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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” autopsies

2. Medico-legal autopsies

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2
Q

What are “hospital” autopsies?

A

Require medical certificate of cause of death
acquire for <10% of all UK autopsies
Requires a medial certificate of cause of death
used for audit, teaching, research, governance

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3
Q

What are medico-legal autopsies?

A

account for >90% of all UK autopsies

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4
Q

2 types of medico-legal autopsies?

A
  1. Coronial autopsies - death is not due to unlawful action

2. Forensic autopsies - death is thought unlawful

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5
Q

what 4 questions does a coronial autopsy answer?

A
  1. Who was deceased?
  2. When did they die?
  3. Where did they die?
  4. How did their death come about?
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6
Q

3 reasons deaths are referred to a coroner?

A
  1. Presumed natural
  2. Presumed iatrogenic
  3. Presumed unnatural
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7
Q

Presumed natural deaths - why referred to a coroner?

A

Patient was not seen by doctor in last illness (within last 14 days)
Cause of death is unknown
Most common reason for referral

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8
Q

Presumed iatrogenic - why referred to a coroner?

A

Anaesthetic deaths
Illegal abortions
Peri/postoperative deaths
Complications of therapy (even if recognised complications)

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9
Q

Presumed unnatural - why referred to a coroner?

A 
Accident 
Unlawful killing 
Neglect 
Suicide 
War/industrial pension 
Custody death
Industrial deaths
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10
Q

Who can refer for an autopsy?

A

Doctors
Registrar of BDM
Others; relatives, police, anatomical pathology technicians, other properly interested parties

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11
Q

Doctors and referring an autopsy

A

GMC provides guidance
Do NOT have a statutory duty to do so
Common law duty

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12
Q

Registrar of BDM and referring an autopsy

A

Have a STATUTORY DUTY to refer

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13
Q

Who can perform autopsies?

A

Doctors
Histopathologists
Forensic pathologists

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14
Q

What autopsies can histopathologists perform?

A

Hospital autopsies

Coronial autopsies; natural deaths, drowning, suicide, road traffic deaths, accidents, fire deaths, industrial deaths, peri/postoperative deaths

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15
Q

What autopsies can forensic pathologists perform?

A

Coronial autopsies; homicide, death in custody, neglect, any other coronial deaths that may have been caused by a third party

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16
Q

what autopsies can doctors perform?

A

All autopsies

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17
Q

5 stages of an autopsy

A
  1. History/ scene
  2. External examination
  3. Evisceration
  4. Internal examination
  5. Reconstruction
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18
Q

What other investigations/ processes does an autopsy entail?

A 
Toxicology 
Microbiology 
Digital photography 
Histology 
Genetics 
Radiology
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19
Q

Purpose and process of an external examination?

A

To ensure having the right body
Identification; formal identifier, gender, age, body habitus, jewellery, body modification, clothing
Disease and treatment
Injuries

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20
Q

Process of the evisceration stage?

A
  • Y-shaped evisceration (behind ears to clavicle)
  • Open all body cavities
  • Examine all organs in situ
  • Remove thoracic and abdominal organs
  • Remove brain
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21
Q

Process of internal examination stage (in specific order)?

A 
All body systems are examined in a specific order
Heart and great vessels 
Lungs, trachea, bronchi 
Liver, gallbladder, pancreas
(avoiding lower GI tract to avoid infection)
Spleen, thymus, lymph nodes 
Genitourinary tract 
Endocrine organs 
Central nervous system
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22
Q

What is inflammation?

A

The local physiological response to tissue injury, it is NOT a disease, but is a MANIFESTATION of disease.
A series of reactions that brings cells and molecules of the immune system to sites of infection or damage.

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23
Q

Beneficial effects of inflammation?

A
  • Destruction of invading microorganisms
  • Walling off of an abscess cavity
  • Prevents spread of infection
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24
Q

How can inflammation produce disease?

A
  • An abscess can act as a space-occupying lesion and compress other vital surrounding structures
  • Fibrosis from chronic inflammation may distort the tissues and permanently alter function
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25
Q

What are the 2 types of inflammation and how are they characterised?

A
  • Characterised by differences in cell types taking part in the inflammatory response.
  • Acute inflammation; neutrophils, granulocytes, resident immune cells already present in involved tissue
  • Chronic inflammation; lymphocytes (around vessel), macrophages (multinucleate giant cell), plasma cells, leukocytes, T lymphocytes, fibroblasts,
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26
Q

What is acute inflammation?

A

The initial and often transient series of tissue reactions to injury.
Lasts few hours - few days.

Complete elimination of a pathogen followed by resolution of damage, disappearance of leukocytes and full regeneration of tissue.

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27
Q

What is chronic inflammation?

A

The subsequent and often prolonged tissue reactions following the initial response.

Persistent, un-resolved inflammation.

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28
Q

Example of acute inflammation

A

Appendicitis

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29
Q

Steps of ACUTE Inflammation

A
  • Initial reaction of tissue to injury
  • Vascular component; dilation of vessels
  • Exudative component; vascular leakage of protein-rich fluid
  • Neutrophil polymorph is the characteristic cell recruited
  • Travels to tissue
  • Outcome; resolution, suppuration (i.e. abscess), organisation, progression to chronic inflammation
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30
Q

Causes of ACUTE inflammation

A
  • Microbial infections; viruses, pyogenic bacteria
  • Hypersensitivity; parasites
  • Physical agents; trauma, ionising agents
  • Chemicals; alkalis, corrosives, acids
  • Bacterial toxins
  • Tissue necrosis; ischaemic infarction
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31
Q

How do microbial infection (viruses and bacteria) lead to acute inflammation?

A
  • Viruses lead to death of individual cells by multicellular multiplication
  • Bacteria release; exotoxins that synthesise chemicals to initiate inflammation OR endotoxins that are associated with their cell walls
  • Organisms can cause immunologically mediated inflammation through hypersensitivity reactions
    Where hypersensitivity is important in Parasitic infections & tuberculous inflammation
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32
Q

How do hypersensitivity reactions lead to acute inflammation?

A
  • Hypersensitivity reaction occurs when an altered state of immunological responsiveness causes an inappropriate or excessive immune reaction that damages the tissues
  • Hypersensitivity reactions all have a cellular/ chemical mediators similar to those involved in inflammation
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33
Q

How do physical agents lead to acute inflammation?

A
  • Tissue damage caused by physical trauma, ultraviolet/ ionising radiation, burns, excessive cooling can lead to inflammation
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34
Q

How do irritant and corrosive chemicals lead to acute inflammation?

A
  • Corrosive chemicals lead to gross tissue damage provoking inflammation
  • Infecting agents release specific chemical irritants that lead to directly to inflammation
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35
Q

How does tissue necrosis lead to acute inflammation?

A
  • Death of tissue through necrosis is a potent inflammatory stimulus
  • Edge of recent infarcts shows acute inflammatory response, in response to peptides released from the red tissue
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36
Q

What is acute inflammation characterised by?

A

Redness, Heat, Immobility (loss of function), Swelling, Pain

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37
Q

Why is redness associated with acute inflammation?

A

Due to inflammation of small blood vessels within the damaged area.

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38
Q

Why is heat associate with acute inflammation?

A

Due to increased blood flow through the region, so vascular dilation and delivery of warm blood to the area
Systemic fever as a result of some of the chemical mediators also contributes to the local temperature.

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39
Q

Why is swelling associated with acute inflammation?

A

There is an accumulation of fluid in the extravascular space as part of the fluid exudate -> Oedema
Swelling results from oedema
Physical mass of inflammatory cells migrating to the area and formation of new connective tissue also contributes to the swelling.

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40
Q

Why is pain associated with acute inflammation?

A

It partly results form the stretching and distortion of tissues due to oedema and from pus under pressure in an abscess cavity.
Other chemical mediators of acute inflammation (bradykinin, prostaglandins, serotonin) also induce pain.

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41
Q

Why is immobility associated with acute inflammation?

A

Movement of an inflamed area is consciously and reflexly inhibited by pain.
Severe swelling may physically immobilise tissues.

