Inflammation & Repair Flashcards

1
Q

Name 4 stimuli for acute inflammation.

A

Infections (viral, bacterial, etc.)

Tissue necrosis

Foreign bodies (trauma)

Autoimmune rxns

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

What vascular changes happen with acute inflammation? (3 of the cardinal signs)

A
  1. Rubor (redness) - increased blood flow
  2. Calor (warmth) - increased blood flow
  3. Tumor (swelling) - edema caused by increased vascular permeability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What happens to hydrostatic and osmotic pressure in blood vessels during inflammation?

A

Increased hydrostatic pressure, decreased osmotic pressure –> leakage across vessels

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

What is transudate? Exudate? (clinical terms for fluid collections outside blood vessels)

A

Transudate - fluid only (low protein, low specific gravity, few inflamm cells)

Exudate - high protein, high specific gravity, many inflammatory cells

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

What is transcytosis? What increases this?

A

Increased transport of fluids across cells

VEGF - vascular endothelial growth factor

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

What molecules do neutrophils use when rolling for weak attachment? What are these molecules upregulated by?

A

Selectins which are upregulated by cytokines TNF and IL-1

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

What molecules do neutrophils use during adhesion for strong attachment?

A

Integrins and CD44

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

Define diapedesis.

A

Transmigration of neutrophils across blood vessels

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

What molecules do neutrophils use during phagocytosis?

A

Opsonins

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

What molecules do neutrophils use to kill?

A

Leukocyte enzymes, oxygen radicals

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

What does leukocyte adhesion deficiency type I involve?

A

Defect in biosynthesis of beta-2 chain on integrins

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

What molecules does leukocyte adhesion deficiency type 2 involve defects in?

A

Defects in E and P selectins

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

Chediak-Higashi syndrome

A

Defective fusion of phagosomes and lysosomes Autosomal recessive Susceptible to infections, albinism, nerve defects, platelet defects

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

Chromic granulomatous disease (CGD)

A

Defects in gene that codes components of phagocyte oxidase - can’t make superoxide Defects in bacterial killing and recurrent infections X-linked

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

What vasoactive amine is a link between clotting and inflammation and is a key component in coagulation?

A

Serotonin

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

What are the broad classes of anti-inflammatory drugs?

A
  1. Cyclooxygenase (COX) inhibitors - inhibit COX-1 and COX-2 which inhibits prostaglandin synthesis
  2. Lipooxygenase (LOX) inhibitors - inhibit leukotriene production or block leukotriene receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What cytokines induce endothelial adhesion molecules?

A

TNF and IL-1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the three types of nitrous oxide? What does it do?

A

Endothelial, neuronal, inducible Promotes vasodilation and inhibits inflammatory responses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How does inflammation get turned off? (3 ways)

A
  1. Short half life for inflammatory mediators. 2. Production of lipoxins 3. Production of TGFbeta
20
Q

4 outcomes of acute inflammation.

A
  1. Resolves completely - regeneration 2. Localizes - abscesses form 3. Heal w/ scarring 4. Progress to chronic inflamm
21
Q

What types of cells dominate in acute inflamm? Chronic?

A

Acute - neutrophils

Chronic - “mononuclear” lymphocytes, plasma cells, macrophages/histiocytes

22
Q

What types of macrophages dominate in the following: Liver Lymph nodes Lungs CNS

A

Liver - Kupfer cells LNs - sinus histiocytes Lungs - alveolar macrophages CNS - microglia

23
Q

What is granulomatous inflammation? Is it an acute or chronic inflammation?

A

Focal collection of “epitheliod” histiocytes - histiocytes that have been activated - large w/ abundant pink cytoplasm that looks like epithelial cells

Type of chronic inflammation

24
Q

What type of necrosis can be seen with granulomatous inflammation?

