it's about the vascular events which occur during inflammation

1. ADITHIYAN UDAYASANKAR

2.  INTRODUCTION
 DEFINITION
 CAUSES
 TYPES
 VASCULAR EVENTS
 REFERNCE
 CONCLUSION

3.  Inflammation is fundamentally a
protective response designed to get
rid the organism of both the initial
cause of cell injury(microbes) and
the consequences of such
injury(necrotic cell & tissues)

4.  Inflammation is a complex reaction
elicited in the vascularised connective
tissues of body by various exogenous or
endogenous stimuli that cause cell
injury. It is a protective response that
tend to isolate , eliminate, dilute
causative factor as well as necrotic
tissue that result from original damage.

5.  HYPOXIA
 PHYSICAL CAUSES
 POISONS
 IMMUNE MEDIATED
 NUTRITIONAL IMBALANCE
 TISSUE NECROSIS
 INFECTIONS

6.  Depending on severity of stimulus &
effectiveness of initial response to neutralize
the agent . It is classified into
ACUTE
•Short duration -several mins, to hrs, to days
•Chacterized by edema
CHRONIC
• Prolonged duration –several days, to months, to
years
• Characterized by infiltration of lymphocytes,
macrophages

7.  ACUTE INFLAMMATION is defined as
immediate or early response to an injurious
stimulus , the critical function of which is to
deliver leukocytes, plasma proteins,
antibodies to the site of injury.
 The events in acute inflammation can be
divided into
1) Vascular events
2) Cellular events

8.  Certain vascular changes take place during
inflammation .These are
Alteration in vascular caliber to increase
blood flow
Alteration in vascular permeability with
emigration of fluid & plasma proteins
Emigration of leukocytes (neutrophils)

9.  The above vascular features are responsible
for 5 cardinal signs of inflammation
 RUBOR-REDNESS
 CALOR-HEAT
 TUMOR-SWELLING
 DOLOR-PAIN
 LOSS OF FUNCTIONS
 Redness &heat are due to increased blood flow
 Swelling is due to edema
 Loss of function is due to tissue damage

10.  ALTERATION INVASCULAR CALIBER &
BLOOD FLOW:
 As the injurious stimulus strikes there is
immediateTRANSIENT vasoconstriction
which lasts for few seconds.
 It is followed by vasodilation
 Which involves arterioles followed by
opening of capillary beds which was carrying
low blood flow ,so there is increased blood
flow.

11.  Increased blood flow is the cause of heat and
redness (erythema).Vasodilation is induced
by the action of histamine & nitric oxide (NO).
 Vasodilation is quickly followed by slowing of
circulation which is due to increased vascular
permeability with the outpouring of protein
rich fluid into extravascular tissues.
 This increases the viscosity of blood and
cause stasis.

12.  STASIS: Dilation of blood vessels packed with
slow moving rbc’s(red blood cells).
 As stasis develops, the laminar blood flow is
interrupted so the leukocytes principally
neutrophils tend to fall out from centre to the
periphery close to endothelial cell,this is
known as MARGINATION.

13.  As there is increased blood flow due
to vasodilation, there is increased
hydrostatic pressure with
outpouring of fluid into
extravascular space.This fluid is
known as transudate.

14.  Normally, the hydrostatic pressure at arteriolar
end is 32mm hg while at venous end is 12mm hg.
The COP of tissues is 25mm hg which is almost
equal to mean capillary pressure. Hence the
outflow is negligible.
 In inflammation due to vasodilation & due to
increased hydrostatic pressure causes transduate
formation.
 Transudate-ultra filtration of plasma due to
increased hydrostatic pressure or decreased
COP without alteration in vascular
permeability.

15.  Transduate contains
1. Low protein content
2. Low fibrinogen
3. Low specific gravity
4. Low cell count
 Transduate is soon followed by increased
vascular permeability with outpouring of
protein rich fluid into interstitium.This fluid
is exduate.

16.  A hallmark of acute inflammation is increased
vascular permeability leading to escape of
protein rich exudate causing edema .
 Exudate –inflammatory extravascular fluid
formed due to increased vasc. Permeability
 Exudate contains
1. High protein content
2. High specific gravity
3. High cell count

17.  Transudate
• increased hydrostatic pressure
I. congestive heart failure
II. venous outflow obstruction
• decreased colloidal osmotic pressure
i. liver cirrhosis
ii. nephrotic syndrome
iii. protein losing enteropathy.
 Exudate – purulent (pus formation)

18.  Several mechanisms are responsible for increased
vascular permeability .
 Endothelial cell contraction: occurs immediately
in response to mediators like serotonin,
bradykinin, substance P, histamine .
 The endothelial cells contract widening the inter
endothelial junction causing increased
permeability
 It is called immediate transient response.
 Short lived (15-30 mins) & reversible
 It Is mainly seen in post capillary venules.

19.  It occurs in response to cytokines like IL-1 ,
TNF alpha .
 They cause structural re-organisation of
endothelial cytoskeleton disrupting the inter
endothelial junction.
 Begins in 2-4 hrs &lasts for 24 hrs.
 Arterioles, capillaries, venules can be
effected.

20.  It may occur with severe injury causing
endothelial cell necrosis & detachment.
 For example burns , lytic bacterial infection .
 The leakage begins immediately & sustained
at high level until vessel is thrombosed or
repaired.This is known as immediate
sustained response.
 Leakage begins in 2-12 hrs &persist for
several hours.

21.  As stasis occurs, leucocytes tend to fall
towards endothelial cells .These leukocytes
are activated &they produce reactive oxygen
species(ROS)& PROTEOLYTIC ENZYME that
can damage endothelial cells.
 For example, pulmonary & glomerular
capillaries.

22.  Inflammation associated with process of
healing & repair in which there is vascular
proliferation in response to mediators like
VEGF .
 The newly formed vascular sprout have a
leaky endothelial junction .
 The fluid can pass through endothelial cells in
form of tiny vesicles.