Module 4 Flashcards

(75 cards)

1
Q

The vascular and cellular responses of living tissue to an injury

A

Inflammation

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2
Q

Inflammation is derived from the words?

A

Derived from “to inflame” or “to set fire to”

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3
Q

Inflammation is described as-

A

• The vascular and cellular responses of living tissue to an injury

• A protective response that serves to destroy, dilute or wall of the injurious agent and injured tissue

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4
Q

A protective mechanism because protective factors such as Ab, complement and phagocytic cells from the blood stream are able to go to the site of the injured tissue in order to destroy the invader

• The reaction is similar regardless of the inciting agent, though it may vary depending on the severity and persistence of the irritant as well as some host factors (e.g. location and type of tissue)

A

Inflammation

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5
Q

Outcome of inflammation according to main description

A

•The outcome of inflammation is also variable, if the response is successful, healing may occur, if not, further tissue reaction which may harm the host can occur

• In order to understand many disease processes and surgical processes, one has to fully understand inflammation and its role in tissue repair and regeneration

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6
Q

Cardinal signs of Inflammation:

A

Rubor (redness)

Tumor (swelling)

Dolor (pain)

Calor (heat)

Loss of function

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7
Q

Purposes of the Inflammation:

A

a. To minimize the effect of the irritant or injury

b. To repair the damaged tissue and restore the tissue to normal

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8
Q

Causes of Inflammation:

A

Pathogenic agents e.g. bacteria, viruses, fungi, protozoa, etc.

Chemical agents or poisons

Physical agents e.g. heat, cold, trauma, irradiation

Immunologic reactions/injury

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9
Q

Summary of events in Acute Inflammation

A

1. Transient or momentary vasoconstriction of arteriole (occurs only for a few seconds to about 5 minutes)

a. Followed by increase blood flow to terminal vascular bed due to dilation of all the blood vessels in the injured area

b. Accompanied by opening of new capillary beds and venules

2. Increase permeability of the terminal vascular bed accompanied by the exudation or outflow of plasma factors into tissues = tissue swelling, retardation of blood flow and hemoconcentration in the vascular bed

3. Margination – when *(leukocytes attach to the wall of blood vessels with migration of leukocytes** and exudation of erythrocytes into the tissues

; the process that attracts cells into the tissues is known as chemotaxis

4. Phagocytosis or removal of injurious agents by leukocytes,
breakdown of necrotic tissues by phagocytes and drainage or reabsorption thru lymph vessels or into the venules

5. Repair and regeneration

a. Regeneration – when dead cells are replaced by similar cells thru mitosis of viable

b. Repair – when fibrous connective tissue replaces damaged tissue if regeneration cannot occur

c. Both a and b can occur in a tissue

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10
Q

when leukocytes attach to the wall of blood vessels with migration of leukocytes and exudation of erythrocytes into the tissues;

A

Margination

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11
Q

when dead cells are replaced by similar cells thru mitosis of viable

A

Regeneration

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12
Q

when fibrous connective tissue replaces damaged tissue if regeneration cannot occur

A

Repair

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13
Q

The Inflammatory process in inflammation

A
  1. Vascular response
  2. Cellular response
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14
Q

increase blood flow or hyperemia in arterioles and capillaries; increase in venous blood causing passive congestion and contributes to vasodilation

A

Dilation of small vessels
(Vascular response)

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15
Q

B. Increase permeability of small vessels probably as a result of direct damage to endothelial cells or due to loosening of their attachments to other cells

• Increase permeability and increase hydrostatic pressure due to increase blood flow = exudation of fluid and plasma factors into the tissue spaces leading to swelling of the inflamed area

A
  1. Vascular response of Inflammatory process
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16
Q

2 Phases of Vascular Permeability:

A

a. An immediate transient phase that lasts than 1 hour followed by a prolonged phase that lasts for 3-4 hours or may be longer if the stimulus persists;

b. A third phase which is delayed in onset but lasts for several days have also been observed

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17
Q

Early stages of inflammation are characterized by margination which is the adherence of platelets and leukocytes to the endothelium

A

Cellular response

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18
Q

Many cells are observed to line the endothelium by a process known as

A

pavementing

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19
Q
  1. Cellular response
    The slowing down of blood flow and sludging of RBCs id due to:
A

a. **Hemoconcentration that results from fluid loss*((or when fluid goes into the extravascular space)

b. Increase resistance to flow = increase adherence of cells to each other and to the endothelium

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20
Q

The cellular response is characterized by migration of the following cells to the injured site =

A

a. Tissue macrophage – considered as the 1st inflammation line of defense during

• During the onset of inflammation, the macrophages present in injured tissues becomes phagocytic • They are activated by inflammatory products so that they enlarge rapidly

• The attached macrophages become mobile and active during the 1st hour of the inflammatory process

• Principal phagocytic cells responsible for completing the destruction of the irritant and clearing the necrotic and degenerating tissues in the site of inflammation

b. Neutrophils – 2nd line of defense; migrates form the blood to the tissues and capable of phagocytosis

• Leukocytes are able to migrate from blood vessels to tissues by pseudopods in the intercellular junctions of endothelial cells thus enlarging the opening to enable them to squeeze thru via diapedesis

• This will also allow RBC to pass via passive extravasation• Leukocytes are attracted to the injured tissue via chemotaxis

• There is leakage of blood from the damaged vessel wall to extravascular tissue = clot formation called hematoma or hematocyst

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21
Q

The process of ingestion or engulfing of particulate matter by the cell.

A

Phagocytosis

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22
Q

Formed when the cell membrane invaginates to enclose a particle.

A

Phagosome

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23
Q

Considered the most important defense system of the body.

A

Phagocytosis

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24
Q

Substances that enhance phagocytosis, they are mainly antibodies and complement components like C3b.

A

Opsonins

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25
The fragment of complement most important as an opsonin.
C3b fragment
26
The type of acids (besides antibodies and complement) that can act as opsonins.
Polypeptides and Basic poly amino acids
27
The **combined structure** formed when a **phagosome fuses with a lysosome.**
Phagolysosome
28
The remnant structure that contains undigested material.
Residual body
29
The oxygen-consuming pathway activated when neutrophils contact a foreign agent.
Respiratory burst
30
The term used to describe the 2–3× increase in oxygen consumption, hydrogen production, shunt activity, and superoxide generation.
Respiratory burst
31
Enumerate the factors that favor phagocytosis.
Opsonins Increased body temperature Entrapment of antigen in inflammatory exudates
32
Enumerate the events of respiratory burst.
a. 2–3× increase in oxygen consumption b. Production of hydrogen c. Increased activity of **hexose monophosphate shunt** d. Generation of **superoxide anion (O₂⁻)**
33
Enumerate the oxygen-dependent killing mechanisms.
a. Bactericidal effect of H₂O₂ (alone or with myeloperoxidase) b. Hydroxyl radical action c. Superoxide anion action d. Single oxygen
34
Oxygen-independent bactericidal agents:
Lysozyme – dissolves bacterial cell membranes Lactoferrin binds Fe and other metals needed by bacteria Phospholipase Granule-associated cationic proteins
35
Effects of lysosomal enzymes:
Produce chemotactic effect Influence clotting mechanism Act as pyrogens (fever-inducing agents)
36
Explain how opsonins increase the efficiency of phagocytosis.
Opsonins coat antigens, making them more recognizable and “grabbable” by phagocytes, thus enhancing engulfment efficiency.
37
What do lysosomal enzymes break down, and what type of molecule resists digestion?
Lysosomal enzymes break down carbohydrates and proteins, but not fats. Fats remain undigested and form the residual body
38
Why are agents resistant to digestion dangerous for the host?
Resistant agents persist inside phagocytes, protected from other defense mechanisms and drugs, prolonging infection.
39
What role do migrating phagocytes play in spreading infection
Migrating phagocytes can carry undigested pathogens into the lymphatics, spreading infection.
40
How can lysosomal enzymes contribute to fever?
Lysosomal enzymes act as pyrogens, inducing fever by influencing the hypothalamic temperature-regulating center.
41
Substances responsible for changes in blood flow, vascular permeability, and the cellular response at the site of injury
Chemical mediators of inflammation
42
Other name for chemical mediators of inflammation
Autacoids
43
Source of exogenous mediators
Outside sources (e.g. bacterial products and toxins)
44
Plasma derived mediators
Plasma-derived endogenous mediators that include **coagulation-fibrinolytic, kinin, and complement system**
45
Cell/tissue-derived mediators (preformed)
Preformed mediators stored in granules such as **histamine and cationic proteins**
46
Cell/tissue-derived mediators (newly synthesized)
interleukin, leukotrienes, and platelet-activating factor
47
Peptide mediators are produced by = Sequential activation of molecules by limited proteolysis
complement, coagulation-fibrinolytic system
48
Lipid mediators are derived from
Arachidonic acid after phospholipase action on membrane phospholipids
49
Collective name for lipid mediators
Eicosanoids
50
Most biologically active mediators of inflammation
Plasma systems and eicosanoids
51
Classification of Chemical Mediators Based on the source:
1. Exogenous mediators – bacterial products, toxins 2. Endogenous mediators – synthesized by the body a. Plasma derived Coagulation-Fibrinolytic system Kinin system Complement system b. Cell or tissue derived Preformed mediators in granules (e.g. histamine, cationic proteins) Newly synthesized (e.g. interleukins, leukotrienes, platelet activating factor)
52
Based on biochemical synthetic pathway:
1. Peptide mediators – complement, coagulation-fibrinolytic system 2. Lipid mediators – arachidonic acid derivatives (eicosanoids)
53
Effects of Mediators A. Vasodilation and Hyperemia – most potent ones:
1. Histamine (from mast cells and basophils) 2. Bradykinin 3. Prostaglandin E1 and I2 4. Leukotriene B4 5. C5 fragment of complement 6. Thromboxane
54
Effects of Mediators B. Vasopermeability:
1. Histamine 2. Serotonin 3. Bradykinin 4. Kallikrein 5. Platelet aggregating factor 6. Lymphokines 7. Anaphylatoxin (C3 and C5 complement fragments) 8. Leukotrienes B4, C4, D4 9. 5-HPETE (5-hydroxyeicosatetranoic acid) 10. Fibrin degradation products
55
C. Leukocyte Emigration and Chemotaxis
Neutrophils: 1. C5a fragment of complement 2. Leukotriene B4 3. Bacterial toxins 4. Platelet aggregating factor
56
Monocytes and Macrophages:
1. C5a fragment of complement 2. Leukotriene B4 3. Bacterial toxins 4. Cationic protein fractions of neutrophils 5. Lymphokines 6. Fibrin degradation products
57
Lymphocytes:
Lymphokines
58
Eosinophils:
1. ECF-A (Eosinophil chemotactic factor of anaphylaxis from mast cells) 2. Prostaglandin O2
59
Fluid and cells that accumulate in tissue spaces during inflammation
Inflammatory exudates
60
2. Main contents of inflammatory exudates
Protein, bacteria or irritant, injured tissues or cells, inflammatory cells, plasma constituents (H₂O, RBC, globulins, fibrinogen, fibrin)
61
Process of engulfing or ingesting the irritant by phagocytes
Phagocytosis
62
Exudate component that traps irritants, covers delicate tissues, and prevents spread through lymphatics
Fibrin
63
Exudate function that provides a scaffold for healing and repair
Fibrin deposition
64
Serum proteins effective against bacteria and viruses found in exudates
Antibodies
65
Antibody that causes bacteria to clump together
Agglutinins
66
Antibody that dissolves cells and bacteria
Lysins
67
Antibody that causes precipitation of antigens
Precipitins
68
Antibody that neutralizes toxins
Antitoxins
69
Antibody that processes bacteria for phagocytosis
Opsonins
70
Exudate contribution that supplies O₂, nutrients, and removes catabolic products
Increased blood plasma flow with nutrients and oxygen
71
Environmental condition maintained by exudates that is ideal for phagocytosis
Hydrogen ion concentration (pH)
72
Exudate property that ensures enzymes and antibodies act effectively
Fluid medium support
73
Contents of Inflammatory Exudates
1. Protein 2. Bacteria or irritant 3. Injured tissues or cells 4. Inflammatory cells 5. Plasma constituents: H₂O, RBC, globulins, fibrinogen, fibrin
74
Functions of Exudates
1. Dilutes irritant – plasma constituents dilute or neutralize irritant, disperse particles (like bacteria), facilitate phagocytosis 2. Mechanically washes or carries irritant away 3. Carries phagocytes to area for phagocytosis 4. Provides nutrient environment for sustaining leukocytes invading the area 5. Carries fibrin to inflamed area for: a. Entrapping irritant and delaying spread until phagocytosed b. Providing protective covering between irritant and delicate tissue cells c. Sealing lymphatic lumen to prevent entry and spread of irritant to lymph nodes/organs d. Helping in healing/repair by scaffolding or apposing wound surfaces e. Stimulating fibroblast proliferation 6. Brings antibodies to site of inflammation 7. Brings oxygen and nutrients for healing and repair; removes catabolic products; maintains ideal pH for phagocytosis; provides fluid medium for enzymes and antibodies
75
C. Types of Antibodies Found in Exudates
1. Agglutinins – cause bacterial clumping 2. Lysins – dissolve cells and bacteria 3. Precipitins – cause precipitation of antigens 4. Antitoxins – neutralize toxins 5. Opsonins – enhance phagocytosis