Inflammation 1-3 🗸

Question 1

Five causes of inflammation

Answer 1

infection
trauma
foreign bodies
immune reaction
necrosis

Question 2

Vascular changes in response to injury

Answer 2

changes in blood flow and blood vessel caliber (vasodilation)
changes mediated by histamine and nitric oxide
results in calor and rubor

Question 3

calor

Answer 3

heat of infected area

Question 4

rubor

Answer 4

redness of inflammation

Question 5

5 responses to injury

Answer 5

stasis
margination
rolling
adhesions
transendothelial migration

Question 6

stasis

Answer 6

blood flow slows as a result of vasodilation

Question 7

margination

Answer 7

slowed blood vessels allow WBCs to accumulate near the blood vessel wall (neutrophils are the main cell of acute inflammation)

Question 8

rolling

Answer 8

selectins stimulate WBCs to roll along the cell wall

Question 9

Adhesions

Answer 9

endothelial expression of cell adhesion molecules (ICAM and VCAM)
Adhesion molecules also expressed on WBCs - integrins and selectins
low affinity initially - affinity increased by proteoglycans + prostaglandins (VCAM and ICAM) and histamine + thrombin (selectins)

Question 10

transendothelial migration

Answer 10

WBCs able to move through vascular endothelium (leaky)
caused by direct damage or endothelial contraction which is mediated by histamine, bradykinin, substance n and leukotrienes
pass through junctions, diapedesis, transcytosis

Question 11

chemotaxis

Answer 11

Occurs after WBC has left the blood vessel
cells follow a chemical gradient and move along in

Question 12

Phagocytosis (inflammation)

Answer 12

recognition and attachment happens first (aided by opsonins)
engulfment, then killing and degradation happens

Question 13

two reactive species that help kill in phagocytosis and what produces them

Answer 13

oxygen - NADPH oxidase
nitrogen - nitric oxide species

Question 14

causes of rubor and calor

Answer 14

increase perfusion
slow flow
increased permeability of vessels

Question 15

tumour (swelling) caused by which vascular changes?

Answer 15

proteins exit the leaky blood vessels causing change in osmotic pressure

Question 16

dolor (pain)

Answer 16

mediated by prostaglandins and bradykinin

Question 17

functio laesa

Answer 17

loss of function

Question 18

What is the outcome of acute inflammation dependant on?

Answer 18

site of injury (capacity for repair)
type of injury (severity, pathogenic organisms)
duration of injury

Question 19

resolution of inflammation

Answer 19

complete restoration of tissue to normal after the removal of inflammatory components

Question 20

erosions and abrasions

Answer 20

injury with basement membrane intact
heat rapidly with complete resolution

Question 21

suppuration

Answer 21

formation of pus - neutrophils, bacteria, inflammatory debris

Question 22

Empyema

Answer 22

space filled by pus and walled off

Question 23

organisation in response to inflammation

Answer 23

scarring

Question 24

What gives increased chances of organisation

Answer 24

lots of necrosis
lots of fibrin
poor blood supply
damage goes beyond the basement membrane

Question 25

Chronic inflammation

Answer 25

characterised by lymphocytes and macrophages

Question 26

when is chronic inflammation favoured?

Answer 26

suppuration, scarring
persistence of injury
infectious agent
type of injury - autoimmune, transplant rejection

Question 27

granuloma

Answer 27

aggregate of epithelioid histiocytes (macrophages)
associated with foreign bodies - endogenous and exogenous
also associated with specific infections e.g. parasites, TB

Question 28

Myocardial infarction causes…

Answer 28

hypoxia = no oxygen = no ATP therefore Na+/K+ ATPase fails and Ca2+ pump fails

Question 29

Inflammation of the cells >20 minutes after MI

Answer 29

mild short-lived damage that doesn’t always result in tissue death, it is reversible
no microscopic changes to myocardium

Question 30

Inflammation of the cells after 20 minutes after MI

Answer 30

cell death - results in necrosis
cell shrink and become red

Question 31

Inflammation of the cells 24 hours after MI

Answer 31

cell contents leaked
complement cascade initiated
acute inflammation
necrosis - mostly coagulative

Question 32

Inflammation of the cells 24-72 hours after MI

Answer 32

total loss of nuclei and striations
heavy neutrophilic infiltrate

Question 33

Inflammation of the cells 3-7 after MI

Answer 33

heart is weakest - most vulnerable to cardiac rupture
Neutrophils fade away and are replaced by macrophages - chronic inflammation

Question 34

Inflammation of the cells 2-6 weeks after MI

Answer 34

macrophages fade away, replaced by fibroblasts
fibroblasts lay down collagen - scarring (poor blood supply)
scarring means heart cant pump as well
nerve bundles may also be damaged

Question 35

Inflammation of the cells 6+ weeks after MI

Answer 35

can’t date MI if took place longer then 6 weeks ago, only scar tissue left