Brainscape's Knowledge GenomeTM

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


See full index

CSI 1c A > 1 > Flashcards

1 Flashcards

1
Q

complications of meningitis

A

sensorrineural hearing loss (most common)
seizure
focal neurological deficit
infective: sepsis or intracerebral abscess
pressure: brain herniation, hydrocephalus

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

AB for under 3 months

A

IV cefotaxime + amoxicillin

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

AB for 3 months to 50 yrs

A

IV cefotaxime or ceftriaxone

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

AB over 50

A

IV cefotaxime or ceftriaxone + amoxicillin

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

AB meningococcal meningitis

A

IV benzyle penicillin or cefotaxime or ceftriaxone

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

AB pneumococcal meningitis

A

IV cefotaxime or ceftriaxone

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

AB haemophilus influenzae meningitis

A

IV cefotaxime or ceftriaxone

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

AB listeria meningitis

A

IV amoxicillin+ gentamycin

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

red light temp

A

over 38 in infant 0-3 months

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

amber light temp

A

tmep over 39 for 3-6 month

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

tachypnea

A

over 60 for 0-5 months
over 50 for 6-12 months
over 40 for over 1 year old

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

tachycardia

A

over 160 if pt under 1 year
over 150 if pt 1-2 years old
over 140 if pt 2-4 years old

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

cap refil

A

more than 3 seconds= dangerous

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

non blanching rash

A

send to ED, but give IM or IV benzyl penilcillin

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

how quickly to see pt

A

life threatning-999
red features but not life threatening= seen by paediatrician within 2 hours
amber: HCP discretion and can safety net
green: managed at home

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

safety net

A

seizure, develop non blanching rash, less well, fever more than 5 days, parent distressed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Colour of skin traffic light

A

Green= normal
Amber= pallor
Red= pale, mottled, ashen, blue

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

Activity traffic light

A

Green; respond well to social ques, smile, stay awake, strong normal crying.
Amber= not responding to social cue, no smile, wake only to prolonged stimulation, dec activity
Red= no response to social cues, appears I’ll, not wake , weak or continuous cry

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

Traffic circulation

A

Green= normal skin and eyes, moist mucous membranes.
Amber= tachy cardia, CRT above 3, dry mucous membranes, poor feeding, reduced urine output
Red= reduced skin turgor

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

Most common cause of meningitis

A

Neisseria meningitidis; meningococcal
Strep pneumonias; pneumococcal
Haemofilus influenzae

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

Common features of meningitis, meningococcal disease, meningicococcal septicaemia

A

Fever, nausea and vomiting, head ache, non blanching rash, altered mental state and can also include lethargy, joint pain, muscle ache

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

Meningitis specific Exam

A

Photophobia
Kernig’s sign
Brudzinskis sign

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

Kernigs sign

A

Lie child on back, flex knee to right angle to body and completely extend leg at knee joint- cause stretching of meninges leading to pain which positive sign

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Brudzinskis sign

A

Flex neck forward, child deletes hips and knees to avoid pain

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

Signs of septicaemia

A

Shock, hypotension, unusual skin colour, cold hands and feet, increased CRT

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

Suspected meningitis or meningococcal septicaemia in primary care

A

Transfer young pt with non blanching rash to hospital
with benzyl penicillin IV or IM

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

Primary care, no rash

A

Send to hospital but don’t give AB

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

How much benzyl penicillin do you give

A

300 mg if under 1 year old, or 600 for 1-9 years old

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

How would you investigate meningitis in hospital

A

Start ceftriaxone ASAP
Full set of bloods including clotting to test for coagulopathy
Blood cultures= N. Meningitits
Please= primary so do unless contraindications but don’t delay ABx,

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

What is contraindicated for LP

A

Raised, ICP, shock or hypovolaemia, neurological signs, unequal pupils or coagulation abnormalities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What do you look for in CSF

A

WBC, check total protein, glucose concentrations, gram staining, microbiology culture

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

Normal CSF

A

5-20 pressure, normal, 0.18-0.46 protein. 2.5-3.5 glucose, normal stain, less than 3 WCC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Bacterial CSf

A

Pressure over 30, turbid appearance, protein more than 1, glucose less than 2.2

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

Viral CSF

A

Normal or mildly increased pressure, clear appearance, less than 1 protein, normal glucose and normal gram stain. Monocytes.

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

Fungal or TB CSF

A

Fibrin web, less protein, less glucose, monocytes

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

SBAR

A

S- pt status, really unwell or stable (need to stabilise with ABC+ Resus)
B= pt details, age, condition, contraindications to GA, drug allergies, treatment received so far
A= recent obs, PEWS
R= anaesthetic review and assessment how to prepare for sedation and procedure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

How do you prepare for operaiton

A

NBM for 6 hrs, water for 2
Pre op assessment
Consent

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

AMPLE

A

Allergies, medication (coagulation) , past history, last meal, events

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

Suspected meningitis and recent travel

A

Vancomycin and ceftriaxone/ cefotaxmine

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

Ca2+ containing infusion

A

Don’t use ceftriaxone use cefotaxime. Also don’t use ceftriaxone III premature babies, babies with jaundice, hypoalbuminuriaor acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

HiB meningitis

A

IV ceftriaxone for 10 days in total

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

S. Pneumonia meningitis

A

IV ceftriaxone for 14 days

43
Q

Group B strep meningitis

A

IV cefotaxime for 14 days

44
Q

L monocytogenes bacterial meningitis

A

IV amoxicillin of ampicillin for 21 days and gentamicin for at least first 7 days

45
Q

Gram negative bacilli bacterial meningitis

A

IV cefotaxime for 21 days unless directed otherwise

46
Q

Over 3 months unconfirmed uncomplicated suspected bacterial meningitis

A

IV ceftriaxone for 10 days

47
Q

Under 3 months

A

Cefotaxime or amox for 14 days

48
Q

Meningococcal

A

IV ceftriaxone for 7 days

49
Q

What should you monitor

A

Hypoglycaemia, acidosis, hypokalaemia, hypocalcaemia, hypo afnesaemia, anaemia, coagulopathy
Assess for shock, raised ICP, dehydration using enteral fluid or feeds or IV isotonic fluids (NaCl 0.9% with glucose or dextrose 5% or 10% for neonates)

50
Q

IV fluid resuscitation

A

Sign of shock= bonus of 20ml/kg NaCl 0.9% over 5-10 min via IV and then reassess

51
Q

Shock persists

A

Second bonus of 20ml/kg of IV of NaCl0.9% or human albumin 4.5% solution over 5-10 min

52
Q

Sign of shock after first 40ml/kg

A

3rd bolus, anaesthetic review, vasoactive treatment (adrenaline-NA?) . May need large fluid bolus

53
Q

how else can you test for bacteria in CSF

A

GRAM STAIn, bacterial Ag

54
Q

how else can you test for whihc virus in CSF

A

PCR

55
Q

how else can you test for TB

A

Ziel Neelsen stain, flourecnesnce test, PCR

56
Q

main cell type in CSF

A

b: neutrophil, V: lymphocyte

57
Q

resp support for resp distress

A

15L face mask O2 via reservoir re breathing mask

58
Q

threat to loss of airway patency or need assisted ventilation, hypoventilation, apoea

A

prepare for tracheal intubation, but prepare for sudden deterioration of pt - anticipate aspiration, pulmonary oedema, worsening shock, GCS under 9

59
Q

feature of resp failure

A

irregular inspiration, hypoxia, decO2 saturation, hypercapnia

60
Q

corticosteroids in pt under 3 months

A

DO NOT USE!

61
Q

when to give dexmethasone for bacterial meningitis

A

ASAP if LP reveals: purulent CSF, WCC over 1,000, raised protein conc, bacteria on gram stain

62
Q

max dose of dexmethasone given

A

0.15 mg/KG max dose 10mg QDS for 4 days straight
administer 1st dose within 4 hours of starting AB but don’t start dexmethasone more than 12 hours after starting ABx

63
Q

meningococal septicaemia

A

DONT GIVE HIGH DOSE STEROIDS can give hydrocortisone 25mg/m2 QDS if pt unresponsive to vasoactive agents

64
Q

what stain is N. meningitidis and does it have vaccine

A

gram negative, coffee bean shaped diplococci
MenB vaccine

65
Q

what stain is strept pneumoniae and does it have vaccine

A

gram positive, mix of single cocci and chains. PCV13 vaccine

66
Q

what stain is group B strep

A

gram posiitve, mix of single cocci and chains no vaccine

67
Q

what protects N. menin.

