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ESA 2 > Infection > Flashcards

Infection Flashcards

1
Q

What colour do gram positive bacteria stain?

A

Purple

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2
Q

What colour do gram negative bacteria stain?

A

Pink

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3
Q

What size peptidoglycan layer do gram positive bacteria have?

A

Thick

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4
Q

What size peptidoglycan layer do gram negative bacteria have?

A

Thin

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5
Q

Which bacteria have an outer membrane?

A

Gram negative

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6
Q

How much lipopolysachharide do gram positive bacteria have?

A

Low levels

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7
Q

How much peptidoglycan content do gram negative bacteria have

A

High content

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8
Q

Which type of bacteria are more resistant?

A

Gram negative

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9
Q

What type of bacteria tend to favour exotoxins instead of endotoxins

A

Gram positive

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10
Q

Which type of bacteria tend to favour endotoxins instead of exotoxins?

A

Gram negative

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11
Q

What are endotoxins?

A

Bacterial toxins consisting of lipids located within a cell

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12
Q

Name some gram positive cocci

A 
Staph aureus
Coagulase negative staph
Streptococcus pneumoniae
Strep pyogenes
Beta and alpha haemolytic strep
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13
Q

Name some gram positive bacilli

A

Clostridium difficile
Listeria monocytogenes
Bacillus anthracis
Bacillus lereus

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14
Q

Name some gram negative cocci

A

Neisseria meningitidis
Neisseria gonorrhoeal
Moraxella catarhalis

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15
Q

Name some gram negative bacilli

A

Escherichia coli
Haemophilus influenza
Klebsiela pneumoniae
Salmonella typhi

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16
Q

What are some key viruses to know?

A 
Adenovirus
Norovirus
Epstein Barr
HIV
Hepatitis
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17
Q

What are 2 classifications of fungi?

A

Yeasts and moulds

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18
Q

What are some examples of yeast infection

A

Candida albicans
Cryptococcus Noeformans
Pneumocystis jiroveci

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19
Q

What are some examples of mould infections?

A

Aspergillus

Dermatophytes (ring worm, athletes foot)

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20
Q

What are single cell fungi

A

Yeasts

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21
Q

What are the 2 classifications of parasites

A

Protozoa

Helminths

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22
Q

What are Protozoa

A

Single cell parasites

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23
Q

What are some examples of Protozoa?

A 
Malaria
Giardia Lambia
Cryptosporidium parvum
Plasmodium falciparum
Trypanesoma cruzi
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24
Q

What are some examples of helminths

A

Roundworms
Tapeworms
Flukes

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25
Q

What is first line defence in inate immunity?

A

Barriers- physical, physiological, chemical, biological

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26
Q

What are some examples of inate immunity physical barriers?

A

Skin
Mucousal membranes
Bronchial cilia

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27
Q

What are some examples of inate physiological barriers

A

Vomiting
Coughing
Sneezing
Diarrhoea

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28
Q

What are some examples of inate immunity chemical barriers?

A

Low PH of vagina, stomach, skin

Antimicrobial- IGA, lysozymes, gastric acid

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29
Q

What are biological barriers in reference to 1st line defecnce

A

Natural flora

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30
Q

What 3 things does the natural flora do that is beneficial for the host?

A

Competes for resources
Produce antimicrobial
Synthesise vitamins

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31
Q

What are some issues with normal flora?

A

Can be displaced out of its normal environment
Can be pathogenic in immunocompromised
Can be depleted by antibiotics

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32
Q

What are second line defences of the inate immune system?

A

Phagocytosis
Opsinisation
Complement system
Cytokinesis

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33
Q

What do pathogens have on them that allow them to be detected non specifically?
What are they

A

Pathogen associated molecular pattern PAMP

Carbohydrates, lipids, proteins, nucleic acids

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34
Q

What is a pamp and what is it recognised by?

A

Pathogen associated molecular pattern

Pathogen recognition receptors PRR

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35
Q

What’s a PRR and what does it recognise

A

Pathogen recognition receptor- PAMPS

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36
Q

Aside from PAMPS what else can a pathogen have that will enhance recognition?

A

Opsonins attached

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37
Q

What are some examples of phagocytes that could be involved in the inate immune response

A 
Macrophages
Monocytes
Neutrophils
Basophils
Eisonophils
NKC
Dendritic cells
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38
Q

What organs are macrophages present in?

A

All of them

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39
Q

What do macrophages present to?

What can they produce?

A

T cells

Cytokines/ chemokines

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40
Q

Monocytes are found where? What can they differentiate into?

A

Found in the blood

Macrophes or dendritic cells

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41
Q

Where are neutrophils found?
How are they recruited in the inate immune response?
What can they ingest?

A

In the blood
Recruited by chemokines
Ingest pyogenic species

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42
Q

Basophils/ mast cells are early actors in what?

A

Inflammation

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43
Q

Eisonophils are our defence mechanism against what?

A

Parasites

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44
Q

What do NKC target?

A

Abnormal host cells (virus, cancer)

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45
Q

What do dendritic cells do?

A

Present microbial antigens to T cells

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46
Q

What are some examples of opsonins

A

Complement: C3b, C4b
Antibodies: IgG, IgM
Acute phase proteins: CRP, mannose binding lectin MBL

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47
Q

Once a PRR has attached to a PAMP what happens?

A

Engulfment
Phagolysosome formation
Oxygen dependent and oxygen independent breakdown

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48
Q

What are some oxygen dependent examples of breakdown in the phagolysosome

A

Respiritory burst with oxygen radicals:
Hydrogen peroxide
Hydroxyl radicals
NO

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49
Q

What are some oxygen independent actions in the phagolysosome

A

Lysozyme
Transferrin
Cationic proteins
Proteolytic enzymes

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50
Q

What are the 2 complement pathways and how are they activate?

A

Alternate: initiated by cell surface microbial

MBL (classic)- when Manose binds to Manose binding lectin

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51
Q

What is the role of C3a and C5a in the complement pathway?

A

Recruit phagocytes

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52
Q

What is the role of C3b-C4b in the complement pathway

A

Opsinisation

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53
Q

What is the role of C5-C9 in the complement pathway

A

Membrane attack complex

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54
Q

Opsonins like IgM and IgG are essential in what? Especially when?

A

Clearing encapsulated bacteria

Especially in asplenic

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55
Q

What signals for cytokine release?

A

Toll like receptors (signalling PRR)

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56
Q

What’s a signalling PRR

A

Toll like receptor

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57
Q

What are the 3 functional categories of cytokines

A

Cytokines that regulate inate
Cytokines that regulate adaptive
Cytokines that regulate haematopoesis

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58
Q

Cytokines that regulate the inate immune system are mostly produced by what

A

Macrophages and dendritic cells

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59
Q

What are some key inate immune response cytokines

A

TNF
IL-1
IL-6

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60
Q

What 4 big affects do the cytokines TNF alpha, IL-1 and IL-6 have in the inate immune response

A

Stimulate liver
Stimulate bone marrow
Stimulate hypothalamus
Stimulate inflammation

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61
Q

What effect does TNF, IL1 and IL6 have on the liver in the inate immune response

A

Production and excretion of CRP and MBL

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62
Q

What effect does TNF, IL1 and IL6 have on the bone marrow in the inate immune response

A

Neutrophil mobilisation

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63
Q

What effect does TNF, IL1 and IL6 have on the hypothalamus in the inate immune response

A

Stimulates an increase in body temp

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64
Q

TNF alpha, IL6 and IL1 stimulate inflammation in the inate immune response, what 4 things does this do

A

Vasodilation
Increased vascular permeability
Adhesion molecules
Neutrophil attraction and invasion

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65
Q

What does a macrophage/dendritic cell do to initiate a adaptive immune response

A

Capture
Process
Present

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66
Q

Where are antigen presenting cells strategically located?

A

Skin (SALT)
Mucous membranes (GALT, NALT, BALT, GUALT)
Lymphoid organs
Blood circulation

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67
Q

What antigen presenting cells are found in the skin

A

Langerhanns

Macrophages

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68
Q

What antigen presenting cells are found in lymphoid organs

A

B cells
Dendritic cells
Macrophages

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69
Q

What antigen presenting cells are found in mucous membranes

A

Dendritic cells

Macrophages

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70
Q

What can the ‘Capture’ Portion of capture process present be?

A

Phagocytosis (whole microbe)

Micropinocytosis (particles)

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71
Q

What does MHC stand for?

A

Major histocompatability complex

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72
Q

Where are MHC genes located

A

Chromosome 6

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73
Q

What HLA genes are present on all nucleated cells

A

HLA A/B/C

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74
Q

What do HLA A/B/C code for>

A

MHC class 1

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75
Q

What cells have HLA Dr/Dq/Dp ?

What does it code for?

A

Dendritic, macrophages, B cells

Class 2 MHC

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76
Q

What are some key features about the expression of class 1 and 2 HLA genes

A

Co dominant expression

Polymorphic genes

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77
Q

What do MHC class 1 present

A

Intracellular- virus, tumour, intracellular bacteria

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78
Q

What do MHC class 1 present to?

A

CD8

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79
Q

What is TAP and what is it to do with?

A

Transport associated presentation. Associated with MHC class 1 processing

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80
Q

Where do intracellular contents bind to the MHC1 molecule before presentation?

A

RER

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81
Q

What is a CD8 cell also known as?

A

T Killer cell

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82
Q

CD8 is associated with what adaptive immune response?

A

Cell dependent

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83
Q

When a CD8 cell beings to a MHC1 complex what is the result

A

Activation to a cytotoxic t lymphocyte.

Perforins and granzymes used on the infected cell

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84
Q

What MHCs are used in the cell dependent response?

A

Both MHC1 and MHC2

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85
Q

What is the role of MHC2 in the cell depdendent response?

A

Recruits CD4 TH1 cells

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86
Q

CD4 TH1 cells:
What part of the adapative immune response?
What do they secrete?
What does that activate?

A

Cell dependent
IFNg
Activate B cells to make IgG antibodies and macrophages to phagocytise

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87
Q

What is costimulation in relation to the adaptive immune response?

A

Naive T helper cells receive cytokines co stimulation as well as MHC
TH1, TH2, TH17

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88
Q

Where are MHC2 proteins exported from?

A

from the ER in a vesicle

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89
Q

What blocks the binding cleft of MHC2 protein?

A

Class2 associated invariant chain peptide CLIP

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90
Q

What removes CLIP to replace it with an antigen peptide, in the processing of an MHC2 protein?

A

HLA-DM

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91
Q

What do MHC class 2s present to?

A

CD4 cells- TH1,2,17

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92
Q

what are CD4 cells

A

T helper cells

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93
Q

What MHC is needed for the humoral response?

A

MHC2

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94
Q

In the humoral response what does MHC2 present to

A

CD4 TH2 and TH17

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95
Q

An important aspect of the binding clefts in MHC molecules is what?

A

They are highly polymorphic

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96
Q

In the humoral response. What CD4 cell attracts neutrophils? What does it use?

A

CD4 TH17 uses IL17 to attract neutrophils

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97
Q

What part of the humoral response recruits eosinophils?
When would this happen
What’s secreted

A

MHC2-> CD4 TH2
To kill parasites
Secreted IL-5 to attract eosinophils

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98
Q

How are B cells and Mast cells recruited in the humoral response?

A

CD4 TH2 (activated by MHC2) secretes IL-4, this attracts both mast cels and B cells

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99
Q

A B cell recruited by a TH2 CD4 cell will do what?

A

Differentiate into B memory
Complete isotype switching and secrete antibodies
Activating phagocytosis and complement

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100
Q

What does a mast cell secrete as an antibody

A

IgE

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101
Q

What is IgG when is it used

A

Antibody, FC dependent

Complement activation, neonatal immunity, toxins/virus neutralisation

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102
Q

What does IgM activate?

A

Complement

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103
Q

What does IgE do?

A

Provides immunity against helminths and mast cell degranulation

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104
Q

What is IgA for?

A

Mucousal immunity

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105
Q

What antibody is highest in initial exposure to a pathogen?

A

IgM

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106
Q

Which antibody is higher in exposure to the same pathogen on the second time?

A

IgG

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107
Q

What is a benefit of higher IgG on second exposure?

A

Faster, longer, higher affinity response

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108
Q

What is septic shock

A

Persisting hypotension, requiring treatment despite fluidn resuscitation

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109
Q

What is sepsis?

A

Life threatening organ dysfunction due to a dysregulated response to infection

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110
Q

What first has to happen before sepsis can begin to be set in motion?

A

The pathogen must enter the blood stream

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111
Q

What becomes amplified and dysregulated (mostly) in sepsis?

A

Cytokine release

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112
Q

What 4 big things does the amplified, dysregulated release of cytokines invoke in sepsis?

A

Increase vasodilation and capillary permeability
Pyrexia induction at hypothalamus
Coagulation, metabolism and neuroendocrine activation
Post hyperinflammation induced immunoparalysis

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113
Q

What are 5 symptoms of sepsis

A 
Decreased BP
Raised HR
Raised RR
Temp up or down
DIC
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114
Q

Why do we get increased HR in sepsis

A

There is a drop in BP, HR rises to compensate

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115
Q

Why is there a drop in BP with sepsis?

A 
Mass vasodilation (distributorry)
DIC
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116
Q

Why does RR rate increase in sepssis

A

As a response to hypoxia

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117
Q

What are the sepsis 6

A

Give 3- iv fluids, oxygen, IV ABx

Take 3- urine, blood cultures, lactate and FBC

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118
Q

Why give IV fluids in sepsis

A

Raise BP

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119
Q

Why give oxygen in sepsis

A

Patient likely hypoxic

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120
Q

Why measure urine output in sepsis

A

Decrease indicated organ failure

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121
Q

What does sepsis result in?

A

Multi organ failure

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122
Q

How can streptocccus be divided by haemolysis?

A 
Alpha haemolytic (partial)
Beta haemolytic (complete)
Gamma haemolytic (no haemolysis)
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123
Q

How many different types of strep are there?

A

6

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124
Q

What haemolytic group is strep pneumonia

A

Alpha haemolytic

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125
Q

What streps are alpha haemolytic? What does this mean? What is seen on agar?

A

Strep pneumoniae and strep viridans
Partially breaks down rbc
Green halo

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126
Q

Does strep pneumoniae have a capsule?

A

Yes

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127
Q

What 4 main diseases can strep pneumonia cause?

A

Meningitis (no 1 cause in adults)
Pneumonia (no 1 cause in adults)
Otitis media
Sinusitis

MOPS

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128
Q

What are the 2 virulence factors that strep pneumonia has?

A

Capsule

IgA protease

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129
Q

Why is is important that strep pneumoniae has a IgA protease?

A

Because IgA is the main antibody in mucousal surfaces, where it mainly infects

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130
Q

What gram stain is strep pneumonia?

A

Gram positive diplodocus

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131
Q

Who is catalase positive? Strep or staph?

A

Staph

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132
Q

Which staph is coagulase positive? Staph aureus or staph epidermis?

A

Staph aureus

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133
Q

What gram stain is staph aureus

A

Gram positive cocci clusters

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134
Q

Why does staph aureus have a golden halo on blood agar?

A

It’s a beta haemolytic and has broken down the RBC completely

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135
Q

What are 3 important endotoxins staph aureus has?

A

Protein A- binds antibodies at FC portion (less opsinisation)
Coagulase- causes coagulation (fibrin strands around bacteria) allows it to cause abscesses
Penicilinase- normal penicillins broken down, methicillin can in theory work but not in MRSA

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136
Q

What are 3 important exotoxins staph aureus has?

A

Exfoliatin- causes scalded skin syndrome
Enterotoxin- cause gastroenteritis
TSST-1- toxic shock syndrome

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137
Q

What disease can staph aureus cause from direct invasion

A 
Almost every system
Meningitis
Acute bacterial endocarditis
Pneumonia
Sepsis
UTI
Osteomyelitis
Septic arthritis
Skin infection/ cellulitis
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138
Q

How do we treat staph aureus

A

Penicillinase resisitant beta lactams or 1st gen cephalosporins

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139
Q

How has MRSA changed to become resistant to Methicilin? What do we treat it with?

A

Developed a new penicillin binding protein

Vancomycin

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140
Q

What is staph epidermidis a normal part of the flora for?

What’s the clinical relevance for this?

A

Normal skin flora

Contaminates samples frequently- urine and bloods

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141
Q

What does staph epidermidis form? Therfore what does it frequently infect?

A

Biofilm

Prosthetic joints, valves, IV lines

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142
Q

How does staph epidermidis cause infection?

How do we treat it? Why

A

By causing a biofilm

Vancomycin as the biofilm makes it very resistant

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143
Q

What gran stain is strep viridans

A

Postitive

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144
Q

What kind of haemolysis does strep viridans produce

A

Alpha

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145
Q

Why is it called strep viridans

A

Green from alpha haemolytic

Green salad gets stuck in your teeth

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146
Q

Where is strep viridans normal flora?

A

Oral and GI flora

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147
Q

How can strep viridans cause dental cavities?

A

Extracellular dextran

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148
Q

What can strep viridans do if it gets in the blood stream eg from dental work?

A

Sub-acute bacterial endocarditis (using dextran) strep sanguinus
Can cause abscess anywhere (blood borne) strep intermedius

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149
Q

Where would the following sub species of strep viridans cause infection?
Strep mutans
Strep sanguinis
Strep intermedius

A

Strep mutans- mouth
Strep sanguines- heart valves
Strep intermedius- blood borne tissue abscess

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150
Q

What is non multidrug resistant?

A

Not succeptible to 1 or less agents in 2 or less antimicrobial classes

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151
Q

What is MDR?

A

Multi drug resistant- non succeptible to at least 1 agent in 3 or more antimicrobial categories

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152
Q

What is XDR?

A

Extensively drug resistant- non succeptible to at least one agent in all but 2 or fewer categories

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153
Q

What is PDR

A

Pan drug resistant- not succeptible to all agents in all categories

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154
Q

What is antimicrobial stewardship

A

Coordinated interventions designed to improve the selection and use of antimicrobials

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155
Q

What kind of studies have demonstrated antibiotic resistance

A

Lab studies
Ecological studies
Individual level studies

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156
Q

What are the 3 main elements of antimicrobial stewardship

A

Persuasive- education, opinion leaders
Restrictive- authorisation needed, stop orders etc
Structural- records, lab tests

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157
Q

What are some examples of process measures in antimicrobial stewardship

A

Defined daily dose/1000 beds
Adherence guidelines
Benchmarking

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158
Q

What are some outcome measures of antimicrobial stewardship

A

Patient outcomes, infection rates, emergence of resistance

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159
Q

What defines a healthcare infection?

A

Onset at least 48 hours after admission

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160
Q

What are the more prevelant healthcare infection sites

A

UTI
GI
Surgical wound site
Chest (pneumonia )

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161
Q

What are some viral examples of healthcare infection

A

HEP B, C, HIV
Norovirus
INfluenza

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162
Q

What are some bacterial examples of healthcare infections?

A 
Staph aureus (MRSA)
CDIFF
ECOLI
Klebsiella
Pseudomonas
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163
Q

What re some fungal healthcare infections?

A

Candida

Aspergillus

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164
Q

The 4 ps that determine the likelihood of an acquired healthcare infection are what

A

4 ps
Patient (are they imminsupressd, diabetic, obese)
Pathogen (its virulence factors, ecological interactions)
Practice (of healthcare workers the polices etc)
Place (fixed and variable)

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165
Q

What are some examples of patient interventions to lower the risk of healthcare infections

A 
Antibiotic prophylaxis
Skin prep
Hand hygiene
Nutrition
Screening
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166
Q

How can we reduce patient to patient transmission

A

Barrier nursing/ isolation

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167
Q

What are some enviromental interventions that can reduce the spread of healthcare infections

A

Layout ie where the sinks, toilets are etc
Correct use of equipment
Positive and negative pressure Rooms

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168
Q

What it the I face in identifying a potentially harmful pathogen?

A 
Identify (A_F)
Isolate
Investigate
Inform
Initiate
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169
Q

What is the A-F in identifying harmful pathogens

A 
Abroad?
Blood borne?
Colonised (MDR)
Diarrhoea and vomiting
Expectorating
Funny looking rashes
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170
Q

What does person to person indirect require?

A

A vector such as a mosquito

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171
Q

What’s an endemic disease?

A

It’s usual background rate

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172
Q

What is an outbreak in relation to disease?

A

Two or more linked cases in time and place

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173
Q

What’s an epidemic in relation to disease?

A

A rate of infection greater than the endemic rate

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174
Q

What is a pandemic in relation to disease?

A

Very high rate of infection spreading across regions

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175
Q

What is a pandemic often due to

A

Antigen shift, abrupt change in dna making everyone succeptible

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176
Q

What’s antigen drift?

A

Slow change in dna of an infectious agent

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177
Q

What is the R0 of a pathogen?

A

The basic reproduction number. The average number of cases generated in a overwise healthy population

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178
Q

If R0 is equal to 1 what does that mean? What if its above 1

A

1=stable number of cases

Above 1 means its increasing

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179
Q

What can lead to an epidemic or pandemic

A

Sudden change in pathogen eg new virulence or resistance
Change in practice or social behaviour
Change in the patient that it can affect eg low immune

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180
Q

What determines how transmissible an organism is?

A

Infectious dose- the number of organisms required to cause infection

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181
Q

How is the infectious dose altered?

A

By the immunity of the hose and the virulence of the microorganism

182
Q

What do we see graphically with epidemics?

A

Epidemic curves as cases slowly increase to peak of susceptibility then decrease

183
Q

What is herd immuity

A

Vaccinating enough people to protect the vulnerable, decreased change of spread to almost 0

184
Q

What does HIV make you more succeptible to?

A

Infections, in particular latent infections, fungus and Protozoa

185
Q

In viruses how can the genetic material be stored?

A

DNA or RNA

Double strand or single strand

186
Q

In Viruses they have a protein shell, whats it called?What shape can it be?

A

Capsid
Helical (rod/coiled)
Icosahedral (spherical)

187
Q

A lipid envelope of a virus is derived from what?

A

Host cell membrane and has viral antigens

188
Q

What does a HIV virus bind to and fuse with?

A

Binds to CD4 receptor and coreceptor (t helper cells, monocytes and macrophages)

189
Q

How is the info/ genetics kept in the HIV virus

A

Single strand RNA (retrovirus)

190
Q

Once the HIV virus has bound to CD4 receptor and coreceptor it empties its cellular contents, what happens?

A

The single strand RNA is converted too DNA by reverse transciptase

191
Q

One HIVs rna has been converted to DNA heat happens in the CD4 cell?

A

The viral DNA is recombined into host DNA with integrase

192
Q

Once HIVs viral DNA has been integrated into the host. What happens?

A

Sets of viral proteins are made

Immature viruses push out the cell taking some of the cell membrane with it

193
Q

Once an immature HIV virus has pushed out of the host cell, how does it mature?

A

Proteases cut the protein chains, these are recombined to make a new mature virus.

194
Q

How is HIV transferred ?

A

Bodily fluids with mucousal tissue/blood or broken skin

195
Q

What happens to viral load with initial infection of HIV?

A

Initial massive increase

196
Q

Why can you not test for HIV initially?

A

The virus is initially in the lymph tissue

197
Q

What happens to CD4 initially with infection, then what happens?

A

Slight drop
Recovers
Slowly drops over time

198
Q

What CD4 count in HIV is unsymptomatic

A

500 and above

199
Q

What CD4 count constitutes AIDS

A

200 or below

200
Q

How do you diagnose HIV, how long before its detectable?

A

Blood serology- HIV antigen, HIV antibody.

4 weeks

201
Q

The rapid HIV tests can be interpreted how?

A

If negative very accurate

If positive serology needed

202
Q

How do anti-retro viral drugs target HIV

A 
Inhibiting at 4 stages 
Entry to cell
Reverse transcriptase
Intergrase
Maturation proteases
203
Q

How do you treat HIV

A

2 nucleoside reverse transcriptase inhibitors and 1 of either: non-nucleoside reverse transcriptase inhibitors, protease inhibitor, integrase inhibitor

204
Q

Why give 3 drugs in HIV retroviral treatment

A

Millions of viral replications and mutations occur, resistance develops quickly

205
Q

What is hepatitis?

A

Inflammation of the liver

206
Q

What systemic viruses cause collateral liver damage?

What is special about hepatitis

A

EBV, CMV

Hepatitis replicates specifically in hepatocytes

207
Q

What HEPS cause chronic illness?

A

B
C
D with B

208
Q

What is different about the structure of hep B compacted to A,C,D,E?

A

It is double stranded DNA and enveloped (c is also enveloped)

209
Q

What genetic material do HEP A,C,D,E all have?

A

Single stranded RNA

210
Q

HEP A C D E all share the fact that they are single stranded RNA.
What seperated C from ADE?

A

C is enveloped icosahedral

ADE nonenveloped icosahedral

211
Q

What is billirubin the breakdown of?

212
Q

What does the liver do to billirubin?

A

Conjugates it

213
Q

How does haem get converted to billlirubin, where does this happen?

A

Haem-> billivurdin-> billirubin

In the RES

214
Q

How does billirubin travel in the blood stream?

A

With albumin

215
Q

Where does conjugated billirubin go?

A

Either excreted as urine or to bile and then into the small intestine

216
Q

What happens to conjugated billirubin in the small intestine (after being secreted as bile)

A

Conjugated billirubin-> urobillin-> stercobillin -> faeces

217
Q

What 3 categories of jaundice are there? Ie where is it occurring

A

Prehepatic
Cholestatic intrahepatic
Cholestatic extrahepatic

218
Q

What is prehepatic jaundice caused by?

A

Haemolysis

219
Q

What are some examples of cholestatic intrahepatic causes of jaundice?

A 
Viral hepatitis
Drugs
Alcoholic hepatitis
Cirrhosis
Autoimmune 
Pregnancy
220
Q

What are some examples of cholestatic extrahepatic jaundice causes

A

Common duct stones, carcinoma of bile duct, billary stricture

221
Q

How can we test liver function

A

billirubin levels
Liver transaminases ALT, AST
Albumin levels
Coagulation

222
Q

What indicates hepatocyte damage?

A

High ALT/AST

223
Q

What does low albumin level indicate?

A

Liver isn’t producing enough albumin

224
Q

In liver damage what happens to coagulation tests

A

INR and prothrombin time rises

225
Q

What does alkaline phosphotase measure?

A

Billary tract cell damage/ cholestasis

226
Q

How is hep b transmitted in 75% of cases, how else can it get transmitted?

A

Vertical transmission 75%

Sexual content, IV, needle stick or blood exposure

227
Q

What are some symptoms of hep B infection

A

Fatigue, jaundice, abdominal pain anorexic, arthralgia

228
Q

What is the incubation period in hep b

A

6 weeks - 6 months

229
Q

What levels ALT/AST is seen in hep b

A

In the 1000s

230
Q

How many cases of hep B develop chroniciity?

231
Q

In hep B serology there are 2 antigens and 4 antibodies. What are these? In order of when they are seen in serology

A 
Surface antigen
E antigen
Core antibody IGM
E antibody HBeAB hep b e antibody 
Surface antibody HBsAB hep b surface antibody 
Core antibody IGG
232
Q

In Hep B serology, what is the first thing to appear (within 6 weeks) what is accomponied with it?

A

Surface antigen appears
Rise in ALT
Hep B virus DNA (PCR to show viral load)

233
Q

After the surface antigen is detectable in serology of hep B, what is next, what is important about this?

A

The E antigen presents HBeAg

Highly infectious

234
Q

What follows the surface antigen and the e antigen in blood serology?

A

The core antibody IGM

235
Q

After the core antibody is detectable in hep B serology, what is present, what does this signal?

A

The E antibody HBeAB. Signals the dissapearnace of the e antigen and its infectivity

236
Q

What is the last antibody to appear in Hep B serology? What does it signal?
What persists for life following hep B infection?

A

Surface antibody last to appear and signals viral clearance

IGG persists for life

237
Q

How are HEP B infected patients managed?

A

Long term antivirals makes patient inactive carrier (low viral load and normal LFTs)

238
Q

What does a hep B vaccine produce in patients?

A

The surface antibody response

239
Q

What would someone who’s recieved a vaccine for hep b have in serology, (what will they not have)

A

Surface antibody present

No surface antigen or core antibody.

240
Q

What are 90% of the cases of hep C attributed to?

241
Q

How many hep C cases become chronically infected?

242
Q

What symptoms are associated with hep c?

A

80% have no symptoms. The rest are vague fatigue, anorexia, nausea, abdo pain

243
Q

How do we test for hep C? When is it positive? What tests for chronic infection ?

A

Hep C antibody only present even after clearance or cure

Viral PCR for chronicity

244
Q

What do we have for hep C that we dont have for hep B?

What do these not stop

A

Direct acting antiviral drugs

Don’t stop reinfection

245
Q

What is HIV PEP

A

Early initiation of anti-retro viral structure to reduce risk of HIV
3 ARVs for 28 days

246
Q

What is a prion?

A

A chemical structure that can generate a copy of themeselves and spread person to person

247
Q

What can prions withstand?

A

High temperatures

248
Q

What are bacteriaphages

A

A virus within a bacteria

249
Q

What bacteria can’t survive outside of host cell?

A

Mycoplasma, chlamydiae

250
Q

What classification system is used for viruses?

What does it seperate them based on?

A

Baltimore classification system
Single strand or double strand
RNA or DNA
+ sense or - Sense

251
Q

What has to happen to + sense strand of RNA? In virus

A

Needs to be converted to be read by mRNA

252
Q

What categories can DNA viruses be grouped into?

A

Single strand non enveloped
Double strand non enveloped
Double strand enveloped

253
Q

RNA viruses can be classified as what

A

Single strand icosahedral + non enveloped
Single strand icosahedral/helical + enveloped
Single strand helical - enveloped
Double strand icosahedral non enveloped

254
Q

What can bacteria have that allow them to replicate and transfer generic information between bacteria?

255
Q

How can cocci arrange?

A

Clusters and chains

256
Q

What are some mechanisms of infection

A 
Contiguous (direct spread)
Ingestion
Inhalation
Vertical 
Via a vector
Haematogenous
Inoculation
257
Q

What’s the general timeline of infectio

A 
Exposure
Adherence
Invasion
Multiplication
Dissemination
258
Q

What’s bacteriology?

A

Specimen growth on agar, use of antigen detection ad nucleic acid detection

259
Q

What’s virology

A

Antigen detection, antibod detection and viral nucleic acid detection

260
Q

What are different types of antimicrobial

A

Antibacterial
Antifungal
Antiviral
Antiprotozoal

261
Q

What are 4 different ways we can classified antibacterials?

A

Bacteriacidal vs bacteriastatic
Broad vs narrow spectrum
Target site/ mech of action
Chemical structure

262
Q

What do you want in an antimicrobial agent

A 
Selective toxicity
Few adverse effects
Oral and iv
Long Half life
No interactions
263
Q

What are the 4 broad mechanisms of action that antibacterials use?

A

Cell wall synthesis
Protein synthesis
Cell membrane function
Nucleic acid synthesis

264
Q

What antibacterials affect cell wall synthesis

A

Beta lactams

Glycopeptide

265
Q

What antibacterials affect protein synthesis

A

Tetracyclines
Aminoglycosides
Macrolides

266
Q

What antibacterials affect cell membrane function

A

Polymixins

267
Q

What antibacterials affect nucleic acid synthesise

A

Quinolones

268
Q

How does penicillin work?

A

Penicillin binding protein acts to make cross links in cell walls, penicillin slots into this cross link section

269
Q

What is vancomycin drug class? What does it inhibit?

A

Glycopeptide

Stops cross linking of cell walls

270
Q

What do fluroquinlone inhibit?

A

The proteins associated with coiling and super coiling of DNA

271
Q

What is intrinsic resistance?

A

There is no target or access for a drug to work. This is permanent

272
Q

What is acquired resistance

A

The mutation or acquisition of genetic material resulting in its reistance (usually permanent)

273
Q

What is adaptive resistance

A

The resistance caused by inducing stress on a microbe, usually reversible

274
Q

What are some different mechanisms for resistance

A

Drug inactivating enzymes
Altered targets with lower affinities for antibacterials
Alter uptake eg pumps that remove antibiotics from cells

275
Q

How can mutations occur?

A

Darwinian model or horizontal transfer

276
Q

How do we measure antibiotic activity?

A

Disk sensitivity test

277
Q

How do we work out the minimum inhibitor concentration?

A

Double the dilution until it isnt killing the organism

278
Q

What fall under the category of beta lactams

A

Penicillins
Cephalosporins
Carbapenems

279
Q

What is a typical broad spectrum beta lactam?

280
Q

What are some different penicillins and what are they active against?

A

Penicillin- mainly streptococcus
Amoxicillin- strep and some gram negatives
Flucloxacillin- staph and strep

281
Q

What do cephalosporins work against?

A

Broad spectrum but no anaerobe activity

282
Q

When would we use glycopeptides like vancomycin

A

For gram positives when other agents arent working as toxic

283
Q

When are tetracycline or doxycycline used?

A

Active against atypical pathogens in pneumonia

284
Q

When is the aminoglycoside gentamicin used?

A

Gram negative. Works well in blood and urine.
Reserved for gram neg sepsis
Nephrotoxic

285
Q

When are macrolides like erythromycin and clarithromycin used?

A

Alternative to penicillin for gram positives

Atypical resp infections

286
Q

When are timethoprim or sulphonamides used?

A

UTI, inhibit folic acid synthesis

287
Q

What do azoles do?

A

Antifungal that inhibit cell membrane synthesis

Flucanazole for candida

288
Q

What do polyenes do?

A

Inhibit cell membrane function in fungi

289
Q

What does aciclovir do? When would you use it?

A

Inhibit viral DNA polymerase

Herpes, encephalitis

290
Q

What does osetamiver do?

A

Inhibits viral neraminidase in influenza a and b

291
Q

Why do alpha haemolytic strep cause a wet appearance

A

Due to capsule

292
Q

What is enterococcus faecalis haemolytic classification

A

Gamma/ non haemolytic

293
Q

What lancefield classification is strep pyogenes

294
Q

What lancefield b strep causes neonatal sepsis?

A

Agalactiae

295
Q

What kind of capsule does strep pyogenes have?

A

Hyaluronic acid capsule- inhibits phagocytosis

296
Q

What does the M protein on strep pyogenes inhibit?

A

Complement pathway

297
Q

What does streptolysin O do?

A

Causes lysis of erythrocytes

298
Q

What does streptokinase do?

A

Dissolution of clots converting plasminogen to plasmin

299
Q

What causes strep pharyngitis?

A

Strep pyogenes

300
Q

What’s a complication of strep pharyngitis?

A

Scarlet fever

Acute rheumatic fever

301
Q

Define sepsis

A

Life threatening organ dysfunction due to the dysregulated host response to infection

302
Q

How do you analyse urine?

The presence of what indicates uti?

A

Dipstick
Nitrites- some gram negs convert nitrate to nitrites
Leukocyte esterase- enzyme released by neutrophils

303
Q

What antibody is present in the mucous membranes

304
Q

What antibodies are releaesed immediately after exposure to a new pathogen?

305
Q

What antibody confers immunity to a disease?

306
Q

What does cdiff exotoxin A do?

A

Damage intestinal mucousa

307
Q

What does cdiff toxin b do?

A

Causes opening of tight junctions of intestinal epithelial

308
Q

What can vancomycin be used for?

A 
IV
Skin infections
Blood stream infections
Endocarditis
Bone and joint infections
Meningitis caused by MRSA
Orally
CDIFF
309
Q

What does vancomycin inhibit?

A

Cell wall synthesis in gram positive bacteria

310
Q

When is ceftriaxone used in meningitis?

A

Caused by pneumococci
Mengiococci
Haemophilus influenza

311
Q

How can ceftriaxone be administered

312
Q

What can ceftriaxone be used to treat?

A 
Middle ear infections
Endocarditis
Meningitis
Pneumonia
UTI
Gonnorheoea
313
Q

What class of antibiotic is ceftriaxone?

A

3rd gen cephalosporin within beta lactam family

314
Q

What kind of bacteria does flucloxacillin treat? Is it narrow or broad spectrum?

A

Narrow spectrum

Gram positive bacteria

315
Q

Would you use flucloxacillin for MRSA

A

No ineffective

316
Q

What class of antibiotics is flucloxacillin

A

Beta lactam, penicillin class

317
Q

What is metronidazole? What is the first line drug for?

A

Antibiotic and antiprotozoal

1st line for C diff and often used for helicobacter pylori

318
Q

What kind of action does metronidazole have?

A

Nitroimidazole- inhibits nucleic acid synthesis mainly in anaerobic cells

319
Q

What is Aciclovir? What is t primarily used for treatment of?

A

Antiviral
Herpes simplex, chickenpox, shingles
Prevention of cytomegalovirus post transplant

320
Q

What kind of spectrum does gentamicin have? What does it mainly target?

A

Broad

Gram negative

321
Q

What bacteria is gentamicin used for? What is it not used for and why?

A

Pseudomonas, proteus, klebsiella, gram positive staph.

Not used for neisseria meningitis or gonorrhoeae as shock risk

322
Q

How does gentamicin work?

A

Irreversibly binds to 30s ribosome subunit inhibiting protein synthesis. Similar to aminoglycosides

323
Q

What is the drug of choice within the beta lactams? Why?

A

Amoxicillin.

Well absorbed

324
Q

What is amoxicillin the first line treatment for?

A

Middle ear infection
Pneumonia that isn’t severe (with macrolide)

Also effective for helicobacter pylori, strep throat, skin infections, UTI, strep, haemophilus, klebsiella

325
Q

What is co-amoxiclav?

A

Amoxicillin with a beta lactamase inhibitor

326
Q

What is trimethoprims primary use?

A

Bladder infections

327
Q

How does trimethoprim work?

A

Inhibits reduction of dihydryfolic acid to tetrahydrofolic acid, essential precursor in thymidine synthesis

328
Q

What’s piperacillin? What’s the primary use?

A

Broad spectrum beta lactam

Serious hospital acquired infections

329
Q

What is meropenem?

What subgroup

A

ULTRA broad spectrum
Carbapenem of beta lactam
Gram pos and neg

330
Q

What is tetracyclines primary use? What are not succeptible to it?

A

UTI, chlamydia, syphilus

Anaerobic

331
Q

How does tetracycline work?

A

Protein synthesis inhibitor- inhibits mRNA ribosome

332
Q

What does doxycycline work on?

A

Bacteria and protozoa
Bacterial pneumonia
Prophylaxis against pneumonia

333
Q

How does erythromycin work?

A

Binds to 50s subunit inhibiting protein synthesis

334
Q

Ciprofloxacin is what class?

What is it active against?

A

Broad spectrum fluoroquinilone

Gram positive and negative

335
Q

Where is ciprofloxacins mechanism of action?

A

Inhibits DNA gyrase inhibiting cell division

336
Q

What is oseltamivir?

A

Antiviral prevents influenza A and influenza B

337
Q

What is flucanazole

A

Antifungal medication

Treats candidiasis

338
Q

What’s amphotericin?

A

Anti fungal for serious fungal infections and leishmaniasis

339
Q

What’s contagious spread?

A

Spread from physical contact or casual contact

Eg secretions, airborne , touch

340
Q

What’s non contagious spread

A

Via intermediate like mosquito pr non casual transfer of bodily fluid like sec

341
Q

If you are vaccinated against hepatitis B what antibody would be seen on serology?

342
Q

If you are not vaccinated but have acquired immunity to hep B what would serology show?

A

HBsAB

HBcAB

343
Q

What fungal infection can be confused with strep pyogenes?

A

Oral candidiasis

344
Q

What do the lesions in oral candidiasis look like?

A

Cottage cheese that bleeds when scraping

345
Q

What cytokines acts on the hypothalamus to induce raised temp in infection?

346
Q

What causes the release of IL-6 to raise core body temp?

A

PAMP being recognised by Toll like receptor

347
Q

What is mononucleosis caused by in 90% of cases?

348
Q

What are some symptoms of mononucleosis?

A

Sore throat, fever, enlarged lymph nodes, tiredness

349
Q

What happens in 1% of mononucleoiss cases?

A

Splenomegally leading to splenic rupture

350
Q

What happens to blood lymphocytes in mononucleosis?

A

10% seen are atypical

351
Q

What is mononucleosis often confused with?

A

Strep throat

352
Q

What are the minority of cases of mononucleosis caused by?

353
Q

Lipopolysachharide is more associated with what stain of bacteria?

A

Gram negative

354
Q

What is the test to see how much antibiotic is needed called?

A

Minimum inhibitor concentration

355
Q

Why is neisseria meningitidis toxic primarily?

356
Q

What is EBV also called?

A

Human herpes 4 virus

357
Q

Other than mononucleosis what is EBV associated with?

A

Hodgkin’s lymphoma
Burkett lymphoma
Higher risk of autoimmune disease

358
Q

How is EBV spread?

A

Via saliva and genital secretions

359
Q

What does EBV infect?

360
Q

What is EBV composed of?

A

Double helix of DNA surrounded by nuclear capsid surrounded by enveloped with lipids and glycoproteins

361
Q

What does EBV demonstrate after not being active?

362
Q

What is CMV also known as?

A

Human herpes 5

363
Q

What does CMV strain for life once infected?

364
Q

What are the main methods of transportation for CMV

A

Vertical

Saliva

365
Q

What can CMV lead to?

A

CMV hepatitis, retitinitis, mononucleosis

366
Q

What is the strong anti phagocytic virulence factor demonstrates by strep? How does it work?

A

M protein

Destroys C3 convertase preventing opsinisation

367
Q

What is the quickest method to guide antibiotic choice?

A

Gram stain

368
Q

What is a medical emergency associated with tonsillitis?

A

Peritonsilar abscess

369
Q

What’s helicobacter gram stain?

Usual location?

A

Gram negative

Stomach 80%

370
Q

What does acute helicobacter pylori present as?

A

Acute gastritis with abdo pain

371
Q

What risks are associated with helicobacter infection?

A

Peptic ulcer

Stomach cancer

372
Q

What are some virulence factors associated with helicobacter pylori?

A 
Hydrogenase that binds to hydrogen
Biofilm
Adhesins
Flagella
LPS
373
Q

How does helicobacter pylori avoid acidic aspect of stomach?

A

Burrows into epithelium

Chemotaxis

374
Q

How does helicobacter pylori cause its symptoms?

A

Distrupting tight junctions causing inflammmation

375
Q

How do you treat helicobacter pylori infection?

A

Protein pump inhibit

Clarithromycin

376
Q

What is isotype switching?

A

Change from IGM to IGG by changing heavy chain but keeping variable region the same

377
Q

What are some reasons for an increase in foreign infections?

A

More exotic travel
Immunocomprimised now able to travel
Lots of migration

378
Q

What are some key areas concerning travel related infection based on the infection model?

A

Calendar time- time with symtoms

Relative time- time since travel re incubation times

379
Q

What foreign pathogen classes are particularly relevant, what do many use?

A

Parasites, bacteria like rickettsia and spirochaette.

Vectors

380
Q

Why is a good travel history important?

A

Recognise imported rare diseases
Recognise different strains of pathogens (antibiotic resistant etc)
Protect lab and ward staff

381
Q

What are some key questions re travel infections when trying to work out what pathogen it could be?

A

Where- what region travelled to
When (symptoms started)
What (symptoms)
How (potential modes of transmission)

382
Q

What are some key aspects of a travel history (which you may not ask in a normal history)

A

Anybody else in the group unwell
An vaccine or prophylaxis use
Recreational activities
Healthcare exposure

383
Q

What are the 4 main species of malaria?

A

Plasmodium falciparum
Plasmodium ovale
Plasmodium vivax
Plasmodium malaria

384
Q

What is the malaria vector?

A

Female anophelos mosquito

385
Q

Where are the 3 locations of the malaria parasites life cycle?

A

Within the mosquito
Within host liver
Within host RBC

386
Q

What’s the minimum and maximum incubation period of malaria?

A

6-7 days min
6 months for P. Falciparum
12 months for P. Ovale and P. Vivax

387
Q

What’s the treatment for malaria?

A

P falciparum- quinine, doxycycline

P. Vivax/ovale chloroquinine

388
Q

What tests are done for malaria

A 
Blood smear (3 neg needed, parasite seen in RBC)
FBC
LFT
Glucose
CT head (risk of haemorrhage)
CXR- risk of ARDS
389
Q

What are signs of malaria onset?

A

Fever with +/- mild splenomegally

+/- myalgia, headache, chills, dry cough

390
Q

What are some outcomes of sever P falciparum infection (2% and up)

A 
ARDS
Confusion/fits
Thrombocytopenia
DIC
AKI
Raised Billirubin (breakdown of RBC pre liver)
391
Q

How can malaria be avoided

A

Ax risk
Bite protect
Chemoprohylaxis

392
Q

What does salmonella typhi cause?

A

Enteric fever

393
Q

How is salmonella typhi transmitted?

A

Fecal oral route

394
Q

What kind of bacteria is salmonella typhi?

A

Enterobacteriae, gram negative bacilli

395
Q

What allows salmonella typhi to adhere? Where does it do this?

A

Fibrimiae to the peyers patches

396
Q

What allows salmonella typhi to grow intracellularly

397
Q

What are signs of enteric fever?

A 
Systemic disease
Fever
Headache
Dry cough
Abdo pain
Constipation
*bradychardia
398
Q

What’s the incubation period for salmonella typhi

399
Q

Whats a complication of enteric fever that can lead to death?

A

Intestinal haemorrhage and perforation

400
Q

How do you investigate enteric fever?

A

Serology is unreliable so a blood culture or faeces culture needed

401
Q

What’s the treatment for enteric fever?

What’s the prevention method”

A

Ceftriaxone or azithromycin

Food and hand hygiene, typhoid vacc

402
Q

What can cause a widespread flat rash with confluent areas?

A

Rickettsia (spotted fever)
Mononucleosis
Childhood virus- measles, rubella
Dengue

403
Q

What’s the most common arbovirus?

A

Dengue fever

404
Q

How many serotypes of dengue fever are there?

405
Q

What happens on 1st infection of dengue fever?

A

Anywhere from asymptomatic to severe afebrile. Lasts 1-5 days and improves 3 to 4 days after rash. Supportive Rx only

406
Q

What happens when you get reinfected with dengue fever but a difference serotype

A

Dengue haemorhagic fever

Dengue shock syndrome

407
Q

What gram stain is TB

A

Neither needs Ziehl-Neelsen staining

408
Q

What is the immunocomprmised host

A

State in which immune system is unable to respond appropriately and effectively to infectious micro-organisms due to defect in one or more components of immune system

409
Q

What are some cells of the inate rapid immune response

A

Granulocytes (BEN), dendritic cells, macrophage, mast, NKC

410
Q

What are the cells of the adaptive slower immune response

A

B cell
T cell CD4 CD8

NKC overlaps

411
Q

Primary immunodefficency is a result of what?

A

Gene defect

Eg chronic granulomatous

412
Q

Secondary immunodefficency us due to what?

A

Underlying disease state or treatment that causes either a decrease in the production of immune components or an increase in the loss or catabolism of immune components

413
Q

What does SPUR refer to in reference to immune defficency

A

Severe
Persistent
Unusual
Recurrent

Infections suggest PID/Secondary

414
Q

What is one of the major comorbidities associated with having an immunodefficency disorder

A

Cancer, in particular lymphoma

Different PID associated with different cancers

415
Q

examples of PID due to antibody defficencies

A 
Brutons disease (x linked recessive)
Common Variable Immunodefficecny (CVID)
Selective IGA defficency (often asymptomatic)
416
Q

When do antibody defficency like CVID commonly present

A

6/12 to 5 years and 5 years up

417
Q

What is an example of a combines T cell and B cell immunodefficency?
When would it present?
Why is it combined?

A

Severe combined immmunodefficency disorder SCID
Presents younger than 6 months
T cell defect therefore B cell due to co-activation

418
Q

What’s an example of a phagocytic defect PID? When would it present?

A

Chronic granulomatous disease
Severe congenital neutropenia
Below 6/12 or 6/12 to 5 years

419
Q

What immunodefficency tend to present after the age of 5

A

B cell
Antibody
Complement
Secondary

420
Q

What would someone with a complement defficency struggle with? Therefore what would the likely presentation be?
A c3 issue would cause what?
A c5-9 would cause what

A

Struggle to clear encapsulated bacteria
Chronic infections with N meningitidis, haemophilus influenza
C3-pyogenic issue
C5-9 meningitis/sepsis

421
Q

What would someone with a phagocytic defect suffer from?

A

Recurrent skin and mucousal layer infections

FUNGAL infection such as aspergilllus

422
Q

Somebody with an antibody defficency would be succeptible to what?

A

Unusual Upper resp tract infections

GIARDIA LAMBLIA GI infection

423
Q

Someone with a T cell defect is succeptible to what?

A

Everything. Herpes simplex in particular

424
Q

What are some supportive Mx for PID?

A

Prophylactic antibiotics
Vit A and D
Prompt Rx

425
Q

What are some specific Mx plans for PID

A

Immunoglobulin therapy- CVID, Burtons

Haemopoetic stem cell transplant - SCID

426
Q

Secondary immunodefficency due to decreased production of immune components can be caused by what?

A 
Malnutrition 
Infection like HIV
Liver disease (compliment made here)
Lymphoproliferative disorders
Asplenic
427
Q

Why is the spleen so important?

What’s OPSI

A

Only organ to remove blood borne pathogen, involved in IGM and IGG response, removes encapsulated bacteria. Removes opsonised microbes.
OPSI- overwhelming post splenectomy infection

428
Q

Haematological malignancies lead to 2nd immunodefficency how?

A

Chemo induced neutropenia
Chemo induced mucousa damage
Vascular catheters

429
Q

An increase in the loss of catabolism of immune components leading to 2nd immunodefficency can be due to what?

A

Protein losing conditions
Neprhopathy
Burns

430
Q

How would you test antibody function

A

Look at response to an already vaccinated microbe

431
Q

What would you look at on the FBC to tell you about the cell mediated component

A

Lymphocytes

432
Q

What would you look at on the FBC to tell you about the phagocytic portion of immune response

A

Neutrophil count

433
Q

Microbes that cause infection can either be what?

A

Exogenous or commensal

434
Q

How is the innate response described?

A

Non specific and rapid

435
Q

What can the innate response recognise? How? What’s a characteristic of this?

A

PAMPS using PRR. Recognises groups of pathogens so is not that specific but detects a wide range. Toll like receptor 4- LPS
Toll like receptor 2- peptidoglycan

436
Q

What bridges the inate and adaptive immune responders

A

Dendritic cells

437
Q

What is immunisation

A

Activating the adaptive immune response with a less virulent analogue

438
Q

What’s the main portal of entry into the blood?

A

Poor dental hygiene-> dental extraction

439
Q

In the inate immune response what 2 things detect invaders?

A

Phagocyte like macrophage and complement in blood

440
Q

CD8 T cell are activated by what MHC? For intra or extra?

A

Intra MHC 1

441
Q

How can B cells respond without T cells? What’s the issue with this?

A

They can detect native proteins, lipids and LPS but need T cells for isotype switching to IGG

442
Q

What’s special about MHC1/2 between individuals?

A

We also process and present differently due to polymortphism

443
Q

What happens in a viral infection to activate adaptive immune respnse

A

MHC1->CD8. CD8 needs co-signal from CD4 to become cytotoxic so MHC2 presents and activates CD4 to activate CD8

444
Q

Why could you have a low CD8 in HIV

A

Low CD4 so less co-activation of CD8

445
Q

How is a bacterial pathogen processed and presented?

A

MHC2-> CD4-> B cell-> antibodies

446
Q

The key microbes for the module are? Gram pos-neg

A

Pos cocci- Staph and strep
Pos bacilli- C Diff
Neg cocci- N meningitidis
Neg Bacilli- E. coli, salmonella typhi, haemophilus influenza, legionella pneumophilia

447
Q

EBV and Herpes zoster share what ?

A

Family- both herpes

Cause latent infections

448
Q

The 4 areas an ARV acts in HIV are?

A

HIV binding
Reverse transcriptase
Integrate (when it combines to host dna)
Protease enzyme when virus protein chains are cut once leaving the cell

449
Q

The Rx for meningococccal sepsis is what?

A

Ceftriaxone its a beta lactam, cephalosporin

450
Q

The Rx for Cellulitis is what? And why?

A

Flucloxacillin- beta lactam, penicillin

Effective against strep and staph

451
Q

The treatment for a UTI is?
Likely causative orgnaism
Action of antibiotic

A

Trimethoprim which inhibits folic acid synthesis

E Coli

452
Q

The Rx for tonsillitis? And likely pathogen

A

Penicillin- beta lactam

Strep pyogenes

ESA 2 (10 decks)

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