II - Acute and Chronic Inflammation

Question 1

It is a response of vascularized tissues to infection and damaged tissues that brings cells and molecules of host defense from the circulation to the sites where they are needed, in order to eliminate the offending agents.

Answer 1

Inflammation

Robbins Basic Pathology, 9th ed. p. 69

Question 2

The first step in a typical inflammatory reaction

Answer 2

Recognition of offending agent

Robbins Basic Pathology, 9th ed. p. 70

Question 3

The main components of inflammation

Answer 3

Vascular reaction and cellular response

Robbins Basic Pathology, 9th ed. p. 72

Question 4

The sequential steps in a typical inflammatory reaction

Answer 4

Recognition of offending agent, recruitment of leukocytes and plasma proteins, removal of agent, regulation of response, repair

Robbins Basic Pathology, 9th ed. p. 70

Question 5

Inflammation which is characterized by exudation of fluid and plasma protein and a predominantly neutrophilic leukocyte accumulation.

Answer 5

Acute inflammation

Robbins Basic Pathology, 9th ed. p. 71

Question 6

Inflammation typified by influx of lymphocytes and macrophages associated with vascular proliferation and deposition of connective tissue.

Answer 6

Chronic inflammation

Robbins Basic Pathology, 9th ed. p. 71

Question 7

Five cardinal signs of inflammation

Answer 7

Heat (calor)redness (rubor)swelling (tumor)pain (dolor)loss of function (functio laesa)

Robbins Basic Pathology, 9th ed. p. 71

Question 8

Initial vascular response to injury

Answer 8

Vasoconstriction

Robbins Basic Pathology, 8th ed. p.33

Question 9

Three major components of acute inflammation

Answer 9

Vasodilation, increased permeability, leukocyte emigration

Robbins Basic Pathology, 9th ed. p. 73

Question 10

An ultrafiltrate of blood which contains little protein, little or no cellular material and low specific gravity as a result of osmotic or hydrostatic imbalance across the vessel wall without increase in vascular permeability.

Answer 10

Transudate

Robbins Basic Pathology, 9th ed. p. 73

Question 11

An extravascular fluid with high protein content. Its presence implies an increased vascular permeability, triggered by tissue injury and ongoing inflammatory reaction.

Answer 11

Exudate

Robbins Basic Pathology, 9th ed. p. 73

Question 12

Denotes an excess fluid in the interstitial tissue or serous cavities

Answer 12

Edema

Robbins Basic Pathology, 9th ed. p. 73

Question 13

Effect of histamine on vascular smooth muscle

Answer 13

Vasodilation

Robbins Basic Pathology, 9th ed. p. 73

Question 14

The most common mechanism of increased vascular permeability.

Answer 14

Contraction of endothelial cells resulting in increased interendothelial spaces

Robbins Basic Pathology, 9th ed. p. 74

Question 15

Proliferation of lymphatic vessels and painful enlarged lymph nodes secondary to inflammation.

Answer 15

Reactive or inflammatory lymphadenitis

Robbins Basic Pathology, 9th ed. p. 74

Question 16

State the molecule in the endothelium responsible for this stage of vascular inflammatory response: Rolling

Answer 16

Selectins

Robbins Basic Pathology, 9th ed. p. 76

Question 17

State the molecule in the lymphocyte responsible for this stage of vascular inflammatory response:Firm adhesion

Answer 17

Integrins

Robbins Basic Pathology, 9th ed. p. 76

Question 18

State the molecule in the endothelium responsible for this stage of vascular inflammatory response:Transmigration

Answer 18

PECAM-1/CD 31

Robbins Basic Pathology, 9th ed. p. 77

Question 19

State the endothelial adhesion molecule responsible for this stage of vascular inflammatory response:Intercellular adhesion

Answer 19

ICAM -1

Robbins Basic Pathology, 9th ed. p. 76

Question 20

State the lymphocytic adhesion molecule counterpart of the following endothelial receptors:E-Selectin

Answer 20

Sialyl-Lewis X modified glycoprotein

Robbins Basic Pathology, 9th ed. p. 76

Question 21

State the lymphocytic adhesion molecule counterpart of the following endothelial receptors:P-Selectin

Answer 21

Sialyl-Lewis X modified glycoprotein

Robbins Basic Pathology, 9th ed. p. 76

Question 22

State the lymphocytic adhesion molecule counterpart of the following endothelial receptors:ICAM-1

Answer 22

Integrins

Robbins Basic Pathology, 9th ed. p. 76

Question 23

State the lymphocytic adhesion molecule counterpart of the following endothelial receptors:CD-31

Answer 23

CD-31

Robbins Basic Pathology, 9th ed. p. 76

Question 24

The process of leukocyte accumulation at the periphery of blood vessels

Answer 24

Margination

Robbins Basic Pathology, 9th ed. p. 75

Question 25

Arrange the following steps in the inflammatory response:A. Recruitment of leukocytesB. Regulation of responseC. Recognition of injurious agentD. Removal of agentE. Resolution

Answer 25

C, A, D, B, E Robbins Basic Pathology, 9th ed. p. 72

Question 26

``` Arrange the steps in leukocyte recruitment: A. Transmigration B. Rolling C. Margination D. Firm adhesion ```

Answer 26

C, B, D, A Robbins Basic Pathology, 9th ed. p. 75

Question 27

Process of coating microorganisms with proteins that facilitate phagocytosis.

Answer 27

Opsonization Robbins Basic Pathology, 9th ed. p. 75

Question 28

A lymphocyte with ingested microorganism fused with lysosome is called _______.

Answer 28

Phagolysosome Robbins Basic Pathology, 9th ed. p. 78

Question 29

The process of migration of the leukocytes through the endothelium.

Answer 29

Transmigration or diapedesis Robbins Basic Pathology, 9th ed. p. 76

Question 30

Process of leukocyte migration toward sites of infection or injury along a chemical gradient.

Answer 30

Chemotaxis Robbins Basic Pathology, 9th ed. p. 77

Question 31

The most important lysosomal enzyme involved in bacterial killing.

Answer 31

Elastase

Question 32

A peptide leukocyte granule constituent which kills microbes by creating holes in their membranes.

Answer 32

Defensins Robbins Basic Pathology, 8th ed. p.40

Question 33

Predominant form of leukocyte during the first 6 - 24 hours of inflammation?

Answer 33

Neutrophils Robbins Basic Pathology, 9th ed. p. 77

Question 34

Predominant form of leukocyte during 24-48 hrs after the onset of inflammation?

Answer 34

Monocytes Robbins Basic Pathology, 9th ed. p. 77

Question 35

Predominant cellular infiltrate in Pseudomonas infection.

Answer 35

Neutrophils Robbins Basic Pathology, 9th ed. p. 77

Question 36

Predominant cellular infiltrate in viral infections

Answer 36

Lymphocytes Robbins Basic Pathology, 9th ed. p. 77

Question 37

Predominant cellular infiltrate in allergic reactions

Answer 37

Eosinophils Robbins Basic Pathology, 9th ed. p. 77

Question 38

Sequential steps in phagocytosis

Answer 38

Recognition and attachment of particle to be ingested, engulfment and formation of phagocytic vacuole, killing or degradation of ingested material Robbins Basic Pathology, 9th ed. P.78

Question 39

First step in phagocytosis

Answer 39

Recognition and attachment of particle to be ingested Robbins Basic Pathology, 9th ed. P.78

Question 40

Substances responsible for leukocyte-induced tissue injury

Answer 40

Lysosomal enzymes, reactive oxygen and nitrogen species

Question 41

Defective synthesis of CD 18 B-subunit of leukocyte integrins LFA-1 and Mac-1 leading to impaired leukocyte adhesion and migration through endothelium.

Answer 41

Leukocyte adhesion deficiency type 1 Robbins Basic Pathology, 8th ed. p.41

Question 42

Caused by a defect in fucose metabolism resulting in absence of sialyl-lewis X, the oligosaccharide on leukocytes that binds to selectins on activated endothelium.

Answer 42

Leukocyte adhesion deficiency type 2 Robbins Basic Pathology, 8th ed. p.41

Question 43

Results from a defect in the protein involved in membrane docking and fusion.

Answer 43

Chediak-Higashi syndrome Robbins Basic Pathology, 8th ed. p.41

Question 44

NADPH deficiency or defect resulting in decreased oxidative burst.

Answer 44

Chronic Granulomatous Disease Robbins Basic Pathology, 8th ed. p.42

Question 45

Type of inflammatory mediators that are normally sequestered in intracellular granules and can be rapidly secreted by granule exocytosis or are synthesized de novo in response to a stimulus.

Answer 45

Cell-derived mediators Robbins Basic Pathology, 9th ed. p. 82

Question 46

Type of mediators that are produced mainly in the liver and are present in the circulation as inactive precursors that must be activated by proteolytic cleavages to acquire their biologic properties.

Answer 46

Plasma-derived mediators Robbins Basic Pathology, 9th ed. p. 83

Question 47

The richest sources of histamine

Answer 47

Mast cells Robbins Basic Pathology, 9th ed. p. 83

Question 48

Effects of histamine of arterioles and venules

Answer 48

Dilation of arterioles and increases permeability of venules Robbins Basic Pathology, 9th ed. p. 83

Question 49

Arachidonic acid metabolites/derivatives

Answer 49

Prostaglandin, prostacyclin, thromboxane, leukotrienes, lipoxin Robbins Basic Pathology, 9th ed. p. 84

Question 50

Arachidonic acid derivative that causes vasoconstriction and promotes platelet aggregration.

Answer 50

Thromboxane A2 (TXA2) Robbins Basic Pathology, 9th ed. p. 84

Question 51

Arachidonic acid metabolite implicated in increased vascular permeability and bronchospasm

Answer 51

LTC4, LTD4, and LTE4 Robbins Basic Pathology, 9th ed. p. 84

Question 52

Arachidonic acid metabolite that causes chemotaxis and leukocyte adhesion.

Answer 52

Leukotriene B4 (LTB4) and hydroxyeicosatetraenoic acid (HETE) Robbins Basic Pathology, 9th ed. p. 84

Question 53

Cytokines that induce systemic acute-phase response associated with infection or injury, and are implicated in sepsis.

Answer 53

TNF, IL-1 (and IL-6) Robbins Basic Pathology, 9th ed. p. 86

Question 54

The cytokines that are important mediators of acute-phase reaction causing fever.

Answer 54

TNF, IL-1 (and IL-6) Robbins Basic Pathology, 9th ed. p. 99

Question 55

3 Functions of complement proteins

Answer 55

Inflammation, opsonization and phagocytosis, and cell lysis Robbins Basic Pathology, 9th ed. p. 89

Question 56

Morphologic hallmarks of acute inflammation

Answer 56

Vasodilation and accumulation of leukocytes and fluid in the extravascular tissue Robbins Basic Pathology, 9th ed. p. 90

Question 57

Type of acute inflammation characterized by the outpouring of watery, relatively protein-poor fluid derived from the serum or endothelial lining of peritoneal, pleural, and pericardial cavities.

Answer 57

Serous inflammation Robbins Basic Pathology, 9th ed. p. 90

Question 58

Fluid in a serous cavity is called ______.

Answer 58

Effusion Robbins Basic Pathology, 9th ed. p. 90

Question 59

This type of inflmmation results from greater vascular permeability that allows larger molecules to pass the endothelial barrier.

Answer 59

Fibrinous inflammation Robbins Basic Pathology, 9th ed. p. 90

Question 60

Histologically, appears as an eosinophilic meshwork of threads or sometimes an amorphous coagulum.

Answer 60

Fibrinous inflammation Robbins Basic Pathology, 9th ed. p. 90

Question 61

This type of inflammation is manifested by the presence of large amounts of purulent exudate consisting of neutrophils, necrotic cells, and edema fluid.

Answer 61

Suppurative (purulent) inflammation Robbins Basic Pathology, 9th ed. p. 90

Question 62

Focal collections of pus that may be caused by seeding pyogenic organisms into a tissue or by secondary infections of necrotic foci.

Answer 62

Abscess Robbins Basic Pathology, 9th ed. p. 90

Question 63

It is an excavation of the surface of an organ or tissue that is produced by necrosis of cells and sloughing of inflammatory necrotic tissue.

Answer 63

Ulcer Robbins Basic Pathology, 9th ed. p. 91

Question 64

Vasoactive amines that are preformed molecules in secretory granules of mast cells, basophils and platelets.

Answer 64

Serotonin, Histamine Robbins Basic Pathology, 9th ed. p. 83

Question 65

Complement fragments which are anaphylotoxins.

Answer 65

C3a, C5a (A for anaphylotoxin) Robbins Basic Pathology, 9th ed. p. 89

Question 66

Complement fragment which aids in opsonization.

Answer 66

C3b (b for binding) Robbins Basic Pathology, 9th ed. p. 89

Question 67

Membrane attack complex

Answer 67

C5b, C6-9 Robbins Basic Pathology, 9th ed. p. 89

Question 68

Deficiency of the terminal components of complement predisposes to what infection.

Answer 68

Neisseria infections Robbins Basic Pathology, 9th ed. p. 89

Question 69

It is the cytolytic endproduct of the complement cascade, which forms a transmembrane channel causing osmotic lysis of target cells.