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42
Q

Describe the early stages of acute inflammation…

A
  • Oedema fluid, fibrin and neutrophil polymorphs accumulate in the extracellular spaces of damaged tissue
  • Neutrophil polymorphs are the first cells on the scene (essential for histological diagnosis of acute inflammation)
  • They capture and destroy invading microorganism via phagocytosis and intercellular degradation, granules and formation of neutrophil extracellular traps that result in pus
  • They also recruit & activate other cells to the scene
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43
Q

What are the 3 processes that the acute inflammatory response involves?

A
  1. Changes in vessel calibre and flow
  2. Increased vascular permeability, formation of the fluid exudate
  3. Formation of cellular exudate - emigration of neutrophil polymorphs into extravascular space
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44
Q

What causes increased vascular permeability?

A
  • Immediate transient chemical mediators; histamine, bradykinin, platelet activating factor
  • Immediate sustained severe direct vascular injury; trauma
  • Delayed prolonged endothelial cell injury; x-rays , bacterial toxins
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45
Q

Formation of the cellular exudate…

A
  • Accumulation of neutrophil polymorphs within extracellular space (diagnostic histological feature of acute inflammation)
  • Leukocytes reach the tissue
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46
Q

How do neutrophil polymorphs emigrate into damaged tissues?

A
  1. Margination of neutrophils
  2. Pavementing of neutrophils
  3. Pass between endothelial cells
  4. Pass through basal lamina and pirate into adventitia
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47
Q

Causes of increased vascular permeability, time course & mechanism

A
  • Immediate transient; chemical mediators, histamine, platelet activating factor, bradykinin, nitric oxide
  • Immediate sustained; severe direct vascular injury i.e. trauma
  • Delayed prolonged; Endothelial cell injury i.e. X-rays, bacterial toxins
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48
Q

Role of chemical mediators involved in acute inflammation

A

Acute inflammation speeds due to chemical substances being released from injured tissues spreading outwards into uninjured areas.
The original inflammatory stimulus releases histamine and thrombin cause up-regulation of adhesion molecules on the surface of endothelial cells.
Overall effect of the molecules = very firm neutrophil adhesion to the endothelial surface.

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49
Q

What are the chemical mediators of acute inflammation called?

A

Endogenous chemical mediators

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50
Q

What do endogenous chemical mediators cause?

A
  • Vasodilation
  • Emigration of neutrophils
  • Chemotaxis
  • Increased vascular permeability
  • Itching and pain
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51
Q

what chemical mediators are released from cells?

A
  • Histamine
  • lysosomal compounds
  • eicosanoids
  • 5-hydroxytryptamine (serotonin)
  • chemokine (chemotactic cytokines)
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52
Q

what 4 enzymatic cascade systems do plasma factors contain?

all are interrelated and produce various inflammatory mediators

A
  • complement
  • the kinins
  • the coagulation factors
  • the fibrinolytic system
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53
Q

what does coagulation factor XII (hageman factor) activate?

A
  • Kinin system
  • Fibrinolytic system
  • Coagulation system
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54
Q

Describe the kinin system pathway…

A

Kinin system –> Kinins –> Complement systems –> Activated complement

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55
Q

Describe the fibrinolytic system pathway…

A

Fibrinolytic system –> Plasmin –> Complement systems –> Activated complement

(Plasmin also degrades fibrin)

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56
Q

Describe the coagulation system pathway…

A

Coagulation –> fibrin –> fibrin split products

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57
Q

What endogenous chemical mediators cause vascular dilation?

A
  • Histamine
  • Prostoglandins
  • PGE2/ I2
  • Nitric Oxide
  • VIP
  • PAF
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58
Q

What endogenous chemical mediators cause increased vascular permeability?

A
  • transient phase; histamine

- prolonged phase; bradykinin, nitric oxide,C5a, leucotriene B4, PAF

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59
Q

What endogenous chemical mediators cause adhesion of leucocytes (up-regulation of adhesion molecules on endothelium)?

A
  • IL-8,
  • C5a,
  • leukotriene B4,
  • PAF,
  • IL-1,
  • TNF-alpha
60
Q

What endogenous chemical mediators cause neutrophil polymorph chemotaxis?

A
  • leukotriene B4

- IL-8

61
Q

Role of neutrophil polymorph in acute inflammation…

A
  • Neutrophil polymorph contains lysosomes
    1. The neutrophil ingests the bacterium
    2. Bacterium lies within a phagocytes vacuole (phagosome)
    3. Lysosomes fuse with phagosome and enzymes digest the bacterium (phagolysosome)
    4. Bacterial debris is released from neutrophil polymorph and lysosomes replenished
62
Q

What descriptive terms are used for appearances of tissue involved in inflammation and the type of agent provoking it?

A
  • Serous
  • Suppurative (purulent) inflammation
  • Membranous inflammation
  • Pseudomembranous inflammation
  • Necrotising (gangrenous) inflammation
63
Q

What are the effects of acute inflammation?

2 types, beneficial or harmful?

A
  • local and systemic effects; both can be beneficial or harmful
  • local effects; usually beneficial i.e. destruction of invading microorganisms, but sometimes appear to serve no obvious function or are harmful
64
Q

harmful effects of acute inflammation?

A
  • Digestion of normal tissues
  • Swelling
  • Inappropriate inflammatory response
65
Q

What are the possible outcomes of acute inflammation?

A
  • Resolution
  • Suppuration (pus forming)
  • Organisation
  • Progression to chronic inflammation
66
Q

What does the outcome of acute inflammation depend on?

A
  • the type of tissue involved
  • amount of tissue destruction
  • nature of the injurious agent
67
Q

What is the usual outcome of acute inflammation?

A

Resolution

68
Q

What is the outcome of acute inflammation if there is excessive exudate?

A

Suppuration –> discharge of pus and repair and organisation

69
Q

What is the outcome of acute inflammation if there is excessive necrosis?

A

Repair and Organisation –> Fibrosis

70
Q

What is the outcome of acute inflammation if the causal agent is persistent?

A

Chronic inflammation –> Fibrosis

71
Q

What are the systemic effects of inflammation?

A
  • Pyrexia (raised body temp.)
  • Constitutional symptoms
  • Weight loss
  • Reactive hyperplasia of the reticuloendothelial system
  • Haematological changes
  • Amyloidosis (abnormal build up of protein, amyloid, in tissues and organs)
72
Q

What are the causes of chronic inflammation?

A
  • Primary chronic inflammation
  • Transplant rejection
  • Progression from acute inflammation
  • Recurrent episodes of acute inflammation
  • Resistance of infective agent to phagocytosis and intracellular killing
  • Endogenous materials; necrotic adipose tissue, bone, uric acid crystals
  • Exogenous materials; silica, abets fibres, suture materials, implanted prostheses
  • Autoimmune diseases; rheumatoid arthritis, contact hypersensitivity reactions
  • Primary granulomatous diseases; Crohn’s disease, sarcoidosis,
  • Diseases of unknown aetiology; chronic bowel disease
73
Q

What is the macroscopic appearance of chronic inflammation?

A
  • Chronic ulcer
  • Chronic abscess cavity
  • Thickening of the wall of a hollow viscus
  • Granulomatous inflammation
  • Fibrosis
74
Q

What are the microscopic features of chronic inflammation?

A
  • cellular infiltrate consists of lymphocytes, plasma cells and macrophages
  • little/no neutrophil polymorphs (some eosinophil polymorphs may be present)
  • some macrophages may form multinucleate giant cells
  • production of new fibrous tissue from granulation tissue (no exudation of fluid)
  • Continuing destruction tissue may be present at the same time as tissue regeneration and repair
  • tissue necrosis (especially in granulomatous conditions; tuberculosis)
75
Q

Explain the paracrine stimulation of connective tissue proliferation…

A
  • healing = regeneration and migration of specialised cells

- repair = angiogenesis, followed by fibroblast proliferation and collagen synthesis –> granulation tissue

76
Q

What regulates the processes of paracrine stimulation of connective tissue proliferation?

