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Pathology block 1 > Inflammation 2 > Flashcards

Inflammation 2 Flashcards

1
Q

Define Cytokines

A

the intercellular messenger substances secreted by cells of the immune systems (innate and acquired) that tell other cells what to do, but they don’t travel too far or else they would be hormones

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2
Q

Define Symptom

A

subjective experience of disease

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3
Q

Define Sign:

A

objective visible, audible, palpable or smell-able manifestation of disease

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4
Q

Define Hickam’s dictum:

A

A patient can have as many diseases as he darn well pleases

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5
Q

Define Tuberculosis:

A

prototype granulomatous disease, Mycobacterium tuberculosis infection

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6
Q

Define Sarcoidosis:

A

multi-system, probably autoimmune granulomatous disease

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7
Q

Define Lymph nodes:

A

processing centers of the acquired immune system, police stations in the lymphatic system

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8
Q

The process of using cytokines begins with what?

A

The process begins with Toll-like receptors on macrophages, neutrophils and endothelial cells

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9
Q

Other than toll like receptors, what other receptors do cytokines use?

A

G-coupled receptors

nucleotide oligomerization domain proteins 1 and 2 (NOD1 and NOD2, which react with intracellular pathogens)

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10
Q

Toll-like receptors and those similar bind to what in order to activate inflammatory cells?

A

bind various microbial cell wall and internal elements,

ex: bacterial cell wall lipoproteins and lipopolysaccharides; fungal wall components; bacterial and viral nucleic acids.

binding activates the inflammatory cells.

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11
Q

The activated inflammatory cells produce what?

A
  • TNF,
  • IL-1,
  • IL-6,
  • IL-8,
  • IL-12,
  • IL-18,
  • interferon-gamma,
  • high mobility group box 1 protein (HMGB1)
  • other pro-inflammatory cytokines.
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12
Q

How do the pro-inflammatory cytokines direct leukocytes to the site of inflammation?

A

These pro-inflammatory cytokines upregulate the expression of endothelial cell adhesion molecules that bind leukocytes, directing them to the site of infection.

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13
Q

Most of the inflammation-associated cytokines are produced by what type of cells?

A

by mononuclear phagocytic cells.

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14
Q

What are the main cytokines involved in the acute phase response?

A
  • IL-6,
  • IL-1,
  • TNF-alpha,
  • interferon-gamma,
  • TGF-beta
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15
Q

What are the main stimulators of fever?

A

IL-1 and TNF

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16
Q

IL-6 is the main stimulator for what?

A

the increased production of most acute phase reactant proteins.

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17
Q

What cytokines secreted by mononuclear phagocytic cells stimulate hepatic Kupffer cells (themselves part of the mononuclear phagocytic system)? What is the result of this stimulation?

A

IL-6, TNF and IL-1

amplify the cytokine response.

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18
Q

How can cytokines further induce the cytokine response?

A

The cytokines also act on monocytes, fibroblasts and endothelial cells, further magnifying the cytokine response.

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19
Q

The central nervous system participates by mediating fever. How?

A

by secreting adrenocorticotrophic hormone (ACTH).

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20
Q

Combined effects of what result in the changes in acute phase protein synthesis?

A

The combined effects of cytokines and glucocorticoids on hepatocytes

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21
Q

Is pain a sign or symptom?

A

Pain is a symptom.

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22
Q

How can fever be both a sign and symptom?

A

If a person experiences an elevated body temperature, that is fever as a symptom.

If measured by another person, fever is a sign.

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23
Q

T/F Patients can have more than one disease at the same time.

A

true

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24
Q

T/F Patients can have a single symptom caused by two or more diseases simultaneously.

A

true

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25
Q

What is dyspnea?

A

shortness of breath

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26
Q

How can heart failure cause dyspnea?

A

with fluid transudating into the airspaces because of high pressure due to the heart’s failure to adequately pump the blood the lung is sending it

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27
Q

As patients age, which is most likely to be true? Occam’s razor or Hickam’s dictum

A

Hickam’s dictum

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28
Q

Define chronic inflammation. What does it consist of?

A

Chronic inflammation is inflammation of prolonged duration (weeks to years).

It generally consists of (1) active inflammation with (2) tissue destruction and (3) attempted repair,

all 3 proceeding simultaneously.

