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semester 2 > Pathology > Flashcards

Pathology Flashcards

1
Q

what is inflammation

A
  • local physiological response to tissue injury

- complex reaction in vascularised connective tissue

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2
Q

role of inflammatory response

A

serves to destroy,dilute or wall of injurious agent (primarily a protective response)

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3
Q

when is inflammation harmful (3)

A
  • life-threatening hypersensitivity reactions
  • chronic inflammatory diseases e.g. rheumatoid arthritis and crohn’s
  • repair by fibrosis may lead to disfiguring scars
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4
Q

types of inflammation (2)

A
  • acute

- chronic

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5
Q

what is acute inflammation

A

the initial and often transient series of tissue reactions to injury (involving several processes)

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6
Q

what is chronic inflammation

A

subsequent and often prolonged tissue reactions following the initial response

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7
Q

principle causes of acute inflammation (5)

A
  • microbial infections (viruses,bacteria such as E.coli, actinomycetemcomitans)
  • hypersensitivity reactions (inappropriate or excessive immune reaction which damages tissues, including reactions to parasites)
  • physical agents (trauma, uv light, thermal agents inc. burns or frostbite)
  • irritant and corrosive chemicals (acids, alkalis, infecting agents releasing chemical irritants)
  • foreign bodies (e.g. splinters,dirt,sutures,restorative material)
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8
Q

physical characteristics of inflammation (5)

A
  • redness (dilation of blood vessels)
  • heat (increase in blood flow, hyperaemia)
  • swelling (due to accum. of fluid exudate in extravasc. space)
  • pain (stretching/distortion of tissues by inc. fluid, also chemical mediators inc. bradykinin produce pain)
  • loss of function (due to swelling and pain,conscious and reflex)
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9
Q

processes of acute inflammation (2)

A
  • vascular phase

- exudative and cellular phase

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10
Q

what occurs in vascular phase of acute inflammation (2)

A
  • dilation (pre capillary bed sphincter opens,most capillaries are full)
  • increased permeability of blood vessels (oxygen carbon dioxide and some nutrients transfer via diffusion, main transfer of fluid and solute is by ultrafiltration as described by starling)
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11
Q

what occurs in exudative/cellular phase of acute inflammation

A

fluid and cells escape from permeable venules

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12
Q

what is oedema

A

the net increase in extravascular fluid

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13
Q

what is within the fluid exudate that builds up in extravascular space (and role of these components) (2)

A
  • proteins including immunoglobins and fibrinogen:
  • > immunoglobins important in destruction of invading organisms
  • > fibrinogen (fibrin on contact with ECM, hence acutely inflamed organ surfaces commonly covered in fibrin)
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14
Q

role of lymphatics in acute inflammation

A

continually remove exudate (it is replaced by new exudate)

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15
Q

how does vascular permeability increase

A
  • via formation of endothelial gaps in venules (lined with single layer of endothelial cells)
  • > endothelial cells contain contractile proteins, which when stimulated by chemical mediators (histamine, bradykinin) they pull open transient pores
  • > endothelial cells are not damaged in this process
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16
Q

which chemical mediators bring about an increase in vascular permeability (2)

A
  • histamine

- bradykinin

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17
Q

location of leaked fluid when vascular permeability increases during acute inflammation

A

confined to POST CAPILLARY VENULES

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18
Q

causes of immediate and transient increased vascular permeability

A
  • chemical mediators:
  • > histamine
  • > bradykinin
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19
Q

causes of immediate and sustained increased vascular permeability

A

severe direct vascular injury e.g. trauma

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20
Q

cause of delayed and prolonged increased vascular permeability

A

endothelial cell injury e.g. X-rays, bacterial toxins

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21
Q

cellular component of acute inflammation

A

neutrophil (diagnostic feature of acute inflammation, accumulates in extracellular space)
->aka polymorphonuclear leucocytes

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22
Q

what type of cell is a neutrophil

A

leukocyte

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23
Q

function of neutrophils (6)

A
  • kill organisms
  • ingest offending agents
  • degrade necrotic tissue
  • produce chemical mediators
  • produce toxic oxygen radicals
  • produce tissue damaging cells
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24
Q

steps involved in neutrophils reaching site of inflammatory stimulus (3)

A
  • margination (flow in plasmatic zone of blood vessels, occurs ONLY in venules)
  • adhesion (interaction between adhesion molecules on its surface and the endothelial surface)
  • transendothelial migration/transmigration (following firm adhesion, neutrophils insert pseudopodia into junctions between endothelial cells, then cross through basement membrane into extravascular space)
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25
Q

predominant molecules involved in migration of neutrophil across basement membrane into extravascular space (4)

A
  • increased expression of selectins on endothelium
  • loose, rolling adhesion between selectins and their receptors on the leucocyte
  • firm adhesion between activated integrins on leucocyte and ICAM-1 (intercellular adhesion molecule 1) on endothelial cell
  • transmigration is mediated by ICAM-1, integrins and PECAM-1 (CD31)
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26
Q

what increases leucocyte surface adhesion molecule expression (3)

A
  • complement component C5a
  • leukotriene B4
  • tumour necrosis factor (TNF)
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27
Q

what increases endothelial cell expression of adhesion molecules to which neutrophils and other leucocytes bond (3)

A
  • IL-1
  • endotoxins
  • tumour necrosis factor (TNF)
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28
Q

how do neutrophils find the site of inflammatory stimulus

A

-process called chemotaxis (‘locomotion orientated along a chemical gradient’)

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29
Q

compounds chemotactic/trigger chemotaxis for neutrophils (4)

A
  • bacterial products
  • complement components
  • cytokines
  • products produced by the neutrophils themselves
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30
Q

what is the result of the series of chemical reactions caused by the binding of chemotactic agents to cell receptors (4)

A
  • release of intracellular calcium
  • influx of extracellular calcium
  • > increased cytosolic calcium triggers assembly of contractile proteins responsible for cell movement
  • > locomotion involves rapid assembly and disassembly of contractile filaments)
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31
Q

role of endogenous chemical mediators (5)

A
  • > drive the process of acute inflammation
  • cause:
  • > vasodilation
  • > emigration of neutrophils
  • > chemotaxis
  • > increased vascular permeability
  • > itching and pain
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32
Q

chemical mediators of inflammation released from cells (6)

A
  • histamine
  • lysosomal compounds
  • serotonin
  • chemokines
  • leukotrienes
  • prostagladins
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33
Q

result of release of chemical mediator histamine from cells

A
  • vacular dilatation

- transient increase in vascular permeability

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34
Q

which cells release histamine (4)

A
  • mast cells
  • eosinophils
  • basophils
  • platelets
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35
Q

where are lysosomal compounds released

A

from neutrophils

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36
Q

result of release of lysosomal compounds

A

may increase vascular permeability and activate complement

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37
Q

type of serotonin present in high conc. in platelets

A

5 hydroxytryptamine

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38
Q

effect of serotonin release from cell

A

causes increased vascular permeability

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39
Q

what are chemokines and role

A
  • proteins which attract various types of leucocyte to the site of inflammation
  • > various chemokine bind to ECM components setting up a gradient of chemotactic molecules fixed to the extracellular matrix
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40
Q

what are leukotrienes synthesised by

A

arachidonic acid, especially in neutrophils

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41
Q

role of leukotrienes

A
  • posses vasoactive properties

- involved in type I hypersensitivity

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42
Q

what are prostaglandins

A

fatty acids synthesised by many cell types

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43
Q

effect of prostaglandins release

A
  • increased vacslar permeability

- stimulate platelet aggregation

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44
Q

plasma factors in inflammation (4 enzymatic cascade systems which mediate various aspects of inflammation in addition to other functions)

A
  • complement system
  • kinin system
  • coagulation system
  • fibrinolytic system
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45
Q

function of the complement system

A

innate and adaptive immunity for defence against microbes

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46
Q

what makes up the compliment system

A

compliment proteins C1-C9 and their cleavage products

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47
Q

what does complement activation cause (3)

A
  • increased vascular permeability (C3a, C5a, C4a)
  • chemotaxis (C5a)
  • opsonization (C3b)
48
Q

what causes complement activation (4)

A
  • bacterial endotoxins
  • products of kinin, coagulation and fibrinolytic systems
  • antigen-antibody complexes
  • enzymes released from dying cells
49
Q

what occurs as a result of complement activation (5)

A
  • oponisation of pathogens (facilitates phagocytosis)
  • increased vascular permeability
  • recruitment of inflammatory cells (neutrophils, monocytes, eosinophils and basophils)
  • killing of pathogens
  • histamin release from mast cells (vasodilation)
50
Q

role of the kinin system

A
  • generates vasoactive peptides from plasma proteins called kininogens by the action of specific kallikreins
  • activation of coagulation factor XII leads to formation of kinin e.g. bradykinin
51
Q

what activates the kinin system

A

coagulation factor XII (hageman factor)

52
Q

what does bradykinin cause (4)

A
  • increased vascular permeability
  • arteriolar dilatation
  • smooth muscle contraction (e.g. bronchial)
  • pain
53
Q

what occurs during the coagulation system

A
  • conversion of soluble fibrinogen into fibrin
  • > hageman factor/coagularion factor XII is activated by contact with extracellular materials and enzymes of bacterial origin
54
Q

fibrin

A

major component of the acute inflammatory infiltrate

55
Q

role of activated XII

A

-can activate the COMPLEMENT, KININ, COAGULATION AND FIBRINOLYTIC systems

56
Q

the fibrinolytic system

A
  • counterbalances coagulation
  • plasminogen factors (from endothelium, leucocytes and other tissues) cleave plasminogen -> plasmin
  • plasmin responsible for fibrin -> fibrin degradation products (may have local effects on vascular permeability)
  • plasmin also cleaves C3
57
Q

role of lymphatic system in acute inflammation

A
  • the lymphatic channels become dilated as they drain away the oedema fluid of the inflammatory exudate (limits extend of oedema in tissues)
  • antigens are carried to regional lymph nodes for recognition by lymphocytes
58
Q

role of the neutrophil polymorph (variation)

A
  • movement (chemotaxis)
  • recognition and adhesion to micro-organisms
  • phagocytosis and intracellular killing of micro-organisms (oxygen dependent and oxygen independent mechanisms)
59
Q

what is opsonisation

A

the process of coating a particle to target it for phagocytosis

60
Q

what do most organisms have to be coated in to be recognised for phagocytosis

A

opsonins

61
Q

eg’s of major opsonins (3)

A

-Fc fragment of IgG (presumably naturally occurring antibody against the ingested particle)
C3b (fragment of C3 generated by complement activation)
-collectins (plasma proteins which bind to microbial cell walls)

62
Q

what do opsonins do

A

bind to specific receptors on leucocytes and greatly enhance phagocytosis

63
Q

what is phagocytosis

A

complex process by which phagocytes such as neutrophils and macrophages engulf and ingest microorganism or other cells and foreign particles

64
Q

3 steps involved in phagocytosis

A
  • recognition (by particles on leucocyte surface receptors) and attachment
  • engulfment
  • killing and degradation
65
Q

what happens to neutrophils following phagocytosis

A

they undergo apoptosis

66
Q

what enhances efficiency of phagocytosis

A

opsonisation of particles

67
Q

what initiates the process of active phagocytosis

A

attachment of a particle to a phagocyte receptor

68
Q

what occurs during engulfment phase of phagocytosis

A
  • cytoplasmic extensions flow around the particle resulting in complete engulfment of the particle within a phagosome made by the cell membrane
  • the phagosome then fuses with the lysosomal membrane, resulting in discharge of the lysosome content into the phagolysosomes
69
Q

2 mechanisms of killing and degradation during phagocytosis

A
  • oxygen dependent (phagocytosis results in products of oxygen reduction which causes intracellular killing of microorganisms)
  • oxygen dependent (via the action of substances in leucocyte granules, e.g. lysosome which attacks bacterial coat)
70
Q

what occurs after killing during phagocytosis

A

acid hydrolase from lysosomes degrade the microorganisms within the phagolysosome

71
Q

where are leucocyte products released during activation and phagocytosis

A

into extracellular space as well as into the phagolysosome

72
Q

key products in neutrophils and macrophages (3)

A
  • lysosomal enzymes
  • oxygen derived active metabolites
  • products of arachidonic acid metabolism including prostaglandins and leukotrienes
73
Q

effect of lysosomal produce release (5)

