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MoD Flashcards

1
Q

What are the 4 types of hypoxia?

A
  1. Hypoxaemic (arterial content of O2 is low)
  2. Anaemic (decreased ability of haemoglobin to carry O2)
  3. Ischaemic (intrusion to blood supply)
  4. Histiocytic (inability to utilise O2, disabled phosphorylation enzymes)
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2
Q

What are the 4 principle targets for cell injury?

A
  1. Cell membranes
  2. Nucleus
  3. Proteins
  4. Mitochondria
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3
Q

Summarise hypoxic cell injury

A

Cell deprived of O2; mitochondrial ATP production stops.
ATP- driven membrane ionic pumps run down, Na+ and H2O seep into cell, causing it to swell, plasma membrane is stretched.
Glycolysis enables cell to limp on for a while, cell initiates heat-shock (stress) response, won’t be able to cope if hypoxia continues.
pH of cell drops due to lactic acid accumulation
Ca2+ enters cell…
ER and other organelles swell
Enzymes leak out of lysosomes, enzymes attack cytoplasmic components
All cell membranes damaged and start to show blebbing
Cell dies (possibly killed by burst of bleb)

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4
Q

Once Ca2+ enters a cell damaged by hypoxia, what 4 things does it activate?

A
  1. Phospholipases - causing cell membranes to lose phospholipid
  2. Proteases - damaging cytoskeletal structures and attacking membrane proteins
  3. ATPase - causing more loss of ATP
  4. Endonucleases - causing the nuclear chromatin to clump
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5
Q

What are the 7 causes of cell injury?

A
  1. Hypoxia
  2. Physical agents
  3. Chemical agents
  4. Micro-organisms
  5. Immune mechanisms
  6. Dietary insufficiency
  7. Genetic abnormalities
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6
Q

What 3 things may ischemia reperfusion injury be due to?

A
  1. Increased production of O2 free radicals
  2. Increased number of neutrophils following reinstatement of blood supply resulting in more inflammation and increased tissue injury
  3. Delivery of complement proteins and activation of the complement pathway
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7
Q

When free radicals attack lipids in cell membranes, what do they cause?

A

Lipid peroxidation

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8
Q

Name the 3 free radicals of particular biological significance

A

Hydroxyl (OH*)
Superoxide (O2-)
Hydrogen Peroxide (H2O2)

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9
Q

What’s the name of the reactions that produce hydroxyl (OH*) radicals?

A

Fenton and Haber-Weiss

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10
Q

What are the vitamins which help reduce biological free radical levels?

A

ACE

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11
Q

What reaction does superoxide dismutase (SOD) catalyse?

A

O2- —-> H2O2

Catalyses complete the process of free radical removal

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12
Q

Give an example of a heat shock protein

A

Ubiquitin

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13
Q

What do heat shock proteins do?

A

Their synthesis is increased when cell is under stress. Concerned with protein repair - important when the folding step goes astray. Recognise incorrectly folded proteins and repair or destroy them.

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14
Q

What are the 3 main alterations that can be seen under the microscope with cell injury?

A
  1. Cytoplasmic changes - reduced pink staining of cytoplasm due to accumulation of water. Followed by increased pink staining due to detachment of ribosomes and accumulation of denatured proteins
  2. Nuclear changes - chromatin is subtly clumped. Followed by various levels of pyknosis, karryohexis, and karryolysis of nucleus.
  3. Abnormal intracellular accumulations
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15
Q

List irreversible electron microscopy changes

A

Nuclear changes (pyknosis, karyolysis, karyorrhexis),swelling and rupture of lysosomes, membrane defects, appearance of myelin figures (damaged membranes), lysis of ER due to membrane defects, amorphous densities in swollen mitochondria

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16
Q

Define oncosis

A

Oncosis: cell death with swellings the spectrum of changes that occur in injured cells prior to death

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17
Q

Define necrosis

A

Necrosis: in a living organism the morphological changes that occur after a cell had been dead for some time (e.g. 4-24hrs).
An appearance, not a process, describes morphological changes.

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18
Q

Define apoptosis

A

Apoptosis: cell death with shrinkage, induced by a regulated intracellular programme where a cell activates enzymes that degrade its own nuclear DNA and proteins

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19
Q

What are the 4 types of necrosis?

A

Coagulative
Liquifactive
Caseous
Fat necrosis

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20
Q

Describe coagulative necrosis

A

Denaturation of proteins dominates, dead tissue has solid consistency and appears white to the naked eye. Histologically cellular architecture is somewhat preserved, creating ‘ghost outline’ of cells (first few days only).

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21
Q

Describe Liquifactive necrosis

A

Enzyme degradation dominates, leading to enzymatic digestion of tissues. Seen in massive neutrophil infiltration (neutrophils release proteases), so often bacterial infections and brain as is fragile tissue

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22
Q

Describe caseous necrosis

A 
Caseous = cheese (latin), to naked eye has cheesy appearance.
Structuresless debris (no ghost outlines). Associated with infections e.g. TB and form of inflammation 'granulomatous'
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23
Q

Describe fat necrosis

A

Occurs when there is destruction of adipose tissue, typically as a consequence of acute pancreatitis as release of lipases. Causes release of free fatty acids, which can react with Ca to form chalky deposits in fatty tissue, these can be seen on X-ray, and to naked eye in surgery/autopsy. Can also occur as a result of direct trauma especially to breast tissue.

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24
Q

Describe gangrene

A

Not a type of necrosis! Clinical term for necrosis visible to the naked eye. Classified into dry (exposed to air, coagulative necrosis) or wet (infected with bacteria, liquifactive). Gas gangrene is wet gangrene where tissue is infected with anaerobic bacteria which produce visible bubbles of gas in the tissue.

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25
Q

Describe infarction

A

Refers to the cause of necrosis, namely ischaemia. An area of tissue death caused by obstruction of the tissues blood supply is an infarct. Can lead to gangrene. Mostly due to thrombosis or embolism. Necrosis resulting can be coagulative or liquifactive.

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26
Q

Describe the 2 types of infarct

A

White (anaemic) - occurs in solid organs, after occlusion of an ‘end’ artery. White due to lack of blood in tissue.
Red (haemorrhagic) - occurs where there is extensive haemorrhage into dead tissue, e.g. In tissues with duel blood supply, if numerous anastomoses are present, loose tissue, previous congestion, raised Venus pressure. Secondary arterial supply insufficient to rescue tissue but does allow blood to enter dead tissue

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27
Q

What do the consequences of an infarct depend on?

A

Whether tissue effected has an alternative blood supply
How quickly ischaemia occurred (if slowly time for development of additional perfusion pathways?)
How vulnerable tissue is to hypoxia
O2 content of blood (more serious if anaemic patient)

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28
Q

List the principal molecules released by injured, dying and dead cells

A

Potassium - Ecell high conc. High concs reaching heart can cause MI. Can cause massive necrosis elsewhere
Enzymes - can indicate organ involved and extent
Myoglobin - released from myocardium/striated muscle, in large conc causes rhadbomyolysis. Can block renal tubules causing renal failure

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29
Q

Does apoptosis involve lysosomal enzymes

A

No

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30
Q

Does apoptosis require energy?

A

Yes

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31
Q

Describe the microscopic features of apoptosis

A

Chromatin condenses, pyknosis, karyorrhexis. Cytoplasmic budding (not blebbing as in oncosis!), progresses to fragmentation into membrane bound apoptotic bodies (containing cytoplasm, organelles and nuclear fragments), eventually removed by macrophage phagocytosis. No leakage of cell contents, so inflammation not induced

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32
Q

Name the key stages of apoptosis

A

Initiation
Execution
Degradation/phagocytosis

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33
Q

What are caspases?

