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Introduction to Clinical Sciences (detailed) Flashcards

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1
Q

Def: Acute inflammation

A

Initial and often transient series of tissue reactions to injury - may last from a few hours to a few days

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2
Q

Def: Chronic inflammation

A

Prolonged inflammatory reactions involving a progressive change in type of cell present

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3
Q

List the main symptoms of inflammation (4)

A

Heat, Redness, Swelling, Pain, (loss of function also a characteristic)

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4
Q

List the 4 stages of Neutrophil polymorph emigration

A

Margination of neutrophils
Adhesion of neutrophils
Neutrophil emigration
Diapedesis

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5
Q

Def: Neutrophil polymorph emigration

A

Accumulation of neutrophil polymorphs within the extracellular space

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6
Q

Describe the margination of neutrophils

A
  • Normal circulation - cells confined to axial flow (central)
  • Due to loss of fluid in inflammation plasma viscosity increases and flow decreases
  • Neutrophils able to flow in plasmatic zone next to endothelial cells
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7
Q

Describe the adhesion of neutrophils

A

○ Known as pavementing
○ Random contact with endothelium results in interactions between WBC and endothelial cells
○ Occurs only in venules
○ Adhesion molecules made more active by chemical inflammatory mediators

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8
Q

Describe neutrophil emigration

A

○ Migrate through the walls of venules and small veins
○ Insert pseudopodia between endothelial cells and move through the gap and through the basal lamina into the vessel wall

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9
Q

Name the chemical mediators involved in vascular dilatation

A

Histamine, Prostaglandin E2, Nitric oxide, PAF (platelet-activating factor), VIP (vasoactive intestinal peptide)

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10
Q

Name the chemical mediators involved in increased vascular permeability

A

Immediate transient: Histamine
Prolonged: Bradykinin, Nitric oxide, C5a, Leukotriene B4 and PAF
Immediate sustained: Severe direct vascular injury
Delayed prolonged: Endothelial cell injury e.g. x-rays, bacterial toxins

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11
Q

Name the chemical mediators involved in adhesion of leukocytes to endothelium

A

IL-8, C5a, Leukotriene B4, Il-1 and TNF-a

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12
Q

Name the chemical mediators involved in neutrophil polymorph chemotaxis

A

Leukotriene B4 and IL-8

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13
Q

Which cells release histamine

A

Basophils and mast cells

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14
Q

What induces the release of histamine from basophils and mast cells

A

C5a, C3a and lysosomal proteins

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15
Q

Name causes of inflammation (6)

A
  • Hypersensitivity reactions
  • Microbial infections
  • Physical agents
  • Chemicals
  • Bacterial toxins
  • Tissue necrosis
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16
Q

Give some examples of physical agents resulting in inflammation

A

Ionising radiation, Heat, Cold, Trauma

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17
Q

Give some examples of chemicals resulting in inflammation

A

Corrosives, Acids, Alkalis, Reducing agents

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18
Q

Name the plasma factors (4)

A

Complement factors
Kinins
Coagulation factors
Fibrinolytic system

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19
Q

What is the basic function of the complement system

A

Removes and destroys pathogens via opsonisation or by direct lysis

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20
Q

What are the 3 pathways of the complement system

A

Classical
Alternative
Lectin

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21
Q

How is the classical pathway (complement system) activated

A

Antibody binds to bacterial antigens -> classical pathway activated -> generates C3b (opsonising properties

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22
Q

How is the alternative pathway (complement system) activated

A

Bacterial lipopolysaccharides detected -> alternative pathway activated -> C3b generated

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23
Q

What do macrophages do in inflammation

A
  • Secrete cytokines IL-1 and TNF-a
  • Cause endothelial, fibroblast and epithelial cells to secrete MCP-1
  • Predominate in later stages
  • Responsible for clearing tissue debris, damaged cells and digestion of inflammatory exudate
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24
Q

What is MCP-1

A

Monocyte chemoattractant protein 1 also known as CCL2 - attracts monocytes, T memory cells and dendritic cells to site of inflammation

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25
Q

How is exudate drained

A

Lymph vessels become dilated and drain fluid to prevent extensive tissue oedema

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26
Q

Describe the process of phagocytosis

A
  • Adhesion of pathogen to cell surface -> opsonisation
  • Ingestion of pathogen - pseudopodia surround and fuse into a phagosome
  • Lysosome fusion with phagosome to form a phagolysosome
  • Intracellular killing
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27
Q

Basic description of oxygen-dependent intracellular killing

A

Reactive oxygen species like hydrogen peroxide react with myeloperoxidase in the presence of a halide to produce a potent microbicidal agent

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28
Q

Basic description of oxygen independent intracellular killing

A

Include lysozymes (muramidase) and lactoferrin

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29
Q

List the benefits of inflammation (5)

A
  • Destruction of invading microorganisms and walling off of abscess cavity, preventing infection spread
  • Dilution and removal of toxins by lymph drainage
  • Entry of antibodies into exudate allows killing of pathogens
  • Fibrin formation from exuded fibrinogen impedes pathogen movement and serves as a matrix for formation of granulation tissue
  • Stimulation of immune response via drained exudate to lymph nodes -> antigens detected
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30
Q

List the limitations of inflammation (5)

A
  • Disease -> abscess in the brain acts as a space-occupying lesion, compressing surrounding structures
  • Fibrosis resulting from chronic inflammation distorts and alters the function of tissues
  • Digestion of normal tissues due to collagenase and protease release
  • Swelling is dangerous in enclosed spaces such as the cranial cavity -> raises pressure to blood flow is restricted, possibly leading to ischaemia
  • Hypersensitivity reactions (e.g. anaphylactic shock)
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31
Q

List the 4 main outcomes of inflammation

A
  • Resolution
  • Suppuration
  • Organisation
  • Progression to chronic inflammation
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32
Q

Describe resolution of inflammation

A

Tissue completely returns to normal after episode of acute inflammation.

