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Acute Inflammation Flashcards

Lecture 4 (115 cards)

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1
Q

What is the primary purpose of inflammation?

A

The primary purpose of inflammation is to protect the body by eliminating the initial cause of cell injury, such as pathogens or damaged cells, and resolving the consequences of cell injury.

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2
Q

Describe the continuum of inflammation.

A

Inflammation occurs in a continuum, starting from the initial inflammatory phase characterized by vascular and cellular responses, progressing through the resolution of inflammation, and concluding with the healing and repair phase.

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3
Q

What are the key components involved in the inflammatory process?

A

-vascular responses (increased blood flow and vascular permeability)

-cellular responses (migration of leukocytes to the affected area),

-the release of chemical mediators (cytokines, prostaglandins) that modulate the inflammatory response.

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4
Q

What are the various stimuli or causes that can trigger an inflammatory reaction?

FIT TIP

A

Foreign bodies (e.g., splinters, dirt, sutures)

Infections (bacterial, viral, parasitic) and microbial toxins

Trauma (blunt and penetrating)

Tissue necrosis (from any cause)

Immune reactions (hypersensitivity reactions)

Physical and chemical agents, thermal injury (burns or frostbite), irradiation, environmental factors

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5
Q

What are the categories of inflammatory responses based on time?

CASH

A

Hyperacute, acute, subacute, and chronic.

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6
Q

How can inflammatory responses be categorized based on the degree of tissue damage?

A

Superficial or deep.

Suppuration, abscess, ulcer, or cellulitis.

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7
Q

What are the characteristic pictures used to categorize inflammatory responses?

A

Specific or non-specific.

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8
Q

What are the immunopathological mechanisms involved in inflammatory responses?

A

Allergic reactions.

Reactions mediated by cytotoxic antibodies.

Reactions mediated by immune complexes.

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9
Q

How are chemical substances released by tissues utilized in the inflammatory response?

A

When injury occurs, chemical substances are released by tissues, creating a “chemical or chemotactic gradient,” which attracts fluid and cells to the site of injury. These mediators can be derived from plasma, cells, tissues, or exogenous sources such as bacteria.

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10
Q

What are immunopathological mechanisms?

A

Chemical substances released by tissues utilized in the inflammatory response

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11
Q

Mediators derived from either:

A

Plasma, cells or tissues or exogenous (bacteria)

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12
Q

What are the two simultaneously occurring phases in the inflammatory response, irrespective of the causative mechanism of injury?

A

Vascular phase:
Cellular phase:

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13
Q

Vascular phase:

A

Involves changes in blood flow within small blood vessels of the microcirculation, including arterioles, venules, and capillaries.

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14
Q

Cellular phase

A

Involves changes in endothelial cells lining the blood vessels.

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15
Q

What is the Triple Response of Lewis, and how does it demonstrate the vascular phase of inflammation?

A

The Triple Response of Lewis is a series of observable changes that demonstrate the vascular phase of inflammation.
White line: Represents transient capillary vasoconstriction.
Red line: Indicates capillary dilatation.
Flare/red halo: Reflects arteriolar dilatation.
Wheal/swelling: Manifests as edema

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16
Q

What are the components of the pathophysiology of the vascular phase of inflammation?

A

i. Transient vasoconstriction followed by vasodilatation.
ii. Increased vascular permeability.
iii. Increased viscosity of blood.
iv. Peripheral orientation of leukocytes.

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17
Q

What initiates the transient vasoconstriction during the vascular phase of inflammation?

A

The transient vasoconstriction is initiated by vasoactive chemical mediators.

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18
Q

How is the initial decrease in blood flow followed by vasodilatation during the vascular phase of inflammation achieved?

A

The initial decrease in blood flow is brought about by vasoconstriction mediated by vasoactive chemical mediators.
Subsequently, there is arteriolar and venular dilatation, leading to increased blood flow and blood pooling.
This increased blood flow results in redness and warmth at the site of inflammation.
Endothelial cells contract and intercellular junctions separate, allowing the formation of endothelial gaps, which contribute to increased vascular permeability.

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19
Q

What is the consequence of increased vascular permeability during the vascular phase of inflammation?

A

leads to the formation of endothelial gaps, resulting in the loss of plasma proteins. This reduces capillary colloid osmotic pressure (COP) and increases interstitial COP, causing fluid and inflammatory cells to accumulate in the tissues. This accumulation leads to swelling or edema, characterized by transudate or exudate formation, and loss of intravascular fluid.

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20
Q

How does increased blood viscosity contribute to the inflammatory response

A

Increased blood viscosity, resulting from the loss of intravascular fluid and haemoconcentration, leads to stasis of blood. This promotes clotting and localizes the offending agent, aiding in the inflammatory response.

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21
Q

What is the significance of the peripheral orientation of leukocytes during the vascular phase of inflammation?

A

Stasis of blood flow leads to the peripheral orientation of leukocytes, where they move to the periphery. Additionally, platelets adhere to the endothelium, and red blood cells adhere to one another, forming Rouleau formation, which enhances clotting.

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22
Q

Summary: What are the key events of the vascular phase of inflammation?

A
  1. Vasoconstriction followed by vasodilatation.
  2. Increased blood flow.
  3. Increased vascular permeability leading to the outpouring of protein-rich fluid.
  4. Fluid accumulation in tissues leading to impaired function.
  5. Fluid loss resulting in the slowing of blood flow and localization of the offending agent.
  6. Leukocytes migrate to the periphery, red blood cells clump and clot, and platelets adhere to the endothelium.
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23
Q

What is the difference between transudate and exudate?

A

Transudate:

Result of hydrostatic or colloid osmotic imbalance.
Ultrafiltrate of plasma.
Low protein content, low cell count, low fibrinogen content, and low specific gravity.

Exudate:

Result of inflammation.
Increased vascular permeability.
High protein content, high cell count, high fibrinogen content, and high specific gravity.

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24
Q

What are the types of Exudates:

Sarah has five mini pies

A

-Serous
-Haemorrhagic
-Fibrinous
-Membranous
-Puriulent

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25
What are the characteristics of serous exudate?
Serous exudate: Watery consistency. Low protein content.
26
What causes the formation of haemorrhagic exudate?
Occurs due to severe tissue injury causing blood vessel damage. Results in the leak of red cells from capillaries.
27
Describe the characteristics of fibrinous exudate.
Contains a large amount of fibrin, forming a thick, sticky meshwork.
28
What is unique about membranous exudate?
Found on mucous membrane surfaces. Made of necrotic cells enmeshed in fibropurulent exudate
29
What components are found in purulent exudate?
Contains pus composed of degraded white cells, proteins, and tissue debris.
30
What are the three patterns of response observed depending on the severity of inflammation?
Immediate but transient response: Immediate and sustained response: Delayed hemodynamic response:
31
Immediate but transient response:
Occurs after minor injury, such as a mosquito bite. Rapid development of changes seen in venules.
32
Immediate and sustained response:
Occurs with serious injuries like burns or products of bacterial infection. Longer duration involvement of arterioles, venules, and capillaries. Direct damage to endothelium.
33
Delayed hemodynamic response:
Begins after 2-12 hours and lasts for several hours to days. Involves venules and capillaries. Leakage mechanism involves direct effects. May accompany radiation injury, such as sunburn.
34
What are the main events in the cellular phase of inflammation?
Main events in the cellular phase of inflammation include: i. Leukocyte migration. ii. Leukocyte adhesion to endothelium. iii. Migration of leukocytes across endothelium. iv. Chemotaxis. v. Activation and phagocytosis.
35
Which cells are involved in acute inflammation **Tip** -PM
Polymorphonuclear leukocytes: neutrophils, eosinophils, basophils. Mononuclear cells: lymphocytes, monocytes/macrophages.
36
Polymophonuclear leukocyes ** Tip BEN**
Neutrophils Eosinophils Basophils
37
Mononuclear cells
Lymphocyes Monocye/macrophages
38
What initiates the movement or recruitment of cells from circulation into tissues during inflammation?
The movement or recruitment of cells from circulation into tissues during inflammation is initiated by endothelial activation due to the effects of TNF and IL-1. This leads to increased vascular permeability, fluid loss, haemoconcentration, and stasis. Heavier white blood cells (WBCs) then roll and marginate for the process of adhesion, pavementing, and emigration or transmigration by diapedesis.
39
How does leucocyte migration or margination occur during inflammation?
occurs due to stasis and slowing of blood flow, as seen in the vascular phase of inflammation. Leucocytes move to the periphery of blood flow and towards the endothelial lining, a process known as margination, where they come to rest on the endothelial cells.
40
How does leucocyte adhesion occur during inflammation?
Leucocyte adhesion occurs in the following steps: 1. Leucocytes come in contact with endothelial cells. 2. Chemical mediators are released, which bind to carbohydrates on the surface of leucocytes. 3.This binding results in a "tethering," "rolling," or "tumbling" effect of cells along the endothelial lining. 4. Leucocytes come to rest due to the strong adhesion of intercellular adhesion molecule (ICAM) on the endothelium.
41
Name three types of adhesion molecules involved in the process of inflammation.
Selectins Integrins Immunoglobulin
42
Selectins
Mediate the adhesion of leucocytes to endothelial cells.
43
Integrins:
Promote cell-to-cell and cell-to-extracellular matrix interactions.
44
Immunoglobulin
Includes intracellular adhesion molecules (ICAM-1, ICAM-2) and vascular adhesion molecule (VCAM), which interact with integrins to mediate the recruitment of leucocytes.
45
What is transmigration, emigration, or diapedesis in the context of inflammation?
Transmigration, emigration, or diapedesis in inflammation involves the following steps: After firm adhesion with the endothelium, leucocytes squeeze out across the basement membrane. They extend pseudopodia between endothelial cell gaps and migrate out of the vessel. In the early response, mostly neutrophils and eosinophils are involved, while in the later response, monocytes and lymphocytes participate.
46
What is chemotaxis in the context of inflammation?
Chemotaxis involves the directed movement of leucocytes towards a chemical stimulus or offending agent. It's a dynamic, energy-dependent process.
47
Once leucocytes are in the interstitial tissue, what guides their movement? (CHEMOTAXIS)
Once in the interstitial tissue, leucocytes are guided by the chemical gradient created by chemoattractants. These chemoattractants include plasma, cells, tissue, and exogenous substances.
48
What are some examples of chemoattractants involved in chemotaxis during inflammation?
Chemoattractants include chemokines such as interleukins and TNF, bacterial and cellular debris, protein fragments (resulting from the activation of the complement system, e.g., C3a, C5a), as well as macrophages and non-immune cells.
49
What is the first step involved in phagocytosis?
The first step in phagocytosis is recognition and adhesion, which involves specific receptors allowing the microbe to adhere to the phagocyte.
50
Describe the second step of phagocytosis.
The second step of phagocytosis is engulfment, where the microbe is entrapped by pseudopodia and ingested by the phagocyte, leading to the formation of the phagosome.
51
What occurs during the intracellular killing phase of phagocytosis?
During the intracellular killing phase of phagocytosis, the phagosome fuses with intracellular lysosomes to form phagolysosomes. Digestion of the ingested microbe occurs by enzymes, leading to the formation of a residual body and discharge of waste material.
52
In acute inflammations, which types of cells are the first to arrive, and which cells follow later?
In acute inflammations, neutrophils are the first to arrive, followed later by monocytes (plasma cells or macrophages).
53
Are there any exceptions to the typical sequence of cell arrival in acute inflammations?
Yes, exceptions to the typical sequence of cell arrival in acute inflammations include: Viral and rickettsial infections: Lymphocytes are the first to arrive. Allergy and parasitic infections: Eosinophils are the first to arrive.
54
What are the beneficial effects of inflammation? BIICA
Increase in fluid: Dilutes the irritant present in the area. Blood cell activity: Engulf and digest bacteria, dead cells that might cause or continue inflammation. Antibody action: Antibodies present in the edema fluid neutralize toxic substances, contributing to the immune response. Clotting with fibrin: Walls off the area and prevents the irritant or inflammation from spreading beyond the affected area. Initiation of healing and regeneration: Initiates the process of healing and regeneration in the affected tissues.
55
Harmful effects of inflammation DIAL
Digestion and destruction of normal tissue: Inflammatory mediators can lead to the digestion and destruction of normal tissue. Inappropriate or exaggerated inflammatory response: Acute manifestations can include life-threatening hypersensitivity reactions, while chronic manifestations can lead to conditions like atherosclerosis, scar formation, and fibrosis. Altered blood supply: Inflammation can lead to altered blood supply, resulting in conditions like anoxia and infarcts. Loss of function: Swelling, tenseness, abscess, and pain can result in loss of function in the affected area.
56
What are the problems associated with the cellular phase of inflammation regarding leucocyte function?
Defective adhesion: -Impaired adhesion characterized by recurrent bacterial infections and impaired wound healing. Defective chemotaxis or phagocytosis: -Resulting in impaired locomotion and impaired lysosomal degranulation. Example: Chediak-Higashi syndrome: Presents with neutropenia, defective degranulation, and delayed microbial killing.
57
Chediak-Higashi syndrome:
Presents with neutropenia, defective degranulation, and delayed microbial killing.
58
Defective adhesion:
Leucocyte function - -Impaired adhesion characterized by recurrent bacterial infections and impaired wound healing.
59
Defective chemotaxis or phagocytosis:
Leucocyte functioning problem -Resulting in impaired locomotion and impaired lysosomal degranulation.
60
What are the problems associated with the cellular phase of inflammation regarding microbial function?
Insufficient hydrogen peroxide production or myeloperoxidase deficiency: Results in chronic granulomatous disease, making individuals susceptible to recurrent infections. Deficiency in the number of circulating cells: Can result from marrow destruction or infiltration by cancer cells, or it can be due to the effects of radiation or chemotherapy.
61
What are the local clinical manifestations of acute inflammation?
1. Calor (heat): 2. Rubor (redness): 3. Tumor (swelling): 4. Dolor (pain): 5. Functio laesa (loss of normal function):
62
Calor (heat):
Increased blood flow to the area from arteriolar dilatation and increased vascularity followed by stasis.
63
Rubor (redness):
Increased blood flow to the area from arteriolar dilatation and increased vascularity followed by stasis., leading to a dusky cyanotic appearance.
64
3. Tumor (swelling):
Caused by exudation of plasma and fluid and cellular migration from the vasculature into the interstitium and its accumulation. Inflammatory processes within rigid or semi-rigid structures (e.g., bones) may lead to increasing pressure in a confined space, potentially compressing and occluding blood vessels, resulting in ischemic necrosis.
65
4. Dolor (pain):
Caused by inflammatory mediators such as bradykinin and prostaglandins (PGE2) irritating nerve endings. Physical tension and swelling within the confines of organs or tissues and stretching of the capsule can also contribute to pain.
66
5. Functio laesa (loss of normal function):
Caused by the noxious influence of the injurious agent and the inflammatory process.
67
What are the systemic effects of acute inflammation collectively called
Acute Phase Reactions,
68
Name 6 Acute Phase Reactions
1. Fever & Rigors 2. Leucocytosis 3. Acute Phase proteins 4. Endocrine changes 5. Lymphadenopathy 6. Raised ESR - erythrocye sedimentation role
69
What are the causes of fever and rigors during acute inflammation?
Fever and rigors during acute inflammation are caused by inflammatory mediators such as TNF, IL-1, or PGE2, triggered by exogenous factors like bacterial or viral products.
70
What is leucocytosis in the context of acute inflammation?
Leucocytosis refers to the increase in the white blood cell count, which is mediated by IL-1 and TNF during acute inflammation.
71
What are acute phase proteins, and how are they produced during acute inflammation?
Acute phase proteins such as fibrinogen and C-reactive proteins are produced in the liver. Their production increases due to changes mediated by IL-1 and TNF during acute inflammation.
72
How are endocrine changes manifested during acute inflammation?
involve the production of glucocorticoid steroid hormones, which are mediated by IL-1 and IL-6.
73
What is lymphadenopathy, and why does it occur during acute inflammation?
Lymphadenopathy refers to enlarged lymph nodes due to lymphatic drainage from local infection during acute inflammation.
74
What causes the raised ESR (erythrocyte sedimentation rate) during acute inflammation?
The raised ESR during acute inflammation is due to alterations in plasma proteins mediated by IL-1 and TNF.
75
What are inflammatory mediators, and how are they released?
Inflammatory mediators are chemical substances released by tissues in response to infection or injury. They create a chemical or chemotactic gradient, which attracts fluid and cells to the site of injury.
76
What causes the acute phase reactions seen in clinical manifestations of inflammation?
The acute phase reactions observed in clinical manifestations of inflammation are caused by inflammatory mediators.
77
What are the properties of inflammatory mediators?
Inflammatory mediators: Are triggered by microbes or host proteins. Act on target cells. Are short-lived.
78
What are the origins of inflammatory mediators?
Plasma-derived mediators: Cell-derived mediators:
79
Plasma-derived mediators:
These mediators are present in precursor form and must be activated by proteolytic cleavages. Sources include the complement system and the kinin system.
80
Cell-derived mediators:
These mediators are sequestered in intracellular granules and can be secreted (e.g., histamine) or synthesized de novo (e.g., prostaglandins, cytokines) upon exposure to a stimulus. Sources include platelets, neutrophils, monocytes/macrophages, mast cells, and mesenchymal cells.
81
How are inflammatory mediators activated?
Inflammatory mediators are produced by microbial products or host proteins and are themselves activated by microbes or damaged tissues. Examples include products of the complement, kinin, and coagulation systems.
82
Cell derived mediators sources
platelets, neutrophils, monocyte/macrophages mast cells, mesenchymal cells (endothelium, fibroblasts, smooth muscle cells)
83
How do inflammatory mediators exert their effects on target cells?
Inflammatory mediators bind to specific receptors on target cells. Most mediators mediate their action in this manner, while a few others mediate action by direct enzyme action or oxidative damage
84
What types of cells do inflammatory mediators act on?
Inflammatory mediators act on single or few target cell types. They may have diverse effects on the same target or differing effects on different types of cells.
85
What is the duration of action of inflammatory mediators?
The action of inflammatory mediators is short-lived and can decay, be inactivated by enzymes, scavenged by inflammatory cells, or inhibited.
86
What are the cellular mediators involved in inflammation?
Two important cellular mediators are histamine and serotonin.
87
What are the sources of histamine?
Histamine: Widely distributed, with high amounts in the lungs, skin, and gastrointestinal tract. Sources include mast cells (connective tissue of blood vessels), basophils, and platelets.
88
What are the sources of serotonin?
Serotonin: Also known as 5-hydroxytryptamine. Sourced from platelets and enterochromaffin cells.
89
What are the stimuli for the release of histamine?
Stimuli for the release of histamine include physical injury (trauma, heat, cold), immune reactions (such as binding to antibodies in allergies), fragments of complements (anaphylotoxins like C3a and C5a), histamine-releasing proteins derived from leukocytes, and neuropeptides and cytokines (such as IL-1 and IL-8).
90
What is the mode of action of histamine?
The mode of action of histamine includes arteriolar and venular dilatation, increased vasopermeability, and endothelial gaps. This is due to its action on H1 receptors on smooth muscles. Its action typically lasts for about one hour.
91
What is the clinical application of antihistamines?
Antihistamines are used in allergic reactions and act as H1 receptor blockers. However, they do not influence the production or release of histamine.
92
What is the mode of action of serotonin?
The mode of action of serotonin is similar to histamine and involves increased vascular permeability. It is released in response to platelet aggregation triggered by factors such as platelets in contact with collagen, thrombin, ADP, antigen-antibody complexes, and platelet-activating factor (PAF) from mast cells.
93
What is the complement system?
The complement system consists of a large number of proteins and cleavage products and functions in both innate and adaptive immunity. It is produced in the liver.
94
What are the modes of action of the complement system? DICO
Direct lysis of organisms: Achieved by the formation of the membrane attack complex from C5b Increased vascular permeability: Mediated by C3a and C5a. Chemotaxis and adhesion: Facilitated by C5a. Opsonization: Enhanced by C3b (can be augmented by IgG).
95
What is the Kinin system?
The Kinin system forms vasoactive peptides (kininogen) from plasma proteins, activated by Hageman factor (XII).
96
What is the role of Bradykinin in inflammation?
Bradykinin is a potent agent in inflammation that causes: Increases vascular permeability (100,000 times greater than histamine) Vasodilation (10,000 times greater than histamine) Pain production by activating nerve endings Non-vascular smooth muscle contraction, such as bronchial smooth muscle.
97
How long does the action of Bradykinin last?
short-lived as it is rapidly inactivated by enzymes known as kininases.
98
What are Eicosanoids?
Eicosanoids are arachidonic acid metabolites.
99
What are the sources of arachidonic acid (AA)?
Arachidonic acid can be obtained from dietary sources or through the hydrolysis of membrane phospholipids, particularly by phospholipase A2 following cell injury.
100
How are Eicosanoids synthesized from arachidonic acid (AA)? CL
Eicosanoids are synthesized from arachidonic acid by: Cyclo-oxygenation, resulting in the formation of prostaglandins and thromboxane. Lipo-oxygenation, leading to the production of leukotrienes (LT).
101
What are the modes of action of Eicosanoids?
Eicosanoids act through various mechanisms: They increase vascular permeability, mediated by leukotrienes E4 and B4, prostaglandin E2 and I2. They serve as chemoattractants, with leukotrienes and prostaglandins playing this role.
102
What is the action of aspirin and NSAIDs?
Aspirin and NSAIDs inhibit the cyclooxygenase pathway, thereby inhibiting prostaglandin synthesis. This action results in pain relief, making them examples of anti-pyretic, analgesic, and anti-inflammatory drugs.
103
What is the action of glucocorticoids?
Glucocorticoids inhibit the release of phospholipase A2, which prevents the release of arachidonic acid and histamine. Additionally, they inhibit the production of pro-inflammatory cytokines such as IL-1 and TNF-α. This overall inhibitory effect leads to a reduction in inflammation. Hydrocortisone and steroids are examples of glucocorticoids.
104
What is Platelet Activating Factor (PAF)?
Platelet Activating Factor (PAF) is a phospholipid derived from sensitized basophils.
105
What are the modes of action of Platelet Activating Factor (PAF)? Pam vanished like bashy bambo
The modes of action of PAF include: 1. Platelet aggregation 2. Vasodilation and increased vascular permeability (110 to 10,000 times greater than histamine) 3. Leukocyte adhesion (via integrins), chemotaxis, and degranulation of mast cells 4.Boosting synthesis of other mediators, such as eicosanoids, by leukocytes 5. Bronchoconstriction
106
What are the modes of action of Cytokines and Chemokines?
The modes of action of Cytokines and Chemokines include: Transient, closely regulated, and multifunctional actions. Increasing endothelial cell adhesion molecules. Regulating immune and hematopoietic cell proliferation and activity. Involvement in the movement of leukocytes through chemokinesis (random movement) and chemotaxis (directional movement).
107
What are Cytokines and Chemokines?
Cytokines and Chemokines are polypeptides derived from different cell types. Examples include lymphokines (from lymphocytes) and monokines (from macrophages). Examples of specific cytokines include Interleukin 1 (IL1) and Tumor Necrosis Factor alpha (TNF-a).
108
What are the mediators responsible for vasoconstriction?
The mediators responsible for vasoconstriction include Thromboxane A2 and Leukotrienes.
109
Which mediators cause vasodilation?
The mediators causing vasodilation include Histamine, Prostaglandin I2, E2, and G2.
110
Which mediators contribute to increased vascular permeability?
Mediators such as Histamine, Bradykinin, Platelet Activating Factor (PAF), and Leukotrienes lead to increased vascular permeability.
111
Which mediators are involved in chemotaxis and leukocyte adhesion?
Leukotrienes and Platelet Activating Factor (PAF) are involved in chemotaxis and leukocyte adhesion.
112
Which mediators are associated with fever?
Prostaglandin E2 (PGE2), Interleukin-1 (IL-1), and Tumor Necrosis Factor alpha (TNF-a) are associated with fever.
113
What mediators contribute to pain sensation?
Prostaglandin I2 (PGI2), Prostaglandin E2 (PGE2), Bradykinin, Interleukin-1 (IL-1), and Tumor Necrosis Factor alpha (TNF-a) contribute to pain sensation.
114
What is the role of the Clotting and Fibrinolytic System in inflammation?
The Clotting and Fibrinolytic System is important in inflammation. It acts by causing clotting of blood, acting as a chemical mediator in inflammation, increasing vascular permeability, and being chemotactic for neutrophils.
115
What are the outcomes of Acute Inflammation?
The outcomes of Acute Inflammation include: Complete resolution: Little tissue damage with the capability of regeneration. Abscess, suppuration, or cellulitis. Scarring and fibrosis: In tissues unable to regenerate, due to the organization of excess fibrin deposition. Chronic inflammation

Pathophysiology (4 decks)

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