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BSNC 1000 > Module 8 > Flashcards

Module 8 Flashcards

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
Q

Abscess

A

localized area of inflammation containing purulent exudate

central necrotic core + surrounding layer of neutrophils

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26
Q

Ulcer

A

localized inflammation of epithelium + subepithelium

epithelium becomes necrotic + eroded

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27
Q

Resolution of Acute inflammation

A

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

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28
Q

Etiology of Chronic Inflammation

A

1) results from acute inflammation

2) continued exposure to a low-grade irritant

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29
Q

Chronic Inflammation Characteristics

A

infiltration of leukocytes
angiogenesis
fibrosis

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30
Q

Causes of chronic inflammation

A

foreign agents
viruses
bacteria
injured tissue
hypersensitive/inappropriate immune reactions
obesity (white adipose tissue = inflammatory)

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31
Q

Granuloma

A

occurs with chronic inflammation

lesion containing macrophages and lymphocytes

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32
Q

Systemic inflammation

A

occurs when inflammatory mediators enter the circulation

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33
Q

Clinical manifestations of systemic inflammation

A 
acute phase response 
white blood cell count
fever
increased heart rate
anorexia
somnolence
malaise
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34
Q

Acute phase response

A

changes in concentrations of plasma proteins
skeletal muscle catabolism
negative nitrogen balance
increased erythrocyte sedimentation rate (ESR)
leukocytosis

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35
Q

C-Reactive Protein

A

major acute phase protein

involved in opsonization.
CRP levels rise during acute inflammation

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36
Q

White Blood Cell Count

A

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

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37
Q

WBC involved in bacterial infection

A

neutrophils

38
Q

WBC involved in allergic/parasitic infection

A

eosinophil

39
Q

WBC involved in viral infection

A

decrease in neutrophils

increase in lymphocytes

40
Q

Fever

A

increase in body temperature due to a resetting of the thermoregulatory center in the hypothalamus

41
Q

Functions of fever

A

create an inhospitable environment for invading microbes (high temp –> denatures proteins)
increase cellular metabolism –> promote healing

42
Q

Atherosclerosis

A

accumulatio of fatty plaques on the tunica intima of medium and large elastic arteries

causes vessel occlusion –> increased resistance –> increased blood pressure

43
Q

Modifiable Risk Factors

A 
Smoking
Diet 
Obesity
Hyperlipidemia (high LDL (bad), low HDL)
Inflammation
Chronic conditions (diabetes, hypertension, chronic renal disease)
44
Q

Non-modifiable Risk Factors

A 
Age
Gender (men at higher risk)
Family History of cardiovascular disease 
Genetic
Poor lipid metabolism
45
Q

Nontraditional Risk Factor

A

Inflammation caused by C-Reactive Protein

46
Q

Effects of smoking

A 
vasoconstriction
increases blood pressure
reduces myocardial oxygen supply
increases inflammation
oxidation of LDL cholesterol
47
Q

3 Types of Atherosclerotic Plaques

A

1) fatty streaks (non-pathological)
2) fibrous atherosclerosis
3) complicated lesion

48
Q

Fatty streaks

A 
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
Q

Complications from atherosclerosis

A 
angina
coronary artery disease
carotid artery disease
stroke 
peripheral vascular disease
thrombosis/thromboembolism
hypertension 
aneurysms 
endothelial injury
renal disease
50
Q

Complicated atherosclerotic lesion

A

occurs when fibrous plaque breaks open –> release of lipids and cellular debris into bloodstream

can cause a blood clot

51
Q

Endothelial Characteristics

A

single layer of endothelial cells
tight cell junctions
selectively permeable
normally anti-thrombotic (expression of cell adhesion molecules –> margination)

52
Q

Where atherosclerotic plaques

A

bifurcated arteries

areas of turbulent blood flow

53
Q

Foam cells

A

when macrophages ingest oxidized LDL they form foam cells that become compacted in atherosclerotic plaques

