Respiratory Flashcards
What is acute bronchitis?
Acute bronchitis is defined as a lower respiratory tract infection which causes inflammation in the bronchial airways.
It is a clinical diagnosis characterized by cough resulting from acute inflammation of the trachea and large airways but with no evidence of pneumonia.
What are the causes of acute bronchitis?
Acute bronchitis is usually caused by a viral infection. The most common viruses associated with acute bronchitis include
-rhinovirus,
-enterovirus,
-influenza A and B,
-parainfluenza,
-coronavirus,
-human metapneumovirus,
-respiratory syncytial virus, and adenovirus.
Bacteria are detected in between 1 in 100 and 1 in 10 cases, including
-Streptococcus pneumoniae,
-Haemophilus influenzae, and
-Moraxella catarrhalis.
What is the prognosis and what are the complications for acute bronchitis?
Is usually a mild, self-limiting illness.
The cough usually lasts about two to three weeks. Most people recover fully with no residual symptoms after an episode of acute bronchitis.
Around a quarter of people will have a cough for more than 4 weeks, and in some, cough will persist for up to 6 months (post-bronchitis syndrome).
Pneumonia may occur as a complication of acute bronchitis, particularly in older people.
What is the pathophysiology of acute bronchitis?
The symptoms of acute bronchitis are due to acute inflammation of the bronchial wall, which causes increased mucus production together with oedema of the bronchus. This leads to the productive cough that is the hallmark of a lower respiratory tract infection. While the infection may clear in several days, repair of the bronchial wall may take several weeks. During the period of repair, patients will continue to cough. Pulmonary function studies of patients with acute bronchitis demonstrate bronchial obstruction similar to that in asthma. As the symptoms of acute bronchitis abate, pulmonary function returns to normal.
Half of all patients with acute bronchitis continue to cough for >2 weeks. In a quarter of patients, cough may last for >1 month. This is termed post-bronchitis syndrome. This period probably reflects ongoing repair to the bronchial walls after the clearance of the acute infection.
How does acute bronchitis typically present?
Patients typically present with cough, which may be productive, and symptoms suggestive of bronchial obstruction (such as intermittent wheeze or dyspnoea). However, the key point is that the cough and bronchial obstructive symptoms are acute and related to other signs of a respiratory infection, such as rhinorrhoea, sore throat, and low-grade fever.
The physical examination may reveal signs of upper respiratory tract infection, such as coryza, nasal congestion, and pharyngeal hyperaemia. There may also be evidence of bronchial obstruction (which can include prolonged expiratory phase) and wheezing, which may be brought out by forced expiration in the prone position, or rhonchi.
How is acute bronchitis investigated?
Pulse oximetry — arrange urgent hospital admission for people who require supplemental oxygen.
C-reactive protein test — if the person has symptoms of a lower respiratory tract infection and a clinical diagnosis of pneumonia has not been made and there is uncertainty about whether antibiotics are indicated.
A chest X-ray if the person has suspected community-acquired pneumonia and they are at risk of underlying lung pathology (for example lung cancer) or the cause is uncertain — chest X-ray may be helpful to rule out pneumonia, but is not normally initially necessary for most people with suspected community-acquired pneumonia who are managed in primary care.
How is acute bronchitis managed?
-Self care: Fluids, antipyretics/analgesics, OTC cough medicines
-Smoking cessation
-Antibiotics (doxycycline or alternative amoxicillin, clarithromycin and erythromycin) ONLY if systemically unwell, at higher risk of complications or CRP>100
Bronchodilators, ICS and mucolytics are NOT indicated unless there is an underlying airway disease.
What is the pathophysiology of tuberculosis?
An infection disease caused by the acid-fast bacillus Mycobacterium Tuberculosis and characterised by the formation of nodular lesions (tubercles) in the tissues.
In pulmonary TB, the bacillus is inhaled into the lungs where it sets up a primary tubercle and spreads to the nearest lymph nodes, known as the primary complex. Natural immune defences may heal it at this stage but alternatively the disease may smoulder for months or years and fluctuate with the patients resistance. Only pulmonary disease is communicable. In some cases, the bacilli spread from the lungs to the bloodstream, setting up millions of tiny tubercles throughout the body (miliary tuberculosis), or it can migrate to the meninges and cause tuberculous meningitis. Bacilli entering by the mouth, usually through infected Cow’s milk, set up a primary complex in abdominal lymph nodes leading to peritonitis and sometimes spread to other organs joints and bones.
Active infection: occurs when containment by the immune system (T cells and macrophages) is inadequate. Can arise from primary infection or reactivation of previously latent disease.
