WEEK 5 infl--5.pptx

8/10/2019 WEEK 5 infl--5.pptx

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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

WEEK 5 infl--5.pptx

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