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General pathology > Inflammation > Flashcards

Inflammation Flashcards

1
Q

what does inflammation aim to do?

A
  • get rid of damaged or necrotic tissue
  • remove microorganisms or other foreign material
  • sets the scene for regeneration to repair of tissues
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2
Q

how can inflammation be harmful?

A
  • hypersensitivity’s
  • autoimmune reactions
  • prolonged inflammation
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3
Q

what are the cardinal signs of inflammation?

A
  • Rubor (redness)
  • Tumor (swelling)
  • Calor (heat)
  • Dolor (pain)
  • Functio laesa (loss of function)
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4
Q

is acute inflammation a rapid or slow response to stimuli?

A

rapid

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5
Q

what 3 things happen in the rapid response to stimuli in acute inflammation?

A
  • increased blood flow
  • increased vascular permeability
  • leukocyte emigration
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6
Q

what stimuli can result in acute inflammation

A
  • microorganisms e.g parasitres or bacteria
  • Necrosis - ischaemia, trauma etc
  • hypoxia
  • Foreign bodies
  • Hypersensitivity reactions / autoimmune disease
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7
Q

How do blood vessels react to acute inflammation?

A

they change to allow plasma proteins and cells out of the circulation into the site of stimulus. They:
- release excess fluid into tissue or body cavities = called OEDEMA
- release of fluid and cells from the circulation is called = EXUDATION

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8
Q

define oedema

A

release excess fluid into tissue or body cavities

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9
Q

define exudation

A

release of fluid and cells from the circulation

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10
Q

what is an exudate?

A

extracellular fluid, rich in protein and contains cells

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11
Q

what is pus (purulent exudate) rich in?

A

leukocytes and debris of dead cell

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12
Q

ultrafiltrates of plasma are caused by what?

A

loss of osmotic pressure or high hydrostatic pressure

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13
Q

what is a transudate?

A

fluid with low protein content and little or no cellular material.

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14
Q

when there is loss of hydrostatic pressure in a vessel what is the result

A

forms transudate fluid, fluid leakage into extracellular fluid

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15
Q

when tissue gets damaged the vessels vasoconstrict and then what and what does it allow for?

A

vasodilation, the arterioles dilate opening new capillary beds in the region
- allows increased blood from to the tissue
causes erythema at the site

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16
Q

what is erythema?

A

heat and redness

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17
Q

what is vasodilation induced by?

A

histamine and nitric oxide acting on the sooth muscles of the vessels

18
Q

with vasodilation there is increased vascular permeability, what does this allow for?

A

allows escape of protein rich exudate into the tissue (oedema)

19
Q

Name the 3 mechanisms that promote the increase in vascular permeability

A
  1. contraction of endothelial cells (increased inter endothelial spaces)
  2. endothelial injury (necrosis and detachment)
  3. Increased transport through endothelial cells (transcytosis)
20
Q

How does contraction of endothelial cells increase vascular permeability

A
  • increased spaces between the endothelial cells
  • typically immediate and transient response, mediated by chemical mediators like histamine
  • sometimes delayed with prolonged leakage
21
Q

how does endothelial injury increase vascular permeability?

A
  • direct damage to endothelial cells leading to necrosis and detachment from basement membrane
  • starts immediately after injury is sustained for several hours until damaged vessels thrombosed or repaired
22
Q

how does transcytosis increase vascular permeability?

A
  • fluids and proteins can be transported through endothelial cells (trasncytosis)
    channels created and vesiculovacuolar organelle allow this transport
23
Q

with increased vascular permeability what happens to proteins? specifically fibrin

A
  • plasma leaving the vessels acts to dilute the stimulus of acute inflammation
  • fibrinogen is one of the proteins which leaves the vessels in exudates
  • fibrinogen polymerise to form fibrin
  • this fibrin stops the stimulus spreading to nearby tissue and allows leukocytes to target cause of inflammation
24
Q

what is stasis?

A

slower blood flow and increased viscosity

25
Q

what is happening for stasis to occur

A

fluid loss and increased vessel diameter results in the slower blood flow

increased concentration of red cells results in increased viscosity of blood

26
Q

stasis is observed as what?

A

vascular congestion

27
Q

how does stasis help with inflammation

A

allows leukocytes to accumulate and adhere on the vascular endothelium and migrate through the vessel wall to the stimulus

28
Q

how do lymphatic vessels react to inflammation?

A
  • lymph flow increased draining oedema fluid
  • proliferate during inflammation
  • can result in other issues: lymphangitis, lymphadenitis
29
Q

what is lymphangitis?

A

secondary inflammation of lymphatic vessels

30
Q

what is lymphadenitis?

A

draining lymph nodes become inflamed

31
Q

what is reactive/inflammatory lymphadenitis

A

lymph nodes increase in size due to hyperplasia of lymphoid follicles

32
Q

describe how leukocytes adhere to the endothelium

A
  • adhesion to endothelium: when stasis occurs there leukocytes make contact with the endothelial surface = margination. these cells start rolling along the endothelium before adhering with it. This adhesion is by complementary adhesion molecules. Cytokines enhance expression of the adhesion molecules

how
- SELECTINS are proteins that mediate rolling:
L-selectin
E-selectin
P-selectin
- the selections bind to ligands
- these selectins and ligands are expressed in response CYTOKINES
- interactions beween these two is LOW-AFFINITY, so that the leukocytes can bind, detach and re-attach quickly so they can ROLL along the endothelium

33
Q

where are these different selections expressed:
L-selectin
E-selectin
P-selectin

A

L selectin = expressed on leukocytes
E selectin = expressed on endothelial cells
P selectin expressed on platelets and endothelial cells

34
Q

Rolling slows down the luekocyte allowing stronger adhesions. What is this mediated by and how?

A

mediated by integrins

ICAM-1 on endothelial cells binds to B2 integrins

VCAM-1 on endothelial cells binds to B1 integrins

this stops the rolling, reorganises the cytoskeleton so that the leukocyte spreads out on the endothelial surface

35
Q

describe how leukocytes migrate across the vessel

A
  • once leukocytes have adhered they need to move through endothelium = diapedesis (or transmigration)
  • migration down a chemokine concentration gradient
  • PECAM-1, JAM A, JAM C mediate (receptors) transmigration
  • The leukocyte gets through basement membrane due toSECRETING COLLAGENASES
  • leukocytes adhere to extracellular matrix using intwgrins and CD44
36
Q

what are leukocyte adhesion deficiencies characterised by?

A

recurrent bacterial infections due to the inability of leukocytes to perform the steps

37
Q

what is chemotaxis?

A

migration of cells along a chemical gradient

38
Q

describe how leukocytes migrate to the stimulus?

A
  • chemotaxis, used by leukocytes migrating towards sites of injury
  • exogenous: bacterial products, such as lipids and peptides
  • endogenous: cytokines, complement system, arachidonic acid metabolites

all of these chemotactic agents bond to receptors on the surface of leukocytes

Downstream signalling alters the cytoskeleton of leukocytes, causing filopodia to move the cell in the direction of the stimulus, along the chemical gradient.

39
Q

Anne and describe the four types of receptors in the recognition of foreign organisms and dead tissue

A
  • G protein-coupled receptors found on leukocytes they recognise short bacterial peptides
  • Toll-like receptors (TLRs) Recognise components of different microbes
  • Cytokine Receptors Leukocytes express these in response to microbes
    -Opsonin Receptors proteins that can be used to kill organisms. The act of coating is called opsonisation. These receptors are present on leukocytes.
40
Q
A

General pathology (2 decks)

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