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MOD Flashcards

0
Q

Five causes of cell death

A

Hypoxia, toxins, immune mechanisms, microorganisms, dietary insufficiency, genetic, heat, cold, trauma.

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1
Q

Definition of disease

A

Consequence of failed homeostasis, with consequent morphological and functional disturbances.

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2
Q

4 targets of cell injury

A

Cell membrane, nucleus, proteins (e.g. Structural proteins), mitochondria.

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3
Q

Describe Reversible hypoxic injury

A

Reduced ATP synthesis, Na+/K+ pump works less well. NA+ and water enters the cell resulting in oncosis. Ca2+ also enters, causing loss of microvilli, blebs and ER swelling. Anaerobic respiration takes place, causing increase in lactate, and decreased pH. This causes ribosomes to detach from ER and fat to accumulate.

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4
Q

Describe Irreversible hypoxic injury.

A

Most cells die due to oncosis. Increased permeability of membrane causing influx of ca2+ which activates enzymes, such as ATPase and Phospholipase. Lysosomes membrane is also damaged, so enzymes leak into the cell. Intracellular substances also leak out.

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5
Q

Why is returning blood flow to a previously ischaemic area harmful?

A

Increased production of ROS, increased neutrophils and activation of complement pathway.

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6
Q

Defences against ROS include…?

A

SOD enzyme, Vit A,C & E.

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7
Q

Role of heat shock proteins,

A

Protection against cell injury. Recognise misfolded proteins and repair them. If not possible to repair, then destroy them. Maintains protein viability.

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8
Q

Appearance of injured cells via light microscopy.

A

Reduced pink staining. Clumped chromatin, then pyknosis (shrinkage), karyorhexis (fragmentation), and karyolysis (dissolution) of the nucleus.

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9
Q

Appearance of injured cells via electron microscopy

A

Swelling, cytoplasmic blebs, clumped chromatin, myelin figures, ER lysis and swollen mitochondria.

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10
Q

What is oncosis

A

Cell death with swelling. (Changes prior to death).

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11
Q

What is necrosis?

A

Morphological changes in living organisms after cell died some time ago.

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12
Q

What is apoptosis?

A

Cell death with shrinkage, induced by regulated Intracellular programme, where enzymes degrade its own DNA and proteins.
Non-random cleavage of DNA. Helps to sculpt during embryological development aswell as removes unwanted/virally infected cells.

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13
Q

Describe the 4 types of necrosis.

A

Coagulative: protein denaturation. Ghost outline of cells. Cell proteins less soluble. Appears white.
Liquefactive: enzyme digestion of tissues. Neutrophil infiltration. Tissue becomes viscous. Pus present.
Caseous: structureless debris. Associated with infection. E.g TB
Fat Necrosis: adipose destruction. Increased release of lipases. FA release, which reacts with Ca2+ to form deposits (calcium soaps).

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14
Q

What is gangrene?

A

Necrosis visible to the naked eye. Can be dry (exposure to air) or wet (infection with bacteria).

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15
Q

What is an infarction?

A

Obstruction to a tissues blood supply. Can cause necrosis.

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16
Q

Where would you find white infarcts?

A

In solid organs such as the spleen, heart and kidneys. Due to end artery occlusion.

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17
Q

Where would you find red infarcts?

A

Looser organs such as lungs and small intestines. Caused by extensive haemorrhage into dead tissue due to dual blood supply.

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18
Q

Appearance of cells post apoptosis.

A

Shrunken, condensed chromatin, cytoplasmic budding, fragmentation forming apoptic bodies that are phagocytosed.

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19
Q

Intrinsic apoptosis process

A

DNA damage activates P53. This increases permeability of the mitochondria. Cytochrome C protein leaks out and binds to APAF. This then associates with Procaspase 9, forming an apoptosome. Caspase becomes activated causing apoptosis to take place.

