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principles of disease > acute inflammation > Flashcards

acute inflammation Flashcards

1
Q

define acute inflammation

A

Series of protective changes occurring in living tissue as a response to injury, can’t happen after death
it is a dynamic homeostatic mechanism limited to higher organisms

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2
Q

list the 5 cardinal signs of inflammation

A
  • Rubor - redness
    • Calor - heat
    • Tumor - swelling
    • Dolor - pain
    • Loss of function
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3
Q

what are the 6 causes of acute inflammation (the aetiology)

A 
microorganisms
mechanical trauma
chemical 
physcical 
dead tissue
hypersensitivity
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4
Q

microorganisms as a cause of acute inflammation

A

viruses, bacteria, fungi, parasites (pathogenic organisms cause infection)

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5
Q

mechanical trauma as a cause of acute inflammation

A

injury to tissue (all injuries even sterile i.e. surgery)

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6
Q

chemical causes of acute inflammation

A

upset stable environment, acid/alkali (upset pH), bile (alkali) and urine (acidic) (irritation when in inappropriate place e.g. peritoneum)

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7
Q

physical causes of acute inflammation

A

extreme conditions e.g. heat (sunburn), cold (frostbite), ionising radiation (e.g. gamma ray source)

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8
Q

dead tissue as a cause of acute inflammation

A

cell necrosis irritates adjacent tissue, acute inflammation at the boundary between the dead and living tissue

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9
Q

hypersensitivity as a cause of acute inflammation

A

several classes of reaction, responses to antigens and antibodies e.g. allergies

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10
Q

what is the process of acute inflammation

A
  • Series of microscopic events - we see the consequences of these effects
    • Localised to affected tissue - generally not about the whole body
      Take place in the microcirculation = capillary beds, fed by arterioles and drained by venules
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11
Q

what are the steps in acute inflammation (pathogenesis)

A
  • Changes in vessel radius - flow
    • Change in the permeability of the vessel wall - exudation i.e. what flows in/out of the vessel
      Movement of neutrophils (acute inflammatory cells) from the vessel to the extravascular space
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12
Q

local changes in vessel radius and blood flow

A
  1. Transient arteriolar constriction - few moments, probably protective
    1. Local arteriolar dilation - active hyperaemia
    2. Relaxation of vessel smooth muscle - ANS or mediator derived
      Called the triple response - flush, flare, wheal
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13
Q

how does increased radius affect flow

A
  • Increased arteriolar radius causes increased local tissue blood flow
    • Results in observed redness and heat (blood is closer to the surface)
      a tiny amount of change in the radius produces a huge change in the amount of substance moving through a vessel
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14
Q

increased permeability in blood vessels

A
  • Localised vascular response (happens in a specific vessel at a specific time)
    • Microvascular bed (doesn’t happen all over)
    • Endothelial leak - fluid and protein not held in vessel lumen (imbalance of Starling forces)
      Locally produced chemical mediators
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15
Q

what are the effects of increased permeability

A

○ Net movement of plasma from capillaries to extravascular space
Process is exudation, what is leaked is exudate - fluid rich in protein (plasma) includes immunoglobulin and fibrinogen
○ Fluid loss –> increased velocity (h)
○ Rate of flow slows - stasis (slowing of the flow)
Stasis produces a change in flow characteristics in vessel because blood is a non-Newtonian fluid

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16
Q

what are the effects of exudation

A

○ Oedema formed - accumulation of fluid in the extravascular space
○ Explains swelling of tissue in acute inflammation
Swelling causes pain –> reduced function

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17
Q

describe normal laminar flow

A

working from the edge of the blood vessel towards the centre: plasma, erythrocytes, WBC

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18
Q

what determines laminar flow

A

Laminar flow is due to the size of the particles floating within the blood. Biggest particles flow through the middle

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19
Q

flow through vessels in inflammation

A
  • Neutrophil polymorphonuclear leukocyte is most important cell
    • Neutrophil; polymorph; NPL
    • Loss of normal laminar flow
    • Red cells aggregate in the centre of the lumen
      Neutrophils found near endothelium
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20
Q

phases of emigration of neutrophils

A
  • Margination - neutrophils move to endothelial aspect of lumen
    • Pavementing - neutrophils adhere to endothelium with adhesion molecules
    • Emigration - neutrophils squeeze between endothelial cells (active process) to extravascular tissues
      Note diapedesis - happens to red cells, passive movement of cells from the vessel lumen into the extravascular space
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21
Q

examples of acute inflammation

A
  • Gingivitis - inflammation of the gums, occurs commonly in leukaemia
    • Pleural inflammation - inflammation on the surface of the lung
    • Appendicitis
    • Acute pyelonephritis - kidney, inflammation in the tubules
      Bacterial endocarditis - inflammation of the heart valves, leads to vegetations, occurs most commonly as a result of septicaemia, seen in drug users who are sharing needles
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22
Q

outline resolution of acute inflammation

A
  • Inciting agent isolated and destroyed
    • Macrophages move in from blood and phagocytose debris then leave
    • Epithelial surfaces regenerate
    • Inflammatory exudate filters away
    • Vascular changes return to normal
      Inflammation resolves
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23
Q

what are the benefits of acute inflammation

A
  • Rapid response to non-specific insult
    • Cardinal signs and loss of function - transient protection of inflamed area
    • Neutrophils destroy organisms and denature antigen for macrophages
    • Plasma proteins localise process
      Resolution and return to normal
24
Q

what are the outcomes of acute inflammation

A
  • Resolution
  • Suppuration - pus formation
  • Organisation - beginning of healing
  • dissemination
    Chronic inflammation - long term result of healing and repair
25
Q

how is inflammation at anatomical locations named?

A 
stucture - itis 
e.g. peritoneal cavity - peritonitis
meninges - meningitis 
EXCEPTIONS: 
lungs - pneumonia
pleural cavity - pleurisy
26
Q

what is the role of neutrophils in acute inflammation

A
  • Mobile phagocytes
    ○ Recognise foreign antigen
    ○ Move towards it - chemotaxis (detect chemical and move towards it, moving up the concentration gradient)
    ○ Adhere to organism
    • Granules possess oxidants (e.g. hydrogen peroxide) and enzymes (e.g. proteases)
    • Release granule contents
    • Phagocytose and destroy foreign antigen
27
Q

what are the consequences of neutrophil action

A

○ Neutrophils die when granule contents released
○ Produce a ‘soup’ of fluid, bits of cell, organisms, endogenous proteins - pus (marker of inflammatory processes)
○ Might extend into other tissues, progressing the inflammation

28
Q

what is the role of plasma proteins in acute inflammation

A
  • Fibrinogen - coagulation factor, forms fibrin (polymer) and clots exudate, localises inflammatory process
    Immunoglobulins in plasma specific for antigen - humoral immune response (see immunology lectures)
29
Q

what are the 4 mediators of acute inflammation

A
  • Molecules on endothelial cell surface membrane
    • Molecules released from cells
    • Molecules in the plasma
      Molecules inside cells
30
Q

what are the collective effects of mediators

A
  • Vasodilatation
    • Increased permeability
    • Neutrophil adhesion (Pavementing)
    • Chemotaxis
      Itch and pain
31
Q

what molecules are released from cells in acute inflammation

A

histamine, serotonin, prostaglandins, cytokines and chemokines, NO, oxygen free radicals

32
Q

what is the role of histamine

A

○ Preformed in granules in mast cells beside vessels, platelets, basophils
○ Released as a result of local injury; IgE mediated reactions
○ Causes vasodilatation, increased permeability
Acts via H1 receptors on endothelial cells

33
Q

what is the role of 5-hydroxytryptamine

A

○ Preformed in platelets in granules
○ Released when platelets degranulate in coagulation
○ Vasoconstriction - reduce radius of the vessel, reduces the flow, makes the vessel easier to block if it is leaking
Also acts as a neurotransmitter

34
Q

what are the role of prostaglandins

A

arachidonic acid metabolites which run through the cyclo-oxygenase pathway
○ Many cells (endothelium and leukocytes)
○ Many promote histamine effects and inhibit inflammatory cells
○ Thromboxane A2 promotes platelet aggregation and vasoconstriction - the opposite effect to PGD2, PGE2, etc
○ Latter: effectiveness of non-steroidal anti-inflammatory drugs

35
Q

what are the roles of cytokines and chemokines

A

○ Small molecules produced by macrophages, lymphocytes, endothelium in response to inflammatory stimuli
○ Pro-inflammatory and anti-inflammatory effects
§ Different molecules have different effects, dynamic balance between the 2 effects
Stimulate intracellular pathways and signalling

36
Q

what is the role of nitric oxide

A

○ Various cells

○ Smooth muscle relaxation, anti-platelet, regulate leukocyte recruitment to inflammatory focus

37
Q

what are the roles of oxygen free radicals

A

H2O2, OH-, O2-
○ Destroy molecules in order to gain electrons, help with the breakdown process
○ Released by neutrophils on phagocytosis
○ Amplify other mediator effects

38
Q

signalling molecules inside cells

A
  • Pattern associated molecular patterns:
    ○ Microbial antigen
    ○ Genetically hard wired to recognise antigens as foreign
    ○ Innate and adaptive immunity (non-specific)
    • Danger associated molecular patterns
      ○ Substances released in response to stimulus
    • Stimulate pattern recognition receptors on cell membranes
    • Activate inflammatory response
39
Q

intracellular inflammatory pathways

A
  • NF-kB (nuclear factor kappa-B) pathway
    • MAPK (mitogen-activated protein kinase)
      ○ Stimulated in inflammation via surface receptors e.g. toll-like receptors (TLRs)
      ○ Regulates pro-inflammatory cytokine production and inflammatory cell recruitment
    • JAK-STAT (Janus kinase - signal transducer and activator to transcription) pathway
      Direct translation of extracellular signal to molecular expression
40
Q

interaction of 4 enzyme cascades in plasma

A
  • Blood coagulation pathways
  • Fibrinolysis
  • Kinin system
  • Complement cascade
41
Q

blood coagulation pathways

A

○ Clots fibrinogen in exudate

Interacts widely with other systems

42
Q

fibrinolysis

A

○ Breaks down fibrin, helps maintain blood supply

Fibrin breakdown products vasoactive

43
Q

kinin system

A

Bradykinin: pain

44
Q

complement cascade

A

○ Ties inflammation with immune system

Active components stimulate increased permeability, chemotaxis, phagocytosis, cell breakdown

45
Q

what are the general effects of mediators

A
  • Vasodilation and constriction
    • Altered permeability
    • Neutrophil adhesion
    • Chemotaxis
    • Itch and pain
    • Mediators have +ve and -ve effects
    • Result is a dynamic balance
    • Favours and inhibits acute inflammation (not usually at the same time)
    • Relative to need (inflammatory response is proportional to the injury caused)
46
Q

what are the immediate systemic effects of acute inflammation

A
  • Pyrexia - raised temperature
    ○ Endogenous pyrogens from white cells act centrally
    • Feel unwell
      ○ Malaise, anorexia, nausea
      ○ Abdominal pain and vomiting in children
    • Neutrophilia - raised white cell count
      ○ Bone marrow releases/produces
47
Q

what are the long term systemic effects of inflammation

A
  • Lymphadenopathy: regional lymph node enlargement (immune response - switch over from innate to adaptive immunity)
    • Weigh loss - catabolic process of making neutrophils, proteins etc
      Anaemia
48
Q

suppuration

A
  • Pus formation: dead tissue, organisms, exudate, neutrophils, fibrin, red cells, debris
    Pyogenic membrane surrounds pus: capillary sprouts grow into the piece of fibrin, neutrophils, fibroblasts. Walls off pus
49
Q

what is an abscess

A
  • Collection of pus (suppuration) under pressure
    • Single locule or multiloculated
    • Points and discharges
    • Collapses - healing and repair
50
Q

describing pus in other places

A
  • Empyema - in a hollow viscus
    ○ Gall bladder, pleural cavity
    Pyaemia - discharge to bloodstream
51
Q

organisation

A
  • Granulation tissue characteristic
    • Healing and repair
      Leads to fibrosis and formation of a scar
52
Q

what is granulation tissue

A

universal patch, repair kit for all damage

Formed of: new capillaries (angiogenesis), fibroblasts and collagen, macrophages

53
Q

dissemination

A
  • Spread to bloodstream - patient ‘septic’
    • Bacteraemia - bacteria in blood
    • Septicaemia - growth of bacteria in blood
      Toxaemia - toxic products in blood
54
Q

what are the effects of systemic infection

A
  • Shock - inability to perfuse tissues
    • Clinical picture of early septic shock
      ○ Peripheral vasodilation –> tachycardia –> hypotension
      ○ Often pyrexia
      Sometimes haemorrhagic skin rash
55
Q

pathogenesis of septic shock

A
  • Systemic release of chemical mediators from cells into plasma
  • increased HR compensates (for loss of SVR and tachycardia to maintain CO)
  • Bacterial endotoxin released - leads to pyrexia
  • Activation of coagulation (resulting in disseminated intravascular coagulation, vasodilatation and haemorrhagic skin rash)
  • WHEN COMPENSATION FAILS:
    ○ Raised HR insufficient to maintain CO, SVR low so BP falls
    ○ Reduced perfusion of tissues: tissue hypoxia, loss of cell tissue and organ function
56
Q

outcome of septic shock

A
  • Rapidly fatal
    • Tissue hypoxia –> cell death (affects kidneys, brain, heart)
    • Haemorrhage
    • Requires urgent intervention and support
      ○ Awareness and early recognition
      ○ Ability of young people to compensate - get very ill very quickly
      ○ Admit to hospital and intensive care

principles of disease (40 decks)

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