L3 - Acute Inflammation Flashcards
List three major causes of acute inflammation
Hypersensitivity Physical trauma Chemical agents Microbial infections foreign bodies necrosis
Give three of the five characteristic clinical signs of acute inflammation
Rubor (redness) Tumor (swelling) Calor (heat) Dolor (pain) Loss of function
The two major stages of acute inflammation are the vascular phase and the cellular phase. Briefly describe these
Vascular phase - vasodilation, increase in vascular permeability and exudate formation
1) changes in blood flow - initial transient vasoconstriction followed by a vasodilation to increase blood flow to the injured area (thus heat and redness).
2) movement of fluid into tissue - vascular permeability increase and an exudate oedema forms, this causes a ‘red cell stasis’ due to the remaining fluid being thick because of the loss of fluid into the surrounding it. Movement of fluid out is due to increased hydrostatic pressure and increased plasma oncotic pressure
Cellular phase
3) infiltration of inflammatory cells into tissue (mainly neutrophils in acute inflammation)
What are the two types of interstitial fluid. Explain the difference
Exudate - result of inflammation via increased vascular permeability. Protein rich.
Transudate - No change in vascular permeability, result of increased hydrostatic pressure or reduced capillary oncotic. Occurs in heart/hepatic/renal failure. Protein poor.
Give three ways in which vascular permeability can be increased
Histamine - causes endothelial contraction (holes between cells)
Cytokines like TNF and IL-1
Enzymes released by leukocytes
What is the characteristic feature of a neutrophil under the microscope
A tri-lobulated nucleus
What are the 4 steps on neutrophils in the blood to escape the blood vessels
Margination - stasis causes neutrophils to line up at the edge of the vessel
Rolling - neutrophils then roll along, intermittently sticking to the vessel wall
Adhesion - they then stick properly
Emigration (diapedesis) - emigration of neutrophils through the blood vessel wall
What are the adhesion molecules on the neutrophils and endothelial wall surface that allow binding?
Endothelium - selectins
Neutrophils - integrins
What process do neutrophils use to move towards areas of inflammation?
Chemotaxis - movement along a chemical gradient left by bacterial peptides
How do neutrophils recognise toxins?
Opsonisation - toxins covered in opsonins (complement), neutrophils have receptors
How do neutrophils kill foreign material?
Phagocytosis
Neutrophils have oxygen dependent and independent pathways depending on the situation. In both pathways, enzymes are released that can also cause damage to host tissue. Give an example of a ROS enzyme released in the oxygen dependent pathway
O.
OH.
H2O2
independent pathway involves fusion with lysosomes, dependent uses oxidative burst
Name some ways in which oedema limits damage to the body
1) diluted toxins
2) delivers plasma proteins to area of injury
3) increases lymphatic draining from area of injury - explanation - drains antigens to lymph nodes for adaptive immune response (lymphocytes)
Give an example of a plasma protein that is delivered by oedema and how it limits damage
Fibrin (forms a mesh to limit toxin spread)
Immunoglobulins
Give some potential local complication of acute inflammation
- swelling can block nearby ducts and tubes
- exudate can compress organs
- loss of fluid in burns
- pain can lead to muscle atrophy and pyscho-social consequences of pain
How is fever caused by inflammation
Endogenous pyrogens such as prostaglandins act on the hypothalamus to alter the baseline temperature - explanation - this maximises ability of WBC’s to work and kills some microbes
Give some examples of systemic complications as the result of acute inflammation
Septic shock (widespread hypovolaemia) Leucocytosis Fever Reduced appetite Malaise (tiredness)
Give some cellular signs of sepsis
Can be remembered by ABCDE
Widespread vasodilation causing Hypotension Breathlessness Tachycardia Multi-organ failure fever Death
What do the cytokines IL-1 and TNF do?
These are cytokines - They act on the bone marrow to increase production of neutrophils (bacterial infection) or lymphocytes (viral infection) and also increase vascular permeability
Would a high lymphocyte count indicate a bacterial or viral infection?
Viral
Appendicitis is the result of a blocked lumen causing an accumulation of bacteria and reduced blood flow. what most commonly blocks the lumen?
A faecolith (poo rock)
Give two symptoms of pneumonia
Shortness of breath Fever Cough Sputum production Chest pain
Name a microorganism causing pneumonia
Streptococcus pneumoniae
Haemophilus influenzae
What are the symptoms of bacterial meningitis
Neck stiffness, fever, photophobia, altered mental state
What is an abcess?
An accumulation of dead and dying neutrophils with associated liquefactive necrosis
More….can cause compression of surrounding structures and nerves (complication of acute inflammation)
Give an example of inherited disorders of acute inflammation
Angio-oedema
Alpha-1 antitrypsin deficiency
Chronic granulomatous disease
See flow chart for acute inflammation
see in lecture ive added very decent pic
Hereditary angio-oedema is a rare autosomal dominant condition which sufferers have a C1-Esterase inhibitor (component of complement system) deficiency. This means complement can’t be turned off, leading to what symptoms
Non-itchy angio-oedema (recurrent swelling of tissue just under skin or mucous membranes) of the skin
recurrent abdominal pain due to abdominal oedema
swelling of airway can cause breathlessness
What does alpha-1 antitrypsin do?
It is a protease inhibitor that deactivates enzymes released by neutrophils at site of inflammation
Give a classical description of a patient with alpha-1 antitrypsin deficiency
Young with emphysema (lung damage from inflammation) and possible liver disease
In chronic granulomatous disease phagocytes can ingest but not destroy bacteria because of a lack of ability to generate superoxide free radicals of their oxidative burst. This means numerous granulomas form leaving abscesses affecting the skin, lymph nodes and lungs to name a few. NADPH oxidase deficiency T/F
T
Look at bacterial meningitis, lobar pneumonia etc extra notes I’ve added to the lecture
Yes
How does acute inflammation bring about an effective response to injury
Vasodilation deliver nutrients and oxygen to damaged cells/
Exudate dilutes the toxins/
Acute phase proteins increase temp/
Delivery of immune cells for phagocytosis of bacteria/
Acute phase proteins stimulate pain and encourage reduction in function and rest
What are the symptoms of acute appendicitis
Vomiting/right iliac fossa pain/ fever - result of a blocked lumen
What is ascending cholangitis? What can it lead to?
Inflammation of the bile duct commonly result of gallstones -> inflammation can spread to the liver and cause liver abcesses
What are some signs and symptoms of ascending cholangitis/liver disease
Jaundice/RUQ pain/ fever
serous exudates are classically seen in blisters and burns, they are clear due to lack of infection
Fibrinous exudates are cloudy as they contain lots of fibrin, seen when blood vessels are damaged with inflammation
haemorrhagic exudate looks bloody - significant blood vessel damage with inflammation
purulent exudates are creamy white as they are rich in neutrophils, seen when there is high infection
seromas are clear and appear post-operatively
T
capillary hydrostatic pressure increases in acute inflammation due to vasodilatation of the artierioles
T
alpha 1 anti-trypsin inhibits the proteases released by neutrophils, what problems do those with a deficiency commonly get?
Emphysema and liver disease
