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Mine ESA 2 > Mechanisms of Disease > Flashcards

Mechanisms of Disease Flashcards

0
Q

What are the cause of hypoxia?

A

-hypoxaemia, anaemia, Ischaemia, histiocytic

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1
Q

What are the causes of cell injury and death?

A
  • hypoxia
  • physical agent
  • radiation
  • Toxins
  • Microorganisms
  • immune mechanisms
  • dietary insufficiencies
  • genetic abnormalities
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2
Q

What does histiocytic mean?

A

Inability to utilise oxygen in cells due to disabled oxidative phosphorlytic enzymes

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3
Q

What principle structures are the target for cell damage?

A

Cell membranes
Nucleus/DNA
Proteins, structural and enzymes
Mitochondria

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4
Q

What are the changes in reversible, hypoxic injury?

A

Loss of activity of sodium potassium ATPase
Cell switches to anaerobic metabolism
Ribosomes detach from ER so protein synthesis is disrupted

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5
Q

What occurs in irreversible hypoxic injury?

A

Profound disturbances in membrane integrity
Massive cystolic accumulations of calcium
Potent enzymes attracted elf. ATPase, endonuclease, proteases
Continuation of lysosomal damage

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6
Q

What is ischaemic reperfusion injury?

A

Blood floe is returned to tissue which has been subjected to Ischaemia but isn’t yet necrotic, the damage sustained by the return of flow can be worse

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7
Q

Possible causes of injury in ischaemic reperfusion injury?

A

Increased production of oxygen free radicals
Increased number of neutrophils, more inflammation and increased tissue injury
Delivery of complement protein and activation of complement pathway

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8
Q

What do chemicals do in chemical injury?

A

Some chemical act by combining with cellular component e.g. Cyanamide binging to mitochondrial cytochrome oxidase inhibiting ET and OP

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9
Q

What are free radicals?

A

Are reactive oxygen species with a single unpaired electron in their outer shell, they are unstable and are very reactive

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10
Q

How are free radicals produced?

A

Chemical and radiation injury
Cellular ageing
Ischaemic reperfusion injury
High oxygen concentration

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11
Q

What do free radicals do that is bad?

A

Attack lipid in cell membranes causing lipid per oxidation
Damage protein and nucleic acids
Know to be mutagenic

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12
Q

What do free radicals to that is good?

A

Produced by leuocytes in immune systems oxidative burst

Used in cell signalling

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13
Q

What are heat shock proteins used for?

A

These are proteins which are concerned with the upkeep of cellular proteins e..g ubiquitin and aim to mend and maintain then retaining cell viability

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14
Q

What is seen under a light microscope during cell injury?

A 
Cytoplasmic: 
Decreased pink staining of cytoplasm, increased blue staining due to detachment of ribosomes from ER 
Nuclear:
Pyknosis, shrinkage 
Karryosensis, fragmentation 
Karryolysis, dissolution of nucleus
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15
Q

What is seen under a electron microscope during cell injury?

A

Reversible:
Swelling, cyctoplasmic blebs, clumped chromatin, ribosomes separated from ER
Irreversible:
Further cell swelling, nuclear changes, swelling and rupture of lysosomes, membrane defects, myelin figures, lysis of ER, amorphorosis densities in swollen mitochondria

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16
Q

Define oncosis

A

Cell death with swelling, the spectrum of changes that occur in injured cells prior to death

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17
Q

Define necrosis

A

The morphological changes that follow cell death in living tissue, largely due to progressive degrading action of enzymes in a lethally injured cell

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18
Q

Define apoptosis

A

Cell death induced by a regulated intracellular programme where a cell activates enzymes that degrade it’s own nuclear DNA and protein. Cell death with shrinkage, individual cell

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19
Q

State the main differences between necrosis/oncosis and apoptosis?

A 
Apoptosis: 
Singer cells affected 
Cell shrinkage 
Pathological or physiological 
Membrane remains intact
Internucelosmal DNA cleavage

Oncosis/necrosis:
Sheets of cells affected
Cell swelling
Always pathological

Membrane breaks down
Diffuse/random DNA damage

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20
Q

Name the types of necrosis?

A

Coagulative
Liquefaction
Caseous
Fat

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21
Q

Describe coagulative necrosis

A

Denaturation of proteins dominates over release of enzymes

Cellular architecture is preserved

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22
Q

Describe liquefaction necrosis

A

Enzyme degradation is greater than desaturation of proteins so see enzymatic degradation of tissues.
See massive neutrophil infiltration
Tissue becomes a viscous mass no and acute inflammation = pus

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23
Q

Describe caseous necrosis

A

Charcetersied by amphomorosis debris, cheesy appearance down microscope
E.g. TB

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24
Q

Describe fat necrosis

A

Destruction of adipose tissue, direct trauma to tissue so breast, acute pancreatitis,

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25
Q

What is gangrene?

A

Not a type of necrosis!

A clinical term used to describe what is visible to the naked eye and is seen in ischaemic limbs

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26
Q

What is dry gangrene?

A

Coagulative necrosis

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27
Q

What is wet gangrene?

A

Liquifactive necrosis normally due to infection and can lead to septicaemia

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28
Q

Give a physiological and pathological example of apoptosis

A 
Physiological = embryogenesis, in the removal of webbing
Pathophysiological = hepatits B (council man bodies), graft vs host disease
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29
Q

Describe intrinsic initiation of apoptosis

A

All apoptotic machinery is inside the cell -> mitochondria
Triggers include DNA damaged withdrawal of GF, hormones
1. Leads to increased mitochondrial permeability resulting in the release of cytochrome C from mitochondria
2. Cytochrome c interacts with APAF1 and Capase 9 to form an apoptdome that activates various downstream capases
3. This clear proteins, breaks up cytoskeleton and starts degradation of DNA

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30
Q

Describe extrinsic initiation of apoptosis

A

Cause by externa ligands!

