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MOD Flashcards

0
Q

What are causes of cellular injury?

A 
Hypoxia
Toxins
Immune response
Free radicals 
Microorganisms
Dietary insufficiency or excess
Physical agent (heat, electricity, trauma etc.)
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1
Q

What are the types of cellular hypoxia?

What are possible causes of each?

A

Hypoxaemic - low arterial oxygen due to lung disease or reduced atmospheric concentration.

Anaemic - decreased ability of the blood to carry oxygen due to the anaemia or co poisoning

Ischaemic - interruption of blood supply to a region due to thrombus or shock

Histiocytic - inability of the cell to utilise oxygen due to poisoning such as cyanide, carbon dioxide or dinitrophenol

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2
Q

What reversible changes happen to a cell as it becomes hypoxic?Why?

A

Lack of oxidative phosphorylation
Fall in ATP
Loss of Na/K ATPase activity
Increased intracellular sodium and calcium and extra cellular potassium
Water follows osmotic gradient into cell causing blebbing of cytoplasm and swelling
Glycolysis increases to raise ATP resulting in lactic acid production lowering pH
This causes clumping of chromatin
Ribosomes detach decreasing protein synthesis

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3
Q

What are the irreversible changes of hypoxic cell injury including the DNA changes?

A 
Cell death by swelling - oncosis
High calcium levels causing inappropriate activation of proteins (e.g. Proteases)
Pyknosis (chromatin shrinking)
Karyohexis  (nucleus fragmentation)
Karyolysis (nucleus dissolution)
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4
Q

How can free radicles be created?

A

Radiation
Fenton reaction
Haber Weiss reaction

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5
Q

What are common mechanisms for cell damage other than hypoxia?

A

Membrane (including organelle) disruption
Nucleus
Proteins (enzymes and structural)
Mitochondria

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6
Q

What are the main mechanisms of free radical injury?

A

Lipid peroxidation - hydroxyl radical reacts with unsaturated hydrocarbon removing one hydrogen to create water. This radical lipid is then react with O2 creating an O2* side group. It can then react with a neighbouring chain creating a OOH side group and making the new chain a radical - this propagates on creating more radical chains.

DNA strand breaking and base alteration

Protein disulphide bridge formation by cysteine oxidation altering structure.

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7
Q

What is the mechanism of reperfusion injury?

A

Increase O2 for free radical production

Influx of inflammatory components such as neutrophils and complement

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8
Q

How do cells protect themselves from injury?

A

Heat shock proteins - mend or mark for degradation misfolded proteins e.g. Ubiquitin

ROS protection - SOD, catalase, glutathione, iron sequestration, antioxidants

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9
Q

Define necrosis

A

The morphological changes that occur after a cells has been dead for some time in a living organism.

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10
Q

What are the four main types of necrosis?

A

Coagulative - cell architecture preserved, proteins denatured
Liquifactive - cell degraded by own active enzymes
Caseous - tb - structureless debris form surrounded by granuloma
Fat - lipids released

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11
Q

What is gangrene? How can it be classified?

A

The clinical description of a mass of necrotic tissue

Dry - coagulative necrosis following arterial occlusion
Wet - liquifactive necrosis typically following infection
Gas - infection usually with Clostridium perfringens

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12
Q

What is infarction?

A

Necrosis resulting from ischaemia (thrombus, emboli, vessel twisting or external compression of vessel).

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13
Q

What are white and red infarcts?

A

White - occurs in solid organs on occlusion of an end artery - no haemorrhage can occur due to solid stroma.

Red - occurs in loose organs, on venous occlusion or where anastamoses or dual supply is present but insufficient to sustain the tissue. There can be haemorrhage into surrounding tissues.

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14
Q

How does potassium release cause damage to the heart?

A

danger around heart as it causes depolarisation towards threshold of myocytes raising the number of inactive vgNa channels slowing upstroke (and has the paradoxical effect of slowing conduction through HCN channels slowing heart rate)

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15
Q

What cell injury mechanisms can lead to hyperkalaemia around the heart?

A

Local - MI

Systemic - crush syndrome burns, tumour lysis sydrome

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16
Q

What toxins can be released from cells that die by oncosis?

A

Potassium
Enzymes (e.g CKMB, ALT)
Myoglobin

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17
Q

What is the main cause and effect of myoglobin release in cell injury?

A

Rhabdomyolysis - damage renal glomeruli causing acute kidney injury.

