Lecture 4 - Inflammation part 2 Flashcards

1
Q

Bactericidal permeability increasing protein (BPI), lysozyme, lactoferrin, and Defensins (punch holes in membranes) are the contents of_____________.

A

leukocytes granules

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2
Q

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) are the defect of what?

A

Leukocyte function of adhesion.

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3
Q

Microtubule assembly defect leads to impaired locomotion and lysosomal degranulation (Chediak-Higashi Syndrome) are the defect of what?

A

Leukocyte function of chemotaxis/ phagocytosis.

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4
Q

Deficiency of NADPH oxidase that generates superoxide… no oxygen-dependent killing mechanism (chronic granulomatous disease) are the defects of what?

A

Leukocyte function of microbicidal activity.

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5
Q

What are the chemical mediators of inflammation? (2)

A

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

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6
Q

What is the systematic effects of inflammation? Give examples.

A

Fever (cytokine- mediated, acute phase reactions including: anorexia, skeletal muscle protein degradation, hypotension)

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7
Q

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. These are the possible outcomes for _____________.

A

Inflammation.

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8
Q

PFA (platelet activating factor) is derived from what? Causes what?

A

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

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9
Q

Prostaglandins and thromboxane: via cyclooxygenase pathway are the specific mediators of _____________ and causes _________and prolong ______ but also protective.

A

Arachidonic acid metabolites; vasodilation; edema

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10
Q

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. This is the ____ system.

A

Kinin system

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11
Q

__________ as a mediator has vasodilatory effects similar to those of histamine, platelet dense-body granules. It is released by the trigger of ___________-, plasma proteases, clotting system, complement, kinins.

A

Serotonin; platelet aggregation

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12
Q

Histamine as a ________ causes vasodilation and venular endothelial cell contraction, junctional widening. It is released by _____, _____, ______ in response to injury.

A

mediator; mast cells; basophils; platelets

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13
Q

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). These are the 4 things about ____________.

A

Chemical mediators

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14
Q

_________ is released by the granules of mast cells, basophils, platelets in response to _______ and ______________-.

A

Histamine; injury; immune reactions

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15
Q

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

A

W/ numbers: C1-C9; 20 factors

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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

Which specific kinds of cytokines are important for inflammation?

A

IL-1, TNF-α and -β, IFN-γ

19
Q

__________ short-acting soluble free-radical gas with many functions. They are produced by __________ and ____________. Causes are _________ and ______________, counteracts platelet adhesion, aggregation, and degranulation.

A

Nitric acid; endothelial cells; macrophages; vascular smooth muscle relaxation; vasodilation

20
Q

What are some possible outcomes of inflammation? (5)

A

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

21
Q

What is an undesirable outcome of inflammation?

A

Fibrosis, in tissues unable to regenerate

22
Q

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. What is this condition?

A

Chronic inflammation

23
Q

Macrophages that are all over. They circulate as monocytes & reach site of injury w/in 24-48 hrs & transform. Become activated by T cell-derived cytokines, endotoxins, and other products of inflammation. These are ______________ (2).

A

mononuclear phagocytes

24
Q

Give 3 lymphocytes.

A

T & B lymphocytes, plasma cells, eosinophils

25
Q

How are T & B lymphocytes activated? Release what?

A

Antigen-activated (via macrophages and dendritic cells); release macrophage-activating cytokines

26
Q

Describe granulomatous inflammation.

A

Clusters of T cell-activated macrophages, which engulf and surround indigestible foreign bodies.

27
Q

Lymphatics drains ______, which causes…

A

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

28
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).

29
Q

What cytokines causes fever?

A

IL-1, IL-6, and TNF

30
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

31
Q

What is Leukocytosis?

A

Elevated white blood cell count.

32
Q

What is Chediak-Higashi Syndrome?

A

Lysosomal degranulation.

33
Q

What does fever do to the immune response and pathogens?

A

Fever speeds up immune responses and makes it difficult for pathogens to survive at elevated temperature.

34
Q

Does granulomas resemble squamous cells, therefore called “epithelioid” granulomas (a microbe that is resistant to destruction)?

A

Yes.