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ESA 2 > Pathology > Flashcards

Pathology Flashcards

1
Q

What is acute inflammation?

A

A response of living tissue to injury. Inate, immediate, stereotyped, that acts to limit tissue damage

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2
Q

What is the purpose of inflammation?

A

Accumulation of fluid exudate and neutrophils in tissue

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3
Q

What can cause acute inflammation?

A

Microbial infections, hypersensitivity reactions, chemicals, necrosis, physica agents (heat, light, radiation)

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4
Q

What are the 5 signs of acute inflammation?

A

Redness, swelling, heat, pain and loss of function

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5
Q

What are the 3 main tissue level changes that occur in acute inflammation?

A

Change in blood flow, exudate of fluid, infiltration of inflammatory cells.

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6
Q

What is the first action that occurs in regards to the change in blood flow in acute inflammation?

A

Transient vasoconstriction (few seconds)

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7
Q

After transient vasoconstriction in acute inflammation what 3 things happen? And what signs of inflammation do they account for?

A

Vasodilation of arterioles then capillaries (heat and red), Increased permeability of blood vessels causing exudation and circulation slowing (swelling), increased concentration of RBC in small vessels and increased viscosity- stasis.

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8
Q

What causes vascular dilation, transient increase in vascular permeability and pain in acute inflammation?

A

Histamine

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9
Q

What releases histamine?

A

Mast cells, basophils and platelets

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10
Q

Mast cells, basophils and platelets release histamine in acute inflammation in response to what stimuli?

A

Physical damage, C3a, C5a, IL-1, factors from neutrophils and platelets

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11
Q

Histamine accounts for the immediate response in inflammation. What accounts for the persistant response in acute inflammation?

A

Leukotrienes and bradykinin (incompletely understood)

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12
Q

What determines fluid flow across vessel walls?

A

Balance of hydrostatic and colloid osmotic pressure

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13
Q

What pressures would increase fluid flow out of the vessel?

A

Increase in hydrostatic pressure, increase of colloid osmotic pressure of interstitium

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14
Q

In acute inflammation what leads to increase in hydrostatic pressure

A

Arteriolar dilation

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15
Q

In acute inflammation what causes an increase in colloid osmotic pressure of the interstitium?

A

Increased permeability of vessel walls leading to loss of protein.

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16
Q

Net fluid out of vessels causes what?

A

Oedema

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17
Q

What is the difference between a transudate and an exudate?

A

Transudate has the same protein level as plasma. An Exudate has more protein than plasma (inflammation)

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18
Q

What is the purpose of oedema?

A

INcreased lymphatic drainage.

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19
Q

When do we get a transudate instead of an exudate and why?

A

The fluid loss is due to hydrostatic pressure imbalance only. IN cardiac failure or venous outflow obstruction

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20
Q

What are the 5 mechanisms of vascular leakage in acute inflammation?

A 
Endothelial contraction-> gaps
Cytoskeleton reorganisation-> gaps
Direct injury
Leukocyte dependent injury
Increased transcytosis (through cytoplasm)
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21
Q

What chemical mediators are responsible for endothelial contraction in the vascular leakage associated with acute inflammation?

A

Histamine, leukotrines

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22
Q

What chemical mediators are responsible for cytoskeleton reorganisation in acute inflammation?

A

Cytokines IL-1 and TNF

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23
Q

What chemical mediator induces iucnreased transcytosis in vascular leakage associated with acute inflammation?

A

VEGF

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24
Q

What plasma protein in particular is important in exudate formation associated with acute inflammation and why?

A

Fibrin– causes a meshwork localising the products of inflammation. Particulary important in serousal surfaces.

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25
Q

What is the primary white blood cell of inflammation and what is another name for it?

A

Neutrophil- polymorph

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26
Q

What is important for the infiltration of neutrophils

A

Stasis

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27
Q

What are the 4 stages of neutrophil infiltration in acute inflammation?/

A

Margination, Rolling, Adhesion, Emigration

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28
Q

What chemicals are important in rolling? And what are important in adhesion?

A

Selectins for rolling

Integrins for adhesion

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29
Q

How do neutrophils move to the site in acute inflammation?

A

Chemotaxis- movement along concentration gradient of chemoattractants

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30
Q

What are some key Chemotaxins

A

C5a, LTB5, bacterial peptides

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31
Q

What chemical signals facilitate the phagocytic work of neutrophils in acute inflammation?

A

Opsonins (FC, C3b)

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32
Q

The 3 categories of chemical mediators in acute inflammation are

A

Proteases (kinins, complement, coagulation system)
Prostaglanding/ Leukotrines
Cytokines/Chemokines

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33
Q

Proteases (kinins, complement, coagulation system) are found where and produced where?

A

Produced in the liver and found in the plasma

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34
Q

Chemokines in acute inflammation come from where? (TNF, IL-)

A

WBC

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35
Q 
The primary chemical mediators in acute inflammation for:
Increased blood flow
Vascular permeability
Neutrophil chemotaxis
Phagocytosis

Are?

A

Blood flow- histamines and prostaglandins
Permeability- histamines and leukotrines
Chemotaxis of neutrophils- c5a, LTB4, Bacterial peptides
Phagocytosis- C3b

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36
Q

2 hallmark features of acute inflammation are

A

Exudate of fluid and infilatrate of inflammatory cells

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37
Q

How does exudation of fluid combat injury in acute inflammation?

A

Delivers plasma proteins
Dilutes toxins
Increases lymphatic drainage

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38
Q

How does infiltration of cells in acute inflammation combat injury?

A

Removes pathogenic organisms and necrotic debris

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39
Q

How does vasodilation in acute inflammation combat injury?

A

INcreases delivery and increase temp

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40
Q

Why is pain and loss of function important in acute inflammation?

A

Enforces rest, reduces chance of further damage

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41
Q

What are some local complications of acute inflammation?

A 
Swelling blocking tubes
Exudate compressing- eg tamponade
Exudate causing serositis
Loss of fluid
Pain and loss of function
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42
Q

What are some systemic effects of acute inflammation?

A

Fever
Leukocytes is
Acute phase response

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43
Q

What induces a fever in acute inflammation? What is commonly used to treat this

A

Endogenous pyrogens- Il-1, TBFalpha, prostaglandins

Aspirin

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44
Q

What is leukocytosis and what causes it?

A

Il-1 and TNF alpha cause accelerated release of macrophages, t lymphocytes from bone marrow.

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45
Q

In a reaction to a bacterial infection, induced leukocytosis causes release of what?
What happens in a viral infection?

A

Bacterial- neutrophils

Viral- lymphocytes

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46
Q

What is the systemic effect of acute phase response in acute inflammation?

A

Decreased apetite, raised pulse, altered sleep

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47
Q

Name some acute phase proteins associated with acute inflammation?

A 
CRP
Alpha 1 antitrypsin
Haptoglobin
Fibrinogen
Serum amyloid A protein
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48
Q

In resolution of acute inflammation what 3 things gradually happen?

A

Neutrophils no longer migrate
Vessel permeability back to normal
Vessel calibrate returns to normal

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49
Q

What needs to be maintained for complete resolution ?

A

Tissue architecture

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50
Q

What happens to the exudate in acute inflammation resolution?
What happens to fibrin?

A

Exudate drained to lymphatics

Fibrin degraded by plasmin and proteases.

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51
Q

What are some key features of mediators that allows resolution of acute inflammation?

A 
Short half lives
Some inactivated by degradation
Some have inhibitors
Some are unstable
Some dilute in exudate.
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52
Q

Why are skin blisters usually full of clear fluid?

A

Relatively few inflammatory cells unless bacterial infection

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53
Q

What is occurring at the centre of an abscess?

A

Liquifactive necrosis

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54
Q

An effusion is what?

A

Exudate within a serous cavity

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55
Q

What is chronic inflammation?

A

A chronic response to injury associated with fibrosis

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56
Q

What is the most important characteristic in chronic inflammation?

A

The type of cell present

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57
Q

What are the 2 main cells in chronic inflammation?

A

Macrophages and Lymphocytes

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58
Q

What are the functions of lymphocytes?

A

B lymphocytes to produce antibodies

T lymphocytes in both control and cytotoxic functions

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59
Q

A well as macrophages and lymphocytes what other cells are involved in the chronic inflammatory response?

A

PLasma cells
Eosinophils
Fibroblasts/myofirbolasts.

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60
Q

What does the presence of plasma cells usually imply in chronic inflammation?

A

Considerable chronicity

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61
Q

When are eosinophils present in acute inflammation?

A

Allergic reactions, parasitic infections and some tumours

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62
Q

What is a giant cell?

A

Multinucleated cell made by fusion of macrophages

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63
Q

What are giant cells a result of?

A

Frustrated phagocytosis

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64
Q

What types of giant cells are there? And what are they associated with?

A

Langhans-> TB
Touton-> fat necrosis
Foreign body type

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65
Q

What sort of shape do you commonly see with a langhan giant cell?

A

Horseshoe

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66
Q

What normally surrounds a Touton giant cell

A

Foamy cytoplasm

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67
Q

What is the main difference in the morphology of chronic inflammation compared to acute?

A

There is a lot more variation in proportions of cells

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68
Q

In RA what proportion of cells would you expect to be higher than in other types of chronic inflammation?

A

Plasma cells

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69
Q

What are the 4 main effects of chronic inflammation?

A

Fibrosis
Impaired function
Atrophy
Stimulation of immune response

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70
Q

In chronic cholecystitis what is the cause of the chronic inflammation?

A

Repeated acute inflammation due to repeated obstruction by gall stones

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71
Q

What symptoms would a patient with IBD present with?

A

diarrhoea, rectal bleeding

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72
Q

What is a big difference between ulcerative colitis and crohns?

A

Ulcerative colitis is superficial (Sx diarrhoea, bleeding)

Crohns is transmural (Sx strictures, fistulae)

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73
Q

Chronic inflammation with fibrosis leads to what?

A

Cirrhosis (disorganisation of architecture with attempted regeneration)

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74
Q

What is granulomatous inflammation

A

Chronic inflammation with granulomas

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75
Q

What is a granuloma

A

Collection of immune cells (histiocytes)-macrophages stuck together

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76
Q

Why would a granuloma form?

A

The immune system attempts to wall of a substance thought to be foreign but is unable to eliminate it

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77
Q

When do granulomas arise?

A

Persistent low grade antigenic stimulation

Hypersensitivity

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78
Q

What are the 3 main causes of granulomatous inflammation?

A

Foreign material
Infections (TB)
Unknown (sarcoid, wegeners)

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79
Q

How does TB cause disease?

A

Persistence and induction of cell mediated immunity

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80
Q

Why is TB so difficult to destroy?

A

Wall lipids (mycosides)

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81
Q

What is special about a tuberculous granuloma

A

Caseous necrosis in the centre

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82
Q

In cell injury, the degree of an injury depends on what 3 things?

A

Type of injury
Severity of injury
Type of tissue

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83
Q

What is the cell injury response continuum (4)

A

Homeostasis-> cellular adaption-> cell injury-> cell death

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84
Q

7 examples of things that can cause cell injury

A 
Hypoxia
Toxins
Physical agents
Radiation
Microorgansims
Immune
Dietary insufficient/ excess
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85
Q

What is the difference between hypoxia and ischaemia

A

Hypoxia means decreased oxygen supply, ischaemia is decreased blood supply (worse as its hypoxia and less nutrients, glucose etc)

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86
Q

What are 4 typical causes of hypoxia

A

Hypoxaemic
Anaemic
Ischaemic
Histiocytic

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87
Q

What is hypoxaemic hypoxia

A

Low arterial content of oxygen (could be reduced inspiration, reduced absorbtion)

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88
Q

What is anaemic hypoxia?

A

Low oxygen due to haemoglobins ability to carry oxygen- anaemia or CO

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89
Q

What is iscaemic hypoxia

A

Low oxygen due to interruption of blood supply- blockage or heart failure

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90
Q

What is histiocytic hypoxia

A

The inability of cells to utilise oxygen due to disable oxidative phosphorlyayion enzymes (Cyanide)

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91
Q

Typically how can the immune system damage its own cells?

A 
Hypersensitivity reactions 
Autoimmune reactions (not recognising self)
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92
Q

What components of the cell are most succeptible to injury

A

Cell membranes (plasma and organelle)
Nucleus (DNA)
Proteins (enzymes)
Mitochondria

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93
Q

What is the first outcome of hypoxia on a cell in a reversible injury?

A

Decreased oxidative phosphorylation

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94
Q

In a reversible cell injury, there is the initial decrease in oxidative phosphorylation. What is the result of this?
What 3 changes does this induce?

A

Decreased ATP
Decreased activity of the Na/K pump
Increased glycolysis
Detachment of ribosomes, decreasing protein synthesis

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95
Q

Due to decreased ATP in a reversible injury to the cell the Na/K pump isn’t working well. What is the resultant electrolyte change and what changes can be seen?

A

Influx of calcium, H2O and Na+. Efflux of K+

Cellular swelling, blebbing, ER swelling, myelin figures

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96
Q

Due to a decrease in ATP in a reversible hypoxic injury there is a increase in glycolysis.
What is the effect of this

A

Decreased PH, decreased glycogen.

Clumping of nuclear chromatin (due to ph Change)

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97
Q

IN a reversible hypoxic injury there is decreased ATP production leading to less protein synthesis.
How is this seen in the cell?

A

Lipid deposition

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98
Q

In prolonged, irreversible hypoxia what is the main agent that accumulates in the cytosol?

A

Calcium

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99
Q

INcreased cytosolic calcium in prolonged hypoxia induces what 5 things? Leading to what?

A

ATPase->decreased ATP
Phospholipase->decreased phospholipids
Protease-> disrupts membranes and cytoskeletons
Endonuclease-> chromatin damage

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100
Q

What primarily damages membranes in hypoxia?

A

Free radicals

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101
Q

What is a free radical?

A

reactive oxygen species with single unpaired electron

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102
Q

3 free radicals of particular biological importance?

A

Hydroxyl OH
Superoxide O2-
Hydrogen peroxide H2O2

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103
Q

What are the 2 physiological mechanisms in which free radicals are produced?

A

In metabolic reactions like oxidative phosphorlyation

In inflammation- oxidative burst of neutrophils

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104
Q

What 3 pathological mechanisms induce free radical production?

A

Contact with unbound metals- iron, copper
Radiation
Drugs and chemicals

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105
Q

What 3 mechanisms does the body have to control free radicals?

A

Anti-oxidant system
Metal carrier and storage proteins
Enzymes that neutralise free radicals

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106
Q

What are the anti-oxidant vitamins and how do they work?

A

A,C,E

Donate electrons

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107
Q

What are some examples of metal carriers that sequester iron and copper?

A

transferrin, ceruloplasmin

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108
Q

What enzymes are responsible for neutralising free radicals

A

superoxide dismutase
Catalase
Glutathione peroidase

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109
Q

What is oxidative imbalance?

A

The number of free radicals overwhelming the anti-oxidant system

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110
Q

What are the most important targets of free radicals in the cell? And what do they cause

A

Lipids- lipid peroxidation

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111
Q

What is an autocatalytic chain reaction in relation to lipid peroxidation

A

The generation of further free radicals

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112
Q

Other than lipid peroxidation what effect can free radicals have on the cell

A

Oxidise proteins, carbohydrates and dna

Beings out of shape or cross linking.

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113
Q

How can the cell protect itself from injury?

A

Heat shock proteins

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114
Q

What is the role of a heat shock protein?

A

Aim to mend misfiled do proteins and maintain cell viability

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115
Q

Heat shock proteins are (2) e.g

A

Unfoldases
Chaperonins
Eg ubiquitin

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116
Q

What does an injured cell look like under a microscope

A

Bit pale and swollen (movement in of sodium and water)

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117
Q

What does a dead cell look like under microscope?

