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N116 > inflammation > Flashcards

inflammation Flashcards

1
Q

inflammation

A

immunologic defence against tissue injury, infection or allergy

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2
Q

function of inflammatory response

A

restitution of normal, functioning cell after injury

fibrous repair when restitution of functioning cells is impossible

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3
Q

injuries that cause inflammation

A

mechanical, thermal, electrical, chemical, radiation, biological assault

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4
Q

steps of inflammatory response (8)

TVSIMEMR

A
  1. tissue injury - release of chemical mediators
  2. vasodilation + increase blood flow
  3. swelling + retraction of endothelial cells
  4. increased vascular permeability + leakage of small plasma proteins
  5. movement of immune response cells to injury site
  6. exudate formation
  7. movement of glucose + oxygen to injury site
  8. release of chemical repair factors from endothelial cells
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5
Q

populations at greatest risk

A

very young
very old
uninsured

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6
Q

exposure to secondhand smoke

A

smoke irritates eyes and mucous membranes of respiratory tract. irritation causes inflammation

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7
Q

excessive exposure to sun

A

results in sun burn (thermal injury)

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8
Q

exposure to infection

A

infection always accompanied by inflammation

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9
Q

rheumatoid arthritis

A

inflammation of joints and surrounding tissues

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10
Q

first line of defence is?

A 
innate immunity (natural)
physical, mechanical, biochemical barriers
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11
Q

second line of defence is?

A

inflammatory response

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12
Q

third line of defence is?

A

adaptive immunity (acquired)

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13
Q

physical barriers
describe
line of defence

A 
1st line of defence
- skin
- lining of gastrointestinal, genitourinary, respiratory tract 
> sloughing of cells
> coughing and sneezing
> flushing - urine
> vomiting
> mucous and cilia
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14
Q

epithelial cell-derived chemical barriers
describe
line of defence

A

1st line of defence

  • secrete saliva, tears, earwax, sweat and mucous
  • antimicrobial peptides
  • normal microbiome
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15
Q

inflammatory response
describe
line of defence

A

nonspecific

regulated by chemical mediators

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16
Q

what materials cause inflammatory response

A

infection, tissue necrosis, ischemia, trauma, physical/chemical injury, foreign bodies, immune reaction

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17
Q

local manifestations of inflammatory response

A

redness, heat, swelling, pain, loss of function

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18
Q

inflammatory response

vascular

A

vasodilation
increased vascular permeability and leakage
WBC adherance to inner wall of vessels

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19
Q

goals of inflammation

A

prevent/limit infection or further damage
limit/control immune response
initiate adaptive immune response
initiate healing

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20
Q

list three protein systems

A

complement
clotting
kinin

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21
Q

complement system

A

produces biologically active fragments that recruit phagocytes, activate mast cells and destroy pathogens

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22
Q

activation of C3 and C5

A

most important to complement system
opsonins
chemotactic factors
anaphylatoxins

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23
Q

pathways of complement system

CAL

A

classical: antigen-antibody reaction
alternative: bacterial endotoxin
lectin: independent of antibody

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24
Q

clotting system

A

forms blood clots at an injured/inflamed site

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25
Q

what do blood clots do

A

prevents spread of infection
localizes micro organisms and foreign bodies
stops bleeding
framework for repair/healing

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26
Q

main substance in clotting system

A

insoluble protein - fibrin

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27
Q

pathways of clotting system

A

extrinsic: activated by tissue factor
intrinsic: factor XII

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28
Q

kinin system

A

activate and assist inflammatory cells

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29
Q

primary kinin

A

bradykinin

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30
Q

what does the kinin system do

A

cause dilation o blood vessels and smooth muscle contraction, induces pain, increase vascular permeability

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31
Q

cellular components of inflammation

EPL

A

erythrocytes
platelets
leukocytes

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32
Q

types of leukocytes

A

granulocytes
monocytes
lymphocytes

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33
Q

cellular receptors of inflammation

A

bind a large spectrum of antigens

different receptors recognize specific molecules

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34
Q

types of receptors

PPDTCSN

A
  • Pattern recognition receptors (PRRs)
  • Pathogen-associated molecular patterns (PAMPs)
  • Damage-associated molecular patterns (DAMPs)
  • Toll-like receptors (TLRs)
  • Complement receptors
  • Scavenger receptors
  • NOD-like receptors (NLRs)
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35
Q

what are cytokines responsible for

A

activating other cells and regulating inflammatory response

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36
Q

cytokines can be either

A

pro-inflammatory (induce)

anti-inflammatory (inhibit)

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37
Q

types of cytokines

CITI

A

chemokines
interleukins
tumor necrosis factor-alpha
interferon

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38
Q

chemokines synthesized by

pro or anti

A

different cells in response to pro-inflammatory cytokines

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39
Q

chemokines induce

A

chemotaxis to promote phagocytes and wound healing

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40
Q

examples of chemokines

A
  • monocyte/macrophage chemotactic proteins
  • macrophage
    inflammatory response
  • neutrophils
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41
Q

interleukins produced by

A

macrophages and lymphocytes in response to stimulationof PRRs or other cytokines
many types

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42
Q

examples of interleukins

A

IL-1 proinflammatory

IL-10 anti-inflammatory

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43
Q

tumour necrosis factor-alfa secreted by

A

macrophages in response to PAMP and toll-like receptor recognition

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44
Q

tumour necrosis factor-alfa induces

A

fever

acts as endogenous pyrogen

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45
Q

tumour necrosis factor-alfa increases

A

synthesis of inflammatory serum proteins

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46
Q

tumour necrosis factor-alfa causes

A

muscle wasting and intravascular thrombosis

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47
Q

high levels of tumour necrosis factor-alfa can be

A

lethal

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48
Q

interferons protect against

A

viral infections

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49
Q

interferons produced and released by

A

virally infected host cells in response to viral DS RNA

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50
Q

types of interferons

A

IFN-a and INF-b:
induce production of antiviral proteins
IFN-y:
increase microbiocidal activity of macrophages

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51
Q

mast cells

A

cellular bags of granules located in the

loose connective tissues close to blood vessels

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52
Q

mast cells contain

A

histamine, cytokines, and chemotaxic factors

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53
Q

mast cells release

A

degranulation

synthesis

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54
Q

mast cell degranulation

A

release of the contents of mast cell granules

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55
Q

mast cells synthesis

A

new production and release of mediators in response to stimulus

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56
Q

mast cell degranulation

histamine

A

-vasoactive amine
causes temporary, rapid constriction of large blood vessels and dilation of postcapillary venules
- retraction of endothelial cells lining the capillaries causing increased vascular permeability

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57
Q

mast cell degranulation

receptors

A

H1 and H2

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58
Q

H1 receptor

A

pro-inflammatory

present in smooth muscle cells of the bronchi

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59
Q

H2 receptor

A

anti-inflammatory
present on parietal cells of the stomach mucosa
induces the secretion of gastric acid

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60
Q

leukotrienes

A

product of arachidonic acid from mast cell membranes

similar effects to histamine in later stages

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61
Q

prostaglandins

A

similar to leukotrienes (induce pain)

aspirin and some NSAIDS block synthesis of prostaglandins

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62
Q

platelet-activating factor

A

similar to leukotrienes and platelet activation

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63
Q

types of phagocytes

A 
neutrophil
eosinophil
basophil
monoctye/macrophage
dendritic
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64
Q

neutrophils

A
  • polymorphonuclear neutrophils (PMNs)
  • predominate in early inflammation
  • ingest bacteria, dead cells and cellular debris
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65
Q

eosinophils

A
  • mildly phagocytic

- defence against parasites and regulation of vascular mediators

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66
Q

basophils

A
  • least prevalent granulocytes

- primary role unknown

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67
Q

monocytes and macrophages

A

monocytes in bone marrow>circulation>migrate to inflammatory site>become macrophages
arrive 24 hours after neutrophils

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68
Q

dendritic cells

A

peripheral organs and skin

migrate through lymph to interact with T lymphocytes to generate acquired immune response

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69
Q

phagocytosis

A

process by which cells ingest and dispose of foreign material

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70
Q

margination

A

adherence of leukocytes to endothelial cells in the walls of capillaries

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71
Q

diapedesis

A

emigration of cells through the endothelial junctions

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72
Q

5 steps of phagocytosis

A
  • adherence
  • engulfment
  • phagosome
  • fusion with lysosomal granules
  • destruction of target
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73
Q

natural killer cells

A

recognize and eliminate cells infected with viruses

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74
Q

local manifestations results of acute inflammation

A

vascular changes and corresponding leakage of circulating components into the tissue

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75
Q

examples of local manifestations of acute inflammation

A

heat, swelling, redness, pain, loss of function

exudative fluids

76
Q

serous exudate

A

watery exudate
indicates early inflammation
ex - blister fluid

77
Q

fibrinous exudate

A

thick, clotted exudate
indicates more advanced inflammation
ex - pneumonia

78
Q

purulent exudate

A

pus
indicates bacterial infection
ex - cyst or abscess

79
Q

hemorrhagic exudate

A

contains blood

indicates bleeding

80
Q

systematic manifestations

A

fever
leukocytes
increased plasma protein synthesis

81
Q

fever caused by

A

exogenous and endogenous pyrogens

act directly on hypothalamus

82
Q

leukocytes

A

increased number of circulating leukocytes (WBC)

83
Q

increased plasma protein synthesis

A

acute phase reactants

84
Q

examples of acute-phase reactants

A
  • C-reactive protein
  • fibrinogen
  • haptoglobin
  • amyloid
  • ceruloplasmin
85
Q

what is chronic inflammation characterized by

A

pus formation, supperation

incomplete wound healing

86
Q

other causes of chronic inflammation

A
  • high lipid and wax content of a micro organism
  • ability to survive inside macrophage
  • toxins
  • chemicals, particulate matter or physical irritants
87
Q

characteristics of chronic inflammation

A
  • dense infiltration of lymphocytes and macrophages
  • granuloma formation
  • epithelioid cell formation
  • giant cell formation
88
Q

hypersensitivity def.

A

altered immunological response to an antigen that results in disease or damage to the host

89
Q

allergy

A

hypersensitivity

deleterious effect of hypersensitivity to environmental antigens

90
Q

autoimmunity

A

disturbance in immunological tolerance of self-antigens

91
Q

4 types of immune mechanisms

A

type I IgE mediated
type II tissue specific
type III immune complex-mediated
type IV cell-mediated

92
Q

type I

A

against environmental antigens

histamine release from mast cell degranulation

93
Q

type I

IgE binds to

A

Fc receptors on surface of mast cells

94
Q

type I manifestations

GI allergy

A

nausea, vomiting, diarrhea, abdominal pain

95
Q

type I manifestations

skin

A

urticaria (hives)

96
Q

type I manifestations

mucosa allergens

A

conjunctivitis, rhinitis,

asthma

97
Q

type I manifestations

lung allergens

A

bronchospasm, edema, thick secretions

98
Q

type II

A

specific cell or tissue is the target of an immune response

99
Q

type II

five mechanisms

A
  1. cell destroyed by antibodies and complement
  2. cell destruction through phagocytosis
  3. soluble antigen enter circulation and deposit on tissues
  4. antibody-dependent cell -mediated cytotoxicity
  5. target cell malfunction
100
Q

type III mediated by

A

immune complex

101
Q

type III antigen-antibody

A

complexes formed in circulation

later deposited in vessel walls or extravascular tissues

102
Q

type IV mediated by

A

cell-mediated hypersensitivity

103
Q

what do type IV not invlove

A

antibodies

104
Q

strain

A

stretching injury

105
Q

strain involves

A

muscle/tendons

106
Q

strain caused by

A

mechanical overload

107
Q

sprain involves

A

ligaments

incomplete or completely torn

108
Q

pain and swelling resolve faster in in sprain or strain

A

strain

109
Q

sprain caused by

A

irregular or excessive movement of a joint

110
Q

symptoms of sprain

A 
pain
rapid swelling
heat
disability
discolouration
limited function
111
Q

sprain strain treatment

A

anti-inflammatory analgesics

gradual return to activity

112
Q

RICE

A

rest
ice
compression
elevate

113
Q

osteoarthritis characterized by

A
  • loss+damage of articular cartilage
  • inflammation
  • new bone formation in joint
  • subchondral bone chanes
  • variable degrees of mild synovitis
  • thickening of joint capsule
114
Q