  1. Ligands bind to death receptors
  2. Leads to Capase activation independent of mitochondria
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31
Q

Describe the final stage of apoptosis: degradation and phagocytosis

A
  1. Cells break down into membrane body fragments called apoptotic bodies
  2. Apoptotic bodies express molecules on their surface that induce their phagocytosis by neighbouring cells or phagosomes
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32
Q

Name the important apoptotic molecules

A 
P53
Cytochrome C, APAF1, Capase 9 
Trail, death ligand 
Trail - R, death receptor
Capases
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33
Q

Describe the structural changes see in apoptosis under a light microscope

A

Apoptotic cells appear shrunken and eosinophilic

Cell shrinkage, chromatic condensation, Pyknosis, nuclear fragmentation

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34
Q

Describe the structural changes see in apoptosis under a electron microscope

A

Apoptotic cells show cytoplasmic stemming, this progresses to fragmentation into membrane bound apoptotic bodies which contains cytoplasm organelles and nuclear fragments

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35
Q

What are the modules release by injured or dying cells

A

Potassium, enzymes, myoglobin,

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36
Q

What is an infarction?

A

An area of tissue death causes by obstruction of a tissue blood supply

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37
Q

Define hypoxia

A

Oxygen deprivation

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38
Q

What causes an infarct?

A

Thrombosis, embolism, external compression of a vessel, twisting of vessels

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39
Q

When do we get white infarcts!

A

Occurs in solid organs which limits the amount of haemorrhaging, occlusion of end artery, coagulative necrosis, white due to lack of blood in tissue

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40
Q

When do do by get a red infarct?

A

Extensive haemorrhaging into dead tissue, so dual blood supply such as the lungs, numerous anastomoses, loose tissue so poor structural support for capillaries, previous congestion e.g. Congestive heart failure, raised venous pressure

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41
Q

Infarcts can have a range of consequences…

A

Tissue affected has an alternate blood supply
How quickly the ischaemia occurs
How vulnerable the tissue is to hypoxia
Oxygen content of blood

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42
Q

What are the main abnormal cellular accumulations?

A

Fluids
Pigments
Lipids
Proteins

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43
Q

What does abnormal accumulation of fluid indicate?

A

Vacuoles and hydrophobic bleeding

Osmotic disturbance severe cellular distress

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44
Q

What are the abdomen cellular accumulations: lipid

A

Steatosis: accumulation of TAG, seen in liver, caused by alcohol abuse, diabetes mellitus, obesity, toxins.

Cholesterol: seen under microscopic as foam cells acquired in hereditary hyperlipideamia

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45
Q

What are the abdomen cellular accumulations: protein

A

Seen as eosinophilic droplets or aggregates in the cytoplasm.
Mallorys hyaline, seen in hepatocytes in liver disease
Alpha 1 anti trypsin deficiency, alpha anti trypsin in liver cannot be packaged by ER therefore accumulates in organelle can get emphysema in lung tissue.

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46
Q

Name an exogenous pigments

A

Carbon/coal dust

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47
Q

Name endogenous pigments

A

Lipofusin: seen in ageing cells, sign of previous free radical injury + lipid perioxidation
Haemosiderin, derived from Hb is formed when there is systemic or local excess of iron
Bilirubin, a bile pigment when deposited in tissues (jaundice, haemolytic anaemia, abnormal liver function)

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48
Q

Describe dystrophic calcification

A

No abnormality in calcium metabolism a serum calcium concentration
Occurs in:
Area of dying tissue, atherosclerotic plaques, ageing or damaged heart values, tuberculous lymph nodes

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49
Q

Describe metabolic calcification

A

Calcium is deposited in tissue when there is hyerpcalcaemia secondary to disturbances in calcium
E.g. Increased secretion of PTH due to parathyroid gland tumorusm ectopic secretion of PTH-rp
Destruction of bone secondary to primary tumours of bone e.g. leukaemia, Paget’s disease

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50
Q

What happens as cellular ageing

A

Damage to cellular constituents, DNA, accumulate lipofusin pigment, abnormally folded proteins, decline to ability to replicate and replicative sensence -> telomere

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51
Q

What is aspirin action?

A

Is a drug that acetates platelets cycooxygenase and blocks platelets ability to make thromboxane A2 which is a substance that activates platelet aggregation.

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52
Q

What harmful effects does aspirin have?

A

Stimulates respiratory centre causing respiratory alkalilous and compensatory mechanisms include metabolic acidosis also interfere with carbohydrate, fat and protein metabolism, decreased platelet aggregation, GI bleeding

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53
Q

Define acute inflammation

A

Response in living tissue to injury whose purpose is to limit the tissue damage

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54
Q

What are the features of a true inflammation?

A

Innate, stereotypes, immediately, occurs in minutes/hours, resolves in a few days, early

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55
Q

What are the causes of acute inflammation? And the purpose of it?

A 
Microbial infections 
Hypersensitivity reactions 
Physical agents 
chemicals
Purpose is to protect and help prevent further damage
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56
Q

What are the macroscopic features of acute inflammation?

A

Redness, swelling, pain, heat

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57
Q

What are the microscopic features of acute inflammation and how do they relate to macroscopic ones?

