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Phase 2a Medicine > Introductory Clinical Sciences > Flashcards

Introductory Clinical Sciences Flashcards

1
Q

Name 2 types of autopsies

A
  • Hospital autopsies

- Medico-legal autopsies

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2
Q

What percentage of UK autopsies do hospital autopsies account for?

A

Less than 10%

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3
Q

What are hospital autopsies used for?

A
  • Teaching
  • Research
  • Governance
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4
Q

What percentage of UK autopsies do medico-legal autopsies account for?

A

More than 90%

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5
Q

What are the two types of medico-legal autopsies?

A
  • Coronial

- Forensic

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6
Q

What four questions do coronial autopsies try to answer?

A
  1. WHO was the deceased?
  2. WHEN did they die?
  3. WHERE did they die?
  4. HOW did they die?
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7
Q

What are forensic autopsies for?

A

Where death is thought unlawful

- e.g. murder

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8
Q

Name three reasons why deaths might be referred to a coroner.

A
  1. Presumed natural
  2. Presumed iatrogenic
  3. Presumed unnatural
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9
Q

What is a ‘presumed natural’ death?

A
  • The cause of death is not known

- Patient hadn’t seen a doctor within 14 days prior to death

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10
Q

Name some examples of presumed iatrogenic deaths.

A
  1. Anaesthetic deaths
  2. Illegal abortions
  3. Complications of therapy
  4. Peri / post- operative deaths
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11
Q

Name some examples of presumed unnatural deaths.

A
  1. Accidents
  2. Industrial deaths
  3. Suicide
  4. Murder
  5. Neglect
  6. Custody death
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12
Q

Who refers patients to a coroner?

A
  1. Doctors
  2. Registrar of BDM
  3. Relatives
  4. Police
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13
Q

Who performs autopsies?

A
  • Histopathologists

- Forensic pathologists

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14
Q

What autopsies do histopathologists do?

A
  1. Hospital autopsies

2. Coronial autopsies (natural deaths, drowning, suicide, etc.)

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15
Q

What autopsies do forensic pathologists do?

A

Coronial autopsies for homicides, deaths in custody, and neglect

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16
Q

Name the stages of an autopsy.

A
  1. History / scene
  2. External examination
  3. Evisceration
  4. Internal examination
  5. Reconstruction
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17
Q

At which stages of an autopsy do you look at the microbiology?

A
  1. External examination
  2. Evisceration
  3. Internal examination
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18
Q

At which stages of an autopsy do you look at toxicology?

A
  1. External examination
  2. Evisceration
  3. Internal examination
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19
Q

At which stages of an autopsy do you X-ray the subject?

A
  1. External examination

2. Evisceration

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20
Q

At which stages of an autopsy do you look at genetics?

A
  1. Evisceration

2. Internal examination

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21
Q

At which stage of an autopsy do you look at histology?

A

Internal examination

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22
Q

What does the external examination look for?

A
  1. Identification points (e.g. gender, age, jewellery, body modification, etc.)
  2. Disease and treatment
  3. Injuries
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23
Q

What does evisceration involve?

A
  1. Y-shaped incision from ears down the midline
  2. Open all body cavities
  3. Examine organs in situ
  4. Remove thoracic and abdominal organs
  5. Remove brain
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24
Q

What do you avoid removing during an internal examination and why?

A

Lower GI tract as this presents an infection risk

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25
Q

Define ‘acute inflammation’, and give an example.

A

The initial and often transient series of tissue reactions to injury. It may last a few hours to a few days.

E.g. appendicitis

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26
Q

What is inflammation?

A

The local physiological response to tissue injury. It is not a disease, but a manifestation of one.

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27
Q

What are the benefits of inflammation?

A
  • Destruction of invading microorganisms

- The walling off of an abscess cavity

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28
Q

What are the limitations of inflammation?

A
  • Disease (e.g. brain abscess) will act as a space-occupying mass compressing surrounding structures
  • Fibrosis resulting from chronic inflammation may distort tissues and permanently alter their function
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29
Q

What is the vascular component of acute inflammation?

A

Dilation of vessels

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30
Q

What is the exudative component of acute inflammation?

A

Vascular leakage of protein-rich fluid

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31
Q

What is a neutrophil polymorph?

A
  • A white blood cell

- It is the characteristic cell recruited to the tissue

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32
Q

What are the four outcomes of acute inflammation?

A
  1. Resolution
  2. Suppuration
  3. Organisation
  4. Progression to chronic inflammation
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33
Q

What is suppuration?

A

Pus formation

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34
Q

What is organisation?

A
  • Healing by fibrosis (scar formation) when there is substantial damage to the connective tissue framework
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35
Q

Describe the steps of organisation.

A
  1. Dead tissues and exudate are removed from the damaged areas by macrophages
  2. The defect becomes filled by the ingrowth of a specialised vascular connective tissue, granulation tissue
  3. Granulation tissue then gradually produces collagen to form a scar
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36
Q

Name six causes of inflammation.

A
  • Microbial infections
  • Hypersensitivity reactions
  • Physical agents
  • Chemicals
  • Tissue necrosis
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37
Q

How do bacteria cause harm?

How do viruses cause harm?

A

Release exotoxins and endotoxins

Cause death of individual cells by intracellular multiplication

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38
Q

What is a hypersensitivity reaction?

A

When an altered state of immunological responsiveness causes an inappropriate or excessive immune reaction that damages the tissues

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39
Q

What are some physical agents that may cause acute inflammation?

A
  • Trauma
  • Ionising radiation
  • Heat
  • Extreme cold (frostbite)
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40
Q

Why does tissue necrosis cause acute inflammation?

A

Peptides released from the dead tissue cause inflammation

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41
Q

What is tissue necrosis?

A

Death of tissues from lack of oxygen or nutrients resulting from inadequate blood flow (infarction)

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42
Q

Name five macroscopic features of acute inflammation.

