CR1 KCP1 Acute Inflammation

Define Acute Inflammation and state its primary goals.

A rapid, protective response of vascularized tissue to injury that brings immune cells/proteins to the site to: 1. Neutralize/eliminate invaders; 2. Remove necrotic tissue; 3. Initiate repair.

List the 4 main causes of acute inflammation.

1. Infections (bacterial, viral, fungal, parasitic); 2. Tissue Necrosis (ischemia, trauma, radiation); 3. Foreign bodies (splinters, sutures); 4. Immune reactions (hypersensitivity, autoimmune).

5 cardinal signs of inflammation and their Latin names.

Redness (Rubor), Heat (Calor), Swelling (Tumor), Pain (Dolor), and Loss of Function (Functio laesa).

What vascular event causes Rubor (Redness) and Calor (Heat)?

Arteriolar vasodilation causing increased localized blood flow.

What vascular event causes Tumor (Swelling)?

Increased vascular permeability causing fluid exudation into extravascular space.

What causes Dolor (Pain) in acute inflammation?

Tissue stretching from edema plus chemical nerve stimulation by Prostaglandin PGE2 and Bradykinin.

What is the initial, temporary vascular response to injury before vasodilation occurs?

Transient arteriolar vasoconstriction (lasting seconds).

Describe the mechanism and timeline of the Immediate Transient Response in vascular permeability.

Endothelial cell contraction opening interendothelial gaps in postcapillary venules, induced by Histamine/Bradykinin. Lasts 15–30 minutes.

Describe the Delayed Prolonged Response in vascular permeability.

Direct endothelial cell injury (burns, severe toxins) causing endothelial necrosis and detachment across venules, capillaries, and arterioles.

Differentiate between Exudate and Transudate based on protein content, specific gravity, and cause.

Exudate: High protein (>3 g/dL), high specific gravity (>1.020), contains cells; caused by increased vascular permeability. Transudate: Low protein (<3 g/dL), low specific gravity (<1.012), clear/few cells; caused by hydro/oncotic pressure shifts.

What are the terms for inflammation of lymphatic vessels vs. lymph nodes?

Lymphangitis (vessels) and Lymphadenitis (nodes).

What adhesion molecules mediate the Rolling phase of leukocyte extravasation?

Selectins (L-selectin on leukocytes; E-selectin and P-selectin on endothelium) binding to Sialyl-Lewis X glycoproteins.

What adhesion molecules mediate the Firm Adhesion phase of leukocyte extravasation?

Integrins (LFA-1, MAC-1, VLA-4 on leukocytes) binding to Immunoglobulins (ICAM-1, VCAM-1, MAdCAM-1 on activated endothelium).

What is Transmigration (Diapedesis) and where does it mostly occur?

Leukocytes squeezing through interendothelial junctions to enter tissue; occurs primarily in postcapillary venules.

Name 4 major chemoattractants involved in leukocyte Chemotaxis.

Bacterial products, Chemokines, Complement fragment C5a, and Leukotriene LTB4.

Contrast the arrival timeline and lifespan of Neutrophils vs. Monocytes in acute inflammation.

Neutrophils: Arrive in 6–24 hours, short-lived (die in 24–48 hours). Monocytes: Arrive in 24–48 hours, long-lived, produce growth factors for repair.

Describe the 3 steps of Phagocytosis.

1. Recognition & Attachment (opsonins bind receptors); 2. Engulfment (forming phagolysosome); 3. Killing & Degradation (via ROS/MPO and NO).

What is the primary oxygen-dependent enzyme system used by neutrophils for intracellular microbial killing?

Myeloperoxidase (MPO) combining H2O2 with Cl- to form Hypochlorite (ClO-, bleach).

What is the primary source and function of Histamine?

Source: Mast cells, basophils, platelets. Function: Arteriolar vasodilation and increased venular permeability.

Which Prostaglandin is responsible for inducing Pain and Fever?

Prostaglandin PGE2.

Contrast the primary functions of Leukotrienes LTC4/D4/E4 vs. LTB4.

LTC4/D4/E4: Vasoconstriction and increased vascular permeability. LTB4: Chemotaxis and neutrophil recruitment.

What are the local actions of TNF and IL-1 on blood vessel endothelium?

Endothelial activation—inducing the expression of adhesion molecules (selectins, integrin ligands) and increasing permeability.

What systemic pathological effects occur when systemic levels of TNF are dangerously high?

Depressed myocardial contractility (low cardiac output), systemic vasodilation, fluid leakage, and septic shock.

Name the 3 Complement activation pathways and their shared convergence enzyme.

Classical, Alternative, and Lectin pathways; all converge on C3 convertase (splitting C3 into C3a and C3b).

What are the distinct functions of Complement fragments C3a/C5a, C3b, and C5b-9 (MAC)?

C3a/C5a: Inflammation/histamine release and chemotaxis (C5a). C3b: Opsonization for phagocytosis. C5b-9 (MAC): Direct cell lysis via membrane pores.

What is the source and major inflammatory action of Bradykinin?

Source: Plasma kininogens (liver). Action: Vasodilation, increased vascular permeability, smooth muscle contraction, and pain.

Describe Serous Inflammation (definition, characteristic feature, example).

Outpouring of thin, watery, protein-poor fluid (serous exudate). Example: Skin blister or body cavity effusion.

Describe Fibrinous Inflammation (pathogenesis, microscopic feature, classic example).

Pathogenesis: Severe vascular injury leaking fibrinogen that converts to fibrin. Microscopic: Pink, eosinophilic thread-like meshwork. Example: Fibrinous Pericarditis ("bread and butter").

Define Suppurative (Purulent) Inflammation and Abscess.

Suppurative: Production of large amounts of pus (neutrophils, dead debris, liquid). Abscess: Localized walled-off collection of pus buried within tissue.

Ulcer.

A local defect/excavation on an organ surface produced by sloughing off inflamed necrotic tissue.

What anti-inflammatory cytokines drive Complete Resolution of inflammation?

IL-10 and TGF-B

What growth factors drive Healing by Scarring (Fibrosis)?

TGF-B, PDGF, FGF-2