Lung Infections Flashcards

1
Q

What is pneumonia?

A

Acute lower respiratory tract infection/infection of lung parenchyma causing inflammation of lungs which results in a build up of fluid in alevoli

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2
Q

Describe the pathophysiology of pneumonia

A
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3
Q

State the different types of pneumonia- giving a brief description of each

A
  • Community acquired: developed before or within 48hrs of hosp admission and not been in hosp in last 14 days
  • Hospital acquired (nosocomial): developed pneuomonia >48hrs after admission to hospital
  • Aspiration pneumonia: developed pneumonia due to aspiration
  • Pneumonia in the immunocompromised: pneumonia caused by atypical organism as pt is immunocompromised

*Can also classify based on infecting organism but often we classive based on source of infection

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4
Q

State the most common causative organisms of each of the following types of pneumonia:

  • CAP
  • HAP
  • Aspiration pneumonia
  • Pneumonia in immunocompromised
A
  • CAP
    • Streptococcus pneumoniae
    • Haemophilius influenza
    • Morazella catarrhalis
    • Staphlococcus aureus
    • Some of the atypical organisms
  • HAP
    • Strep pneumoniae
    • Gram negative bacteria
    • MRSA
    • Pseudomonoas aeruginosa
    • Staphylococcus aureus
  • Aspiration pneumonia
    • Oral flora
    • Anaerobes
  • Pneumonia in immunocompromised/opportunistic
    • Pneumocystis jiroveci
    • Aspergillus spp
    • Cytomegalovirus

*CAN ALSO GET VIRAL PNEUMONIA

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5
Q

Alongside the 4 widely accepted categories of pneumonia mentioned previously, pneumonia can be also be caused by atypical organisms; state 3

A
  • Mycoplasma pneumonia *MOST COMMON
  • Chlamydia pneumoniae
  • Legionella pneumophilia
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6
Q

State some risk factors for devleoping pneumonia

A
  • Chronic respiratory disease (especially COPD)
  • Smoking
  • Age
  • Lives in nursing home
  • Immunocompromised
  • Chronic alcohol use/abuse
  • Contact with children
  • Smoking
  • Other chronnic comorbidities e.g. diabetes, CVD
  • Poor oral hygiene

*Ones in bold= strong risk factors

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7
Q

State the symptoms of pneumonia

A
  • Fever
  • Cough
  • Sputum production
  • Dyspnoea
  • Pleuritic chest pain
  • Confusion (elderly)
  • Rigors/night sweats
  • Malaise
  • Myalgia
  • Anorexia
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8
Q

We have already said that pneumonia can be caused by atypcial organisms; for each of the following atypical organisms state some symptoms, risk factors and/or test results that may indicate that organism is the cause:

  • Klebsiella
  • Pseudomonas
  • Legionella
  • Mycoplasma
  • PCP
  • Chlamydia
A

Klebsiella

  • Red current jelly like sputum
  • Alcoholics & aspiration

Psuedomonas

  • Green sputum
  • Need stagnant mucus

Legionella

  • Flu like symptoms precede dry cough
  • Colonises water tanks at <60degrees (e.g. hotel air conditioning, hot water systems)
  • D&V, hepatitis
  • Hyponatraemia
  • Urine antigen present

Mycoplasma

  • Flu-like symptoms followed by a dry cough later on
  • Cold agglutins

Pneumocystis jiroveci pneumonia

  • ​Dry cough
  • SoBoE (over few days become rapidly SOB on exertion)
  • Treatment= co-Trimoxazole

Chlamydia

  • Pharyngitis, hoarseness, otits followed by pneumonia
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9
Q

State what you might find on clinical examination of someone with pneumonia

A
  • Pyrexia (although elderly can be hypothermic)
  • Cyanosis
  • Tachynnoea
  • Tachycardia
  • Hypotension
  • Signs of consolidation:
    • Dull percussion
    • Increse vocal resonance
    • Bronchial breathing
    • Pleural rub
    • Reduced chest expansion
    • Reduced air entry
    • Crackles
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10
Q

