Bryan - General Pathology - Chronic And Acute Inflammation - Spring 2010

Front 1

T or F:
Inflammation occurs only in a living host.

Back 1

True!

Front 2

The release of fluid and/or cells as part of an inflammatory process is called...

Back 2

exudation

Front 3

T or F:
Infection and inflammation are synonymous.

Back 3

False!

Front 4

Which of the following statements are false?
Inflammation is protective.
Inflammation can be the mechanism of injury.
Inflammation can exacerbate a disease.
Acute inflammation is an exudative process.
All are true.

Back 4

All are true!

Front 5

What cell type (leukocyte species) is typical of acute inflammation?

Back 5

Neutrophils

Front 6

What cell type (leukocyte) is typical of chronic inflammation?

Back 6

Macrophages

Front 7

Acute and chronic inflammation are also known as ___________ and ___________ inflammation.

Back 7

Exudative
Proliferative

Front 8

What are the cardinal signs of inflammation?

Back 8

Heat (calor)
Redness (rubor)
Swelling (tumor)
Pain (dolor)
Loss of function

Front 9

What is the "hallmark" of acute inflammation?

Back 9

Exudate!

Front 10

If hyperemia is a component of acute inflammation, why does vascular flow slow in an inflamed area?

Back 10

Vascular leakage of water (edema) leads to more viscous plasma

Front 11

What are some mechanisms for vascular leakage?

Back 11

Endothelial contraction
Cytoskeletal reorganization
Direct injury
Neutrophil-dependent injury
Increased transcytosis

Front 12

What are two main sources of bradykinin in the injury/inflammatory response?

Back 12

Endothelial cells
Leukocytes

Front 13

What are some of the major mediators of vascular inflammatory events?

Back 13

Histamine
Complement
Proteases
Arachidonic acid metabolites (prostacyclins)
Kinins
Serotonin

Front 14

T or F:
An inflammatory exudate is rich in proteins.

Back 14

True!

Front 15

T or F:
An inflammatory exudate always includes fluid and cells.

Back 15

False! Always fluid but not always cells.

Front 16

What are some factors directing the nature of an inflammatory exudate?

Back 16

Type of injury
Intensity of injury
duration of injury
duration of inflammatory response

Front 17

What are the main categories of exudate in acute inflammation?

Back 17

Serous
Fibrinous
Mucus (not a true exudate)
Neutrophilic
Combinations of the above

Front 18

What are the components of a serous exudate?

Back 18

Albumin rich
IgGs
Plasma proteins
ACELLULAR

Front 19

What is the exudate indicative of mild, acute injuries?

Back 19

Serous exudate

Front 20

What are the two fates of a serous exudate?

Back 20

1) Reabsorption
2) Progression to fibrinous exudate

Front 21

What are some of the benefits to a fibrinous exudate?

Back 21

Prevents spread by blocking lymph drainage
Provides framework for healing and phagocytosis
Fibrin split products are chemotactic

Front 22

What type of material comprises intestinal "casts"?

Back 22

Fibrinonecrotic material (fibrin)

Front 23

What is the histological appearance of fibrinous exudate?

Back 23

eosinophilic meshwork ("cobwebs")

Front 24

What are the two possible resolutions for a fibrinous exudate?

Back 24

1) Fibrinolysis (with plasmin)
2) Organization resulting in fibrosis

Front 25

Which of the following is not a true exudate?
Serous
Fibrinous
Mucous
Neutrophilic
All of the above are true exudates

Back 25

Mucous exudate is NOT a true exudate

Front 26

What is the mechanism for the formation of a mucous "exudate"?

Back 26

Injury leading to goblet cell hyperplasia

Front 27

T or F:
A mucous "exudate" is restricted to mucous membranes.

Back 27

True!

Front 28

Mucous exudate + neutrophils =

Back 28

Mucopurulent exudate or Catarrhal

Front 29

What are two terms synonymous with a neutrophilic exudate?

Back 29

Suppurative or purulent

Front 30

What type of bacteria is characterized by forming a neutrophilic exudate?

Back 30

Pyogenic bacteria

Front 31

What three components make up pus?

