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Phase 2a Medicine > Pathology > Flashcards

Pathology Flashcards

1
Q

What are the 2 types of autopsy?

A

Hospital autopsies

Medico-legal autopsies

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2
Q

What can medico-legal autopsies be classified into?

A

Coronial and forensic autopsies

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3
Q

What are the 3 reasons for deaths being referred to a coroner?

A

Presumed natural, presumed iatrogenic, presumed unnatural

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4
Q

Why would a presumed natural death be investigated?

A

Cause of death not known, not seen a doctor in last 14 days

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5
Q

Why would a presumed iatrogenic death be performed?

A

Concern that patient’s care led to death

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6
Q

Who performs autopsies and what sort of autopsy does each perform?

A

Histopathologists (coronial and hospital autopsies) and forensic pathologies (coronial autopsies)

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7
Q

What questions does a coronial autopsy answer?

A
  1. Who was the deceased?
  2. When did they die?
  3. Where did they die?
  4. How did they die?
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8
Q

What are 4 main laws during autopsy?

A
  1. Coroners Act 1988
  2. Coroners Rules 1984
  3. Amendment Rules 2005
  4. Coroners and Justice Act 2009
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9
Q

Which law comes into place when coroner has finished with body?

A

Human Tissues Act 2004

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10
Q

What does an autopsy consist of?

A
  1. History/scene
  2. External examination
  3. Evisceration
  4. Internal examination
  5. Reconstruction
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11
Q

Describe acute inflammation

A

A reaction to injury or infection involving cells like neutrophils and macrophages

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12
Q

What is inflammation?

A

A local physiological response to tissue injury

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13
Q

How is acute inflammation classified?

A

Initial and often transient series of tissue reactions to injury. Sudden onset, short duration and usually resolves.

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14
Q

How is chronic inflammation classified?

A

Subsequent and often prolonged tissue reactions following initial tissue response. Slow onset or sequel to acute, long duration and may never resolve.

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15
Q

Which cells are involved in acute inflammation?

A
  1. Neutrophil polymorphs
  2. Macrophages
  3. Lymphocytes
  4. Endothelial cells
  5. Fibroblasts
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16
Q

Which cells are first to present in acute inflammation?

A

Neutrophil polymorphs

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17
Q

How do neutrophil polymorphs kill bacteria?

A

Cytoplasmic granules full of enzymes

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18
Q

How do macrophages kill bacteria?

A

Phagocytosis

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19
Q

Which cell type presents antigens to lymphocytes?

A

Macrophages

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20
Q

What is the function of lymphocytes?

A

Immunological memory for past infections and antigens

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21
Q

What cell type becomes sticky in areas of inflammation?

A

Endothelial cells, so inflammatory cells adhere to them

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22
Q

What is the function of fibroblasts?

A

Form collagen in areas of chronic inflammation and repair

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23
Q

What are the steps of acute inflammation?

A
  1. Initial reaction of tissue to injury
  2. Dilation of blood vessels
  3. Vascular leakage of protein-rich fluid
  4. Neutrophil polymorphs recruited to tissue
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24
Q

What are the causes of acute inflammation?

A
  1. Microbial infections
  2. Hypersensitivity reactions
  3. Physical agents
  4. Chemicals
  5. Bacterial toxins
  6. Tissue necrosis
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25
Q

What infections is hypersensitivity important in?

A

Parasitic infections and TB inflammation

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26
Q

Give 3 examples of physical agents causing inflammation

A

Physical trauma, UV, burns, excessive cooling

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27
Q

What are the clinical manifestations of acute inflammation?

A
  1. Rubor - redness
  2. Calor - heat
  3. Tumor - swelling
  4. Dolor - pain
  5. Loss of function
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28
Q

What is a granuloma?

A

An aggregate of epithelia histiocytes

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29
Q

What cells are involved in chronic inflammation?

A
  1. Plasma cells
  2. Lymphocytes
  3. Multinucleate giant cell
  4. Capillary endothelium
  5. Macrophage
  6. Fibroblast
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30
Q

What are the causes of chronic inflammation?

