Inflammation Flashcards
name a vascular change that occurs in inflammation
vasodilation
what mediates vasodilation in inflammation?
histamine
nitric oxide
what vessels undergo vasodilation in inflammation?
arterioles first, then capillaries
name five cellular changes that occur during inflammation
stasis white cell margination rolling adhesions migration
what is white cell margination?
when white cells move peripherally due to slowed rate of blood flow because of vasodilation
why do blood cells stick to vessel walls in inflammation?
the vessels express proteins on their luminal surface which have matching proteins on the WBC’s
what proteins cause blood cells to stick to the vessel walls in inflammation?
selectins (bind to VCAM)
integrins (bind to ICAM)
VCAM
ICAM
what does ICAM and VCAM stand for?
vascular cell adhesion molecule
intracellular adhesion molecule
what effect do chemokines have on blood cells sticking to the lumen?
they increase the affinity of the ligands, making the bonds longer lasting
what two things increase expression of selectin in inflammation?
histamine
thrombin
what two things increase endothelial cell expression of VCAM and ICAM in inflammation?
TNF
IL-1
what does vascular permeability due to inflammation cause?
loss of proteins
change in osmotic pressure, as water follows the proteins out
this results in swelling
name two ways that blood vessels can become permeable
endothelial cell contraction resulting in gaps between cells
direct injury
what substances cause endothelial cell contraction?
histamine
bradykinin
substance P
leukotrienes
what do blood cells do after they leave the vessel and what is this called?
they follow a chemical gradient
chemotaxis
what are the three phases in phagocytosis?
recognition + attachment
engulfment
killing + degradation
what do phagocytes use to engulf foreign material?
extensions of the cytoplasm called pseudopods
what do phagocytes produce that kill pathogens?
reactive oxygen species
reactive nitrogen species
name an ROS made by phagocytes
NADPH oxidase
name an RNS made by phagocytes
nitric oxide synthase
what are clinical features of inflammation?
rubor
calor
tumor
dolor
what is rubor?
redness
what is calor?
heat
what is tumor?
swelling
what is dolor?
pain
what cell characterises acute inflammation?
neutrophil
name four possible outcomes of acute inflammation
resolution
suppuration
organisation
chronic inflammation
what two outcomes of inflammation can progress to fibrosis?
suppuration
chronic inflammation
what does the outcome of acute inflammation depend on?
the site of injury
the type of injury
the duration of injury
what is resolution?
the complete restoration of the tissue to normal
when is resolution likely to occur?
when there is:
- minimal cell death
- capacity for tissue repair
- a good vascular supply
- easily removed injurious agent
what is suppuration?
production of pus
what is a walled off space filled with pus called?
empyema
why do abscesses and empyemas need to be removed?
they have no blood supply so cells needed for repair and antibiotics cannot reach the area
what is organisation?
scarring of damaged tissue
when does organisation occur?
lots of necrosis
lots of fibrin produced
poor blood supply
tissue damaged can regenerate
what outcome is more likely if damage goes beyond the basement membrane and why?
organisation
if it is not damaged it acts as a scaffold for resolution
what is the common response to injury in all tissues?
formation of granulation tissue
how is granulation tissue formed?
capillaries and myofibroblasts infiltrate area
deposit collagen and smooth muscle that tissues can build on top of
why does granulation tissue appear very red?
due to the new vascular supply forming
what can organisation of a large area cause?
loss of function and contraction as normal cells are replaced with fibrosis
what happens if the regenerative capacity of the liver is overwhelmed?
the liver becomes cirrhotic and can fail, meaning it can’t remove toxins from the blood and make proteins
what characterises chronic inflammation?
the presence of a lymphocyte
what is a granuloma?
an aggregate of epithelioid histiocytes
what can cause granulomas to form?
foreign body’s
endogenous substances (bone, keratin)
exogenous substances (talc, asbestos)
infections
what do granulomas caused by mycobacterium TB cause?
caseous necrosis
what is infarction?
death of tissue after loss of oxygen
what does the heart require to contract?
ATP
therefore it also needs oxygen
what fails if no ATP is produced?
the sodium potassium pump
the calcium pump
what happens when the sodium potassium pump fails?
hyperkalaemia
swelling
what happens when the calcium pump fails?
hypercalcaemia
what does hypercalcaemia stimulate?
ATPase phospholipase proteases endonuclease increased mitochondrial permeability
how long is the window before serious damage occurs in MI?
20 minutes, after which damage is irreversible and cell death starts via necrosis
what can be seen that identifies an MI in the first 20 mins?
only changes on an ECG
what are the first changes due to MI that can be seen microscopically?
pyknosis
redness
shrunken, dark nucleus
presence of contraction bands
what happens within the first day after an MI?
cell contents leak and initiate the complement cascade
causes acute inflammation, which can cause gross changes
what are the three types of necrosis?
caseous
liquefactive
coagulative
when is there the greatest risk of cardiac rupture post MI?
3-7 days after
what replaces neutrophils in cardiac tissue?
macrophages
these create a yellow appearance and can be seen on microscopy
when can’t an MI be dated and why?
if it happened more than 6 weeks ago
collagen is laid down after 2 weeks and is completed at 6 weeks