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20
Q

Extrinsic apoptosis process

A

External Ligands such as TRAIL bind to death receptors on the outer cell membrane. Procaspase 8 binds, leading to activation of caspase 8. This initiates apoptosis.

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21
Q

What is pathological calcification?

A

Abnormal calcium salt deposition in tissues.

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22
Q

The two types of pathological calcification?

A

DYSTROPHIC: Only in area of dying tissue. Causes nucleation of hydroxyapatite crystals. Causes organ dysfunction.

METASTATIC: Affects whole body. Due to calcium metabolism disturbance. Can be lethal. Caused by PTH over secretion.

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23
Q

Relevance of cellular ageing?

A

Cells cannot replicate indefinitely as telomeres shorten. (Except germ cells as they contain telomerase to maintain telomeres)

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24
Q

3 effects of chronic alcohol intake on the liver

A

1) Fatty change, causing steatosis. (Reversible)
2) Acute alcoholic hepatitis. Malory bodies form and neutrophils infiltrate.
3) cirrhosis. Leads to a hard, shrunken, knobbly liver. Irreversible and potentially fatal.

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25
Q

What is acute inflammation?

A

The response to injury of vascularised tissue. It is innate, immediate and has a short duration.

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26
Q

What are 5 causes of acute inflammation?

A
  • foreign bodies
  • infections and microbial toxins
  • trauma
  • immune reactions
  • tissue necrosis
  • physical and chemical agents
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27
Q

What are the 5 clinical signs of acute inflammation?

A 
Rubor - redness
Tumour - swelling
Color - heat 
Dolor - pain
Loss of function, enforcing rest
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28
Q

What causes the pain during acute inflammation?

A

Stimulation of nerve endings by mediators, especially bradykinin.

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29
Q

Describe the change in blood flow during acute inflammation.

A

Vasoconstriction then vasodilation of arterioles and capillaries, increasing blood flow.
Increased permeability of blood vessels allowing plasma to escape.
Slowing of circulation.
Histamine released from mast cells causing increased vascular permeability and vasodilation.

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30
Q

Explain exudation of fluid into tissues during acute inflammation.

A

Membranes become leaky, arterioles dilate and plasma proteins escape into tissue. Increasing the fluid flow out of vessels, leading to oedema (increased fluid in tissue spaces).

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31
Q

What is exudate oedema?

A

Fluid loss in inflammation. High protein content.

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32
Q

What is transudate?

A

Fluid loss due to hydrostatic pressure imbalance. Low protein content.

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33
Q

How is excess fluid drained during acute inflammation.

A

Via lymphatic system ,taking microorganisms and antigens too. These are then presented to the immune system in the lymph nodes.

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34
Q

What is the role of opsonins?

A

They coat foreign material for phagocytosis.

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35
Q

What does neutrophil presence indicate?

A

A bacterial/parasitic invasion.

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36
Q

What are the 6 stages of a neutrophil?

A

1) chemotaxis
2) activation
3) margination
4) diapedesis
5) recognition-attachment
6) phagocytosis

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37
Q

What is chemotaxis?

A

The directional movement towards a chemical attractant.

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38
Q

How are neutrophils activated?

A

Ca2+ and Na+ ions rush into the cell. The cell swells and reorganises its cytoskeleton. The cell then sends out pseudopodia (cell extensions)

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39
Q

How do leukocytes leave venules?

A

Diapedesis- they produce collagenase that digests the basement membrane, allowing them to move towards their target.

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40
Q

Explain the recognition-attachment stage of neutrophils

A

They recognise bacteria via opsonins/ microbial surface antigens, and phagocytose them.

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41
Q

What are the two types of phagocytosis?

A
  • oxygen-dependent: uses oxygen derived free-radicals which are then released into the phagosome = oxygen bursts.
  • oxygen-independent: uses enzymes e.g. Proteases, nucleases, lysozymes.
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42
Q

Name 3 types of chemical mediators

A

Proteases (e.g. Kinins, complement system)
Prostaglandins/leukotrienes
Cytokines/chemokines (made by WBCs)

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43
Q

Which two chemical mediators cause increased blood flow?

A

Histamine and prostaglandins

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44
Q

Which chemical mediators increase vascular permeability?

A

Histamine and leukotrienes

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45
Q

Which chemical mediators induce neutrophil chemotaxis?

A

C5a, bacterial peptides.

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46
Q

Which chemical mediators induce phagocytosis?

A

C3b

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47
Q

What are some local complications of acute inflammation

A
  • blockage of tubes e.g. Bile duct
  • compression of vital structures e.g. Cardiac tamponade
  • damage to normal tissue
  • loss of fluid as it continuously leaks from skin wounds e.g. Burns
  • pain and Loss of function
48
Q

Name three systemic consequences of acute inflammation.

A

Fever
Leukocytosis
Shock
Acute phase response

49
Q

Why is fever a consequence of acute inflammation?

A

Exogenous pyrogens stimulate macrophages to produce pyrogenic cytokines. These increase the synthesis of prostaglandin E2 in the hypothalamus.

50
Q

Explain shock

A

Spread of microorganisms and toxins in the blood stream cause a dramatic drop in blood pressure due to vasodilation and increase in vascular permeability.

51
Q

Describe resolution post acute inflammation.

A

When stimulus is removed, mediators are no longer present. So normal vascular permeability returns, there’s cessation of neutrophil emigration and exudate is reabsorbed via lymphatic drainage. Fibrin is degraded by plasmin. Neutrophils die and are phagocytosed via macrophages. Degenerated tissue may be able to regenerate, if not, scar tissue forms.

52
Q

What are possible sequelae of acute inflammation?

A

Complete resolution
Death
Abscess
Fibrous repair

53
Q

How does chronic inflammation arise?

A
  • may take over from acute inflammation if damage not resolved
  • may arise from scratch e.g. Some autoimmune conditions
  • may develop alongside acute inflammation
54
Q

Which cell types are present in chronic inflammation?

A
  • macrophages for phagocytosis, antigen presenting and synthesis of cytokines/complement components/clotting factors Etc.
  • lymphocytes: B to produce antibodies & T for control/cytotoxic function
  • eosinophils: role in allergic reactions/parasite invasions/some tumours
  • fibroblasts/myofibroblasts to produce collagen (fibrosis)
55
Q

What are giant cells?

A

Multinucleate cells made by fusion of macrophages during frustrated phagocytosis. Langhan’s (TB), foreign body type and touton (fat necrosis).

56
Q

Give four effects of chronic inflammation.

A
  • fibrosis
  • impaired function
  • atrophy
  • stimulation of immune response
57
Q

Ulcerative Collitis vs. Crohn’s Disease

A

UC: superficial, diarrhoea, rectal bleeding. Treat with immunosuppressants/colectomy

CD: transmural, strictures, fistulae, treat via lifestyle modifications/immunosuppressants

58
Q

What is chronic cholecystitis?

A

Repeated gall bladder obstruction due to gallstones, leading to chronic inflammation/fibrosis of the gall bladder wall.

59
Q

What is cirrhosis?

A

Chronic inflammation with fibrosis leading to disorganisation of architecture and attempted regeneration. Commonly caused by alcohol/fatty liver disease/drugs. Cannot be revered. Treatment only prevents further damage.

60
Q

What is granulomatous inflammation?

A
  • chronic inflammation with granulomas.
  • granulomas made when body can’t deal with particles that are difficult to eliminate. E.g. Thorns/splinters/TB
  • granulomas form around the particle, and concentrates mononuclear cells within it to destroy the particle. E.g. Macrophages.
61
Q

What is TB?

A

Tuberculosis is caused by a mycobacterium, and causes disease by persistence and induction of cell-mediated immunity.

