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Phase 2a > ICS > Flashcards

ICS Flashcards

1
Q

What are the 2 types of autopsy?

A

Hospital (very few)

Medico-legal (most, coronial and forensic)

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2
Q

Which deaths are referred to the coroner?

A

Presumed natural
Presumed iatrogenic
Presumed unnatural

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3
Q

Who can make a referral to the coroner?

A

Doctors (common law duty)
Registrars of BDM (statutory duty)
Relatives, police, anatomical pathology physicians

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4
Q

What are the 4 questions to be answered by a coronial autopsy?

A

Who
When
Where
How

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5
Q

What is the structure of an autopsy?

A

History/scene, external examination, evisceration, internal examination, reconstruction

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6
Q

What is looked for in an external examination in an autopsy?

A

Gender, age, jewellery, body mods…
Injuries
Signs of disease/treatment

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7
Q

What happens in evisceration?

A

Y-shaped incision
Open all body cavities
Examine then remove thoracic and abdominal organs and brain

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8
Q

Give a (rough) definition of inflammation

A

reaction to injury or infection involving certain cells

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9
Q

When can inflammation be good?

A

Injury

Infection

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10
Q

When can inflammation be bad?

A

Autoimmunity

When involved in over-reaction to a stimulus

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11
Q

What are the two classes of inflammation?

A

Acute and chronic

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12
Q

Give some characteristics of acute inflammation

A

Sudden onset
short duration
usually resolves

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13
Q

Give some characteristics of chronic inflammation

A

Slow onset or sequel to acute
Long duration
May never resolve

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14
Q

What are the main cells involved in inflammation?

A 
Neutrophil polymorphs 
Macrophages 
lymphocytes 
endothelial cells 
fibroblasts
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15
Q

Give some features of neutophil polymorphs

A

First on the scene of acute inflammation
Short lived
Usually die onsite (=pus)
Cytoplasmic granules full of enzymes to destroy bacteria
release chemicals to attract other inflamm cells

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16
Q

Give some features of macrophages

A 
Weeks to months 
phagocytic properties
ingest bacteria and debris 
may present antigen to lymphocytes
many types eg Kupffer cells
Single big nucleus
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17
Q

Five some features of lymphocytes

A 
Years 
Produce chemicals to attract other inflamm cells 
Immunological memory (t)
Control inflammation 
Mostly nucleus in appearance 
b cells produce antibodies
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18
Q

Give features of endothelial cells in inflammation

A

Become ‘sticky’ so inflammatory cells can adhere
Becomes porous so inflammatory cells ca pass into tissue
Grow into areas of damage to form new capillaries
Precapillary sphincters open

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19
Q

Give some features of fibroblasts in inflammation

A

Long lived

form collagen in areas of chronic inflammation and repair

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20
Q

Give an example of acute inflammation

A

Acute appendicitis

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21
Q

Give an eg of chronic inflammation

A

tuberculosis

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22
Q

What is a granuloma?

A

Collection of epitheliod cells (macrophages but pale)

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23
Q

What can granuloma suggest?

A

The appearance of granulomas may be augmented by the presence of caseous necrosis (as in tuberculosis)
The association of granulomas with eosinophils often indicates a parasitic infection (e.g. worms)
Small traces of elements such as beryllium induce granuloma formation

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24
Q

Name the 4 macroscopic appearances of acute inflammation

A

Rubor (redness)
Calor (heat)
Tumor (swelling)
Dolor (pain)

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25
Q

What causes rubor in inflammation?

A

Dilation of small blood vessels

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26
Q

What causes calor in inflammation?

A

Only in superficial parts

Hyperaemia leads to dilation of blood vessels leads to increased flow of hot blood

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27
Q

What causes tumor in inflammation?

A

Proteins leak out meaning fluid will not move back in at end of capillary bed

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28
Q

what causes dolor in inflammation?

A

stretching and distortion of tissues

some chemical mediators (bradykinin, prostaglandins, serotonin)

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29
Q

Name a fifth feature of acute inflammation

A

Loss of function

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30
Q

Name steps of acute inflammation.

A

Changes in vessels and flow
increased vascular permeability
formation of exudate fluid
migration of neutrophil polymorph cells to extravascular space

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31
Q

Name some causes of acute inflammation

A 
Microbial infection (virus=death of cells, bacteria= release of toxins)
Hypersensitivity (xs immune reaction to change in immunological responsiveness)
Physical agents (damages tissues) 
Chemicals 
Tissue necrosis (peptides from dying tissue)
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32
Q

Name some systemic effects of inflammation

A 
pyrexia
weight loss 
reactive hyperplasia 
haematologial changes
amyloidosis
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33
Q

Name the four outcomes of acute inflammation

A

Resolution
Suppuration
Repair and organisation
Chronic inflammation

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34
Q

Name some causes of chronic inflammation

A

Primary chronic inflammation
Transplant rejection
Progression from acute inflammation
Recurrent episodes of acute inflammation

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35
Q

Name some macroscopic features of chronic inflammation

A 
Chronic ulcer
Chronic abscess cavity
Thickening of the wall of a hollow viscus
Granulomatous inflammation
Fibrosis
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36
Q

Name some microscopic features of chronic inflammation

A

The cellular infiltrate consists characteristically of
lymphocytes plasma cells and macrophages.
Some of the macrophages may form multinucleate giant
cells.
Exudation of fluid is not a prominent feature, but there may be production of new fibrous tissue from granulation
tissue.
There may be evidence of continuing destruction
at the same time as tissue regeneration and repair.
Tissue necrosis may be a prominent feature, especially in granulomatous conditions such as tuberculosis.

