inflammation Flashcards
- Inflammations: definition, causes, Celsian Signs
Definition:
An inflammation is an unspecific reaction of the organism towards the harmful action of inflammatory factors:
• by an inflammatory reaction the tissue tends to locate and eliminate inflammatory agents, altered metabolic cells, germs and foreign particles, which do not belong to the normal structure of that tissue.
Inflammation terminology:
inflamed organ = the suffix is “itis”
Inflammations can be:
acute: short duration ( up to a few days)
chronic: long duration (over six months)
The clinical signs of acute inflammations are the Celsian signs
Rubor: redness of the area because of local congestion
Tumor: the tumefaction of the area because of the local inflammatory edema
Calor: the heating up of the area because of the arterial blood deposit in the capillary bed
Dolor: pain in the inflamed area, under the action of the chemical mediators set loose locally and because of compression, through an edema, of the local nervous fillet
Funtio laesa (Gallenus added this element in 2nd century AD): the decrease of the functional capacity of the inflamed area because of the pain and the local edema
- Pathological features of inflammations: alteration, exudation, proliferation
WHAT ARE THE PATHOLOGICAL FEATURES OF INFLAMMATIONS?
The pathological characteristics of inflammations are:
alteration
exudation
proliferation
1. Alteration:
the dystrophic influence of the cells from the inflammatory point (hydropic dystrophy, fatty dystrophy or necrosis).
The parenchymatous organs are more frequently influenced:
the myocardium, the liver, the kidneys.
It is more evident in acute inflammations.
Etiopathogenesis:
the direct toxic action of the phlogogenic agents on the cells (toxic substances, toxic microbes)
hypoxia produced by vascular modifications
2. Exudation:
vascular modifications and extravasation of some haematic elements that appeared in acute inflammations
Vascular modifications
Caliber and blood flux modifications
• The arteriolar vein-construction phase: is short and appears under the action of some neurogenic agents and chemical mediators.
• The arteriolar vein-dilatation phase: the precapillar sphincter and the new capillar beds; in this situation the active hyperemia (congestion)
• The stasis phase (passive hyperemia): appears after a few hours and lasts a few hours
The increase in vascular permeability
• normally, between the endothelial vascular cells there are junctions and only very small molecules can pass between them (plasmatic ultrafilterred)
• Increased permeability of the capillaries and the venules appears in acute inflammations through the active contraction of the actin filaments of the endothelial cells. These retract, intercellular junctions separate and endothelial intercellular spaces appear, which allows a significant increase of permeability
Inflammatory exudation (inflammatory edema)
• a large quantity of liquid moves from the blood into the interstitium due to hyperemia and the rise of vascular permeability
• the composition of the exudate is similar to that of the plasma containing immunoglobulin, complement and fibrinogen (the exudated fibrinogen is transformed into fibrin under the influence of the thromboplastin tissue)
• unlike exudate, transuded represents a way out of the liquid from blood-vessels by raising the hydrostatic pressure under normal vascular permeability
Cellular response
Types of cells implicated in inflammations:
• polymorphonuclear cells (PMN), especially neutrophilic cells which dominate the first phase (24 hours) and are present in the inflammatory process for a few days.
• after 24-48 hours the macrophage cells and the immunologically active cells (lymphocytes and the plasmocytes) appear.
The neutrophilic cell margination
• normally, the blood’s figurative elements circulate axially (towards the center of the blood-vessel) being separated from the endothelial cells by the haematic plasma.
• in hyperemia of acute inflammation, the blood circulation is modified: the red blood-cells gather in rolls and the neutrophilic cells move to the margin (the marginalization of the leucocytes) and some cling to (pavement) endothelial cells.
The migration of the neutrophilic cells
• the attached neutrophilic cells actively go through intercellular junctions, then through the basal membrane, then into the interstitial spare (the penetration of the wall takes 2-10 minuntes)
Chemotactic agents
• in the interstitium, the neutrophilic cells move actively towards the inflamed area under the influence of the chemotactic agents (which cling to the leucocytes and “drag” them towards the infected area)
Phagocytoses
• phagocytoses is the property to recognize, ingest and digest alien structures from the body (inflammatory agents, cellular detritus, etc.)
• it occurs in three stages:
– 1: the recognition of the pathogen agent,
– 2: the ingestion of the pathogen agent (they surround it with a membrane, form a phagosome, which then adheres to the lysosome forming the phagolysosome),
– 3: the destruction of the micro-organism by cellular bactericide agents
Proliferation
• the cell deposit at the inflamed area
• it can be diffuse in the organism or localized (granulomatous inflammations)
• it is more characteristic of chronic inflammations
In the inflamed area, the following accumulates:
Cells of sanguine origin:
• PMN (are characteristic of acute bacterial inflammations)
• Monocyte macrophage specialized macrophage cells such as: epithelioid cells, Langhans gigantic cells, alien body gigantic cells, etc. (they are characteristic of chronic inflammations)
• B lymphocytes immunoblast plasmocyte and T lymphocyte immunoblast T lymphocyte sensitized (they are characteristic of acute inflammations caused by viruses, bacterial toxins, parasites, chronic inflammations of any etiology)
Local cells: reactive proliferation
• Examples:
– epithelial pavement cells in acuminate condylomas (under the influence of the Papilloma virus)
– epithelial secretion cells in chronic gastritis
- Inflammations of the pavimentous epithelium: serous, fibrinous and suppurative examples of inflammation
SEORUS - On surfaces
On pavimentos epithelium (the tegument and mucous tissues)
Etiology;
• chemical and physical factors
• viruses (varicella-zoster v., herpetic v.)
• type I reactions of hypersensitivity (urticaria)
Macroscopic feature:
• macula (flat, red area)
• papula (higher, red area)
• vesicle (liquid deposit, less than 1 cm diameter)
• bulla (liquid deposit, more than 1 cm diameter)
Microscopic feature:
macula: blood-vessel congestion in the superficial derma
papula: the liquid deposited in the epidermis removes the keratinocytes (intercellular edema), this situation is also called spongiosis
vesicule : liquid deposit in the epidermis (epidermis vesicle), deposit also at the dermo-epidermis junction (dermo-epidermis vesicle)
The evolution of the vesicle\bulla:
on the tegument : the vesicle breaks and an ulceration remains, a crust forms on top of it, the epithelium recovers and the lesion heals
on the mucous : the vesicle breaks, but the ulceration is not covered with the crust but with fibrin (fibrin pseudomembrane)
in profound ulcerations, lesions are called aphtha (aphthous inflammations), they are lesions that heal slowly
The evolution of the serous inflammation:
it heals
it worsens if the sero-fibrinous sero-purulence, sero-haemorrhagic, sero-fibrinous-haemorrhagic inflammation appears
FIBRINOUS - On surfaces The diphtheria croup Etiology: • the diphtheria bacillus Localization: • at the level of the superior airy wave Macroscopically: • thick, white-grayish pseudomembranes at the throat (the pharynx, the larynx, the trachea) Microscopically: • fibrin pseudomembranes, at the subjacent level there is the congestive mucous, the edema, the PMN infiltrate Evolution: • the pseudomembranes can detach themselves producing larynx obstructions
SUPPURATIVE - On surfaces
The pustule:
vesicles with suppurative content
The folliculate:
superficial inflammation of the hair follicle
The furuncle:
the inflammation affects several hair follicles and subcutaneous cellular tissue
Carbuncle:
it is an agglomeration of furuncles
Suppurative hydrosadenitis:
it affects the deep follicular structures and the sudoriparous glands (situated mostly under the armpit)
- Morphology of the pus: macroscopy, microscopy
The macroscopic feature of the pus: yellow, creamy fluid (staphylococcus) whitish or haemorrhagic liquid (streptococcus) grayish, bad smelling (b.coli) blueish (pyocianic)
The microscopical feature of the pus:
pathogen agents (microbial colonies, with basophil aspect in H.E. tint)
cellular detritus (necrosed, local cells)
PMN which can be:
• normal aspect
• with a phagocytized pathogen agent
• piocitos or pus globules (PMN with fatty dystrophy under the action of the pathogen agent)
• necrosed (under the influence of the pathogen agent)
- Abscesses: acute, chronic
The abscess: circumscribed suppurative inflammation Etiology: • staphylococcus aurae (more frequent) Localization: • the brain, • the lung, • the myocardium, • the kidneys, • the liver
The recent abscess (acute)
Macroscopic feature:
• the area is well defined ; it is round and yellow-whitish
Microscopic feature:
• local PMN deposit, microbial colonies, cellular detritus
• on the periphery of the abscess : congestion, xanthomatous granulation tissue
Evolution:
• healing (with AB treatment)
• It becomes chronic
The old (chronic) abscess
Macroscopic feature:
• the well defined and round area
• in the middle of the area there is pus
• on the periphery: the conjunctive capsular wall
Microscopic feature:
• the central area: pus (necrosis of liquefaction) made up of PMN variants, the etiological agent, the local cellular detritus
• on the periphery: conjunctive tissue (the organization of the granular tissue) coated by a fibrin pseudomembrane. In its eyes there are microbial colonies (the pyogenic membrane).
Evolution:
• Surgical treatment: the incision and excision of the pyogenic membrane, and then AB treatment
• Spontaneous fistulization: the pus under pressure migrates along the lines of minimal resistance and it is evacuated towards the surface, the cavity closes and cicatrizes.
An infected tooth as seen in an x-ray.The dark circle
around the root tip is an advanced dental abscess.
- Complications of the suppurative inflammation
Complications of the suppurative inflammation:
bacteriemia:
the free circulation of bacteria in the blood without serious consequences to healthy people
septicemia:
the circulation and multiplication of the microbes in the blood (clinically : hemocultures +)
septicopyemia:
the circulation and the multiplication of microbes in the blood, with secondary suppurative effects upon various organs.
- The catharal inflammation
WHAT ARE CATARRHAL INFLAMMATIONS? Definition: the catarrhal inflammation is an exudative inflammation which appears on the surface of the oral-cilindric mucous tissues. The exudation is called catarrh (it means: to drain on the surface). The catarrh can be: serous mucous suppurative hemorrhagic mixed (mucous-suppurative, serous-haemorrhagic, etc)
Etiology:
physical agents (the cold), chemical (the alcohol)
viruses, bacteria
allergy agents
Acute catarrhal inflammation:
Macroscopic:
• congestioned mucous tissue, sometime with ulcerations and haemorrhages and the surface exudates is most often mixed.
Microscopically:
• congestion, edema, small areas with ulcerations, inflammatory cells, hyperplasia of the mucous tissue cells, mucus hyperproduction.
Catarrhal stomatitis
- Granulomatous inflammations: tuberculoid and foreign body granulomas
The predominantly proliferative inflammations can be:
Diffuse:
• the inflamed cells are diffuse in the organ. Ex. glomerulonephritis, myocarditis, hepatitis, etc.
Local:
• the inflammatory proliferation has a nodular aspect, the lesions are called granuloma, and the inflammation is called granulomatous inflammation.
Examples of granulomas:
Tuberculoid granuloma
it is characteristic of tuberculosis, but it has the same aspect in other lesions as well: sarcoidosis, syphilis, beryllosis, the cat claws disease, Crohn disease, granulomatous orchitis, granulomatous prostatitis, granulomatous thyroiditis.
macroscopiscally:
• nodular lesion, pseudo-tumoural
microscopically:
• the central area with total necrosis, eosinophilia, surrounded by epitheliod cells (long, situated in groups like the epithelial cells) and gigantic Langhans cells (large cells with numerous nuclei situated on the periphery of the cell) and on the periphery of the granuloma there are numerous lymphocytes (the lymphocytic “crown”)
Foreign body granuloma
It appears around foreign bodies that came from outside the body (talc/chalk, catgut, parasytes, silicium, coal, calcium etc.) or from inside the body (cholesterol chrystals, urates, cytosteatonecrosis, hemosiderin, etc)
the granuloma is made up of:
• PMN, macrophages, epitheliod cells, foreign body gigantic cells (large cells with numerous nuclei randomly situated in the cell), lymphocytes, plasmocytes, xantomathous cells, siderophage cells.
Candidiasis
WHAT IS CANDIDOSIS?
Definition:
candidosis is an inflammation caused by a fungus
Etiology:
Candida albicans which can be:
• Saprophyte: in the oral cavity, in the digestive tract, in the respiratory tract, in the vagina, on the tegument
• Pathogen: when the immune defense mechanism does not function
Local favourable factors:
traumatisms, burns, ulcerations, surgical interventions, catheterism
a wet environment and rubber clothes
treatments with antibiotics
General favourable factors:
AIDS patients, hereditary deficiencies of the cellular immunity
Diabetes melitus, malignant tumors, leukemia, anemia, polyendocrine disorders
Pregnancy, birth control pills
Treatments with corticoids, cytostatic immune-suppressors
Types of candidosis:
Superficial Candidosis
It appears in wet, warm areas that undergo maceration
On the skin:
• in the axilar region and in the inguinal area, under the mammar area, in the interdigital area or between the buttocks
• eczematous and granulomatous lesions, abscesses
At fingernails
• onychomycosis at the finger nail and paronychia of the perinail tissue
On the mucous membranes
• The oral cavity, the tongue, the mucous membrane of the cheek, the oral comissures
• It is a whitish and soft deposit which can be removed by scratching, and underneath the mucous membrane is irritated, red (the leukoplasia is also white but it cannot be removed by scratching)
• It also appears on the esophagus, the stomach, the intestines (candidosis on the esophagus signals AIDS)
• the vulva and the vaginal mucosa is also affected
Invasive candidosis at the heart: • vegetative endocarditis kidneys, lungs, liver, brain: • abscesses it can also cause: • meningitis, enteritis, arteritis, osteomyelitis
Microscopical feature: under the shape of levuri : small round structures under the form of pseudohyphae under the form of hyphae: like bamboo sticks, narrow, septate, without branches Colorations/Stains H-E: red PAS: red Methenamine sylver: black
Evolution:
the antimycotic treatment and the removal of the cause
- Regeneration of the epithelias and healing of wounds
HOW DOES THE REGENERATION OCCUR?
The regeneration of the epithelia
Cilindric single-layer epithelium
• When the basal membrane of the epithelium is not affected, the epithelium is regenerated through the replication of the cells from the margin of the drawback
stratified epithelium ( squamous)
• when the spinal cells (keratinocytes) are affected, the epithelium is rebuilt from the level of the basal cells which multiply and differentiate replacing the affected cells.
• when the basal cells are also affected, the basal stratus is first reconstructed and then it is differentiated upwards (spiny strata) to the surface of the epithelium
the visceral epithelium
the liver:
• when the hepatocytes are affected and the basal membrane stay intact, the hepatocytes divide on the path of the basal membrane, rebuilding the liver structurally and functionally.
• when the basal membrane are also affected, the hepatocytes regenerate in a disorderly way, they have a nodular unfunctional aspect (ex. cirrhotic nodules).
the kidney :
• when the cells of the urinary tubes are affected without harming the basal membrane of the tubes, the epithelial cells recover along the basal membranes, restructuring the kidney functionally
• when the tubular basal membranes are also affected, the epithelial cells multiply chaotically without rebuilding the kidney’s structure and function
the lung
• the pneumocytes can regenerate functionally when the alveolar BM are intact
• if the alveolar BM is affected, pulmonary fibrosis appears
HOW DOES THE HEALING PROCESS OCCUR?
The healing of the wounds
The « per primam intentionem » healing
• in small, aseptical surgical wounds with regular and close margins
• the lesion affects the epidermis and the derma.
• The healing stages :
– hemorrhage with the formation of a clot that fills the drawback, a crust forms on the surface (by dehydration)
– the basal cells proliferate from the margin of the wound under the crust rebuilding the basal stratum from which in time the spinous strata will be differentiated
– PMN and Mf invade the clot and form a granulation tissue
– collagen is produced from the periphery of the wound in order to tie the margins of the wound
– the lesional area is transformed into scarred conjuctive tissue
« per secundam intentionem » healing
• between the lips of the wound there are infections, foreign bodies, cellular remains
• in the first stage the surgical cleaning of the wound occurs (clean and straight margins)
• in the second stage the actual healing begins as in the previous case