A

polysaccharide capsule- coat bacteria and allow it to hide from phagocytes
factor H binding protein
super oxide dismutase to inactivate ROS

68
Q

what protects strep pneumoniae

A

polysaccharide capsule
neuraminidase
IgA protease
pneumolysin (porin)- pore forming toxin which punch hole in immune cell and lyse cell

69
Q

what protects group B strep

A

polysaccharide capsule
ScpB-C5a peptidase
IgA protease: degrades IgA
sod A
nuclease A degrade NETs

70
Q

what is reverse vaccinology

A

genome based approach to identify vaccine candidates
antigens induce humoral AB located in extracellular or outer membrane region

71
Q

Men B vaccine

A

Research through genome database and look for transcripts of proteins that are presented on surface of bacteria so presented out into extra cellular space (where IS interacts with them). In theory these can be used as antigens in humoral response.
Need to find a target which is important for bacteria so unable to down regulate it or hide it, without compromising their own survivability
We find 4 antigens that fit target and now made into multi component vaccine- mix different antigens together and different epitopes from antigens are combines with an attachment and adjuvant.

72
Q

Group A stroptococcus infection pathway

A

GAS or s.pyogenes
asymptomatic carrier
non invasive infection
systemic comlications
immune sequelae
invasive infection

73
Q

waht is non invasive infection of GAS

A

EG PHARYNGITIS OR STREP THROAT

74
Q

systemic complications of GAS

A

scarlet fever where GAS produces streptococcal pyrogenic exotoxins A,B and C (SPE) which can induce inflammation

75
Q

invasive infection in GAS

A

super antigens (strep pyrogenic exotocins) lead to super antigens so cause massive inflammation in host so direct systemic inflammation eg necrotiisng fascitis

76
Q

immune sequelae GAS

A

M protein in pathogen similar to cardiac myosin so cause acute rheumatic fever
If unchecked, can result in immune sequelae where responses against toxins such as result in autoimmune responses resulting in rheumatic heart disease and glomerular nephritis.

77
Q

necrotising fascitis

A

rapidly progressive infection that destroys deep soft tissues eg muscle fascia
M: surgical debridement of necrotic tissue and broad spec ABx (peniiclin)

78
Q

pathology of necrotising fascitis H292

A

border of venule lumen, inside blood cells and tissues. bacteria surrounding it but neutrophils not able to get out and attack pathogen.
abnormal as 1st line defence= neutrophils but neutrophils unable to find pathogen and get into tissues

79
Q

H292 hypothesis

A

molecule that interferes with neutrophil recruitment
so cell neutrophils unable to go and attack host due to H292 strain of GAS which results in fatality

80
Q

neutrophil specific chemoattractant

A

CXCL8/IL8
C5a

81
Q

how can you assay for levels of CXCL8

A

ELISA
western blot

82
Q

CXCL8 degradation

A

Blood from invasive and throat from s. pyogenes outlets and measured rate of degradation of neutrophil attracting chemokine 68/ IL8 after incubating it with bacteria, degraded CXCL8 so suggests something in islets of invasive GAS which is degrading CXCL8
inactivation of CXCL8 (assessed by IL8 on ELISA) by blood isolates

83
Q

Q. What molecules might H292 be producing?

A

A CXCL8-specific protease.
cleaved (cuts of C terminal 13 amino acid) then digested by H292- mass migration (stops this from happening?)

84
Q

Q. How might we assess the effects of such a protease ?

A

SDS-PAGE analysis of CXCL8 digested with H292.

Mass spectrometry.

