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T1 - Phase 2 - Systems Modules (I) > Inflammation - Mechanisms of Disease - Cell Injury, Death, & Repair; Acute & Chronic Inflammation > Flashcards

Inflammation - Mechanisms of Disease - Cell Injury, Death, & Repair; Acute & Chronic Inflammation Flashcards

1
Q

The etiology of disease refers to what?

A

The cause

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2
Q

Identify the defined term: ____________ changes.

“Structural alterations in tissues or cells, recognized by gross and microscopic exam.”

A

Morphologic

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3
Q

What is the initial cellular response to stress?

What occurs if the stress is excessive or prolonged?

A

Cell adaptation;

cell injury

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4
Q

The hallmarks of reversible cell injury are:

_________ oxidative phosphorylation

_________ depletion

Cellular _________

A

The hallmarks of reversible cell injury are:

Reduced oxidative phosphorylation

ATP depletion

Cellular swelling

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5
Q

The hallmarks of reversible cell injury are:

Reduced ________

ATP ________

________ swelling

A

The hallmarks of reversible cell injury are:

Reduced oxidative phosphorylation

ATP depletion

Cellular swelling

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6
Q

What two signs of reversible cellular injury are visible under light microscopy?

A

Cellular swelling;

fatty change

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7
Q

Name some of the ultrastructural signs of reversible cell injury in regards to the following cellular structures:

Plasma membrane

Mitochondria

ER

Nucleus

A

Plasma membrane - blebbing / microvilli loss / blunting

Mitochondria - swelling / amorphous densities

ER - dilation

Nucleus - granular and fibrillar disaggregation

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8
Q

Are the following examples of cellular adaptations to reversible or irreversible injury?

Hypertrophy

Hyperplasia

Atrophy

Metaplasia

A

Reversible

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9
Q

The cellular adaptation hypertrophy is typically seen in stressed cells that no longer _________.

A

Divide

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10
Q

What tissue adaptation is characterized in this endometrial micrograph?

A

Hyperplasia

(normal endometrium shown below)

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11
Q

Hypertrophy is typically caused by an increase in cellular _________ synthesis.

Atrophy is typically caused by a decrease in cellular _________ synthesis an an increase in cellular _________.

A

Protein;

protein, proteolysis

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12
Q

What is the typical, generic stimulus for metaplastic tissue change?

A

Chronic irritation

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13
Q

Metaplastic tissue changes may predipose to _________ changes.

What is an example of this?

A

Neoplastic;

Barrett’s esophagus

(metaplasia predisposes to esophageal adenocarcinoma)

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14
Q

An injurious stimulus may lead to reversible cellular changes.

Irreversible cell injury will occur if the stimulus is ________ and/or ________.

A

Excessive, prolonged

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15
Q

What are some potential causes of tissue atrophy?

A

Loss of innervation or blood supply;

underusage;

loss of nutrition or endocrine stimulation;

pressure

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16
Q

What ultrastructural marker of irreversible cell injury is shown in this electron micrograph?

A

Myelin figures

(whorled phospholipid masses derived from damaged cell membranes)

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17
Q

What ultrastructural marker of irreversible cell injury is shown in this electron micrograph?

A

Mitochondrial dilation + amorphous densities (precipitated Ca2+ / globulins)

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18
Q

What are the three nuclear changes (in order) of a cell undergoing irreversible cell injury (leading to necrosis)?

A

Pyknosis –> karryorhexis –> karyolysis

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19
Q

In what order do the following nuclear changes occur in an irreversibly damaged cell undergoing necrosis?

Karryorhexis, Pyknosis, Karyolysis

A

Pyknosis –> Karryorhexis–>Karyolysis

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20
Q

Define: pyknosis.

A

Shrunken, hyperchromatic nucleus

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21
Q

Define: karryorhexis.

A

Nuclear fragmentation

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22
Q

Define: karyolysis.

A

Fading of the nucleus

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23
Q

True/False.

Apoptotic nuclear changes are as follows:

Pyknosis –> Karryorhexis –> Karyolysis

A

False.

Necrotic nuclear changes are as follows:

Pyknosis –> Karryorhexis –> Karyolysis

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24
Q

How does apoptosis affect the nucleus?

