Lecture 4 - Inflammation part 2 Flashcards

1
Q

List the contents of leukocytes granules.

A

Bactericidal permeability increasing protein (BPI), lysozyme, lactoferrin
Defensins (punch holes in membranes).

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

List the defects of leukocyte function of adhesion.

A

LFA-1 and Mac-1 subunit defects lead to impaired adhesion (LAD-1),
Absence of sialyl-Lewis X, and defect in E- and P-selectin sugar epitopes (LAD-2)

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

List the defects of leukocyte function of chemotaxis/phagocytosis.

A

Microtubule assembly defect leads to impaired locomotion and lysosomal degranulation (Chediak-Higashi Syndrome).

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

List the defects of leukocyte function of microbicidal activity.

A

Deficiency of NADPH oxidase that generates superoxide… no oxygen-dependent killing mechanism (chronic granulomatous disease)

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

What are the chemical mediators of inflammation?

A

Plasma derived: Complement, kinins, coagulation factors, many in “pro-form” requiring activation.
Cell-derived: Preformed, sequestered and released (mast cell histamine), synthesized as needed (prostaglandin)

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

What are the systematic effects of inflammation?

A

Fever (One of the easily recognized cytokine- mediated, acute phase reactions including: anorexia, skeletal muscle protein degradation, hypotension)
Fever speeds up immune responses and makes it difficult for pathogens to survive at elevated temperature.
Leukocytosis: Elevated white blood cell count

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

List the possible outcome of inflammation.

A

Complete resolution, little tissue damage capable of regeneration, scarring (fibrosis), in tissues unable to regenerate, excessive fibrin deposition organized into fibrous tissue, abscess formation occurs with some bacterial or fungal infections

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

What is the specific mediators of PFA (platelet activating factor) Causes what?

A

Derived also from cell membrane phospholipid; causes vasodilation, increased vascular permeability, increases leukocyte adhesion

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

What are the specific mediators of arachidonic acid metabolites? Causes what?

A

Prostaglandins and thromboxane: via cyclooxygenase pathway
cause vasodilation and prolong edema but also protective.

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

Describe the Kinin system.

A

Leads to formation of bradykinin from cleavage of precursor (HMWK), vascular permeability Arteriolar dilation, non-vascular smooth muscle contraction (e.g., bronchial smooth muscle), causes pain

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

What does serotonin do as a mediator? Released by what?

A

Has vasodilatory effects similar to those of histamine, platelet dense-body granules; release is triggered by platelet aggregation, plasma proteases, clotting system, complement, kinins

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

What does histamine do as a mediator? Released by what?

A

Causes vasodilation and venular endothelial cell contraction, junctional widening; mast cells, basophils, platelets in response to injury

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

State 4 things about chemical mediators.

A

May or may not utilize a specific cell surface receptor for activity; may signal target cells to release other effector molecules that either amplify or inhibit initial response; are tightly regulated; quickly decay, inactivated enzymatically (kininase), or are scavenged (antioxidants)

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

Where is histamine released by? In response to what?

A

The granules of mast cells, basophils, platelets; to injury and immune reactions

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

How are the complement factors in the complement system named? How many factors are there?

A

W/ numbers: C1-C9; 20 factors

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

Prostaglandins and thromboxane: via cyclooxygenase pathway causes what? But is also ________

A

vasodilation and prolong edema; protective: gastric mucosa

17
Q

PAF stands for? Derived from? Causes?

A

Platelet activating factor; from cell membrane phospholipid; causes vasodilation, increased vascular permeability, increases leukocyte adhesion (integrin conformation)

18
Q

Leukotrienes: via lipoxygenase pathway are… causes…

A

are chemotaxins, vasoconstrictors; cause increased vascular permeability, and bronchospasm

19
Q

Which specific kinds of cytokines are important for inflammation?

A

IL-1, TNF-α and -β, IFN-γ

20
Q

Nitric oxide are… produced by… causes…

A

short-acting soluble free-radical gas with many functions; by endothelial cells, macrophages; vascular smooth muscle relaxation and vasodilation, kills microbes in activated macrophages, counteracts platelet adhesion, aggregation, and degranulation

21
Q

What are some possible outcomes of inflammation?

A

Complete resolution,
Little tissue damage Capable of regeneration
Scarring (fibrosis)
Progression to chronic inflammation

22
Q

What is an undesirable outcome of inflammation?

A

Fibrosis, in tissues unable to regenerate

23
Q

Describe chronic inflammtion.

A

Lymphocyte, macrophage, plasma cell infiltration, tissue destruction by inflammatory cells, attempts at repair with fibrosis and angiogenesis (new vessel formation). When acute phase cannot be resolved, persistent injury or infection. Prolonged toxic agent exposure (silica). Can cause autoimmune diseases.

24
Q

Describe mononuclear phagocytes

A

Macrophages that are all over. They circulate as monocytes & reach site of injury w/in 24-48 hrs & transform. Then become activated by T cell-derived cytokines, endotoxins, and other products of inflammation.

25
Q

Give 3 lymphocytes.

A

T & B lymphocytes, plasma cells, eosinophils

26
Q

How are T & B lymphocytes activated? Release what?

A

Antigen-activated (via macrophages and dendritic cells); release macrophage-activating cytokines (in turn, macrophages release lymphocyte- activating cytokines until inflammatory stimulus is removed)

27
Q

Describe granulomatous inflammation.

A

Clusters of T cell-activated macrophages, which engulf and surround indigestible foreign bodies. Resemble squamous cells, therefore called “epithelioid” granulomas (a microbe that is resistant to destruction)

28
Q

Lymphatics drains ______, which causes…

A

tissues; flow to increase in inflammation, antigen is transported to the lymph node

29
Q

What are the patterns of acute and chronic inflammation ?

A

Serous (Watery, protein-poor effusion), fibrin accumulation (entirely removed or becomes fibrotic), suppurative (presence of pus), and ulceration (Necrotic and eroded epithelial surface).

30
Q

What are the systemic effects of inflammation?

A

Fever (speeds up immune responses & makes it difficult for pathogens to survive at elevated temp), leukocytosis (elevated white blood cell count)

31
Q

What cytokines causes fever?

A

IL-1, IL-6, and TNF

32
Q

How does white blood cell count increases?
Differentiation indicates what?
An elevation of neutrophils suggest what? Eosinophils? Lymphocytes?

A

By proliferation/cell division.
The level of white blood cells.
Suggests bacteria infections; parasitic infection; viral