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Unit 4: LGS > Week 1 > Flashcards

Week 1 Flashcards

1
Q

4 classes of microbes

A
  • Virus
  • Bacteria
  • Fungus
  • Parasite
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2
Q

Morphology of bacteria

A
  • Cocci
  • Bacilli
  • Spirals
  • Pleiomorphic
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3
Q

Cocci

A

circle

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4
Q

Staph

A

cluster

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5
Q

Strep

A

string

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6
Q

Bacilli

A

rod

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7
Q

What is used to look at cell wall?

A

Gram stain

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8
Q

Gram +

  • color
  • peptidoglycan
A
  • purple

- thick peptidoglycan, traps 1st dye

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9
Q

Gram -

  • color
  • peptidoglycan
A
  • pink
  • thin peptidoglycan layer
  • has layer of lipopolysaccharide
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10
Q

Porins

A

how drug gets into bacteria

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11
Q

Function of flagella

A

motility

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12
Q

Function of pilli

A

for genetic transmission between bacteria; sexual transfer–importance in antibiotic resistance

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13
Q

Function of fimbriae

A

for adhesion

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14
Q

Why is morphology important?

A

If taking a sample it will be some of the first information that will clue you in to what organism it is

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15
Q

What is Pleiomorphic?

  • found?
  • what do we get?
A
  • varied shapes
  • extreme environments
  • enzymes to run some of diagnostic testing
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16
Q

Cell wall

A
  • used for protection

- target of beta-lactamases

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17
Q

Layers of cell protection

A

cell membrane, cell wall, capsule

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18
Q

Bacteria that will not stain

A

Syphilis, chlamydia

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19
Q

Importance of lipopolysaccharide layer in gram -

A

important in virulence of bacteria

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20
Q

E. coli

A

-has flagella, pilli, H antigen, O antigen, K antigen

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21
Q

Virulence factors of E. coli

A
  • pilli
  • flagella
  • LPS
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22
Q

H antigen

A
  • flagella

- used for testing in serology

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23
Q

O antigen

A
  • antigenic variation
  • seen in flu
  • used for testing in serology
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24
Q

K antigen

A

-capsule

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25
Q

Importance of capsule

A
  • antiphagocytic property
  • can help with adherence
  • can help form biofilm
  • can dry out quickly
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26
Q

Bio-film

A

-ale to avoid complement/anti-body because it acts as barrier between the bacteria and the immune system

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27
Q

1st test when suspecting bacteria

A

gram stain

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28
Q

E. coli gram stain

A

-gram negative rods

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29
Q

How to test for aerobic/anaerobic

A
  • catalase test

- culture

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30
Q

Plates used for E. coli

A
  • Eosine methylene blue: will have metallic green sheen because it ferments lactose very quickly
  • MacConkey agar: hazy bright pink
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31
Q

What does eosine methylene blue inhibit?

A

growth of gram + bugs

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32
Q

MacConkey agar

A
  • Lactose negative- no color

- Lactose positive- pink

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33
Q

Catalase testing

A
  • tests bacteria for catalase enzyme

- will add hydrogen peroxide to sample, looking to see if enzyme will cleave hydrogen peroxide into water and gas

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34
Q

Cytochrome C oxidase testing

A
  • Cytochrome C oxidase is enzyme used in ETC of aerobic bacteria
  • will be positive if the test turns blue
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35
Q

What kind of respiration does E. coli use?

A
  • faculatative anaerobe

- can survive in aerobic environment, but prefers anaerobic respiration

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36
Q

Why would bacteria not want to be aerobic?

A

-Oxygen damages cell with radicals

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37
Q

Indole test

A
  • looking for red ring

- breaks down tryptophan

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38
Q

Indole test and e. coli

A

positive

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39
Q

Acid fermentation test

A

-e. coli is mixed acid fermenter and produces gas

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40
Q

VP test

A

-looks for glucose fermenters

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41
Q

VP and E. coli

A
  • negative; because only one substrate added

- however, E. coli can use glucose in aerobic environment

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42
Q

Methyl red test

- e. coli

A
  • looks for mixed acid fermenters

- positive

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43
Q

Can body naturally degrade bacterial cell wall?

A

yes; with lysozymes

-cleaves between NAG/NAM complexes

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44
Q

NAG and NAM

A
  • creates chain linked fance formation for cell wall
  • always attached to different AA
  • building blocks of chain made from NAG-NAM complex which binds to another complex with an AA bridge
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45
Q

lysostaphin

A
  • natural body mechanism
  • knocks out the cross bridges making the cell wall less stable
  • used in gram +
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46
Q

How to get rid of lipopolysacharide

A

-dry it out

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47
Q

Things to consider when choosing anti-biotic

A
  1. Disease state of patient
  2. Prior adverse reaction
  3. Impaired elimination
  4. Patient age
  5. Pregnancy status
  6. Epidemiologic exposure
  7. Pharmacologic factors
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48
Q

Why is disease state of patient important?

A

-antibiotics are chemotherapeutic drugs because they are trying to kill/stop growth of living cell

49
Q

Why is disease state of patient important?

A
  • antibiotics are chemotherapeutic drugs because they are trying to kill/stop growth of living cell
  • looking out for immuno-compromised individuals
50
Q

Why is impaired elimination important?

A

-If you cannot get rid of of drug then it could cause toxicity

51
Q

Why is age important?

A
  • older: side effects of dizziness- can cause falls

- neonates: increased bili

52
Q

Epidemiologic exposure

A

If patient lives in close contact with someone else and is infected with highly contagious organism then the people they live with need to be tested

53
Q

Bacteriacidal

A

Kills the cell

54
Q

Bacteriacidal

A
  • Kills the cell

- targets the cell wall

55
Q

Bacteriostatic

A
  • Stops cell growth

- targets proteins

56
Q

Post antibiotic effect

A
  • in absence of anti-biotic there is still anti-biotic effect, lasts 1.5 hours to 6 hours
  • can occur because as medication is excreted as long as concentration stays above MIC there is still antibacteria like effect
57
Q

Minimal inhibitory concentration

A

Minimum amount of drug that will stop visible growth of bug

58
Q

Minimal bacteriocidal concentration

A

Minimum concentration of drug that will kill the bug

59
Q

How to choose proper drug

A

-empirically treat and then

60
Q

Antimicrobials with activity against e coli

A 
• Penicillin: Most commonly given
• Cephalosporin: Most commonly given
• Aminoglycosides: It’s a synergistic drug
• Sulfonamides
• Trimethoprim
-fluoroquinolones
61
Q

Physical barriers to infection

A

-mechanical, chemical, microbiological

62
Q

Skin barriers

A
  • m: epi cells are joined by tight junction, longitudinal flor of air/fluid
  • c: fatty acids, antimicrobial peptides
  • M: normal flora
63
Q

Gut barriers

A
  • m: epi cells are joined by tight junction, longitudinal flor of air/fluid
  • c: low pH, antimicrobial enzymes, antimicrobial peptides
  • M: normal flora
64
Q

Lungs

A
  • m: epi cells are joined by tight junction, movement of mucus by cilia
  • c: pulmonary surfactant, antimicrobial peptides
  • M: normal flora
65
Q

Eye, nose, oral cavity

A
  • m: epi cells are joined by tight junction,tears, nasal cilia
  • c: antimicrobial enzymes in tears and saliva
  • M: normal flora
66
Q

How do antimicrobial peptides kill?

A

Disrupting pathogen membranes

67
Q

Function of pentraxins

A

bind microbes and target them to phagocytes

68
Q

Cells of innate immune system

A

-eosinophil, basophil, neutrophil, NK, T cell, mast cell, monocyte, macrophage, dendritic cell

69
Q

Granulocytes

A

Eosinophil, basophil, neutrophil, NK cell

70
Q

Phagocytic cells

A

-neutrophil, monocyte, dendritic cell, macrophage

71
Q

Tissue resident cells

A

dendritic cell, macrophages, mast cell, plasma cell

72
Q

lymphocytes

A

T cell, B cell

73
Q

recognition mech of innate immunity

A

-rapid response, fixed, limited # of specificity, constant during response, multiple cell types

74
Q

recognition mech of adaptive immunity

A

-slow response, variable, numerous highly selective specificities, improve during response, lymphocytes only

75
Q

complement role in first line defense

A

Complement coats the surface of bacteria and extracellular virus particles and makes them more easily phagocytosed. Without such a coating, many bacteria resist phagocytosis, especially those that are enclosed in thick polysaccharide capsules.

76
Q

Complement pathways

A
  • alternative, lectin, classical

- all lead to activation of C3

77
Q

Alternative pathway

A
  • works at start of infection

- innate immunity

78
Q

Lectin pathway

A
  • innate immunity

- requires time

79
Q

Classical pathway

A
  • part of both innate and adaptive immunity
  • requires the binding of either antibody or an innate immune-system protein called C-reactive protein to the pathogen’s surface.
80
Q

Macrophage effector functions

  • bacteria binding to macrophage
  • bacterial component binding to macrophage
A
  • induces engulfment and degradation

- induces the synthesis of inflammatory cytokines

81
Q

Neutrophils moving to infection

-steps

A
  • rolling adhesions, tight binding, diapedesis, migration
  • Neutrophils have CXCL8 receptors and endothelial cells of vasculature near site of infection will express CXCL* so the neutrophils can bind to that site and then move though the vessel to get to the infection
82
Q

TLR-4

  • binds to?
  • cells carrying receptor
  • location
A
  • binds to LPS of gam - bacteria
  • macrophage, dendritic cell, mast cells, eosinophils
  • plasma membrane
83
Q

NF Kappa B

  • used in
  • function
  • what occurs when non function
A
  • TLR’s and NLR
  • transcription factor that transcribes proinflammatory cytokines
  • non function then you cannot combat against bacterial agents because you cannot produce defensins and cannot recruit WBC to help with fighting bacteria
84
Q

NLR

A

-important for activation of the inflammasome and very important in transcribing definsins

85
Q

NEMO disease

A
  • A subunit of one of the IkB kinases in the NF-kB pathway is missing therefore
    NF Kappa B cannot be released from inhibitory marker to induce transcription
    -leads to abnormality in skin, hair, teeth and makes patient susceptible to bacterial infections
86
Q

Neutrophils

A

-express many bacterial and fungal receptors making them super phagocytes

87
Q

Dendritic cells and NK cells

A
  • activate NK cells and help them to proliferate
  • once NK cells are abundant and outnumber dendritic cells then they kill dendritic to regulate further activation of NK cells
  • once NK cells are scarce and are outnumbered by the dendritic cells they drive the dendritic cells to mature into the form that initiates adaptive immunity
88
Q

Netosis

A

unique form of cell death that is characterized by the release of decondensed chromatin and granular contents to the extracellular space.

89
Q

Absence of — would prevent complement cascade from amplification?

A

cleavage of C3 by C3bBb

90
Q

What molecule directly prevents formation of C3 convertase?

A

Factor I

91
Q

Molecule that most directly stimulates migration of neutrophils from blood to tissues

A

C5a

92
Q

Molecule that directly mediates destruction of complement-coated microbes

A

C3b

93
Q

C3 deficiency

A
  • When you don’t have C3, you don’t opsonize bacteria as well, so phagocytes are not phagocytizing as well. This leads to increased susceptibility of infection
  • lack of opsonization and inability to utilizr the membrane attack pathway
94
Q

Factor H/I deficiency

A

-causes uncontrolled activation of C3 via the alternative pathway resulting in depletion of C3 and causing C3 deficiency and susceptibility to bacterial infection

95
Q

What is mechanism of joint pain in C3 deficiency?

A

stems from buildup of immune complexes in the joint

96
Q

Factor D deficiency

A

Factor D cleaves factor B, so a deficiency in this factor would lead to factor B not being cleaved, and you can’t make C3 convertase. If you can’t make C3 convertase, you can’t cleave C3 which results in decreased opsonization because you can’t place C3b on pathogen’s surface. Pts with Factor D deficiency are at risk for serious infections.

97
Q

Factor P deficiency

A

the factor 3 convertase from alternative pathway will not be stabilized so it will disintegrate very quickly and opsinozation will not work effectively

98
Q

lymph capillary

  • other name
  • description
  • role
A
  • initial terminal capillaries
  • discontinuous, anchored to the ECM, single layer of epithelial cells,
  • role is the formation of the lymph.
99
Q

collectine lymphatics

A

-contain smooth muscles so they are able to propel the lymph from one portion to the other.

100
Q

lymph node

A

capsulated, it filters and it’s a reservoir for WBC.

101
Q

lymphatic trunks

A

drain from the nodes to the ducts

102
Q

lymphatic ducts

A

where the lymphatic is entering back into the venous system

103
Q

What contributes to net flow rate in lymphatics

A

Formation and propulsion.

104
Q

driving forces of lymphatic formation

A

Oncotic pressure and hydrostatic pressure. They help to move the fluid into the interstitial space and then from the interstitial space to the lymphatics.

105
Q

driving forces of lymphatic propulsion

A

Systemic forces like blood pressure, respiration, exercise and massage. These systemic forces create a change in pressure which is important because fluid moves from high pressure to low pressure.

106
Q

arteries and lymphatics

A

Lymphatic vessels are next to arteries which pulsate and that pulsating causes the lymphatic vessels and collecting vessels to continue to move.

107
Q

Importance of GAGS in lymph formation

A
  • highly negatively charged so they repel each other and because of that they are able to establish interstitial volume and neutrality which helps to create osmotic gradient leading to lymphatic formation so that the lymphatics can pick up the fluid.
  • if disrupted there is less lymphatic formation in the interstitial terminal lymphatics.
108
Q

anchoring filaments

A
  • anchoring filaments pull open the terminal lymphatic capillaries and help to create a tissue pump or a second valve, increasing the luminal volume, causing the fluid to get in and forming the lymph and then sending them to the collecting lymphatics
  • if damaged edema can be formed
109
Q

sterling forces

A

needed to get the fluid from the capillaries into the interstitial space are hydrostatic and oncotic pressures

110
Q

net filtration

A
  • hydrostatic forces are greater than the oncotic forces

- hyrdostatic pressure is pushing pressure and will push the liquid from the capillaries to the interstitial space

111
Q

net resorption

A
  • oncotic forces are greater than hydrostatic forces

- oncotic pressure is pulling pressure and will pull the liquid from the interstitial space back to the capillary

112
Q

venous insufficiency effect on lymph

  • why?
  • treatment
A
  • Venous insufficiency means she’s cant move blood back to the heart so there is increased hydrostatic pressure in capillary on venous end, therefore less liquid from interstitum can be pulled back into the capillary and the fluid in interstitum is too much from lymph to completely drain which creates edema
  • Also has fibrotic tissue which is leading to remolding of her ECM which could be affecting her Gags and anchoring filaments that affects lymphatic formation
  • exercise and compression socks
113
Q

thymus

A

-primary lymphoid tissue where the T-cells originate

114
Q

activation of adaptive immune response

A

-dendritic cell will follow lymphatics from tissue to nearest lymph node, then present the antigen from the bacteria to the t-cells, t-cells will activate b cells which will turn into plasma calls and being making anti-bodies to bind antigen

115
Q

what happens if antigen/pathogen is inserted directly in blood?

A

-it will travel to spleen first and be filtered out there since the spleen is abundant in lymphocytes (specifically T cells)

116
Q

what cells are located in the peri-articular sheath of the spleen?

A

-t-cells

117
Q

effect of Wuchereria bancrofti

A

-live in efferent lymphatics which causes a mechanical obstruction in those vessels, so there is a build up and no forward flow in the collecting lymphatics, the smooth muscles get stretched out further and stop working, the pressure builds up, the collecting lymphatics starts to distend. hydrostatic pressure in the lymphatics increases so fluid goes into the tissues instead of being moved through lymph vessels

118
Q

what is primary cause of edema?

A

-genetic defect, specifically one in VEGF formation which will usually stimulates the formation of new capillaries (both arterial/venous and lymph) so a mutation will lead to absence of terminal lymphatics and absence of lymph formation, causing build up of fluid in interstitum

Unit 4: LGS (7 decks)

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