Brs Chapter 2 Inflammation

Front 1

platelet-derived growth factor (PDGF) promotes _____.

Back 1

the proliferative response of fibroblasts and smooth m cells

Front 2

What synthesizes PDGF?

Back 2

platelets and other cells

Front 3

PDGF promotes chemotactic migration of ___, ___, and ___.

Back 3

fibroblasts, smooth m cells, and monocytes

Front 4

A progression factor that promotes the growth of endothelial cells, fibroblasts, and epithelial cells.

Back 4

epidermal growth factor (EGF)

Front 5

Promotes the synthesis of extracellular matrix protein (fibronectin) by fibroblasts, endothelial cells, and monocytes.

Back 5

fibroblast growth factors (FGFs)

Front 6

Fibronectin is chemotactic for ___.

It promotes ___.

What does it link?

Back 6

fibroblasts and endothelial cells

angiogenesis

links extracellular matrix components and macromolecules to cell surface integrins

Front 7

This is a growth inhibitor for many cell types and may aid in modulating the repair process.

It is also a chemotactic factor for ___ and ___.

Back 7

transforming growth factor (TGF-b)

macrophages and fibroblasts

Front 8

What are the macrophage-derived growth factors and what do they promote?

Back 8

IL-1 and TNF; proliferation of fibroblasts, smooth m cells, and endothelial cells

Front 9

Granulation tissue is composed of ___ and ___.

What type of tissue is it?

Back 9

capillaries and fibroblasts


connective tissue

Front 10

Granulation tissue fills defects created by ___.

Scarring is made by the addition of ___ which is produced by ___.

Back 10

liquefaction of cellular debris


collagen; fibroblasts

Front 11

List 4 examples of labile cells.

Back 11

epidermis, GI tract mucosa, genitourinary tract, hematopoietic cells of the bone marrow

Front 12

List 4 examples of stable cells.

Back 12

hepatocytes, renal tubules, parenchymal tissue of glands, mesenchymal cells

Front 13

List 2 examples of permanent cells.

Back 13

neurons and myocardial cells

Front 14

Which type of cell is capable of division when needed?

Back 14

stable cells

Front 15

What is an example of a disease causing caseous granulomatous infection?

Back 15

tuberculosis

Front 16

What is an example of a disease causing noncaseating granulomatous infection?

Back 16

sarcoidosis

Front 17

What are granulomas and what usually surrounds them?

Back 17

nodular collections of specialized macrophages called epitheliod cells; surrounded by a rim of lymphocytes

Front 18

what are the two types of giant cells derived from macrophages?

Back 18

langhans giant cell and foreign body giant cell

Front 19

how are giant cells formed?

Back 19

during granulomatous inflammation, activation of macrophages by T lymphocytes, interaction with T-cell receptor triggers release of cytokines which transform monocytes and macrophages into giant cells

Front 20

Chronic nonspecific inflammation is mediated by ____.

Back 20

the interaction of monocytes-macrophages with lymphocytes

Front 21

how are the nuclei arranged in a langhans giant cell? foreign body giant cell?

Back 21

horseshoe shaped pattern; scattered nuclei

Front 22

leukocyte adhesion deficiency (LAD) 1 is characterized by ___ and is caused by ____. .

Back 22

recurrent bacterial infections; deficiency of B2 integrins

Front 23

leukocyte adhesion deficiency (LAD) 2 is characterized by ___ and is caused by ___.

Back 23

recurrent bacterial infections; mutations in the gene that codes for fucosyltransferase, required for the synthesis of sialyl Lewis X on neutrophils

Front 24

What characterizes Chediak-Higashi syndrome?

It is marked by the appearance of abnormal ___.

What happens functionally?

Back 24

autosomal recessive disorder; neutropenia, albinism, cranial and peripheral neuropathy, and repeated infections
WBC
abnormal microtubule formation causing impaired chemotaxis and mirgration

Front 25

This disease is characterized by deficient activity of an enzyme involved in NAPDH oxidase activity and is marked by phagocytic cells that ingest but do not kill catalase-positive organisms.

Back 25

chronic granulomatous disease of childhood

Front 26

What happens when catalase-positive organisms are not killed?

Back 26

they will destroy H2O2 generated by bacterial metabolism, H2O2 is no longer available for myeloperoxidase, thus the myeloperoxidase-halide system of bacterial killing fails

Front 27

This is a cavity filled with pus, it is often walled off by fibrous tissue, and results from tissue destruction by lysosomal products

Back 27

abscess

Front 28

An ulcer is the loss of ___.

Back 28

surface epithelium

Front 29

what produces NO?

what does it do?

Back 29

endothelial cells

relaxes smooth m, inhibits platelet aggreation, and participates in microbial killing

Front 30

This system consists of plasma proteins that participate in immune lysis of cells and play a significant role in inflammation

Back 30

complement system

Front 31

C3a and C5a are known as ____.
1. They mediate degranulation of ___ and ___, causing the release of ___.
2. C5a is ___ and mediates release of ___ from ___.
3. C5a also induces expression of ___.
4. C5a activates the ___ pathway to ___ metabolism.

Back 31

anaphylatoxins
1. basophils and mast cells; histamine
2. chemotactic- mediates release of histamine from platelets
3. leukocyte adhesion molecules
4. lipoxygenase; arachidonic acid

Front 32

C3b is an ____.

Back 32

opsonin

Front 33

What activates the kinin system?

activation of this system in turn activates the ____.

Back 33

Hageman factor (factor XIIa)

complement

Front 34

The kinin system converts ___ to ___.

Back 34

prekallikrein to kallikrein

Front 35

In the kinin system, kininogen is cleaved by ____ resulting in ____.

Back 35

kallikrein; bradykinin

Front 36

Bradykinin mediates ___, ___, and ___.

Back 36

vascular permeability, arteriolar dilation, and pain

Front 37

The cytokines IL-1 and TNF are secreted by ___ and have several effects on ___.

Back 37

monocytes-macrophages; inflammation

Front 38

IL-1 and TNF reduce ___ properties of the endothelium, thus promoting ___.

Back 38

thromboresistant; thrombosis

Front 39

IL-1 and TNF induce ___ responses.

Back 39

acute phase

Front 40

Arachidonic acid is metabolized in two pathways. What are they?

Back 40

cyclooxygenase and lipoxygenase pathways

Front 41

what stimulates the release of arachidonic acid from membrane phospholipids?

Back 41

phosopholipase- A2

Front 42

what catalyzes the cyclooxygenase pathway?

what inhibits this pathway?

Back 42

COX-1 and COX-2

asprin and anti-inflammatory drugs

Front 43

the cyclooxygenase pathway yields ___ and ___.

Back 43

thromboxane A2 (TxA2) and prostacyclin (PGI2) (prostaglandins)

Front 44

what does platelet thromboxane A2 (TxA2) do?

Back 44

powerful vasoconstrictor and platelet aggregant

Front 45

what does endothelial PGI2 do?

Back 45

vasodilator and inhibitor of platelet aggregation

Front 46

What does the lipoxygenase pathway yield?

Back 46

HPETE and its derivates

Front 47

5-HPETE gives rise to ____ and ____ which are both ____ for neutrophils.

Back 47

HETE and leukotrienes (LTB4); chemotactic factors

Front 48

Histamines are liberated by degranulation from ___, ___, and ___.

Back 48

basophils, mast cells, and platelets

Front 49

What does histamine mediate?

Back 49

increase in capillary permeability associated with the contraction of endothelial cells in post cap venules; PRODUCES ENDOTHELIAL GAPS

Front 50

List 4 stimuli for the release of histamine from basophils and mast cells.

Back 50

1) binding of antigen to membrane bound IgE
2) binding of C3a and C5a to receptors
3) physical stimuli (heat or cold)
4) cytokine IL-1

Front 51

how is histamine released from platelets

what triggers this?

Back 51

platelet aggregation and the release reaction

endothelial injury or platelet-activating factor (PAF)

Front 52

What is the role of PAF and what does it cause the release of?

Back 52

activates and aggregates platelets with the release of histamine and serotonin

Front 53

List the steps involved in oxygen-dependent killing via the myeloperoxidase-halide system.

Back 53

phagocytosis causes an oxidative burst supplying electrons to NADPH oxidase, producing the superoxide anion, which is converted to hydrogen peroxide, and further broken down to hydroxyl. In the presence of myeloperoxidase and chloride, hydrogen peroxide oxidizes bacteria disrupting their cell walls.

Front 54

What are the most important opsonins?

Back 54

IgG and C3b

Front 55

what is the role of opsonins?

Back 55

immobilize the particles on the surface of the phagocyte; coat the microbe, making it a target for phagocytosis

Front 56

tensile strength of a wound can be expected to reach ___% compared to the unwounded skin.

Back 56

70-80%

Front 57

how long does the wound take to reach its maximum tensile strength?

Back 57

3 months

Front 58

what is the normal hemoglobin measurement in males and females?

Back 58

15 and 13

Front 59

what is the normal red count for males and females?

Back 59

5 and 4.5

Front 60

what is the normal hematocrit amount for males and females?

Back 60

45 and 40

Front 61

In addition to activating the kinin system, what is significant about factor XIIa (Hageman)?

Back 61

it links the kinin, coagulation, plasminogen, and complement systems

Front 62

what is the role of leukotrienes?

What is another name for leukotrienes?

Back 62

vasoconstrictors and mediators of increased capillary permeability

slow-reacting substance of anaphylaxis

Front 63

During the adhesion part of emigration, ___ on leukocytes bind to ___ on endothelial cells.

Back 63

integrins; immunoglobulin-family adhesion proteins

Front 64

Which adhesion molecules mediate rolling of leukocytes?

Back 64

selectins- they loosely bind to leukocytes

Front 65

What mediates transmigration of leukocytes across the endothelium?

Back 65

platelet endothelial cell adhesion molecule-1 (PECAM-1)

Front 66

What is chemotaxis?

Back 66

the process by which leukocytes are attracted to and move toward an injury

Front 67

What are four chemotactic factors for neutrophils?

Back 67

1) products from bacteria
2) complement C5a
3) arachidonic acid metabolites: LTB4 and HETE
4) kallikrein

Front 68

Where are neutrophils released from during acute inflammation?
There is a larger proportion of which cells?

Back 68

bone marrow postmitotic reserve pool
band neutrophils (less mature)

Front 69

What are some causes of monocytosis?

Back 69

tuberculosis, brucellosis, typhus, and salmonella

Front 70

Along with monocytes-macrophages, what cell are present in large quantities in chronic inflammation?

Back 70

lymphocytes

Front 71

What are some causes of lymphocytosis?

Back 71

viral infections such as influenza, mumps, rubella, and infectious mononucleosis and bacterial infections such as wooping cough and tuberculosis

Front 72

What are the predominant cells in allergic reactions and parasitic infestations?

Back 72

eosinophils

Front 73

What are the most important causes of eosinophilia?

Back 73

allergies- asthma, hay fever, and hives, and parasitic infections

Front 74

What are some important causes of basophilia?

Back 74

chronic myelogenous leukemia and other myeloproliferative diseases

Front 75

What marks the conversion from acute to chronic inflammation?

Back 75

1. replacement of neutrophils and monocytes with plasma cells, macrophages, and lymphocytes.
2. proliferation of fibroblasts and angiogenesis, with resultant scarring and distortion of architecture.

Front 76

Deficiency of complement components leads to ___.

Back 76

increased susceptibility to infection

Front 77

In nonspecific inflammation, ___ are activated by macrophage-presented antigen with results in formation of ___.

Back 77

B lymphocytes; antibody-producing cells

Front 78

What are the 4 acute phase responses elicited by IL-1 and TNF?

Back 78

1) system effects of inflammation, including fever and leukocytosis
2) hepatic synthesis of acute phase proteins
3) synthesis of adhesion molecules
4) neutrophil degranulation

Front 79

leukotrienes LTC,D,E4 are responsible for what?

Back 79

vasoconstriction and increased capillary permeability