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Pathology > Pathology 3 > Flashcards

Pathology 3 Flashcards

1
Q

What is inflammation?

A

A nonspecific host response to something injurious

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2
Q

What are the main causes of inflammation (6)?

A
  1. Infection
  2. Tissue necrosis
  3. Immune reaction
  4. Trauma
  5. Foreign bodies
  6. Physical and chemical agents
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3
Q

What are the four signs and symptoms of acute inflammation?

A
  1. Redness
  2. Swelling
  3. Heat
  4. Pain
    * Sometimes loss of function is added to this list
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4
Q

T or F: Acute inflammation has a rapid onset and a short duration.

A

T

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5
Q

What are the five forms of inflammation?

A
  1. Purulent
  2. Abscessing
  3. Fibrinous
  4. Serous
  5. Granulomatous
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6
Q

What are the three components of inflammation?

A
  1. Vascular response
  2. Leukocyte (WBC) response
  3. Systemic response
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7
Q

What happens in the vascular response of inflammation?

A

Dilation and increased permeability, which permits an outpouring of fluid, plasma proteins, and leukocytes from the blood into the extracellular space

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8
Q

What is serum and why is it thin?

A

Serum is the liquid portion of blood that has clotted and been centrifuged to separate the clotted cells and proteins. It’s thin because it has a low protein content and no cells.

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9
Q

What is plasma?

A

The liquid portion of blood that has been anti coagulated and centrifuged, leaving a protein-rich liquid portion including the blood clotting factors

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10
Q

What is serous inflammation?

A

A form of usually acute inflammation marked by an outpouring of think fluid from blood vessels or mesothelium or a skin blister

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11
Q

What is fibrinous inflammation?

A

A form of usually acute inflammation characterized by deposition of fibrin-rich exudate on pleura, pericardium, peritoneum, or meninges

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12
Q

Exudate

A

An inflammatory ECF with high protein content, cells, cellular debris, and specific gravity > 1.020.

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13
Q

Transudate

A

Thin serous acellular fluid

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14
Q

What is purulent (aka supparative) inflammation?

A

Usually acute inflammation featuring production of abundant pus. It’s commonly caused by infection with pyogenic bacteria.

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15
Q

What is pus?

A

Purulent exudate rich in neutrophils, cellular debris, and commonly microbes. It’s thick, opaque, and variably colored.

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16
Q

What are some causes of congenital leukocyte defects?

A

Leukocyte adhesion deficiency 1 and 2, chronic granulomatous disease, myeloperoxidase deficiency, chediak-higashi syndome, and cryopyrin-associated periodic fever syndromes

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17
Q

What are some causes of acquired leukocyte defects?

A

Diabetes mellitus, hemodialysis, malnutrition, and leukemia

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18
Q

What are the four most important systemic effects of acute inflammation?

A
  1. Fever or hypothermia
  2. Tachychardia
  3. Hyperventilation
  4. Leukocytosis (more WBC in circulation in blood)
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19
Q

Acute inflammatory response is largely mediated by _________.

A

Cytokines, especially IL-1, TNF, and IL-6

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20
Q

Acute inflammation results in an increase in what?

A

CRP, Amyloid-A, Fibrinogen, Epinephrine, Norepinephrine, Glucagon, WBC and platelet counts

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21
Q

Acute inflammation results in a decrease in what?

A

Albumin, Serum iron and zinc, RBC production, Skeletal muscle

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22
Q

What is neutrophilia and what is it associated with?

A

More neutrophils in circulation in the blood; associated with bacterial infections

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23
Q

What are the types of leukocytosis?

A
  1. Neutrophilia
  2. Lymphocytosis
  3. Eosinophilia
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24
Q

What is lymphocytosis and what is it associated with?

A

Leukocytosis consisting of lymphocytes; associated with viral infections

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25
Q

What is eosinophilia and what is it associated with?

A

Leukocytosis consisting of eosinophils; associated with allergies and parasites

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26
Q

Severe acute inflammation can cause neutrophils to have _______ and _____.

A

Dohle bodies and toxic granulations

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27
Q

What are Dohle bodies and what do they look like?

A

Patches of dilated endoplasmic reticulum that appear as “sky-blue peripheral cytoplasmic puddles”

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28
Q

What do toxic granulations look like?

A

They’re dark blue or purple granules that are bigger and coarser than the small, faintly stained neutral granules in segmented neutrophils

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29
Q

Toxic granulations are more common in (immature/mature) neutrophils.

A

Immature

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30
Q

Acute phase reactants include ________.

A 
Fibrinogen
Complement proteins
Amyloid-A
CRP
Alpha-1-antitrypsin
Hepcidin
Ferritin
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31
Q

What does amyloid A do?

A

Plays a role in recycling and reusing cholesterol from destroyed and damaged cells. It replaces apolipoprotein A in HDL and targets delivery of HDL to macrophages, suppressing ACAT and enhancing neutral cholesterol esterase and ABC transporters in macrophages.

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32
Q

What does fibrinogen do?

A

It causes sticky erythrocytes and an increased ESR

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33
Q

What influences the erythrocyte sedimentation rate (ESR)?

A

Inflammation, age, size/shape/concentration of erythrocytes

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34
Q

What does CRP do?

A

It binds to phosphocholine residues that are unique to bacteria, and once bound it becomes a ligand for complement C1 binding, initiating the classical complement cascade.

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35
Q

What cytokine induces CRP synthesis?

A

IL-6

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36
Q

T or F: Bacterial and viral infections raise the CRP level.

A

F: CRP goes up with bacterial but not viral infection

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37
Q

What characterizes systemic inflammatory response syndrome (SIRS)?

A

2 or more of the following:

  1. Temperature >100.4 or 90/minute
  2. Respiratory rate >20/minute or PCO2 12000 or 10% bands
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38
Q

The majority of patients with sepsis have (positive/negative) blood cultures.

A

Negative

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39
Q

What are acute phase reactants?

A

Proteins produced in abundance with inflammation

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40
Q

What are the 5 big signs of the flu?

A
  1. Fever
  2. Malaise
  3. Myalgia
  4. Nasal congestion
  5. Sore throat
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41
Q

Which cell type predominantly defines acute inflammation?

A

Neutrophil

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42
Q

Which cell type predominantly defines chronic inflammation?

A

Mononuclear cells like lymphocytes and monocytes

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43
Q

Fever seen in acute infections and acute inflammatory responses is due primarily to ____ and ___.

A

IL-1 and TNF

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44
Q

What does the ESR measure and what does it tell you?

A

ESR = erythrocyte sedimentation rate. It is a test for inflammatory response. When acute phase reactant proteins are present, RBCs stick together and act as larger profile bodies and they sediment in the serum more quickly than individual red cells.

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45
Q

What is the Hof in a plasma cell?

A

Clearing in the cytoplasm where the Golgi apparatus resides

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46
Q

Emigration of ______ from the microcirculation into the site of injury is the characteristic event occurring early in the acute response to injury.

A

Leukocytes

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47
Q

What is responsible for the redness and warmth that you see in an inflamed area?

A

Vascular dilation

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48
Q

What is the VERY first thing that happens in the vascular response to inflammation?

A

Vasoconstriction until ATP runs out and vessels relax, letting blood flow

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49
Q

The result of transudation and exudation is ______.

A

Edema

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50
Q

When a vessel leaks, generally you see (exudate/transudate) first.

A

Transudate

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51
Q

What is the most characteristic cause of increased vascular permeability? Where is this seen?

A

The creation of gaps between endothelial cells by contraction of those cells
Seen in post capillary venules

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52
Q

Endothelial cell retraction occurs under the effect of ___________ (3).

A

IL-1, TNF, and hypoxia

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53
Q

What is the immediate sustained response?

A

Vessel are injured by effects such as burns, toxins, or certain chemicals, and the endothelial cells die. They undergo necrosis, cell death, and detachment and leave large gaps and holes.

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54
Q

T or F: Endothelial cell retraction is reversible.

A

T

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55
Q

What is leukocyte dependent injury?

A

As leukocytes travel carrying chemicals, their cargo is occasionally leaked or spilled into the endothelium.

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56
Q

What is transcytosis? What mediates it?

A

Mechanism by which materials can pass through the endothelial cell without damaging or injuring it. Mediated by VEGF.

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57
Q

What are the steps of how leukocytes respond to the process of phagocytosis?

A
  1. Neutrophil engulfs bacteria into a phagosome
  2. Phagosome is attached to a primary granule
  3. Secondary granule comes in, and ROS are formed in an oxidative burst
  4. Dead bacteria fragments undergo exocytosis into tissues and circulation
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58
Q

What modulates leukocyte rolling and adhesion?

A

Selectins

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59
Q

What modulates leukocyte adhesion and transmigration?

A

Integrins

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60
Q

What is margination?

A

Leukocyte accumulation at the periphery of blood vessels

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61
Q

What is rolling?

A

Leukocytes are pushed out of the central axial column by flowing blood

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62
Q

What is pavementing?

A

Leukocytes line up along the blood vessel wall

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63
Q

Where do you find E-selectin, P-selectin, and L-selectin.

A

E-selectin: endothelium
P-selectin: endothelium and platelets
L-selectin: most leukocytes

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64
Q

What is diapedesis?

A

Leukocytes move between endothelial cells and through the basement membrane into the extravascular spaces

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65
Q

What modulates diapedesis?

A

Molecules of the immunoglobulin superfamily on endothelial cells that interact with integrins on leukocyte cell surfaces

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66
Q

What are the endothelial adhesion molecules?

A

ICAM-1 and VCAM-1

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67
Q

What are examples of integrins?

A

LDA-1 and Mac-1: bind to ICAM-1

VLA-1: binds to VCAM-1

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68
Q

The adhesion molecules that cause the leukocytes to firmly adhere to the endothelial surface are ______.

A

Integrins

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69
Q

T or F: Transmigration through the endothelial and basement membrane is a passive process.

A

F

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70
Q

Transmigration through the endothelial and basement membrane is modulated by ________.

A

PCAM-1

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71
Q

What is the order of cellular events in acute inflammation?

A
  1. Margination and rolling
  2. Adhesion and transmigration
  3. Chemotaxis and cell activation
  4. Phagocytosis and degranulation
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72
Q

What is chemotaxis?

A

Movement of cells or organisms in response to chemicals

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73
Q

What can produce the chemical gradient needed for leukocyte chemotaxis?

A

Soluble bacterial products, complement (C5a), LTB4, and cytokines such as the chemokine family including IL-8

74
Q

What are pseudopods?

A

Formations by which cells travel along a chemical gradient

75
Q

In chemotaxis, there is G protein-mediated activation of _______.

A

Phospholipase C

76
Q

In leukocyte activation, activation of protein kinase C results in __________.

A

Degranulation and secretion of lysosomal enzymes and the generation of the oxidative burst

77
Q

What are the 3 steps of phagocytosis?

A
  1. Recognition and attachment
  2. Engulfment
  3. Killing and degradation
78
Q

During phagocytosis, engulfment is triggered by ______.

A

The binding of opsonized particles

79
Q

What are azurophilic granules?

A

Granules located in the cytoplasm of granulocytes that are responsible for the production of perchlorate

80
Q

Dead microorganisms are degraded by _______.

A

Lysosomal acid hydrolases

81
Q

T or F: Pro-inflammatory cytokines upregulate the expression of endothelial cell adhesion molecules that bind leukocytes, directing them to the site of infection.

A

T

82
Q

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

A

IL-6, IL-1, TNF-alpha, IFN-gamma, and TGF-beta

83
Q

What is the main stimulator for the increased production of most acute phase reactant proteins?

