Prepared By Cahat Ali for LearningHints.Com
The immune complexes and complement activation fragments also attract neutrophils Ultimately, it is the activated complement and the release of neutrophilic enzymes and other toxic molecules (e.g, oxygen metabolites) that cause the tissue damage in immune complex disease.
Type I, Hypersensitivity ( Allergy and Anaphylaxis)
Definition: Immunological reaction, developing withen minutes after combination of an antigen with antibody bound on mast cells or basophils, in already sensitized individuals. Depending upon the portal of entry:
Local reaction (Ag confined to particular site) that is merely annoying (hay fever, seasonal rhinitis) or severely debilitating (asthma)
The initial response , characterized by vasodilation vascular leakage , and smooth muscle spasm, usually evident within 5-30 minutes after exposure to an allergen and subsiding by 60 minutes.
A second late phase reaction that sets in 2-8 hrs later and lasts for several days.
The late phase reaction in characterized by more intense infiltrationof tissues with eosinophil and other acute and chronic inflammatory cells as well as by tissue destruction in the form of mucosal epithelial cell damage.
Molecule leading to cross linking of igE FcReceptors
Leukotriene (C4,D4 are vasoactive &spasmogenicWhile B4 chemotactic for NP ‘Ep Monocytes)
Prostaglandin : Bronchospasm & increased mucous Secretion)
PAF (platelet aggregation , release of histamine , Bronchospasm vasodilation , chemotactic)
Ctokines :TNF , IL-1 ,IL -3,4,5,6,
Milk & food Allergy
(e.g, drug metabolites)
Occur in the following situations:
maternal antibodies against Rhin a sensitized Rh negative mother cross the placenta and cause destruction of Rh-positivefetal red cells.
Against desmosomal proteins that lead toDisruption of epidermal intercellularJunctions
Mediated Cytotoxicity (ADCC)
Types that bear receptors for The FC portion of IgG; targets
Coated by antibody are lysedWithout phagocytosis orComplement fixation
certain instances (e.g, eosinophil mediated killing of parasites; lgE antibodies are used.
Motor end-plates of skeletalmuscles impair neuromusculartransmission with resultantweakness.
thyroid epithelial cellsand result in hyperthyroidism
Systemic Immune complex Disease
-Size of Immune complex
Removed from the circulation by mononuclear phagocyticcells and are there before relatively harmless.
Excess and are small are of intermediate size, and are cleared
Less avidly by phagocytosis cells, and therefore circulate
Longer-Status of mononuclear phagocyte system (over load or dysfunction.
Local Immune Complex Disease
Localized area of tissue necrosis resulting fromImmune complex vasculitis involving lgG&lgM
It is immunologic response to variety of intracellular microbe e.g
Mycobacterium, virus, protozoa,fungi,as well as condition like contact
Dermatitis, graft reiection.
- intracellular bacteria (Mycobacterium) and Viruses
-Extra cellular agents-Protozoa, fungi, and parasites
-Contact skin sensitivity(poison ivy)
-Transplant rejection and tumor immunity
Type IV Hypersensitivity can be subdividedInto
CD4+ T cells (tuberculine reaction, granulomatous Inflamation)
The Sequence of events
“ Reaction of vascularized living tissue to local injury”
Purpose: inflammation is a complicated defensive and protective mechanism of the body against and irritant which involves vascular, cellular as well as local tissue reaction.
In this process the blood flow to the effective area is increased and more blood is poured at the site so as to dilute the irritant, localized its effective or even destroys it.
Cardinal signs of inflammation:
Great increase in blood at inflamed area as the result of Hyperima.
Mainlydue to Hyperimia.
At site of inflammation there is increased heat . This also results from the increased blood . flow through area.
The inflamed are is pain full. Pain occur as increased the pressure upon and injury to nerve ending.
This is due to partly to mechanical swelling and partly to distribution of tissue.
Tissue Changes in the Inflammatory Process:
Immediately upon application of the irritant to the issue, the blood vessels are constricted. This is very short.
The momentary conditions of the vessels is quickly followed by their direction. Which occurs in arteriolesand vennules, and not capillaries.
Process of “Inflammation”:
1.Stimulus is recognized by the inflammatory cells . process i- e Macrophages, Histocytes. Mastocytes (PRRs) “Pattern recognizing Receptors’.
Changes in blood vessels:
As stimulus apply the blood vessels constrict.
As the endothelial cells lining swell now the blood flow diminished.
Due to flow of passage of plasma out of blood cause blood viscosity.
Now “Leukocytes” move towards endothelial Linning and make it rough and
“Margination”the leukocytes or no attract by “salectians are adhesion male cedes that ad here with integrinsmalecvles of Navtrqonils.
It now reduce the blood flow and stasis occur.
Changes in Blood Secretions:
The normal blood consist on two zone.
As the permeability of vessel leaked out as fan inflammatory Exudate.
Emigration of leukocytes: Extravasations
The process of moving of leukocytes out side of vessels is Called “ Emigration”
When the nasals is dial ate by grandees mast cells Phage stair
Diapedesis of Erythrocytes:
Distribution of erythrocytes RBCs toward peripheral and then leakage through the capillaries wall is called “Diapedesis”.
Out all cellular and internaladebri and having immune globulins which Phagocytosed. The pathogen, and enzymatic ally digested the cellular debries.
Plasma is blood is product g phoyocytosis form exudates.
This exudates cause swelling g pain .
Servos, RBCs, WBCs break down products, fibrinogen, tissue debris.
1.Acute non – Suppurative Inflammation:
Non- Suppurative inflammation is Characterized by the absence of pus formation .
(i) Serous enudafe comprises of lumph and occurs most often in serous cavities such as joints, tendons , sheath, pericardial sac, plural and peritoneal cavities, ventricles of the brain and meningeal space.
(ii) It occurs also in skin and mucous membranes in the from of blisters or vesicles
(iii) It is often the first enudate to appear on mucous surface in catarrhal inflammation.
(iv) the casuse is often a relatively milled irritant.
(i).Catarrhal exudates is thin, clear or slightly viscid in consistency produces by milled irritant acting upon mucous membrane .
(ii) it consist of lymph, mucin and descumated epithelial cells and leukocytes.
(iii) the most prominent element is mucin produce by the stimulatory action of an irritant on the mucous surface. During early stage, catarrhal enudate contains much lymph but later it mined with many leukocytes.
(i)Fibrous exudates may occur within tissue, upon mucous and serous surface.
(ii) where it has the appearance of a pale yellow or white membrane.
(iii) when associated with edema it imparts a jelly like consistency and is often called “ Gelatinous inflammation”
Haemorrhagic exudates is the result of injury to blood vessels by severe irritant. Such as bacillus anthraces. Member of pasturella group and some coccidian.
It the irritant is so severe as to cause out right necrosis of a tissue the condition is called Acute necrotic inflammation.
Chronic or non suppurative inflammation:
(ii) the most conspicuous cells of chronic inflammation is the fibroblast.
Which shows intensive proliferation.
(iii) During the early stage chronic lesions are quite cellular, but as time passes they become less cellular and proliferative changes take the upper hand.
(iv) Finally, the connective tissue cells become mature and the process no long remain inflammation. It is fully healed lesion which become firm and is designated of a pale yellow or white membrane as fibrous indurated, or organized tissue a fibroused quarter of cow udder fallowing chronic mastitisis good enample of this type .
Acute and fchronicsuppurative inflammation
(i) A large number of micro organisms are associated with pus formation.i.e they are capable of causing suppurative inflammation among them are staphylococci,Escherichia coli, corynaebacteriumpyogenes, Actinobaccillyusequnli, actinomycesbovis, and action bacillus lignieresi\
(ii) Beside pus formation organisms, some inorganic and forganic chemicals such as mercuric chloride, turpentine and croton oil, exert as similar influence.
(iii) Acute suppurative inflammation being in the same way as the same way as the non-suppurative inflammation .the principal difference of being that the predominant cells in the enuclate are neutrophils which are called microphages
(iv) The neutrophil which die during the inflammatory process liberate certain proteolysis enzyme from Lysosomes. Diget the dead tissue and fconvert it to semifluid, creamy mass called Abscess.
5. Chronic Suppurative inflammation confined to the rle in that the vascular change become less prominent and proliferative changes predominate.
Ordinarily that exudative changes are nto so prominent encept in a few cases such chronic suppurative rhinitis and chronic suppurativemeteritis.
(i) Although most of these cases of inflammation are of non. Suppurative or suppurative nature the granulamatous type is associated with certain specific infectious diseases transmissible to man and animals. These discases are caused by micro organisms which are either than bacteria, yeast, mould , fungi or protozoa produce chronic granulamatons reaction.
(ii) it granulamatous lesion the vascular changes ae at the minimum where as exudates changes are characterized by a small amount to fluid and excessive accumulation of inflamatexy cells. Particularly the large mononuclear leukocytes.
(iii) there is tendency for nodules formation at the site of local inflammatory reaction due to entensive proliferation of tissue macrophage or histiocytes.
The cellular reaction in chronic granulomatious inflammation this comprises of encessive proliferation of large mononuclear leucoytes.
Resolution. When blood nesses comes to the nomalayer the inflammation called nasality.
On the basis of duration:
O – 4 hours (A.I )
Fever is the abnormal elevation of body temperature is one of the most prominent systemic manifestations. especially when the inflammation is
associated with infection.
Fever is a syndrome in which there is beside rise of body temperature (pyrexia). A disturbance in metabolism and various functional distmbances such as increased in pulse rate. Anorexia nausea. Vomiting constipation increased these scanty urine and dehydrating.
Pathogen sis of fever:
Recently new facts have come to light regarding the production of fever its is new established that the venous factors mimed above do not withes produced Fever Direly hut that they act entirely by releasing endogens progens (Eps ) From the leucocytes.
It is know thought that cytokines. Mainly interleukin –I (ii-i)and tumor neurosis factor(TNE) are Involved in the origin of the fever . these cytokines are produce by leukocytes and perhaps also by the other cells in response to infections agents. Or to Immunology and toxic reactions and reactions and release to circulation. They reach the brain and interact with Vascular receptors in the thermoregulatory centre of the Hypothalamus. Either by direct action of the cytokines or more likely. Through local prostaglandin (PGE ) )Production. Information is transmitted from Hypothalamus. To the vasomotor cent. This result in sympathetic never stimulation. Vasoconstriction of the skin vessels. Decease in heart dissipation and fever
Among the most common causes of fever are bacteria,
CIRCULATION: increased pulse rate. Lowered blood pressure
RESPIRATION: increased respiration. This may be brought about by the action of CO2 on the respiratory rate. Due to increased metabolism of fever more Co2 produced.
The Course f the fever
Cold and region occur due to contraction of cancerous blood vessels.
These are beneficial and include: