Brainscape's Knowledge GenomeTM

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


See full index

Term III: Pathology > Inflammation & Repair > Flashcards

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?

A

Caseous

25
Q

Describe what a granuoma looks like.

A

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
Q

What are the two final processes of repair?

A

Regeneration - replacement by cells identical to those lost

Fibrosis (scarring) = replacement of lost cells by collagen

27
Q

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

A. Cells that are always dividing

28
Q

Where are labile cells present?

A

Cells that are always dividing (in cell cycle)

Skin, bone marrow, GI mucosa

29
Q

What are stable cells - where are they present in the body?

A

Cells that can enter the cell cycle and divide

Hepatocytes, renal tubular cells, endothelial cells

30
Q

What are permanent cells, where are they found?

A

Cells that can’t divide

Neurons, skeletal & cardiac muscle cells

31
Q

What inhibits cell growth? Promotes it?

A

Inhibits - contact inhibition

Promotes - Cytokines like EGF/TGFalpha, PDGF, FGFs, VEGF, TGFbeta

32
Q

What produces epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-alpha)?

What are they mitogenic for?

A

Keratinocytes, macrophages, inflammatory cells

Mitogenic for epithelia

33
Q

What is hepatocyte growth factor (HGF) mitogenic for? What produces it? What is its receptor?

A

Mitogenic for hepatocytes and biliary epithelium, lung, kidney, and mammary gland cells

Produced by fibroblasts and most mesenchymal cells

Receptor: c-MET

34
Q

Where is platelet-derived growth factor (PDGF) stored? What is it mitogenic for?

A

Platelets

Mitogenic for fibroblasts, smooth muscle cells, and any tumor cells

35
Q

What is vascular endothelial growth factor (VEGF) mitogenic for?

A

Blood vessel formation (angiogenesis) - allows for healing of wounds

36
Q

What processes does fibroblast growth factor (FGF) contribute to?

A

Wound healing, hematopoiesis, angiogenesis, development

37
Q

What does transforming growth factor beta (TGF-beta) contribute to?

A
  1. Growth inhibitor for epithelia
  2. Potent fibrogenic agent
  3. Strong anti-inflammatory effects
38
Q

What is the most common protein in the animal world? What cell type produces it?

A

Collagen, produced by fibroblasts

39
Q

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
A
  1. Fibronectin
  2. Laminin
  3. Integrins
40
Q

What are the 4 main steps of the repair process?

A
  1. Angiogenesis
  2. Migration & proliferation of fibroblasts
  3. Deposition of ECM
  4. Remodeling
41
Q

When do myofibroblasts cause wound contraction - healing by 1st or 2nd intention?

Which one has scab formation?

A

Wound contraction - 2nd intention

Scab formation - 1st intention

42
Q

What type of tissue forms over wounds?

A

Granulation tissue - small vessels with a lot of edema and inflammation and fibroblasts

Leads to scars

43
Q

Define/describe the following:

  1. Serous inflammation
  2. Fibrinous inflammation
  3. Suppuration
  4. Ulcer
  5. Lymphangitis
  6. Cellulitis
A
  • 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
Q

What are the local effects of inflammation? (5)

A
  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
Q

What are the two systemic effects of inflammation?

A
  1. Fever - acute phase (cytokine mediated)

(also chills, anorexia, somnolence, malaise)

  1. Leukocytosis - increased WBCs in peripheral blood + “left shift” - presence of immature WBCs in peripheral blood
46
Q

What is the difference between fibrosis and healing

A
  • Fibrosis - implies persistent tissue damage & inflammation
  • Healing - implies a single/self-limited tissue injury
47
Q

What is the difference between granulomas and granulation tissue?

A

•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

Term III: Pathology (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions