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Pathological Basis of Disease I > Acute Inflammation - SRS > Flashcards

Acute Inflammation - SRS Flashcards

1
Q

What are the three outcomes of acute inflammation?

A
  1. It resolves
  2. Leads to chronic inflammation
  3. ummm… leads to chronic inflammation

Okay, so I listened to this part a couple of times and it sounded like he said it led to chronic inflammation two of the three possible outcomes. If I missed something here please correct this slide.

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2
Q

What are the five general sequential steps by which the inflammatory reaction develops and subsides?

A
  1. Offending agent (in extravascular tissues) is recognized by host cells and molecules
  2. Leukocytes and plasma proteins are recruited from the circulation to the site where the agent is located.
  3. Leukocytes and proteins are activated and work together to destroy the offending substance.
  4. The reaction is controlled and terminated
  5. The damaged tissue is ​repaired
    1.
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3
Q

What type of necrosis is seen in TB?

How does the body deal with a TB infection?

A

Caseous necrosis

Since the immune system can’t kill the TB it walls it off from everything, including O2, with granulomatous tissue. This causes a dead area within the walled off section.

(granuloma encases the pathogen - leading to caseous necrosis)

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4
Q

What cell type is primarily associated with acute inflammatory reactions?

A

Neutrophils

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5
Q

What cell type is mostly associated with chronic inflammation?

A

Macrophages

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6
Q

Is asthma an acute or chronic inflammatory reaction?

A

It is both.

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7
Q

What cytokine is responsible for pulmonary fibrosis?

A

TGF-B

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8
Q

What are the 5 cardinal signs of inflammation?

A

Calor - Heat

Rubor - Redness

Tomor - Swelling

Dolor - Pain

Functio-laesa - Loss of function

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9
Q

What are the four primary causes of inflammation?

A
  1. Infections
  2. Tissue necrosis (due to Trauma, chemical, thermal injuries)
  3. Foreign Bodies
  4. Hypersensitivity (Immune reactions
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10
Q

What causes the inflammatory response seen in celiac disease?

A

GI flora that get in the lymph system or cause an antigenic change the immune system responds poorly to.

(Also this for Inflammatory Bowel Disease)

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11
Q

What type of necrosis is causing this inflammation?

A

Coagulative necrosis

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12
Q

What is the source of inflammation in this image?

A

Foreign body - This is a suture granuloma (refractile tissue surrounded by multinucleated giant cells)

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13
Q

What is this inflammatory response caused by/called?

A

Urticaria - caused by a hypersensitivity reaction

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14
Q

What are the steps of inflammation?

A

The five R’s

  1. Recognition of injurious agent
  2. recruitment of leukocytes
  3. removal of agent
  4. regulation of response
  5. Resolution (repair)
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15
Q

What are the 3 major components of acute inflammation?

A
  1. Dilation of small vessels, leading to increase in blood flow
  2. Increased permeability of the microvasculature enabling plasma proteins and leukocytes to leave the circulation
  3. Emigration of the leukocytes from the microcirculation, their accumulation in the focus of injury, and their activation to eliminate the offending agent
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16
Q

In super basic terms what is the process by which leukocytes diapedese?

A

Stop

Drop

Roll

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17
Q

Characterize the magnitude of hydrostatic pressure vs. colloid osmotic pressure and the net flow of fluid, under normal conditions.

A

Hydrostatic pressure exceeds colloid osmotic pressure normally, so there is a small net outflow from the vessels. (Per Dr. Hertz)

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18
Q

What causes exudate?

A

Increased vascular permeability due to increased interendothelial spaces

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19
Q

What are the typical contents of exudate?

A
  1. High Protein
  2. Some white cells
  3. Some red cells
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20
Q

What causes transudate?

A

Fluid leakage due to significantly increased hydrostatic pressure or decreased osmotic pressure.

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21
Q

Describe the contents of transudate.

A

Low protein

Few cells

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22
Q

A two year old girl’s urinalysis detects elevated protein levels. A sample of fluid is taken from the patients edemetous regions. What type of fluid is this?

What is this condition called?

A

Transudate

Nephrotic Syndrome

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23
Q

In a patient with liver cirrhosis would you see transudate or exudate?

A

Transudate, due to drop in protein production leading to diminished colloid osmotic pressure

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24
Q

If a patients heart function tanks, will we see exudate or transudate?

A

Transudate - due to increased hydrostatic pressure in the venous system.

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25
Q

Between transudate and exudate which is benign?

A

Transudate is benign.

Exudate is bad.

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26
Q

A 52 year old male is delivered unconscious to your ED with bilateral hemothorax and no evidence of trauma. What is the most likely diagnosis?

