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Phase 2a > Intro To Clinical Sciences > Flashcards

Intro To Clinical Sciences Flashcards

1
Q

What are the 2 types of autopsy?

A
  1. Hospital Autopsy

2. Medico-legal autopsies

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2
Q

Describe what a Hospital Autopsy entails…

A
  • Account for less than 10% of UK autopsies
  • Requires a medical certificate of cause of death
  • Used for teaching research & governance
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3
Q

Describe what a Medico-legal Autopsy entails…

A
  • Account for more than 90% of UK autopsies
  • Coronial Autopsies: where death is not due to unlawful action
  • Forensic autopsies: where death is thought unlawful, e.g. murder
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4
Q

What 4 questions does the Coronial autopsy answer?

A
  1. Who was the deceased?
  2. When did they die?
  3. Where did they die?
  4. How did their death come about?
    (essentially performs the same role as the coroner)
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5
Q

What deaths will be refereed to the coroner?

A
  • Presumed Natural
  • Presumed iatrogenic
  • Presumed unnatural
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6
Q

What does a Presumed Natural death entail?

A
  • Cause of death unknown
  • Patient hasn’t seen doctor within 14 days prior to death
  • Most common reason for referral
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7
Q

What does a Presumed Iatrogenic death entail?

A
  • Peri/postoperative deaths
  • Anaesthetic deaths
  • Illegal abortions
  • Complications or therapy (even if recognised complication)
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8
Q

What does a Presumed Unnatural death entail?

A
  • Accidents
  • Industrial death
  • Suicide
  • Unlawful killing i.e. murder
  • Neglect
  • Custody death
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9
Q

Who can refer for a coronial autopsy?

A

Doctors:

  • do NOT have statutory duty to refer
  • common law duty
  • guidance provided by GMC

Registrar of BDM:
- Statutory duty to refer

Others:
Police
Relatives

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10
Q

What autopsies do Histopathologists perform?

A 
Hospital autopsies 
Coronial autopsies:
- Natural deaths 
- Drowning 
- Suicide 
- Accidents 
-  Road traffic deaths 
- Fire deaths 
- Industrial deaths 
- Peri/postoperative death
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11
Q

What autopsies do Forensic pathologists perform?

A

Coronial Autopsies:

  • Homicide
  • Death in custody
  • Neglect
  • Any from the coronial list of the histopathologist that may be due to the action of a third party
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12
Q

What are the 5 different steps of an autopsy?

A
  1. History/ Scene
  2. External Examination
  3. Evisceration
  4. Internal examination
  5. Reconstruction
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13
Q

What examinations/processes does an autopsy entail?

A
  • Microbiology
  • Toxicology
  • Radiology
  • Genetics
  • Histology
  • Digital photography
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14
Q

What is looked for at the step of external examination?

A
  1. Identification:
    Formal identifiers, gender, age, body habitus (build), jewellery, body modification, clothing
  2. Disease & treatment
  3. Injuries
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15
Q

What happens within the evisceration stage?

A
  • Y-shaped cut; from behind the ears down to clavicles then down to mid-line
  • Open all body cavities
  • Examine all organs in situ
  • Remove thoracic and abdominal organs
  • Remove brain
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16
Q

What does the internal examination stage entail?

A
  • Heart & great vessels
  • Lungs, trachea & bronchi
  • Liver, gallbladder, pancreas
    (avoid lower GI tract to prevent infection risk)
  • Spleen, thymus, lymph nodes
  • Genitourinary tract (common site of cancer)
  • Endocrine organs
  • Central nervous system
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17
Q

What is the definition of Acute Inflammation?

A

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

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18
Q

Give an example of acute inflammation

A

Appendicitis

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19
Q

What is inflammation?

A
  • The local physiological response to tissue injury

- Nota disease itself, but instead usually a manifestation of disease

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20
Q

What are the benefits of inflammation?

A

Destruction of invading microorganisms and the walling off of an abscess cavity, thereby preventing the spread of an infection.

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21
Q

What are the limitations of inflammation?

A
  • Disease; e.e.g abscess in the brain can act as a space-occupying lesion that can compress surrounding structures
  • Fibrosis resulting from chronic inflammation may distort tissues and permanently alter their function
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22
Q

Describe the steps of cute inflammation

A
  1. Initial reaction of tissue to injury.
  2. Vascular component dilation of vessels
  3. Exudative component: vascular leakage of protein-rich fluid
  4. Neutrophil polymorph is recruited to the tissue.
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23
Q

What are the possible outcomes of acute inflammation?

A
  • Resolution; goes away
  • Suppuration; pus formation e.g. abscess
  • Organisation
  • progression to Chronic inflammation
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24
Q

Explain in detail the Organisation outcome of acute inflammation…

A
  • This is healing by fibrosis (scar formation)
  • substantial damage to connective tissue framework and the tissue lacks the ability to regenerate specialised cells
  • Macrophages remove dead tissue and acute inflammatory exudate from the damaged areas
  • The defect then becomes infilled by the growth of a specialised vascular connective tissue (granulation tissue)
  • the granulation tissue gradually produces collagen to form a fibrous (collagenous) scar constituting the process of repair
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25
Q

What are the causes of acute inflammation?

A
  • Microbial infections: pyogenic bacteria, viruses
  • Hypersensitivity reactions: parasites, tubercle bacilli
  • Physical agents: trauma, ionising radiation, heat, cold (frost-bite)
  • Chemicals: corrosives, acids, alkalis, reducing agents
  • Bacterial toxins
  • Tissue necrosis: ischaemic infarction
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26
Q

Explain Microbial infections as a cause of acute inflammation

A
  • One of the most common causes
  • Viruses lead to death of individual cells by intracellular multiplication
  • Bacteria release specific exotoxins (chemicals synthesised by them to initiate inflammations)
    or can release specific endotoxins (associated with their cell walls)
  • some organisms can cause hypersensitivity reactions via immunologically mediated inflammation
  • Parasitic infections & tuberculous inflammation = hypersensitivity is VITAL
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27
Q

Explain hypersensitivity reactions as a cause of acute inflammation

A
  • Occur when an altered state of immunological responsiveness causes an inappropriate or excessive immune reaction that damages tissues
  • Involve cellular or chemical mediators (similar to those involved in inflammation)
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28
Q

Explain physical agents as a cause of acute inflammation

A
  • Physical trauma, ultravoilet or other ionising radiation, burns or excessive cooling may cause tissue damage that leads to inflammation
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29
Q

Explain irritant & corrosive chemicals as a cause of acute inflammation

A
  • Corrosive chemicals provoke inflammation through gross tissue damage
  • Infecting agents can release specific irritants that lead directly to inflammation
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30
Q

Explain tissue necrosis as a cause of acute inflammation

A
  • Death of tissues due to lack of oxygen/ nutrients as a result of infarction is a potent inflammatory stimulus
  • The edge of a recent infarction often shows an acute inflammatory response due to the peptides released from dead tissue
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31
Q

What are the 4 essential macroscopic appearances of acute inflammation?
(and 1 that is also characteristic)

A
  1. Redness; Rubor
  2. Heat; Calor
  3. Swelling; tumour
    4 Pain; Dolor
  • Loss of function is also characteristic
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32
Q

AI; what causes redness (rubor)?

A
  • Acutely inflamed tissue appears red due to the dilation of small blood vessels within the damaged area
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33
Q

AI: what causes heat (dolor)?

A
  • only seen in the peripheral parts of the body i.e. skin
  • due to increased blood flow (hyperaemia) through the region, resulting in vascular dilation
  • increase in temp can also be caused by systemic fever resulting from chemical mediators of inflammation
34
Q

AI: what causes swelling (tumour)?

A
  • due to accumulation of fluid in the extravascular space as part of the fluid exudate - oedema
  • very slightly due to the mass of inflammatory cells migrating into the damaged area
  • formation of new connective tissue also contributes to the swelling (once the inflammation response has started to progress)
35
Q

AI: what causes pain (dolor)?

A
  • due to the stretching and distortion of tissues due to inflammatory oedema and pus under pressure in an abscess cavity
36
Q

AI: what causes loss of function?

A
  • movement of an inflamed area is consciously and reflexly inhibited by pain
  • severe swelling my physically immobilise the tissues too
37
Q

What happens in the early stages of acute inflammation?

A
  • Oedema fluid, fibrin and neutrophil polymorphs accumulate in the extracellular space of the damaged tissue
  • Cellular component presence of neutrophil polymorphs is essential for the histological diagnosis of acute inflammation
38
Q

What are the 3 steps of the acute inflammatory response process?

A
  1. Changes in vessel calibre (gets wider) and consequently increased vessel flow
  2. Increased vascular permeability and formation of the fluid exudate
  3. Formation of the cellular exudate - emigration of the neutrophil polymorphs into the extravascular space
39
Q

Explain the vascular changes that occur in acute inflammation:

A
  • Precapillary sphincters in arteriolar walls relax, so increase blood flow through capillaries; contributing to redness and heath
  • Capillary hydrostatic pressure is increased and there is escape of plasma proteins into the extravascular space (due to increased pressure), so osmotic pressure is increased - resulting in more fluid leaving the vessels than returning into them = increased vascular permeability
40
Q

What is the net escape of protein-rich fluid called?