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29
Q

Causes of chronic inflammation include what? (4)

A

(1) persistent infections such as tuberculosis,
(2) prolonged toxin exposure as in silicosis,
(3) autoimmunity with, for instance, systemic lupus erythematosus
(4) conditions of unknown etiology,

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30
Q

Who are the key cellular players in most chronic inflammation? What activates them?

A

Macrophages

They are activated by cytokines such as interferon-gamma, bacterial endotoxins and other factors.

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31
Q

What do they secrete and leak at the site of inflammation?

A

secrete neutrophil chemotactic factor and growth factors (TGF-beta, PDGF and FGF),

leak proteases and reactive oxygen species at sites of chronic inflammation.

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32
Q

Macrophages are drawn to sites of inflammation by what process? What molecules drive this process?

A

by chemotaxis

MCP-1, C5a, PDGF, TGF-alpha, fibrinonectin and fibrinopeptide fragments.

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33
Q

What is important in maintaining chronic inflammation?

A

Macrophage proliferation and immobilization

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34
Q

Why are Lymphocytes important in many chronic inflammatory conditions?

A

They have bidirectional interactions with macrophages, who present antigens to T cells with costimulators and produce cytokines (IL-12) that stimulate T cells.

Activated T cells secrete interferon-gamma, which activates macrophages.

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35
Q

T/F All chronic inflammatory diseases have a predominance of macrophages,

A

false, Some chronic inflammatory diseases have a predominance of macrophages, while others have a predominance of lymphocytes.

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36
Q

Examples of macrophage predominant diseases include what?

A
  • atherosclerosis,
  • subacute phase pneumonia,
  • Gaucher disease,
  • gout
  • usual interstitial pneumonia;
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37
Q

Examples of lymphocyte predominant diseases include what?

A

thyroiditis (most forms),

rheumatoid arthritis

myocarditis (most forms).

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38
Q

What is a granuloma?

A

an aggregate of activated macrophages working together

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39
Q

granulomatous diseases are a subset of what type of predominant disease?

A

granulomatous diseases are really a subset of macrophage predominant diseases

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40
Q

Examples of granulomatous diseases include what?

A
  • tuberculosis (the prototype),
  • leprosy,
  • syphilis (some forms),
  • cat-scratch disease
  • sarcoidosis
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41
Q

Tuberculous granulomas resemble what?

A

resemble tiny potatoes (tubercles), commonly cheesy (caseous) ones.

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42
Q

Tell where TB is most common and where it spreads

A

Tuberculosis is most common in the lungs, from which it spreads to local lymph nodes.

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43
Q

Decribe where cat-scratch disease begins and its spread. Tell the overall visual on it

A

Cat-scratch disease starts in skin and spreads to nearby lymph nodes.

Cat-scratch disease granulomas tend to be rounded or stellate, with central necrotic granular debris and neutrophils.

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44
Q

Tell where sarcoidosis is most common then where does it spread. Tell the appearance of it

A

Sarcoidosis is most common in the lungs and spreads to nearby lymph nodes.

Sarcoidosis tends to have non-necrotizing (non-caseating) tight naked granulomas without a rim of lymphocytes.

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45
Q

The lymphatics are what of the body?

A

sewer system of the body,

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46
Q

Describe the lymph vessels and why is this important

A

lined by endothelium with scant basement membrane and constituting a secondary line of defense with police stations (lymph nodes) at intervals.

allows cells to escape with relative ease to filter through the tissue

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47
Q

What is lymphangitis?

What is lymphadenitis?

A

Inflammation of lymphatic channels

Inflammation of lymph nodes

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48
Q

Define lymphadenopathy

A

Enlargement of lymph nodes

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49
Q

Chronic infections tend to go where? why?

A

to lymph nodes because they are the processing centers of the immune system in the lymphatic sewer system of the body.

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50
Q

T/F Chronic inflammation has systemic effects on the patient as a whole person exactly the same as acute inflammation.

A

Chronic inflammation has systemic effects on the patient as a whole person similar to, but not exactly the same as acute inflammation.

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51
Q

Describe the SED rate wrt the different inflammations

A

Chronic inflammation can increase the erythrocyte sedimentation rate.

**Immunoglobulins make erythrocytes sticky, but not as much as fibrinogen, so the “sed rate” tends not to be as elevated by chronic inflammation as by acute inflammation. **

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52
Q

Chronic inflammation causes what disease that is not found in acute inflammation unless special circumstances are present?

A

anemia,

not a feature of acute inflammation unless this is complicated by bleeding, hemolysis (breakdown of erythrocytes) or disseminated intravascular coagulation.

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53
Q

The most important systemic effects of inflammation, acute or chronic, are alterations of what 4 things?

A

(1) body temperature,
(2) heart rate,
(3) respiratory rate
(4) white blood cell count, usually increases in them.

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54
Q

Describe body temperature throughout the day, wrt gender, and locations taken

A

body temperature is normally lower in the morning by about 0.6 degrees C (1 degree F),

normally lower in men by about 0.3 degrees C (0.2 degrees F),

normally lower taken orally than by tympanic membrane reading by around 0.8 degrees C (1.4 degrees F),

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55
Q

Elevated body temperature is what?

A

fever

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56
Q

Fever as a component of the systemic inflammatory response is due to what?

A

the release of pyrogens (fever producing substances) from the mononuclear phagocyte system.

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57
Q

The main such endogenous pyrogens are what?

A

IL-1 and TNF-alpha.

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58
Q

Fever is mediated by what? Where do these molecules act?

A

mediated by prostaglandins, particularly PGE2 which acts directly on the hypothalamus.

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59
Q

Causes of fever include what?

A
  • infection,
  • infarction,
  • tumors,
  • non-infectious inflammation (gout, rheumatoid arthritis, etc.),
  • hemorrhage,
  • brain damage,
  • drug reactions
  • heatstroke.
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60
Q

Describe the process of a heatstroke. What is the result if left untreated?

A
  • When environment is hot and humid, even mild exercise may cause a significant rise in body temperature.
  • If rise is too high, heat regulating center becomes depressed so temp rises more.
  • metabolic rate increases, more heat is generated and temperature rises to 41 degrees C (105.8 degrees F) or more.
  • This hyperthermia is termed heatstroke.
  • Unless treated promptly, the temperature may continue to rise reaching 43 degrees C at which point the person becomes comatose. Death may ensue.
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61
Q

T/F Brain damage can increase body temperature in the absence of inflammation.

A

true

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62
Q

The hormone can raise body temperature? and is probably responsible for the elevated temperature when?

A

The hormone progesterone can raise body temperature

probably responsible for the elevated temperature at the time of ovulation.

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63
Q

It should be remembered that a fully anesthetized patient is what wrt temperature?

A

poikilothermic (has ambient temperature).

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64
Q

nstead of fever, the systemic inflammatory response may cause an abnormally low body temperature, called what? Who is this most common in?

A

hypothermia

This is most common at the extreme of life in neonates and the elderly.

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65
Q

What are the 2 most common types of anemia?

A
  1. iron deficiency
  2. Anemia of chronic disease
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66
Q

What often seen with chronic infections, autoimmune disorders and cancer?

A

anemia of chronic disease

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67
Q

In the anemia of chronic disease, mononuclear phagocytic system cells have what function?

A

there is increased uptake and retention of iron by mononuclear phagocytic system cells.

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68
Q

The body acts as if all chronic inflammation is due to what? What is the body’s response to chronic anemia?

A

infection with microbes competing for our iron and hides it from them, but also from our own red blood cell production.

The body is limits the anemia of chronic disease so that it does not cause hemoglobin to fall to less than 10 g/dl.

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69
Q

Pathophysiologic steps of anemia (1)

What down-regulates the expression of ferroportin? Why is this important?

A

Interferon, lipopolysaccharide, and TNF-alpha

Ferroportin is the only iron export protein in iron-transporting cells, so this decreases the release of iron from these cells.

70
Q

pathophys anemia (2)

Interleukin-6 and lipopolysaccharide stimulate what? What is the result?

A

the hepatic production of the acute phase protein hepcidin,

which inhibits duodenal absorption of iron and macrophage iron recycling

71
Q

Pathophys anemia (3)

Hepcidin binds to ferroportin and leads to what?

A

its degradation.

72
Q

Pathophys anemia (4)

The invasion of microorganisms, the emergence of malignant cells, or autoimmune dysregulation leads to activation of what?

A

T cells (CD3+) and monocytes.

73
Q

Pathophys anemia (5)

T cells (CD3+) and monocytes induce immune effector mechanisms, causing what?

A

thereby producing cytokines such as interferon-gamma (from T cells) and TNF-alpha, interleukin-1, interleukin-6, and interleukin-10 (from monocytes or macrophages).