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18
Q

How does the process of apoptosis differ from oncosis?

A 
Controlled
Few cells 
Requires energy
Membrane integrity maintained
Ordered process
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19
Q

Give some examples of physiological apoptosis

A

Remodelling of an embryo
Distraction of a virus infected cell
Decreasing breast tissue after lactation

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20
Q

Give an example of pathological apoptosis

A

Parkinsons disease
Amylotrophic lateral sclerosis
Alzheimers

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21
Q

How is apoptosis initiated?

A

Intrinsic - DNA degradation or withdrawal of growth factors, increased mitochondrial permeability, release of cytochrome C, activation of capases

Extrinsic - binding of TRAIL to receptor, activates capases

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22
Q

How do cells degenerate in apoptosis?

A

Break into small membrane bound fragments called apoptotic bodies.

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23
Q

How are apoptotic bodies removed?

A

Phagocytosis by neighbouring cells or phagocytotic cells like macrophages.

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24
Q

What is the effector molecule of apoptosis?

A

Capases

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25
Q

What molecules accumulate in cells abnormally?

A

Lipids - fatty liver, xantholasma, athrosclerosis
Proteins - mallory hyaline in liver disease, misfolded proteins
Pigments - coal dust, tattooing ink, bilirubin, haemosiderin lipofusin

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26
Q

What are the two forms of calcification?

A

Malignant - raised serum calcium

Dystrophic - normal serum calcium

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27
Q

Why do cells age?

A

Telomeres shorten with every replication.

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28
Q

What is it termed when telomeres ‘run out’ for a cell?

A

Replicative senescence

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29
Q

What cells telomeres are immortal? Why?

A

Germ cells, some cancer cells

Telomerase enzyme

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30
Q

What enzymes are involved in the metabolism of alcohol?

A

Alcohol dehydroginase

Aldehyde dehydroginase

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31
Q

What is the intermediate and product in alcohol metabolism? What is created?

A

Acetylaldehyde

Acetic acid

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32
Q

Why are women more sensitive to alcohol?

A

Lower levels of alcohol dehydroginase

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33
Q

What are the effects of chronic alcohol intake?

A

Fatty liver from increased acetyl coA and NAPDH

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34
Q

What could occur in acute very excessive alcohol intake?

A

Acute alcoholic hepatitis

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35
Q

What is produced when normal paracetamol metabolism is saturated?
What effect does this have?

A

NAPQI which is conjugated to glutathione
NAPQI is directly toxic binding to sulphydryl groups
Glutathione depletion leaves cells vulnerable to ROS

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36
Q

What patients are high risk in paracetamol overdoses?

A 
Taken with alcohol
Alcoholics
Malnourished
Hiv/aids
Enzyme inducing drug patients
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37
Q

How does n-acetyl cystine work?

A

Prodrug precursor to l-cysteine which is precursor to glutathione

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38
Q

What occurs in an aspirin OD?

A

Stimulation of resp centre causing a resp alkalosis
Body compensates with a metabolic acidosis
Decreased platelet aggregation causes bleeding

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39
Q

What are the four signs of inflammation?

A

Calor
Rubor
Dolor
Tumor

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40
Q

What are the two phases of acute inflammation?

A

Vascular

Cellular

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41
Q

What occurs in the vascular phase of acute inflammation?

A

Brief vasoconstriction
Vasodilation increasing blood flow and capillary hydrostatic pressure
Increased permeability of blood vessels
Leakage of exudate
Raised cellular concentration of blood slowing it down

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42
Q

What triggers the vascular phase of acute inflammation?

A

Histamine released from mast cells, basophils and platelets due to:
Damage
C3a C5a and IL-1 from neutrophils and platelets
Immunologic reactions

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43
Q

What causes pain in vascular phase of acute inflammation?

A

Histamine

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44
Q

What chemical mediators cause increased vascular permeability in acute inflammation?

A 
Histamine
Il-2 
TNF alpha
Direct damage
ROS
Leukotrines
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45
Q

Differentiate transudate from exudate

A

Exudate contains proteins and is only formed when vessel permeability increases as well as hydrostatic and osmotic pressure

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46
Q

What proteins leave the vascular compartment during the vascular phase of acute inflammation? What effect does this have?

A

Fibrin - formation of fibropurilent exudate to contain inflammation
General proteins - increase oncotic pressure increasing exudate formation

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47
Q

What occurs in the cellular phase of acute inflammation?

