Chapter 3: Acute inflammation Flashcards
The typical inflammatory reaction develops through a
series of sequential steps. Describe in five simple steps what happens to an offending agent when it arrives at a certain tissue.
- The offending agent is recognized by host cells and molecules.
- Leukocytes and plasma proteins are recruited from the blood circulation to the site of infection.
- Leukocytes and proteins are activated and work together to destroy and eliminate the offending agent.
- This reaction is eventually terminated.
- The damages tissue is repaired.
What are characteristics of acute inflammation?
- It’s of short duration (few hours-few days)
- Exudation of fluid and plasma proteins.
- Emigration of leukocytes (neutrophils).
What happens when the reaction of acute inflammation progresses?
It becomes a chronic inflammation.
What are five clinical manifestations of an inflammation?
Exsudation (edema), heat (calor), redness (rubor), swelling (tumor), pain (dolor) and loss of function (functio laesa).
What sort of inflammation can cause a disease/illness?
Excessive inflammation and defective inflammation.
Wat are the differences between acute and chronic inflammation (name difference in onset, cellular infiltrates, how bad tissue injury)?
Onset: acute inflammation is fast (minutes-hours), chronic inflammation is slow (days).
Cellular infiltrate: in acute inflammation mainly neutrophils, in chronic infl. monocytes/macrophages and lymphocytes.
Arrange the following diseases in either acute or chronic inflammation:
arthritis, pulmonary fibrosis, glomerulonephritis, septic shock, asthma, acute respiratory distress syndrome, atherosclerosis.
Acute inflammation: acute respiratory distress syndrome, asthma, glomerulonephritis, septic shock.
Chronic inflammation: arthritis, asthma, atherosclerosis and pulmonary fibrosis.
Why is inflammation terminated when the offending agent is eliminated?
When the offending agent is eliminated, cells are no longer stimulated to produce mediators like cytokines and so can no longer activate and stimulate other cells like leukocytes. The cells that still surround the injured tissue will be broken down and cells like leukocytes die because of their short lifespan. Also, there are anti-inflammatory mechanisms that are activated when the offending agent is eliminated.
Why are anti-inflammatory mechanisms important?
Because they control the respons and prevent it from causing excessive damage to the host.
What happens when the tissue is being repaired?
Here injured tissue is replaced through regeneration of surviving cells and where there are no more effective cells it’s replaced with connective tissue (scarring).
Name four causes of inflammation.
Infections (bacterial, viral, fungal, parasitic), tissue necrosis, foreign bodies, immune reactions.
Is there always inflammation during tissue necrosis? Or does it depend on the cause of cell death?
No it doesn’t depend on the cause of cell death. Regardless of this, it always elicits inflammation.
Where are Toll-like receptors located in cells and what do they recognize/bind?
The ones located on the plasma membranes recognize bacterial product (e.g. LPS). The ones located in endosomes recognize viral and bacterial DNA/RNA.
What happens when a Toll-like receptor is activated through binding of a pathogen?
It activates transcription factors for stimulation and expression of membrane proteins. These proteins are mediators of inflammation, (anti-viral) cytokines and proteins that promote lymphocyte activation.
Where are NOD-like receptors located and what do they recognize?
They’re located in the cytosol. They recognize products of necrotic cells (uric acid and ATP), ion disturbances (loss of K+) and some microbial products.
What is the inflammasome?
A protein complex that is activated through a NOD-like receptor, which in turn activates caspase-1.
What happens when a NOD-like receptor is activated?
It activates the inflammasome, which in turn activates caspase-1. Caspase-1 activates IL-1.
What does IL-1 do?
It’s a mediator of inlammation, recruits leukocytes and induces fever.
In which type of inflammation does the inflammasome play a role in?
In chronic disorders with chronic inflammation.
Where are C-type lectin receptors located, what do they recognize and what do they do upon recognition?
They’re located on the plasma membranes of macrophages and dendritic cells. They recognize fungal glycans and create an inflammatory respons against it.
What are the two cytosolic receptors called, what do they recognize and what do they do upon recognition?
RIG-I and cytosolic DNA sensor. They recognize nucleic acids of virusses (respectively RNA and DNA) and stimulate the prodction of anti-viral cytokines.
Where are G protein-coupled receptors located, what do they recognize and what do they do upon recognition?
They’re located on leukocytes like neutrophils and macrophages and recognize bacterial peptides (N-formylmethionyl residuen). They stimulate a chemotactic respons.
What do mannose receptors recognize and what do they do upon recognition?
They recognize microbial sugars (mannose and fucose) and induce phagocytosis
What is exudation and what is typical for an exudate?
Fluid, proteins and blood cells leave the bloodvessel into interstitial tissues. An exudate has a high concentration proteins and cell debris.
What clue gives the presence of an exudate us?
The blood vessels’ permeability has increased.
What is a transudate and how does it arise?
Fluid with a low concentration of proteins or cell debris. It arises due to an osmotic or hydrostatic imbalans.
Did the permeability of the blood vessel change if there’s a transudate present?
No.
Is edema transudate of exudate?
It can be either exudate or transudate.
What is the definition of pus?
It’s an inflammatory exudate with a high concentration leukocytes and cell- and microbe debris.
What are the first few steps during the start of inflammation?
Due to the inflammation different mediators are produced which cause vasodilation of vascular smooth muscle -> increased bloodflow -> increased permeability -> fluid from blood vessel goes into extravascular tissue (forms an exudate) -> combination of vasodilation and loss of fluid causes a decrease in bloodflow and an increased viscosity -> stasis bloodflow and congestion of red blood cells -> accumulation of neutrophils and production of mediators -> leukocytes will bind to the endothelium and leaves the blood vessel
What are factors that are responsible for an increase in permeability during inflammation?
Retraction of endothelium, endothelial injury and transcytosis.
Does retraction of endothelium happen in every vein/artery?
No, it occurs mostly in post-capillary venules.
Name examples of mediators that stimulate endothelial retraction.
Histamin, NO, bradykinin, leukotrienes
What is meant by endothelial injury?
This is necrosis and detachment of endothelial cells.
What is meant by transcytosis?
Increased transport of fluids and proteins. It’s probably caused by factors like VEGF, channels are formed that stimulate vascular leakage.
What is the function of lymphatic vessels and nodes during an inflammation?
They drain accumulated oedema.
Why can inflammation result in lymphangitis or lymphadenitis?
Like blood vessels, lymphatic vessels proliferate to keep up with the increased workload. This can result in inflammation of the lymphatic vessels or nodes.
Which blood cells move in the center of a blood vessel and which blood cells move more outwards during circulation? Why?
Red blood cells are light-weighted and smaller and so tend to move faster than the larger white cells. Therefore red cells are confined to the central axial column and white cells are pushed out toward the wall of the vessel.
Why can’t white blood cells bind to the endothelium when they’re so close to it?
The fast bloodflow prevents them from binding.
What is the definition of margination?
Redistribution of leukocytes to a more peripheral position.
