Acute Inflammation

Question 1

What is inflammation

Answer 1

Response of living tissue to injury

Question 2

Features of acute inflammation

Answer 2

Immediate 
Short duration
Innate 
Stereotyped- same respomse regardless what the injury is
Limits damage

Question 3

What are the two phases of acute inflammation called and what happens

Answer 3

Vascular phase- all about changes in blood flow. Accumulation of exudate
Cellular phase - delivery of neutrophils

Question 4

What is acute inflammation controlled by

Answer 4

Chemical mediators

Question 5

What causes inflammation

Answer 5

1) trauma/foreign body
2) micro-organisms
3) hypersensitity
4) other illnesses (e.g necrosis)

Question 6

What are the clinical signs

Answer 6

Rubor-redness
Tumor- swelling
Dolor- pain
Calor-heat

Question 7

Describe the vascular phase of inflammation

Answer 7

1) vasoconstriction for a few seconds
2) vasodilation for minutes- more blood can flow to affected area causing heat and redness
3) increased permeability of vessels , they become leaky.fluids and cells can escape.

Question 8

What is the starling’s law

Answer 8

Movement of fluid is controlled by the balance of hydrostatic pressure( pressure exerted on a vessel wall by fluid) and the oncotic pressure ( pressure exerted by proteins).

Question 9

What happens to hydrostatic and oncotic pressure in acute inflammation

Answer 9

Vasodilation- more blood flowing through vessels so increased capillary hydrostatic pressure
Increased vessel permeability- plasma proteins move into interstitium and increases interstitial oncotic pressure.

Question 10

What does the movement of fluid out of vessel cause

Answer 10

Increased viscosity of blood

Reduced flow through vessel- stasis

Question 11

What are the two types of interstitial fluid? Compare them

Answer 11

Exudate- increased vascular permeability
Protein rich fluid ( delivers proteins to area of injury). Occurs in inflammation. May contain some white and red cells.
Transudate- vascular permeability unchanged. Fluid movement due to increased capillary hydrostatic pressure and reduced capillary oncotic pressure. This occurs in heart failure/ hepatic failure/ renal failure

Question 12

how does a vessel wall become permeable

Answer 12

1) retraction of endothelial cells as they shrink. this is brought about by chemical mediators such as histamine, nitric oxide, leukotrienes
2) or by direct injury- by burns , toxins and direct trauma
3) leucocyte dependent injury- wbc activated in acute inflammation and release enzymes and free radicals

Question 13

how is the vascular phase effective?

Answer 13

presence of interstitial fluid dilutes toxins reducing capability to cause damage
exudate delivers proteins e.g fibrin- mesh limits spread of toxin to other parts of the body. immunoglobulins from adaptive immune response that specifically target certain antigens, microbes or toxins
fluid carries the microbes to lymph nodes and presents them to APCs stimulating an adaptive immune response.

Question 14

which white blood cell is involved in the cellular phase of acute inflammation and how can it be identified

Answer 14

neutrophils

trilobed nucleus

Question 15

what is the end goal of cellular phase

Answer 15

getting neutrophils out into the tissue so they can go out and deal with the trauma/infection etc

Question 16

how do neutrophils escape vessels

Answer 16

1) margination- movement of neutrophils from middle of blood vessels to the edge
2) rolling - brought about by weak intermittent bonds between neutrophils and endothelial cells. selections on activated endothelial cells are responsible for this
3) adhesion -brought together by tight strong bonds between neutrophils and endothelial cells. integrins on neutrophil surface are responsible for this. they have a conformational change changing them from low to high affinity state and tether in the high affinity state
4) emigration (diapedesis)- movement of neutrophils out into interstitial space.

Question 17

how do the neutrophils move through the interstitium

Answer 17

chemotaxis
movement along an increasing chemical gradient of chemoattractants.
chemoattractant are released by either the area of injury or the pathogens.
examples are bacterial peptides, inflammatory mediators.
they rearrange the neutrophil cytoskeleton to propel it to an area of high chemoattractant conc.

Question 18

what do neutrophils do ?