A
  1. Primary chronic inflammation
  2. Transplant rejection
  3. Progression from acute inflammation
  4. Recurrent episodes of acute inflammation
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31
Q

What are the clinical manifestations of chronic inflammation?

A
  1. Chronic ulcer
  2. Chronic abscess cavity
  3. Thickening of wall of a hollow viscus
  4. Granulomatous inflammation
  5. Fibrosis
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32
Q

Describe the microscopic appearance on chronic inflammation

A
  1. Cellular infiltrate [lymphocytes, plasma cells, macrophages, eosinophil polymorph]
  2. Granulation tissue becomes fibrous tissue, tissue damage & necrosis
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33
Q

What are the systemic effects of acute inflammation?

A
  1. Pyrexia
  2. Weight loss,
  3. Lymphadenopathy
  4. Increased WBC count 5. Amyloidosis
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34
Q

What does healing involve?

A

Regeneration and migration of specialised cells

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35
Q

What are the features of repair?

A

Angiogenesis followed by fibroblast proliferation and collagen synthesis which forms granulation tissue

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36
Q

What regulates the cell proliferation processes in repair?

A

Growth factors

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37
Q

What 2 cell types are in lymphocytic tissue?

A

B lymphocytes and T lymphocytes

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38
Q

What happens when B lymphocytes contact antigens?

A

They transform into plasma cells

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39
Q

What is the function of plasma cells?

A

Antibody production

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40
Q

What happens when T lymphocytes contact antigens?

A

They produce cytokines

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41
Q

How do macrophages kill organisms?

A

Lysosomal enzymes

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42
Q

What happens when macrophages particulate in hypersensitivity reactions?

A

They die leading to necrosis

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43
Q

What is the mononuclear phagocyte system also called?

A

Reticuloendothelial system

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44
Q

What is a granuloma?

A

An aggregate of epithelioid histiocytes

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45
Q

Give an example of granulomatous disease

A

TB, leprosy

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46
Q

Describe epithelioid histiocytes

A

Large vesicular nuclei, plentiful eosinophilic cytoplasm, elongated

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47
Q

How are epithelioid histiocytes arranged?

A

In clusters

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48
Q

What is a secretory product of epithelioid histiocytes?

A

Angiotensin converting enzyme (ACE)

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49
Q

How is the appearance of granulomas augmented?

A

Presence of caseous necrosis or by conversion of histiocytes into multinucleate giant cells

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50
Q

What can association of granulomas with eosinophils indicate?

A

Parasitic infection

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51
Q

What is a feature of stimuli which induce granulomatous inflammation?

A

Indigestibility of particulate matter by macrophages

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52
Q

What could cause histiocytic giant cells to form?

A

Inert minerals e.g. silica, bacteria e.g. tubercle bacilli

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53
Q

When may histiocytic giant cells form?

A

When foreign particles are too large to be ingested by one macrophage, and 2+ fuse and unite

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54
Q

What histiocytic giant cell forms in TB?

A

Langhans’ giant cells

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55
Q

What histiocytic giant cell are seen in particulate foreign body material?

A

Foreign body giant cells

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56
Q

What histiocytic giant cell are seen in dermatofibromas of skin?

A

Touton giant cells

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57
Q

When is acute inflammation involved in CVS?

A

In response to acute MI and some of its complications e.g. cardiac rupture

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58
Q

How is chronic inflammation involved in carcinogenesis?

A

Has a role in initiation and propagation of cancer and its progression

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59
Q

When is chronic inflammation involved in CVS?

A

In myocardial fibrosis following MI

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60
Q

Name a neurodegenerative disorder of the CNS which inflammation is involved in

A

Multiple sclerosis - perivascular cuffing by plasma cells and T lymphocytes is seen in zones of white matter where macrophages break down myelin

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61
Q

What is resolution?

A

Where a tissue is undamaged or able to regenerate, and the initiating factor has been removed

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62
Q

What is repair?

A

The initiating factor is still present, tissue is damaged and unable to regenerate

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63
Q

What happens when the liver is persistently damaged?