  • tuberculosis granulomas contain caseous necrosis.
  • outcomes include fibrosis/scarring, erosion into bronchus, TB emphysema etc.
62
Q

What is regeneration/resolution?

A

The growth of cells and tissue to replace lost structures. Damage to the tissue cannot be extensive.

63
Q

What are the three types of tissue?

A
  • Labile: proliferate throughout life, replacing destroyed cells. E.g. Surface epithelia.
  • Stable: low level of replication, but can divide in response to stimuli. (cells are in G0 but can enter G1) e.g. Hepatocytes/fibroblasts
  • Permanent: cells have left the cell cycle and cannot undergo mitosis. E.g. Nerve cells/cardiac myocytes.
64
Q

What are the three types of stem cells?

A
  • Unipotent: can only give rise to one type of adult cell e.g. Epithelia
  • Multipotent: can produce several types of differentiated cells e.g. Haematopoietic.
  • Totipotent: can produce any type of cell.
65
Q

Describe fibrous repair.

A

-takes place when permanent tissue undergoes necrosis or when collagen framework of Labile/stable cells is destroyed.

1) phagocytosis of necrotic tissue debris
2) proliferation of endothelial cells, giving new capillary growth
3) proliferation of fibroblasts and myofibroblasts to synthesis collage and cause wound contraction, forming granulation tissue
4) granulation tissue becomes less vascular and matures to fibrous scar
5) scar matures and shrinks due to contraction of fibrils in myofibroblasts

66
Q

What are some of the roles of extracellular matrix?

A 
Supports/anchors cells.
Separates tissue compartments
Sequesters growth factors
Allows communication between cells
Facilities cell migration
67
Q

What are the stages of angiogenesis?

A

1) Endothelial proteolysis of basement membrane
2) Migration of endothelial cells via chemotaxis
3) Endothelial proliferation
4) Endothelial maturation and tubular modelling
5) Recruitment of periendothelial cells

68
Q

Give three conditions involving defects of collagen synthesis.

A

1) Scurvy (Vit C deficiency). This required for hydroxylation of alpha-chains. Lacks strength and vulnerable to degradation.
2) Ehlers-Danlos. Inherited. Collagen fibres lack tensile strength so skin is hypertensible, fragile and easily injured. Also poor wound healing.
3) Osteogenesis Imperfecta. Brittle bones and blue sclera due to too little collagen.
4) Alport syndrome. Type 4 collagen abnormal, so dysfunction of the glomerula membrane, cochlea of ear and lens of eye.

69
Q

What are the three types of cell communication?

A
  • autocrine: cells respond to signalling molecules that they produce themselves
  • paracrine: a cell produces the signalling molecule, which acts on adjacent cells,
  • endocrine: hormones synthesised by cells in an endocrine organ are conveyed in the bloodstream to target tissue.
70
Q

What are growth factors?

A

Polypeptides that act on specific cell surface receptors. Coded for by proto-oncogenes. Stimulate cell proliferation or inhibition, by stimulating the transcription of genes that regulate the entry of the cell into the cell cycle.

71
Q

What is contact inhibition?

A

Normal cells replicate until they have cells touching them and then they will stop. It is altered in malignant cells.
Cells adhere to each other via cadherins and they bind to extracellular matrix via integrins.

72
Q

What is healing by primary intention and what are the stages?

A

Occurs in closed, incisional, non-infected wounds, where there is only death of limited number of epithelial and CT cells.

1) Haemostasis. Severed arteries contract. Blood clot forms.
2) Inflammation. Neutrophils at margins, warding off bacteria.
3) Migration of cells. Macrophages scavenge dead neutrophils as well as secrete cytokines to attract fibroblasts/endothelial cells. Basement membrane components deposited.
4) Regeneration. Granulation tissue invades, epidermal layer thickens and scab falls off. Collagen produced and angiogenesis progresses.
5) Early scarring. Fibroblasts proliferate and produce collagen forming scar. White cells infiltrate. Oedema and increased vascularity.
6) Scar maturation. Scar becomes fibrous tissue with collagen fibres, few cells, few vessels and few elastic fibres.