Latent infection: infection without disease due to persistent immune system containment i.e granuloma formation prevents bacteria growth and spread. Positive blood and skin testing shows evidence of infection but the patient is asymptomatic, non-infectious and would have a normal sputum and CXR.
Lifetime risk of reactivation is 5-10%. Risk factors for reactivation are: if the infection is new (<2 years), HIV, Organ transplantation, immunosuppression including corticosteroids, silicosis, illicit drug use, high risk settings eg homeless shelter and prison, low socioeconomic status and haemodialysis.
What are the possible clinical manifest
How is TB investigated?
- Latent TB: offer testing to close contacts of pulmonary or laryngeal TB, immune dysfunction, healthcare workers and high risk populations (prisoners, migrants, homeless)
-Mantoux test: tuberculin skin test. Give intradermal injection of purified protein derivative tuberculin, size of skin induration determines positivity depending on vaccination history and immune status
-Interferon-gamma release assays (IGRAS): diagnoses exposure to TB by measuring the release of interferon gamma from T cells reacting to TB antigen. Higher specificity than skin testing if patient has had BCG vaccination.
Neither test can diagnose or exclude active disease, clinical evaluation is required. Immunosuppression decreases sensitivity of both tests - Active pulmonary TB:
-CXR: fibronodular or linear opacities in upper lobe (typical), cavitation, calcification, miliary disease, effusion and lymphadenopathy
-Sputum smear: can be spontaneously produced or induced with nebulised saline and precautions to prevent transmission. 3 specimens needed including early morning sample. Stained for AFB (all mycobacteria are acid fast). If AFB are seen, treatment should be commenced and the patient isolated.
-Sputum culture: more sensitive than smear, takes 1-3 weeks in liquid media or 6-8 weeks in solid media. Can be used to assess drug sensitivity
-Nucleic acid amplification test (NAAT): direct detection of M Tuberculosis in sputum by DNA or RNA amplification. Rapid diagnosis (< 8 hours) and can also detect drug resistance
Extrapulmonary TB:
-Investigate for coexisting pulmonary disease, obtain material for aspiration or biopsy from the lymph nodes or pleura or bone or synovium, or the GI or GU tract to enable AFB staining histological examination to look for caseating granuloma and/or culture.
-NAAT can be carried out on any sterile body fluid including CSF and pericardial fluid
How is TB managed?
- Rifampicin: 2 months intensive, 4 months continuation (enzyme inducer, care with Warfarin, oestrogen and phenytoin, colours body secretions orange, altered liver function)
- Isoniazid: 2 months intensive, 4 months continuation (inhibits formation of active pyridoxine (B6) which causes peripheral neuropathy so increased risk with diabetes, CKD, HIV or malnutrition so give with prophylactic B6, risk of hepatitis)
- Pyrazinamide: 2 months intensive (idiosyncratic hepatotoxicity, decrease dose if eGFR < 30)
- Ethambutol: 2 months intensive (colour blindness, decreased visual acuity, optic neuritis, check acuity at start of treatment and monitor throughout, monthly visual check if treatment > 2 months, careful if eGFR <30)
All forms of active TB are statutorily notifiable to public health.
What are the causes of community acquired pneumonia?
- Community-acquired pneumonia (CAP): may be primary or secondary to underlying disease. Typical organisms are
- Streptococcus pneumoniae (most common),
- Haemophilus influenzae,
- Moraxella catarrhalis.
Atypical:
- mycoplasma pneumoniae,
- Staphylococcus Aureus,
- Legionella species and
- Chlamydia.
Gram-negative bacilli and anaerobes are rarer. Viruses account for up to 15%
What are the causes of hospital-acquired pneumonia?
- Hospital-acquired pneumonia (HAP): defined as pneumonia developed > 48 hours after hospital admission. Most commonly gram-negative enterobacteria or Staphylococcus Aureus.
Also Pseudomonas Klebsiella bacteroides and Clostridia.
What are the causes of aspiration pneumonia?
- Aspiration pneumonia: those with stroke, myasthenia gravis, bulbar palsies, decreased consciousness eg post-ictal or intoxicated, poor dental hygiene and oesophageal disease (achalasia, reflux) risk aspirating oropharyngeal anaerobes
What are the clinical features of pneumonia?
KEY: Cough, Chest pain, Fever
SYMPTOMS:
-Symptoms of infection: fever, malaise, headaches, rigors
-Cough
-Chest pain (pleuritic)
-Anorexia
-Dyspnoea
-Purulent sputum
-Haemoptysis
SIGNS:
-Pyrexia
-Cyanosis
-Confusion (can be the only sign in the elderly)
-Tachypnoea
-Tachycardia
-Hypotension
-Signs of consolidation: reduced expansion, dullness to percussion, increased tactile vocal fremitus/ vocal resonance, bronchial breathing
-Pleural rub
How is pneumonia investigated?
