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Medicine > Infectious Disease > Flashcards

Infectious Disease Flashcards

1
Q

What are bacteria?

A
  • Single celled organisms
  • Some pathogenic + cause disease
  • Anaerobic (don’t need O2) or aerobic (do)
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2
Q

What are gram positive bacteria?

A
  • Thick peptidoglycan wall

- Stains with crystal violet stain

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3
Q

What are gram negative bacteria?

A
  • No peptidoglycan cell wall
  • Doesn’t stain with crystal violet stain but will with others
  • Counterstain-> binds to cell membrane so turns pink/red
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4
Q

What are atypical bacteria?

A

Not stained or cultured in the normal way (eg crystal violet or other stains)

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5
Q

What is the anatomy of bacteria?

A
  • Cell wall
  • Outer membrane
  • Nucleic acid-> DNA
  • Ribosomes-> where proteins synthesised
  • Folic acid-> needed for synthesising + regulating DNA
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6
Q

Why do bacteria need folic acid?

A

needed for synthesising + regulating DNA

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7
Q

What are examples of gram positive cocci?

A

Staph, strep, enterococcus

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8
Q

What are examples of gram positive rods?

A
  • Corneybacteria
  • Mycobacteria
  • Listeria
  • Bacillus
  • Nocardia
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9
Q

What are examples of gram +ve anaerobes?

A
  • Clostridium
  • Lactobacillus
  • Acintomyces
  • Propionibacterium
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10
Q

What are examples of gram negative bacteria?

A
  • Neisseria meningitidis
  • Neisseria gonorrhoea
  • H/influenzae
  • E.coli
  • Klebsiella
  • Pseudomonas aeruginosa
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11
Q

What are examples of atypical bacteria?

A

Leigonella, psittaci, mycoplasma pneumoniae, chlamydydophilia pneumoniae, Coxiella burnetti

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12
Q

What is MRSA?

A
  • Methicillin-resistant staph aureus
  • Resists beta-lactams-> penicillins, cephalosporins, carbapenems,
  • Colonised on skin + resp tract
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13
Q

How is MRSA prevented?

A
  • Screen via nasal + groin swabs on admission for surgery/treatment
  • Chlorhexidine washes + antibacterial nasal creams
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14
Q

How can MRSA be treated?

A

Doxycycline, clindamycin, vancomycin, linezolid, teicoplanin

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15
Q

What are ESBLs?

A
  • Extended Spectrum Beta-Lactamase bacteria
  • Resistant to beta-lactams-> produce beta-lactamase and destroy
  • Often E.coli + Klebsiella
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16
Q

What infections do ESBLs often cause?

A

E.coli + Klebsiella-> UTIs + pneumonia

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17
Q

How can ESBL infection be treated?

A

Carbapenems-> eg meropenem

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18
Q

How do bacteriostatic antibiotics work?

A

Stop bacterial reproduction + growth

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19
Q

How do bacteriacidal antibiotics work?

A

Kill bacteria directly

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20
Q

How does penicillin work?

A

Inhibits cell wall synthesis + has beta-lactam ring

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21
Q

How do carbapenems work?

A

Inhibits cell wall synthesis + has beta-lactam ring

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22
Q

How do cephalosporins work?

A

Inhibits cell wall synthesis + has beta-lactam ring

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23
Q

How does vancomycin work?

A

Inhibits cell wall synthesis + doesn’t have beta-lactam ring

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24
Q

How does teicoplanin work?

A

Inhibits cell wall synthesis + doesn’t have beta-lactam ring

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25
Q

How does trimethoprim work?

A

Inhibits folic acid metabolism

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26
Q

How do macrolides (eg clarythromycin) work?

A

Inhibit protein synthesis by targetting ribosomes

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27
Q

How does clindamycin work?

A

Inhibit protein synthesis by targetting ribosomes

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28
Q

How do tetracyclines (eg doxycycline) work?

A

Inhibit protein synthesis by targetting ribosomes

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29
Q

How does gentamicin work?

A

Inhibit protein synthesis by targetting ribosomes

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30
Q

How does chloramphenicol work?

A

Inhibit protein synthesis by targetting ribosomes

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31
Q

How does metronidazole work?

A
  • Is reduced to active form in anaerobic cells then inhibits nucleic acid synthesis
  • Effective against anaerobes
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32
Q

How many people with penicillin allergy also have cephalosporin + carbapenem allergy?

A

Around 1%

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33
Q

What is the treatment pathway for a hospital patient with infection?

A
  • Start with amoxicillin-> strep, listeria, enterococcus
  • Switch to co-amoxiclav-> staph, haemophilus, E.coli
  • To tazocin-> pseudomonas
  • To meropenem-> ESBLs
  • Add teicoplanin/vancomycin-> MRSA
  • Add clarithromycin or doxycycline-> atypicals
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34
Q

What is the pathophysiology of sepsis?

A
  • Pathogen recognised by macrophages, lymphocytes + mast cells
  • Release cytokines etc-> activate other systems + make endothelial BV lining more permeable
  • Fluid into extracellular space-> oedema + less IV volume-> space between blood + tissues-> less O2 to tissues
  • NO release-> vasodilation
  • Coagulation activation-> fibrin circulating-> less tissue perfusion + platelets consumed to form clots-> DIC (thrombocytopaenia + haemorrhages)
  • Hypoperfusion-> raised lactate (anaerobic resp)
  • Disregulated immune response
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35
Q

What is sepsis?

A

Disregulated immune response to infection causing systemic inflammation

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36
Q

What is septic shock?

A
  • Systolic BP <90 after fluid resus
  • Lactate >4mmol/L (hypoperfused tissues)
  • Circulatory, cell + maetabolic abnormalities
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37
Q

How is septic shock managed?

A

IV fluids, ICU, inotropes (noradrenaline- stimulate CV system)

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38
Q

What are the features of severe sepsis?

A

Hypoxia, oliguria, AKI, thrombocytopaenia, coagulation dysfunction, lactate >2mmol/L

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39
Q

What are the risk factors for developing sepsis?

A
  • Age <1 or >75
  • Chronic conditions
  • Chemo, steroids, immunosuppressants
  • Recent burns
  • Pregnant or pregnant in last 6 weeks
  • trauma or surgery in last 6 weeks
  • Catheters + central lines
  • IVDU
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40
Q

What infections commonly cause sepsis?

A

Pneumonia, UTI, abdominal, skin/soft tissue

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41
Q

What are the signs of sepsis?

A
  • Tachypnoea often first
  • Picked up on NEWS score
  • Infection, non-blanching rash, reduced UO, mottled skin, cyanosis
  • New onset AF
  • Obs might be normal in neutropaenic or immunosuppressed patients
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42
Q

At what NEWS score should you be worried about sepsis?

A

Definitely 5+ but depends on patient

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43
Q

What are the red flag features of being at high risk for sepsis?

A

If 1+ should suspect…

  • New onset or altered mental state
  • Systolic BP <90 or >40 change
  • HR >130
  • RR >25
  • SpO2 92% on oxygen
  • Lactate >2
  • AKI
  • Recent chemo
  • No PU in 18 hours
  • Non blanching rash
  • Mottled skin
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44
Q

What are the amber flag features of being at risk for sepsis?

A

Investigate + review within 1 hour if 2+ are present…

  • Mental status concerns
  • Systolic BP 91-100
  • HR 91-130
  • RR 21-24
  • Immunosuppressed or recent trauma/surgery
  • Acute deterioration of functional ability
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45
Q

When might lactate be falsely elevated?

A

Alcoholics, liver disease, adrenaline nebs

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46
Q

How is sepsis investigated?

A
  • Bloods-> FBCs, U+Es, LFTs, CRP, clotting
  • Blood culture
  • Blood gas-> lactate
  • Locate source-> urine dip + culture, CXR, CT abdomen, LP
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47
Q

How is sepsis managed?

A
  • Sepsis 6 (BUFALO)-> blood culture, urine output, fluids, antibiotics (broad spec), lactate, oxygen
  • IV crystalloids-> stat boluses but call critical care if oedema or 2L+ given
  • Local guidelines for antibiotics-> co-amoxiclav in South Yorkshire
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48
Q

What is neutropaenic sepsis and what features might suggest it?

A
  • Neutrophils <1 x 10^9/L

- Temperature 38+

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49
Q

What can cause neutropaenic sepsis?

A
  • Chemo
  • Clozapine
  • Immunusuppressants eg methotrexate or infliximab
  • -Carbimazole
  • Quinine
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50
Q

How is neutropaenic sepsis treated?

A

Tazocin (piperallicin + tazobactam)

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51
Q

What are common causes of chest infections?

A
  • Viral most common
  • Strep pneumoniae (50%)
  • H.influenzae (20%)
  • Moraxella catarrhalis-> COPD
  • P.aeruginosa-> CF, bronchiectasis
  • S.aureus-> CF
  • Atypicals eg leigonella
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52
Q

What antibiotics are usually used in chest infections?

A
  • Amoxicillin
  • Erythromycin
  • Clarithromycin
  • Doxycycline
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53
Q

What bacteria/pathogens usually cause UTIs?

A
  • E.coli
  • Klebsiella
  • Enterococcus
  • P.aeruginosa
  • Candida albicans
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54
Q

What often causes bacteria/pathogens to enter the urethra and cause UTIs?

A
  • Faeces-> intestinal bacteria
  • Incontinence or hygiene issues
  • Urinary catheters
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55
Q

How do lower UTIs present?

A
  • Dysuria, frequency, urgency, incontinence
  • Suprapubic pain/discomfort
  • Cloudy/smelly urine
  • Haematuria
  • Confusion
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56
Q

How does pyelonephritis present?

A
  • Fever, unwell, vomiting, loss of appetite
  • Loin, suprapubic, back pain-> uni or bilateral
  • Haematuria
  • Renal angle tenderness
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57
Q

What are nitrites?

A
  • Nitrates are a waste product of urine
  • Are broken down by gram negative bacteria into nitrites
  • Indicator of UTI
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58
Q

What does a urine dip result of +ve for nitrites and WBCs indicate?

A

Diagnostic of UTI

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59
Q

What does a urine dip result of +ve for nitrites only indicate?

A

Diagnostic of UTI

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60
Q

What does a urine dip result of +ve for WBCs only indicate?

A

Not UTI unless clinical evidence

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61
Q

Why might RBCs be present in urine?

A

UTI, nephritis, cancers

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62
Q

When is it important to include MSU (midstream urine sample for culture) in investigations for UTI?

A

Complicated UTI-> pregnancy, UTIs, atypical symptoms, when not improved with antibiotics

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63
Q

How is UTI managed (simple, in women)?

A

3 days of trimethoprim or nitrofurantoin or amoxicillin

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64
Q

How is UTI managed (men, pregnancy or catheter-associated)?

A

7 days of trimethoprim or nitrofurantoin or amoxicillin

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65
Q

How is UTI managed (immunosuppressed, abnormal anatomy, kidney issues)?

A

5-10 days of trimethoprim or nitrofurantoin or amoxicillin

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66
Q

When should nitrofurantoin be avoided?

A

eGFR <45

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67
Q

What risks do UTIs pose in pregnancy?

A

Pyelonephritis, PrOM, pre-term labour risks

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68
Q

How is UTI in pregnancy managed?

A
  • 7 days antibiotics even if asymptomatic
  • Nitrofurantoin-> NOT in 3rd trimester (haemolytic anaemia of newborn risk)
  • Trimethoprim-> not in 1st trimester (anti-folate and neural tube defect risks)
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69
Q

When and why should trimethoprim be avoided in pregnancy?

A

in 1st trimester (anti-folate and neural tube defect risks)

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70
Q

When and why should nitrofurantoin be avoided in pregnancy?

A

in 3rd trimester (haemolytic anaemia of newborn risk)

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71
Q

How is pyelonephritis managed?

A
  • 7-10 days of cefalexin, co-amoxiclav, trimethoprim or ciprofloxacin
  • Investigate renal abscess or stones if doesn’t respond
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72
Q

What are the side effects of ciprofloxacin?

A

Tendon damage + lowers seizure threshold

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73
Q

How is chronic pyelonephritis investigated?

A

DMSA scan-> scarring/damage areas not taken up so obvious where

74
Q

What bacteria causes cellulitis?

A
  • Staph aureus
  • Group A strep eg s.pyogenes
  • Group C strep
  • MRSA
75
Q

What causes cellulitis?

A
  • Infection of skin + soft tissue
  • Skin trauma, eczema, fungal nail infection, ulcers-> point of entry where skin breaks
  • Often staph aureus or group A strep
76
Q

How does cellulitis present

A

Erythema, warm, tense, thickened, oedematous, bullae (fluid-filled blisters)

77
Q

What causes impetigo?

A

Group A strep or staph aureus

78
Q

What is the Eron classification for cellulitis?

A

Assesses severity…

  • Class 1-> no systemic toxicity/comorbidity
  • 2-> systemic toxicity/comorbs
  • 3-> Significant systemic
  • 4-> sepsis, life-threatening
79
Q

What antibiotics are usually used in cellulitis?

A
  • Flucloxacillin
  • Clarithromycin
  • Clindamycin
  • Co-amoxiclav
80
Q

What usually causes tonsillitis?

A
  • Virus

- Group A strep eg s.pyogenes

81
Q

What are ENT infections commonly caused by?

A
  • Virus
  • Group A strep eg s.pyogenes
  • H.influenzae
  • M.catarrhalis
  • S.aureus
82
Q

What are the Centor criteria for tonsillitis?

A

1 point for…

  • Fever 38+
  • Tonsillar exudates
  • No cough
  • Tender anterior cervical LNs

3+-> should give antibiotics

83
Q

What is the feverPAIN score for tonsillitis?

A
  • Fever
  • Purulent tonsils
  • Absence of cough/coryza
  • Inflammation
  • New symptoms (<3 days)

Consider delayed antibiotics if score 2/3 and consider immediate if 4+

84
Q

What antibiotic is usually used in tonsillitis?

A

Penicillin V (phenoxymethylpenicillin) for 10 days

85
Q

What are the symptoms of otitis media?

A
  • Ear pain
  • Bulging red tympanic membrane
  • Discharge if perforates
86
Q

How is otitis media managed?

A
  • Usually resolves in 3-7 days by self
  • Amoxicillin
  • If doesn’t resolve in 2 days-> co-amoxiclav
87
Q

How is sinusitis managed?

A
  • Usually resolves in 2-3 weeks without treatment
  • No antibiotics within <10 days
  • No improvement-> 2 weeks high dose steroid nasal spray
  • Still none-> penicillin V for 5 days, co-amoxiclav switch if none after 2 days
88
Q

What bacteria usually cause intra-abdominal infections?

A
  • Anaerobes-> bacteriodes, clostridium
  • E.coli
  • Klebsiella
  • Enterococcus
  • Strep
89
Q

What bacteria is co-amoxiclav effective and not effective against?

A

Yes-> Gram +ve, gram -ve and anaerobic

No-> pseudomonas, atypical

90
Q

What bacteria is ciprofloxacin (and other quinolones) effective and not effective against?

A

Yes-> gram +ve, gram -ve, atypicals

No-> anaerobes

91
Q

What bacteria is metronidazole effective and not effective against?

A

Yes-> anaerobic

No-> aerobic

92
Q

What bacteria is gentamicin effective and not effective against?

A

Yes-> gram -ve, some gram +ve (eg staph)

93
Q

What bacteria is vancomycin effective and not effective against?

A

Yes-> gram +ve, MRSA, gram -ve (when + gentamicin), anaerobes (+ metronidazole)

94
Q

What bacteria are cephalosporins effective and not effective against?

A

Yes-> gram +ve and gram -ve (broad spec)
No-> anaerobes
Risk of C.diff

95
Q

What antibiotics are commonly associated with C.diff?

A

Cephalosporins

96
Q

What bacteria is tazocin effective and not effective against?

A

Yes-> gram +ve, gram -ve, anaerobic, usually when unresponsive to other antibiotics
No-> atypical or MRSA

97
Q

What bacteria is meropenem effective and not effective against?

A

Yes-> gram +ve, gram -ve, anaerobic, usually when unresponsive to other antibiotics
No-> atypical or MRSA

98
Q

When does spontaneous bacterial peritonitis occur?

A

Liver failure

99
Q

What is used to treat spontaneous bacterial peritonitis?

A
  • Tazocin 1st line
  • Cefotaxime
  • Levofloxacin + metronidazole
100
Q

What bacteria usually cause septic arthritis?

A
  • S.aureus
  • N.gonorrhoea-> gonococcal, when sexually active
  • Group A strep
  • H.influenza
  • E.coli
101
Q

What commonly causes septic arthritis?

A

Hip/knee replacement-> higher risk in revision surgery

102
Q

What is the presentation of septic arthritis?

A
  • Single joint-> often knee

- Hot, swollen, painful, limited ROM, systemic

103
Q

What are the differentials for septic arthritis?

A
  • Gout-> negatively birefringent urate crystals
  • Pseudogout-> calcium pyrophosphate crystals, positive birefringent
  • Reactive arthritis-> conjunctivitis or urethritis etc
  • Haemoarthrosis
104
Q

How is septic arthritis managed?

A
  • Hot joint policy-> who admitted and which antibiotics
  • Aspirate-> gram stain, crystal microscopy, culture & sensitivity
  • Empirical IV antibiotics-> flucloxacillin + rifampicin 1st line
105
Q

What is the influenza virus?

A
  • RNA virus with 3 types-> A, B, C

- A type has H+N subtypes-> H1N1 (swine flu) etc

106
Q

Who is eligible for free influenza vaccines?

A

65+, kids, pregnant, HC workers, chronic conditions (asthma, COPD, HF, DM)

107
Q

How does influenza present?

A

Fever, coryzal symptoms. lethargy, fatigue, anorexia, loss of appetite, muscle aches, joint aches, headache, dry cough, sore throat

108
Q

How is influenza diagnosed?

A
  • Viral nasal or throat swabs for PCR

- Give public health data to monitor cases

109
Q

How is influenza managed?

A
  • Self care if low risk
  • High risk-> oral oseltamivir for 5 days or inhaled zanamivir for 5 days
  • PEP for high risk-> within 48 hours of close contact
110
Q

What are the potential complications of influenza?

A

Otitis media, sinusitis, bronchitis, viral pneumonia, worsening of chronic conditions, febrile convulsions, encephalitis

111
Q

What is gatroenteritis?

A

Inflammation of stomach + intestines causing nausea, vomiting and diarrhoea

112
Q

What pathogens commonly cause gastroenteritis?

A
  • Viruses-> rotavirus, norovirus, adenovirus
  • Bacteria-> E.coli, campylobacter jejuni, Shigella, salmonella, bacillus cerus etc
  • Parasites-> Giardiasis
113
Q

How is E.coli gastroenteritis spread?

A
  • Faeces, water, unwashed salad

- Normal intestinal bacteria + some strains cause GE

114
Q

What is the pathophysiology of E.coli gastroenteritis?

A

E.coli 0157-> produces Shiga toxin

115
Q

How does E.coli gastroenteritis present?

A
  • Abdominal cramps, bloody diarrhoea, vomiting

- Risk of HUS-> destroys RBCs

116
Q

How is E.coli gastroenteritis managed?

A
  • Conservative

- Avoid antibiotics-> increased HUS risk

117
Q

What is campylobacter jejuni?

A
  • Gram negative curved/spiral bacteria

- Commonly causes traveller’s diarrhoea and bacterial gastroenteritis

118
Q

How does campylobacter jejuni gastroenteritis spread?

A

Raw poultry, untreated water, unpasteurised milk

119
Q

How does campylobacter jejuni gastroenteritis present?

A
  • Abdominal cramps, diarrhoea, bloody stools, vomiting, fever
  • Incubates for 2-5 days
  • Resolves in 3-6 days
120
Q

When are antibiotics used in campylobacter jejuni gastroenteritis?

A
  • When organism isolated
  • When severe or risk factors (HIV etc)
  • Azithromycin or ciprofloxacin used
121
Q

What is the pathophysiology of shigella gastroenteritis?

A
  • Produces Shiga toxin-> can cause HUS

- Spread via faeces, swimming pools, food

122
Q

How does shigella gastroenteritis present?

A
  • Bloody diarrhoea, abdominal cramps, fever
  • Incubates 1-2 days
  • Resolves in 1 week
123
Q

How is shigella gastroenteritis managed?

A
  • Conservative

- Severe-> azithromycin or ciprofloxacin

124
Q

How is salmonella spread?

A

Raw eggs, poultry, food contaminated with faeces

125
Q

How does salmonella present?

A
  • Watery diarrhoea, mucus, blood, abdominal pain, vomiting
  • Incubation 12 hours-3 days
  • Symptoms resolve in 1 week
126
Q

How is salmonella managed?

A

Only give antibiotics when severe + guide by stool culture

127
Q

What is bacillus cereus infection?

A
  • Gram positive rod
  • Spread through inadequately cooked food-> often rice
  • Cerulide toxin produced-> watery diarrhoea in intestines
128
Q

How does bacillus cereus gastroenteritis present?

A
  • Abdominal cramping and vomiting-> wIthin 5 hours of ingestion
  • Watery diarrhoea-> 8 hours after
  • Resolves in 24 hours
129
Q

What is yersinia enterocolitica infection?

A
  • Gram negative bacillus

- Spread through contamination with urine/faeces or eating uncooked pork

130
Q

How does yersinia enterocolitica infection present?

A
  • Young kids
  • Watery/bloody diarrhoea, abdominal pain, fever, lymphadenopathy
  • Incubation-> 4-7 days
  • Can last 3+ weeks
  • Mesenteric lymphadenitis-> right sided abdo pain
131
Q

How is staph aureus gastroenteritis spread?

A
  • Dairy, eggs, meat

- Enterotoxins-> small intestine inflammation

132
Q

How does staph aureus gastroenteritis present?

A
  • Diarrhoea, vomiting, abdominal cramps, fever
  • Within hours of digestion
  • Lasts 12-24 hours
133
Q

What is giardiasis?

A
  • Gastroenteritis due to giardia lamblia parasite
  • Lives in animals’ intestines-> release cysts in stools-> contaminate food + water-> infect host
  • Faecal-oral
134
Q

How does giardiasis present?

A

Chronic diarrhoea, no symptoms

135
Q

How is giardiasis managed?

A
  • Stool microscopy

- Metronizadole

136
Q

How is gastroenteritis managed (generally)?

A
  • Isolate + infection control
  • Samples-> MC&S
  • Fluid challenge, rehydration (dioralyte), IV fluids
  • Stay off work/school for 48 hours until symptoms resolved
  • Antidiarrheal in some types (eg loperamide)
  • Antiemetics
  • Antibiotics when high risk
137
Q

How long should people stay off work/school when they have gastroenteritis?

A

48 hours after symptoms resolve

138
Q

What complications can gastroenteritis have?

A

Lactose intolerance, IBS, reactive arthritis, GBS

139
Q

What bacteria usually cause meningitis?

A
  • Neisseria meningitidis (meningococcus)

- Group B strep-> neonates (from vagina during birth)

140
Q

What is meningococcal septicaemia?

A
  • Meningococcus in bloodstream

- Causes DIC-> non-blanching rash

141
Q

How does meningitis present?

A
  • fever, neck stiffness, vomiting, headache, photophobia, LOC, seizures
  • non-blanching rash-> meningococcal septicaemia
  • Neonates-> hypotonia, poor feeding, lethargy, hypothermia, bulging fontanelle
142
Q

What is the criteria for getting a lumbar puncture in suspected meningitis?

A
  • <1 month with fever
  • 1-3 months with fever + unwell
  • <1 year with unexplained fever + features of serious illness
143
Q

What is Kernig’s test and what does it show?

A
  • Patient on back + flex 1 hip and knee to 90 degrees
  • Straighten knee + keep hip flexed 90 degrees
  • Stretch meninges
  • Spinal pain/resistance-> meningitis
144
Q

How is meningitis managed initially in the community?

A

Urgent stat IM/IV benzylpenicillin-> different dose for different ages

145
Q

How is meningitis managed in hospital?

A
  • Blood culture + LP before antibiotics unless acutely unwell
  • Local policy
  • <3 months-> cefotaxime + amoxicillin
  • > 3 months-> ceftriaxone
  • Vancomycin-> when risk of pneumococcal (eg travel)
  • Steroids-> dexamethasone for 4 days in >3 months to prevent hearing + neuro damage
  • Inform PHE
146
Q

What antibiotics are used in meningitis?

A
  • In community-> Urgent stat IM/IV benzylpenicillin
  • Local policy
  • <3 months-> cefotaxime + amoxicillin
  • > 3 months-> ceftriaxone
  • Vancomycin-> when risk of pneumococcal (eg travel)
147
Q

Why are steroids used in meningitis management?

A

prevent hearing + neuro damage

148
Q

When and what is used for PEP in meningitis?

A
  • Single dose ciprofloxacin
  • Within 24 hours of pt diagnosis
  • Risk when prolonged contact within 7 days of illness onset
  • No symptoms after 7 days-> unlikely to have
149
Q

How is viral meningitis managed?

A
  • CSF sample + viral PCR from LP

- Acyclovir if HSV

150
Q

What causes viral meningitis?

A

HSV, enterovirus, VZV

151
Q

How is LP performed in meningitis?

A
  • Into L3/4-> cord ends at L1/2
  • Send-> bacterial culture, viral PCR, cell count, protein, glucose
  • Blood glucose-> compare CSF
152
Q

How does bacterial meningitis show on an LP?

A
  • Cloudy
  • High protein
  • Low glucose
  • High WCCS + neutrophils
  • Positive culture
153
Q

How does viral meningitis show on an LP?

A
  • Clear
  • Mildly raised or normal protein
  • Normal glucose
  • High WCC + lymphocytes
  • Negative culture
154
Q

What are some complications of meningitis?

A

Hearing loss, seizures, epilepsy, cognitive impairment, LD, memory loss, focal neuro (limb weakness + spasticity)

155
Q

What is tuberculosis caused by?

A

Mycobacterium tuberculosis-> acid fast bacilli (unable to gram stain as resistant)

156
Q

How is mycobacterium tuberculosis stained?

A

Zeihl-Neelsen stain-> red on blue background

157
Q

Who is tuberculosis more prevalent in?

A
  • Non-UK born patients
  • Immunocompromised
  • Close contacts from high prevalence areas
  • Homeless
  • Drug users
  • Alcoholics
158
Q

What is the disease course of tuberculosis?

A
  • Spread by inhaling saliva droplets
  • Into lymphatics + blood-> granulomas
  • Active-> can kill + clear
  • Latent-> encapsulated + progress stopped
  • Secondary-> reactivation of latent
  • Miliary-> immune system can’t control so disseminates
  • Extrapulmonary-> LNs, pleura, CNS, pericardium, GI, GU, bones, skin
159
Q

Why is tuberculosis hard to treat?

A
  • Slowly divides
  • High oxygen demand
  • Hard to culture
  • Can become latent
160
Q

How does the BCG vaccine work?

A
  • Live-attenuated
  • Intradermal
  • Need negative Mantoux test + immunosuppression tests before-> due to live vaccine risks
161
Q

Who gets the BCG vaccine?

A
  • Neonates in high risk areas or relatives from
  • FH
  • Unvaccinated with close contacts
  • HC workers
162
Q

How does tuberculosis present?

A
  • Chronic + gradually worsening
  • Cough, haemoptysis, LNopathy
  • Lethargy, fevers, night sweats, weight loss, erythema nodosum
  • Spinal pain-> Pott’s disease of the spine
163
Q

How is tuberculosis investigated?

A
  • Ziehl-Neeslen stain
  • Mantoux test
  • Interferon-gamma release assays (IGRAs)-> when +ve Mantoux test
  • CXR-> primary, reactivated and miliary have different signs
  • Sputum culture-> eg from bronchoscopy
  • Blood cultures
  • LN aspiration/biopsy
  • Nucleic acid amplification test-> when high risk
164
Q

How does the Mantoux test work?

A
  • Inject intradermally
  • Bleb under skin
  • Back in 72 hours
  • +ve if >5mm
165
Q

What CXR findings might be present in tuberculosis?

A
  • Primary-> patchy consolidation, effusions, hilar LNopathy
  • Reactivated-> patchy/nodular consolidation, cavitation
  • Milary-> ‘millet seeds’
166
Q

How is active tuberculosis managed?

A
  • Rifampicin-> 6 months
  • Isoniazid-> 6 months
  • Pyrazinamide-> 2 months
  • Ethambutol-> 2 months
  • Also notify PHE, isolate for 2 weeks, test for HIV etc
167
Q

What are the side effects of the tuberculosis drugs?

A
  • Rifampicin-> red/orange urine/tears, hepatotoxicity
  • Isoniazid-> peripheral neuropathy, hepatotoxicity
  • Pyrazinamide-> hyperuricaemia, gout, hepatotoxicity
  • Ethambutol-> colour blind + reduce acuity
168
Q

What is the pathyphysiology of Human Immunodeficiency Virus?

A
  • HIV-> RNA retrovirus, types 1 (most) + 2
  • Enters + destroys CD4 T-helper cells
  • Transmitted by sex, vertical (mum to baby), mucous membranes + open wounds (eg needles)
169
Q

How does Human Immunodeficiency Virus progress?

A
  • Seroconversion illness-> flu like, within a few weeks of infection
  • Asymptomatic
  • Progresses-> immunocompromised + AIDS-defining illnesses
170
Q

How does screening for Human Immunodeficiency Virus worK?

A
  • Antibody test, HIV antigen (P24), PCR (HIV RNA + viral load)
  • Everyone in hospital or with RFs in community
  • Need consent
  • Antibodies can be -ve for 3 months after exposure-> repeat
171
Q

How is Human Immunodeficiency Virus monitored?

A
  • Viral load-> copies per ml of bleed, 50-100/ml counts as undetectable
  • CD4 count-> 500-1200cells/mm3 normal, <200 is AIDS
172
Q

What are AIDS-defining illnesses?

A
  • Kaposi’s sarcoma
  • CMV
  • Pneumocystis jivorecii pneumonia
  • Candidiasis of oesophagus/bronchi
  • Lymphomas
  • TB
173
Q

How is Human Immunodeficiency Virus managed?

A
  • Antiretrovirals-> 2 nucleotide reverse transcriptase inhibitors (NRTIs) + 1 other agent
  • Eg-> tenofovir + emtricitabine + protease inhibitor
  • Aims-> normal CD4 + undetectable viral load
  • Tailored on bloods but all get treatment-Other-> co-trimoxazole (PCP prevention), cervical smears (HPV risk), vaccines (eg annual flu)
  • Newborn with HIV +ve mum-> ART for 4 weeks after birth
  • Contraception-> condoms + dams, risks with unprotected even with undetectable load
  • Can conceive-> IVF, sperm washing etc
174
Q

What is PEP for Human Immunodeficiency Virus?

A
  • Use in <72 hours of exposure
  • ART combo-> tenofovir + emtricitabine + reltegravir for 28 days
  • Test 3 months after
175
Q

What causes malaria?

A
  • Plasmodium-> protozoan parasites eg falciparum, vivax, ovale
  • Female anopheles mosquito-> bite
  • Spores injected when bite human-> mature in liver to merozoites-> infect RBCs in blood-> reproduce in 48 hours-> RBCs rupture + release merozoites to blood-> haemolytic anaemia + high spiking fevers every 48 hours
  • Can be dormant for years in vivax + ovale
176
Q

How does malaria present?

A
  • Incubation 1-4 weeks
  • Fever, sweats, malaise, myalgia, headache, vomiting
  • Pallor, hepatosplenomegaly, jaundice
177
Q

How is malaria diagnosed?

A
  • Blood film-> parasites

- 3 samples over 3 days-> 48 hour cycle of release

178
Q

How is malaria managed?

A
  • Admission in falciparum-> can deteriorate
  • Doxycycline, quinine, riamet, malarone
  • IV if severe-> quinine, artesunate
179
Q

What are the complications of falciparum malaria?

A

Cerebral malaria, seizures, LOC, AKI, pulmonary oedema, DIC, severe haemolytic anaemia, multi-organ failure

180
Q

What is used for malaria prophylaxis?

A
  • High risk locations-> on BNF
  • Sprays + nets
  • Doxycycline-> 2 days before, during, 4 weeks after-> beware on sunlight
  • Malarone or mefloquine
181
Q

What antibiotics are associated with the development of Clostridium difficile infection?

A

Clindamycin, ciprofloxacin, cephalosporins

Medicine (13 decks)

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