A
  1. Cirrhosis
  2. Fibrous scarring
  3. Regenerative nodules
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64
Q

What can cause persistent damage to the liver?

A

Alcohol, hepatitis B/C

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65
Q

What is lobar pneumonia?

A

Acute inflammation of one lobe of the lungs full of neutrophil polymorphs

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66
Q

Describe abrasion

A
  1. Heals well as haven’t removed all of the epithelium
  2. Scab forms over surface
  3. Epidermis grows out from adnexa
  4. Sweat glands and hair follicles remain intact
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67
Q

Describe healing by 1st intention

A

Looks white as collagen is present which is made by fibroblasts

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68
Q

Give an example of how healing by 1st intention occurs

A

Surgical wound

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69
Q

Describe healing by 2nd intention

A
  1. Hair follicles removed

2. Fibroblasts make collagen so get bigger scar

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70
Q

Describe granulation tissue

A
  1. Very big wound which looks granular as blood vessels grow up
  2. Big scar with pale fibrous tissue
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71
Q

What is repair?

A

Replacement of damaged tissue by fibrous tissue

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72
Q

What produces collagen?

A

Fibroblasts

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73
Q

Which cells can regenerate?

A
  1. Hepatocytes
  2. Pneumocytes
  3. All blood cells
  4. Gut epithelium
  5. Skin epithelium
  6. Osteocytes
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74
Q

Which cells can’t regenerate?

A
  1. Myocardial cells

2. Neurons

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75
Q

What is laminar flow?

A

Cells travel in centre of arterial vessels and don’t touch sides

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76
Q

What happens when the endothelium is damaged?

A

Platelet aggregation: platelets stick to epithelium and each other, releasing aggregating factors causing a positive feedback loop

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77
Q

What happens when laminar flow is disrupted?

A

RBC may get trapped into platelets

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78
Q

How is a fibrin mesh formed?

A

Fibrin deposition occurs as platelets release chemicals causing fibrinogen to form fibrin. This holds cells together in a fibrin mesh and can trap RBC

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79
Q

What is thrombosis?

A

The formation of a solid mass of blood constituents formed within intact vascular system during life

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80
Q

What are the components of the thrombosis triad?

A
  1. Change in vessel wall
  2. Change in blood flow (laminar to turbulent)
  3. Change in blood constituents
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81
Q

How do thrombus form in veins?

A

If the endothelium becomes sticky, slow blood flow can cause thrombus formation when blood constituents touch the sticky endothelium

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82
Q

Why are pulmonary embolisms common in hospital?

A

Venous thrombus are common as people are bed bound

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83
Q

What is thrombus formation in veins called?

A

Stasis, due to slow blood flow

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84
Q

What is the prevention for thrombosis?

A

Exercise, stockings, aspirin

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85
Q

Why is aspirin prescribed to over 50s?

A

It inhibits platelet aggregation so a smaller embolism will form

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86
Q

What is an embolus?

A

The formation of a mass of material in vascular system able to become lodged within a vessel and block it

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87
Q

What is ischaemia?

A

Reduction in blood flow

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88
Q

What is infarction?

A

Reduction in blood flow with subsequent death of cells

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89
Q

What is a reperfusion injury?

A

When a patient has had ischaemia and blood is let back in, superoxide radicals are also let in which causes damage to cells

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90
Q

How can reperfusion injuries be prevented?

A

Keep patients in an induced coma when they are adjusting to having blood

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91
Q

Which organs have dual blood supply?

A

Lungs, liver, some parts of brain

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92
Q

Why is the heart more susceptible to infarction?

A

It is at the limit of 2 different blood supplies (watershed areas)

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93
Q

When does atherosclerosis tend to arise?

A

40-50 years old

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94
Q

What is the early stage of atherosclerosis?

A

Fatty streak - when macrophages fill with lipids

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95
Q

Where is atherosclerosis commonly found?

A

High pressure systems e.g. aorta and systemic arteries

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96
Q

What is in a plaque?

A
  1. Fibrous tissue
  2. Lipids - cholesterol
  3. Lymphocytes
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97
Q

What are the common risk factors for atherosclerosis?

A
  1. Smoking
  2. Hypertension
  3. Diabetes
  4. Hyperlipidaemia
  5. CHD in men
  6. More deprived industrial areas of UK
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98
Q

What is the pathogenesis of atherosclerosis?

A
  1. Endothelial cells are delicate, metabolically active and produce NO
  2. Endothelial cells are damaged
  3. Recurrent injuries to endothelial cells causes micro-haemorrhages which burst
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99
Q

What is the mechanism of damage from smoking?

A

Free radicals, nicotine, CO

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100
Q

How does hypertension cause atherosclerosis?

A

Shearing forces on endothelial cells esp. at bifurcation points

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101
Q

How does diabetes cause atherosclerosis?

A

Superoxide anions, glycosylation products

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102
Q

How does hyperlipidaemia cause atherosclerosis?

A

Direct damage to endothelial cells

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103
Q

What are some complications of atherosclerosis?

A
  1. Cerebral infarction
  2. Carotid atheroma
  3. MI, cardiac failure
  4. Acute aneurysms
  5. Peripheral vascular disease with intermittent claudication
  6. Gangrene
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104
Q

Why are blood clots rare?

A
  1. Laminar flow

2. Endothelial cells aren’t sticky when healthy

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105
Q

What is the first stage of thrombosis?

A

Platelet aggregation

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106
Q

What can be an embolism?

A

A thrombus break off, air, cholesterol crystals, tumour, amniotic fluid, fat

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107
Q

Where will the embolus travel if it enters the venous system?

A

To the vena cava, through the RHS of the heart and will lodge in pulmonary arteries

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108
Q

Where can the emboli travel if it enters the arterial system?

A

To anywhere downstream of its entry point

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109
Q

What usually causes infarction?

A

Thrombosis of an artery

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110
Q

What is apoptosis?

A

Programmed cell death

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111
Q

What happens in apoptosis?

A
  1. Enzymes are released with a cell that cause it to shrink
  2. Nucleus shrivels up
  3. Organelles enter vesicles which are engulfed by macrophages
112
Q

What is a common cause of apoptosis?

A

DNA damage e.g. UV in skin

113
Q

What is the gatekeeper of the genome?

114
Q

What does p53 do?

A

Detects DNA damage and produces chemicals that may switch on apoptosis

115
Q

What are caspases?

A

Enzymes which chew up things and are effectors of apoptosis

116
Q

What caspase turns off apoptosis?

117
Q

What caspase stimulates apoptosis?

118
Q

Wha receptor and ligand are involved in switching on caspases?

A

Fas ligand and Fas receptor

119
Q

Why is apoptosis needed in development?

A

Needed to make things work e.g. webbed fingers becoming digits

120
Q

Why is apoptosis needed in normal function?

A

To remove cells at end of useful life in tissues with high cell turnover

121
Q

What disease has a lack of apoptosis?

A

Cancers due to p53 mutation for example

122
Q

What disease has too much apoptosis?

123
Q

What is necrosis?

A

Traumatic cell death affecting large areas of cells

124
Q

Give clinical example of necrosis

A
  1. Toxic spider venom
  2. Frostbite
  3. Cerebral infarction
  4. Avascular necrosis of bone
  5. Pancreatitis
125
Q

Describe coagulative necrosis

A

Thick and gooey

126
Q

Describe liquefactive necrosis

A

Thin and liquid

127
Q

Describe caseous necrosis

A

Has multinucleate giant cells, looks like soft cheese and is linked with TB

128
Q

What proportion of conceptions survive 1 month and why?

A

25%

Chromosomal abnormalities

129
Q

What are the degrees of exposed spinal cord at birth?

A
  1. Spina bifida
  2. Meningocele
  3. Myelomeningocele
130
Q

What causes heart murmur?