A
  • these products may cause endothelial and tissue damage
  • > activates coagulation factor XII
  • > attracts other leucocytes into the area
  • > damages local tissues
  • > increases vascular permeability
  • > pyrogens producing systemic fever
74
Q

macroscopic appearances of acute inflammation (6)

A
  • necrotising (septic necrosis, bacterial putrefaction)
  • serous (thin protein rich fluid exudate)
  • catarrhal (mucus hyper secretion)
  • fibrinous (exudate contains plentiful fibrin)
  • suppurative (production of pus)
  • membranous (epithelium coated by fibrin)
75
Q

what is suppuration and cause

A

=formation of pus

->stimulus almost always infective agent (e.g. pyogenic bacteria such as staphylococci)

76
Q

components of pus (3)

A
  • dead neutrophils
  • bacteria
  • cellular debris
77
Q

drainage of abscess

A
  • has central collection of pus with an adjacent zone of preserved neutrophils surrounded by membrane of sprouting capillaries and vascular dilation and occasional fibroblasts
  • > on draining abscess cavity collapses and is obliterated by organisation and fibrosis
  • > deep seated abscesses may drain along a sinus tract or fistula
78
Q

formation of ulcer (ulceration)

A

-local defect or excavation of the surface of an organ/tissue that is produced by the sloughing of inflammatory necrotic tissue

79
Q

frequent locations of ulcers

A
  • mucosa of mouth, GI tract, GU tract

- low limbs (chronic ulcers) in those with circulatory disturbance

80
Q

beneficial effects of acute inflammation (6)

A
  • dilution of toxins (can be carried away by lymphatics)
  • entry of antibodies (due to increased vascular permeability)
  • stimulation of the immune response (fluid exudate containing antigens reaches local lymph nodes)
  • fibrin formation (impedes movement of micro-organisms)
  • delivery of nutrients and oxygen (aided by blood flow)
  • transport of drugs (e.g. antibiotics)
81
Q

harmful effects of inflammation (3)

A
  • digestion of normal tissues
  • swelling (eg. laryngeal oedema, brain swelling)
  • inappropriate inflammatory response (e.g.. type I hypersensitivity)
82
Q

systematic effects of acute inflammation (5)

A
  • fever
  • constitutional symptoms
  • weight loss
  • reactive hyperplasia of the reticuloendothelial system
  • haematological changes
83
Q

coordination of fever

A
  • coordinated by the hypothalamus

- it is a coordinated endocrine, autonomic and behavioural response

84
Q

endocrine response of fever (3)

A
  • secretion of acute phase proteins by the liver including C-reactive protein (CPR) and serum amyloid protein (SAA)
  • > these proteins act as opsonins and bind complement
  • increased production of glucocorticoids activating a stress response
85
Q

autonomic response of fever (3)

A
  • blood is redirected from the skin to deep vascular beds to minimise heat loss through skin
  • increased pulse and blood pressure
  • decreased sweating
86
Q

behavioural response of fever (4)

A
  • rigors (shivering)
  • anorexia (loss of appetite)
  • somnolence (drowsiness)
  • malaise
87
Q

why is fever beneficial during inflammation

A

-elevation in temp. of even a few degrees may improve the efficiency of leukocyte killing and probably impairs replication of many offending micro-organisms

88
Q

constitutional systems of acute inflammation

A
  • malaise
  • anorexia
  • nausea
89
Q

how does acute inflammation cause weight loss

A

due to negative nitrogen balance, particularly when there is extensive chronic inflammation

90
Q

reactive hyperplasia of the reticuloendothelial system (systematic effect of acute inflammation)

A

-nodal enlargement caused by hyperplasia of lymphoid follicles and hyperplasia of the phagocytic cells lining the sinuses

91
Q

haematological changes as a systematic effect of acute inflammation

A
  • increased erythrocyte sedimentation rate (ESR)
  • anaemia (eg. blood loss, haemolysis, chronic disorders)
  • leucocytosis (eg. lymphocytosis, neutrophilia, eosinophilia)
92
Q

what is leucocytosis and what causes it

A
  • increased total number of WBC’s
  • > usually due to accelerated release of cells from the bone marrow reserve pool (IL-1 and TNF)
  • > prolonged infection will induce proliferation of precursors in the bone marrow also mediated by IL-1 and TNF
93
Q

which type of WBC do most bacterial infections produce (leucocytosis)

A

neutrophilia

94
Q

which type of WBC can viral infections produce (leucocytosis)

A

lymphocytosis

95
Q

which type of WBC is usually produced during allergic disorders/parastitic infections (leucocytosis)

A

eosinophilia

96
Q

sequelae of acute inflammation (5)

A
  • resolution
  • suppuration (->discharge of pus)
  • repair and organisation
  • fibrosis
  • chronic inflammation
97
Q

what is resolution following inflammation

A

resolution means the complete restoration of the tissues to normal after an episode of acute inflammation

98
Q

factors favouring resolution (4)

A
  • minimal cell death/tissue damage
  • occureence in an organ/tissue with regenerative capacity (e.g.. liver)
  • rapid destruction of the causal agent
  • rapid removal of fluid and debris by good local vascular drainage
99
Q

what is organisation following inflammation

A

organisation of tissues is their replacement by granulation tissue

100
Q

factors favouring organisation (3)

A
  • large amounts of fibrin formed
  • substanital necrosis
  • exudate and debris cannot be removed or discharged
101
Q

formation of granulation tissue during organisation

A
  • capillaries grow into the inflammatory exudate accompanied by macrophages and fibroblasts
  • > predominate features of repair are angiogenesis (formation of new blood cells), followed by fibroblast proliferation and collagen synthesis
102
Q

what regulates the processes involves in organisation/formation of granulation tissue

A

growth factors

103
Q

role of growth factors

A

stimulate cell proliferation regeneration and angiogenesis (e.g. TNF,EGF, FGF)

104
Q

when does acute inflammation progress to chronic inflammation

A

if the agent causing acute inflammation is not removed

105
Q

what occurs in progression of acute inflammation to chronic inflammation (2)

A
  • organisation of the tissue

- change of cellular exudate character

106
Q

how may chronic inflammation arise (2)

A
  • develop from acute inflammation

- primary chronic inflammation (more common)

107
Q

factors favouring the progression from acute to chronic inflammation (3)

A
  • indigestible substances such as glass and suture material may result in chronic suppuration (foreign body reaction)
  • deep seated suppurative inflammation in which drainage is delayed or inadequate will result in a thick abscess wall composed of fibrous/granulation tissue (the rigid walls fail to come together after drainage, pus within the cavity becomes organised and eventually results in a fibrous scar)
  • recurrent episodes of acute inflammation and healing may eventually result in clinicopathological entity of chronic inflammation
108
Q

osteomyelitis

A

mandible

109
Q

chronic cholecystitis

A

replacement of wall by fibrous tissue and lymphocytes rather than neutrophils predominate

110
Q

predominant cells of chronic inflammation (3)

A
  • lymphocytes
  • plasma cells
  • macrophages
111
Q

examples of primary chronic inflammation (6)

A
  • resistance of infective agent to phagocytosis and intracellular killing (e.g. tuberculosis, leprosy brucellosis, viral infections)
  • foreign body reactions ito endogenous materials (e.g. gout, may be acute or chronic)
  • foreign body reactions to exogenous materials (e.g.. asbestos fibres)
  • some autoimmune diseases (e.g. rheumatoid arthritis)
  • specific diseases of unknown aetiology (e.g. ulcerative colitis)
  • primary granulomatous diseases (e.g. sarcoidosis)
112
Q

macroscopic appearances of chronic inflammation (4)

A
  • chronic ulcer (mucosa is breached, base is lined by granulation tissue, fibrous tissue extends through muscle layers)
  • chronic abscess cavity (eg. osteomyelitis)
  • thickening of the wall of a hollow viscus by fibrous tissue (e.g.. intestine)
  • granulomatous inflammation (eg. tuberculosis, caseous necrosis)
113
Q

most prominent feature of chronic inflammatory reaction

A
  • may be fibrosis (formation of granulation tissue results in fibrosis)
  • > when most of the chronic inflammatory cell infiltrate has subsided, fibrosis may lead to distortion and stricture formation (narrowing) eg. crown’s disease
114
Q

ulcerative colitis

A

chronic inflammatory bowel disease

115
Q

formation of macrophage in chronic inflammation

A

blood monocyte -> tissue macrophage

semester 2 (9 decks)

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