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Anat Path > Inflammation: Acute > Flashcards

Inflammation: Acute Flashcards

1
Q

DEFINITION of inflammation

A

Inflammation is a response of vascularized tissues to infections and damaged tissues that brings cells and molecules of host defense from the circulation to the sites
where they are needed, in order to eliminate the offending agents

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2
Q

The inflammatory responses are divided into two

A

A. VASCULAR RESPONSES
B. CELLULAR RESPONSES

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3
Q

Celsus in the first century AD, listed the 4 cardinal features of inflammation
(and the 5th by virchow)

A
  • rubor(redness)-dilation of vessels
  • tumour(swelling)-extravascular fluid accumulation
  • calor(heat)- increased blood flow
  • dolor(pain).-increased pressure exerted by accumulation of interstitial fluid and mediators such as bradykinin
  • functio laesa (loss of function)- 5th sign (Virchow 1793)-
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4
Q

AIM OF INFLAMMATION

A
  • To bring plasma protein,leucocytes and tissue macrophages to the site of injury.
  • To curtail the effect of injury (checkmate infection and prevent festering sores).
  • To initiate wound healing
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5
Q

Which 2 Nobel prize winners shared a prize in in 1908 and for what discoveroes?

A

Elie metchnikoff —- Phagocytosis
Paul Ehrlich=– humoral theory of immunity

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6
Q

TYPES OF INFLAMMATION

A

• ACUTE
• CHRONIC

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7
Q

Briefly Describe Acute inflammation

A

The initial, rapid response to infections and tissue damage
Acute inflammation-rapid onset (seconds or minutes)
-relatively short duration(lasting for minutes, several hours or a few days)

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8
Q

Inflammatory reaction underlies some common chronic diseases such as (consequences of inflammation)

A

rheumatoid arthritis, atherosclerosis, lung fibrosis, hypersensitivity reactions to insect bites, drugs, and toxins.

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9
Q

Chronic inflammation may be responsive for the following:

A

• Atherosclerosis, type 2 diabetes, degenerative disorders like Alzheimer disease, and cancer.

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10
Q

Innate and adaptive immunity are associated with which types of inflammation respectively?

A

Acute inflammation is one of the reactions of the type of host defense known as innate immunity, and
chronic inflammation is more prominent in the reactions of adaptive immunity

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11
Q

Acute inflammation has three major components:

A

(1) dilation of small vessels leading to an increase in blood flow

(2) increased permeability of the microvasculature enabling plasma proteins and leukocytes to leave the
circulation

(3) emigration of the leukocytes from
the microcirculation, their accumulation in the focus of injury, and their activation to eliminate the offending agent (phagocytosis)

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12
Q

CAUSES OF ACUTE INFLAMMATION

A

• Infections: bacterial, viral, fungal, parasitic and microbial toxins

• Tissue necrosis : ischemia (myocardial infarct), trauma, hypoxia and physical and chemical injury (thermal injury, burns,frostbite, irradiation,environmental chemicals).

• Foreign bodies: splinters, dirts, sutures.

• Immune reactions: hypersensitivity reactions or autoimmune diseases.

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13
Q

EXUDATION

A

EXUDATION:The movement of fluid, proteins, and blood cells from the vascular system into the interstitium or body cavities.

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14
Q

Exudate

A
  • Exudate: Are extravascular fluid having high protein concentration, contains cellular debris, and has a high specific gravity.
  • Is an inflammatory response at site of injury due to increase permeability of small blood vessels.

Exudate – fluid with high specific gravity
>1.020.

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15
Q

Transudate

A

Transudate: Are fluid with low protein content (albumin), no cellular material, and low specific gravity.

  • Is blood plasma ultrafiltrate resulting from osmotic or hydrostatic imbalance across the vessel wall without an increase in vascular permeability.

Transudate- fluid with low specific gravity <1.012

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16
Q

Edema

A

Edema : Excess fluid in the interstitium or serous cavities
• This can either be an exudate or a transudate.

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17
Q

Purulent Inflammation, Purulent exudate,

A
  • Purulent exudate, inflammatory exudate rich in leukocytes, the debris of dead cells debris and microbes
  • Purulent (Suppurative) Inflammation, Abscess

Purulent inflammation is characterized by the production of pus, an exudate consisting of neutrophils, the liquefied
debris of necrotic cells, and edema fluid.

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18
Q

VASCULAR CHANGES during inflammation

A
  1. After an injury, there is initial transient constriction of arterioles for a few seconds.
  2. Then vasodilation mediated by histamine and nitric oxide occurs. This leads to increased blood flow in the injured site(HEAT and REDNESS).
  3. Increased permeability of vascular walls lead to extravasation of protein rich fluid from blood vessels to the interstitial tissue.
    note: increased vascular permeability is the hallmark of acute inflammation
  4. Stasis: due to extravasation of fluid, the red blood cells become concentrated in the dilated vessels causing increased viscosity and slowed flow of blood.
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19
Q

PATHOGENESIS OF VASCULAR LEAKAGE

What are the mechanisms are responsible for the increased permeability of postcapillary venules?

A
  1. Contraction of endothelial cells resulting in increased interendothelial spaces in venules ( through which fluid escapes) elicited by many chemical mediators: histamine, bradykinin, leukotrienes, the neuropeptide substance P.

It is called the immediate transient response because it occurs rapidly after exposure to the mediator and is usually short-lived (15 to 30 minutes) and it is the most common.

  1. Direct endothelial injury BY APOPTOSIS due to burns, microbes and toxins. In most instances leakage starts immediately
    after injury and is sustained for several hours until the damaged vessels are thrombosed or repaired. Delayed prolonged leakage, and affecting venules and arterioles.
  2. Leukocyte mediated endothelial injury. Neutrophils that adhere to the endothelium during inflammation may also injure the endothelial cells and thus amplify the reaction above.
  3. Increased transcytosis. Transport of fluids and proteins through the endothelial cell. This process may involve intracellular channels that may be stimulated by certain factors, such as vascular endothelial growth factor (VEGF), that promote vascular leakage. Vesiculovacuolar organelles located near intercellular junctions leads to leakage from the vessel via VEGF.
  4. Leakage from newly formed blood vessels which have immature intercellular junctions.
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20
Q

Major Components of Acute Inflammation (Haemodynamic Changes/ Vascular event) & Cellular Component/ Event

A

Haemodynamic Changes/ Vascular event
* Initial vasoconstriction
* Vasodilatation (Histamine, Bradykinin & PGs)
* Increased vascular permeability (Vas, bradykinin & LT)

Cellular Component/ Event
* Neutrophil polymorph is the main cell of AI
* Macrophages
* Chemical Mediators
* Chemical substances that drives the inflammatory response

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21
Q

CELLULAR EVENTS OF INFLAMMATION

A
  • Stasis disturb the axial flow of the blood cellular elements in the midline and plasmatic fluid at the periphery
  • Margination
  • Pavementing
  • Emigration
  • Chemotaxis
  • Phagocytosis:
    endocytosis formation of phagosome (vesicle containing bacteria)
    opsonization (a process by which a pathogen is marked for phagocytosis through coating of a target cell with antibodies) formation of
    cellular killing
    phagolysosome

LEUCOCYTE EXTRAVASATION AND PHAGOCYTOSIS

22
Q

What are the different molecules that play predominant roles in the different steps of extravasation?

A
  • Selectins in rolling
  • Chemokines to activate the neutrophils increase avidity of integrins.
  • Integrins - firm adhesion.
  • CD31 (PECAM-1) - transmigration.
23
Q

Types of selectins and how do they bind?

A

There are
three types of selectins:

one expressed on
1. leukocytes
(L-selectin), one on

  1. endothelium (E-selectin), and one in
  2. platelets and on endothelium (P-selectin).

Selectins bind, through their lectin domain, to sialylated forms of oligosaccharides

24
Q

The immunoglobulin family molecules include two endothelial adhesion molecules:

A
    1. ICAM-1 (intercellular adhesion molecule 1) attaches to LFA-1 and mac-1.
    1. VCAM-1 (vascular cell adhesion molecule 1), on the blood vessel wall, attaches to VLA-4 integrin on the leukocyte surface.

Both these molecules (VCAM and Lcam) serve as ligands for integrins found on leukocytes

These strengthen the adhesion interaction, causing a chnage in sytoskeleton so the leukocyte can squeeze out into the tissue space

25
Q

What are Integrins?

A

Integrins are transmembrane heterodimeric glycoproteins, made up of α and β chains, that are expressed on many cell types and bind to ligands on endothelial cells, other leukocytes, and the extracellular matrix.

26
Q

Cytokines

A

Cytokines: tumor necrosis factor (TNF), interleukin-1 (IL-1), chemokines are secreted by macropahges, mast cells, endothelial cells on encoutering microbes and dead tissue AT THE POST CAPPILLARY VENULES

  • Within 1-2 hours the endothelial cells begin to express E-selectin and the ligands for L-selectin.
27
Q

Action of other mediators

A

Other mediators such as histamine, thrombin, and platelet-activating factor (PAF), stimulate the redistribution of P-selectin from its normal intracellular stores in endothelial cell granules (called Weibel-Palade bodies) to the cell surface.
* Leukocytes express L-selectin,.
* Express ligands for E- and P-selectins, bind to the complementary molecules on the endothelial cells.

28
Q

Transmigration or Diapedesis

A

Is migration of the leukocytes through the endothelium aiding by PECAM-1 (platelet endothelial cell adhesion molecule) or CD31

  • Occurs mainly in post-capillary venules via Chemokines aiding migration through interendothelial spaces.
  • leukocytes pierce the basement membrane by secreting collagenases, and enter the extravascular tissue.
29
Q

Steps of Leukocyte Extravasation (to the site of injury)
Define chemotaxis

A

It involves the following steps :

  1. In the lumen: margination, pavementing,rolling, and adhesion to endothelium.
    Inflammation activate endothelium to bind leukocytes aiding extravasation.

Margination: Blood flow slows early in inflammation (stasis), hemodynamic conditions change (wall shear stress decreases), and more leukocytes (which are normally in the center) assume a peripheral position along the endothelial surface.
This process of leukocyte redistribution is called margination

Rolling: leukocytes adhere transiently to the endothelium, detach and bind again, thus rolling on the vessel wall. Rolling is mediated by selectins (P & E-Selectin) are found on activated endothelial cells (by mediators TNF, IL-1). L-Selectin is found on the surface of leukocytes. Corresponding ligand for all 3 are sialyated oligosaccharides e.g. Sialyl-Lewis X

Adhesion: The cells finally come to rest at some point where they adhere firmly.
Leukocytes will express integrins whilst the endothelial cells express integrin ligand (V-CAM-1 & ICAM-1) which results in binding and firm adhesion. Expression of these molecules is enhanced by cytokines (TNF & IL-1).

  1. Migration across endothelium and vessel
    wall (transmigration/ diapedesis). It is brought about by adhesion molecules on the endothelial cells and leukocytes (PECAM-1 /CD31) on both. After traversing the endothelium, leukocytes pierce the
    basement membrane, probably by secreting collagenases, and enter the extravascular tissue.
  2. Migration within the interstitium towards a chemotactic stimulus (chemotaxis): The cells then migrate toward the chemotactic gradient created by chemokines and other chemoattractants and accumulate in the extravascular site.

Chemotaxis: Locomotion along a chemical
gradient.

30
Q

What is chemotaxis?
What are chemotactic factors for neutrophils at site of injury?

A
  • Unilateral movement of leucocytes toward a chemical attractant.
  • Chemotactic factors for neutrophils at site of injury include:
  • Bacteria products.
  • Complement component - C5a
  • Arachidonic acid metabolites esp. leukotiene B4(LBT4), HETE-hydroxyeicosatetraenoic acid and kallikrein.
  • Cytokines -IL8.
31
Q

Action of chemoattractants

A
  1. Chemotactic agents bind to specific seven transmembrane G protein-coupled receptors on the surface of leukocytes.
  2. Signals induce polymerization of actin and localization of myosin filaments at the
    back.
  3. The leukocyte moves by extending filopodia that pull the back of the cell in the direction of extension
  4. The net result is that leukocytes migrate toward the inflammatory stimulus in the direction of the locally produced chemoattractants.
32
Q

What is phagocytosis and the processes it includes?

A
  • 1.Opsonization (identification and marking of pathogens for phagocytosis)
    1. endocytosis
  • 3.formation of phagosome
  • 4.formation of phagolysosome
  • 5.cellular killing

Phagocytosis: Ingestion of particulate material by phagocytic cells (neutrophils & monocyte-macrophages).

33
Q

Opsonisation and examples pf opsonin

A

Is the coating of a particulate material by opsonin to facilitate phagocytosis.

These opsonin include:
* Antibodies-Immunoglobulin G (IgG) subtype
* Complement protein -C3b.
* Plasma lectin

34
Q

Phagocytosis involves three distinct but interrelated steps:

A
  1. Recognition and attachment of the particle to be ingested by the leukocyte
  2. Engulfment -formation of a phagocytic vacuole
  3. Killing or degradation of the ingested material.
35
Q

Ocl-) destroys microbes by

A
  1. Halogenation.
  2. Oxidation of protein
  3. Lipid peroxidation
36
Q

Phagocytosis: Killing and Degradation

A
  • Occur effectively after phagocyte activation.
  • ROS (e.g. hydrogen peroxide) and Reactive nitrogen species (e.g. nitric oxide) are involved in killing and digestion of microbe
  • Phagocytosis initiate activity of hexose monophosphate shunt, causing an oxidative burst and supplying electron to a NADPH oxidase in the phagosomal membrane.
  • The neutropils convert O2 to Superoxide anion (O2-), which is further converted to hydrogen peroxide (H2O2) by spontaneous dismutation .

In the presence of myeloperoxidase and halide such as chloride, H2O2 is converted to hypochlorite
* Hypochlorite (OCl-) potent antimicrobial agent

  • oxidizes microbial protein and disrupts cell wall.

H2o2 can be converted to hydroxyl radical (-OH).

37
Q

What is the most efficient bactericidal system of neutrophils?

A

The H2O2-MPO-Halide system

38
Q

Serum, tissue fluids, and host cells possess antioxidant mechanisms that protect against these potentially harmful
oxygen-derived radicals

A
  • Superoxide dismutase
  • Catalase
  • Glutathione peroxidase
  • Copper containing serum protein ceruloplasmin.
  • Serum transferrin
39
Q

NO react with superoxide anion to generate______

A
  • NO react with superoxide anion to generate peroxynitrite (ONOO).
  • Function same as hypochlorite.
  • Microbial killing can also occur through action of substances in leukocyte granules i.e elastase, defensin, cationic arginine-rich granule peptide, lysozyme,lactoferrin ,cathelicidins etc
40
Q

Examples of leukocyte induced injury: Acute

A
  • Acute respiratory distress syndrome
  • Acute transplant rejection
  • Asthma
  • Glomerulonephritis
  • Reperfusion injury
  • Septic shock
  • Vasculitis
41
Q

Examples of leukocyte induced injury: Chronic

A
  • Arthritis
  • Asthma
  • Atherosclerosis
  • Chronic lung disease
  • Chronic rejection
42
Q

Defects in leukocyte function

A

Impairment of virtually every phase of leukocyte function from adherence to vascular endothelium to microbicidal activity has been identified, and the existence of clinical genetic deficiencies in each of the critical steps in the process has been described.

43
Q

Leukocyte Adhesion Deficiencies (LAD)

A

Genetic deficiencies in leukocyte adhesion molecules(impaired leucocyte adhesion and defective inflammation) could result:
Recurrent bacterial.
Individuals with LAD could present as :
1.leukocyte adhesion deficiency type 1 have a defect in the biosynthesis of the β2 chain shared by the LFA-1 and Mac-1 integrin

Defective leukocyte adhesion because of
mutations in β chain of CD11/CD18 integrinss (ICAM-1).

2.Leukocyte adhesion deficiency type 2 is caused by mutations in fucosyl transferase required for
synthesis of sialylated oligosaccharide (receptor
for selectins)

  1. Chediak Higashi syndrome - Defect in phagolysosome function, associated with infection susceptibility, nerve defect, bleeding disorder and albilism.
  2. Chronic granulomatous diseases- Defect in microbial activity - (X-link and autosomal recessive type), decreased oxidative burst
44
Q

Morphologic Patterns of Acute Inflammation is determined by

A

Acute inflammatory reactions are characterized by vascular changes and leukocyte infiltration-

. the severity of the reaction
. its specific cause
. the particular tissue and site involved determine the morphologic patterns observed.

45
Q

Morphologic Patterns of Acute Inflammation include

A

Serous
Fibrous
Purulent
Ulcers

46
Q

Serous Inflammation

A

Serous inflammation is marked by the outpouring of a thin fluid that, depending on the size of injury, is derived from either the plasma or the secretions of mesothelial cells lining the peritoneal, pleural, and pericardial cavities (called effusion).

The skin blister resulting from a burn or viral infection represents a large accumulation of serous fluid, either within or immediately beneath the epidermis of the skin

47
Q

Fibrinous Inflammation

A

With more severe injuries and the resulting greater vascular permeability, larger molecules such as fibrinogen pass the vascular barrier, and fibrin is formed and deposited in the extracellular space. A fibrinous exudate is characteristic of inflammation in the lining of body cavities, such as the meninges (meningitis), pericardium (pericarditis) and pleura (pleuritis).

48
Q

Suppurative or purulent Inflammation

A

Suppurative or purulent inflammation is characterized by the production of large amounts of pus or purulent exudate consisting of neutrophils, necrotic cells, and edema fluid. Certain bacteria (e.g., staphylococci) produce this localized suppuration and are therefore referred to as pyogenic (pus-producing) bacteria e.g. in an abcess, acute appendicitis etc.

49
Q

Ulcers

A

An ulcer is a local defect, or excavation, of the surface of an organ or tissue that is produced by the sloughing (shedding) of inflammatory necrotic tissue.

Ulceration can occur only when tissue necrosis and resultant inflammation exist on or near a surface.

50
Q

Outcomes of inflammation

A
  • Complete resolution.
  • Healing by connective tissue (fibrosis)
  • Chronic inflammation.
51
Q

A hallmark of acute inflammation is_______

A

production of protein-rich exudate - edema

52
Q

Types of chemoattractants and examples

A

Exogenous chemoattractants are:
bacterial products, including peptides that possess an N-formylmethionine terminal amino acid and some lipids.

Endogenous chemoattractants include several
chemical mediators:

(1) cytokines, particularly those of the chemokine family (e.g., IL-8);
(2) components of the complement system, particularly C5a; and
(3) arachidonic acid (AA) metabolites, mainly leukotriene B4 (LTB4)

Anat Path (26 decks)

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