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Found. of Path. Processes - Block 1 > 6 - Acute and Chronic Inflammation > Flashcards

6 - Acute and Chronic Inflammation Flashcards

1
Q

What is inflammation and what is it’s purpose?

A

Tissue response to damage or infections - brings host defense cells and molecules from the circulation to the site of damage.

Protective: destroys or contains harmful agent, prepares for healing/repaid.

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2
Q

What are the four cardinal signs of inflammation?

A
  1. Heat
  2. Redness
  3. Swelling
  4. Pain
  5. Loss of function
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3
Q

What is the sequence of events that occurs in an inflammatory reaction?

A
  1. Recognition by mø, dendritic cells, and mast cells causing release of medatiors that cause…
  2. Recruitment of leukocytes (PMNs and monocytes)
  3. Vasodilation and increased vasc. perm. causing edema
  4. Elimination of microbes, dead tissue
  5. Repair
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4
Q

For acute inflammation, what is the onset, cellular infiltrate, tissue injury/fibrosis, and local/systemic signs?

A

Onset: fast (min to hours)

Infiltrate: mainly PMNs

Injury/fibrosis: mild and self-limited

Local and systemic signs: prominent

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5
Q

For chronic inflammation, what is the onset, cellular infiltrate, tissue injury/fibrosis, and local/systemic signs?

A

onset: slow (days)

Infiltrate: monocytes/macrophages and lymphocytes

Injur/fibrosis: severe and progressive

Local and systemic signs: less prominent, may be subtle

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6
Q

How can inflammation be harmful? What are two examples?

A

Damage to site of injury and nearby normal tissue

  • can tissue without permanent damage in acute inflamm
  • may cause permanent damage with long-standing infection

Autoimmune diesaes: inflamm response against self-antigens

Allergies: inflamm response against harmless antigens

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7
Q

What are some causes of inflammation?

A
  1. Infection and microbial toxins
  2. Tissue necrosis: ischemia, trauma, physical or chemical injury
  3. Foreign bodies
  4. Immune (hypersensitivity) reactions: environment or self antigens
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8
Q

An abnormal stimulus such as an extracellular microbe, other antigen, or dead cells, is recognized by what? Where are these found?

A

Receptors that detect presense of infectious pathogens:

-Epithelial cells: skin, lining of GI/Resp tract

-Dendritic cells: derived from BM progenitors, in epithelia of most organs

-Phagocytes: PMNs and monocytes/mø in connective tissue and organs

-Toll-like receptors: in PM and endosomes and recognize pathogens on cell surface and in cytoplasm

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9
Q

What are the sensors of cell damage?

A
  • Receptors that sense structures present with cell damage such as uric acid, ATP, reduced intracell K+, cytosolic DNA
  • Inflammasome: cytoplasmic complex that recognizes parts of dead cells to trigger caspase-1 to activate IL-1 to recruit leukocytes
  • circulating proteins: complement system
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10
Q

What are three components of acute inflammation?

A

1. Vascular change: dilation of small vessels

2. Vascular change: increased permeability of small vessels and responses of lymphatic vessels and lymph nodes

3. Emigration of leukocytes from circulation, leukocyte activation

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11
Q

Describe the initial vascular changes in acute inflammation? How is this induced?

A

Vasodilation induced by chemical mediators like histamine and NO.

Affects arterioles first, then capillaries and leads to stasis of blood flow that causes warmth and erythema.

Margination of leukocytes (leaving the blood)

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12
Q

Describe the vascular changes in acute inflammation that result in increased vascular permeability? How is this induced?

A

Endothelial cell contraction (histamine and bradykinin) causes immediate transient response impacting venules.

Endothelial cell injury - directly injured by burns, microbes, PMNS causes rapid trancytosis (transport of proteins through cell) and this is a delayed prolonged response.

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13
Q

What is the lymphatic vessel response to inflammation?

A

Increased flow allows drainage of edema fluid and cellular debris

Occasionally lymphangitis/lymphadenitis occurs

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14
Q

Define transudate and exudate? What is each caused by?

A

Transudate: hypocellular and low protein count - noninflammatory extravascualr fluid (low specific gravity <1.012)

-caused by osmotic or hydrostatic pressure imbalance

Exudate: cellular and protein rich - inflammatory extravascular fluid (high specific gravity >1.020)

-caused by alteration in normal vessel permeability

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15
Q

What is pus? What is specific gravity?

A

Purulent exudate rich in leukocytes

Specific gravity: ratio of density of a substance to a reference substance

-indirect measure of protein count, most often a measure of urine concentration

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16
Q

What is the function of histamine, nitric oxide, and bradykinin? What are they relseased in response to?

