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BSNC 1000 > Module 8 > Flashcards

Module 8 Flashcards

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1
Q

Definition

A

inflammation is a normal immunological response to tissue damage (injury or infection)

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2
Q

Inflammatory cells

A 
Neutrophils
Eosinophils
Basophils
Mast cells 
Platelets
Monocytes/Macrophages
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3
Q

Inflammatory Mediators

A

cytokines that contribute to an inflammatory response
located in the plasma or produced by local cells

prostaglandins
leukotrienes
histamine

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4
Q

Histamine

A

released by basophils and mast cells
early acute inflammatory response

vasodilation
increase vascular permeability
pain production

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5
Q

Prostaglandins/Leukotrienes

A

derived from plasma membrane phospholipids
produced by various tissue cells
later acute inflammatory response

vasodilation
increase vascular permeability
anaphylactic hypersensitive reactions

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6
Q

Bradykinins

A

plasma protein

vasodilation
increase vascular permeability
pain production

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7
Q

Types of Inflammation

A

Acute
Chronic
Systemic

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8
Q

Stages of Acute Inflammation

A

Vascular

Cellular

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9
Q

5 Cardinal Signs of Inflammation

A 
Redness
Swelling
Pain
Warmth
Partial loss of function
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10
Q

Vascular stage of AI

A

1) stimulation of local mast cells/tissue areas –> release of inflammatory mediators (prostaglandins, leukotrienes, histamine)
2) inflammatory mediators –> retraction of endothelial cells –> leaking of exudate –> edema (swelling, pain)
3) inflammatory mediators –> relax smooth muscle –> vasodilation –> increased blood flow (warmth, redness)

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11
Q

Cellular stage of AI

A

1) margination: inflammatory mediators cause endothelial cells to present cell adhesion molecules (proteins) on membrane. circulating WBC’s attach to CAMs and begin to “roll” down endothelium
2) adhesion: WBCs eventually fully adhere to endothelial lining due to cell adhesion molecules (selectin)
3) transmigration: white blood cells begin to squeeze through intercellular gaps caused by endothelial retraction
4) chemotaxis: release of chemokines attract white blood cells to injured area
5) activation + phagocytosis: neutrophils + macrophages

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12
Q

Function of Inflammation

A

1) clear cellular debris
2) dilute toxin/infectious agent
3) promote healing / prepare tissue for repair

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13
Q

Opsonization

A

molecules bind to antigens and flag them for phagocytosis. facilitate the adhesion of microbes and phagocytes

complement proteins, antibodies,

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14
Q

Plasma-derived inflammatory mediators

A

liver proteins

1) complement proteins –> involved in various functions of the immune system
2) clotting proteins –> hemostasis
3) acute phase proteins –> involved in systemic infection

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15
Q

Cell-derived inflammatory mediators

A

preformed granules found in local cells or synthesized by cells upon stimulation
produced by

mast cells
neutrophils
platelets
monocytes/macrophages

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16
Q

Serotonin

A

inflammatory mediator released by platelets

vasodilation
increased vascular permeability

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17
Q

Prostaglandin formation

A

formed from arachidonic acid + cyclooxygenase enzyme

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18
Q

Leukotriene formation

A

formed from arachidonic acid + lipooxygenase enzyme

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19
Q

Cytokines

A

proteins expressed by immune and other cells involved in chemical messaging
modulate function of nearby cells
paracrine (outside cells) + autocrine (same cell) function

produced by
macrophages + lymphocytes
endothelial cells
epithelial cells
fibroblasts
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20
Q

Cytokines released by macrophages

A

activated macrophages release tumor necrosis factor alpha (TNF-a) and interleukin-1 in response to inflammation

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21
Q

TNF-a & IL-1 Effects

A

cause endothelial cells to express cell adhesion molecules
stimulate release of cytokines, chemokines, reactive oxygen species
margination of neutrophils
activate systemic inflammation acute-phase response

