Brainscape's Knowledge GenomeTM

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


See full index

CMOD-Path Block 1 > (04-08) Inflammation > Flashcards

(04-08) Inflammation Flashcards

1
Q

What are the two methods of release for inflammatory mediators?
- list them.

A

Preformed Granules:

  • Histamine
  • Serotonin

Newly Synthesized:

  • Prostaglandins
  • Leukotrienes
  • Platelet-activating factor
  • Reactive Oxygen Species
  • Nitric Oxide
  • Cytokines
  • Neuropeptides
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What arachidonic acid metabolites act to vasodilate?

A
  • Prostaglandins PGI2, PGE1, PGE2, PGD2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What arachidonic acid metabolites act to to vasocontrict?

A
  • Thromboxane A2, Leukotrienes C4, D4, E4
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What arachidonic acid metabolites act to increase vascular permeability?

A

Leukotrienes C4, D4, E4

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

What arachidonic acid metabolites act in chemotaxis and leukocyte adhesion?

A

Leukotriene B4, HETE

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

What is the function of Platelet-Activating Factor?

- Receptor type?

A
  1. Stimulates Platelets
  2. POTENT BROCHOCONSTRICTION
  3. Inflammation via:
    - Leukocyte adhesion
    - Chemotaxis
    - Leukocyte Degranulation
    - Respiratory Burst

Acts on a G-protein coupled receptor

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

What are two general roles of cytokines?

A
  1. Mediate Inflammation and immune response

2. Interleukins mediate leukocytes

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

What the the major cytokines of ACUTE inflammation?

A
  • TNF
  • IL-1
  • IL-6
  • chemokines (chemoattractant cytokines)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What Characterizes Chronic Inflammation?

  • Major Cell of chronic Inflammation
  • Major cytokines of CHRONIC inflammation?
  • Common causes?
A

Characteristics:

  • Infiltration of mononuclear cells MACROPHAGES mainly (aka not neutrophils)
  • Tissue Destruction
  • Repair, Angiogenesis, and FIBROSIS

Mediators:

  • Interferon-gamma (IFN-gamma)
  • IL-12

Common Causes:

  • Persistent Infections (ie TB)
  • Immune-mediated Inflammatory Diseases (autoimmune, allergic)
  • Prolonged Exposure to toxic agents
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What does IL-17 do?

A

Recruits neutrophils

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

What cell(s) make(s) TNF and IL-1?

  • How to they contribute to local inflammation
  • What are their protective effects
  • What are their pathologic effects
A

Produced by alternatively activated MACROPHAGES, mast cells, and endothelial cells

Local Inflammation:

  • Increase expression of Adhesion molecules
  • Increase Vascular Permeability
  • Activate Leukocytes (to produce IL-1, and IL-6)

Protective Effects:

  • FEVER
  • Acute Phase Proteins (IL-6 mainly)
  • Production of Leukocytes

Pathologic Effects:

  • Low Blood output from heart
  • Thrombosis
  • Insulin Resistance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What causes Hereditary Angiodema?

A
  • Loss of C1 inhibitor

- Production of Kinins Secondary to complement activation results in edema of multiple tissues including larynx

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

What is DAF?

  • what does it do?
  • what is caused by a deficiency in this?
A

DAF = Decay Accelerating Factor

Limits the Formation of C3 and C5 convertases

Loss of this = Paroxysmal Nocturnal Hemoglobinuria (occurs at night because of rise in blood pH)

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

What is Factor H?

- what disease(s) result(s) if you lack it?

A
  • Plasma Protein that limits convertase Formation
  • Hemolytic Uremic Sydrome
  • Macular Degeneration (from spontaneous vascular permeability)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the general Role of Kinins?

A

Mediates Vascular Reaction and Pain

*Produced by Proteolytic Cleavage of Precursors

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

Differentiate between cells found in Granulomas and Abscesses.

A

Granulomas:
- Histiocytes should be present, these are macrophages that look similar to epithelial cells

Abscesses:
- Neutrophils will be present

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is a definitive marker of CHRONIC rhinitis?