  • Minimal cell death
  • Good local vascular drainage
  • Occurs in organ capable of regeneration
  • Rapid destruction of causal agent
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33
Q

Describe suppuration and the outcomes it can have

A

Formation of pus:

  • Pus surrounded by pyogenic membrane
  • Abscess (collection of pus)
  • Bacteria in the membrane is inaccessible to antibodies and antibiotic drugs
  • Empyema - pus filled socket in hollow organ created by the fusion of an outflow tract by fibrin
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34
Q

Describe conditions that favour organisation after inflammation

A

Replacement of normal tissues with granulation tissue

  • Lots of fibrin formed (enzymes not able to remove all)
  • Tissue becomes necrotic or fibrous tissue not easily digested
  • Exudate not removed or discharged
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35
Q

Describe what happens in organisation (inflammation) (4)

A
  • New capillaries grow into exudate
  • Macrophages migrate
  • Fibroblasts proliferate under influence of TGF-b
  • Defect filled by ingrowth of granulation tissue
  • Granulation tissue produces collagen, forming a fibrous scar
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36
Q

Describe progression to chronic inflammation

A
  • Causative agent not removed

- Cell exudate changes composition

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37
Q

What is the change in cell exudate in progression to chronic inflammation

A

Instead of neutrophil polymorphs there are lymphocytes, macrophages, multinucleate giant cells and fibroblasts

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38
Q

3 main responses in acute inflammation

A

Increased vessel dilatation
Increased vascular permeability
Formation of exudate

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39
Q

What does release of lysosomal products result in

A
  • Damage to local tissues by proteolysis (elastase, collagenase)
  • Activates coagulation factor XII
  • Attracts other leukocytes
  • Some increase vascular permeability and others are pyrogens (induces systemic fever by acting on the hypothalamus)
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40
Q

What is the role of the mast cell in acute inflammation

A
  • Stimulated by C3a/C5a
  • Release preformed inflammatory mediators like histamine
  • Metabolise arachidonic acid into leukotrienes, prostaglandins and thromboxanes
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41
Q

Descriptive terms for inflammation (5)

A
  • Serous (lots of fluid release)
  • Suppurative (purulent)
  • Membranous
  • Pseudomembranous
  • Necrotising (gangrenous)
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42
Q

Name some systemic effects of inflammation (5)

A
  • Pyrexia
  • Constitutional symptoms
  • Reactive hyperplasia of the reticuloendothelial system
  • Haematological changes
  • Amyloidosis
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43
Q

How is pyrexia induced in acute inflammation

A
  • Stimulated by phagocytosis, endotoxins and immune complexes
  • Neutrophil polymorphs and macrophages produce endogenous pyrogens (of which IL-2 ha the greatest effect
  • Pyrogens act on the hypothalamus to set thermoregulatory mechanisms at a higher temperature
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44
Q

What are the constitutional symptoms of acute inflammation

A
  • Malaise
  • Anorexia
  • Nausea
  • Weight loss (negative nitrogen balance due to energy required to produce inflammatory mediators)
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45
Q

Describe reactive hyperplasia of the reticuloendothelial system

A
  • Local or systemic lymph node enlargement

- Splenomegaly is found in certain specific infections e.g. malaria and infectious mononucleosis

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46
Q

What are the haematological changes seen in acute inflammation

A

Increased levels of WBC
- increased neutrophils seen in pyogenic infections and tissue destruction
- Increased eosinophils in allergic and parasitic infection
- Increased lymphocytes seen in chronic infection and viral infections
- Increased monocytes seen in certain bacterial infections e.g. TB and typhoid
Anaemia may result due to blood loss into inflammatory exudate or haemolysis due to bacterial toxins

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47
Q

Describe amyloidosis

A

Long-standing chronic inflammation may cause amyloid to be deposited into various tissues, resulting in secondary amyloidosis
e.g. rheumatoid arthritis, TB, bronchiectasis

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48
Q

What is amyloid

A

Abnormal protein that builds up in organs/tissues and can eventually lead to their failure

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49
Q

Which cells predominate in chronic inflammation

A

Lymphocytes
Plasma cells
Macrophages

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50
Q

Name the types of chronic inflammation (4)

A
  • Primary chronic inflammation
  • Transplant rejection
  • Progression from acute inflammation
  • Recurrent episodes of acute inflammation
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51
Q

