Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Block II Pathology > Week 2: Chronic Inflammation > Flashcards

Week 2: Chronic Inflammation Flashcards

1
Q

What are the four general features of chronic inflammation? How is chronic inflammation disease characterized?

A

Inflammation is not a disease, but a response to insult or injury. It involves the steps of:

Insidious onset

Prolonged duration

Tissue destruction

Ongoing healing and fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are common etiologies of chronic inflammation?

A

Viral infections and other persistent infections

Toxic substances

Hypersensitivity diseases like asthma, autoimmune disorders, inflammatory bowel disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the “five R’s” that make up the general steps to inflammation pathways?

A

Recognition

Recruitment

Removal

Regulation

Repair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

___________ play a role in both innate and adaptive immunity

A

Macrophages

Innate = general phagocytosis

Adaptive = APC for B cells/T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What immune cells are generally associated with acute and chronic inflammation?

A

Acute = neutrophil

Chronic = lymphocytes (B/T cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the technical term for scarring? What is being deposited?

A

Fibrosis, which is the deposition of collagen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are some main forms of toxic substances that cause chronic inflammation?

A

Prolonged exposure to toxic substances like silicone, asbestos, or endogenous particles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is this an example of?

A

This is the skin of a patient with rheumatoid arthritis, an hypersensitivity disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the main differences in chronic and acute inflammation?

A

Cells involved:

acute = neutrophils (early), macrophages (late)

chronic = macrophages, lymphocytes, plasma cells

Tissue changes:

acute = vascular changes

chonic = tissue destruction

Long vs. short term:

acute = edema

chronic = fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the main roles of macrophages?

A

Activated by various stimuli (sometimes lymphocytes)

Microbial removal

Initiation of repair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What signals stimulate inflammation in macrophages? Which stimulate tissue repair and anti-inflammatory effects?

A

Inflammation = microbes, IFN-gamma

Repair/anti-inflammatory effects = IL-13, IL-4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe the recruitment and roles of lymphocytes

A

Lymphocytes are mobilized by cell-mediated and antibody-mediated immune reactions

They respond to signaling by activated macrophages, which display antigens for lymphocytes (APCs)

Lymphocytes also produce cytokines that produce T-cell responses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe the recruitment and roles of plasma cells

A

Plasma cells develop from activated B cells, and produce antibodies against altered tissue components or against a persistent antigen. They act as the humoral mediators of leukocyte immunity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are mast cells and what roles do they play in the inflammatory process?

A

Mast cells are cytokine-producing granulocytes that play roles in both acute and chronic inflammation

Acute = anaphylactic reactions

Chronic = cytokine production that may contribute to fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are eosinophils and what roles do they play in inflammation?

A

Eosinophils are granulocytes that play a role in parasitic infections and immune reactions mediated by IgE.

They respond to eotaxin, a cytokine responsible for recruitment of eosinophils to a site of infection

They also include major basic protein, a nerve toxin that helps kill parasites.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What causes tissue damage in chronic inflammation?

A

Toxins or injurious stimuli

Products secreted by macrophages

T-lymphocytes

Fibroblasts

17
Q

What is granulomatous inflammation?

A

A subtype of chronic inflammatory reaction

Tuberculosis is an example. It occurs when a nodule of specialized macrophages form a giant cell and can recruit other inflammatory cells, including TDTH cells

There are epitheloid (very large) and spindled (thinned out) forms.

18
Q

What are the two main forms of granulomatous inflammation, and how does each occur?

A

Foreign body type granulomas - initiated by inert foreign bodies like sutures, asbestos slivers, or splinters

Immune granulomas - poorly degradeable or particulate agents, T-lymphocytes and macrophages induce transformation of macrophages

Involves IL-2, TNF and interferons

19
Q

What is caseating granulomatous inflammation?

A

A type of inflammation associated with mycobacterial infection–for example, tuberculosis, a prototype of this kind of inflammation

Activated macrophage accumulates to attempt to destroy the infective agent. We observe central necrosis (caseous) in the middle of the granuloma (pink area)

20
Q

What is non-caseating granulomatous inflammation?

