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NURS 324 Pathophysiology > Innate Immunity - Inflammation and Wound Healing > Flashcards

Innate Immunity - Inflammation and Wound Healing Flashcards

1
Q

What is the body’s first line of defense ?

A

Innate Immunity (AKA natural/innate)

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2
Q

Is it worse to have damage to a single cell or to multiple cells ?

A

Multiple cells - damage to a single cell can be easily repaired while damage at the level of multiple cells or tissues or organs can result in disease and potentially the death of the individual

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3
Q

Innate immunity consists of what kind of barriers ?

A

Physical, biochemical, and mechanical barriers

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4
Q

Innate immunity contains barriers and what other line of defense?

A

Inflammation

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5
Q

Group of microorganisms within the body that can protect us from pathogens

A

Normal flora or Normal Microbiome

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6
Q

If surface barriers are breached, The second line of defense is …………………

A

The inflammatory response

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7
Q

The inflammatory response does what ?

A

It protects the body from further injury, prevents infection of the injured tissue and promotes healing

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8
Q

What is the third line of the body’s defenses ?

A

adaptive Immunity

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9
Q

Unique about adaptive immunity

A

It is a specific response - it is a relatively slower response but is targeted to the pathogen
it also involves memory

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10
Q

When are the natural defenses of innate immunity in place ?

A

At birth

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11
Q

What kind of cells provide the first line of defense as physical barriers ?

A

Tightly packed epithelial cells of the skin and of the linings of the gastrointestinal, genitourinary and respiratory tracts

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12
Q

Epithelial cells secrete what kind of substances to aid in defense?

A

Mucus, saliva, sweat, tears and earwax

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13
Q

Lysozyme

A

An enzyme contained in sweat, tears, and saliva

that attacks the cell walls of gram positive bacteria

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14
Q

Microbes of the Normal Microbiome colonize what areas of our body ?

A

Skin, mucous membranes of our eyes, upper and lower Gi tracts, upper respiratory tract, urethra and vagina

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15
Q

Benefits of Normal Microbiome

A

Produce enzymes that aid in digestion, produces usable metabolites such as vitamin K and vitamin B, defends against pathogens through antibacterial factors

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16
Q

Danger of prolonged use of broad spectrum antibiotics

A

Can alter the normal microbiome, decreasing its protective activity and lead to an overgrowth of pathogenic microbes

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17
Q

What are opportunistic microorganisms ?

A

Those that are normally a part of the normal microbiome but that can cause disease if the individuals defenses are compromised

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18
Q

Inflammation is programmed to response to ………………..

A

cellular or tissue damage

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19
Q

Is inflammation a specific or nonspecific response ?

A

Nonspecific

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20
Q

Inflammatory response- where does it occur ?

A

In any tissues with a blood supply (vascularized)

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21
Q

Is the inflammatory response rapid or slow ?

A

It is a rapid response

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22
Q

The inflammatory response depends on what ?

A

Cellular and chemical components

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23
Q

Signs of acute inflammation

A

Redness, swelling, pain, heat , loss of function

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24
Q

Rubor

A

redness

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25
Q

Erythema

A

Redness

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26
Q

Steps of inflammation

A

1) Dilation of blood vessels and increased blood flow
2) Leakage of plasma proteins
3) Leukocyte (neutrophil) recruitment and migration

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27
Q

Dilation of blood vessels and increased blood flow leads to

A

erythema and warmth

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28
Q

Leakage of fluid from the vessels to the injured tissue area leads to ………………….

A

edema of the area

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29
Q

What are the three plasma protein systems ? What are they essential for ?

A

The complement system, the clotting system and the kinin system. They are needed for an effective inflammatory response in order to contain and destroy bacteria

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30
Q

The complement cascade system consists of what ?

A

A large number of proteins that constitute about 10% of the total circulating serum protein

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31
Q

The cascade system activates _____ and ____________. This results in a variety of molecules that are ___________, _________________ or ________________

A

C3 and C5; opsonins; chemotactic factors; anaphylatoxins

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32
Q

How many different pathways can the complement system be activated by ?

A

3 - classical, alternative and leptin pathways

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33
Q

What is the clotting system ?

A

A group of plasma proteins that when activated sequentially form a blood clot

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34
Q

What is the final product of the kinin system ?

A

Bradykinin

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35
Q

What does Bradykinin do ?

A

Causes dilation of blood vessels, acts with prostaglandins to induce pain, causes smooth muscle cell contraction and increases vascular permeability

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36
Q

Physical barriers

A

Skin, GI, GU, respiratory tract

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37
Q

mechanical barriers

A

dead skin cells, coughing, sneezing, vomiting

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38
Q

Biochemical barriers

A

mucus, sweat, saliva and earwax

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39
Q

Inflammatory process is caused by

A

infection, tissue necrosis ,trauma, physical/chemical injury, ischemia

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40
Q

Adaptive immunity can be divided between

A

Cell mediated and Humoral mediated immunity

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41
Q

Difference between infection and inflammation

A

Inflammation is a response to tissue injury that aims to restore health and promote healing

Infection is a failure of inflammatory defenses and involves invasion of host tissues by disease causing agents, colonization and multiplication and the reaction of host tissues to organisms and the toxins they produce

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42
Q

Goals of Inflammatory process

A

Limit and control the inflammatory process
Prevent and limit infection and further damage
Initiate adaptive immune response - brings more macrophages and lymphocytes to the site of injury
Initiate healing

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43
Q

The plasma protein systems are __________

A

interdependent. Activation of one can activate the other

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44
Q

Granulocytes consist of

A

Neutrophils, basophils and eosinophils

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45
Q

Neutrophils are

A

the first responder’s to inflammation/infection, are highly mobile

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46
Q

BANs

A

immature neutrophils

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47
Q

Segmented neutrophils are

A

mature neutrophils

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48
Q

A shift to the left

A

refers to an increased number of BANs in circulation, commonly found in patients with acute bacterial infection

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49
Q

An elevation in BANs and WBC could indicate an

A

acute bacterial infection

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50
Q

Do BANs have an effect on fighting infections ?

A

No because they are immature

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51
Q

Eosinophils respond to

A

allergic reactions and help control inflammatory mediator release

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52
Q

Basophils

A

respond to allergic reactions where IgE is present

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53
Q

agranulocytes

A

monocytes and macrophages

Monocytes mature into the macrophages

produce prostaglandins

have longer phagocytic reactions than granulocytes

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54
Q

T cells mature in the

A

thymus

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55
Q

B cells mature in the

A

bone marrow

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56
Q

Plasma cells develop from the

A

B lymphocytes

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57
Q

Leukocytosis

A

elevated levels of WBC’s, mostly neutrophils

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58
Q

phagocytosis

A

where one cell ingests another - Primarily the job of granulocytes (neutrophils, basophils, eosinophils) and monocytes

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59
Q

Inflammation - think about ___________ and ________

A

leukocytosis and phagocytosis

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60
Q

Cytokines

A

are another response to inflammation and infection

small, low MW signaling proteins produced during all phases of the immune response - Primarily made by T cells and macrophages (lymphokines/monokines) and act primarily on other immune cells in response to presence of viral or bacterial infection

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61
Q

Cytokines can be

A

pro inflammatory and anti-inflammatory

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62
Q

Mast cell degranulation

A

immediate release of chemotactic factors that attract neutrophils and eosinophils

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63
Q

Histamine

A

increases permeability of vessels

64
Q

Leukotrienes

A

induce smooth muscle contraction, constricts pulmonary airways, increases microvascular permeability

65
Q

Prostaglandins

A

induce vasodilation, induce fever, increase vascular permeability, chemotaxis, and pain by direct effects on nerves

66
Q

Platelet Activating Factor

A

Activates platelets

67
Q

Cyclooxygenase pathway (COX) leads to

A

Synthesis of prostaglandins and thromboxane

68
Q

thromboxane

VCPF

A

causes vasocontriction, bronchoconstriction and promotes platelet function

69
Q

Lipoxygenase pathway

A

Synthesis of leukotrienes

Constricts pulmonary airways

70
Q

Corticosteroids prevent the release of ____________

A

arachidonic acid - this would reduce inflammation

71
Q

arachidonic acid

A

no production of leukotrienes, prostaglandins and thromboxane

72
Q

Primary phagocyte within the blood

A

Neutrophil

73
Q

Phagocytosis steps

A

Production of adhesion molecules
Margination (pavementing)
- Adherence of leukocytes to endothelial cells
Diapedesis (emigration)
- Emigration of cells through the endothelial junctions
Chemotaxis
- Leukocytes are attracted and accumulate at the site