A

IL-6

84
Q

Which cytokines stimulate hepatic Kupffer cells, thereby amplifying the cytokine response.

A

IL-6, TNF, and IL-1

85
Q

How does the central nervous system participate in acute phase response?

A

By mediating fever and by secreting ACTH

86
Q

Hickam’s dictum

A

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

87
Q

T or F: The older the patient, the less likely Occam’s razor will be correct and the more likely that Hickam’s dictum will apply.

A

T

88
Q

Chronic inflammation consists of what three simultaneous processes?

A
  1. Active inflammation
  2. Tissue destruction
  3. Attempted repair
89
Q

What are the 4 main causes of chronic inflammation?

A
  1. Persistent infections
  2. Prolonged toxin exposure
  3. Autoimmunity
  4. Conditions of unknown etiology
90
Q

What are the key cellular players in most chronic inflammation?

A

Macrophages

91
Q

What are macrophages activated by?

A
  • Secretion of acid and neutral proteases
  • Plasminogen activator
  • Complement components
  • Coagulation factors
  • Arachindonic acid metabolites
  • ROS
  • NO
  • IL-1 and TNF
92
Q

Macrophages are drawn to sites of inflammation by chemotaxis by _______.

A

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

93
Q

Macrophage proliferation and immobilization are important in maintaining chronic inflammation, especially in _____.

A

Atherosclerosis

94
Q

Activated T cells secrete _______, which activates macrophages.

A

IFN-gamma

95
Q

What are some examples of macrophage predominant diseases?

A

Atherosclerosis, subacute phase pneumonia, Gaucher disease, gout and usual interstitial pneumonia

96
Q

What are some examples of lymphocyte predominant diseases?

A

Thyroiditis, rheumatoid arthritis, and myocarditis

97
Q

What is a granuloma?

A

An aggregate of activated macrophages working together

98
Q

What are some examples of granulomatous diseases?

A

TB, leprosy, syphilis, cat-scratch disease, and sarcoidosis

99
Q

What do cat-scratch disease granulomas look like?

A

They tend to be rounded or stellate with central necrotic granular debris and neutrophils

100
Q

What do sarcoidosis granulomas look like?

A

The tend to have non-necrotizing tight naked granulomas without a rim of lymphocytes

101
Q

What are lymphatics lined by?

A

Endothelium with scant basement membrane

102
Q

Inflammation of lymphatic channels is known as ________.

A

Lymphangitis

103
Q

Inflammation of lymph nodes is known as ________.

A

Lymphadenitis

104
Q

Enlargement of lymph nodes is known as _______.

A

Lymphadenopathy

105
Q

Why do chronic infections tend to go to lymph nodes?

A

Because they are the processing centers of the immune system in the lymphatic sewer system of the body

106
Q

T or F: Chronic inflammation can increase the ESR.

A

T

107
Q

Which typically elevates the ESR more: acute or chronic inflammation?

A

Acute inflammation

108
Q

Fever as a component of the systemic inflammatory response is due to _______.

A

The release of pyrogens from the mononuclear phagocyte system

109
Q

What are the main endogenous pyrogens?

A

IL-1 and TNF-alpha

110
Q

What are the main causes of fever?

A

Infection, infarction, tumors, non-infectious inflammation, hemorrhage, brain damage, drug reactions, and heatstroke

111
Q

Which hormone can raise body temperature?

A

Progesterone

112
Q

In regard to body temperature, fully anesthetized patient is __________.

A

Poikilothermic – has ambient temperature

113
Q

What is the general basis of anemia of chronic disease?

A

The body acts as if all chronic inflammation is due to infection with microbes competing for our iron and hides it from them.

114
Q

If a chronically ill patient has a hemoglobin of less than 10 g/dl, what should you look for?

A

Something besides anemia of chronic disease, like bleeding

115
Q

What down-regulates the expression of ferroportin?

A

IFN, LPS, TNF-alpha

116
Q

What is ferroportin?