A

Ventricular spinal defect

131
Q

What is a congenital condition? Give an example

A

Present at birth - could be genetic or not

Club foot

132
Q

What is an inherited condition? Give an example

A

Caused by an inherited genetic abnormality and may not manifest until later in life
Huntington’s disease

133
Q

Give an example of a chromosomal abnormality

A

Down’s syndrome

134
Q

What type of inheritance is linked to Mendelian inheritance?

A

Autosomal inheritence

135
Q

What type of inheritance is linked to most genetic diseases?

A

Polygenic inheritance (multiple genes influence)

136
Q

What is an acquired disease? Give an example

A

Caused by non-genetic environmental factors but may be congenital
Foetal alcohol syndrome

137
Q

What genes can cause dwarfism?

A

COL2AI (type 2 collagen)

Fibroblast growth factor receptor 3 gene

138
Q

What is hypertrophy?

A

Increase in size of a tissue caused by an increase in size of constituent cells

139
Q

What is the function of myostatin gene?

A

Forms a protein that stops muscles growing once they reach a certain size

140
Q

What is an example of hypertrophy?

A

Making biceps bigger

141
Q

What is hyperplasia?

A

Increase in size of a tissue caused by an increase in the number of constituent cells

142
Q

Give an example of hyperplasia

A

Increase in number of smooth muscle cells in prostate

143
Q

What is atrophy?

A

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

144
Q

Give an example of atrophy

A

Loss of brain tissue in Alzheimer’s, muscle atrophy after bone breaks

145
Q

What is metaplasia?

A

Change in differentiation of a cell from one fully differentiated type to a different fully differentiated type

146
Q

Give an example of metaplasia

A

Ciliated columnar epithelium to squamous epithelium in bronchi of smokers

147
Q

What is dysplasia?

A

Imprecise term for morphological changes seen in cells in progression to becoming cancer

148
Q

Give an example of dysplasia

A

Focal cortical dysplasia

149
Q

What allows DNA replication?

150
Q

What happens to telomeres over time?

A

They shorten with each division so cells eventually stop dividing

151
Q

What is progeria?

A

Premature ageing of children with short telomeres as cells can no longer divide prematurely

152
Q

What causes damage?

A
  1. Crosslinking proteins
  2. Loss of Ca influx
  3. Damage to mitochondrial DNA
  4. Loss of DNA repair mechanism
  5. Peroxidation of membranes
  6. Free radical generation
  7. Activation of ageing and death genes
  8. Telomere shortening
  9. Accumulation of toxic by-products of metabolism
  10. Crosslinking or mutations of DNA
153
Q

What can stop damage?

A

Calorific restriction

154
Q

What causes dermal elastosis?

A

UV-B light protein cross linking causing collagen crosslinks and loss of elasticity

155
Q

What causes osteoporosis?

A
  1. Increased bone resorption

2. Decreased bone formation

156
Q

Why is osteoporosis more common in women?

A

Due to the lack of oestrogen after menopause

157
Q

What causes cataracts?

A

UV-B light protein crosslinking

158
Q

What causes senile dementia?

A
  1. Atrophy of brain
  2. Neuronal loss
  3. Plaques
  4. Neurofibrillary tangles
159
Q

What causes sarcopaenia?

A
  1. Decreased growth hormone
  2. Decreased testosterone
  3. Increased catabolic cytokines
160
Q

What causes deafness?

A

Loss of hair cells

161
Q

Why can basal cell carcinoma of skin be cured?

A

It only invades locally

162
Q

What causes basal cell carcinoma of skin?

163
Q

What are the systemic symptoms of leukaemia?

A

Weight loss
Fever
Frequent infections

164
Q

Name 10 other symptoms of leukaemia

A
  1. Easy SOB
  2. Muscle weakness
  3. Bone/joint pain
  4. Fatigue
  5. Loss of appetite
  6. Lymph node swelling
  7. Spleen enlargement
  8. Night sweats
  9. Easy bleeding and bruising
  10. Purplish patches or spots
165
Q

What 2 types of leukaemia are treated with chemotherapy?

166
Q

What type of cancer spreads from blood to bone?

A

Carcinomas

167
Q

What cancers commonly spread to bone?