A

Exudation; Fluid exudate

41
Q

What are the causes of increased vascular permeability?

A
  • Immediate transient; Chemical mediators ie. histamine, bradykinin (vasodilators), complements,, platelet activating factor
  • Immediate sustained; severe direct vascular injury
  • Delayed prolonged; endothelial cell injury
42
Q

What is the diagnostic histological feature of acute inflammation?

A

The accumulation of neutrophil polymorphs with the extracellular space.

43
Q

What are the stages of neutrophil polymorph emigration?

A
  1. Margination of neutrophils
    - loss of intravascular fluid and increase in plasma viscosity with slowing of flow at the site of AI means neutrophils can flow into the plasmatic zone
  2. Adhesion of neutrophils
    - attach to the vascular endothelium at the site of AI –> ‘pavementing’
    - at site of injury pavementing occurs early in the AI response (only in VENULES)
    - interaction between paired adhesion molecules on leucocyte & endothelial surfaces results in increased leucocyte adhesion
  3. Neutrophil emigration
    - leucocytes migrate through walls of venules and small veins (not commonly exit from capillaries)
    - neutrophils, eosinophil polymorphs & macrophages insert pseudopodia between endothelial cells
    - allows migration through the gaps between endothelial cells through basal lamina into the vessel wall
  4. Diapedesis
    - RBCs also escape from vessels, the process is passive, depends on hydrostatic pressure forcing cells out
    - large numbers of RBCs in extracellular space = severe vascular injury
44
Q

What allows the spread of AI from the site of damage?

A

Due to the release of chemical substances from the injured tissues spreading outwards into surrounding uninjured areas.

45
Q

What chemical mediators are released early in the response? and by what? and what do they cause?

A

Histamine and Thrombin.
Released by the original inflammatory stimulus.
Cause the up-regulation of adhesion molecules on the surface of endothelial cells.

46
Q

What is the overall effect of chemical mediators of acute inflammation?

A

Very firm neutrophil adhesion to the endothelial surface

47
Q

What do the endogenous chemical mediators cause?

A
  • Vasodilation
  • Emigration of neutrophils
  • Chemotaxis (attraction of neutrophil polymorphs towards certain chemicals)
  • Increased vascular permeablity
  • Itching and pain
48
Q

Histamine release in AI, effects, source, stimulated by…

A

Causes:
- vascular dilation
- immediate transient phase of increased vascular permeability
- has an immediate effect due to storage in preformed granules = instant release
Sources:
- Mast cells
- Basophil and eosinophil leucocytes
- Platelets
Stimulated by:
- Complement components C3a & C5a
- Lysosomal proteins released from neutrophils

49
Q

What other chemical mediators are there?

A
  • Lysosomal compounds
  • Eicosanoids (prostoglandins)
  • 5-hydroxytryptamine (serotonin)
  • Chemokine (chemotactic cytokines)
50
Q

What are the 4 enzymatic cascade systems that plasma contains?

A
  1. Complement
  2. The Kinins
  3. Coagulation factors
  4. Fibrinolytic system
    All interrelated and produce various inflammatory mediators.
51
Q

What is the complement system?

A

A complex series of interacting plasma proteins. They form a major effector system for antibody-mediated immune reactions.
Remove/ destroy antigens either by direct lysis or by opsonisation.

52
Q

What is opsonisation?

A

The enhancement of phagocytosis by factors (opsonins) in various ways.

53
Q

How is the complement system activate during the AI reaction?

A

Tissue necrosis; enzyme that activates complement are released from dying cells
Infection; formation of antigen-antibody complexes activate complement via the classical pathway.
Endotoxins of gram-negative bacteria activate complement via the alternative pathway.

54
Q

Describe the effect of Coagulation factor XII (Hageman factor) on the different enzymatic cascade systems.

A 
(See flow chart) 
Activates...
- Kinin system 
- Fibrinolytic system 
- Coagulation system
55
Q

Describe the Kinin system

A

Activated factor XII and plasmin activate the conversion of prekallikrein to kallikrein.
This in turn stimulates the conversion of kininogens to kinins (ie. bradykinin - causes vasodilation).
Prekallikrein can also be activated by leucocyte proteases.
(see flow chart for more detail).