73
Q

What is healing by secondary intention?

A

In excisional wounds/wounds with tissue loss and separated edges. As well as in infected wounds.
-opened wound filled with granulation tissue from the wound margins. There is more intense inflammation. Wound contraction to close defect, mostly done by myofibroblasts. Substantial scar forms, with a thinner new epidermis.

74
Q

How do bone fractures heal?

A

Haematoma forms, followed by a fibrin mesh and granulation tissue. Cytokines released, promoting osteoclastic/osteoblastic activity. Soft callus forms, consisting of fibrous tissue and cartilage, forming bulge. Hard callus appears due to osteoblasts. Woven bone to lamellar bone. Remodelling.

75
Q

Give 4 local and 4 systemic factors that affect wound healing.

A

Local: size/location/type of wound, blood supply, infection, foreign bodies, protection (dressings)

Systemic: age, anaemia, obesity, diabetes, malignancy, genetic disorders, drugs, vitamin c deficiency.

76
Q

Give three complications of fibrous repair.

A

Formation of fibrous adhesions, loss of function, overproduction of scar tissue, excessive scar contraction.

77
Q

Can liver cells regenerate?

A

Yes. There is compensatory growth of liver tissue if part of liver is removed. Almost all hepatocytes replicate during regeneration.

78
Q

Can peripheral nerves regenerate?

A

When a nerve is severed, the axons degenerate. The proximal stumps of the degenerated axons sprout and elongate. They use Schwann cells to guide them back to the tissue that the nerve innervates. Axon growth = 1-3mm/day

79
Q

What is Haemostasis?

A

The body’s response to stop bleeding and loss of blood.

  • the blood vessels constrict to limit blood loss
  • platelets adhere to damaged vessel wall and to each other, forming a platelet plug.
  • coagulation cascade activates components. Prothrombin to thrombin activates conversion of fibrinogen to fibrin
  • fibrinolysis breaks down fibrin via plasminogen.
80
Q

What is thrombosis and what is it caused by?

A

=the formation of a solid mass of blood within the circulatory system during life.
Caused by virchow’s triad:
-changes in blood flow e.g. Stagnation/turbulence
-changes in vessel wall e.g. Atheroma
-changes in blood components e.g. Smokers/post-partum

81
Q

What are the five possible outcomes of thrombosis?

A

1) lysis- complete dissolution of thrombus, blood flow re-established.
2) propagation- spread of thrombosis, distally in arteries, proximally in veins
3) organisation- reparative process with ingrowth of fibroblasts and capillaries. Lumen remains obstructed.
4) recanalisation- blood flow re-established, usually incompletely. One of more channels formed through organising thrombus.
5) embolism- part of the thrombus breaks off and travels through bloodstream and lodges at a distant site.

82
Q

What is an embolism?

A

The blockage of a blood vessel by a solid/liquid/gas at a site distant from its origin. 90% are thrombo-emboli. Others include air, amniotic fluid, nitrogen and tumours.

83
Q

Where will thrombo-emboli from systemic veins lodge?

A

The lungs (pulmonary emboli) as they wont get stuck in large veins near heart.

84
Q

What can cause fat embolisms?

A

Long bone fractures/lacerations of adipose.

85
Q

What is disseminated intravascular coagulation?

A

Pathological activation of coagulation mechanisms that happen in response to disease. Small clots form throughout the body, disrupting normal coagulation as they use up all the clotting factors. Abnormal bleeding occurs from the skin. Triggers include infection, trauma, liver disease and obstetric complications.

86
Q

Describe haemophilia.

A

Type A (factor 8 deficiency). Type B (factor 9 deficiency).

  • X-linked recessive due to nonsense point mutation.
  • haemorrhage into major joints, synovial hypertrophy, pain.
  • muscle bleeding causes necrosis and pressure on nerves
  • replace clotting factors.
87
Q

What is thrombocytopenia?

A

Platelet count well below normal. Due to either platelet production failure/increase in platelet destruction.
Usually accompanied by bone marrow dysfunction.

88
Q

What is atherosclerosis?

A

The thickening and hardening of arterial walls as a consequence of Atheroma.

89
Q

What is Atheroma?

A

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

90
Q

What is arteriosclerosis?

A

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

91
Q

How are atherosclerotic lesions formed?

A
  • injury to endothelium of an artery wall.
  • endothelial cells undergo functional alterations to allow inflammatory cells and lipids to enter intimal layer and form plaque.
  • foam cells die via apoptosis and empty lipids into lipid core.
  • tissue repair. Growth factors stimulate proliferation of intimal smooth muscle cells and collagen synthesis. Fibrous cap encloses lipid-rich core.
92
Q

Atheroma appearance macroscopically.

A
  • fatty streaks, composed of lipid-laden macrophages
  • simple plaque with irregular outline that enlarges
  • complicated plaque e.g. Due to haemorrhage/calcification etc.
93
Q

Atheroma appearance microscopically.

A
  • early stages: proliferation of smooth muscle cells, accumulation of foam cells and extracellular lipid
  • later changes: fibrosis/necrosis. Cholesterol clefts and +/- inflammatory cells.
94
Q

Give four CHD risk factors.

A

Gender (women protected before menopause), hyperlipidaemia, alcohol, cigarette smoking, hypertension, diabetes mellitus.

Also genetic predispositions and infection.

95
Q

What is the unifying hypothesis of antherogenesis?

A
  • endothelial injury due to raised LDLs, toxins, hypertension etc.
  • endothelial injury causes platelet adhesion, PDGR release, SMC proliferation, uptake of lipid by macrophages and migration of monocytes into intima.
  • stimulated SMC produce matrix material
  • foam cells secrete cytokines causing further SMC proliferation and recruitment of other inflammatory cells.
96
Q

What is the role of the restriction point in the cell cycle?

A

It is a checkpoint that decides whether or not cell should continue in cell cycle. If activation occurs, p53 protein suspends cell cycle and trigger DNA repair mechanisms. If unrepairable, then apoptosis.

97
Q

How is progression through cell cycle regulated?

A

By cyclin proteins and cyclin-dependent kinases. Activated CDKs drive the cell cycle by phosphorylating proteins.
The mechanism is regulated by CDK inhibitors that are shut off by some growth factors.

98
Q

Give five different types of cellular adaptations.

A
  • regeneration (replacement of cell losses by identical cells)
  • hyperplasia (increased cell number, increasing tissue/organ size)
  • hypertrophy (increased cell size, increasing tissue/organ size)
  • atrophy (decrease in size/number of cells,decreasing tissue/organ size)
  • mataplasia (reversible change of one cell type to another)
  • hypoplasia (incomplete development of tissue at embryonic stage)
  • aplasia(compete failure of tissue/organ to develop at embryonic stage)
  • involution (normal programmed shrinkage of an organ e.g. Uterus)
  • atresia (body orifice/passage abnormally closed/absent)
  • dysplasia (abnormal maturation of cells within a tissue)
99
Q

What is neoplasm?

A

Abnormal growth of cells that persists after the initial stimulus us removed.
Malignant neoplasms also invade the surrounding tissue, with potential to spread to distant sites.

100
Q

What is a tumour?

What is a cancer?

A

Tumour is any clinically detectable lump or swelling.

Cancer is any malignant neoplasm.

101
Q

What is metastasis?

What is dysplasia?

A

Metastasis: a malignant neoplasm that has spread from original site. The place to which it has spread is called the secondary site.

Dysplasia: pre-neoplastic alteration in which cells show disordered tissue organisation, it is reversible.

102
Q

Property of a benign neoplasm?