A

Histamine: released from mast cells in connective tissue near vessels in reasponse to IL-1, trauma, complement. Causes vasodilation and increased vasc. permeability.

Nitric oxide: released by endothelial cells in response to injury and causes vasodilation

Bradykinin: plasma protein resulting from activation of kinin system and causes vasodilation, increased perm., and pain.

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17
Q

What is the origin, lifespan, and response to stimuli of PMNs at sites of inflammation?

A

Origin: from hematopoietic stem cells in marrow

Lifespan: 1-2 days

Rapid, short-lived response to stimuli

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18
Q

What is the origin, lifespan, and response to stimuli of macrophages at sites of inflammation?

A

Origin: hematopoietic stem cells in marrow (in inflamm) and many tissue-resident macrophages (stem cells during development)

Lifespan of inflamm mø: days or weeks; tissue-resident: years

Response to stimuli: more prolonged, slower, depends on gene transcription

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19
Q

What occurs with vasodilation and stasis of blood flow?

A

Leukocytes marginate and move close to the vessel wall.

Adhesion molecules help with rolling and adhesion to endothelial cells.

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20
Q

What are two types of adhesion molecules?

A

Selectins: on endothelial cells, platelets, and leukocytes

  • Not present on cell surfaces until cell activated by mediators
  • Aids in rolling and loose attachment of leukocytes to endothelial cells

Integrins: on leukocytes: expression of chemokines on endothelial cells activate integrins

  • TNF and IL-1 secreted by mø at sitem increase endothelial cell ligand expression
  • Results in stable attachment of leukocytes to endothelium
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21
Q

How do leukocytes get through the vessel wall and get to the site of injury?

A

Transmigration: movement of leukocytes through vessel (diapedesis), cells squeeze betweenendothelial cells. Driven by CD31 (PECAM1) on leukocytes and endothelial cells.

Chemotaxis: after crossing vessel wall, migrates to site of injury. Chemotactic factors: chemokines, complement, leukotrienes,

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22
Q

What are the activators involved in leukocyte (PMNs, mø) activation that occurs after recruitment to the site of injury? What is a result of this activation?

A

Activators: microbes, necrotic tissue, mediators (LTB4, C5a, IL-8)

Results: phagocytosis, intracellular destruction, release of substances that destroy dead tissue and microbes, and more mediator production (amplify inflamm rxn).

23
Q

How does the recognition of the microbe by the leukocyte occur? What happens after recognition?

A

Opsonins (mark microbe as target) and engulfment. Then formation of a phagocytic vacuole within the leukocyte (fusion with lysosome).

Killing and degredation by ROS within the phagolysosome and secretion of enzymes by leukocytes such as elastase into the extracellular space.

24
Q

What mediators are involved in vasodilation during the inflammatory process?

A

Histamine

NO

25
Q

What mediators are involved in increased vascular permeability during the inflammatory process?

A

Histamine

Bradykinin

26
Q

What mediators are involved in chemotaxis, leukocyte recruitment, and activation during the inflammatory process?

A

IL-1, TNF, and bacterial products

27
Q

What mediators are involved in fever during the inflammatory process?

A

IL-1, TNF (released by mø to increase COX activity)

PGE2 increases temp set point

28
Q

What mediators are involved in pain during the inflammatory process?

A

Bradykinin

29
Q

What mediators are involved in tissue damage during the inflammatory process?

A

Reactive oxygen species and NO

30
Q

What are the two types of leukocyte-induced tissue injury? What is the mechanism of injury?

A

1. Innocent bystanders - adjacent tissue to site of infection damaged

2. Autoimmune disease - inflammatory response directed against host inappropriatrly

Mechanism: same as those that eliminate microbes/dead tissue

31
Q

What are the three types of defects in leukocyte functoin? What are examples of each?

A

Acquired:

  • Defect in production: BM suppression from chemo/rediation
  • Defect in adhesion and chemotaxis: sepsis, DB, dialysis
  • Defect in phagocytosis and microbicidal activity: sepsis, DB, anemia

Genetic: rare

32
Q

What happens after an acute inflammatory response?

A

Termination of response:

  • mediators degrade
  • vascular permeability returns to normal
  • PMN die via apoptosis
  • Debris cleared by mø

OR progression to chronic inflamm —> scarring/fibrosis

33
Q

What is the morphologic pattern of acute inflammation? What are subtypes?

A

Accumulation of leukocytes (PMN/mø) and fluid in EC tissue; dilation of small blood vessels

Suptypes:

  1. Serous
  2. Fibrinous
  3. Suppurative
34
Q

What is serous inflammation? What are examples?

A

Mildest form of acute inflammation.

Outpouring of thin fluid with very few cells or proteins from plasma or serosal cavity linings due to injury of surface epithelia.

Exp: pleural effusions, skin blisters from burns, viral infections, or trauma (friction)

35
Q

What is fibrinous inflammation? What does it effect?

A

Secondary to more severe injury - large vascular leaks result in passage of fibrinogen and conversion to fibrin (protein leaking).

Affects linings like meninges, pericardium, pleura, peritoneum.

36
Q

What is the most severe type of acute inflammation? What are characteristics and some examples?

A

Suppurative inflammation: large #’s of PMNs present with necrotic cells, edema fluid, and bacteria = PUS.

Infections; some bacteria more common causes (pyogenic - staph).

Causes abcesses.

Exp: acute appendicitis, acute bronchopneumonia, acute meningitis.

37
Q

What is an ulcer? What are examples?

A

Local defect on the surface of organs or tissue.

Sloughing off of surface covering and necrotic inflammatory tissue.

Exp: peptic ulcers, skin ulcers (DB)

38
Q

Abcesses are usually filled with _______ and _______ debris. These are usually walled off by ______.

A

Filled with PMNs and necrotic debris.

Walled off by fibroblasts.

39
Q

What are characteristics of chronic inflammation? What are some causes?

A

Active inflammation, tissue injury, and healing occuring at the same time- weeks to years.

Causes:

-Persistent infections

-Prolonged exposure to toxic agents

-Hypersensitity disease (autoimmune/allergic)

40
Q

What cells are involved in chronic inflammation?

A

Infiltration by mononuclear cells: mø, lymphocytes, and plasma cells.

Tissue destruction caused by inflamm cells

Attempts at healing: angiogenesis and fibrosis (collagen)

41
Q

How are macrophages involved in chronic inflammation? What do macrophages do?

A

Macrophages persist in tissues because of steady release of dead cells/microbes

  • secrete ROS, NO, and lysosomal enzymes that cause tissue injury
  • other mø stimulated by cytokines to perform repair
42
Q

How is the adaptive immune system activated during chronic inflammation?

A
  1. Lymphocytes amplify and propogate chronic inflammation
  2. Eosinophils in parasitic infection and IgE mediated inflammation (allergies) - MBP toxic to parasites and epithelial cells
  3. Mast cells are found in connective tissue and are involved in allergic and anaphylactic reactions
43
Q

What are the morphological features of chronic inflammation?

A
  1. Mononuclear cell infiltrate: macrophages, lymphocytes, and plasma cells.

  1. Tissue descruction and ongoing attempt at replacement and repair
    - angiogenesis and fibrosis
44
Q

What is granulomatous inflammation? What are the two types?

A

Distinct pattern of chronic inflmmation: activated mø with epithelioid appearance.

Types:

  1. Immune granulomas caused by persistent microbe/self-antigen (T cell response)
  2. Foreign body granulomas: no T cell mediated response
45
Q

What is the morphological appearance of granulomatous inflammation? What disease is this seen in?

A

Epithelioid histiocytes (macrophages)

Multinucleated giant cells caused by IFN-Y induced fusion of macrophages.

Tuberculosis (filled with caseous necrosis) and foreign bodies or other infections such as leprosy, syphilis.

46
Q

What is the main cell type involved in acute suppurative inflammation?

A

Neutrophils.

47
Q

What are the acute phase responses (systemic effects) to inflammation?

A

1. Fever

2. Elevated levels of acute-phase proteins

3. Leukocytosis

48
Q

Why does fever occur in chronic inflammation?

A

In response to pyrogens that cause production of prostaglandins (PGE2) that stimulates hypothal to reset at higher temp

Can be:

exogenous: LPS from bacteria

endogenous: leukocyte release, IL-1 and TNF

49
Q

Why do acute-phase protein levels elevate in chronic inflammation? What are they are what do they do?

A

Stimulated by IL-6.

CRP, fibrinogen, serum amyloid A protein

Bind microbe for elimination. Fibrin binds RBCs causing stacks that sediment > increase in the erythrocyte sedimentation (sed) rate (ESR).

50
Q

Describe the leukocytosis that occurs in chronic inflammation? What stimulates it? What does it indicate?

A

WBC count increased between 15000-20,000; accel release from BM.

-stimulated by TNF and IL-1.

Type of leukocytosis indicates underlying cause.

  • PMN: bacterial
  • Lymphocytosis: viral
  • Eosinophilia: allergies, asthma, parasite
  • Leukopenia: typhoid, rickettsiae, protozoans
51
Q

What is a localized area of pyogenic inflammation with liquefactive necrosis located in solid tissue termed?

A

An abscess

52
Q

What fuses to become a multinucleated giant cell in granulomatus inflammation?

A

Epithelioid macrophage

53
Q
A

Found. of Path. Processes - Block 1 (18 decks)

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