Back 31

Fluid + fibrin + neutrophils

Front 32

A walled-off neutrophilic exudate is known as a/an _____________.

Back 32

Abscess

Front 33

What is pus in a body cavity called?

Back 33

Empyema

Front 34

Widely dispersed pus between tissue planes is called __________.

Back 34

Cellulitis

Front 35

What is the histological appearance of a neutrophilic exudate?

Back 35

Neutrophil neutrophil neutrophil neutrophil neutrophil neutrophil neutrophil neutrophil....yeah...lots of neutrophils

Front 36

What are some problems associated with a neutrophilic exudate?

Back 36

Neutrophil-induced tissue destruction (tissue lysis)
Fibrosis

Front 37

What is the main enzyme released by neutrophils causing tissue destruction?

Back 37

Elastase

Front 38

A neutrophilic exudate with lots of fibrin is called...

Back 38

Fibrinopurulent

Front 39

An exudate including blood and fibrin is called...

Back 39

fibrinohemorrhagic

Front 40

A "shaggy" in appearance proliferative event of the mesothilium is called...

Back 40

fibrinoproliferative

Front 41

Which component of the acute inflammatory response dilutes and isolates the irritant?

Back 41

Exudate

Front 42

What is the first inflammatory cell to arrive at an injury site?

Back 42

Neutrophil

Front 43

Is the neutrophil half life in the blood short or long?

Back 43

short

Front 44

T or F:
Staph infections induce neutrophilia.

Back 44

True!

Front 45

T or F:
Neutrophils are released from the marrow upon demand.

Back 45

False!
They are released continuously but their release increases with demand

Front 46

The collateral neutrophilic damage incurred by the host is called the ____________ effect.

Back 46

bystander

Front 47

What are two major mechanisms of neutrophilic killing?

Back 47

Respiratory burst (via ROIs)
Phagocytosis

Front 48

Is the eosinophil half life in the blood short or long?

Back 48

short

Front 49

What are the major components of the eosinophil granules and what do they do?

Back 49

Basic protein - neutralize heparin; induce histimine release; kill parasites
Cationic protein - kill parasites
Arylsulfatase B - inactivate leukotrienes

Front 50

What are chemotactic factors that attract eosinophils?

Back 50

ECF-A
SRS-A
C5a
Ag-Ab complexes

Front 51

What chemotactic factor released by mast cells stimulates eosinophils?

Back 51

ECF-1 (eosinophilic chemotactic factor-anaphylaxis)

Front 52

What cell is similar to a mast cell?

Back 52

basophil

Front 53

Is the half-life for macrophages short or long?

Back 53

long

Front 54

Where can macrophage cells be generated?

Back 54

Bone marrow
Liver (kupffer cells)

Front 55

What type of macrophage is typical of tuberculosis?

Back 55

Multinucleate giant cells

Front 56

Which of the following is not a function of macrophages?

Antigen presentation
Control of intracellular parasites
Orchestrate healing response
Kill tumor cells
Hypersensitivity reaction
Stimulate angiogenesis

Back 56

Hypersensitivity reaction - LYMPHOCYTE involved!

Front 57

T or F:
Macrophages can only operate in an aerobic environment.

Back 57

False!
They have anaeorbic metabolism too!

Front 58

An example of inflammation involving only plasma cells is called plasma cell ___________.

Back 58

Stomatitis

Front 59

With respect to neutrophil emigration from the circulation, ________ cause the neutrophil to roll, ___________ cause the neutrophil to bind, and ________________ cause the neutrophils to trans-mitgrate.

Back 59

Selectins
Integrins
Intercellular Adhesion Molecules

Front 60

From among lymphocytes, neutrophils, and macrophages, which is the most responsive to chemotaxis? Which is second?

Back 60

#1 neutrophils
#2 macrophages

Front 61

What is an artificial chemotaxin that has positive response in humans but not in bovids?

Back 61

f-met-leu-phe

Front 62

What components of the neutrophilic response allows for target differentiation from host?

Back 62

C3b receptors and Fc opsonins

Front 63

T or F:
Most hydrophobic surfaces (fibrin fragments and necrotic tissue) do not require opsonization before phagocytosis.

