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Pathophysiology > Chapter 9 > Flashcards

Chapter 9 Flashcards

1
Q

Cardinal Signs of Inflammation

A 
Rubor (redness)
Tumor (swelling)
Calor (heat)
Dolor (pain)
Functio Laesa (loss of function)
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2
Q

Acute Inflammation

A

Early host protective response
Short (few minutes to several days)

Characterized by exudation off fluid and plasma components, emigration of leukocytes (neutrophils) into extra vascular tissues

Self limited and short in duration

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3
Q

Chronic inflammation

A

Longer (days to years)

Characterized by presence of lymphocytes and macrophages, proliferation of BV’s, fibrosis, tissue necrosis

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4
Q

Endothelial cells

A

Single cell-thick epithelial lining of BV’s
Form a selective permeable barrier between circulating blood and surrounding tissues

Regulate blood flow

Produce: anti platelet, anti thrombotic agents, vasodilator, vasoconstrictors

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5
Q

What are the phases of acute inflammation?

A

Vascular phase
Cellular phase (marination, adhesion, and transmigration)
Leukocyte activation and phagocytosis

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6
Q

Vascular phase

A

Acute Inflammation

Vasoconstriction of arterioles at site of injury —> vasodilation —> increase capillary flow —> increase vascular permeability —> decrease capillary osmotic pressure/ increase interstitial osmotic pressure —> stagnation of flow and clotting of blood (due to increased concentration of blood constituents)

Symptoms: heat, redness (erythema), swelling, pain, impaired function

Exudation dilutes offending agent

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7
Q

Exudate

A

Protein-rich fluid

Will move into extravascular spaces during tissue injury

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8
Q

Cellular Phase

A

Acute inflammation

Leukocytes (neutrophil PMN’s) —> endothelial activation —> adhesion —> marination —> transmigration —> chemotaxis

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9
Q

Thrombocytes

A

Platelets
Involved in coagulation and the inflammatory response

increase vascular permeability

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10
Q

Neutrophils

A

Primary phagocyte
early arrival at tie of inflammation (within 90 minutes)

AKA PMN

Able to generate hydrogen peroxide and nitrogen oxide

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11
Q

Granulocyte

A

White blood cell itch distinctive cytoplasmic granules

Contain enzymes and antibacterial material used in destroying engulfed microbes and dead tissues

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12
Q

Leukocytosis

A

Increase in circulating white blood cells from normal value (4000-10000) to upwards of 10000-20000

Elevated during tissue injury and infection

Important to maintain levels of neutrophil

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13
Q

Monocytes

A

Largest circulating leukocytes

Act as macrophages, destroy causative agent, aid in immunity, resolve inflammatory process, initiate healing

Produce vasoactive mediators (prostaglandins, leukotriene, platelet-activating factor, inflammatory cytokines, growth factors)

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14
Q

Eoasinophils

A

Induce inflammation, especially important in hypersensitivity and allergic disorders

Recruited to tissues and control release of specific chemical mediators

Contain proteins toxic to parasitic worms

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15
Q

Basophils

A

Blood granulocytes derived from bone marrow progenitors, circulate in blood

Contain histamine and other inflammatory mediators

Bind antibody IgE —> release of histamine/ vasoactive agents (same occurs with mast cells)

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16
Q

Mast Cells

A

Activate when leave circulation and lodge in tissue sites —> release of performed contents in granules (histamine, proteoglycans, protease, cytokines, lipid mediations, stimulation of cytokines and chemokine)

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17
Q

Vascular response patterns

A

Immediate transient response
Immediate sustained response
Delayed hemodynamics response

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18
Q

Immediate Transient Response

A

Minor injury
Short in duration and occur immediately

leakage affects venues

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19
Q

Immediate sustained response

A

More serious injury for several days

Affects arterioles, capillaries, and venules

Due to direct damage of endothelium

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20
Q

Delayed hemodynamic response

A

Increased permeability occurs in venules and capillaries

Often from injuries due to radiation (eg: sunburns) leading to delayed endothelial cell damage

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21
Q

Marination

A

Proces of leukocyte accumulation

Adherence tightly to endothelium and movement along periphery of blood vessels

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22
Q

What type of cell communication molecules are released during margination?