A
  • low molecular weight proteins = growth factors

- they bind to specific receptors on cell membranes and trigger a series of events culminating in cell proliferation

77
Q

What 2 main types of lymphocyte does the lymphatic tissue infiltrate involved in chronic inflammation contain?

A
  • B-lymphocytes

- T lymphocytes

78
Q

What role do B lymphocytes play in chronic inflammation?

A

On contact with antigen, they come progressively transformed into plasma cells (production of antibodies).

79
Q

What role do T lymphocytes play in chronic inflammation?

A

Responsible for cell-mediated immunity. ON contact with antigen, T lymphocytes produce a range of soluble factors, cytokines, which are responsible for recruitment and activation of other cell types.

80
Q

What are the growth factors involved in healing and repair associate with inflammation?

A
  • Epidermal growth factor; EGF
  • Transforming growth factor-alpha; TGF-alpha
  • Transforming growth factor-beta; TGF-beta
  • Platelet-derived growth factor; PDGF
  • Fibroblast growth factor; FGF
  • Insulin-like growth factor-1; IGF-1
  • Tumour necrosis factor; TNF
81
Q

What is the functions or epidermal growth factor?

A

Regeneration of epithelial cells

82
Q

What is the role of transforming growth factor-alpha?

A

Regeneration of epithelial cells

83
Q

What is the role of transforming growth factor-beta?

A

Stimulates fibroblast proliferation and collagen synthesis.

Controls epithelial regeneration.

84
Q

What is the role of platelet-derived growth factor?

A

Mitogenic and chemotactic for fibroblasts and smooth muscle cells.

85
Q

What is the role of fibroblast growth factor?

A

Stimulates fibroblast proliferation, angiogenesis and epithelial cell regeneration

86
Q

What is the role of insulin-like growth factor?

A

Synergetic effect with other growth factors (works together with other growth factors).

87
Q

What is the role of tumour necrosis factor?

A

Stimulates angiogenesis.

88
Q

Describe the role of macrophages in chronic inflammation…

A
  • Macrophages move by amoeboid motion through tissues
  • they respond to certain chemotactic stimuli
  • ingest a more materials than polymorphs
  • are long-lived, s can harbour viable organisms if cannot successfully kill them with their lysosomal enzymes
  • participate in delayed-type hypersensitivity, but often die in the process, contributing to the large areas of necrosis by release of their lysosomal enzymes
  • Macrophages in inflamed tissues are derived from blood monocytes that have migrated out of vessel and transformed in tissues
  • are part of the mononuclear phagocyte system; reticuloendothelial system
89
Q

What is a granuloma?

A

An aggregate/collection of epithelioid histiocytes (activated macrophages), but can also contain other cell types such as lymphocytes and histolytic giant cells.

90
Q

Give examples of granulomatous diseases:

A
  • Tuberculosis
  • Leprosy
  • Crohn’s disease (unknown aetiology)
  • Sarcoidosis (unknown aetiology)
91
Q

What are epithelioid histiocytes?

A
  • vague histological resemblance to epithelial cells
  • have large vesicular nuclei, eosinophilic cytoplasm, elongated
  • tend to be arranged in clusters
  • little phagocytes activity
  • but have secretory function; one product is angiotensin converting enzyme
  • amount of activity of this enzyme in the blood acts as a marker for systemic granulomatous disease
92
Q

What does the association of granuloma with eosinophils indicate…

A

A parasitic infection

93
Q

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

A

Indigestibility of particulate matter by macrophages

94
Q

Describe the mononuclear phagocyte system:

A

Haemopoietic stem cell –> Promonocyte (bone marrow) —> monocyte (blood) —> tissues (many different types of cells

95
Q

What cells do monocytes differentiate into once they have migrated into tissues?

A
  • Connective tissue histiocyte
  • Alveolar macrophage
  • Peritoneal macrophage
  • Kupffer cell of liver
  • Lipophage
  • Osteoclast in bone
  • Microglial cell in brain
  • Specialised histiocytes (epithelioid cell)
  • Histiocytic giant cell
96
Q

What are histocytic giant cells?