A

Proteases that mediate the cellular effects of apoptosis. Act by cleaving proteins breaking up the cytoskeleton and initiating the degradation of DNA

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34
Q

Name the 2 key mechanisms for triggering apoptosis

A

Intrinsic and extrinsic

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35
Q

What is p53?

A

The ‘guardian of the genome’ - mediates apoptosis in response to DNA damage

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36
Q

What are cytochrome c, APAF1 and caspase 9 together?

A

Together they are the apotosome

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37
Q

Give an example of a death ligand

A

TRAIL

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38
Q

Give an example of a death receptor

A

TRAIL-R

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39
Q

Name the 5 main groups of intracellular accumulations

A
  1. Water and electrolytes
  2. Lipids
  3. Proteins
  4. ‘Pigments’
  5. Carbohydrates
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40
Q

What is lipofuscin

A

‘Age pigment’. Brown pigment seen in aging cells, sign of previous free radical injury. Yellow-brown grains in cytoplasm

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41
Q

What is haemosiderin?

A

Iron storage molecule. Forms when systemic (deposited everywhere, haemosiderosis, seen in conditions such as haemolytic anaemia of hereditary haemochromatosis)or local excess of iron.

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42
Q

Name the two types of pathological calcification

A

Dystrophic and metastatic

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43
Q

Describe dystrophic calcification

A

Occurs in dying tissue. No abnormality of Ca2+ metabolism, local changes to tissue favours nucleation of hydroxyapatite crystals. Can cause organ disfunction.

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44
Q

Describe metastatic calcification

A

Disturbance is body-wide. Hydroxyapatite crystals deposited in normal tissue throughout body. Hypercalcaemia secondary to disturbances in Ca2+ metabolism (e.g. Increased secretion of PTH, destruction of bone tissue)

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45
Q

Why can germ/stem cells replicate indefinitely?

A

Contain an enzyme called telomerase which maintains the original length of telomeres

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46
Q

Name 3 major effects of excessive alcohol on the liver

A

Fatty change
Acute alcoholic hepatitis
Cirrhosis

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47
Q

What is the main reparative mechanism in the CNS?

A

Gliosos

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48
Q

List some causes of acute inflammation

A 
Microbial infections
Hypersensitivity reactions
Physical agents 
Chemicals
Tissue necrosis
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49
Q

List the 4 main clinical signs of acute inflammation

A
  1. Rubor - redness
  2. Tumor - swelling
  3. Calor - heat
  4. Dolor - pain

Resulting loss of function

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50
Q

What are the 3 steps of acute inflammation?

A
  1. Changes in blood flow
  2. Exudate on of fluid into tissues
  3. Infiltration of inflammatory cells
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51
Q

What are the changes in blood flow which occur during acute inflammation?

A
  1. Initial brief vasoconstriction of arterioles
  2. Vasodilation of arterioles then capillaries (increased blood flow, heat and redness)
  3. Increased permeability of blood vessels (exudate on of protein rich fluid to tissues, slowing of circulation. Swelling)
  4. Increased viscosity of blood (increased conc. of RBC. = stasis)
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52
Q

Which cells release histamine? In response to what stimuli?

A

Mast cells, basophils and platelets

In response to physical damage, immunologic reactions, factors from neutrophils and platelets

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53
Q

What does histamine cause?

A

Vascular dilation
Transient increase in vascular permeability
Pain

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54
Q

Define oedema

A

Increased fluid in tissue spaces. Leads to increased lymphatic drainage

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55
Q

Describe the 2 forms of oedema

A

Transudate (same amount of protein as blood, present due to hydrostatic pressure imbalance)
Exudate (more protein than blood, type present in inflammation).

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56
Q

Describe the 5 mechanisms of vascular leakage

A
  1. Endothelial contraction (>gaps) - histamine, leukotrienes
  2. Cytoskeletal reorganisation (>gaps) - cytokines IL-1 and TNF
  3. Direct injury - toxic burns, chemicals
  4. Leukocyte (WBC) Dependent Injury - toxic O2 species and enzymes from leukocytes
  5. Increased transcytosis - channels across endothelial cytoplasm - VEGF
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57
Q

Give a synonym of ‘neutrophil’

A

Polymorph

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58
Q

Describe the 4 stages of neutrophil infiltration

A
  1. Marination - stasis causes neutrophils to line up at the edge of blood vessels, along the endothelium
  2. Rolling - neutrophils roll along endothelium, sticking intermittently
  3. Adhesion - neutrophils stick more avidly
  4. Emigration - neutrophils emigrate through blood vessel wall, infiltrate tissues
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59
Q

What is ‘diapedesis’

A

The digestion of the basement membrane by an infiltrating neutrophil

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60
Q

Define chemotaxis

A

Movement along concentration gradients of chemoattractants

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61
Q

Name some opsonins that aide phagocytosis by neutrophils

A

Fc (fixed component present in all antibodies)

C3b (form of complement)

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62
Q

What are the 2 major killing mechanisms of neutrophils?

A

O2 dependent - produces superoxide a and H2O2.

O2 independent - lysozyme and hydrolases, bacterial permeability increasing protein (BPI), cationic proteins

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63
Q

Name 2 chemical mediators that increase blood flow

A

Histamine

Prostaglandins

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64
Q

Name 2 chemical mediators that increase vascular permeability

A

Histamine

Leukotrienes

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65
Q

Name 3 chemical mediators which aide neutrophil chemotaxis

A

C5a
LTB4
Bacterial Peptides

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66
Q

Name a chemical mediator which aides phagocytosis by neutrophils

A

C3b

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67
Q

How does exudation of fluid help combat injury?

A

Delivers plasma proteins to site of injury (e.t. immunoglobulins, inflammatory mediators, fibrinogen)
Dilutes toxins
Increases lymphatic drainage

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68
Q

How does infiltration of cells help combat injury?

A

Removes pathogenic organisms and necrotic debris

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69
Q

Give 4 local complications of acute inflammation

A
  1. Swelling - could block tubes
  2. Exudate - serositis, compression
  3. Loss of fluid e.g. Burn
  4. Pain and loss of function
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70
Q

Name 3 systemic effects of acute inflammation

A

Fever
Leukocytosis
Acute phase response

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71
Q

Give 4 possible things which could occur after acute inflammation

A
  1. Complete resolution
  2. Continued acute inflammation with chronic inflammation - abscess
  3. Chronic inflammation with fibrous repair, tissue regeneration
  4. Death
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72
Q

What is chronic inflammation?

A

Chronic (>12wk) response to injury with associated fibrosis

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73
Q

List 3 ways chronic inflammation may arise

A
  1. Takes over from acute inflammation
  2. Arises de novo e.g. Chronic infection (TB), autoimmune (RA), chronic low level irritation (eg silica)
  3. Develop alongside acute inflammation e.g. On going bacterial infection.
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74
Q

List 5 cell types present in chronic inflammation

A
  1. Macrophages
  2. Lymphocytes (T&B)
  3. Eosinophils
  4. Plasma cells
  5. Fibroblasts/myofibroblasts
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75
Q

Name and describe 3 types of giant cell (formed by fusion of macrophages)

A
  1. Langhans (TB) - peripheral nuclei
  2. Foreign body type - random nuclei. Engulf foreign body if it’s small enough, otherwise sticks to edge of body.
  3. Touton (fat necrosis) - nuclei in ring towards centre. Form leisions where there is a high lipid content e.g. Fat necrosis, xanthomas.
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76
Q

List 4 consequences of chronic inflammation

A
  1. Fibrosis
  2. Impaired function
  3. Atrophy
  4. Stimulation of immune response
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77
Q

What is a granuloma?