A

This is a granuloma that forms without central necrosis, and is associated with syphilis, cat-scratch disease, and sarcoidosis

21
Q

What are the systemic, general effects of inflammation?

A

Systemic inflammatory response syndrome (acute phase response)

Reaction to cytokine production

Fever, leukocytosis and acute phase proteins

22
Q

What is involved in the acute phase response of inflammation?

A

“ACute End For Luke”

Acute phase reactions: fever, sleep, decreased appetite, neutrophilia, hemodynamic shock

Endothelial effects: increased leukocyte adherence, procoagulant activity, decreased anticoagulant activity, increased IL-1,6,8 production, PDGF production

Fibroblast effects: increased proliferation and collagen synthesis, increased collagenase and protease, increased PGE synthesis

Leukocyte effects: increased cytokine secretion (IL-1,6)

23
Q

What steps of the acute phase response leads to fever?

A

“P-IL for Thursday Night Fever”

Pyrogens

IL-1 and TNF

Conversion of AA to prostaglandins

Action on the hypothalamus to reset the temperature set point

Can relieve with NSAIDS

24
Q

What helps us assess leukocytosis, and what are the two major elements involved?

A

Neutrophilia is an increase in neutrophils, and lymphocytosis is an increase in lymphocytes.

You can assess these values with a CBC (complete blood count) of:

Hemoglobin

Hematocrit

WBC count

Platelet count

25
Q

What are the acute phase proteins that are relevant to the immune response? What do we look for in this process and what might it mean?

A

Crack For SAAle En Montana

Proteins:

C-reactive protein

Fibrinogen

Serum amyloid A protein

Look for:

Erythrocyte sedimentation rate

Might mean:

Markers for inflammatory disorders

26
Q

What are the symptoms of the acute phase response?

A

The People aRe Chilly And Mad

Tachycardia

Peripheral vasoconstriction

Rigors

Chills

Anorexia

Malaise

27
Q

What is the difference between regeneration and repair?

A

Regeneration occurs when there is intact tissue framework (superficial wounds, parenchyma damage), and allows normal tissue to reform

Repair occurs when the tissue framework is damaged (deep wounds, parenchyma and mesenchyma damage), and creates scar formation

28
Q

What occurs with persistent tissue damage?

A

Fibrosis (NOT the same as scarring)

Chronic inflammatory diseases like:

Cirrhosis

Chronic pancreatitis

Pulmonary fibrosis

29
Q

What are the major components (5) of wound healing?

A

Inflammation

Angiogenesis

Fibroblastic proliferation

Collagen deposition (scarring) from angiogenesis and the formation of granulation tissue

Tissue remodeling (maturation and wound contraction)

30
Q

What is angiogenesis?

A

Neovascularization where pre-existing vessels give rise to new vessels. It involves many growth factors (VEGF) and ECM (Notch) proteins direct endothelial cell growth.

31
Q

How does deposition of connective tissue occur?

A

Fibroblasts migrate and proliferate at the site of the wound due to growth factors and cytokines. They secrete collagen and other ECM factors.

Vessel and fibroblast proliferation are components of granulation tissue.

32
Q

What are the major components of granulation tissue?

A

New vessel formation and fibroblastic proliferation

33
Q

What are the two main forms of cutaneous wound healing?

A

Primary intention - uncomplicated, clean incision, little scar formation

Secondary intention - large, deep wounds with excessive granulation tissue and scarring, wound contracture

Main steps to either: Inflammation, Proliferation, Maturation (remodeling and contraction)

34
Q

What systemic and local factors influence healing?

A

Systemic:

Nutrition and metabolism, blood supply, hormones

Local:

Infection, mechanical stretching, foreign bodies, size of wound, location of wound

35
Q

What is fibrosis?

A

Abnormal deposition of collagen in internal organs that occurs with chronic disease.

Ongoing inflammation and stimulation of fibroblasts

Block II Pathology (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions