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Year 3 Medicine > Infectious Diseases > Flashcards

Infectious Diseases Flashcards

1
Q

Definition of pneumonia

A

Infection of lung tissue causing inflammation and sputum filling the airways and alveoli.

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2
Q

What are the types of pneumonia

A
  • Community Acquired Pneumonia (CAP)
  • Hospital Acquired Pneumonia (HAP)
  • Aspiration pneumonia
  • Atypical pneumonia
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3
Q

Symptoms of pneumonia

A
  • SOB
  • cough with purulent sputum
  • fever
  • haemoptysis
  • pleuritic chest pain
  • delirum
  • sepsis
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4
Q

Signs of pneumonia

A

Characteristic chest signs
* bronchial breath sounds = harsh breath sounds due to consolidation
* focal coarse crackles = air passing through sputum
* dullness to percussion - lung collapse &/or consolidation

Sepsis secondary to pneumonia
* tachypnoea
* tachycardia
* hypoxia
* hypotension

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5
Q

How is the severity of pneumonia assessed?

A

CURB-65 (CRB-65 out of hospital)
* Confusion: abbreviated mental test ≤8 or disorientated
* Urea >7
* RR ≥ 30
* BP: SBP <90 or DBP ≤60
* Age ≥65

0-1 = mild, consider treatment at home
≥2 = moderate, consider hospitalisation
≥3 = severe, consider intensive care assessment

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6
Q

Common bacterial causes of pneumonia

A
  • streptococcus pneumoniae (50%)
  • haemophilus influenzae (20%)
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7
Q

Other bacterial causes and associations of pneumonia

A
  • moraxella catarrhalis in the immunocompromised or chronic pulmonary disease
  • pseudomonas aeruginosa in patients with cystic fibrosis or bronchiectasis
  • staphylococcus aureus in patients with cystic fibrosis
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8
Q

Causes of atypical pneumonia

A

Mycoplasma pneumoniae
* can cause rash = erythema multiforme (pink ring, pale centre)
* can cause neurological symptoms

Chlamydophila pneumoniae = mild to moderate chronic pneumonia and wheeze

Coxiella burnetii = typically contracted from contact with infected birds

Legionella pneumophila
* caused by infected water supplies or air conditioning units
* Can cause SIADH = hyponatraemia

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9
Q

Investigations for pneumonia

A
  • Basic Obs
  • CXR
  • Bloods: FBC, U+E, LFT, CRP, blood culture
  • Sputum culture
  • O2 sats, ABG if <92% or severely unwell
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10
Q

Abx for CAP

A
  • Mild-moderate: amoxicillin PO. Clarithromycin or doxycycline if allergic.
  • Severe: co-amoxiclav, cefuroxime, or cefotaxime IV (or levofloxacin if allergic), plus clarithromycin IV
  • If hospitalised, start within 4 hrs. Monitor response to treatment with CRP
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11
Q

Abx for HAP

A
  • Piperacilin/tazobactam, 3rd generation cephalosporin, meropenem, or levofloxacin IV.
  • Co-amoxiclav is a PO alternative or stepdown
  • Add vancomycin or teicoplanin or linezolid if MRSA suspected
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12
Q

Abx for aspiration pneumonia

A

clindamycin, levofloxacin, or piperacilin/tazobactam

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13
Q

Duration of abx in pneumonia

A
  • 5 days total usually sufficient
  • longer if remains febrile or unstable, or for certain pathogens e.g. pseudomonas
  • If starting IV, review after 48 hrs for possible PO stepdown
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14
Q

Supportive care in pneumonia

A
  • oxygen
  • fluids
  • paracetamol
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15
Q

Prognosis of pneumonia

A
  • fever should resolve within 1 week
  • cough and SOB may take up to 6 weeks to resolve
  • fatigue may persist up to 3 months
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16
Q

Complications of pneumonia

A
  • Respiratoy failure
  • sepsis and septic shock
  • uncomplicated parapneumonic pleural effusion, empyema, or lung abscess
  • Death: 1% in community, 10% if admitted
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17
Q

Pathophysiology of infective endocarditis

A
  • infection of the endocardium, usually a (prosthetic or native) valve (mitral or aortic), usually following transient bacteraemia and turbulent flow past valve
  • leads to formation of vegetation on valves containing bacteria, fibrin and platelets
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18
Q

Causes of infective endocarditis

A
  • bacterial: strep viridans, staph aureus
  • fungal: candida, aspergillus
  • non-infective: cancer, SLE
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19
Q

Key features of infective endocarditis

A

Murmer (85%) + fever

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20
Q

Septic signs and symptoms of infective endocarditis

A
  • fevers, rigors and night sweats
  • malaise
  • weight loss
  • splenomegaly
  • clubbing
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21
Q

Signs of subacute infective endocarditis

Usually due to immune-complex depositions and vasculitis

A
  • Petechiae and splinter haemorrhages
  • Janeway lesions: painless plantar/palmar lesions
  • Osler’s nodes: painful infarcts in distal phalanges
  • Roth spots: retinal haemorrhages with pale centre
  • Glomerulonephritis
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22
Q

Risk Factors for infective endocarditis

A

Increased turbulent flow
* valve disease
* prosthetic valves
* structural disease: unrepaired PDA, VSD
* rheumatic heart disease

Increased pathogen entry and bacteraemia
* IV drug use
* haemodialysis
* dermatitis

Chronic disease
* Diabetes
* Kidney disease

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23
Q

Investigations in infective endocarditis

A

Blood cultures
* 3 sets from different sites before starting abx
* within 6 hours if subacute, within 1.5 hrs if acute
* 90% sensitive

Bloods
* FBC: normocytic anaemia
* ↑ neutrophils
* ↑ ESR/CRP
* Rheumatoid factor may be +ve (due to IE itself or RA)

Heart investigations
* Echo: transthoracic, then transoesophageal if -ve
* CXR: cardiomegaly
* ECG: ↑PR interval. Monitor to decide whether surgery required

Urinalysis: microhaematuria

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24
Q

Duke Criteria in Infective Endocarditis

A

Diagnosis requires any 1 of:
* 2 major
* 1 major plus 3 minor
* 5 minor

Major Criteria
* +ve blood culture x2 or persistent
* +ve echo: vegetation, abscess, new regurgitation, or prosthetic valve dehiscence

Minor criteria
* RF +ve
* fever
* vascular immune-complex signs
* +ve blood culture (x1)
* +ve echo for other abnormality