A

A cohesive group of macrophages and other inflammatory cells

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78
Q

Under what circumstances do granulomas arise?

A

Persistent, low-grade antigenic stimulation or Hypersensitivity.
E.g.
Mildly irritant foreign material
Infections (some fungi, mycobacteria e.g. TB, leprosy)
Unknown causes, sarcoid, Crohn’s disease

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79
Q

Name 2 types of TB

A 
Miliary TB (many bugs)
Single organ TB (few bugs)
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80
Q

Which type of giant cell has peripheral nuclei?

A

Langhans

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81
Q

Which type of giant cell has randomly arranged nuclei?

A

Foreign body giant cells

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82
Q

Which type of giant cell has nuclei arranged in a ring towards the centre of the cell?

A

Touton

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83
Q

Define regeneration

A

The replacement of dead or damaged cells by functional, differentiated cells. Normal structure is restored.

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84
Q

Define repair

A

Response to injury involving both regeneration and fibrosis (scar formation). Normal structure is permanently altered.

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85
Q

Name and describe the 3 groups tissues of the body are divided into on the basis of their proliferative activity.

A
  1. Liable tissues (continuously dividing) - proliferate throughout life replacing cells that are destroyed e.g. Surface epithelia
  2. Stable tissues (quiescent tissues) - normally have a low level of replication but can undergo rapid division in response to stimuli and can reconstruct tissue of origin. E.g. Parenchymal cells of liver/kidney.
  3. Permanent tissues (non-dividing tissue) - contain cells that have left the cell cycle and can’t undergo mitotic division in postnatal life. E.g. Neurones, cardiac muscle cells.
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86
Q

Define unipotent

A

Can only produce one type of differentiated cell e.g. Epithelia

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87
Q

Define multipotent

A

Can produce several types of differentiated cell e.g. Haematopoietic

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88
Q

Define totipotent

A

Can produce any type of cell i.e. embryonic stem cells

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89
Q

Describe what an autocrine signal is

A

Cell responds to signal made by itself

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90
Q

Describe what a paracrine signal is

A

Cell produces signal which acts on nearby cells

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91
Q

Describe what an endocrine signal is

A

Endocrine organ produces signal which acts on cells far away

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92
Q

List the main components of fibrous repair

A

Cell migration
Blood vessels - angiogenesis
Extracellular matrix production & remodelling

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93
Q

What does VEGF stand for and what does it do?

A

Vascular Endothelial Growth Factor

Proangiogenic factor, initiates angiogenesis

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94
Q

Describe the 5 major stages of angiogenesis

A
  1. Endothelial proteolysis of basement membrane
  2. Migration of endothelial cell via chemotaxis
  3. Endothelial proliferation
  4. Endothelial maturation and tubular remodelling
  5. Recruitment of periendothelial cells.
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95
Q

Describe the 5 main stages of fibrous repair

A
  1. Phagocytosis of necrotic tissue debris
  2. Proliferation of endothelial cells which results in small capillaries that grow into the area (angiogenesis)
  3. Proliferation of fibroblasts and myofibroblasts that synthesise collagen and cause wound contraction (repair tissue at this stage is granulation tissue)
  4. Granulation tissue becomes less vascular and matures into a fibrous scar
  5. Scar matures and shrinks due to contraction of fibrils within myofibroblasts
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96
Q

List 5 functions of the extracellular matrix in wound repair

A
  1. Supports and anchors cells
  2. Separates tissue compartments
  3. Sequesters growth factors
  4. Allows communication between cells
  5. Facilitates cell migration
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97
Q

What types of collagen are fibrillar?

A

1-3

E.g. Dermis, bone

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98
Q

What types of collagen are amorphous?

A

4-6

E.g. Basement membrane

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99
Q

Describe the mechanism of fibrous repair

A
  1. Inflammatory cells infiltrate (blood clot forms, acute/chronic infection)
  2. Clot replaced by granulation tissue (angiogenesis, myo/fibroblasts migrate and differentiate, producing extracellular matrix)
  3. Maturation (relatively long lasting, collagen increases, cell pop. falls, myofibroblasts contract, vessels differentiate and are reduced, left with fibrous scar)
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100
Q

How are inflammatory cells recruited?

A

Chemotaxis

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101
Q

When are angiogenic cytokines produced?

A

In response to hypoxia

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102
Q

Describe healing by primary intention

A

Occurs in clean wounds with opposed edges. BM minimally obscured/minimal damage to BM. Minimal contraction &a scarring.
Risk of trapping infection (abscess) by epidermis regenerating over wound

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103
Q

Describe healing by secondary intention

A

Large wound, ulcer, infarct, abscess. Unapposed wound edges. Considerable contraction required to close wound edges (initially by blood clot, then myofibroblasts. Epidermis regenerates from the base up.
Much more granulation tissue produced than in primary intention, so takes much longer to heal.

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104
Q

List 6 local factors that might influence wound healing

A
  1. Type/size/location of wound
  2. Apposition (lack of movement)
  3. Blood supply (arterial/venous)
  4. Infection (suppuration, gangrene, systemic)
  5. Foreign material
  6. Radiation damage
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105
Q

List 6 general factors which might influence wound healing

A
  1. Age
  2. Drugs (e.g. Steroids) and hormones
  3. General dietary deficiencies (e.g. Protein)
  4. Specific dietary deficiencies (Vit. C, essential amino acids)
  5. General state of health (chronic diseases?)
  6. General cardiovascular status
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106
Q

What is wound dehiscence?

A

Separation of wound edges e.g. Abdominal insicion

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107
Q

List 5 possible complications of fibrous repair

A
  1. Formation of fibrous adhesions
  2. Loss of function due to replacement of specialised functional parenchymal cells by non-functional collagenous scar tissue
  3. Disruption of complex tissue relationships within an organ i.e. Distortion of architecture interfering with normal function
  4. Overproduction of fibrous scar tissue e.g. Keloid scar.
  5. Excessive scar contraction causing obstruction of tubes, disfiguring scars following burns or joint contracture a (fixed flextures)
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108
Q

What 4 factors does successful haemostasis depend upon?

A
  1. Vessel wall (constricts to limit blood loss)
  2. Platelets (adhere to damaged wall/each other)
  3. Coagulation system
  4. Fibrinolytic system (prevents too much haemostasis occurring)
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109
Q

Name the ‘important’ stages of the coagulation cascade

A

Prothrombin —> Thrombin
|
|
Fibrinogen —> Fibrin

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110
Q

Give 3 fundamental predisposing factors to thrombosis. What are these known as?

A
  1. Abnormalities of blood flow (stagnation, turbulence)
  2. Abnormalities of blood vessel wall (atheroma, direct injury, inflammation)
  3. Abnormalities of the constituents of the blood (smokers, post-partum, post-op)

Known as Virchow’s triad.

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111
Q

Tight regulation of thrombin is required (1ml of blood can generate enough thrombin to convert all the fibrinogen in the body to fibrin!). How is this achieved?

A

Balance of procoagulant and anticoagulant forces.
E.g. Thrombin inhibitors:
Anti-thrombin III
Protein C and S

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112
Q

What is fibrinolysis?

A

The breakdown of fibrin

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113
Q

What do plasminogen activators do?

A

Convert plasminogen into its active form, plasmin, which is then used in fibrinolysis.

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114
Q

Define thrombosis

A

The formation of a solid mass of blood within the circulatory system DURING LIFE

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115
Q

Describe the appearance of an arterial thrombi

A

Pale
Granular
Lines of Zahn
Lower cell content

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116
Q

Describe the appearance of venous thrombi

A

Soft
Gelatinous
Deep red
Higher cell content

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117
Q

What are the 5 possible outcomes of thrombosis?

A

Lysis (complete dissolution of thrombus, fibrinolytic systems activate, bloodflow re-established. Most likely when thrombi are small)
Propagation (progressive spread of thrombosis, in direction of blood flow)
Organisation (reparative process, ingrowth of fibroblasts and capillaries, lumen remains obstructed)
Recanalisation (bloodflow re-established but usually incompletely, one or more channels formed through organising thrombus)
Embolism (part of thrombus breaks off, travels through bloodstream, lodges at distant site)

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118
Q

What are the effects of arterial thrombosis?

A

Ischaemia
Infarction
Depends on site and collateral circulation

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119
Q

What are the effects of venous thrombosis?

A

Congestion
Oedema
Ischaemia
Infarction (rare, consequence of built up tissue pressure)

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120
Q

Define embolism

A

The blockage of a blood vessel by solid, liquid or gas, at a site distant from its origin.

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121
Q

What % of emboli are thrombo-emboli?

A

> 90%

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122
Q

Name 6 possible types of embolism

A 
Thrombo
Air
Amniotic fluid
Nitrogen ('benz')
Medical equipment
Tumour cells
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123
Q

List predisposing factors for deep vein thrombosis

A 
Immobility
Post-operative
Pregnancy and post-partum
Oral contraceptives
Severe burns
Cardiac failure
Disseminated cancer
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124
Q

How can deep vein thrombosis be treated?

A

Intravenous heparin

Oral warfarin

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125
Q

Define atheroma

A

The accumulation of intracellular and extracellular lipid in the intima and media of large and medium sized arteries

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126
Q

Define atherosclerosis

A

The thickening and hardening of arterial walls as a consequence of atheroma

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127
Q

Define arteriosclerosis

A

The thickening of the walls of arteries and arterioles usually as a result of hypertension or diabetes mellitus

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128
Q

Describe the macroscopic features of atheroma

A

Fatty streak - yellow, slightly raised, lipid deposits in intima
Simple plaque - raised yellow/white, irregular outline, widely distributed, enlarge and coalesce
Complicated plaque - thrombosis, haemorrhage into plaque, calcification, aneurysm formation

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129
Q

List common sites for atheroma

A 
Aorta (especially abdominal)
Coronary arteries
Carotid arteries
Cerebral arteries
Leg arteries
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130
Q

Describe the microscopic early changes of atheroma

A

Proliferation of smooth muscle cells
Accumulation of foam cells
Extracellular lipid

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131
Q

Describe the later microscopic changes of atheroma

A 
Fibrosis
Necrosis
Cholesterol clefts
Inflammatory cells
Disruption of internal elastic lamina
Damage extends into media
Ingrowth of blood vessels
Plaque fissuring
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132
Q

What is intermittent claudication? (With reference to peripheral vascular disease)

A

Pain in legs due to reduced blood supply. Pain goes away on resting.

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133
Q

List risk factors for atheroma

A 
Age
Gender (women protected before menopause)
Hyperlipidaemia
Hypertension (endothelial damage)
Infection
Obesity
Lack of exercise
Oral contraceptives
Genetics/family history
Alcohol
Diabetes mellitus
Smoking
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134
Q

What (6) cells are involved in atheroma formation?

A 
Endothelial cells 
Platelets
Smooth muscle cells
Macrophages
Lymphocytes
Neutrophils
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135
Q

What role do endothelial cells have in atheroma formation?

A

Key role in haemostasis
Altered permeability to lipoproteins
Production of collagen
Stimulation of proliferation and migration of smooth muscle cells

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136
Q

What role do platelets have in the formation of atheroma?

A

Key role in haemostasis

Stimulate proliferation and migration of smooth muscle cells

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137
Q

What role do smooth muscle cells have in the formation of atheroma?

A

Take up LDL and other lipid to become foam cells

Synthesise collagen and proteoglycans

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138
Q

What role do macrophages have in the formation of atheroma?

A

Oxidise LDL
Take up lipid to become foam cells
Secrete proteases which modify matrix
Stimulate proliferation and migration of smooth muscle cells

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139
Q

What role do lymphocytes have in the formation of atheroma?

A

TNF may affect lipoprotein metabolism

Stimulate proliferation and migration of smooth muscle cells

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140
Q

What role do neutrophils have in the formation of atheroma?

A

Secrete proteases leading to continued local damage and inflammation

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141
Q

Describe the unifying theory of atheroma formation

A

Endothelial damage occurs
Endothelial damage causes platelet adhesion, smooth muscle cell (SMC) proliferation and migration. Insudation of lipid, LDL oxidation, so uptake of lipid by SMC and macrophages
Stimulated SMC produce matrix material
Foam cells secrete cytokines causing further SMC stimulation and recruitment of other inflammatory cells

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142
Q

What may cause endothelial damage?

A

Raised LDL
Toxins, e.g. Cigarette smoke
Hypertension
Haemodynamic stress

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143
Q

What do the size of cell populations depend upon?

A

Rate or cell proliferation, cell differentiation and cell death by apoptosis

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144
Q

What regulates normal cell proliferation?

A

Proto-oncogenes

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145
Q

Give the possible outcomes of signalling biochemistry (4 points)

A

Divide (enter the cell cycle)
Differentiate (take on a specialised form and function)
Survive (resist apoptosis)
Die (undergo apoptosis)

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146
Q

List the 3 ways cell to cell signalling can be via

A
  1. Hormones
  2. Local mediators
  3. Direct cell-cell or cell-stroma contact
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147
Q

Signalling molecules binding to receptors results in what?

A

Modulation of gene expression

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148
Q

List functions of a cell that growth factors can affect

A 
Cell proliferation and inhibition
Locomotion
Contractility
Differentiation
Viability
Angiogenesis
Activation
149
Q

How does an increase in cell growth occur once cells are instructed to divide?

A

Shortening cell cycle

Conversion of quiescent cells to proliferating cells, making them enter the cell cycle too

150
Q

What is the most critical ‘checkpoint’ in the cell cycle?

A

The restriction point, towards the end of G1

151
Q

What are labile cell populations?

A

Stem cells that divide persistently to replenish losses

152
Q

What are stable cell populations?

A

Stem cells, normally quiescent or proliferate very slowly, but proliferate persistently when required

153
Q

What are permanent cell populations?

A

Stem cells present, but cannot mount an effective proliferative response to significant cell loss.

154
Q

Name the 5 important types of cell adaptation

A
  1. Regeneration - cells multiply to replace loses
  2. Hyperplasia - cells increase in number above normal
  3. Hypertrophy - cells increase in size
  4. Atrophy - cells become smaller
  5. Metaplasia - cells are replaced by cells of a different type
155
Q

Are regenerated cells as good as the original cells?

A

Usually, but not always, and not immediately

156
Q

What is aplasia?

A

Complete failure of a specific tissue or organ to develop, embryological developmental disorder. Term also used to describe an organ whose cells have ceased to proliferate.

157
Q

What is hypoplasia?

A

Congenital underdevelopment/incomplete development of a tissue or organ at the embryological stage. Inadequate number of cells within tissue present.

158
Q

What is involution?

A

Normal programmed shrinkage of an organ (overlaps with atrophy) e.g. Uterus after childbirth

159
Q

What is atresia?

A

‘No orifice’, congenital inperforation of an opening

160
Q

What is dysplasia?