A

Oedema, swelling
Vasodilation, swelling, redness, heat
Neutrophil margination and migration, swelling

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58
Q

In acute inflammation name the mediators responsible for increased blood flow

A

Histamine and prostaglandins

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59
Q

In acute inflammation name the mediators responsible for vascular permeability

A

Histamine, leukotrienes

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60
Q

In acute inflammation name the mediators responsible for neutrophil chemo taxis

A

Bacterial peptides, C5a, LTB4

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61
Q

In acute inflammation name the mediators responsible for phagocytosis

A

C3b

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62
Q

Describe the microscopic changes in acute inflammation and how they are brought about

A
  1. Changes in blood flow
  2. Infiltration of inflammatory cells
  3. Exudate on of fluid into tissue, starlings law
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63
Q

Describe oxygen dependant mechanism in acute inflammation

A

Produces superoxide and hydrogen peroxide

And H2O2 mydroperoxidase halide system produces HOCL

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64
Q

Describe oxygen independent mechanism in acute inflammation

A

Lysoenzyme and hydroyalases
Bacterial permeability increasing protein, BPI
Cationic proteins

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65
Q

Why does the exudation of fluid constituent an effective response to injury in acute inflammation?

A

Delivers plasma proteins to area of injury
Dilutes toxins
Increases lymphatic draining, delivering microorganisms to phagocytes and antigens to immune systems and lymph nodes

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66
Q

Why does the infiltration of cells an effective response to injury in acute inflammation?

A

Removes pathogenic organisms and neurotic debris

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67
Q

Why does vasodilation constituent an effective response to injury in acute inflammation?

A

Increases delivery and increases temperature

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68
Q

Why does pain and loss of function constituent an effective response to injury in acute inflammation?

A

Enforces rest and reduces chance of further traumatic damage

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69
Q

What are the systematic effects of acute inflammation?

A

Fever,
Leukocyte, increase in WBC content do blood
Acute phase response, decreased appetite, raised pulse rate, altered sleep pattern, changes in plasma concentrations of acute phase proteins

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70
Q

Describe the resolution of acute inflammation

A
  • neutrophils no longer marginate
  • vessel permeability returns to normal
  • exudate drains to lymphatic
  • fibrin is degraded by plasmin and other proteases
  • neutrophils die, break up, carried away, phagocytosed
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71
Q

What is the mechanism behind resolution in acute inflammation?

A 
All mediators have short half lives
Maybe inactivated by degradation 
Maybe unstable 
Maybe dilute in the exudate 
Specific inhibitors of acute inflammatory changes e.g. Endothelium
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72
Q

Aorta from resolution what are the outcomes of acute inflammation?

A

Chronic inflammation -> absecss

GI, fibrous repair and tissue regeneration, death

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73
Q

What is labour pneumonia and what microorganism causes it?

A

A form of pneumonia that effects a large and continuous area of lobe of lung, see inflammation of lungs, exudate, breathless, hypoxic patients,
Caused by streptococcus pneumoniae

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74
Q

What is hereditary angio oedema?

A

Absence of C1 esterase inhibitor

Main clinical features are swelling on the lips, eyes, tonque

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75
Q

Define chronic inflammation

A

Chronic response to injury with associated fibrosis

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76
Q

When does chronic injury arise?

A

May take over form acute inflammation
May arise de novo
May develop alongside acute inflammation

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77
Q

What are the two most important cells in chronic inflammation?

A

Lymphocytes

Macrophages

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78
Q

What are the three types of giant cells that you can get?

A

Touton, foamy cytoplasm, neatly organised nuclei
Langerhans, multinucleated but nuclei in a peripheral horse shoe shape
Foreign body type, multinucleated, haphazard positioning of nuclei

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79
Q

What are possible, complication of chronic inflammation?

A

Fibrosis
Impaired function
Atrophy
Stimulation of an immune response

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80
Q

What is granulomatous inflammation?

A

Chronic inflammation with granuloma

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81
Q

What is the main cell type in a granuloma?

A

Main cell: epitheliod histiocytes, which are modified immobile macrophages
Lymphocytes

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82
Q

What are the main causes of granulomatous inflammation?

A
  • mildly irritant foreign material
  • infections: mycobacterium , leprosy, TB, syphyilis
  • unknown causes, sarcoid, Crohn’s disease
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83
Q

Describe TB chronic inflammation

A 
Cause by mycobacterium, produces number of toxins or lysis enzymes,  
See langerhans giant cells 
1. Arrest, fibrosis scarring 
2. Erosion into bronchioles 
3. Tuberculous emphysema 
4!. Erosion into the blood stream
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84
Q

Describe sarcoidosis inflammation

A 
Idiopathic
Causes small patches of red and swollen tissue grnwulomas 
Non cascating granulomatous, giant cell 
Lymph nodes and lungs involved 
Variables clinical maniefesto tins
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85
Q

Define resolution

A

Restoration of normality

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86
Q

Define regeneration

A

The replacement of dead or damaged cells by functional, differentiated cells. In order to maintains the size of a tissue or organ.
It can occur after injury if the harmful agent is removed and there is linked tissue damage.

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87
Q

What factors contribute to controlling regeneration?

A
  1. Growth factors, promote proliferation in stem cell population, expression of genes controlling cell cycle, Extracellular signals transduced into cell
  2. Contact between basement membranes -> signalling down by adhesion molecules, inhibits proliferation in intact tissue, so loss of contact promotes prliferation I.e. Contact inhibition
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88
Q

Define fibrous repair

A

The replacement of functional tissue by scar tissue

- occurs in necrosis of labile and stable cells if collage framework is destroyed or in necrosis of permanent cells

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89
Q

What are the three points in fibrous repair

A
  1. Cell migration of inflammatory cells, endothelial cells, fibroblast/myofibroblasts
  2. Angiogenesis
  3. Extra cellular matrix
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90
Q

What is the function of the extra cellular matrix in healing and repair?

A

Supports and anchors cell
Separates tissue comportment
Sequesters growth factors
Allows communication between cells facilities cell migration

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91
Q

What is Ethlers Danlos syndrome?