A
  1. Rubor (redness)
  2. Calor (heat)
  3. Tumor (swelling)
  4. Dolor (pain)
  5. Loss of function
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43
Q

Why does rubor occur in acute inflammation?

A

Dilation of small blood vessels in the damaged area, causing tissue to appear red

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44
Q

Why does calor occur in acute inflammation?

A
  • Hyperaemia through a region, resulting in vascular dilation and the delivery of warm blood to the area
  • Only occurs in superficial body parts (e.g. skin)
  • Systemic fever contributes
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45
Q

Why does tumor occur in acute inflammation?

A

Swelling resulting from oedema, due to the accumulation of exudate in the extravascular space

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46
Q

Why does dolor occur in acute inflammation?

A
  • Stretching and distortion of tissues due to oedema and pressurised pus
  • Some chemical mediators (e.g. bradykinin, serotonin, etc.) induce pain
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47
Q

Why does loss of function occur in acute inflammation?

A

Movement of an inflamed area is consciously and reflexively inhibited by pain

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48
Q

Describe the acute inflammatory response process.

A
  1. Vessel calibre increases (vasodilation), increasing vessel flow
  2. Formation of fluid exudate - Increased vascular permeability
  3. Formation of cellular exudate - emigration of neutrophil polymorphs into the extravascular space
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49
Q

What forms precapillary sphincters? And what is their job?

A

Smooth muscle of arteriolar walls regulate blood flow through capillary bed

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50
Q

What happens to precapillary sphincters in acute inflammation?

A

They relax, increasing blood flow to the capillary bed, resulting in rubor and calor

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51
Q

Under normal circumstances, what is the consequence of high osmotic pressure inside the vessel? What causes this high osmotic pressure?

A

Plasma proteins cause the high osmotic pressure, which favours fluid returning to the vascular compartment

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52
Q

Under normal circumstances, what is the consequence of high hydrostatic pressure at the arteriolar end of the capillaries?

A

Fluid is forced out into the extravascular space

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53
Q

Which end of the capillary bed has low hydrostatic pressure, and what does this favour?

A

The venous end, which favours fluid returning to the vessel

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54
Q

What happens to capillary hydrostatic pressure in acute inflammation?

A

Increases

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55
Q

What is the movement of plasma proteins in acute inflammation? Why? How does this affect osmotic pressure?

A

> Increased hydrostatic pressure
forces plasma proteins out of the vessel into the extravascular space
increasing osmotic pressure in the extravascular space

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56
Q

What is the name of the protein-rich fluid that leaves the vessel during acute inflammation?

A

Fluid exudate

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57
Q

Name three causes of increased vascular permeability in acute inflammation.

A
  1. Immediate transient - chemical mediators
  2. Immediate sustained - severe direct vascular injury
  3. Delayed prolonged - endothelial cell injury
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58
Q

What are some examples of chemical mediators causing increased vascular permeability?

A
  • Histamine
  • Bradykinin
  • Nitric oxide
  • C5a
  • Leukotriene B4
  • Platelet activating factor
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59
Q

What are some things that cause endothelial cell injury, resulting in increased vascular permeability?

A

X-rays and bacterial toxins

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60
Q

What are the four stages in neutrophil polymorph emigration?

A
  1. Margination of neutrophils
  2. Pavementing of neutrophils
  3. Neutrophil emigration
  4. Diapedesis
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61
Q

Describe the margination of neutrophils in neutrophil polymorph emigration.

A
  • In normal circulation, cells circulate in the axial stream in blood vessels, and not in the plasmatic zone near the endothelium
  • Loss of intravascular fluid, increase in plasma viscosity, and slowing of blood flow near site of inflammation causes neutrophils to flow in the plasmatic zone
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62
Q

What is the axial stream in blood vessels?

A

The central part of the blood stream

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63
Q

What is the plasmatic zone in blood vessels?

A

The blood flowing nearest the endothelium

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64
Q

Describe the pavementing of neutrophils in neutrophil polymorph emigration.

A
  • Neutrophils adhere to endothelium in venules
  • Increased leucocyte adhesion results from interaction between paired adhesion molecules on the cell and endothelial surfaces
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65
Q

What happens if neutrophils come into contact with endothelial cells in normal tissues?

A

They do not adhere

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66
Q

Describe the neutrophil emigration stage of neutrophil polymorph emigration.

A
  • Neutrophils, eosinophil polymorphs, and macrophages insert a pseudopodia between endothelial cells
  • They migrate through the gap they created between the cells
  • They then migrate through the basal lamina into the vessel wall
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67
Q

Where does neutrophil emigration normally happen?

Where does it happen in acute inflammation?

A
  • Venules and small veins

- Capillaries

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68
Q

What is diapedesis?

A

The movement of red blood cells out of the vessel

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69
Q

Describe the diapedesis stage of neutrophil polymorph emigration.

A

Due to increased hydrostatic pressure, red blood cells are forced out of the vessel

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70
Q

What does the presence of large numbers of red cells in the extracellular space suggest?

A

There is severe vascular injury, such as a tear in the vessel wall

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71
Q

What causes the the spread of the acute inflammation response to uninjured tissues?

A

Chemical substances (endogenous chemical mediators) released from injured tissues spreading outwards

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72
Q

What do histamine and thrombin cause in acute inflammation?

A

The up-regulation of adhesion molecules on the surface of endothelial cells, leading to increased pavementing / adhesion

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73
Q

Name two examples of endogenous chemical mediators.

A

Histamine and thrombin

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74
Q

What 5 things do endogenous chemical mediators cause?

A
  1. Vasodilation
  2. Emigration of neutrophils
  3. Chemotaxis (attraction of neutrophil polymorphs towards certain chemicals at inflammation site)
  4. Increased vascular permeability
  5. Itching and pain
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75
Q

What does histamine cause?

A
  • Vasodilation

- Immediate transient phase of increased vascular permeability

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76
Q

How is the response of histamine so rapid?

A

Histamine is stored in preformed granules so can be released immediately when stimulated

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77
Q

What cells are the primary source of histamine? What other cells is histamine also present in?

A

Primary source: Mast cells

Other sources: basophil and eosinophil leucocytes, and platelets

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78
Q

What 2 things trigger the release of histamine?

A
  • Complement components C3a and C5a

- Lysosomal proteins released from neutrophils

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79
Q

Name five chemical mediators released from cells.

A
  1. Histamine
  2. Lysosomal compounds
  3. Eicosanoids - a type of prostaglandin
  4. 5-hydroxytrypamine (serotonin)
  5. Chemokine
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80
Q

What four enzymatic cascade systems are within the plasma?

A
  1. Complement system
  2. Kinin system
  3. Coagulation system
  4. Fibrinolytic system
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81
Q

Define the complement system.

A

A complex series of interacting plasma proteins which form a major effector system for antibody-mediated immune reactions

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82
Q

What is the main purpose of the complement system?

A

To remove and destroy antigens

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83
Q

How does the complement system destroy / remove antigens?

A

Direct lysis or opsonisation

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84
Q

How is the complement system activated in tissue necrosis?

A

Enzymes capable of activating complement factors are released from dying cells

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85
Q

How is the complement system activated during infection?

A
  • The formation of antigen-antibody complexes activates the complement system via the classical pathway
  • Endotoxins of gram-negative bacteria activate it via the alternative pathway
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86
Q

Which systems are activated by coagulation factor XII?

A
  1. Kinin system
  2. Fibrinolytic system
  3. Coagulation system
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87
Q

What is the product of the kinin system?

A

Kinins

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88
Q

What is the product of the fibrinolytic system?

A

Plasmin

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89
Q

What is the product of the coagulation system?

A

Fibrin

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90
Q

What is fibrin degraded by?

A

Plasmin

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91
Q

What activates the complement system?

A

Kinins and plasmin

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92
Q

Which system is the conversion of prekallikrein to kallikrein involved in?

A

The kinin system

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93
Q

What 3 things activate the conversion of prekallikrein to kallikrein?

A
  • Activated factor XII (aka. XIIa)
  • Plasmin
  • Leucocyte proteases (e.g. trypsin)
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94
Q

What does kallikrein stimulate?

A

The conversion of kininogens to kinins

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95
Q

Which kinin is a common vasodilator?

A

Bradykinin

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96
Q

What are the 2 important chemical mediators released by macrophages?

A
  1. Interleukin-1 (IL-1)

2. Tumour necrosis factor (TNF-alpha)

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97
Q

What acts first; histamine and thrombin or IL-1 and TNF-alpha?

A

Histamine and thrombin

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98
Q

What is the role of IL-1 and TNF-alpha?

A

They stimulate endothelial cells, fibroblasts, and epithelial cells to secrete MCP-1

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99
Q

What does MCP-1 do?

A

It’s a powerful chemotactic protein that attracts neutrophil polymorphs

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100
Q

What happens when blood monocytes leave the blood vessel at the site of inflammation?

A

They become more metabolically active, motile, and phagocytic = macrophages

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101
Q

What is opsonisation? What two things are involved in the opsonisation of microorganisms?

A

It is the marking of a substance for destruction

Antibodies and complements are involved in opsonisation

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102
Q

What are macrophages responsible for?

A

Clearing away tissue debris and damaged cells

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103
Q

Macrophages and neutrophils discharge their lysosomal enzymes into the ECF. Why?

A

It aids the digestion of the inflammatory exudate

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104
Q

Which vessels are blind-ended? What does this mean?

A

Terminal lymphatic vessels are blind-ended which means they are closed off at one end

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105
Q

In a given tissue, which is more numerous; lymphatics or capillaries?

A

Neither, they are similar in number

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106
Q

What do terminal lymphatics drain into?

A

Collecting lymphatics

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107
Q

Describe how collecting lymphatics drain lymph into lymph nodes.

A
  • Presence of valves
  • Contraction of neighbouring muscles
  • Very similar to veins
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108
Q

What happens to lymphatic channels in acute inflammation?

A

They become dilated as they drain oedema fluid away from the inflammatory exudate

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109
Q

Why is lymph drainage important in the immune response?

A

Antigens are carried to regional lymph nodes for recognition by lymphocytes in lymph channels

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110
Q

What does the staining of neutrophil polymorphs with HandE look like?

A

Nucleus - blue

Cytoplasm - pink/purple

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111
Q

What are bacterial lipopolysaccharides?

A

Endotoxins from gram-negative bacteria

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112
Q

How do endotoxins activate complement? What does this generate? What is the role of the product?

A

> Activates complement via the alternative pathway
Generates component C3b
C3b has opsonisation properties

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113
Q

How do antibodies activate complement? What does this generate?

A
  • Antibodies bind to bacterial antigens
  • Activates complement via the classical pathway
  • Generates C3b
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114
Q

What happens when immunoglobulins bind to microorganisms?

A

Immunoglobulins bind to microorganisms with their Fab components, which leaves the Fc fragment of immunoglobulins exposed

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115
Q

What is the significance of the Fc fragment on immunoglobulins?

A

Neutrophils have surface receptors for the Fc fragments, so bind to the microorganism prior to phagocytosis

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116
Q

What is the first step of phagocytosis?

A

Adhesion

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117
Q

What happens during the adhesion stage in phagocytosis?

A

The particle to be phagocytosed is held to the cell surface of a neutrophil polymorph or macrophage

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118
Q

How does a phagocyte start the process of engulfing a particle?

A

It sends out pseudopodia, which meet and fuse, engulfing the particle into a phagosome

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119
Q

What are lysosomes?

A

Membrane bound packets containing toxic compounds

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120
Q

How are phagolysosomes formed?

A

Lysosomes fuse with phagosomes

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121
Q

Where does intracellular killing take place?

A

In phagolysosomes

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122
Q

What substances are contained within neutrophil polymorphs that are similar to bleach?

A

Noxious microbicidal agents

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123
Q

What are the two classes of noxious microbicidal agents?