Describe primary chronic inflammation and give some examples

A

Where there is no initial phase of acute inflammation

- TB, Asbestos fibres, Rheumatoid arthritis, Crohn’s disease

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52
Q

Describe granulomatous inflammation

A

Immune system attempts to wall off substance but is unable to eliminate it, forming a granuloma

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53
Q

What is a granuloma

A

Collection of epithelioid histiocytes - stationary phagocytic cell found in tissue

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54
Q

Def: Angiogenesis

A

Formation of new blood vessels

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55
Q

Which cells are derived from monocytes (10)

A 
Connective tissue histiocyte
Alveolar macrophage
Peritoneal macrophage
Kupffer cell
Melanophage of skin
Lipophage
Osteoclast
Microglial
Specialised histiocyte e.g epithelioid cell
Histiocytic giant cell
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56
Q

What changes does a macrophage undergo as they migrate into an area of inflammation (5)

A

Increase in size, protein synthesis, mobility, phagocytic activity, and content of lysosomal enzymes

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57
Q

Give some examples of cytokines produced by macrophages (6)

A

Interferon alpha and beta
IL-1, 6, 8
Tumour necrosis factor alpha (TNF-a)

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58
Q

What stain is used to identify TB and what colour does is turn

A

Ziehl-Neelsen stain goes bright red

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59
Q

List characteristics of epithelioid histiocytes

A
  • Histologically similar to epithelial cells
  • Large vesicular nuclei
  • Plentiful eosinophilic cytoplasm
  • Elongated
  • Arranged in clusters
  • Little phagocytic activity
  • Secretory function (inc. ACE)
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60
Q

What is caseous necrosis

A

Tissue maintains cheese-like appearance - soft and white

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61
Q

When do histiocytic giant cells form

A
  • Accumulation of particulate matter indigestible by macrophages
  • Foreign particles too large to be ingested by one macrophage
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62
Q

List some characteristics of langerhans giant cells (2)

A
  • Horseshoe arrangement of peripheral nuclei at one pole of cell
  • Seen in TB and other granulomatous conditions
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63
Q

Describe healing by first intention

A
  • Small blood vessels occluded by thrombosis
  • Fibrin locally deposited binds sides of the wound
  • Coagulated blood on the surface forms a scab keeping the wound clean
  • Capillaries proliferate and fibroblasts secrete collagen as they migrate into fibrin network
  • After ~ 10 days repair is sufficient enough for removal of suture
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64
Q

Describe healing by second intention (tissue loss)

A
  • Phagocytosis to remove any debris
  • Granulation tissue to fill in lesions and repair lost specialised tissue
  • Epithelial regeneration to cover the surface
  • Timescale depends on size of defect and final cosmetic result depends on how tissue loss there has been
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65
Q

Def: Atheroma

A

the build up of materials that adhere to arteries (fat, cholesterol, calcium, connective tissue, inflammatory cells). Can lead to stenosis of the arteries, resulting in atherosclerosis

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66
Q

Describe the pathogenesis of an atheroma (pt.1)

A
  • Endothelial damage due to irritants
  • Cholesterol collects in endothelium forming fatty streaks
  • Cholesterol oxidised, activating an inflammatory response
  • Monocytes migrate to area of damage and transform into macrophages
  • Macrophages engulf large volumes of cholesterol, undergo apoptosis and become foam cells
  • Foam cells release cytokines and growth factors, attracting more monocytes
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67
Q

Describe pathogenesis of an atheroma (pt.2)

A
  • Smooth muscle cells migrate into the plaque due to platelet derived growth factor and secrete elastin and collagen, forming a fibrous cap
  • Presence of foam cells stimulates smooth muscle cells to secrete calcium - hardens the plaque
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68
Q

What secretes growth factors

A

Platelets, injured endothelium, macrophages and smooth muscle cells

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69
Q

List risk factors for atherosclerosis

A
  • Hypercholesterolaemia
  • Smoking
  • Hypertension
  • Diabetes
  • Male
  • Increasing age
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70
Q

Def: fatty streak

A

Flat or slightly elevated yellow lesion in an artery wall containing intracellular accumulation of lipids

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71
Q

What does a fibrous cap contain

A

Smooth muscle cells, macrophages, lymphocytes, foam cells, collagen, elastin

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72
Q

List 4 clinical manifestations of an atheroma

A
  • Lumen narrowing due to plaque stenosis
  • Acute atherothrombotic occlusion
  • Embolisation of distal arterial bed
  • Ruptured abdominal atherosclerotic aneurysm
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73
Q

Outcomes of lumen narrowing

A
  • Reversible tissue ischaemia (especially during exercise)
  • Ischaemic pain may develop at rest
  • Large intraplaque haemorrhage may increase rate of stenosis
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74
Q

Describe acute atherothrombotic ischaemia

A
  • Plaque rupture exposes highly thrombogenic material - collagen and elastin
  • Activation of coagulation cascade and thrombotic occlusion
  • Total occlusion -> irreversible ischaemia leading to infarction
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75
Q

Why are small infarctions in the heart dangerous

A

Can lead to dangerous arrhythmias

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76
Q

Def: thrombosis

A

The solidification of blood contents that forms within the vascular system during life

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77
Q

When does a thrombus form

A

A pathological thrombus forms when there is an imbalance between natural coagulant and anticoagulant factors and the coagulation and fibrinolytic system