A

Extravasation of neutrophils

Phagocytosis of debris and pathogens

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48
Q

How do neutrophils enter the tissue fluid?

A

Margination - slow blood leads to cells moving to vessel walls
Rolling - adhere to selectins and roll along wall
Adhesion - adhere tightly to adherins
Emigration - squeeze through gaps between cells digesting basement membrane as they do.

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49
Q

How are neutrophils attracted to areas of acute inflammation?

A

Chemotaxis along concentration gradients of C5a and bacterial peptides

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50
Q

How does acute inflammation aid us?

A

Swelling and pain - enforces rest
Exudation of fibrin - contains damage
Fluid exudation - dilutes toxins
Increased lymph drainage - removes pathogens
Exudation of immune cells - destroy pathogens and debris
Vasodilation - faster delivery of fluid and cells

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51
Q

What are local complications of acute inflammation?

A

Tube compression
Prolonged pain
Loss of function

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52
Q

What are systemic complications of acute inflammation?

A

Fever
Dehydration
Altered plasma proteins
Shock

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53
Q

What are outcomes of acute inflammation?

A

Resolution
Progression to chronic inflammation
Repeated acute inflammation
Death

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54
Q

What aids acute inflammation resolution?

A 
Lymphatic drainage
Short half life of mediators
Proteolytic degradation
Binding of inhibitors
Dilution
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55
Q

How does inflammation cause fever?

A

ILs, prostaglandins and TNF alpha are pyrogens that effect the hypothalamus

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56
Q

Why does chronic inflammation occur?

A

Take over from acute inflammation if damage is too severe to be repaired within a few days
Alongside acute inflammation in repeat irritation
Without acute inflammation in some conditions eg. RA, TB, small foreign body

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57
Q

Hw does chronic inflammation differ from acute?

A

More variable course
Macrophages, lyphocytes, plasma cells and eosinophils
Giant cells

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58
Q

What is the function of macrophages in chronic inflammation?

A

Phagocytosis
Antigen presentation
Release of cytokines, complement and clotting factors

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59
Q

Hw are lymphocytes identified histologically, what is their role in chronic inflammation?

A

Near invisible plasma membrane and cytoplasm

Specific response to a particular antigen

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60
Q

How do plasma cells appear histologically?

A

Clock face nuclei (clumped peripheral chromatin)

White halo of golgi

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61
Q

How do eosinophils appear histologically?

A

Bilobed nuclei in red staining cytoplasm (sunburnt face with sunglasses)

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62
Q

What are the types of giant cells?

A

Langerhans - TB - ordered crescent of nuclei peripherally
Foreign body type - FB! - disordered nuclei, evidence of debris
Toutons - fat - ordered crescent of nuclei with foamy appearance outside of cell

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63
Q

What causes giant cell formation?

A

Frustrated macrophages unable to phagocytose pathogen / debris joins with others.

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64
Q

How does chronic inflammation cause fibrosis? In what conditions does this occur?

A

Mediator production by macrophages cause fibroblast recruitment resulting in collagen production. This causes fibrosis.
This impairs function.
Found in cirrhosis, repeated choleocystitis, fibrotic lung disease

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65
Q

When does chronic inflammation result in up-regulation of function?

A

Graves disease

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66
Q

What is a granuloma?

A

A focal discrete collection of immobile macrophages (epitheloid macrophages) surrounded by lymphocytes.

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67
Q

What causes granuloma formation?

A

Persistent low grade irritation that cant be removed - e.g TB or idiopathic like wegners granulomatoisis and chrones disease

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68
Q

What are the different classifications of stem cells

A

Unipotent
Multipotent
Pluripotent
Totipotent

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69
Q

How can cell division be classified?

A

Labile - actively dividing, no entry to g0
Stable - divides when signalled but usually at rest
Permanent - unable to divide fixed in g0

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70
Q

What factors upregulate cell division? Give examples

A 
Growth factors
Pdgf
Egf
Gh
Oestrogen
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71
Q

What factors downregulate cell division?

A

Adhesion molecules in neighbouring cells and basement membrane (contact inhibition)

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72
Q

When would a tissue repair by fibrous repair not regeneration?

A

Necrosis of permanent cells

Loss of collagen framework of necrosed labile or stable cells

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73
Q

What are the three stages of fibrous repair?