A
  • Presence of esosinophils at near the basal side of the respiratory epithelium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the role of Macrophages in host defense and the inflammatory response (4)?

A
  1. Phagocytosis
  2. Tissue Repair
  3. Secrete Mediators of Inflammation
  4. APC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What T-lymphocyte is involved in the the classical pathway of macrophage activation?

  • How?
  • what type of inflammation results from this pathway?
A

TH1

  • TH1 secretes IFN-gamma
  • ACUTE inflammation results
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What T-lymphocyte is involved in the the alternative pathway of macrophage activation?

  • How?
  • what type of inflammation results from this pathway?
A

TH2

  • TH2 secretes IL-4, IL-5, and IL-13, which recruits and activates EOSINOPHILS, and alternatively activated macrophages
  • CHRONIC inflammation results from this pathway
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What inflammatory Mediators are important in vasodilation?

A
  • Prostaglandins
  • Nitric Oxide
  • Histamine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What inflammatory Mediators are important in increasing vascular permeability?

A
  • Histamine and Serotonin
  • C3a and C5a (indirectly)
  • Bradykinin
  • Leukotrienes C4, D4, E4
  • PAF
  • Substance P
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What inflammatory Mediators act as chemotaxins?

A
  • TNF, IL-1
  • Chemokines
  • C3a, C5a
  • Leukotriene B4
  • Bacterial Products
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What inflammatory Mediators are important in Fever?

A

IL-1, TNF

Prostaglandins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What inflammatory Mediators are imporant in pain?

A

Prostaglandins

Bradykinin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What inflammatory Mediators cause tissue damage?

A

Lysosomal Enzymes of Leukocytes
ROS
NO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Granulomatus Inflammation

  • Cells involved
  • common diseases where these are formed
A

Macrophages surrounded by Lymphocytes (TH1)

Common Diseases:

  • TB
  • Chrohn Disease
  • Sarcoidosis
  • Response to foreign bodies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Acute-Phase Reaction:

  • Cytokines involved
  • Characteristics
A

Aka Systemic Inflammatory Response Syndrome

Cytokines:

  • TNF
  • IL-1
  • IL-6

Physiologically:
Fever - caused by TNF and IL-1 stimulating production of prostaglandins in the hypothalmus

High BP and HR

Elevated Acute phase proteins (IL-6 mediated) - more CRP, SAA

Erythrocyte Sedimentation Rate (ESR) increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the 3 clinical markers of septic shock?

- Chemokines that cause this

A
  1. Hypotensive
  2. Acidosis
  3. Dissemenated Intravascular Coagulation (DIC)

Chemokines:

  • TNF (coagulation and fever)
  • IL-12
  • IL-1
30
Q

What are the 5 indicators of Inflammation?

- causes of each of them?

A

Calor
- Increased Blood Flow

Rubor
- Increased Blood Flow

Tumor
- Extravasation of Leukocytes from Increased Vascular Permeability

Dolor
- Bradykinin, Prostaglandins

Loss of Function

31
Q

What are the 5 R’s of inflammation?

A
  1. Recognition
  2. Recruitment of Leukocytes
  3. Removal of Agent
  4. Regulation of response
  5. Resolution
32
Q

Differentiate the characteristic of Acute and Chronic Inflammation.

  • time
  • cell type
  • degree of injury
  • Signs
A

Acute:

  • Fast onset Minutes or Hours
  • Mainly Neutrophils
  • Injury Usually Mild
  • PROMINENT signs locally and systemically

Chronic:

  • Slower onset?
  • Monocytes/Macrophages and Lymphocytes
  • Tissue injury and Fibrosis is often sever and progressive
  • Local and systemic signs are more often less prominent and subtle
33
Q

What is vascular Statsis?

A
  • Slowing of the blood in the bloodstream with vasodilation and fluid exudation to allow chemical mediators and inflammatory cells to collect and respond to the stimulus
34
Q

What chemokine plays a key role in obesity related type 2 diabetes and artherosclerosis?

A

IL-1

35
Q

What is an inflammasome?

A
  • Protein complex that recognizes products of dead cells
36
Q

Diffentiate between Transudate and Exudate.