A

They are confined to their site of origin and so do not produce metastasis. They have a pushing outer margin. Rarely dangerous.

103
Q

Property of a malignant neoplasm?

A

Have potential to metastasise. They have an irregular outer margin and shape and may show signs of necrosis and ulceration.

104
Q

Well differentiated vs. poorly differentiated

A

Well differentiated: e.g. Benign neoplasm has cells that closely resemble parent tissue = low grade.

Poorly differentiated: e.g. Malignant neoplasm have cells that show no resemblance to any tissue = high grade = anaplastic.

105
Q

Give three things that neoplasms can show under the microscope.

A
  • increasing nuclear size and nuclear to cytoplasmic ratio.
  • nuclear hyperchromasia (dark stainings)
  • more mitotic figures
  • increasing variation of size and shape of cells and nuclei (pleomorphism)
106
Q

What do initiators and promotors do?

A

Mutations are caused by initiators, which are mutagenic agents, e.g. Chemicals, infections and radiation.
Promotors cause cell proliferation.
Together they result in an expanded, monoclonar populations of mutant cells.

107
Q

What does the term monoclonal neoplasm mean?

A

The cells originate from a single founding cell.

Proven via a study of x-linked gene for G6PD enzyme in tumour tissue from women.

108
Q

What is the suffix for naming benign and malignant tumours?

A

Benign: -oma
Malignant: -carcinoma (if epithelial)
-sarcoma (if stromal)

109
Q

Give the benign and malignant names for neoplasms of smooth Muscle, fibrous tissue, bone, cartilage, fat and glial cells.

A

Smooth muscle: B= leiomyoma M= leiomyosarcoma
Fibrous tissue: B= fibroma M= fibrosarcoma
Bone: B= osteoma M= osteosarcoma
Cartilage: B= chondroma M= chondrosarcoma
Fat: B= lipoma M= liposarcoma
Glial cells: B= glioma M= malignant glioma

110
Q

In terms of neoplasm, what is invasion and what is metastasis?

A 
Invasion= the ability of cells to break through the basement membrane & spread.
Metastasis= the spread of a malignant tumour to a distant site.
111
Q

Describe malignant cell invasion.

A

Requires 3 alterations to allow epithelial cells to appear like mesenchymal cells:

1) altered adhesion- reduce E-cadherin expression, aswell as changes in integrin expression to alter adhesion between malignant cells and stromal proteins.
2) stromal proteolysis- altered expression of proteases, notably matrix metalloproteinases.
3) altered motility- changes in actin cytoskeleton via signalling through integrins. Changes take place via small G-proteins.

112
Q

Give three ways that malignant cells can transport to distant sites.

A

1) via blood vessels, enter capillaries. Angigenesis also allows entrance.
2) via lymphatic vessels
3) spread via fluid in body cavities = transcoelomic spread

113
Q

What must malignant cells do at secondary site?

A
  • leave vessel (extravasation) and grow (colonisation).

- some malignant cells lodge at secondary site but die/fail to grow= micrometastases. (Tumour dormancy).

114
Q

Give three common sites of blood borne metastasis.

A

Lung
Bone
Liver
Brain

115
Q

Give three neoplasms that commonly spread to bone.

A 
Breast
Bronchus
Kidney
Thyroid 
Prostate
116
Q

Give three local effects of neoplasms.

A

Due to Direct invasion and Destruction of normal tissue.

  • bleeding
  • compression of adjacent structures
  • blocking tubes and orifices
117
Q

Give three systemic effects of neoplasms.

A

-increasing tumour burden leads to parasitic effect on host.

118
Q

4 causes of hypoxia

A

Hypoxaemic- arterial oxygen conc. is low
Anaemic- decreases Hb ability to carry oxygen
Ischaemic- blood supply interruption
Histiocytic- inability to use O2 in cells due to disabled oxidative phosphorylation enzymes

ESA 2 (7 decks)

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