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25
Q

Acute Management of Infective Endocarditis

A

Abx as soon as blood cultures taken:
* 4-6 weeks, including at least 2 weeks IV initially
* Empiric therapy and for streptococci: benzylpenicillin (or amoxicillin) + gentamicin
* staph. aureus: flucloxacillin if native valve, add rifampicin and gentamicin if prosthetic valve

Surgery:
* Debridement, repair or replacement required in 20%
* Indications: refractory HF, persistant sepsis or emboli, or fungal IE

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26
Q

Bacterial causes of meningitis

A
  • <3 months old = Group B strep
  • 3 months - 45 yrs = neisseria meningitidis
  • > 45yrs = strep. pneumoniae
  • other causes = staph. aureus, e. coli, h. influenzae
  • Listeria monocytogenes: may occur in pregnancy, neonates, the alcohol misusers
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27
Q

Viral causes of meningitis

A
  • enteroviruses; coxsackie, echovirus
  • herpes simplex, HSV2 more than HSV1
  • Mumps
  • Measles
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28
Q

Fungal causes of meningitis

A
  • Cryptococcus neoformans
  • it has an insidious onset
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29
Q

Non-infectious causes of meningitis

A
  • cancer: carcinomatous meningtitis
  • drugs: co-amoxiclav, NSAIDs, IVIg, azathioprine
  • Inflammatory and autoimmune sarcoidosis, SLE, Behcet’s
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30
Q

Epidemiology of meningitis

A
  • 40% of cases of bacterial meningitis are in children aged <15 years
  • Commonest in first few months of life, affecting 1/2000 per year, then incidence drops to around 1/100,000 per year for the rest of life
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31
Q

Symptoms of meningitis

A
  • Classic triad: fever, stiff neck, headache/altered mental status
  • vomitting
  • photophobia
  • mottled skin
  • confusion
  • seizures
  • rigors
  • cold hands and feet
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32
Q

Signs of meningitis

A
  • Kernig’s sign: with hip and knee flexed, pain limits passive extension of the knee
  • Brudzinskis sign: neck flexion leads to involuntary hip and knee flexion
  • Both are around 10% sensitive and 90% specific for meningitis
  • Cerebral oedema = loss of consciousness, papilloedema, and focal CNS signs

Meningococcaemia
* petechiae and purpura: look carefully all over including backs of legs etc
* septic shock: hypotension, ↓ capillary refill
* DIC

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33
Q

Risk Factors for meningitis

A
  • immunosuppression, including complement deficiencies and asplenia
  • Skull fracture or anatomical defects
  • crowding: university halls, military barracks, Hajj
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34
Q

Investigations for meningitis

A

Bloods
* ↑WBC, ↑CRP
* U&Es and LFTs
* Blood culture +/- N. meningitidis PCR
* Coag: DIC

Lumbar puncture:
* CT and opthalmoscopy 1st if ↑ICP suspected
* Bacterial CSF: ↑polymorphs, ↑proteins, ↓glucose, bacteria on culture, gram stain. Listeria can be mixed polymorphs and lymphocytes
* TB CSF: ↑lymphocytes, ↑protein, ↓glucose, ZN stain +ve
* Viral CSF: ↑lymphocytes, viral PCR +ve

Other investigations
* Throat swab for N. meningitidis
* CXR: pneumococcal pneumonia, TB

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35
Q

Acute Management of meningitis

A
  • resuscitate, including oxygen and fluids
  • broad spectrum IV abx stat, e.g. cefotaxime. Add amoxicillin if age>50 or <3 months. Benzylpenicillin IM if pre-hospital
  • dexamethasone IV if >3months old: ↓neurological complications, but doesn’t affect mortality
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36
Q

Public health measures for meningitis

A
  • notify public health about any case of meningitis or meningococcaemia
  • isolate patient
  • prophylactic abx: single dose of ciprofloxacin or 2 days of rifampicin. Give to all close contacts from the last 7 days, regardless of vaccination status
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37
Q

Complications of meningitis

A
  • short term: ↑ICP, shock, DIC, subdural effusions, SIADH, seizures, venous sinus thrombus
  • long term: cranial nerve palsies, deafness, limb amputation, memory or cognitive problems
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38
Q

Prognosis of meningitis

A
  • 5% mortality rate in meningococcal
  • 25% mortality rate in pneumococcal
  • 35% mortality rate for listeria
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39
Q

What is encephalitis

A

Inflammation of the brain

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40
Q

Viral Causes of encephalitis

A

Most common
* Herpes simplex (HSV1>HSV2)
* VZV
* EBV

Others
* CMV
* HIV seroconversion
* measles
* mumps
* arboviruses (west Nile, Japanese, tick borne, St Louis)
* rabies

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41
Q

Other causes of encephalitis

A
  • Autoimmune
  • Idiopathic
  • bacterial meningitis –> meningoencephalitis
  • TB
  • protozoa: malaria
  • fungal: Aspergillus,Cryptococcus
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42
Q

Epidemiology of encephalitis

A
  • annual incidence: 1/20,000
  • Most common under 1 year old or over 65
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43
Q

Signs and Symptoms of Encephalitis

A
  • Initially non-specific: fever, headache, nausea, vomiting, malaise
  • Neuro symptoms: seizures, odd behaviour or confusion, ↓level of consciousness, focal signs
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44
Q

History for Encephalitis

A

include travel and bite exposure

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45
Q

Investigations for encephalitis

A

Bloods
* blood culture
* serum viral PCR
* If suspected: toxoplasma IgM, malaria film

Image with MRI or contrast-enhanced CT
* Temporal lobe inflammation: usually HSV or autoimmune
* meningeal irritation: meningoencephalitis

Special tests
* LP: ↑protein (most causes), ↑lymphocytes (viral, autoimmune), ↑PMNs (bacterial), ↓glucose (bacterial). Identify pathogen with viral PCR and gram stain
* EEG: optional

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46
Q

Management of Encephalitis

A
  • Aciclovir IV stat to cover HSV. Continued for 14-21 days if HSV confirmed
  • Consider ganciclovir for CMV if immunocompromised
  • anticonvulsants for seizures
  • autoimmune encephalitis: immunosuppressants (steroids, IVIg, plasma exchange) and treat for any underlying cancer
  • If infectious notify public health authorities
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47
Q

Complications of encephalitis

A
  • Short term: seizures, ↑ICP, SIADH, diabetes insipidus
  • Long term: neurological complications, including motor and cognitive problems
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48
Q

Prognosis of encephalitis

A
  • 10% mortality overall
  • For HSV, treatment reduces mortality from >50% to 20%
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49
Q

Pathogens that cause gastroenteritis

A
  • Viral: norovirus, rotavirus, astrovirus, adenovirus
  • Bacteria: campylobacter jejuni, salmonella (usually S. enteriditis), shigella, E. coli, vibrio cholera, clostridium difficile
  • protozoa: giardia, cryptosporodium, cyclospora, entamoeba
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50
Q

Transmission of gastroenteritis

A
  • most are faecal-oral, and can be person to person, water-borne or foodborne
  • some are zoonotic
  • campylobacter, shigella and giardia can be sexually transmitted, especially in MSM
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51
Q

Signs and symptoms of gastroenteritis

A
  • acute diarrhoea and/or vomitting
  • anorexia
  • malaise
  • fever
  • weight loss
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52
Q

Investigations in gastroenteritis

A
  • most cases require minimal if any
  • stool culture and microscopy if there is bloody stool, the patient is immunocompromised, there is recent travel to the developing world, or symptoms are prolonged (>7 days)
  • Basic bloods if unwell: FBC (↑WBC), U&E (dehydration), CRP, LFT
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53
Q

Management of gastroenteritis

A

most cases do not require admission and can be managed at home with regular oral fluid intake

Inpatient management
* fluids (PO or IV)
* anti-emetics or anti-diarrhoeals if severe (do not give in dysentry)
* abx if systemically unwell or immunocompromised. Ciprofloxacin (campylobacter, salmonella, shigella) or tetracycline (V. cholera)

Infection control
* isolate patients with D+V
* any food poisoning or suspected food poisoning is a notifiable disease

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54
Q

Complications of gastroenteritis

A
  • lactose intolerance
  • Guillian-Barre syndrome
  • Reactive arthritis
  • Haemolytic uraemic syndrome after E. coli
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55
Q

Pathophysiology of C. diff infection

A
  • gram +ve anaerobic bacillus
  • transmitted by spores from people or the environment
  • often follows abx course, especially clindamycin, cephalosporins or quinolones, which eliminate gut commensals (usually post 4-9 days, but can be up to 8 wks)
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56
Q

Presentation of C. diff infection

A
  • Profuse watery diarrhoea. Bloody stool can occur but is rare
  • abdominal pain and tenderness
  • fever
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57
Q

Investigations in C. diff infection

A
  • ↑WBC, sometimes very elevated. ≥15 = severe c. diff
  • U&E. AKI = severe c. diff
  • Stool PCR ± toxin immunoassay to confirm
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58
Q

Management in c. diff infection

A
  • Stop any abx which may be causing it
  • none-severe and sever: vancomycin PO = 1st line, fidaxomicin PO if vancomycin ineffective
  • Life-threatening (shock, ileus, or megacolon): vancomycin PO/PR ± metronidazole IV. May need colectomy if there is toxic megacolon
  • Consider faecal microbiota transplantation for recurrent disease
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59
Q

Complications of C. diff infection

A
  • pseudomembranous colitis
  • toxic megacolon
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60
Q

What is bacteriuria

A

bacteria in urine. may or may not be symptomatic

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61
Q

What is a UTI

A

significant bacteriruria (≥100,000 colony forming units/mL in MSU) + symptoms

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62
Q

What is a complicated UTI

A

UTI in the presence of certain risk factors, including renal or urinary tract abnormality, voiding difficulty, ↓ kidney function, indwelling catheter, immunosuppression, or virulent organism

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63
Q

Pathogens that cause UTIs

A
  • E. coli (90%)
  • Staph. saprophytics: occurs in sexually active women
  • proteus mirabilis: suggests kidney stones
  • enterococcus facealis: causes prostatis
  • Klebsiella: usually in catheterised patients
  • Staph. aureus: from haematogenous spread
  • STIs: chlamydia, gonorrhoea
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64
Q

Epidemiology

A
  • annual incidence: 1/10 women, 1/100 men
  • Lifetime risk: 1/2 women, 1/20 men
  • Risk increases with age
  • Although less common in men, they account for 40% of UTI hospitalisations
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65
Q

Symptoms of UTIs

A
  • cystitis (lower UTI): frequency, urgency, dysuria, nocturia, haematuria, suprapubic ache
  • acute pyelonephritis (upper UTI): fever ± rigors, loin pain, systemically unwell (e.g. vomiting)
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66
Q

Signs of UTIs

A
  • fever
  • suprapubic or loin tenderness
  • cloudy or smelly urine
  • swollen, boggy, tender prostate (prostatitis)
  • Discharge (STI urethritis)
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67
Q

Risk Factors for UTIs

A
  • demographic: female, age
  • pregnancy
  • pathogen exposure: sexually active, catheter
  • stagnant flow: obstruction (prostate, stones), retention, extended holding
  • infection prone states: diabetes, immunosuppression
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68
Q

Other differential diagnoses alongside UTI signs/symptoms

A
  • overactive bladder
  • STIs
  • non-infectious inflammation: atrophic vaginitis, interstitial cystitis
  • vaginitis
  • stones
  • bladder or renal cancer
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69
Q

Investigations for UTIs

A

Urine dipstick:
* nitrites or leukocytes esterase +ve
* if +ve: start treatment and send MSU for M,C&S
* If -ve: send MSU anyway if strong clinical suspicion, male, child, pregnant or immunosuppressed

MSU MC+S
* Microscopy shows leukocytes ± bacteria
* If <100,000 CFU/mL but pyuria (>20 WBC/mm3) = sterile pyuria (prev. treated UTI, prostatitis, STI, TB, appendicitis, bladder tumour, stones, PKD)
* if many different organisms, suspect contaminated (not mid-stream) and repeat MSU

Further investigations if indicated
* pyelonephritis: FBC, U+E, CRP, blood cultures
* Blood glucose to rule out diabetes
* Imaging: kidney US (obstruction/hydronephrosis), post-void bladder US, CT KUB (stones)

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70
Q

General Approach to manage UTIs

A
  • Abx if symptomatic
  • paracetamol +/or NSAIDs for symptom relief
  • remove catheter if present
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71
Q

Treatment of lower single UTI in women

A
  • nitrofurantoin (if eGFR≥45) or trimethoprim PO for 3 days
  • pregnancy: treat even if asymptomatic. Nitrofurantoin 1st line (unless at term), amoxicillin or cefalexin 2nd line, all PO for 7 days
  • any other complicated UTI: trimethoprim or nitrofurantoin PO for 7 days
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72
Q

Preventing recurrent UTI in women

A
  • behavioural and lifestyle: increase daily water intake, pre/post coital washing, avoid spermicides and diaphragm
  • consider vaginal oestrogen if post-menopausal
  • prophylactic abx if very disruptive: nitrofurantoin if eGFR≥45 or trimethoprim PO taken post-coitus if sex-related, otherwise daily
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73
Q

Urology referral and imaging indications for UTI

A
  • failure of other measures
  • has risk factors for urinary tract abnormality: obstructive symptoms, history of stones, urinary tract surgery, gynae cancer
  • immunosuppressed
  • recurrent UTI with haematuria: urgent referral for suspected cancer
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74
Q

Treatment of lower UTI in men

A
  • nitrofurantoin (if eGFR≥45) or trimethoprim PO 7 days for cystitis
  • ciprofloxacin PO for 2-4 wks if there if prostatis, IV if severely unwell
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75
Q

Treatment for upper UTI

A
  • most upper UTIs are uncomplicated and can be managed with PO abx (cefalexin or ciprofloxacin for 7-10 days)
  • if there is no response within 24hrs, signs of sepsis or in complicated UTI = hospitalisation and consider IV abx, e.g. 2nd-3rd generation cephalosporin or ciprofloxacin
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76
Q

Complications of UTIs

A
  • infectious spread: pyelonephritis, perinephric or intrarenal abscess, prostatis, sepsis
  • Kidney: AKI, hydronephrosis
  • recurrence: 1 in 3 women, usually reinfection (new pathogen)
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77
Q

Prognosis of UTIs

A

symptoms resolve in 3-4 days with an effective abx, vs 5-7 days without treatment (or with a resistant organism)

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78
Q

What is cellulitis

A

Inflammation of dermis and subcutaneous tissue. Most commonly group A strep, then staph aureus

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79
Q

Signs and symptoms of cellulitis

A

Skin:
* inflammation: painful, red, hot, swollen
* poorly demarcated
* precipitating lesion: trauma, ulcer, bite, skin damage from chronic condition
* may have associated skin abscess

non-dermal features:
* lymphadenopathy
* systemic symptoms: fever

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80
Q

Common sites for cellulitis

A
  • lower legs (NOTE: bilteral lower leg cellulitis is rare, consider venous eczema)
  • canula site
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81
Q

Risk factors for cellulitis

A
  • previous cellulitis
  • chronic disease: diabetes, chronic kidney disease or liver disease, cancer
  • immunodeficiency
  • venous insufficiency
  • age
  • skin disease, e.g. tinea pedis
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82
Q

Investigations for cellulitis

A

Affected area:
* look for portal of entry and ask about trauma
* draw around edge of area to monitor progress
* swab for culture only needed for severe/resistant infections, or unusual exposures (penetrating injury, water-born, acqiured abroad)

Bloods if systemic symptoms:
* ↑WBC and ↑CRP
* Blood cultures

Investigate associated conditions
* foot Xray for osteomyelitis
* D-dimer, ultrasound and Well’s score if suspected DVT

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83
Q

Management of cellulitis

A

Abx
* flucloxacillin PO for 5-7 days 1st line for most
* if penicillin allergyc, doxycycline or clarithromycin PO
* if near eyes or nose, or for human/animal bite wounds, co-amoxiclav PO
* if severe, cefuroxime, ceftriaxone, flucloxacilling, co-amoxiclav, or clindamycin IV
* if MRSA, vancomycin, tecioplanin or linezolid IV

Analgesia
* simple analgesia PO
* leg elevation can ease pain

If at cannula site
* remove cannula, resite, and culture needle tip

84
Q

Complications of cellulitis

A
  • thrombophlebitis
  • sepsis
  • toxic shock syndrome
  • lymphangitis and secondary lymphoedema
  • cavernous sinus thrombosis if facial
85
Q

pathophysiology of necrotizing fasciitis

A
  • Bacteria enters through a break in the skin following surgery, trauma, IV injection, or insect bite
  • Infection spreads rapidly across fascial layer, leading to tissue death of fascia and subcutaneous tissue
86
Q

Types of necrotizing fasciitis and common causes

A
  • Polymicrobial (type 1)
  • Monomicrobial (type 2) = Group A strep, with tissue destruction driven by exotoxins A, B & C
87
Q

Risk factors for necrotizing fasciitis

A
  • IV drug use
  • diabetes
  • obesity
88
Q

Signs and symptoms of necrotizing fasciitis

A
  • Rapidly expanding, inflammed area of skin. May progress to bullae and dusky, purplish discolouration
  • severe pain out of proportion to skin signs
  • skin crepitus: crackly on palpation
  • sepsis and systemic symptoms
89
Q

Investigations in necrotizing fasciitis

A
  • Bloods: ↑WBC, ↑CK, ↑lactate
  • XR, CT, or MRI may help aid diagnosis, showing gas in soft tissue
90
Q

Management of necrotising fasciitis

A
  • urgent surgical debridement
  • IV abx: carbapenem + clindamycin ± MRSA coverage (e.g. vancomycin)
91
Q

What is septic arthritis

A

bacterial infection of a joint that can rapidly destroy it

92
Q

common pathogens that cause septic arthritis

A
  • staph. aureus
  • N. gonorrhoea
  • gram -ve bacilli
93
Q

Signs and symptoms of septic arthritis

A
  • acute monoarthritis: hot, red, swollen, painful joint. May be immobile
  • Most commonly affects knee
  • Fever, systemically unwell
94
Q

Risk factors for septic arthritis

A
  • RA
  • diabetes
  • immunosuppression
  • kidney failure
  • joint replacement
95
Q

Investigations for septic arthritis

A

Bloods and microbiology
* FBC and CRP
* Joint aspiration: gram stain and culture
* blood culture

Imaging
* XR should be done but is often normal
* CT and MRI is more sensitive but only used if there is diagnostic uncertainty

96
Q

Management of septic arthritis

A
  • Abx for 4-6 weeks , initially IV for 2 weeks. Flucloxacillin for staph. aureus, vancomycin for MRSA, or cefataxime for N. gonorrhoea or gram -ve bacilli. Start after joint aspiration
  • drainage of joint if severe. This may involve serial aspirations if the joint is easily accessible (knee, elbow), or open washout in theatre if less accessible (e.g. hip)
  • splinting
97
Q

Pathophysiology of osteomyelitis

A
  • Infection can come from direct/contiguous spread (cellulitis, abscess, trauma, surgery prosthesis), or haematogenous spread, which is commoner in kids, patients with urinary catheters, or TB
  • Once infected, leukocytes enter bone, releasing enzymes which cause bone lysis and leave necrotic areas known as sequestra. New bone often forms around this
  • Chronic osteomyelitis if >6 months of infection
98
Q

Pathogens that cause osteomyelitis

A
  • Staph. aureus = most common
  • Less common = strep. pyogenes (kids), H. influenzae (kids), gram -ve bacilll (elderly)i, pseudomonas aerguinosa (IV drug users)
99
Q

General features of osteomyelitis

A
  • Local inflammation
  • pain
  • slight effusion of neighbouring joints
  • systemic symtoms
  • can be asymptomatic in diabtes due to neuropathy
100
Q

Signs and symptoms of vertebral osteomyelitis

A
  • localised spine inflammation
  • Chronic back pain, which may be worse at rest and at night
  • there is often associated discitis
101
Q

Risk factors for osteomyelitis

A

Portal for pathogen entry
* Trauma: open fracture or orthopaedic surgery
* surgical prostheses
* IVDU

Diseases
* TB
* diabetes
* peripheral vascular disease
* immunosuppression
* alcoholism
* sickle cell disease

102
Q

Investigations for osteomyelitis

A

Blood and microbiology
* ↑WBC/ESR/CRP
* bone culture is gold standard
* also culture blood, pus, and local joint effusion
* look for cause e.g. urine

Imaging
* X-ray: dark area in bone, soft tissue swelling. Signs may be minimal in acute infection
* MRI provides clearer picture if diagnosis is uncertain

103
Q

Management of osteomyelitis

A
  • abx for 6 weeka, IV then PO, Flucloxacillin ± fusidic acid or rifampicin in first 2 weeks
  • Debridement to drain pus and remove sequestra if severe
  • chronic osteomyelitis may require 12 weeks of abx and extensive surgery
104
Q

Complications of osteomyelitis

A
  • septic arthritis
  • fracture
  • deformity
105
Q

Epidemiology of malaria cases imported to the UK

A
  • 1500 cases annually, many from those visiting family members in country of origin

Species
* Plasmodium falciparum: 80%, usually Africa
* Plasmodium vivax: 10%, usually South Asia
* Plasmodium ovale & Plasmodium malariae: 10%

106
Q

General signs and symptoms of malaria

A
  • Fever: all tertian (48-hourly) except quartan (72-hourly) in P. malariae. These classic patterns aren’t always seen
  • rigors
  • headache
  • diarrhoea and vomitting
  • hepatosplenomegaly
107
Q

Signs and symptoms of falciparum malariae

A
  • Flu-like prodrome: myalgia, malaise, headache, anorexia
  • irregular fever initially
  • Jaundice
108
Q

Signs and symptoms of complicated falciparum malaria

A
  • Mortality approaches 100% if sever and untreated
  • cerebral malaria: altered mental status, seizures, coma, decerebrate posturing, ↑plantars, teeth-grinding
  • AKI
  • Bleeding: haemoglobinuria (blackwater fever), DIC, retinal haemorrhages
  • Metabolic: hypoglycaemia, metabolic acidosis
  • ARDS and pulmonary oedema
  • splenic rupture
  • shock
109
Q

Investigations to diagnose malaria

A

Blood films
* serial testing: up to 3 times if 1st -ve
* Thick film - quick yes or no malaria - and thin film - which subtype
* Also shows parasitaemia (%RBCs afected) and stage, with imminent decline in patient condition due if there are ↑shizofonts. Dangerous if parasitaemia >2%, life threatening if >5%
* Simple but less sensitive antigen detection kits are available too

110
Q

Investigations to do in malaria patients

A

Bloods:
* FBC: anaemia, low platelets (due to increased spenic activity during haemolysis = increased clearance)
* Coag: DIC
* Hypoglycaemia
* ABG: metabolic acidosis
* U+E: AKI

Other tests:
* urinalysis: blood
* blood cultures to rule out bacterial sepsis

111
Q

Prophylaxis for malaria

A
  • Start 1 week before to check for side effects, and continue until 4 weeks after

Areas without chloroquinine resistance
* chloroquinine (daily) + proguanil (weekly)

Areas with chloroquinine resistance (any 1 of)
* atovaquone/proguanil. Few side effects and is taken from 1 day before
* doxycycline
* mefloquine (Larium): once weekly

Also
* long sleeves dusk till dawn
* mosquito nets
* DEET repellent

112
Q

Treatment for malaria

A
  • P. vivax, P.ovale & P. malariae: chloroquinine + primaquine
  • Uncomplicated P. falciparum: 1st line artemether/lumefantrine (Riamet). 2nd line: quinine/doxycycline, or atovaquone/proguanil
  • Complicated P. falciparum (cerebral, renal, or shock): artesunate IV (preferably), or quinine IV + doxycycline IV/PO. Careful monitoring of fluid, lactate, U+E. Transfuse if anaemic
113
Q

Complications of malaria

A
  • P. vivax & P. ovale can remain dormant in the liver as hypnozoites and relapse years later. Cause tropical splenomegaly syndrome if recurrent
  • P. malariae can lielow in blood for years, with or without symptoms
114
Q

Side effects of chloroquine

A
  • Headache
  • psychosis
  • retinopathy
  • Contraindication: epilepsy
115
Q

Side effects of primaquine

A
  • epigastric pain
  • triggers haemolysis in G6PD deficiency (check 1st and give atovaquone/proguanil if +ve)
116
Q

Side effects of atovaquone/proguanil

A
  • abdo pain
  • nausea
  • dizziness
117
Q

Side effects of mefoquine

A
  • nauea
  • dizziness
  • insomnia
  • vivid dreams
  • psychosis
  • Contraindication: epislepsy, psychosis
118
Q

Side effects of doxycycline

A
  • photosensitivity
  • diarrhoea
  • oesophagitis
119
Q

What pathogen causes TB

A

Infection by one of the Mycobacterium tuberculosis complex: M. tuberculosis, M. bovis, or M. africanum

120
Q

How is TB spread

A

Respiratory transmission

121
Q

Histological finding in TB

A

Caseating granuloma that can spread to local lymph nodes

122
Q

Systemic features of TB

A
  • fatigue
  • malaise
  • fever
  • night sweats
  • weight loss
  • anorexia
  • immunosuppression
123
Q

Signs and symptoms of pulmonary TB

A
  • Chronic productive cough ± haemoptysis, clubbing
  • can progress to pneumonia, pleural effusion, lobar collapse, and bronchiectasis
  • accounts for 60% of TB causes in UK
124
Q

