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Mechanism Of Disease > Lecture 2 and 3 objectives > Flashcards

Lecture 2 and 3 objectives Flashcards

1
Q

list the disease etiologies

A

Microorganisms, hypoxia/ischemia, nutritional deficiencies, trauma/surgery, radiation, caustic chemicals, extreme heat or cold

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2
Q

What is the first line of defense?

A

skin and mucous membranes (tears, saliva, gut flora, stomach acid)

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3
Q

What is the second line of defense?

A

inflammatory response (nonspecific, acute inflammation is an expected response to injury)

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4
Q

What is the third line of defense?

A

immune reponse

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5
Q

When does immediately transient response occur?

A

following a minor injury, active for a few minutes or hours (slap to the face)

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6
Q

When does immediate sustained occur>

A

following a major injury, vascular, and active for a few days because more extensive damage has occurred (pathogen response while blistering)

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7
Q

When does a delayed hemodynamic occur?

A

approximately 4-24 hours after an injury (Sun burn)

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8
Q

What do vascular changes in the acute inflammation process entail?

A

increased blood flow to the injury site and increased blood vessel permeability at the injury site

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9
Q

What two major anatomic changes happen in vascular response?

A

vasodilation, increased permeability

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10
Q

What are the benefits of increasing permeability during the vascular response?

A

helps plasma and cells get to the site of injury while also making it difficult for infectious agents o move away from the injury site-prevents the spread of the foreign/offending agents

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11
Q

How does increased permeability occur?

A

endothelial cells that are lining the vessels contract, separating the intercellular junction

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12
Q

What marks the start of the cellular response

A

Movement of phagocytic white blood cells into the area of injury

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13
Q

How long does it take neutrophils to arrive to site of injury? How long can they survive?

A

arrive within 90 minutes. They survive approximately 10 hours

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14
Q

Benefits of neutrophils arriving to scene?

A

Causes increase in circulating WBCs, immature forms of neutrophils may be released

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15
Q

what is leukocytosis?

A

increase in numbers of WBC

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16
Q

When do Eosinophils pull up?

A

Allergic reactions and parasitic infections

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17
Q

When do basophils pull up? what do they do?

A

inflammation and allergic reactions, release histamine, bond with IgE

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18
Q

When do Mast Cells pull up? What do they do?

A

Similar to basophils, but in Connective Tissue. Found in mucosal surfaces-lung, GI tract, dermis. They’re in the Sentinel position. Allergic reaction, parasitic infections. Also bond with IgE

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19
Q

When do monocytes pull up?

A

approximately 24 hours after injury

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20
Q

Characteristics of Monocytes

A

Largest WBCs, significantly longer lifespan than PMNs, arrive 24 hours after injury, they are the predominant cell in injury cite approximately 48 hours after injury, engulf larger and greater quantities of foreign material than neutrophils, play a role in adaptive immune response

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21
Q

List the four steps in cellular response

A

Margination/adhesion
Migration (diapedesis)
Chemotaxis
Phagocytosis

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22
Q

What happens during margination/adhesion

A

injury causes relapse of chemical mediators (cytokines)
Increased expression of adhesion molecules (selectins)
Leukocytes slow migration and begin marginating (pavementing) along periphery of vessels
Adhesion to vessel walls allows us to advance to the next step

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23
Q

What happens during diapedesis?

A

Leukocytes extend pseudopods and pass through the capillary wall via ameboid movement

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24
Q

What happens during chemotaxis?

A

Leukocytes travel through the tissue to the site of injury
Cytokines and complement (cytokines are released by damaged cell)

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25
Q

What happens during Phagocytosis?

A

Recognition and attachment +opsonization
engulfment
intracellular killing

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26
Q

What is the most important kinin in the inflammatory response?

A

Bradykinin

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27
Q

What functions does bradykinin have?

A

Vasodilation and increased permeability, smooth muscle contraction, involved with pain response

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28
Q

what are kinins broken down by?

A

kininase and angiotensin-converting enzyme

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29
Q

Key protease enzyme in the clotting process?

A

Thrombin

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30
Q

What are fibrinopeptides and thrombin functions?

A

Expression of endothelial adhesion molecules, production of prostaglandins, PAF, and chemokines

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31
Q

Where are complements found?

A

They’re present in inactive form in plasma

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32
Q

What do complement proteins do once activated?

A

Activated to become proteolytic enzymes that degrade other complement proteins in a cascade

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33
Q

what are some complement functions?

A

Vasodilation, increased vascular permeability, smooth muscle contraction, leukocyte activation, adhesion, and chemotaxis, augmentation of phagocytosis, and mast cell degredation

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34
Q

Most important complements

A

C3a, C5a

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35
Q

What cells release histamines?

A

mast cells, basophils, and platelets?