A
  1. Breast
  2. Prostate
  3. Lung
  4. Thyroid
  5. Kidney
168
Q

How can a breast cancer diagnosis be confirmed?

A
  1. Mammograms

2. Core biopsy

169
Q

What happens if breast cancer spreads to the axilla?

A

Axillary nodes are cleared

170
Q

What would not be seen on scans following a tumour excision?

A

Micro metastases

171
Q

What is adjuvant therapy?

A

Extra treatment given after surgical excision to prevent local recurrence

172
Q

What therapy can improve survival and recurrence in breast cancer?

A

Anti-oestrogen therapy

173
Q

How many breast cancers are HER2 positive?

174
Q

What is a side effect of anti-oestrogen therapy?

A

Premature menopause

175
Q

What drug is used in HER2 positive breast cancers?

176
Q

What is carcinogenesis?

A

The transformation of normal cells to neoplastic cells through permanent genetic alterations or mutations

177
Q

What does carcinogenesis apply to?

A

Malignant neoplasms

178
Q

What are carcinogens?

A

Agents known or suspected to cause tumours

179
Q

Why are carcinogens known as mutagenic?

A

They act on DNA

180
Q

What % of cancer risk is environmental?

181
Q

What are the main problems with identifying carcinogens?

A
  1. Latent interval may be decades
  2. Complexity of environment
  3. Ethical constraints
182
Q

Where is hepatocellular carcinoma common?

A

In areas with more hepatitis B/C and mycotoxins

183
Q

Where is oesophageal cancer common?

A

Japan, China, Turkey, Iran

184
Q

What are the risks oesophageal cancer?

A

Drinking very hot coffee, diet

185
Q

What are the behavioural risks for lung cancer?

A

Smoking

Blue asbestos

186
Q

What are the occupational risks or bladder cancer?

A

Aniline dye in printing, rubber industries

187
Q

What is the risk for scrotal cancer?

A

Polycyclic aromatic hydrocarbons in chimney sweeps

188
Q

Radioactive iodine is a risk factor for which cancer?

A

Thyroid cancer

189
Q

Thorotrast is a risk for which cancer?

A

Angiosarcoma

190
Q

What are the issues with experimental models in cancer?

A
  1. Bacterial mutation may not = carcinogenicity

2. Animals/cultures may metabolise agents differently to humans

191
Q

What are the classes of carcinogens?

A
  1. Chemical
  2. Viral
  3. Ionising and non-ionising radiation
  4. Hormones, parasites and mycotoxins
  5. Miscellaneous
192
Q

What is the common metabolic conversion for chemical carcinogens?

A

Pro-carcinogens to ultimate carcinogenic

193
Q

What can the metabolic conversion from pro-carcinogens to ultimate carcinogenic cause?

A

Cancer in a place different to the exposure site

194
Q

What does exposure to UV-A or UV-B increase risk of?

A

Basal cell carcinoma, melanoma, squamous cell carcinoma

195
Q

What is xeroderma pigmentosum?

A

Failure in the ability of DNA to repair mutations in skin

196
Q

What does oestrogen increase the risk of?

A

Mammary/endometrial cancer

197
Q

What do anabolic steroids increase the risk of?

A

Hepatocellular carcinoma

198
Q

What does aflatoxin B1 (grain mould) cause?

A

Hepatocellular carcinoma

199
Q

What cancer does Chlonorchis sinensis cause?

A

Cholangiocarcinoma (bile duct cancer)

200
Q

What does Shistosoma cause?

A

Bladder cancer (SCC)

201
Q

What are the host factors in carcinogenesis?

A
  1. Race
  2. Diet
  3. Constitutional factors e.g. age, sex
  4. Premalignant legions
  5. Transplacental exposure
202
Q

Why is oral cancer is more common in SE Asia?

A

Reverse smoking, betal chewing, chewing tobacco

203
Q

Why is skin cancer less common in black people?

A

They have more melanin

204
Q

Give 2 examples of cancers with inherited predisposition

A
  1. Familial polyposis coli

2. Retinoblastoma

205
Q

Name a cancer which is affected by gender?