Answer 18

phagocytosis- neutrophil wraps around bacteria forming phagosome which then fuses with lysosomes. this produces secondary phagolysosomes .
they also release inflammatory mediators

Question 19

how do neutrophils recognise what to phagocytose

Answer 19

opsonisation
toxin will be covered in C3b and Fc (opsonins)
receptors for these are on the neutrophil surface

Question 20

how do neutrophils destroy pathogens

Answer 20

oxygen dependent- reactive oxygen intermediates (superoxide anion, hydroxyl radicals , hydrogen peroxide) or reactive nitrogen intermediates ( Nitric oxide, nitrogen dioxide)
oxygen independent - lysozyme, hydrolytic enzymes , defensins

Question 21

how is the cellular phase effective

Answer 21

removal of pathogens and necrotic tissue

releases inflammatory mediators

Question 22

what do inflammatory mediators do and where do they originate from

Answer 22

they are chemical messengers that control coordinate the inflammatory response. they originate from activated inflammatory cells, platelets, endothelial cells and toxins

Question 23

which inflammatory mediators bring about vasodilation

Answer 23

histamine
serotonin
prostaglandin
nitric oxide

Question 24

which inflammatory mediators increase vascular permeability

Answer 24

histamine
bradykinin
leukotrienes
C3a & C5a

Question 25

which inflammatory mediators are involved in chemotaxis

Answer 25

C5a TNF-a IL-1 bacterial peptides

Question 26

which inflammatory mediators bring about systemic response ( hot, sweating fever etc)

Answer 26

IL-1 IL-6 TNF-a

Question 27

which inflammatory mediators bring about pain

Answer 27

bradykinin Substance P Prostaglandin

Question 28

what are the local complications of acute inflammation

Answer 28

swelling - can lead to compression of tubes exudate build up in pericardial space resulting in a pressure called cardiac tamponade loss of fluid in burns as the exudate evaporates pain -muscle atrophy, psychical consequences

Question 29

what are the systemic complications of acute inflammation

Answer 29

fever -some inflammatory mediators(prostaglandins,IL-1,IL-6,TNF-a) are pyrogens and act on the hypothalamus to alter temp. NSAIDs are used reduce fever and pain symptoms as they block cyclo-oxygenase enzymes(involved in the production of prostaglandins) leucocytosis- increased production of abc. acute phase response- malaise(discomfort), reduced appetite , altered sleep, tachycardia. this all induces rest for healing septic shock - huge release of chemical mediators , widespread vasodilation, hypotension ,tachycardia, multi-organ failure

Question 30

what does a high CRP count suggest

Answer 30

inflammation

Question 31

what happens after acute inflammation

Answer 31

1) complete resolution- mediators dilated, vessels back to normal, neutrophils undergo apoptosis and get phagocytose, exudate is drained via lymphatics 2) fibrosis-repair with connective tissue 3) progression to chronic inflammation

Question 32

what is appendicitis, how does it present

Answer 32

inflamed appendix blocked lumen between caecum and appendix accumulation fo bacteria and exudate increasing pressure leading to perforation vague abdominal pain, sharp ;localised pain a few days later appendix is yellow/green this is the fibrin and exudate

Question 33

examples of acute inflammation

Answer 33

appendicitis pneumonia bacterial meningitis

Question 34

causes of pneumonia, signs and symptoms ,risk factors

Answer 34

streptococcus penumoniae, haemophilus influenzae shortness of breath cough sputum fever risk factors ; smoking , pre existing lung condition

Question 35

what is bacterial meningitis, what causes is and what are the signs and symptoms

Answer 35

inflammation of the meninges. this is a protective layer between brain and skull. brain is compressed caused by group b streptococcus, e.coli, neisseria meningitides headache, neck stiffness photophobia , altered mental state

Question 36

what is abscess

Answer 36

accumulation of dead or dying neutrophils | can cause compression of surrounding structures cause pain and blockage of ducts

Question 37

how do serous cavities becomes inflamed

Answer 37

exudate pours into them

Question 38

name some disorders of acute inflammation

Answer 38

hereditary angio-oedema alpha-1 antitrypsin deficiency chronic granulomatous disease