A

Multinucleate giant cells (may contain over 100 nuclei) that have little phagocytic activity and no known function.

97
Q

Where do histiocytic giant cells tend to form?

A

Form where particulate matter that is indigestible by macrophages accumulates, or when foreign particles are too large to be ingested by just one macrophage.
Thought to develop by accident when 2 macrophages attempt to simultaneously engulf the same particle; causing the cell membranes to fuse and the cells unite.

98
Q

Describe the structure & arrangement of Langhans’ giant cells and what conditions they are seen in

A
  • have a horseshoe arrangement of peripheral nuclei at one pole of the cell
  • seen in tuberculosis, and other granulomatous conditions
99
Q

Describe the structure and arrangement of ‘Foreign body giant cells’ and what conditions they are seen in

A
  • large cells with nuclei randomly scattered throughout their cytoplasm
  • seen in relation to particulate foreign body material
100
Q

Describe the structure & arrangement of Touton giant cells and what conditions they are seen in

A
  • a central ring of nuclei, peripheral to which there is lipid material
  • see when macrophages attempt to ingest lipids and in xanthomas/ dermatofibromas of the skin
101
Q

What role does inflammation play in contributing to the development of atheroma?

A
  • Macrophages adhere to the endothelium, migrate into the arterial intimacy and with T lymphocytes, express cell adhesion molecules
  • These molecules recruit other cells into the are a
  • The macrophages also process the lipids that accumulate in artheromatous plaques
102
Q

What role does inflammation play in tissue injury associated with neurodegenerative disorders of the cell nervous system?

A
  • Chronic inflammation is involved in MS (a relatively common chronic demyelinating neurodegenerative disorder)
  • Perivascular cuffing by plasma cells and T lymphocytes is seen in zones of white matter where macrophages break down myelin
103
Q

What is the difference of Acute and Chronic inflammation?

A
  • Acute; a relatively rapid onset and commonly resolution, neutrophil polymorphs are the most abundant cells
  • Chronic; a relatively insidious onset, prolonged course, slow resolution and lymphocytes, plasma cells and macrophages (sometimes can also be seen with granuloma formation)
104
Q

What is the difference of exudate and transudate?

A
  • Exudates; have a high protein content as they result from increased vascular permeability
  • Transudates; a low protein content, because the vessels have normal permeability characteristics
105
Q

What is the difference between granuloma and granulation tissue?

A
  • Granuloma; an aggregate of epithelioid histiocytes and a feature of some specific chronic inflammatory disorders
  • Granulation tissue; important component of healing, compromises small blood vessels in a connective tissue matrix with myofibroblasts
106
Q

What is the difference between monocytes, macrophages and histiocytes?

A
  • Monocytes; newly formed cells of the mononuclear phagocyte system, spend a few hours in the blood and the enter tissues and undergo further differentiation into MACROPHAGES
  • Some macrophages have specific names and features others are referred to as histiocytes
107
Q

What is the difference between fibrin and fibrous?

A
  • Fibrin; is deposited in blood vessels and tissues or on surfaces as a result of the action of thrombin on fibrinogen
  • Fibrous; the texture of a non-mineralised tissue of which the principle component is collagen
108
Q

What is resolution?

A
  • The initiating factor (factor causing damage) is removed
  • The tissue is left undamaged or able to regenerate
  • Tissue is left with how it was to begin with
109
Q

What is repair and give examples?

A
  • The initiating factor is still present
  • The tissue is damaged and unable to regenerate
  • Replacement of damaged tissue by fibrous tissue
  • Collagen produced by fibroblasts
  • Occurs where tissues can’t regenerate
  • Examples; heart after myocardial infarction, brain after cerebral infarction (results in gliosis - fibrosis of glial cells), spinal cord after trauma
110
Q

Give an example of a type of tissue that is able to regenerate

A

Liver, hepatocytes can continue to grow even after half are removed (hepatocyte proliferation)

111
Q

What happens to a liver that experiences continuous damage?