A

Fragmentation into nucleosome-like fragments

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25
Q

In apoptosis, the plasma membrane is __________ and cellular contents are __________.

In necrosis, the plasma membrane is __________ and cellular contents are __________.

A

Intact, contained;

disrupted, released

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26
Q

Which of the following (or both) are characterized by frequent cases of adjacent inflammation?

(I.e. the process damages surrounding tissues.)

Apoptosis

Necrosis

A

Necrosis only

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27
Q

Which of the following (or both) are sometimes normal during physiological processes?

(I.e. non-pathological)

Apoptosis

Necrosis

A

Apoptosis only

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28
Q

Describe the basic cellular changes of apoptosis.

A
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29
Q

Describe the basic cellular changes of necrosis.

A
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30
Q

What nuclear change is displayed in this micrograph?

A

Pyknosis

(shrunken, hyperchromatic)

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31
Q

What nuclear change is displayed in this micrograph?

A

Karyorrhexis

(fragmentation)

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32
Q

This micrograph displays a normal renal tubule. How might a necrotic tubule appear?

A
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33
Q

What are the five main types of necrosis?

A

Coagulative,

liquefactive,

caseous,

fat,

fibrinoid

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34
Q

Ischemia in any tissue except the brain will cause what type of necrosis?

A

Coagulative necrosis

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35
Q

What kind of situations are most likely to cause liquefactive necrosis?

A

Brain ischemia,

abcesses

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36
Q

What is the main difference between coagulative and liquefactive necrosis?

A

Tissue architecture preserved in coagulative necrosis

(protein denaturation leads to decreased proteolytic activity)

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37
Q

What type of necrosis is characteristic of TB infection?

A

Caseous necrosis

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38
Q

What type of necrosis is characterized by saponification of lipids by calcium?

A

Fat necrosis

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39
Q

Saponification occurs in fat necrosis and is due to ___ reacting with free fatty acids.

A

Ca2+

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40
Q

Fibrinoid necrosis involves immune antigen-antibody complexes in the ________________ combining with fibrin.

A

Blood vessels

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41
Q

___________ necrosis involves immune antigen-antibody complexes combining with fibrin in the blood vessels.

A

Fibrinoid

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42
Q

Name the type of necrosis indicated in each of the following cases:

Ischemic non-neural tissue

Blood vessel immune reaction

Abcess

A

Coagulative

Fibrinoid

Liquefactive

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43
Q

Name the type of necrosis indicated in each of the following cases:

Tuberculosis

Ischemic neural tissue

Pancreatic autodigestion

A

Caseous

Liquefactive

Fat

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44
Q

Which type of necrosis is immune in nature?

Which type of necrosis preserves tissue architecture?

A

Fibrinoid;

coagulative

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45
Q

Why does coagulative necrosis preserve tissue architecture?

A

Protein denaturation –> decreased proteolysis

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46
Q

What are apoptotic bodies?

A

Fragments of nucleus/cytoplasm

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47
Q

What is happening to this prominent epidermal cell?

A

Apoptosis

(cellular swelling + dense cytoplasm)

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48
Q

True/False.

Apoptosis is only caused by normal physiologic stimuli.

A

False.

DNA damage, misfolded proteins, certain infections, and glandular duct destruction are all examples of potential pathologic causes of apoptosis.

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49
Q

Injurious cellular stressors such as UV rays, heat, and ROS can all trigger apoptosis via accumulation of what?

A

Misfolded proteins

(and other damaged cellular contents; e.g., lipids and DNA)

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50
Q

What are the two main pathways of apoptosis initiation?

A

Mitochondrial (intrinsic);

death receptor (extrinsic)

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51
Q

What is the main anti-apoptotic protein that maintains most cells?

A

Bcl-2

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52
Q

What proteins sense cellular stress?

What channel do they activate if the stress is excessive? (Where?)

A

Bim, Bid, Bad (BH3 family);

Bax/Bak (mitochondrial pores)

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53
Q

What is the end result of this pathway:

Excessive cell stress –>

BH3 family activated (Bim, Bid, Bad) –>

Bax/Bak activated –>

???

A

Mitochondrial channels formed –>

cytochrome C released –>

caspases activated –>

apoptosis

(Note: this is the intrinsic pathway of apoptosis)

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54
Q

Activation of what protein type is the end result of both the intrinsic and extrinsic pathways of apoptosis?

A

Caspases

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55
Q

What do caspases do?

A

Degrade the nuclear matrix –> fragmentation

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56
Q

What are the two main triggers for the surface membrane death receptors of the extrinsic pathway of apoptosis?

A

TNF;

Fas-L

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57
Q

What process is basically programmed necrosis and resembles necrosis morphologically and apoptosis mechanistically?

A

Necroptosis

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58
Q

Is necroptosis dependent on caspases?

What complexes control the process?

A

No;

RIP1 / RIP3

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59
Q

How does the RIP1/RIP3 complex induce necroptosis?

A

Reduced ATP –> increased ROS production –> rupture of lysosomal membranes

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60
Q

True/False.

Necroptosis is programmed cell death that results in a non-inflammatory reaction resembling necrosis.

A

False.

Necroptosis is programmed cell death that results in an inflammatory reaction resembling necrosis.

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61
Q

Define: pyroptosis.

A

Infected cells activate caspase-1

(infection-induced apoptosis)

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62
Q

True/False.

Increases in intracellular Ca2+ can cause decreased mitochondrial permeability and decreased cellular enzyme activity.

A

False.

Increases in intracellular Ca2+ can cause increased mitochondrial permeability and increased cellular enzyme activity.

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63
Q

Mitochondrial damage leads to leakage of pro-___________ proteins.

A

Apoptotic

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64
Q

Why is lysosomal damage dangerous to cell survival?

A

Release of lytic enzymes

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65
Q

Explain why ATP depletion causes the following cellular effects:

Cell / ER swelling

Chromatin clumping

Lipid accumulation / protein depletion

A

Decreased Na/K ATPase activity (cell / ER swelling)

Lactic acidosis (chromatin clumping)

Ribosomal detachment (lipid accumulation / protein depletion)

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66
Q

What are the three main damaging effects of ROS?

A

Protein/enzyme misfolding,

membrane disruption,

DNA damage

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67
Q

Define: autophagy (a form of cell death).

A

A non-apoptotic, non-necrotic form of cellular recycling

(the cells are scrapped for parts/nutrients)

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68
Q

Why can excessive/prolonged Ca2+ influx be damaging to cell survival?

A

Enzymatic activation

(e.g. proteases, phospholipases, phosphatases, glucosidases, ATPases, RNases, DNases, etc.)

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69
Q

Where are pro-apoptotic protein clusters (e.g. cytochrome C) contained within the mitochondria?

A

The intermembrane space

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70
Q

What are the main serum markers for cardiac injury?

And bile duct epithelial injury?

And hepatic injury?

A

CK-MB, troponins;

ALP;

AST, ALT

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71
Q

Describe the pathophysiology of ischemia-reperfusion injury.

A

Increased [ROS] and [RNS] –> increased inflammation / complement activation

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72
Q

What are some examples of categories of materials that can accumulate in a cell?

A

Energy storage (e.g. lipids, glycogen);

misfolded proteins (e.g. amyloid, α1-antitrypsin);

endogenous (e.g. lipofuscin or due to lysosomal storage diseases);

exogenous (e.g. heavy metals)

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73
Q

Dystrophic calcification occurs in __________ tissues when calcium levels are __________.

A

Damaged;

normal

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74
Q

Metastatic calcification occurs in __________ tissues when calcium levels are __________.

A

Normal;

elevated (e.g. PTH excess)

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75
Q

Nephrocalcinosis is an example of ___________ (dystrophic/metastatic) calcification.

A

Metastatic

(due to elevated calcium levels)

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76
Q

__________ calcification occurs in normal tissues when serum calcium levels are significantly elevated.

A

Metastatic

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77
Q

__________ calcification occurs in damaged tissues when serum calcium levels are normal.

A

Dystrophic

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78
Q

What body areas are most likely to be affected by metastatic calcification?

A

Areas of acid secretion

(e.g. gastric mucosa, kidneys, lungs, blood vessels)

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79
Q

A calcified aortic valve is an example of what kind of calcification?

A

Dystrophic

(as opposed to metastatic)

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80
Q

What are the cardinal S/Sy of inflammation?

A

Pain (dolor),

redness (rubor),

loss of function (functio laesa),

swelling (tumor),

heat (calor)

81
Q

What suffix signifies inflammation?

A

‘-itis’

82
Q

What is the purpose of inflammation?

A

To bring cells and molecules of host defense from the circulation to the sites where they are needed

83
Q

How long does acute inflammation usually take to set in?

How long does it usually last?

A

Minutes;

hours to days

84
Q

What are the major steps of inflammation according to accomplished function?

A
  1. Increase in blood vessel permeability
  2. Leukocyte chemotaxis
  3. Leukocyte activation
85
Q

What main substance is released in acute inflammatory situations by endothelial cells to promote vasodilation?

How long is its half-life?

A

Nitric oxide;

seconds

86
Q

In acute inflammatory settings, nitric oxide is secreted by _____________ cells to promote _____________.

A

Endotheilal;

vasodilation

87
Q

What main substance is released in acute inflammatory situations by mast cells / basophils / platelets to promote an increase in vascular permeability (and vasodilation)?

A

Histamine

88
Q

In acute inflammatory settings, histamine is secreted by _____________ cells to promote _____________.

A

Mast cells / basophils / platelets;

vascular permeability / vasodilation

89
Q

What substance is the major mediator of vasodilation in acute inflammation?

What substance is the major mediator of vascular permeability in acute inflammation?

A

Nitric oxide;

histamine

90
Q

True/False.

All of the following are examples of stimuli that cause mast cell degranulation:

Trauma, cold, heat, allergic reactions, anaphylatoxins C3a and C5a, other histamine-releasing proteins, neuropeptides (e.g., substance P), and cytokines IL-1 / IL-8

A

True.

91
Q

Histamine results in dilation of __________ and increased permeability of __________.

A

Arterioles;

venules

92
Q

What happens rapidly to endothelial cells in cases of acute inflammation and typically lasts for 15 - 30 min?

A

Endothelial contraction

93
Q

Besides endothelial contraction, what are some other processes that increase the inter-endothelial space?

A

Endothelial damage (direct or leukocyte-mediated);

increased transcytosis

94
Q

True/False.

Lymphatic vessels proliferate during acute inflammation.

A

True.

95
Q

Upon examining a patient’s swollen forearm, you notice red streaks on the patient’s skin radiating outwards away from a purulent sore.

What is causing the red streaks?

A

Lymphangitis

96
Q

What term refers to inflammation of the lymph nodes?

What term refers to inflammation of the lymph vessels?

A

Lymphadenitis;

lymphangitis

97
Q

What are the two general types of edematous fluid?

Put the higher osmolality one first.

A

Exudate;

transudate

98
Q

Transudate is edematous fluid characterized by ___ protein content and ___ specific gravity.

A

Low;

low

99
Q

Ascites is an example of what type of fluid?

A pus-laden plural effusion is an example of what type of fluid?

A

Transudate;

exudate

100
Q

The steps of leukocyte recruitment are the following:

  1. ______________________.
  2. Extravasation (diapedesis).
  3. In-tissue chemotaxis.
A

The steps of leukocyte recruitment are the following:

  1. Margination, rolling, & adhesion to endothelium.
  2. Extravasation (diapedesis).
  3. In-tissue chemotaxis.
101
Q

The steps of leukocyte recruitment are the following:

  1. Margination, rolling, & adhesion to endothelium.
  2. ______________.
  3. In-tissue ___________.
A

The steps of leukocyte recruitment are the following:

  1. Margination, rolling, & adhesion to endothelium.
  2. Extravasation (diapedesis).
  3. In-tissue chemotaxis.
102
Q

What is leukocyte margination?

A

Leukocytes moving to vessel wall

103
Q

After marginating to the endothelium, via what endothelial proteins do leukocytes begin to roll? Be specific.

A

E-selectins (endothelium),

P-selectins (endothelium & platelets),

L-selectins (leukocytes)

104
Q

True/False.

Endothelial selectins bind X-modified integrins on leukocyte surfaces.

A

False.

Endothelial selectins bind X-modified Sialyl-Lewis glycoproteins on leukocyte surfaces.

105
Q

What are Weibel-Palade bodies?

What causes their release to the cell surface?

A

P-selectin granules (in endothelial cells);

histamine, thrombin, and platelet-activating factor

106
Q

True/False.

The cytokines TNF and IL-1 increase the expression of selectins and their ligands on endothelial cells and leukocytes.

A

True.

107
Q

Leukocyte rolling causes what to occur for leukocytes?

A

Slowing down / stronger endothelial binding

108
Q

Chemokines increase leukocyte adhesion by converting (1) __________ to a high-affinity state.

Cytokines such as IL-__ and ___ induce endothelial VCAM-1 and ICAM-1 expression for the (1) __________ to bind.

A

(1) Integrins;

IL-1, TNF

109
Q

True/False.

Leukocyte CAMs bind endothelial integrins during leukocyte adhesion.

A

False.

Leukocyte integrins bind endothelial CAM__s during leukocyte adhesion.

110
Q

Name where each of the following are found, respectively:

E-selectins

P-selectins

L-selectins

A

E-selectins — endothelium

P-selectins — platelets; endothelium

L-selectins — leukocytes

111
Q

The cytokines of acute inflammation mainly increase the expression of endothelial adhesion molecules such as ___________ and ___________.

The cytokines of chronic inflammation mainly increase the expression of enzymes associated with ___________ remodeling and ___________.

A

Selectins, integrins;

matrix, thrombogenicity

112
Q

___, IL-__, and IL-__ are major mediators of acute inflammation.

IFN-__, IL-__, and IL-__ are major mediators of chronic inflammation.

A

TNF, 1, 6;

γ, 2, 17

113
Q

How are chemokines grouped?

α

β

γ

A

According to conserved cysteine (C) residues

α - C-X-C

β - C-C

γ - C

114
Q

What do cell type(s) do each of the following chemokine groups act on, respectively?

α (C-X-C)

β (C-C)

γ (C)

A

α (C-X-C) - mostly neutrophils

β (C-C) - attract monocytes, eosinophils, basophils, and lymphocytes

γ (C) - specific for lymphocytes

115
Q

What chemokine promotes strong adhesion of monocytes and T cells to endothelial cells?

A

CX3C (fractalkine)

116
Q

True/False.

Chemokine receptors are mostly tyrosine kinase receptors.

CXCR-4 and CCR-5 are involved in ____ infection.

A

False.

Chemokine receptors are mostly GPCRs.

CXCR-4 and CCR-5 are involved in HIV infection.

117
Q

Endothelial P- and E-selectins are involved in leukocyte ____________.

Endothelial ICAM-1 and VCAM-1 are involved in leukocyte ____________.

A

Rolling;

adhesion

118
Q

____________ P- and E-selectins are involved in leukocyte rolling.

____________ sialyl-Lewis X-modified proteins are involved in leukocyte rolling.

A

Endothelial;

leukocyte

119
Q

_____________integrins are involved in leukocyte adhesion.

_____________ ICAM-1 and VCAM-1 are involved in leukocyte adhesion.

A

Leukocyte;

endothelial

120
Q

What are the endogenous and exogenous agents of chemotaxis?

A

Endogenous — Cyto/chemokines, complement, arachidonic acid metabolites

Exogenous — Bacterial products

121
Q

How does chemotaxis work on a cellular level?

(I.e., what do the signals induce at the front and back of the cell?)

A

Front: actin polymerization

Back: myosin filament localization

122
Q

What is the timeline of the following pieces in acute inflammation?

Neutrophil

Monocyte/Macrophages

Edema

A

< 1 day –> Edema

6 - 24 hours –> Neutrophils

~2 days –> Monocytes/macrophages

123
Q

Some ___________ infections produce continous recruitment of neutrophils for several days.

________ infections tend to have more lymphocytes

A

Bacterial;

viral

124
Q

How do leukocyte intracellular conditions change when they become activated?

A

Increased cytosolic calcium;

enzyme activation / ROS production

125
Q

What are the steps of phagocytosis?

1) ___________ and attachment of particle to be ingested by the leukocyte
2) ___________ with subsequent formation of phagocytic vacuole
3) ___________ of the ingested material

A

Recognition;

engulfment;

degradation

126
Q

Name a few of the recognition/attachment receptors of phagocytosis.

A
  • Macrophage mannose receptors
  • Scavenger receptors
  • Macrophage integrins
  • Receptors for opsonins
127
Q

Neutrophils use the ____________ to create ROS in order to destroy phagocytosed materials.

A

Respiratory burst

128
Q

What are the intermediates of the respiratory burst?

A

O2 –> O2- –> H2O2 –> ClO-

(Oxygen –> superoxide –> hydrogen peroxide –> hypochlorite)

129
Q

What are the enzymes of the respiratory burst?

A

NADPH oxidase (O2 –> O2-);

superoxide dismutase (O2- –> H2O2);

myeloperoxidase (H2O2 –> ClO-)

130
Q

What defect causes leukocyte adhesion deficiency type I (a cause of recurrent bacterial infections)?

A

β2

(shared by LFA-1 and Mac-1 integrins)

131
Q

What defect causes leukocyte adhesion deficiency type II (a cause of recurrent bacterial infections)?

A

Sialyl-Lewis X

(E- and P-selectins ligand)

(may be a defect of fucosyl transferase)

132
Q

The basic cause of Chediak-Higashi syndrome is defective fusion of __________ with _________.

A

Phagosomes;

lysosomes

133
Q

What enzyme is deficient in chronic granulomatous disease?

What is the most common inheritance?

A

NADPH oxidase;

X-linked

134
Q

What type of cell is especially rich in inflammatory responses in chronic granulomatous disease?

A

Macrophages

(neutrophil response is inadequate)

135
Q

Leukocyte adhesion deficiency I and II, Chediak-Higashi syndrome, and chronic granulomatous disease are all characterized by recurrent _______________ infections.

A

Bacterial

136
Q

Name a few examples of conditions that might induce leukocyte dysfunction.

A

Chemotherapy;

leukemia;

diabetes;

dialysis

137
Q

The effects of acute inflammation include:

fever, leukocytosis and left shift, chills, malaise

This is mainly due to what two factors?

A

IL-1, TNF

(also IL-6, CRP, hepcidin, fibrinogen)

138
Q

Bacterial infections cause ________ia.

Viral infections cause _______osis.

Parasites, allergies, and asthma cause ________ia.

A

Bacterial infections cause netrophilia.

Viral infections cause leukocytosis.

Parasites, allergies, and asthma cause eosinophilia.

139
Q

True/False.

Septic shock is mainly mediated by IL-2 and CRP.

A

True/False.

Septic shock is mainly mediated by IL-1 and TNF.

140
Q

What is the difference between septic shock and systemic inflammatory response syndrome (SIRS)?

A

SIRS is due to non-infectious causes

141
Q

True/False.

Neutrophils and the mediators of acute inflammation have short half-lives.

A

True.

142
Q

When acute inflammation has ended, the pro-inflammatory signals switch to what?

A

Anti-inflammatory signals

143
Q

_____________ inflammatory fluid occurs in effusions and blisters.

A

Serous

144
Q

_____________ inflammatory fluid occurs in inflammation of body cavities (e.g. meninges, pericardium, pleura).

A

Fibrinous

145
Q

_____________ inflammatory fluid occurs in inflammation that produces pus.

It is typically of a bacterial origin.

A

Suppurative (purulent)

146
Q

An abcess is a localized collection of ____________ tissue surrounded by a zone of viable ____________.

A

Purulent (suppurative);

neutrophils

147
Q

An ulcer is a local defect of the surface tissue with the co-existence of _______ and _______ inflammation, with potential scar formation.

A

Acute;

chronic

148
Q

True/False.

Chronic inflammation always follows acute inflammation.

A

False.

Chronic inflammation can arise insidiously.

149
Q

How long does chronic inflammation last?

A

Weeks or months

150
Q

Acute inflammation is mostly managed by what cell type(s)?

Chronic inflammation is mostly managed by what cell type(s)?

A

Neutrophils;

macrophages, lymphocytes, plasma cells

151
Q

Angiogenesis and fibrosis are attempts at healing seen in ________ inflammation.

A

Chronic

152
Q

What type of pulmonary inflammation is shown here?

(Acute or chronic?)

A

Acute

153
Q

What type of pulmonary inflammation is shown here?

(Acute or chronic?)

A

Chronic

154
Q

What is the half-life of macrophages in circulation?

And in tissues?

A

1 day;

months-to-years

155
Q

Which of the following would NOT be a significant component of a typical chronic inflammatory process?

A. Lymphoid follicles

B. Plasma cells

C. Neutrophils

D. Macrophages

A

C. Neutrophils

156
Q

The two types of macrophage activation are the _________ pathway and the _________ pathway.

A

Classical;

alternative

157
Q

What is the difference in macrophage function between the classical and alternative activation pathways?

A

Inflammation (classical);

repair (alternative)

158
Q

What cytokines cause classical macrophage activation?

A

IFN-γ; microbes

159
Q

What cytokines cause alternative macrophage activation?

A

IL-4;

IL-13

160
Q

True/False.

The adaptive immune system has little-to-no role in chronic inflammation.

A

False.

CD4+ T cells and B cells play prominent roles.

161
Q

What are the two most basic causes of granulomatous inflammation?

A

Foreign bodies (foreign body granulomas);

a difficult inciting agent to eradicate (immune granulomas)

162
Q

Epithelioid and giant cells are very common in _____________ granulomas.

Persistent T cell-mediated immune activity is characteristic of _____________ granulomas.

A

Foreign body;

immune

163
Q

What are the two methods of tissue repair?

Which is characteristic of wound healing?

Which is characteristic of chronic inflammation?

Which is characteristic of epithelial tissues?

A

Regeneration, scar formation;

scar;

scar;

regeneration

164
Q

Which of these tissues are stable tissues (as opposed to labile or permanent)?

Kidney

Pancreas

Adrenal

Lung

Endothelial cells

A

All of them

165
Q

Which tissue type is the most important tissue source of growth factors?

Which cell type is the most important cellular source of growth factors?

A

ECM;

macrophages

166
Q

How long does it take for a liver remnant to double after 60% of the liver is resected?

A

1 month

167
Q

What mediators of chronic inflammation are produced following stimulation by the following mediators of acute inflammation?

IL-6

IL-1 and TNF

A

IL-6 –> CRP and fibrinogen

IL-1 and TNF –> serum amyloid A

168
Q

What are the effects of elevated CRP, fibrinogen, and serum amyloid A on tissues (due to chronic inflammation)?

A

CRP / fibrinogen –> elevated ESR;

SAA –> amyloidosis (in severe cases)

169
Q

Inflammation causes a _____ shift leukocytosis.

A

Left

170
Q

What are some of the systemic effects of septic shock due to elevated TNF and IL-1?

1. _________ in blood pressure

2. D__________ i__________ c__________

3. __________ abnormalities (e.g. insulin resistance, hyperglycemia)

A

1. Decrease in blood pressure

2. Disseminated intravascular coagulation

3. Metabolic abnormalities (e.g. insulin resistance, hyperglycemia)

171
Q

What growth factors are involved in angiogenesis?

A

VEGF;

FGFs;

angiopoeitins I and II

172
Q

True/False.

Angiogenesis requires both extensive endothelial-ECM interactions and also ECM destruction by metalloprotease activity.

A

True.

173
Q

What are the two main forms of angiogenesis?

A

From pre-existing vessels;

de novo

174
Q

Name some of the systemic effects associated with acute phase inflammatory responses.

A

Elevated heart rate, BP, and temperature;

decreased sweating;

presence of chills, rigors, anorexia, malaise, somnolence

175
Q

What are the two forms of tissue healing?

A

Tissue regeneration;

scar formation

176
Q

Scar formation involves the following processes:

_______genesis.

Formation of ________ tissue.

Remodeling of ________ tissue.

A

Scar formation involves the following processes:

Angiogenesis.

Formation of granulation tissue.

Remodeling of connective tissue.

177
Q

______ is produced by cells in granulation tissue and acts to increase collagen/fibronectin synthesis and decrease metalloprotease activity.

A

TGF-β is produced by cells in granulation tissue and acts to increase collagen/fibronectin synthesis and decrease metalloprotease activity.

178
Q

Is this granulation tissue or a mature scar?

A

Granulation tissue

(mature scar below)

179
Q

True/False.