74
Q

Pathophys anemia (6)

Interferon-gamma, lipopolysaccharide or both have what effect wrt macrophages and iron?

A

increase the expression of divalent metal transporter 1 on macrophages and stimulate the uptake of ferrous iron (Fe 2+).

75
Q

Pathophys anemia (7)

What up-regulates transferrin receptor expression and increases transferrin-receptor–mediated uptake of transferrin bound iron into monocytes?

A

The anti-inflammatory cytokine interleukin-10

76
Q

Pathophys anemia (8)

a process that is further induced by TNF-alpha for the turnover of iron is done how?

A

activated macrophages phagocytose and degrade senescent erythrocytes for the recycling of iron,

77
Q

Pathophys anemia (9)

Describe how iron export form macrophages is inhibited.

A

Interferon-gamma and lipopolysaccharide down-regulate the expression of the macrophage iron transporter ferroportin 1, thus inhibiting iron export from macrophages, a process that is also affected by hepcidin.

78
Q

Pathophys anemia (10)

What induces ferritin expression and stimulate the storage and retention of iron within macrophages?

A

TNF-alpha , interleukin-1, interleukin-6, and interleukin-10

79
Q

Pathophys anemia (11)

What inhibits the production of erythropoietin in the kidney?

A

TNF-alpha and interferon-gamma

80
Q

Pathophys anemia (11)

What directly inhibits the differentiation and proliferation of erythroid progenitor cells?

A

TNF-alpha , interferon-gamma and interleukin-1

81
Q

Chronic inflammation results in what depending on age?

A

adults=>anemia

children=> retarded growth.

82
Q

What results in cachexia?

A

Chronic excess stimulation of TNF release in advanced cancer results in cachexia.

83
Q

What is Arachidonic acid?

A

a cell membrane fatty acid whose metabolites are short-acting intracellular and short-range extracellular mediators of inflammation.

84
Q

What converts arachidonic acid into the precursors for a group of inflammatory mediators and inhibitors? and what are these groups specifically?

A

Lipoxygenases

the leukotrienes and lipoxins.

85
Q

What converts arachidonic acid into prostaglandins?

A

cyclooxygenase

86
Q

Corticosteroids can mask signs and symptoms of inflammation, causing opportunistic infections. How?

A

block production of arachidonic acid and all the metabolites made from it

87
Q

Non-steroidal anti-inflammatory drugs have more limited side effects. How?

A

block only prostaglandin production

88
Q

Prostaglandins mediate wrt inflammation?

A

much of the pain, fever and other signs and symptoms of inflammation.

89
Q

Describe (NSAIDs) wrt pain, fever and mucosa

A

(NSAIDs) are analgesics (pain killers) and antipyretics (fever breakers), but also interfere with prostaglandin-mediated gastric mucosal protection, leading to gastric bleeding.

90
Q

Describe the function of cyclooxygenase if it is found in endothelial cells or platelets.

A

Cyclooxygenase in endothelial cells makes prostacyclin, which is a vasodilator and inhibitor of platelet aggregation.

cyclooxygenase in platelets makes thromboxane, which is a vasoconstrictor and platelet aggregation promoter.

91
Q

What blocks cyclooxygenase?

A

NSAIDs

92
Q

Most NSAIDs block cyclooxygenase reversibly, except aspirin, which does what?

A

irreversibly inactivates it.

93
Q

If a physician prescribes aspirin therapy, what does he want to happen?

A

The result is a net increase in vasodilation and platelet aggregation inhibition.

94
Q

Describe how aspirin increases vasodilation and inhibits platelet aggregation. How long does this last? why?

A

On aspirin therapy, endothelium makes more enzyme, which makes more prostacyclin, which causes vasodilation and platelet aggregation inhibition.

Platelets, however, cannot make new enzyme because they lack DNA, so platelets zapped by aspirin are prevented from making thromboxane for as long as they live (average 10 days).

95
Q

Know this slide. especially highlights

A 
Mononuclear phagocytes (Mo) secrete
 IL-1, TNF and IL-6

IL-1 and TNF make brain make fever

IL-6 makes hepatocytes (Hep) make acute phase proteins

96
Q

What is this slide an example of?

A

Foamy macrophages at the rupture site of an
atheroma in coronary atherosclerosis

97
Q

What is this an example of?

