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P.O.D own flashcards > Acute inflammation > Flashcards

Acute inflammation Flashcards

1
Q

what are the main causes (aetiologies) of acute inflammation?

A 
micro-organisms
injury/ trauma to tissue
chemical
extreme conditions
dead tissue
hypersensitivity
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2
Q

microorganisms and acute inflammation

A

e.g bacteria, fungi, viruses, parasites- Pathogenic organisms that cause infection

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3
Q

Recognise the benefits of acute inflammation

A

rapid response to injury site
cardinal signs (redness, swelling, pain and heat) and loss of function
neutrophils move from blood vessels to E.C space -destroy organisms and denature antigen for macrophages- can eradicate the infection
plasma proteins localise the process
resolution and return to normal

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4
Q

what are the cardinal signs of inflammation? ie simple sign of symptoms

A 
Rubor (redness)
Calor (heat)
Tumor (swelling)
dolor (pain)
loss of function
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5
Q

Injury/trauma to tissue and acute inflammation

A

All injuries, even sterile (e.g surgery) cause acute inflammation
‘mechanical’= a blow, crush, cut, or penetrating wound

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6
Q

Chemical cause for acute inflammation

A

upset stable environment (e.g acid or alkali, bile (alkaline) and urine cause irritation when in inappropriate place)

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7
Q

Extreme conditions (physical) cause for acute inflammation

A

e.g sunburn from heat, frostbite from cold, ionising radiation

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8
Q

Hypersensitivity for acute inflammation

A

several classes of reaction

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9
Q

dead tissue cause of acute inflammation

A

in tissue that dies, cell necrosis irritates adjacent tissue

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10
Q

what microvascular changes occur because of acute inflammation?

A
  • change in vessel radius/ flow
  • change in vessel permeability as blood vessels dilate and more gaps arise for things to infiltrate it.
  • movement of neutrophils from the vessel to the extra-cellular ‘space’ compartment
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11
Q

increased blood flow?

A

blood vessels dilate which increases the blood flow to the site of inflammation. RESULT= observed redness and heat

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12
Q

Increased permeability?

A

an increase in permeability of the capillaries allows fluid and plasma proteins to move into the interstitial spaces. This process is called EXUDATION. What is leakes is called exudate. Exudation causes the formation of an oedema (accumulation of fluid in the extra-vascular space).
This explains the swelling of tissue in acute inflammation. Swelling causes pain and reduces function.

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13
Q

Define exudation?

A

process by which there is an increase in permeability of the capillaries, allowing fluid and plasma proteins to move into the interstitial spaces

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14
Q

Exudate?

A

a mass of cells and fluid rich in protein that has seeped out of blood vessels. It contains immunoglobulin and fibrinogen.

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15
Q

Migration of neutrophils

A
  1. margination- the neutrophils (WBCs) move to endothelial aspect of lumen (lining)
  2. pavementing/adhesion- neutrophils adhere (stick) to endothelium
  3. emigration- neutrophils squeeze between endothelial cells to extravascular tissues- guided to site of infection
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16
Q

describe sequence of events in exudate formation

A

An increase in permeability of capillaries during acute inflammation allows exudate to leak into extravascular space. It explains the swelling of tissue in acute inflammation. Can lead to oedema, which is the accumulation of fluid in the extravascular space. This swelling causes pain, due to pain receptors being stretched, and loss of function.

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17
Q

What are the local effects of acute inflammation?

A
  1. Transient (lasting only a short time) arteriolar constriction. Lasts a few moments, probably protective
  2. local arteriolar dilation. Relaxation of smooth muscle of vessel.
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18
Q

List the systemic effects of acute inflammation

A
  1. pyrexia- raised temperature
  2. feel unwell (malaise) anorexia, nausea, abdominal pain and vomiting in children
  3. neutrophilia- raised white cell count, produced and released by bone marrow
  4. septic shock
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19
Q

Outcomes of acute inflammation

A 
suppuration (pus formation)
abscess
organisation
dissemination
chronic inflammation
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20
Q

suppuration

A

sup backwards = pus
pus formation, made up of dead tissue, organisms, exudate, neutrophils, fibrin, red cell and debris. ‘membrane’ surrounds pus to keep it contained locally. May extend into other tissues (still contained) and progress inflammation further
many neutrophils die at the site of their action so form the pus that is found at infection site

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21
Q

abscess

A

a collection of pus (suppuration) under pressure. Can be a single locule, or multiloculated (when pus bursts through the pyogenic membrane and forms new cavities)

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22
Q

dissemination

A

spread to the bloodstream, and the patient becomes ‘septic’
bacteraemia= bacteria in the blood
septicaemia= growth of bacteria in blood
toxaemia= toxic products in blood

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23
Q

inflammation leads to the following stages

A

granulation tissue- occurs after a large amount of damage, or an ability to remove dirt from wound-
capillaries grow into the inflammatory mass. Means plasma proteins, macrophages and fibroclasts which lay down collagen to repair damage have access
-healing and repair
-scar formation