56
Q

Describe the role of tissue macrophages in AI

A
  • Secrete numerous chemical mediators when stimulated (local infection/injury)
  • Interleukin-1 and tumour necrosis factor alpha; their stimulatory effects on endothelial cells occur after histamine and thrombin, cause endothelial cells, fibroblasts and epithelial cells to secrete MCP-1
  • MCP-1 = powerful chemotactic protein that attracts neutrophil polymorphs
  • Blood monocytes go to site of AI, on leaving the blood vessels transform into macrophages
  • Phagocytosis of microorganisms is enhanced by opsonisation by antibodies or by complement
  • macrophages appear within a few hours after inflammation, do not predominate until neutrophils have diminished and macrophage population has enlarged by local proliferation
  • macrophages; clear away tissue debris and damaged cells
  • macrophages and neutrophils may discharge lysosomal enzymes into the extracellular fluid (aids digestion of inflammatory exudate)
57
Q

Describe terminal and collecting lymphatics

A

Terminal lymphatics;
- blind-ended, endothelium lined tubed present in most tissues
- drain in collecting lymphatics
Collecting lymphatics;
- have valves , so propel lymph passively aided by contraction of neighbouring muscles (to the lymph nodes)

58
Q

What is the role of lymphatics in acute inflammation?

A
  • lymphatic channels become dilated in AI as they drain away the oedema fluid of the inflammatory exudate
  • drainage tends to limit the extent of oedema in the tissues
  • antigens are carried to the regional lymph node for recognition by lymphocytes
  • vital part of the immune response
59
Q

What is a neutrophil polymorph?

A
  • the most common white blood cell
  • under H&E stain, nucleus stains blue and cytoplasm stains pink/purple
  • characteristic cell of acute inflammatory infiltrate
60
Q

Role of neutrophil polymorph in AI?

A
  • Neutrophil polymorph ingests the antigen
  • The antigen lies within a phagocytic vacuole (phagosome)
  • Lysosomes then fuse with the phagocytic vacuole and enzymes digest the antigen (phagolysosome)
  • Antigen debris released from neutrophil polymorph and lysosomes are replenished
61
Q

How does adhesion to microorganisms occur?

A
  • Microorganisms are opsonised; rendered more amenable to phagocytosis either by immunoglobulins or by complement components
  • bacterial lipopolysaccharides activate complement via the alternative pathway, via the alternative pathway, generating component C3b (opsonising properties)
  • antibody binding to bacterial antigens activates complement via the classical pathway (generating C3b)
  • binding of immunoglobulins to microorganisms by their Fab components leaves the Fc component exposed - neutrophils have surface receptors for the Fc fragment of immunoglobulins and consequently bind to the microorganisms prior to ingestion
62
Q

Describe the process of phagocytosis

A
  • Implemented by neutrophil polymorphs and macrophages
  • first step = adhesion of particle to be phagocytosed to the cell surface (opsonisation)
  • phagocyte ingests the attached particle by sending out pseudopodia around it; they meet and fuse so particle is within a phagosome bound by ecll membrane
  • lysosomes fuse with the phagosome to form pahgolysosomes - within this intracellular killing takes place
63
Q

Describe the process of intracellular killing of microorganisms

A

Noxious microbicidal agents within neutrophil polymorphs are used. These are:

  1. Oxygen-dependent; Hydrogen peroxide reacts with myeloperoxidase in cytoplasmic granules of the neutrophil polymorph in the presence of a halide - produces a potent microbicidal agent
  2. Oxygen-independent; lysozyme (muramidase) & lactoferrin
64
Q

what are the effects of release of lysosomal products?

A
  • Damage local tissues by proteolysis via enzymes (elastase and collagenase)
  • Activate coagulation factor XII
  • Attract other leukocytes to the area
  • Some compounds increase vascular permeability,
  • Others are pyrogens; induce systemic fever by acting on hypothalamus
  • life span of 1 to 3 days
65
Q

Role of mast cells in AI

A
  • Are stimulated by C3/ C5a complement components
  • Release preformed inflammatory mediators stored in their granules
  • Metabolise arachidonic acid into newly synthesised inflammatory mediators (i.e. leukotrienes, prostaglandins, thromboxanes)
66
Q

What are the special macroscopic appearances of AI?

A

Cardinal signs are modified according to the type of tissue involved and what type of agent is provoking the inflammation.

  • Serous inflammation
  • Suppurative inflammation (lots of pus)
  • Membranous inflammation
  • Pseudomembranous inflammation
  • Necrotising (gangrenous) inflammation
67
Q

What are the effect of AI?

