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Patho > Infection, Inflammation, Innate & Specific Immune Responses > Flashcards

Infection, Inflammation, Innate & Specific Immune Responses Flashcards

1
Q

Does bacteria go into a cell nucleus?

A

no

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2
Q

Do viruses go into a cell nucleus?

A

yes

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3
Q

What does the intestinal flora help do for the body?

A

Synthesize vit K

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4
Q

Non-specific inflammatory response example

A

fever & Inflammation

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5
Q

Specific inflammatory response example

A

Antigen-Antibody response

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6
Q

How fast does a Non-specific inflammatory response occur?

A

Immediate

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7
Q

How fast does a specific inflammatory response occur

A

develops slowly

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8
Q

What type of cells are involved in a specific inflammatory response

A

specific cells to combat a particular pathogen

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9
Q

antibody (immunoglobulin)

A

protein that neutralizes pathogens to get them out of the body

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10
Q

Antigen

A

A toxin

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11
Q

Non-specific mechanical first line of defense examples

A

skin, mucus membranes, urine, pooping, vomiting

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12
Q

non-specific: chemical factors: first line of defense examples

A

acid pH of skin, Lysozymes, gastric juice, unsaturated fatty acids

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13
Q

Lysozymes

A

an enzyme that catalyzes the destruction of the cell walls of certain bacteria

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14
Q

Non-specific: internal defenses: second line defense

A

antimicrobial proteins, natural killer cells, phagocytes, inflammation, fever

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15
Q

Phagocytes

A

WBC that can ingest & destroy microorganisms

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16
Q

Complement system

A

group of 20 proteins circulating in the blood looking for invaders

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17
Q

Interferons

A

WBC communicators, proteins produced by WBC when the immune response is triggered

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18
Q

Function of lymph nodes

A

proliferation (increase) of immune cells, filter lymph fluid & remove bacteria/toxins from circulation

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19
Q

Thymus function & location

A

produces t-lymphocytes, located in mediastinum

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20
Q

spleen function

A

reservoir for blood, largest lymph organ, carries platelets

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21
Q

tonsils function

A

produce lymphocytes, gaurd against airborne & ingested pathogens

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22
Q

red bone marrow function

A

houses stem cells that develop into lymphocytes

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23
Q

B cell function and where they are made

A

split into plasma cells that make antibodies and memory b cells; made in the bone marrow

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24
Q

where are T cells made

A

Made in the thymus

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25
Q

Tissue macrophages function

A

clean up blood

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26
Q

examples of tissue mactophages

A

Lung: alveolar macrophages, Liver: Kupffer’s cells, spleen, lymph node, intestine: Peyer patches, CNS: microglial cells

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27
Q

Granulocytes examples

A

Neutrophils, Basophils, Eosinophils

“polys” or “segs”

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28
Q

Neutrophils

A

fight infection by phagocytosis (engulfing miccroorganisms), most common type of WBC,

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29
Q

Phagocytosis

A

the process of engulfing and destroying microorganisms and other foriegn materal

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30
Q

The 3 Phagocytes

A

Neutrophils, monocytes and macrophages

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31
Q

What do granulocytes release?

A

Heparin and histimine

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32
Q

Bands

A

baby neutophils

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33
Q

Basophils & Eosinophils respond to what kind of infections?

A

respond to parasitic & allergic infections

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34
Q

Agranulocytes examples

A

Monocytes, lymphocytes

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35
Q

Lymphocyte examples

A

B-cells and T-cells

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36
Q

Lymphocytes respond to which type of diseases?

A

viral

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37
Q

Monocytes function and respond to which type of infections?

A

take over for neutrophils, respond to severe infections

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38
Q

Relative WBC

A

percentage

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39
Q

Absolute WBC

A

actual number

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40
Q

Aboslute value equals what?

A

Absolute value = % x WBC

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41
Q

Relative WBC values will always equal what?

A

100% (If one type of cell increases then the other types must decrease

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42
Q

Which count is more important? Relative of absolute?

A

Absolute

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43
Q

Terminology: Increased value of WBC

A

“cytosis” except & “philia”

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44
Q

Terminology: Decreased value of WBC

A

“penia”

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45
Q

What can cause a low WBC count?

A

Attack on bone marrow
dietary deficiencies
autoimmune diseases

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46
Q

What does it mean if there is a drastic decrease in WBC count?

A

bone marrow failure & risk for infection

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47
Q

Do newborns & infants have a high or low WBC count?

A

high

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48
Q

How are the elderly affected by WBC count?

A

They may not have an increase in WBC with a severe infection

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49
Q

Erythrocyte Sedimentation Rate (ESR)

A

rate that RBC’s settle out of anticoagulated blood in 1 hour

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50
Q

C-Reactive protein (CRP)

A

an abnormal protein made in the liver, it occurs rapidly

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51
Q

What kind of cell wall does Gram + cocci have?

A

a THICK peptidoglycan cell wall, soak up purple stain

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52
Q

Gram + Cocci examples

A

Staph aureus, staph epidermidisstrep pna, Group A beta-hemolytic streptococcus

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53
Q

Where are Staph aureus & Staph epidermidis found?

A

wounds, surgical sites, indwelling catheters

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54
Q

Where is strep pna found?

A

community acquired pna, adult bacterial meningitis

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55
Q

Example of Group A beta-hemolytic streptococcus

A

rheumatic fever

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56
Q

What kind of a cell wall do a Gram - pathogens have? and what are they impermeable to?

A

A protective outer coat (lipopolysaccharide + transmembrane protein pores) that are impermeable to penicillin’s & cephalosporins

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57
Q

Gram - examples

A

Escherichia, Neisseria, Pseudomonas, most noscomial infections

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58
Q

Anaerobes are made from which gram? + or -?

A

both

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59
Q

Anaerobe examples

A

Bactericides fragilis, CDIFF

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60
Q

“itis”

A

inflammation

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61
Q

Does colonization (presence of microorganisms) cause inflammation?

A

No

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62
Q

What initiates the inflammatory process?

A

cell injury

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63
Q

can you be hypoxic without having ischemia?

A

yes

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64
Q

Can you have ischemia without being hypoxic?

A

no

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65
Q

signs of inflammation

A

rubor (red), calor (heat, Dolor (pain), Tumor (swelling), Functio laesa

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66
Q

rubor

A

red

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67
Q

calor

A

heat

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68
Q

Dolor

A

pain

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69
Q

Tumor

A

swelling

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70
Q

Functio laesa

A

Loss of function

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71
Q

Leukocyte emigration

A

the passage of leukocytes through the endothelial gap junctions of blood vessels

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72
Q

Leukocyte Margination

A

increases expression of adhesion of molecules so they can get to where they need to go to

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73
Q

Chemotaxis

A

The process by which leukocytes (WBC, phagocytes)wander through the bloodstream and our attracted to chemical signals brought on by an inflammatory response

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74
Q

During inflammation, what happens on a vascular level?

A

arteriolar vasoconstriction followed by vasodilation (brings back O2) which produces swelling & erythema & hyperemia

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75
Q

What happens to the capillary permeability during an inflammatory response?

A

It increases causing swelling and dilutes toxins

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76
Q

Who are the first responders in an inflammatory response?

A

Neutrohils (24 hr life)

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77
Q

When do macrophages respond in an inflammatory response

A

after 48 hours, they do more work than neutrphils

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78
Q

Mast cell function

A

release heparin to maintain blood flow to area

79
Q

5 steps in the phagocytosis process

A

1) Attachment
2) Ingestion
3) Fusion of the lysosome & phagosome
4) Digestion
5) Release of digested products

80
Q

Histamine is released by

A

Basophils, platelets & mast cells

81
Q

What else does Histamine stimulate?

A

Bronchoconstriction (H1 receptors) & Gastric acid secretion (H2 receptors)

82
Q

What is the purpose of vasodilation in an inflammatory response?

A

to increase blood flow and increase capillary permeability

83
Q

Kinins function

A

an inflammatory mediator that:

1) increases capillary permeability
2) induces vasodilation
3) act as chemotatic agents for phagocytes

84
Q

Kinin example

A

Bradykinin —> increases capillary permeability & causes pain

85
Q

How are Kinins formed?

A

from inactive precursors (proteins that are inactive and can be turned on), kininogens, in blood

86
Q

What do Prostaglandins do? what are they?

A
  • Inflammatory Mediator made from lipids -They cause fever in response to infection,
  • stimulate pain receptors, increase effects of histamine & Kinins
87
Q

What are prostaglandins blocked by?

88
Q

What are prostaglandins produced by

A

arachodonic acid found in cell membranes

89
Q

what are Leukotrienes produced by?

A

basophils & mast cells during breakdown of membrane phospholipds

90
Q

What is the key role in bonchoconstriction in asthma? Its associated with leukotrienes

A

SRSA- slow Reacting Substance of Anaphylaxis

91
Q

What are Leukotrienes at their function

A

They are Inflammatory Mediators

  • increase vascular permeability
  • increase adhesion of WBC to capillary during injury/infection
  • Acts as chemo-attractants
92
Q

What are complements?

A

Inflammatory Mediators

-consist of 20 circulating proteins

93
Q

What is the function of complements?

A

Increase:

  • Vascular permeability
  • Chemostasis
  • Phagocytosis
  • Lysis of foreign cells
94
Q

Where do Platelet Activating Factors come from and what are they?

A

made from a complex lipid in cell membranes. They are inflammatory mediators

95
Q

Platelet activating factors function

A
  • Induces PLT aggregation (put together)
  • Activates neutrophils
  • Potent eosinophil chemo-attractant
96
Q

Non-inflammatory cells

A

fibroblasts & endothelial cells

97
Q

Cytokines function

A

proteins produced by different cell types to bind to receptors to remove

98
Q

another name for Interleukin

99
Q

non-inflammatory cells

A

fibroblasts & endothelial cells

100
Q

Cytokines: ILs

A

activates t-cells and induces fever

101
Q

Cytokines: IF-y

A

induces MHC 1 and 2, activates macrophages & endothelial cells

102
Q

Cytokines: TNF

A

cytokine for tumor cells

103
Q

Cytokines: CSF

A

promotes neutrophilic, eosinophilic and macrophage bone marrow colonies, activates mature granulocytes

104
Q

chemical mediator for Leukocytosis

A

TNF and IL-8

105
Q

chemical mediator for Fever

A

IL-1 and IL-6

106
Q

chemical mediator for Pain

A

prostaglandins & bradykinin

107
Q

chemical mediator for chemotaxis

A

complement fragments

108
Q

chemical mediator for Tissue damage

A

lysosomal enzymes & products released from neutrophils, & macrophages

109
Q

chemical mediator for swelling, redness & tissue warmth

A

histamine, prostaglandins, leukotrienes, bradykinin, platelet-activating factor

110
Q

what does an Abscess look like?

A

inflammation with purulent exudate

111
Q

what does an ulceration look like?

A

inflammation where epithelial surface has become necrotic &eroded

112
Q

what happens in an acute inflammation response is unsuccessful at riding the body of invading foreign particles?

A

chronic inflammation & granuloma formation

113
Q

Granuloma formation examples

A
  1. ) 1-2mm lesions
  2. ) foreign bodies such as splinters
  3. ) giant cells engulf large foreign particles
  4. ) “cheesy” necrotic center from TB
114
Q

What happens in the acute phase inflammatory response when WBC proteins are broken down?

A

negative nitrogen balance

115
Q

During an acute inflammatory response during bacterial infections, what is increased?

A

of leukocytes, neutrophilia (shift to left)

116
Q

Lymphadenopathy

A

increase in size of lymph nodes

117
Q

Lymphadenitis

A

tender lymph nodes/inflammed

118
Q

non-painful lymph nodes=what

119
Q

what will patients temp be like after surgery

A

low grade for first 48-72 hours

120
Q

Fever coming from outside

A

hyperthermia

121
Q

pyrogens

A

fever producers

122
Q

Endogenous pyrogens stimulate the release of PgE (prostaglandin E) from where?

A

hypothalmus

123
Q

Endogenous pyrogens are produced where? examples

A

from within the the cell; malignancies, graft rejections

124
Q

Exogenous pyrogens are produced where? examples

A

from outside the cell; fungus, endotoxins, gram +/- bacteria

125
Q

stages of fever: prodromal

A

before fever; malaise, feeling achy

126
Q

stages of fever: stage 1

A

cold or shaking stage, occurs 10-40 min w/ rapid steady rise of temp b/c of shaking

127
Q

stages of fever: stage 2

A

flush; thermostat reset, skin warm and flushed—> cellular dehydration occurs

128
Q

stages of fever: stage 3

A

defervescence (heat loss), sweating occurs-fever breaks

129
Q

patterns of fever: intermittent

A

returns to normal at least q24hr

130
Q

patterns of fever: remittent

A

varies a few degrees in either direction

131
Q

Fever of unknown origin

A

temp >101 present for ?3 weeks

132
Q

what are causes of fevers of unknown origin

A

malignancies, infections & cirrhosis

133
Q

apoptosis

A

ability to program cell dealth for the good of the person

134
Q

Hapten &Hapten-carrier complex

A

penicillin binding to plasma protein example

135
Q

Major Histocompatibility complex (MHC) 1:

A

it can differentiate self from non self, on all nucleated cells in body

136
Q

Major Histocompatibility complex (MHC) 2

A

They present the antigen to helper t-cells- “here it it-take it away!”

137
Q

AKA Human Leukocyte Antigens (HLA)

A

4 linked groups of genes on chromosome 6

138
Q

Who gets AKA Human Leukocyte Antigens (HLA)

A

receive a set (haplotype)from each parent

139
Q

who has issues with Major Histocompatibility Complex (MHC)?

A

patients with transplants

140
Q

processing of antigens

A 
ingestion
digestion
fusion
binding
insertion
141
Q

main responders to viral infections

A

lymphocytes (B & T-cells)

142
Q

regulatory lymphocytes

A

coordinate & organize calling to battle

143
Q

effector lymphocytes

A

final stage in immune response, raise alarm by releasing cytokines

144
Q

B-lymphocytes (10-20%)mature where and occur when?

A

mature in bone marrow, found in humoral or antibody-mediated immunity

145
Q

T-lymphocytes (60-70%)mature where and occur when?

A

mature in thymus, occur in cell-mediated immunity

146
Q

cell-mediated immunity

A

the destruction of target cells through secretion of lymphokines

147
Q

types of t-cells

A

killer, helper, suppressor (you have to turn off immune response at some point), memory

148
Q

Humoral or Immunoglobulin-mediated immunity

A

B cell mature into plasma cells which produce antibodies, wants to eliminate bacteria & prevent viral infections

149
Q

cell-mediated immunity chart

A
  • antigen
  • macrophage engulf antigen
  • antigen MHC expression -release of cytokines
  • production of cytotoxic cells
150
Q

what do lymphocytes activate

A

T-cels & B-cells

151
Q

T4 Lymphocyte

A

regulate & amplify B & T-cell response

152
Q

Cytotoxic T- cells bond to MHC I or !!? and what is the code for them

A

MHC I (CD8)

153
Q

Helper T-cells bond to MHC I or II? and what is the code for them

A

MHC2 (CD4)

154
Q

Suppressor t-cells

A

reduce the humoral response

155
Q

memory T-cells

A

remain dormant until 2nd exposure

156
Q

Natural killer cells

A

CD15 & CD56, non-specific that kill tumor cells &virusus

157
Q

How are natural killer cells able to kill cells?

A

they are inhabited by contact with MHC self molecules, depends on production of perforinsm enzymes & toxic cytokines (they punch holes into cells and destroy it)

158
Q

what enhances natural killer cells?

159
Q

macrophages

A

ingest antigen–>present antigen-MHC complex to T-lymphocytes—>activate T-lymphocytes

160
Q

what do macrophages secrete?

A

cytokins: tumor necrosis factor (TNF) & interleukin-1 (IL-1) which produces fever

161
Q

humoral immunity chart

A

clones of B &T cells occur

162
Q

basis of humoral immunity

A

B-lymphocytes

163
Q

antigen binds with receptor,–>differentiates into plasma cell–>secretes immunoglobulins

A

B-Lymphocytes

164
Q

what regulates B-lymphocytes?

A

T-Lymphocytes & cytokines

165
Q

Antibody structure: Fab (antigen binding fragment) is specific for what?

A

each antibody

166
Q

Antibody structure:Fc (constant fragment)

A

non-specific, all immunoglobins

167
Q

What activates constant fragment (Fc) antibody structures?

A

the binding of a antigen binding fragment (Fab)

168
Q

IgG (75%)

A

most common in all body fluids, stays higher during second exposure, crosses placenta—“Its like the grass the field”

169
Q

IgM (10%)

A

first responder–too larger to cross membranes, lasts a week, doesn’t get higher during 2nd exposure –“Its like the maple trees in the grass field

170
Q

IgA (15%)

A

found in body secretions, saliva, sweat, tears, mucus, bile & colostrum —“Its the Area of wetness in the grass field”

171
Q

IgD (0.2%)

A

found in plasma & easily broken down, found on B cells that help B cell grow —“The baby dear that needs to grow up in the grass field”

172
Q

IgE (0.004%)

A

found in allergic reactions, RARE, found on Fc region on basophils & mast cells–“Its like the elm trees in the grass field”

173
Q

natural immunity

A

innate resistance, age, health, race, sex

174
Q

active immunity

A

acquired through immunizations OR having the disease

175
Q

passive immunity

A

short term protection

examples: bit by a snake & antidote given, breast milk, gamma globulins, antitoxin

176
Q

The complement Cascade

A

20 inactive proteins circulating

177
Q

how does the complement cascade cause inflammation?

A

by increasing vascular permeability, cheostasis, phagocytosis & lysis of foreign material

178
Q

the initial step of the classic pathway in the complement cascade (C1-C10?)

179
Q

Anaphylaxis

A

degranulation of mast cells with release of histamine & other chemical mediators

180
Q

Opsonization

A

targeting of antigen so it can be easily engulfed & digested by macrophages

181
Q

cytolysis

A

destruction of cell membranes

182
Q

Adherence of immune cells

A

Adhesion of Ag-Ab complexes to surface of cells

183
Q

C1-C5

A

stimulate mast cell degranulation (release of chemical mediators)

184
Q

C6-10

A

bacterial cell lysis by making cell wall “leaky”

185
Q

the initial step of the alternatepathway in the complement cascade

186
Q

Type 1 hypersensitivity disorder involves what immunoglobin

A

IgE allergic , IMMEDIATE

ex. anaphylaxis, allergy

187
Q

Type 2 hypersensitivity disorder

A

IgM & IgG, cytoxic rxns

ex. blood transfusions

188
Q

Type 3 hypersensitivity disorder

A

immune complex rxns

ex. post-strptococal glomerulonephritis

189
Q

Type 4 hypersensitivity disorders

A

cell-mediated rxns

ex. contact dermatitis

190
Q

which type of hypersensitivity disorders involve antibodies?

191
Q

goodpasture’s syndrome, erythroblastosis fetalis, autoimmune hemolytic anemia, hemolytic transfusion rxn are examples of which type of hypersensitivity disorder?

192
Q

serum sickness, post-streptococcal glomerulonephritis are examples of which type of hypersensitivity disorder?

193
Q

Contact dermatitis, HVGD and GVHD, allograft rejection are examples of what hypersensitivity disorder?

Patho (20 decks)

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