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22
Q

Chemokines

A

type of cytokine involved in chemotaxis

chemoattracts that recruit + direct inflammatory + immune cells

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23
Q

Exudate

A

fluid that leaks from blood vessel –> interstitial fluid

fluid, plasma proteins, leukocytes

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24
Q

Types of exudate

A 
fibrous (high levels of fibrinogen --> fibrin)
serous (watery, blister)
hemorrhagic (blood)
purulent (pus)
sanguinous (oozing)
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25
Abscess
localized area of inflammation containing purulent exudate central necrotic core + surrounding layer of neutrophils
26
Ulcer
localized inflammation of epithelium + subepithelium epithelium becomes necrotic + eroded
27
Resolution of Acute inflammation
1) recovery --> normal function restored 2) progression to chronic inflammation --> occurs when offending agent not removed 3) scarring/fibrosis --> results from significant injury or nonregenerative tissue
28
Etiology of Chronic Inflammation
1) results from acute inflammation | 2) continued exposure to a low-grade irritant
29
Chronic Inflammation Characteristics
infiltration of leukocytes angiogenesis fibrosis
30
Causes of chronic inflammation
foreign agents viruses bacteria injured tissue hypersensitive/inappropriate immune reactions obesity (white adipose tissue = inflammatory)
31
Granuloma
occurs with chronic inflammation lesion containing macrophages and lymphocytes
32
Systemic inflammation
occurs when inflammatory mediators enter the circulation
33
Clinical manifestations of systemic inflammation
``` acute phase response white blood cell count fever increased heart rate anorexia somnolence malaise ```
34
Acute phase response
changes in concentrations of plasma proteins skeletal muscle catabolism negative nitrogen balance increased erythrocyte sedimentation rate (ESR) leukocytosis
35
C-Reactive Protein
major acute phase protein involved in opsonization. CRP levels rise during acute inflammation
36
White Blood Cell Count
in response to infection, bone marrow is stimulated to increase production of WBCs to defend against infection values increase from 4000-10000 cells/uL to 15000-20000 cells/uL
37
WBC involved in bacterial infection
neutrophils
38
WBC involved in allergic/parasitic infection
eosinophil
39
WBC involved in viral infection
decrease in neutrophils | increase in lymphocytes
40
Fever
increase in body temperature due to a resetting of the thermoregulatory center in the hypothalamus
41
Functions of fever
create an inhospitable environment for invading microbes (high temp --> denatures proteins) increase cellular metabolism --> promote healing
42
Atherosclerosis
accumulatio of fatty plaques on the tunica intima of medium and large elastic arteries causes vessel occlusion --> increased resistance --> increased blood pressure
43
Modifiable Risk Factors
``` Smoking Diet Obesity Hyperlipidemia (high LDL (bad), low HDL) Inflammation Chronic conditions (diabetes, hypertension, chronic renal disease) ```
44
Non-modifiable Risk Factors
``` Age Gender (men at higher risk) Family History of cardiovascular disease Genetic Poor lipid metabolism ```
45
Nontraditional Risk Factor
Inflammation caused by C-Reactive Protein
46
Effects of smoking
``` vasoconstriction increases blood pressure reduces myocardial oxygen supply increases inflammation oxidation of LDL cholesterol ```
47
3 Types of Atherosclerotic Plaques
1) fatty streaks (non-pathological) 2) fibrous atherosclerosis 3) complicated lesion
48
Fatty streaks
``` yellow lines found on major arteries do not cause atherosclerosis but can progress into fibrous plaques develop early (8 years old) but do not cause clinical complications ``` made up of smooth muscle cells filled with cholesterol + macrophages
49
Complications from atherosclerosis
``` angina coronary artery disease carotid artery disease stroke peripheral vascular disease thrombosis/thromboembolism hypertension aneurysms endothelial injury renal disease ```
50
Complicated atherosclerotic lesion
occurs when fibrous plaque breaks open --> release of lipids and cellular debris into bloodstream can cause a blood clot
51
Endothelial Characteristics
single layer of endothelial cells tight cell junctions selectively permeable normally anti-thrombotic (expression of cell adhesion molecules --> margination)
52
Where atherosclerotic plaques
bifurcated arteries | areas of turbulent blood flow
53
Foam cells