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78
Q

Name the 3 components of Virchow’s triad

A
  • Changes in vessel wall
  • Changes in blood flow
  • Changes in blood constituents
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79
Q

Describe normal blood flow

A

Laminar. Cells flow in the centre of the lumen and endothelial cells are not sticky

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80
Q

Describe pathogenesis of thrombosis

A
  • Artery is narrowed and blood becomes turbulent
  • Results in damage to endothelial cells and collagen is exposed
  • Stimulates coagulation cascade
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81
Q

Describe the extrinsic pathway in coagulation cascade

A

○ TF activates VII to VIIa, forming a complex which then activates X to Xa (also activates IX to IXa which goes on to activate X through the intrinsic pathway)
○ Xa activates prothrombin to thrombin which activates fibrinogen to fibrin
○ Thrombin activates XI, V (cofactor with Xa), and VIII

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82
Q

Describe the intrinsic pathway in the coagulation cascade

A

○ XII activated by contact with collagen fibres
○ XIIa catalyses activation of XI
○ XIa catalyses activation of IX
○ IXa catalyses activation of X

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83
Q

Where does venous thrombosis usually occur

A
  • Valves -> produce a natural degree of turbulence and can be damaged by trauma, stasis or occlusion
  • Atheromas don’t form in veins due to low BP
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84
Q

When does venous thrombosis usually occur

A
  • Can be in young active individuals with no predisposing factors
  • If BP drops (due to surgery, following MI) blood cells more likely to touch damaged vessel walls
  • Immobilisation -> venous return relies on muscle contractions
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85
Q

4 fates of thrombi

A
  • Resolved (fibrinolytic system dissolves it)
  • Organisation (macrophages clear thrombus and fibroblasts replace it with collagen. scar forms and narrowed lumen)
  • Recanalisation (capillaries grow through thrombus and fuse to form larger vessels - blood flow restored)
  • Embolisation (fragments of thrombus break off into circulation)
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86
Q

Def: embolus

A

Mass of material in the vascular system able to lodge in a vessel and block its lumen

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87
Q

Types of embolus (5)

A
  • Thrombus (most common)
  • Air
  • Cholesterol crystals
  • Tumour amniotic fluid (pregnant women with rapid labour)
  • Fat
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88
Q

Result of a small pulmonary embolism

A
  • Lysed within the lung, unnoticed
  • Organised and permanent -> small respiratory deficiency
  • Accumulation over time may cause idiopathic pulmonary hypertension
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89
Q

Result of a large pulmonary embolism

A
  • Acute respiratory and cardiac problems (may resolve with or without treatment)
  • Symptoms = chest pain and shortness of breath
  • Lung function impaired and patients more likely to have another embolism from the same source
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90
Q

Result of a massive pulmonary embolism

A
  • Sudden death

- Usually from long thrombi from DVT

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91
Q

Where do most systemic emboli originate from

A

The heart and atherosclerotic plaques

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92
Q

How do thrombi form in the heart

A
  • Cardiac muscle dies in MI and collagen left exposed to circulating platelets
  • AF -> blood stagnates in atria so thrombi form and when natural rhythm is re-established fragments may break off
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93
Q

Def: ischaemia

A

Reduction in the blood flow to a tissue or part of the body due to constriction or occlusion of the blood vessels supplying it

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94
Q

Extent of ischaemia depends on ….

A
  • Duration of ischaemic period

- Metabolic demands of the tissue

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95
Q

Def: infarction

A

The death of part or the whole of an organ that occurs when the artery supplying it becomes obstructed

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96
Q

Supply of an organ by only 1 artery

A

End arterial supply

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97
Q

Which organs have dual arterial supply

A

Liver - Portal hepatic vein and hepatic artery
Lungs - Pulmonary veins and bronchial arteries
Brain - Circle of Willis

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98
Q

Describe the pathology of reperfusion injury

????????

A
  • ## During ischaemia transport mechanisms across the cell membrane are disrupted
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99
Q

Def: gangrene

A

Tissue necrosis where whole areas of a limb or region of the gut have their arterial supply cut off and large areas of mixed tissue die in bulk

100
Q

Describe dry gangrene

A

Tissue dies and is mummified, healing occurs above it. Dead area drops off eventually - sterile process

101
Q

Describe wet gangrene

A

Bacterial infection supervenes as a secondary complication. Gangrene spreads proximally and patient dies from sepsis

102
Q

Describe pathology of disseminated intravascular coagulation

A
  • Balance of thrombotic and thrombolytic mechanisms disturbed
  • Thrombosis activated without effective counterbalance
  • Small thrombi form throughout the body
  • This causes bleeding in other areas of the body because clotting factors have been used up
103
Q

Def: watershed areas

A

Tissue at the interface between adjacent territories supplied by 2 different arteries. Prone to infarction if there is impairment of blood/oxygen supply

104
Q

Give 3 examples of watershed areas

A
  1. Splenic flexure between inferior and superior mesenteric
  2. Cerebral hemispheres at the interface between major cerebral arteries
  3. Myocardium between tissue supplied directly by ventricles and coronary arteries
105
Q