prevalence of ____ increased with age

A

osteoarthritis

115
Q

risk factors of osteoarthritis

A
  • increased age
  • joint trauma
  • long-term mechanical stress
  • obesity
116
Q

manifestations of osteoarthritis

A 
pain
stiffness
enlargement of joint
tenderness 
limited motion
muscle wasting
partial dislocation
deformity
117
Q

conservative treatment of osteoarthritis

A

exercise and weight loss
drugs (analgesics and anti-inflammatory)
nutritional supplements

118
Q

surgical treatment of osteoarthritis

A

used to improve joint movement, correct deformity or malalignment, or create new joint with artificial implants

119
Q

prostaglandins

A

lipids that promote inflammation and are found in all tissues

120
Q

cyclooxygenase

A

key enzymes in the biosynthesis of prostaglandins

121
Q

two forms of cyclooxygenase

A

cyclooxygenase-1

cyclooxygenase-2

122
Q

cyclooxygenase-1

location

A

all tissues

123
Q

cyclooxygenase-1

function

A

protects against gastric mucosa, support kidney function, promote platelet aggregation

124
Q

cyclooxygenase-1

inhibited by medications

A

undesirable:increase risk for gastric bleeding and kidney failure

125
Q

cyclooxygenase-2

location

A

all sites of injury

126
Q

cyclooxygenase-2

function

A

mediates inflammation, sensitizes pain receptors, mediates fever in brain

127
Q

cyclooxygenase-2

inhibited by medications

A

desirable: results in suppression of inflammation

128
Q

NSAIDs

A

nonsteroidal anti-inflammatory drugs

129
Q

NSAIDs action

A

inhibit cyclooxygenase->blocking inflammation

130
Q

NSAIDs drug of choice for

A

mild to moderate pain, inflammation, fever

131
Q

properties of all NSAIDs

A

antipyretic
analgesic
anti-inflammatory

132
Q

use of NSAIDs

A 
relief of:
mild/moderate headache
myalgia
neuralgia
arthralgia
post-op pain
arthritis pain
treatment of gout and hyperuricemia
133
Q

celecoxib (celebrex®)

A

NSAID cyclooxygenase inhibitor

134
Q

adverse effects of NSAIDS

A 
heartburn to severe GI bleeding
acute kidney injury 
noncardiogenic pulmonary edema 
altered hemostasis
hepatotoxicity
skin eruption
tinnitus
135
Q

tinnitus

A

hearing loss

136
Q

misoprostal

A

prevents GI bleed

synthetic prostaglandin E1 analogue that inhibits gastric acid secretion

137
Q

NSAIDs nursing considerations

A 
take with food/milk
avoid alcohol
assess for GI bleed
monitor I&O
no children
138
Q

glucocorticoids action

A

suppresses histamine release and inhibits syntheses of prostaglandins by inhibiting COX-2

139
Q

glucocorticoids released by

A

adrenal cortex

natural hormone

140
Q

glucocorticoids helps control inflammatory response by

A

stabilizing cell membranes of inflam cells (lysosomes). decreases migration if WBC into already inflamed areas

141
Q

prednisone

A

Apo-Prednisone

glucocorticoids prototype

142
Q

glucocorticoids routes

A

inhaled or injected

143
Q

glucocorticoids inhaled

A

control of steroid-responsive bronchospastic states

144
Q

glucocorticoids nasal admin

A

manage allergic rhinitis and prevent recurrence of polyps after surgical removal

145
Q

glucocorticoids topical

A

used in management of inflammation of eye ear skin

146
Q

methylprednisolone sodium succinate

A

most common injectable glucocorticoid

147
Q

hydrocortisone sodium succinate and dexamethasone sodium succinate

A

second most common injectable glucocorticoids

148
Q

glucocorticoids - prednisone

action

A

potent anti-inflam: short acting systemic corticosteroid

149
Q

glucocorticoids - prednisone

contraindications

A

active untreated infections, lactation, hypersensitivity to alcohol, bisulfate or tartrazine (food additive)

150
Q

glucocorticoids - prednisone

dosage

A

5-60 mg/day

week to a month

151
Q

glucocorticoids - prednisone

adverse effects

A

depression, euphoria, headache, personality change, psychosis, restlessness, increased intraocular pressure, increased BP, peptic ulcers, anorexia, nausea, vomiting, delayed wound healing, increased blood glucose, decreased potassium, weight gain, osteoporosis, moon face

152
Q

acetaminophen

A

Tylenol
pain reliever
max dose 4g/24 hrs

153
Q

opioid analgesic

A

Ultram (tramadol)

  • extended release
  • synthetic - similar to morphine
  • considered weak
  • binds to receptors in brain responsible for transmitting pain signals and inactivates them
  • manage moderate to severe pain
154
Q

Ultracet or Tramacet

A

contains acetaminophen

155
Q

viscosupplementation

A
  • injected like cortisone
  • available OTC oral supplement
  • ex synvisc, orthovisc
156
Q

eczema

A

“atopic dermatitis”

  • inflam condition
  • chronic (relapse and exacerbation)
  • non contagious
  • genetic predisposition
  • eviron trigger
  • immune dysregulation
  • disturbance to epidermis
  • stress
157
Q

eczema manifestations

A 
dry skin
itching
erythema
papules
infiltration
158
Q

eczema therapy

A 
symptomatic
emollients
oil bath
topical moisturizer
anti-inflam
UV therapy 
topical antifungal 
systemic antibiotics
severe: systemic immunosuppressives (cyclosporine)
159
Q

anaphylaxis

A

most severe hypersensitivity
occurs within minutes of exposure
systemic or cutaneous

160
Q

desensitization

A

reduce the severity of allergic reaction

can cause anaphylaxis

161
Q

antihistamines

A

drugs that directly compete with histamines for receptor sites

162
Q

properties of antihistamines

A

antihistaminic
anticholinergic
sedative

163
Q

histamine antagonists

A

H1 and H2

164
Q

H1 antagonist examples

A

ex: chloropheniramine, fexofenadine (Allegra®), loratadine (Claritin®), cetirizine
(Reactine®), desloratadine (Aerius®),
diphenhydramine (Benadryl®)

165
Q

H2 antagonist examples

A

cimetidine, ranitidine (Zantac®),

famotidine (Pepcid AC®), nizatidine (Axid®)

166
Q

H2 antagonists used to

A

reduce gastric acid in peptic ulcer disease

167
Q

Diphenhydramine hydrochloride

A 
traditional antihistamine (Benadryl)
acts both peripherally and centrally
168
Q

Diphenhydramine hydrochloride also has

A

anticholinergic and sedative effects

169
Q

anaphylaxis pharmacotherapy

A

symptomatic

support cardiovascular system and prevent further hyper-response

170
Q

what does an epipen do

A

rapidly reverse hypotension

171
Q

what is in an epipen

A

epinephrine

andrenergics

172
Q

common diagnostic tests

lab

A 
CBC
WBC with differential
CRP
ESR
serological test to detect specific antibodies or viruses
173
Q

common diagnostic test

radiographic

A

MRI
CAT
PET scan
colonoscopy

174
Q

CBC

A

complete blood count

175
Q

WBC

A

white blood cell

176
Q

CRP

A

C-reactive protein

177
Q

ESR

A

erythrocyte sedimentation rate

178
Q

MRI

A

magnetic resonance imaging

179
Q

CAT

A

Computerized Axial Tomography

180
Q

PET

A

positron emission tomography

181
Q

pregnancy risk category for medications

A

A

adequate
well controlled studies
not shown risks to fetus

182
Q

pregnancy risk category for medications

B

A

no adequate well controlled studies in women

studies in animals not found risks to fetus

183
Q

pregnancy risk category for medications

C

A

no adequate well controlled studies in women
animal studies found harmful effect on fetus
or not studied in women or animals
caution advised, benefits may outweigh risks

184
Q

no adequate well controlled studies

D

A

clear risk to human fetus

benefits may outweigh risks for pregnant women with serious condition

185
Q

no adequate well controlled studies

X

A

clear evidence that medication causes abnormalities in fetus

N116 (11 decks)

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