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Pathology > Inflammation > Flashcards

Inflammation Flashcards

1
Q

What is inflammation

Causes

A

-vascular and cellular response of the body to injury or invasion by pathogens

  • physical trauma
  • chemical trauma
  • hypersensitivity reaction
  • microorganisms infection
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2
Q

What is gram negative outer layer that’s bad to people

What molecules can make antigens

A
  • endotoxins lipid A
  • a liposaccharide
  • proteins
  • sugars
  • glycoprotein
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3
Q

Conditions to classify substance as antigen

A
  • immunologic : must stimulate immune response in specific cells
  • reactive : must stimulate plasma cells to produce specific antibodies
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4
Q

Describe how incomplete antigens are converted to compete and their incomplete name

How does cell membrane damage come about ( pathogens and physical )

A

-haptens bind to skin surface and become compete antigens

/bacteria release endotoxins which damage cell membrane
-physical trauma damages

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5
Q

How are mast cells activated by bacteria and how they respond

A

-endotoxins produced by bacteria bind to receptors on mast cells ( immunoglobulin E ) and this activates them

/release inflammation molecules

  • histamine
  • prostaglandins
  • leukotrines
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6
Q

Describe how bradikirins are formed

A

/in plasm are proteins called factor 7

  • enzyme coverts them to prekalikarin
  • enzyme converts to kalikarin
  • kalikarin converts kinenogen in tissue into bradikirins
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7
Q

Other route for leukotrine and prostaglandin acquisition besides mast cells

A

/when membrane is damaged it releases enzyme phospholipase AC and it breaks down phospholipids into arachadonic acid

  • lipo-oxygenase ( LPO ) converts arachadonic acid into leukotrines
  • Cox 1 and 2 ( cyclo-oxygenase) coverts arachadonic acid into prostaglandins
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8
Q

Hallmarks of acute inflammation

A 
1 edema ( swelling )
2 pain 
3 joint immobilized 
4 redness ( erythema )
5 heat
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9
Q

What do the mast cell molecules do to the endothelial

A

-activates them for inflammation

1 bind to receptor causing wiebel palade bodies inside cell to migrate to membrane and place p selectins

2 bind to receptors causing endothelial cells to contract and create gaps

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10
Q

How does edema come about

A

-after vasculature has been increases in permeability, plasma ( mainly water ) leaks into interstitial tissue , accumulates and causes swelling

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11
Q

How does pain come about in inflammation

A
  • the edema applies pressure on pain receptors in interstitial tissue and this activates them producing pain
  • bradikirins bind to pain receptors activating them and causing pain
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12
Q

What happens to smooth muscle during inflammation and the effects ( how does redness and heat come about )

Benefits of the heat

A
  • mast molecules bind to smooth muscle causing relaxation
  • allows vasculature to expand ( vasodilation)
  • more blood flows to site of inflammation ( erythema )
  • more heat present is vasodilated vessels ( heat )

/to increase metabolic processes to fight against inflammation

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13
Q

List the 3 steps of how WBC enter tissue at site of inflammation

A

1 margination
2 diapedesis
3 chemotaxis

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14
Q

Describe margination

A

-WBC have ligands on surface which bind to p/selectins on endothelial causing them to roll slowing

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15
Q

Describe how diapedesis occurs

A

-endothelial cells have PCAM which are expressed after cytokines and leukotrine influence which bind to WBC integrins to aid them in squeezing through vasculature openings

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16
Q

Describe chemotaxis

Types of chemoattractants and examples

A

-mast molecules stimulate WBC to migrate to site of inflammation

  • exogenous ( molecules from bacteria )
  • endogenous ( IL-8 , arachadonic metabolites , components of contemporary system )
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17
Q

What secretes IL-1 and TNF-alpha and their functions

A
  • macrophages

- bind to endothelial to produce e-selectins which WBC bind to

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18
Q

Function of IL-8

A

-chemotaxis

  • binds to endothelial to stimulate ICAM and VCAM production
  • binds to endothelial receptors and activates WBC integrins so they can bind to ICAM and VCAM during diapedesis
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19
Q

How does fever come about and its function

A

/IL-1 and TNF-alpha migrate to brain ( hypothalamus )and causes release of PGF-2 which resets body temps and causes fever

-increase body metabolism
/heat detrimental to some organisms

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20
Q

Effect of IL-1 and TNF-alpha at liver and it’s uses

Which other chemokine the same effect

A
  • cause production of acute phase reactant proteins ( APRP )
  • if blood test done and ARPR shows up as C-reactive protein aids in deduces presence of inflammation in body
  • IL-6
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21
Q

Effect of IL-1 and TNF-alpha on bone

Name of the process

A
  • stimulates production of WBC’s

- leukocytosis

22
Q

How does WBC fight infection
Describe

What remains !? Or can’t be digested

A

/engulf bacteria with pseudopodia into membrane bound vesicle inside cell ( phagocytosis)

  • phagosome membrane and lysosome membrane fuse forming phagolysosome
  • hydrolytic enzymes of lysosome degrade bacteria wall and cell components

-Antigens

23
Q

What are antigen presenting cells and list them

A

/cells that present antigens on membrane

  • macrophages
  • b lymphocytes cells
  • dendritic cells
24
Q

How do neutrophil extrude antigens

A

-phagolysosome membrane fuses with with membrane and antigen released via exocytosis

25
Q

How do neutrophils deal with bacteria resistant to lysosomes

A

-they sacrifice themselves
/intake O2 and converts it into reactive oxygen species ( superoxide , peroxide , hypochlorite acid ) which kill the bacteria but with cell also ( oxidative respiratory burst )

