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Phase 2A > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What is tuberculosis?

A

an infectious disease caused by the mycobacterium tuberculosis bacteria

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2
Q

What is the most common cause of TB?

A

mycobacterium tuberculosis is the most common causative organism and is an aerobic acid-fast bacilli which is turned bright red against a blue background using the Ziehl-Neelson stain

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3
Q

What are some other mycobacteria which cause TB?

A

M. africans
M. microtis
M.bovis

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4
Q

What are the risk factors for TB?

A

Immunocompromised (e.g. HIV or immunosuppressive meds)
Close contacts with TB
Recent travel or immigration from areas of high TB prevalence
People with relatives or close contacts from countries with a high rate of TB
Homeless people, drug users, alcoholics
IVDU
Older age

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5
Q

What is active TB?

A

active infection in various areas within the body

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6
Q

What is latent TB?

A

where the immune system encapsulates sites of infection and stops the progression of disease

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7
Q

What is miliary TB>

A

severe, disseminated disease when the immune system is unable to control the spread/progression

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8
Q

What is extrapulmonary TB?

A

When infection spreads outside of the lungs (most common site of infection) to lymph nodes, pleura, CNS, pericardium, GI system, GU system, bones + joints, skin (cutaneous TB)

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9
Q

What is the immune response to TB?

A
  1. TB phagocytosed but resist killing –> formation of granulomas
  2. T cells are recruited and central region of granuloma undergoes caseating necrosis (primary Ghon focus, in upper parts of the lung)
  3. Ghon focus spreads to nearby lymph nodes –> Ghon complex (focus + lymph node spread)
  4. in most cases, infection is contained within granulomas –> latent TB
  5. If TB spreads systemically –> miliary TB
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10
Q

What are the key presentation sof TB?

A

chronic, gradual onset of symptoms
lethargy
fever or night sweats
weight loss
cough +/- haemoptysis
lymphadenopathy
erythema nodosum
spinal pain in spinal TB (Pott’s disease of spine)

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11
Q

What are the investigations for TB?

A

1st line: Purified Protein Derivative (PPD) - intradermal skin test which looks for previous immune response to TB
GS: Interferon Gamma Release Assay
Other: CXR , cultures

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12
Q

What are the CXR signs of primary TB?

A

patchy consolidation, pleural effusions and hilar lymphadenopathy

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13
Q

What are the CXR signs of reactivated TB?

A

patchy or nodular consolidation with cavitation typically in the upper zones, disseminates

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14
Q

What are the CXR signs of miliary TB?

A

‘millet seeds’ distributed uniformly throughout the lung fields

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15
Q

What are the 4 drugs used to treat acute pulmonary TB?

A

R - rimfampicin (6mo)
I - isoniazid (6mo)
P - pyrazinamide(2mo)
E- ethambutol (2mo)

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16
Q

What is TLCO?

A

Total lung diffusion capacity for carbon monoxide - shows how much carbon monoxide is taken into body during inhalation/exhalation

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17
Q

What is the BCG vaccination?

A

intradermal infection of live attenuated Tb which offers protection against severe and complicated TB but is less effective at protecting against pulmonary TB (for patients at higher risk of contact with TB)

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18
Q

What is pneumonia?

A

infection of the lung tissue which causes inflammation of the lung tissue and sputum filing the airways and alveoli

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19
Q

What are the causes of pneumonia?

A

streptococcus pneumoniae (50%)
haemophilus influenzae (20%)
moraxella catarrhalis (in immunocompromised patients/pts with chronic disease)
pseudomonas aeruginosa (pts with CF or bronchiectasis)
staphylococcus aureus (pts with CF)

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20
Q

What are the risk factors for pneumonia?

A

Bronchiectasis
Asthma
Cystic fibrosis
COPD
Malnutrition
Diabetes
Heart failure
Sickle cell disease
Liver or kidney disease
Hospitalisation
Older age

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21
Q

What is pleuritic chest pain?

A

pain on deep inspiration (feels like sandpaper on lungs during breathing)

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22
Q

What is the definition of hospital acquired pneumonia?

A

pneumonia which develops more than 48hrs after hospital admission

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23
Q

What are the key presentations of pneumonia?

A

Shortness Of breath
Cough productive of sputum
Fever
Haemoptysis (coughing up blood)
Pleuritic chest pain (sharp chest pain worse on inspiration)
Delirium (acute confusion associated with infection)
Sepsis

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24
Q

What are the signs of pneumonia?

A

Tachypnoea
Tachycardia
Hypoxia
Hypotension
Fever
Confusion

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25
Q

What are the characteristic chest signs of pneumonia?