A

Breast cancer (F:M 200:1)

206
Q

What are premalignant conditions?

A

Identifiable local abnormalities associated with increased risk of malignancy at that site

207
Q

Name a premalignant condition

A
  1. Colonic polyps
  2. Cervical dysplasia
  3. Ulcerative colitis
  4. Undescended testis
208
Q

What is a tumour?

A

Any abnormal swelling

209
Q

What can be classed as a tumour?

A
  1. Neoplasm
  2. Inflammation
  3. Hypertrophy
  4. Hyperplasia
210
Q

What is a neoplasm?

A

A lesion resulting from the autonomous or relatively autonomous abnormal growth of cells which persists after the initiating stimulus has been removed

211
Q

Describe neoplasm

A
  1. Autonomous
  2. Abnormal
  3. Persistent
  4. New growth
212
Q

What proportion of deaths do neoplasms account for?

213
Q

Where is borderline neoplasm commonly found?

214
Q

What cancer is often subclinical?

A

Thyroid cancer

215
Q

Where do neoplastic cells derive from?

A

Nucleated cells

216
Q

What is the function of stroma?

A
  1. Supportive
  2. Mechanical support
  3. Nutrition
217
Q

What does success as a neoplasm depend on?

A

Tumour angiogenesis

218
Q

At what size does a neoplasm need a blood supply?

219
Q

What drives the growth of tumour blood supply?

A

Vascular endothelial growth factor

220
Q

Why must neoplasms be classified?

A
  1. To determine appropriate treatment

2. To provide prognostic information

221
Q

How can neoplasms be classified behaviourally?

A
  1. Benign
  2. Borderline
  3. Malignant
222
Q

How can benign tumour causes morbidity and mortality?

A
  1. Pressure on adjacent structures
  2. Obstruct flow
  3. Production of hormones
  4. Transformation to malignant neoplasm
  5. Anxiety
223
Q

Describe benign neoplasms

A
  1. Localised, non-invasive
  2. Slow growth rate
  3. Low mitotic activity
  4. Resemble normal tissue
  5. Circumscribed or encapsulated
224
Q

How do malignant neoplasms cause morbidity and malignancy?

A
  1. Destruction of adjacent tissue
  2. Metastases
  3. Blood loss from ulcers
  4. Obstruction of flow
  5. Hormone production
  6. Paraneoplastic effects
  7. Anxiety and pain
225
Q

What are the common features of malignant neoplasms?

A
  1. Metastases
  2. Invasive
  3. Rapid growth rate
  4. Poorly defined border
  5. Increased mitotic activity
  6. Variable resemblance to normal tissue
  7. Poorly circumscribed
226
Q

Describe the nuclei of malignant neoplasms

A
  1. Hyperchromatic - darker than normal

2. Pleomorphic - different sized nuclei

227
Q

What is histogenesis?

A

Specific cell of origin of a tumour

228
Q

Where may neoplasms arise from?

A

Epithelial cells, connective tissues, lymphoid/haemopoietic organs

229
Q

What is the suffix of neoplasms?

230
Q

What is a papilloma?

A

Benign tumour of non-glandular non-secretory epithelium

231
Q

What is an adenoma?

A

Benign tumour of glandular or secretary epithelium

232
Q

What is a carcinoma?

A

Malignant tumour of epithelial cells

233
Q

What is an adenocarcinoma?

A

Carcinoma of glandular epithelium

234
Q

How are benign connective tissue neoplasms named?

A

According to the cell of origin and are suffixed by -oma

235
Q

What is a lipoma?

A

A benign neoplasm of adipocytes

236
Q

What is a chondroma?

A

A benign neoplasm of cartilage

237
Q

What is an osteoma?

A

A benign neoplasm of bone

238
Q

What is an angioma?

A

A benign vascular neoplasm

239
Q

What is a rhabdomyoma?

A

A benign neoplasm of striated muscle

240
Q

What is a leiomyoma?

A

A benign neoplasm of smooth muscle

241
Q

What is a neuroma?