/as it is dying in release it’s chromatin which binds to bacteria and actives enzymes ( cathepsin G ) wc degenerate bacteria ( NETS ) neutrophil extracellular trap

26
Q

How is antigen presented to membrane

When is a cell now called an antigen presenting cell

Which chromosomes codes for MHC molecules

A
  • MHC-2 molecules complimentary to antigen transport it to membrane via binding
  • when MHC-2 bound to antigen is at membrane
  • chromosomes 6
27
Q

Diff of MHC 1 and 2 and what does 1 have

A

/1 is found in all nucleated cells and 2 only on antigen presenting cells

-2 has a self antigen present

28
Q

How many genes code for MHC molecules, name them and how do they cater for numerous antigen structures

What is recombination

A
  • MHC 1 : A B C
  • MHC 2 : DP , DR , DQ

/through recombination ( shuffling of nucleotides to produce diff proteins accommodate for numerous antigen structures )

29
Q

Where do antigens go

A

-released into lymph nodes

30
Q

Characteristics of acute inflammation

A

/short duration
- rapid onset

-remove injurious agent
/prevent spread
/initiate healing
-remove all necrotic tissue and cells

31
Q

What happens to lymphatic vessels during acute inflammation

A

/increased lymph flow to accommodate all excess interstitial fluid

/proliferation of lymph cells to handle increased load

32
Q

List briefly cellular response and vascular response of acute inflammation

A

/increased blood flow
-increased permeability

  • recruiting of cells
  • recognition of foreign pathogen
  • removal of foreign pathogen
33
Q

How do WBC dissolve basement membrane

A

-release collagenases

34
Q

How do leukocytes recognize foreign pathogen. List the receptors involved

A

1 toll receptors - recognize bacterial lipopolysaccharides , proteoglycans and RNA

2 GPCR - substances produced by host cells ( leukotrines , PDGF , short bacteria polypeptides

3 opsinon receptors- recognize opsinon proteins ( lectin , antibodies , complement proteins )

4 cytokines receptor - cytokines ( IL-8 )

35
Q

What is opsinosation

A

-coating of bacteria during inflammation with proteins to increase phagocytosis activity

36
Q

How is acute response terminated after injurious agent removed

A

1 stimulus for inflammation no longer persists
2 mediators for response have short half life
3 neutrophils have short duration after leaving circulation
4 leukotrines converted into anti/inflammation lipoxins
5 macrophages release anti-inflammation cytokines IL-10 and TGF
6 neural impulses inhibit inflammation response

37
Q

4 characteristic properties of chronic inflammation

A

1 ongoing tissue destruction
2 ongoing attempt to repair tissue by fibrosis
3 prolonged duration
4 has significant morbidity due to ongoing tissue damage

38
Q

Causes of chronic inflammation

A 
1 Persistent infection 
2 persistent indigestible matter 
3 immune mediated responses 
4 following acute inflammation 
5 repeated acute inflammation episodes
39
Q

What causes persistent infection , examples and what does it evoke

A

-organism difficult to remove
/mycobacterium tuberculosis
/mycobacterium leprde

-evokes hypersensitivity reaction type 4 ( containment of infection for long time by chemical mediators)

40
Q

2 Types of persistent indigestible matter and examples

A

-exogenous
/ silica , asbestos fibers

-endogenous
/ necrotic bone , urid acid deposits

41
Q

Types of immune mediated responses that causes chronic inflammation

A

/auto immune reaction
-organ transplant reaction
/unregulated immune response
-hypersensitivity reactions ( body fighting harmless antigens )

42
Q

How does a acute abscess cause chronic inflammation

A
  • if it cannot be removed by body or surgically it causes chronic abscess
43
Q

Macroscopical changes due to damage via chronic inflammation

A
  • ulcers on epithelium
  • cavitatory lesions On parenchyma tissue
  • chronic abscess
  • formation of sinuses
  • formation of fistula
44
Q

What is an abscess

How is a sinus formed

How is a fistula formed

A
  • pus filled cavity surrounded by pyogenic membrane
  • formed when abscess evades and corrodes surrounding tissue towards surface to try and drain abscess
  • 2 epithelium surfaces connected by chronic damage
45
Q

List and describe macroscopic changes due to fibrosis of chronic damage

A

/hollow organs thicken causing stricture ( hallowing of tube )

-distortion of organ : fibrous tissue tends to contract due to myofibroblasts to reduce size of scar but excessive contraction causes distortion

46
Q

List what is seen microscopically due chronic inflammation

A

1 mononuclear cell infiltration
2 tissue necrosis
3 tissue regeneration
4 multi nucleic giant cells

47
Q

Clinical manifestations of chronic inflammation

A

1 fistula
2 stricture
3 distortion of organs
4 ulcers
5 cavitatory lesions
6 chronic abscess
7 sinuses
8 end artery oblicans ( end arteries closing up )
9 metaplasia of epi surface
10 low grade long term fever due to cytokines
11 loss of appetite and weight due to inhibitatory effect of TNF-alpha

48
Q

How are macrophages recruited to site of chronic inflammation

A

1 via blood by TGF ( transforming growth factors ) , PDGF
2 proliferation of macrophages at site of inflammation
3 immobilized macrophages at site via MIF ( migration inhibition factors ) from T lymphocytes

49
Q

What does TFN/gamma do

What secretes it

A

/activate macrophages so that they can perform their function

-t cells and pathogen endotoxins

50
Q

What do macrophages do at site of chronic inflammation

A 
/released destructive agents 
1 reactive oxygen species 
2 nitric oxide 
3 proteases
4 arachnoid metabolites 
5 growth factors PDGF and VEGF to promote repair

Pathology (13 decks)

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