A

Bronchial breath sounds = harsh breath sounds equally loud on expiration and inspiration caused by consolidation of the lung tissue around the airway
Focal coarse crackles = air passing through sputum in the airways
Dullness to percussion due to lung tissue collapse and/or consolidation

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26
Q

What are the investigations for pneumonia?

A

CURB 65, CXR, FBC, U+Es, CRP
Sputum cultures, blood cultures, legionella and pneumococcal urinary antigens

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27
Q

What are the implications of CURB 65 scores 0-5?

A

0-1 = mild, only admit if social circumstances or single worrying feature
2 = moderate, admit to hospital
3-5 = severe, admit and monitor closely
4-5 = consider admission to critical care unit

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28
Q

What are the mortality percentages for CURB 65 scores?

A

0=0.7%
1=2.1%
3=9.2%
4-5=15-40%

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29
Q

What is the management for pneumonia?

A

Mild CAP = 5 day course of oral antibiotics (amoxicillin or macrolide)
Moderate - severe CAP = 7-10 day course of dual antibiotics (amoxicillin and macrolide)

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30
Q

What are the potential complications of pneumonia?

A

sepsis, pleural effusion, empyema, lung abscess, bronchiectasis, death

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31
Q

What is CURB-65?

A

An algorithm for assessment of pneumonia severity
C - confusion (new disorientation in person, place or time)
U - urea >7
R - respiratory rate ≥ 30
B - blood pressure <90 systolic or ≤ 60 diastolic
65 - age ≥ 65

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32
Q

What is cystic fibrosis?

A

autosomal recessive genetic condition affecting mucus glands which has multi-systemic effects

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33
Q

What is the prevalence of CF in children?

A

1 in 2500

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34
Q

What is the aetiology of CF?

A

Caused by a mutation of the CF transmembrane conductance regulatory gene on chromosome 7 (CFTR)
There are many variants of this mutation, the most common being delta-F508 mutation which codes for cellular channels, particularly a type of chloride channel

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35
Q

What are the risk factors for CF?

A

FHx
Caucasians

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36
Q

What are is the pathophysiology of CF?

A

Thick pancreatic and biliary secretion which cause blockage of the ducts, resulting in a lack of digestive enzymes such as pancreatic lipase in the digestive tract
Low volume thick airway secretions that reduce airway clearance, resulting in bacterial colonisation and susceptibility to airway infections
Congenital bilateral absence of the vas deferens in males

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37
Q

What are the key presentations of CF?

A

Meconium ileus (seen in 20% of babies with CF)
Recurrent lower respiratory tract infections
Failure to thrive (poor weight and height gain)
Pancreatitis
Chronic cough
Thick sputum production
Recurrent respiratory tract infections
Loose, greasy stools (steatorrhoea) due to a lack of fat digesting lipase enzymes
Abdo pain and bloating

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38
Q

What are the signs of CF?

A

Very salty sweat
Nasal polyps
Finger clubbing
Crackles and wheezes on auscultation
Abdominal distension

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39
Q

What are the investigations for CF?

A

Newborn blood spot testing
GS: Sweat test (pilocarpine patch and electrodes used to test chloride concentration) - >60mmol/L = CF
Genetic testing CFTR gene can be performed during pregnancy by amniocentesis or chorionic villous sampling

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40
Q

What is the management for CF?

A

Chest physiotherapy (multiple times daily)
Exercise → improved resp function + reserve, helps clear sputum
High caloric diet
CREON tablets to digest fats in patients with pancreatic insufficiency
Prophylactic flucloxacillin
Treat chest infections
Bronchodilators (salbutamol inhalers)
Nebulised DNase (enzyme which breaks down DNA material in secretions → easier to clear)
Nebulised hypertonic saline
Vaccinations for pneumcoccal, influenza, varicella
Lung transplant in ESRespF
Liver transplant in liver failure
Fertility treatment involving testicular sperm extraction for infertile males

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41
Q

What are some common infections in CF patients?

A

S. aureus
H. influenzae
P. aeruginosa

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42
Q

What are the complications of CF?

A

90% CF patients develop pancreatic insufficiency
50% develop diabetes
30% develop liver disease
Most males are infertile due to absent vas deferens

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43
Q

What is bronchiectasis

A

permanent dilation of bronchioles (+ excessive mucus in them)

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44
Q

What are the causes of bronchiectasis?