A
  1. Oxygen-dependent

2. Oxygen-independent

124
Q

How are oxygen-dependent microbicidal agents formed?

A

Hydrogen peroxide reacts with myeloperoxidase inside cytoplasmic granules, in the presence of a halide (e.g. Cl-)

125
Q

Name two examples of oxygen-independent microbicidal agents.

A
  • Lysozyme

- Lactoferrin

126
Q

What three things do lysosomal products do when they’re released?

A
  1. Damage local tissues by proteolysis
  2. Activate coagulation factor XII
  3. Attract leucocytes to the area
127
Q

What are pyrogens?

A

Substances which induce a systemic fever by acting on the hypothalamus

128
Q

What is the lifespan of neutrophil polymorphs?

A

1-3 days

129
Q

What three ways are neutrophil polymorphs removed from the site of inflammation?

A
  1. They die at the site
  2. They leave via lymphatics
  3. Removed by apoptosis
130
Q

What complement components stimulate mast cells to release histamine?

A

C3a and C5a

131
Q

Is histamine stored or synthesised on demand?

A

Stored in granules

132
Q

What else do mast cells synthesise? And how do they do it?

A

They metabolise arachidonic acid into leukotrienes, prostaglandins, and thromboxanes

133
Q

What factors influence the macroscopic appearance of acute inflammation?

A
  1. The tissue involved

2. The type of agent causing the inflammation

134
Q

What are the five descriptive terms used to describe inflammation appearances?

A
  1. Serous - lots of fluid released
  2. Suppurative - lots of pus
  3. Membranous
  4. Pseudomembranous
  5. Necrotising
135
Q

Beneficial effects of the fluid exudate:

Describe the ‘dilution of toxins’.

A

The fluid exudate dilutes toxins produced by bacteria, allowing them to be carried away in the lymphatics

136
Q

Beneficial effects of the fluid exudate:

Describe ‘entry of antibodies’.

A

Antibodies enter the extravascular space due to increased vascular permeability, which can result in;

  • lysis of microorganisms via the complement system
  • phagocytosis via opsonisation
  • neutralisation of toxins
137
Q

Beneficial effects of the fluid exudate:

Describe ‘transport of drugs’.

A

The increased vascular permeability means that drugs can be transported to the site where bacteria are multiplying

138
Q

Beneficial effects of the fluid exudate:

What are the two ways in which fibrin acts beneficially in acute inflammation?

A
  • Fibrin impedes the movement of microorganisms by trapping them
  • Forms a matrix for the formation of granulation tissue
139
Q

Beneficial effects of the fluid exudate:

How does the fluid exudate aid the delivery of nutrients and oxygen?

A

Increased fluid flow through the area, which is essential for neutrophils which have high metabolic activity

140
Q

Beneficial effects of the fluid exudate:

Why is the fluid exudate important for the immune response?

A

The fluid exudate stimulates the immune response by draining into the lymphatics, allowing particulates and soluble antigens to reach the lymph nodes

141
Q

Name the seven ways the fluid exudate is beneficial in acute inflammation.

A
  1. Dilution of toxins
  2. Entry of antibodies
  3. Transport of drugs
  4. Fibrin formation (trapping)
  5. Fibrin matrix (granulation tissue)
  6. Delivery of nutrients and oxygen
  7. Stimulation of immune response
142
Q

Name the three ways the fluid exudate in acute inflammation can be harmful.

A
  1. Digestion of normal tissues
  2. Swelling
  3. Inappropriate inflammatory response
143
Q

Harmful effects of the fluid exudate:

Describe ‘digestion of normal tissues’.

A
  • Enzymes (e.g. collagenases and proteases) may digest normal tissues
  • May result in vascular damage (i.e. type III hypersensitivity)
144
Q

Harmful effects of the fluid exudate:

Describe ‘swelling’ as a harmful effect in acute inflammation.

A
  • Can be harmful in children (e.g. if the epiglottis swells due to influenza it may obstruct the airway)
  • Serious when in enclosed spaces, such as the cranial cavity (e.g. acute meningitis or cerebral abscess) which can result in ischaemic damage
145
Q

Harmful effects of the fluid exudate:

What is inappropriate inflammatory response?

A

When the provoking antigen (e.g. pollen in hay fever) poses no real threat to the individual

146
Q

What are the four main outcomes of acute inflammation?

A
  1. Resolution
  2. Suppuration
  3. Repair / organisation
  4. Progression to chronic inflammation
147
Q

What does the outcome of acute inflammation depend on?

A
  1. The type of tissue involved
  2. The amount of tissue destruction
  3. The nature of the causal agent
148
Q

Define ‘resolution’.

A

The complete recovery of the tissues to normal after an episode of acute inflammation

149
Q

Name four circumstances / conditions that favour resolution.

A
  1. Minimal cell death and tissue damage
  2. Occurrence in an organ capable of regeneration (e.g. the liver, not the CNS)
  3. Rapid destruction of the causal agent
  4. Rapid removal of fluid and debris by good local vascular drainage
150
Q

What is an example of an acute inflammatory condition that completely resolves?

A

Acute lobar pneumonia

151
Q

Define ‘suppuration’.

A

The formation of pus - a mixture of living, dying, and dead neutrophils and bacteria, cellular debris, and sometimes globules of lipids

152
Q

Is the causative stimulus in suppuration usually short-term and quick to attack, or prolonged and persistent?

A

Prolonged and persistent

153
Q

What happens when pus begins to accumulate in a tissue?

A

It becomes surrounded by a pyogenic membrane consisting of sprouting capillaries, neutrophils, and fibroblasts (sometimes)

  • Results in granulation tissue and scarring
154
Q

What is an abscess? What is the effect of an abscess on drugs and antibodies?

A
  • A collection of pus

- Bacteria within an abscess cavity are relatively inaccessible to antibodies and antibiotics

155
Q

What happens if pus accumulates inside a hollow organ?