A

Cytokines —> endothelial lining cells express cell adhesion molecules (selectins) —> bind leukocytes —> transmigration through vessel wall and into tissue spaces

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23
Q

Chemotaxis

A

Energy-directed cell migration through chemoattractants (chemokines), bacterial/ cellular debris, protein fragments (complement system)

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24
Q

Chemokines

A

Small proteins that direct the trafficking of leukocytes during early stages of inflammation or injury

Bind to proteoglycans on surface of endothelial cells/ ECM —> high concentration of chemokine stay at site of injury/ infection —> chemotactic gradient

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25
Steps of phagocytosis
1- Recognition and adherence 2- Engulfment 3- Intracellular killing
26
Plasma derived mediators acute inflammation
Acute phase proteins, factor XII, complement proteins Synthesized in liver
27
Clinical manifestations of acute-phase proteins
Fever | Inflammation
28
Clinical manifestations of factor XII
Clotting, Kirin
29
Clinical manifestations of complement proteins
Activation of complement system
30
Cell-derived mediators in acute inflammation
Preformed mediators (mast cells, platelets, neutrophils/ macrophages) and newly synthesized (leukocytes, macro phase, lymphocytes, endothelial cells) Originate from cells
31
Clinical manifestations of mast cells as preformed mediators
Release of histamine
32
Clinical manifestations of platelets as preformed mediators
Release of serotonin
33
Clinical manifestations of neutrophils and macrophages as preformed mediators
Release of lysozymal enzymes
34
Clinical manifestations of leukocytes as newly synthesized mediators
Release of prostaglandins, leukotrienes, PAF
35
Clinical manifestations of leukocyte and macrophages as newly synthesized mediators
Release of NO or oxygen-derived free radicals
36
Clinical manifestations of macrophages/ lymphocytes/ endothelial cells as newly synthesized mediators
Release of cytokines
37
Histamine
Preformed stores, first mediator to be released in acute reaction Connective tissues near BV’s, basophils, platelets, principal mediator immediate transient phase Released ion reaction involved IgE antibodies Manifestations: dilation of blood arterioles, increase permeability of venules
38
Arachidonic acid
Unsaturated fatty acid in phospholipids of cell membranes Cascade of reactions lead to production of eicosanoid family of inflammatory mediators
39
Eicosanoid family of inflammatory mediators
Prostaglandins, LT, related metabolites
40
Eicosanoid synthesis
Cycloxygenase pathways —> synthesis of prostaglandins and thromboxane (prostanoids) Lipoxygenase pathway —> synthesis of LT
41
Clinical manifestations of Cyclooxygenase pathways
Prostaglandins —> induce vasodilation and bronchoconstriction, inhibits inflammatory cell function Thromboxane —> vasoconstriction, bronchoconstriction, promotes platelet function
42
Examples of drugs that interfere in the cyclooxygenase pathways
Aspiring, NSAIDS
43
Clinical manifestations of lipoxygenase pathway
Leukotrines —> smooth muscle contraction, pulmonary airway constriction, micro vascular permeability increase
44
Platelet activating factor (PAF)
Complex lipid in cell membranes Induced platelet aggregation, activates neutrophils, potent eosinophils chemoattractant
45
Clinical symptoms from inhalation of PAF
Bronchospasm, eosinophil infiltration, nonspecific bronchial hyperactivity
46
Protease-activated receptors (PARs)
Final link between coagulation system and inflammation Induce inflammation through production of chemokine, expression of endothelial adhesion molecules, induction of prostaglandin synthesis, production of PAF
47
Complement system
20 inactive component proteins (plasma) Become activated to become proteolytic enzymes that degrade each other Form a cascade that works in immunity and inflammation by increasing vascular permeability, improving phagocytosis, and causing vasodilation
48
Kinin system
Creates vasoactive peptides from kininogens (type of plasma proteins) Activation leads to release of bradykinin —> increase in vascular permeability —> contraction of smooth muscle, dilation of blood vessels/ paint when injected into skin Inactivated by kininase or by angiotensin-converting enzyme in the lung