A

Abnormal maturation of cells within a tissue. Potentially reversible, although often pre-cancerous

161
Q

Define neoplasm

A

An abnormal growth of cells that persists after the initial stimulus is removed

162
Q

Define malignant neoplasms

A

‘An abnormal growth of cells that persists after the initial stimulus is removed’ AND invades surrounding tissue with potential to spread to distant sites.

163
Q

What is a tumour?

A

Any clinically detectable lump or swelling

A neoplasm is just one type of tumour

164
Q

What is cancer?

A

Any malignant neoplasm

165
Q

What is a metastasis?

A

A malignant neoplasm that has spread from its original site to a new non-contiguous site.
Original location = Primary site
New location = Secondary site

166
Q

What is dysplasia?

A

A pre-neoplastic alteration in which cells show disordered tissue organisation. Not a neoplastic change as is reversible

167
Q

What is a benign neoplasm?

A

Remains confined to its site of origin, does not produce metastases

168
Q

What is a malignant neoplasm?

A

Has the potential to metastasise

169
Q

Describe the appearance of a benign neoplasm, to naked eye and microscopically

A

Eye: Confined to local area, so have pushing outer margin.
Microscopically: Cells closely resemble the parent tissue (still well differentiated)

170
Q

Describe the appearance of a malignant tumour, to the naked eye and microscopically

A

Eye: Have an irregular outer margin and shape. May show areas of necrosis and ulceration (if on a surface).
Microscopically: range from well to poorly differentiated.

171
Q

What are cells that show no resemblance to any tissue called?

A

Anaplastic

172
Q

Describe what one would see in worsening cell differentiation

A

Increasing nuclear size
Increasing nuclear to cytoplasmic ratio
Increased nucleus staining (hyperchromasia)
More mitotic figures
Increased variation in size and shape of cells and nuclei (pleomorphism)

173
Q

Define neoplasm

A

An abnormal growth of cells that persists after the initial stimulus is removed

174
Q

Define malignant neoplasms

A

‘An abnormal growth of cells that persists after the initial stimulus is removed’ AND invades surrounding tissue with potential to spread to distant sites.

175
Q

What is a tumour?

A

Any clinically detectable lump or swelling

A neoplasm is just one type of tumour

176
Q

What is cancer?

A

Any malignant neoplasm

177
Q

What is a metastasis?

A

A malignant neoplasm that has spread from its original site to a new non-contiguous site.
Original location = Primary site
New location = Secondary site

178
Q

What is dysplasia?

A

A pre-neoplastic alteration in which cells show disordered tissue organisation. Not a neoplastic change as is reversible

179
Q

What is a benign neoplasm?

A

Remains confined to its site of origin, does not produce metastases

180
Q

What is a malignant neoplasm?

A

Has the potential to metastasise

181
Q

Describe the appearance of a benign neoplasm, to naked eye and microscopically

A

Eye: Confined to local area, so have pushing outer margin.
Microscopically: Cells closely resemble the parent tissue (still well differentiated)

182
Q

Describe the appearance of a malignant tumour, to the naked eye and microscopically

A

Eye: Have an irregular outer margin and shape. May show areas of necrosis and ulceration (if on a surface).
Microscopically: range from well to poorly differentiated.

183
Q

What are cells that show no resemblance to any tissue called?

A

Anaplastic

184
Q

Describe what one would see in worsening cell differentiation

A

Increasing nuclear size
Increasing nuclear to cytoplasmic ratio
Increased nucleus staining (hyperchromasia)
More mitotic figures
Increased variation in size and shape of cells and nuclei (pleomorphism)

185
Q

How does neoplasia arise?

A

Caused by accumulated mutations in somatic cells. Mutations are caused by initiators (mutagenic agents), and promoters (which cause cell proliferation).

186
Q

What is progression?

A

The process through which a neoplasm emerges via a monoclonal population. Characterised by the accumulation of yet more mutations

187
Q

What does monoclonal mean?

A

Body of cells all originates from a single cell

188
Q

What is the bronchial circulation and what does it do?

A

Part of the systemic circulation, meets the metabolic requirements of the lungs

189
Q

What is the average pressure in the pulmonary artery? In mmHg

A

15-30
___________
4-12

190
Q

What is the average pressure in the right ventricle? In mmHg

A

15-30
__________
0-8

191
Q

What is the average pressure in the aorta? In mmHg

A

100-140
______________
60-90

192
Q

What is the average pressure in the left ventricle? In mmHg

A

100-140
_____________
1-10

193
Q

What is the average pressure in the left atrium? In mmHg

A

1-10

194
Q

What is the average pressure in the right atrium? In mmHg

A

0-8

195
Q

What are the features and function of the pulmonary circulation?

A

Supplies blood to alveoli for gas exchange. Works with low pressure (prevents rupture of thin alveolar linings) and low resistance (many parallel capillaries, relatively little smooth muscle in arterioles, short wide vessels)

196
Q

What is the V/Q ratio?

A

Ventilation/perfusion ratio

197
Q

What is the optimum value for the V/Q ratio? Maintaining this means what?

A

0.8

Maintaining this means diverting blood from alveoli which are not well ventilated

198
Q

Describe hypoxic pulmonary vasoconstriction

A

Alveolar hypoxia results in vasoconstriction of pulmonary vessels. Ensures perfusion matches ventilation, poorly ventilated alveoli are less well perfused. Most important mechanism regulating pulmonary vascular tone, helps to optimise gas exchange

199
Q

When might chronic hypoxic vasoconstriction occur, and what can it cause?

A

Can occur at altitude or as a consequence of lung disease. Can cause right ventricular failure (chronic increase in vascular resistance leads to chronic pulmonary hypertension, leads to high after load on right ventricle..)

200
Q

Describe the effects of exercises on pulmonary circulation

A

Increases cardiac output
Small increase in pulmonary arterial pressure
Opens apical capillaries
Increased O2 uptake by lungs
As bloodflow increases, capillary transit time is reduced (from ~1s at rest to ~0.3s without compromising gas exchange)

201
Q

What minimises the formation of lumping lymph (pulmonary oedema) normally?

A

Low capillary pressure (9-12mmHg normally)

202
Q

What is mitral valve stenosis, and what might it cause?

A

Abnormal narrowing of the mitral valve

Can lead to pulmonary oedema

203
Q

What can you do to relieve symptoms of pulmonary oedema?

A

Use diuretics to relieve symptoms. Treat underlying cause if possible

204
Q

What % of cardiac output does the brain demand?

A

15%

205
Q

How is the cerebral circulation demand for O2 met?

A

High capillary density
High basal flow rate (x10 for rest of body)
High O2 extraction (35% above average)

206
Q

How long before hypoxia leads to irreversible damage to neurones?

A

~4mins

207
Q

How is s secure cerebral blood supply ensured?

A

Structurally - anastomoses between basilar and internal carotid arteries
Functionally - myogenic auto regulation maintains perfusion during hypotension

208
Q

Below what blood pressure will cerebral autoregulation of bloodflow fail?

A

Below 50mmHg

209
Q

What is hypercapnia?

A

Increase in concentration of CO2 in the blood

210
Q

What is hypocapnia?

A

Decrease in the concentration of CO2 in the blood

211
Q

What is the response of the cerebral vessels to hypercapnia?

A

Vasodilatation

212
Q

What is the response of the cerebral vessels to hypocapnia?

A

Vasoconstriction

213
Q

What is adenosine?

A

A powerful vasodilator of cerebral arterioles

214
Q

Describe cushings reflex

A

Increases in intracranial pressure impairs cerebral blood flow. Impaired bloodflow to vasomotor control regions of the brainstem increases sympathetic vasomotor activity (increasing arterial blood pressure, helping to maintain cerebral blood flow)

215
Q

What is the bronchial circulation and what does it do?

