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Flashcards in MOD 2 Deck (85)
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What are 5 major causes of acute inflammation?

1. Infections (bacterial, viral, parasitic) and microbial toxins
2. Acute phase hypersensitivity reactions
3. Physical agents (thermal, irradiation)
4. Chemicals
5. Tissue necrosis (any cause)
6. Foreign bodies (splinters, dirt, sutures)


What are the 5 cardinal signs of tissue necrosis?

Rubor - redness
Tumour - swelling
Calor - heat
Dolor - pain
Loss of function - enforces rest and reduces the chance of further damage


How are changes to vascular flow brought about in acute inflammation?

Vasodilators (such as histamine) cause arterioles to dilate, increasing flow to the capillaries and capillary pressure. Venules become more leaky


How does a fluid exudate form in acute inflammation? Use Starling's Law in your explanation.

1. Semi-permeable capillary and venule membrane becomes more leaky
2. Capillary pressure increases (main driving force for fluid out of the vessels)
3. Plasma proteins escape into tissue spaces, increasing the interstitial oncotic pressure, so it roughly equals blood oncotic pressure


How does neutrophil emigration occur in acute inflammation?



What tissues changes cause rubor?

Vasodilation of arterioles in the damaged area.


What tissue changes cause tumour?

After the vasodilation of arterioles, venules become leaky and plasma can escape through tiny gaps between endothelial cells. The decrease in viscosity of the blood (increased haematocrit) within the venules, increases the resistance to blood flow in the venules, hampering the outflow of blood from the area of injury and increasing blood pressure upstream.This greater pressure increases the outflow of fluid and plasma proteins into the space within the tissues and so the inflamed area swells.


What tissue changes cause calor?

Vasodilation of arterioles by vasodilators such as histamine increases the flow and therefore the capillary pressure rises. Capillaries that are normally empty fill.

Temperature increase during inflammation only occurs at the skin, as internal organs are already the same temperature as blood.


What tissue changes cause dolor?

Pain occurs when specialised nerve endings are stimulated by mediators, especially bradykinin.


What tissue changes cause loss of function?

Reduced movement due to swelling and pain?


What are the benefits to the tissue changes seen in acute inflammation?

1. Delivery of:nutrients, oxygen, cells, plasma proteins (such as antibodies), inflammatory mediators, fibrinogen.
2. Dilution of toxins - excess fluid drains into lymph vessels and is presented to immune system in nodes
3. Maintenance of temperature
4. Stimulation of immune response
5. Destruction and removal of dead or foreign material
6. Pain and loss of function -> enforcing rest.


How do neutrophils undergo margination?

The stick to the blood vessel walls as they heed the chemotactic signal and roll along the wall until they adhere. They roll along by binding to receptors on the blood vessel surface called selectins and adhere finally using integrins (such as ICAM-1). Chemotaxins and inflammatory mediators increase the concentration of selectins and activate integrins.


How do neutrophils phagocytose material?

They engulf it -> phagosome creation. The cell's bacteriocidal granules then move toward the phagosome and fuse with it injecting their bacteriocidal substance into it (degranulation). These granules fuse with the phagosome before it is completely enclosed, therefore bacteriocidal substances leak out into the surrounding tissue interstitium, causing local tissue damage. Neutrophils can also phagocytose local necrotic tissue debris.


What are the two main mechanisms that neutrophils kill phagocytosed microbes?

oxygen dependent and oxygen independent methods


List four important chemical mediators in acute inflammation?

Complement system


What produces histamine? What is its role in acute inflammation?

Histamine is a vasoactive amine (these tend to be the first mediators to appear during inflammation) that is stored in granules in basophils, mast cells and platelets. It is released in response to many stimuli (e.g. physical damage, immune reactions and complement components) and causes myoepithelial cells to contract causing gaps to form between endothelial cells allowing plasma proteins to pass. It also causes pain, increases venule leakage and vasodilation of arterioles.


What produces bradykinin? What is its role in acute inflammation?

It is produced from circulating plasma precursors. It stimulates specialised nerve endings causing pain and increases vascular permeability.


What produces prostaglandin? What is its role in acute inflammation?

Prostaglandins are produced from membrane phospholipids. They cause vasodilation, make the skin more sensitive to pain and cause fever.


What produces proteins of the complement system? What is their role in acute inflammation?

They circulate in blood as a number of disassembled proteins. In acute inflammation they assemble into a tube which can punch holes in and kill bacteria. Assembly of this tube produces by products which are powerful inflammatory mediators e.g. C3a and C5a (chemotaxins) and C3b (opsonin).


List the local complications of acute inflammation:

1. Damage to normal tissue
2. Obstruction of tubes, compression of vital structures
3. Loss of fluid
4. Pain and loss of function


What are the systemic consequences of acute inflammation?

1. Fever
2. Leucocytosis
3. Acute phase response
4. Shock


How does resolution of acute inflammation occur?

1. Mediators have short half-lives and are degraded after release
2. As triggers of inflammation are removed the normal vascular permeability returns and there's cessation of neutrophil emigration
3. Exudate is reabsorbed into venules or flows away through lymph vessels
4. Fibrin is degraded
5. Neutrophils undergo apoptosis and are phaogcytosed along with necrotic debris by the macrophages
6. If damaged parenchymal cells can regenerate or if unable to regenerate they can form a fibrous scar.


In acute appendicitis what is the causative organisms and its affects?

Appendicitis is caused by a blockage of the hollow portion of the appendix,most commonly by a calcified "stone" made of feces. However, inflamed lymphoid tissue from a viral infection, parasites, gallstone, or tumors may also cause the blockage. This blockage leads to increased pressures within the appendix, decreased blood flow to the tissues of the appendix, and anaerobic bacterial growth inside the appendix causing inflammation. Necrosis can lead to rupture of appendix and release of contents into peritoneum.


In bacterial meningitis what is the causative organisms and its affects?

Children - Group B streptococcus, E coli, Listeria monocytogenes and Streptococcus pneumoniae
Adults - Streptococcus pneumoniae and Neissaria meningitidis
It causes inflammation of the brain and therefore a rise in intracranial pressure which can lead to neurone damage , occlusion of blood vessels leading to ischaemia and optic nerve damage, causing vision problems.


In ascending cholangitis and liver abscess what is the causative organisms and its affects?

This is an infection of the bile duct, usually caused by bacteria ascending from its junction with the duodenum. It tends to occur if the bile duct is already partially obstructed by a gallstone. It's caused mainly by gram-negative bacteris which live in the intestinal tract e.g. enterobacterus, E.coli etc...


What is the inherited disorder, hereditary angio-oedema?

A rare autosomal dominant condition in which sufferers have an inherited deficiency of C1-esterase inhibitor (a component of the complement system). Patients have attacks of non-itchy cutaneous angio-odemea (rapid oedema of the dermis, subcutaneous tissue, mucosa and submucosal tissues). They also experience recurrent abdominal pain which is due to intestinal oedema. There is often a family history of sudden death which is due to laryngeal involvement.


What is the inherited disorder, alpha-1 antitryspin deficiency?

A autsomal recessive disorder with varying levels of severity in which there are low levels of alpha-1 antitrypsin, a protease inhibitor which deactivates enzymes released by neutrophils at the site of inflammation. Patients with the disorder develop emphysema as proteases released from neutrophils within the lung act unchecked and destroy normal parenchymal tissue. Liver diease also occurs as the hepatocytes produce an abnormal version of the protein which is incorrectly folded. It polymerises and cannot be exported from the endoplasmic reticulum. This causes hepatocyte damage and eventually cirrhosis.


What is the inherited disorder, chronic granulomatous disease?

A genetic condition in which phagocytes are unable to generate the free radical superoxide, due to a genetic defect in NADPH oxidase. Therefore bacteria are phagocytosed but are unable to be killed as they are incapable of producing a respiratory burst. This results in the formation of chronic infections in the first years of life. Numerous granulomas and abscesses affecting the skin, ;lymph nodes an sometimes the lung, liver and bones occur, however they are ineffective at eminiating the infectious agent.


What is inflammation?

It is the response to injury of vascularised living tissue. It's purpose is to deliver defensive materials to a site of injury, to protect the body against infection (particularly bacterial), to clear damaged tissue and to initiate tissue repair.


What is the time scale of acute inflammation as compared to chronic inflammation?

Acute: hours or days
Chronic: months or even years