Inflammation Flashcards
PGG2
Prostaglandin 2
- inhibit HCL production in stomach
- regulate blood pressure (
COX-1 inhibitors
Ibuprofen
Naproxen
Acetaminophen
Indomethacin
COX-2 inhibitors
Viox CAUSES THROMBOSIS!
Celebrex
Meloxicam
Steroids inhibit what?
Phosophlipases from synthesizing arachidonic acid which prevents all other reactions
Most powerful steroid?
Prednisone
TXA2
Thromboxane
TXA2
Vasoconstriction
Platelet aggregation
Produced by platelets
PGI2
Prostacyclin
PGI2
Causes vasodilation
Inhibits platelet aggregation
Produced by endothelial cells
PGD2
Lungs
BRONCHOSPASM
mast cells
Baldness (alopecia)
PGE2
Kidney
Hyperalgesia (pain)
Fever
Uterine contraction (induces labor)
PGF2
Corpus luteum
- ->Luteolysis
- –> stops production of progesterone
- —> induces labor
Bronchospasm
Histamine
PGD2
Leukotrienes
Lipoxin A4 & B4
Vasodilation
Inhibit neutrophil chemotaxis
Stimulate monocytes adhesion
Enzyme 12-lipoxygenase
Arachadonic acid becomes?
Cyclooxygenase Cox1 cox2
5-lipoxygenase
Cyclooxygenase becomes?
Prostaglandins
5-lipoxigenase becomes?
Leukotrienes
NSAIDS
COX-1 inhibitors
Lead to kidney problems and stomach irritation/ulceration because no COX-1 is produced
No COX-1 = HCL levels increase
Ex: ibuprofen (Advil), naproxen (aleve) , indomethacin, and aspirin
Leukotrienes
Vasoconstriction- balances out vasodilation
Bronchospasm
Increased permeability
Enzyme 5-lipoxygenase
Tumor necrosis factor
Produced by activated macrophages
Induces inflammatory response
Medications for RA, ankylosis get spondylitis, etc, inhibit TNF and may lead to lymphomas etc
HUMERA INHIBITS TNF
IL-1 and IL-6
(Interleukin)
Produced by T helper cells
Induces acute inflammatory
Acute phase responses
Fever
Increase ability of the body to fight against intruders
Decreased appetite (anorexia )
Increased sleep
Important to autoimmune disease
Increased Acute phase proteins ( C-RP=C reactive protein) and (ESR= erythrocytes sedimentation rate)
Vasodilation (may lead to shock)
Neutrophilia- increase amount of neutrophils
Creates an environment that aids the body in dealing with the cause of inflammation
Kinin cascade
Hageman factor (CF XII)--> Prekallikrein--> Kallikrein--> Kininogen--> Bradykinin
Prekallikrein
Vasodilation
Promotes the vascular component of the inflammation
Short lived: 5-10 minutes
C3a, C4a, C5a
Refers to fragment that has been separated from the complement part
Promotes secretion of histamine from mast cell granules
Participate in inflammation sometimes
In nature they are derived from plasma
Bradykinin
Causes vasodilation
Promotes vascular component of inflammation
Increased permeability
Increased permeability of the vessel via prostacyclin and NO
Small peptide with short life
5-10 minutes
Lymphangitis
Appears as a red Ropey line
Lymphatic capillaries —> inflammation of lymphatic vessels
Enlarged and painful lymph nodes
Lymphadenitis
Enlarged and painful inflamed lymph nodes
Accumulation of bacteria
Painless= cancer (metastasis of lymph nodes)
Bacteremia
Infection if bacteria in blood
Very dangerous
Septicemia-accumulation of bacteria metabolism toxic products
Leukocyte is
Increased leukocytes in blood
>9,000 per 1 cubic mm
Due to infected blood
Neutrophilia
Normal 55-60
Acute bacterial infection (such as appendicitis)
Can increase up to 80-90% of circulating wbc’s
Lymphocytosis
Normal 20-25
VIRAL INFECTION
Eosinophils
Normal 2-4 Allergic reactions (type 1 hypersensitivity) PARASITIC INFECTION (worms)
Long term soft tissue inflammation
Results in osteopenia
Bones in vicinity lose their density
Juvenile rheumatoid arthritis
Hands and joins swollen lots of pain
Inflammation can destroy tissue—>
repair–> fibrillation and connective tissue around
Inflammation can destroy bone
Chronic inflammation
Duration 6-8 weeks minimum
Character of exudate but NOT exudate (usually does not have this because it is found in acute not chronic)
Cell content: ONLY MACROPHAGES AND LYMPHOCYTES
produce immunoglobulins
Selected agents typically involved in chronic inflammation:
Mycobacterium tuberculosis
M. Leprae
Listeria
Treponema pallidum
Bruxelles
Chronic inflammation arises in the following settings
Viral infection
Persistent microbial infection prolonged exposure to potentially toxic agents
Autoimmune diseases
Nonspecific chronic inflammation
A diffuse accumulation of macrophages and lymphocytes develops at the site of injury
Granulomatous inflammation
Formation of granuloma From inside out: Epitheliod cells (changed macrophages)---> lymphocytes-->fibroblasts-->connective tissue Multinucleated giant cell in the center Develops from TB
Pneumoconiosis - silicosis and asbestosis
Kung disease from inhalation of industrial toxic fumes
Tissue damage and replacement by scar tissue