Chapter 3 - Inflammation: Reaction to Injury Flashcards
Inflammation
Local reaction to vascularized tissue to injury
- Acute
- Chronic
Acute inflammation
Usually a rapid response with a short duration
- Shows neutrophils and edema
- Associated with bacterial infection
- Inflammation continues until repair or scar replace is damaged tissue
Chronic inflammation
Usually a later response with a long duration
- Acute inflammation may not proceed
- Usually shows lymphocytes and macrophages
- Often associated with viral or fungal infections
- Injury is ongoing: injury, inflammation and repair coexist
Inflammatory cells
White blood cells or leukocytes; involved in immunity
- Granulocytes
- Mononuclear cells
Granulocytes
Polymorphonuclear leukocytes
- Contain granular cytoplasm
- Involved mainly an acute inflammation
- Neutrophils
- Eosinophils
- Basophils
Neutrophils
65% of WBC’s
- Also called “polys” or “PMNs” (polymorphonuclear neutrophils), “segs” (for segmented, referring to two - five segmented nuclei)
- First to gather at damage site
- Motile: can respond to chemotaxis
- Phagocytosis: canon golf extracellular material (main task of neutrophils)
- Bacteriocidal: have specific bacteriocidal enzymes to kill bacteria
- Release chemical factors which stimulate the inflammatory response, including attracting more WBCs, stimulate bone marrow to produce neutrophils, and act on brain to increased body temperature and cause malaise
Eosinophils
3% of WBCs
- Main cell in parasitic infection (worms, rarely protozoa or fungi)
- Only slightly motile or phagocytic
- Important in allergies (hay fever) attracted by basophils; roll not clear
- Microphage: neutrophils and eosinophils
Basophils (in blood) > mast cell (in tissue)
< 1% WBCs
- Release histamine, one of the chemical factors of inflammation and allergies
- Cause swelling, itching, congestion, and mucus production
Mononuclear cells
Agranulocytes. Contain no granules with nonsegmented nuclei
- Important in chronic inflammation
- Monocytes
- Lymphocytes
Monocytes (in blood) > macrophages (in tissue)
5% of WBCs
- Most prominent in later stages of acute inflammation and chronic inflammation
- Motile: slower than neutrophils
- Phagocyte: scavengers of body; only neutrophils and monocytes are highly phagocytic
- Release inflammatory chemical factors
- Release and science which helped agreed and clear away debries
- Fixed macrophage - Kupffer cells (liver); microglia (brain); Langerhan cells (skin)
Lymphocytes
About 23% of WBCs
- Appear very late in acute inflammation and chronic inflammation
- Main cells of immune system: B and T cells according to their origin
- Activated B cells are called plasma cells and produce antibodies and are present in chronic inflammation
Molecular mediators of inflammation
- Plasma derived mediators
- Cell-derived molecular mediators
Plasma derived mediators
- Clotting system
- Complement system
- Kinin system
Clotting system
- About 12 proteins that cause blood clotting
- Stimulates complement and kinin systems
Complement system
Initiated by immune system or microbial products
- About 24 proteins
- Cause vasodilation
- Attract WBCs
- Directly attack and destroy microbes
Kinin system
Closely related to clotting system
- About 12 proteins that generate molecules
- Cause vasodilation
- Cause increased endothelial cell permeability
Cell derived molecular mediators
Most cause vasodilation
- Vasoactive Amines
- Cell membrane factors
- Cytokines
- Prostaglandins
- Reactive oxygen compounds
Vasoactive amines
Preformed molecule stored in granulocyte lysosomes
- Cause local capillaries to vasodilate and become “leaky”
- Histamine: released from mast cells, basophils, platelets
- Serotonin: released from platelets
Cell membrane factors
From phospholipids and cell membrane of injured cells
- Paracrine factors (local hormones) : attractive WBCs and cause vasodilation
