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Inflammation

Today​ ​we​ ​are​ ​going​ ​to​ ​talk​ ​about​ ​“INFLAMMATION”,​ ​which​ ​comes​ ​after​ ​we​ ​have​ ​talked​ ​about
with​ ​Dr.Mohammad​ ​and​ ​Dr.Samir,​ ​cell​ ​injury..

Inflammation​ ​is​ ​divided​ ​into​ ​two​ ​types​ ​(​Acute​​ ​and​ ​Chronic​),​ ​Dr.Najlaa​ ​is​ ​going​ ​to​ ​ ​cover​ ​the​ ​first
type.

Now​ ​let​ ​us​ ​begin​ ​with​ ​our​ ​lecture…

What​ ​is​ ​inflammation?


It​ ​is​ ​a​ ​dynamic​ ​process​ ​of​ ​chemical​ ​and​ ​cytological​ ​reactions​ ​that​ ​occur​ ​as​ ​a​ ​response​ ​to
stimuli​ ​which​ ​cause​ ​cell​ ​injury​ ​in​ ​vascularized​ ​and​ ​viable​ ​tissue​.​ ​In​ ​simpler​ ​words
‘’Inflammation​ ​occurs​ ​because​ ​I​ ​want​ ​the​ ​soldiers​ ​in​ ​my​ ​body​ ​to​ ​go​ ​to​ ​the​ ​injured​ ​area
and​ ​get​ ​rid​ ​of​ ​the​ ​harmful​ ​agents’’.
Inflammation​ ​results​ ​in:
Accumulation​ ​of​ ​leukocytes,​ ​and​ ​fluid​ ​(Exudation)​ ​containing​ ​antibodies,​ ​plasma
proteins,​ ​chemical​ ​mediators,​ ​and​ ​chemicals​ ​in​ ​extravascular​ ​tissue;​ ​all​ ​resulting​ ​in​ ​the
process​ ​of​ ​inflammation​ ​at​ ​the​ ​site​ ​of​ ​injury.
And​ ​sometimes​​ ​–not​ ​always-​ ​inflammation​ ​is​ ​associated​ ​with​ ​systemic​ ​effects​ ​like​ ​fever,​ ​loss​ ​of
appetite​ ​or​ ​anorexia,​ ​and​ ​malaise.

Effects​ ​of​ ​Inflammation:


1-​Inflammation​ ​eliminates​ ​the​ ​cause​ ​of​ ​cell​ ​injury;​ ​a​ ​battle​ ​between​ ​the​ ​immune​ ​system
and​ ​the​ ​injurious​ ​agent.

2-​Inflammation​ ​eliminates​ ​the​ ​necrotic​ ​cells(​ ​that​ ​have​ ​resulted​ ​from​ ​the​ ​inflammatory
response​ ​).

​ ​ ​ ​ ​ ​ ​ ​3-​Inflammation​ ​paves​ ​the​ ​way​ ​for​ ​repair;​ ​replacing​ ​normal​ ​cells,​ ​including​ ​epithelial​ ​cells
and​ ​leukocytes,​ ​that​ ​have​ ​been​ ​lost​ ​in​ ​the​ ​process.

4-​Inflammation​ ​sometimes​​ ​leads​ ​to​ ​harmful​ ​results.

So​ ​inflammation​ ​is​ ​a​ ​bridge​ ​between​ ​our​ ​immunity​ ​and​ ​the​ ​injurious​ ​agent,​ ​for​ ​example​ ​:a​ ​heart
which​ ​contains​ ​necrotic​ ​cells,will​ ​eliminate​ ​this​ ​necrotic​ ​cells​ ​by​ ​elimination,​ ​“necrosis​ ​will​ ​not
remain​ ​forever”,​ ​and​ ​these​ ​necrotic​ ​cells​ ​will​ ​be​ ​replaced​ ​with​ ​epithelial​ ​cells,​ ​leukocytes…

Sometimes​ ​it​ ​might​ ​happen​ ​as​ ​a​ ​wrong​ ​response​ ​(autoimmune​ ​diseases)​ ​,​ ​or​ ​it​ ​might​ ​get​ ​out​ ​of
control​ ​and​ ​cause​ ​harmful​ ​effects(no​ ​negative​ ​feedback​ ​stopped​ ​it),​ ​so​ ​we​ ​can​ ​describe
inflammation​ ​as​ ​a​ ​“Double-edged​ ​sword”.
Nomenclature

In​ ​medical​ ​terminology​ ​inflammation​ ​is​ ​easily​ ​known​ ​by​ ​the​ ​suffix​ ​–i​ tis​ ​,​ ​it​ ​reflects​ ​the
inflamed​ ​organ.