A

Defective conversion of procollagen to tropocollagen

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92
Q

What is alports syndrome?

A

Cause by defects in type IV collagen a major structural competent of the basement membrane in kidney, ear, eye. See he’s urea, progressive renal failure, hearing loss, chronic kidney disease

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93
Q

What controls fibrous repair?

A

Inflammatory cells are mediated by chemotaxis
Angiogenesis by platelets, GF -> VEGF, BEGF
Macrophages produce various pro fibrotic cytokines e.g. TNF

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94
Q

Describe the mechanisms of fibrosis repair (split into 3 stages)

A
  1. Inflammatory cells infiltrate
    - blood clot forms and immediate protective layer
    - acute inflammation around edges
    - chronic inflammation, Macrophages and lymphocytes migrate into clot
  2. Clot replaced by granulation tissue
    - angiogenesis, capillaries and lymphatic is sprout and infiltrate
    - myo/fibroblasts migrate and differentiate
    - ECM is produced by them
  3. Maturation
    - cell proliferation falls
    - collagen increase, matures and remodels
    - myofibroblasts contract, reducing volume of defect
    - vessels differentiate and are reduced
    - > left with a fibrous scar
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95
Q

Describe healing of a clean incised skin wound/healing by primary intention

A
  • opposed edges
  • minimal clot and granulation tissue
  • epidermis regenerates, dermis undergoes fibrous repair, transition from granulation to scar tissue
  • see minimal contraction, scaring and good strength
    But risk of trapping infection, abscess
96
Q

Describe healing of a large skin defects/healing by secondary intention

A

E.g. Infarct, Abcess to any large skin wound

  • un opposed wound edges
  • large clot, get a scab!
  • epidermis regenerates form the base up
  • greater contraction
  • produces a large scar
  • takes longer
97
Q

Local factor influencing the efficacy of healing and repair

A
  • type, size and location of wound
  • opposition
  • lack of movement
  • blood supply
  • infections
  • foreign material
  • radiation damage
  • protection
98
Q

Systemic factors influencing the efficacy of healing and repair

A

Age
Drugs
General and specific dietary deficiencies e.g. Vitamin C
General state of health, DM, immunodeficiency
Cardiovascular status

99
Q

Define Haemostasis

A

Is the process that stops bleeding

100
Q

What does successful haemostats depend on?

A

Vessel walls, constrict to limit blood loss
Platelets, adhere to damaged vessel wall and each other and undergo platelet release reaction
Coagulation system, cascade allowing for amplification and tight regulation, intrinsic and extrinsic pathways, balance of pro and anticoagulant factors
Fibrinolytic system, further check on clotting

101
Q

Name some laboratory tests to asses coagulation

A
  • erythrocyte sedimentation rate
  • full blood count
  • platelet aggregation test
  • measure for specific clotting factors in the blood
  • prothrombin time and activated partial thromplastic time
102
Q

Define thrombosis

A

Is the formation of a solid mass from the constituents of the bloods thin the circulatory system during life

103
Q

When can you get abnormalities of the constituents of the blood?

A 
Smokers, have higher pro coagulant balance 
Postpartum 
Post operative 
Major trauma 
DM 
Dehydration (major burns) 
Thrombocytopenia 
Liver failure, produces additional clotting factors
104
Q

Describe the appearance of an arterial thrombi

A

Pale, granular, liens of zahn, lower cell content

105
Q

Describe the appearance of a venous thrombi

A

Soft, gelatinous, deep red, higher cell content

106
Q

What are the two effects you see in venous thrombosis that you don’t see in arterial thrombus?

A

Congestion and oedema

See Ischaemia and infarction in both

107
Q

What are the 5 possible outcomes of a thrombosis?

A
  1. Lysis
  2. Propagation
  3. Organisation, repairs time process where you get the ingrowth of fibroblasts and capillaries but the lumen remains obstructed
  4. Recanalisation, blood flow is established but is usually incomplete, so 1 or more channels through the thrombosis
  5. Embolism, part of thrombus breaks off, travels and lodges at a distant site
108
Q

Define a embolism

A

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

109
Q

What are the other types of embolism?

A
  • air
  • amniotic fluid
  • nitrogen -> the bends
  • tumour cells (renal)
  • fat embolism (break bone, damage yelled bone marrow)
  • atheroma
  • medical equipment
  • cerebral embolism, AF causes
110
Q

How does heparin work?

A

Is given subcutaneously and acts by binding to the enzyme inhibitor anti-thrombin III which produced a conformation change activating it. In then inactivates thrombin and other proteases, Xa

111
Q

What does warfarin do?

A

Blocks the effects of vitamin K, which is the cofactor used in the addition of COOH groups to glutamate residues to form Gla domains which then interact with calcium at sites of damage.

112
Q

Describe prophylaxis in general

A

Is any treatment ore health care given whose purpose is to prevent disease rather than curing or preventing their symptoms.

113
Q

Define disseminated intravascular coagulation

A

Widespread activation of clotting cascade therefore clotting factors and platelets have been consumed with subsequent activation of fibrinolytic system

114
Q

Define thrombophilia

A

Is a term describing inherited or acquired defects of homeostasis leading to a predisposition to venous or arterial thrombosis.

115
Q

Define thrombocytopenia

A

Reduction in the platelet count below the normal lower limit

116
Q

Haemophilia a is what?

A

Deficiency in clotting factor VIII

117
Q

Haemophilia B is what?

A

Deficiency in clotting factor IX

118
Q

Define atheroma

A

Is the accumulation if intracellular and Extracellular lipid in the intima and media of large and medium sized arteries

119
Q

Define atherosclerosis

A

Is the thickening and hardening of arterial walls as a consequence of atheroma

120
Q

Define Arteriosclerosis

A

The thickening of the walls of arteries and Arterioles as a result of hypertension or DM

121
Q

What is multi infarct dementia?