A

Cell migration
Angiogenesis
Extracellular matrix production

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74
Q

What are the cells involved in fibrous repair? What do they do?

A

Inflammatory cells - phagocytosis and mediator release
Endothelial cells for angiogenesis
Fibroblasts and myofibroblasts for matrix production and wound closure.

75
Q

What occurs in the angiogenesis phase of fibrous repair?

A

Growth factors (eg VEGF) trigger preexisting vessels to sprout new vessels

  • endothelial proteolysis of basement membrane
  • migration of endothelial cells by chemotaxis
  • endothelial proliferation
  • maturation and remodelling with recruitment of pericytes
76
Q

Explain the rabbit ear chamber model of fibrous repair

A
  • blood clot forms with acute inflammation progressing to chronic inflammation
  • clot replaced with granulation tissue with anginogenesis, (myo)fibroblast infiltration, ECM production and decline in immune cell levels
  • granulation tissue matures - cell populations decline, collagen increases, myofibroblasts reduce volume.
77
Q

Differentiate healing by primary and secondary intention

A

Primary - edges in apposition, little granulation tissue formation, epidermis regenerates over injury, minimal scarring, there is risk of abcess formation if infection trapped under regenerating epidermis

Secondary - edges not in apposition, clot forms creating an eschar, granulation tissue forms from bottom up forming large scar and wound contraction

78
Q

What local factors could influence wound healing?

A 
Movement/joint
Size of wound
Blood supply
Infection
Radiation
Foreign materials
79
Q

What systemic factors could influence wound healing?

A

Age
Comorbidities - diabetes, CHF, PVD, connective tissue disease, immunosuppressive disease
Medications - steroids, hormones
Dietary deficiency - proteins, vitamins, essential amino acids

80
Q

What are the complications of insufficient wound healing?

A

Dehiscence
Herniation
Ulceration

81
Q

What are the complications of excessive wound healing

A 
Scarring
Keloids
Cirrhosis
Fibrosis
Strictures
Contractures
82
Q

What is the initial response to blood vessel damage?

A

Vasoconstriction and venoconstriction

83
Q

How does a platelet plug form?

A
  • Platelets adhere to connective tissue vessel walls activating them
  • Release of calcium from ER
  • Activation of GPIIb/IIIa receptors which bind to fibrinogen creating cross links to other active platelets
  • Release of vesicles containing ADP and TXA2
  • ADP inhibits adenyl cyclase reducing cAMP reducing inhibition of calcium release
  • TXA increases IP3 increasing calcium release
84
Q

How is inappropriate platelet activation inhibited?

A

Release of prostacyclin by endothelium which activates adenyl cyclase increasing cAMP reducing calcium release

85
Q

How can coagulation be activated?

A

Intrinsic pathway - damaged endothelial cells activating factor XII-XIIa
Extrinsic pathway - release of tissue factor causes factor VII-VIIa - very fast activation.

86
Q

What is the common pathway of coagulation

A

X-Xa
Prothrombin - thrombin
Fibrinogen - fibrin and XIII-XIIIa

87
Q

What are some controls of the coagulation cascade?

A

Antithrombin III - binds thrombin inactivating it
Protein C - binds thrombin becoming APC
APC - deactivates factors Va and VIIIa
Fibrinolysis - plasmin converted to plasminogen breaking down fibrin
Thrombomodulin - increases activation of PC to APC

88
Q

What is a thrombosis?

A

A solid mass of blood in the circulatory system

89
Q

What raises risk of thrombosis?

A

Virchows triad
Abnormal vessel wall (athroma, injury, inflammation)
Abnormal coagulability (stagnation, turbulence)
Abnormal blood flow (smoker, post partum, post op, disease)

90
Q

What is the difference between arterial and venous thrombi?

A

Arterial more platelet based - pale, granular, striated with lines of Zahn
Venous more thrombin based - red and gelatinous

91
Q

What are the outcomes of thrombosis?

A

Lysis
Propagation (proximally in veins, distally in arteries - direction of flow)
Recanalisation
Embolism
Reorganisation (ingrowth of fibroblasts and capillaries - granulation like tissue)

92
Q

What is an embolism?

What is the commonest cause?

A

A blockage of a blood vessel by a solid, liquid or gas distant from its site of origin.
90% are thromboembolisms

93
Q

What are common origins and sites of embolisms?