25
Describe what a granuoma looks like.
Giant cell - collection of T-cell activated epithelioid histiocytes that have engulfed indigestible material (like foreign bodies including TB, fungus, etc.) surrounded by inflammatory cells - lymphocytes
26
What are the two final processes of repair?
Regeneration - replacement by cells identical to those lost Fibrosis (scarring) = replacement of lost cells by collagen
27
What is a labile cell: A. Cells that are always dividing B. Cells that are in G0 but can't enter cell cycle C. Cells that are undergoing apoptosis D. Cells that can't divide
A. Cells that are always dividing
28
Where are labile cells present?
Cells that are always dividing (in cell cycle) Skin, bone marrow, GI mucosa
29
What are stable cells - where are they present in the body?
Cells that can enter the cell cycle and divide Hepatocytes, renal tubular cells, endothelial cells
30
What are permanent cells, where are they found?
Cells that can't divide Neurons, skeletal & cardiac muscle cells
31
What inhibits cell growth? Promotes it?
Inhibits - contact inhibition Promotes - Cytokines like EGF/TGFalpha, PDGF, FGFs, VEGF, TGFbeta
32
What produces epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-alpha)? What are they mitogenic for?
Keratinocytes, macrophages, inflammatory cells Mitogenic for epithelia
33
What is hepatocyte growth factor (HGF) mitogenic for? What produces it? What is its receptor?
Mitogenic for hepatocytes and biliary epithelium, lung, kidney, and mammary gland cells Produced by fibroblasts and most mesenchymal cells Receptor: c-MET
34
Where is platelet-derived growth factor (PDGF) stored? What is it mitogenic for?
Platelets Mitogenic for fibroblasts, smooth muscle cells, and any tumor cells
35
What is vascular endothelial growth factor (VEGF) mitogenic for?
Blood vessel formation (angiogenesis) - allows for healing of wounds
36
What processes does fibroblast growth factor (FGF) contribute to?
Wound healing, hematopoiesis, angiogenesis, development
37
What does transforming growth factor beta (TGF-beta) contribute to?
1. Growth inhibitor for epithelia 2. Potent fibrogenic agent 3. Strong anti-inflammatory effects
38
What is the most common protein in the animal world? What cell type produces it?
Collagen, produced by fibroblasts
39
What is the protein name of the following extracellular matrix components that are important in repair: 1. Cell glue 2. Basement membrane, cell attachments 3. Signaling, organization of actin in cytoskeleton
1. Fibronectin 2. Laminin 3. Integrins
40
What are the 4 main steps of the repair process?
1. Angiogenesis 2. Migration & proliferation of fibroblasts 3. Deposition of ECM 4. Remodeling
41
When do myofibroblasts cause wound contraction - healing by 1st or 2nd intention? Which one has scab formation?
Wound contraction - 2nd intention Scab formation - 1st intention
42
What type of tissue forms over wounds?
Granulation tissue - small vessels with a lot of edema and inflammation and fibroblasts Leads to scars
43
Define/describe the following: 1. Serous inflammation 2. Fibrinous inflammation 3. Suppuration 4. Ulcer 5. Lymphangitis 6. Cellulitis
* Serous inflammation - lots of fluid - effusions, blisters * Fibrinous inflammation - more severe vascular leak - larger molecules leak out * Suppuration - formation of pus * Ulcer - loss of surface epithelium * Lymphangitis - inflammation of lymphatics * Cellulitis - diffuse inflammation of soft tissues
44
What are the local effects of inflammation? (5)
1. Redness (rubor) - inc. blood flow 2. Warmth (calor) - inc. blood flow 3. Edema (tumor) - inc. blood flow 4. Pain (dolor) - cytokines 5. Loss of function - swelling and pain limit motion
45
What are the two systemic effects of inflammation?
1. Fever - acute phase (cytokine mediated) (also chills, anorexia, somnolence, malaise) 2. Leukocytosis - increased WBCs in peripheral blood + "left shift" - presence of immature WBCs in peripheral blood
46
What is the difference between fibrosis and healing
* Fibrosis - implies persistent tissue damage & inflammation * Healing - implies a single/self-limited tissue injury
47
What is the difference between granulomas and granulation tissue?
•Granulomas (granulomatous inflammation) –Specialized type of chronic inflammation characterized by epithelioid histiocytes •Granulation tissue –Loose, edematous, highly vascular tissue present in the initial phases of healing