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PP > L3 - Acute Inflammation > Flashcards

L3 - Acute Inflammation Flashcards

1
Q

List three major causes of acute inflammation

A 
Hypersensitivity
Physical trauma
Chemical agents 
Microbial infections
foreign bodies 
necrosis
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2
Q

Give three of the five characteristic clinical signs of acute inflammation

A 
Rubor (redness)
Tumor (swelling)
Calor (heat)
Dolor (pain)
Loss of function
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3
Q

The two major stages of acute inflammation are the vascular phase and the cellular phase. Briefly describe these

A

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)

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4
Q

What are the two types of interstitial fluid. Explain the difference

A

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.

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5
Q

Give three ways in which vascular permeability can be increased

A

Histamine - causes endothelial contraction (holes between cells)
Cytokines like TNF and IL-1
Enzymes released by leukocytes

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6
Q

What is the characteristic feature of a neutrophil under the microscope

A

A tri-lobulated nucleus

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7
Q

What are the 4 steps on neutrophils in the blood to escape the blood vessels

A

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

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8
Q

What are the adhesion molecules on the neutrophils and endothelial wall surface that allow binding?

A

Endothelium - selectins

Neutrophils - integrins

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9
Q

What process do neutrophils use to move towards areas of inflammation?

A

Chemotaxis - movement along a chemical gradient left by bacterial peptides

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10
Q

How do neutrophils recognise toxins?

A

Opsonisation - toxins covered in opsonins (complement), neutrophils have receptors

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11
Q

How do neutrophils kill foreign material?

A

Phagocytosis

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12
Q

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

A

O.
OH.
H2O2

independent pathway involves fusion with lysosomes, dependent uses oxidative burst

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13
Q

Name some ways in which oedema limits damage to the body

A

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)

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14
Q

Give an example of a plasma protein that is delivered by oedema and how it limits damage

A

Fibrin (forms a mesh to limit toxin spread)

Immunoglobulins

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15
Q

Give some potential local complication of acute inflammation

A
  • 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
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16
Q

How is fever caused by inflammation

A

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

17
Q

Give some examples of systemic complications as the result of acute inflammation

A 
Septic shock (widespread hypovolaemia)
Leucocytosis 
Fever
Reduced appetite
Malaise (tiredness)
18
Q

Give some cellular signs of sepsis

Can be remembered by ABCDE

A 
Widespread vasodilation causing 
Hypotension
Breathlessness
Tachycardia
Multi-organ failure
fever
Death
19
Q

What do the cytokines IL-1 and TNF do?

A

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

20
Q

Would a high lymphocyte count indicate a bacterial or viral infection?

A

Viral

21
Q

Appendicitis is the result of a blocked lumen causing an accumulation of bacteria and reduced blood flow. what most commonly blocks the lumen?

A

A faecolith (poo rock)

22
Q

Give two symptoms of pneumonia

A 
Shortness of breath
Fever
Cough 
Sputum production
Chest pain
23
Q

Name a microorganism causing pneumonia

A

Streptococcus pneumoniae

Haemophilus influenzae

24
Q

What are the symptoms of bacterial meningitis

A

Neck stiffness, fever, photophobia, altered mental state

25
Q

What is an abcess?

A

An accumulation of dead and dying neutrophils with associated liquefactive necrosis

More….can cause compression of surrounding structures and nerves (complication of acute inflammation)

26
Q

Give an example of inherited disorders of acute inflammation

A

Angio-oedema
Alpha-1 antitrypsin deficiency
Chronic granulomatous disease

27
Q

See flow chart for acute inflammation

A

see in lecture ive added very decent pic

28
Q

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

A

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

29
Q

What does alpha-1 antitrypsin do?

A

It is a protease inhibitor that deactivates enzymes released by neutrophils at site of inflammation

30
Q

Give a classical description of a patient with alpha-1 antitrypsin deficiency

A

Young with emphysema (lung damage from inflammation) and possible liver disease

31
Q

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

A

T

32
Q

Look at bacterial meningitis, lobar pneumonia etc extra notes I’ve added to the lecture

A

Yes

33
Q

How does acute inflammation bring about an effective response to injury

A

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

34
Q

What are the symptoms of acute appendicitis

A

Vomiting/right iliac fossa pain/ fever - result of a blocked lumen

35
Q

What is ascending cholangitis? What can it lead to?

A

Inflammation of the bile duct commonly result of gallstones -> inflammation can spread to the liver and cause liver abcesses

36
Q

What are some signs and symptoms of ascending cholangitis/liver disease

A

Jaundice/RUQ pain/ fever

37
Q

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

A

T

38
Q

capillary hydrostatic pressure increases in acute inflammation due to vasodilatation of the artierioles

A

T

39
Q

alpha 1 anti-trypsin inhibits the proteases released by neutrophils, what problems do those with a deficiency commonly get?

A

Emphysema and liver disease

PP (19 decks)

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