A

Lots of tiny infarcts which cause a series of small strokes resulting in dementia

122
Q

Consequences of atherosclerosis in the Mesenteric arteries

A

Mesenteric Ischaemia

  • ischaemic colitis, inflammation and injury of the large intestine as a result of inadequate blood supply
  • malabsorption from small intestine
123
Q

What is lerriche’s syndrome?

A

Is one of the effects of atherosclerosis in the leg arteries,
It is an atherosclerotic occlusive disease involving the bifurcation (splitting into 2 parts) of the abdominal aorta as it transitions into the iliac arteries
-> claudication of the buttocks + thigh, absent or decreased femoral pulse, impotence in males

124
Q

Describe the encrustation hypothesis to atheroma formation

A

Propose that plaque initiation and progression are the consequence of repeated cycles of thrombosis and remodelling
BUT:
- autopsy shoe not an initial event but a feature of advanced disease
- does not explain lipid or smooth muscle

125
Q

Describe the monoclonal hypothesis in atheroma formation

A

Each plaque is in fact a smooth muscle cell derived to produce more smooth muscle cells, might represent abnormal growth control, possibility that each plaque is a benign tumour

126
Q

Describe the insudation theory in atheroma formation

A

Endothelial injury
Inflammation
Increased permeability to lipid from plasma into arterial wall

127
Q

Describe Reaction to injury hypothesis in atheroma formation

A

Plaques form in response to endothelial injury
Injury result in increased permeability and allows platelet adhesion
Monocytes then pentameter endothelium
Smooth muscle cells proliferate and migrate endothelial injury may be subtle and unable to see visually
LDL especially oxidised may damage endothelium

128
Q

What do endothelial cells do in atheroma formation?

A

Key role in Haemostasis
Alter permeability to lipoproteins
Secretion of collagen
Stimulation of proliferation and migration of smooth muscle cells

129
Q

What do platelets do in atheroma formation?

A

Key role in Haemostasis

Sit quiet proliferation and migration of smooth muscle cells, PDGF

130
Q

What do smooth muscle cells do in atheroma formation?

A

Take up LDLs and other lipid to become foam cells

Synthesise collagen and proteoglycans

131
Q

What do lymphocytes do in atheroma formation?

A

TNF may affect lipoprotein metabolism

Stimulation and proliferation and migration of smooth muscle cells

132
Q

What do neutrophils do in atheroma formation?

A

Secrete proteases leading to continued local damage and inflammation

133
Q

What do macrophages do in atheroma formation?

A

Oxidise LDLs
Take up lipids to become foam cells
Secrete proteases which modify matrix
Sit au,the proliferation and migration of smooth muscle cells

134
Q

What are uni potent cells?

A

Cells that can produce 1 type of differentiate cells e.g. Epithelial

135
Q

What are multi-potent cells?

A

Cells that can produce several types of differentiated cells e.g. Haematopoietic cells

136
Q

What are toti-potent cells?

A

Cells that can produce any type of cell

137
Q

Name the point between G1 and S in the cell cycle

A

Restriction checkpoint

If activated this delays the cell cycle and triggers DNA repair mechanisms. Most commonly altered in cancer cells

138
Q

Name where the checkpoints are in the cell cycle

A

Restriction checkpoint
G1/S
G2/M

139
Q

What is the main thing controlling the cell cycle?

A

Cyclins:
A cyclin dependant kinase will become active by binding to and compiling with cyclins to drive the cell through the cell cycle by phosphorylation.
Some GFs work by stimulating the production of cyclins or by shutting down CDK inhibitors

140
Q

What controls cells growth?

A

Autocrine, paracrine , endocrine .

Then have GF, vascular and metabolic factors: hormones, local mediators and direct cell to cell stroma contact

141
Q

How are adult stem cells different to embryonic stem cells?

A

They are lineage specific

142
Q

Describe growth factors

A

Local mediators involved in cell proliferation
Polypeptides that act on cell surface receptors
Coded by proto-oncogenes
Bind to specific receptors, stimulating transcription of genes that regulate enters into cell cycle and cells passage through it

143
Q

What do growth factors affect?

A

Cell proliferation, inhibition, locomotion, contractility, differentiation, viability, activation and angiogenesis

144
Q

Give a pathological example of hypertrophy?

A

Is an increase in tissue or organ size due to an increase in cell size
Elf. Smooth muscle hypertrophy in the uterus of a pregnant women

145
Q

What generally tends to cause hyperplasia or hypertrophy?

A

Increased functional demand

Hormones stimulation

146
Q

Give a pathological and a physiological example of hyperplasia?

A

Pathological: enlargement of thyroid gland, psoriasis
Physiological: increased bone marrow production of enterocytes in response to low oxygen, proliferation of endometrial lining of uterus under influence of oestrogen

147
Q

What occurs in atrophy at the level of the cell?

A

Involves shrinkage of the size of the cell to a size where survival is still possible but the cell contains a reduced number if structural components and has a reduced function. It is an adaptive response that may result in cell death

148
Q

Give a pathological and a physiological example of atrophy

A

Physiological:
Decrease in size of uterus post partum
Ovarian atrophy in post menopausal women
Pathophysiological:
Reduced functional demand e.g atrophy of issue
Senile atrophy
Denervation atrophy e.g. Wasted hand muscles after median nerve damage
Pressure e.g. Tissue surrounding an enlarged benign tumour

149
Q

Define Hypoplasia

A

The underdevelopment or incomplete development of a tissue or organ resting in a inadequate number of cells within the tissue that us present.
E.g. Testicular Hypoplasia in klinefleters
- is a congenital condition and an embryonic development disorder

150
Q

Define metaplasia

A

This is a reversible change of 1 differentiated cell type to another. One adult cell type is replaced with an other
E.g. Epithelial tissue
Pseudostratified ciliated epithelium to stratified squamous epithelium in cigarette smoke

151
Q

Define dysplasia

A

The abnormal maturation do cells within a tissue. This is potential reversible but is a pre cancerous condition/pre neoplastic alteration which cels shows disordered tissue organisation

152
Q

What happens is a harmful agent persists or there is extensive tissue damage which occurs in permanent tissue

A

Then regeneration and resolution is not possible and instead the tissue heals with a scar
E.g. In the liver after a partial hepatectomy
Replacement of epidermis by keratinocytes following a skin burn

153
Q

Give an example of a labile cell?