Name areas vulnerable to ischaemia and infarction

A
  • Watershed areas

- Tissue supplied by portal system

106
Q

Name some areas supplied by portal vasculature

A
  • Anterior pituitary receives blood from hypothalamus
  • Renal tubular system receives blood from glomerular capillaries
  • Parts of exocrine pancreas and receive blood already supplying the islet of Langerhans cells
107
Q

List 5 other causes of ischaemia and infarction

A
  1. Spasm
  2. External compression
  3. Steal
  4. Hyperviscosity
  5. Vasculitis
108
Q

Describe pathology of spasm in ischaemia and infarction

A
  • Transient arterial narrowing
  • Can be due to decrease in nitric oxide production by vascular endothelium (cell injury or loss)
  • Spasm of coronary arteries can lead to angina
109
Q

Describe pathology of external compression in ischaemia and infarction

A
  • Vessels partially or totally occluded by external compression
  • intentionally done in surgery by ligation to prevent haemorrhage
  • Veins more susceptible due to thin wall and low intraluminal pressure
  • Common in strangulated hernia, testicular and ovarian torsion
110
Q

Describe pathology of steal in ischaemia and infarction

A
  • Blood diverted ‘stolen’ from a vital territory
  • Atheroma causes blood to be diverted to competing area
  • Tissue distal to the atheroma becomes ischaemic
111
Q

Describe pathology of hyperviscosity in ischaemia and infarction

A
  • Most impact in small vessels

- Can be due to plasma cell tumour - abnormally high conc of antibodies

112
Q

Describe pathology of vasculitis in ischaemia and infarction

A
  • Inflammation of vessel wall narrows the lumen and increases chance of thrombus formation
113
Q

Def: TIA

A

Transient ischaemic attack = a stroke that lasts for <24 hours and is associated with full recovery

It is a risk marker for cerebral infarction

114
Q

Causes of cerebral infarction (

A
  1. Atheroma in intra/extracranial arteries -> arterial thrombosis
  2. Embolic arterial occlusion
  3. Head injury -> hypoxia, vascular occlusion/rupture
  4. Subarachnoid haemorrhage
  5. Generalised arterial disease (e.g. vasculitis)
  6. Critical reduction of cerebral blood flow
  7. Critical reduction of arterial oxygenation
  8. Venous thrombosis
115
Q

What is a subarachnoid haemorrhage caused by (6)

A
  1. Spontaneous rupture of saccular aneurysm in circle of Willis (most common)
  2. Trauma
  3. Hypertensive haemorrhage
  4. Vasculitis
  5. Tumours
  6. Coagulation disorders
116
Q

Def: apoptosis

A

Programmed cell death

117
Q

List inhibitors of apoptosis (4)

A
  1. Growth factors
  2. Extracellular matrix
  3. Sex steroids
  4. Some viral proteins
118
Q

List inducers of apoptosis (8)

A
  1. Growth factor withdrawal
  2. Loss of matrix attachment
  3. Glucocorticoids
  4. Some viruses
  5. Free radicals
  6. Ionising radiation
  7. DNA damage
  8. Ligand binding at ‘death’ receptors
119
Q

What role to Bcl-2 and Bax have in apoptosis

A
  • Bcl-2 inhibits factors inducing apoptosis and Bax-Bax dimers enhance apoptotic stimuli
  • Ratio determines cell susceptibility to apoptotic stimuli
120
Q

Describe the intrinsic pathway of apoptosis

A
  • Responds to growth hormone withdrawal and biochemical stress
  • DNA damage = stress
  • p53 induces cell cycle arrest and induces apoptosis via Bcl-2 family activation
121
Q

Describe the extrinsic pathway of apoptosis

A
  • Ligand binding death receptors
  • Binding promotes clustering of receptor molecules on the cell surface and initiates signal transduction cascade
  • Activation of caspases
122
Q

Execution phase of apoptosis

A
  • pro-caspases activated by intrinsic/extrinsic pathway
  • These are initiator caspases that cleave other pro-caspases
  • Activated caspases cause degradation of many targets
  • Cells phagocytosed immediately or fragment into apoptotic bodies which are phagocytosed later
123
Q

Give some examples of apoptosis in disease (3)

A
  • AIDs -> HIV proteins activate CD4 on uninfected T helper cells (induces apoptosis) - immunodepletion and dysfunction
  • Neurodegenerative disorders
  • Anaemia of chronic disorders
124
Q

Def: Necrosis

A

Traumatic cell death which induces inflammation and repair

125
Q

Describe coagulative necrosis

A
  • Most common form and occurs in most organs
  • Proteins coagulate and metabolic activity ceases
  • Macrophages digest dead cells
  • Necrotic tissue evokes inflammatory response
126
Q

Describe liquifactive/colliquative necrosis

A
  • Occurs in the brain

- Lack of supporting stroma means necrotic neural tissue liquifies

127
Q

Describe caseous necrosis

A
  • Dead tissue is structureless like soft cheese

- Characteristic in TB

128
Q

Describe gangrene (necrosis)

A
  • Rotting of tissues due to bacterial infection (especially clostridia)
  • Tissue appears black due to iron sulfide released from degraded haemoglobin
129
Q

Def: atrophy

A

Decrease in the size of a tissue cause by a decrease in size of individual cells or a decrease in number of constituent cells