49
Symptoms of the acute-phase response
``` Fever Anorexia Hypotension Increased HR Corticosteroid and ACTH release ```
50
Example of cytokines that mediate inflammation
TNF-a and IL-1 Induce endothelial cells to express adhesion molecule and release cytokines, chemokine, ROS
51
Types of chemokines
Inflammatory —> produced in response to bacterial toxins and inflammatory cytokines Homing —> direct chemotaxis to responsive cells
52
Role of NO in the inflammatory response
Smooth muscle relaxation Antagonism of platelet adhesion, aggregation, degranulation Serves as leukocyte recruiter Antimicrobial actions
53
Role of oxygen free radicals in the inflammatory response
Species combine with NO to form ROS intermediates which can increase inflammation and no cause more tissue injury Release extra cellular after exposure to microbes, cytokines, immune complexes during phagocytosis
54
Serous exudate
Water fluids low in protein content that result from plasma entering the inflammatory site
55
Hemorrhagic exudate
occurs in severe tissue injury that damages blood vessels There is significant leakage of red cells from capillaries
56
Fibrinous exudate
Large amounts of fibrinogen form thick and stick mesh work (much like blood clot)
57
Membranous or pseudomembranous exudate
Develop on surface of mucous membranes Composed of necrotic cells in a fibrinopurulent exudate
58
Purulent/ suppurations exudate
Contains pus,composed of degraded white blood cells, proteins, tissue debris Microorganisms like staph are more likely to induce these
59
Abscess
Localized area of inflammation containing purulent exudate that might be surrounded by a neutrophil layer Fibroblasts may wall off area of abscess Clinical interventions: abscess must be drained since antimicrobial agents cannot penetrate fibroblast walls
60
Ulceration
Site of inflammation where an epithelial surface becomes necrotic and eroded Often associated with sub epithelial inflammation
61
What might cause ulceration?
Any traumatic injury to the epithelial surface (eg: peptic ulcer) Vascular compromise (foot ulcers associated with diabetes)
62
Chronic Inflammation
Self-perpetuating and may last for weeks Infiltration by mononuclear cells (macrophages) and lymphocytes as opposed to neutrophils in acute Involved proliferation of fibroblasts as opposed to exudates in acute
63
Cause chronic inflammation
May occur from recurrent and progressive acute responses or anything that fails to evoke an acute response Low grade persistent infections or irritants that are unable to penetrate deeply or spread rapidly Foreign bodies (talc, silica, abestos, surgical suture material) Viruses; bacteria ; larger parasites with lower virulence Injured tissue
64
Is the risk of scarring and deformity greater in acute or chronic inflammation?
Chronic due to proliferation of fibroblasts
65
Two patterns chronic inflammation
Nonspecific Granulomatous
66
Nonspecific Chronic inflammation
Diffuse accumulation of macrophages and lymphocytes at site of injury Ongoing chemotaxis —> macrophages infiltrate inflamed site —> accumulation—> fibroblasts proliferation—> scars replace normal connective tissue causing disease process
67
Granulomatus Lesion
Distinctive form of chronic inflammation Massing of macrophages surrounded by lymphocytes (resemble epithelial cells, aka epitheloid cells) Associated with splinters, sutures, silica, other foreign bodies, microorganisms (tb, syphilis), fungal infection due to the bodies poor digestion and poor immune control of these bodies
68
Epitheloid cells
Derived from blood monocytes Clump in masses, forming a mononucloid giant (foreign body giant cells)that tries to surround foreign agents —> dense connective tissue encapsulates lesion —> isolates lesion
69
Systemic manifestations of inflammation
Usually localized, but in the acute phase response, alterations in white blood cell counts, and fevers may lead to wide spread inflammation Localized acute and chronic inflammation can spread to lymphatic system —> lymph node reaction that drain the affected area
70
Acute phase response
Changes in concentration of plasma proteins (acute phase proteins, skeletal muscle catabolism, negative nitrogen balance, ESR, increased numbers of leukocytes due to release of cytokines Occurring hours or days after onset of inflammation Generally, this mechanism coordinates various changes in body function to enable an optimal host response
71
Obvious signs of acute phase response
Fever due to release of cytokines that affect thermoregulatory center in hypothalamus Anorexia, somnolence, mailaise (due to Il1 and TNFa on the CNS)
72
What induce and increase in the number of circulating neutrophils during the acute phase response?
Il2 and other cytokines by stimulating their production in the bone marrow
73
Purpose of skeletal muscle catabolism during acute phase response
To provide AAs that can be used for the immune response and tissues repair
74
What causes systemic inflammatory response syndrome?
Severe bacterial infections (sepsis)—> large amounts of microorganisms in blood —> uncontrolled inflammatory response and release of tons of inflammatory cytokines (il1 and tnf-a) Symptoms: generalized vasodilation, increased vascular permeability, intravascular fluid loss, myocardial depression, circulatory shock
75
Acute phase proteins
Liver increases production of these during APR Fibrinogen, CRP, and serum amyloid A (SAA), upregulated by cytokines
76
CRP
C-reactive protein, important inflammatory bio marker (eg: acute myocardial infarction, malignancies, autoimmune) Function: protective by by binding to surface of invading microorganisms and targeting them for destruction by complement and phagocytosis Increase when there is an acute inflammatory repsonse
77
What in coronary arteries predisposes individuals to thrombosis and MI?
Inflammation of atherosclerotic plaques
78
Pathologically, why is ESR increased during a systemic inflammatory response?
APR —> high density lipoprotein transferred form liver cells to macrophages —> rise in fibrinogen —> red cells to form stacks (rouleaux) that sediment quicker then a erythrocytes
79
Neutrophilia
Selective increase in neutrophils often caused by bacterial infections
80
Eosinophilia
Selective increase in eosinophils Caused by parasitic or allergic reposnse
81
What causes neutropenia and lymphocytosis together?
Viral infections Neutropenia: decrease in neutrophils Lymphocytosis: increase in lymphocytes
82
Leukopenia
Decrease in white blood cells as a result of overwhelming infections or inability to produce WBCs
83
Lymphadenitis
Enlargement of lymph nodes that drain the affected area due to a nonspecific response to mediators released from the injured tissues or an immunological response to a specific antigen
84
Tissue Repair
Cell migration, proliferation, differentiation, interaction with ECM response to tissue injury, attempting to maintain normal body structure and function Regeneration: injured cells replaced with cells of same type Replacement: connective tissue which leaves a permanent scar
85
Tissue regeneration
Replacement of injured tissue with cells of the same type
86
What are the three types of cells based on their ability to undergo regeneration?
Labile, stable, permanent
87
Two structures in body organs and tissue
Parenchymal: tissues containing the function cells of an organ or body part Stromal: tissues consist of supporting connective tissues, blood vessels, ecm , and nerve fibers
88
Labile cells
Continue to divide and replicate throughout life Replace cells that are destroyed eg: surface epithelial cells of the skin, GI tract, uterus, bone marrow, etc.
89
Stable cells
Stop dividing when growth ceases, but capable of undergoing regeneration with appropriate stimulus and capable of reconstituting tissue of origin (eg; parenchymal cells of liver and kidney, smooth muscles cells, vascular endothelial cells)
90
Permanent or fixed cells
Cannot undergo mitosis division (eg: nerve cells, skeletal muscle cells, cardiac muscle cells) Do not normally regenerate and will be replaced with fibrous scare tissue that lacks functional characters of the destroyed tissue
91
Fibrous Tissue Repair
When repair cannot be accomplished with regeneration alone Rapier occurs by replacement with connective tissues —> generation of granulation and formation of scar tissue
92
Granulation tissue