A

Subacute pneumonia, presumptively bacterial,
with foamy macrophages replacing the
neutrophils and filling the airspaces

98
Q

What is this an example of?

A

Gaucher disease

99
Q

What is this an example of?

A

Usual interstitial pneumonia

Chronic inflammation with predominantly
macrophages infiltrating the interstitium
between airspaces

100
Q

What is this an example of?

What does the arrow point to?

A

Lymphocytic Thyroiditis*

Degenerating thyroid follicle

101
Q

What is this an example of? What type of disease is it commonly?

A

Myocarditis*

predominantly lymphocytic, but some macrophages, (presumptively viral)

rare

102
Q

Name the organ and disease

A

Spleen

myriads of granulomas

103
Q

What is this an example of?

A

Granuloma (in lung)

104
Q

T/F Caseating necrosis resembles cheese grossly only

A

true

105
Q

What is indicated by the green arrow?

A

Tubercles in pulmonary hilar lymph node

106
Q

What is this an example of?

A

Tuberculous granuloma with amorphous
pink necrosis in the center

107
Q

What is this an example of?

A

Multinucleated giant cells at necrosis edge

108
Q

What is this an example of?

A

Rounded-stellate, centrally necrotic granulomas
of cat scratch disease in a lymph node

109
Q

What is this an example of?

A

Tight naked granuloma of sarcoidosis

110
Q

If you have a chronically ill patient, What is the level of hemoglobin for a physician to look for something besides the anemia of chronic disease? what should you look for?

A

hemoglobin <10 g/dl,

bleeding

111
Q

in some patients, Chronically elevated serum amyloid A results in what?

A

secondary amyloidosis

112
Q

Draw a flow chart where arachidonic acid is produced and and what it will lead to

A
113
Q

Prostaglandins mediate which parts of inflammation mainly?

A
  • pain,
  • fever
  • other signs and symptoms of inflammation
114
Q

What is this an example of?

A

Gastric mucosal hemorrhages

115
Q

What is this an example of?

A

1 = esophagus 2 = stomach

arrow: gastric mucosal hemorrhage

116
Q

What is this an example of?

A

acute MI

117
Q

Describe in general chemical mediators of inflammation

A

Plasma-derived mediators
Cell-derived mediators
Usually bind to specific cell receptors
May stimulate release of secondary effector molecules
Mediator function is highly regulated

118
Q

Describe plasma-derived chemical mediators of inflammation

A
  1. Complement
  2. Kinins
  3. Coagulation factors => Clotting, Fibrinolysis

All three characteristically circulate as inactive precursors

119
Q

Describe the Cell-derived chemical mediators

A
  • Normally sequestered in intracellular granules
  • Secreted upon activation: histamine in mast cells
  • Or synthesized de novo in response to a stimulus: prostaglandins
120
Q

What are some chemical mediators?

A

Vasoactive amines
Histamine and serotonin
Neuropeptides
Plasma proteases
Kinin, clotting, and complement systems
Arachidonic acid metabolites
Platelet-activating factor
Cytokines
Interleukin-1 and tumor necrosis factor
Chemokines
Nitric oxide and oxygen-derived free radicals
Lysosomal constituents

121
Q

Describe how histamine is produced, its release triggers, and the result of its production

A

Released by tissue mast cells, circulating platelets and basophils

Release triggers: physical injury (trauma, heat or cold); binding of IgE to FcRs on mast cells; C3a and C5a (anaphylatoxins); leukocyte-derived histamine-releasing proteins; substance P; and certain cytokines; IL-8

Arteriolar dilation and immediate phase of increased vascular permeability

122
Q

Describe the Vasoactive amine: Serotonin

A

Preformed vasoactive mediator
5-hydoxytryptamine
Platelet dense body granules
Released during platelet aggregation
Effects are similar to histamine

123
Q

Describe neuropeptides

A
  • Include substance P
  • Usually small proteins
  • Transmit pain signals
  • Regulate vascular tone
  • Nerve fibers that secrete neuropeptides are prominent in the lung and GI tract.
124
Q

Describe plasma proteases

A
  • Kinin system
  • Clotting system
  • Complement system

All three systems are linked by Hageman factor (factor XII)

Synthesized by the liver
Activated by collagen, basement membrane, or platelets

125
Q

Describe the clotting system wrt plasma proteases

A
  • Factor XIIa results in activation of the clotting cascade
  • Results in generation of thrombin: forms insoluble clot and enhances leukocyte adhesion to endothelium
  • Activated thrombin cleaves fibrinogen into fibrin
  • Factor Xa causes increased vascular permeability and leukocyte emigration
  • Fibrinopeptides: increase vascular permeability and are chemotactic
126
Q

Describe the kinin system wrt plasma proteases

A
  • Activation leads to formation of bradykinin from circulating precursor, HMWK
  • Causes increased vascular permeability, arteriolar dilation and bronchial smooth muscle contraction; pain upon skin injection
  • Rapidly inactivated by kininases in plasma and tissue
  • Kallikrein, an intermediate in the kinin system, is a potent activator of Hageman factor—amplifies the whole set of plasma proteases
127
Q

Draw the kinin and clotting cascades wrt plasma proteases

A
128
Q

Describe the fibrinolytic system wrt plasma proteases

A
  • Counter-regulates clotting by cleaving fibrin; solubilizes clots
  • Without it: continuous and irreversible clotting!
  • Plasminogen activator (endothelium, leukocytes and tissue) and kallikrein cleave plasminogen into plasmin
  • Cleaves fibrin and lyses clots
  • Cleaves C3 into C3a
  • Can also activate Hageman factor
129
Q

Describe the Plasma proteases: Complement system

A
  1. MAC generation
  2. C3 cleavage
  classic pathway (Ag-Ab complexes)
 alternate pathway (endotoxin)
130
Q

Draw a chart describing the complement systems

A
131
Q

Describe the mechanisms and effects of the complement system

A
132
Q

Plasma proteases: Summary

A
133
Q

What are the Arachidonic Acid Metabolites?

A
  • AA: component of phospholipid cell membrane
  • Cyclooxygenase pathway: prostaglandins and thromboxane A2
  • Lipoxygenase pathway: leukotrienes
  • Lipoxins: natural endogenous negative regulators of leukotriene actions
134
Q

Draw a flow chart with the arachidonic acid metabolites

A
135
Q

Name the results of each of the arachidonic acid metabolites

A

**Vasoconstriction: ** TXA2; LT C4, D4 and E4
**Vasodilation: ** Prostacyclin, PGE1, PGE2, PGD2, lipoxins
Increased vascular permeability: LTC4, D4 and E4
Chemotaxis and leukocyte adhesion: LTB4, lipoxins

136
Q

What is platelet activating factor?

What are the results of them?

A

PAF: can aggregate platelets and cause degranulation

  • Phospholipid derived mediator
  • Can also cause vasoconstriction and bronchoconstriction
  • 100X more potent than histamine in inducing vasodilation and increased vascular permeability
137
Q

What is a Polypeptide products of many cell types which Modulate the function of other cell types
Include colony stimulation factors, interleukins and chemokines? Describe its secretion and effects

A

Cytokines

“Messenger molecules of the immune system”

Secretion is typically transient and highly regulated

**Effects are pleiotropic: ** different cells are affected differently by the same cytokine

138
Q

What are the possible cellular effects of cytokines?

A
  • Autocrine: cytokine acts on the same cell that produces it
  • Paracrine: cytokine acts on cells in the immediate vicinity
  • Endocrine: cytokine acts systemically (enters bloodstream to act on cells far away)
139
Q

IL-1 and TNF are produced by activated macrophages. What is the effect of these together?

A

Secretion is stimulated by endotoxin, ab-ag complexes, toxins, physical injury and other inflammatory mediators

Both activate endothelial cells and tissue fibroblasts

140
Q

TNF causes what?

A

aggregation and activation of neutrophils;

hypotension in septic shock

141
Q

IL-1 and TNF induce systemic acute phase responses: give examples

A
  • fever,
  • lethargy,
  • hepatic synthesis,
  • cachexia,
  • ACTH release,
  • neutrophilia
142
Q

What are the functions of Chemokines-A Subgroup of the Cytokines?

A

Activators and chemoattractants for leukocytes

Recruit particular cell populations

143
Q

What are the 2 groups of Chemokines-A Subgroup of the Cytokines? Name their function

A

**CXC (alpha chemokines): ** IL-8; attract neutrophils

**CC (beta chemokines): ** attract monocytes, macrophages and eosinophils

144
Q

What are the effects of Nitric oxide–NO?