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37
Q

In resolution of damage is the initiating factor removed?

A

Yes

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38
Q

In repair of damage is the initiating factor removed?

A

no

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39
Q

When would resolution occur after damage?

A

WHen tissue is undamaged

When tissue is able to regenerate

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40
Q

When would repair occur?

A

If tissue is damaged and unable to regenerate

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41
Q

Can hepatocytes regenerate? And so can liver ‘grow back’ if part cut out?

A

yes

yes

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42
Q

What happens if continuous damage occurs to liver?

A

Repair occurs leading to cirrhosis

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43
Q

What happens in lobar pneumonia?

A

Acute inflammation of single lobe, air spaces filled with neutrophil polymorphs

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44
Q

With treatment, can lobar pneumonia resolve?

A

Yes

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45
Q

Do skin wounds usually go back to normal?

A

no due to fibrosis leaving a scar

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46
Q

What are the types of skin wound resolution?

A

Abrasion
Healing by 1st intention
Healing by 2nd intention

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47
Q

Does an abrasion wound usually heal well?

A

Yes as usually don’t remove all epithelium and hair cells

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48
Q

What is healing by 1st intention?

A

Sewing up a wound if the two ‘ridges’ can be pulled together.
Produces neat scar
Faster
Weak fibrin clot forms then fibroblasts produce collagen forming scar

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49
Q

What is meant by healing by 2nd intention?

A

Can’t suture two edges together so has to be left un-sutured
Heals slowly and messy big scar formed
Capillaries and fibroblasts grow p from bottom of injury and plug pit

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50
Q

Give a definition(ish) of repair

A

Replacement of damaged tissue by fibrous tissue. Occurs in tissues where cells can’t regenerate

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51
Q

Name some cells that can regenerate

A

Hepatocytes, pneumocytes, all blood cells, gut epithelium, skin epithelium and oseocytes

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52
Q

Name some cells that can’t regenerate

A

Myocardial cells

Neurons

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53
Q

Name 2 factors that prevent clots forming in health

A 
Laminar flow (blood only in centre of vessel)
Endothelial cells aren't 'sticky' in health
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54
Q

What is thrombosis?

A

solid mass of blood constituents formed within intact vascular system in life

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55
Q

What would you use to diagnose a thrombus?

A

Doppler ultrasound

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56
Q

State how a thrombus is formed

A

Endothelial lining of vessel is disrupted, exposing collagen fibres
Platelets bind and aggregate, releasing platelet aggregation factor leading to more platelets binding
Thrombus begins to grow which disrupts laminar flow, trapping some RBCs
Platelets also release clotting factors leading to fibrin mesh forming
Positive feedback for the gainz (in thrombus size)

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57
Q

How could a thrombosis occur in vein when resting for long periods?

A

Vein flow is slow and non pulsitile
Vein blood flow (in legs especially) heavily relies on skeletal muscle pump
When resting this reduces flow even more meaning disruption of laminar flow
More likely for platelets to bind to collagen

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58
Q

Name the three main causes of thrombosis

A

Change in vessel wall
Change in blood constituents
Change in blood flow

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59
Q

Name the possible outcomes of a thrombus

A

Broken down (consider damage to organ)
Organisation (vessel collapses and scars over)
Re-canalisation (capillaries grow through clot)
Embolism

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60
Q

Name some ways of avoiding thrombosis

A

Exercise (to keep blood flowing)
Stockings (push blood out of legs)
Aspirin (reduces aggregation)

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61
Q

What is an embolus?

A

Mass of material in vascular system able to become lodged in a vessel and block it

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62
Q

Name some common emboli

A

Usually a thrombus

cholesterol crystal, air, tumour, amniotic fluid and fat

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63
Q

Where will an embolus usually end up if in the venous circulation?

A

Lodge in pulmonary arteries

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64
Q

Where will an embolus go in the arterial circulation?

A

Anywhere downstream

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65
Q

What is ischaemia?

A

Reduction of blood flow to a tissue w/ no other complications
Cells further from capillaries more likely to be ‘unhappy’

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66
Q

What is a re-perfusion injury?

A

Reintroduction of blood to tissue with severe limitation of blood flow leads to ‘nasties’ being produced, like superoxide radicals, that damage cells

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67
Q

What is infarction?

A

Death of cells due to lack of blood supply

It is a subset of ischaemia

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68
Q

What is end artery supply?

A

When an organ has only one artery supplying it

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69
Q

Name some organs with dual arterial supply

A

liver lungs and some parts of the brain

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70
Q

What are watershed areas?

A

When tissue has two blood supplies but is at the end of both these areas, like some areas of the brain

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71
Q

Which cancer never metastasises?

A

Nasal cell carcinoma of skin

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72
Q

What is the name of a malignant rumour of striated muscle?

A

Rhabdomyosarcoma

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73
Q 
Which of the following rarely metastasises to bone? 
Breast 
Lung 
Prostate 
Liposarcoma
A

Liposarcoma

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74
Q

What term describes a cancer that hasn’t invaded the basement membrane?

A

Carcinoma in situ

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75
Q

What is the name of a benign rumour of glandular epithelium?

A

Adenoma

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76
Q

What is the time course for atherosclerosis?

A

Fatty streak builds from around 20 years and symptoms are around 50 years

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77
Q

Is there much atherosclerosis in the pulmonary arteries?

A

No as lower pressure

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78
Q

Name some contents of a plaque

A

lipids
fibrous tissue
cholesterol
lymphocytes

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79
Q

Name some risk factors associated with atherosclerosis

A 
smoking 
hypertension
diabetes (uncontrolled)
hyperlipidemia 
being male 
lower se background
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80
Q

How does smoking increase the risk of atherosclerosis?

A

Smoke contains chemicals that damage the endothelium of vessels

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81
Q

How does hypertension increase the risk of atherosclerosis?

A

Shearing forces on endothelium damage

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82
Q

How is vaping better than smoking

A

Less free radicals and NO BUT same nicotine

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83
Q

How does uncontrolled diabetes increase the risk of atherosclerosis?

A

Produces chemicals that damage endothelium

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84
Q

How does hyperlipidemia increase the risk of atherosclerosis?

A

Damages endothelium

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85
Q

Which theory is the correct theory for atherosclerosis?

A

Endothelial damage theory

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86
Q

Describe endothelial damage theory

A

Damage to endothelium causes platelet aggregation and disruption of laminar flow, catching blood constituents
This heals over (endothelium grows over) and forms lump in lumen
This process of endothelium damage repeats
Chronic inflammation
Atheroma builds up and hardens

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87
Q

Suggest a preventative measure for atheroma

A

asprin as decreases platelet aggregation

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88
Q

Name some complications of atherosclerosis

A

infarcts
gangrene
ischaemia

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89
Q

What is the difference between atherosclerosis and thrombosis?

A

Atherosclerosis is defined as a condition where cholesterol plaques are developed on the endothelium of the blood vessels.
Thrombus refers to a blood clot which is attached to the inner walls of the blood vessels without getting calcified like atherosclerotic plaques.

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90
Q

What is apoptosis?

A

Programmed cell death in which no cellular contents are released, so no inflammatory reaction

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91
Q

Name the main cause for apoptosis

A

DNA damage

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92
Q

State the different ways dna can be changed to cause apoptosis

A

single strand break
double strand break
base alteration
cross linkage

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93
Q

Which protein is responsible for checking for DNA damage

A

p53

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94
Q

What does apoptosis look like microscopically?

A

Death of individual cell

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95
Q

Name the two ways apoptosis can be induced

A 
Bax protein (intrinsic pathway)
Fas ligand binding to fas receptor (extrinsic)
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96
Q

Which protein can reduce apoptosis?

A

BCL2

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97
Q

Which enzymes are primarily responsible for apoptosis?

A

Caspases

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98
Q

Describe briefly how apoptosis occurs

A

Enzymes destroy cell into vesicles

Macrophages mop up

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99
Q

Name a way apoptosis is used in development

A

Fingers becoming unwebbed

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100
Q

How does Juliet maintain a constant body temperature?

A

Romeostsis

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101
Q

Name a function of apoptosis in health

A

death of cells in tissues with high cell turnover rg. the gut

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102
Q

Name a function of apoptosis in disease

A

Lack of apoptosis in cancer

Too much apoptosis in HIV

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103
Q

What is necrosis? :(

A

Poorly controlled form of cell death in which membrane integrity is lost w/ leakage of contents = inflammatory response
traumatic cell death of big swathes of tissue

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104
Q

What would necrosis (generally) look like microscopically?

A

Large swathes of cells dying

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105
Q

Name some clinical egs of necrosis

A 
toxic spider venom
frostbite
cerebral infarction 
avascular necrosis of bone (scaphoid and head of femur)
pancreatitis
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106
Q

Name the types of necrosis

A

Caseous
liquefactive
coagulative

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107
Q

What is caseous necrosis

A

most common type
loss of nuclei but preservation of underlying structure
macroscopically = pale and firm

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108
Q

What is liquefactive necrosis

A

Complete loss of cell structure
Macroscopically= liquidy
Usually following cerebral infarction

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109
Q

What does caseous necrosis look like?

A

Cream cheese

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110
Q

What condition is caseous necrosis associated with?

A

TB

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111
Q

Why is there many disorders of development?

A

Many steps so many places to go wrong

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112
Q

What percentage of fertilisations survive to 1 month?

A

35%, deaths usually due to chromosomal abnormalities

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113
Q

What is spina bifida?

A

Missing spinous process on vertebrae

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114
Q

What a meningocele?

A

Meninges protruding out during development, can usually be treated

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115
Q

What is a myleomeningocele?

A

Meninges and spinal cord protruding out of fetus, usually results in paralysis of lower body

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116
Q

Name some developmental disorders

A

spina bifida
cleft palate
ventriculoseptal defect
Down’s syndrome

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117
Q

What are homeobox genes?

A

Highly conserved genes which code for specific body parts

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118
Q

What is Down’s syndrome?

A

Trisomy 21

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119
Q

Which chromosome is the gene for beta amyloid on?

A

21

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120
Q

What is mendelian inheritance?

