Flashcards in Module 1 -Path Continued Deck (33):
What are the five cardinal signs in inflammation?
Redness (histamine and vasodilation)
Loss of Function
What are the steps in acute inflammation?
Transient vasoconstriction (neurogenic) --> vasodilation (via histamine) --> increased vascular permeability/exudation (margination (rouleaux formation of RBCs pushes WBCs to periphery) --> rolling (mediated by selectins P and E) --> adhesion/emigration via integrins (ICAM-1 and VCAM) --->after this diapedisis or transmigration (movement of WBC from vessels to interstitial space)
What are the chemotactic factors for PMNs/neutrophils?
C5a (most important)
Bacterial Products (most important for macrophages)
Arachidonic Acid Metabolites (Leukotriene B4)
Cytokine --> IL-8
What are the chemotactic factors for macrophages?
MCP1 (CCL-2) , dead neutrophils and bacterial products
Acute Inflammation vs Acute Congestion, which is transudate and which is exudate?
Acute Inflammation = Exudate
Acute Congestion = Transudate
What are features of exudate fluid?
high proteins, white cells and specific gravity
What forces drive the formation of a transudate?
What are the four chemical mediators of fever?
For any viral infection, if they ask what is the first inflammatory cell on site, what is it?
(EBV, MONO, HPV, Etc)
For any bacterial infection or coagulative necrosis, what cells are there first?
What is the process of phagocytosis?
1. Recognition and Attachment --> coated with opsonins (IgG and C3b)
2. Engulfment --> formation of phagolysome requires presence of Ca2+ and Mg2+
3. Killing/Degradation -->
-O2 dependent mechanisms: H2O2-myeloperoxidase-halide system
and MPO independent killing (most potent radial OH)
--O2 independent mechanisms: decreased pH due to lactic acid
What are the 4 types of inflammation?
Serous --> Albumin containing exudate; seen in blister, pulmonary TB
Fibrinous --> contains Fibrin; seen in rheumatic fever (bread and butter pericarditis)
Suppurative/purulent --> liquefactive necrosis caused by pyogens (pus w/neutrophils); seen in acute appendicitis
Sanguinous --> contains large number of RBCs; tumor invasion
What are the changes in vascular permeability in acute inflammation?
Increased intravascular hydrostatic pressure (vasodilation) or decreased intravascular osmotic pressure (decreased albumin) --> increase interstitial fluid (edema)
What are the steps in vascular permeability?
1. Endothelial Cell Contraction-> histamine in venules ---> immediate transient response
2. Junctional Contraction -->Cytokine mediated (TNF and IL-1)
3. Direct Endothelial Injury --> Endothelial detachment in capillaries and venules; immediate sustained response
4. Leukocyte dependent Endothelial Injury --> inflammatory cells release ROS causing endothelial detachment in venules and pulmonary capillaries
5. Increased Transcytosis --> in prescence of VEGF --> increased permeability
What are the cell derived mediators of increased vascular permeability?
Arachidonic Acid Metabolites --> derived from cell membrane phospholipids
-Prostaglandins: vasodilation and increased permeability
-Leukotrienes: increased permeability and chemotactic activity
-PAF-vasodilation, increased permeability and chemotactic activity
-Amines: vasodilation and increased permeability (venules only) (includes histamine and sertonin)
-Endothelins: powerful vasoconstrictors
What are the plasma derived mediators of increased vascular permeability?
Kinins and coagulation cascade: bradykinin (vasodilation, vascular permeability and pain)
Clotting system: prevents infection spread, end product = fibrin
Complement system: opsinizing bacteria=C3b; attracting leukocytes (Chemotaxis)=C5b, 6,7 complex and C5a; mast cell activators = degranulation and histamine release= C3a, C5a; C6-C9=create pores in bacterial walls
Chronic Inflammation, what is an example?
What is the pathogenesis for chronic inflammation?
Previous acute inflammation (>/= 2 weeks)
De Novo: Granulomatous Inflammation (TB) and autoimmune disease
What the main cells for bacterial chronic inflammation?
CD4 T cells Monocytes and Macrophages, lymphocytes, plasma cells, fibroblasts and endothelial cells
What is the hallmark of chronic inflammation?
Hallmark = fibrosis by fibroblasts leading to loss of function
PMNs (neutrophils) are absent
What is the presentation for chronic inflammation?
No pain normally because no more bradykinin, but every chronic inflammation can have an episode of acute on chronic inflammation which does cause pain
(happens alot in crohns, RA, gout and psoriasis)
What has to be secreted in order to get fibroblasts?
In chronic inflammation, collagen is initially type III and with blood vessels and angiogensis and this forms granulation tissue. how long does it take to form granulation tissue?
In chronic inflammation how long does it take for collagen to get transformed from type III to type I ?
2 months process called cicratization (which means scaring)
In acute on chronic flare, what cells would you see?
PMNs (because this is a flare) and you would see all the signs of acute inflammation as well
is there pain with chronic inflammation?
nope just loss of function
In the picture of the intestine for peptic ulcer, what is the white stuff, red and dark red?
White stuff --> fibrosis
Red --> chronic inflammation
Dark red --> acute flare
What type of collagen is a keloid?
type III (thats why keloid looks super soft)
What type of collagen in a hypertrophied scar?
In regards to caseating granuloma, how is the central area of caseous necrosis formed?
No nuclei in center -> walled off by chronic inflammatory cells (macrophages, T cells, plasma cells, fibroblast, giant cells, epitheloid cells but no PMNs)
What are examples of non-caseating granulomas?
no central area of necrosis
(Crohns, Sarcoidosi and Berylliosis)
What are examples of pyogenic/suppurative granulomas?
purulent (has PMNs/neutrophils) granulomas
Cat Scratch Disease and Lymphogranuloma Venterum (LGV) --> STI caused by chlamydia