Introduction to Inflammation

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1

inflammation

local response to tissue injury (exogenous and endogenous injurious agents)

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causes of inflammation

  • physical agents

  • chemical substances

  • microbial infections

  • tissue necrosis

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Celsus signs

heat, swelling, redness, pain, loss of fxn

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vascular rxn to inflammation

accumulation of fluid in extravascular space

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cellular rxn to inflammation

migration and activation of leukocytes

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systemic rxns to inflammation

regeneration + scarring

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triple response injury

flush (cap dilation), flare (arterial dilation) + wheal (edema)

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Phases of inflammation

  1. tissue injury

  2. Vasodilatation and exudation

  3. Proliferative phase

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Tissue injury phase

reversible or irreversible lesions upon to a cell, a tissue or an organ

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10

exogenous causes of tissue injury

  • mechanical, physical, chemical, foreign bodies

  • infectious organisms

  • exo/endotoxins

  • immune mechanism

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11

endogenous causes of tissue injury

  • tissue necrosis, enzymes activation

  • immune-mediated processes

  • storage of substances

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12

Proteolysis from tissue injury causes

metabolite storage, release of chem mediators, activation of coag. system and self-antigen formation

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Storage of metabolites due to tissue injury leads to

acidosis, hyperionia (K+ ), hyperosmosis

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14

release of chemical mediators due to tissue injury from _________, ________ and ___________ leads to :

from neural terminations, platelets and mast cells vascular reaction

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15

Vasodilatation and exudation stage breaks into 3 parts

  1. vascular rxn

  2. formation of the inflammatory exudate and phagocytosis

  3. migration of neutrophils and bacterial phagocytosis

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Vascular rxn of Vasodilatation and exudation stage

  • arterioles + arteries - catecolamines cause spasm (vasoconstrict), serotonin releases -> paralytic dilation

  • capillaries - stasis -> poststasis all leads to hyperemia and cap congestion

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exudate vs. transudate

Exudate

  • extravascular fluid with high protein content and cellular debris (implies increased permeability and therefore inflammation)

Transudate

  • extravascular fluid with low protein content, little to no cellular debris (no increased permeability and therefore NO inflammation)

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Formation of the inflammatory exudate of Vasodilatation and exudation stage

Hyperionia, hyperosmosis, acidosis (h20 exudate) and Increasing of vascular permeability (serum+plasma exudate and leukodiapedesis)

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Phagocytosis of Vasodilatation and exudation stage

Migration of neutrophils and monocytes

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Secondary lymph vessels involvement (lymphangitis, lymphadenitis, lymphadenopathy) occurs in what stage of inflammation?

Vasodilatation and exudation stage

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21

How does neutrophil migrate and bacteria is phagocytosed in the Vasodilatation and exudation stage

neutrophil ingests bacterium (in a phagosome), lysosomes fuse w/ vacuole and enzymes digest bacterium, bacterial debris released

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Chemical mediators of vasodilatation

histamine, noradrenaline (a. spasm), serotonin, chemokines, anaphylatoxins, complements, prostaglandins

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Chemical mediators of chemotaxis (exo + endogenous)

bacterial peptides (exo) plasma and cell factors, lysosomal enzymes, lymphokines

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Proliferative phase

repair of injured tissue

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Early proliferative phase

granulation tissue forms, exudate removed, immunocompetent cells activated, migration of macrophages and fibroblasts, proliferation of the capillaries

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Late proliferative phase

connective scar forms, proliferation of fibroblasts + connective fibers, decreasing # immunocompetent cells + capillaries

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Acute inflammation

initial response of tissue to injury, rapid onset, pain + fever, leukocytosis, neutrophils migrate + edema + tissue injury

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spread of acute inflammation

  1. direct

  2. into cavities

  3. canalicular - asc/desc

  4. into blood

  5. into lymph vessels

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healing of acute inflammation

regeneration complete resolution (restoration) reparation - fibrosis

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Chronic inflammation

prolonged tissue reactions following the initial response, proliferation of immunocompetent cells + fibrosis

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Complications of chronic inflammation

healing (fibrosis), scar, acutization (recurring), tissue atrophy

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Types of chronic inflammation

exudative (-itis) vs productive (non-/specific + foreign body)

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Systemic effects of inflammation

fever, SAPR, leukocytosis, stress-related phase

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34

Fever - exogenous pyrogens are ________ and endogenous pyrogens are ____________

exo - bacteria endo - leukocytes

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Systemic acute phase response

proteins of negative acute phase - albumin, transferin proteins of positive acute phase - globulines

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Leukocytosis

increase in WBC, I: neutrophils II: monocytes macrophages III: lymphocytes

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Alterative inflammation

tissue injury, lack of the exudation and proliferative phase, from metabolic disorders, can lead to necrosis

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Causes of alterative inflammation

physical + chem substances pathogens anergy (lack of immunological response)

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Evolution of alterative inflammation

severe functional disorders healing with fibrosis

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40

serous exudative inflammations

abundant protein-rich serous exudate

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causes of serous (exudative) inflammation

perifocal inflammation, uremia, collagen diseases, allergies

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evolution of serous (exudative) inflammation

  • healing (absorption of exudate)

  • transformation in serous-fibrinous, serous -purulent inflammation

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43

rivalta probe is neg for ______ and pos for ______--

transudate, exudate

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Catarrhal inflammation

serous (exudative) inflammation of mucosae (hyperemia + edema), hypersecretion

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causes of catarrhal inflammation

  • physical factors, chemical agents

  • viruses (common cold)

  • bacteria

  • allergy

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evolution of catarrhal inflammation

  • healing (complete restitution)

  • superinfection muco-purulent inflammation

  • chronic transformation

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47

in serous (exudative) inflammation, papules are due to __________- blisters - vesicles are due to __________ and bullae are due to __________

allergies, viruses, burns

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48

fibrinous exudative inflammation

fibrinogen polymerization (fibrinous exudate in extracell space), on serosal surfaces there is thick fibrin coat

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49

types of membranes - fibrinous pericarditis: _____________ fibrinous pleuritis: _________ fibrinous peritonitis, arthritis: _________

villous, winding, smooth

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50

causes of fibrinous (exudative) inflammation

  • perifocal inflammation)

  • uremia, rheumatic fever, collagen diseases

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51

evolution of fibrinous (exudative) inflammation

healing resolution organization (adherences) transformation into another type of inflammation

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52

Fibrinous inflammations of mucosa (pseudomembranous)

  • dirty false membrane (fibrin+neutrophils+mucus), causes asphyxiation and during typhoid fever - Payer's plaques necrotic

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causes of Fibrinous inflammations of mucosa (pseudomembranous)

diphtheria, uremia

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evolution of Fibrinous inflammations of mucosa (pseudomembranous)

lysis of the membrane and healing, ulceration, obstruction

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55

Purulent exudative inflammation

leukodyapedesis = pus = neutrophils, infecting organisms, liquefactive tissues and serum, on serosal surfaces

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causes of purulent (exudative) inflammation

perifocal inflammation or perforation pyogenic bacteria

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evolution of purulent (exudative) inflammation

healing, organization - adhesions or capsulling of the pus septicemia

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Purulent (exudative) inflammation of mucosa

hyperemic and swollen mucosa + covered w/ pus (empyema)

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causes of Purulent (exudative) inflammation of mucosa

pyogenic bacteria + superinfection

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evolution of Purulent (exudative) inflammation of mucosa

complete resolution (healing) chronic transformation pyemia death

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61

Phlegmon

diffuse acute purulent inflammation of tissues and organs, can lead to abscess or death

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Abscess

a localized cavity with pus + necrotic tissue within a tissue or organ (purulent exudative inflammation)

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acute vs chronic abscess

acute abscess: ill-defined cavity surrounded by neutrophils chronic abscess: surrounded by a "pyogenic" membrane

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types of abscesses

primary abscesses (solitary, multiples) metastatic abscesses - during pyemia - multiple abscesses cold abscesses - for TB, no celsus or neutrophils

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evolution of abscess

  • resolution, scarring or capsuling, calcification

  • spontaneous discharge - fistula

  • ulceration, pyemia, septicopyemia

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66

Necrotizing and gangrenous (exudative) inflammation

presence of necrosis + bacterial putrefaction necrotizing - fetid exudate + putrefaction gangrenous - putrefaction w/o exudate

