proliferate and small capillaries grow into the thrombus - fuse to make larger vessels - recanalised - functional again)
  4. embolism (infarction)
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72
Q

What are some preventative methods to a thrombus?

A

aspirin: prevents platelet aggregation at low doses, prevents them being sticky
warfarin: used in severe cases, inhibits vitamin K
exercise
elastic stockings

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73
Q

What is an embolus?

A

mass of material in the vascular system able to lodge in a vessel and block it

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74
Q

What are the causes of an embolus?

A

most common: piece of thrombus broken off
air: IV fluids/bloods
cholesterol crystals: from atheromatous plaque
fat: severe trauma with multiple fractures

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75
Q

How does a venous embolism occur?

A

venous system - vena cava - right side of heart - pulmonary arteries - pulmonary embolism

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76
Q

Why can’t a venous embolism reach the arterial circulation?

A

lungs split down into capillary size so act as a filter for venous emboli

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77
Q

What happens to small venous emboli?

A

unnoticed

or are organised (scar = some narrowing)

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78
Q

What are the effects of a bigger emboli?

A

respiratory and cardiac problems: chest pain and shortness of breath
may become infarcted and increase the risk of another emboli

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79
Q

What are the effects of a massive emboli?

A

sudden death

usually from leg veins and travel to the bifurcation of the pulmonary arteries

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80
Q

Where do arterial emboli originate?

A

heart

atheromatous plaque

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81
Q

Where can an arterial emboli travel to?

A

from heart: anywhere

from cholesterol crystals: lower limbs + renal arteries

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82
Q

Why do arterial emboli form in the heart?

A

after a MI

atrial fibrillation

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83
Q

What is ischaemia?

A

reduction in blood flow to a tissue due to constriction/blockage of vessel supplying it

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84
Q

Which cells are most susceptible to ischaemia?

A

cells furthest from the vessel

still don’t necessarily die

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85
Q

Ischaemic damage is reversible depending on?

A

duration of ischaemia

metabolic demands of tissue (heart and brain most vulnerable)

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86
Q

What is infarction?

A

death of ells due to an obstructed artery (type of ischaemia)
usually caused by a thrombus

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87
Q

What factors increases the susceptibility of an infarction?

A
  • most organs have a single artery supply (end arterial supply)
  • watershed areas: at limits of 2 different blood supplies (occurs at a decrease in BP)
  • portal vasculature: organs where blood as already passed through 1 set of capillaries (decreases IV pressure = decreases oxygen saturation in 2nd set)
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88
Q

Which organs have a lower susceptibility to ischaemia?

A

those with a dual supply

  • liver (portal venous and hepatic arteries)
  • lungs (pulmonary venous and bronchial arteries)
  • some parts of the brain (circle of willis)
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89
Q

What is repurfusion injury?

A

damage from ischaemia occurs mostly when perfusion is reestablished

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90
Q

How does reperfusion cause injury after ischaemia?

A
  • blood returns + encounters tissue where transport mechanisms are damaged (especially impariment of Ca out of the cell)
  • triggers activation of oxygen dependant free radical systems that clear away dead cells = damage
  • macrophages + neutrophils clear away debris + import their own oxygen free radicals = damage
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91
Q

What is gangrene?

A

whole areas of limbs or guts have their arterial supply cut off + large areas of tissue die in bulk

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92
Q

What are the 2 types of gangrene?

A
  1. dry gangrene: tissues dies, mummifies and healing occurs over it = dead tissue drops off
  2. wet gangrene: bacterial infection occurs as a complication, spreads proximally = overwhelming sepsis = death
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93
Q

Where do MIs most commonly occur?

A

regional transmural MI (between endocardium and epicardium)

subendocardial MI: inner layer of heart more susceptible as blood comes in from outside = reduces BP

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94
Q

What are the other key causes of ischaemia and infarction?

A
  • spasm of smooth muscle
  • external compression
  • steal (blood diverted from vital territories when other artery is atherosclerotic)
  • hyperviscosity
  • vasculitis (inflammation of vessel wall)
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95
Q

What is apoptosis?

A

cellular process where a defined and programmed sequence of intracellular events lead to the removal of a cell without release of harmful substances

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96
Q

What steps are involved in apoptosis?