A

Systemic veins - lungs
Carotid arteries - cerebral arteries
Abdominal aorta - arteries of the leg
Heart - cerebral arteries

94
Q

What are risk factors for DVTs?

A 
Immobility 
Post op hypercoagubility
Pregnancy hypercoagubility
COCP 
Heart failure
Cancer
95
Q

What are mitigations for DVT risk?

A 
Heparin / anticoagulation
Compression stockings
Early mobilisation
Filters in IVC
Intermittent leg compression during surgery
96
Q

Differentiate athroma, athroscleosis and arteriosclerosis

A

Athroma - accumulation of extra and intra cellular lipids in the intima and media of medium and large arteries

Athrosclerosis - hardening of arteries as a consequence of athroma

Arteriosclerosis - thickening hardening of arteries, e.g. Hypertension, DM

97
Q

What are the stages of atroma formation?

What is the macroscopic appearance of each?

A

Fatty streak - slightly raised white or yellow streak
Simple plaque - raised yellow or white plaque
Complex plaque - raised plaque with haemorrhage, infarction, aneurysm and calcification

98
Q

How does a complicated athroma appear histologically?

A

Fibrosis, necrosis, cholesterol clefts, disruption of internal elastic lamina, ingrowth of blood vessels, fissues.

99
Q

What is the histological appearance of simple athroma?

A

Proliferated smooth muscle cells and foam cells

100
Q

What are common locations of athromas with related consequences

A

Coronary arteries - angina / mi
Cerebral arteries - cva / cve
Superior mesenteric artery - ischemic colitis
Legs - pvd

101
Q

What are risk factors for athroma formation?

A 
Age
Gender
Hyperlipidemia 
Smoking
Htn
Diabetes
Alcohol
Infection
102
Q

What is the process of athroma formation?

A

Endothelial injury
Adhesion of platelets and release of PDGF
Proliferation of smooth muscle, macrophage arrival
Phagocytosis of lipids and ldl by smc and macrophage (foam cells)
Macrophages move into intima
Lipoproteins undergo glycosylation
Smc produce unstable matrix weakening plaque
Cytokines from macrophages recruit more inflammatory cells
Neutraphils secrete proteases causing local damage weakening plaque
Lymphocytes stimulate smooth muscle cells

103
Q

What cells are involved in athroma formation?

A

Smooth muscle cells
Macrophages
Lyphocytes
Neutrophils

104
Q

What are possible outcomes of a cell to growth signals?

A

Survive
Die
Divide
Differentiate

105
Q

What are the categories of cell growth signals?

A

Endocrine
Autocrine
Paracrine
Contact

106
Q

What are growth factors?

What are the odd things they effect?

A

Local mediators that bind to receptors to stimulate transcription of genes causing increased return from, G0 and shortening interphase.
Locomotion, contractility, differentiation, viability, angiogenesis.

107
Q

Give some examples of growth factors

A

Epidermal growth factor
Vascular endothelial growth factor
Platelet derived growth factor
Granulocyte colony stimulating factor

108
Q

What are the checkpoints in the cell cycle?

A

G1 end checkpoint - restriction point

G2 end checkpoint

109
Q

What does the restriction point do in the cell cycle?

A

Checks cell size, environment and for dna damage

110
Q

What does the g2 checkpoint do in the cell cycle?

A

Ensures all dna has replicated and the cell is of sufficient size.

111
Q

Which cell checkpoint is the most important in the cell cycle?

A

Restriction point

112
Q

How is cell movement through the cell cycle controlled?

A

Cyclins

113
Q

What cyclins move the cell through the different stages?

A

S to G2 is A
G2 to M is B
M to G1 is D (low)
G1 to S is E

114
Q

How do cyclins work to control cell cycle?

A

Bind to a cyclin dependant kinase which phosphorylates a regulatory protein.

115
Q

How do growth factors effect cyclins?

A

Increase cyclin dependent kinase

Decreased cyclin dependent kinase inhibitors

116
Q

How are cell losses in tissues replaced?

A

Division of a stem cell - one daughter cell remaining undiferentiated, one daughter cell replacing the lost cell.

117
Q

In what ways can cells adapt to stress?

A 
Regeneration
Hypertrophy 
Hyperplasia
Atrophy
Metaplasia
118
Q

What feature of regeneration aids immunity?

A

Replacement cells aren’t immediately mature / fully functional and therefor infection may not be able to colonise or replicate within them.

119
Q

What body parts can reconstitute?

