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Pathology > Inflammation > Flashcards

Inflammation Flashcards

1
Q

What are the 5 cells you would expect to see during inflammation? How can you differentiate between them histologically?

A
  1. Eosinophils
    - red staining granules in cytoplasm due to increase proteins
    - bilobular nucleus
  2. Lymphocytes
    - v large nucleus
  3. Macrophages
    - large amount of cytoplasm
    - nucleus not round
  4. Neutrophil
    - multilobular nucleus (5 lobes)
    - granules
  5. Plasma cell
    - paranuclear hoff= pale area in cytoplasm near nucleus due to there being numerous ribosomes to enable high transcriptional activity
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2
Q

What are the cardinal signs of inflammation?

A 
Heat 
Redness 
Swelling 
Pain 
Loss of function
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3
Q

What are the basic differences between acute and chronic inflammation? (Incl different cell types)

A

Acute:

  • fast onset
  • mainly neutrophils involved
  • mild, self-limited tissue injury/fibrosis
  • prominent local and systemic signs

Chronic:

  • slow onset
  • lymphocytes and plasma cells
  • severe and progressive tissue injury
  • less prominent local and systemic signs
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4
Q

What are the main causes of acute inflammation?

A 
Infection 
Burns 
Chemicals 
Tissue death 
Immune response
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5
Q

What are the 4 stages of acute inflammation response?

A
  1. Recognition of PAMPs and DAMPs
  2. Vascular changes
  3. WBC recruitment
  4. Elimination of microbial and cellular debris
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6
Q

How are PAMPs and DAMPs involved in acute inflammation?

A

Leads to activation of macrophages, dendritic cells, mast cells and epithelial cells via methods of recognition:

  • complement
  • Toll-like receptor s
  • Inflammasome complex= Intracellular complex for recognising bacteria
PAMPS= recognise pathogen 
DAMPS= recognise extracellular ATP released from cytoplasm during cell lysis
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7
Q

How are chemical mediators involved in the vascular changes of acute inflammation?

A

Released in response to DAMPs/PAMPs

Histamine + prostaglandins= vasodilation
C3a + C5a + leukotrienes= increased vascular permeability

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8
Q

What are the vascular changes associated with acute inflammation?
How do these changes lead to blood stasis? Why is this important?

A
  1. Vasodilation
  2. Increased permeability
  3. Leukocyte margination

-Increased permeability leads to plasma entering extracellular space
-concentration for erythrocytes increased which results in congestion and increased blood viscosity
= blood flow decreased -> blood stasis
Enables leukocytes to migrate to endothelium

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9
Q

What enables leukocyte margination in acute inflammation?

A

Blood stasis

Loss of axial streaming due to vasodilation causing plasma to enter extracellular space i.e. would normally preferentially occupy periphery of blood stream

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10
Q

Describe the processes involved in the 5 stages of WBC recruitment in acute inflammation and the adhesion molecules involved.

Which molecules establish the chemotactic gradient?

A
  1. Margination= WBC move to blood periphery
    - no specific adhesion molecules involved i.e. relies on blood stasis and loss of axial streaming
  2. Rolling= weak binding to endothelium
    - selectins
  3. Adhesion= firm adhesion
    - integrins
  4. Transmigration= Movement to extravascular space
    - platelet endothelial cell adhesion molecule-1 (PECAM-1)
  5. Chemotaxis
    - chemotactic substances= bacterial products/complement components/leukotrienes/chemokines
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11
Q

How are microbes eliminated as part of acute inflammation?

A
  1. Phagocytosis
    Opsonins (IgG or C3b) recognise and ATTACH microbe to leukocyte
    Pseudopods ENGULF particle to form phagocytic vacuole
    RO species and lysosomal enzymes released to KILL AND DEGRADE
  2. NETs
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12
Q

What are the histological features of acute inflammation?

A

Increased cell wall diameter

Marginalisation of neutrophils to endothelium

Congested, dilated vessels

Scattered macrophages

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13
Q

What is the difference between purulent exudate and an abscess?

A

PE= formed from neutrophils, liquefactive necrosis and oedema fluid

Abscess= walled-off collection of pus

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14
Q

What are causes chronic inflammation? Try to give examples.

A
  1. Progression from acute inflammation
    Eg Repeated acute inflammatory episodes (peptic ulcer)
    Eg Persistence of injury without resolution (undrained abscess)
2. Primary chronic inflammation 
Eg Intracellular infection (Hep B and C)
Eg Foreign body reaction (exogenous and endogenous)
Eg Autoimmune disease 
Eg Rejection of organ transplant
Eg Unknown aetiology
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15
Q

What are the 3 components of chronic inflammation?

A
  1. Tissue infiltration by mononuclear cells
  2. Tissue distribution
  3. Healing and repair
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16
Q

Give examples of mononuclear cells. What are their roles in chronic inflammation?

A

T lymphocytes

  • CD4+ = activate effector cells and co-operate humoral response
  • CD8+ = effector cells i.e. direct apoptosis or cytotoxic cytokines production

B lymphocytes
-differentiate into plasma cells which secrete Igs

Macrophages
-Activated by cytokines or inflammatory mediators
NOTE: also present in late stages of acute inflammation to remove tissue debris + promoting tissue repair

17
Q

What are the 2 possible origins of macrophage in chronic inflammation?

What are the characteristics of an activated macrophage?

A
  1. Circulating monocytes= diff in tissue
  2. Resident tissue population eg Kupffer cells in liver and Alveolar macrophages in lungs

Increased size
Mobility
Phagocytic activity
Production of substances promoting angiogenesis and fibrosis

18
Q

Which 3 CD4+ TC subsets are associated with chronic inflammation? What cytokines are release and what functions do they mediate?

A

Th1

  • IFN-gamma
  • M1 polarisation

Th2

  • IL-4/5/13
  • eosinophil recruitment (associated with IgE response i.e. parasite response)
  • M2 polarisation

Th17

  • IL-17
  • neutrophil recruitment
19
Q

What is a granuloma and what are possible causes?

A

Aggregation of macrophages with epitheliod morphology, large vesicular nuclei and eosinophilic cytoplasm (can fuse to form giant cells)

  1. Infection eg TB/Fungi/parasites/Syphilis
  2. Foreign body (exogenous or endogenous)
  3. Drugs eg Phenylbutazone (NSAID) + sulfonamides (antibiotics) cause hepatic granulomas
  4. Crohn’s disease
  5. Sarcoidosis
20
Q

What are examples of time when acute inflammation involves lymphocytes rather than neutrophils?

A

Acute viral hepatitis
Viral meningitis
Viral myocarditis
Acute AI hepatitis

21
Q

When is chronic inflammation associated with neutrophils?

A

Acute on chronic inflammation eg cholecystitis

Immune complex mediated glomerulonephritits

22
Q

What are the local and system effects of inflammation? What causes the systemic effects to occur

A

LOCAL:

  • tissue injury
  • fibrosis
  • neoplasia

SYSTEMIC:

  • Fever= IL-1 and TNF increase prostaglandin prod -> affect temp balance in hypothalamus
  • Acute phase proteins (CRP/Fibrinogen/Serum amyloid A)= IL-6, IL-1 and TNF increase prod in hepatocytes
  • Leucocytosis
  • Pain= prostaglandins and bradykinin

Pathology (12 decks)

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