24
Q

how can process of acute inflammation be detrimental to patient

A
  • release of lysosomal enzymes by inflammatory cells may have harmful effects
  • digestion of normal tissue
  • swelling
  • inappropriate inflammatory response
25
Q

digestion of normal tissue effect on patient

A

enzymes such as collagenases and proteases may digest normal tissues, resulting in their destruction. This may result particularly in vascular damage e.g type III hypersensitivity

26
Q

Swelling:- effect on patient

A

Swelling of acutely inflamed tissues may be harmful. Inflammatory swelling is especially serious when it occurs in an enclosed space such as the cranial cavity. Thus, acute meningitis or a cerebral abscess may raise intacranial pressure to the point where blood flow into the brain is impaired.

27
Q

Inappropriate inflammatory response:- effect on patient

A

Sometimes acute inflammatory responses appear inappropriate, such as those which occur in type I hypersensitivity reactions (e.g hay fever) where the provoking environmental antigen (e.g pollen) otherwise poses no threat to the individual. Such allergic inflammatory responses may be life- threatening, for example extrinsic asthma.

28
Q

mediators of vasodilation and vasoconstriction

A

histamine causes vasodilation while serotonin causes vasoconstriction. These two molecules contradict each other in terms of vasodilation and vasoconstriction and so balance each other out through homeostasis

29
Q

mediators of altered permeability

A

prostaglandins and leukotrienes produce molecules that aid and prevent increased permeability, and so balance each other out

30
Q

mediators of neutrophil adhesion

A

molecules can either aid or inhibit the process of neutrophil adhesion

31
Q

what effect do mediators have?

A

mediators can have positive and negative effects, and result in a dynamic balance. They can favour or inhibit acute inflammation relative to need.

32
Q

Is inflammation a quick response?

A

Yes

33
Q

Oedema

A

accumulation of fluid in the extravascular space- swelling

34
Q

What flow is there in a normal vessel?

A

laminar flow

velocity of the fluid through vessel is constant at any point in the fluid

35
Q

Margination

A

movement of neutrophils from centre of vessel to the vessel wall

36
Q

Diapedesis

A

movement of white blood cells out of through capillary walls

37
Q

Inflammation terminology

A

(add -itis usually)
meninges- meningitis
appendix- appendicitis

others:- pneumonia
pleural cavity

38
Q

effector mechanism of inflammation- cell?

A

neutrophil

39
Q

neutrophils

A
  • can recognise foreign antigens

they move towards the antigen by chemotaxis

40
Q

When do neutrophils die?

A

when granule contents are released
they produce pus
although it’s contained, it might extend into other tissues- progressing inflammation

41
Q

fibrinogen

A

helps blood to coagulate in vessels and clot exudate outwith vessels
performs like a plug
localises inflammatory process- stops spreading

42
Q

chemotaxis

A

movement of neutrophils in response to inflammation

Move up a conc. gradient to where the messenger is coming from- requires energy

43
Q

mediators of acute inflammation

A 
vasodilation and vasoconstriction
altered permeability
neutrophil adhesion
chemotaxis 
itch and pain
44
Q

What can septicemia cause/lead to?

A

septic shock- tachycardia, peripheral vasodilation, hypotension (low bp)

shock is the inability to perfuse tissues

45
Q

what effects can mediators have on acute inflammation

A

they can promote/ inhibit inflammatory response

46
Q

Summary of outcomes of acute inflammation

A 
resolution
suppuration
organisation
dissemination
chronic inflammation
47
Q

Histamine

A

it’s a neurotransmitter. it’s in form of granules that are released from inside mast cells
IgE and antigen reaction changes mast cell membrane

the histamine binds to H1 receptors and causes vasodilation, increased permeability

48
Q

Anti-histamines

A

work by blocking/inhibiting H1 receptors (histamine receptors)

49
Q

pyrexia

A

raised temperature

50
Q

Abscess

A

collection of pus under pressure
single locule, multiloculated
can release discharge
collapses- healing and repair
depending on size small may drain naturally, or simply shrink, dry up and disappear
Large- may need antibiotics to clear the infection + pus may need to be drained.

51
Q

multiloculated abscess

A

pus bursts through pyogenic membrane and forms new cavities

52
Q

Pyaemia

A

discharge to bloodstream

53
Q

what is normal laminar flow like?

A

white blood cells in the middle surrounded by red blood cells

54
Q

flow in inflammation

A

neutrophils found near endothelium so capillary walls (margination)
RBCs aggregate in centre of lumen (rouleaux)

55
Q

what do neutrophils do in terms of granule release?

A

their granules possess oxidants eg H2O2 and enzymes eg proteases

they release the granule contents
phagocytose/destroy foreign antigens
when neutrophils release their contents they die and produce pus

P.O.D own flashcards (34 decks)

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