A

enzymatic digestion of nuclear and cytoplasmic contents by macrophages
= enzymes cause organelles to shrink and die
breakdown products phagocytosed within cell membrane

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97
Q

What is the main difference between necrosis and apoptosis?

A

necrosis is unintended

apoptosis suppressed the inflammatory response caused by necrosis

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98
Q

Where is apoptosis normal?

A

in the gut

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99
Q

How can apoptosis cause cancer?

A

defective apoptosis leads to neoplasia = cancer as cells live longer

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100
Q

Give 3 examples of diseases caused by apoptosis?

A

AIDS, neurodegenerative disorders, anaemia

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101
Q

How does apoptosis lead to AIDS?

A

HIV proteins activate CD4 on uninfected T-helper lymphocytes
lymphocytes are apoptosed
= immunodepletion

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102
Q

What is apoptosis inhibited by?

A

growth factors
extracellular cell matrix
sex steroids
some viral proteins

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103
Q

What is apoptosis induced by?

A 
growth factor withdrawal
loss of matrix
glucocorticoids
some viruses
free radicals
ionising radiation
DNA damage
ligands binding to death receptors
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104
Q

How does the intrinsic pathway of apoptosis work?

A

Bcl-2: inhibits factors that induce apoptosis
Bax: enhances apoptopic stimuli
ratio of these determines a cell’s susceptibility to apoptosis
inhibit/activate caspases (enzymes which chew stuff up) which inhibits/activates apoptosis

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105
Q

What part does the p53 gene play in the intrinsic pathway of apoptosis?

A

induces cell cycle arrest + starts DNA damage repair

if damage is too difficult to repair, p53 induces apoptosis by activating Bax

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106
Q

How does the extrinsic pathway of apoptosis work?

A

activated by ligand binding at death receptors eg Fas ligand binds to a Fas receptor
activates caspases via a signal transduction cascade
= apoptosis

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107
Q

What is necrosis?

A

traumatic cell death which induces inflammation and repair

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108
Q

Why does necrosis happen?

A

due to failure to produce ATP

loss of plasma membrane integrity

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109
Q

What conditions can necrosis lead to?

A

frostbite, cerebral infarction, pancreatitis

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110
Q

What is coagulative necrosis?

A

commonest form, occurs in most organs
caused by ischaemia
tissues is firm then becomes soft as macrophages are digested
necrotic tissue causes an inflammatory response

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111
Q

What is liquifactive necrosis?

A

occurs in brain due to lack of supporting stroma

neural tissue liquifies

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112
Q

What is caseous necrosis?

A

dead tissue is structureless, like soft cheese

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113
Q

What is gangrene?

A

type of necrosis with rotting of tissue

tissue goes black

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114
Q

Why does tissue go black in gangrene?

A

deposition of iron sulphide from degraded Hb

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115
Q

Why is a possible cause of gangrene?

A

some certain bacteria

eg clostridia

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116
Q

What can caseous necrosis be a diagnosis for?

A

TB

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117
Q

What is the difference between the induction of apoptosis and necrosis?

A

apoptosis: physiological or pathological stimuli
necrosis: usually pathological injury

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118
Q

What is the difference between the extent of apoptosis and necrosis?

A

apoptosis: single cells
necrosis: cell groups

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119
Q

What is the difference between the biochemical events of apoptosis and necrosis?

A

apoptosis: energy-dependent fragmentation of DNA by endonucleases, lysosomes intact
necrosis: energy failure, impairment of homeostasis, lysosomes leak lytic enzymes

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120
Q

What is the difference between the cell membrane integrity of apoptosis and necrosis?

A

apoptosis: maintained
necrosis: lost

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121
Q

What is the difference between the morphology of apoptosis and necrosis?

A

apoptosis: cell shrinkage and fragmentation = apoptopic bodies with dense chromatin
necrosis: cell swelling and lysis

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122
Q

What is the difference between the inflammatory response of apoptosis and necrosis?

A

apoptosis: none
necrosis: usual

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123
Q

What is the difference between the fate of dead cells of apoptosis and necrosis?

A

apoptosis: ingested by neighbouring cells
necrosis: ingested by neutrophil polymorphs and macrophages

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124
Q

What is the difference between the outcome of apoptosis and necrosis?

A

apoptosis: cell elimination
necrosis: defence and preparation for repair

125
Q

What is a congenital disorder?

A

present at birth

126
Q

What kind of conditions class as a congenital disorder?

A

chromosomal disorders
hereditary or spontaneous genetic disorders
non-genetic failures of differentiation/morphogenesis

127
Q

Give 2 examples of a genetic condition?

A

cystic fibrosis - autosomal recessive

huntington’s - present at birth but manifests later

128
Q

What is a genetic disorder?

A

an inherited genetic abnormality or spontaneous mutation

129
Q

Give 3 examples of spontaneous mutations?

A

Down’s - T21
Edward’s - T18
Palau - T13

130
Q

What is a non-genetic disorder?

A

caused by environmental factors

eg fetal alcohol syndrome

131
Q

Give some examples of acquired disorders?

A

non-genetic

TB, lung cancer, AIDS, bone fracture

132
Q

Give 2 examples of multifactorial disorders?

A

neural tube defects

cleft palate

133
Q

What are the 3 main neural tube defects?

A

spina bifida: exposed spinal cord due to failure of neural tube to close

anencephaly: absence of major portion of brain
hydrocephaly: build up of fluid on the brain

134
Q

How does the body adapt to increased demand?

A

hypertrophy or hyperplasia

135
Q

What is hypertrophy?

A

increased cell size without cell division

136
Q

Give 2 examples of when hypertrophy might happen?

A

in muscles of athletes: limbs and left ventricle

uterine smooth muscle in pregnancy

137
Q

What is hyperplasia?

A

increase in cell number by mitosis

138
Q

Which cells can carry out hyperplasia?

A

only cells that can divide

not myocardial and nerve cells

139
Q

Give an example of when hyperplasia might happen?

A

bone marrow cells that produce rbc in people who live at high altitudes

140
Q

What is atrophy?

A

decrease in size of organ/cell by a decrease in cell size or number

141
Q

When does atrophy occur?

A

when the requirements of the body decrease

can occur naturally eg in development of GU tract

142
Q

When does atrophy occur in disease?

A

alzheimer’s
decreased function eg limb in a cast = muscle atrophy (fibres decrease in size)
lack of innervation to muscle
lack of nutrition = atrophy in adipose tissue

143
Q

What is metaplasia?

A

change in differentiation of a cell: fully differentiated type to another fully differentiated type

144
Q

Why does metaplasia occur?

A

due to alterations to the environment

145
Q

Give an example of metaplasia?

A

ciliated respiratory epithelium to squamous epithelium in trachea and bronchi of smokers
= chronic bronchitis

146
Q

What is dysplasia?

A

morphological changes seen in cells in progression to cancer - not cancer but nearly
or a lack of development (in the bones and brain)

147
Q

What does dysplasia look like under a microscope?

A

mytotic cells, jumbled, larger than normal

148
Q

Why does ageing occur?

A

cells ability to divide decreases with age

149
Q

Which kind of cells have the most potential to divide?

A

fetal cells

150
Q

What is a telomere?

A

non-coding random repetitive DNA sequence at the tip of a chromosome

151
Q

What happens to telomeres in ageing?

152
Q

How does telomere shortening occur?

A
  • telomere is not fully copied in DNA synthesis = single stranded tail of DNA left at tip of chromosome
  • tail is excised
  • with each cell division the telomere shortens
  • becomes so short that DNA polymerase can’t bind = no more replication
153
Q

How is telomere length inherited?

A

from the father

154
Q

What are the main symptoms of ageing in the elderly?

A

senile dementia, deafness, dermal elastosis, loss of teeth, cataracts, balding
osteoporosis, sarcopenia, degenerative joint disease
diverticular disease of colon, prostatic hyperplasia
impaired immunity
hypertension + IHD

155
Q

Why does senile dementia occur in the elderly?

A

brain atrophy - nerve cells can’t replicate

156
Q

Why does deafness occur in the elderly?

A

loss of hair cells in the ear

157
Q

What is dermal elastosis and why does it happen in the elderly?

A

wrinkling due to UV light damage = loss of collagen and elastin in the skin = increased fragility

158
Q

Why does osteoporosis occur in the elderly?

A

lack of oestrogen

low vitamin D and calcium in earlier life

159
Q

What is sarcopenia and why does it happen in the elderly?

A

muscle loss due to age (40+)

due to decreased growth hormone + testosterone and increased catabolic cytokines

160
Q

Why does immunity become impaired in the elderly?

A

reduction in production of immune cells eg T cells

161
Q

Why does cataracts occur in the elderly?

A

UV light damage = cross-linking proteins in the eye

162
Q

What factors wear cells out?

A 
cross-linking/mutations of DNA
cross-linking of proteins
loss of Ca influx controls
damage to mitochondrial DNA
loss of DNA repair mechanism
peroxidation of membranes
free radical generation
activation of ageing and death genes
telomere shortening
accumulation of toxic by-products of metabolism
163
Q

Where do basal cell carcinomas invade and how are they treated?

A 
invade locally (in skin) and never spread
complete local excision = cure
164
Q

What causes basal cell carcinomas?

A

usually UV light

once a person has had it once, likely to recur

165
Q

What are some of the symptoms of leukemia?

A 
weight loss, fever, frequent infections
shortness of breath
muscular weakness
pain or tenderness in bones and joints
fatigue, loss of appetite
swelling of lymph nodes
enlargement of spleen/liver
night sweats, easy bleeding and bruising, purplish patches
= NON-SPECIFIC
166
Q

Why does leukemia spread so quickly?

A

tumours of wbc
wbc circulate around the body and does the tumour
acute: cells divide much quicker than normal

167
Q

Where do carcinoma’s spread to first?

A

lymph nodes that drain the site of the carcinoma

eg breast carcinoma to axillary lymph nodes

168
Q

Which cancers most commonly spread to bone (via the blood)?

A

breast, prostate, lung, thyroid, kidney

169
Q

What is the breast cancer treatment pathway?

A

confirm diagnosis
has is spread to axilla? check with ultrasound and biopsy: yes = axillary node clearance
no = has it spread? check with bone scan and CT
yes = systemic chemotherapy
no = surgery with/without axillary lymph node clearance

170
Q

Why do excised tumours often recur?

A

micro metasteses may still remain

tumours less than 1cm are unlikely to be detected

171
Q

What is adjuvant therapy?

A

extra treatment after surgical excision

172
Q

What are the adjuvant therapies for breast cancer?

A
  1. radiotherapy after a lumpectomy: removes micro mets, almost always recommended
  2. if oestrogen receptor +ve = anti-oestrogen therapy eg tamoxifen
  3. if HER2 gene amplified = herceptin given
173
Q

What is carcinogenesis?

A

transformation of normal cells to neoplastic cells through permanent genetic alterations/mutations
multi-step process

174
Q

What kind of neoplasms does carcinogenesis apply to?

A

malignant only

175
Q

What is oncogenesis?

A

benign and malignant tumours

176
Q

What is a neoplasm?

A

a lesion due to autonomous abnormal growth of cells which persists after the stimulus is removed = a new growth

177
Q

What are the 4 characteristics of a neoplasm?

A

abnormal
autonomous
persistent
new growth

178
Q

What is a carcinogen?

A

something that is known or suspected to cause tumours

179
Q

What is the difference between a carcinogen and an oncogen?

A 
carcinogen = cancer causing
oncogen = tumour causing
180
Q

How do carcinogens act?

A

act on DNA = mutagenic

181
Q

How much cancer risk is environmental and inherited?

A

85% environmental

182
Q

Why can’t carcinogens just be removed?

A

latent interval can be decades - take a while to have an effect (eg asbestos = 30 years)
complex environment
ethical constraints

183
Q

What are the 5 classes of carcinogens?

A 
chemical
viruses
radiation
biological
miscellaneous
184
Q

What needs to happen for a chemical to be carcinogenic?

A

most need to be converted from pro-carcinogens to ultimate carcinogens

185
Q

Where are polycyclic aromatic hydrocarbons found and what tumours do they cause?

A

strong link with smoking + repeated exposure to mineral oils

lung and skin cancer

186
Q

Where are aromatic amines found and what tumours do they cause?

A

in rubber and dye workers

bladder cancer

187
Q

What tumours do nitrosamines cause?

A

gut cancer

188
Q

What tumours do alkylating agents cause?

189
Q

Who is at an increased risk of viral carcinogens?

A

young people and immunosuppressed people

190
Q

Give an example of a viral carcinogen and what tumour it causes?

A

HPV = cervical cancer

191
Q

What is the major cause of skin cancer?

A

UV light

UVB more than UVA

192
Q

Which types of carcinoma does UV light increase the risk of?

A

basal cell and squamous cell carcinoma

193
Q

What condition significantly increases the risk of skin cancer?

A

xedoderma pigmentosum

= reduction in DNA repair enzymes

194
Q

Give 3 examples of the long term effects of radiation on cancer risk?

A

thyroid cancer in Ukrainian children after Chernobyl
skin cancer in radiographers
lung cancer in uranium miners

195
Q

What are the 3 types of biological carcinogens?

A

hormones
parasites
mycotoxins

196
Q

Give 2 examples of hormonal carcinogens?

A

oestrogen = mammary and endometrial cancer

anabolic steroids = hepatocellular carcinoma

197
Q

Give 2 examples of parasitic carcinogens?

A

shistosoma = bladder cancer

chonorchis sinensis = cholangiocarcinoma

198
Q

Give an example of a mycotoxin carcinogen?

A

alfatoxin B1 = hepatocellular carcinoma

199
Q

Give 2 examples of miscellaneous carcinogens?

A

asbestos = mesothelioma and carcinoma of the lung

metals

200
Q

What is a host factor?

A

a factor that influences carcinogenesis

201
Q

What are the 5 host factors for carcinogenesis?

A 
race
diet
constitutional
premalignant conditions
transplacental exposure
202
Q

How does race influence carcinogenesis?

A

skin cancer reduced in black people (due to melanin)

oral cancer higher in India, SE Asia (chew betel nut, tobacco)

203
Q

How does diet influence carcinogenesis?

A

high fat and red meat = colorectal

alcohol = breast + oesophageal

204
Q

What are the constitutional factors that effect carcinogenesis?

A

inherited predisposition eg BRCA1/2 = breast, RB1 abnormality = retinoblastoma
age
gender eg women = breast, men = prostate

205
Q

What is a premalignant condition to carcinogenesis?

A

identifiable local abnormality associated with an increased risk of malignant tumours

206
Q

What are the premalignant conditions that influence carcinogenesis?

A

colonic polyps, cervical dysplasia, ulcerative colitis, undescended testes

207
Q

How does transplacental exposure influence carcinogenesis?

A

diethylstiboestrol to mothers increases vaginal cancer in children

208
Q

What is a tumour?

A

abnormal swelling (neoplasm, inflammation, hypertrophy, hyperplasia)

209
Q

What are the 3 most common cancers in men?

A

prostate, lung, bowel

210
Q

What are the 3 most common cancers in women?

A

breast, lung, bowel

211
Q

What are either sides of the spectrum of cancer?

A

malignant/fatal to benign/subclinical

some are borderline

212
Q

Name a borderline type of cancer?

213
Q

What is the structure of a neoplasm?

A

neoplastic cells supported by a stroma

214
Q

What are the features of neoplastic cells in a neoplasm?

A

derived from nucleated cells
usually monoclonal
growth pattern related to parent cell
continue to synthesise cell products eg collagen, keratin which accumulate in the tumour

215
Q

What is the stroma in a neoplasm and what does it contain?

A

a connective tissue framework

contains fibroblasts and collagen

216
Q

What are the 3 roles of the stroma in a neoplasm?

A

mechanical support
nutrition to neoplastic cells
intracellular signalling

217
Q

What is a neoplasm?

A

autonomous, abnormal, persistent new growths

218
Q

What is tumour angiogenesis?

A

when a tumour becomes large enough for blood vessels to perfuse into it
essential for growth - provides oxygen and nutrients to the tumour

219
Q

What is angiogenesis induced by in a tumour?

A

factors produced by the tumour cells

eg vascular endothelial growth factor

220
Q

When is tumour angiogenesis opposed?

A

in cancer treatment

by factors such as angiostatin

221
Q

What are the 2 types of tumour classifications?

A
  1. behavioural: benign/malignant

2. histogenetic: cell of origin

222
Q

What are the main behavioural features of a benign neoplasm?

A

localised and non-invasive
slow growth rate = few mitotic figures
looks like normal tissue
often encapsulated by a layer of connective tissue (or circumscribed)
nuclear morphometry often normal
necrosis and ulceration rare
outward growths on mucosal surfaces = exophytic lesion

223
Q

How can benign neoplasms cause morbidity and mortality?

A 
pressure on adjacent structures
obstruct flow
production of hormones
turns malignant
anxiety
224
Q

What are the main behavioural features of borderline tumours?

A

rare

defy precise classification

225
Q

What are the main behavioural features of malignant neoplasms?

A

invasive: neoplastic cells penetrate vessel and lymphatic walls (metasteses: 2ndary tumours)
rapid growth
irregular border: do not resemble parent cell as much as benign
crab-like structure: tongues of tissue penetrate normal tissue and destroy it
hyperchromatic nuclei: stain dark
pleomorphic nuclei: vary in shape and size
lots of mitotic activity
necrosis and ulceration common
growths on mucosal surfaces often endophytic (grow inward)
poorly circumscribed

226
Q

How do malignant neoplasms cause morbidity and mortality?

A 
destruction fo adjacent tissue
metasteses
blood loss from ulcers
obstruction of flow
hormone production
paraneoplastic effects (debility and weight loss)
anxiety and pain
227
Q

Are all malignant neoplasms invasive and do all metastasise?

A

ALL are invasive
NOT ALL metastasise
eg basal cell carcinoma

228
Q

What is histogenetic classification of tumours?

A

shows the specific cell of origin of a tumour

found by histopathological exam

229
Q

Where are the 3 places neoplasms derive from?

A
  1. epithelial cells
  2. connective tissues
  3. lymphoid tissue (only malignant and/or haemopoietic organs)
230
Q

What do neoplasms always end in?

231
Q

How is histological grading used for benign and malignant tumours?

A

not usually used for benign due to close resemblance to parent tissue
important for malignant as correlates with prognosis

232
Q

What are the 3 histological grades of malignant neoplasms?

A

well differentiated = grade 1 (resembles parent tissue)
moderately differentiated = grade 2
poorly differentiated = grade 3 (least close to parent tissue)

233
Q

What is the most aggressive grade of malignant tumours?

A

grade 3 - poorly differentiated

234
Q

What are anaplastic neoplasms?

A

so poorly differentiated they lack histogenetic features

= extremely aggressive

235
Q

What is a papilloma? Give an example.

A

benign epithelial neoplasm
tumour on non-glandular, non-secretory epithelium
eg squamous cell papilloma

236
Q

What is an adenoma? Give an example.

A

benign epithelial neoplasm
tumour of glandular or secretory epithelium
eg colonic adenoma

237
Q

How do you name benign epithelial neoplasms?

A 
prefix = cell type of origin
suffix = -oma
238
Q

What are malignant epithelial neoplasms called?

A

carcinomas

239
Q

How are carcinomas named? Give an example.

A

prefix = name of epithelial cell

eg transitional cell carcinoma

240
Q

What is a carcinoma of glandular epithelium called? How are they named?

A

adenocarcinoma

coupled with name of origin tissue eg adenocarcinoma of the prostate

241
Q

What is an intraepithelial carcinoma?

A

epithelial neoplasm exhibiting all signs of malignancy bus has not invaded the epithelial basement membrane so cannot metastasise

242
Q

What are benign connective tissue neoplasms named after?

A

cell of origin and behavioural classification

suffix: -oma

243
Q

What is a benign connective tissue neoplasm of the adipocytes called?

244
Q

What is a benign connective tissue neoplasm of the vessels called?

245
Q

What is a benign connective tissue neoplasm of the cartilage called?

246
Q

What is a benign connective tissue neoplasm of the striated muscle called?

A

rhabdomyoma

247
Q

What is a benign connective tissue neoplasm of the bone called?

248
Q

What is a benign connective tissue neoplasm of the smooth muscle called?

249
Q

What is a benign connective tissue neoplasm of the nerves called?

250
Q

What are malignant connective tissue neoplasms called?

251
Q

How are sarcomas named?

A

prefix: cell of origin

252
Q

What is a malignant connective tissue neoplasm of the adipose tissue called?

A

liposarcoma

253
Q

What is a malignant connective tissue neoplasm of the smooth muscle called?

A

leiomyosarcoma

254
Q

What is a malignant connective tissue neoplasm of the striated muscle called?

A

rhabdomyocsarcoma

255
Q

What is a malignant connective tissue neoplasm of the bone called?

A

osteosarcoma

256
Q

What is a malignant connective tissue neoplasm of the cartilage called?

A

chondrosarcoma

257
Q

What is a malignant connective tissue neoplasm of the blood vessels called?

A

angiosarcoma

258
Q

Carcinomas and sarcomas can be further classified by what?

A

their degree of differentiation

259
Q

Not all -omas are neoplasms. Name the 3 key exceptions?

A

granuloma: chronic inflammation
mycetoma: fungus in the body
tuberculoma: mass of TB

260
Q

Not all malignant tumours are carcinomas or sarcomas. Name the 3 key exceptions?

A

melanoma: malignant neoplasm of melanocytes
mesothelioma: malignant tumour of mesothelial cells
lymphoma: malignant neoplasm of lymphoid cells

261
Q

Some tumours are named after the person that discovered them. Name the key 5 exceptions that follow this rule?

A

Burkitt’s lymphoma: B-cell lymphoma due to Epstein Barr virus
Ewing’s sarcoma: malignant tumour of bone
Hodgkin’s lymphoma: malignant lymphoma with Reed-Sternberg cells
Kaposi’s lymphoma: malignant neoplasm from vascular endothelium
Grawitz tumour

262
Q

What is a teratoma?

A

exception to the classification rules

neoplasm of germ cell origin: forms cells representing all 3 germ cell layers

263
Q

What is a carcinosarcoma?

A

exception to the classification rules

mixed malignant tumours showing characteristics of epithelium and connective tissue

264
Q

What is a APUDoma?

A

exception to the classification rules

amine content and/or precursor uptake and decarboxylation

265
Q

What is the most important criterion for malignancy?

266
Q

What is a carcinoma in situ?

A

not invaded anywhere and can be excised

267
Q

What is a micro-invasive carcinoma?

A

can reach vessels and lymphatics but risk is still low

268
Q

What is an invasive carcinoma?

A

outside basement membrane

269
Q

What are the 3 key factors that influence tumour invasion?

A

decreased cellular adhesion
secretion of proteolytic enzymes
abnormal or increased cellular motility

270
Q

What is the key group of proteolytic enzymes released by malignant neoplastic cells? How do they work?

A

matrix metalloproteinases

chew through basement membrane

271
Q

What are the 3 main families of matrix metalloproteinases?

A

interstitial collagenases
gelatinises
stomelysins

272
Q

Which tissues are extremely resistant to tumour invasion?

A

cartilage

fibrocartilage of the intervertebral discs

273
Q

What is carcinomatosis?

A

extensive metastatic disease

274
Q

Which type of carcinoma never metastasises?

A

basal cell carcinoma

275
Q

Liposarcomas normally metastasise to where?

276
Q

How does a metastatic tumour form?

A
  1. detachment of tumour cells form neighbour
  2. invasion of surrounding connective tissue to reach vessels/lymphatics
  3. intrainvasion into lumen of vessels
  4. evasion of defence mechanisms in blood
  5. adherence to endothelium at remote location
  6. extra invasion of cells from vessel to surrounding tissue
277
Q

What drug was designed to inhibit angiogenesis? What is it used for now?

A

avastin - inhibits VGEF
blocks formation of new blood vessels and reduces likelihood of them leaking
useful for macular degeneration

278
Q

How do tumours metastasise via the haemotogenous route?

A

by blood stream

goes to organs perfused by blood drained from the tumour

279
Q

Tumours usually metastasise to which organs via the haemotogenous route?

A

liver, brain, lung, bone

280
Q

Where do tumours rarely metastasise to via the haemotogenous route?

A

skeletal muscle
spleen
(despite rich blood supply)

281
Q

How do tumours metastasise via the lymphatic route?

A

2ndary tumours in regional lymph nodes
reached via afferent lymphatic channels
can interrupt lymphatic flow = oedema

282
Q

How do tumours metastasise via the transcoelemic route?

A

neoplastic effusion: abnormal build up of fluid between pleura due to a tumour

283
Q

Metastases travel to which pleural cavities via the transcoelemic route? From which tumours originally?

A

pleural and pericardial cavities: common consequence from carcinomas of the breast and lung
peritoneal cavity: from abdominal tumours

284
Q

Which metastatic spread do carcinomas favour?