-Assess oxygenation: oxygen saturation by pulse oximetry, test BP
-ABG: if saturation is less than 92% or if you suspect severe pneumonia
-Blood tests: FBC, U&E, LFT, CRP
-Chest Xray: look for lobar or multilobar infiltrates, cavitation, pleural effusion.
-Sputum test: for microscopy and culture
-Urine: check for legionella or pneumococcal urinary antigens
-Atypical organism and viral serology
-Pleural fluid: may be aspirated for culture
CURB-65
Assesses the severity of disease
Confusion: abbreviated mental test <8
Urea: >7mmol/L
Respiratory rate: >30/min
Blood pressure: <90 systolic and/or <60 diastolic
Age: >65
May underscore the young, clinical judgement necessary.
How is pneumonia managed?
Management is based on CURB-65 score:
0-1: oral antibiotics and home treatment
2: Hospital therapy
>3: Severe, indicates mortality 15-40%, consider ITU
ANTIBIOTICS
1. Community acquired:
Mild: not previously required treatment, CURB 0-1 (Strep pneumoniae, Haemophilus Influenzae)
-Treat with oral amoxicillin or clarithromycin or doxycycline (5 day course)
Moderate: CURB 2 (Strep pneumoniae, Haemophilus influenzae, mycoplasma pneumoniae)
-Oral amoxicillin AND clarithromycin or doxycycline (7 day course)
Severe: CURB >3 (Same organisms as for moderate)
-IV co-amoxiclav or cephalosporins (cefuroxime) AND clarithromycin IV (7 days)
-Add flucloxacillin +/- Rifampicin if Staph is suspected (10 days)
-Vancomycin if MRSA is suspected (10 days)
Atypical:
-Fluoroquinolone + clarithromycin or rifampicin only in Legionella pneumophila
-Tetracycline for Chlamydophila species
-High dose co-trimoxazole for Pneumocystis Jirovecii
- Hospital acquired: caused by gram negative bacilli, pseudomonas, anaerobes
-IV aminoglycosides (gentamicin) and anti-pseudomonal penicillin or 3rd generation cephalosporin - Aspiration pneumonia: Streptococcus pneumoniae and anaerobes
-IV cephalosporin AND IV metronidazole - Neutropenic patients:
-IV aminoglycosides and anti-pseudomonal penicillin or 3rd generation cephalosporin for gram positive cocci or for gram negative bacilli
-Consider anti-fungals after 48 hours in fungal infections
-Oxygen if required
-IV fluids in severe cases
-VTE prophylaxis
-Analgesia if pleurisy
-Consider ITU if shock, hypercapnia or persistently hypoxic. Follow up at 6 weeks with CXR
What is the aetiology of crohn’s disease?
Aetiology is unknown but there is some association with TB
Represents the outcome of 3 essential interacting cofactors:
- Genetic susceptibility: more genetic association than in UC
- Environment: Smoking increases risk twofold, stress and depression might precipitate relapses, invading bacteria might affect enteric microflora
- Host immune response: defective mucosal immune system produces an abnormal response to luminal antigens
What is the pathophysiology of crohn’s disease?
-Begins with crypt inflammation and abscesses which progress to tiny focal apthoid ulcers
-These mucosal lesions can develop into deep ulcers with intervening mucosal oedema creating a characteristic ‘cobblestoned’ appearance
-Transmural inflammatory spread leads to lymph oedema and thickening of bowel wall and mesentery. Mesenteric lymph nodes often enlarge
-Extensive inflammation may cause hypertrophy of the muscularis mucosa, fibrosis and stricture formation which can cause bowel obstruction
-Abscesses are common, fistulas often penetrate into adjoining structures including other loops of bowel, the bladder or the psoas muscle
-Granulomas can occur in lymph nodes, peritoneum, liver and all layers of bowel
-Segments of disease bowel are sharply demarcated from adjacent normal bowel, called ‘skip lesions’
What are the clinical features of Crohn’s disease?
KEY: Abdominal pain, Malabsorption, Diarrhoea and bleeding
SYMPTOMS: Depend on the region of bowel involved.
Small bowel: abdominal pain with weight loss, tiredness and fatigue
Colonic disease: Diarrhoea, bleeding, pain related to defecation
Peri-anal disease: anal tags, fissures, fistulae and abcess formation
Less commonly: Terminal ileal disease can present as an acute abdomen of right iliac fossa pain mimicking appendicitis
SIGNS: Tender abdomen, mass or fullness may be palpable, Anaemia, Fever
During flares: marked tenderness, guarding, rebound tenderness
Stenotic segments may cause bowel obstruction with associated colicky pain, distension, obstipation and vomiting