A

A benign neoplasm of nerves

242
Q

How is a malignant connective tissue neoplasm named?

A

Sarcoma prefixed by cell type of origin

243
Q

What is an anaplastic tumour?

A

Where the cell type of origin of a tumour is unknown

244
Q

What is a malignant neoplasm of melanocytes called?

245
Q

What is a malignant tumour of mesothelial cells called?

A

Mesothelioma

246
Q

What is a malignant neoplasm of lymphoid cells called?

247
Q

What is a carcinoma in situ?

A

When a membrane is full of cancer cells but they haven’t invaded anywhere else

248
Q

How do cancer cells cross the basement membrane?

A

With proteases

249
Q

What is the function of collagenases in intravasation?

A

Chew through vessel walls to allow the tumour to enter it

250
Q

How do tumours evade the host immune defence?

A
  1. Aggregation with platelets
  2. Shed surface antigens
  3. Adhesion to other tumour cells
251
Q

What contributes to extravasation?

A
  1. Adhesion receptors
  2. Collagenases
  3. Cell motility
252
Q

What is needed to allow vessel growth?

A

Angiogenesis promotors

253
Q

What are the angiogenesis inhibitors?

A
  1. Angiostatin
  2. Endostatin
  3. Vasculostatin
254
Q

Where does a tumour in the lower body often metastasise to?

255
Q

What is it called when metastases in the lungs break off and metastasise to further sites?

A

Cannonball metastases

256
Q

What sort of tumour often metastasise to the lungs?

A

Sarcomas and any common cancers

257
Q

Which tumours commonly metastasise to the liver?

A

Colon
Stomach
Pancreas
Carcinoid tumours of intestine

258
Q

Which tumours commonly metastasise to bone?

A

Prostate, breast, thyroid, lung, kidney

259
Q

What are some common side effects of chemotherapy?

A
  1. Myelosuppression
  2. Hair loss
  3. Diarrhoea
260
Q

Which chemotherapies work by binding directly to DNA to inhibit DNA synthesis crosslinking?

A
  1. Ifosamide

2. Cisplatin

261
Q

How does Vinblastine work?

A

Binds microtubules to stop them contracting

262
Q

How does etoposide work?

A

Inhibits topoisomerase II so it can’t replicate DNA

263
Q

What contribute to tumour size increases?

A
  1. Cell division

2. Lack of apoptosis

264
Q

What type of tumour is conventional chemotherapy useful for?

A

Fast dividing tumours (most)

265
Q

What are the benefits to targeted chemotherapy?

A
  1. More effective

2. Less side effects

266
Q

What techniques can be used to differentiate between normal and cancer cells?

A
  1. Gene arrays
  2. Proteomics
  3. Tissue microarrays
267
Q

What is cetuximab?

A

A monoclonal antibody against epidermal growth factor receptor

268
Q

What is the effect of tyrosine kinase activity on EGFR?

A
  1. Epidermal GF binds
  2. IC signalling proteins released
  3. Transcriptional upregulation
  4. Proliferation
  5. Angiogenesis
  6. Cell motility/invasion
269
Q

What is herceptin?

A

A monoclonal antibody against human epidermal growth factor receptor 2: Her2

270
Q

What is the result of over expression of HER2 in breast cancer?

A
  1. Increased dimerisation

2. More IC signalling proteins so more transcriptional upregulation so more proliferation

271
Q

What drug causes endocytosis of Her2?

272
Q

How common is HER2 gene amplified in breast cancer?

A

20-30% of cases

273
Q

What are the characteristics of a HER2 upregulated tumour?

A
  1. Large size
  2. High grade
  3. Aneuploidy
  4. Negative oestrogen receptor status
  5. Independent adverse prognostic factor
274
Q

What is an adjuvant therapy?

A

When a drug e.g. herceptin is given following tumour removal to eliminate any remaining metastases

275
Q

What is gleevec?

A

An inhibitor of c-kit tyrosine kinase

276
Q

What can gleevec treat?

A

Chronic myelogenous leukaemia

Phase 2a Medicine (15 decks)

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