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causes of necrotizing + gangrenous (exudative) inflammation

  • anaerobic bacilli + body anergy

  • hematological disorders

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68

Hemorrhagic (exudative) inflammation

severe vascular injury or depletion of coagulation factors

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evolution of hemorrhagic (exudative) inflammation

erythrodiapedesis -> sanguineous exudate

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70

subserosal hemorrhages are caused by

TB, metastases

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71

Hemorrhagic inflammation of skin -

anthrax + variola (smallpox)

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hemorrhagic inflammation of organs -

pneumonia, encephalitis, DIC, anthrax, plague

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Primary (Inherited) Immunodeficiencies

antibody deficiency T-cell defects

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acquired immunodeficiencies

leukemia HIV/AIDS imunosuppressive drugs transplant malnutrition

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Opportunistic infections in immunocompromised

  • CMV and Pneumocytis carinii (in aids)

  • cystic fibrosis

  • bacterial infections

  • T-cell defects

  • S. Pneumoniae (asplenism), Neisseria, S. Aureus, Herpes virus

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76

Granulation tissue

reparation w/ inflammatory cells fibroblasts, capillary endothelial cells + collagen fibers proliferate fibroblasts became myofibroblasts capillary neoformed vessels

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Granuloma

aggregation of lymphocytes and macrophages, sometimes w/ giant cells

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Scarring/fibrosis

substitution of damaged tissue with connective tissue

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Organization

replacement of the chronic exudate by the formation of a fibrous scar

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80

process of healing

  1. Elimination of lytic cells

  2. Migration of immunocompetent cells

  3. Genesis of new blood vessels - neoformed capillaries

  4. Proliferation of fibroblasts

  5. Fibrous tissue remodelling

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81

Angiogenesis

formation of new blood vessels, process of healing injury, dev of collateral circulations @ ischemia + allowing tumors to grow

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Wound healing by first intention

incised wound, platelets aggregate + scab forms, neutrophils/macrophages chemotaxis, proliferation of epidermal then dermal cells - secrete collagen

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Wound healing by second intention

open wound, foreign material in it, persistent bleeding, infection

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risk factors of open wounds

diabetes, atherosclerosis, nutritional deficiencies, steroid drugs

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steps of wound healing by second intention

tissue loss neutrophil/macrophage chemotaxis phagocytosis to remove the debris granulation tissue organization and scar formation epithelial regeneration

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keloid nodules

In healing by second intention, excessive fibroblast proliferation and collagen production

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Chronic ulcers

loss of the tissue continuity in organs covered by mucosa or on leg

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stages of chronic ulcer healing

surface - covered with fibrin layer + necrotizing exudate phagocytosis of the dead tissue granulation tissue regeneration of the mucosa connective scar

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89

Productive inflammation of the mucosa and organs - leads to

chronic inflammations, hyperplasia, mucosal fold thickening + atrophy

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90

labile tissues

formed by cells which retained the ability to proliferate in post-natal life and have a high rate of turnover (hematopoietic cells)

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stable tissues

good regenerative ability but low rate of turnover (hepatocytes, bone, renal tubes)

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permanent/differentiated tissues

formed by cells which have lost the ability to proliferate being divided only during fetal life (neurons, muscle cells)

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physiological regeneration

epithelial cells, hematopoietic cells

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regeneration in liver

only hepatocyte loss (they are stable cells)

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95

regeneration of kidney

tubular epithelium can be regenerated but not architecture

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96

foreign body granuloma

chronic granulomatous inflammation (accumulation of activated macrophages and inflammatory cells around foreign bodies which cannot be phagocytosed)

  • giant multinucleated cells (macrophage fusion)

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97

lipogranuloma vs oleogranuloma

lipo - lipid deposits oleo - from oil injection

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Tuberculosis

tubercles (specific granulomatous inflammation)

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Mycobacterium tuberculosis - phtyonic acid

central caseous necrosis and epithelioid hystiocytes (langhans)

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exudative tubercle

in anergy and normal immunity, caseous necrosis, evolves to liquefaction and cavity

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