A

The liver changes and results in cirrhosis

112
Q

What leads to liver cirrhosis?

A

Architecture damage –> fibrous scarring (fibrosis) of regenerative nodules (occurs instead of regeneration as initiating factor is persistent)–> cirrhosis

113
Q

What does a cirrhotic liver look like?

A

Full of nodules of tissue and lumps, microscopically can see a lot of fibrous tissue

114
Q

What are the 2 main outcomes of infection?

A

Resolution (preferably) or Repair

115
Q

What is lobar pneumonia?

A

Infection of the lung, can affect anyone of any age, and only affects one lobe, microscopically that should be air spaces are filled with neutrophil polymorphs (acute inflammation)

116
Q

How can lobar pneumonia resolve?

A

Pneumocytes (cells that line the alveoli) can regenerate, as long as lung structure is not damaged (i.e. elastin in walls), happens when alveoli are filled with inflammatory cells and then get rid of them = conditions for pneumocyte regeneration

117
Q

Why does scarring of skin wounds occur?

A

Due to fibrosis and repair

118
Q

How do abrasion (skin wounds) heal?

A
  • Generally heal pretty well
  • As commonly, not all the epithelium has been removed, i.e. hair follicles and sweat glands still remain and the surrounding cells can grow and regenerate the epithelium
  • Scabs come off and skin is back to normal
119
Q

Skin wounds; process of healing by 1st intention

A
  • The whole thickness of the epithelium is cut
  • The gap is filled with fibrin from the blood which makes a weak joint that holds it together
  • Fibroblasts then enter the cut and synthesises collagen
  • Leaves a really strong join that appears white (due to the collagen)
120
Q

Skin wounds; process of healing by 2nd intention

A
  • Where you cannot get the edges of the damaged epithelium together, missing a bit of skin (a deficit)
  • Epithelium will grow across, but nothing to grow up into the gap as hair follicles have been removed
  • Capillaries and fibroblasts fill the gap
  • The fibroblasts produce collagen
  • Eventually epithelium is regenerated from the edges, but it is a slow process that results in a slightly bigger scar with pale fibrous tissue (as it is repair not regeneration)
121
Q

What is granulation tissue?

A

Tissue that appears granular due to the blood vessels in the bottom of the wound, in a connective tissue matrix with myofibroblasts

122
Q

What body cells can regenerate?

A
  • Hepatocytes
  • Pneumocytes (lining of the alveoli)
  • All blood cells (allows for chemotherapy)
  • Gut epithelium
  • Skin epithelium (but needs to be in the right place)
  • Osteocytes (allows repair of fractured bones and bone remodelling)
  • PNS neurones, as long as they have a sheath to go down
123
Q

What body cells do not regenerate?

A
  • Myocardial cells

- CNS neurones

124
Q

Where does thrombosis and embolism occur?

A

In the blood

125
Q

Explain the process of thrombosis in arteries….

A
  • Blood flow in arteries is pulsatile, as left heart is contracting through valve
  • Artery is lined by epithelial cells (that stop things sticking)
  • Have lamina blood flow through artery, so cells are at edges and do not stick to sides (especially important for platelets)
  • When endothelium gets damaged, the collagen beneath it is exposed
  • Platelets stick to the collagen and when they stick they release platelet activating factor, that in turn causes more platelets to aggregate (positive feedback loop)
  • As the endothelium has flapped up, it has disturbed the lamina flow of blood, so red blood cells can get trapped with the platelets underneath the epithelium
    = the start of thrombus formation (a blood clot in a vessel that is not damaged, apart from the epithelium)
  • Platelets release protease thrombin into the blood that cause fibrinogen to polymerise into fibrin (leads to fibrin deposition)
  • Fibrin = big protein molecule that holds the trapped platelets and red blood cells in a fibrin mesh, and also causes more fibrinogen to polymerase (2nd positive feedback loop)
  • These positive feedback loops continue to happen and can lead to the artery occluding = Thrombus
126
Q

What is the definition of thrombosis?

A

A solid mass of blood constituents formed within the intact vascular system during life.