A
  • Half-life measured in seconds
  • Used by macrophages to kill microbes and tumor cells
  • Relaxes smooth muscle in blood vessels
  • Antagonizes all stages of platelet activation
  • Reduction of leukocyte recruitment
145
Q

How is NO made? What are the types of NO?

A

Synthesized from L-arginine, molecular oxygen, NADPH, and other cofactors by the enzyme nitric oxide synthase (NOS)

NOS types: endothelial (eNOS), neuronal (nNOS), and cytokine inducible (iNOS)

146
Q

Oxygen-derived free radicals are synthesized where? What do they release?

A

Synthesized via NADPH oxidase pathway

147
Q

What are the effects of Oxygen-derived free radicals wrt inflammation, negative effects and protective systems?

A

Can amplify inflammation: increased chemokines, cytokines and adhesion molecule expression

Negative effects: thrombosis; increased permeability; direct cell injury

Antioxidant protective systems: catalase, superoxide dismutase and glutathione

148
Q

Lysosomal constituents can be acid or neutral proteases. Describe this concept

A

Acid proteases: require acidic pH for activity; usually only active within phagolysosome

**Neutral proteases **in ECM

  • elastase, collagenase, cathepsin
  • can cause deforming tissue injury
  • can cleave C3 and C5 to C3a and C5a
  • antiproteases check action: alpha-2-macroglobulin (serum), alpha-1-antitrypsin (tissue)
149
Q

What are the outcomes of acute and chronic inflammation? How are they related?

A
150
Q

Describe chronic inflammation

A
  • Inflammation of prolonged duration (weeks to months to years)
  • Infiltration with mononuclear cells: macrophages, lymphocytes and plasma cells
  • Tissue destruction
  • Repair, angiogenesis, and fibrosis
151
Q

Chronic inflammation: clinical settings can be presented how?

A
  • Viral infections
  • Persistent microbial infections
  • Prolonged exposure to toxic agents
  • Autoimmune diseases
152
Q

What are the Chronic Inflammatory Cells?

A

Macrophages: derived from circulating monocytes; resident macrophages

153
Q

What mechanisms can activate the chronic inflammatory cells?

A
  • Activation
  • Acid and neutral protease secretion
  • Plasminogen activator
  • Complement components
  • Coagulation factors
  • AA metabolites
  • Reactive oxygen species and NO
  • Cytokines: IL-1 and TNF
  • Growth factors
154
Q

Describe how a macrophage is activated and what it can cause wrt fibrosis or tissue injury

A
155
Q

Other than macrophages, name other chronic inflammatory cells and what they are usually associated with.

A
  • *Lymphocytes:** viral infections; any specific immune stimulus
  • *Plasma cells: ** rheumatoid arthritis; syphilis
  • *Eosinophils: ** parasitic infections; allergic inflammation
  • *Mast cells: ** allergic inflammation; TB
156
Q

Describe the differences in Granulomatous Inflammation

A
157
Q

What is this an example of?

A

Tuberculosis

158
Q

What is this an example of?

A

Tuberculosis

159
Q

What is the purple arrow pointing to?

A

Foreign body granuloma

160
Q

What is this an example of?

A

Serous inflammation

161
Q

Describe fibrinous inflammation

A
162
Q

What is this an example of? What does the red area indicate? grayish-white? yellow?

A

This is an example of fibrinous
pericarditis.

The red areas
indicate hemorrhage.

The grayish-white
areas indicate fibrin deposition.

Most of the yellow areas are
fatty tissue.

163
Q

Describe suppurative information

A

Large amounts of purulent exudate (pus: neutrophils and cellular debris)
Characteristically produced by pyogenic organisms: Staphylococcus

164
Q

What is an abscess?

A

Abscess: localized, walled-off collection of pus

165
Q

What is a sinus?

A

Sinus: cavity formed by a draining abscess

166
Q

What is a sinus tract?

A

Sinus tract: pathway of a draining sinus to skin or body cavity

167
Q

What is a fistula?

A

Fistula: channel between two spaces

168
Q

What is an empyema?

A

Empyema: collection of pus in a cavity

169
Q

What is this an example of?

A

Hepatic Abscess

170
Q

What is this an example of?

A

This is an example of purulent
tracheobronchitis.

The frothy fluid is an exudate
that contains pus (neutrophils
plus cellular debris).

171
Q

What are these examples of?

A

Pelvic inflammatory disease

172
Q

What type of inflammation is this?

A

Ulcerative inflammation

Pathology block 1 (24 decks)

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