Cytokines
Paracrine factors that attract WBCs, cause vasodilation and stimulate phagocytosis
- Chemokines: cytokines that cause chemotaxis to site of injury
Prostaglandins
Paracrine factors that enhance vasodilation and vascular permeability
- Fever: increases body temperature
Reactive oxygen compounds
- Nitric oxide: causes vasodilation and is bacteriocidal
- Oxygen superoxide: bacteriocidal
Acute inflammation causes
- Microbial infection: especially bacteria
- Physical or chemical injury: thermal or chemical burns
- Immune injury: poison ivy or oak dermatitis
*** Note on most immune injuries
Produces chronic inflammation
Phases of acute inflammation
- Vascular phase: occurs first
- Cellular phase: occurs second
Vascular phase
- Vasoconstriction
- Vasodilation
- Increased vascular permeability
Vasoconstriction
- Limits spread of injurious agents
- Lasts only a short time: seconds to minutes
Vasodilation
- Results in increased blood flow in arterioles
- Creates the redness and heat of the four cardinal signs
Increased vascular permeability
Due to histamine
- Results in protein rich fluid moving into intravascular tissue
- Edema: swelling
- Loss of fluid from vessels makes blood more concentrated, slowing blood flow
Cellular phase
Migration of WBCs (mainly neutrophils) to extra vascular tissue
- Margination
- Extravasation
- Chemotaxis
- Phagocytosis
Margination
Neutrophils stick to lining a blood vessel
Extravasation
Neutrophils squeeze between endothelial cells
Chemotaxis
Neutrophils move towards injured area
Phagocytosis
Neutrophils eat foreign substances
- Opsonin: complement the coats foreign material making it easier to swallow
Clinical signs of acute inflammation
- Cardinal signs: “rubor, calor, tumor, dolor”
- Inflammatory exudates
Redness
Due to vasodilation “hyperemia”
Heat
Due to vasodilation
Pain
Due to irritation of nerve endings, increased tissue tension or prostaglandins
Inflammatory exudated
- Serous
- Fibrinous
- Purulant
- Catarrhal
Serous
Contains albumin, very little fibrinogen, relatively few WBCs
- Blister following a burn
Fibrinous
High protein fluid with fibrinogen, which becomes fibrin
- Scab and skin injuries; uremic pericarditis
Purulent
Numerous neutrophils and debries and fibrinous exudates “pus”
- Neutrophils give white color to puss; also called pyogenic and suppurative exudates
- Staphylococcus aureus: prone to form puss
- Empyema: collection of pus and body cavity (pleural empyema)
- Abscess; bacterial pneumonia
Catarrhal
Large quantities of mucus, but relatively few cells
- Common cold
Consequences of acute inflammation
- Repair
- Scarring
- Abscess
- Chronic inflammation
Repair
Short term injury results and regeneration of tissue
- Sunburn
Scarring
From severe or repeated acute inflammatory episodes
- Severe sunburn
Abscess
Local accumulation of edema, necrotic debries and dead WBCs
- Results when pace of local inflammation and liquefactive necrosis outstrips the inflammatory process to remove the material (cellulitis)
Causes of Chronic Inflammation
- Persistent infection
- Autoimmune disease
- Persistent exposure to injurious agents
Persistent infection
Caused by microbes
- Syphillis: treponema pallidum
- Tuberculosis: myobacterium tuberculosis
Autoimmune disease
Immune system accidently attacks self, it’s own tissues
- All autoimmune disease is chronic
- If you Alyssa acute inflammation (arteritis)
- Rheumatoid arthritis: immune system attacks ones own joints
Persistent exposure to injurious agent
- Starts acute, then becomes chronic
- Silica exposure: rock dust
- Smoking: cigarettes
Clinical signs of chronic inflammation
Less intense than acute inflammation
- Decreased intensity
- Chronic inflammatory cells
- Granulomatous inflammation
Decreased intensity
Less than an acute inflammation
- Not as red, swollen, hot and tender
- Shrunken by scar, atrophy or necrosis
Chronic inflammatory cells
Mononuclear cells (misnomer: due to multinuclear appearance of neutrophilic nuclear lobes, which are technically mono nuclear too)
- Macrophages
- Lymphocytes
Macrophages
Very important thousand and chronic inflammation
- Derived from blood monocytes
- Migrate to tissues and it reside for months to years
- Known by various names in different tissues (Kupffer, microglia)
- Phagocyte: ingest and either digest or present it to lymphocytes
Lymphocyte
The principal reactive cell in chronic inflammation
- T lymphocytes
- B lymphocytes
T lymphocytes
Originate in thymus, cellular immunity, attack directly
B lymphocytes
Originate in bone marrow
- Humeral immunity
- Secrete anti-bodies that circulate and blood as immunoglobulin
- When stimulated by antigens they change appearance and are known as plasma cells
Granulomatous inflammation
- Granuloma
- Epitheloid cell
- Giant cell
- Tuberculosis
Granuloma
Collection of chronic inflammatory cells, especially epitheloid cells or giant cells, and often surrounded by a rim of lymphocytes
Epitheloid cells
Modified macrophages
- Long oval nuclei and abundant cytoplasm
- Not epithelial cells, but look like them
Giant cells
Large cells with multiple nuclei
- Form by the fusion of macrophages
Tuberculosis
The most common cause of granulamotous inflammation
- Other disease associated with this include: syphilis, leprosy, fungal infections, foreign body reactions, parasites
Consequences of chronic inflammation
- Resolution to a scar
- Persistent chronic inflammation
Distant effects of inflammation
- Lymphatic system
- Systematic effects
Lymphatic system
One way dream from tissue to blood for inflammatory fluid, microbes and debris
- Lymphangitis
- Lymphadenitis
Lymphangitis
Inflamed lymphatic vessels due to infection
- Causes red streak’s up from infection site, but not dangerous as in blood poisoning
Lymphadenitis
Lymph nodes draining an injured or infected site may become infected
- Lymph nodes and large and are tender due to infection
- Reactive hyperplasia
- Lymphadenopathy
Reactive hyperplasia
Often lymph nodes are not infected, but rather reacting to inflammatory products draining away from infection or injury
Lymphadenopathy
Enlarged and tender lymph nodes irrespective (don’t know the cause) of suspected diagnosis, Biette infection, malignancy or other benign reactions
Systematic effects of inflammation
Seidel cans can find their way into the blood to induce systematic effects on the:
• Brain
• Liver
• Leukocytes
Brain
- Fever:
• body temperature regulated by hypothalamus
• Set point change to a higher temperature
• Increased phagocytosis and interferon production - Malaise, drowsiness and decreased appetite
Liver
Chronic inflammation causes increased production of:
• Reactant proteins: C – reactive protein CRP – elevates with even minor inflammation; systematic
- Associated with atherosclerosis, cancer, obesity and Alzheimer’s disease
• Fibrinogen: increased fibrinogen cause RBCs to settle rapidly measured by ESR (erythrocyte sedimentation rate) ; RA – have high ESR (sed rate)
Leukocytosis
Increased WBC count in peripheral blood
- Specific type of WBC gives clues as to cause of inflammation:
• Neutrophils: increased neutrophils, bacterial infection
• Lymphocytosis: increased lymphocytes, viral infection
• Eosinophils: increased eosinophils, helminth (worms) infection
Abscess
Localized collection of pus
Pustule
Small elevation of the skin containing pus
Boil
Deep infection of S. aureus associated with hair follicles that produce pus
- Neck, axilla, buttocks, thigh, eyelid (stye) or furuncle
Carbuncle
Same as boil, except coalescing infections produce drainage sinuses: usually the neck
Pyo, py
Prefix meaning pus
Ulcer
Open sore on the skin or mucous membranes (decubitus ulcer)
Fistula
Abnormal tube or passage from a normal cavity to a free surface or another cavity