All of the following points describe metalloproteases.

  1. ECM-degrading.
  2. Copper-dependent.
  3. Produced by fibroblasts only.
  4. Released as zymogens.
A

False.

All of the following points describe metalloproteases:

  1. ECM-degrading
  2. Zinc-dependent.
  3. Produced by neutrophils, synovial cells, fibroblasts, and macrophages, and some epithelial cells.
  4. Released as zymogens.
180
Q

How do vascular regression and fibroblast differentiation (into myofibroblasts) promote scar maturation?

A

Scar contraction

181
Q

Which of the following can delay wound healing?

Glucocorticoids

Diabetes mellitus

Vitamin deficiencies (e.g. vitamin C)

Poor perfusion

Foreign bodies

A

All of them

182
Q

Healing of primary intention involves reconnection of the superficial _________ cutaneous layer by __________.

A

Healing of primary intention involves reconnection of the superficial epithelial cutaneous layer by regeneration.

183
Q

Healing of ________ intention involves reconnection of the superficial epithelial cutaneous layer by regeneration.

A

Healing of primary intention involves reconnection of the superficial epithelial cutaneous layer by regeneration.

184
Q

Describe the time frame for the following processes that occur after a cutaneous injury:

- Clot formation / Neutrophil entry into wound -

- Macrophage entry into wound / angiogenesis / granulation tissue formation -

- Scab removal / healed surface / no inflammation -

A
  • 24 hours -
  • 3 - 7 days -
  • Weeks -
185
Q

How long will it take most cutaneous scars to make it back to 100% of the tensile strength the skin held before injury?

A

Never

186
Q

Healing of _________ intention is used for less extensive tissue loss/destruction when the normal edges can still be approximated.

Healing of _________ intention is used for more extensive tissue loss/destruction when the normal edges cannot still be approximated.

A

Healing of primary intention is used for less extensive tissue loss/destruction when the normal edges can still be approximated.

Healing of secondary intention is used for more extensive tissue loss/destruction when the normal edges cannot still be approximated.

187
Q

In what way are the components of healing by secondary intention significantly different from healing by primary intention?

A

Quantity

(larger clot, more debris, more inflammation, more time, larger scar)

188
Q

Initial granulation tissue is made of type ___ collagen.

This is replaced by type ___ collagen at ~__ weeks.

A

Initial granulation tissue is made of type III collagen.

This is replaced by type I collagen at ~2 weeks.

189
Q

Granulation tissue _______ (is/is not) vascular.

A

Granulation tissue is vascular.

190
Q

What is the main cell type that causes wound contracture?

A

Myofibroblasts

191
Q

True/False.

Over the first six weeks of healing, large skin wound contractures can lead to a reduction of 10-15% in the size of the healed area from original size.

A

True.

Over the first six weeks of healing, large skin wound contractures can lead to a reduction of 10-15% in the size of the healed area from original size.

192
Q

After 1 week, wound strength is ___% of unwounded skin.

Plateaus at ___% after about 3 months.

A

After 1 week, wound strength is 10% of unwounded skin.

Plateaus at 70-80% after about 3 months.

193
Q

After __ _______, wound strength is 10% of unwounded skin.

Plateaus at 70-80% after about __ _______.

A

After 1 week, wound strength is 10% of unwounded skin.

Plateaus at 70-80% after about 3 months.

194
Q

________ is to internal organs as scarring is to the skin.

A

Fibrosis is to internal organs as scarring is to the skin.

195
Q

What term refers to wound rupture after partial healing?

A

Wound dehiscence

196
Q

What is ‘proudflesh?’

A

Excessive granulation tissue

(forms large scar that does not reapproximate original skin surface)

197
Q

Match the following bolded terms with their respective italicized definitions:

keloid, proudflesh, contractures

restricted movement due to wound tightening, excessive scarring, excessive granulation tissue

A

Keloid - excessive scarring

Proudflesh - excessive granulation tissue

Contractures - restricted movement due to wound tightening

198
Q

What cell type is most important in mediating wound healing?

What cell type is most important in the actual process of wound healing?

A

Macrophages;

fibroblasts

T1 - Phase 2 - Systems Modules (I) (27 decks)

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