acute inflammation Flashcards
Types of inflammation:
Serous inflammation
Effusion of thin watery exudate that can be found in the peritoneal, pleural, or pericardial cavities, or be seen as blisters on the skin
No bacteria, it comes from vascular permeability or tissue damage
Types of inflammation:
Fibrinous inflammation
Accumulation of fibrin-rich exudate in meninges, pericardium, or pleura. This can either be resolved or lead to scarring.
Ex. Fibrinous pericarditis ass with MI or Rheumatic fever
Types of inflammation:
Purulent (Suppurative) inflammation
Production of pus, neutrophils, necrotic tissue, and edema
Ex. Acute pancreatitis
Types of inflammation:
Ulcers
Local defect/excavation in the surface of an organ due to necrotic tissue shedding off
common areas are mouth, duodenum, and skin
Types of infection:
Pseudomembranous inflammation
Bacterial toxin-induced damage of mucosal linings (causes a shaggy membrane)
Ex clostridium difficile (pseudomembranous colitis) & corynebacterium diphtheriae
Mediators of acute-phase response of inflammation are?
TNF
IL-1,6
INFs
Mechanisms of fever are mediated by which pyrogenic cytokines?
IL1, 6
TNF
INFs
Liver-made plasma proteins that mediate acute inflammation include:
C-reactive protein
Fibrinogen
Hepcidin
Serum amyloid A protein
IL-6 stimulates ______&_____
C-reactive protein
&
Fibrinogen
Erythrocyte sedimentation rate is due to which acute-phase protein?
Fibrinogen
It binds to RBCs and causes them to form stacks (rouleaux)
Leukocytosis is described as a ______ reaction with leukocyte levels avg ____ -_____
Leukemoid reactions showing levels 40,000 to 100,000 leukocyte counts
Neutrophilia
increase in neutrophil count usually due to bacterial infections
Lymphocytosis
Increase in number of lymphocytes in viral infections
Eosinophilia
Allergies & parasitic infections which increase the number of eosinophils
What are the 3 outcomes of acute inflammation?
Resolution
Scarring/fibrosis
Chronic inflammation
Myeloperoxidase deficiency
Auto REC condition, no HOCL production leads to recurrent fungal infections (candida)
The acquired form of MPO usually happens due to
Myelomonocytic leukemia & acute myeloid leukemia
Chediak Higashi Syndrome
An AUTO REC
Defect in protein trafficking due to mutated CHS1 gene for Lysosomal transport protein
*Albinism
*Leukocytes with GIANT granules
*Hemostasis
*Impaired phagolysosome (recurrent infections)
*Peripheral neuropathy
Chronic Granulomatous disease
Deficient NADPH oxidase
(due to mutated CYBB) absent respiratory burst. It causes deep tissue bacterial and fungal abscesses in macrophage-rich organs (lymph nodes, liver, lungs etc)
Most common are catalase + (S. aureus, Nocardia, Aspergillus, & Candida)
What test is used for CGD and what results indicate what?
Nitroublue Tetrazolium dye test
Blue = NADPH okay
Colorless = NADPH is fucked
LAD (Leukocyte Adhesion Deficiency)
AUTO REC condition
Caused by deficient B2 integrin
-Delayed umbilical separation
- Hyperleukocytosis (>30,000)
- Poor wound healing
- Severe gingivitis
- Ulcers in genital area
LAD 2
AUTO REC
messed up selectin-leukocyte rolling
defective Sialyl-Lewis X glycoproteins
LAD 3
AUTO REC
Defective kindlin (which helps activate the ligands affinity of B2 integrins)
Phagocytic receptors:
Mannose receptor
A lectin that binds the terminal mannose and fucose residues of glycoproteins and glycolipids on microbial cell walls
Phagocytosis process (3 steps)
- Recognition/attachment of particle
- Engulfment + formation of phagocytic vacuole
- Killing/degradation
Chemotactic factors of leukocytes include:
IL-8
C5a
LTB4
Leukocyte Recruitment to inflammation steps (5)
- Margination
- Rolling
- Adhesion
- Transmigration/diapedesis
- Migration in interstitial tissue to injury