Back 63

True!

Front 64

T or F:
All bacteria (intracellular and extracellular) are opsonized before phagocytosis.

Back 64

False!
Intracellular bacteria are not opsonized.

Front 65

What are two examples of bacteria discussed in class that prevent leukocyte degranulation?

Back 65

Mycobacteria
Histophilus (formerly hemophilus)

Front 66

What are some examples of oxygen-independent leukocytic killing?

Back 66

Glycolysis (decreased pH)
Granule activity (enzymes)

Front 67

What are some examples of oxygen-dependent leukocytic killing?

Back 67

Respiratory burst producing ROIs

Front 68

T or F:
Macrophages and neutrophils produce ROIs by different means.

Back 68

True. Macrophages lack myeloperoxidase.

Front 69

T or F:
Respiratory burst activity of neutrophils produces the greatest bystander effect.

Back 69

False. The hypochlorus acid produced has little bystander damage.

Front 70

Shipping fever is more correctly known as __________________ pneumonia.

Back 70

Mannheimia

Front 71

T or F:
The organism implicated in shipping fever is normal lung flora causing an inappropriate phagocyte response.

Back 71

False. Mannheimia hemolitica is a normal NASAL flora that, if it gets into the lungs, causes tuberculosis in a phagocyte-mediated process.

Front 72

What are some diseases and/or conditions discussed in class where recurrent bacterial infections are a symptom?

Back 72

Chronic granulomatous disease
Leukocyte adhesion deficiency
Hyper IgE syndrome
Cyclic hematopoiesis
Burn patients
End stage renal dz/uremia
Chediak-Higashi Syndrome

Front 73

Why do burn patients have recurrent bacterial infections?

Back 73

Abnormal chemotaxis of neutrophils
Decreased secondary granules
Chemotaxis inhibition factors released

Front 74

Why do patients with hyper IgE syndrome have recurrent bacterial infections?

Back 74

Chemotaxis inhibition factors released
Decreased IFN gamma production by T cells causes reduced neutrophil activation

Front 75

What symptoms characterize Chediak-Higashi Syndrome?

Back 75

Partial albinism
Giant neutrophil granules
Decreased neutrophils, decreased chemotaxis, decreased phagocytosis, and decreased fusion
RECURRENT BACTERIAL INFECTIONS

Front 76

What are the three main interrelated systems involved in acute inflammation that result in vascular permeability changes and leukocyte stimulation? What factor is common to all three?

Back 76

Kinins
Complement
Coagulation/fibrinolysis
Factor XII is the common factor

Front 77

What four things does activated factor XII stimulate?

Back 77

Clotting/coagulation
Fibrinolysis (plasmin)
Kinins
Complement

Front 78

The precursor ______________ is acted on by factor XIIa to form ___________, which is converted by ____________ into Bradykinin.

Back 78

The precursor PREKALLIKREIN is acted on by factor XIIa to form KALLIKREIN, which is converted by HMWK into Bradykinin.
HMWK = high molecular wt. kininogen

Front 79

What are downstream effects of bradykinin?

Back 79

Increase vascular permeability
Vasodilation
Smooth muscle contraction
PAIN!!
arachodonic acid metabolism
mast cell degranulation

Front 80

Bradykinin is rapidly inactivated by what enzymes?

Back 80

Plasma kinase
C1 esterase (in the lungs)

Front 81

What are the three major pathways to complement activation?

Back 81

Lectin
Classical
Alternative

Front 82

What is the major activator of the classical complement pathway?

Back 82

Antigen/Antibody complex (IgG or IgM) recognized by C1

Front 83

T or F:
In the alternative complement pathway, C3 is cleaved into C3a and C3b by specific antigens independent of antibodies.

Back 83

True!

Front 84

Which complement fragements functionas anaphylatoxins? Which is the strongest/weakest?

Back 84

C5a>C3a>>C4a

Front 85

Which complement fragment is similar to bradykinin?

Back 85

C2 kinin

Front 86

Which complement fragment activates arachidonic acid metabolism and is involved in chemotaxis?

Back 86

C5a

Front 87

Which complement fragment opsonizes fungi?

Back 87

C3e

Front 88

Which complement promotes blood coagulation?

Back 88

C6

Front 89

What is the body's protective mechanism against elastase activity?

Back 89

Alpha-1 protease inhibitor (alpha-1 antitrypsin)

Front 90

What are two disease states discussed where the loss of alpha 1 protease inhibitor is an issue?

Back 90

COPD
Emphysema

Front 91

What inhibits the production of arachidonic acid from membrane phospholipids?

Back 91

Corticosteroids

Front 92

What inhibits the production of cyclooxygenases (Prostaglandins) from arachidonic acid?

Back 92

NSAIDs

Front 93

What inhibits the production of leukotrienes and lipoxygenases from arachidonic acid?

Back 93

LPX inhibitors

Front 94

What are the main products of arachidonic acid metabolism?

Back 94

Prostaglandins
Leukotrienes

Front 95

What are some functions of prostaglandins?

Back 95

Vasoactive
reduce inflammatory responses
pyrogen

Front 96

What are some functions of leukotrienes?

Back 96

chemotaxis
endothelial cell activation
vasoconstriction
increased vascular permeability

Front 97

T or F:
Some leukocyte products can increase vascular permeability and act as chemotaxins?

Back 97

True

Front 98

Name a ton of chemical mediators for acute inflammation.

Back 98

Amines
Kinins
Complement
Proteinases
Arachidonic acid metabolites
Lysosomal components
ROIs
PAF, IL-1, TNF

Front 99

What is the main factor causing the switch from acute to chronic inflammation?

Back 99

Persistent stimulus and macrophages

Front 100

T or F:
Foci of chronic inflammation are grossly indistinguishable from tumors.

Back 100

True (sometimes)

Front 101

T or F:
Neutrophils are necessary for fibroblast function in repair.

Back 101

False!
This describes MACROPHAGES

Front 102

T or F:
One hallmark of granulomatous inflammation is the presence of granulation tissue.

Back 102

FALSE DUMBbo!
Granulomatous inflammation has nothing to do with granulation tissue!

Front 103

What cells characterize granulamatous inflammation (there are like 6 types at least)?

Back 103

Macrophages
Lymphocytes
Plasma cells
Connective tissue
Epithelioid cells
Multinucleate cells

Front 104

What is generally found in the core of a granuloma?

Back 104

Antigen
Macrophages
Neutrophils

Front 105

What surrounds the core of a granuloma?

Back 105

Lymphocytes
Plasma cells

Front 106

What creates the capsule of a granuloma?

Back 106

Fibroblasts
Vessels

Front 107

Chronic inflammation of the mucosal folds of a ruminant intestine is a characteristic of which disease?

Back 107

Yoni's Disease

Front 108

Which is drier? Chronic or acute inflammation?

Back 108

Chronic (no exudate)

Front 109

How do macrophages commonly present histologically in chronic inflammation?

Back 109

Pale cells in background
Sometimes multinucleate giant cells
Sometimes foamy macrophages

Front 110

Regions of acute inflammation embedded within chronic inflammation characterizes which type of inflammation?

Back 110

Pyogranulomatous inflammation

Front 111

What pyrexia inducing substances do macrophages release in response to multiple stimuli (and makes you feel bad)?

Back 111

IL-1
TNF
Prostaglandins

Front 112

What are the benefits of pyrexia?

Back 112

increased phagocytosis
increased metabolism
decreased viral and bacterial replication

Front 113

Match the following to the inflammation manifestation:

Hyperemia Pain
Exudation Redness
Kinins Swelling
Pressure Heat

Back 113

Hyperemia Heat, Redness
Exudation Swelling
Kinins Pain
Pressure Pain

Front 114

What factors mediate the acute phase response?

Back 114

TNF
IL-1

Front 115

T or F:
Acute phase response occurs in systemic and local injury.

Back 115

True

Front 116

What is the liver's role in the acute phase response?

Back 116

Upregulate synthesis of:
proteases, complement and fibrinogen (2-3x)
SAA, CRP, alpha macroglobulin (100-1000x)

Front 117

What is a marker used to measure inflammation?

Back 117

CRP