A

Hemmorhagic exudate w/o trauma = Cancer - until proven otherwise

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27
Q

How does vascular flow and caliber change during inflammation? (The process, not just the results)

A
  1. Histamine and several other mediators cause vasodilation by acting on smooth muscle
  2. This swiftly leads to increased permeability of microvasculature and the outpouring of protein rich fluid into the extravascular tissues
  3. The loss of fluid and increased vessel diameter lead to slower blood flow, concentration of RBC’s in small vessels and increased viscocity of blood
  4. This leads to stasis, allowing blood leukocytes - mostly neutrophils -accumulate along the vacular endothelium
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28
Q

What are the three ways that vascular permeability may be increased?

A
  1. Contraction of endothelial cells resulting in increased interendothelial spaces. (most common)
  2. Endothelial injury, resulting in endothelial cell necrosis and detachment.
  3. Increased transport of fluids and proteins, called transcytosis, through the endothelial cell.
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29
Q

What is lymphangitis?

A

Secondary inflammation of lymphatics

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30
Q

What is lymphadenitis?

A

Inflammation of the lymph nodes

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31
Q

Why are inflamed lymph nodes often enlarged? What is this constellation of changes termed?

A

Due to hyperplasia of the lymphoid follicles and increased numbers of lymphocytes and macrophages.

This constellation of pathological changes is called reactive, or inflammatory lymphadenitis

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32
Q

What does the presence of red streaks near a wound signify?

A

Infection in the wound. The streaks follow the lymphatic channels and are diagnostic of lymphangitis.

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33
Q

Lymphangitis may be accompanied by painful swelling of the draining lymph nodes, indicating what?

A

Lymphadenitis.

He seemed to indicate these lymph questions would be high yield, for boards and possibly our exam.

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34
Q

What is this? Which of the hallmarks of inflammation is visible here?

A

Lymphadenitis

  1. Calor
  2. Dolor
  3. Tomor
  4. Rubor
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35
Q

What is this?

A

Lymphangitis

  • The lymph tracts are inflammed and probably infected
  • Red streak = time to treat

(This image is going to be on the exam in some capacity)

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36
Q

What causes erythema and stasis of blood flow?

A

Vasodilation induced by chemical mediators such as histamine

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37
Q

What stops the flow of leukocytes?

A

Selectins

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38
Q

What hooks the leukocyte to endothelium in preperation for diapedesis?

A

Integrins

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39
Q

What cells are selectins found on?

A

Endothelium

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40
Q

What cells have integrins on them?

A

Leukocytes

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41
Q

What mediates the attachment of leukocytes to endothelium?

A

complemetary adhesion molecules (selectins and integtins)

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42
Q

After diapedisis, what directs leukocyte movement?

A

Leukocytes follow cytokines and chemokines through chemotaxis

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43
Q

What organ is this tissue from?

What do you see that is abnormal?

A

The heart

Shows early infiltrates (neutrophils) and congested blood vessels

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44
Q

This is from heart tissue also. What do we see here that should not be?

A

Later cellular infiltrates - mononuclear

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45
Q

On your pathology rotation you are assisting in an autopsy - the pathologist shows you this sample from the cadaver and asks you what the time frame from the onset of the MI was.

You answer?

A

6-8 hours, due to the presence of neutrophils and absence of macrophages.

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46
Q

What are two cytokines that increase the expression of selectins and integrin ligands on endothelium?

A

TNF and IL-1

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47
Q

What type of cell is this?

Is it active or dormant?

How do you know these things?

A

Neutrophil - multilobed nucleus

Has recently been activated - we see toxic granulation here.

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48
Q

What type of cell is this?

Is it active?

What are the signs we see in this cell specific for?

A

Still a neutrophil

Active - the clear spaces we see are toxic vacuoles. The presence of these is highly specific for sepsis.

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49
Q

What does the arrow indicate on this neutrophil?

A

The arrow points to an inclusion - called a Dohle body, which is precipitated RNA. This indicates the cell is constructing proteins.

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50
Q

What are the steps of phagocytosis?

A
  1. Recognition and attachment of the particle to be ingested by the leukocyte
  2. Engulfment, with subsequent formation of a phagocytic vacuole
  3. Killing or degradation of the ingested material.
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51
Q

How is the intracellular destruction of microbes and debris typically accomplished?

A

ROS - reactive oxygen species (or intermediates) and reactive nitrogen species - primarily nitric oxide (NO).

AND, lysosomal enzymes.

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52
Q

What are we looking at here?

A

NETs - neutrophil extracellular traps.

Extracellular fibrillar networks that provide a high concentration of antimicrobial substances at sites of infection and prevent the spread of the microbes by trapping them in the fibrils.

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53
Q

NETs are essentially just fancy…?

A

Biofilms

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54
Q

What are three examples of leukocyte mediated injury

A
  1. Collateral damage - as part of a normal reaction against microbes. In cases where a pathogen is difficult to eradicate, the host response can contribute more to the disease pathology than the microbe itself.
  2. Autoimmune disease - When the inflammatory response is inappropriately directed against host tissues.
  3. Excessive reaction ​to usually harmless environmental substances as in allergies and asthma.
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55
Q

The termination of the acute inflammatory response occurs because of what three things?

A
  1. Mediators of inflammation are produced in rapid bursts only as long as the stimulus persists.
  2. Have short half lives
  3. are degraded after their release
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56
Q

What are the most important mediators of acute inflammation?

A
  1. Vasoactive amines and lipid products
    1. Prostaglandins
    2. leukotrienes
  2. Cytokines and chemokines
  3. Products of complement activation
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57
Q

How are cell derived mediators of inflammation stored normally?

A

Sequestered in intracellular granules. OR synthesized de novo in response to a stimulus

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58
Q

What are the major cell types that produce mediators of acute inflammation?

A
  1. macrophages
  2. dendritic cells
  3. mast cells
59
Q

Can neutrophils, platelets, endothelial and epithelial cells be induced to elaborate mediators of inflammation?

A

Yup

60
Q

Where are plasma derived mediators of inflammation produced and present?

A

Produced in the liver

Present in circulation as inactive precursors that must be activated

61
Q

What is this?

A

Mast cell

62
Q

What is the arrow pointing to?

A

Histamine granule of a mast cell

63
Q

Most inflammatory mediators are short lived, why?

A
  1. Decay quickly
  2. inactivated by enzymes
  3. scavenged
  4. inhibited
64
Q

What is the source of histamine?

A
  1. Mast cells
  2. basophils
  3. platelets
65
Q

What is the action of histamine?

A
  1. Vasodilation
  2. Increased vascular permeability
  3. endothelial activation
66
Q

What produces prostaglandins?

A
  1. Mast cells
  2. Leukocytes
67
Q

What is the action of prostaglandins?

A
  1. Vasodilation
  2. pain
  3. fever
68
Q

What produces leukotrienes?

A
  1. Mast cells
  2. Leukocytes
69
Q

What cells produce cytokines (TNF, IL-1, IL-6)?

A
  1. Macrophages
  2. endothelial cells
  3. mast cells
70
Q

What are the actions of leukotrienes?

A
  1. Increased vascular permeability
  2. chemotaxis
  3. leukocyte adhesion
  4. activation
71
Q

What are the actions, both systemic and local of cytokines? (TNF, IL-1, IL-6)

A

Local - endothelial activation: expression of adhesion molecules

Systemic - Fever, metabolic abnormalities and hypotension (shock)

72
Q

What cells produce chemokines?

A
  1. Leukocytes
  2. activated macrophages
73
Q

What is the action of chemokines?

A
  1. Chemotaxis
  2. leukocyte activation
74
Q

What are the two major vasoactive amines?

A
  1. Histamine
  2. Serotonin
75
Q

What does histamine do to arterioles and venules?

A

Dilates arterioles

Increases permeability of venules

76
Q

From what precursor are prostaglandins and leukotrienes produced?

A

Arachadonic acid (AA)

77
Q

At what point in the prostaglandin/leukotriene synthesis pathway do steroids work to inhibit the process?

Production of what end molecules is precluded?

A

The work to inhibit phospholipases from converting cell membrane phospholipids to AA.

Thus this precludes formation of both leukotrienes and prostaglandins

78
Q

At what point in the prostaglandin/leukotriene synthesis pathway doe aspirin work to inhibit the process?

Production of what end molecules is precluded?

A

Aspirin (and Ibuprofen) is a COX-1 (cyclooxegenase-1) inhibitor. This inhibits conversion of AA to Prostaglandin G2 (PGG2).

Thus, only prostaglandins are inhibited.

79
Q

Where do celebrex and Vioxx work on the AA –> leukotriene and prostaglandin pathway?

Production of which end product is inhibited?

A

These are COX-2 inhibitors

Thus only prostaglanding production is precluded.

80
Q

What enzymes convert AA to prostaglandins?

What are prostaglandins involved in?

A

Cyclooxegenases

COX-1

COX-2

Prostaglandins are involved in the pathogenesis of pain and fever in inflammation

81
Q

What pathogenic processes are leukotrienes involved in?

A

Inflammation

Bronchoconstriction

Airway obstruction

Cell infiltration

82
Q

What enzyme converts AA to leukotrientes?

A

Lipoxygenase

83
Q

What are TNF antagonists used for?

A

Treatment of psoriasis and periarthritis

84
Q

Which are more common in the body, COX-1 or COX-2?

A

COX-1 are ubiquitous in the body.

COX-2 are more limited

85
Q

What is an example of a leukotriene inhibitor?

A

Singulair (I believe he said this is also a steroid inhaler)

86
Q

Lipoxins are generated by the AA lipoxygenase pathway. How do they differ from prostaglandins and leukotrienes?

A

Lipoxins suppress inflammation by inhibiting the recruitment of leukocytes.

87
Q

How do NSAIDs affect lipoxygenase?

A

They do not.

88
Q

What are inhibitors of leukotriene production good for?

A

Asthma treament

89
Q

Another type of asthma treatment (besides preclusion of leukotriene production) is?

A

Leukotriene receptor antagonists (Montelukast)

90
Q

Corticosteroids are broad spectrum antiinflammatory agents that reduce?

A

The transcription of genes encoding

  1. COX-2
  2. phospholipase A2
  3. proinflammatory cytokines (IL-1, TNF)
  4. iNOS
91
Q

How is fish oil beneficial to human beings?

A

Blocks AA product metabolism by working even before steroids do.

Increases HDL’s

Decreases LDL’s

Decreased risk of cardiovascular disease

92
Q

What are the principle sources of TNF?

A
  1. Macrophages
  2. Mast cells
  3. T lymphocytes
93
Q

What is the principle action of TNF in inflammation?

A

Stimulates expression of endothelial adhesion molecules and secretion of other cytokines.

Has systemic effects like fever and hypotension

94
Q

What are the principle sources of IL-1?

A

Macrophages

Endothelial cells

Epithelial cells (some)

95
Q

What are the principle actions of IL-1 in inflammation?

A

Similar to TNF

Greater role in fevers

96
Q

How do TNF and IL-1 play a critical role in leukocyte recruitment?

A

Promotion of adhesion of leukocytes to endothelium and migration through vessels.

97
Q

What is a common treatment protocol for Rheumatoid arthritis?

A

TNF blockers

98
Q

What are the five key actions attributed to TNF alpha?

A
  1. Increased inflammation
  2. Increased cell infiltration
  3. Increased angiogenesis
  4. Increased CRP in serum
  5. Articular cartilage degredation
99
Q

What are four actions of IL-1?

A
  1. Inflammation -> through activation of monocytes and macrophages
  2. Induces fibroblast proliferation -> Synovial Pannus formation
  3. Activates chondrocytes -> Cartilage breakdown
  4. Activates osteoclasts -> Bone resorption
100
Q

What can synovial pannus formation lead to?

A

It is overgrowth of synovium in the joint space. This occurs in Rheumatoid arthritis

101
Q

TNF augments the responses of neutrophils and stimulates the micobicidal activity of macrophages, in part by?

A

Inducing production of NO

102
Q

What impact does IL-7 have on fibroblasts?

A

Activates them to synthesize collagen and stimulate proliferation of synovial and other mesenchymal cells.

103
Q

IL-7 also stimulates TH17 responses, leading to?

A

induction of acute inflammation

104
Q

Sustained production of TNF contributes to?

A

Cachexia, by supressing appetite and promoting lipid and protein mobilization.

105
Q

What does an increased RBC sedimentation rate indicate?

A

Patient is sick.

Increased TNF and IL-1 lead to RBC’s sticking together due to elevated acute phase reactants.

106
Q

What are the local cytokine effects of TNF and IL-1?

A

Increased expression of adhesion molecules

Leukocyte activation

107
Q

What are the systemic protective effects of TNF, IL-1 and IL-6 on the Brain, liver and bone marrow?

A

Brain: Fever

Liver: acute phase protein production (IL-1 and IL-6 only)

Bone marrow: Leukocyte production

108
Q

What is the impact of TNF on the heart?

Endothelial cells and blood vessels?

TNF and IL-1 on skeletal muscle?

A
  1. Decreased CO
  2. Thrombus formation
  3. Insulin resistance
109
Q

What conditions are TNF antagonists remarkably effective in treating?

A

Chronic inflammatory diseases

  1. rheumatoid arthritis
  2. psoriasis
  3. Inflammatory bowel disease
110
Q

What is the primary action of chemikines?

A

Chemoattractant for specific types of leukocytes

111
Q

What cell has a large amount of tryptases?

A

Mast cells

112
Q

What are the two types of chemokines we were presented?

A

Inflammatory chemokines

homeostatic chemokines

113
Q

Inflammatory chemokines are the ones whose production is induced by microbes and other stimuli. What do they do to leukocytes?

A
  1. Increase affinity of integrins
  2. Stimulate migration to site of infection or damage
114
Q

Homeostatic chemokines are produced constitutively in tissues. What do these do?

A

Organize various cell types in different regions of tissues such as T and B lymphocytes in discrete areas of the spleen and lymph nodes

115
Q

What would you measure for identifying nephritic syndrome?

A

C3 and C4

116
Q

How does the alternative pathway of complement kick off?

A

Direct recognition of microbes, complex polysaccharides, venom and other substances in the absence of antibody.

117
Q

What are the three outcomes of complement?

A
  1. Inflammation
  2. Phagocytosis
  3. Lysis
118
Q

What is the critical step in complement activation?

A

Proteolysis of the third (and most abundant) component?

C3

119
Q

By what is the classical pathway triggered?

A

Fixation of C1 to antibody (IgM or IgG) that has combined with antigen

120
Q

How does the lectin pathway start up?

A

Plasma mannose-binding lectin binds to carbohydrates on microbes and directly activates C1

121
Q

What are C3a and C5a called? What do they do?

A

Anaphylatoxins - cause inflammation

122
Q

All three pathways of complement lead to the formation of what? Which splits into what?

A

C3 convertase

C3a and C3b

123
Q

C3b and its cleavage product iC3b, when fixed to a microbial cell wall do what?

A

Act as opsins and promote phagocytosis by neutrophils and macrophages, which have cell surface receptors for complement fragments

124
Q

What is this condition? What is this child missing?

A

Hereditary angioedema

C1 INH (inhibitor) - which normally blocks activation of C1, the first protein of the classical complement pathway

125
Q

This person with angioedema was just given a drug. What drug was it most likely?

A

Beta blocker

126
Q

What is this called? What causes this?

A

Dermatographism

Scratching causes the release of histamine - which cannot be eliminated due to missing C1Q, leading to inflammation.

127
Q

What is the term for the cell indicated by the red arrow?

What does this indicate?

A

Spherocyte - RBC that has lost central pallor

Indicates hemolytic anemias

128
Q

In paroxysmal nocturnal hemoglobinuria what causes the lysis of RBC’s at night?

A

Decreased respiration during sleep leads to decreased pH. Acid pH enables compiment to pop the RBC’s

129
Q

What are the principle mediators of vasodilation?

A

Histamine

Prostaglandins

130
Q

What are the principle mediators of increased vascular permeability?

A

Histamine

serotonin

Leukotrienes C4, D4, E4

131
Q

What are the principle mediators of chemotaxis, luekocyte recruitment and activation?

A
  1. TNF
  2. IL-1
  3. Chemokines
  4. C3a
  5. C5a
  6. Leukotriene B4
132
Q

What are the principle mediators of fever?

A

IL-1

TNF

Prostaglandins

133
Q

What are the principle mediators of pain?

A

Prostaglandins

Bradykinin

134
Q

What are the principle mediators of tissue damage?

A

Lysosomal enzymes of leukocytes

reactive oxygen species

135
Q

A 53 year old obese male who loves to drink and eat steak. What is this called?

A

Tophus - deposition of uric acid crystals —> ulceration

136
Q

This is pulled out of a lung… What kind of fluid is this?

A

Exudate

137
Q

This patient presented with chest pain and an audible rub. What do you see in the picture?

A

“Bread and butter” fibrinous pericarditis

138
Q

What is an abcess? What type of exudate is associated with an abcess?

A

Abcess - localized collections of purulent inflammatory tissue

Purulent or rotten exudates

139
Q

What kind of inflammation is associated with meningitis?

A

Purulent (suppurative) inflammation

140
Q

What are the arrows pointing to in the picture on the left?

The slide on the right is a sample from one of the arrowed items. What does it contain?

(This is tissue from the bronchus)

A

Bacterial abcesses in a case of bronchopneumonia.

Abcess contains cellular debris, and neutrophils. Is surrounded by congested blood vessels

141
Q

Patient comes in complaining of numbness of the feet. What is the likely cause?

A

Diabetic peripheral neuropathy

142
Q

This is a gastric ulcer. What is a likely candidate for a drug that could have caused this?

A

Ibuprofin

143
Q

What are the three outcomes of acute inflammation?

A
  1. Complete resolution
  2. Healing by connective tissue replacement (scarring or fibrosis) AKA - Organization
  3. Chronic inflammation

Pathological Basis of Disease I (11 decks)

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