Connective tissue with new capillaries, proliferating fibroblasts, and residual inflammatory cells Development: angiogenesis, fibrogenesis, and formation of scar tissue
93
Angiogenesis
Formation of new capillaries from pre-existing vessels Eventually will differentiate into arterioles and venules
94
Fibrogenesis
Influx of activated fibroblasts —> secrete ECM components (fibronectin, hyaluronic acid, proteoglycans, collagen)
95
Scar formation
emigration and proliferation of fibroblasts into site of injury —> disposition of ECM by these cells
96
Final consistency of scar
Inactive spindle-shaped fibroblasts, dense collagen fibers, fragment of elastic tissue, ECM components
97
Chemical mediators in tissue regeneration
ILs, interferons, TNF-a, and arachidonic acid derivatives (prostaglandins and L) that participate in inflammatory response
98
ECM
Secreted locally Assembles into a network of spaces surrounding tissues cells Three components: fibrous structural proteins (collagen and elastin fibers), water-hydrated gels (proteoglycans and hyaluronic acid) that permit resilience and lubrication, adhesive glycoproteins (fibronectin, laminitis) that connect matrix element to each other and to other cells
99
ECM locations
1- basement membrane that surrounds epithelial, endothelial, smooth muscle cells 2- interstitial matrix: present in spaces between cells in connective tissue and between epithelium and supporting cells of blood vessels
100
Functions of ECM
Provides tutor to soft tissue and righty to bone Supplies substratum for cell adhesion Regulation of growth, overeat, an differentiation of surrounding cells Storage and presentation of regulatory molecules that control repair process Provides scaffolding for tissue renewal
101
What type of ECM is critical for regeneration?
Intact ECM, especially the basement membrane
102
What is the primary focus of the healing process?
Fill the gap created by tissue destruction and to restore the structural continuity of the injured part
103
Primary intention
Sutured surgical incision
104
Healing by secondary intention
Larger wounds (burns and surface wounds) have a greater loss of tissue and contamination; wounds that may have become infected and healed by secondary intention Slower, resulting in formation of larger amount of scar tissue
105
Phases of wound healing
1- inflammatory phase 2- proliferating phase 3- wound contraction and remodeling phase Each phase mediated by cytokines and growth factors
106
Inflammatory phase of wound healing
Begins at time of injury with formation of blood clot and migration of phagocytosis white blood cells into wound cite —> neutrophils arrive, ingest, rand remove bacteria/ cell debris —> macrophages arrive, ingest cell debris and produce growth factors Involves hemostasis
107
Proliferative phase of wound healing
Building of new tissue to fill wound space Fibroblast: connective tissue that synthesizes and secretes the collagen, proteoglycans, and glycoproteins needed for wound healing - Produce growth factors that induce angiogenesis and endothelial cells proliferation and migration Epithelialization: epithelial cells at wound edges proliferate to form a. New surface layer that is similar to that which was destroyed by the injury
108
Wound contraction and remodeling phase of wound healing
3 weeks after injury- 6 months or later Decrease in vascularity, continued remodeling of scar tissue by simultaneous synthesis of collagen by fibroblasts Lysis by collagen are enzymes
109
Factors that affect wound healing
Malnutrition, impaired blood flow, oxygen delivery, impaired inflammatory and immune response, infection, wound separation, foreign bodies, age effects, specific disorders (diabetes, peripheral artery disease, venous insufficiency, nutritional disorders)
110
Vitamins essential in the healing process
Vitamin C and A (collagen synthesis and sitsmualting epitelializtaion, capillary formation) Vitamin B: cofactors in enzymatic reactions Vitamin K: prevents bleeding disorders that contribute to hematoma
111
Implications of hypoxia on wound healing
Prevents would healing due to it causing a decrease in fibroblast growth, collagen production, and angiogenesis

Pathophysiology (9 decks)

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