when macrophages ingest oxidized LDL they form foam cells that become compacted in atherosclerotic plaques
54
Clinical Manifestation
atherosclerosis is typically asymptomatic until it causes a significant medical event myocardial infarction stroke
55
Role of macrophages
increased cholesterol levels increase macrophage & endothelial cellular reactions macrophages burrow into tunica media --> release inflammatory mediators that result in local inflammation oxidation of LDL --> endothelial injury when macrophages ingest oxidized LDL --> foam cells
56
Atherosclerosis of large elastic arteries
thrombus formation | aneurysm
57
Atherosclerosis of medium elastic arteries
ischemia | infarction
58
Commonly affected organs
brain --> stroke heart --> coronary artery disease, myocardial infarction kidneys --> renal disease lower extremities
59
Pathophysiological process
1) damage to endothelium 2) migration of inflammatory cells 3) lipid accumulation + smooth muscle proliferation 4) formation of plaque structure
60
Causes of endothelial damage leading to atherosclerosis
``` hypertension hyperlipidemia high levels of blood insulin due to diabetes smoking inflammation ```
61
Hyperlipidemia
elevated levels of cholesterol and triglycerides in blood
62
Dyslipidemia
elevated levels of LDL cholesterol or low levels of HDL cholesterol
63
Lipoproteins
spherical particles made up of cholesterol, proteins and phospholipids that transport lipids in the bloodstream
64
Four types of lipoproteins
chylomicron very low density lipoprotein low density lipoprotein high density lipoprotein
65
Chylomicron
made in the small intestine transports dietary lipids from small intestine --> adipose tissue
66
Very low density lipoprotein
made in the liver transports triglycerides made in the liver --> adipose cells around body
67
Low density lipoprotein
formed in the blood by the removal of triglycerides from VLDLs transports 75% of cholesterol in the bloodstream high LDL cholesterol contributes to atherosclerosis
68
High density lipoprotein
made in the liver transports excess cholesterol from body tissues to liver for destruction high HDL cholesterols contributes to heart health
69
What is atherosclerosis
is an inflammatory diseases leading to the build up of fatty plaques in large and medium arteries
70
What blood vessels does atherosclerosis affect
large and medium sized elastic arteries
71
Where do atherosclerotic plaques typically form
bifurcated arteries curves in area areas of disturbed blood flow
72
Shear stress
parallel frictional force that blood exerts on the endothelial surface
73
Laminar blood flow
normal blood flow. concentric layers moving in a parallel direction to the blood vessel laminar blood flow = high shear stress
74
Turbulent blood flow
occurs when blood flow pathway becomes disorganized caused by atherosclerosis, aneurysm, bifurcated arteries turbulent blood flow = low shear stress
75
Stages of Atherosclerosis
1) endothelial injury 2) migration of LDL into subendothelial space 3) oxidation of LDL 4) migration of monocytes/macrophages 5) phagocytosis and development of foam cells 6) apoptosis of foam cells --> build up of fatty plaque --> release of cytokines that attract more WBCs 7) growth factors released by macrophages stimulate smooth muscle proliferation + development of fibrous cap 8) smooth muscle cells cause calcification of fatty plaque
76
Treatment
risk factor treatment (chronic conditions) smoking cessation dietary modification lifestyle changes physical activity pharmacotherapy (antiplatelet, antiatherogenic)
77
Plaque Stability Factors
plaque composition (contents) wall stress (fibrous cap strength) size and location of core configuration of plaque in relation to blood flow
78
Recommended blood cholesterol levels
5.18 mmol/L
79
Elevated blood cholesterol
5.19-6.18 mmol/L
80
High blood cholesterol
>6.22 mmol/L
81
Recommended HDL levels
1.55 mmol/L
82
Low HDL levels
1.0-1.55 mmol/L
83
Very low HDL levels
<1.0 mmol/L
84
Recommended LDL levels
<2.59 mmol/L
85
Elevated LDL levels
2.59-4.12 mmol/L
86
High LDL levels
>4.15 mmol/L
87
Recommended Triglyceride levels
<1.70 mmol/L
88
Elevated Triglyceride levels
>1.70 mmol/L
89
Acute phase proteins
synthesized in the level | serum proteins whos levels decrease/increase by >25% in response to inflammation
90
Positive acute phase proteins
``` C-reactive protein Fibrinogen Alpha-1 antitrypsin Procalcitonin Interleukin-1 receptor antagonist Haptoglobin Hepodin ```
91
Negative acute phase proteins
Albumin Transferrin Transthyretin

BSNC 1000 (10 decks)

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