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36
Q

Histamine functions

A

one of the first mediators of inflammation, major role in vascular inflammatory response via the H1 receptor, Increase vasodilation, increase vascular permeability

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37
Q

List of cytokines (5)

A

chemokine, interferons (IFNs), interleukins (ILs), lymphokines, and tumor necrosis factor (TNF)

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38
Q

what are two cytokines that are major mediators of early inflammatory response?

A

Interleukin-1 and Tumor necrosis factor-alpha

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39
Q

what are IL-1 and TNF-alpha responsible for?

A

fever, adhesion of leukocytes to vessel epithelial, chemotaxis, and acute phase response. Also involved in pain response.

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40
Q

What is arachidonic acid?

A

a fatty acid precursor

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41
Q

where is arachidonic acid derived from?

A

phospholipids in the cell membrane

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42
Q

What is arachidonic acid a precursor for?

A

prostaglandins, leukotrienes, thromboxane

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43
Q

what is derived from the cyclooxyrgenase pathway?

A

prostaglandins and thromboxane

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44
Q

what is derived from the lipooxygenase pathway?

A

leukotrienes

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45
Q

What are prostaglandins responsible for?

A

vascular permeability and vasodilation, involved in pain response, also makes Prostaglandin E1, and Prostaglandin E2 (both induce inflammation and potentiate effects of other inflammatory mediators, especially histamine, thromboxane A2-promotes platelet aggregation and vasoconstriction

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46
Q

What inhibits the cyclooxygenase pathway for prostaglandin and thromboxane synthesis?

A

NSAIDS and Aspirin

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47
Q

What do PGE1 and PGE2 do?

A

induce inflammation and potentiate effects of other inflammatory mediators, especially histamine

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48
Q

What does Thromboxane A2 do?

A

promote platelet aggregation and vasoconstriction

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49
Q

What do leukotrienes do?

A

similar function to histamine
vascular permeability, adhesion of endothelial cells, chemotaxis, further histamine release
Slow reacting substance of anaphylaxis (SRS-A) group of leukotrienes-causes slow and sustained constriction of bronchioles

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50
Q

What are the leukotriene receptor antagonists used for?

A

used for the treatment of asthma

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51
Q

what blocks the lipoxygenase pathway from synthesizing leukotrienes

A

5-lipoxygenase inhibitor

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52
Q

Where are platelet activating factors derived from ?

A

cell membrane phospholipids

53
Q

What is the function of Platelet activating factor?

A

induces platelet aggregation, stimulates platelets to release vasoactive mediators and synthesize thromboxane, increased vascular permeability, neutrophil activation, chemoattractant for eosinophils

54
Q

What does nitric oxide do?

A

Smooth muscle relaxation, antagonism of platelet functions (adhesion, aggregation, degranulation), reduction of leukocyte recruitment, assists in microbicidal action by phagocytes

55
Q

Lymphadenitis etiology

A

inflamed lymph nodes that are draining an injured area, caused by the filtering lymph fluid that contains infectious or necrotic material form the local, injured/infected area.

(free and non moving lymph node: not good-can be cancer)

56
Q

Etiology of lymphangitis

A

inflammation of infection of lymph channels draining in an injured area.

Entire lymph vessel is inflamed and points to the site of injury

57
Q

Pathogenesis of lymphadenitis

A

Swollen, tender, mobile/moving, rubbery, may be erythematous, or fluctuant

58
Q

Pathogenesis of lymphangitis

A

MCC streptococcus pyogenes and appears as red, tender streaks that extend proximally

59
Q

Treatment of lymphadenitis or lymphangitis

A

antimicrobial therapy, anti-inflammatories, analgesics, cool compress

60
Q

What happens in Erythrocyte sedimentation rate?

A

increased levels of acute-phase proteins, especially fibrongen, causes an increase in the erythrocyte sedimentation rate

61
Q

C-reactive protein

A

binds to surface of invading microorganisms to assist their destruction
also aids with regulating immune response, clearance of necrotic cells
can help diagnose or measure activity of inflammatory or autoimmune disease
elevated CRP is associated with increased cardiovascular disease risk

62
Q

what conditions can cause an elevation in C-reactive protein?

A

hypertension, diabetes, smoking, aging, obesity, depression,

63
Q

what is an elevated C-reactive protein count indicative of?

A

inflammation

64
Q

what are the 5 cardinal signs of inflammation?

A

erythema, heat, swelling, pain, loss of function

65
Q

what cases erythema?

A

vasodilation

66
Q

what causes heat to be a cardinal sign of inflammation

A

blood is warm

67
Q

what causes swelling?

A

increased vascular permeability and increased fluid in extracellular space

68
Q

what causes pain in inflammation?

A

compression in tissue due to swelling; direct elicitation of pain due to inflammatory mediators

69
Q

what causes loss of function from inflammation?

A

direct damage to tissue from injury, decreased function due to pain and swelling

70
Q

5 major types of shock

A

cariogenic, hypovolemic, anaphylactic, neurogenic, septic

71
Q

what are the three types of distributive shock

A

anaphylactic, septic, neurogenic

72
Q

what causes cardiogenic shock?

A

inability of heart to pump the required amount of blood. caused by cardiac arrhythmias, damaged heart muscle or valves, pressure around heart inhibiting cardiac movement, rupture of heart muscle

73
Q

what causes hypovolemic shock?

A

deceased intravascular volume leading to decreased perfusion of vital organs. Can be caused by hemorrhage or fluid loss

74
Q

What causes septic shock?

A

systemic vasodialtion secondary to infection and dysregulation of inflammatory response

75
Q

what largely mediates septic shock?

A

Interleukin 1 and tumor necrosis factor alpha

76
Q

what causes anaphylactic shock?

A

severe, rapid allergic or hypersensitivity reaction with potential to be fatal

77
Q

What causes neurogenic shock?

A

damage to the autonomic pathways within the CNS

78
Q

How does septic shock affect the circulatory system?

A

severe hypotension and hypo perfusion
excessive vasoactive mediators, decreasing vascular reisstance
third spacing of fluid, increased vascular permeability

79
Q

How does septic shock affect the lungs?

A

Pulmonary edema and hypoxia

80
Q

how goes septic shock affect the GI tract?

A

increased intestinal permeability allowing bacteria and bacterial endotoxins in gut to enter systemic circulation

81
Q

how does septic shock affect the liver

A

impaired elimination of bacteria and endotoxins from gut due to direct cellular injury

82
Q

how does septic shock affect the kidney?

A

impaired filtration of toxins and waste products from blood due to hypo perfusion and direct renal damage

83
Q

how does septic shock affect the nervous system?

A

encephalopathy due to changes in cell signaling caused by inflammatory mediators dysfunction of blood-brain barrier

84
Q

four steps of tissue repair in terms and the approximate time table

A
  1. hemostasis (right away)
  2. inflammation (approx 90 min)
  3. proliferation
  4. remodeling
85
Q

what does hemostasis include?

A

clotting, vascular response

86
Q

what does proliferation include?

A

epithelial healing, scar formation

87
Q

what does remodeling include?

A

scar remodeling includes decrease in fibroblasts, decrease in blood vessels, increase in collagen

88
Q

what are the three possible outcomes of scar remodeling

A

resolution, regeneration, replacement

89
Q

when does resolution occur?

A

very mind injury, with minimal disruption (rapid healing, minimal to no scaring)

90
Q

when does regeneration occur?

A

primary with labile or stable cell types
cells can either:
proliferate (reproduce and grow)
differentiate (local cells mature and become specialized)
Diapedesis may occur (local similar cells migrate to replace lost or damaged cells)

91
Q

What happens during replacement?

A

production of scar tissue when regeneration is not possible (usually seen in injuries to permanent cells, extensive or major injuries)

92
Q

List the four types of growth factors

A

Vascular endothelial growth factor
Platelet derived growth factor
fibroblast growth factor
Epithelial growth factor

93
Q

what do the growth factors do?

A

mediate proliferation, differentiation, and cell metabolism, mediate inflammatory response, promote chemotaxis of leukocytes and fibroblasts, stimulate angiogenesis, contribute to generation of ECM

94
Q

What types of cells produce vascular endothelial growth factor?

A

oxygen deficient cells

95
Q

what are the 4 major steps of angiogenesis

A
  1. Proteolytic degradation of parent vessel basement membrane (capillary sprout forms)
  2. Migration of endothelial cells from parent vessel towards the angiogenic stimulus
  3. Proliferation of endothelial cells behind the leading edge of migrating cells
  4. maturation of endothelial cells and vessel walls
96
Q

what is angiogenesis?

A

formation of new capillaries

97
Q

what is diapedesis?

A

cells moving from the blood vessels to the tissue

98
Q

What are interns?

A

transmembrane proteins that allow for attachment to the ECM and communication between intracellular and extracellular environments

99
Q

What do fibroblasts do in respect to wound healing?

A

Fibroblasts secrete collagen, produce growth factors that encourage the healing process, help convert provisional matrix to granulation tissue, lay down new collagen during remodeling process

100
Q

What do endothelial cells do in respect to wound healing?

A

aid in re-epitheliazation and laying down new borders of the epithelium between the wound and external environment, also important in angiogenesis

101
Q

what do macrophages do in respect to wound healing?

A

remove foreign matter and invading organisms, extracellular debris, damaged fibrin and cell fragments
they release growth factors to stimulate cell growth, fibroblast attraction and angiogenesis
also help convert the provisional matrix to granulation tissue

102
Q

What does collagen do in respect to wound healing?