A

The mucosal layers of the outflow tract may become fused together by fibrin, resulting in an empyema (a pus filled pocket)

156
Q

Define ‘organisation’.

A

Organisation of tissues is their replacement by granulation tissue

157
Q

What is granulation tissue?

A

Tissue forming in response to injury, containing lots of new blood vessels and, in its later stages, large numbers of fibroblasts

158
Q

Give three conditions that favour organisation.

A
  1. Large amounts of fibrin are formed, which cannot be completely removed by fibrinolytic enzymes
  2. Substantial volumes of tissue becoming necrotic, or if the dead tissue is not easily digested
  3. Exudate and debris cannot be removed or discharged
159
Q

What happens during organisation?

A
  • New capillaries grow into the exudate
  • Macrophages migrated into the area
  • Fibroblasts proliferate under the influence of TGF-beta, resulting in fibrosis and scar formation
160
Q

When does acute inflammation progress onto chronic inflammation?

A

When the agent causing acute inflammation is not removed

161
Q

How does the cellular exudate change in the progression from acute to chronic inflammation?

A

Neutrophil polymorphs are replaced with;

  • lymphocytes
  • plasma cells (make antibodies)
  • macrophages (eat debris and bacteria)
  • multinucleate giant cells
  • fibroblasts (lay down collagen)
162
Q

Does acute inflammation always precede chronic inflammation?

A

No, chronic inflammation often occurs as a primary event

163
Q

Name five systemic effects of inflammation.

Just the categories, not the specific points

A
  1. Pyrexia
  2. Constitutional symptoms
  3. Reactive hyperplasia of the reticuloendothelial system
  4. Haematological changes
  5. Amyloidosis
164
Q

What is pyrexia?

A

A fever

165
Q

What do neutrophil polymorphs and macrophages produce that cause pyrexia? What do they act on?

A

Endogenous pyrogens act on the hypothalamus

166
Q

What do endogenous pyrogens do?

A

They act on the hypothalamus to set the thermoregulatory mechanisms at a higher temperature

167
Q

Which pyrogen has the greatest effect?

A

Interleukin-2 (IL-2)

168
Q

What stimulates the release of pyrogens?

A
  1. Phagocytosis
  2. Endotoxins
  3. Immune complexes
169
Q

What are the four constitutional symptoms?

A
  1. Malaise
  2. Anorexia
  3. Nausea
  4. Weight loss - as there is a negative nitrogen balance
170
Q

What is reactive hyperplasia of the reticuloendothelial system?

A

Local or systemic lymph node enlargement, including splenomegaly (spleen enlargement)

171
Q

When do you see increased levels of neutrophils?

A
  • Pyogenic infections

- Tissue destruction

172
Q

When do you see increased levels of eosinophils?

A
  • Allergic disorders

- Parasitic infections

173
Q

When do you see increased levels of lymphocytes

A
  • Chronic infection
  • Viral infections
  • Whooping cough
174
Q

When do you see increased levels of monocytes?

A
  • Bacterial infections
175
Q

Why would anaemia occur in acute inflammation?

A
  • Blood loss into the inflammatory exudate

- Haemolysis due to bacteria toxins

176
Q

What is amyloidosis?

A

In long-standing chronic inflammation, elevation of serum amyloid A protein (SAA) may cause amyloid to be deposited in various tissues, resulting in secondary amyloidosis

177
Q

What is amyloid?

A

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

178
Q

Define chronic inflammation.

A

The subsequent and often prolonged tissue reactions to injury following the initial response

179
Q

Which cells predominate chronic inflammation?

A
  • Lymphocytes
  • Plasma cells
  • Macrophages
180
Q

What is primary chronic inflammation?

A

When there is no initial phase of acute inflammation

181
Q

Is transplant rejection acute or chronic inflammation?

A

Chronic

182
Q

What is the most common type of acute inflammation to progress into chronic inflammation?

A

Suppurative inflammation

183
Q

How can acute suppurative inflammation progress into chronic inflammation?

A

> Pus forms abscess cavity that is deep-seated
drainage is delayed or inadequate
abscess develops thick wall composed of granulation and fibrous tissue
rigid walls of abscess cavity fail to come together after drainage
stagnating puss becomes organised by ingrowth of granulation tissue
replaced by a fibrous scar

184
Q

Give an example of a chronic abscess.

A

Osteomyelitis - chronic abscess in a bone

185
Q

Give four examples of indigestible materials that favour chronic inflammation and explain why.

A
  • Keratin (from ruptured cysts)
  • Fragments of necrotic bone
  • Surgical sutures
  • Wood, metal, glass, etc.
  • They are inert and are resistant to the action of lysosomal enzymes
186
Q

What type of inflammation do indigestible foreign bodies give rise to?

A

Chronic suppuration which leads to granulomatous inflammation, which causes macrophages to form multinucleate giant cells

187
Q

What happens if you get reoccurring acute inflammation in one location?

A

It progresses to chronic inflammation

  • e.g. gallstones causing chronic cholecystitis
188
Q

What are the five potential macroscopic appearances of chronic inflammation?

A
  1. Chronic ulcer
  2. Chronic abscess cavity
  3. Thinking of the wall of a hollow organ
  4. Granulomatous inflammation
  5. Fibrosis
189
Q

What is granulomatous inflammation?

A

When the immune system attempts to wall off a substance but is unable to completely eliminate it, which forms a granuloma

190
Q

What is a granuloma?

A

A collection of epithelioid histiocytes (a stationary macrophage found in tissue)

It may contain other cell types such as lymphocytes and histiocytes

191
Q

What is fibrosis?

A
  • Thickening or scarring of connective tissue

- Becomes most prominent when majority of chronic inflammatory cell infiltrate has subsided

192
Q

What are the six potential microscopic features of chronic inflammation?

A
  1. Cellular infiltrate consists of lymphocytes, plasma cells, and macrophages
  2. Eosinophil polymorphs may be present (but neutrophil polymorphs are rare)
  3. Some macrophages form multinucleate giant cells
  4. May be production of new fibrous tissue from granulation tissue
  5. Potential evidence of continuing destruction of tissue, simultaneous to tissue regeneration and repair
  6. Potential tissue necrosis
193
Q

What are the three predominant features of tissue repair?

A
  1. Angiogenesis (formation of new blood vessels)
  2. Fibroblast proliferation
  3. Collagen synthesis
    - 2 and 3 result in granulation tissue
194
Q

What regulates tissue repair?

A

Growth factor proteins, which bind to specific receptors on cell membranes and trigger a series of events culminating in cell proliferation

195
Q

What does the lymphocytic tissue infiltrate contain?

A

B and T lymphocytes

196
Q

What happens when a B lymphocyte comes into contact with an antigen?

A

It becomes progressively transformed into plasma cells

197
Q

What are the T lymphocytes responsible for?

A

Cell-mediated immunity

198
Q

What happens when a T lymphocyte comes into contact with an antigen?

A

It produces a range of soluble factors called cytokines

199
Q

What do cytokines do?

A

They recruit and activate other cells (e.g. macrophages)

200
Q

How do macrophages move through tissues?

A

By amoeboid motion

201
Q

What happens when a neutrophil ingests a microorganism?

A

It self-destructs within 3 days

202
Q

What are some differences between macrophages and neutrophil polymorphs, with regards to;

  • range of materials ingested
  • lifespan
A
  • Macrophages can ingest a wider range of materials

- Macrophages are long lived, NPs live for 3 days

203
Q

Give an example of a foreign body which can survive inside a macrophage.

A

Mycobacteria, e.g. mycobacterium tuberculosis

204
Q

What happens if a macrophage dies during a delayed-type hypersensitivity response?

A

It releases its lysosomal enzymes and contributes to widespread necrosis

205
Q

What are macrophages in inflamed tissues derived from?

A

Blood monocytes that have migrated out of vessels and become transformed

206
Q

Describe the first four stages of the reticuloendothelial system.

A

Haemopoietic stem cell > promonocyte > bone marrow monocyte > blood monocyte

207
Q

What does the activation of macrophages as they migrate into an area of inflammation involve?

A
  1. Increase in size
  2. Protein synthesis
  3. Mobility
  4. Phagocytic activity
  5. Content of lysosomal enzymes
208
Q

Give some examples of cytokines macrophages produce.

A
  • Interferon-alpha and -beta
  • Interleukin-1, -6, and -8
  • Tumour necrosis factor alpha (TNF-alpha)
209
Q

Name four examples of granulomatous diseases.

A
  • Tuberculosis
  • Leprosy
  • Crohn’s disease
  • Sarcoidosis
210
Q

What stain do you use to identify tuberculosis? What colour does it turn in a positive sample?

A

Ziehl-Neeson turns bright red with TB

211
Q

Describe the histology of epithelioid histiocytes with regards to;

  1. Similar to…
  2. Nuclei
  3. Eosinophilic / basophilic cytoplasm
  4. Shape
  5. Arrangement
  6. Phagocytic activity
  7. Function
A
  1. Similar to epithelial cells
  2. Large vesicular nuclei
  3. Eosinophilic cytoplasm
  4. Elongated shape
  5. Arranged in clusters
  6. Little phagocytic activity
  7. Adapted for secretory function - secretes ACE
212
Q

What does the presence of granulomas and eosinophils suggest?

A

Parasitic infection

213
Q

What is a common feature of a stimuli that induce granulomatous inflammation?

A

They are indigestible particulate matter

214
Q

Give four causes of granulomatous inflammation.

A
  1. Specific infections, e.g. TB
  2. Materials that resist digestion, e.g. bone
  3. Specific chemicals, e.g. beryllium
  4. Drugs, e.g. allopurinol
215
Q

When do histiocytic giant cells form?

A

When foreign particles are too large to be ingested by one single macrophage

216
Q

When do multinucleate giant cells form? How many nuclei can they have?

A

When two or more macrophages attempt to engulf the same particle at the same time

They can have over 100 nuclei

217
Q

What is the function of multinucleate giant cells?

A

Nothing - they have little phagocytic activity

218
Q

What is the key histological feature of a Langerhans giant cell?

A

Horseshoe arrangement of peripheral nuclei at one pole of the cell

219
Q

Which infection are you likely to see Langerhans giant cells in?

A

Tuberculosis

220
Q

What is the key histological feature of a foreign body giant cell?

A

Large cells with nuclei randomly scattered throughout cytoplasm

221
Q

What is the key histological feature of a Touton giant cell?

A

Central ring of nuclei, peripheral to which there is lipid material

222
Q

When are you likely to see a Touton giant cell?

A

When macrophages attempt to ingest lipids and in xanthomas / dermatofibromas

223
Q

What type of inflammation is associated with an MI?

What type of inflammation is associated with myocardial fibrosis after an MI?

A
  • Acute inflammation

- Chronic inflammation

224
Q

What is the role of inflammation in the development of an atheroma?

A

> Macrophages adhere to the endothelium
migrate into the arterial intima
express cell adhesion molecules
which recruit other cells into the area

225
Q

What are labile cells?

Give an example

A

Cells with a good capacity to regenerate

e.g. surface epithelial cells

226
Q

What are stable cell populations?

Give two examples

A

Cells which divide at a very slow rate, but still retain their capacity to divide when necessary

e.g. hepatocytes and renal tubular cells

227
Q

What are permanent cells?

Give an example

A

Cells with no effective regeneration

e.g. nerve cells and striated muscle cells

228
Q

What are stem cells used for?

A

When cells are lost through injury or normal ageing, they are replaced from the stem cell pool present in many labile and stable cell populations

229
Q

How do stem cells divide and multiply?

A

One of the daughter cells progresses along a differentiation pathway according to the needs and functional state of the tissue, the other retains the stem cell characteristics

230
Q

Where are stem cells found in the epidermis?

A
  • The basal layer immediately adjacent to the basement membrane
  • In hair follicles
  • In sebaceous glands
231
Q

Where are stem cells found in the intestinal mucosa?

