The respiratory system - Lung infections Flashcards

1
Q

How is cystic fibrosis (CF) inherited?

A

It is an autosomal dominant - both parents must be carriers for child to have it

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2
Q

What gene is affected in CF?

A

Mutations to the cystic transmembrane conductance regulator (CFTR) gene on the long arm of chromosome 7

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3
Q

What is the role of the cystic fibrosis transmembrane conductance regulator (CTFR) gene?

A

The CTFR gene encodes for an epithelial chloride channel regulated by cyclic AMP. This channel help maintain the right balance fluid in the airways.

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4
Q

What is the most common CF mutation

A

Delta F508

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5
Q

What is the description for the following classes of CFTR mutation:

a) stage I

b) Stage II

c) Stage III

d) Stage IV

e) Stage V

A

a) No functional CFTR is made

b) Defective protein processing

c) Defective regulation

d) Defective conduction

e) Reduced functional CFTR

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6
Q

Describe the pathogenesis of cystic fibrosis

A
  1. Defects in the CTFR gene lead to defects in the normal ion transport
  2. This result in dehydration of airway surface resulting in mucociliary dysfunction
  3. This leads to reduced mucus clearance, airway obstruction and predisposition to infection
  4. Recurrent infection leads to chronic bronchitis, damage to the bronchi and eventually bronchiectasis
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7
Q

What are the clinical features of CF in new-borns

A

Meconium ileus (a bowel obstruction that occurs when the meconium in a child’s intestine is even thicker and stickier than normal meconium)

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8
Q

What are the clinical features of CF in infants/children

A
  • Pancreatic insufficiency (Failure to thrive)
  • Hepatic steatosis (Fatty stools)
  • Recurrent chest infections
  • failure to thrive
  • Rectal prolapse
  • Dehydration
  • Allergic bronchopulmonary aspergillosis (ABPA)
  • Renal calculi
  • Distal intestinal obstruction syndrome (DIOS)
  • Hyponatraemic hypochloraemic metabolic alkalosis
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9
Q

What are the clinical feature of CF in adolescence/adulthood

A
  • Chronic sinusitis
  • Nasal polyps
  • Bronchiectasis
  • Liver disease
  • Steatorrhea
  • Constipation
  • Distal intestinal obstruction syndrome (DIOS)
  • Male infertility
  • Arthritis/arthralgia
  • Delayed puberty, Osteoporosis
  • Finger clubbing
  • Gallstons
  • Pancreatic insufficiency
  • Pancreatitis
  • Diabetes
  • Renal calculi, renal failure
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10
Q

Exacerbation of pulmonary infections in patients with cystic fibrosis

a) Symptoms

b) Signs

A

a)
- Increased frequency and duration of cough
- Increased sputum production
- Change in appearance of sputum
- Increased SOB
- Decreased exercise tolerance
- Decreased appetite
- Feeling of increased congestion in the chest

b)
- Increased respiratory rate
- Use of accessory muscles for breathing
- Intercostal retractions
- Change in results of auscultatory examination of chest
- Decline in measures of pulmonary function consistent with presence of obstructive airway disease
- Fever and leukocytosis
- Weight loss
- New infiltrate on chest radiograph

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11
Q

Describe the 4 common clinical manifestations of cystic fibrosis

A

Respiratory disease
- Most common
- Persistent, daily, productive cough
- Recurrent infections result in bronchiectasis
- Complications: cor pulmonale, haemoptysis and pneumothorax

Pancreatic disease
- CF-related disease
- Fatty stools
- Malabsorption

Gastrointestinal disease
- Most common cause of meconium ileum in infants
- Constipation
- Distal intestinal obstruction syndrome (DIOS))

Malignancies
- Increased risk of GI malignancies

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12
Q

Why do CF patients get fatty stools and malabsorption?

A

Thick secretions block the outflow of exocrine digestive enzymes leading to insufficiency with fatty stools and malabsorption

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13
Q

Describe the screening of CF in the UK

A

CF is screened for as part of new-born heel prick test

Conducted at day 5 after birth

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14
Q

Give 3 tests that can be used to diagnose CF

A

Heel prick test (detects immunological-reactive trypsin)

Sweat test

Genetic testing

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15
Q

What are the diagnostic result of the sweat test in CF?

A

Sodium chloride of > 60 mmol/L is diagnostic

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16
Q

Describe the CXR changes in CF

A

Hyperinflation

Reticulonodular shadowing

Collapse/atelectasis

Bronchiectasis

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17
Q

Describe the management of pulmonary disease in CF

A

Conventional
- airway clearance techniques
- Chest physiotherapy

Pharmacological (Mucoactive agents)
1. rhDNase - 1st line and given via nebuliser
2. Hypertonic sodium chloride - may be used alone or with rhDNase. Given via nebuliser
3. Mannitol dry power inhalation - used in patients intolerant, ineligible or not responding to rhDNase. It is inhaled

Pulmonary infection
- Prophylactic antibiotics/antifungal + steroids e.g., ABPA

Lung transplantation
- Can be considered in patients with progressive respiratory failure and usually both lungs

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18
Q

How are CF patients with new infections (psudeomonas aeruginosa) treated?

A

Treat with eradication therapy with oral/IV antibiotics and inhaled antibiotics.

If clinically unwell then only IV and inhaled antibiotics used

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19
Q

What antibitoic can be offered in CF children from age 3-6 years?

A

Oral flucloxacillin

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20
Q

Describe the management of nutrition and pancreatic insufficiency in CF

A

Nutrition
- Nutritional assessment and reviews offered with a specialist dietician
- If wight loss/inadequate weight gain increase portion size + eat high-energy foods. Nutritional supplements can be considered if unsuccessful
- Ongoing deficit may need enteral feeding or trial of oral appetite stimulant

Pancreatic insufficiency
- Oral pancreatic enzyme replacement (e.g., CREON)

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21
Q

Describe the management of liver disease in CF

A
  • Patients screen regularly
  • Ursodeoxycholic acid can be given
  • Transplantation: may be indicated in those with liver failure (completed alone or as a liver-lung or liver-pancreas transplant)
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22
Q

Describe the management of CF-related diabetes

A
  • Should be screened annually from age of 10 and at any times where symptoms are suggestive
  • Treat diabetes e.g., insulin
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23
Q

.Several new therapies for the management of cystic fibrosis known as CFTR modulators have been approved for use in the UK.

a) Describe their mechanism of action

b) Name the 4 drugs available in the UK

A

a) Target the underlying mechanism in cystic fibrosis

b) Kalydaco, Orkambi, Symkevi and Kaftrio

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24
Q

What is bronchiectasis?

A

Bronchiectasis is the irreversible and abnormal dilatation of the airways

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25
Q

Describe the epidemiology of bronchiectasis

A
  • Females are more affected than males
  • Prevalence increases with age
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26
Q

Describe the pathophysiology of bronchiectasis

A

Normally results from the inflammatory destruction of the elastic and muscular components of thew airways

This leads to abnormally dilated airways, persistent sputum productive with insufficient clearance and current chest infections

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27
Q

Describe the aetiology of bronchiectasis

A

Immunodeficiency (predisposed patients ot infection
- Primary: IgA and ig deficiency
- Secondary: HIV, malignancy

Mechanical obstruction
- Foreign bodies, mucus plugging, stenosis, tumours or lymph nodes

Mucociilary cleareance dysfunction
- CF
- Primary ciliary dyskinesia (autosomal recessive pattern, characterised by immotile cilia often resulting in recurrent infections and bronchiectasis)
- Young syndrome (characterised by male infertility, sinusitis and bronchiectasis)

Congenital airways defects
- Williams-Campbell syndrome: a rare disease characterised by defective cartilage in the airways resulting bronchiectasis
- Mounier-Kuhn syndrome: also termed tracheobronchomegaly, it is a rare disease characterised by dilatation of the trachea itself as well as the bronchi

Other causes - RhA, ABPA, COPD, inflammorty bowel disease

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28
Q

Clinical features of CF

a) Symptoms

b) Signs

A

a)
- Persistent sputum production
- Persistent cough
- Haemoptysis
- Weight loss

b)
- Crackles
- High pitched inspiratory squeaks
- Wheeze
- Clubbing (rare)

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29
Q

The clinical course of bronchiectasis may be interrupted by acute infective exacerbations.

What are the clinical features of an acute infective exacerbation?

A

Worsening of chronic features (dyspnoea, cough and sputum production)

Systemic infection features e.g., fever, malaise

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30
Q

Describe the investigations for bronchiectasis

A

Bloods - FBC, renal function, serum immunoglobulines

Cultures - sputum cultures, blood culture

Asperigullis fumigates - serum total IgE, sensitisation assessment (specific IgE or skin prick test)

Other
- In patterns with features of arthritis, vasculitis or CTD: RF, anti-CCP, ANA and ANCA
- Bronchoscopy
- Tets for primary ciliary dyskinesia
- Spirometry - decreased FEV1/FVC ratio

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31
Q

Imaging for bronchiectasis

a) 1st line

b) Diagnostic modality

A

a) CXR

b) High-resolution CT - diagnostic modality of choice

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32
Q

High resolution CT changes of bronchiectasis

A

Thickened bronchial walls

Tram-track/tram-line airways

Ring shadows

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33
Q

Describe the management of bronchiectasis

A

Conservative
- Airway clearance techniques
- chest physiotherapy
- Patient education
- Support group
- Smoking cessation

Medical
1. Mucoactives - Isotonic and hypertonic saline, Oral carbocisteine, (recombinant human DNase not recommended in adults with bronchiectasis)
2. Prophylactic antibiotics (treatment depends on whether or not the patient is colonised by P. aeruginosa)
3. Bronchodilators - used in patients with coexisting asthma/COPD/ABPA or in those wit significant breathlessness

Surgery
- Lung resection
- Lung transplant

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34
Q

What are the indications of lung transplant in bronchiectasis

A

Patients aged 65 or younger, with an FEV1 < 30% and clinical instability or rapidly deteriorating lung function despite medical intervention

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35
Q

Patients with recurrent exacerbations despite education, treatment of underlying cause, physiotherapy (+/- mucoactives) should be considered for long-term antibiotics.

Treatment depends on whether or not the patient is colonised by P. aeruginosa. What is the treatment if:

a) P.aeruginosa colonised

b) Non-P.aeruginosa colonised

A

a)
1st line - Colisistn and gentamicin
2nd line - Oral azithromycin or erythromycin (considered in those who don’t tolerate inhaled therapy or in addition to inhaled therapy where it is ineffective)

b)
1st line - Azithromycin or erythromycin
2nd line - Inhaled gentamicin can be considered second line.

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36
Q

Describe the complications of bronchiectasis

A
  • Infective exacerbation
  • Chronic respiratory failure
  • Haemoptysis
  • Cor pulmonale
  • Pneumothorax
  • Chest bag
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37
Q

What is Pneumonia?

A

Inflammation of the parenchyma of the lung

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38
Q

Describe the pathophysiology of pneumonia

A
  1. Infection the lung (e.g., bacteria, virus)
  2. Inflammatory response initiated
  3. Alveolar oedema + exudate formation
    3.Alveoli and respiratory bronchioles fill with serous exudate, blood cells, fibrin, bacteria
  4. Consolidation of lung tissues
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39
Q

Pneumonia

a) Symptoms

b) Signs

A

a)
- Fever
- Malaise
- Productive cough
- Dyspnoea
- Pleuritic pain
- Haemoptysis
- Rigors

b)
- Dull percussion
- Reduced breath sounds
- Bronchial breathing
- Coase crepitaitons
- Increased tactile vocal fremitus
- Tachycardia
- Pyrexia
- Hypotension
- Confusion
- Cyanosis
- Pleural rub

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40
Q

Name the 3 classifications of penumonia

A

Community acquired

Hospital acquired

Immuno-compromised

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41
Q

Name 5 typical bacterial/viral pathogen of community acquired pneumonia

A
  • Streptococcus pneumoniae (most common)
  • Haemophilus influenza
  • Moraxella catarrhalis
  • Influenza-Staph.A super infection
  • Respiratory viruses
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42
Q

Name 6 atypical bacterial/viral pathogens

A
  • Chlamydophila psittaci
  • Coxiella burnetii - Q fever
  • Mycoplasma pneumonia
  • Legionnaires disease
  • Mycobacterium tuberculosis
  • Pneumocystis jirovecii
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43
Q

How can bacterial pneumonia and viral pneumonia be differentiated?