State the investigations you would do if you suspectd pneumonia, include:

  • Bedside
  • Bloods
  • Imaging

*For each, justify why

A

Bedside

  • Usual observations as always (attention SpO2)
  • ?ABG: assess PaO2 and PaCO2 to guide O2 therapy
  • Sputum sample: determine causative organism & antibiotic sensitivity
  • Oropharyngeal swab: PCR for atypical organisms
  • Urine culture: check for pneunomoccal and/or legionella antigens

Bloods

  • FBC: WCC
  • U&Es: need urea for CURB65
  • LFTs: may be abnormal if basal pneumonia infiltrate liver. Hypoalbuminaemia also marker of severity. Chronic liver disease risk factor for complications
  • CRP: infection
  • ESR: infection
  • Cold agglutins: check for mycoplasma
  • Blood culture: determine causative organism

Imaging

  • CXR: classical features of pneumonia. Rule out other causes
  • ?Aspiration pleural fluid: if have pleural effusion. Can show causative organsis also. May need to drain
  • ?Bronchoscopy or bronchoalevolar lavage: if symptoms persist after 6 weeks treatment
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11
Q

Discuss what you would find on CXR of someone with pneumonia

A

Consolidation will be seen; place varies dependent on subtype:

  • Lobar pneumonia
    • Homogenous consodlidation of affected lobe
    • Air bronchograms may be seen where consolidation is
  • Bronchopneumonia
    • Patchy consolidation
  • Interstitial pneumonia
    • Consolidation in ground glass appearnce in central distribution

May also pleural effusions, cavitations

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12
Q

Compare lobar, broncho and interstital pneumonia

A

*

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13
Q

State some common differentials for consolidation on a CXR

A
  • Pneumonia
  • TB (usually upper lobe)
  • Lung cancer
  • Lobar collapse (due to blockage of bronchi)
  • Haemorrhage
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14
Q

We use the CURB65 score to assess the severity of pneumonia; explaint the CURB65 score

A

One point for each.

  • 0-1= antibiotic/home therapy
  • 2= hosp
  • 3 or more= severe pneumonia- consider ITU

CURB65:

  • Confusion: abbreviated mental test <8
  • Urea: >7mmol/L
  • Resp rate: >30/min
  • BP: <90mmHg systolic, <60mm/Hg diastolic
  • 65: aged 65 or over

*NOTE: CURB65 may underscore the young so use clinical judgement also

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15
Q

Brielfly/broadly discuss the immediate management of pneumonia

A

Always do ABCDE to make sure pt stable. Then main treatment plan is antibiotics in accordance with local guidelines (if CURB65 >2 give IV antibiotics)

Also consider:

  • Oxgyen
  • Fluids
  • VTE prophylaxis
  • Analgesia
  • Consider ITU
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16
Q

Discuss what antibiotics you would use to treat CAP; include treatment for mild, moderate & severe disease

A

Mild

  • Oral amoxicillin or oral doxycycline or oral clarithromycin (5 days)

Moderate

  • Oral amoxicillin + oral doxycycline or oral clarithromycin (7-10 days)

Severe

  • IV co-amoxiclav + IV doxycycline or IV clarithromycin (7-10 days)
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17
Q

Discuss what antibiotics you would use for HAP; include treatment for mild-moderate and severe

A

Mild-moderate

  • Oral co-amoxiclav

Severe

NICE reccomends following IV antibiotics:

  • Piperacillin/tazobactam
  • Ceftazamide
  • Ceftriazone
  • Meropenem
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18
Q

Discuss the follow up management of someone with pneumonia

A
  • Arrange follow up 6 weeks later and repeat CXR to ensure resolution
    • Consider bronchoscopy in pts with persisting symptoms or abnormal radiological findings at 6 week follow up
  • Other follow up tests:
    • HIV test
    • Immunoglobulins
    • Pneumococcal IgG serotypes
    • Haemophilius influenza b IgG
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19
Q

State some causes of non-resolving pneumonia

**Think CHAOS

A
  • Complication: empyema, lunga abscess
  • Host: immuncompromised
  • Antibiotic: inadequete dose, poor oral absorption
  • Organism: resistant or unexpected organisms not covered by antibiotics
  • Second diagnosis: PE, cancer, organising pneumonia
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20
Q

What do we mean by atypical pneumonia?

