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Life Protection > Acute inflammation > Flashcards

Acute inflammation Flashcards

1
Q

What is acute inflammation?

A

initial rapid response to injury/infection
- takes mins - hours to develop
- short duration (hours - days)
Type of innate immune response
Non-specific, responds to all types of injury

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2
Q

What are the main triggers of acute inflammation?

A

infections
tissue damage (physical, chemical and mechanical agents/ischaemia)
foreign bodies

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3
Q

What are the main functions of acute inflammation?

A
  • alert the body
  • contain infection to prevent it from spreading
  • Protect injured site from becoming infected
  • eliminate dead cells/tissue
  • Healing and repair
    Acute inflammation is a physiological response
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4
Q

What are the 5 R’s of acute inflammation?

A 
Recognition
Recruitment
Removal 
Regulation (of response)
Resolution/Repair
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5
Q

What are the 5 cardinal signs of acute inflammation?

A 
Rubor (redness)
Calor (heat) 
Tumor (swelling)
Dolor (pain)
Functio laesa (loss of function)
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6
Q

Where does acute inflammation primarily mediate its effect?

A

locally to site of infection/injury
affecting the capillaries and tissue adjacent initially
(this may have systemic implications)

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7
Q

What systemic changes may be implicated in acute inflammation?

A

Fever: release of endogenous (IL-6, TNFa) or exogenous pyrogens (microbial toxins)

Neutrophils: G-CSF stimulation of bone marrow. Replenish and release of immature neutrophils = increase in neutrophil count.

Acute phase reactants: CRP, fibrinogen, complement, serum amyloid A protein (SAP)
synthesised in liver, triggered by IL-6, IL-1, TNFa (pro-inflammatory cytokines)
increased fibrinogen -> rouleaux/stacking of RBCs -> increased ESR

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8
Q

What is the mechanism behind elevated ESR in chronic accumulation?

A

during inflammatory processes, elevated cytokines are released which cause increases in fibrinogen
Fibrinogen deposits on RBCs which causes them to rouleaux
This makes them stickier and heavier, and increases their sedimentation rate. This parameter is known as ESR
ESR has a long duration effect (longer than CRP, which will only be elevated in conditions of acute inflammation)

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9
Q

What are rare consequences of acute inflammation?

A

Systemic Inflammatory Reaction Syndrome (SIRS)
e.g. sepsis
this is widespread and can cause severe manifestations
SIRS can result in further complications e.g. shock, AKI and multi organ failure

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10
Q

What are the 2 main types of events associated with acute inflammation?

A
  • vascular

- cellular

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11
Q

What vascular events occur in acute inflammation?

A
  • vasodilation (of small vessels)
  • Increased blood flow (to injured site)
  • increased vessel permeability (fluid leakage results in oedema)
    These are driven by release of prostaglandins such as histamine and serotonin
    Function of these events is to promote the transport of leukocytes and plasma proteins from the blood to injury site
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12
Q

How does histamine and serotonin affect the endothelium in blood vessels directly?

A

Causes contraction of the endothelial cells
Exposing gaps between cells where tight junctions normally reside
these gaps are used by immune cells to enter the surround ‘inflamed’ tissue (and also promotes fluid leakage)

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13
Q

What is inflammatory exudate?

A

produced under inflammatory conditions dues to mediators such as histamine
fluid composed of serum, fibrin and leukocytes
Formed due to increased vessel permeability

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14
Q

How is transudate different from exudate?

A

transudate formed in non-inflammatory conditions
formed due to increased peripheral pressures (e.g. hypertension) causing fluid to leak out of vessels e.g. lymphoedema
In transudate, the vascular permeability is normal

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15
Q

What are pyrogens?

A

molecules/mediators that result in an increase in local or systemic temperature
In humans, they usually act at the hypothalamus to initiate a fever

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16
Q

What are the main types of inflammatory exudate?

A

Serous
Purulent
Fibrinous
Haemorrhagic

17
Q

What is serous (inflammatory) exudate?

A

few cells
little or no microbes
fluid derived from plasma or secreted by endothelial cells
found in serous cavities (pleura, peritoneum, pericardium)
skin blisters (burns, viral infections)

18
Q

What does serous fluid usually refer to?

A

any body fluid resembling serum
typically pale yellow, transparent and benign in nature
Secretion of serous fluid from cavities is generally termed as an effusion
e.g. pleural effusion

19
Q

What is purulent (inflammatory) exudate?

A

= fibrino-purulent
PUS contains many leukocytes (usually neutrophils), dead cells and microbes
pus-producing bacteria (pyrogenic) e.g. staph. A
e.g. in acute appendicitis
e.g. abscess is a collection of (pus) purulent inflammation

20
Q

What is the long term complications of fibrino-purulent exudate on serous cavities?

A

This type contains less fluid that other types of exudate
therefore, it is difficult to eliminate
especially in deep structures e.g. pleura
this causes INCREASED FRICTION on epithelial cells

21
Q

What is fibrinous (inflammatory) exudate?

A

results in fibrin deposition (from fibrinogen in plasma, increased during acute inflammation in response to IL-6, TNFa)
Forms via large vascular leaks -> fibrinogen exits blood and enters tissue
Present in serous cavities e.g. pleura, meninges
Can lead to chronic scar tissue -> fibrosis -> impaired function
Fibroblasts also may deposits collagen (e.g. stellate cells)

22
Q

What is haemorrhagic (inflammatory) exudate?

A

contains RBCs mostly
formed via blood vessel rupture
and trauma

23
Q

What are the main cellular steps that occur in acute inflammation?

A
  1. migration and accumulation of cells e.g. neutrophils
  2. removal of pathogens + injured/dead cells
  3. migration and accumulation of monocytes
24
Q

What are the 5 steps of neutrophil recruitment?

A

1) Margination and rolling
2) Integrin activation (by chemokines e.g. IL-8)
3) Firm attachment to endothelium (Integrin-ICAMs)
4) Transmigration through endothelium into tissue
5) Chemotaxis to inflamed site (e.g. IL-8 for neutrophils)

25
Q

Describe the molecules involved in weak and firm attachment of neutrophils to the vessel endothelium

A

Weak/preliminary: Selectins

Firm attachment: Integrins and ICAMs

26
Q

What are ICAMs?

A

= immunoglobulin superfamily cell adhesion molecules
role in mediating firm attachment of neutrophils to endothelium post-rolling phase
bind activated integrin molecules on neutrophil PM surface

27
Q

How are selectins involved in the neutrophil recruitment process?

A

2 main types involved:
- P-selectin (constituively expressed, mobilised to PM under acute inflammation. Occurs within minutes, stored in pre-formed granules).
- E-selectin (expression induced following IL-1/TNFa, synthesis and translocation to PM takes longer to occur)
=> These types mediate rolling action of neutrophils prior to firm attachment mediated by ICAMs/integrins

Also L-selectin: expressed on leukocytes (neutrophils, monocytes, lymphocytes) with cognate ligands on endothelium

28
Q

Which ligands, present on the PM surface of neutrophils, bind selectins P and E?

A

P-selectin: PSGL-1 (P-selectin glycoprotein ligand-1)

E-selectin: sialylated carbohydrates (siacyl Lewis)

29
Q

What is margination and how does it initiate the rolling process?

A

acute inflammation
release of pro-inflammatory mediators (e.g. histamine)
vasodilation -> increased vessel diameter, reduced speed of WBC flow
WBCs move from central lumen and start flowing closer to the marginal zones/endothelium edge (MARGINATION)
Allows interaction of selectins and cognate ligands to occur and for rolling to be initiated (ROLLING)

30
Q

Why are the interactions between P- and E-selectins and their associated ligands lead to rolling?

A 
Low-affinity interactions
blood flow weakens these causing disruption 
repetitive attachment and detachment 
slows down flow of WBCs even further
Appear to be "rolling"
31
Q

What are the ligands for P- and E-selectin?

A

P-selectin: PSGL-1

E-selectin: sialyl - Lewis

32
Q

Why does integrin activation occur?

A

Integrin activation leads to high affinity interaction between neutrophil and endothelium

33
Q

What is Koebner phenomenon? In which conditions is it seen?

A

It describes skin lesions which appear at the site of injury

Found in:

  • psoriasis
  • vitiligo
  • warts
  • lichen planus
  • lichen sclerosus
  • molluscum contagiosum
34
Q

What can be observed in blood smears in DIC?

A

DIC - disseminated intravascular coagulapathy

schistocytes: fragmented RBCs
most often found to be microcytic with no area of central pallor

35
Q

In sepsis, why does the tissue exudate have a higher protein content than normal tissue?

A
  • inflammation causes increased permeability of capillary walls
  • exudation of plasma proteins
36
Q

What are the vascular changes that occur during acute inflammation?

A

VASOCONSTRICTION (transient)
caused by thromboxane A1 and reflex from pain receptors

VASODILATION
histamine release from mast cells and NO from endothelial cells. Will also cause inflammatory exudate and oedema

PLASMA DEHYDRATION
as fluid leaves the blood, making blood hyperviscous and slower moving

NEUTROPHIL MARGINATION
stasis and reduced fluid flow allows migration of neutrophils to site of injury/infection

Life Protection (30 decks)

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