A

Stem cells so…
Surface epithelial, bone marrow

Normal state is active cell division, usually with rapid proliferation

154
Q

Give an example of a stable cell

A

Is in the resting state, GO so the speed of regeneration is variable but can enter the cell cycle
E.g. Liver hepatocytes, osteoclasts, fibroblasts, vascular endothelial cells

155
Q

Give an example of permanent cells

A

Brain neurones: space filled with glial cells
Cardiac myocytes: heals with a scar of fibrous tissue
Skeletal muscle:
So unable to divide and enter Go, can to regenerate if proliferate if there is significant cell loss

156
Q

Define a neoplasm

A

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

157
Q

Define a malignant neoplasm

A

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

158
Q

Define a tumour

A

A clinically detectable lump or swelling

159
Q

Define a cancer

A

Is any malignant neoplasm

160
Q

Define a metastasis

A

Is a malignant neoplasm that has spread from its rogisnls ite to a new non contiguous site

161
Q

Describe a benign neoplasm

A

Remains confined to their sites of origin
Grows in a confined local area and has a pushing outer margin
Cells will closely resemble the parent tissue and are well differentiated

162
Q

Describe a malignant neoplasm

A

Have the potential to mestastise
Tumours have an irregular outer margin and shape and may show areas or necrosis and ulceration if are on a surface
Range from well to poorly differentiated

163
Q

What do we see in poorly differentiated tissues which have a high grade?

A

An increasing nuclear size
Increases nuclear to cytoplasmic ratio
More Mitotic figures
Increasing variation in size and shadow of cells and nuclei -> Pleomorphism

164
Q

What does monoclonal mean?

A

That all the cells originate from a single founding cell, discovered using a study of glucose-6-phosphate dehydrogenase found have heat stable isoenzymes and heat labile isoenzymes. In normal cells see a patchwork of each type but not in neoplasms

165
Q

Define invasion

A

The process of infiltration and active destruction of surrounding tissues, is a property of malignant neoplasms

166
Q

Define metastasis

A

Transfer of disease from 1 organ or part of the body to another not directly connect with it due to the transfer of cells. All malignant tumours do this

167
Q

Describe the journey of a malignant neoplasm

A
  1. Grown and invade at the primary site
  2. Enter a transport system
  3. Grow at the secondary site to form a new tumour -> colonisation
168
Q

What three alterations do you need of invasion?

A
  1. Altered adhesion
    Involves a reduction in E-Catherin expression
    Between malignant cells and stroma proteins, involves changes in inter grin expression
  2. Stoma proteolysis
    Cells must degrade basement membrane and Stroma to invade so release proteases, MMPs. Take advantage of newly formed non neoplastic cells by forming a cancer niche providing growth factors and proteases
  3. Motility
    Involves changes in the actin cytoskeleton
    Signalling though intergrins is important this occurs via small g-proteins
169
Q

Transport to different sites of neoplasms occurs by

A

Blood vessels, sarcoma -> stromal malignancy
Lymphatic vessels, carcinoma -> epithelial malignancy
Transcolemic spread

170
Q

Describe micrometastase’s

A

Is the name for the surviving microscopic deposits that fail to grow because of immune attack, secondary site is hostile, have to re learn angiogenesis at the new site
Hence sometimes called tumour dormancy

171
Q

What are the common sites of blood borne metastasis? So carcinoma -> epithelial malignancy

A

Lung
Liver
Bone
Brain

172
Q

What are the neoplasms that frequently spread to bone?

A 
Breast 
Bronchioles 
Thyroid 
Prostate 
Kidney
173
Q

What are the local effects of a neoplasm?

A
  1. Direct invasion and destruction of normal tissue
  2. Ulceration at surface leading to bleeding
  3. Compression of adjacent structures
  4. Blocking of tubes and orifices I.e. Obstruction
174
Q

What are the systemic affects of neoplasms?

A

Reduced appetite and weight loss -> cachexia
Immunosuppression
Thrombosis
Endocrine effects due to hormone release, ectopically, insufficiency or destruction by pressure
Haemotologically -> anaemia, DIC
Can be caused by an increase in tumour burden, or secreted factors e.g. Cytokines, hormones

175
Q

What are the intrinsic risk factors for cancer?

A

Hereditary
Age
Gender due to hormones

176
Q

What are the extrinsic risk factors for cancer?

A

Chemical
Radiations
Infections

177
Q

What are the five behavioural and dietary risks?

A
  1. High BMI
  2. Low fruit and vegetable intake
  3. Lack of physical activity
  4. Tobacco use
  5. Alcohol use
178
Q

What is the difference between initiators and promoters and what follow them?

A

Initiators are mutagens where as promoters cause prolonged proliferation in the target tissue. This results in monoclonal expansion of mutant cells and the neoplasm becomes fully malignant by progression.

179
Q

Name the main types of chemical carcinogens

A 
Polycyclic aromatic hydrocarbons 
Aromatic amines 
N-nitro compounds 
Alkylating agents 
D....... Natural products
180
Q

What are the direct causes of DNA damage by radiation?

A

Altered DNA bases and single double strand DNA breaks

181
Q

What are the indirect causes of DNA damage by radiation?

A

Free radicals

182
Q

How can infections be indirectly carcinogens and other direct carcinogens?

A

Direct: affects genes that control cell growth
e.g. HPV which expresses E6 and E7 which inhibit P53 and pRB

Indirect: cause chronic tissue injury so the resulting regeneration acts a s a promoter for any pre existing mutations or causes new mutations from DNA replication errors
E.g. Hepatits B and C: viral DNA is integrated into host cells genome, or epistein Barr which infect epithelial cells and B cells and it’s virus genes deregulate normal and proliferate survival signals

183
Q

Why does reduced immunity cause a neoplasm?

A

It lowers the immunity allowing other potential carcinogenic infections to occur. An example of a virus is HIV

184
Q

Define tumour suppressor genes

A

Genes tang inhibit neoplastic growth

185
Q

Define oncogenes

A

Genes that enhance neoplastic growth and are abnormally activated proto oncogenes

186
Q

What are proto oncogenes?

A

Genes that are the opposite to oncogenes so they prevent neoplastic growth however you only need to turn 1/2 into an oncogene. Does not follow two hit hypothesis like tumour suppressor genes

187
Q

Want is xerodermapigmentosum?

A

Is an autosomal recessive, due to maturation in genes that effect DNA nucleotide excision repair. So patient is very sensitive to UV damage and will develop skin cancer at a you age due to nucleotide instability.

188
Q

What is HNPCC, hereditary non polyposis colon cancer?

A

Is an autosomal dominant germ line mutation where 1 DNA mismatch repair genes is mutated, leading to colon carcinoma

189
Q

What does the BRCA1, BRCA2 genes do?

A

Are mutations for repairing double strand DNA breaks resulting in chromosome instability so can get familial breast carcinoma,

190
Q

Define progression

A

The name given to this steady accumulation of multiple mutations

191
Q

What are 6 hallmarks cellular behaviours in cancer?

A
  1. Self sufficient growth signals
  2. Resistant to anti-growth signals
  3. Grown indefinitely,
  4. Be capable of inducing new blood vessels/angiogenesis
  5. Be resistance to apoptosis
  6. Invade and produce metastases
192
Q

What is FAP/familial adenomatous polyposis?

A

An autosomal dominant mutation of adenomatous polyposis coli tumour suppressor gene.
Patients develop, polyposis adenomas of the colon
100% will develop colon cancer by the age of 50
Multiple adenomas may be present elsewhere
Tend to undergo prophylactic colerectomy

193
Q

What is ataxia telangiectasia?

A

Is tej gradual lost of purkinje cells in the cerebellum producing cerebellar ataxia
See Telangiectasia in conjunctiva and skin
Have defective lymphocyte maturation and proliferation resulting in immunodeficiency, acute sensitivity to ionising radiation and profund susceptibility to lymphoid malignancies
Tend to die in 2nd decade

194
Q

What is the ATM gene?

A

The ATM protein senses double strand DNA breaks, damage caused by ionising radiation but in ataxia telangiectasia DNA damaged cells will continue to proliferate and are prone to transformation

195
Q

What does RAS do?

A

Is a protein situated in the cytoplasmic side of plasma membrane and when activated transmit growth producing signals to the nucleus.
If mutated then is permanently activated e.g. In. Retinoblastoma

196
Q

What does the C-myc oncogene do?

A

MYC is rapidly induced when quiescent cells receive a signal to divide. MY c protein acts on the nucleus as a potent transcriptional activator

197
Q

What does C-erbB-2 ( HER-2) do?

A

Is a growth factor receptor and is present in 25% of breast cancer. Which use monoclonal agonists ERB and B2 are used in therapy against this.

198
Q

What does retinoblastoma TSG do?

A

Key role in regulatory cell cycle, if absent then molecular breaks in cell cycle are removed

199
Q

What is p53?

A

The guardian of the genome!
Mutations of to are found in 50% of tumours
Role is in response to DNA damage it causes cell cycle arrest, induction of DNA repair or induced apoptosis if repair fails

200
Q

What is ulcerative colitis?

A

Long term condition where the colon and the rectum become inflammed, so see DNA damage, micro satellite instability.
Symptoms can mimic those of cancer however there is an increased risk of colonic adenomacarcinoma

201
Q

What is cancer is cirrhosis associated with?

A

85/90% cause of heptaocellular carcinoma

202
Q

What does chronic atrophic gastritis do?

A

Can cause gastric cancer,
Can be autoimmune:
So autoantibodies to components of parietal cells leading to gland destruction and mucosal atrophy which reduced acid producing on and increases risk of gastric carcinoma and carcinoid tumour
Can be caused by helicobacter pylori,
Strong causal association with gastric carcinoma and cause of gastric MALT lymphoma
Will cause atrophy, intentional metaplasia, dysplasia carcinoma

203
Q

Describe the geographical variation in gastric cancer

A

2nd most common in the world and leads deaths
High: Japan, Chile, Costa Rica, Columbia, China, Portugal, Russia, Bulgaria
Low: US, UK, Canada, Australia, NZ, Franca and Sweden

204
Q

Describe the geographical variation in breast cancer?

A

High in US and EU.
Increased risk if younger age of first period, menopause is late, increase oestrogen exposure, Causian women
Lower risk if younger when have first live brith and breast feed

205
Q

Describe the geographical variation of burkitts lymphoma

A

Most common tumour in central Africa and New Guinea

Higher risk if epistein Barr

206
Q

What are the commonest types of neoplasm in adults?

A

Breast, lung, bowel, prostate

207
Q

What are the commonest type of cancer in children?

