Inflammation & Pathology Review

• Pathology involves the study of disease, including its causes, nature, and effects on tissues.
• Pathology includes definition and Etiology which are involved in the causes of disease.
• Pathogenesis is the mechanism of the development of a disease.
• Pathology includes the pathological picture, which is either the gross picture (naked-eye changes), the microscopic picture (changes seen by microscope), or the fate (end results of the disease).
• The fate in pathology involves the end results of the disease, whether healing, complications, or death.

Causes of Cell Injury

• Living irritants, like bacteria, their toxins, viruses, parasites and fungi, can cause cell injury.
• Physical hazards like excess heat, cold, or radiation are considered non-living irritants that can damage cells.
• Chemical examples such as acids, alkalis and poisons cause cell injury as a non-living irritant.
• Non-living mechanical irritants include trauma and friction, which can damage cells.
• Hypoxia, the decrease in oxygen supply, as in anemia, can cause cell injury.
• Ischemia, the decrease in blood supply, as in arterial occlusion, causes cell injury.
• Immunological reactions can also cause cell injury
• Nutritional disturbances will cause cell injury
• Genetic disorders cause cell injury

Inflammation

• Inflammation is a biological and protective reaction of living tissues to an irritant, and it can be acute or chronic.
• Inflammation results from all causes of cell injury, with living irritants being the main cause.
• The suffix "itis" is added to an organ's name to denote its inflammation.

Acute Inflammation

• Acute inflammation has a rapid onset and short duration.
• Acute inflammatory reaction includes local tissue damage, where central cells undergo necrosis and surrounding cells undergo degeneration.
• The second feature of acute inflammatory reaction is local vascular reactions, including transient vasoconstriction.
• Transient vasoconstriction occurs as a direct vascular smooth muscle response to an injurious stimulus, lasting seconds or minutes. -Vasodilatation results from the effect of chemical substances like histamine, serotonin, bradykinin, and kallikrein.
• Vasodilatation leads to increased blood input and hydrostatic pressure and slowing of circulation.
• Increased vascular permeability results from the effect of inflammatory mediators like histamine, bradykinin and leukotrienes, mainly in venules.
• Increased vascular permeability accompanies vasodilation, leading to the formation of protein-rich exudate and tissue edema.
• Inflammatory fluid exudates form due to increased capillary permeability, intravascular and extravascular hydrostatic & osmotic pressures, and increased fluidity of the ground substance.
• Formation of inflammatory fluid exudate and vascular leakage is due to:
  • Increased capillary permeability
  • Increased intravascular hydrostatic pressure
  • Increased extravascular osmotic pressure
  • Increased fluidity of the ground substance.

Function & Fate of Inflammatory Fluid Exudates

• Inflammatory fluid exudates dilute irritants with their toxins and bring antibodies from blood
• Fibrinogen coagulates into fibrin to localize the irritant and form a network for phagocytic/repair cells to move on.
• Inflammatory fluid exudates also bring nutrition to cells and remove waste products.
• Fluid exudates that drain into lymphatics can carry bacteria & toxins, causing lymphangitis and acute lymphadenitis, enlarging the nodes.
• Exudates can carry bacteria/toxins causing toxemia, bacteremia, or septicemia.

Cellular Exudates

• Inflammatory cellular exudates are key to this process.
• Margination and Pavementing happens as polymorphs and monocytes emigrate
• Diapedesis, in which red cells move through the capillaries, also happens.
• Chemotaxis involves the unidirectional movement of polymorphs/macrophages towards the irritant via fibrin threads.
• Chemotactic substances: bacterial products, complement fractions as C3a and C5a, lymphokines, prostaglandin E1, lectins leukotriene B4 and chemokines as IL-8
• Phagocytosis is the act of ingesting/destroying bacteria and necrotic tissue by phagocytic cells, either polymorphs or macrophages.
• Polymorphs in cellular exudates are neutrophils.
• Macrophages in cellular exudates are blood monocytes and tissue histiocytes.

Chemical Mediators

• The kinin system (bradykinin) in plasma, the complement system (C5a & C3a), and the coagulation and fibrinolytic systems.
• vasoactive amines like histamine and serotonin are factors released from tissues
• Arachidonic acid metabolites can be released as prostaglandins and leukotrienes from tissues.
• Lysosomal components, lymphokines, and monokines is released from tissue cells.
• Chemical mediators increase vascular permeability, vasodilation and chemotaxis

The Course & Fate of Acute Inflammation

• Acute inflammation can have a complete resolution to normal, can regress or heal.
• Progression and spread occur when the bacteria overcome a body's defense mechanism, and chronicity can occur.
• General changes include leukocytosis (above 10,000/mm3), fever, and high erythrocyte sedimentation rate(ESR).
• Signs/symptoms include hotness, swelling, redness, pain, and loss of function.