Adherence
Engulfment 
Phagosome formation
Fusion with lysosomal granules
Destruction of the target
74
Q

Acute Inflammation

A

Self-limiting
Local manifestations—result from vascular changes and corresponding leakage of circulating components into the tissue
Heat, swelling, redness, pain
Exudative fluids

75
Q

Serous exudate indicates

A

early inflammation- it is watery and has low protein

76
Q

Fibrinous exudate indicates

A

Thick, clotted exudate: indicates more advanced inflammation, large amounts of fibrinogen

77
Q

Purulent exudate indicates a

A

bacterial infection

78
Q

Hemorrhagic exudate

A

contains bloood and indicates bleeding and a severe leakage of red cells from capillaries

79
Q

Systemic Manifestations of Acute Inflammation

A

Fever, Leukocytosis, increased plasma protein synthesis (proteins can be proinflammatory or anti-inflammatory)

80
Q

Chronic Inflammation

A

lasts longer than 2 weeks- Often related to an unsuccessful acute inflammatory response
Characterized by pus formation, purulent discharge, and incomplete wound healing

81
Q

Other causes of chronic inflammation

A

High lipid and wax content of a microorganism
Ability to survive inside the macrophage
Toxins
Chemicals, particulate matter, or physical irritants

82
Q

Temperature raising responses

A

vasoconstriction
shivering
piloerection
increased metabolism

83
Q

Temperature reducing responses

A

vasodilation
sweating
increased ventilation

84
Q

Pharmocologic treatment of fever

A

Antipyretic medications
NSAID’s (non-steroidal anti-inflammatory drugs)
Aspirin
Ibuprofen (Motrin, Advil, etc)

Antipyretic only (Not anti-inflammatory drug)
Acetaminophen (Tylenol)
85
Q

How do Antipyretic medications reset the temperature set point ?

A

By blocking the activity of COX (and prostaglandins)

86
Q

Agents of Infection

A

Bacteria
Fungi
Virus
Parasitic

87
Q

Staphylococcus aureus

A 
Life threatening 
Major cause of nosocomial infection
Common on normal skin and nasal passages
Opportunistic
Biofilms associated with colonization
Secretes exotoxins
Antibiotic resistance is a major problem
88
Q

biofilms consist of

A

mixed species of microorganisms - this makes it harder to fight against certain bacteria

89
Q

bacteremia

A

bacteria are present in the blood

90
Q

septicemia

A

infection in the blood

91
Q

Bacteremia and Septicemia are both results of the

A

failures of the body’s defense mechanisms

92
Q

DIC

A

Disseminated Intervascular Coagulation - we have used up all of our clotting factor so we start bleeding - perhaps from the eyes or the site of an IV. This can happen when endotoxins are released from the blood because of bacteremia

93
Q

Gram negative organisms produce

A

endotoxins that release the TLR-4. This triggers the septic syndrome to start.

94
Q

SIRS

A

systemic inflammatory response - fever, tachycardia, tachypnea, leukocytosis)

95
Q

SIRS + bacteremia =

A

sepsis

96
Q

IF we dont treat our patients with fluids, oxygen, get cultures and antibiotics then sepsis can ___________ into a bigger issue. What can result ?

A

Vasodilation, hypotension, tissue inflammation, tissue hypoperfusion

97
Q

More severe Sepsis results in

A

myocardial depression, worsening hypoperfusion (cold shock) increase in lactic acid >2

98
Q

Septic shock has lactic acid levels greater than

A

4

99
Q

Viruses can live on their own. True or false?

A

False- viruses hijack other cells and depend on these cells for replication. It is not capable of independent production

100
Q

Viral Invasion and Replication Steps

A 
Attachment
Penetration
Uncoating
Replication
Assembly
Release
101
Q

Antigenic drift

A

refers to a virus than can change yearly. The influenza virus undergoes antigenic drift leading to new strains

102
Q

Characteristics of Fungi

A

Large microorganisms with thick, rigid cell walls without peptidoglycans (resist penicillin and cephalosporins)
Eukaryotes
Exist as single-celled yeasts, multicelled molds, or both
Reproduce by simple division or budding
Pathogenicity
Adapt to host environment
Wide temperature variations, digest keratin, low oxygen
Suppress the immune defenses
Usually controlled by phagocytes, T lymphocytes

103
Q

Most common cause of fungal infections

A

Candida Albacans

Opportunistic
Found in normal microbiome of skin, GI tract, vagina
Localized infection if overgrowth occurs
Disseminated infection if immunocompromised
May involve deep infection
High mortality rates

104
Q

Factors for Infection: Communicability

A

Ability to spread from one individual to others and cause disease: measles and pertussis spread very easily; HIV is of lower communicability

105
Q

Factors for Infection: Infectivity

A

Ability of pathogen to invade and multiply in the host

Involves attachment to cell surface, release of enzymes, escape of phagocytes, spread through lymph and blood to tissues

106
Q

Factors for Infection: Virulence

A

Capacity of a pathogen to cause severe disease; for example, measles virus is of low virulence while rabies virus is highly virulent

107
Q

Factors for Infection: Pathogenicity

A

Ability of an agent to produce disease

Success depends on communicability, infectivity, extent of tissue damage, and virulence

108
Q

Factors for Infection: Portal of entry

A

Route by which a pathogenic microorganism infects the host

109
Q

Factors for Infection: Toxigenicity

A

Ability to produce soluble toxins or endotoxins, factors that greatly influence the pathogen’s degree of virulence

110
Q

Role of Biofilm in common infections

A

Bacteria prefer to stick to and colonize environmental surfaces

Biofilm is a structured community of bacteria
Access to nutrients- elimination of wastes
Intracellular signaling and communication
Implicated in as much as 80% of infections
Locations:
Dental plaque, catheter infections, implanted medical devices

111
Q

We dislike foley catheters because of _________

A

biofilms

112
Q

Treating Infectious diseases

A

Antibiotics, antifungals and antivirals

113
Q

Requirements of medications and actions take to fight and eliminate infection

A

Organism must be susceptible to concentrations of drug at infected site
Dose and route of administration must result in adequate levels of drug at infected site for sufficient time
Local factors must not interfere with drug activity
Host defenses must facilitate microbial clearance
Adjunctive therapies (such as surgical drainage of abscess) must be used when necessary

114
Q

Antibacterial drugs consist of

A

Narrow spectrum antibiotics: target few types of bacteria
Broad spectrum antibiotics: target many types of bacteria
Anti-mycobacterial drugs

115
Q

Antiviral drugs consist of

A

Antivirals

Anti-retroviral

116
Q

Classifications of Antibiotics by mechanism of action

A 
Inhibits bacterial cell wall synthesis
Inhibits protein synthesis
Inhibits nucleic acid synthesis
Interrupts metabolic pathways
Disrupts cell membrane permeability
Inhibits enzymes important in microorganism’s function
117
Q

A patient might be on several antibiotics because

A

of the range of actions that these antibiotics may take towards the invading bacteria

118
Q

Bactericidal

A

drug actually kills bacteria

119
Q

Bacteriostatic

A

drug inhibits bacterial reproduction so host defenses can kill

120
Q

Selective Toxicity

A

Drug is toxic to microbe but not to human host

121
Q

Organism Sensitivity

A

Drug is toxic to the microorganism causing the infection. Culture and sensitivity testing will determine this.

122
Q

If someone comes in with a infection, the best thing we can do is

A

get a culture and sensitivity. Culture will let us know what antibiotic bacterium is sensitive to

123
Q

Tests for identifying infecting microbe can be

A

rapid or take days depending on the test

124
Q

Frequently therapy is initiated with ____________ antibiotics and then switched to a more specific ______________ when the organism is identified.

A

broad spectrum; antibiotic

125
Q

We worry about _____________ resistance.

A

Antibiotic

126
Q

Antibiotic resistance is caused by

A 
Genetic mutations
Inactivation of antibiotic
Penicillin resistance
Modification of target molecule
Increasing active efflux of antibiotic
Caused by:
Lack of compliance with therapeutic regimen
Overuse
Destruction of normal microbiome
127
Q

Adverse effects of antibiotic therapy

A

Normal gut flora are killed - diarrhea and can pave the way for colonization with pathogenic bacteria (clostridium difficile )
Supra-infection: Infection with a second (antibiotic resistant) organism that occurs during antibiotic therapy.
Pseudomembranous colitis: bowel is colonized with Clostridium difficile, producing a severe diarrhea that is sometimes fatal.
Allergy – most common with the penicillins (up to 7%)
Cross over allergy > Cephalosporins (cousin to penicillin) (small 1%)

128
Q

Supra infection

A

Infection with a second (antibiotic resistant) organism that occurs during antibiotic therapy

Pseudomembranous colitis: bowel is colonized with Clostridium difficile, producing a severe diarrhea that is sometimes fatal.

129
Q

Allergy is most common with

A

penicillins

130
Q

Cross over allergy

A

allergic to one drug means one may be allergic to another drugs “cousin”

Cephalosporins (cousin to penicillin) (small 1%)

131
Q

We can identify a pathogen through

A

culture, gram stain

132
Q

What is the important principle of antimicrobial selection and administration ?

A

Match “drug with bug”

133
Q

Antibiotics should be given

A

around the clock. We need the higher, consistent levels in order to kill the bacteria

134
Q

Synergistic

A

Antibiotics work well with each other

135
Q

In some instances, antibiotic resistance is discouraged by _____________

A

combinations

136
Q

In some instances, antibiotic resistance is discouraged by _____________

A

combinations

137
Q

Ways to decrease risk for antibiotic based infections

A

don’t take antibiotics to prevent illness
washing hands
follow directions
do not request antibiotic for flu or cold
finish course
do not take left over antibiotics

138
Q

With a “shift to the left” what are we worried about ?

A

BANS level are usually 0-4%. With increased levels we are looking at acute inflammatory response or acute infection.

139
Q

What is chemotaxis ?

A

Chemotaxis is the movement of an organism in response to a chemical stimulus.
Somatic cells, bacteria, and other single-cell or multicellular organisms direct their movements according to certain chemicals in their environment.

a chemically induced signally process that leads to the migration of WBC

140
Q

Margination of WBC refers to

A

an accumulation of WBC near the vessel wall

141
Q

chemotaxis occurs after

A

a WBC has left circulation via the process of diapedesis

142
Q

diapedesis

A

WBC squeezes through the vessel wall

143
Q

diapedesis gives rise to

A

chemotaxis as chemical signals direct the WBCs to the site of injury

144
Q

What is hyperemia ?

A

an excess of blood in the vessels supplying an organ or other part of the body.

145
Q

Corticosteroids, NSAIDS and acetylsalicylic acid act to inhibit various steps in what pathway?

A

The cyclooxygenase pathway and the Lipoxygenase pathway

146
Q

When cells are activated by injury, the arachidonic acid in the cell membrane is rapidly converted to produce what substances ?

A

Prostaglandins, thromboxane and leukotrienes

147
Q

Prostaglandins are considered pro-inflammatory and are potent ____________ contributing to increased __________ and ________

A

vasodilators; blood flow; edema formation

148
Q

Prostaglandins- do they dilate or constrict vessels ?

A

Dilate vessels

149
Q

Arachidonic acid is important because

A

it produces Prostaglandins and thromboxane and leukotrienes, all which play important roles in the inflammatory response

150
Q

roles of Prostaglandin

A

vasodilator
sensitizing pain receptors to arousal by stimuli
stimulate temperature regulating area of hypothalamus, helping to produce fever

151
Q

Thromboxane roles

A

powerful vasoconstrictor
platelet aggregating agent
causes brief vasoconstriction and skin pallor at the injury site and promotes clot formation

152
Q

Leukotrienes

A

form the slow reacting substance of anaphylaxis, which constricts smooth muscles of bronchi, causing narrowing of the airway, and increases capillary permeability leading to airway edema
- stimulate chemotaxis

153
Q

Histamine role

A

causes vasodilation and increased capillary permeability

154
Q

A biochemical substance that attracts leukocytes to the site of inflammation is a(n):

A

chemotactic factor

155
Q

Leukotrienes act like histamine and cause smooth muscle contraction, ________________ vascular permeability, and chemotaxis.

Prostaglandins cause increased vascular permeability, chemotaxis, and pain.

Adhesion molecules increase the _____________ between cells.

A

increased; stickiness

NURS 324 Pathophysiology (6 decks)

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