A

Bacterial pneumonia - sudden onset of symptoms and rapid illness progression

Viral pneumonia - slow onset of URTI and wheezing

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44
Q

Describe the treatment of community acquired pneumonia

A

Penicillin (Amoxicillin, Tazobactam) pLUS macrolied (Clarithomycine)

Antivirals e.g., oseltamivir for 7 days (but within 3-5 days of symptoms)

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45
Q

Describe the prevention of community acquired pneumonia

A

Smoking cessation

Vaccines

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46
Q

What is hospital acquired pneumonia defined by NICE?

A

HAP is defined by NICE as a contracted > 48 hours after hospital admission that was not incubating at the time of admission

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47
Q

Give 5 risk factors of hospital acquired pneumonia

A
  • Antibiotics
  • Surgery
  • Chronic lung disease
  • Advanced age
  • Immunosuppression
  • Tracheal intubation
  • Mechanical ventilation
48
Q

What are the 4 types of hospital acquired pneumonia?

A
  • Ventilator associated pneumonia
  • Aspiration pneumonia
  • Environment source
  • Hospital transmission
49
Q

Name 5 ventilator associated hospital acquired pneumonias

A
  • Pseud. aeruginosa (most common)
  • Acinetobacter sp.
  • Stenotrophomonas maltophilia
  • Haemophilus spp
  • S. aureus – MRSA
  • Escherichia coli /Kleb. Pneumonia/ Enterobacter sp.
  • Streptococcus spp/Strep pneumoniae
  • Fungi (Candida spp., Aspergillus)
50
Q

Name 5 organisms associated with aspiration pneumonia

A
  • Gram negative organisms (Pseud. aeruginosa, E. coli
  • Haemophilus spp
  • Anaerobes
  • Mouth related (upper GI) streptococci
  • Strep. Pneumoniae
51
Q

Give 4 risk factors of aspiration pneumonia

A
  • Stroke
  • Myasthenia gravis
    -Bulbar palsy
  • Alcoholism
  • Achalasia
52
Q

Name 5 likely causative organisms of pneumonia in immunocompromised patients

A

Bacterial pathogens: myobacterium complex and non-tuberculosis myobacterium
Fungal pathogens: pneumocytosis jirovii, Aspergillus fumigatus and crypto coccus neoformans
Viral pathogens: Marcella zoster virus and cytomegalovirus
Parasitic pathogens: parasitic pneumonias are very rare and seen almost exclusively in the immunocompromised

53
Q

Streptococcus pneumonia

a) classification

b) Clinical features

c) Colour of sputum

A

a) Gram-positive alpha-haemolytic streptococci

b) Productive cough, pleuritic pain, and pyrexia, and may be accompanied by reactivation of cold sores (associated with herpes labials)

c) Rust colour sputum

54
Q

Haemophilus influenza

a) Classification

b) Sputum colour

c) What time of patients is it associated with?

A

a) Gram-negative coccobacilli

b) Green sputum

c) Associated with patients with COPD

55
Q

Staphylococcal pneumonia

a) Classification

b) What type of patients is it found in?