Examples:

• Appendix ​ ​ ​ ​ ​ ​ ​ ​ ​ ​ ​ ​ ​ ​ ​ ​ ​ ​Appendicitis

• Dermis ​ ​ ​ ​ ​ ​ ​ ​ ​ ​ ​ ​ ​ ​ ​ ​ ​ ​ ​ ​ ​Dermatitis

• Gallbladder ​ ​ ​ ​ ​Cholecystitis

• Duodenum ​ ​ ​ ​Duodenitis

• Meninges ​ ​ ​ ​ ​ ​ ​ ​ ​ ​ ​ ​ ​ ​Meningitis

Causes​ ​of​ ​Inflammation:


The​ ​causes​ ​of​ ​cell​ ​injury​ ​are​ ​the​ ​same​ ​causes​ ​of​ ​inflammation

1-​Microbial​ ​infections​:​ ​ ​bacteria,​ ​viruses,​ ​fungi,​ ​parasites...etc


2-​Immunologic​: hypersensitivity when contacting allergens, causing autoimmune
reactions​ ​like​ ​asthma*​ ​and​ ​eczema.
3-​​ ​Physical​ ​agents​:​ ​ ​trauma,​ ​heat,​ ​cold,​ ​ionizing​ ​radiation.
4-​​ ​Chemical​ ​agents​:​ ​acids,​ ​alkali,​ ​bacterial​ ​toxins,​ ​metals.
5-​​ ​Foreign​ ​material​:​ ​sutures,​ ​dirt.
6- ​Tissue necrosis​: ischemic necrosis (or any type of necrotic debris/tissue) is eliminated
from the body and replaced by many alternations, mostly by fibrous connective tissue
formed​ ​by​ ​fibrosis.

*Asthma: inhaling certain allergens initiates a local reaction and leads to bronchospasm;
which​ ​is​ ​an​ ​inflammatory​ ​response.
The​ ​participants​ ​in​ ​Inflammation:
“inflammation is a war between my body and cellular injury,, the ​Soldiers are the
participants”

-White​ ​blood​ ​cells​ ​and​ ​platelets​​ ​(​The​ ​major​ ​participant​)

​ ​ ​ ​ ​ ​ ​ ​ ​ ​ ​Ex:​ ​Neutrophils,​ ​monocytes,​ ​lymphocytes,​ ​eosinophils,​ ​basophils..

-​Plasma proteins are proteins that are synthesized in the liver, but their inactive form is
found in the serum, and once stimulated by inflammation, they are activated, producing
other proteins and chemical mediators (we will talk about them in details in the future
InshaaAllah), each of these proteins will give active byproducts that have a specific role
in​ ​the​ ​inflammatory​ ​process.

​ ​ ​ ​ ​ ​ ​ ​ ​Ex:​​ ​Coagulation​ ​/fibrinolytic​ ​system,​ ​kinin​ ​system,​ ​complement​ ​system.

-Endothelial cells and smooth muscles of vessels (needs chemical regulators​) ​*epithelial
cells​ ​surround​ ​the​ ​smooth​ ​muscles​ ​in​ ​blood​ ​vessels​ ​anatomy*

-Extracellular​ ​matrix​ ​and​ ​stromal​ ​cells


Ex: ​Mast cells, fibroblasts, macrophages & lymphocytes​, ​Structural fibrous proteins,
adhesive​ ​ ​ ​ ​ ​ ​ ​ ​ ​glycoproteins,​ ​proteoglycans,​ ​basement​ ​membrane.

You​ ​need​ ​to​ ​know​ ​if​ ​a


participant​ ​is​ ​located
inside​ ​or​ ​outside​ ​a
vessel.
As​ ​mentioned​ ​in​ ​the​ ​beginning​ ​of​ ​the​ ​sheet,​ ​there​ ​are​ ​2​ ​types​ ​of​ ​inflammation;​​ ​acute
and​ ​chronic.​ ​And​ ​here​ ​is​ ​a​ ​brief​ ​comparison​ ​between​ ​these​ ​two​ ​types:

Acute Chronic
Duration:​ ​starts​ ​instantly;​ ​within​ ​minutes Duration:days​ ​to​ ​years
and​ ​lasts​ ​for​ ​days​ ​*early​ ​response* (​ ​starts​ ​after​ ​days​ ​and​ ​lasts​ ​for​ ​years)

Predominance​ ​of​ ​neutrophils Predominance​ ​of​ ​lymphocytes​ ​and


macrophages

Fluid​ ​&​ ​plasma​ ​protein​ ​exudation​ ​(more Vascular​ ​proliferation​ ​and​ ​fibrosis
fluids)
More​ ​swollen.

Notes:

-If​ ​the​ ​acute​ ​inflammation​ ​failed​ ​to​ ​eliminate​ ​the​ ​injurious​ ​agent​ ​it​ ​will​ ​change​ ​to​ ​the
chronic​ ​inflammation​ ​type.

-Fibrosis​ ​is​ ​the​ ​distinct​ ​feature​ ​of​ ​the​ ​chronic​ ​inflammation.

-Certain​ ​diseases​ ​are​ ​based​ ​on​ ​inflammation;​ ​a​ ​patient​ ​may​ ​live​ ​his​ ​life​ ​with​ ​an​ ​ongoing
inflammatory​ ​process.

-Presence​ ​of​ ​neutrophils​ ​is​ ​a​ ​very​ ​important​ ​indicator​ ​of​ ​acute​ ​inflammation.

Acute​ ​Inflammation:

Is​ ​an​ ​early​​ ​response​ ​of​ ​vascularized​ ​tissue​ ​to​ ​injury.


The​ ​aim​​ ​of​ ​acute​ ​inflammation​ ​:
1- The​ ​recruitment​ ​of​ ​neutrophils​​ ​to​ ​the​ ​injured​ ​area​ ​especially​ ​during​ ​the​ ​first​ ​3​ ​days,​ ​and
then​ ​ ​monocytes​​ ​(​macrophages)​​ ​(after​ ​3​ ​days)​ ​arrive​ ​to​ ​clear​ ​the​ ​cause​ ​of​ ​injury​ ​and
remove​ ​necrotic​ ​tissue/debris​ ​and​ ​pave​ ​the​ ​way​ ​for​ ​repair​ ​.
NOTE:​​ ​In​ ​normal​ ​conditions​ ​we​ ​do​ ​not​ ​find​ ​neutrophils​ ​outside​ ​blood​ ​vessels,
-these​ ​cells​ ​are​ ​synthesized​ ​in​ ​the​ ​bone​ ​marrow​ ​and​ ​after​ ​that​ ​stay​ ​inside​ ​blood
vessels-.
​ ​ ​ ​2-​​ ​Deliver​ ​plasma​ ​proteins​:​ ​Antibodies,​ ​plasma​ ​proteins,​ ​complement​ ​proteins,
chemical​ ​mediators,​ ​and​ ​others.

When​ ​any​ ​type​ ​of​ ​injury​ ​that​ ​causes​ ​inflammation​ ​happens​ ​there​ ​will​ ​be​ ​two​ ​events​ ​or
components​​ ​occurring:

1- Vascular​ ​change​​ ​(​In​ ​the​ ​area​ ​of​ ​injury​ ​we​ ​would​ ​have:​ ​Vasodilatation​​ ​followed​ ​by
increased​ ​blood​ ​flow​​ ​then​ ​ ​increased​ ​vascular​ ​permeability​(extravasation​ ​of​ ​fluids)
and​ ​lastly​ ​stasis​.

Stasis:​ ​Normal​ ​blood​ ​is​ ​composed​ ​of​ ​cells​ ​and​ ​plasma,​ ​but​ ​as​ ​an​ ​inflammatory​ ​response​ ​the​ ​fluid
leaks​ ​out​ ​of​ ​the​ ​vessel​ ​and​ ​the​ ​cells​ ​stay​ ​inside,​ ​this​ ​slows​ ​the​ ​flow​ ​and​ ​increases​ ​the​ ​viscosity
inside​ ​the​ ​vessels.

​ ​*​ ​A​ ​student​ ​asked​ ​about​ ​the​ ​defense​ ​mechanism​ ​which​ ​is​ ​driven​ ​by​ ​the​ ​leukocytes,​ ​how​ ​is​ ​it
accomplished​ ​if​ ​the​ ​cells​ ​stay​ ​inside​ ​the​ ​vessels?​ ​The​ ​doctor​ ​said​ ​that​ ​the​ ​leukocytes​ ​emigrate
out​ ​of​ ​the​ ​cells​ ​after​ ​the​ ​exudation​ ​of​ ​fluids​.

2- Cellular​ ​events;​ ​Emigration​ ​of​ ​cells​ ​from​ ​microvessels​​ ​*this​ ​is​ ​a​ ​very​ ​complicated​ ​event
that​ ​needs​ ​chemical​ ​mediators*​ ​ ​and​ ​accumulation​ ​at​ ​sites​ ​of​ ​injury).

Here​ ​is​ ​a​ ​sample​ ​taken​ ​from​ ​a​ ​patient​ ​who


suffers​ ​from​ ​acute​ ​inflammation​ ​of​ ​lungs
(pneumonia).
Notice​ ​that​ ​alveoli​ ​in​ ​normal​ ​people​ ​are
empty​ ​containing​ ​only​ ​air,​ ​but​ ​here​ ​due​ ​to​ ​an
inflammatory​ ​response​ ​it​ ​is​ ​not,​ ​instead​ ​it​ ​is
full​ ​of​ ​fluid,​ ​inflammatory​ ​cells,​ ​fibrin,
neutrophils​ ​and​ ​static​ ​RBCs​ ​ ​etc..
The​ ​five​ ​classic​ ​signs​ ​of​ ​acute​ ​inflammation:​ ​take​ ​any​ ​example

• Heat.

• Redness.

• Swelling​ ​(due​ ​to​ ​the​ ​accumulation​ ​of​ ​exudate​ ​fluid).

• Pain.

• Loss​ ​of​ ​function.

Vascular​ ​changes
Arteriolar​ ​dilatation​ ​follows:
​ ​1-​transient​ ​vasoconstriction​ ​(the​ ​doctor​ ​said​ ​it​ ​is​ ​not​ ​important​ ​as​ ​it​ ​occurs​ ​so​ ​fast)
​ ​2-​vasodilation​ ​and​ ​after​ ​that​ ​there​ ​will​ ​be​ ​an​ ​increase​ ​in​ ​the​ ​vascular​ ​permeability.
3-​Increased​ ​vascular​ ​permeability​ ​and​ ​stasis:
• Early​ ​phase​ ​Arteriolar​ ​vasodilatation​ ​→​ ​↑​hydrostatic​ ​pressure,​ ​resulting
in​ ​transudate.
● Late​ ​phase​:​ ​Leaky​ ​vessels​ ​results​ ​in​ ​the​​ ​loss​ ​of​ ​proteins​ ​(​ ​due​ ​to​ ​the
difference​ ​in​ ​oncotic​ ​pressure)→​ ​exudate​ ​(protein​ ​rich​ ​fluid)​ ​and​ ​stasis.
#​ ​The​ ​protein-poor​ ​fluid​ ​(​ ​due​ ​to​ ​the​ ​increase​ ​of​ ​ ​hydrostatic​ ​pressure​ ​across​ ​ ​blood
vessels)​ ​is​ ​called​​ ​transudate​ ​(inside​ ​the​ ​vessels).
#​The​ ​protein-rich​ ​liquid​ ​due​ ​to​ ​the​ ​increase​ ​of​ ​oncotic​ ​pressure​ ​is​ ​called​​ ​exudate
(outside​ ​the​ ​vessels).
4-​Margination​ ​of​ ​leukocytes;​ ​the​ ​process​ ​by​ ​which​ ​leukocytes​ ​migrate​ ​from​ ​inside​ ​the
blood​ ​vessel​ ​to​ ​the​ ​outside.
{​ ​In​ ​summary​ ​:​ ​when​ ​an​ ​injury​ ​occurs,​ ​the​ ​small​ ​blood​ ​vessels​ ​in​ ​the​ ​area​ ​constrict
(vasoconstriction)​ ​very​ ​momentarily.​ ​The​ ​blood​ ​vessels​ ​then​ ​dilate,​ ​causing​ ​an​ ​increase​ ​in​ ​blood
flow​ ​into​ ​the​ ​area.​ ​Blood​ ​vessels​ ​walls​ ​that​ ​normally​ ​allow​ ​only​ ​water​ ​and​ ​salts​ ​to​ ​pass​ ​through
become​ ​more​ ​permeable.​ ​Increasing​ ​the​ ​hydrostatic​ ​pressure​ ​results​ ​in​ ​transudate​ ​in​ ​the​ ​early
phase,​ ​followed​ ​by​ ​the​ ​late​ ​phase​ ​which​ ​creates​ ​exudate​ ​as​ ​a​ ​result​ ​of​ ​increasing​ ​oncotic
pressure.​ ​The​ ​final​ ​step​ ​is​ ​the​ ​migration​ ​of​ ​leukocytes​ ​from​ ​inside​ ​of​ ​blood​ ​vessel​ ​to​ ​site​ ​of
injury.​ ​}

How​ ​does​ ​inflammation​ ​lead​ ​to​ ​leakiness​ ​of​ ​endothelial​ ​cells?


Different​ ​mechanisms,​ ​depending​ ​on​ ​the​ ​cause​ ​of​ ​the​ ​injury​​ ​and​ ​the​ ​type​ ​of​ ​the
chemical​ ​mediator​ ​that​ ​is​ ​released​ ​as​ ​a​ ​result​ ​of​ ​this​ ​type​ ​of​ ​injury.
-​There​ ​are​ ​a​ ​couple​ ​of​ ​mechanisms​ ​of​ ​leakage​ ​or​ ​(vascular​ ​permeability)​ ​in​ ​acute
inflammation.

The​ ​1st​​ ​ ​mechanism


​ ​ ​ ​*​Endothelial​ ​cell​ ​contraction
● The​ ​ ​endothelial​ ​cells​ ​are​ ​packed​ ​tightly,​ ​but​ ​here​ ​these​ ​cells​ ​contract​ ​so
gaps​ ​will​ ​be​ ​formed​ ​between​ ​them​ ​and​ ​thus​ ​allowing​ ​the​ ​fluid​ ​to​ ​leak​ ​out
and​ ​causing​ ​edema​.​ ​This​ ​mechanism​ ​is​ ​usually​ ​reversible​​ ​once​ ​mediators
stop​ ​working​,​ ​and​​ ​it​ ​is​ ​called​​ ​Immediate​ ​transient​ ​response​ ​with​ ​short
life​,​ ​because​ ​it​ ​starts​ ​within​ ​seconds​ ​and​ ​lasts​ ​to​ ​minutes(15-30​ ​minutes)
● The​ ​chemical​ ​mediators​ ​that​ ​induce​ ​this​ ​reaction​ ​are:​ ​histamine,
bradykinin,​ ​leukotrienes,​ ​neuropeptide​ ​substance​ ​P.
● ​ ​Happens​ ​mostly​ ​in​ ​postcapillary​ ​venules.
The​ ​2nd​
​ ​ ​ ​mechanism

*Endothelial​ ​cell​ ​retraction


• Externally​ ​it​ ​looks​ ​like​ ​the​ ​first​ ​mechanism​ ​because​ ​gaps​ ​are​ ​formed
between​ ​endothelial​ ​cells,​ ​but​ ​structurally​ ​it​ ​is​ ​different​ ​and​ ​takes​ ​longer
time​ ​to​ ​appear​ ​because​ ​beside​ ​the​ ​change​ ​in​ ​the​ ​endothelial​ ​cells,​ ​the
cytoskeleton​ ​volume​ ​changes​ ​due​ ​to​ ​actin​ ​filaments​ ​rearrangement​ ​(outer
structure);​ ​it​ ​also​ ​takes​ ​more​ ​time​ ​to​ ​be​ ​reversed​ ​(Starts​ ​4-6​ ​hours​ ​after
injury​ ​and​ ​stays​ ​for​ ​24​ ​hours).
• Induced​ ​by:​ ​IL-1​ ​and​ ​TNF,​ ​IFN-​​ ​γ.