127
Q

What 3 things predispose a vessel to thrombosis?

A
  • Change in vessel wall (endothelial damage)
  • Change in blood flow (from lamina flow to tubular flow)
  • Change in blood constituents (i.e. too many platelets)
128
Q

What can damage to the blood vessels lead to?

A

Artherosclerosis

129
Q

Explain the process of thrombosis in veins…

A
  • slightly different, as blood has been through capillaries and is travelling at a slow rate back to the heart, powered by muscles contracting the vein walls (stasis)
  • combination of sticky endothelial cells and slow blood flow means blood constituents can stick to this area and cause thrombus formation
  • bits of thrombus can break off and travel through veins and cause a pulmonary embolism
130
Q

What can occur after the thrombus had been broken down?

A
  • Lysis and resolution;
  • Organisation (and repair, leaves collagen scar tissue, so vessel is no longer patent but is stuck to itself)
  • Recanalization (capillaries growing through it)
  • Embolism (break off and spread to other places)
131
Q

How to prevent thrombosis?

A
  • Exercise
  • Elastic stockings
  • Aspirin, anti-platelet drug; inhibits platelet aggregation, stops platelets being so sticky, means only a few platelets will stick and so prevents thrombus formation
132
Q

What is the definition of an embolus?

A

A mass of material in the vascular system able to become lodged within the vessel and block it.

133
Q

What is the most common cause of an embolus?

A

A broken off piece of thrombus has travelled through the blood and has become lodged in a vessel that is too small to let it pass.

134
Q

How to identify a thrombus?

A

Doppler ultra-sound.

135
Q

Where can a thrombus from the left side of the heat go?

A

Anywhere in the body, as it enter the systemic blood circulation from the left side of the heart.

136
Q

What is the definition of ischaemia?

A

A reduction in blood flow.

137
Q

Explain the process of ischaemia…

A
  • Reduced blood flow through a vessel means that the cells furthest away from the capillaries are most susceptible to not receiving sufficient oxygen, so become ischaemic
  • The greater the reduction in blood flow, the greater the number of cells effected
  • if the cells have not died, and blood flow is increased and oxygen levels are restored to cell, the cells will return to their non-ischaemic state
  • Does NOT imply that cells have died
138
Q

What is the definition of infarction?

A

Is a reduction in blood flow with subsequent death of cells.
Death of tissue due to lack of blood supply.

139
Q

What is reperfusion injury?

A

Occurs after ischaemia, if blood supply is severely limited but cells have not died, then blood flow is restored, cells produce ROS’s that chew up cells., and cause damage.
Cells are deoxygenated too quickly.
Reason why sometimes patients are kept in an induced coma, and in a cold environment.

140
Q

What is an end artery supply?

A

When an organ has only one artery supplying blood to it. ( a cul-de-sac)

141
Q

Why is a thrombus in an end artery more severe?

A

Because, the blood in that artery has nowhere to go, so the organ is going to infarct (die) as it is not getting any blood. (i.e. kidney)

142
Q

Why is infarct of the liver or lung and some parts of the brain not common?

A

As it as 2 blood supplies, dual blood supply, so if one has an embolism, blood is till being supplied to it. Both supplies need to be blocked to experience infarct.

143
Q

What are watershed terriotries?

A

Tissues that are at the limits of 2 different blood supplies. Right at the ends of 2 different blood supplies.

144
Q

What causes an infarct in watershed areas?

A

A drop in blood pressure, despite dual blood supply, not enough blood is reaching the area.

145
Q

What is the definition of apoptosis?

A

It is programmed cell death.

146
Q

What is Artherosclerosis?

A

A disease of the arteries characterised by the deposition of fatty material on inner cell walls.

147
Q

Explain the vascular changes that occur in acute inflammation?

A
  • Capillaries = no smooth muscle in their walls to control calibre, are narrow so that red blood cells pass through them in single file
  • Arteriolar walls = precapillary sphincters which regulate blood flow through the capillary bed
  • Acute inflammation –> sphincters relax, so blood flow is increased and contributes to redness and heat

Phase 2a (8 decks)

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