Signs and symptoms of genitourinary TB

A
  • frequency, dysuria, loin/back pain, haematuria
  • can progress to renal TB, salpingitis, epididymitis, and cystitis
  • 2nd most common TB presentation in UK
125
Q

Other types of TB (apart from pulmonary and genitourinary)

A
  • Skeletal TB: most commonly affects spine (Pott’s disease). Can lead to vertebral collapse
  • Skin TB (aka lupus vulgaris): rough nodules, often on the face or shin which are +ve for AFB, scrofula (cold cervical lymphadenopathy), erythema nodosum, erythema multiforme
  • Peritoneal TB: abdomincal pain, diarrhoea, vomiting, ascites
  • TB meningitis: neurological signs are usually preceded by weeks of systemic symptoms
  • TB pericarditis: acute or constrictive pericarditis
126
Q

Signs and symptoms for miliary TB

A
  • affects multiple organs so symptoms are varied
  • there are often retinal signs
127
Q

Risk factors for TB

A
  • contact with infected individuals
  • South Asian or African
  • Homeless
  • Immunosuppressed, including HIV and extremes of age
128
Q

What is the first line investigation in TB

A

CXR, get it even in extrapulmonary TB

129
Q

CXR findings in primary TB infection

A
  • Distinct Ghon fous in the middle zone, or an area of patchy consolidation. Sometimes the parenchymal focus is too small to detect
  • Extra-parenchymal findings: ipsilateral hilar lymphadenopathy (especially in kids), effusion (especially in adults)
  • these signs may resolve following successful immune response, leaving just calcified nodies in 1/3
130
Q

CXR findings in secondary TB infection

A
  • cavitating lesion (air-filled) in the apices, especially in the right
  • other signs including patchy consolidation and linear or nodular opacities
131
Q

CXR findings in miliary TB

A
  • Diffuse 1-10mm shadows throughout lung fields
  • The term miliary is used to describe a CXR where there are more nodules than can be easily counted
132
Q

Microbiological Investigation in TB

A

Getting samples:
* pulmonary: 3 sputum samples (including 1 early morning), idaelly spontaneous. Otherwise induce with nebulised saline or do bronchoalveolar lavage.
* extra-pulmonary: aspirate or biopsy lymph nodes, ascites, organs, pus, urine, or CSF

Investigations
* MC+S: AFB smear and microscopy usually involves Ziehl-Neelson staining which is around 65% sensitive. Culture in a Lowenstein-Jenson medium typcially takes 4-8 weeks and is around 80% sensitive
* NAAT allow diagnosis a week earlier than culture, with a similar sensitivity
* PCR for rifampicin resistance
* Histology of biopsies for caseating granuloma

133
Q

Immunological testing in TB

A

Methods
* Mantoux (aka PPD): a tuberculin skin test. A delayed hypersensitivity response to tuberculin develops from 2-10 weeks after primary infection. Also +ve post BCG vaccination
* Interferon gamma release assays (IGRA): measures T cell response to TB antigens.

Uses and limitations
* Bother are around 80% sensitive
* cannot distinguish between latent and active TB
* more useful for screening contacts than diagnosis. Mantoux usually first, then confirmed with IGRA, or use IGRA first in those with previous BCG

134
Q

Other investigations for TB (apart from CXR, Microbiological & Immunological testing)

A
  • HIV screening
  • Basic bloods - FBC, LFT, U+E - may show systemic and extrapulmonary disease, and are required for baseline values before starting treatment
  • imaging for suspected extrapulmonary TB: CT/MRI (CNS, abdo, bone), US (pericardial, lymph nodes, GU), XR (bone)
135
Q

Infection control in active TB

A
  • Notify public health authorities
  • screen close contacts
  • for pulmonary TB, isolate patient in a single room, ideally negative pressure, for first 2 weeks of treatemnt. Have them wear msak if they leave the room.
  • Masks and gowns for healthcare workers are only needed for aerosol-generating procedures like sputum induction of bronchoscopy, or for multiple drug resistant TB
136
Q

Drug treatment in active TB

A
  • Treat before confirmation by culture if clinical suspicion is high. Consider continuing treatment even if culture is negative but clincal signs are strong
  • 6 months treatment with RIPE (rifampicin, isoniazid, pyranizamide & ethambutol) = 4 for 2 months, 2 for 4 months
  • Add further 6 months of dual therapy for meningeal TB
  • Add steroids for meningeal and pericardial disease
  • consider directly observed therapy (DOT) to increase adherance
137
Q

management in latent TB

A

Offer treatment to those with latent TB plus any 1 of:
* close contacts with active TB
* At high risk of progression to active TB: immunosuppressed, aged <5yrs, alcoholic, IVDU, diabetes or CKD
* immigrants from high incidence countries
* healthcare workers

Drug options
* 3 months isoniazid + rifampicin
* 6 months isoniazid monotherapy if need to avoid rifampicin e.g. on antiretrovirals

138
Q

Prevention of TB

A

Mantoux/IGRA screening for:
* Healthcare workers who are unvaccinated or from high incidence countries
* close contacts (household partner) of people with active TB
* Immigrants from high incidence countries

Actions
* If -ve, give BCG
* If +ve, asses for active TB and treat latent/active TB as needed
* in older immigrants, benefits of BCG (if age >35) and latent TB treatment (if age >65) may be smaller so are not routinely indicated

BCG vaccine
* redues infection risk by 25% and active TB risk by 70% (in children)
* in addition to those identified through screening, give to children at risk
* also offer to those at high risk through occupational exposure

139
Q

Side effects of rifampicin

A
  • hepatitis (so stop if increase bilirubin)
  • orange urine/tears
  • P450 inducer (inactivates warfarin and contraceptive pill)
  • flu-like symptoms
140
Q

Side effects of isoniazid

A
  • hepatitis
  • agranulocytosis
  • P450 inhibitor
  • peripheral neuropathy can result from pyridoxine depletion, so give supplements to all
141
Q

Side effects of pyrazinamide

A
  • hepatitis
  • arthralgia
142
Q

Side effects of ethambutol

A
  • optic neuritis
  • colour vision goes first, so check it using Ishihara charts before starting
143
Q

What type of virus is HIV

A

A single stranded, RNA retrovirus

144
Q

How is HIV transmitted

A
  • sex (including oral)
  • IV drug use
  • blood transfusions
  • vertically
145
Q

How does HIV enter cells

A
  • attaches to CD4 T cells and macrophages
  • Then integrates into DNA
  • moves to lymph nodes
146
Q

Time of course of HIV infection

A
  • 1-6 weeks post-infection, seroconversion illness occurs, similar to infectious mononucleosis
  • Then latent as the immune system mounts partial response but CD4 count drops progressively. During this time 30% develop persistent (> 3mnths) generalised lymphadenopathy
  • after around 10 years, infections and cancers begin to develop
147
Q

Stages of HIV

A

Normal CD4 count is about 800 cells/mm3
* Stage 1 ≥ 500
* Stage 2 < 500
* Stage 3 < 200

148
Q

Signs and symptoms of seroconversion illness

A
  • lymphadenopathy
  • pharyngitis
  • systemic: fever, malaise
  • pain: myalgia, headache
  • maculopapular rash
  • lasts 1-2 weeks
149
Q

Respiratory presentation of HIV

A
  • Pneumocystis jiroveci. Fungal infection that causes dry cough, sweats, SOB and desaturation on exertion, but no chest signs
  • Other fungal infections: aspergillus, cryptococcus, histoplasma
  • TB: pulmonary TB or atypical and disseminated forms such as miliary TB and TB meningitis
  • Strep and staph pneumonia
  • CMV
150
Q

Neurological presentation of HIV

A
  • Toxoplasma encephalitis: protozoal infection. Focal neurological signs
  • Cryptococcal meningitis: fungal infection. Causes insidous, chronic meningitis, usually without stiff neck
  • Primary cerebral lymphoma
  • progressive multifocal leukoencephalopathy: JC virus infection
  • HIV dementia: neurological decline in multiple domains, in the absence of other infection
  • HIV peripheral neuropathy
151
Q

Skin presentation of HIV

A
  • Kaposi’s sarcoma: due to human herpes virus 8. Purple papules on the face, mouth, back, lower limbs, or genitalia. Can also affect GI and respiratory tract
  • Multi-dermatomal zoster (shingles)
  • Recalcitrant psoriasis
152
Q

HIV presentation in the mouth

A
  • oral and oesophageal candidiasis
  • oral hair luekoplakia: non-malignany white growths on the lateral tongue due to EBV
  • HSV and aphthous mouth ulcers
153
Q

GI presentation of HIV

A
  • Cryptosporidiosis: protozoa. Chronic diarrhoea
  • CMV colitis
  • HIV wasting syndrome: unexplained weight loss >10%
  • Mycobacterium avium complex (MAC): GI, lung or disseminated
  • Fungal: cryptococcus, histoplasma
  • Other bacteria: salmonella, shigella
  • Hepatitis B and C
154
Q

Cancers in relation to HIV

A

B-cell lymphoma: EBV related
Cervical and anal cancers: HPV related
Lung cancer
Head and neck cancers

155
Q

HIV presentation in the eye

A

CMV retinitis. Mozarella pizza sign on fundoscopy

156
Q

Infections by CD4 level in HIV

  • 200 - 500:
  • 100 - 200:
  • 50 - 100:
  • <50:
A
  • 200 - 500: TB, candida, VZV, Kaposi’s, other pneumonias
  • 100 - 200: PCP, histoplasmosis, PML
  • 50 - 100: atypical TB, CMV, retinitis/colitis, toxoplasmosis, cryptosporidiosis, cryptococcal meningitis
  • <50: MAC
157
Q

Investigations to make a HIV diagnosis

A
  • Serum HIV combined antibody + p24 antigen test screen, then confirm with Western Blot. 50% detectable within 1 month of infection, and nearly all by 6 months
  • If +ve, screen for: TB, hepatitis A-C, syphilis, Toxoplasma, CMV
  • Genotype testing to guide drug treatment
  • Pregnancy test for women
  • Baseline bloods: FBC, U&E, LFT, lipids, glucose
158
Q

Tests for specific presentations in HIV

  • PCP:
  • Toxoplasma:
  • Cryptococcal meningitis:
A
  • PCP: CXR shows bilateral interstitial infiltrates
  • Toxoplasma: contrast-enhancing lesions on CT/MRI brain
  • Cryptococcal meningitis: cryptococcal antigen in CSF and serum
159
Q

Monitoring in HIV

A
  • 3 to 6 months: CD4 count, HIV quantitative RNA PCR (viral load), FBC
  • Annual: U&E and LFTs, lipids, glucose
160
Q

Lifestyle and preventative management of HIV

A
  • counseling to prevent high-risk sexual behaviour. Lifelong condom use traditionally recommended, but good evidence that those with undetectable viral load cannot transmit even during condomless sex.
  • Assistance with partner notification and contact tracing
  • Vaccines: heptatitis A and B, annual flu, pneumococcal vaccine, HPV. Avoid live ones if CD4<200
161
Q

Combination antiretroviral therapy for HIV

A
  • Triple therapy: {2 x NRTI} + {NNRTI or protease inhibitor or integrase inhibitor}
  • Research suggests clear benefits of starting treatment as soon as diagnosis is made
162
Q

Common side effects of antiretroviral therapy

A

GI
* Diarrhoea and vomiting
* Hepatitis, especially nevirapine

Skin
* Mild rash
* In rare cases, hypersensitivity or SJS/TEN

Metabolic
* Lipodystrophy: fat reduction peripherally (head and limbs) but gain centrally. Seen with protease inhibitors, but possible with all

163
Q

Common drug interactions with ART

A
  • AEDs: phenytoin and carbamezapine should be avoided
  • Sildenafil: use lower dose
  • Lorazepam should be avoided
164
Q

Definition of Pyrexia of Unknown Origin (PUO)

A
  • Temperature >38 degrees for > 3 weeks, which is still undiagnosed after 1 week of hospital investigation
  • Sub-types of fever of unknown origing: neutropenic, HIV, nosocomial
165
Q

Causes of PUO

A
  • Infection: abscess (chest/abdo/pelvic), infective endocarditis, TB, osteomyelitis, UTI, biliary infection, non-bacterial
  • Connective tissue disease: polymyalgia rheumatica, temporal arteritis, adult-onset Still’s disease, SLE, RA, PAN
  • Cancer: lymphoma, leukaemia, renal cell cancer
  • Others: drugs, IBD, PE, sarcoidosis, amyloidosis, thyrotoxicosis, Addison’s
166
Q

Important infections to rule out for fever in a returning traveller

A
  • malaria
  • typhoid and paratyphoid fever
  • influenza, HIV, viral hepatitis
167
Q

Fever in a returning traveller: DDx if short incubation (<10 days)

A
  • influenza
  • Arboral: yellow fever, dengue
  • Rickettsial infection
  • relapsing fever
  • leptospirosis
168
Q

Fever in a returning traveller: DDx if intermediate incubation (10-21 days)

A
  • malaria
  • enteric fever: typhoid and paratyphoid
  • viral haemorrhagic fever
  • leptospirosis
169
Q

Fever in a returning traveller: DDx if long incubation (>3 weeks)

A
  • malaria
  • acute shistosomiasis
  • Viral: hepatitis A-E, HIV seroconversion
  • Protozoal: african trypansomiasis, amoebic liver abscess
  • TB
  • rabies
170
Q

Fever in a returning traveller: DDx if Carribean and Latin America

A
  • arboviruses: dengue, Zika, yellow fever
  • malaria in certain areas
  • bacterial: bartonellosis
  • Fungal: histoplasmosis
171
Q

Fever in a returning traveller: DDx if South Asia

A
  • arboviruses: dengue
  • bacterial: enteric fever
  • malaria
172
Q

Fever in a returning traveller: DDx if Sub-saharan Africa

A
  • Malaria
  • bacterial: Ricketsial infection, enteric fever
  • arboviruses: dengue, yellow fever
  • helminths: acute shistosomiasis
  • viral haemorrhagic fever: Ebola, Marburg, Lassa
173
Q

What are the 5 moments of hand hygiene

A

BARFS
* Before patient contact
* Before Asceptic technique
* Right after patient contact
* After body Fluid contact
* After patient Surroundings contact

174
Q

What are some notifiable diseases

A
  • CNS: meningitis, encephalitis
  • Respiratory: TB, Legionnaires, whooping cough, anthrax, SARS
  • GI: food poisoning, haemolytic uraemic syndrome, infectious bloody diarrhoea, cholera, diptheria, enteric fever (typhoid, paratyphoid)
  • Skin: leprosy, plague, small pox
  • Neurological: rabies, botulism, tetanus
  • malaria
  • measles, mumps, rubella
  • Infectious group A strep infections
  • yellow fever
  • viral haemorrhagic fever
175
Q

Examples of gram +ve cocci

A
  • staphylococcus
  • streptococcus
  • enterococcus
176
Q

Examples of gram +ve bacilli

A
  • clostridium (anaerobe)
  • listeria monocytogenes
177
Q

Examples of gram -ve cocci

A
  • neisseria
  • moraxella
178
Q

examples of gram -ve bacilli

A
  • E. coli
  • Shigella
  • Salmonella
  • Campylobacter jejuni
  • helicobacter pylori
  • haemophilus influenzae
179
Q

Mechanism of Action of penicillins

A
  • inhibits synthesis of peptidoglycan layer of bacterial cell wall
  • Some bacteria produce beta-lactamase and require the use of beta-lactamase resitant (BLR) penicillins
180
Q

Side effects of penicillins

A
  • Rash
  • diarrhoea (esp. co-amoxiclav)
  • hypersensitivity: anaphylaxis, serum sickness
  • encephalopathy
  • renal: AIN, crystalluria (amoxicillin)
  • liver: cholestasis (flucloxacillin)
181
Q

Contraindications of penicillins

A
  • hypersensitivity
  • reduce dose in renal impairment
182
Q

Examples of penicillins

A
  • amoxicillin
  • co-amoxiclav
  • flucloxacillin
183
Q

Mechanism of Action of cephalosporins

A

beta lactam = inhibits synthesis of peptidoglycan layer of bacterial cell wall

184
Q

Contraindications of cephalosporins

A
  • hypersensitivity
  • potentiates warfarin
  • don’t cover anaerobes
  • autoimmune haemolytic anaemia
185
Q

Examples of cephalosporins

A
  • cefalexin
  • cefuroxime
  • ceftriaxone
  • cefepime
186
Q

Mechanism of action of carbapenems

A

beta lactam = inhibits synthesis of peptidoglycan layer of bacterial cell wall - with beta-lactamase resistance

187
Q

Side effects of carbapenems

A
  • neuro: headache, dizziness, seizure
  • GI: diarrhoea and vomiting
  • haematological: anaemia, eoisinophilia, decreased WBCs
188
Q

Contraindications of carbapenems

A
  • pregnancy
  • breast feeding
189
Q

Examples of carbapenems

A
  • imipenem
  • meropenem
190
Q

Mechanism of action of aminoglycosides

A

inhibits protein synthesis at the bacterial 30S ribosome site

191
Q

Contraindications and interactions of aminoglycosides

A
  • pregnancy
  • furosemide
  • myasthenia gravis: exacerbates weakness
192
Q

side effects of aminoglycosides

A
  • ototoxicity
  • nephrotoxicity
193
Q

examples of aminoglycosides

A
  • gentamicin
  • streptomycin
194
Q

Mechanism of action of tetracyclines

A

inhibits protein synthesis at the bacterial 30S ribosome site

195
Q

Side effects of tetracyclines

A
  • photosensitivity
  • diarrhoes and vomiting
196
Q

Contrainidications of tetracyclines

A
  • pregnancy
  • breast feeding
  • children <12 yrs
  • kidney failure
197
Q

Examples of tetracyclines

A
  • doxycycline
  • tetracycline
  • tigecycline
198
Q

Mechanism of action of macrolides

A

inhibits protein synthesis at the bacterial 50S ribosome

199
Q

Side effects of macrolides

A
  • GI: nausea, vomiting, and diarrhoea
  • hepatotoxicity
  • rash
200
Q

contraindications for macrolides

A

potentiates
* warfarin
* statins
* theophylline
* ergotamine
* carbamezapine

201
Q

Examples of macrolides

A
  • azithromycin
  • erythromycin
  • clarithromycin
202
Q

Mechanism of action of quinolones

A

inhibits bacterial DNA synthesis via topoisomerase II or DNA gyrase inhibition

203
Q

contraindications of quinolones

A

pregnancy

204
Q

Side effects of quinolones

A
  • GI: diarrhoea and vomiting, C. diff
  • Neuro: headache, dizziness, seizure risk in those with epilepsy, peripheral neuropathy
  • MSK: tendon rupture, arthralgia
  • CV: increased QT, aortic dissection and rupture
  • rash
  • raised LFTs
205
Q

Examples of quinolones

A
  • ciprofloxacin
  • levofloxacin
  • moxifloxacin
206
Q

Mechanism of action of glycopeptides

A

inhibits synthesis of peptidoglycan layer of bacterial cell wall

207
Q

examples of glycopeptides

A
  • vancomycin
  • teicoplanin

Year 3 Medicine (3 decks)

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