Acute Inflammation

Question 1

what is inflammation

Answer 1

vascular phase

• changes in blood flow
• accumulation of exudate

cellular phase
-delivery of neutrophils

Question 2

what causes inflammation

Answer 2

trauma/ foreign body
microorganisms
hypersensitivity
other illnesses

Question 3

what are the clinical signs of acute inflammation

Answer 3

rubor
calor
tumour 
dolor
loss of function

Question 4

vascular changes to blood flow

Answer 4

vasoconstriction (seconds)
vasodilation ( minutes)- heat and redness
increased permeability - fluid and cells can escape

Question 5

what is starlings law

Answer 5

movement of fluid controlled by the balance of hydrostatic pressure and oncotic pressure

hydrostatic pressure- pressure exerted on a vessel wall by fluid- pushes fluid away

oncotic pressure- the pressure exerted by proteins- draws fluid towards

Question 6

what is stasis

Answer 6

reduced flow through vessel

Question 7

what is exudate

Answer 7

increased vascular permeability
protein rich fluid (delivers proteins to area of injury)
occurs in inflammation

delivers proteins

Question 8

what is transudate

Answer 8

vascular permeability unchanged
fluid movement due to:
-increased capillary hydrostatic pressure
-reduced capillary oncotic pressure

occurs in
-heart failure
-hepatic failure
renal failure

Question 9

how do neutrophils escape vessels

Answer 9

1) margination- movement from middle of blood vessel to periphery of blood vessel
2) rolling- stasis reduced flow of blood allow neutrophil to marginate
3) adhesion - they get tethered to one another
4) emigration ( diapedesis) - movement of neutrophil cell into interstitium through to the middle or between

Question 10

what are selectins

Answer 10

expressed on activated endothelial cells
cells activated by chemical mediators
responsible for rolling

Question 11

what are integrins

Answer 11

found on neutrophil surface
change from low affinity to high affinity state
responsible for adhesion

Question 12

how do neutrophils move through the interstitium

Answer 12

chemotaxis
movement along an increasing chemical gradient of chemoattractants:
-bacterial peptides, inflammatory mediators
-rearragement of neutrophil cytoskeleton

Question 13

what is opsoniation

Answer 13

when the C3b and Fb protein bind to the the C3b receptor on the neutrophil

Question 14

systemic complications of inflammation

Answer 14

fever
NSAIDs
leucocytosis 
malaise
reduced appetite
altered sleep
tachycardia 
Acute phase proteins: C-reactive protein release 
septic shock

Question 15

what happens after acute inflammation

Answer 15

complete resolution
repair with connective tissue- fibrosis
progression to chronic inflammation- prolonged inflammation with repair

Question 16

what causes appendicitis

Answer 16

blocked lumen- faecolith
accumulation of bacteria and exudate
increased pressure leads to perforation

Question 17

what causes pneumonia

Answer 17

strepococcus pneumoniae

Haemophilus influenzae

Question 18

signs and symptoms of pneumonia

Answer 18

shortness of breath
cough
sputum
fever

Question 19

what causes bacterial meningitis

Answer 19

inflammation of meninges
Group B strepococcus
E coli
neisseria meningitides

Question 20

signs and symptoms of meningitis

Answer 20

headache
neck stiffness
photophobia
altered mental state

FATAL

Question 21

What is absess

Answer 21

accumulation of dead and dying neutrophils
associative liquefactive necrosis
cause compression of surrounding structures

pain
blockage of ducts

Question 22

stages of pneumonia

Answer 22

congestion
red hepatisation
grey hepatisation
resolution

Question 23

inherited angio-oedema

Answer 23

autosomal dominant 
recurrent attacks of swelling over regions in the body 
allergens can trigger swelling
problem with C1 esterase inhibitor 
prolonged inflammation

Question 24

chronic granulomatous disease

Answer 24

defects in phagcytes
this phagocytes are unable to produce radicals to allow oxidative damage in pathogens
corticosteriods given to reduce inflammation
antibiotics

Question 25

alpha-1-antitrypsin deficiency

Answer 25

alpha-1-antitrypsin protects body tissues from damage by immune response against pathogens
increased risk of COPD, liver disease and panniculitis and swelling of vessels
shortness of breath
extensive cough

Question 26

how is exudate formed

Answer 26

Tissue injury is followed by the release of vasoactive mediators.

These induce arterioles to dilate and capillary hydrostatic pressure therefore increases.

Inflammatory mediators also cause endothelial cells to contract and the walls of venules to become leaky.

Fluid and plasma proteins pass out into the extravascular space as a result of the increase in capillary hydrostatic pressure and the leaky vessel walls.

As plasma proteins have passed into the extravascular space the interstitial fluid colloid osmotic pressure increases and this holds the fluid in the extravascular space.

Question 27

name some diseases in which a granuloma can be seen

Answer 27

• Tuberculosis
• Syphilis
• Leprosy
• Cat scratch disease
• Sarcoidosis
• Wegener’s granulomatosis
• Aspergillosis

Question 28

what inflammatory mediators cause vasodilation

Answer 28

histamine
serotonin
prostaglandins
nitric oxide

Question 29

which inflammatory mediators cause increased vascular permeability

Answer 29

histamine
bradykinin
leukotrienes
C3a and C5a

Question 30

which inflammatory mediators are involved in chemotaxis

Answer 30

C5a
TNF-a
IL-1
bacterial peptide

Question 31

which inflammatory mediators cause pain- increased nerve endings

Answer 31

bradykinin
substance P
prostaglandins

Question 32

which inflammatory mediators cause fever

Answer 32

IL-1
IL-6
TNF-a