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MDENT110 > Inflammation > Flashcards

Inflammation Flashcards

1
Q

List the common causes of acute inflammation

A

Infection due to:
• bacteria: exotoxins & endotoxins, enzymes
• viruses: intracellular replication causing cell damage
• parasites

Trauma

Physical & chemical agents

Tissue necrosis (death of part of tissue)
• Usually occurs due to lack of blood supply

Foreign bodies:
• splinters, dirt, sutures

Immune reactions (hypersensitivity

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2
Q

•Describe the clinical features of acute inflammation

A

Red

Hot

Swollen

Pain

Loss of function

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3
Q

•List and explain the main features of the acute inflammatory
response

A

Arterioles vasoconstrict - area becomes white (Local axon reflex)

arteriolar, capillary and venule dilation allows all the immune cells and chemical mediators to arrive- area becomes red and warm (Histamine,
serotonin, nitric
oxide,
prostaglandins)

Increased vascular permeability - causes swelling due to oedema (Histamine, C3a &
C5a, leukotrienes) (increases in spaces between endothelial cells so white cell can get to the tissues in emigration - which causes swelling)

vascular stasis - loss of fluid due to decreases in blood concentration as everything is in the tissues now, slows the blood flow

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4
Q

What 3 functions does inflammation have?

A
  • Protective
    • Destroy, wall off or dilute injurious agent
    • Initiate repair
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5
Q

What are the differences in acute and chronic inflammation?

A 
Acute
• Onset: immediate
• Short lived
• Usually single episode
• Neutrophils and other
granulocytes
Chronic
• Gradual onset
• Prolonged
• Frustrated healing
• Macrophages and
lymphocytes
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6
Q

what are some examples of acute inflammation in the oral cavity?

A
  • Abscess
  • Acute pulpitis - response to bacteria
  • Lacerations
  • Acute herpetic gingivostomatitis - caused by Herpes simplex virus
  • Parotitis - bacterial infection due to parotid gland stones
  • Reactions to piercings
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7
Q

What does increased vascular permeability occur as a result of? (3 things)

A
  1. Retraction of endothelial cells.
  2. Endothelial injury
  3. Increased transport of fluid and proteins through
    endothelial cells, known as transcytosis.
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8
Q

What type of fluid is seen in oedema of inflammation?

A

Exudate: Extravascular fluid with a high protein

content. This is what we see in inflammation

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9
Q

What is transudate?

A

Extravascular fluid with low protein content - increase in pressure of vessel but no spaces between endothelial cells , can’t get white blood cells out but fluid gets out

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10
Q

What is the role of oedema (excess fluid in the tissues) in acute inflammation?

A
  1. contains complement - proteins (membrane receptors) found in the plasma - normally inactivated, when activated form pathway, each protein turns into enzyme and amplifies itself down the pathway - enzyme cascade
    - protylysis of c3 important
  2. may contain antibodies which act as an opsonin and aids phagocytosis as the white cells have a receptor which can bind to that antibody
  3. contains clotting cascade - fibrin forms a barrier to spread of infection (fibrinogen
    converted to fibrin by thrombin).
    • Coagulation may also promote inflammation
  4. Contains Kininogens: these are converted to kinins by
    proteases (e.g.thrombin). Bradykinin- similar effect to
    histamine (vasodilation)
  5. Dilutes bacterial & other toxins
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11
Q

Which molecule is a key molecule in vasodilation and how is it stimulated?

A

trauma, complements and cytokines act on mast cells which release histamine - key molecule in vasodilation

also serotonin and nitric oxide

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12
Q

What is transcytosis?

A

Increased transport of fluid and proteins through

endothelial cells

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13
Q

What are the 3 pathways of complements linked to oedema?

A

Classical pathway - c1 activated by normal antibodies binding to antigen
alternative pathway
- pathogen produces LPS that activated c1
Lectin pathway - Lectin activates c1

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14
Q

What is the membrane attack complex?

A

series of c5-c9 proteins that punch holes in cells

MAC forms
transmembrane
channels. These disrupt
the phospholipid bilayer
= cell lysis and death
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15
Q

What does c3a stimulate?

A

Dilation and increased vascular permeability

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16
Q

What does c3a and c5a stimulate?

A

Stimulate histamine release
promotes formation of leukotrienes (attracts neutrophils) and prostaglandins (vasodilation)

attracts phagocytes - neutrophils

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17
Q

Which complement has a role in opsonisation?

A

c3b can bind to outside of pathogens and phagocytes have a c3b receptor with which to bind to this - phagocytose more easily

18
Q

What are the stages of the cellular response?

A
  1. Margination- due to vascular stasis (blood vessels dilate and WBC drop to the edge of the vessels)
  2. . Pavementation- neutrophils adhere to the endothelial cells using adhesion molecules on
    vessel wall known as selectins (bind lightly, roll and stop). Neutrophils then bind more
    strongly using integrins on their cell surface to ICAM (receptors) on endothelial
    cells (promoted by IL-1, TNF alpha)
  3. Emigration- movement of neutrophils between endothelial cells via
    chemotaxis via chemotactic gradient (e.g. IL-8, C5a)
  4. the cells aggregate in the tissues where needed
  5. Phagocytosis- neutrophils and macrophages engulf and destroy
    microorganisms/necrotic tissue
    Pseudopodia (projection of their cytoplasm) surrounds microorganism to form phagosome, and
    destroyed by reactive oxygen species and hydrolytic enzymes in lysosomes - phagolysosome forms
19
Q

Why do white blood cells not adhere to endothelial cells all the time?

A

Don’t have ICAM receptors on endothelial cells all the time

cytokines - iL-1 and TMF -alpha promotes the process which isn’t always present

20
Q

What molecules attract the white blood cells to the tissues in emigration?

A

IL-8 and c5a

21
Q

What are the 3 methods of neutrophils to destroy pathogens?

A 
Phagocytosis
• Degranulation (defensins,
lysozyme, lactoferrin)
• NETS (Neutrophil
extracellular traps)
22
Q

What type of inflammation is an abscess?

A

acute inflammation - neutrophils, dead/dying bacteria and cell debris

23
Q

What are NETs?

A

Neutrophile extracellular traps
CHROMATIN released as the neutrohpils die - attracts the enzymes and free ozygen radicals and pathogens
The DNA acts as a meshwork containing proteases

It increases the concentration of antimicrobials in an area - limits tissue damage in other area as they only gather in specifc area

24
Q

Why is there pain in acute inflammation? (2 reasons)

A
  • Increase in tissue pressure due to oedema
    • Inflammatory mediators stimulate pain fibres e.g.
    bradykinin and prostaglandins
25
Q

What are the 3 outcomes of acute inflammation?

A
  • Complete resolution - common response to trauma, bacteria gone, tissue goes back to normal, oedema drains away e.g. ulcer - cells turn over so quickly so heals well
  • Healing by fibrosis - common on skin and in specialised tissue e.g. heart and brain - cells don’t turn over as quick, pathogen removed but granulation tissue depositis - (endothelial cells and fibroblasts) which matures to become dense scar tissue that has lots of collagen

• Progression to chronic inflammation - • Acute inflammatory response fails to get rid of
injurious agent e.g. foreign-body or there is an interference with normal healing e.g. neutropenia (low wbc) or radiotherapy e.g. dental abscess causes by bacteria in tooth, acute inflamm goes away but bacteria is still there so can progress to chronic - chronic perapical granuloma or radicular cyst

26
Q

List the common causes of chronic inflammation

A

Acute inflammation failed to resolve e.g.

  • chronic and low grade rom the outset usually in response to chronic low grade stimuli

persistent injury

viral infections

chronic infections

autoimmune diseases

27
Q

Describe the clinical features of chronic inflammation

A

• minimal vascular changes

• infiltration by chronic inflamm cells -macrophages, lymphocytes
and plasma cells

• Repair- vascular granulation tissue
(fibroblasts + endothelial cells)-
may mature to give scarring

• Continued tissue destruction inflammatory agent or inflammatory
cells from host response and pathogen

28
Q

What is chronic inflammation?