A

Very pink cytoplasm (denature and coagulation)

Nucleus changes

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118
Q

What 3 changes in the mucleus can be seen in dead cells

A

Pyknosis
Karyorrhexis
Karyloysis

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119
Q

Under an electron microscope what can be seen in the cell in a state of reversible injury?
( can already see general swelling and pale staining under microscope)

A 
Blebs
Clumping of chromatin
ER swelling
Dispersion of ribosomes
Mitochondrial swelling
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120
Q

Under electron microscope of a dead cell, what additional features can we see compared to the microscope?
(Already seen change in nucleus (pyknnosis, karyohexis or karyolysis) and increased staining

A

Rupture of lysosomes, cell membrane defects, lysis of ER, myelin figures

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121
Q

How do we diagnose cell death?

A

INjection of dye- dead cells cant keep it out

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122
Q

What is necrosis

A

Morphological changes that occur after a cell is dead

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123
Q

What is oncosis

A

Cell death with swelling, the spectrum of changes prior to death

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124
Q

What are the 2 main types of necrosis and the 2 special types

A

Main: coagulative, liquifactive
Special: Caseous, fat

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125
Q

Where does coagulative necrosis occur?

A

Ischemia in solid tissues

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126
Q

What process dominates in coagulative necrosis?

A

Protein desaturation

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127
Q

Where does liquifactive necrosis occur and what is there a prescence of?

A

Loose tissue

Neutrophils

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128
Q

What predominated in liquifactive necrosis?

A

Enzyme release

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129
Q

What does coagulative necrosis look like?

A

Cellular architecture preserved
Darker staining
Protein desaturation> proteases

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130
Q

What does liquefactive necrosis look like?

A

Loss of cell architecture

Essentially dissolved away

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131
Q

What does caseous necrosis contain ?

A

Structureless debris

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132
Q

What is caseous necrosis associated with?

A

TB

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133
Q

What does fat necrosis look like? What causes it

A

Large fat drops surrounded by macrophages

Leaking of lipid that combine with calcium to form calcium soaps.

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134
Q

What is gangrene

A

Necrosis visible to the naked ete

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135
Q

What is an infarction

A

Necrosis caused by reduction of arterial blood flow

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136
Q

What is an infarct

A

An area of ischaemic necrosis

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137
Q

What is dry gangrene?

A

Necrosis modified by exposure to air (coagulative)

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138
Q

What is wet gangrene?

A

Necrosis modified by infection (liquifactive)

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139
Q

What are the commonest causes of infarction?

A

Thrombosis

Embolism

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140
Q

Why are some infarcts white?

A

Occlusion of end artery. Coagulative necrosis. Often wedge shaped

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141
Q

Why are some infants red?

A

Loose tissue
Dual blood supply
Raised venous pressure
Re-perfusion

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142
Q

What is ischaemia-reperfusion injury?

A

Paradoix- blood flow returned to damaged but not yet necrotic tissue inducing more damage

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143
Q

3 important things that leak out in cell death-

A

Potassium
Enzymes
Myoglobin

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144
Q

Why is the release of K in cell death dangerous

A

Hyperkalemia leading to cardiac arrest

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145
Q

If myoglobin leaks out, what can be a clinical sign?

A

Rhabdo

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146
Q

What is the biggest macroscopic difference in the cell undergoing apoptosis compared to necrosis

A

The cell shrinks rather than swells

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147
Q

Is apoptosis an active or passive process?

A

Active

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148
Q

What happens to the membrane in apoptosis?

A

Membrane integrity is maintained

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149
Q

are lysosomal enzyme involved in apoptosis?

A

NO

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150
Q

Is apoptosis pathological or physiological?

A

Both

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151
Q

What happens to dna and proteins in apoptosis

A

Enzymes degrade them

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152
Q

When does pathological apoptosis occur?

A

Cytotoxic T cells killing virus/neoplastic cell
Damaged cell (particulary dna)
Graft v host

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153
Q

3 stages of apoptosis

A

Initiation (Condensation), execution (fragmentation),degradation and phagocytosis (apoptic bodies)

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154
Q

What 2 mechanisms trigger initiation and execution of apoptosis?

A

Intrinsic and extrinsic

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155
Q

The intrinsic and extrinsic activation of apoptosis result in what?

A

Activation of caspases

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156
Q

What is the role of caspases?

A

Control and mediate apoptosis

Cause cleavage of dna and proteins

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157
Q

What are the most common triggers for the intrinsic pathway?

A

Irreparable dna damage, withdrawal of growth factors

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158
Q

What do the triggers in the intrinsic pathway of apoptosis activate? And what’s its effect?

A

P53, makes mitochondrial membrane leaky

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159
Q

What is released from a leaky mitochondrial membrane in apoptosis? And what does it do?

A

Cytochrome C- causes activation of caspases

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160
Q

What is the trigger to the extrinsic pathway of apoptosis? An example of a signal?

A

Cells that are a danger- tumour, virus

TNF alpha

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161
Q

What does TNF alpha, secreted by a T killer cell do to induce apoptosis?

A

Bind to death receptor, resulting in activation of caspases

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162
Q

How are apoptotic bodies phagocytosed

A

Express proteins on surface recognised by phagocytes

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163
Q

What are the 5 main groups of intracellular accumulation?

A 
Water and electrolytes
Lipids
Carbohydrates
Proteins
Pigments
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164
Q

What does fluid accumulation in cells indicate? Where is this a particular problem

A

Cellular distress. Na+ and water into cell.

The brain

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165
Q

What is steatosis?

A

Accumulation of triglycerides

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166
Q

Where is lipid accumulation often seen?

A

Liver. (Major organ of fat metabolism)

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167
Q

What can cause fatty liver?

A

Alcohol
Diabetes
Obesity

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168
Q

Why does cholesterol accumulate in cells in vesicles?

A

Insoluble, eliminated only though the liver

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169
Q

Where does cholesterol accumulate if in excess?

A

Smooth muscle cells and macrophages in plaques (foam cells). Macrophages in skin and tendons- xanthomas

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170
Q

How are protein accumulations seen?

A

Eosinophilic droplets in cytoplasm

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171
Q

What conditions can result in protein accumulation in cells?

A

Alcoholic liver disease

Alpha 1 antitrypsin deficency.

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172
Q

What are examples of pigment accumulations?

A

Carbon
Coal
Dust
Soot

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173
Q

Why do pigment accumulations occur?

A

Phagocytosis by macrophages

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174
Q

What is an example of an endogenous pigment accumulation?

A

Haemosiderin in a bruise

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175
Q

What is haemosiderin?

A

Iron storage molecule derived from haemoglobin

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176
Q

In haemochromatosis where is iron deposited and what is it often associated with?

A

Skin, liver, pancreas, heart

Scarring

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177
Q

What are 4 mechanisms of intracellular accumualtion?

A

Abnormal metabolism
Alteration in protein folding and transport
Deficency in critical enzyme
Inability to phagocytosis particles

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178
Q

What is dystrophic calcium deposition

A

deposition of calcium salts in an area of dying tissue

Plaques, heart valves, lymph nodes

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179
Q

Is dystrophic calcification associated with abnormality in calcium metabolism or calcium concentrations in serum?

A

NO

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180
Q

Why does dystrophic calcification occur?

A

Local change that favours nucleation of hydroxyapatite crystals

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181
Q

Why does metastatic calcification occur?

A

Due to hypercalcaemia secondary to disturbance in calcium metabolism

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182
Q

What 2 things cause hypercalcaemia?

A

Increased secretion of parathyroid hormone

Destruction of bone tissue

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183
Q

What is disease characterised as?

A

Pathological condition of a body part, organ or system characterised by identifiable group of signs and symptoms

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184
Q

What is pathology?

A

Understanding the process of disease and why you have symptoms

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185
Q

What is cytopatholoy?

A

Looking at diaggregated cells rather than tissues

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186
Q

What is the purpose of microscopic diagnosis?

A

Aid in definitive diagnosis and guide extent of intervention

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187
Q

What’s the difference between cytology and histology?

A

Cytology is the cellular level, histology is the architecture of the tissue

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188
Q

What are some clinical examples of histology?