Types of Acute Inflammation

• Acute inflammation can manifest as suppurative (pus-forming) or non-suppurative.

Suppurative inflammation

• In ACUTE SUPPURATIVE INFLAMMATION (Pyogenic or Septic) the definition entails severe acute inflammation that is characterized by pus formation.
• Causes entail pyogenic microorganisms- staphylococcus aureus and streptococcus hemolyticus are some examples.
• Pyogenic microorganisms cause necrosis and bring on polymorphonuclear leukocytes. Pyogenic microorganisms ultimately liquify necrotic tissue and fibrin threads
• Resulting the fluid material mix with inflammatory process products forming the pus.
• Pus consist of bacteria and toxins, liquefied necrotic tissue, inflammatory cellular exudates and inflammatory fluid exudate.
• Types of suppurative inflammation are localized and diffuse.
• Some examples of localized are: abscess, furuncle, and carbuncle.
• Some examples of diffuse are: cellulitis, suppurative appendicitis, and suppurative peritonitis.

Localized Suppurative Inflammation

• Abscess is a localized suppurative inflammation that results in the formation of an irregular cavity containing pus.
• Abscess is commonly caused by staphylococcus aureus that produce coagulase enzyme that helps fibrin formation and localization.
• Definition of a boil is a small abscess related to hair follicles/sebaceous glands.
• Definition of Carbuncle is a localized suppuration that forms multiple communicating suppurative foci in the skin/subcutaneous fat.
• Cause of Carbuncle is staphylococcus aureus, which is commonly present in those with diabetes mellitus and can be located on the back of the neck, scalp, and buttocks.

Diffuse Suppurative Inflammation

• Cellulitis involves acute diffuse suppurative inflammation.
• Cellulitis is caused by streptococcus hemolyticus which produces the enzymes Fribrinolysin(streptokinase) and Hyaluronidase(spreading factor.)
• Fibrinolysin dissolves fibrin.
• Hyaluronidase dissolves hyaluronic acid and helps with bacteria and toxin spread.
• Loose connective tissue is in areas such as subcutaneous tissue, orbit, pelvis, scrum and wall of appendix.
• Complications entail, lymphatic/blood spread of infection causing ailments/septicemia.
• Septic thrombophlebitis causes pyemia.
• Inadequate drainage and treatment affects transition abscess to a chronic one.
• Complications of healing in the form of chronic ulcer,sinus, fistula and keloid Putrefaction and gangrene.
• Toxaemia involves bacterial toxins circulating in the blood and will have toxic manifestations which include fever, rigors, headache, weakness, acute heart failure, anemia & sceptic shock.
• Bacteraemia refers to transit presence of some bacteria in the blood- w/out toxic manifestation
• Septicaemia refers to the circulation and multiplication of large numbers of virial bacteria/toxins. It is highly fatal.
• Pyaemia is circulation of septic emboli in the blood which results in multiple and small abscesses around the body. This ailment is highly fatal and associated with Septicemia.

Acute Non-Suppurative Inflammation

• In Catarrhal Inflammation, mucous membranes are inflamed non-suppuratively and mildly, characterized characterized by excess mucus secretion and examples include rhinitis, bronchitis, and appendicitis.
• Membranous or Pseudomembranous Inflammation includes server acute non-suppurative inflammation, involves mucous membrane, and creates pseudomembrane, with examples including Diphtheria and bacillary dysentery
• Serofibrinous Inflammation is acute inflammation characterized by excess fluid exudates rich in firbrinogen which affect cerous membranes such as the pleura, pericardium, and peritonium.
• Fibrinous is characterized by exhibiting exudates that are excessive in fibirin with and example being lobar pneumonia.
• Serous inflammation is excessive in cerous exudate and examples including burns and herpes.
• Hemorrhagic Inflammation is recognized by exudates rich in red blood cells due vascular damage, with an example entailing small pox.
• Necrotizing Inflammation entails marked tissue necrosis that can be characterized by marked tissue necrosis with cancrum oris being an example.
• Allergic inflammation derives from a antigen/antibody reaction such as as an reaction with allergic rhinitis..

Test your knowledge of inflammation, its causes, and related pathological processes. Questions cover cell injury, etiology, pathogenesis, and specific types of inflammation. Review key concepts in general pathology.