85
Q

chemokine

A

40 soluble proteins
each binds to specific GPCR to elicit responses indluding chemotaxis, adhesion, release of anti microbial

86
Q

cepA

A

gene encoding SpyCEP is upregulated in strains associated with necrotising disease
serine protease with homolgy to S8 proteases
catalytic triad
cell wall anchored by LPXTG motif

87
Q

cepA -mine

A

cepA: can kill its own host and usually bacteria don’t want that as they loose their home. Mutation in regulatory part of the gene which lifts that expression.
Catalytic triad important for breaking apart substrate and chemokine. so the triad seen in very rare cases of necrotising GAS

88
Q

what does SpyCep do molecularly

A

cleaves all ELR+ neutrophil recruiting chemokines (end terminal -ELR- important to recognise substrate) then proteases break down neutrophil recruiting chemokines

89
Q

how do neutrophils usually work

A

migration (measured via live cell assay) measure neutrophile chemotaxis via chemokine gradient. recruit cells to CXCL8- very strong directional response

90
Q

how does SpyCEP interfere with neutrophil function

A

SpyCEP has catalytic triad which digest the chemokines so fewer cells recruited and so less gradient so bacteria more likely to survive.
prove this with animal model that knocks in SpyCEP and see the impact of it

91
Q

knock out SpyCEP - H575

A

necrotising strain in mice not kill them, because not on cell wall. SpyCEP knocked out, so not spread as much and not spread to lymph nodes so no fatality

92
Q

SpyCEP knocked in-l.lactis

A

Knock in spycep gene- becomes deadly. Inject into thigh- allow bacteria to survive in tight and then spread to lymph nodes, liver and spleen

93
Q

SpyCEP summary

A

Invasive strains of GAS produce SpyCEP.

SpyCEP selectively cleaves CXCL8, impairing neutrophil recruitment.

Knockout of cepA results in impaired GAS survival and spread to the regional lymph nodes.

Knock-in of cepA into L. lactis results in enhanced survival and rapid spread to organs.

94
Q

AB and SpyCEP

A

AB available that recognises intact form of CXCL8 but none that recognise inactivated form.
CXCL8 incubated with bacterial lysate (so lyse cxcl8- inactive) and so then inject inactivated CXCL8 to mice, produce antibodies that complement inacitve CXCL8 and collect those AB.
then add the inactive cxcl8 with catalytic triad so that nocks out the enzymatic function wihhout losing structure (so makes competetive antagonist)

95
Q

Km

A

the Michaelis Constant and is defined as the concentration of substrate at which a particular enzyme works at half its maximal velocity
compar strenght of enzyme substrate complexs
lowe KM means tight binding of substrate to enzyme
high KM: low affinity

96
Q

K cat

A

number of substrate molecules processed per second.

97
Q

Km of SpyCEP

A

Spycep very strong- only need small amount to be potent because CXCL9 is very strong
Different concentrations of CXCL8 degraded them with spycep over time, translate with mass spec, to work out Kcat
Km very low: as very high potency of CXCL8 (active even if tiny concentration), enzymes need to be sooo strong to cut all the CXCL8, so enzyme sooo potent

98
Q

inhibitor of SpyCEP

A

Inhibitor 1: add to neutrophils, not reduce migration.
Spycep: add to neutrophils then reduces migration but then inhibitor 1 rescues that migration back so able to defeat pathogen

99
Q

Spycep +inhibitor 1

A

infection of mice with l.lactic+ spycep knocked in
-spycep: ensures neutrophils don’t get rid of l. lactis so l.lactis can grow
-inhibitor 1: promotes local tissue clearance of SpyCEP bacteria

100
Q

mice vaccination

A

Look at immunogenicity of recombinant spycep.
Took catalytically dead spycep (with catalytic traid shape but non functioning) and injected into mice to induce immune response and then measure anti spycep IgG took out antibodies from mice. So these antibodies stop CXCL8 from being cleaved by competitively antagonizing (so antibodies can now bined to spycep –as it was based on non functioning spycep- and stop it from working)

101
Q

human vaccine

A

Best Epitope to be put in vaccine using crystallography and NMR to see which epitope are exposed on surface of vaccine on proteins and include them in vaccine

102
Q

q

A

unclear how catalytic triad cooperate with each other
unclear how CXCL8 us bound and gets access to catalytic traid
need to generate structure which has CXCL8 bound to spycep

103
Q

what awill be put in vaccine

A

deat mutants of spycep complexed with CXCL8

104
Q

C5a

A

SCPA- c5a peptidase affect symptoms in beginning of infection. copy the techniques so both scpA and SpyCEP (CXCL8 peptidase- late stage or necrotising infections) in 1 vaccine

CSI 1c A (1 decks)

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