A

Core biopsies, cancer resection, endoscopic biopsies

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189
Q

What are some examples of clinical cytology

A

Fine needle aspirates- breast, thyroid, lung, sputum, urine, cervical smear

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190
Q

What is more invasive typically cytology or histology?

A

Histology

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191
Q

What is generally cheaper cytology or histology?

A

Cytology

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192
Q

What is an issue with cytology?

A

Generally has higher error rates

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193
Q

What is a major advantage of cytology

A

Fast and cheap

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194
Q

What is the cancer staging mnemonic

A

TNM

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195
Q

What does TNM stand for in cancer staging

A

Tumour, Nodes, Metastisis

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196
Q

What would be the worst cancer staging?

A

T3N2M(high number)

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197
Q

What is the first thing that needs to be stopped when preparing a slide for histology?

A

Autolysis

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198
Q

What is autolysis when preparing a slide?

A

Self digestion (begins to occur once blood supply lost)

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199
Q

How is autolysis inhibited in slide preparation?

A

With use of fixatives

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200
Q

What do fixatives do, in refereance to slide preperation

A

Inactivate tissue enzymes and denature proteins, present bacterial growth and harden tissue

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201
Q

What is the normal fixative used in slide preparation?

A

Formalin

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202
Q

What is trimming?

A

Slicing of a specimen into stamp size pieces to be put in a cassette

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203
Q

What happens after trimming in slide preparation?

A

Water is removed from the tissue

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204
Q

How is water removed from tissue in slide preparation?

A

Alcohol

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205
Q

How is alcohol removed from a slide (added to remove water)

A

use of xylene

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206
Q

What is paraffin wax used for in slide preparation? When is it added?

A

Embedding

After xylene has been added

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207
Q

What happens once a tissue has been embedded in paraffin wax in slide preparation?

A

Blocking- placed on freezing surface.

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208
Q

The slide is now embedded and has been blocked. What happens now before the slide is stained?

A

Cut with microtome. Water bath to remove wrinkles

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209
Q

What is the normal tissue stain, what does it stain

A

H (nuclei purple)

E (cytoplasm pink)

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210
Q

What is immunohistochemistry?

A

Labelling with specific antibodies to demonstrate a substance is present

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211
Q

In immunohistochemistry an antibody is normally joined to what? Why?

A

Peroxidase enzyme- catalyses colour change

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212
Q

How are things like her2, cadherins, actin demonstrated in a tissue slide?

A

Immunohistochemistry

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213
Q

What is the use of cytokeratins in cancer diagnosis?

A

Can indicate primary site (difference cytokeratins)

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214
Q

What cytokeratins are form the lung, breast, endometrium, ovary or thyroid?

A

CK7+ / CK20-

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215
Q

What cytokeratins are from the large bowel

A

CK7- / Ck20+

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216
Q

What can molecular pathology use FISH for?

A

Look at amount of gene copies (aids in treatment choice)

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217
Q

In molecular pathology what is more useful to look at than the gene or amount of gene copies when using it to guide treatment? Why?

A

MRNA expression. Better shows what gene is being transcribed

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218
Q

What is a tumour signature?

A

The mRNA expression from the tumour. Aids in prediction of its behaviour

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219
Q

To what accuracy does a frozen section have?

A

96%

220
Q

Why do we still use post mortems given the advent of modern imagining and biochemistry?

A

Discrepancies still in modern imaging

221
Q

When does an autopsy not require consent?

A

When its on behalf of HM cornonor

222
Q

What are some examples of reasons to have a HM coroner autopsy?

A

If deceased unknown
Deceased not seen by a doctor within 14 days of death
Attending doctor cant give cause of death
Unnatural death
Relation to occupational disease or accident
Related to medical treatment
Forensic

223
Q

When is consent required for an autopsy?

A

In hospital autopsies that aren’t on Hm coronoers orders

224
Q

What occurs in an autopsy?

A 
External exam and internal looking at all systems
Histology
Toxicology
Biochemistry
Microbiology
Molecular dna based ax
225
Q

Who can perform a paediatric autopsy?

A

Someone trained in paediatric surgical pathology and autopsy

226
Q

What would a paediatric pathologist look at in autopsy (type)

A

In utero, perinatal, death in infants and children that are suspicious

227
Q

A hit on the head leading to a ‘slow leak’ is likely what kind of haemorrhage

A

Extradural

228
Q

What kind of haemorrhage is a berry aneurysm

A

Sub-arachnoid

229
Q

What are the two types of stroke?

A

Ischaemic and haemorrhagic

230
Q

What types of intracranial haemorrhage are there?

A

Extramural, subdural, subarachnoid, intracerebral

231
Q

What happens in diffuse atonal injury

A

Axons are broken

232
Q

What can raised ICP cause

A

Resp and cardiac issues.

Decreased consciousness

233
Q

What happens in a tension pneumothorax

A

Air is within the pleural cavity, when the lung expands more air moves into pleural cavity

234
Q

When is hypovolemia life threatening

A

20% blood volume

235
Q

What are some systemic effects of burns?

A

Increased vascular permeability
Reduced myocardial contractility and end organ hypoperfusion
Non specific down regulation of the immune system

236
Q

What are some clinical features of sepsis?

A 
Mottled skin
Cap refill less than 3
Decreased urine output
Lactate above 2 mol
Cardiac dysfunction
Change in mental state
Platelets above 100
Troponin leak
ARDS
DIC
237
Q

What is ARDS

A

Acute resp distress syndrome

Neutrophil sequestration and migration into alveolus causing oedema and necrosis of type 1 cells

238
Q

What are the 3 basic processes involved in wound healing? And why?

A

Haemostasis - the vessels are open
Inflammation- there is tissue injury
Regeneration- structures have been injured or destroyed

239
Q

Regeneration in wound healing can be either what?

A

Resolution of restitution

240
Q

What is healing by primary intention

A

Restitution with no or minimal evidence of previous injury

241
Q

When does healing by primary intention occur?

A

Superficial abrasion

242
Q

Generally on a skin level what is the difference between an abrasion and an ulceration?

A

Abrasion the top few layers of skin

Ulceration is something deeper

243
Q

In the gut what specifically is the difference between an abrasion and an ulceration?

A

An ulceration penetrates the muscularis layer

244
Q

What cells replicate in regeneration

A

Stem cells

245
Q

What 3 things do stem cells display?

A

Prolonged proliferative activity
Asymmetric replication
Internal repair system

246
Q

Where are stem cells located in the epidermis?

A

Basal layer adjacent to basement membrane

247
Q

Where are stem cells located in the intestinal mucosa?

A

Bottom of crypts

248
Q

Where are stem cells located in the liver?

A

Between hepatocytes and bile ducts

249
Q

What are most adult stem cells?

A

Unipotent

250
Q

What does being a unipotent stem cell entail?

A

Able to produce one type of differentiated cell

251
Q

What is a multipotent stem cell? And an example?

A

Produces several types of differentiated cell

Haematopoeitc stem cell

252
Q

An embryonic stem cell is what type of stem cell

A

Totipotent

253
Q

What can a totipotent stem cell do?

A

Produce any type of cell and therefore any type of tissue

254
Q

What tissues cant undergo mitosis and have no or few stem cells?

A

Permanent tissues

255
Q

What are some examples of permanent tissues

A

Skeletal muscle
Neural tissue
Cardiac muscle

256
Q

What tissues contain short lived cells?

A

Labile tissues

257
Q

What are some examples of labile tissues?

A

Surface epithelial, haematopoeitc tissues

258
Q

What tissues have low levels of replication but can undergo rapid proliferation of needed?

A

Stable tissues

259
Q

What are some examples of stable tissues?

A

Liver parenchyma, bone, fibrous tisssue, endothelium

260
Q

What are the 3 tissue type (labile, stable and permanent) divided based upon?

A

Proliferation activity (based on cell cycle)

261
Q

What 3 circumstances are needed for regeneration to occur

A

The tissue is label/ stable
The tissue damage is not extensive
Intact connective tissue scaffold

262
Q

What is fibrous repair?