  • Causes
  • Contents
  • do these occur during inflammatory conditions or not?
A

Transudate
Causes:
- High Hydrostatic Pressure
- Low osmotic pressue

Contents:
- not proteins in this because epithelial cells are still tightly linked

Conditions:

  • Heart Failure
  • Liver or Kidney disease

Exudate
Causes:
- Increased Vascular Permeability

Contents:
- Protein and Cells

Conditions:
Inflammation

37
Q

T or F: both transudate and Exudate cause edema

A

True

38
Q

What 4 possible causes of increased vascular permeability?

A
  1. Endothelial Cell contraction leading to INTERCELLULAR GAPS in POSTCAPILLARY venules
  2. Endothelial Cell Injury
  3. Increased Transcytosis of proteins through channels formed by intracellular vesicles
  4. Leakage from new blood vessels from tissue repair
39
Q

List the 4 Steps in Diapedsis and molecules involved.

A
  1. Margination
  2. Rolling
    P-selectin and E-selectin on endothelial cells binds CD34
  3. Adhesion
    LFA-1 binds to ICAM-1
    IL-8 on endothelial cell, binds IL-8 receptor on Neutrophil
  4. Diapedesis
    CD31 binds to CD31
40
Q

Which cells will be present at early and late stages in inflammation?

A

Early:
- Infiltrates of neutrophils and congest blood vessels

Late:
- Mononuclear Cellular infiltrates

41
Q

Elastase

  • Inhibitor
  • Implications Inability to inhibit
  • Disease
A

Inhibitor:
Alpha-1 antitrypsin (A1AT)

Loss of A1AT leads to inability to prevent elastase from chopping up elastic tissue

Disease:
A1AD - Results from inability to get A1AT out of vesicles that are inside of the liver.

42
Q

T or F: leukocytes can regularly excrete elastase Extracellularly.

A

False, they only do they can no longer ingest particles, or if there is damage to the phagolysosome

43
Q

What are the steps in the formation of NETS?

A
  1. Production of ROS
  2. Migration of the Protease Neutrophil Elastase (NE)
  3. Myeloperoxidase (MPO) was transformed from granules to the nucleus
  4. Processing of Histones
  5. Cell Rupture
44
Q

Chediak-Higashi

  • defect?
  • Symptoms, Explain them
  • Histological Features
A
  • Microtubule Defect

Symptoms:

  • Albinism - Melanin granules can’t be expelled from melanocytes
  • Occulocutaneous Albinism - eye and skin
  • Recurrent Pyogenic Infections - neutrophils can degranulate

Histological Features:
GIANT GRANULES in Nuetrophils

45
Q

Differentiate between Transudate and Exudate.

A

Exudate:
- PROTEIN RICH, YELLOWISH fluid

Trandusate:
CLEAR with LITTLE protein or cells

46
Q

Differentiate between seroanguinous and serofibrinous exudate.

A

Seroanguinous:
- Red blood cells in exudate

Fibrinous:
- Fibrin protein rich exudate

47
Q

What characterizes purulent exudate?

- aka?

A
  • Many PMN’s present

- also known as empyema

48
Q

Differentiate Between Purulent and Chylous effusion.

A

Purulent:
- More Yellow and filled with Neutrophils

Chylous:
- White and filled with lymphocytes

49
Q

Indicate what is happening at the different points in time in Cell and Tissue Regeneration:
Day 1, Day2/3, Day4/5, Week 2

A

Day 1:
- Inflammation and Fibrin

Day 2/3:
- Macrophages and Granulation tissues

Day 4/5:
Neovascularization

Week 2:
- Collagen with less prominent vessels and inflammation

50
Q

What kinds of insults lead to scar formation in non-regenerative tissue and in regenerative tissue?

A

Non-regenerative tissue - any damage will lead to scar formation

Regenerative - leads to scar formation only if the regenerating cells are damaged (e.g. damaging skin stem cells in the basal lamina)

51
Q

What is the main role of a scar?

A

Provide structural Support

52
Q

What factors drive tissue regeneration?

A

Chemical Factors:
VEGF - very important
FGF - also very important

Proteins:
- Cyclin-dependent Kinases

53
Q

The 3 components of Regeneration include the remaining tissue, Vascular Endothelial Cells, and Fibroblasts. How do each of these contribute to the regeneration process?

A

Remaining Tissue:
- Sends out signals to bring in things like fibroblasts

Vascular Endothelial Cells:
- Granulation Tissue gets very VASCULAR then goes away

Fibroblasts:
- Principal cell remaining to proliferate after granulation tissue goes away

54
Q

Differentiate between Lable, Stable, and Permanent tissues.

A

Label:
- Continuously Dividing Cells in the Tissue

Stable:
- Quiescent and have some replicative activity

Permanent:
- Terminally differentiated and non-proliferative

55
Q

What are some examples of Labile tissues?

A

Bone Marrow
Surface Epithelia
Uterus

56
Q

What are some examples of Stable tissues?

A

Most of you internal organs…

LIVER (large regenerative capacity) 
Kideny (can undergo hyperplasia, contralateral to removed kidney) 
Endothelial Cells
Smooth Muscle
Fibroblasts
57
Q

What tissues of the body are permanent>

A

Neurons
Heart
General Skeletal Muscle

58
Q

What are the 2 forms of ECM and what do they do/what are they?
- What type of collagen can you find in the basement membrane?

A
  1. Interstitial Matrix
    - Space between cells in connective tissue
  2. Basement Membrane
    “Glue holding endothelium to matrix”
  • TYPE IV collagen
59
Q

What are the components of the basement membrane of and of the interstitial matrix?

A

Basement Membrane

  • Type IV collagen
  • Laminin
  • Proteoglycan

Interstitial Matrix:

  • Fibrillar collagen
  • Elastin
  • Proteoglycan and Hyaluronan
60
Q

What are the 3 steps in scar formation?

A
  1. Angiogenesis
  2. Migration and Proliferation of Fibroblasts and Depsosition of CT (some vessels and leukocytes still present) = GRANULATION TISSUE
  3. Maturation and remodeling of fibrous tissue to form a fibrous scar
61
Q

What histological Features can help you differentiate granulation tissue from mature scar tissue?

A

Scar Tissue will be much more blue in color with Trichrome stain

***Granulation tissue will have fibroblasts and will appear VERY VASCULAR, not very much collagen (less blue)

62
Q

What 3 growth factors drive wound repair and what is the role of each?

A

TGF-ß

  • Stimulates Collagen, Proteoglycan, and Fibronectin Production
  • LIMITS inflammatory response

PDGF

  • Stimulates growth and proliferation of Fibroblasts and Smooth muscle
  • may help in movement of macrophages

FGF
- angiogenesis

63
Q

What group of proteins break down collagen?

  • Co-factor
  • Inhibitor
A

Metalloproteases
- ZINC co-factor

Inhibitor = TIMPs

64
Q

**How do steriods inhibit scar formation?

A
  • Inhibit TGF-ß production and Reduce Fibrosis
65
Q

What is the biggest factor that determines if a scar will form or not?

A

Infection

Others:
- Nutrition (vit. C), Glucocorticoids, Mechanical Variables (surgical vs. laceration), Perfusion, Foreign bodies)

66
Q

T or F: Keloids form from an over-production of ECM.

A

True

67
Q

*****What is the biggest difference in healing by 1st intention vs. healing by second intention?

A
  • Healing by 1st intention will result in a FIBROUS union as the end product
  • Healing by 2nd intention requires MYOFIBROBLASTS to contract the wound so that healing can occur
  • *More Scarring this way
68
Q

What should you look for when determining whether or not a tissue has undergone fibrosis?

A

Spindled shaped cells (fibroblasts)

69
Q

What interleukin promotes eosinophil activation?

- what is the job of eosinophils?

A

IL-5

Eosinophils:
- Modulate Effects of the Mast Cell: Histaminase, and aryl Sulphatase (inactivating histamine and leukotrienes)

  • Also release major basic protein and eosinophilic cationic protein that break down tissue
70
Q

What does fibronectin do?

A

Links Integrins to collagen

CMOD-Path Block 1 (10 decks)

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