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Phase 3 > Week 6 > Flashcards

Week 6 Flashcards

1
Q

Describe the difference between gram positive and negative bacteria

A

positive have a thick peptidoglycan wall

negative have thin peptidoglycan wall and periplasm and outer membrane

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2
Q

Where can antibiotics target?

A

cell wall peptidoglycan
metabolism
DNA
ribosome

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3
Q

Describe the action of bactericidal antibiotics

A

achieve sterilisation of the infected site by directly killing bacteria
lysis of bacteria can lead to release of toxins and inflammatory material

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4
Q

Describe the action of bacteriostatic antibiotics

A

suppresses growth but do not directly sterilise infected site
requires additional factors to clear bacteria - immune mediated killing

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5
Q

What is meant by the antibiotic spectrum?

A

refers to the range of bacterial species effectively treated by the antibiotics

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6
Q

Describe the spectrum of meropenum

A

active against almost all gram positive and negative species. Resistance is rare except for MRSA

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7
Q

Describe the spectrum of benzyl-penicilin

A

highly active against streptococci. most other disease causing bacteria are resistant

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8
Q

Describe broad spectrum antibiotics

A

active against a wide range of bacteria

treat most causes of infection but also have a substantial effect on colonising bacteria

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9
Q

Describe narrow spectrum antibiotics

A

active against limited range of bacteria
useful where cause of infection is well defined
much more limited effect on colonising bacteria

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10
Q

What are the main gram positive bacteria?

A

clostridum
streptococcus
enterococcus
staphylococcus

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11
Q

What are the main gram negative bacteria?

A 
bacteroides
psuedomonas
haemophilus 
neisseria
e.coli
other coliform
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12
Q

What is guided therapy?

A

depends on identifying cause of infection and selecting agent based on sensitivity testing

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13
Q

What is empirical therapy?

A

best guess therapy based on clinical/epidemiological acumen

used when therapy can’t wait for culture

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14
Q

What is prophylactic therapy?

A

preventing infection before it begins

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15
Q

What can the disruption of bacterial flora lead to?

A

overgrowth with yeasts - thrush
overgrowth of bowel - diarrhoea
development of C.dif colitis
future colonisation and infection with resistant organisms

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16
Q

What are the main classes of beta-lactam antibiotics?

A

penicillins
cephalosporins
carbapenems
monobactams

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17
Q

Describe the overall mechanism of action of b lactams

A

all share same structural feature
Beta-lactam motif analogue of branching structure of peptidoglycan
inhibits cross linking of cell wall peptidoglycan
causes lysis of bacteria - bacteriocidal

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18
Q

What are beta-lactamases?

A

enzymes that lyse and inactivate beta-lacta drugs
commonly secreted by gram negatives and S.aureas
confer high level resistance to antibiotic - high doses will not overcome it

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19
Q

Describe the pharmacology of beta-lactams

A

poorly absorbed in GI tract
usually excreted unchanged in urine, some also via bile
half life varies enormously
effectively distributed to infection sites

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20
Q

Which beta-lactams can be effective orally?

A

amoxicillin, flucloxacillin

vomiting limits dose

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21
Q

Describe the cross reactivity of penicillin allergy

A

patients allergic to a penicillin will usually be allergic to others
cross reactivity with other antibiotic classes is much lower

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22
Q

What are common penicillin?

A

benzyl-penicillin
amoxicillin
flucloxacillin

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23
Q

What is a common cephalosporins?

A

ceftriaxone

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24
Q

What is a common carbapenem?

A

meropenem

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25
Q

WHat is a common monobactam?

A

aztreonam

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26
Q

What are common beta lacteal/beta lactase inhibitor combinations?

A

co-amoxiclav

piperacillin/tazobactam

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27
Q

Describe benzylpenicillin

A

chemically similar to original penicillin
IV
remains first choice antibiotic for serious strep infection
narrow spectrum

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28
Q

Describe amoxicillin

A

semi-synthetic
greatly increased activity against gram negative organisms
much more orally bioavailable than natural peniclins
widely used in the treatment of a wide range of infections
non severe respiratory tract infections

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29
Q

Describe fluloxacillin

A

synthetic penicillin developed to be resistant to beta-lactase produced by staph
highly active against staph.aureus and streptococci
no activity at all against gram negative organism
orally but nausea limits the dose

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30
Q

Describe beta-lactamase inhibitors

A

effectively inhibit some beta lactamases
co-administered with penicillin antiobiotic
greatly broadens spectrum of penicillins against gram negatives and S.aureus
some uninhibited beta lactamases may still lead to antibiotic failure

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31
Q

Describe cepahlosporins

A

found to have good activity against gram negatives and positives
less susceptible to beta-lactamases than penicillins

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32
Q

Describe the activity of cetriaxone

A

wide spectrum
not enterococcus
not pseudomonas
not MRSA

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33
Q

Describe carbapenems

A

ultra broad spectrum beta-lactam antibiotics
excellent spectrum of activity against gram positives and negatives
no activity against MRSA
new beta lactamases are emerging which lyse carbapenems

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34
Q

Describe the activity of meropenem

A

everything but MRSA

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35
Q

Describe monobactams

A 
aztreonam only member of this class
no cross reactivate to penicillins so can be given ti those with penicillin allergy (except anaphylaxis)
only given IV
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36
Q

Describe the activity go aztreonam

A

all gram negative bacteria except bacterioides

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37
Q

Describe vancomycin

A

inhibits cell wall formation in gram positives
no gram negative action
not dependent on PBP so effective against resistant organisms
always IV except for C.dif
resistance is very uncpmmpn

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38
Q

What are the side effects associated with vancomycin?

A

nephrotoxicity
red-man syndrome if injected too rapidly
ototoxicity

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39
Q

Why is therapeutic drug monitoring carried out with vancomycin?

A

narrow therapeutic range

aim higher in severe illnesses

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40
Q

Give examples of protein synthesis inhibitors

A 
50s
macrocodes
clindamycin
chloramphenicol
30S
aminoglycosides
tetracyclines
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41
Q

Give examples of macrolides

A

erythromycin
clarithromycin
azithromycin

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42
Q

Give an example of an aminoglycoside

A

gentamicin

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43
Q

Give an example of a tetracycline

A

doxycycline

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44
Q

Describe macrolides

A

good spectrum of activity against gram positives and respiratory gram negatives
active against atypicals - legionella, mycoplasma, chlamydia
excellent oral absorption - even on sever infection

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45
Q

What are the adverse effects associated with macrocodes?

A

diarrhoea and vomiting
QT prolongation
hearing loss with long term use

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46
Q

Describe the drug interactions with macrolides

A

clarihromycin - over 400 drug interactions
simvastatin - avoid co-prescription
atorvastatin
warfarin

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47
Q

Describe clinamycin

A 
similar to macrolides
same mechanism of action
excellent oral absorption
principle actin against gram positives 
no action against aerobic gram negatives or atypicals 
excellent activity against anaerobes
added to patients with gram positive toxin mediated disease - toxic shock syndrome, necrotising fascitis 
causes C.dif
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48
Q

Describe C.differgic antibiotics

A

antibiotics dramatically alter the colonic flora
c.dif commonly colonises the human colon
forms spores which can be difficult from hospitals
has developed resistance to common antibiotics classe

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49
Q

What are the 4 Cs in C.differgic antibiotics?

A

clindamycin
co-amoxiclav
cephalosporins
ciprofloxacilin

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50
Q

Describe chloramphenicol

A

inhibits 50S ribosome
excellent spectrum of activity
toxic - bone marrow, aplastic anaemia, pptic neuritis

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51
Q

What are the modern uses of chloramphenicol?

A

topical therapy to eyes

bacterial meningitis with beta-lactam allergy

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52
Q

Describe gentamicin

A

reversibly binds to the 30S ribosome - bacteriostatic actions
poorly understood action on the cell membrane - bactericidal action

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53
Q

What are the side effects of gentamicin?

A

nephrotoxicity
ototoxicity
neuromuscular blockade

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54
Q

Describe tetracylcines

A

similar spectrum of activity of macrolides
also active against atypical organisms
relatively non toxic
avoid in children and pregnant women

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55
Q

What are examples of quinolones?

A

cirprofloxacin

levofloxacilin

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56
Q

What type of antibiotics affect DNA repair and replication?

A

quinolones and rifampcin

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57
Q

Describe quinolones

A

broad spectrum, bactericidal antibiotics
excellent oral biovavilabiliy
active against many atypical pathogens including legionella

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58
Q

Describe the activity of ciprofloxacin

A

good against gram negatives, weaker against gram positives. Cmonly used in UTI/abdominal infection

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59
Q

Describe the activity of levofloxacin

A

sacrifices some gram negative activity for stronger gram positive activity - respiratory tract

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60
Q

What are the side effects of quinolones

A 
GI toxicity
QT prolongation
Tendonitis 
Resistance emerging on therapy
tendon damage
C.diff infection
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61
Q

Describe rifampicin

A

principally used for two indications in UK - TB, in addition in serious gram positive infection (especially staph.a)
drugs interactions are important

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62
Q

Describe the issues with TB

A

slow growing
high bacterial burden
limited access of drugs to granuloma

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63
Q

What is the solution to TB?

A

prolonged courses of therapy

combination therapy to prevent resistance and resting kill growing and resting organisms

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64
Q

What is the standard short course therapy of TB?

A

isoniazid
rifampicin
pyrazinamide
ethambutamol

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65
Q

How to folate synthesis inhibits work?

A

inhibition of folate metabolism pathway leads to impaired nucleotide synthesis and therefore impaired DNA replication

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66
Q

Describe trimethoprim

A

orally administered
good range of action against gram positives and negative
resistance is Major problems
limited to use in uncomplicated UTI

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67
Q

Describe the toxicity of trimethoprim

A

elevation of serum creatinine - does not reflect fall in GFR
related to action on proximal tubules
Elevation of serum K+ - problematic in patients with chronic renal impairment
Rash and GI disturbance uncommon

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68
Q

Describe metronidazole

A

enters by passive diffusion and produces free radicals
effective against most anaerobic bacteria
often added to therapy in intra-abdominal infections, especially with abscess

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69
Q

What are the side effects of metronidazole?

A

causes unpleasant reaction with alcohol

peripheral neuropathy with long term use

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70
Q

Describe an uncomplicated UTI

A

Lower urinary tract symptoms
absence of sepsis or evidence of upper tract involvement
treatment only needs to sterilise the urine
low risk infection so can wait for culture results

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71
Q

Describe the use of trimethoprim in lower UTI

A

currently fist line in most cases
avoid in 1st trimester of pregnancy
penetrates well into prostate so good choice for men

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72
Q

Describe the use of nitrofuratoin in UTI

A

excellent broad spectrum activity
concentrated in urine so no effect on other tissues
failure to concentrate in urine in renal failure
relatively non-toxic in short courses- pulmonary fibrosis with long term use

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73
Q

Which antibiotics are thought to be safe in pregnancy?

A

most beta lactams
broad spectrum agents may be associated with NEC in premature infants
macrolides
anti-tuberculants

74
Q

What antibiotics are not considered safe during pregnancy ?

A 
tetracyclines 
trimethoprim
nitrofurantoin
aminoglycosides
quinolones
75
Q

What is inherent antibiotic resistance?

A

lack a pathway or target which a drug interacts with, or the drug is unable to gain access to the target

76
Q

What is acquired antibiotic resistance?

A

where a drug which was previously sensitive has gained some genetic material encoding for resistance

77
Q

Describe vertical gene transfer

A

genetic information passed from parent cell to progeny

78
Q

Describe horizontal gene transfer

A

genes transferred other than through traditional reprodocution

79
Q

Describe spontaneous mutation

A

resistance mutations occur in bacteria exposed to drugs
spontaneous mutations occur at a lower rate than acquisition of mobile pieces of DNA
treatment of some infections with 2 drugs acting in different ways is based on the principle that if a mutation occurs in one drug target the other drug will still the organism

80
Q

Describe conjugation

A

requires cell to cell contact between two bacteria
small pieces of DNA called plasmids are transferred
most important mechanism of horizontal gene transfer

81
Q

Describe plasmids

A

plasmids are pieces of circular double stranded DNA
Genetic information that can be carried on plasmidscan include resistance to antibiotics, heavy metals, UV light
can carry genes which encode pili and mediate adherence and can encode toins

82
Q

Describe transduction

A

this is where small pieces of DNA are transferred between bacteria by a virus
bacteriophages are viruses which infect bacteria

83
Q

Describe fitness cost and selection pressure

A

genetic material acquired may affect more than just drug susceptibilty
this reduced growth is called a fitness cost
in an environment without a selective pressure these slower growing mutants will be outgrown by their wild type colleagues and will slowly die awy
the time this takes depends on the significance of the fitness cost
sometimes other mutations may develop which compensate for the fitness cost allowing the mutated bacteria to compete with the wild type colleagues

84
Q

Describe resistance in coliforms

A

gut commensals e.g E.coli and klebsiella
cause of infections such as UTI, intra-abdominal sepsis and HAP
antibiotics commonly used to treat these include amoxicillin, ciprofloxacin, cephalosporins and gentamicin

85
Q

Describe beta-lactase inhibitors

A

clavlanate and tazobactam
these are compounds which in themselves have only weak antibacterial activity but which mainly acts by bidding the beta-lactamase
thus allowing the beta-lactam to continue to act

86
Q

Describe extended spectrum beta-lactamases

A

ESBLs
usaully plasmid encoded
these are enzymes which are able to hydrolyse the beta-lactam ring of not only penicillins but also cephalosporins

87
Q

what are the treatment options for ESBLs?

A

ciprofloxacin
temocillin
gentamicin
meropenem

88
Q

What are non-genetic mechanisms of resistance?

A

protected environment
resting stage
presence of a foreign body

89
Q

How can the spread of resistance be prevented?

A

narrow spectrum where possible
follow empirical prescribing guidance
short courses - 3 days for UTI
5-7 days for LRTI

90
Q

What are non-genetic mechanisms of resistance?

A

protected environment
resting stage
presence of a foreign body

91
Q

WHat are the four main mechanisms of antibiotic resistance?

A

target change, inactivation, decreased entry and increased exit

92
Q

What are conventional pathogens?

A

endogenous flora
hospital acquired
envionmental organisms

93
Q

What are opportunistic pathogens in immunosuppressed patients?

A

CoNS (cannulas)

aspergillus (mould)

94
Q

Describe primary immunodeficiencies

A

inherited
exposure in utero to environmental factors
rar

95
Q

Describe secondary immunodeficiency

A

underlying disease state
treatment for disease
common

96
Q

Why is there an increasing population of profoundly immunocompromised patients?

A 
improved survival at extremes of life
improved cancer treatment 
development in transplant techniques
developments in intensive care
management of chronic inflammatory conditions
steroids
97
Q

Describe neutropaenia

A

can be caused by chemotherapy or therapeutic irradiation

decreased proliferation of marriw

98
Q

What is the definition of neutropenia?

A

<0.5X10 to the power of 9/

<1.0 X10 the power of 9 and falling

99
Q

Describe chronic granulomatous disease

A

inherited X linked disorder
defect in gene coding for NADPH oxidase
deficiency in production of oxygen radicals
defective intracellular killing
recurrent bacterial and fungal infections > abscesses lung, lymph nodes, skin
inflammatory responses with widespread granuloma formation

100
Q

What can suppress cellular immunity?

A 
DiGeroge syndrome
malignant lymphoma
cytoxic chemotherapy 
extensive irradiation
immunosupressive drugs 
allogeneic stem cell transplants 
infections - HIV, mycobacterial infections, measles, EBV, CMV
101
Q

What can suppresses humoral immunity?

A

bruton agammaglobulinaemia
Antibody production decreased in CLL< myeloma
usually preserved in acute leukaemia
intensive radio and chemotherapy

102
Q

Describe splenic function

A

splenic macrophages eliminate non-opsonised microbes - encapsulated bacteria
site of primary immunoglobulin response
specific opsonising antibody required for phagocytosis of encapsulated bacteria
impairs activity of all phagocytic cells

103
Q

What infections are those with humeral deficiency, splenectomy or hypospenism predisposed to?

A

strep. pneumonia
haemophilus influenza type B
neisseria meningitidis

104
Q

What are the important physical barrier in the immune system?

A

skin
conjunctivae
mucous membranes - gut, respiratory, GU

105
Q

Why is the skin a good physical barrier to infection?

A 
desquamates
dry
pH 5-6
temp is 5 degrees lower
secretory IgA in sweat
106
Q

Describe mucosal barrier injury and colonisation resistance

A

High mitotic inde - affected by chemo and radiation
GI lymphoid tissue responds with inflammatory response
mucositis
pain, dysphasia etc
impairment of GI function, altered nutrition status
H2 antagonists, PPIS, antibiotics, diarrhoea can lead to an altered microbiome

107
Q

wHat is the definition of severe nutritional deficiency?

A

<75% ideal body weight

or rapid weight loss and hypoalbuminaemia

108
Q

What are the causes of impaired nutritional status?

A

anorexia
nausea and vomiting
mucositis
metabolic derangements

109
Q

What effect foes iron deficiency have on host defences?

A

reduces microbicidal capacity of neutrophils and T cell function

110
Q

How can concurrent illness effect the immune system?

A

stress- reduced T cell function

diabetes mellitus - reduced opsonisation, chemotaxis

111
Q

Why are premature babies so prone to infection?

A 
no maternal immunoglobulin
immature T cells
lines
ventilation
urinary catheter 
prolonged time in hospital - resistant organisms
112
Q

What are the non-infectious causes pf febrile neutropenia?

A 
malignancy
chemotherapy
transfusion
antibiotics
colony stimulating factors 
allergies
113
Q

What is the definition of a fever?

A

pyrexia or hypothermia (>38 or <36)

114
Q

What is SIRS?

A

systemic inflammatory response
sweats, chills, riggers, malaise, tachypnoea (>20) tachycardia (>90), hypotension (patients may seem well perfused despite hypotension)

115
Q

What is sepsis?

A

Evidence of infection (including SIRS) and organ dysfunction (1 of hypotension, confusion or tachypnoea (RR>22)

116
Q

What is septic shock?

A

sepsis induced hypotension requiring inotropic support or hypotension that is unresponsive (within 1hr) to adequate fluid resuscitation (<90 or >40 less from baseline)

117
Q

What is neutropenic sepsis or febrile neutropenia?

A

neutrophil count <0.5 or <1 if recent chemotherapy

plus fever/hypothermia or SIRS or sepsis/septic shock

118
Q

What should standard risk patients with febrile neutropenia receive?

A

piperacillin/tazobactam

or vancomycin or ciprofloxacin if penicillin allergic

119
Q

What should high risk patients with febrile neutropenia receive?

A

piperacillin/tazobactam and gentamicin

120
Q

How else should febrile neutropenia be managed?

A 
if skin/soft tissue - vancomycin
if atypical pneumonia- clarithromycin
if previous ESBL= merepenem
consider PCP
refer to seniors
121
Q

What is the key factor in selecting for resistance?

A

pressure or volume (duration of course X number of courses_

122
Q

What is the individual effect in collateral damage due to antibiotics?

A

antibiotic resistance
drug reaction/ toxicity/ interactions
diarrhoea - cliff
vascular site infection - S.aureas bacteraemia

123
Q

What are the population effects of the unintended consequences of antibiotics?

A

antibiotic resistance

clostridium dificile

124
Q

what is antimicrobial stewardship?

A 
programme to ensure safe and appropriate use of ABx
optimize outcomes
minimise unintended consequences
reduce AMR and c.dif
patient at centre of Rx decision making
125
Q

How is antimicrobial stewardship achieved?

A 
monitoring/surveillance
guidelines/protocols
specific restrictions
specific interventions
MDT working
126
Q

What is under surveillance in AMS?

A 
volume of antibiotic prescribing
quality of antibiotic prescribing 
antimicrobial resistance
c.dif
other adverse events related to prescribing /interventions
127
Q

What is the role of the lab in AMS programme?

A

optimisation of lab diagnosis - sampling ,testing and minimisation of over diagnosis
restricted reporting of organisms to prevent over treatment
restricted reporting of sensitivities to reduce use of inappropriate agents
Co-ordination of clinical advice with guidance
data on resistance and CDI

128
Q

When should antibiotics not be prescribed?

A

viral and self limiting bacterias infections (OM, sinusitis, LRTIs, COPD, URTIs)
asymptomatic bacteruria, uncomplicated cystitis
ingrown toe nails
varicose ecxema
systemic inflammatory response due to cancer, ischaemia, inflammation

129
Q

What non-antibiotic measures can be used?

A

reassurance / explanation
symptomatic measures - fluids, analgesia
delayed script
review date/opportunity - safety netting

130
Q

What are symptoms and signs of bacterial infection?

A 
fever
sweats
rigors
shivers
shakes
131
Q

What are localising symptoms and signs of bacterial infection?

A

dysuria and freuency
dyspnoea, cough and green/brown sputum, crepitations
erythema, heat, swelling
sore threat with exudate and adenopathy

132
Q

What antibiotics should be used in non sever LRTI?

A

amoxicillin or doxycycline

133
Q

Which antibiotics should be used in non severe UTIs?

A

trimethoprim or nitrofurantoin

134
Q

Which antibiotics should be used in cellulitis?

A

flucloxacillin

135
Q

Which antibiotics should be used in severe or life-threatening infection?

A

usually IV combination (beta lacteal and gentamicin) initlally
use of protected Abx if risk of MDR

136
Q

What are the human factors in knowledge and experience and prescribing antiobiotics?

A

perception of resistance
misconception that spectrum of activity = efficacy
lack of confidence in diagnosis
fear of failure

137
Q

What are the human factors in the prescribing culture of antibiotics?

A

peer practice
speed of escalation of Rx
brand familiarity
fear of litigation

138
Q

Describe scarlet fever

A

group A strep

strawberry tongue

139
Q

What is the eagle effect?

A

in very severe strep
mass of strep stop expressing PBP . Mitochondria produce endotoxins which cause low BP and rash. Clindamycin acts on mitochondria and prevents the production of endotoxins

140
Q

What is the sepsis 6?

A 
blood cultures
antibiotic administration
oxygen to achieve target saturation
measure lactate and JHb
IV fluids
monitor urinary output hourly
141
Q

What are the indications for IV antibiotic therapy?

A

sepsis, SIRS or rapidly progressing infection
special conditions - endocarditis, CNS infection, bacteraemia, osteomyelitis
mod-severe skin and soft tissue infection
infection and oral route compromised
no oral formulation of antibiotic available

142
Q

What is cellulitis normally caused by?

A

beta haemolytic strep
staph - wound infections
gram negatives uncommon

143
Q

What is the treatment of cellulitis

A

oral 5 days flucloxacillin if milf
IV if modernly severe 7-10 days
very severe IV clindamycin and gentamicin

144
Q

What is necrotising fasciitis normally caused by?

A

beta haemolytic strep
staph
rarely gram negative

145
Q

Describe necrotising fasciitis

A

pain out with appearance
masked by NSAIDs
rapidly progressive with multi organ faiilure
EAGLE effect - static growth ophase with excess toxin production
surgery, immunoglobulin

146
Q

What needs to be done when there is S.aureus bacteraemia?

A

find and remove source of infection
ECHO and other investigation for underlying source
reread Bfs after 48-96 hours of effective IVABRx

147
Q

What is the treatment of S.aureus bacteraemia?

A

flucloxacillin
vans as per guidance
if persistent fever or no improvement nor further positive blood culture then do TOE
TOE also for negative TTE if PV or if endocarditis still suspected
Rx all with IV therapy for >2 weeks

148
Q

What history is important in a returning febrile traveller?

A 
past medical history
current medications
pre travel advice
vaccines / malarial tablets
where travelled to (in world, rurual/urban)
means of travel
time- longer stay increased risk of some illnesses / decreased risk of others)
activities - swimming, sex safari
149
Q

What are the most common cases of traveller illnesses?

A

GI, febrile illness and dermatological diseases are the vast majority of cases

150
Q

What is the management of travellers diarrhoea?

A

fluids!!!!!
antibiotics (only in some cases) (quinolones, azithromycin)
anti motility agents (use with caution)
investigation for other cause if persistent

151
Q

What type of travellers illness is the most concerning?

A

undifferentiated fever

152
Q

What are the most common causes of undifferentiated fever?

A

malaria
dengue - particularly southeast asia, carribean
Typhoid - south central asia

153
Q

Which mosquitos are most likely to bite at different parts of the day?

A

aedes - day biter. can live in most polluted cities

anopheline - night biter

154
Q

What are the physical avoidance strategies to prevent mosquito bites?

A

indoors - AC, screens
Impregnated netting
clothing - cover up, spray/soak clothing

155
Q

How is malaria diagnosed?

A

antigen testing and thin film

PCR is helpful for detect low levels of parasite

156
Q

What are the clinical features of malaria?

A

fever, malaise, headache, myalgia, diarrhoea
anaemia
jaundice
renal impariment

157
Q

Describe severe malaria

A 
parisitaemia >2%
cerebral malaria
severe anaemia
renal failure
shock
DIC
acidosis 
pulmonary oedema
158
Q

What is the treatment of malaria?

A

traditionally quinine and doxycicline

artemehter compounds are more used now

159
Q

What are the main chemoprophylaxis options against malaria?

A

mefloquine
doxycicline
malarone

160
Q

Describe mefloquine

A

once weekly

psychiatric side effects (vivid dreams to psychosis)

161
Q

Describe doxycicline

A

daily

photosensitisation

162
Q

Describe malarone

A

minimal side effects

cost

163
Q

What is enteric fever?

A

S.typhi and S.paratyphi

164
Q

Describe enteric fever

A

human reservoir only

human to human spread and contaminated food / water

165
Q

What is the incubation period of typhoid?

A

5-21 days

166
Q

What does the incubation period for tyhpoid depend on?

A

age
gastric acidity
immune status
infectious load

167
Q

What are the clinical features of typhoid?

A 
fever
myalgia 
headache
cough
abdo pain
constipation
diarrhoea
168
Q

What can typhoid lead to?

A

septic shock

death

169
Q

What are the GI symptoms of thyphoid?

A

diarrhoea/constipation
abdominal pain
rectal bleeding
bowel perforation

170
Q

What are the neurological symptoms of thyphoid ?

A

headahce
enteric encephalopathy - altered consciousness/ confusion
increased mortality
steroids

171
Q

How is typhoid diagnosed?

A

travel history - area visited, food and drink, pre travel vaccination / advice
blood culture (60-80% positive)
stool culture and serology not very sensitive

172
Q

What is the treatment of typhoid?

A

quinolones - resistance
cephalosporins
azithromycin

173
Q

What type of mosquito is dengue fever spread by?

A

aedes

174
Q

What are the clinical features of dengue fever?

A 
headache
fever
retro-orbital pain
arthralgia / myalgia
rash
cough
sore throat
nausea 
diarrhoea
175
Q

What is likely to be seen in lab tests in dengue fever?

A

leucopenia
thrombocytopenia
transaminitis

176
Q

What is the treatment of dengue fever?

A

symptomatic
no specific anti-viral treatment
horrible self limiting fever

177
Q

What is dengue haemorrhagic fever?

A

increased vascular permeability
thombocytopaenia
fever
bleeding

178
Q

What types of viral haemorrhagic fevers are there?

A 
lassa
ebola / marburg
CCHF
SAVHFs
RVF
DHF
yellow fever
179
Q

What are the clinical features of viral haemorrhagic fever?

A

febrile, non specific, pharyngitis, conjunctival infection, chest pain, prostration
haemorrhage - petichiae, mucosal surfaces
oedema, effusions
low WCC, low platelets, prolonged TT, prolonged APTT

180
Q

What VHF is spread by rats?

A

lassa

181
Q

What is ebola spread by?

A

bata

182
Q

What is CCHF spread by?

A

ticks

Phase 3 (15 decks)

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