Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

ESA 2 > Infection > Flashcards

Infection Flashcards

1
Q

What colour do gram positive bacteria stain?

A

Purple

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What colour do gram negative bacteria stain?

A

Pink

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What size peptidoglycan layer do gram positive bacteria have?

A

Thick

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What size peptidoglycan layer do gram negative bacteria have?

A

Thin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Which bacteria have an outer membrane?

A

Gram negative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How much lipopolysachharide do gram positive bacteria have?

A

Low levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How much peptidoglycan content do gram negative bacteria have

A

High content

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which type of bacteria are more resistant?

A

Gram negative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What type of bacteria tend to favour exotoxins instead of endotoxins

A

Gram positive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

Gram negative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are endotoxins?

A

Bacterial toxins consisting of lipids located within a cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Name some gram positive cocci

A 
Staph aureus
Coagulase negative staph
Streptococcus pneumoniae
Strep pyogenes
Beta and alpha haemolytic strep
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Name some gram positive bacilli

A

Clostridium difficile
Listeria monocytogenes
Bacillus anthracis
Bacillus lereus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Name some gram negative cocci

A

Neisseria meningitidis
Neisseria gonorrhoeal
Moraxella catarhalis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Name some gram negative bacilli

A

Escherichia coli
Haemophilus influenza
Klebsiela pneumoniae
Salmonella typhi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are some key viruses to know?

A 
Adenovirus
Norovirus
Epstein Barr
HIV
Hepatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are 2 classifications of fungi?

A

Yeasts and moulds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are some examples of yeast infection

A

Candida albicans
Cryptococcus Noeformans
Pneumocystis jiroveci

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are some examples of mould infections?

A

Aspergillus

Dermatophytes (ring worm, athletes foot)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are single cell fungi

A

Yeasts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the 2 classifications of parasites

A

Protozoa

Helminths

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are Protozoa

A

Single cell parasites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are some examples of Protozoa?

A 
Malaria
Giardia Lambia
Cryptosporidium parvum
Plasmodium falciparum
Trypanesoma cruzi
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are some examples of helminths

A

Roundworms
Tapeworms
Flukes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is first line defence in inate immunity?

A

Barriers- physical, physiological, chemical, biological

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are some examples of inate immunity physical barriers?

A

Skin
Mucousal membranes
Bronchial cilia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are some examples of inate physiological barriers

A

Vomiting
Coughing
Sneezing
Diarrhoea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are some examples of inate immunity chemical barriers?

A

Low PH of vagina, stomach, skin

Antimicrobial- IGA, lysozymes, gastric acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are biological barriers in reference to 1st line defecnce

A

Natural flora

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

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

A

Competes for resources
Produce antimicrobial
Synthesise vitamins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are second line defences of the inate immune system?

A

Phagocytosis
Opsinisation
Complement system
Cytokinesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is a pamp and what is it recognised by?

A

Pathogen associated molecular pattern

Pathogen recognition receptors PRR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What’s a PRR and what does it recognise

A

Pathogen recognition receptor- PAMPS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

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

A

Opsonins attached

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What organs are macrophages present in?

A

All of them

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What do macrophages present to?

What can they produce?

A

T cells

Cytokines/ chemokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Monocytes are found where? What can they differentiate into?

A

Found in the blood

Macrophes or dendritic cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Basophils/ mast cells are early actors in what?

A

Inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Eisonophils are our defence mechanism against what?

A

Parasites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What do NKC target?

A

Abnormal host cells (virus, cancer)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What do dendritic cells do?

A

Present microbial antigens to T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What are some examples of opsonins

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Once a PRR has attached to a PAMP what happens?

A

Engulfment
Phagolysosome formation
Oxygen dependent and oxygen independent breakdown

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What are some oxygen dependent examples of breakdown in the phagolysosome

A

Respiritory burst with oxygen radicals:
Hydrogen peroxide
Hydroxyl radicals
NO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are some oxygen independent actions in the phagolysosome

A

Lysozyme
Transferrin
Cationic proteins
Proteolytic enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

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

A

Recruit phagocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

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

A

Opsinisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

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

A

Membrane attack complex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

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

A

Clearing encapsulated bacteria

Especially in asplenic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What signals for cytokine release?

A

Toll like receptors (signalling PRR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What’s a signalling PRR

A

Toll like receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What are the 3 functional categories of cytokines

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

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

A

Macrophages and dendritic cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What are some key inate immune response cytokines

A

TNF
IL-1
IL-6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

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

A

Neutrophil mobilisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

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

A

Capture
Process
Present

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Where are antigen presenting cells strategically located?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What antigen presenting cells are found in the skin

A

Langerhanns

Macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What antigen presenting cells are found in lymphoid organs

A

B cells
Dendritic cells
Macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What antigen presenting cells are found in mucous membranes

A

Dendritic cells

Macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

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

A

Phagocytosis (whole microbe)

Micropinocytosis (particles)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What does MHC stand for?

A

Major histocompatability complex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Where are MHC genes located

A

Chromosome 6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What HLA genes are present on all nucleated cells

A

HLA A/B/C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What do HLA A/B/C code for>

A

MHC class 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What cells have HLA Dr/Dq/Dp ?

What does it code for?

A

Dendritic, macrophages, B cells

Class 2 MHC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

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

A

Co dominant expression

Polymorphic genes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What do MHC class 1 present

A

Intracellular- virus, tumour, intracellular bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What do MHC class 1 present to?

A

CD8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What is TAP and what is it to do with?

A

Transport associated presentation. Associated with MHC class 1 processing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

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

A

RER

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What is a CD8 cell also known as?

A

T Killer cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

CD8 is associated with what adaptive immune response?

A

Cell dependent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What MHCs are used in the cell dependent response?

A

Both MHC1 and MHC2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

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

A

Recruits CD4 TH1 cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Where are MHC2 proteins exported from?

A

from the ER in a vesicle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What blocks the binding cleft of MHC2 protein?

A

Class2 associated invariant chain peptide CLIP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

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

A

HLA-DM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What do MHC class 2s present to?

A

CD4 cells- TH1,2,17

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

what are CD4 cells

A

T helper cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What MHC is needed for the humoral response?

A

MHC2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

In the humoral response what does MHC2 present to

A

CD4 TH2 and TH17

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

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

A

They are highly polymorphic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

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

A

CD4 TH17 uses IL17 to attract neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

What does a mast cell secrete as an antibody

A

IgE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

What is IgG when is it used

A

Antibody, FC dependent

Complement activation, neonatal immunity, toxins/virus neutralisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

What does IgM activate?

A

Complement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What does IgE do?

A

Provides immunity against helminths and mast cell degranulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

What is IgA for?

A

Mucousal immunity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

What antibody is highest in initial exposure to a pathogen?

A

IgM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

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

A

IgG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

What is a benefit of higher IgG on second exposure?

A

Faster, longer, higher affinity response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

What is septic shock

A

Persisting hypotension, requiring treatment despite fluidn resuscitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

What is sepsis?

A

Life threatening organ dysfunction due to a dysregulated response to infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

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

A

The pathogen must enter the blood stream

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

What becomes amplified and dysregulated (mostly) in sepsis?

A

Cytokine release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

What are 5 symptoms of sepsis

A 
Decreased BP
Raised HR
Raised RR
Temp up or down
DIC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

Why do we get increased HR in sepsis

A

There is a drop in BP, HR rises to compensate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

Why is there a drop in BP with sepsis?

A 
Mass vasodilation (distributorry)
DIC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

Why does RR rate increase in sepssis

A

As a response to hypoxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

What are the sepsis 6

A

Give 3- iv fluids, oxygen, IV ABx

Take 3- urine, blood cultures, lactate and FBC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

Why give IV fluids in sepsis

A

Raise BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

Why give oxygen in sepsis

A

Patient likely hypoxic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

Why measure urine output in sepsis

A

Decrease indicated organ failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

What does sepsis result in?

A

Multi organ failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

How can streptocccus be divided by haemolysis?

A 
Alpha haemolytic (partial)
Beta haemolytic (complete)
Gamma haemolytic (no haemolysis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

How many different types of strep are there?

A

6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

What haemolytic group is strep pneumonia

A

Alpha haemolytic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

Does strep pneumoniae have a capsule?

A

Yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

What are the 2 virulence factors that strep pneumonia has?

A

Capsule

IgA protease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

What gram stain is strep pneumonia?

A

Gram positive diplodocus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

Who is catalase positive? Strep or staph?

A

Staph

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

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

A

Staph aureus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

What gram stain is staph aureus

A

Gram positive cocci clusters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

What are 3 important exotoxins staph aureus has?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

How do we treat staph aureus

A

Penicillinase resisitant beta lactams or 1st gen cephalosporins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

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

A

Biofilm

Prosthetic joints, valves, IV lines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

What gran stain is strep viridans

A

Postitive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

What kind of haemolysis does strep viridans produce

A

Alpha

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

Why is it called strep viridans

A

Green from alpha haemolytic

Green salad gets stuck in your teeth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

Where is strep viridans normal flora?

A

Oral and GI flora

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

How can strep viridans cause dental cavities?

A

Extracellular dextran

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

What is non multidrug resistant?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

What is MDR?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

What is XDR?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

What is PDR

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

What is antimicrobial stewardship

A

Coordinated interventions designed to improve the selection and use of antimicrobials

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

What kind of studies have demonstrated antibiotic resistance

A

Lab studies
Ecological studies
Individual level studies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

What are some examples of process measures in antimicrobial stewardship

A

Defined daily dose/1000 beds
Adherence guidelines
Benchmarking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

What are some outcome measures of antimicrobial stewardship

A

Patient outcomes, infection rates, emergence of resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

What defines a healthcare infection?

A

Onset at least 48 hours after admission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

What are the more prevelant healthcare infection sites

A

UTI
GI
Surgical wound site
Chest (pneumonia )

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

What are some viral examples of healthcare infection

A

HEP B, C, HIV
Norovirus
INfluenza

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

What are some bacterial examples of healthcare infections?

A 
Staph aureus (MRSA)
CDIFF
ECOLI
Klebsiella
Pseudomonas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

What re some fungal healthcare infections?

A

Candida

Aspergillus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

How can we reduce patient to patient transmission

A

Barrier nursing/ isolation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

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

A 
Identify (A_F)
Isolate
Investigate
Inform
Initiate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

What is the A-F in identifying harmful pathogens

A 
Abroad?
Blood borne?
Colonised (MDR)
Diarrhoea and vomiting
Expectorating
Funny looking rashes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q

What does person to person indirect require?

A

A vector such as a mosquito

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q

What’s an endemic disease?

A

It’s usual background rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
172
Q

What is an outbreak in relation to disease?

A

Two or more linked cases in time and place

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
173
Q

What’s an epidemic in relation to disease?

A

A rate of infection greater than the endemic rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
174
Q

What is a pandemic in relation to disease?

A

Very high rate of infection spreading across regions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
175
Q

What is a pandemic often due to

A

Antigen shift, abrupt change in dna making everyone succeptible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
176
Q

What’s antigen drift?

A

Slow change in dna of an infectious agent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
180
Q

What determines how transmissible an organism is?

A

Infectious dose- the number of organisms required to cause infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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?

A

Haem

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?

A

10%

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?

A

IVDU

241
Q

How many hep C cases become chronically infected?

A

80%

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?

A

Plasmids

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?

A

Meropenem

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

A

A

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

A

IgA

304
Q

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

A

IGM

305
Q

What antibody confers immunity to a disease?

A

IGG

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

A

IV or IM

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?

A

HBsAB

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?

A

IL-6

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?

A

EBV

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?

A

CMV

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?

A

LPS layer

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?

A

B cells

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?

A

Latency

362
Q

What is CMV also known as?

A

Human herpes 5

363
Q

What does CMV strain for life once infected?

A

T cells

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

A

Invasion

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

A

7-14 days

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?

A

4

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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions