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II-Non suppurative Inflammation
1- Serous InflammationAcute inflammation characterized by
excess serous exudate
This is characterized by an outpouringof a thin fluid that is derived from
either the blood serum or secretion ofmesothelial cells lining serous cavities.
e.g. burns and herpes simplex whichshow epidermal vesicles full of serous
containing few inflammatory cells.Serous inflammation usually observed
in the serous membranes
e.g. pleura, pericardium, synovialmembrane and peritoneum.
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2. Catarrhal InflammationDefinition:Mild acute inflammation of the mucousmembranes characterized by excessmucus secretione.g. catarrhal rhinitis, bronchitis, ... etc.
Gross Picture:
(a) Early the mucous membrane appears red, hot,swollen and dry. Dryness is due to temporarycessation of mucus secretion.
(b) Then excess waterymucoid discharge appears,composed of inflammatory fluid exudate, mucus,small number of polymorphonuclear leucocytes andshaded epithelial cells. When the polymorphs
increase the discharge becomes thick and yellowish.
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Microscopic Picture
Microscopic Picture:
(a) Mucosal cells appearswollen and rounded due to
mucus accumulation(mucoid change) and mayrupture or desquamate.
(b) The submucosa showshyperaemia, inflammatoryoedema and mildpolymorphonuclearleucocytic infiltration.
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3-Fibrinous Inflammation
Acute inflammation
characterized by anexudate rich infibrinogen which
converted to fibrin.The fibrin mixed with
inflammatory cellsmainly neutrophils,macrophages andplasma cells.
Occurred in mucous
and serous membrane.
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4-Membranous Inflammation
(Pseudomembranous or Diphtheritic)Definition: Severe acute inflammation
characterized by the formation of apseudomembrane on the affected surface e.g.diphtheria
Pathogenesis: The bacteria produce powerful
exotoxin which causes patchy mucosal necrosis.The exotoxin is absorbed in the blood streamcausing severe toxaemia.
Gross Picture:
Early the mucosa is congested and shows smallgrayish yellow patches of necrosis.
Next a yellowish white slightly elevatedpseudomembrane is formed on the surface.
The membrane is adherentand its removal leavesa bleedin surface
Pseudome
mbranouscolitis
Diphtheroid
pseudomem
brane
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Microscopic Picture
(a) The pseudomembrane is formed of
necrotic cells, bacteria and acute
inflammatory cells held together by a
fibrin network.
(b) The submucosa shows hyperaemia,
inflammatory oedema, fibrin network
and acute inflammatory cells in the
form of polymorphonuclear leucocytes,
pus cells, macrophages and RBCs.
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5- Sero-Fibrinous Inflammation
Definition: Acute inflammationcharacterized by the formation ofexcess fluid exudate rich in fibrine.g. inflammation in serous sacs(pleura, pericardium andperitoneum).
Gross Picture:
(a) Earlythe serous surfaces showmany hyperaemic vessels.
(b) Next the visceral and parietallayers become thickened, opaque,grayish yellow
(c) An inflammatory serous fluidcollects in the serous sac.
t
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croscop c cture(a) The fibrinogen changes
to fibrin forming a
network on visceral and
parietal layers entangling
acute inflammatory
(polymorphs, pus cells,
macrophages and RBCs).
(b) The serosa shows
hyperaemia, inflammatory
oedema, fibrin and acute
inflammatory cells.
Polymorpho--
nuclear leucocytes
fibrin network
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6- Haemorrhagic Inflammation
Acute inflammation
characterized by cellular
exudate rich in the bloodcells due to vascular
damage
e.g. smallpox andstreptococcal hemolyticus
infection.
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7- Necrotizing Inflammation
Acute inflammation
characterized by
marked tissuenecrosis e.g. Viral
hepatitis, Typhoid
fever.
Appendix
Gallbladder
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8-Allergic Inflammation
It is a type of acuteinflammation characterized
by cellular reaction mainly
eosinophils andmast cells.
The main cause of allergy is
progressive reaction of
human body against certain
foreign protein e.g.
bronchial asthma, drug,
food, pollution.
Eosinophilic myositis
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COURSE OF ACUTE INFLAMMATION 1) Resolution: Means complete restoration of the
inflamed area to normal.
(2) Regression and Healing: The body defenseovercomes the irritant. Part of the necrotic tissue, deadcells and fibrin are removed by the macrophages. Theliquefied part together with the fluid exudate are
drained by the lymphatics and veins. (3) Progression and Spread: The bacteria overcome
the defense mechanism and inflammation spreadsdirectly, by lymphatics and by blood causing fatal
septicaemia. (4) Chronicity: The causative agent is partially
overcome, but the body is unable to get rid of itcompletely. It remains as a weak irritant acting on the
tissue for a long time, thus acute inflammation changesto a chronic one.
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(3) Neurofibromatosis
A hereditary familialdisease transmitted as adominant trait. The disease
is characterized by:
(a) Multiple neurofibromas
which appear as small firmnodules in the skin alongthe course of the
cutaneous nerves.
(b) Cafe au lait skinpigmentation.
(c) Pigmented irishamartomas called Lisch
nodules.
Malignant tumours:Malignant Schwannoma
(neurofibrosarcoma).
Multiple neurofibromas
Cafe au lait skin
Malignant NeurofibromaPlexiform Neurofibroma