A

The only iron export protein in iron-transporting cells

117
Q

_______ binds to ferroportin and leads to its degradation.

A

Hepcidin

118
Q

What stimulates the production of hepcidin, and what does hepcidin do?

A

IL-6 and LPS stimulate hepcidin production, and hepcidin inhibits the duodenal absorption of iron and macrophage iron recycling

119
Q

Which cytokine upregulates transferrin receptor expression and increases transferrin-receptor-mediated uptake of transferrin bound iron into monocytes?

A

IL-10

120
Q

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

A

Cachexia (wasting syndrome)

121
Q

Chronically elevated serum amyloid A can result in ________ in some patients.

A

Secondary amyloidosis

122
Q

Lipooxygenases convert arachidonic acid into ___________.

A

Leukotrienes and lipoxins

123
Q

Cyclooxygenase converts arachidonic acid into ________.

A

Prostaglandins

124
Q

How do corticosteroids work?

A

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

125
Q

How do NSAIDs work?

A

They block prostaglandin production

126
Q

T or F: NSAIDs block cyclooxygenase reversibly.

A

Most do, except aspirin, which prevents platelets from making thromboxane for the rest of their lives

127
Q

Cyclooxygenase (1/2) is constitutively expressed and cyclooxygenase (1/2) is inducible.

A

1: constitutively expressed
2: inducible

128
Q

_______ might have all the anti-inflammatory effects of other NSAIDs with less gastric bleeing (but more heart attacks)

A

Rofecoxib – a COX-2 inhibitor

129
Q

Cyclooxygenase in ________ makes prostacyclin.

A

Endothelium

130
Q

Cyclooxygenase in _______ makes thromboxane.

A

Platelets

131
Q

What are release triggers of histamine?

A
  • Physical injury
  • Binding of IgE to Fc receptors on mast cells
  • C3a and C5a anaphylatoxins
  • Leukocyte-derive histamine releasing proteins
  • Supstance P
  • Certain cytokines
  • IL-8
132
Q

T or F: Effects of serotonin are similar to histamine.

A

T

133
Q

Serotonin is present in ________ and released during ________.

A

Present in platelet dense body granules and is released during platelet aggregation

134
Q

What are neuropeptides important for?

A

Their ability to transmit pain signals

135
Q

One of the most important neuropeptides is ________.

A

Substance P

136
Q

Nerve fibers that secrete neuropeptides are prominent in ___________.

A

The lung and GI tract

137
Q

The kinin system, clotting system, and complement system are linked by _______.

A

Hageman factor (factor XII) – synthesized by the liver and activated by collagen, basement membrane, or platelets

138
Q

________ sits at the top of the kinin cascade and the clotting cascade, both of which are important in inflammation.

A

Activated Hageman Factor (XIIa)

139
Q

How does the kinin cascade influence the fibrinolytic system?

A

Through kallikrein activation of plasminogen to plasmin

140
Q

How is plasmin related to the complement cascade?

A

Plasmin affects the activation of complement C3 to C3a

141
Q

Activation of the kinin system leads to formation of ______ from _____.

A

Formation of bradykinin from high MW kininogen

142
Q

Physiologically, activation of the kinin system leads to _________.

A

Increased vascular permeability, arteriolar dilation, and bronchial smooth muscle contraction

143
Q

Pain is a feature of injection of ______ and ______ into skin.

A

Bradykinin and Kininogen

144
Q

____________ amplifies the whole set of plasma proteases in the clotting system.

A

Kallikrein

145
Q

________ forms insoluble clots and enhances leukocyte adhesion to endothelial cells.

A

Thrombin

146
Q

What do fibrinopeptides do?

A

They’re a part of the clotting system and they increase vascular permeability and play a role in chemotaxis

147
Q

What would happen if we didn’t have the fibrinolytic system?

A

There would be continuous and irreversible clotting

148
Q

How does the fibrinolytic system counter-regulate clotting?

A

By cleaving fibrin, which lyses clots.

149
Q

What is the central role of the Hageman factor?

A

It activates the kinin, clotting, fibrinolytic, and complement systems

150
Q

Which plasma proteases contribute to vascular permeability?

A

Bradykinin, C3a, C5a

151
Q

Which plasma protease is important in chemotaxis?

A

C5a

152
Q

What functions is the lipooxygenase pathway responsible for?

A

Vasoconstriction, bronchospasm, and increased vessel permeability

153
Q

What functions is the cycloocygenase pathway responsible for?

A

Prostacyclin: vasodilation, inhibition of platelet aggregation
Thromboxane: vasoconstriction, platelet aggregation

154
Q

_________(3) potentiate edema through vasodilation.

A

PGD2, PGE2, and PGF2

155
Q

5-HETE and Leukotriene B4 are involved in _______.

A

Chemotaxis

156
Q

Which arachidonic acid metabolites mediate vasoconstriction?

A

TXA2 and LT C4, D4, and E4

157
Q

Which arachidonic acid metabolites mediate vasodilation?

A

Prostacyclin, PGE1, PGE2, PGD1, Lipoxins

158
Q

Which arachidonic acid metabolites are involved in increased vascular permeability?

A

LTC4, D4, and E4

159
Q

Which arachidonic acid metabolites are involved in chemotaxis and leukocyte adhesion?

A

LTB4, Lipoxins

160
Q

What does platelet-activating factor do?

A

It can aggregate platelets and cause degranulation and it is 100x more potent than histamine in inducing vasodilation and increased vascular permeability
-But it scan also cause vasoconstriction and bronchoconstriction

161
Q

Autocrine cytokines

A

Act on the same cell that produces it

162
Q

Paracrine cytokines

A

Act on cells in the immediate vicinity

163
Q

Endocrine cytokines

A

Act systemically (enter bloodstream to act on cells that are far, far away)

164
Q

Secretion of IL-1 and TNF is stimulated by _______.

A

Endotoxin, antigen-antibody complexes, toxins, physical injury, and other inflammatory mediators

165
Q

______ causes aggregation and activation of neutrophils and causes hypotension in septic shock.

A

TNF

166
Q

T or F: IL-1 and TNF induce systemic acute phase responses.

A

T

167
Q

What are the major groups of chemokines?

A
  • CXC (alpha chemokines): attract neutrophils

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

168
Q

What role does nitric oxide play in inflammatory response?

A
  • It is used by macrophages to kill microbes and to kill tumor cells that the macrophages have engulfed
  • It relaxes smooth muscles and blood vessels and antagonizes all stages of platelet activation
169
Q

NO is synthesized from _________ by _______.

A

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

170
Q

How can free radicals amplify inflammation?

A
  • By increased chemokines, cytokines, and adhesion molecule expression
  • Initiate thrombosis and increased permeability in direct cell injury
171
Q

What are the antioxidant protective systems?

A

Catalase, superoxide dismutase, glutathione

172
Q

Where are acid proteases active?

A

Usually only in the phagolysosome

173
Q

Neutral proteases can be found in the ECM in the form of _________(3).

A

Elastase, collagenase, and cathepsin

174
Q

What do antiproteases do and what are examples of these?

A

They check and help reverse the action of neutral proteases

-Examples: alpha-2-macroglobulin in the serum and alpha-1 antitrypsin in tissue

175
Q

_______ is the most important of the peroxidases.

A

Myeloperoxidase

176
Q

Peroxidase negative granules contain substances such as ______ and ______.

A

Lactoferrin and lysozyme

177
Q

What are characteristics of hypersensitivity granulomas?

A

Multinucleated giant cells that are aggregates of activated macrophages (epitheloid macrophage)
-Associated with T cell responses to certain microbes

178
Q

What are characteristics of foreign body granulomas?

A

No epitheloid macrophages

Have multinucleated giant cells

179
Q

What is an empyema?

A

Collection of pus in a cavity

180
Q

What is a sinus and what is a sinus tract?

A

Sinus: cavity formed by a draining abscess

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

Pathology (4 decks)

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