A

Near the bottom of the crypts

232
Q

Where are stem cells found in the liver?

A

Between the hepatocytes and bile ducts

233
Q

Describe complete restitution.

Describe the process for a minor skin abrasion.

A

Loss of part of a labile cell population can be completely restored

> epidermis is lost over an area, but at the margins are cells that can multiply to cover the defect
cells proliferate and spread out as a thin sheet over the area
when a confluent layer has formed, the stimulus to proliferate is switched off - CONTACT INHIBITION
the epidermis is built up from the base until it is indistinguishable from normal

234
Q

Why is contact inhibition important?

A

It is an important control mechanism for growth and movement

235
Q

What happens to contact inhibition in neoplasia?

A

It is lost, allowing the continued proliferation of tumour cells

236
Q

What is organisation?

A

The repair of specialised tissues by the formation of a fibrous scar

237
Q

Briefly describe the process of organisation.

A

> Granulation tissue is formed
dead tissue is removed by macrophages and NPs
granulation tissue contracts and accumulates collagen
scar is formed

238
Q

What is the macroscopic difference between tissue before and after organisation?

A

The organised area is firmer than normal, shrunken, and puckered

239
Q

What happens if specialised tissue (e.g. nervous tissue) is destroyed?

A

It cannot be reconstructed, so repair occurs with the formation of granulation tissue

240
Q

Describe the formation of granulation tissue.

A
  1. Capillary endothelial cells proliferate and grow into the area, becoming vessels arranged in loops arching into the damaged area
  2. Fibroblasts are stimulated to divide and secrete collagen and other matrix components
    - They acquire bundles of muscle filaments and attach to adjacent cells
    - These complexes are called myofibroblasts

The combination of capillary loops and myofibroblasts is granulation tissue

241
Q

How much can a tissue contract when it is being repaired?

A

A scar can cause the tissue to contract by up to 80%

242
Q

Why does a granulation tissue cause tissue contraction?

A

Myofibroblasts in granulation tissue are attached to each other and to the adjacent matrix component, drawing in the surrounding tissues

243
Q

What turns granulation tissue into a scar?

A

The addition of collagen

244
Q

What are some potential consequences of wound contraction?

A
  • If damage is circumferential around a lumen (e.g. a vessel or the gut), it may cause stenosis or obstruction
  • Permanent functional inhibition if a muscle is shortened = contracture
  • Cosmetic damage, especially with burns
245
Q

How is an incised wound healed?

A

Healed by first intention

246
Q

Describe healing by first intention.

A
  1. An incision (e.g. by a scalpel) causes little damage to tissue on either side of cut
  2. Deposited fibrin binds the two sides of the wound
  3. Coagulated blood on wound surface forms a scab which helps keep the wound clean
    - Scabs are weak, but are an important framework for later stages
  4. Capillaries proliferate sufficiently to bridge the gap, and fibroblasts secrete collagen as they migrate into the fibrin network
247
Q

How is tissue loss healed? Why is it healed this way?

A

Healed by second intention, because the wound margins are not apposed

248
Q

Give some examples of things that might result in healing by second intention.

A
  • Tissue loss
  • Haemorrhage keeping wound margins separated
  • Infection in the gap
249
Q

What are the three steps to healing by second intention/?

A
  1. Phagocytosis to remove debris
  2. Granulation tissue to fill in defects and repair specialised tissue loss
  3. Epithelial regeneration to cover the surface
250
Q

What does the final cosmetic result of repair depend on?

A

How much tissue loss there was

251
Q

When is complete restitution possible in liver damage?

A

When there is only hepatocyte loss

252
Q

When is complete restitution not possible in liver damage?

A

When the hepatocytes and liver architecture are damaged

253
Q

What is cirrhosis?

A

The imbalance between hepatocyte regeneration and reconstruction of architecture

254
Q

Define ‘thrombosis’.

A

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

255
Q

What is the difference between a clot and a thrombus?

A

A clot is outside of the vascular system or after death, a thrombus is inside the CVS and during life

256
Q

Why don’t thrombi form all the time?

A
  1. Laminar flow - cells travel in axial stream so don’t touch the endothelial cells
  2. Endothelial cells aren’t stick when healthy
257
Q

What are platelets derived from?

A

Megakaryocytes in the bone marrow

258
Q

Which two types of granules do platelets contain?

A

Alpha granules and dense granules

259
Q

What substances are in alpha granules?

A
  • Fibrinogen
  • Fibronectin
  • Platelet growth factor
260
Q

What is the role of alpha granules?

A

Release substances that causes platelet adhesion to damaged vessel walls

261
Q

What is in dense granules?

A

ADP

262
Q

What is the role of dense granules?

A

Releases ADP which causes platelets to aggregate

263
Q

When are platelets activated?

A

When they come into contact with collagen, which is exposed in damaged vessel walls

264
Q

How do platelets result in a thrombus?

A

If platelet granules release their contents in an intact vessel, the platelets form a mass against the wall, resulting in a thrombus

265
Q

What is the first step in thrombus formation? What does this trigger?

A

Platelet aggregation, which starts the clotting cascade

266
Q

What forms during the clotting cascade?

A

Fibrin, which makes a mesh to trap red blood cells

267
Q

What three factors may cause thrombosis?

A
  1. Changes in vessel wall
  2. Changes in blood flow
  3. Changes in blood constituents
268
Q

What is arterial thrombosis? How does it form?

A

An atheromatous plaque will result in a change in the vessel wall, and therefore a change in blood flow nearby, resulting in a thrombus

269
Q

Describe the stages of arterial thrombosis.

A
  1. An atheromatous plaque may consist of a slightly raised fatty streak on the intimal surface of an artery
  2. The plaque will grow and visibly protrude into the lumen, thus causing turbulence
  3. Turbulence results in loss of intimal cells, exposing plaque surface
  4. Fibrin is deposited and platelets aggregate, due to the exposed collagen
  5. The plaque grows in size, causing more turbulence, therefore the cycle repeats
  6. Laminar flow is disrupted, and greatest degree of turbulence occurs downstream of the thrombus
270
Q

Why is platelet aggregation during arterial thrombosis self-perpetuating?