The​ ​3rd​
​ ​ ​mechanism

*Direct​ ​endothelial​ ​injury


• Severe injury (like a 3​rd degree burn); all vessels in that area will be
damaged​ ​or​ ​destroyed.
• Immediate sustained response (immediate because it starts immediately
and sustained because it needs a long time to repair the damaged blood
vessels).
• All​ ​microvessels​ ​can​ ​be​ ​affected.

The​ ​4th​
​ ​ ​mechanism
● *​Delayed prolonged response​“Delayed” reflects that it needs time to occur
which​ ​is​ ​2-12​ ​hours,​ ​however​ ​it​ ​lasts​ ​for​ ​hours​ ​or​ ​days.​ ​.
• Many types of injury could lead to this response but mostly is caused by thermal
injury, UV radiation and bacterial toxins; injuries that are ​not severe enough to
destroy​ ​all​ ​vessels.

The​ ​5th​
​ ​ ​mechanism

Leukocyte-dependent endothelial injury​(especially in the lungs when we


have adipocytes clustered there); called dependent because certain chemical
substances (mediators) can’t be released without the presence of leukocytes,
the​ ​leukocytes​ ​is​ ​the​ ​cause​ ​this​ ​endothelial​ ​injury.
The​ ​6th​
​ ​ ​mechanism
• Increased​ ​Transcytosis
• (endocytosis+exocytosis) through vesiculo vacuolar pathway Stimulated
by ​VEGF special mediator only (Vascular Endothelial Growth Factor) it will
lead to increase the permeability by forming channels inside endothelial
cells themselves ​(not in the gaps) ​and thus increasing transcytosis
(endocytosis)

As​ ​a​ ​general​ ​rule;​ ​any​ ​newly​ ​formed​ ​blood​ ​vessel​ ​will​ ​be​ ​leaky​,​ ​because​ ​the​ ​tight
junctions​ ​between​ ​the​ ​endothelial​ ​cells​ ​and​ ​the​ ​supportive​ ​tissue​ ​surrounding​ ​it​ ​are​ ​not
yet​ ​formed​ ​properly.

​ ​*A​ ​student​ ​asked,​ ​do​ ​any​ ​RBCs​ ​leak​ ​out​ ​of​ ​the​ ​vessels?​ ​The​ ​doctor​ ​said​ ​yes​ ​in​ ​a​ ​small
amount​ ​but​ ​the​ ​plasma​ ​is​ ​more​ ​in​ ​volume,​ ​and​ ​when​ ​the​ ​leakage​ ​of​ ​RBCs​ ​increase​ ​its
called​ ​a​ ​hemorrhage,​ ​not​ ​leakage.*

​ ​Exudation​ ​of​ ​fluid


*​ ​Fluid​ ​that​ ​is​ ​accumulated​ ​out​ ​of​ ​blood​ ​vessels​ ​in​ ​a​ ​location​ ​is​ ​called​ ​Edema​​ ​(one
of​ ​the​ ​consequences​ ​of​ ​ ​vascular​ ​changes​ ​in​ ​acute​ ​inflammation).
*​ ​Sometimes​ ​it​ ​is​ ​mild​ ​and​ ​tolerable,​ ​as​ ​illustrated​ ​on​ ​the​ ​right​ ​side,
​ ​ ​ ​ ​and​ ​sometimes​ ​it​ ​is​ ​a​ ​dangerous,​ ​life​ ​threatening,​ ​infectious​ ​and​ ​fatal
​ ​ ​especially​ ​if​ ​it​ ​occurs​ ​in​ ​a​ ​critical​ ​organ.​ ​For​ ​example;​ ​edema​ ​in​ ​the​ ​larynx​ ​or
​ ​epiglottis​ ​blocks​ ​the​ ​airway​ ​and​ ​damages​ ​ ​blood​ ​vessels.
{e.g: after burning your hand it becomes red and painful after awhile you will see a
blister​ ​which​ ​is​ ​extravasated​ ​fluid​ ​(transudate:​ ​protein​ ​poor​ ​fluid)}

