Infection and Immunity Wk 8 - Lesson 58

What is inflammation?

the body's response to injury to eliminate the inciting cause, rid the area of debris, and restore hemoestasis

What are the five cardinal signs of inflammation?

redness, heat, swelling, pain, loss of function

How is inflammation recognized clinically?

by the five cardinal signs of inflammation

What is the process of inflammation?

injury, chemical mediators, cellular response and vascular response, exudate

What are the categories of inflammation causes?

pathogenic organisms, poisons and toxins, mechanical and thermal injuries, immune reactions and hypersensitivities

What are examples of pathogenic organisms?

bacteria, fungus, viruses, and parasites

What are poisons and toxins?

chemicals that enter the body and inhibit homeostasis

What are mechanical and thermal injuries?

penetrating and blunt injuries, chemical and thermal burns

What are immune reactions and hypersensitivities?

excessive responses directed against the body's own cells

What does the cellular response consist of?

granulocytes and mononuclear cells activated

What cells are granulocytes?

neutrophils, eosinophils, basophils, mast cells

What cells are mononuclear cells?

monocytes/macrophages, lymphocytes

What cells activate for acute response?

granulocytes

What cells activate for chronic response?

mononuclear cells

What is the function of neutrophils?

first responding cell; fight off infection by phagocytizing pathogens and releasing extracellular enzymes

What do eosinophils respond to?

parasites and hypersensitivities

What is the function of macrophages?

phagocytize and wall off pathogens and eat-up dead cells

What is the function of basophils and mast cells?

release chemical mediators to activate more inflammation

What are the five main steps in the vascular response?

vasodilation, increased vascular permeability, change in blood flow, leukocyte margination, rolling and adhesion, leukocyte emigration

What is the order of vessels getting vasodilated?

arterioles then capillaries, then venules

What is vasodilation initiated by?

predominantly histamine and bradykinin

What is hyperemia?

excess blood in the vessels during inflammation

Why is vasodilation beneficial to the inflammatory response?

increased flow of cells, nutrients, oxygen, fluid, and other factors to the site of injury

What affects mechanism of vascular permeability?

type of injury

What are the types of injuries that cause vascular permeability?

increased blood pressure (hydraulic pressure), physiologic response due to chemical mediators, direct damage to blood vessels, damage from responding WBCs

What is the vascular permeability like in homeostasis?

amount of plasma that leaves the arterioles largely returns in the venules

What is the vascular permeability like in inflammation due to increased blood pressure?

net flow of plasma is out of arterioles, capillaries, and venules to get cells and fluid out to site of injury

What chemical mediators can change vascular permeability?

histamine, serotonin, bradykinin, prostaglandins, leukotrienes

How do chemical mediators affect vascular permeability?

bind to endothelium and cause retraction of endothelial cells and formation of widened inter-cellular gap junctions

What leaks into the interstitial space?

fluid and RBCs

What affects the location of vascular permeability?

depends on severity

How does mild injury affect vascular permeability?

leakage of post capillary venules

How long does vascular permeability change with mild injury?

transient 30-60 mins; monophasic

What is vascular permeability for mild injury mediated by?

histamine and serotonin

How does moderate injury affect vascular permeability?

leakage of post capillary venules and capillaries

How long does vascular permeability change with moderate injury?

immediate and lasts minutes to days; biphasic

How does severe injury affect vascular permeability?

leakage of post capillary venules, capillaries, and arterioles

What is vascular permeability for moderate injury mediated by?

kinin, prostaglandins, leukotrienes

How long does vascular permeability change with severe injury?

prolonged and sustained response; biphasic

What is vascular permeability for severe injury mediated by?

kinin, prostaglandins, leukotrienes, histamine, serotonin

What are examples of direct injury to blood vessels?

penetrating injuries, burns, toxins

What does direct injury to blood vessels result in?

resulting in fluid and cells released into interstitial space

Where is damage from responding white blood cells common in?

lung and glomeruli

What is hemorrhage by diapedesis?

physiologic response can cause RBCs to escape through widened cellular junctions

What is true hemorrhage?

damaged or ruptured vessels can cause hemorrhage of RBCs

Where does blood flow slow?

site of injury

What causes the increase in viscosity of blood?

loss of plasma and influx of cells and protein

What is tombstoning?

endothelial cells signaled by histamine to contract to increase vascular permeability and stick further into blood vessel causing drag

What does is the benefit of change in blood flow?

allows more nutrients, oxygen, etc. to accumulate in the vessel in the general area of injury

How does normal blood flow affect the flow leukocytes?

results in WBCs and RBCs being sucked from the periphery into the central axial zone

How does inflammation affect the flow of leukocytes?

blood stagnation results in margination as more WBCs and RBCs flow in the periphery of the vessel

What causes leukocytes to roll and adhere in the blood vessel?

WBCs make contact with cell adhesion molecules on endothelium

What is the process of transmigration?

stuck WBCs use cell-cell adhesion and pseudopodia to traverse basement membrane into the extra-vascular space

What is the process of emigration?

WBCs follow a chemical gradient from the site of extravasation to the area of injury

What chemicals can form the gradient that emigration follows?

chemokines, interleukins, complement factors, pathogen products

What affects the time it takes for emigration?

acute vs chronic inflammation

What cardinal sign does vasodilation cause?

redness and heat

What cardinal sign does increased vascular permeability cause?

swelling

What is the one mechanism of vascular response that is not involved in swelling?

stasis of blood flow

What is the difference between inflammation and congestion?

-inflammation is an active process that has increased inflow

-congestion is a passive process with decreased outflow

What is exudate?

the active part of inflammation

What is the chemical component of exudate?

factors that drive and regulate inflammation

What is the fluid component of the exudate?

medium for cells, nutrients, and other factors

What is the cellular component of exudate?

granulocytes and mononuclear cells

How are we classifying exudates?

by timeframe; acute and chronic

What are the exudates with acute inflammation?

serous, serohemorrhagic, fibrinous, catarrhal, and purulent/suppurative

What are the exudates with chronic inflammation?

granulomatous and lymphoplasmacytic

What is serous exudate composed of?

blood plasma with very few cells

How is serous exudate grossly seen?

in cavities, skin, lungs, and mucosal surfaces as clear or straw colored fluid

When is serous exudate seen?

mild or early injury that causes increased vascular permeability

How does serous exudate look microspcopically?

homogenous and pink because high in soluble protein; very few inflammatory cells but may see few red blood cells

When is serohemorrhagic exudate seen?

widespread diapedesis or mild vascular damage

How does serohemorrhagic exudate grossly look?

similar to serous fluid but with a more pronounced red-tinge

What is the benefit of serohemorrhagic exudate?

dilution, flushing, and influx of nutrient rich fluid

What is the cost of serohemorrhagic exudate?

can be problematic when fills cavities or in respiratory tract

What is the resolution to serohemorrhagic exudate?

fluid is relatively easy to reabsorb if inciting cause is eliminated but may be an indicator of more to come

When is fibrinous exudate seen?

with more pronounced inflammation that serous exudate due to increased leakiness or damage of vessels

What protein causes fibrinous exudate?

fibrinogen escaping the vasculature and is converted to fibrin

How does fibrinous exudate grossly look?

fibrin appears yellow, rough or stringy depending on the distribution

How does fibrinous exudate look microscopically?

appears haphazardly arranged in pink strands with enmeshed leukocytes

What is the benefit of fibrinous exudate?

protect surfaces from damage, blood loss, traps pathogens

What is the cost of fibrinous exudate?

severe fibrinous exudate can restrict organ function and movement

What is the resolution for fibrinous exudate?

may resolve and get reabsorbed or if inflammation is prolonged it becomes a framework for formation of fibrous scar tissue

What can fibrous scar tissue cause?

contracts as it matures and can result in more severe organ restriction and adhesions

What is the difference between fibrinous and fibrous?

-fibrinous describes fibrin, involved in clotting; can be pulled off like string

-fibrous describes connective (scar) tissue; involved in healing; cannot be pulled off

What causes catarrhal exudate?

inflammation of a mucous membrane can cause goblet cell hypertrophy and hyperplasia that secret mucus

What tissues can have catarrhal exudate?

respiratory, gastrointestinal, urogenital

What does catarrhal grossly look like?

clear with a snot-like consistency

What does catarrhal exudate microscopically look like?

deeply purple, thick, entrapped in air and fat and leukocytes

What is the benefit of catarrhal exudate?

layer of mucus protects surfaces, traps pathogens, contains inflammatory factors, and flushes foreign material

What is the cost of catarrhal exudate?

thick exudate that can be hard to clear

What is the resolution for catarrhal exudate?

if inciting cause is resolved, mucus is discharged or flushed through the system

Do goblet cells return to normal?

once inciting issue is gone, yes

What does purrulent/suppurative exudate grossly look like?

thick, yellow, opaque fluid grossly

What does purulent/suppurative exudate microscopically look like?

lots of neutrophils admixed with liquefactive necrosis; often associated with bacterial component

What prefix is associated with purulent exudate?

pyro

What is an abscess?

discrete areas of suppurative inflammation

How do you treat abscess under the skin with possible bacterial infection?

antibiotics, drain, flush, and keep empty

What are the benefits of purulent exudate?

highly effective, non-specific method of neutralizing and breaking down many pathogens and material

What is the cost of purulent exudate?

can cause massive destruction of host tissue