A

aid in the remodeling of scar tissue

103
Q

What affects healing process?

A

type of tissue damaged, extent of injury, underlying host factors, age, foreign bodies, blood flow and oxygenation

104
Q

What is parenchyma tissue? + an example

A

functioning cells of an organ or body part?

(IE myocyte, hepatocyte, nephron)

105
Q

what is stromal tissue? + an example

A

connective, supportive framework that supports the function of the parenchymal tissue

(IE connective tissue, extracellular matrix)

106
Q

What are labile cells? + an example

A

cells that continually divide and replicate
(IE epithelial cells- skin, oropharynx, GI tract, Bone marrow)

107
Q

what are stable cells? +an example

A

normally stop dividing when growth ceases, but can regenerate when given appropriate stimulus
must have supporting stromal framework to regenerate properly

(IE hepatocytes, smooth muscle cells)

108
Q

What are permanent cells +an example

A

Cannot regenerate or divide

(IE neurons, cardiac myocytes, ocular lens)

109
Q

What is Vitamin C used for?

A

collagen

110
Q

What are the systemic manifestation of chronic inflammation?

A

fever, malaise, fatigue, anemia, anorexia (weight loss)

111
Q

Explain the pathogenesis of chronic granulomatous inflammation and associated diseases and distinguish it from granulation tissue.

A

+Nodular inflammatory lesions that encase substance that are not easily destroyed by usual inflammatory and immune responses
-Foreign bodies or pathogens
+Macrophages adapt to address the foreign body
-Giant cells (multinucleated, surround large particles) or epithelioid cells (surround and contain the offending agent and the macrophages processing it)
+Fibrous tissue eventually surrounds and encapsulates the inflamed area: macrophages phagocytize harmful substances within granuloma and fill with necrotic remains to limit the foreign material from spreading to the rest of the body

112
Q

Explain how chronic inflammation causes disease in terms of the cellular mechanisms, cytokine effects, and tissue pathology.

Nonspecific chronic inflammation:

A

-Diffuse accumulation of macrophages and lymphocytes at the site of injury
-Cytokines produced leads to persistent chemotaxis of leukocytes/fibroblasts
-Significant scar tissue forms and replaces normal stromal/parenchymal tissues -This causes loss of normal structure/function of tissue
n in the body by blocking ferroportin which carries RBC, this causes anemia
-IL-1, TNF-alpha and IFN-gamma also play a role in inhibiting erythropoietin release and augmenting RBC phagocytosi

113
Q

Explain how chronic inflammation causes disease in terms of the cellular mechanisms, cytokine effects, and tissue pathology.

+Cancer and inflammation:

A

-Inflammatory response to abnormal or damaged cells. Tumor cells often have abnormal markers and outgrow their supply of nutrients which leads to cell distress/ischemia
-Cytokine response leads to angiogenesis and influx of new nutrients
-Growth factors promote reproduction of cancer cells and new vessels
-Proteases and ECM remodeling enhances ability to grow and spread

114
Q

Explain how chronic inflammation causes disease in terms of the cellular mechanisms, cytokine effects, and tissue pathology.

+Anemia and inflammation:

A

-Prolonged inflammation leads to IL-6 production which increase hepcidin by the liver
-Hepcidin reduces iron in the body by blocking ferroportin which carries RBC, this causes anemia
-IL-1, TNF-alpha and IFN-gamma also play a role in inhibiting erythropoietin release and augmenting RBC phagocytosis

115
Q

Types of plasma proteins?

A

Complement proteins, kinins, and clotting system

116
Q

What is involved in pain response?

A

cytokines, prostaglandins, bradykinins

117
Q

what release histamines?

A

Mast cells, basophils, and platelets

118
Q

What stops cell membrane phospholipids from making arachidonic acid?

A

corticosteroid medication

119
Q

what are chemical mediators?

A

cytokines

120
Q

list out the types of cytokines

A

chemokine, interferons, interleukins, lymphokines, and tumor necrosis factor

121
Q

list out inflammatory mediators

A

plasma proteins, histamine, interleukin and other cytokines, platelet activating factor, prostaglandins, leukotrienes.

122
Q

where are c-reactive proteins made?

A

liver

123
Q

where are fibrinogens created?

A

liver

124
Q

what is granulation tissue made up of?

A

new capillaries, proliferating fibroblasts, and residual inflammatory cells

125
Q

What do fibroblasts secrete for ECM components?

A

fibronectin, hylauronan, proteoglycans, and collagen

126
Q

what are proteins used for?

A

needed for mediation of inflammatory phase, fibroblast proliferation, collagen synthesis, angiogenesis, and remodeling

127
Q

what are carbohydrates used for?

A

needed for energy for WBCs and reduce use of proteins for energy

128
Q

What are fats used for?

A

needed for synthesis of new cells

Mechanism Of Disease (3 decks)

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