*A​ ​student​ ​asked:​ ​Is​ ​the​ ​exudate​ ​fluid​ ​sterile​ ​or​ ​not?
The​ ​doctor​ ​answered:
It depends on the cause of the leakage, for example if it was a
burn​ ​it​ ​is​ ​sterile,
unless a secondary infection occurs, but if it was due to a
bacterial​ ​infection​ ​for​ ​example,​ ​it​ ​isn’t​ ​sterile.​ ​*
TRANSUDATE EXUDATE

• Mechanism:​ ​Hydrostatic​ ​pressure • Mechanism:​ ​An​ ​alteration​ ​in​ ​normal


imbalance​ ​across​ ​the​ ​vascular permeability​ ​of​ ​small​ ​blood​ ​vessels​ ​in
endothelium. the​ ​area​ ​of​ ​injury.

• Fluid​ ​of​ ​low​ ​protein​ ​content • Fluid​ ​of​ ​high​ ​protein​ ​content​ ​(>3g/dl)
(ultrafiltrate​ ​of​ ​blood​ ​plasma). &​ ​increased​ ​cellular​ ​debris.

• Specific​ ​gravity​ ​<1.012. • Specific​ ​gravity​ ​>1.020.

*Notes:
-Transudate​ ​does​ ​not​ ​contain​ ​microorganisms.
-Specific​ ​gravity:​ ​measured​ ​by​ ​a​ ​machine,​ ​it​ ​reflects​ ​the​ ​amount​ ​of​ ​protein​ ​in​ ​the
fluid

0
Cellular​ ​Events

❖ Margination,​ ​rolling​ ​and​ ​adhesion


■ *Margination:​ ​the​ ​blood​ ​contains​ ​cells​ ​and​ ​plasma​ ​fluid,​ ​and​ ​in
normal​ ​blood​ ​flow,​ ​the​ ​plasma​ ​fluid​ ​is​ ​the​ ​component​ ​that​ ​comes​ ​in
contact​ ​with​ ​the​ ​endothelial​ ​cells.​ ​But​ ​in​ ​inflammation​ ​the​ ​fluid
leaks​ ​from​ ​the​ ​vessels,​ ​so​ ​the​ ​leukocytes​ ​now​ ​come​ ​in​ ​contact​ ​with
the​ ​endothelial​ ​cells.​ ​(Peripheral​ ​orientation​ ​of​ ​the​ ​leukocytes​ ​from
the​ ​center​ ​of​ ​the​ ​blood​ ​stream​ ​will​ ​move​ ​to​ ​periphery​ ​and​ ​come​ ​in
contact​ ​with​ ​the​ ​endothelial​ ​cells)​.
■ Margination​ ​decreases​ ​the​ ​speed​ ​of​ ​cells,​ ​as​ ​cells​ ​keep​ ​trying​ ​to
attach​ ​until​ ​weak​ ​adhesion​ ​is​ ​formed(rolling),​ ​this​ ​is​ ​followed​ ​by
firm​ ​adhesion;​ ​cells​ ​become​ ​fixed​ ​to​ ​endothelial​ ​cells).
❖ Transmigration​ ​between​ ​endothelial​ ​cells.
❖ Migration​ ​in​ ​the​ ​interstitium​ ​toward​ ​the​ ​site​ ​of​ ​stimulus​ ​(inflammation​ ​area).
❖ Phagocytosis​ ​and​ ​degranulation​​ ​(degrades​ ​offending​ ​agent).
❖ Release​ ​of​ ​leukocyte​ ​products.

Neutrophil​ ​migration

- This​ ​was​ ​the​ ​first​ ​time​ ​for​ ​me​ ​to​ ​publish​ ​a​ ​sheet​ ​to​ ​the​ ​whole​ ​batch,​ ​so​ ​please​ ​forgive​ ​me​ ​for​ ​any
unintentional​ ​mistakes,​ ​if​ ​you​ ​have​ ​any​ ​question​ ​do​ ​not​ ​hesitate​ ​to​ ​ask​ ​and​ ​I​ ​will​ ​try​ ​my​ ​best​ ​to​ ​help,
​ ​ ​ ​ ​Your​ ​colleague​ ​Malak​ ​Khasawneh