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FPP Block 1 > Acute and Chronic Inflammation > Flashcards

Acute and Chronic Inflammation Flashcards

1
Q

What is inflammation and what are 3 general ways that it provides a protective response?

A
  • tissue response to damage or infections that bring host defense cells and molecules from the ciruclation to the site of damage
  • Protective response bc:
    • destroys/ contains harmful agent
    • Prepares for occurence of healing/repair
    • Without inflammation, infections and wounds would not heal
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2
Q

What are the four cardinal signs of inflammation?

A

Calor (heat)

Rubor (red)

Tumor (swelling)

Dolor (pain)

Functio lase (loss of function0

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3
Q

Describe the general sequence of events for an inflammatory reaction. 5 steps

A
  1. recognition by macrohages etc in cells and tissues
  2. mediators (amines, cytokines) released by macrophages, DCs and mast cells recruit leukocytes
  3. vasodilation and increased vascular permeability-leads to edema
  4. elimination of microbes and dead tissue by lymphocytes
  5. repair via cytokines and growth factors
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4
Q

How are acute and chronic inflammation different? Describe:

onset

cellular infiltrate

tissue inury, fibrosis

local ad systemic signs

A
  • ONSET
    • Acute: fast minutes
    • Chronic: slow days
  • CELLULAR INFILTRATE:
    • Acute: PMNs (neutrophils)
    • Chronic: monoctes/macrophage and lymphocytes (T/B)
  • TISSUE INJURY:
    • Acute: mild and self limited
    • Chronic: severe and progressive
  • LOCAL AND SYSTEMIC SIGNS:
    • Acute: prominent
    • Chronic: less prominent, may be subtle
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5
Q

Damage to the sit of injury/adjacent normal tissue may occur. What are 4 ways which this can occur?

A
  1. acute inflammation: resolves w/o permanent damage
  2. long standing infection (chronic): permanent damage possible
  3. autimmune disease (ex lupus)
  4. Allergies: inflammation against something that should be a toleragen
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6
Q

What recognizes abnormal stimulus in the body?

A
  1. Cells with receptors that detect the presence of infectous pathogens (Epithelial cells, Dendritic cells, phagocytes, and usually the receptor is a TLRs)
  2. sensors of cell damage that are activated by: uric acid, ATP, reduced intracellular K, cytosolic DNA. The sensors activate inflammasome
  3. circulating complement proteins
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7
Q

What is inflammasome?

A
  • sensors of cell damage would activate it
  • cytoplasmic complex recognizing parts of dead cells that trigger the activation of caspase-1 which activates IL-1 triggering leukocte recruitment
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8
Q

What are the three components of actue inflammation? (what things change)

A
  1. Dilation of small vessels
  2. increased permebility of small vessels (influenceing lymph vessels & nodes)
  3. Emigration of leukocytes from circulation, leukocyte activation
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9
Q

Describe how dilation of small vessels occurs during acute inflammation. What does this lead to?

A
  • histamine and NO induce vasodilation
  • first affects arterioles then capillary beds
  • vasodilation leads to stasis of flow/congestion resulting in erythema and calor
  • margination of leukocytes
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10
Q

How does vascular permeability increase during acute inflammation?

A
  1. endothelial cell contraction due to histamine and bradykinin
    • ​​predominately affect venules
  2. You might also get endothelial cell injury from burns or things traveling through it-increased transcytosis
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11
Q

How do lymph vessels respond to acute inflammation?

A
  • edema fluid and cellular debris drain
  • sometimes secondary lymphandentitis occurs
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12
Q

What is edema?

A
  • excess fluid in interstitia, or serosal cavities
    *
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13
Q

WHat is transdudate?

A
  • Hypocellular and low protein contetnt leading to fluid leakage
    • ex: non-inflammatory extravascular fluid, ultrafiltrate or plasma with a low specici gravity
  • Usually not from inflammation but is from liver failure or heart failure. whereas exudate is typically from inflammation/trauma. less serious thatn exudate. increased hydroststaic or decreased colloid pressure.
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14
Q

What is Exudate? What causes it?

A
  • cellular (white and RBCs) and protein rich
  • inflammatory extravasculr fluid with high specific gravity
  • caused by alteration in normal vessel permeability usually from inflammation
  • this is more serious than transudate which doesn’t have much more than fluid.
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15
Q

What is pus?

A

pirulent exudate rich in leukocytes-infected

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16
Q

Histamine:

where is it released from, in response to what, and what does it cause?

A

HIstamne:

  • released from mast cells in connective tissue near vessels
  • released in response to IL-1, trauma, complement
  • causes vasodilation and increases vascular permeability
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17
Q

Nitric Oxid (NO) where is it released from, in response to what, and what does it cause?

A
  • released by endothelial cells in response to injury and causes vasodilation
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18
Q

Bradykinin where is it released from, in response to what, and what does it cause?

A

Bradykinin is a plasma protein resulting from activation of kinin system due to exposure to a site of endothelial injury. leading to vasodilation, increased permeability and ***pain***

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19
Q

What is the origin of neutrophils

A

from hematopoetic stem cell marrow

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20
Q

What is the origin of macrophages

A
  • from hematopoietic cells in marrow (in inflammatory reactions)
  • many tissue resident macrophages (stem cells during development)
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21
Q

WHat is the life span of neutrophils?

A

1-2 days

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22
Q

What is the life span of macrophages?

A

inflammatory macrophages: days or weeks

tissue-resident macrophages: years

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23
Q

How do neutrophils respond to stimuli?

A

rapid, short-lived responses

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24
Q

how do macrophages respond to stimuli

A

more prolonged, slower, dependent on new gene transcription

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25
Q

Describe how leukocytes ahere to th endothelium

A
  • leukocytes marginate close to wall as the blood flow slows (due to vasodilation)
  • Molecules roll and adhere to endothelial cels with the help of adhesion molecules
    • Selectins: on endothelial cells, platelets, leukocytes
    • Integrins: on leukocytes
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26
Q

WHat is the role of selectin/how does it work?

A
  • exists on endothelial cells, pltelets, leukocytes
    • P-selectin, L-selectin etc.
    • not present on cell surfaces until cell activated by mediators ( histamine, thrombin, etc.
    • aid in rolling and loose attachment to endothelial cells
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27
Q

What is the role of integrin and how does it work?

A
  • integrin is on leukocytes
  • activated by expression of chemokines on endothelial cells
  • TNF and IL-1, secreted by macropages at the site of injury, increase endothelial cell ligand expression
  • results in stable attachment of leukocytes to endothelium
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28
Q

What is the difference in attachment between selectin and integrin?

A

selectin aids in loose attachment and integrins aid in stable attachment

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29
Q

What is DIapedesis?

A

movement of leukocyte through vessel wall

30
Q

Describe the process of transmigration in actue inflammation

A
  • leukocytes squeeze between endothelial walls
  • this is driven by chemokine: CD31 (PECAM) on leukocytes and endothelial cells
31
Q

How is chemotaxis involved in acute inflammation?

A
  • Chemotaxis is the movement along a chemical gradient
  • after crossing the vessel wall, cell migrate towards the injury site based upon chemotactic factor like chemokines, complement and leukotrienes
32
Q

Leukocytes are involved in acute inflammation. What activates them? when does activation occur and what are the 4 results of leukocyte activation?

A
  • Leukocytes are nuetrophils and macrophages
  • they are activated by microbes, necrotic tissue, mediators
  • activation occurs after recruitment to site of injury
  • the results are:
    • Phagocytosis
    • intracellular destruction
    • release of substances that destroy dead tissue and microbes
    • more mediator production (amplify inflammatory reaction)
33
Q

How does phagocytosis occur in inflammation?

A
  • leukocyte recognizes a microbe via a specific surface receptor or opsonins marking the microbe as a target
  • Engulfment and formation of pahgocytotic vacuole within leukocyte and fusion with a lysosome
34
Q

How are microbes are killed and degraded?

A

within a phagolysosome via ROS and leukocytes secreting enzymes into the extracellular space to degrade microbes and dead tissue

35
Q

What mediators are associated with vasodilationand what is the source?

A

HIstamine, Nitric Oxide

Source: mast cells, basophils, platelets, endothelium, macrophages, mast cells, leukocytes

36
Q

What mediators are associated with increased vascular permeability?

A

histamine, bradykinin

source: mast cells, basophils, platelets, plasma, leukocytes

37
Q

What mediators are associated with chemotaxis, leukocyte recruitment and activation

A

IL-1, TNF, Bacterial products

38
Q

What mediators are associated with fever?

A

IL-1, TNF

source: macrophages, endothelial cells, mast cells

39
Q

What medators are associated with pain?

A

bradykinin

source: mast cells, leukocytes, plasma

40
Q

What mediators are associated with tissue damage?

A

Reactive oxygen species, NO

41
Q

Describe the key steps in acute inflammation

A
  1. Recognition of injurious agent by receptors on epithelial cells and endothelial cells
  2. initiation of the inflammatory response: release of Il-1 and TNF activates endothelial cells
  3. Recruitment of leukocytes:
    1. margination: leukocyte accumulation at periphery of vessels
    2. RollingL weak and transient adhesions to endothelium (selectins)
    3. Adhesion: firm adhesion to endothelium (Integrins)
    4. Transmigration: movement through endothelium to interstitium (CD31)
  4. Leukocytes move towards site of infection (chemotaxis) and are activated by microbes, necrosis, mediators
  5. Phagocytosis and killing
42
Q

What are the 3 causes of leukocyte functional defects?

A
  • defect in leukocyte production: bone marrow suppression due to chemotherapy and/or radiation
  • defect in adhesion and chemotaxis: sepsis, diabetes, dialysis, malignancy
  • defect in phagocytosis and microbial activity: sepsis, diabetes, anemia, malnutrition
43
Q

How does acute inflammation resolve?

A
  • Resolution:
    • mediators degrade
    • vascular permeability returns to normal
    • neutrophils die (by apoptosis)
    • debris cleared by macrophages
  • OR progession to chronic inflammation
  • OR scarring or fibrosis
44
Q

What does the morphology of inflammed tissue reflect?

A

severtity of inflammation, specific cause, and tissue affected

45
Q

What are general conditions of all actue inflammation?

A
  • accumulation of leukocytes (neutrophils and macrophages) and fluid in extracellular tissue
  • dilation of small blood vessels
46
Q

List the 3 subtypes (morphologic patterns) of inflammation

A
  • serous
  • fibrinous
  • suppurative
47
Q

Describe Serous inflammation and list examples

A
  • Mildest form of acute inflammation
  • outpouring of thin fluid (very few cells or proteins) from plasma or serosal cavity linings due to injury of surface epithelia
  • examples:
    • peritoneal, pleural, or pericardial effusions-CHF, fluid overload
    • Skin blister from burn, viral infection or trauma
48
Q

Describe Fibrinous inflammation and list examples

A
  • occurs secndary to more severe injury
  • larger vascular leaks, passage of fibrinogen, conversion to fibrin
  • affects linings: meninges, pericardium, pleura, peritoneum
  • May resolve completely or may organize leading to scarring
  • examples:
    • fibrinous pericarditis from uremia, a transmural myocardial infarct, or acute rheumatic fever
    • fibrinous pleuritis
    • fibrinous peritonitis
49
Q

Describe suppurative (purulent) inflammation

A
  • when large numbers of neutrophils are present along with necrotic cells, edema fluid, bacteria, usually liquified and called PUS
  • occurs with infections: pyogenic bacteria are most llikely (ex staph)
  • abscess
  • ex: acute appendicitis, acute bronchopneumonia, acute meninngitis
50
Q

What is an abscess?

A

central area of necrotic tissue surrounded by preserved neutrophils, dilated vessels and fibroblastic proliferation

51
Q

What is an ulcer?

A
  • local defect
  • surface of organ or tissue
  • sloughing of surface covering and necrotic inflammatory tissue
  • occurs when tissue necrosis and inflammation are present on or near a surface (skin, GI tract) may be acute or chronic
  • ex: pepic ulcer, skin ulcer
52
Q

What kind of inflammation is this?

A
  • fibrous inflammation
  • usually caused by uremia
53
Q

What kind of infection is this?

A

suppurative

Look at all of the neutrophils!

54
Q

Please summarize the initation of inflamm response

A
  • recognition of injury by cell recepors resulting in cytoking ( Il-1, TNF) production and leukocyte recruitment
55
Q

What causes chronic inflammation?

A
  • persistent infection
  • prolonged exposure to toxic agents
  • hypersensitivity disease: autoimmune, allergy
56
Q

What is chronic inflammation characterized by?

A
  • infiltration by mononuclear cells: macrophages, lymphocytes and plasma cells
  • tissue destruction from continous inflammation
  • attempts at healing: angiogenesis (blood vessel formation) and fibrosis (deposition of collagen)
57
Q

What is the role of macrophages in chronic inflammation?

A
  • macrophages persist bc of release of dead cells and stimulation by cytokines
  • they secrete products that result in continued tissue injury
58
Q

How are lymphocytes involved in chronic inflammation?

A
  • amplify and propagate chronic inflammation
    • T&Bs migrate to site and Plasma cells produce immunoglobi against persistent antigen and there is bidirectional interaction with macrophages
59
Q

What is the role of eosinophils in chronic inflammation?

A

parasitic infection and IgE mediation inflamation (allergies) using Major basic protein

60
Q

WHat are mast cells

A
  • they are found in conenctive tissue
  • they have a receptor for IgE that is specific for environmental antigen and release histamine and arachidonic acid metabolites and they are central in allergies
61
Q

What are the morphologic features of chronic inflammation?

A
  • mononuclear cell infiltrates-macrophages, lmphocytes, plasma cells
  • tissue destruction
  • attempted tissue repair: angiogenesis and fibrosis
62
Q

Describe granulomatous inflammation

A
  • aggregate of epithelioid histocytes (macrophages)
  • multinucleated giant cells
    • fusion of many macrophages, IFN-y induces giant cell formation
  • surrounding fibrosis
  • in TB: central caseous necrosis
63
Q

What is this arrow showing?

A

Angiogenesis

64
Q

What type of inflammation is typically seen in appendicitis?

A

acute suppurative inflammation

  • neutrophils through wall surface
  • no giant cells usually
65
Q

What are the systemic effects of inflammation?

A
  • Called acute phase response
  • fever
  • elevated levels of acute-phase proteins
  • leukocytosis
66
Q

What type of inflammation is this?

A

granulomatous- bc you can se the giant cell!

67
Q

WHat causes a fever and what does a fever cause?

A
  • in response to pyrogens both exgenous (endotoxins lipopolysaccharides) and endogenous (Leukocytes release IL-1 and TNF)
  • cause production of prostaglandins (PGE2) which stimulate the hypothalamu to repeat higher temepratures
68
Q

What are the effects of acute phase proteins in inflammation?

A
  • C-reactive protein, firbinogen
  • bind to microbe wall to aid in elimination
  • fibrinogen binds to erythrocytes causing stacks that sediment more rapidly than normal and therefore increased sed rate is used to monitor activity of inflammation
69
Q

What is leukocytosis?

A
  • stimulated by TNF, IL-1
    • WBC count is high (15,000-20,000)
  • neutrophilia-bacterial infection
  • lymphocytosis-viral infections
  • eosinophilial allergies, asthma, prasitic infections
  • Leukopenia-typhoid, rickettsiae
70
Q
A

FPP Block 1 (18 decks)

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