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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
Q

Steps of phagocytosis

A

1- Recognition and adherence
2- Engulfment
3- Intracellular killing

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26
Q

Plasma derived mediators acute inflammation

A

Acute phase proteins, factor XII, complement proteins

Synthesized in liver

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27
Q

Clinical manifestations of acute-phase proteins

A

Fever

Inflammation

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28
Q

Clinical manifestations of factor XII

A

Clotting, Kirin

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29
Q

Clinical manifestations of complement proteins

A

Activation of complement system

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30
Q

Cell-derived mediators in acute inflammation

A

Preformed mediators (mast cells, platelets, neutrophils/ macrophages) and newly synthesized (leukocytes, macro phase, lymphocytes, endothelial cells)

Originate from cells

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31
Q

Clinical manifestations of mast cells as preformed mediators

A

Release of histamine

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32
Q

Clinical manifestations of platelets as preformed mediators

A

Release of serotonin

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33
Q

Clinical manifestations of neutrophils and macrophages as preformed mediators

A

Release of lysozymal enzymes

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34
Q

Clinical manifestations of leukocytes as newly synthesized mediators

A

Release of prostaglandins, leukotrienes, PAF

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35
Q

Clinical manifestations of leukocyte and macrophages as newly synthesized mediators

A

Release of NO or oxygen-derived free radicals

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36
Q

Clinical manifestations of macrophages/ lymphocytes/ endothelial cells as newly synthesized mediators

A

Release of cytokines

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37
Q

Histamine

A

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

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38
Q

Arachidonic acid

A

Unsaturated fatty acid in phospholipids of cell membranes

Cascade of reactions lead to production of eicosanoid family of inflammatory mediators

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39
Q

Eicosanoid family of inflammatory mediators

A

Prostaglandins, LT, related metabolites

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40
Q

Eicosanoid synthesis

A

Cycloxygenase pathways —> synthesis of prostaglandins and thromboxane (prostanoids)

Lipoxygenase pathway —> synthesis of LT

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41
Q

Clinical manifestations of Cyclooxygenase pathways

A

Prostaglandins —> induce vasodilation and bronchoconstriction, inhibits inflammatory cell function

Thromboxane —> vasoconstriction, bronchoconstriction, promotes platelet function

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42
Q

Examples of drugs that interfere in the cyclooxygenase pathways

A

Aspiring, NSAIDS

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43
Q

Clinical manifestations of lipoxygenase pathway

A

Leukotrines —> smooth muscle contraction, pulmonary airway constriction, micro vascular permeability increase

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44
Q

Platelet activating factor (PAF)

A

Complex lipid in cell membranes

Induced platelet aggregation, activates neutrophils, potent eosinophils chemoattractant

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45
Q

Clinical symptoms from inhalation of PAF

A

Bronchospasm, eosinophil infiltration, nonspecific bronchial hyperactivity

46
Q

Protease-activated receptors (PARs)

A

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
Q

Complement system

A

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
Q

Kinin system

A

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
Q

Symptoms of the acute-phase response

A 
Fever
Anorexia
Hypotension
Increased HR
Corticosteroid and ACTH release
50
Q

Example of cytokines that mediate inflammation

A

TNF-a and IL-1

Induce endothelial cells to express adhesion molecule and release cytokines, chemokine, ROS

51
Q

Types of chemokines

A

Inflammatory —> produced in response to bacterial toxins and inflammatory cytokines

Homing —> direct chemotaxis to responsive cells

52
Q

Role of NO in the inflammatory response

A

Smooth muscle relaxation
Antagonism of platelet adhesion, aggregation, degranulation
Serves as leukocyte recruiter
Antimicrobial actions

53
Q

Role of oxygen free radicals in the inflammatory response

A

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
Q

Serous exudate

A

Water fluids low in protein content that result from plasma entering the inflammatory site

55
Q

Hemorrhagic exudate

A

occurs in severe tissue injury that damages blood vessels

There is significant leakage of red cells from capillaries

56
Q

Fibrinous exudate

A

Large amounts of fibrinogen form thick and stick mesh work (much like blood clot)

57
Q

Membranous or pseudomembranous exudate

A

Develop on surface of mucous membranes

Composed of necrotic cells in a fibrinopurulent exudate

58
Q

Purulent/ suppurations exudate

A

Contains pus,composed of degraded white blood cells, proteins, tissue debris

Microorganisms like staph are more likely to induce these

59
Q

Abscess

A

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
Q

Ulceration

A

Site of inflammation where an epithelial surface becomes necrotic and eroded

Often associated with sub epithelial inflammation

61
Q

What might cause ulceration?

A

Any traumatic injury to the epithelial surface (eg: peptic ulcer)

Vascular compromise (foot ulcers associated with diabetes)

62
Q

Chronic Inflammation

A

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
Q

Cause chronic inflammation

A

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
Q

Is the risk of scarring and deformity greater in acute or chronic inflammation?

A

Chronic due to proliferation of fibroblasts

65
Q

Two patterns chronic inflammation

A

Nonspecific

Granulomatous

66
Q

Nonspecific Chronic inflammation

A

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
Q

Granulomatus Lesion

A

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
Q

Epitheloid cells

A

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
Q

Systemic manifestations of inflammation

A

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
Q

Acute phase response

A

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
Q

Obvious signs of acute phase response

A

Fever due to release of cytokines that affect thermoregulatory center in hypothalamus

Anorexia, somnolence, mailaise (due to Il1 and TNFa on the CNS)

72
Q

What induce and increase in the number of circulating neutrophils during the acute phase response?

A

Il2 and other cytokines by stimulating their production in the bone marrow

73
Q

Purpose of skeletal muscle catabolism during acute phase response

A

To provide AAs that can be used for the immune response and tissues repair

74
Q

What causes systemic inflammatory response syndrome?

A

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
Q

Acute phase proteins

A

Liver increases production of these during APR

Fibrinogen, CRP, and serum amyloid A (SAA), upregulated by cytokines

76
Q

CRP

A

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
Q

What in coronary arteries predisposes individuals to thrombosis and MI?

A

Inflammation of atherosclerotic plaques

78
Q

Pathologically, why is ESR increased during a systemic inflammatory response?

A

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
Q

Neutrophilia

A

Selective increase in neutrophils

often caused by bacterial infections

80
Q

Eosinophilia

A

Selective increase in eosinophils

Caused by parasitic or allergic reposnse

81
Q

What causes neutropenia and lymphocytosis together?

A

Viral infections

Neutropenia: decrease in neutrophils
Lymphocytosis: increase in lymphocytes

82
Q

Leukopenia

A

Decrease in white blood cells as a result of overwhelming infections or inability to produce WBCs

83
Q

Lymphadenitis

A

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
Q

Tissue Repair

A

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
Q

Tissue regeneration

A

Replacement of injured tissue with cells of the same type

86
Q

What are the three types of cells based on their ability to undergo regeneration?

A

Labile, stable, permanent

87
Q

Two structures in body organs and tissue

A

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
Q

Labile cells

A

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
Q

Stable cells

A

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
Q

Permanent or fixed cells

A

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
Q

Fibrous Tissue Repair

A

When repair cannot be accomplished with regeneration alone

Rapier occurs by replacement with connective tissues —> generation of granulation and formation of scar tissue

92
Q

Granulation tissue

A

Connective tissue with new capillaries, proliferating fibroblasts, and residual inflammatory cells

Development: angiogenesis, fibrogenesis, and formation of scar tissue

93
Q

Angiogenesis

A

Formation of new capillaries from pre-existing vessels

Eventually will differentiate into arterioles and venules

94
Q

Fibrogenesis

A

Influx of activated fibroblasts —> secrete ECM components (fibronectin, hyaluronic acid, proteoglycans, collagen)

95
Q

Scar formation

A

emigration and proliferation of fibroblasts into site of injury —> disposition of ECM by these cells

96
Q

Final consistency of scar

A

Inactive spindle-shaped fibroblasts, dense collagen fibers, fragment of elastic tissue, ECM components

97
Q

Chemical mediators in tissue regeneration

A

ILs, interferons, TNF-a, and arachidonic acid derivatives (prostaglandins and L) that participate in inflammatory response

98
Q

ECM

A

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
Q

ECM locations

A

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
Q

Functions of ECM

A

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
Q

What type of ECM is critical for regeneration?

A

Intact ECM, especially the basement membrane

102
Q

What is the primary focus of the healing process?

A

Fill the gap created by tissue destruction and to restore the structural continuity of the injured part

103
Q

Primary intention

A

Sutured surgical incision

104
Q

Healing by secondary intention

A

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
Q

Phases of wound healing

A

1- inflammatory phase
2- proliferating phase
3- wound contraction and remodeling phase

Each phase mediated by cytokines and growth factors

106
Q

Inflammatory phase of wound healing

A

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
Q

Proliferative phase of wound healing

A

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
Q

Wound contraction and remodeling phase of wound healing

A

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
Q

Factors that affect wound healing

A

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
Q

Vitamins essential in the healing process

A

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
Q

Implications of hypoxia on wound healing

A

Prevents would healing due to it causing a decrease in fibroblast growth, collagen production, and angiogenesis

Pathophysiology (9 decks)

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