ACUTE INFLAMMATION Slides Pathology. pdf

Acute Inflammation

1. Acute
Inflammation
Dr IramKhurshid
MBBS, FCPS (Histopath)
Assistant Professor, CKMC

3. Learning objectives
1.Define acute Inflammation
2.Enlist the stimuli for inflammation
3.Enlist the morphological and
functional changes in inflammation
4.Enlist the components of vascular
and cellular events in inflammation
and explain their mechanisms and
regulation

4. Inflammation
▪Inflammation is a response of
vascularized tissues to infections
and tissue damage that brings cells
and molecules of host defense from
the circulation to the sites where
they are needed, to eliminate the
offending agents.
▪The main components:
Vascular reaction and a cellularresponse;

5. Stepsoftheinflammatory
response(5Rs):
1)Recognition of the injurious
agent,
2)Recruitment ofleukocytes,
3)Removal of theagent,
4)Regulation (control) of the
response,and
5)Resolution(repair).

6. TYPES OF INFLAMMATION
 2 main types:
1. Acute Inflammation
2. Chronic Inflammation

7. ACUTEINFLAMMATION
❑Acuteinflammationisaninitial,
rapidresponsetoinjury,microbesand
otherforeignsubstances thatis
designedtodeliverleukocytesand
plasmaproteinstositesofinjury.
❑Ittypicallydevelopswithinminutesor
hoursandisofshortduration,lastingfor
severalhoursorafewdays

8. Stimuli for Acute Inflammation
1)Infections(bacterial, viral, fungal,
parasitic) and microbial toxins are among
the most common causes.
2)Trauma: Thermal injury, as in burns or
frostbite; irradiation).
3)Physical and chemicalagents
(exposure to some environmental
chemicals)
4)Tissue necrosis:Ischemia (Several
molecules released from necrotic cells are
known to trigger inflammation)

9. Stimuli for AcuteInflammation
5) Foreign bodies:
(splinters, dirt, sutures) may
elicit inflammation by
themselves or because they
cause traumatic tissue injury
or carry microbes.

10. 6) Immune reactions: The
injurious immune responses
may be directed against self
antigens, causing autoimmune
diseases, or may be
inappropriate reactions against
environmental substances, as in
allergies, or against microbes

12. Recognition of Microbes, Necrotic
Cells, and Foreign Substances
Recognition of injurious agent occurs by
various receptors.
Located on surface of phagocytes,
dendriticcells and many other cells, such
as epithelial cells.
Toll-like receptors (TLRs) recognize
products of bacteria (such as endotoxin
and bacterial DNA), viruses, and other
pathogens.

13. The inflammasomeis a
multi-protein cytoplasmic
complex that recognizes
products of dead cells, such
as uric acid and extracellular
ATP, as well as crystals and
some microbial products.

15. Externalmanifestations: The
external manifestations of inflammation,
often called its cardinal signsare:
1)Heat(calor),
2)Redness(rubor),
3)Swelling(tumor),
4)Pain (dolor)and
5)Loss of function (functio
laesa).

16. Components taking part in
inflammation?

17. Two majorcomponents
A. Vascularchanges:
1. Vasodilatation
2. Increased vascular
permeability.
Both designed to maximize the
movement of plasma proteins and
leukocytes out of the circulation and into
the site of infection or injury.

18. Twomajorcomponents
2.Cellularevents:
Cellular recruitment and
activation.
Theprincipalleukocytesinacuteinflammationare
neutrophils (polymorph nuclearleukocytes).

19. A.ChangesinVascularCaliber
andFlow
Begin rapidly after infection orinjury
Dependingonthenatureandseverity
oftheoriginal inflammatorystimulus.
◦After Transient vasoconstriction(lasting
only forseconds),
◦Arteriolarvasodilationoccurs,induced by
the action of several mediators, notably
histamine, on vascular smooth muscle

20. Vasodilationfirst involves the
arterioles and then leads to the
capillary beds in the area. The result is
increased blood flow, which is the
cause of heat and redness
(erythema) at the site of
inflammation.
Vasodilationis quickly followed by
increased permeability of the
microvasculature, with the outpouring
of protein-rich fluid (an exudate) into
the extravasculartissues.

22. Microvasculature
permeable
RBC become
more
concentrated
Slowing of the
circulation
ChemotaxisMargination
Stasis
Protein-rich
fluid moves out
EV tissues
Increasingblood
viscosity

23. Increased vascularpermeability
Several mechanisms are responsible for
increased vascular permeability in acute
inflammation including:
1) Retraction of endothelial cells:
**leadingtointercellulargaps
It occurs rapidly after exposure to the
mediator (within 15 to 30 minutes) and is
usually short-lived; hence, referred to as the
immediate transient response.

24. Endothelial cellcontraction
Reversibleprocess
Histamine,bradykinin,leukotrienes,
and many other chemical
mediators.

25. 2. Endothelial injury
resulting in endothelial cell necrosis
and detachment.
Direct damage to the endothelium is
encountered in severe injuries, for
example, in burns, or is induced by
the actions of microbes and
microbial toxins that target
endothelial cells.

26. Immediate sustained response:
leakage begins immediatelyafter
theinjuryandpersistsforseveral
hours (or days) until the
damaged vessels are thrombosed
or repaired.

27. ❑Direct injury to endothelial cells may
also induce a delayedprolongedleakage
thatbeginsafteradelayof2 to 12 hours,
lasts for several hours or even days, and
involves venules andcapillaries.
❑Examplesincludemildtomoderate
thermalinjury,certain bacterial toxins,
and x-orultravoilet irradiation
❑In a thermal burn, leakage results
from chemically mediatedendothelial
contractionaswellasfromdirect injury
and leukocyte-mediated endothelial
damage.

28. Consequences of vascular
permeability
•Swollen finger or , swollen knee are
results of accumulation of fluid due
to inflammation
➢Exudate: due to inc vascular
permeability (inflammation)
➢Transudate: due to inc IVHP and
decreased oncoticpressure. (Edema)

31. Difference b/w transudate and exudate
Transudate Exudate
Found in fluid accumulation
without inflammation
Found in inflammation
Results from incIVHP or dec
colloid pressure
Results from increased
vascular permeability
Protein poor <2.5gm/dl Protein rich >2.9gm/dl
Specific gravity < 1.012) Specific gravity > 1.020
Neutrophils absent Neutrophils present
Very low cell count Cells are abundant
Clear Cloudy

32. Responses of Lymphatic
Vessels
In addition to blood vessels, lymphatic
vessels also participate in acute
inflammation.
Lymphaticsdrain the small amount of
extravascularfluid that seeps out of
capillaries under normal circumstances.
In inflammation, lymph flow is increased to
help drain edema fluid that accumulates
because of increased vascular
permeability.

33. Insevereinflammatoryreactions,
especiallytomicrobes,the lymphaticsmay
transport the offending agent.
Lymphangitis&lymphadenitis.
InflamedLymphnodesareoften
enlarged,becauseofhyperplasiaof
thelymphoidfolliclesandincreased
numbers oflymphocytesand
phagocyticcellsliningthesinusesof
thelymphnode.