A

Part of the systemic circulation, meets the metabolic requirements of the lungs

216
Q

What is the average pressure in the pulmonary artery? In mmHg

A

15-30
___________
4-12

217
Q

What is the average pressure in the right ventricle? In mmHg

A

15-30
__________
0-8

218
Q

What is the average pressure in the aorta? In mmHg

A

100-140
______________
60-90

219
Q

What is the average pressure in the left ventricle? In mmHg

A

100-140
_____________
1-10

220
Q

What is the average pressure in the left atrium? In mmHg

A

1-10

221
Q

What is the average pressure in the right atrium? In mmHg

A

0-8

222
Q

What are the features and function of the pulmonary circulation?

A

Supplies blood to alveoli for gas exchange. Works with low pressure (prevents rupture of thin alveolar linings) and low resistance (many parallel capillaries, relatively little smooth muscle in arterioles, short wide vessels)

223
Q

What is the V/Q ratio?

A

Ventilation/perfusion ratio

224
Q

What is the optimum value for the V/Q ratio? Maintaining this means what?

A

0.8

Maintaining this means diverting blood from alveoli which are not well ventilated

225
Q

Describe hypoxic pulmonary vasoconstriction

A

Alveolar hypoxia results in vasoconstriction of pulmonary vessels. Ensures perfusion matches ventilation, poorly ventilated alveoli are less well perfused. Most important mechanism regulating pulmonary vascular tone, helps to optimise gas exchange

226
Q

When might chronic hypoxic vasoconstriction occur, and what can it cause?

A

Can occur at altitude or as a consequence of lung disease. Can cause right ventricular failure (chronic increase in vascular resistance leads to chronic pulmonary hypertension, leads to high after load on right ventricle..)

227
Q

Describe the effects of exercises on pulmonary circulation

A

Increases cardiac output
Small increase in pulmonary arterial pressure
Opens apical capillaries
Increased O2 uptake by lungs
As bloodflow increases, capillary transit time is reduced (from ~1s at rest to ~0.3s without compromising gas exchange)

228
Q

What minimises the formation of lumping lymph (pulmonary oedema) normally?

A

Low capillary pressure (9-12mmHg normally)

229
Q

What is mitral valve stenosis, and what might it cause?

A

Abnormal narrowing of the mitral valve

Can lead to pulmonary oedema

230
Q

What can you do to relieve symptoms of pulmonary oedema?

A

Use diuretics to relieve symptoms. Treat underlying cause if possible

231
Q

What % of cardiac output does the brain demand?

A

15%

232
Q

How is the cerebral circulation demand for O2 met?

A

High capillary density
High basal flow rate (x10 for rest of body)
High O2 extraction (35% above average)

233
Q

How long before hypoxia leads to irreversible damage to neurones?

A

~4mins

234
Q

How is s secure cerebral blood supply ensured?

A

Structurally - anastomoses between basilar and internal carotid arteries
Functionally - myogenic auto regulation maintains perfusion during hypotension

235
Q

Below what blood pressure will cerebral autoregulation of bloodflow fail?

A

Below 50mmHg

236
Q

What is hypercapnia?

A

Increase in concentration of CO2 in the blood

237
Q

What is hypocapnia?

A

Decrease in the concentration of CO2 in the blood

238
Q

What is the response of the cerebral vessels to hypercapnia?

A

Vasodilatation

239
Q

What is the response of the cerebral vessels to hypocapnia?

A

Vasoconstriction

240
Q

What is adenosine?

A

A powerful vasodilator of cerebral arterioles

241
Q

Describe cushings reflex

A

Increases in intracranial pressure impairs cerebral blood flow. Impaired bloodflow to vasomotor control regions of the brainstem increases sympathetic vasomotor activity (increasing arterial blood pressure, helping to maintain cerebral blood flow)

242
Q

When does bloodflow through the left coronary arterie occur mainly?

A

Diastole

243
Q

How is the demand for O2/nutrients met by the coronary circulation?

A

High capillary density facilitates efficient O2 delivery

Diffusion distance

244
Q

Coronary arteries dilate due to hyperaemia. List some vasodilators of coronary arteries…

A

Adenosine
High [K+]
Low pH

245
Q

What type of arteries are coronary arteries?

A

Functional end arteries

246
Q

How is the large range or bloodflow to skeletal muscle achieved?

A

High vascular tone (permits lots of dilation)

At rest, only 1/2 of capillaries are perfused at any one time, allows for increased recruitment

247
Q

List vasodilators for skeletal muscle

A 
High [K+]
Increased osmolarity
Inorganic phosphates
Adenosine
Adrenaline (skeletal muscle specific via beta2 receptors)
High [H+]
248
Q

What are artereovenous anastomoses and what do they do?

A

Blood vessels under skin involved in temperature regulation. Under (sympathetic) neural control (decrease in core temperature increases sympathetic tone in AVAs, decreasing blood flow to apical skin)

249
Q

What are the major contents of the extracellular matrix, and what do they do?

A

Matrix glycoproteins - organise and orientate cells, e.g. Figronectin, laminin
Proteoglycans - matrix organisation, cell support, regulation of growth factors e.g. Heparin
Elastin - provides tissue elasticity

250
Q

What is most likely to kill you with a malignant neoplasm?

A

Tumour burden - vast numbers of ‘parasitic’ malignant cells (number of which greatly increased by ability to spread to distant sites)

251
Q

What 3 main stages are there in the process of malignant cells getting from a primary site to a secondary site?

A
  1. Grow and invade at the primary site
  2. Enter a transport system and lodge at a secondary site
  3. Grow at the secondary site to form a new tumour (colonisation)
252
Q

Why is the process of malignant cells getting from a primary site to a secondary site inefficient?

A

Cells must evade destruction by immune cells at all points

253
Q

Reduction in expression of what enables altered adhesion between malignant cells?

A

E-cadherin

254
Q

Altered adhesion between malignant cells and stromal proteins involves changes in what expression?

A

Integrin

255
Q

What proteins are involved in the degradation of basement membrane and stroma in the invasion of malignant neoplasms?

A

Altered expression of proteases, notably matrix metalloproteinases (MMPs)

256
Q

What is a cancer niche and what does it do?

A

Nearby cells taken advantage of by malignant cells (together form cancer niche). Provide some growth factors and proteases.

257
Q

How does signalling through integrins occur?

A

Via small G-proteins e.g. Members of the Rho family

258
Q

What does altered motality in malignant neoplasms involve?

A

Changes in the actin cytoskeleton

259
Q

Transport to distant sites can occur via malignant cells entering:

A

Blood vessels via capillaries and venules
Lymphatic vessels
Fluid in body cavities (pleura, peritoneal, pericardial, brain ventricles), known as transcoelomic spread

260
Q

What is extravasation?

A

The process by which a malignant neoplastic cell gets out of a vessel at secondary site

261
Q

What are micrometastases?

A

Surviving microscopic deposits that fail to grow

262
Q

What is tumour dormancy?

A

An apparently disease free person may harbour many micrometastases

263
Q

What does the secondary site of a neoplasm depend on?

A

Regional drainage of blood (often next capillary bed), lymph (lymph nodes), or coelomic fluid (other areas in coelomic space)
‘Seed and soil’ - due to interactions between malignant cells and the local tumour environment (is niche) at secondary site.

264
Q

How do carcinomas typically spread via first?

A

Lymphatics first

265
Q

How do sarcomas generally spread via?

A

Blood stream

266
Q

What are common sites for blood borne metastasis?