Answer 69

Membrane attack complex (C5b,C6-9) Robbins Basic Pathology, 9th ed. p. 89

Question 70

Platelet-activating factor (PAF) is a phospholipid-derived mediator that is now known to have multiple inflammatory effects. What are these?

Answer 70

Platelet aggregration, vasoconstriction (vasodilation in low concentration), bronchoconstriction, and increased venular permeability. Robbins Basic Pathology, 9th ed. p. 89

Question 71

Enzyme blocked by NSAIDS.

Answer 71

Cyclooxygenase 1 and 2 Robbins Basic Pathology, 9th ed. p. 85

Question 72

Enzyme inhibited by glucocorticoids

Answer 72

Phospholipase A2 Robbins Basic Pathology, 9th ed. p. 85

Question 73

Polypeptide products of many cell types that function as mediators of inflammation and immune response.

Answer 73

Cytokines Robbins Basic Pathology, 9th ed. p. 86

Question 74

They are a family of small structurally related proteins that act primarily as chemoattractants for different subsets of leukocytes.

Answer 74

Chemokines Robbins Basic Pathology, 9th ed. p. 87

Question 75

Major cytokines in acute inflmmation.

Answer 75

TNF and IL-1 Robbins Basic Pathology, 9th ed. p. 86

Question 76

A short-lived, soluble, free-radical gas produced by endothelial cells causing smooth muscle relaxation and vasodilation.

Answer 76

Nitric oxide Robbins Basic Pathology, 9th ed. p. 80

Question 77

This component of the coagulation cascade initiates four systems involved in the inflammatory response, namely the kinin, clotting, fibrinolytic and complement systems.

Answer 77

Activated Hageman Factor / Factor XIIa Robbins Basic Pathology, 8th ed. p.52

Question 78

Inflammation characterized by infiltration with mononuclear cells, tissue destruction and repair involving angiogenesis and fibrosis.

Answer 78

Chronic Inflammation Robbins Basic Pathology, 9th ed. p. 93-94

Question 79

Macrophages in the liver

Answer 79

Kupffer cells Robbins Basic Pathology, 9th ed. p. 94

Question 80

Macrophages in the spleen and lymph nodes

Answer 80

Sinus histiocytes Robbins Basic Pathology, 9th ed. p. 94

Question 81

Macrophages in the CNS

Answer 81

Microglial cells Robbins Basic Pathology, 9th ed. p. 94

Question 82

Pathway of macrophage activation induced by microbial products such as endotoxin, cytokines, or foreign substance to produce substance for host defense and inflammatory reactions

Answer 82

Classical pathway Robbins Basic Pathology, 9th ed. p. 94

Question 83

Pathway of macrophage activation induced by cytokines produced by T lymphocytes and other cells with the principal function of tissue repair.

Answer 83

Alternative pathway Robbins Basic Pathology, 9th ed. p. 95

Question 84

Macrophages in the lungs

Answer 84

Alveolar Macrophages Robbins Basic Pathology, 9th ed. p. 94

Question 85

A focus of epitheloid cells, rimmed by fibroblasts, lymphocytes, histiocytes, occasional giant cells.

Answer 85

Noncaseating tubercle, Tuberculosis Robbins Basic Pathology, 8th ed. p.56

Question 86

Central amorphous granular debris, loss of all cellular detail, acid-fast bacilli

Answer 86

Caseating tuberculosis Robbins Basic Pathology, 8th ed. p.56

Question 87

Acid-fast bacilli in macrophages, noncaseating granulomas

Answer 87

Leprosy Robbins Basic Pathology, 8th ed. p.56

Question 88

Microscopic to visible lesion, enclosing wall of histiocytes, plasma cell infiltrates, necrotic central cells without loss of cellular outline

Answer 88

Gumma (Syphilis) Robbins Basic Pathology, 8th ed. p.56

Question 89

Rounded or stellate granuloma containing central granular debris and recognizable neutrophils, giant cells uncommon.

Answer 89

Cat-scratch Disease Robbins Basic Pathology, 8th ed. p.56

Question 90

Noncaseating granulomas with abundant activated macrophages

Answer 90

Sarcoidosis Robbins Basic Pathology, 8th ed. p.56

Question 91

Occasional noncaseating granulomas in intestinal walls, with dense chronic inflammatory infiltrate

Answer 91

Crohn's disease Robbins Basic Pathology, 8th ed. p.56

Question 92

Cells with pink, granular cytoplasm with indistinct boundaries.

Answer 92

Epitheloid cells Robbins Basic Pathology, 9th ed. p. 98

Question 93

40-50 um in size, consisting of a large mass of cytoplasm and many nuclei.

Answer 93

Giant cells Robbins Basic Pathology, 9th ed. p. 98

Question 94

Necrotic material which appears amorphous, structureless, granular debris, with complete loss of cellular details.

Answer 94

Caseous necrosis Robbins Basic Pathology, 9th ed. p. 98

Question 95

Cytokines which stimulate prostaglandins in the hypothalamus, producing fever.

Answer 95

TNF, IL-1 Robbins Basic Pathology, 8th ed. p.57

Question 96

A form of chronic inflammation characterized by collections of activated macrophages, often with T lymphocytes.

Answer 96

Granulomatous inflammation Robbins Basic Pathology, 9th ed. p. 98

Question 97

Diseases with granulomatous inflammation

Answer 97

TB, Leprosy, syphilis, cat-scratch disease, sarcoidosis, Crohn's disease, systemic mycoses Robbins Basic Pathology, 9th ed. p. 98

Question 98

True or false. Schistosomiasis may cause granulomatous inflammation

Answer 98

True

Question 99

True or false. Histoplasmosis may cause granulomatous inflammation

Answer 99

True

Question 100

A 5 y/o child touches a lit candle and develops a small blister on his right hand. The blister is an example of what type of inflammation?

Answer 100

Serous inflammation

Question 101

The hallmark of chronic inflammation

Answer 101

Tissue destruction

Question 102

A 20 y/o male was admitted due to RLQ pain of 18 hours duration. Appendectomy and revealed an edematous and erythematous appendix. An infiltrate of what cells would be most likely seen?

Answer 102

Neutrophils

Question 103

Heat and redness in acute inflammation is due to what pathogenetic mechanism?

Answer 103

Increased blood flow Robbins Basic Pathology, 9th ed., p. 74

Question 104

An 18 year old college student accidentally scalds his hand while ironing, where a large unruptured blister forms. What is seen in the blister? (A) protein poor fluid (B) eosinophilic meshwork of amorphous coagulum (C) large necrotic center surrounded by neutrophils (D) epithelioid macrophages and giant cells

Answer 104

protein poor fluid (Morphologic patterns of acute inflammation) Robbins Basic Pathology, 8th ed. Pp 43-44

Question 105

A 64 year old stroke patient at the ICU with a chest radiograph showing a cavitary lesion in the right lower lung lobe with fluid levels. What is seen in that lobe? (A) protein poor fluid (B) eosinophilic meshwork of amorphous coagulum (C) extensive necrosis and neutrophilic infiltrates (D) epithelioid macrophages and giant cells

Answer 105

large necrotic center surrounded by neutrophils (Morphologic patterns of acute inflammation) Robbins Basic Pathology, 8th ed. Pp 43-44

Question 106

A rheumatologist auscultates a friction rub in a 33 year old admitted lupus patient. What is seen in her pericardial cavity? (A) protein poor fluid (B) eosinophilic meshwork of amorphous coagulum (C) large necrotic center surrounded by neutrophils (D) epithelioid macrophages and giant cells

Answer 106

eosinophilic meshwork of amorphous coagulum (Morphologic patterns of acute inflammation) Robbins Basic Pathology, 8th ed. Pp 43-44

Question 107

A 33 year old female who underwent partial thyroidectomy for a colloid nodule 5 years ago underwent a completion thyroidectomy for persistent enlargement. On her present thyroid specimen, the original excision site shows a sutured area. Microscopic examination of that area will show (A) epithelioid cells with occasional giant cellssurrounding a necrotic center (B) neutrophils surrounding a necrotic center (C) protein poor fluid (D) giant cells surrounding refractile bodies

Answer 107

giant cells surrounding refractile bodies (Granulomatous Inflammation) Robbins Basic Pathology, 8th ed. P 56

Question 108

What is expected in the involved intestine of a patient with Chron disease? (A) eosinophilic network of amorphous coagulum (B) foci of neutrophils with necrotic debris (C) occasional noncaseating granulomas with dense chronic inflammatory infiltrate (D) pockets of protein poor fluid

Answer 108

occasional noncaseating granulomas with dense chronic inflammatory infiltrate (Granulomatous Inflammation) Robbins Basic Pathology, 8th ed. p.56