130
Q

3 pathological manifestations of atrophy

A
  • Decreased function (immobilised limb due to cast -> muscle atrophy)
  • Loss of innervation of a muscle
  • Lack of nutrition (atrophy of adipose tissue, gut and pancreas)
131
Q

What is the response of an individual cell to increased functional demand

A

Increase size by hypertrophy, hyperplasia, or both

132
Q

Def: hypertrophy

A

Increase in cell size without cell division

133
Q

Give 2 examples of hypertrophy

A
  • In athletes: skeletal muscles due to increased activity and in left ventricle due to sustained outflow resistance
  • Uterine smooth muscle at puberty and pregnancy (oestrogen)
134
Q

Def: hyperplasia

A

Increase in cell number by mitosis

135
Q

Give 2 examples of hyperplasia

A
  • Living at high altitudes stimulates bone marrow hyperplasia (inc. erythropoietin)
  • Benign/cancerous hyperplasia of prostate smooth muscle
136
Q

Def: dysplasia

A

Imprecise term for the morphological changes seen in cells in the progression to becoming cancer. Also refers to lack of development

137
Q

Def: metaplasia

A

The change in differentiation of a cell from one fully-differentiated cell type to a different fully-differentiated cell type

138
Q

3 examples of metaplasia

A

Metaplasia occurs as a result to change in cell environment

  1. Smoking - ciliated epithelium in the trachea transforms to squamous epithelium
  2. Stone blocking - epithelium in salivary glands and pancreas + bile ducts transforms to squamous epithelium
  3. Barrett’s oesophagus - prolonged exposure to stomach acid changes squamous epithelium to columnar epithelium
139
Q

Def: telomere

A

Non-coding section of randomly repetitive DNA at the tip of each chromosome

140
Q

What is the significance of telomeres in ageing

A
  • Telomeres not fully copied in DNA replication so shorten with each divide
  • Eventually shorten to the extent that DNA polymerase is unable to engage
141
Q

Where can telomerase be found

A

Germ cells and embryos

142
Q

Def: sarcopaenia

A

Muscle loss due to ageing

143
Q

When does sarcopaenia start and accelerate

A

Starts around 40, accelerates around 80

144
Q

What is sarcopaenia caused by (basic)

A

Decreased growth hormone and testosterone and increased catabolic cytokines

145
Q

Give 6 changes due to ageing and their causes

A
  1. Deafness - hair cell loss
  2. Senile dementia - brain atrophy (nerve cells unable to replicate)
  3. Cataracts - UV light damage that cross links proteins in the eye
  4. Osteoporosis - brittle bones due to oestrogen, vit D and calcium deficiency in early life
  5. Dermal elastosis - wrinkling caused by UV
  6. Impaired immunity - immunological changes result in lowered production of immune cells
146
Q

Def: carcinogenesis

A

The transformation of normal cells to neoplastic cells through permanent genetic alterations or mutations. Only refers to malignant neoplasms

147
Q

Def: neoplasm

A

A lesion resulting from the autonomous or relatively autonomous abnormal growth of cells which persists after the initiating stimulus has been removed

148
Q

Def: neoplasia

A

The presence or formation of a new, autonomous, abnormal, persistent growth

149
Q

Where can’t neoplasm arise from

A

Erythrocytes (no nucleus so no DNA to mutate)

150
Q

Def: tumour

A

Any abnormal swelling

151
Q

4 types of tumour

A
  1. Neoplasm
  2. Inflammation
  3. Hypertrophy
  4. Hyperplasia
152
Q

How can tumours be classified

A

By behaviour and histologically

153
Q

5 ways benign tumours can cause morbidity/mortality

A
  1. Pressure on adjacent structures
  2. Obstruction of fluid
  3. Production of hormone (thyroid tumour)
  4. Transformation into malignant tumour
  5. Anxiety and stress (patient hears tumour = cancer)
154
Q

7 ways malignant tumours can cause morbidity/mortality

A
  1. Pressure on and destruction of adjacent tumours
  2. Formation of secondary tumours
  3. Blood loss from ulcerated surfaces
  4. Obstruction of fluid
  5. Hormone production
  6. Paraneoplastic effects resulting in weight loss and debility
  7. Anxiety and pain
155
Q

Growth rate of malignant tumours

156
Q

Nuclear morphology of malignant tumour

A
  • Enlarged
  • Hyperchromatic (stains darkly)
  • Irregular outline
  • Multiple nucleoli
  • Pleomorphic (vary in size and shape)
157
Q

Describe the border of a benign tumour

A

Often circumscribed (restricted within limits) or encapsulated

158
Q

Describe the border of a malignant tumour

A

Often poorly defined or irregular

159
Q

Direction of growth of benign tumours

A

Often exophytic

160
Q

Direction of growth of malignant tumours

A

Often endophytic (invasive inwards direction of growth)

161
Q

Def: histogenesis

A

The specific cell or origin of a tumour

162
Q

Def: tumour grade

A

An assessment of tumour’s degree of malignancy or aggressiveness

163
Q

Factors to assess in tumour grading

A
  1. Mitotic activity
  2. Nuclear size (hyperchromasia & pleomorphism)
  3. Degree of resemblance to the origin tissue
164
Q