A

Uterine lining

End of a finger tip below a certain age

120
Q

How does the cns ‘regenerate’

A

Origional tissue not restored but plasticity allows for new pathways to form.

121
Q

Why might the cns not regenerate?

A

It may disrupt memory formation

122
Q

Give examples of physiological and pathological hyperplasia

A

Physiological - endometrial proliferation,

Pathological - goitre, eczema

123
Q

Give some physiological and pathological examples of hypertrophy

A

Phys - muscle bulk

Pth - cardiac hypertrophy, prostatic hypertrophy

124
Q

At what point does atrophy become irreversable?

A

When a large number of functional cells are lost

125
Q

Give some examples of atrophy

A

Denervation atrophy

Thin skin in pvd

126
Q

How does metaplasia occur.

A

One differentiated cell type replaced from stem cells by another of the same germ layer

127
Q

What is a neoplasm?

A

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

128
Q

What is a malignant neoplasm?

A

A neoplasm that invades surrounding tissues and has the potential to spread to distant sites

129
Q

What is a tumour?

A

A clinically detectable lump or swelling

130
Q

What is cancer?

A

A malignant neoplasm

131
Q

What is dysplasia?

A

Disordered but reversible cell organisation. Pre neoplastic

132
Q

How do benign neoplasms appear macroscopically?

A

A growing mass with a smooth capsule of compressed tissues

Slow growing

133
Q

What are macroscopic features of malignant neoplasm?

A

Infiltration of surrounding tissues, irregular outer margin, ulceration, necrosis

134
Q

What are microscopic features of benign and malignant neoplasms?

A

Progression from highly differentiated cells to poorly differentiated. More likely to be malignant if poorly differentiated.

135
Q

What cellular cells can be seen in malignant neoplasms?

A

Nuclear hyperchromaisa
Increased nucleus size
Mitotic figures
Pleomorphism (variation in cell size and shape)

136
Q

When are cellular changes very important in malignacy diagnosis?

A

On a needle biopsy.

137
Q

What makes the majority of ca. Risk? Interinsic or extrinsic factors?

A

85% extrinsic

138
Q

What is the initiator promotor model of cancer?

A

Initiators are mutagens that result in a primary mutation. Promotors then cause replication of the cell creating many monoclonal copies.

139
Q

What is the evidence that neoplasms are monoclonal?

A

In a female (xx) look at 2 isoenzymes for g6p dehydroginase (x linked) some cells produce one, some the other. Stain. All neoplasms create just one isoenzyme.

140
Q

What are malignant epilthilial neoplasms called?

A

-carcinoma

141
Q

What are malignant mesenchymal neoplasms called?

A

-sarcoma

142
Q

What is a leukemia?

A

A malignacy of blood forming bone marrow

143
Q

What is a malignancy of lymph nodes?

A

Lymphoma

144
Q

What is a germ cell neoplasm?

A

A malignancy of pluripotent cells

145
Q

What is a blastoma?

A

A neoplasm of imature precusor cells

146
Q

What is a tumour of smooth muscle?

A

Leiomy -oma/sarcoma

147
Q

What is a glioma?

A

A benign tumour of glial cells

148
Q

What is a malignant neoplasm of glial cells?

A

Malignant glioma

149
Q

What are the three steps to metastasis?

A

Grow at primary site
Enter transport systems and lodge at secondary site
Grow at secondary site

150
Q

In order to invade at a primary site what changes must tumour cells undergo and how?

A

Alter adhesion - e-cadherin and integrin must change
Lyse basement membrane - alter niche cells to cause proteolysis
Change cell mobility - alter cytoskeleton such as. Changes to rho family proteins

151
Q

What are the changes in a primary epithelial malignant tumour preparing for metastasis called?

A

Epithelial to mesenchymal transition

152
Q

What is the difference between e-cadherin and integrin?

A

E-cadherin is cell to cell anchoring

Integrin is cell to basement membrane anchoring

153
Q

What routes can tumours spread?

A

Blood
Lymphatics
Transcelomic

154
Q

What is the easiest route for metastasis? Why?

A

Lymphatics - thin membranes

155
Q

What are the common sites of secondaries (very generally!) in each of the three routes of metastasis?

A

Lymph - regional lymph nodes
Blood - first capillary bed reached
Transcoelomic - gravity assisted (eg. Pouch of Douglass)

156
Q

What explains variation in then common rules of tumour metastasis distribution?