A

Alpha granules release platelet derived growth factors, which causes the proliferation of arterial muscle cells - an important constituent of the atheroma

271
Q

What is propagation?

A

Thrombi growing in the direction of blood flow

272
Q

Why don’t atheroma form in veins?

A

Lower blood pressure

273
Q

Where in the veins do venous thrombi begin forming? Why?

A

At the valves, as there is natural turbulence, and they may be damaged by trauma, stasis, or occlusion

274
Q

Where is the greatest degree of turbulence with regards to venous thrombi?

A

Upstream side of the thrombus

275
Q

Why might low blood pressure result in venous thrombosis?

A

Laminar flow is disrupted as blood flow is slower, so blood cells are able to contact the vessel walls

276
Q

Why might immobility result in venous thrombosis?

A

Venous return from the legs is reliant on muscle contraction and relaxation to push the blood heartwards, therefore immobility may result in formation of deep vein thromboses (DVT)

277
Q

What are the three clinical effects of arterial thrombosis?

A
  1. Loss of pulse distal to thrombus
  2. Area becomes cold, pale, and painful
  3. Eventually, if untreated, the tissue will die and become gangrenous
278
Q

What are the three clinical effects of venous thrombosis?

A
  1. Tenderness, due to ischaemia
  2. Rubor
  3. Swelling
279
Q

Give four ‘fates’ of thrombi.

A
  1. Lysis and resolution
  2. Organisation
  3. Recanalisation
  4. Embolism
280
Q

Describe lysis and resolution of thrombi.

A

The thrombus may resolved as a result of the body dissolving it and clearing it away

281
Q

Describe organisation of thrombi.

A

Thrombus may be organised into scar tissue by the invasion of macrophages and fibroblasts.

  • Macrophages = clear it away
  • Fibroblasts = replace it with collagen
282
Q

Describe recanalisation of thrombi.

A

Intimal cells of vessel may proliferate and form small sprouts of capillaries through the thrombus which then fuse on the other side of the thrombus to form larger vessels

283
Q

Describe embolisation of thrombi.

A

Fragments of the thrombus may break off into the circulation

284
Q

How does aspirin effect clotting?

A

It inhibits platelet aggregation

285
Q

Define an embolus.

A

A mass of material in the vascular system able to lodge in vessels and block its lumen

286
Q

What types of emboli can you get? Which is the most common?

A
  1. Thrombus - most common
  2. Air
  3. Cholesterol crystals - from plaques
  4. Tumour amniotic fluid
  5. Fat
287
Q

What is the result of a venous embolism?

A

A pulmonary embolism

288
Q

How does a pulmonary embolism form?

A

A venous embolism travels to the vena cava, through the right side of the heart, and will lodge in the pulmonary arteries

289
Q

What are the effects of small venous emboli?

A
  • May go unnoticed and be lysed in the lung
  • May become organised and cause permanent respiratory deficiency - multiple events of this may cause ‘idiopathic pulmonary hypertension’
290
Q

What are the effects of slightly larger venous emboli?

A
  • May result in acute respiratory and cardiac problems that result without treatment
  • Chest pain, and SOB - potential infarction
  • Impaired lung function
291
Q

What are the effects of massive venous emboli?

A

Sudden death

292
Q

What is the result of arterial embolism?

A

A systemic embolism

293
Q

Why might a myocardial infarction result in systemic emboli?

A

Areas affected by myocardial infarction will have lost normal endothelial lining, so will expose collagen to platelets, causing a thrombus

294
Q

How does atrial fibrillation cause thrombosis in the heart?

A

Ineffective movement of blood causes it to stagnate in the atrial appendages

When normal heart rhythm is re-establised, emboli may break off the thrombus

295
Q

Define ischaemia.

A

A reduction in blood flow to a tissue or part of the body caused by a constriction or blockage of the blood vessels supplying it

296
Q

What do the effects of ischaemia on a tissue depend on?

A
  1. Duration of the ischaemic period

2. Metabolic demands of the tissue

297
Q

Define infarction.

A

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

298
Q

Why are the liver, lungs, and brain less susceptible to infarction?

A

They have dual arterial supply

299
Q

What is reperfusion injury?

A

Many of the tissue damage of ischaemic injury does not occur until after perfusion is re-establised

This is because much of the damage is oxygen-dependent so requires blood flow to restart

300
Q

Describe the process of reperfusion injury.

A
  1. Blood flow is re-established after an ischaemic event
  2. Blood encounters tissues where transport mechanisms across membrane has been disrupted
  3. This triggers the activation of oxygen-dependent free radicals that begin clearing away dead cells
  4. Neutrophil polymorphs and macrophages also enter and clear away debris, adding more oxygen free radicals
301
Q

What is gangrene?

A

When 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

302
Q

Describe dry gangrene.

A

The tissue dies and becomes mummified and healing occurs above it

Eventually dead areas drop off

303
Q

Describe wet gangrene.

A

Bacterial infection supervenes as a secondary complication

Gangrene spreads proximally and patient dies from sepsis

304
Q

What is capillary ischaemia?

A

Severe constriction of capillaries (e.g. in extremely cold temperatures), causing ischaemia and infarction of tissues

305
Q

What is disseminated intravascular coagulation?

A

An interruption in the balance of thrombotic and thrombolytic mechanisms

306
Q

What are watershed areas?

A

Tissue at the interface between the adjacent territories of two arteries, where there is impairment of blood or oxygen supply

307
Q

What is portal vasculature?

A

Some tissues are perfused by blood which has already passed through a capillary bed

There is a drop in intravascular pressure and oxygenation int he second capillary bed, making the this tissue vulnerable to ischaemic injury

Phase 2a Medicine (5 decks)

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