54
Q

Clinical Manifestation

A

atherosclerosis is typically asymptomatic until it causes a significant medical event

myocardial infarction
stroke

55
Q

Role of macrophages

A

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
Q

Atherosclerosis of large elastic arteries

A

thrombus formation

aneurysm

57
Q

Atherosclerosis of medium elastic arteries

A

ischemia

infarction

58
Q

Commonly affected organs

A

brain –> stroke
heart –> coronary artery disease, myocardial infarction
kidneys –> renal disease
lower extremities

59
Q

Pathophysiological process

A

1) damage to endothelium
2) migration of inflammatory cells
3) lipid accumulation + smooth muscle proliferation
4) formation of plaque structure

60
Q

Causes of endothelial damage leading to atherosclerosis

A 
hypertension 
hyperlipidemia
high levels of blood insulin due to diabetes
smoking
inflammation
61
Q

Hyperlipidemia

A

elevated levels of cholesterol and triglycerides in blood

62
Q

Dyslipidemia

A

elevated levels of LDL cholesterol or low levels of HDL cholesterol

63
Q

Lipoproteins

A

spherical particles made up of cholesterol, proteins and phospholipids that transport lipids in the bloodstream

64
Q

Four types of lipoproteins

A

chylomicron
very low density lipoprotein
low density lipoprotein
high density lipoprotein

65
Q

Chylomicron

A

made in the small intestine

transports dietary lipids from small intestine –> adipose tissue

66
Q

Very low density lipoprotein

A

made in the liver

transports triglycerides made in the liver –> adipose cells around body

67
Q

Low density lipoprotein

A

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
Q

High density lipoprotein

A

made in the liver

transports excess cholesterol from body tissues to liver for destruction
high HDL cholesterols contributes to heart health

69
Q

What is atherosclerosis

A

is an inflammatory diseases leading to the build up of fatty plaques in large and medium arteries

70
Q

What blood vessels does atherosclerosis affect

A

large and medium sized elastic arteries

71
Q

Where do atherosclerotic plaques typically form

A

bifurcated arteries
curves in area
areas of disturbed blood flow

72
Q

Shear stress

A

parallel frictional force that blood exerts on the endothelial surface

73
Q

Laminar blood flow

A

normal blood flow. concentric layers moving in a parallel direction to the blood vessel
laminar blood flow = high shear stress

74
Q

Turbulent blood flow

A

occurs when blood flow pathway becomes disorganized
caused by atherosclerosis, aneurysm, bifurcated arteries
turbulent blood flow = low shear stress

75
Q

Stages of Atherosclerosis

A

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
Q

Treatment

A

risk factor treatment (chronic conditions)
smoking cessation
dietary modification
lifestyle changes
physical activity
pharmacotherapy (antiplatelet, antiatherogenic)

77
Q

Plaque Stability Factors

A

plaque composition (contents)
wall stress (fibrous cap strength)
size and location of core
configuration of plaque in relation to blood flow

78
Q

Recommended blood cholesterol levels

A

5.18 mmol/L

79
Q

Elevated blood cholesterol

A

5.19-6.18 mmol/L

80
Q

High blood cholesterol

A

> 6.22 mmol/L

81
Q

Recommended HDL levels

A

1.55 mmol/L

82
Q

Low HDL levels

A

1.0-1.55 mmol/L

83
Q

Very low HDL levels

A

<1.0 mmol/L

84
Q

Recommended LDL levels

A

<2.59 mmol/L

85
Q

Elevated LDL levels

A

2.59-4.12 mmol/L

86
Q

High LDL levels

A

> 4.15 mmol/L

87
Q

Recommended Triglyceride levels

A

<1.70 mmol/L

88
Q

Elevated Triglyceride levels

A

> 1.70 mmol/L

89
Q

Acute phase proteins

A

synthesized in the level

serum proteins whos levels decrease/increase by >25% in response to inflammation

90
Q

Positive acute phase proteins

A 
C-reactive protein
Fibrinogen
Alpha-1 antitrypsin
Procalcitonin
Interleukin-1 receptor antagonist
Haptoglobin
Hepodin
91
Q

Negative acute phase proteins

A

Albumin
Transferrin
Transthyretin

BSNC 1000 (10 decks)

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