A

Seed and soil theory - metastases can only settle where the niche is correct (e.g. Why bronchial tumours metastasis are found in the adrenals but not the kidneys)

157
Q

What is the main route of carcinoma spread

A

Lymphatics

158
Q

What is the main route of sarcoma spread?

A

Blood

159
Q

What common cancers cause bone mets?

A 
Breast
Bronchus
Kidney
Thyroid
Prostate
160
Q

What is growth at secondary site of cancer also known as?

A

Colonisation

161
Q

What is the theory behind cancer relapse?

A

Formation of micrometastases at secondary sites that dont develop can reactivate

162
Q

What are causes of micrometastases dormancy?

A

Immune response
Hostile niche
Failure of angiogenesis

163
Q

What are local clinical effects of neoplasms?

A

Direct invasion and tissue destruction
Blockage of tubes and ducts
Ulceration
Compression of adjacent structures

164
Q

What are the systemic effects of neoplasm?

A

Increased tumour burden - weight loss, malaise, immunosuppression, thrombosis

Hormone production (especially well differentiated tumours, therefore more common in benign tumours)

Poorly understood issues such as clubbing, fever, myositis

165
Q

What are extrinsic causes of cancer?

A 
Environmental factors (e.g. UV exposure) 
Lifestyle factors (e.g. Smoking, overweight, alcohol, low exercise, low fruit and veg)
166
Q

What are examples of intrinisic risk factors for cancer?

A

Age
Sex
Ethnicity
Hereditary defects

167
Q

What are the three categories of extrinsic carcinogens?

A

Chemicals
Radiation
Infection

168
Q

What are the typical characteristics of chemical carcinogens?

A

Long delay between exposure and cancer
Increased risk with increased dose
Can be organ specific

169
Q

Give some examples of chemical carcinogens

A

Asbestos - mesothelioma

Tobacco - bronchial carcinoma

170
Q

What is the term for a chemical which is a initiator and a promotor of cancer?

A

Complete carcinogen

171
Q

What are the types of nuclear radiation?

A

Alpha
Beta
Gamma

172
Q

What are the electromagnetic carcinogenes?

A

UV
Xray
Gamma ray

173
Q

Which radiationn carcinogens cause ionisation?

A

Alpha, beta and gamma as well as xrays.

174
Q

Which electormagentic carcinogen has the shortest wavelenght?

A

Gamma rays

175
Q

How does ionising radiation work?

A

Strips electrons off atoms

176
Q

What are examples of direct and indirect damage from radiation?

A

Direct - alteration of bases etc

Indirect - production of ROS

177
Q

What are direct and indirect carcinogenic mechanisms of infection?

A

Direct - influencing protooncogene and tsg

Indirect - cause chronic injury necessitating regeneration (acting as a promotor)

178
Q

How does HPV cause cancer?

A

Expresses proteins E6 (inhibits p53) and E7 (inhibits RB)

179
Q

What infections cause cancer by the indirect route?

A

Hep b/c
H pylori
Liver flukes

180
Q

How does hiv raise cancer risk?

A

Lower immune system therefore increased risk of carcinogenic infection such as karposi’s sarcoma

181
Q

What is knudsons two hit hypothesis?

A

Both copies of a gene must be defective for a tumour suppressor gene to be deactivated. If one is defective due inherited mutation then you are much much more likely to experience the deactivation as only one further mutation is required.

182
Q

How many copies of a gene need to be mutated to turn a protoncogene into an oncogene

A

One, it is upregulation.

183
Q

What do protoncogenes commonly code for?

A 
Growth factors (e.g. Pdgf)
Growth factor receptors (e.g. HER2)
Signal transducers (e.g. RAS activating cyclin D)
Cyclins
Transcription factors
184
Q

Other than oncogenes and protooncogenes what other mutations can increase cancer risk?
Give examples

A

Dna repair genes
Xeroderma pigmentosum - mutation in nucleotide excision repair gene responsible for repairing UV damage
HNPCC - mutation in mismatch repair gene
Familial Ca breast - BRCA1/2 repair double stranded DNA breaks therefore mutation increases risk of translocation or gene loss.

185
Q

What are the 6 hallmarks of cancer?

A 
Self sufficient growth 
Ignore stop growth signals
Ignore apoptosis signals
No limit to number of divisions
Ability to undergo angiogenesis
Ability to metastasise

PPE (12 decks)

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