A

Healing with formation of fibrous connective tissue (Scar)

263
Q

What tissue is often lost for fibrous repair to occur

A

Specialised tissue

264
Q

When does fibrous repair occur?

A

Significant tissue loss

Permanent or complex tissue is injured

265
Q

What is the first stage in scar formation? What time frame?

A

Haemostasis

Seconds-minutes

266
Q

What is the second stage in scar formation? What time frame

A

Acute inflammation

Minutes to hours

267
Q

What is the third stage in scar formation? What time frame

A

Chronic inflammation

1-2 days

268
Q

What’s the fourth stage in scar formation? After chronic inflammation, and roughly when does that begin

A

Granulation tissue forming at 3 days

269
Q

When does early scar fomration take place ?

A

7-10 days

270
Q

Over what time period does scar maturation occur?

A

Weeks- 2 years

271
Q

What does granulation tissue consist of?

A

Developing capillaries
Fibroblasts and myofibroblasts
Chronic inflammatory cells

272
Q

What is the function of granulation tissue?

A

Fills the gap
Capillaries bring oxygen and nutrients
Contracts and closes gap

273
Q

In fibrous repair a blood clot initially forms. What cells follow this?

A

Neutrophils to digest clot

Macropages and lymphocytes

274
Q

In fibrous repair what is synthesised from the vascular network?

A

Collagen

275
Q

What does the collagen do once deposited in fibrous repair

A

Matures, contracts and remodels

276
Q

What are the 3 cell/ cell groups involved in fibrous repair

A

Inflammatory cells
Endothelial cells
Fibroblasts/myofibroblasts

277
Q

What is the role of inflammatory cells in fibrous repair?

A

Phagocytosis Debi’s and produce chemical mediators

278
Q

What is the purpose of the endothelial cells in fibrous repair

A

Angiogenesis

279
Q

Fibroblasts and myofibroblasts do what in fibrous repair?

A

Produce extracellular matrix

Responsible for wound contraction

280
Q

Why are scars white?

A

No regeneration of melanocytes

281
Q

What do scars tend to stretch?

A

We dont lay down elastin with them

282
Q

What can tends to be absent on scar tissue ?

A

Sweat glands and hair follicles

283
Q

Why is a scar initially red?

A

Lots of blood vessels present

284
Q

What are amorphous collagens and what are they for?

A

Collagens 4-9 things like basement membrane

285
Q

What collagen is most common and where’s it found?

A

Type 1- bones, ligaments, skin, blood vessels

286
Q

What collagen makes up basement membranes

A

Type 4

287
Q

What are some symptoms of scurvy

A

Unable to heal wounds
Tooth loss
Old scars break open

288
Q

What do the collagen fibres in Ehlers danlos lack?

A

Tensile strength

289
Q

What change in the eye is seen with osteogenesis imperfecta?

A

Blue sclerae- too little collagen within them

290
Q

What is abnormal in Alport syndrome

A

Type 4 collagen

291
Q

What are growth factors?

A

Polypeptides that act on cell surface receptors

292
Q

What are growth factors coded by/

A

Porto-oncogenes

293
Q

What do growth factors stimulate?

A

Transcription of genes that regulate entry of cell into cell cycle

294
Q

Other than cell proliferation what effects can growth factors have?

A 
Inhibition of division
Locomotion
Contractility
Differentiation 
Viability 
Angiogenesis
295
Q

Name 4 growth factors

A

Tumour necrosis factor
Platelet derived growth factor
Vascular endothelial growth factor
Epidermal growth factor

296
Q

What do cadherins do?

A

Bind cells to each other

297
Q

What do integrins do?

A

Bind cells to extracellular matrix

298
Q

What does contact inhibition do?

A

Inhibits proliferation in intact cells, encourages it in damaged cells

299
Q

When can contact inhibition be altered?

A

Malignant cells

300
Q

What is healing by primary intention?

A

Incision, closed, non-infected and sutured wounds.
Small number of disrupted cells
Minimal clot and granulation tissue

301
Q

What is healing by secondary intentions?

A

Excisional wound with tissue loss and seperated edges.

Filled by abundant granulation tissue, grows in from wound margins

302
Q

In secondary intention healing the new epdidermis is often what?

A

Thinner than usual

303
Q

Skin grafts are taken at what thickness?

A

Split thickness

304
Q

What are some general factors that influence wound healing?

A 
Age
Obesity
Diabetes 
Vitamin deficiencies and malnutrition
Anaemia, hypoxia, hypovolaemia
Drugs
305
Q

What can occur if there is insufficient fibrosis (scarring) in fibrous repair?

A

Wound dehiscence, hernia, ulceration

306
Q

What are some complications of fibrous repair

A 
Adhesion formation
Loss of function (replacement of specialised tissue)
Disruption of complex tissue
Overproduction of scar
Excessive contraction of scar
307
Q

What is the general purpose of haemostasis

A

To prevent bleeding
To prevent unesscesary coagulation
To allow blood flow

308
Q

What is haemostasis the process of ?

A

Making a clot, controlling the clotting and breaking the clot down

309
Q

What are the 3 stages of the clotting process

A

Initiation
Formation
Fibrinolysis

310
Q

In clot initiation what is happening? Re platelets

A

Platelet aggregation to vessel wall and activation of coagulation

311
Q

In clot formation once the platelets have aggregated against the vessel wall what is the key conversion that occurs in the activation of the coagulation pathway?

A

Thrombin converts fibrinogen to fibrin which forms fibrin polymers

312
Q

In fibrinolysis what is occurring generally?

A

Retraction of fibrin polymers and breakdown of fibrin fragments

313
Q

How do platelets look on a H and E

A

Non nucleated purple staining dots

314
Q

What produces platelets

A

Megakaryocytes (bud off from cytoplasm)

315
Q

What is the normal platelet range

A

150-400 x 10^9

316
Q

What is the normal lifespan of platelets

A

7-10 days

317
Q

What drug is an antiplatelet?

A

Aspirin

318
Q

When damage to vessel walls occurs what encourages platelet adhesion? Via what receptor?

A

Exposed collagen

VWF receptor

319
Q

What activated other platelets once platelet adhesion has occurred?

A

Secretion of ADP and thromboxane

320
Q

What do the platelets do once they have aggregated against a damaged vessel wall

A

Cross link to form platelet plug

321
Q

What is the platelet plug mediated by?

A

Von willebrands factor, fibrinogen, collagen, thromboxane and thrombin

322
Q

How does the clotting process itself limit clotting?

A

Negative feedback loop where the clot destroys proteins activated by the clotting cascade

323
Q

What do we have naturally occurring the inhibit the activation of the clotting cascade?

A

Natural anticoagulants

324
Q

Both coagulation factors and natural anticoagulants are made where?

A

Liver

325
Q

What 2 clotting pathways are there? Where do they converge?

A

Intrinsic and extrinsic

X

326
Q

Which clotting pathway involves factor

A

Extrinsic (PT)

327
Q

Which clotting pathway involves factors 8,9,11,12?

A

Intrinsic/ APPT

328
Q

What clotting factors do both the intrinsic and extrinsic involve?

A

V, X, prothrombin, fibrinogen

329
Q

What is APTT a measure of?

A

The intrinsic pathway

330
Q

What is PT a measure of?

A

The extrinsic pathway

331
Q

In clotting tissue factor exposure activates what ?

A

FVII

332
Q

When the activation of FVII occurs and thrombin is made. What happens to massively amplify the process?

A

Thrombin burst. (Lots of clotting factors and thrombin)

Thrombin feeding back in the cascade

333
Q

What is Von willebrands factor involved in?

A

Platelet adhesion to vessel wall. Platelet aggregation

Carries factor VIII

334
Q

What is activated in fibrinolysis to breakdown fibrin mesh?

A

Plasminogen activated to plasmin

335
Q

What does plasmin breakdown? To what?

A

Fibrin to D dimers

336
Q

What are some natural anticoagulants?

A

Protein C
Protein S
Antithrombin

337
Q

Deficency in protein c, protein s or anti thrombin results in what?