A

single gene inheritance

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121
Q

Name an example of autosomal recessive condition

A

Cystic fibrosis

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122
Q

Name an autosomal dominant condition

A

polycystic kidney disease

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123
Q

Name an autosomal co-dominant example

A

blood groups

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124
Q

What is polygenic inheritance

A

many genes contribute to one feature or condition

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125
Q

Are more diseases polygenetic or monogenetic

A

poly

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126
Q

What does congenital mean?

A

Present at birth (can be environmental or genetic)

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127
Q

What does inherited mean?

A

Caused by inherited genetic abnormality, may not manifest until later in life however eg. huntingdon’s

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128
Q

What does acquired mean?

A

Caused by non-genetic factors, however may be congenital

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129
Q

Name a congenital acquired condition

A

Fetal alcohol syndrome

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130
Q

Name some conditions of growth

A

Growth hormone deficiency, and too much GH

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131
Q

What is hypertrophy?

A

Increase in size of tissue caused by increased size of cells, as cells can’t replicate

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132
Q

Name main organ where hypertrophy occurs

A

Skeletal muscle (gainz)

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133
Q

Which gene prevents muscle growth after a certain size?

A

Myostatin

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134
Q

What is hyperplasia?

A

Increase in size of tissue due to increased number of constituent cells

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135
Q

Name some common examples of where hyperplasia occurs

A

prostate
smooth muscle
endometrium (too much oestrogen:progesterone)

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136
Q

During pregnancy does the uterus undergo hyperplasia or hypertrophy?

A

LOL-both

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137
Q

What is atrophy?

A

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

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138
Q

Can nerves atrophy?

A

Oui Oui

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139
Q

What is metaplasia?

A

Change in differentiation of cell from one to another fully differentiated cell

140
Q

Give an example of metaplasia

A

When smoking, in bronchi ciliated columnar to squamous (like skin)
So resistant to irritants but doesn’t produce mucus or sweep mucus

141
Q

What is dysplasia?

A

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

142
Q

What is neoplasia?

A

Abnormal and excessive growth of cells, can be benign or malignant

143
Q

Name something that doesn’t age

A

Plasmodium as just divides by binary fission

144
Q

Why do multicellular organisms show ageing?

A

Many cells in highly ordered structures

Some cells can’t divide and order becomes less ordered

145
Q

Do elderly cells have as much potential t divide as younger cells?

A

Yes

146
Q

Do elderly cells divide as much as younger cells (of the same type)?

A

No

147
Q

What is progeria?

A

A progressive genetic disorder where symptoms of ageing are manifested at an early age

148
Q

In dividing cells, why does ageing occur?

A

Telomeres shorten over life meaning there’s a limit as to how many times a cell can divide

149
Q

In non-dividing cells, how does change occur with time?

A

Cells can’t divide so born with all you’ll ever have

Free radicals, loss of DNA repair mechanisms, damage to DNA… all lead to loss of cells meaning lower functioning

150
Q

Is there a way to slow ageing in non-dividing cells?

A

Yes, calorie restricted diet

151
Q

What causes dermal elastosis?

A

UV-B causes protein cross linking= wrinkles

152
Q

What causes osteoporosis?

A

Reduction in bone matrix due to increased bone resorption and decreased bone formation
Due to lack of oestrogen

153
Q

What causes cataracts?

A

Foggy lens due to UV-B causing proteins to cross-link and become opaque

154
Q

What causes senile dementia?

A

Atrophy of brain, especially memory parts

Plaques, amyloid and tangles

155
Q

What causes sarcopenia (lack of muscle)?

A

Decrease growth hormone and testosterone

increase in catabolic cytokines

156
Q

What causes deafness in ageing?

A

Cilia/ hair cells in ear (non-replaceable) destroyed

157
Q

Does basal cell carcinoma spread to other parts of the body?

A

No it only invades locally

158
Q

What is a complete cure for basal cell carcinoma?

A

Surgical removal

159
Q

What causes basal cell carcinoma?

A

UV light, increased risk if have had it previously

160
Q

Will a tumour of white blood cells spread?

A

Yes as WBC circulate

161
Q

Where do carcinomas primarily spread to?

A

Lymph nodes that drain the site

162
Q

Can carcinomas spread through the blood to bone/lung?

A

Yes

163
Q

Which cancers most commonly spread to the bone?

A

Breast, prostate, lung, thyroid and kidney

164
Q

What can be left behind even if a tumour is completely excised?

A

Micro-metastases

165
Q

What is adjuvant therapy?

A

Extra treatment given after surgical excision to try to clear micro-metastases

166
Q

What is leukaemia?

A

Cancer of WBC

167
Q

Give some systemic symptoms of leukaemia

A

Weight loss, fever, frequent infection

168
Q

Give symptoms of leukaemia related to the lung

A

Easy shortness of breath

169
Q

Give symptoms of leukaemia related to the muscles

A

Weakness

170
Q

Give symptoms of leukaemia related to the bones

A

Pain/ tenderness

171
Q

Give symptoms of leukaemia related to psychology

A

fatigue and decreased appetite

172
Q

Give symptoms of leukaemia related to the lymph nodes and spleen/liver

A

Enlargement

173
Q

Give symptoms of leukaemia related to the skin

A

Night sweats
easy bleeding and bruising
purplish patched and spots

174
Q

Describe the plan of treatment for breast cancer

A
  • Confirm diagnosis
  • Has it spread to axilla? YES= axillary node clearance, NO and YES= has it spread to rest of body
  • Has it spread to rest of body? YES=systemic (chemo) therapy, NO= surgery (with or without lymph node clearance depending on above)
175
Q

Name some ways of confirming breast cancer diagnosis

A

Needle core biopsy

Screening/ mammograms

176
Q

Why do we need to confirm diagnosis in plan of treatment for cancer?