A

lymphatic (at least initially)

285
Q

Which metastatic spread do sarcomas favour?

A

haemotogenous

286
Q

Which tumours commonly metastasise to the lung?

A

sarcomas

any common cancer

287
Q

Which tumours commonly metastasise to the liver?

A

colon, stomach, pancreas, carcinoid tumours of intestine

288
Q

What is the difference between carcinomas formed in smokers and non-smokers?

A

non-smokers: adenocarcinoma

smokers: squamous cell carcinomas

289
Q

What are the 4 key drugs used in conventional chemo and how do they work?

A
  1. vinblastine: anti-microtubule agent, binds to micro0tubules and stops them contracting to stop cell division
  2. etoposide: inhibits topoisomerase II (enzyme needed to replicate DNA)
  3. ifosamide
  4. cisplatin
    3 + 4: bind directly to DNA, inhibits DNA synthesis by cross linking
290
Q

Which type of cancer is often treated with cisplatin in conventional chemo?

291
Q

What are the main problems with conventional chemo?

A

not selective for tumour cells - hits any dividing cells, including normal ones e.g. bone marrow
side effects because of this: myelosuppression, hair loss, diarrhoea
won’t hit tumour cells that aren’t dividing

292
Q

How do tumours increase in size? How does this alter the effectiveness of conventional chemo?

A
  1. cell division - faster
  2. lack of apoptosis
    if cells divide slowly and don’t apoptose = NOT GOOD FOR CHEMO
293
Q

Which types of tumour does conventional chemo work best for? Give 5 examples.

A 
fast dividing tumours - all quite rare
germ cell tumours of testis
lymphomas
embryonal paediatric tumours
acute leukaemias
choriocarcinomas
294
Q

Which types of tumour does conventional chemo not work well for?

A

slow dividing tumours

295
Q

How does targeted chemo work?

A

exploits differences between cancer cells and normal cells

296
Q

How is targeted chemo better than conventional chemo?

A

more effective

less side effects

297
Q

How are differences in cancer cells found in targeted chemo?

A

gene arrays, proteomics, tissue microarrays

e.g. if a gene is up/down regulated, more/less protein is produced

298
Q

How does a growth factor cell signal usually work?

A

growth factor binds to growth factor receptor
intracellular signalling proteins are switched on
signal leads to transcriptional up regulation
leads to proliferation

299
Q

What are the 2 ways growth of a cell can become abnormal and form a tumour?

A
  1. over expression of growth factor receptors
  2. continuous activation of growth factor receptors: nothing has to bind to it
    due to mutations
300
Q

What are the 2 treatments used in targeted chemo?

A

monoclonal antibodies

small molecular inhibitors

301
Q

Which types of tumour can monoclonal antibodies be used to treat in targeted chemo?

A

does work in over expressed growth factor receptors: more antibodies needed
does not work with continuously activated receptors: nothing has to bind to it so has not effect

302
Q

What is a small molecular inhibitor?

A

small molecule that binds to the inside of a growth factor receptor

303
Q

What types of tumours can small molecular inhibitors be used to treat in targeted chemo

A

both types:
over expressed growth factor receptors: if given enough
growth factor receptors that are continuously activated

304
Q

What are the advantages and disadvantages of using monoclonal antibodies in targeted chemo?

A

+ easy to make

  • large: must be given by infusion
  • does not work with continuously activated receptors
305
Q

What are the advantages and disadvantages of using small molecular inhibitors in targeted chemo?

A 
\+ more effective
\+ work with both type of tumour
\+ small: can be taken as a tablet
- hard to make
- have to produce thousands and screen them to see which work
306
Q

Give an example of a monoclonal antibody used in targeted chemo? How does it work?

A

cetuximab

MAB against epidermal growth factor receptor

307
Q

When is cetuximab used for targeted chemo patients?

A

selected by immunohistochemistry: check tumour has enough EGFR
for use in CRC patients who have failed conventional chemo

308
Q

Why can’t monoclonal antibodies produced in mice be used for human treatment?

A

body always recognises foreign proteins

have to produce a chimeric IgG humanised MAB

309
Q

When epidermal growth factor is upregulated due to a tumour, what increases?

A

angiogenesis

cell motility/invasion

Phase 2a (5 decks)

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