A

Lung, bone, liver, brain

267
Q

Name some neoplasms that commonly spread to bone

A

Breast, bronchus, kidney, thyroid, prostate

268
Q

What is likelihood of metastasis dependent on?

A

Type of malignant tumour

Size of primary neoplasm (basis of cancer scaling)

269
Q

What are direct local effects of a neoplasm caused by?

A

Due to primary &/or secondary neoplasm

270
Q

What are indirect systemic effects of a neoplasm caused by?

A

Increasing tumour burden
Secreted hormones
Miscellaneous

271
Q

What are indirect systemic effects of a neoplasm sometimes referred to?

A

Paraneoplastic syndromes

272
Q

Give examples of local effects caused by neoplasms

A

Direct invasion and destruction of normal tissue
Ulceration at a surface, leading to bleeding
Compression of adjacent structures
Blocking tubes & orifices

273
Q

What is most likely to kill you with a malignant neoplasm?

A

Tumour burden - vast numbers of ‘parasitic’ malignant cells (number of which greatly increased by ability to spread to distant sites)

274
Q

What 3 main stages are there in the process of malignant cells getting from a primary site to a secondary site?

A
  1. Grow and invade at the primary site
  2. Enter a transport system and lodge at a secondary site
  3. Grow at the secondary site to form a new tumour (colonisation)
275
Q

Why is the process of malignant cells getting from a primary site to a secondary site inefficient?

A

Cells must evade destruction by immune cells at all points

276
Q

Reduction in expression of what enables altered adhesion between malignant cells?

A

E-cadherin

277
Q

Altered adhesion between malignant cells and stromal proteins involves changes in what expression?

A

Integrin

278
Q

What proteins are involved in the degradation of basement membrane and stroma in the invasion of malignant neoplasms?

A

Altered expression of proteases, notably matrix metalloproteinases (MMPs)

279
Q

What is a cancer niche and what does it do?

A

Nearby cells taken advantage of by malignant cells (together form cancer niche). Provide some growth factors and proteases.

280
Q

How does signalling through integrins occur?

A

Via small G-proteins e.g. Members of the Rho family

281
Q

What does altered motality in malignant neoplasms involve?

A

Changes in the actin cytoskeleton

282
Q

Transport to distant sites can occur via malignant cells entering:

A

Blood vessels via capillaries and venules
Lymphatic vessels
Fluid in body cavities (pleura, peritoneal, pericardial, brain ventricles), known as transcoelomic spread

283
Q

What is extravasation?

A

The process by which a malignant neoplastic cell gets out of a vessel at secondary site

284
Q

What are micrometastases?

A

Surviving microscopic deposits that fail to grow

285
Q

What is tumour dormancy?

A

An apparently disease free person may harbour many micrometastases

286
Q

Give examples of local effects caused by neoplasms

A

Direct invasion and destruction of normal tissue
Ulceration at a surface, leading to bleeding
Compression of adjacent structures
Blocking tubes & orifices

287
Q

What are indirect systemic effects of a neoplasm sometimes referred to?

A

Paraneoplastic syndromes

288
Q

What are indirect systemic effects of a neoplasm caused by?

A

Increasing tumour burden
Secreted hormones
Miscellaneous

289
Q

What are direct local effects of a neoplasm caused by?

A

Due to primary &/or secondary neoplasm

290
Q

What is likelihood of metastasis dependent on?

A

Type of malignant tumour

Size of primary neoplasm (basis of cancer scaling)

291
Q

Name some neoplasms that commonly spread to bone

A

Breast, bronchus, kidney, thyroid, prostate

292
Q

What are common sites for blood borne metastasis?

A

Lung, bone, liver, brain

293
Q

How do sarcomas generally spread via?

A

Blood stream

294
Q

How do carcinomas typically spread via first?

A

Lymphatics first

295
Q

What does the secondary site of a neoplasm depend on?

A

Regional drainage of blood (often next capillary bed), lymph (lymph nodes), or coelomic fluid (other areas in coelomic space)
‘Seed and soil’ - due to interactions between malignant cells and the local tumour environment (is niche) at secondary site.

296
Q

What are the 5 leading behavioural & dietary risks which lead to 30% of cancer deaths?

A 
High BMI
Low fruit and veg
Lack of physical activity
Tabacco use
Alcohol use
297
Q

What are the 3 main categories for extrinsic cancer risk factors?

A

Chemicals
Radiation
Infections

298
Q

What characteristics are shown for exposure to some extrinsic factors causing cancer?

A

Risk of cancer depends on total carcinogen dosage
Long delay between carcinogen exposure used and malignant neoplasm onset
Sometimes organ specificity for particular carcinogens is seen

299
Q

What organ specificity does the cancer induced by 2-napthylamine (industrial carcinogen used in dyes)

A

Bladder cancer

300
Q

What are initiators?

A

Mutagens

301
Q

What do promotors cause?

A

Prolonged proliferation in target tissues

302
Q

What are the 5 ways to classify mutagenic chemical carcinogens

A 
Polycyclic aromatic hydrocarbons
Aromatic amines
N-nitroso compounds
Alkylating agents
Natural products
303
Q

What in the liver converts pro-carcinogens to carcinogens?

A

Cytochrome P450 enzymes

304
Q

What are compete carcinogens?

A

Carcinogens which act as both initiators and promotors

305
Q

What is radiation?

A

Any form of energy travelling through space

306
Q

How may radiation damage DNA?

A

Can damage DNA bases
Cause single, and double strand DNA breaks
Indirect DNA damage via free radicals

307
Q

Give an example of a virus that acts as a direct carcinogen

A

HPV (Human Papilloma Virus)

Expresses E6 & E7 proteins that inhibit p53 & pRB protein function (important for cell proliferation)

308
Q

Give 2 examples of 2 infections that can indirectly cause cancer?

A

Hep B & C - cause chronic liver cell injury & regeneration
HIV - lowers immunity, enabling other potentially carcinogenic infections to occur

309
Q

How many alleles must be inactivated in order for tumour suppressor genes to permit cancer growth?

A

Both alleles

310
Q

How many alleles must be inactivated in order for proto-oncogenes to permit cancer growth?

A

Only one allele

311
Q

What is RAS?

A

An oncogene that encodes a small G protein that relays signal into the cell, eventually pushing cell past cell cycle restriction point

312
Q

What does the RB gene do?

A

Restricts cell proliferation by inhibiting passage through restriction point

313
Q

What is xeroderma pigmentosum (XP)?

A

Autosomal recessive. Mutation in DNA repair genes (nucleotide excision repair). Patients are very sensitive to UV light

314
Q

Describe hereditary non-polyposis colon cancer (HNPCC) syndrome

A

Autosomal dominant

Associated with colon carcinoma and the germline mutation affects 1 of several DNA mismatch repair genes

315
Q

Familial breast carcinoma is associated with which genes? What do they do?

A

BRCA1 or BRCA 2

Important for repairing double stranded DNA breaks

316
Q

What is progression?

A

Mutations occur during sequence (time frame often decades); step wise accumulation of mutations in malignant neoplasms

317
Q

What are the 6 hallmarks of cancer? Plus one enabling factor

A
  • Self-sufficiency in growth signals
  • Resistance to growth stop signals
  • No limit on the number of times a cell can divide (cell immortalisation)
  • Sustained ability to induce new blood vessels (angiogenesis)
  • Resistance to apoptosis
  • Ability to invade and produce metastasis
    + Genetic instability
318
Q

Name 7 factors protooncogenes/tumour suppressor genes may effect

A
  • Growth factors
  • Growth factor receptors
  • Plasma membrane signal transducers
  • Intracellular kinases
  • Transcription factors
  • Cell cycle regulators
  • Apotosis regulators
319
Q

What are the 4 types of cancer that make up 54% of all cancer incidence in the UK?