A

The lump could be one of many things, with different degrees of severity

177
Q

How to check if cancer has spread to axilla?

A

Ultrasound of axilla, then can needle core biopsy the nodes

178
Q

How to check if cancer has spread to rest of body?

A

Bone scan

CT liver and lungs

179
Q

After surgery for breast cancer, what can be done if probability that tumour could recur/still there is high?

A

ADJUVANT therapy
Radiotherapy (recommended in all breast cancer pts)
Tests on tumour to see if express receptors
- if oestrogen receptor +ive, use antioestrogen treatment
HER2 protein stain

180
Q

Define carcinogenesis

A

Transformation of normal cells to neoplastic cells through PERMANENT genetic alterations or mutations

181
Q

Does carcinogenesis apply to benign tumours?

A

Nae

182
Q

What process applies to both malignant and benign tumours?

A

Oncogenesis

183
Q

Is carcinogenesis a single step process

A

NOOOOO

184
Q

What is a carcinogen?

A

An agent known or suspected to cause tumours/cancer

185
Q

What does carcinogenic mean?

A

Cancer causing

186
Q

What does oncogenic mean?

A

Tumour causing

187
Q

What do carginogens act on?

A

DNA

188
Q

What percentage of cancer risk is environmental?

A

85%

189
Q

What factors make identifying carcinogens hard?

A

Carcinogens take tens of years to take effect
V complex environment= many potential ones
Ethical constraints, can’t pour asbestos on people to see what happens

190
Q

What evidence can be used to try to identify carcinogens?

A

Epidemiological- then look for links
Experimental
Direct evidence

191
Q

Give an example of using epidemiological evidence to ID a carcinogen

A

Increased liver cancer in areas with high prevalence of Hep. B and C

192
Q

What are the advantages of experimental evidence in identifying carcinogens?

A

Can explore incidence in lab animals

Can test in cultures

193
Q

What are the -ives of experimental evidence in IDing carcinogens?

A

Different metabolism to species using in lab
A bacterial mutation may not lead to cancer, where as it may in hoomans
Multicellular vs. singlecellular organisms

194
Q

Name some examples of direct evidence in IDing carcinogens

A

Thyrotrast- used to be used for imaging for vasc. system but caused cancer
Thyroid irridation -Chernobyl

195
Q

Name the 5 classifications of carcinogens

A 
Chemical 
Viral 
Radiation (ionising and non)
Biological (hormones, parasites and mycotoxins)
Miscellaneous
196
Q

State features of chemical carcinogens (4)

A

No common structural features
Some act directly
Most require conversion from pro- to ultimate-
Enzyme required to convert may be confined to organs

197
Q

What cancer are polycylic aromatic hydrocarbons associated with? And whats their source?

A

Lung cancer smoking

Skin cancer Mineral oils

198
Q

What cancer are aromatic amines associated with? And whats their source?

A

Bladder rubber/dye workers

199
Q

What cancer are nitrosamines associated with? And whats their source?

A

Gut cancer Processed meats

200
Q

What cancer are alkylating agents associated with?

A

Leukaemia small risk

201
Q

Name some examples of radiant energy as a carcinogen

A

UVA/B
X-rays (radiographers)
Lung cancer in uranium miners (uranium converts to radon)
Chernobyl (thyroid)

202
Q

Name some examples of biological carcinogens

A 
Increased oestrogens = mammary/endometrial cancer
Increased anabolic steroids= herpatocellular carcinoma 
Alfatoxin B1 (mycotoxin)= herpatocellular carcinoma 
Chlonorchis sinensis (parasite) = cholangiocarcinoma (bile duct)
203
Q

Name some miscellaneous carcinogens

A

Asbestos

Metals eg arsenic

204
Q

What host factors can have an impact on risk of developing cancer?

A 
Race 
Constitutional 
Premalignant tumours 
Diet 
Transplacental exposure
205
Q

What is tumour?

A

Any abnormal swelling

206
Q

Give some examples of tumour

A

Neoplasm
Inflammation
hypertrophy
hyperplasia

207
Q

Define neoplasm

A

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

208
Q

Give the key words for neoplasm

A

Autonomous
Abnormal
Persistent
New

209
Q

Why are neoplasms such a big issue?

A

25% of population affected, of all ages
Risk increases with age
High death/mortality rate
20% of all death

210
Q

What are the two spectra of disease for neoplasms?

A

Malignant/borderline/benign

Fatal/subclinical (may have but don’t know)

211
Q

What are the two components of a neoplasm

A

Neoplastic cells

Stroma

212
Q

State some characteristics of neoplastic cells in the neoplasm (4)

A

Derive from nucleated cells
Usually monoclonal at start
Growth pattern related to parent
Synthetic activity related to parent (eg. collagen, mucin, keratin, hormones)

213
Q

State some characteristics of the stroma of a neoplasm (4)

A

Connective tissue framework
Mechanical support
Nutrition
Not neoplastic or autonomous, grow due to growth factors from neoplastic cells

214
Q

What does a stroma consist of

A

Fibroblasts and blood vessels

215
Q

What is angiogenesis in relation to neoplasms

A

Tumour becoming vascularised, malignant tumour often tends to outgrow rate of angiogenesis and die

216
Q

Why do we classify neoplasms?

A

To determine appropriate treatment

Provide prognostic info

217
Q

What are the two methods of classifying tumours

A

Behavioural (malignant/benign)

Histogenic (cell of origin)

218
Q

Are benign tumours invasive

A

nah

219
Q

Benign tumour growth rate and mitotic activity

A

Slow and low

220
Q

Does benign tumour look close to normal tissue?

A

Yes look at borders to distinguish difference

221
Q

Are benign tumours circumscribed?

A

Yah

222
Q

Are necrosis and ulceration rare in benign tumours?

A

Yas

223
Q

Which way do benign tumours grow on mucosal surfaces?

A

Up and out (exophytic)

224
Q

Name some dangers/effect of benign tumours (5)

A 
Pressure on adj. structures
Obstruct flow 
Produce hormones 
go malignant 
anxiety
225
Q

Are malignant tumours invasive?

A

YES, they must be, can be metastatic

226
Q

Growth rate and mitotic activity of malignant tumours?

A

Fasttttt and high

227
Q

Does malignant tumour look like normal?

A

Variable

228
Q

Are malignant tumours well defined?

A

No, irregular border

229
Q

What makes malignant tumour nuclei stand out?

A

Hyperchromatic and pleomorphic

230
Q

Are necrosis and ulceration common in malignant tumours?

A

Yas

231
Q

Which way do malignant tumours grow on mucosal surfaces?

A

In and down (endophytic)

232
Q

Name some dangers of malignant tumours (8)

A 
Encroach upon and invade surrounding structures 
Metastasise 
Poorly circumscribed
Blood loss from ulcers 
Para-neoplastic effects 
Anxiety and pain 
Hormone production 
Obstruction of flow
233
Q

What is histogenesis?

A

The specific cell origin of a tumour

234
Q

Where may a neoplasm arise from (3)

A

Epithelial cells
Connective tissue
Lymphoid/haemopoietic organs

235
Q

What is the main ending for neoplasms?

A

-oma

236
Q

What are (generally) the two types of benign epithelial neoplasms?

A

Papilloma and adenoma

237
Q

What tissue does a papilloma originate from?

A

Non-glandular or secretory epithelium (BENIGN)

238
Q

What suffix is used for papillomas and adenomas?

A

Cell of origin

239
Q

What tissue does an adenoma originate from?

A

Glandular or secretory epithelium (BENIGN)

240
Q

What are the two main malignant epithelial neoplasms?`

A

Carcinoma and adenocarcinoma

241
Q

What tissue does a carcinoma stem from?

A

Non glandular or secretory epithelium (MALIGNANT)

242
Q

What tissue does an adenocarcinoma come from?

A

Glandular epithelium (MALIGNANT)

243
Q

What is the general rule for benign connective tissue neoplasm?

A

Tissue it looks like -oma

244
Q

What is rhabdomyoma?

A

Benign of striated muscle

245
Q

What is neuroblastoma?

A

Benign neoplasm of nerves

246
Q

What is leiomyoma?

A

Benign neoplasm of smooth muscle

247
Q

What is hibernoma?

A

Benign neoplasm of brown fat

248
Q

What is angiolipoma?

A

Benign neoplasm of blood vessels and adipocytes

249
Q

What is the general rule for malignant connective tissue neoplasms?

A

Cell it looks like-sarcoma

250
Q

What are carcinomas and sarcomas further graded by?

A

Degree of differentiation

251
Q

What is anaplastic?

A

Cell type unknown/ doesn’t look like any cell

252
Q

Name some exeptions to the general classification rule by Burton

A

Not all -omas are neoplasms (granuloma, tuberculoma)
Not all malignant are carcinoma or sarcoma (lyphoma, mesothelioma)
Eponymous named (Burkitt’s lymphoma, Ewing’s sarcoma, Grawitz tumour)
Teratoma
Embryonal blastomas
Mixed tumours
APUDomas
Carcinosarcomas

253
Q

Name the main effector cell in acute inflammation

A

Neutrophil polymorph

254
Q

What is the name of the cell that produces collagen in fibrous scarring?

A

Fibroblast

255
Q

Give an example of acute inflam?

A

Appendicitis

256
Q

What crystals are deposited into joints in gout?

A

Uric acid, body tries to ‘gobble up’ leads to acute inflam

257
Q

Name some conditions in which granulomatous inflammation occurs

A

Chron’s diesease
TB
Sarcoidosis

258
Q

What type of inflammation occurs in lobar pneumonia?

A

Acute

259
Q

What is the name of calcification in diseased tissues?

A

Dystrophic calcification

260
Q

Name a condition that is chronic inflam from the start

A

Infectious mononucleosis

261
Q

What cells produce antibodies?

A

Plasma cells

262
Q

What do cancer cells use to invade basement membrane?

A 
Proteases
Collagenase 
Cathepsin D 
Urokinase-type activator 
Cell motility  
Basically stuff to 'chew through basement membrane'
263
Q

Name the seven steps involved in metastases

A 
Invasion of basement membrane 
Tumour cell motility 
Inravasation 
Evasion of host immunity 
Extravasation 
Growth at metastatic site 
Angiogenesis
264
Q

What causes tumour cell motility?