A

Inflammation, repair and continued tissue
destruction occur simultaneously

Duration
• Lasts weeks, months or years.

Systemic features (fever, general malaise)
• Typically less in comparison to acute
29
Q

What are 3 examples of where acute inflammation fails to resolve?

A 
foreign body, grit, retained
sutures
• Non-vital tooth causing
continued chronic
inflammation at the root apex
• Poor healing due to
inadequate blood supply e.g. osteoradionecrosis, areas of dead bone can't respond
30
Q

What are 3 examples of chronic and low grade inflammation from the outset?

A

• Certain micro-organisms such as
mycobacteria responsible for tuberculosis
• Prolonged exposure to toxins e.g. silica
responsible for silicosis; atherosclerosisresponse to lipids in plasma
• Autoimmune disease- body mounts an
inflammatory reaction against a component of
‘self. e.g. rheumatoid arthritis

31
Q

What are 3 examples of chronic and low grade inflammation from the outset?

A

• Certain micro-organisms such as
mycobacteria responsible for tuberculosis
• Prolonged exposure to toxins e.g. silica
responsible for silicosis in the lungs; atherosclerosis response to lipids in plasma
• Autoimmune disease- body mounts an
inflammatory reaction against a component of
‘self. e.g. rheumatoid arthritis

32
Q

What are the roles of the activated macrophages in chronic inflammation?

A

Antigen
presentation stimulate
immune
response - activated T cells, then differentiates into cytotoxic T cells, T helper cells can activate B cells - plasma cells - antibodies, T cells activate macrophages (IFN-gamma)

produces growth factors.
Stimulation of
fibroblasts +
endothelial cells to
promote healing

Phagocytosis

produces cytokines (activate lymphocytes) + chemokines
attract inflammatory
cells + regulate
inflammatory response

33
Q

What are macrophages derived from?

A

Blood monocytes

activated by IFN-gamma produced by T cells

34
Q

What colour cytoplasm so eosinophils contain?

A

Pink
Major basic protein in granulues
important in parasitic infections

35
Q

Why is there ongoing tissue destruction in chronic inflammation?

A 
• Products of activated
macrophages such as free
oxygen, proteases
• Necrotic tissue promotes further
inflammation - further necrosis etc 
• Release of enzymes by
neutrophils
• Cytotoxic T cells
• Products of micro-organisms
36
Q

What two mechanisms does repair occur via?

A
  1. Regeneration: complete resolution
    to normal tissue - oral cavity
  2. Connective tissue deposition
    and scar formation: occurs in
    tissues not capable of complete
    regeneration e.g. heart/brain or where there has been
    prolonged, severe damage e.g. periodontal disease
37
Q

What is granulation tissue made up of?

A
  • Fibroblasts
  • Endothelial cells

stimulated by growth factors from macrophages to come to the area

38
Q

What is granulomatous inflammation? - type of chronic inflammation

A

collections of macrophages and giant cells (lots of macrophages combined together multinucleated) in an area combine, surrounded by a rim of lymphocytes e.g. in TB, chron’s diseases, orofacial granulomatism

  • epitheliod macrophages (round, big and pink)
  • multinucleate giant cell
  • lymphocytes
39
Q

What are the 2 types of multinucleate giant cells?

A

Foreign body type e.g. in response to stitches - nuclei randomly aranged in the cell

Langhans type - nuclei in a horse shoe shape around edge

40
Q

What are the causes of Granulomatous inflammation?

A

• Certain micro-organisms- e.g.
mycobacterium which causes
tuberculosis, syphilis, leprosy

• Certain immune reactions- e.g.
Crohn’s disease; OFG

• Response to foreign material
e.g. sutures

41
Q

How is a granulomatous inflammation different to periapical granuloma and granulation tissue?

A

periapical granuloma - no collection of macrophages, granulation tissue and chronic inflammation

granulation tissue is just granulation tissue

42
Q

What is a caseating granuloma?

A

There is some necrosis in the middle - specifically in Tb

MDENT110 (26 decks)

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