A

Both local and systemic effects, that can both be beneficial or harmful.

68
Q

What are the beneficial effects of the fluid exudate?

A
  • Dilution of toxins; can then be carried away via lymphatics
  • Entry of antibodies due to increased vascular permeability into the extravascular space
  • transport of drugs to specific site
  • Fibrin formation from exuded fibrinogen; can impede microorganism movement
  • Delivery of nutrients and oxygen
  • Stimulation of immune response via drainage of fluid exudate into the lymphatics
69
Q

What are the harmful effects of AI?

A
  • Digestion and destruction of normal tissues; collagensases and proteases
  • Swelling; most serious when in enclosed spaces i.e. cranial cavity
  • Inappropriate inflammatory response
70
Q

What are the possible outcomes of AI?

A

Usual result –> Resolution
Excessive exudate –> Suppuration–> discharge of pus
Excessive necrosis –> repair and organisation –> fibrosis
Persistent causal agent –> Chronic inflammation –> fibrosis

71
Q

What is Resolution of AI?

A
  • Complete restoration of the tissues to normal after an episode
  • favoured by the following conditions:
  • minimal cell death and tissue damage
  • occurred in organ capable of regeneration
  • rapid destruction of causal agent
  • rapid removal of fluid and debris by goo local vascular drainage
    example: acute lobar pneumonia
72
Q

What is Suppuration of AI?

A
  • Formation of pus, mixture of living, dying and dead neutrophils/ bacteria/ cellular debris
  • causative stimulus fairly persistent, virtually always an infective agent
  • pus accumulating in tissue: is surrounded by a ‘pyogenic membrane’ = sprouting capillaries, neutrophils and occasional fibroblasts = start of healing
  • results in granulation tissue and scarring
  • bacteria within an abscess are relatively inaccessible to antibodies and to antibiotic drugs
73
Q

What is the resolution of an abscess?

A
  • Usually points then bursts; abscess cavity collapses and is obliterated by organisation and fibrosis - leaves a scar
  • sometimes requires surgical drainage to eliminate
  • if accumulates inside a hollow organ, mucosal layers of outflow tract of the organ may become fused together by fibrin and result in an empyema
74
Q

What is Organisation of AI?

A
  • the replacement of tissues by granulation tissue as part of the repair process
  • new capillaries grow into the inflammatory exudate, macrophages migrate into the area and fibroblasts proliferate (under the influence of TGF-beta) = result in fibrosis and possible scar formation
    Favoured by the following conditions:
  • large amounts of fibrin, that cannot be removed completely by fibrinolytic enzymes
  • substantial volumes of tissue becoming necrotic or if dead tissue is not easily digested
  • exudate debris unable to be removed or discharged
    example: pleural space following acute lobar pneumonia
75
Q

What is the process of progression to chronic inflammation following AI?

A
  • Causal agent is not removed
  • Nature of cellular exudate changes, neutrophil polymorphs are replaced by lymphocytes, plasma cells, macrophages, multinucleate giant cells and fibroblasts
76
Q

What are the systemic effects of inflammation?

A
  • Pyrexia (fever)
  • Constitutional symptoms: malaise, anorexia, nausea, weight loss
  • Reactive hyperplasia of the reticuloendothelial system
  • Haematological changes
  • Anaemia
  • Amyloidosis
77
Q

What is pyrexia (fever)?

A
  • Endogenous pyrogens are produced by neutrophil polymorphs and macrophages
  • these act on the hypothalamus to set the thermoregulatory mechanisms at a higher temp.
  • Pyrogen interleukin-2 has the greatest effect
  • Release of pyrogens is stimulated by phagocytosis, endotoxins and immune complexes
78
Q

What is reactive hyperplasia of the reticuloendothelial system?

A
  • local or systemic lymph node enlargement commonly accompanies inflammation
  • splenomegaly found in specific infections
79
Q

What haematological changes are seen with inflammation?

A
  • Increased levels of white blood cells in the blood: neutrophils - pyogenic infections, eosinophils - allergic disorders and parasitic infection, lymphocytes - chronic infection, whooping cough, many viral infections, monocytes - bacterial infections
  • Anaemia due to blood loss into the inflammatory exudate or haemolysis
80
Q

What is amyloidosis?

A
  • Caused by long-standing chronic inflammation, by elevating serum amyloid A protein (SAA)
  • Causes amyloid to be deposited in various tissues
  • Can lead to secondary (reactive) amyloidosis

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