A

Thrombophillia

338
Q

Are bleeding disorders inherited or acquired?

A

Both

339
Q

Where can abnormalities be to lead to a bleeding disorder?

A

Vessel wall
Platelets
Coagulation factors

340
Q

Haemophilia A is a disorder of what?

A

Clotting factor 8

341
Q

Haemophilia B is a disorder of what

A

Clotting factor 9

342
Q

What acquired disorders can lead to clotting disorders?

A

Liver disease
Vitamin k deficency (needed for 2,9,10,7)
A

343
Q

What symptoms would a coagulation factor disorder present with?

A

Muscle haematomas
Recurrent haemarthroses
Joint pain and deformity
Excessive post surgical bleeding

344
Q

Haemophilia A has what generic pattern

A

X linked recessive

345
Q

How is haemophilia A treated

A

Recombinant factor 8

346
Q

Someone presents with skin and mucous membrane bleeding. But doesn’t report haemartroses or muscle haematoma.
What would you think it is?

A

Von willebrands disease

347
Q

What occurs in Von willebrands disease?

A

Abnormal platelet adhesion and reduced factor 7 activity

348
Q

What symptoms are associated with a vessel wall abnormality (haemostasis)

A

Easy bruising, spontaneous small bleeds. Mainly skin but also mucous membrane

349
Q

Name a congential disease associated with vessel wall abnormality

A

Hereditary haemorrhagic telangiectasia

350
Q

What are some acquired diseases of the vessel wall?

A

Senile purpura
Meningococcal
Measles

351
Q

Platelet disorders can either be what?

A

Qualitative or quantitative

352
Q

A quantitative disorder of the platelets is known as

A

Thrombocytopenia

353
Q

What can a low platelet count be a result of generally

A

Reduced production or increased removal

354
Q

The increased removal of platelets inducing thrombocytopenia could be due to what?

A

Immune destruction
Non immune destruction
Splenic pooling

355
Q

If the production of platelets is low what should you look at?

A

Bone arrow and the megakaryocytes

356
Q

What is an example of immaterial destruction of platelets?

A

Immune thrombocytopenia purpura

357
Q

In Immune thrombocytopenia purpura what is happening? What can it be secondary to?

A

Antibodies against glycoproteins on platelet surface are produces.
Secondary yo disease like lupus or lymphoma

358
Q

How would you treat Immune thrombocytopenia purpura

A

Immune supression

359
Q

What is an example of non immune destruction of of platelets?

A

Microangiopathic haemolytic states like DIC

360
Q

What thrombocytopenias are due to low production of platelets?

A

B 12 defficency
Bone marrow cancer
Chemo
HIV

361
Q

What could happen if platelet count falls below 30?

A

Mucousal bleeding

Intracranial haemorrhage

362
Q

What is more common an acquired platelet function disorder or hereditary

A

Acquired

363
Q

What are some common examples of acquired platelets function disorder causes

A

Aspirin
NSAIDS
Uraemia
Myeloproliferative disorder

364
Q

What is DIC an example of

A

Microangiopathic haemolytic anaemia

365
Q

What are formed in DIC

A

Microthrombi

366
Q

Why are microthrombi formed in DIC

A

Pathological activation of coagulation

367
Q

In DIC what would clotting tests show and why?

A

Increased clotting times as clotting factors and platelets are used up
Raised d dimers from breakdown of clots

368
Q

Is DIC a diagnosis?

A

No there is always a trigger

Malignancy, infection, obstetric cause etc

369
Q

What is atheroscelerosis an accumulation of?

A

Intracellular and extracellular lipid

370
Q

Where does atherosclerosis occur?

A

Intima and media of medium to large arteries

371
Q

What is the result of atherosclerosis?

A

Thickening and hardening of the walls of arteries

372
Q

What is the time line of atherosclerosis?

A

Fatty streak-> simple plaque-> complicated plaque

373
Q

What is the macroscopic appearance of the fatty streak in atherosclerosis formation?

A

Lipid deposits in intima, yellow and slightly raised

374
Q

What’s the macroscopic appearance of the simple plaque in atherosclerosis?

A

Raised yellow/white with irregular outline and wide distribution

375
Q

What is the complicated plaque in atherosclerosis?

A

Thrombosis followed by haemorrhage into plaque, calcification and the formation of an aneurysm

376
Q

Where are some common sites of atherosclerosis?

A

Aorta (especially abdominal), coronary arteries, carotid arteries, cerebral arteries, arteries of the leg.

377
Q

What is the normal structure of an artery (out to in)

A

Endothelium, internal elastic lamina, muscularis media, external elastic lamina, adventitia

378
Q

What are some early microscopic features of atherosclerosis?

A

Smooth muscle proliferation
Accumulation of foam cells
Extracellular lipid

379
Q

What are some mid stage- late changes in atherosclerosis microscopically?

A

Fibrosis
Necrosis
Cholesterol clefts
Occasional inflammatory cells

380
Q

What are the late stages of atherosclerosis as seen microscopically

A

Disruption of internal elastic lamina
Damage into media
Ingrowth of blood vessels
Plaque fissuring

381
Q

What are some clinical consequences to atherosclerosis of coronary arteries?

A

Ischaemic heart disease-

MI, Angina pectoris, Arrythmias, Cardiac failure

382
Q

What does a myocardial infarction look like macroscopically

A

Yellow with red border, known as hyperaemic border

383
Q

What are some clinical effects of cerebral atherosclerosis

A

Cerebral ischemia leading to
TIA
Cerebral infarct
Multi-infarct dementia

384
Q

How are cerebral infarcts seen macroscopically

A

Small area of infarct and a large area of haemorrhage

385
Q

What would the clincal effect of mesenteric ischaemic manifest itself as?

A

Ischaemic colitis, malabsorption, intestinal infarction

386
Q

What can peripheral vascular disease lead to?

A

Intermittent claudication
Leriche syndrome (buttocks and impotence)
Ischaemic rest pain
Gangrene

387
Q

What are some risk factors for atherosclerosis?

A 
Age
Gender (women protected before menopause)
Hyprelipidemia
Cigarette smoke
HTN
DM
Alcohol
Infection
388
Q

Why is the initial endothelial injury taking place in atherosclerosis?

A

Raised LDL
Toxins
HTN
Haemodynamic stress

389
Q

What is the first thing to happen in atherosclerosis development?

A

Endothelial injury

390
Q

After endothelial injury in atherosclerosis what happens re platelets?

A

Platelet adhesion
Platelet derived growth factor release
Smooth muscle proliferation and migration

391
Q

After endothelial injury in atherosclerosis what happens re lipids?

A

Insudation of lipid
LDL oxidation
Uptake of lipid by smooth muscle cell and macrophage

392
Q

After endothelial injury in atherosclerosis what happens re monocytes

A

Migrate to intima

393
Q

In atherosclerosis, once endothelial damage has occurred. The platelets have adhered, the lipid has insudated and the monocytes have migrated, what do smooth muscle and foam cells do?

A

SMC produce matrix material

Foam cells secrete cytokines that cause further SMC stimulation and recruit inflammatory cells

394
Q

What’s a thrombosis?

A

Solid mass of blood within circulatory system during life

395
Q

What’s the difference between a clot and a thrombosis

A

Clot occurs at skin level/ test tube/ breakage of the continuity of vessel

396
Q

What causes thrombosis

A

Wircoffs triad
Abnormalities in vessel wall
Abnormalities in blood flow
Abnormalities in blood components

397
Q

What are some vessel abnormalities that might lead to a thrombosis

A

Atheroma (plaque)
Direct injury (not a cut)
Inflammation (like in vasculitis)

398
Q

What kin of abnormalities in blood flow might cause a thrombus

A

Stagnation (eg DVT)

Turbulence (eg aortic stenosis)

399
Q

What kind of abnormalities in blood components can assist in causing a thrombosis

A

Post partum
Post op
Smoking

400
Q

What is the macroscopic appearance of a thrombis in an artery?

A

Pale, granular with lines of zahn, a lower cell contents

401
Q

What creates the lines of zahn seen in a thrombosis in the arteries?

A

At times there are less red cells being laid down making it appear paler.

402
Q

Macroscopically how would a thrombus appear in a vein?

A

Soft, gelatinous, deep red with a high cell content

403
Q

What are 5 potential outcomes of thrombosis ?

A 
Lysis
Propogation
Organisation
Recanalisation
Embolism
404
Q

What is lysis in reference to a thrombosis

A

The complete dissolution of thrombus thanks to the fibrolytic system, bloodflow re-established

405
Q

What is organisation in reference to a thrombosis?

A

Reparative process
Ingrowth of fibroblasts and capillaries much like granulation tissue
Lumen remains obstructed

406
Q

What does the tissue of an organised thrombus resemble?

A

Granulation tissue

407
Q

What is propogation in relation to thrombosis? What direction would this travel

A

Progressive spread of thrombosis
Dismally in arteries
Proximal in veins

408
Q

What is recanalisation in reference to thrombosis

A

Blood flow is re-established but is usually incompetent

One or more channels form through organising thrombus

409
Q

What is thrombo-embolism?

A

Part of thrombus breaks off, travels through blood stream lodging at distant site

410
Q

Where do arterial and venous thrombo-embolisms travel

A

Veins back towards the heart.(usually ending in the lungs)

Arteries away from the heart (commonly renal and mesenteric)

411
Q

What does an arterial thromboembolism usually result in (that a venous one is less likely to)

A

Ischaemia, infarction

412
Q

When will an infarction not develop from an arterial embolism?

A

If there is collateral circulation sufficient enough to not allow ischamia to take place

413
Q

What is a venous embolism likely result in? When may this develop to ischaemia and infarction?

A

Usually congestion and oedema due to increased hydrostatic pressure.
Ischaemia and infarction develop if pressure reaches the same as the arterial side.

414
Q

What is an embolism?

A

Blockage of blood vessel by solid, liquid, gas from distant site of origin (90% thrombo embolism) next most common is air

415
Q

How much air is needed to induce an air embolism? What does it do to blood

A

150ml

Makes blood froffy and hard to pump

416
Q

Where would the fat in a fat embolism be released from?

A

Bone marrow typically

417
Q

What are the 3 determinants of cell population ?

A

Rate of proliferation
Rate of differentiation
Rate of apoptosis

418
Q

Cell proliferation can be pysiological or pathological, what is prostatic hypertrophy an example of?

A

Physiological developing into pathological

419
Q

What regulated normal cell proliferation?

A

Porto-onco genes

420
Q

What controls cell proliferation, altering the expression of proto-onco genes

A

Chemical signals from the micro-environment

421
Q

How does a chemical signal alter the expression of proto-oncogenes

A

Singalling molecule eg steroid, binding to a receptor, usually located in cell membranes in cytoplasm or nucleus and then either activation or inhibition of a genes expression

422
Q

What are the basic 4 things a chemical signal can tell a cell to do re cell growth

A

Survive
Die (apoptosis)
Divide
Differentiate

423
Q

To increase the cell population, what 2 options are available?

A

Shorten cell cycle

Recruit quiescent cells back into cell cycle

424
Q

What can looking for mitosis tell us about a cancer?

A

Aid to grade how aggressively they are dividing

425
Q

In the normal cell, what stops it replicating with damaged dna?

A

Cell cycle checkpoints

426
Q

What is the most critical cell cycle checkpoint?

A

The R point

427
Q

Why is the R point the most critical cell checkpoint?

A

The majority of cells that pass the R point will complete cell cycle
No external signals are needed

428
Q

Before the R point, what signals is the cell responsive to?

A

Mitogenic growth factors

TGF-beta

429
Q

What is the most commonly altered checkpointt in cancers?

A

R point

430
Q

At the R point what can delay the cell cycle, activate repair mechanisms or apoptosis

A

P53

431
Q

What molecules internally control the cell cycle

A

Cyclin and cycli dependent kinases

432
Q

How do cyclins and cyclin dependent kinases work?

A

Cyclin binds to the substrate (target protein), Cyclin dependent kinase phosphorylates it to give the desired action

433
Q

What is the Leonard hayflick number

A

The number of times cells can divide

61

434
Q

What is hyperplasia

A

Increase in cell number

435
Q

What tissues does hyperplasia occur in

A

Labile and stable tissue

436
Q

Why does physiological hyperplasia occur

A

Increased functional demand or hormone stimulation

437
Q

What’s the difference between physiological and pathological hyperplasia

A

Physiological is reversible as it is under control

438
Q

What does pathological hyperplasia increase the risk of?

A

Mutations

439
Q

What’s an example of physiological hyperplasia and pathological hyperplasia

A

Bone marrow response in hypoxia at altitude

Goitre in iron defficency

440
Q

What is hypertrophy

A

Increase in cell size

441
Q

What tissues does hypertrophy occur in?

A

Labile, stable and permanent (especially)

442
Q

Why does hypertrophy occur?

A

Increased demand or hormonal stimulation inducing more cell structural component

443
Q

What is hypertrophy usually accompanied by in labile and stable tissues

A

Hyperplasia

444
Q

What’s compensatory hypertrophy

A

Another organ becoming enlarged as the result of poor function elsewhere

445
Q

What’s an example of pathological and physiological hypertrophy

A

Phys- gainz

Path- hypertrophy in HTN of cardiac muscle

446
Q

What is atrophy

A

Decrease in size and or number of cells

447
Q

What is tissue atrophy often a combination of?

A

Cellular atrophy and apoptosis

448
Q

What happens at a cellular level in atrophy

A

Autophagosomes get rid of cellular components it doesnt need- forming residual bodies

449
Q

What is an example of physiological atrophy

A

Ovarian atrophy post menopause

450
Q

What is metaplasia?

A

Reversible change of cell type

451
Q

What is metaplasia due to?

A

Altered stem cell differentiation

Adaptive substitution of cells sensitive to stress

452
Q

What is metaplasia often a prelude to?

A

Dysplasia and cancer

453
Q

What tissues can undergo metaplasia

A

Labile and stable

454
Q

What does metaplasia not occur across?

A

Germ layers

455
Q

What are examples of metaplasia?

A

Change in bronchial pseudostratified to stratified squamous in cigarette smoking
Change from stratified squamous in gut to glandular epithelium in acid reflux

456
Q

What is aplasia?

A

Complete failure of tissue or organ to develop

Organ who’s cells wont proliferate

457
Q

What is hypoplasia?

A

In spectrum with aplasia, it is the incomplete development of an organ or tissue

458
Q

What is involution?

A

Overlaps with atrophy, it is the normal programmed shrinkage of a tissue eg uterus post birth

459
Q

What is reconstitution?

A

Replacement of lost body part

460
Q

What is atresia?

A

Lack of orrifice

461
Q

What is dysplasia?

A

Abnormal maturation of cells within a tissue, often pre-cancerous

462
Q

What is a neoplasm

A

Abnormal group of cells that persists after the initial stimulus is removed

463
Q

What is a malignant neoplasm

A

Abnormal group of cells persisting after initial stimulus removed + invades surrounding tissue with potential to spread

464
Q

What’s a tumour?

A

Clinically detectable lump of swelling

465
Q

What is a neoplasm an example of?

A

A tumour

466
Q

What is a cancer

A

Any malignant neoplasm

467
Q

What is a metastasis

A

A malignant neoplasm that has spread from original site to a non continuos site

468
Q

A pre-neoplasticism alteration in which cells show disordered tissue organisation is what

A

Dysplasia

469
Q

Why is dysplasia not neoplastic?

A

The change is reversible

470
Q

Tumours can be dividied into what 2 main categories

A

Neoplastic and non neoplastic

471
Q

What is important for something to be a benign neoplasm

A

Confined to original site of origin, doesnt produce metastasis

472
Q

What is important differntiating factor about a malignant neoplastic tumour

A

It has the potential to metastasise

473
Q

How do benign tumours grow

A

In a confined local area with pushing outer margins

474
Q

How do malignant tumours grow

A

Irregular outer margins and may show areas of necrosis and ulceration

475
Q

If something is well differentiated, what does that mean in terms of neoplasm

A

Closely resembles parent tissue

476
Q

Benign neoplasms have what kind of differentiation

A

They are well differentiated

477
Q

Malignant neoplasms show what kind of differentiation?

A

Poorly differentiated

478
Q

What does it mean if a neoplasm is anaplastic

A

No resemblance to any tissue

479
Q

What features are seen with worsening differentiation in neoplasm?

A

Increase nuclear size (nuclear to cytoplasm ratio)
Increased nuclear staining (hyperchromasia)
More mitotic figures
Pheomorphism (change in size and shape of cells and nuclei)

480
Q

If a neoplasm is poorly differentiated, what kind of grading is it?

A

High

481
Q

Mild, moderate and severe dysplasia are measures of what?

A

Worsening differentiation

482
Q

In mutations you have initiators and promoters. What combination of mutations is needed for neoplasia to develop

A

Initial mutagenic initiatior followed by promoters of cell proliferation

483
Q

What is progression in relation to neoplasms?

A

A neoplasm emerging from accumulation of more mutations

484
Q

Are neoplasms monoclonal or polyclonal?

A

Monoclonal

485
Q

How do we know neoplasms are monoclonal

A

Studies where lyonisation has occurred (cells that have random allele in cells in mixed tissues)
Neoplastic tissues only express the one isoenzyme

486
Q

In neoplasms, what do the initial genetic alterations affect?

A

Proto-oncogenes

Tumour suppressor genes

487
Q

How are proto-oncogenes affected in neoplasia

A

They become abnormally activated, then known as oncogenes

488
Q

How are tumour suppressor genes altered to favour neoplasm formation

A

They become inactivated

489
Q

What do benign neoplasms end in?

A

Oma

490
Q

What do malignant neoplasms end in if they are epithelial

A

Carcinoma

491
Q

What do malignant neoplasms get called if it is stromal

A

Sarcoma

492
Q

What is a carcinoma known as if it doesnt invade epithelial basement membrane

A

In situ

493
Q

If a carcinoma penetrate the basement membrane what is it

A

Invasive

494
Q

What’s leukaemia?

A

Malignant neoplasms of blood forming cells arising in the bone marrow

495
Q

What are lymphomas

A

Malignant neoplasms of lymphocytes, mainly affecting lymph nodes

496
Q

What is a myeloma

A

Malignant neoplasm of plasma cells

497
Q

What do germ cell neoplasms arise from

A

Pluripotent cells mainly in testis and ovary

498
Q

What’s a blastoma?

A

Neoplasms mainly in children from immature precursor cells

499
Q

What would a benign fat neoplasm get termed

A

Lipoma

500
Q

What would a benign nerve neoplasm get termed

A

Neuroma

501
Q

What would a benign cartilage neoplasm get called

A

Chondroma

502
Q

What would a malignant neoplasm of bone get called

A

Osteosarcoma

503
Q

What can increase tumour burden

A

The ability of malignant cells to invade distant sites

504
Q

What is the 3 step process if invasion and metastasis and what do they need to avoid at all points

A
  1. Grow and invade primary
  2. Enter a transport system and lodge at secondary
  3. Grow and form colonisation

At all points avoiding destruction by immune cells

505
Q

What 3 important alterations do carcinoma cells require to invade into surrounding tissues?

A

Altered adhesion
Stromal proteolysis
Motility

506
Q

If a carcinoma cell gets the ability to adhere, be motile and have stromal proteolysis what cell phenotype does it more closely resemble. What therefore is this transition called?

A

Mesenchymal

Epithelial- mesenchymal transition EMT

507
Q

What cells does a malignant neoplastic cell have to avoid from the immune system?

A

NKC

CD8

508
Q

Altered adhesion between malignant cells involves what?

A

Reduction in E- Catherine expression

509
Q

Altered adhesion between malignant and stromal cells involves what?

A

Change in integrin expression

510
Q

How does a malignant cell degrade basement membrane and stroma in order to invade a site?

A

Altered expression of proteases. Notably matrix metalloproteinases MMPs

511
Q

What is a cancer niche?

A

When malignant cells take advantage of non-neoplastic cells that provide growth factors and proteases.

512
Q

What does altered motility in a malignant cell involve?

A

Change in the actin skeleton

513
Q

What are the 3 routes that malignant cells can be transported in?

A

Blood vessels- capillaries and venules
Lymphatic vessels
Fluid in body cavities (pleura, peritoneal, pericardial, brain ventricles)

514
Q

What is transcoelomic spread

A

Travel via fluid in body cavities of malignant cells

515
Q

What is the greatest barrier to successful formation of metastasis

A

Failed colinisation

516
Q

What are micrometastases

A

These are surviving microscopic deposits that fail to grow into mets at distant sites

517
Q

What is tumour dormancy and what can it result in?

A

It’s the apparent disease free person harbouring micro mets

These are typically causes of relapses years after apparent cure

518
Q

What are the 2 main determinants of where a secondary neoplasm ends up

A

The regional drainage of the area

The seed and soil phenomenon

519
Q

In terms of secondary neoplasm. In regional drainage, where would the spread be from lymphatic metastisis?

A

The the draining lymph node of the site

520
Q

In transcoelemic spread of mets, what is the likely met site?

A

Adjacent organs

521
Q

In blood borne spread of mets, what is typically the region of the met?

A

To the next capillary bed

522
Q

What is the seed soil phenomena and what does it help explain

A 
The interaction (niche) between certain malignant cells and the environment
Helps explain the seemingly unpredictable nature of blood borne mets?
523
Q

What route do carcinomas tend to spread in first?

A

Lymphatics

524
Q

How do sarcomas tend to spread

A

In the blood stream

525
Q

Where are common sites of blood borne mets?

A

Lung
Bone
Liver
Brain

526
Q

What neoplasms frequently spread to bone mets?

A

Breast, bronchus, kidney, thyroid, prostate

527
Q

What malignant neoplasm is very aggressive and metastisie early?

A

Small cell bronchial carcinoma

528
Q

What cancer rarely metastisies?

A

Basal cell carcinoma of skin

529
Q

What is the likelihood of mets based on?

A

Size of the primary neoplasm

530
Q

How can effects of neoplasms on host be divided?

A

Direct local effects and indirect systemic effects

531
Q

What are the local effects of primary and secondary neoplasms?4

A

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

532
Q

What are some of the systemic effects of neoplasms

A

Tumour burden
Secreted factors such as cytokines, both lead to weight loss malaise, thrombosis and immunosupression
Hormone secretion

533
Q

What neoplasms commonly secrete hormones

A

Neoplasms of endocrine glands

534
Q

What are some of the more miscelannious systemic effects that neoplasms may cause

A 
Neuropathies affecting brain and peripheral nerves
Skin problems like pruritis
Abnormal pigmentation
Fever
Finger clubbing
Myositis
535
Q

What is exophytic growth?

A

Tending to grow outward beyond the surface epithelium

536
Q

What is endophytic growth?

A

Tending to grow inwards towards tissue

537
Q

What is a sarcoma?

A

Malignant tumour of connective tissue

538
Q

What does anaplastic mean?

A

Poor cellular differentiation, losing characteristic of mature cells and there orientation with respect to each other and to endothelial cells

539
Q

What is an adenocarcinoma?

A

Malignant tumour from glandular tissue

540
Q

What is a leiomyoma

A

Benign smooth muscle tumour

541
Q

What is a leiomyosarcoma?

A

Smooth muscle connective tissue tumour

542
Q

What is a lymphoma

A

A group of white blood cell tumours that develops from lymphocytes

543
Q

What are the 2 main categories of lymphoma?

A

Hodgkin’s and non hodgkins

544
Q

What makes it a Hodgkin’s lymphoma?

A

Prescence of reed sternburg cells

545
Q

What does polyploidy mean?

A

More than 2 paired sets of chromosomes

546
Q

What does sessile mean?

A

Attached directly via broad base

ESA 2 (10 decks)

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