A

a) Gram-positive coccus

b) IV drug users, elderly patients, or patients who already have an influenza infection

56
Q

Klebsiella pneumonia

a) Classification

b) Sputum colour

c) At risk groups

A

a) Gram-negative anaerobic rod

b) Red-currant jelly sputum

c)
- Patients with weakened immune system such as elderly, alcoholics, diabetes
- Patients with malignancy
- COPD
- Long term steroid use
- Renal failure

57
Q

Mycoplasma pneumonia

a) Classification

b) Clinical features

c) Complications

d) Gold-standard investigation

e) Treatment

A

a) Gram negative rod-shaped bacterium (that lack a cell wall)

b) Flu like symptoms consisting of flu, arthralgia, myalgia, dry cough, headache, auto-immune manifestations (due to cold agglutinins) causing an autoimmune haemolytic anaemia

c) Erythema multiforme (target-shaped skin legions); Stevens-Johnsons Syndrome, Guillain-Barré syndrome and meningoencephalitis

58
Q

Legionella pneumonia

a) Classification

c) Clinical features

d) What is it associated with?

e) Give 2 important investigations and their findings

f) CXR findings

A

a) Gram-negative

b) Fever, myalgia, malaise, dyspnoea and dry cough

c) Associated with Legionnaire’s disease, usually in patients who have been exposed to poor hotel air conditioning or unsanitary water

d)
- LFTs and U&Es - look for hyponatraemia and deranged LFTS
- Urinary antigen enzyme immunoassay - Legionella antigen may be present in the urine

f) Non-specific but show patchy or bi-basal consolidation, pleural effusions

59
Q

Chlamydophilia psittaci pneumonia

a) Classification

b) How is it acquired?

c) Clinical features

A

a) Intracellular gram-negative bacteria

b) Acquired from contact with infected birds such as parrots, cattle, horse and sheep

c) Diarrhoea, vomiting, lethargy, arthralgia, headache, anorexia, dry cough and fever + hepatitis, splenomegaly, nephritis, infective endocarditis, meningoencephalitis and a rash

60
Q

Pneumocystis jirovecii pneumonia

a) Classification

b) What type of patients is it associated with?

c) Clinical features

d) Diagnostic test and findings

A

a) Fungus

b) Immunosuppressed patients

c) Exertion dyspnoea, dry cough, fever

d) Silver stain - cyst walls or trophozoites can be detected

61
Q

Pseudomonas aerginosa pneumonia

a) Classification

b) Sputum colour

c) What patients is associated with

d) Clinical features

e) Treatment

A

a) Gram negative bacillus/rod (typically causes HAP)

b) Green

c) Immunosuppressed patients and those with chronic lung disease such as, patients with bronchiectasis (e.g., CF) –> cause CAP

d) Symptoms classically associated with pneumonia - fever, fatigue, productive cough etc

e) Cephlosporin and amino glycoside. Aerosolised antibiotics may be used in patients with cystic fibrosis.

62
Q

Complications of pneumonia

a) Pulmonary

b) Extrapulmonary

A
63
Q

Complications of pneumonia

a) Pulmonary

b) Extrapulmonary

A

a)
- Parapneumonic effusion
- Pneumothorax
- Abscess
- Empyema

b)
- Sepsis
- AF

64
Q

Investigations should not delay antibiotic treatment for pneumonia. When should antibiotics be administrated upon admission or diagnosis

A

Antibiotic treatment which should be administrated within 4 hours of admission or diagnosis (and < 1 hour where sepsis is suspected)

65
Q

Describe the investigations for pneumonia

A

Bedside
- Observations
- Sputum sample: for microscopy and culture
- Urinary sample: for MC&sS
- Urinary antigens: consider pneumococcal and legionella urianry antigen test to help guid antibiotics
- ECG

Bloods - FBC, U&Es, CRP and blood cultures

PCR - For mycoplasma pneumonia

Imaging - CXR

66
Q

Describe the CXR findings in pneumonia

A
  • Consolidation
  • May also show: parapneumonic effusions, pneumothorax, abscess and empyema
67
Q

Describe the role of the CRB-65 and CURB-65

A

CRB-65 = Calculated in primary care to assess severity of the infection and need for hospital admission

CURB-65 = calculated when patients present to hospital and helps establish best place of care

68
Q

a) What are the parameters of the CRB-65 score? and how much does each parameter score?

b) What do the scores mean?

A

a)
C- confusion
R - respiratory > 30
B - blood pressure < 90 SYS, or <60 DIA
65 - age > 65

b)

0: outpatient
1-2: secondary care
3: urgent admission

69
Q

a) What are the parameters of the CURB-65 score? and how much does each parameter score?

b) What do the scores mean?

A

a)
C- confusion
R - respiratory > 30
B - blood pressure < 90 SYS, or <60 DIA
65 - age > 65

b)

0-1: outpatient
2: secondary care
3: ICU

70
Q

Describe the supportive management of pneumonia

A

Oxygen - titrated sats to 94-98% and 88-92% if CO2 retainer

IV fluids

Analgesia - paracetamol, NSAIDs (with caution), opioids

71
Q

Antibiotic treatment for community-acquired pneumonia

a) Low severity

b) Intermediate severity

c) High severity

A

a) Oral therapy with a broad-spectrum beta-lactate (e.g., amoxicillin) for 5-7 days. A tetracycline or macrolide may be used in those with a penicillin allergy (doxycycline or clarithromycin)

b) Dual therapy with a becta-lactam e.g., amoxicillin) and a macrolide (e.g., clarithromycine) for 7-10 days. Doxycycline may be used as an alternative in those with penicillin allergy

c) IV beta-lactamase stable beta-lactam (e.g., co-amoxiclav) and a macrolide (e.g., clarithromycin) for 7-10 days. May be extended to 14 or 21 days depending on clinical circumstances

72
Q

Describe the management of hospital-acquired pneumonia

A
  • Should follow local guidelines based upon local microbial knowledge
  • Co-amoxiclav 625mg orally TDS may be used in mild infection
  • Tazocin (piperacillin/tazobactam) 4.5g IV TDS may be used in severe infection
73
Q

a) When should a CXR post-pneumonia be taken and in which type of patients?

b) What us the reason for this

A

a) A CXR at 6-8 weeks post-event in 50+

b) To screen for underlying lung cancers

74
Q

Prevention of infection

a) Primary

b) Secondary

c) Tertiary

A

a)
- Prevent or reduce exposure
- Immunisation (Pneumococcus, Influenza)

b)
- Chemoprophylaxis
- Contact tracing

c)
- Minimise disability arising from infection
- Effective treatment
- Physiotherapy

75
Q

Empyema

a) What is it?

b) How does it usually present in a patient with pneumonia

c) Diagnostic investigation

d) Management

A

a) When pus forms in the pleural space

b) Tends to present as either failure to recover fully with antibiotics alone or with a characteristic “swinging fever”

c) Pleural aspirate

d) Chest drain under radiological guidance

76
Q

What is tuberculosis?

A

TB is an infectious disease caused by bacteria of the mycobacterium tuberculosis complex

77
Q

Risk factors of TB

A

Ethnic minority groups (most commonly those from sub-Saharan Africa and South Asia). The risk is highest if returned from a high-prevalence country in last 5 years

The homeless - associated with overcrowding, poor living conditions and malnutrition

Drug and alcohol abuse - associated with overcrowding, poor living conditions, and malnutrition

Close contact with infected patient

Immunosuppression - results in reactivation of latent disease or primary military infection

Young or old - due to immature immune systems in the very young

78
Q

Describe 3 characteristics of mycobacterium tuberculosis

A

Obligate aerobes - require oxygen to grow

Facultative intracellular - can grow outside the cell but finds it advantageous to be intracellular

Acid fast bacilli (AFB) - resistant to decolorisation of staining by acid

79
Q

What are the 4 clinical paths of TB?

A
  1. Infection cleared
  2. Primary TB
  3. Progressive primary TB - when primary infection is nos suppressed and prolonged
  4. Post-primary TB (reactivation TB) - occurs in patients with latest TB
80
Q

Describe clinical feature of pulmonary TB

A

Asymptomatic

Triad: Cough, fever, weight loss

Night sweats

SOB

Haemoptysis

Failure of antibiotic therapy

81
Q

Describe the extra-pulmonary features of TB

A

Lymph-node TB
- Enlarged
- Firm
- Non-tender

Genitourinary TB
- ‘Sterile’pyuria
-

82
Q

Name the extra-pulmonary manifestations of TB

A

Lymph-node TB

Genitourinary TB

Miliary TB

CNS TB

Vertebral TB

Cutaneous TB

Adrenal TB

83
Q

Describe the extra-pulmonary features of TB

A

Lymph-node TB
- Enlarged
- Firm
- Non-tender

Genitourinary TB
- ‘Sterile’ pyuria
- Salpingitis
- Epididymo-orchitis
- Renal abscess

CNS TB
- TB meningitis: fever, malaise and headache

Vertebral TB - aka Potts syndrome
- Fever
- Weight loss
- Back pain
- Development of spinal deformities, typical kyphosis

Cutaneous TB
- Manifestations include: lupus vulgaris and scrofuloderma, erythema nodosum

Pericardial TB
- Pericardial effusions or constrictive pericarditis

Adrenal TB
- can cause Addison’s disease

Gastrointestinal TB
- can affect the intestines: terminal ileitis
- Peritoneal spread may lead to ascites

84
Q

What type of patients are screened for latent TB?

A
  • Contact risk
  • Immunocompromised
  • Prior to medication that may reactivated TB e.g., anti-TNF-alpha
  • New entrants to the UK from high-risk areas
  • NHS workers
85
Q

Describe the role of the mantoux/tuberculin

A

The mantoux test involves an intradermal injection of tuberculin, a purified protein derivative from M.tuberculosis

If a patient has had an exposure to TB, they exhibit a delayed (type IV) skin hypersensitivity reaction.

Diagnosis is based on the degree of the local epidermal reaction

Usually offered to contacts of infected patients

86
Q

What is the disadvantage of the mantoux/tuberculin test?

A

It is positive in those who have had the BCG vaccine

87
Q

Describe the role of the interferon-gamma release assay

A

It tests for the T-cell interferon-gamma response to M.tuberculosis antigens

88
Q

Interferon-gamma release assay

a) Advantages

b) Disadvantages

A

a)
- Results are obtained rapidly
- Not affected by prior BCG

b)
- Cannot tell difference between active and latent TB
- Not useful in very young or immunosuppressed

89
Q

Describe the investigations for the diagnosis of active tB

A
  • CXR
  • Sputum samples for microscopy and sensitivity
  • Samples from non-pulmonary sites
  • PCR
90
Q

a) How many sputum samples are needed for microscopy and sputum

b) What is seen after microscopy and sensitivity of sputum samples

A

a) at least 3

b) acid-fast bacilli (rod shaped) which is M.tuberculosis

91
Q

What type of vaccine is Bacilli Calmetter-Guerin (BCG)? and what does it protect against?

A

Live attenuate vaccine

Protects against tuberculosis and leprosy

92
Q

Describe the management of latent tB

A

6 months of isoniazid (with pyridine (6H)

OR

3 months of isoniazid (with pyridine and rifampicin (3H)

93
Q

Describe the management of active TB without CNS involvement

A

Rifampicin, Isoniazid (with pyridoxine), pyrazinamide and ethambutol for 2 months followed by rifampicin and isoniazid for a further 4 months - RIPE

94
Q

Describe the management of active TB with CNS involvement

A

Rifampicin and isoniazid (with pyridoxine) for 12 months whilst pyrazinamide and ethambutol are given for the first 2 months (2HRZE, 10HR).

offered dexamethasone or prednisolone at the start of treatment which is then weaned over 4-8 weeks

95
Q

Side effects of Rifampicin

A

Stains secretions pink, may cause hepatoxicity

96
Q

Side-effects of Isoniazid

A

Peripheral neuropathy (but these are rare at normal doses - it is given with pyridoxine which is a vitamin B6 replacement to reduce this risk), hepatotoxicity, optic neuritis, and gout

97
Q

How is peripheral neuropathy prevented when Isoniazid is given to treat TB?

A

By given it with pyridoxine

98
Q

Side-effects of pyrazinamide

A

May cause hepatotoxicity, gout

99
Q

Side-effects of ethambutol

A

Toxic optic neuropathy (optic retrobulbar neuritis) e.g., colour blindness, decreased visual acuity

100
Q

What is acute bronchitis?

A

Inflammation of airways

101
Q

What type organism is usually causes acute bronchitis

A

Viral

102
Q

Name 4 causative organisms of acute bronchitis

A
  • Rhinovirus
  • Parainfluenza
  • Influenzas A/B
  • Respiratory syncytial virus
  • Coronavirus
  • Human metapneumovirus
103
Q

Describe the presentation of acute bronchitis

A
  • Non-productive/minimally productive cough - accompanied/preced by URTI symptoms
  • Subjective dyspnoea due to chest pain tightness with breathing
  • Wheezing
  • Clear, purulent sputum
  • Mild fever
104
Q

What patients are at risk of acute bronchitis

A
  • Smokers
  • COPD
  • Cystic fibrosis
  • Conditions leading to bronchiectasis
105
Q

Describe the management of acute bronchitis

A

Symptomatic treatment
- Paracetamol
- Salbutamol

Antitussives - if cough interfering with sleep

Inhaled albuterol (B2 antagonist) or ipatropium (anti-cholinergic) - for patients wheezing

Inhaled corticosteroids - if cough persists > 2 weeks

Oral antibiotics
- (Amoxicillin 500mg PO 7 days/ Doxycycline 100mg PO 7 days) used in patients with pertussis OR COPD with at least 2 of…
1. Increased cough
2. Increased dyspnoea
3. Increased sputum purulence

106
Q

Describe the virus that causes influenza

A

Negative-sense, single-stranded RNA virus

107
Q

Name 5 at risk patients of influenza

A
  • The elderly (65+)
  • Young children
  • Pregnant women
  • Diabetics
  • Those with existing cardiovascular and respiratory conditions
  • Immunodeficiency
108
Q

Describe the presentation of influenza

A

Respiratory symptoms
- Congestion/runny nose
- Hoarse voice
- Non-productive cough
- Sore throat

General symptoms
- Headache
- Chills
- Shivering
- Malaise
- Fatigue
- Muscle aches
- Loss of appetite
- Fever

Gastrointestinal symptoms
- Gastroenteritis
- Diarrhoea
- Nausea
- Vomiting

109
Q

Describe the management of influenza

A
  • Conservative
  • Antiviral drugs (oral oseltamivir or inhaled zanamivir) indicated if influenza current known to be circulation AND are in an at-risk group
  • Free influenza vaccine for at-risk groups
110
Q

Define upper respiratory infections

A

Defined as an acute infection which involves the nasal cavity, pharynx, and larynx

111
Q

What is the most common cause of URTI?

A

Viruses, mainly rhinovirus

112
Q

What are the risk factors of URTI?

A
  • Close contact with children
  • Medical disorder: people with asthma and allergic rhinitis
  • Smoking
  • Immunocompromised individuals
  • Anatomical anomalies including facial dysmorphic changes or nasal polyposis
113
Q

Describe the presentation of URTIs

A
  • Acute URTIs include rhinitis, pharyngitis/tonsillitis and laryngitis. This also leads to sinusitis, ear infection and sometimes bronchitis
  • Nasal discharge
  • Nasal congestion
  • Sore throat
  • Cough
  • Headache
  • Low grade fever
  • Malaise
  • Colour or consistency changes in mucous discharge to yellow, thick or green are the natural course of a viral URTI and are not an indication for antibiotics
114
Q

How are URTIs diagnosed?

A

The presence of classical features for UTRI, coupled with absence of signs of bacterial infection or serious respiratory illness is sufficient to make a diagnosis of UTRI

Diagnostic test is not usually necessary

Rapid strep swabs can be used to rule out bacterial pharyngitis

115
Q

Describe the treatment of URTIs

A
  • Analgesia: paracetamol, ibuprofen
  • Decongestants can limit cough, congestion, and other symptoms in adults
  • Avoid cough preparations for children
  • Early antiviral treatment for high-risk patients
  • Influenza vaccination