Which abx do they respond to?

A

Pneumonia caused by an organism that can’t be cultured in the normal way or detected using a gram stain.

They don’t respond to penicillins. Can be treated with marcolides (e.g. clarithromycin), fluoroquinolones (e.g levofloxacin) or textracyclines (e.g. doxycycline)

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21
Q

State the 5 causes of atypical pneumonia

HINT: can remember by “Legions of psittaci MCQs”

A
  • Legionella pneumophilia (Legionnaire’s disease)
  • Chlamydia psittaci
  • Mycoplasma pneumonia
  • Chlamydydophilia pneumoniae
  • Q fever (coxiella burnetii)
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22
Q

For each of the causes of atypical pneumonia, discuss:

  • Where pt gets infection from
  • Any symptoms/signs associated with infection by the atypical organism
A

Legionella pneumophilia (Legionnaire’s disease)

  • Infected water supplies or air conditioning
  • Can cause SIADH causing hyponatraemia

Chlamydia psittaci

  • Infected birds
  • MCQ pt often a parrot owner

Mycoplasma pneumoniae

  • Milder pneumonia which can cause erythema multiforme rash and neurological symptoms in young pts

Chlamydydophilia pneumoniae

  • Mild to moderate chronic pneumonia and wheeze in school aged children

Q fever (coxiella burnetti)

  • Exposure to animals and their bodily fluids
  • Typical MCQ is farmer with flu-like symptoms
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23
Q

For fungal pneumonia, discuss:

  • Who usually presents in
  • Most common causative fungi
  • Presentation
  • Treatment
A
  • Immuncompromised; it is particularly important to consider in poorly controlled or new HIV with a low CD4 count
  • Pneumocystis jiroveci (PCP)
  • Present subtly with dry cough, SOBoE and night sweats
  • Treatment: co-trimoxazole (trimethoprim/sulfamethoxazole) known by bran name Septrin

*NOTE: pts with low CD4 counts prescribed prophylactic oral co-trimoxazole to protect against PCP

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24
Q

State some potential complications of pneumonia

A
  • Sepsis
  • Pleural effusion
  • Empyema
  • Lung abscess
  • Death
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25
Q

State 4 ‘at risk’ groups who are offered the flu vaccination

A
  • Elderly >65yrs
  • Chronic heart, liver, renal, lung conditions
  • Immunosupressed
  • Diabetes mellitus not controlled by diet
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26
Q

State 4 at risk groups who are offered pneumococcal vaccination

A
  • babies
  • people aged 65 and over
  • anyone from the ages of 2 to 64 with a health condition that increases their risk of pneumococcal infection (generally same people who are eligible for flu vaccination)
  • anyone at occupational risk, such as welders
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27
Q

What is tuberculosis?

A

Infection with Mycobacterium tuberculosis. It commonly involves the lungs and is communicable in this form, but may affect almost any organ system including the lymph nodes, central nervous system, liver, bones, genitourinary tract, and gastrointestinal tract.

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28
Q

Describe the pathogenesis of tuberculosis (recap from resp sem 3)

A
  1. Inhale MTB which deposits in alveoli. TB likes to deposit in fissures and subpleural spaces
  2. Macrophages try to remove MTB but cannot. Leads to activation of cell mediated immunity leading to emergence of macrophages with enhanced ability to kill MTB- takes about 6 weeks
  3. Macrophages then kill MTB in the alveoli forming a subpleural focus of tubercles called the ‘Ghon or Primary focus’. NOTE: tubercle= spherical granuloma with central caseating necrosis
  4. Some of the macrophages, which have engulfed TB, travel to a hilar lymph node and kill MTB causing a granuloma in lymph node aswell. The Ghon focus & enlarged hilar lymph node that has caseous granuloma also called the primary complex. This occurs over 3-8 weeks and causes an inflammatory reaction.
  5. Some TB bacilli may enter blood stream and heamatogenous spread can oocur leading to TB forming tubercles in other parts of lungs and extra-pulmonary sites
  6. There are then three options after this:
  • Bacteria continues to multiply leading to progressive primary infection
  • Bacteria is completely cleared (heals/self cure)
  • Some TB bacilli persist in host without causing disease (TB bacilli could be in lungs or other extra-pulmonary sites) this can be reactivated in time causing secondary progressive/post primary TB
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29
Q

What is meant by miliary TB?

A

TB that has spread via blood both in lungs(leading to many discrete foci of granulomas in lungs) and to other organs in body; leading to millet seet appearance on CXR

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30
Q

State some risk factors for TB

A
  • Past history of TB
  • Known history of TB contact
  • Born in country with high TB incidence
  • Foreign travel to country with high TB incidence
  • Immunosupression

*High TB incidence: Asia, Africa, South America, Eastern Europe

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31
Q

State the symptoms of TB

*remember to think about respiratory & non-respiratory TB

A
  • Fever
  • Night sweats (drenching)
  • Weight loss
  • Malaise

Respiratory TB

  • Cough +/- prurulent sputum
  • Haemoptysis
  • Pleurisy

Non-respiratory TB:

  • Skin: erythema nodosum, lupus vulgaris, scrofuloderma
  • GI: pain, vomit, bowel obstruction
  • Lymph: lymphadenopathy (cervical & supraclavicular)
  • Bone: spinal pain & tenderness
  • CNS: meningitis, abscess
  • Cardiac: pericarditis
  • Renal: haematuria, pyruria
32
Q

Discuss what you might find on clinical examination of a pt with TB

A
  • Crepitations or bronchial breathing if there is pulmonary changes/pleural effusion
  • Pericardial rub if there is pericardial involvement
  • Finger clubbing
  • Erythema nodosum
33
Q

State some differential diagnoses of haemoptysis

A

Infection

  • Pneumonia
  • TB
  • Bronchiectasis
  • CF
  • Cavitating lung lesion (fungal)

Malignancy

  • Lung cancer
  • Metastases

Haemorrhage

  • Bronchial artery erosion
  • Vasculitis
  • Caogulopathy

Others

  • PE
34
Q

State what investigations you would want for someone with suspected TB, include:

  • Bedside
  • Bloods
  • Imaging

*For each, justify why

A

Bedside

  • Sputum culture & acid-fast bacilli smear: need three specimens, including at least one early morning sample (ideally all early morning)
  • Nucleic acid amplifciation test: do for sputum but can use any bodily fluid- useful if detect extrapulmoonary TB
  • ?ABG

Bloods

  • FBC: WCC, aneamia in some
  • U&Es: renal func
  • LFTs: liver func
  • CRP: infection
  • Vit D levels
  • HIV test

Imaging

  • CXR: features of TB
  • Chest CT: if suspect TB but CXR not typcial
  • ?MRI brain/spine & lumbar puncture: if suspect miliary TB
35
Q

Explain the difference between a sputum smear, sputum sample and nucleic acid amplification test (NAAT)

A
  • Sputum smear: stain with Ziehl Neelsoon stain- stains acid fast bacilli e.g. Mycobacterium tuberculosis
  • Sputum sample: grow Mycobacterium tuberculosis (culture can take 1-3 weeks or 4-6 dependent on media)
  • NAAT: detect DNA in sample- rapid detection
36
Q

Do each of the following differentiate between mycobacterium and non-mycobacterium TB:

  • Smear test
  • Culture
  • NAAT
A
  • Smear test: does not differentiate
  • Culture & NAAT: do differentiate
37
Q

Discuss what you might find on CXR of someone with TB

A
  • Cavitations
  • Pleural effusion
  • Medistinal/hilar lymphadenopathy
  • Parenchymal infiltration
38
Q

What might you see on CT scan of a pt with TB?