Def: tumour stage

A

Extent of a tumour’s spread determined by histopathological and clinical examination

165
Q

What are the 3 component of the TNM tumour grading system

A

Tumour size
Node status
Metastases

166
Q

What is T(NM)

A

Primary tumour size
Number given that assesses the size of tumour and the organ harbouring it
Large number = large tumour

167
Q

What is (T)N(M)

A

Lymph node status

Number denotes the number of lymph nodes or groups of nodes containing metastases

168
Q

What is (TN)M

A

Anatomical extent of metastases

169
Q

Nomenclature: benign non glandular, non secretory epithelium

170
Q

Nomenclature: benign glandular or secretory epithelium

171
Q

Nomenclature: Malignant epithelium

172
Q

Nomenclature: Malignant glandular epithelium

A

Adenocarcinoma

173
Q

Benign adipocyte tumour

174
Q

Benign striated muscle tumour

A

Rhabdomyoma

175
Q

Benign smooth muscle cell tumour

176
Q

Benign cartilage tumour

177
Q

Benign bone tumour

178
Q

Benign vascular tumour

179
Q

Benign nerve tumour

180
Q

Malignant adipocyte tumour

A

Liposarcoma

181
Q

Malignant striated muscle tumour

A

Rhabdomyosarcoma

182
Q

Malignant smooth muscle tumour

A

Leiomyosarcoma

183
Q

Malignant cartilage tumour

A

Chondrosarcoma

184
Q

Malignant bone tumour

A

Osteosarcoma

185
Q

Malignant vascular tumour

A

Angiosarcoma

186
Q

Malignant nerve tumour

A

Neurosarcoma

187
Q

3 -oma that are not neoplasms

A
  1. Granuloma - chronic inflammation
  2. Mycetoma - fungus in the body
  3. Tuberculoma - mass of TB
188
Q

Malignant neoplasm of melanocytes

189
Q

Malignant tumour of mesothelial cells

A

Mesothelioma

190
Q

Malignant neoplasm of lymphoid cells

191
Q

Burkitt’s lymphoma

A

B-cell lymphoma caused by Epstein-Barr virus

192
Q

Ewing’s sarcoma

A

Malignant tumour of the bone

193
Q

Hodgkin’s lymphoma

A

Malignant neoplasm characterised by presence of Reed-Sternberg cells

194
Q

Kaposi’s sarcoma

A

Malignant neoplasm derived from vascular endothelium, commonly associated with AIDs

195
Q

Def: Teratoma

A

Neoplasm of germ cell origin that forms cells representing all 3 germ cell layers of the embryo (endoderm, mesoderm, ectoderm)

196
Q

What is a carcinosarcoma

A

Mixed malignant tumours showing characteristics of both epithelium and connective tissue

197
Q

Def: oncogenesis

A

Refers to both benign and malignant tumours

198
Q

Def: carcinogens

A

An environmental agent participating in the causation of tumours. Act on DNA

199
Q

Def: carcinogenic

A

Cancer causing carcinogen

200
Q

Def: oncogenic

A

Tumour/neoplasm causing carcinogen

201
Q

Name the classes of carcinogens (7)

A
  1. Chemical
  2. Viruses
  3. Ionising/non-ionising radiation
  4. Hormones
  5. Parasites
  6. Mycotoxins
  7. Miscellaneous
202
Q

Characteristics and examples of chemical carcinogens

A
  • No common structural features
  • Most require conversion from pro-carcinogens
  • Examples: polycyclic hydrocarbons, aromatic amines
203
Q

Characteristics and examples of viral carcinogens

A
  • More common in younger people
  • Epstein-Barr leads to Burkitt’s lymphoma
  • Human papillomavirus leads to cervical cancer
204
Q

Examples of ionising/non-ionising carcinogens

A
  • UV (UVB more so) exposure gives higher change of basal and squamous cell carcinoma
  • Tissues more susceptible to ionising radiation = thyroid, breast, bone, haemopoietic tissue
205
Q

Examples of hormonal carcinogens

A
  • Oestrogen increases incidence of mammary and endometrial cancer
  • Anabolic steroids increase incidence of hepatocellular carcinoma
206
Q

Examples of parasites as carcinogens

A
  • Schistosoma haematobium leads to bladder cancer

- Clonorchis sinesis results in adenocarcinoma of bile ducts (choleangiocarcinoma)

207
Q

Example of mycotoxin as a carcinogen

A

Alfatoxins produced by Aspergillus flavus -> hepatocellular carcinoma

208
Q

2 Examples of asbestos linked tumours

A

Malignant mesothelioma and lung carcinoma

209
Q

5 host factors influencing carcinogenesis

A
  1. Race
  2. Diet
  3. Constitutional factors (age, gender etc.)
  4. Premalignant lesions
  5. Transplacental exposure
210
Q

How does race influence carcinogenesis

A
  • Skin cancer uncommon in black people - melanin protects from UVB
  • Oral cancer more common in India + South-East Asia (chewing tobacco)
211
Q

How does diet influence carcinogenesis

A
  • High dietary fat, red/processed meat -> colorectal cancer
  • Alcohol -> breast/oesophageal cancer
  • Dietary fibre protects against colorectal cancer
212
Q

How do constitutional factors influence carcinogenesis

A
  • Inherited presdispostion -> BRCA1/2, RB1 genes
  • Age -> incidence increases
  • Gender -> breast cancer 200x more likely in women, prostate cancer more common in men
213
Q

Premalignant lesions that lead to cancer (5)

A
  • Colonic polyps - bowel cancer
  • Cervical dysplasia - cervical cancer
  • Ulcerative colitis - bowel cancer
  • Undescended testes - testicle tumours
214
Q

3 stages of carcinogenesis

A

Initiation, promotion, progression

215
Q

Initiation stage of carcinogenesis

A

Carcinogen induces genetic alterations that give the cell neoplastic potential

216
Q

Promotion stage of carcinogenesis

A

Stimulation of clonal proliferation of the initiated transformed cell

217
Q

Progression stage of carcinogenesis

A

Culminating in malignant behaviour characterised by invasion and its consequences

218
Q

Genetic alterations needed to transform normal cells into neoplastic cells

A
  1. Telomerase expression
  2. Loss or inactivation of both copies of tumour suppression gene (removes inhibitory control of cell replication)
  3. Activation or normal expression of oncogenes to self stimulate cell proliferation
  4. Genomic instability
219
Q

Name 2 types of tumour suppressor gene

A

Caretaker and gatekeeper

220
Q

What do caretaker genes do and give an example

A

Repair DNA damage

BRCA1/2

221
Q

What do gatekeeper genes do and give 2 examples

A

Inhibit proliferation or promote death of cells with DNA damage
p53
RB1

222
Q

Role of p53 gene

A
  • Transcription factor that responds to DNA damage
  • Repairs damaged DNA before S phase
  • If DNA damage too extensive, initiates apoptotic cell death
223
Q

How can p53 lose normal function

A
  • Non sense or missense mutations
  • Complexes of normal and mutant p53 that prevent normal function
  • Binding of normal p53 to proteins encoded by oncogenic DNA viruses
224
Q

Role of RB1

A
  • Transcriptional regulator that controls G1/S checkpoint

- Associated with retinoblastomas

225
Q

5 types of oncogene products

A
  1. Growth factors
  2. Receptors for growth factors
  3. Signalling mediator with tyrosine kinase activity
  4. Signalling mediator with nucleotide binding activity
  5. Nuclear-binding transcription factor oncoprotein
226
Q

How is an oncogene activated by translocation

A

Oncogene translocated from untranscribed site to one adjacent to an actively transcribed gene

227
Q

How is an oncogene activated by point mutation

A

Substitution of a single base changes an amino acid resulting in hyperactivity of the oncogene

228
Q

How is an oncogene activated by amplification

A

Insertion of multiple copies of the oncogene resulting in cellular proliferation stimulated by excessive copies

229
Q

Factors leading to invasion of tumour

A
  • Decreased cell adhesion to adjacent cells
  • Secretion of proteolytic enzymes
  • Abnormal or increased cellular motility (more motile and loses contact inhibition mechanism)
230
Q

Matrix metalloproteinases

A

Most important proteinase secreted by malignant neoplastic cells to digest surrounding tissues

231
Q

3 major metalloproteinases

A
  1. Interstitial collagenases
  2. Gelatinases
  3. Stromelysins
232
Q

What do interstitial collagenases digest

A

Collagens I II III

233
Q

What do gelatinases digest

A

Collagen IV and gelatin

234
Q

What do stromelysins digest

A

Collagen IV and proteoglycans

235
Q

What inhibits matrix metalloproteinases

A

Tissue inhibitors of metalloproteinases (TIMPs)

236
Q

Tissues with less resistance to tumour invasion

A

Perineural and vascular lamina

237
Q

Tissues with high resistance to tumour invasion

A

Cartilage and fibrocartilage of intervertebral discs

238
Q

Def: Metastasis

A

The process whereby malignant tumours spread from their site of origin to form other tumours at distant sites

239
Q

Def: Carcinomatosis

A

Extensive metastatic disease

240
Q

Which tumour never metastasises

A

Basal cell carcinoma (cure = excise the whole thing)

241
Q

Where does liposarcoma metastasise to

242
Q

Sequence of metastasis

A
  1. Detachment of tumour cells from adjacent cells
  2. Invasion of surrounding connective tissue to reach pathway for metastasis (lymphatics/blood vessel)
  3. Intravasation into the lumen
  4. Evasion of host defence mechanisms (e.g. natural killer cells)
  5. Adherence to endothelium
  6. Extravasation into surrounding tissue
243
Q

Routes of metastasis (3)

A
  1. Haematogenous
  2. Lymphatic
  3. Transcoelomic
244
Q

Metastases in the bone are often from :

A
  1. Lung
  2. Breast
  3. Thyroid
  4. Kidney
  5. Prostate
245
Q

Describe transcoelomic metastasis

A
  • Pleural, pericardial and peritoneal cavities

- Effusion contains neoplastic cells -> spread to any organ in cavity

246
Q

How do carcinomas most often spread

A

Lymphatics

247
Q

How do sarcomas most often spread

A

Haematogenous

PHASE 2 (6 decks)

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