A

Tumour cell derived motility factors

Breakdown of extracellular matrix

265
Q

what happens in intravasation?

A

Tumour cell moved into vessel using collagenases and cell motility

266
Q

How does the tumour cell evade host immunity?

A

Aggregation w/ platelets
Shedding of surface antigens
Adhesion to other tumour cells

267
Q

What happens in extravasation?

A

Tumour cell uses adhesion receptors, collagenases and cell motility to move out of vessel

268
Q

What allows growth at metastatic site?

A

Growth factors produced by tumour

Can grow up to 1mm diameter until need blood supply

269
Q

What happens in the angiogenesis step of metastasis?

A

Blood vessels grow into tumour to provide support
Promoters- vascular endothelial growth factors, basic fibroblast growth factors
Inhibitors- Angiostatin, endostatin, vasculostatin

270
Q

State 3 main routed of metastasis

A

Vena cava -> heart->lungs (small capillaries filter)
Intestines-> liver via hepatic portal vein
Tumours to bone

271
Q

Name common tumours to metastasise to lungs

A

Sarcomas, any common cancers

272
Q

Name some common tumours to metastasise to liver

A

Colon, stomach, pancreas and carcinoid tumours of intestine

273
Q

Name some common tumours that metastasise to bone

A

Prostate breast thyroid lung kidney

Some eat holes in bone some produce new bone

274
Q

What is vinblastine?

A

Conventional chemo. Antimicrotubule agent

275
Q

What is etoposide ?

A

Conventional chemo. inhibits topoisomerase ii

276
Q

What is ifosamide?

A

Conventional chemo, binds to dna and prevents replication by cross linking

277
Q

What is cisplatin?

A

Conventional chemo, binds to dna and prevents replication by cross linking

278
Q

Is conventional chemo selective for cancer cells?

A

No, only fast dividing cells

279
Q

What can conventional chemo cause?

A

Myelosupression, hair loss, diarrhoea, vomiting fatigue

280
Q

What is conventional chemo good for?

A

Fast dividing tumours

281
Q

Name some fast dividing tumours

A

Germ cell of testis, acute leukaemias, lymphomas, embryonal paediatric tumours and choriocarcinoma

282
Q

What is conventional chemo not so good for?

A

Slower dividing tumours

283
Q

How is targeted chemo different from conventional chemo?

A

Targeted exploits some differences between normal cells and cancer cells

284
Q

Name 3 ways we can identify differences in tumour cells

A

Gene arrays
Proteomics
Tissue microarrays

285
Q

How do cells usually increase proliferation?

A

Growth factor binds to receptor
Receptor releases intracellular signalling proteins
This causes transcriptional upregulation

286
Q

Name two ways in which cancer cells greatly increase proliferation, evasion and angiogenesis

A

Over-expression of growth factor receptor

Constitutive activation of growth factor receptor (receptor always on)

287
Q

Name two ways of blocking cancer cells from increasing proliferation

A

Monoclonal antibodies against the receptor

Small molecular inhibitor of growth factor receptor

288
Q

How do monoclonal antibodies against gf receptor work

A

Bind to extracellular component of receptor blocking gf from binding

289
Q

How do small molecular inhibitors work?

A

Bind to the intracellular component of the receptor, preventing release of intracellular signalling molecules

290
Q

What is Cetuximab (erbitux)?

A

Monoclonal antibody against epidermal growth factor receptor (EGFR)
Chimeric IgG humanised monoclonal antibody
Blocks production of VEGF, interleukin 8 and bFGF

291
Q

What is herceptin (trastuzumab)?

A

Monoclonal antibody against epidermal growth factor receptor 2 (Her-2)
Chimeric mouse-human monoclonal antibody

292
Q

How does herceptin work?

A

Her-2 receptors need to ‘bum’ into eachother or into Her-3 with ligand to work
Herceptin binds to Her-2 and causes endolytic removal and antibody cell cytotoxicity (lymphocytes kill Her-2)
Decreases chance of bumping

293
Q

What breast cancers is Her-2 associated with?

A 
Her-2 amplified in 20-30% of breast cancers 
Large size
High grade 
Anaploidy 
Negative oestrogen receptor status
Independent adverse prognostic factor
294
Q

What is gleevec?

A

Small molecular inhibitor of C-kit
Inhibitor of c-kit tyrosine kinase
Works on mutated receptor and over-expressed receptor

295
Q

State some ways to detect protein amplification

A

Fluorescent in-situ hybridisation (FISH)- looking for gene (Gene for Her-2 on ch 17)
Immunohistochemistry - look for protein

296
Q

What is anti PD1?

A

Anti programmed cell death protein 1
Includes pembrolizumab and nivolumab
PD1 usually surprsses immune response to prevent autoimmune diseases, but also stops killing cancer cells, removing it allows to kill cancer

297
Q

Name some other cancer treatments

A

EGFR TK- gefitinib (inhibitor of EGFR tyrosine kinase)

Chimeric T cell receptors (dna into viral vector, produce t cell which react with antigens on cancer cells to kill them)

298
Q

What are the big names in lung cancer?

A

Small cell lung cancer (BAD)
Squamous cell carcinoma
Adenocarcinoma

299
Q

What do TNM and R stand for in cancer grading?

A 
Tumour 
Node 
Metastases 
Recection
higher number = worse
300
Q

What is the main factor to reduce bleeding immediately?

A

Vessel spasm due to damage

301
Q

Which neoplasm never metastasises?

A

Basal cell carcinoma

302
Q

What is the name of malignant tumour of striated muscle

A

Rhabdomyosarcoma

303
Q 
Which does not commonly metastasise to bone? 
Breast 
lung
prostate
liposarcoma
A

Liposarcoma

304
Q

What term describes a cancer that hasn’t invaded a basement membrane

A

Carcinoma in situ

305
Q

What is the name of a benign tumour of glandular epithelium

A

Adenoma

306
Q 
Which of these does not have a screening programme 
breast
colorectal
cervical
lung
A

Lung

307
Q 
Which of the following is not known to be a carcinogen 
Aspergillus niger
Hap. c 
ionising radiation 
aromatic amines
A

Aspergillus niger

308
Q

What is a benign tumour of fat cells called

A

lipoma

309
Q

What is a malignant tumour of glandular epithelium called

A

Adenocarcinoma

310
Q 
Which is not a feature of malignant tumour 
Vascular invasion 
metastasis
increased cell division 
growth related to overall body growth
A

Last one

311
Q

A transitional cell carcinoma of bladder is malignant?

A

True

312
Q

A leiomyoma is a benign tumour of smooth muscle

A

True

313
Q

Radon gas is a cause of lung cancer?

A

True

314
Q

Asbestos is a human carcinogen?

A

True

315
Q 
Which lifestyle factor is most likely to cause cancer 
Wine bevs 
Being obese
Running 
SMoking
A

Smoking

316
Q 
Which has the shortest median survival 
Basal cell carcinoma 
Malignant melanoma 
Breast cancer 
Anaplastic carcinoma of thyroid
A

Anaplastic carcinoma of thyroid

317
Q

Ovarian cancer commonly spreads to peritoneum

A

True

318
Q

What must the immune system do?

A

discriminate self from non self

319
Q

State some features of innate imunity (4)

A

Does not depend on lymphoctes
Present from birth
Instinctive
Non-specific

320
Q

State some features of adative immunity (3)

A

Acquired/learned immunity
requires lymphocytes
antibodies

321
Q

What are the three layers of blood sample when centrifuged?

A 
Upper layer (plasma, straw coloured, water, electrolytes, proteins, lipids and sugars)
Buffy coat (WBC)
Lower layer (RBC and platelets)
322
Q

What is serum

A

Plasma without fibrinogen and other clotting factors

323
Q

What are leukocytes?

A 
White cells
lymphocytes 
phagocyte 
neutrophil 
eosinophil 
basophil
324
Q

What are the types of lymphocytes? and what soluable mediators do they secrete?

A

B (produces antibodies)
T (cytokines)
Large granular lymphocytes (=> cytokines)

325
Q

What are the types of phagocytes? and what soluable mediators do they secrete?

A

mononuclear phagocyte (cytokines and complement)
neutrophil
eosinophil

326
Q

What are the types of axillary cells? and what soluable mediators do they secrete?

A

Basophil
Mast cell
Platelts
All secrete inflammatory mediators

327
Q

Which soluble mediators do tissue cells secrete?

A

Interferons

Cytokines

328
Q

What is the origin of blood cells

A

Multipotent haemopoietic stem cell (haemocytoblast)

329
Q

What two cells are produced by haemocytoblasts?

A

Common myeloid progenitor cells

Common lymphoid progenitor cells

330
Q

Which cells do common myeloid progenitor cells produce?

A

magakaryocyte (platelets)
erythrocyte
myeloblast

331
Q

Which cells do common lymphoid progenitor cells produce?

A

Lymphocytes (B and T)

332
Q

Which are the polymorphonuclear leukocytes?

A

Neutrophil eosinophil basophil

333
Q

Which cells are the mononuclear leukocytes?

A

Monocytes (=> macrophage)
t cells (=>tregs, thelper and cytotoxic)
bcells (plasma)

334
Q

Name two types of antigen presenting cells?

A

Macrophages and dendritic cells

335
Q

What is complement C’?

A

20 serum proteins secreted by liver that need to be activated
As part of immune response

336
Q

What are the outcomes of the complement system?

A

Direct lysis
Attract more leukocytes
Increase opsonisation and increase phagocytosis

337
Q

What do antibodies do?

A

Bind specifically to antigens

338
Q

What are immunogobulins?

A

Soluable secreted glycoproteins bound to antibodies as part of B-cell antigen receptor

339
Q

What are the 5 classes of Ig

A

G, M, A, D and E

340
Q

Which are the most numerous Ig’s?

A

G and M

341
Q

What are the functions of IgG?(3)

A

Binds to pathogen (agglutination and osponisation)
Activates classical pathway of complement system
Neutralises toxins

342
Q

Where are IgMs mainly found?

A

In the blood as too big to cross endothelium

343
Q

What is the function of IgM

A

Initial contact with antigen

344
Q

Describe IgA

A

Most is in monomer form

Main Ig in mucous secretion (breast milk, tears and sputum)

345
Q

Where is IgD present

A

Bcells

346
Q

Where are IgE receptors found?

A

Mast cells and basophils

347
Q

What does binding of IgE to receptors cause?

A

Release of histamine

Phase 2a (1 decks)

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