A

Leukaemias, CNS tumours and lymphomas

208
Q

What are the biggest cancer killers?

A

Pancreas, lung, oesophagus, brain, stomach

209
Q

What do we use to predict the outcome?

A

Age, general health status, tumour site, tumour type, tumour grade, tumour stage, availability of effective treatments

210
Q

What is stage and the main staging system used?

A

Stage = measure of the malignant neoplasm overall burden
T: site of primary tumour
N: extent of regional node mestastasis
M: extent of distant metastatic spread
Used in breast, prostate, bladder and rectum

211
Q

What is the staging used in bowel cancer/colorectal carcinoma?

A

Duke staging
Dukes A: invasion into but not through bowel
Dukes B: invasion through the bowel wall
Dukes C: involvement of lymph nodes
Dukes D: distant metastases

212
Q

What is the staging sued in lymphoma/Hodgkin’s disease?

A

Ann arbour
Stage 1: lymphoma in a single node region
Stage 2: 2 separate region on same side of diaphragm
Stage 3: spread to both sides of diaphragm
Stage 4: diffuse of disseminated involvement of 1 or more extra lymphatic organs e.g. Bone marrow or lungs

213
Q

What cancer is the bloom Richardson system used for?

A

Breast cancer

Is used to asses tubule formation, nuclear variation, number of mitoses

214
Q

Haven is tumour grade more important?

A

For planning treatment, estimating prognosis in certain types of malignancy e.g. Brian tumours, soft tissue sarcoma, lymphoma, breast, prostate cancer

215
Q

What does a tumour grade of G1 mean?

A

That the cells are week differentiated e.g. Resemble cell it came from

216
Q

What does a tumour grade of G4 mean?

A

That the cells are poorly differentiated or anaplastic I.e. We cannot feel which tissue it is from

217
Q

What is neoadjuvant treatments?

A

Is given to reduce the size of the primary tumour prior to surgical excision

218
Q

What is adjuvant treatment?

A

Is given after surgical removal of a primary tumour to eliminate any sub clinical disease

219
Q

Hated els radiotherapy do?

A

Kills rapidly dividing cells especially those in G2 of the cell cycle.

  1. Cause free radical id cued DNA damage which can be detected at cell cycle checkpoint leading to apoptosis
  2. causes damage to chromosomes which prevents the M phase form completing correctly
220
Q

What are the types of chemotherapy drugs?

A 
Anti metabolites 
Alkalyting and platinum based drugs 
Antibiotics
Plant derived drugs  
 They  all affect rapidly proliferating cells that  are not specific for cancer e.g. Air follicles, bone marrow is suppressed, affect gi tract so get bleeding and diarrhoea, sore mouth
221
Q

What do anti metabolites do?

A

Mimic normal substrates involved in DNA synthesis and come other for enzymes

222
Q

What do alkylating and platinum based drugs do?

A

Cross link the two strands of the DNA helix

223
Q

What do antibiotics do?

A
  1. Inhibits DNA topoimerase which is needed for DNA synthesis
  2. Causes doubled strand DNA breaks
224
Q

What do plant derived drugs do?

A

Blocks micro tubule assembly and interfere with Mitotic spindle formation

225
Q

What is hormone therapy?

A

Is used in cancer as a non-toxic treatment for certain malignant tumours.

226
Q

Give an example of a sue of hormone therapy in cancer?

A

Selective oestrogen receptor modulators -> tamoxifen
1. Binds to oestrogen receptors
2. Prevents oestrogen from binding
3. Helps prevent growth of neoplasms
Only use in post menopausal women use another one for pre

Androgen blockade -> casadex
Used in testicular cancer and stops testosterone from reaching the cells

227
Q

We are starting to see oncogenes being targets by cancer therapy give an example of this

A

Herceptin:
Blocks HER-2 signalling by HER-2 gene which is over expressed in 25% of breast cancer
Imatinib (gleevic):
Is used in chronic myeloid leukaemia which shows a chromosomal arrangement of t9:22 -> Philadelphia chromosome where the oncogenic fusion protein BCR-ABL is encoded.
This inhibits the fusion protein

228
Q

What is the use of tumour markers?

A

Have a slight role in diagnosis but are used mostly to measure tumour burden during treatment and follow up.

229
Q

What is carcinoembryonic antigen a measure of?

A

Is a glycoprotein present in normal mucosa cells.

Colorectal cancer/adenocarcinoma

230
Q

What is hCG used for?

A

Is released in testicular tumours -> teritoma

231
Q

What is alpha feto protein a measure of?

A

Major protein of fetal serum but is usually undetectable after birth.
Seen in hepatocellular carcinoma, germ cell tumours, gastric cancer, biliary tract cancer, pancreatic cancer

232
Q

What tumour marker is sued in prostate cancer?

A

Prostate specific antigen

233
Q

What is the mucin/glycoprotein used in ovarian cancer as a tumour marker?

A

CA-125

234
Q

What are the problems with cancer screening?

A

Lead time bias
Lengths bias
Over diagnosis

235
Q

What cancers do we screen for in the uk?

A

Breast -> mammogram 50-70
Ovarian -> liquid base cytology test with a small sample of cells from inside your cervix 25-60
Colorectal cancer -> foecal adult blood test/stool test or flexible sigmoidscopy 60-70

236
Q

What is Chrons disease?

A

Have a cobbled stone appearance in the intestine but is a long term condition that causes inflammation of the digestive system

237
Q

What is inflammatory bowel disease?

A

Term used to describe ulcerative colitis and Crohn’s disease.
Main difference is that ulcerative colitis tends to be just the inner lining and only occurs in the large intestine of the gut where as chrons disease can spread through the whole wall of the intestine and can effect any part of the gut.

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