A

Lung
Breast
Prostate
Bowel

320
Q

What are the most common types of cancer in children under 14?

A

Leukaemias
CVS tumours
Lymphomas

321
Q

What is ‘Ann Arbor’ staging used for?

A

Lymphoma

322
Q

What is ‘Dukes staging’ used for?

A

Colorectal carcinoma

323
Q

Describe the Ann Arbor staging system

A

Stage 1: lymphoma in a single node region
Stage 2: lymphoma in separate regions, on one side of the diaphragm
Stage 3: lymphoma spread to both sides of the diaphragm
Stage 4: diffuse or disseminated involvement of one or more extra-lymphatic organs e.g. bone marrow, lungs

324
Q

Describe the Dukes staging system

A

Dukes A: invasion of lamina propria (not through bowel)
Dukes B: invasion of muscularis propria (through bowel wall)
Dukes C: involvement of lymph nodes
Dukes D: distant metastasis

325
Q

What is grading used to determine?

A

How differentiated a carcinoma is

326
Q

Describe the general grading system

A

G1: well differentiated
G2: moderately differentiated
G3: poorly differentiated
G4: anaplastic (undifferentiated)

327
Q

What is the Bloom-Richardson system used for?

A

Grading of breast carcinoma

328
Q

Describe the Bloom-Richardson grading system

A

Grade 1: tubules
Grade 2: mitoses
Grade 3: nuclear pleomorphism

329
Q

What is adjuvant treatment?

A

Treatment given after surgical removal of a primary tumour to eliminate subclinical disease

330
Q

What is neoadjuvant treatment?

A

Treatment given to reduce the size of a primary tumour prior to surgical excision

331
Q

Why is radiotherapy given in fractionated doses?

A

Minimise normal tissue damage

332
Q

What form of radiation is used in radiotherapy?

A

Ionising radiation (e.g. X-rays)

333
Q

How does radiotherapy kill cells?

A

High doses causes direct, or feed radical induced DNA damage, that is detected by the cell cycle check points, triggering apoptosis (especially in G2 of cell cycle).
Double stranded DNA breakages cause damaged chromosomes that prevents M phase from completing correctly

334
Q

How do antimetabolite chemotherapy drugs work?

A

Mimic normal substrates involved in DNA replication

335
Q

How do alkylation and platinum based chemotherapy drugs work?

A

Cross lint the 2 strands of DNA helix

336
Q

How do plant-based chemotherapy drugs work?

A

Blocks microtubule assembly, interfering with mitotic spindle formation

337
Q

How might antibiotic chemotherapy drugs work?

A

Inhibit DNA topoisomerase (doxorubicin)

Cause double stranded DNA breaks (bleomycin)

338
Q

How might hormone therapy be used to treat breast carcinoma?

A

Hormone receptor-positive breast cancer.
Selective oestrogen receptor modulators (SERMs) bind to oestrogen receptors, preventing oestrogen from binding (e.g. Tamoxifen)

339
Q

What is oncogene targeting?

A

Identifying cancer-specific alterations e.g. Oncogene mutations, provides an opportunity to target drugs specifically at cancer cells

340
Q

What can tumour markers be used for?

A

Diagnosis

Monitoring tumour burden during treatment and follow up

341
Q

What might tumour markers be?

A

Hormones
‘Oncofetal’ antigens
Specific proteins
Mucins/glycoproteins

342
Q

What are possible problems caused by cancer screening?

A

Lead time bias
Length bias
Over diagnosis (might never effect patient at all anyways)

343
Q

What cancers are screened for in the UK?

A

Cervical
Breast (50-70yrs, every 3 yrs)
Bowel (60-74yrs, every 2 yrs)

344
Q

What is karryohexis?

A

The destructive fragmentation of the nucleus of a dying cell, whereby the chromatin is distributed irregularly throughout the cytoplasm

345
Q

What is karyolysis?

A

Dissolution of a cell nucleus

346
Q

What is pyknosis (karyopyknosis)?

A

The irreversible condensation of chromatin in the nucleus of a cell undergoing necrosis or apoptosis. Followed by karyorrhexis (fragmentation of nucleus)

347
Q

What is a sarcoma?

A

Cancer of soft tissue, connective tissue or bone

348
Q

What is the normal capillary pressure in the lungs?

A

9-12mmHg

349
Q

What is human chorionic gonadotropin a tumour marker for?

A

Trophoblastic tumours

Non-seminomatous germ cell tumours of the testes

350
Q

What is calcitonin a tumour marker for?

A

Medullary carcinoma of the thyroid

351
Q

What are catecholamines and metabolites tumour markers for?

A

Phaeochromocytoma and related
Liver cell carcinoma
Non-seminomatous germ cell tumour of the testes

352
Q

What is carcinoembryonic antigen a tumour marker for?

A

Colon cancer

353
Q

What is prostate specific antigen a tumour marker for?

A

Prostate cancer

354
Q

What is CA-125 a tumour marker for?

A

Ovarian cancer

355
Q

What is CA19.9 a tumour marker for?

A

Pancreatic cancer

356
Q

What must first happen to neutrophils before infiltration?

A

They must be activated (switched to a higher metabolic state)

357
Q

What are the signs and symptoms of the acute phase response?

A

Decreased appetite, raised pulse rate, altered sleep patterns, changes in plasma concentrations of acute phase proteins

358
Q

When is complete resolution impossible?

A

When tissue architecture has been damaged/destroyed

359
Q

What are the 4 types of exudate?

A

Pus/abscess - creamy white, rich in neutrophils. Typical of infection by chemotactic bacteria
Haemorrhagic - contains many RBCs, indicates vascular damage, seen in destructive infections or when exudate is a result of infiltration by a malignant tumour.
Serous - clear, contains plasma proteins but few lymphocytes indicating no infection, e.g. Blister
Fibrinous - significant deposition of fibrin e.g. In pericardial/pleural spaces. Heard as a rubbing sound

360
Q

How is the endothelium naturally anti-thrombotic?

A

Contains plasminogen activators (NO, thrombomodulin, prostacyclin)

361
Q

What causes Alpert syndrome?

A

Type 4 collagen is abnormal, basement membrane is dysfunctional

362
Q

How does gliosis work?

A

Neural tissue is replaced by proliferation of CNS supportive elements (glial cells)

363
Q

Describe how peripheral neurons repair

A

Axons degenerate, proximal stumps sprout/elongate and are guided back to tissue by Schwann cells

364
Q

What factors control regeneration?

A

Growth factors - promote proliferation in stem cell population. Extracellular signals transduced into cell, promote expression of genes controlling cell cycle. Protein/hormone
Contact between basement membrane and adjacent cells - signalling through adhesion molecules. Inhibits proliferation in intact tissue (contact inhibition), less contact promotes proliferation (deranged in cancer)

365
Q

When does initiation and promotion lead to neoplasm formation?

A

When they effect protooncogenes and tumour supressor genes

366
Q

What are ‘caretaker genes’?

A

Genes that maintain genetic stability

367
Q

Describe the sequence of progression leading to colon carcinoma

A

Adenoma –> primary carcinoma –> metastatic carcinoma

Stepwise Sequence of acquisition of mutations

368
Q

What is androgen blockade used as a treatment for?

A

Treatment of prostate cancer (example of hormone therapy)

369
Q

What could tumour markers be?

A

Hormones, ‘oncofetal’ antigens, specific proteins or mucins/glycoproteins

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