A

Lymphadenopathy (nodes with central necrosis are more suggestive)

39
Q

If you are unsure between a diagnosis of pneuomonia and TB, what should you do?

A
  • Sputum samples prior to any antibiotics
  • Start antitbiotics for pneumonia whilst investigating possibility of TB
40
Q

If a pt is critically unwell (hence no time to wait for sample resutlts) and there is high likelihhood of TB, what would you do?

A
  • Start anti-TB treatment after samples sent
41
Q

What is meant by the paradoxical reaction in TB?

A

When pts start treatment, there is an increase in inflammation as bacteria die causing worsening of symptoms. If TB is affecting sites where additional swelling cannot be tolerated (e.g. meningeal TB, spinal TB or pericardial TB) then steroids are given at start of treatment

42
Q

Discuss the management/treatment of ACTIVE TB

A
  • ABCDE to make sure pt stable
  • Admit to side room & start infection control
  • Start anti-TB therapy (ATT) *NOTE: often start this before get samples back as samples can take a while

Anti-TB Therapy

  • Rifampicin (6 months)
  • Isoniazid (6 months)
  • Pyrazinamide (2 months)
  • Ethambutamol (2 months)
  • Pyridoxine also given whilst on isoniazid to protect against peripheral neuropathy

If pt has miliary/disseminated TB teratment will be longer (12 months). May also give steroids dependent on where TB is and if paradoxical reaction in these areas would cause harm.

43
Q

What must you check before starting ethambutamol?

A

Visual acuity (it can cause colour blindness, decreased visual acuity, optic neuritis..). Hence check for visual acuity at start and monitor monthly

44
Q

What blood test is it EXTREMELY important to check regularly in someone taking anti-TB medication?

A

LFTs

45
Q

State some of the major side effects of the 4 anti-TB drugs

A
  • Rifampicin: hepatitis, rashes, febrile reaction, orange/red body secretions (includes saliva, sweat, tears etc.. hence can stain contact lenses), enzyme inducer therefore interacts wtih many drugs including warfarin & COCP
  • Isoniazid: hepatitis, rashes, peripheral neuropathy, psychosis
  • Pyrazinamide: hepatitis, rashes, vomitting, athralgia
  • Ethambutamol: retrobulbar neuritis
46
Q

Which of the TB drugs is most hepatotoxic?

A

Pyrazinamide

47
Q

Do we treat latent TB? If so, how do we treat it?

A

Yes, we treat active TB to reduce risk of post-primary TB. Treat with either:

  • Rifampicin & isoniazid (and pyridoxine) for 3 months
  • Isoniazid (and pyridoxine) for 6 months
48
Q

Compare and contrast the two ways in which we can screen for TB

A

Mantoux/Tuberculin Skin Testing

  • Intradermal injection of tuberculin. Measure size of induration about 48-72hrs later. Induration indicates previous exposure to TB

Interferron-Gamma Release Assays (IGRAs)

  • Collect blood sample from pt and incubate with mycobacterium tuberculosis antigens. If pts been exposed to TB before then T lymphocytes in pts blood will produce interferron gamma in response

Neither can distinguish between latent and active TB. HOWEVER, IGRAs can distinguish between MTB and non-MTB & BCG vaccine (because the antigens in test are not present in non-MTB or the bacilli used in BCG vaccine).

Both can produce false negatives in immuncompromised pts. TST can produce false positives in those who have had BCG.

49
Q

What pt groups do we screen for latent TB?

A

Use interferon gamma test in asymptomatic pts with risk factors for latent TB:

  • Immigrants from high prevelance countries
  • Healthcare workers
  • HIV positive pts
  • Pts starting on immunosuprresion
50
Q

Is any monitoring required post TB treatment?

A

Have CXR at end of treatment. Other than that no routine follow up post treatment unless pt had multi-drug resistant TB in which case close follow up required for 2 years (CXR & sputum every 4-6 months).

51
Q

Discuss the infection control rules surrounding TB, consider:

  • Isolation
  • PPE for staff and pt
  • MDR TB
A
  • Pts with non-resistant pulmonary TB should be nursed in side room until 2 weeks of treatment is completed. At this point they are generally considered non-infectious to immuncompetent individuals. If ward manages immuncompromised pts then TB pt must remain in side room until discharge.
  • Pts who are smear positive can be discharged home but need to quarantine until they have completed two weeks of treatment
  • Staff do no need to wear masks/aprons unless MDR TB is suspected or they are performing an aeorsol generating procedure
  • Pts with smear positive TB do need to wear a mask when leaving their room until they have completed 2 weeks of treatment
  • PTs with MDR TB must ne managed in a negative pressure room and staff should wear PPE when dealing with them
52
Q

State some examples of lower respiratory tract infections

A

LRTI means any infection below voicebox/larynx

  • Pneumonia
  • Flu
  • TB
  • Bronchitis
  • Bronchiolitis
53
Q

What is influenza?

A

Acute respiratory viral infection which is caused by seasonal influenza virus A,B or C; it can cause both upper & lower respitory tract infections

54
Q

Remind yourself of the following from the influenza lecture in infection module:

  • Shape
  • DNA or RNA
  • Double or single stranded
  • Negative or positive genetic material
  • Enveloped or non-enveloped
  • Two surface antigens & their role
A
  • Spherical
  • RNA
  • Single
  • Negative
  • Enveloped
  • Haemaglutinin (binds to cells of infected person) & neuraminidase (release virus from host cell surface)
55
Q

Remind yourself of the following from the influenza lecture in infection module in sem 2:

  • Which of influenza A,B and C shows antigenic shift and drift
  • Which causes most severe disesse
  • Which causes most outbreaks
A

Influenza A

  • Shift & drift
  • Varying intensity- potential for severe disease
  • Annual outbreaks, epidemics every few years, potential for pandemic

Influenza B

  • Drift
  • Usually less severe than A
  • Outbreaks every few years

Influenza C

  • Drift
  • Mild disease no seasonality
56
Q

State some risk factors for developing influenza

A
  • Age
  • Immunocompromised
  • Winter
  • Unvaccinated
  • Outbreak
57
Q

Dicuss the symptoms of influenza

A
  • Fever
  • Dry cough
  • Sore throat
  • Headache
  • Malaise
  • Myalgia
  • Conjunctivitis
  • Eye pain +/- photphobia
58
Q

State what you might find on clinical examination of someone with influenza

A
  • Fever
  • Lymphadenopathy

Physical examination may be normal. If lots of findings on clinical examination might make you think of other causes e.g. pneumonia

59
Q

If you suspect influenza, do you always test for it?

A

No, diagnosis is clinical and only do testing if results are likely to infect diangosis, treatment or for public surveillance.

If needed testing you could do viral culture of any of the following samples: throat swab, nasal swab, sputum etc..)

60
Q

Discuss how you treat uncomplicated influenza

A
  • Symptomatic treatment e.g. paracetamol
  • Only give antivirals if high risk e.g. chronic disease, immunocompromised, pregnant, >65yrs, <6months, BMI>40
61
Q

Discuss how you treat complicated influenza

A

Complicated influenza is when pt needs hosp admission often and/or exacerbates underlying condition.

  • Antiviral inhibitors of neuraminidase e.g. Oseltamivir first line. Zanamavir second line.
62
Q

If a high risk pt has been exposed to influenza (e.g. someone in a nursing home gets influenza and so rest of residents were exposed) what might you consider giving them?

A
  • Prophylaxis IF HIGH RISK AND NOT PROTECTED BY VACCINATION. Consider oseltmavir for 10 days
63
Q

State soem potential complications of influenza highlighting which is most common

A
  • Bacterial pneumonia
  • Viral pneumonia
  • Otitis media (common in children)
  • Croup (children)
  • Myositis
  • Encephalitis
  • Reye syndrome
64
Q

Bronchiolitis is an example of a LRTI. Summarise the following:

  • What it is
  • Who it is common in
  • Symptoms
  • Treatment
  • Prophylaxis
A
  • Inflammation bronchioles
  • Children. Caused by RSV (respiratroy sycytial virus) which infects almost all children by age of 3 but only minority develop bronchiolitis
  • Symptoms: cough, tachypnoea, wheezing, retractions, grunting, nasal flaring
  • Treatment: supportive (oxygen, fluids. Seniors will be involved for further treatment)
  • Prophylaxis is given in first year of life for babies who are at increased risk
65
Q

Acute bronchitis is an example of a LRTI, summarise:

  • What it is
  • Symptoms
  • Diagnosis
  • Treatment
A
  • Infections which cause inflammation of airways (whereas in comparison pneumonia is infection causing inflammation of lung parenchyma)
  • Symptoms: productive cough <30 days (in pt with no history of chronic resp illness)
  • Diagnosis: exclusion of other resp infections e.g. pneumonia
  • Usually resolves on its own in 4 weeks advise fluids and analgesia. Consider antibiotic therapy (doxycycline 1st line, amoxicillin if can’t use doxycycline) if patients:
    • are systemically very unwell
    • have pre-existing co-morbidities
    • have a CRP of 20-100mg/L (offer delayed prescription) or a CRP >100mg/L (offer antibiotics immediately)
    • NICE Clinical Knowledge Summaries/BNF currently recommend doxycycline first-line
66
Q

What is meant by a pleural infection (also known as empyema)?

A

Pus in pleural space. Often occurs when there has been pleural effusion and an infection then occured due to the stagnant fluid.

67
Q

State some risk factors for developing empyema

A
  • Pneumonia
  • Iatrogrenic invasion of pleural space
  • Immunosupression
68
Q

State some symptoms of empyema

A
  • SOB
  • Fever
  • Rigors
  • Pleuritc chest pain
  • Productive cough
69
Q

What might you find on clinical examination of someone with empyema

A
  • Decreased breath sounds
  • Decreased vocal resonance
  • Dullness to percussion
  • Signs of sepsis
70
Q

What investigations would you do if you suspect empyema, include:

  • Bedside
  • Bloods
  • Imaging
A

Bedside

  • Sputum culture: see if still evidence of infection e.g. pneumonia
  • Thoracocentesis: aspirate and check sample for multiple things e.g. colour

Bloods

  • FBC: WCC
  • CRP: marker infection
  • Blood culture: ?sepsis

Imaging

  • CXR: may see empyema, may see consolidation if pneumonia is cause
71
Q

Discuss the treatment for empyema

A
  • Empirical antibiotics IV (all should start on IV, then move to oral)
  • Chest drain
  • Supportive care e.g. fluids, oxygen
  • If above doesn’t work may consider surgery or intrapleural fibrinolytics
72
Q

What score is used in primary care to assess severity of pneumonia?

Interpret this score

A
73
Q

What is the point-of-care CRP test in regards to CAP?

A

NICE also mention point-of-care CRP test. This is currently not widely available but they make the following recommendation with reference to the use of antibiotic therapy:

  • CRP < 20 mg/L - do not routinely offer antibiotic therapy
  • CRP 20 - 100 mg/L - consider a delayed antibiotic prescription
  • CRP > 100 mg/L - offer antibiotic therapy
74
Q

What should all cases of pneumonia have 6 weeks after diagnosis?

A

All cases of pneumonia should have a repeat chest X-ray at 6 weeks after clinical resolution to ensure that the consolidation has resolved and there is no underlying secondary abnormalities (e.g. a lung tumour).

75
Q

Describe the typical resolution of symptoms/progression/time course of pneumonia

A