A

Recurrent pulmonary infection leads to progressive bronchial damage
Post infectious (18% of adult patients)
COPD (15% of adult patients)
Asthma (7%)
Connective tissue disorders (9%)
Allergic bronchopulmonary aspergillosis (5%)
Immunodeficiency (5%)
Aspiration or inhalation injury (4%)
Genetic
IBD
Focal bronchial obstruction
Idiopathic (29%)
Other (e.g. Marfan, Ehlers-Danlos…)

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45
Q

What are the risk factors for bronchiectasis?

A

Post infection (e.g. TB, pneumonia)
CF
HIV
ABPA (allergic bronchopulmonary aspergillosis - fungal infection of lung)
Congenital airway disorders

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46
Q

What is the pathophysiology of bronchiectasis ?

A

Irreversible dilation, loss of cilia + mucus hypersecretion ↑risk of infection (as ↓mucociliary clearance)

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47
Q

What are the key presentations of bronchiectasis?

A

Productive cough with lots of sputum + dyspnoea
Fever
Fatigue
Haemoptysis
Wheezing

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48
Q

What are the signs of bronchiectasis on auscultation?

A

Crackles, high pitched inspiratory squeaks and rhonchi (low pitched wheezes)

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49
Q

What is the management for bronchiectasis?

A

Non-curative
conservative : chest physio (+stop smoking)
Drug: bronchodilators
Consider abx if infection

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50
Q

What is pleural effusion?

A

Collection of fluid in the pleural cavity which can be exudative (high protein count >35g/L)
Or transudative (lower protein count <35g/L)

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51
Q

What are the exudative causes of pleural effusion?

A

Exudative causes are related to inflammation which leads to protein leakage out of tissue into the pleural space:
Lung cancer
Pneumonia
Rheumatoid arthritis
Tuberculosis

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52
Q

WHat are the transudative causes of pleural effusion?

A

Transudative causes relate to fluid moving across into the pleural space:
Congestive cardiac failure
Hypoalbuminemia
Hypothyroidism
Meigs syndrome

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53
Q

What are the key presentations of pleural effusion

A

SOB
Dullness to percussion over the effusion
Reduced breath sounds
Tracheal deviation away from the effusion if it’s massive

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54
Q

What are the signs of pleural effusion?

A

Reduced chest wall expansion
Quiet breath sounds
Stony dull percussion
Reduced tactile/vocal fremitus
Mediastinal shift away from affected side

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55
Q

WHat are the investigations for pleural effusion?

A

CXR (blunting of costophrenic angle, fluid in the lung fissures, larger effusions have a meniscus, tracheal and mediastinal deviation)
Thoracocentesis (sample of pleural fluid, pH, lactate, WCC, microscopy, transudate or exudate)

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56
Q

What are the signs seen on CXR in pleural effusion?

A

Blunting of costophrenic angle
Fluid in the lung fissures
Larger effusions have a meniscus
Tracheal and mediastinal deviation

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57
Q

What is Light’s criteria?

A

measurements of a number of factors including protein used to show whether pleural effusion is transudative or exudative)

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58
Q

What are the different appearances of fluid aspirate taken from lungs in pleural effusion and what do they indicate?

A

Straw coloured/clear - transudate/exudate
turbid /foul smelling - empyema/parapneumonic effusion
Milky - chylothorax
Blood stained - trauma/cancer/PE
Food particles - esophageal rupture

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59
Q

What is the management for pleural effusion?

A

Conservative ; small effusions will resolve with treatment of the underlying cause
Pleural aspiration (needle into lungs to remove fluid)
Chest drain (drain the effusion, prevents recurrence)

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60
Q

What is empyema?

A

infected pleural effusion
- suspected when the patient has improving pneumonia but new or ongoing fever
- plueral effusion shows pus, acidic pH, low glucose and high LDL

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61
Q

What is the treatment for empyema?

A

chest drain to remove pus
6 weeks antibiotics

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62
Q

What is the treatment for malignant effusions?

A

depends on symptoms, treatment for underlying cancer and prognosis
drain + pleurodesis –> chest drain (talc via drain), thoracoscopy (spray talc)
if recurrent and problematic –> indwelling pleural catheter

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63
Q

WHat is haemothorax?

A

blood in pleural cavity

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64
Q

What are the causes of haemothorax?

A

trauma, post-operative, bleeding disorders, lung cancer, PE, aortic rupture, thoracic endometriosis

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65
Q

What is the management for haemothorax?

A

large bore chest drain, possible vascular intervention, surgical opinion

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66
Q

What is hydropneumothorax?

A

air and fluid in pleural space

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67
Q

WHat are the causes of hydropneumothorax?

A

iatrogenic, gas forming organisms, thoracic trauma

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68
Q

What is pneumomediastinum?

A

where air from the lungs/trachea/oesophagus escapes into neck/face and abdomen

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69
Q

What causes pneumomediastinum?

A

surgical emphysema/pneumothorax
oesophageal rupture (Boerhaave’s syndrome)

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70
Q

What are the causes of pleural thickening?

A

related to asbestos exposure
following infection/empyema/chest trauma/haemothorax
cancer (consider if nodular /1 cm depth)

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71
Q

What is pneumothorax?

A

excess air accumulation in the pleural space, causing ipsilateral collapse

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72
Q

What is the aetiology of pneumothorax?

A

Can be primary (spontaneous (rupture of apical pleural bleb), no underlying cause) or secondary (to trauma or pathology)

Secondary pathological causes:

Known lung disease
-60% COPD
-Asthma/ILD/CF/Lung cancer
-Cystic lung disease

Infection
-PCP/TB
-lung abscess

Genetic predisposition
-Marfan’s syndrome, Birt-Hogg Dube
-LAM - Lymphangioleiomyomatosis

Catamenial Pneumothorax

Traumatic causes:
Penetrating chest wall injury
Puncture from rib
Rupture bronchus/oesophagus

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73
Q

What are the risk factors for primary spontaneous pneumothorax?

A

male, smokers, tall, age 20-40yrs, previous occurrence

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74
Q

What is the pathophysiology of pneumothorax?

A

Pleural space is normally a vacuum (no air)
Breach in pleura (trauma/CT disorders) e.g. subpleural bullae burst –> fistula between pleural space + airways → air in the pleural space
THis causes intrapleural pressure to be negative which leads to air being sucked into cavity leading to partial or total lung collapse

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75
Q

What are the key presentations in pneumothorax?

A

SOB
One sided sharp pleuritic chest pain
Decreased breath sounds
Hyperresonant percussion ipsilaterally (increased air)
Can be asymptomatic

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76
Q

What are the signs of pneumothorax?

A

Often no clinical signs except in severe cases
Tachypnoea
Hypoxia
Unilateral chest wall expansion
Reduced breath sounds
Hyper-resonant percussion note
Red flags (tension pneumothorax)
Deviated trachea
Surgical emphysema
Distended neck veins
Cardiovascular compromise

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77
Q

WHat are is the management for pneumothorax?

A

Small = self-resolving
Larger - needle decompression (remove air with syringe), chest drain
Surgical (if recurrent) - pleurodesis (insertion of a mildly irritant drug into pleural space to close space and prevent further collection of air or fluid)

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78
Q

What is tension pneumothorax?

A

air can flow into pleural space but can’t leave –> intrapleural pressure increases with every breath (can even press on heart –> cardiac disorder symptoms)

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79
Q

What are the signs of a tension pneumothorax?

A

tracheal deviation away from side of pneumothorax, reduced air entry to affected side increased resonance to percussion on affected side, tachycardia, hypotension

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80
Q

What is the treatment for tension pneumothorax?

A

insert large bore cannula into 2nd intercostal space at the midclavicular line, needle decompress and then chest drain

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81
Q

What forms the triangle of safety for chest drains?

A

The 5th intercostal space (inferior nipple line)
Mid-axillary line (or the lateral edge of the latissimus dorsi)
Anterior axillary line (lateral edge of the pectoralis major)

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82
Q

What is pulmonary hypertension?

A

Resting mPAP >25mmHg measure with right heart catheterisation
*often results in RHS heart failure; cor pulmonale

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83
Q

What are the causes of pulmonary hypertension?

A

Pre-capillary → pulmonary emboli, primary pulmonary hypertension
Capillary + lung → COPD, asthma
Post-capillary → LV failure
Chronic hypoxemia → COPD, altitude

84
Q

What is the pathophysiology of pulmonary hypertension?

A

Increasing the pressure and resistance in the pulmonary arteries causes strain on the right side of the heart trying to pump blood through the lungs which also causes a back pressure of blood into the systemic venous system → RVH + dilated pulmonary arteries

85
Q

What are the key presentations of pulmonary hypertension?

A

SOB
Syncope
Tachycardia
Raised JVP
Hepatomegaly
Peripheral oedema

86
Q

WHat are the investigations for pulmonary hypertension?

A

ECG (RVH→ larger R waves (V1-V3) and S waves (V4-V6), right axis deviation, RBBB)
GS: CXR (dilated pulmonary arteries, RVH)
NT-proBNP blood test (raised)
Echo

87
Q

What is the management for pulmonary hypertension?

A

Primary:
IV prostanoids (e.g. epoprostenol)
Endothelin receptor antagonists (e.g. macitentan)
Phosphdiesterase-5 inhibitors (e.g. sildenafil)

Secondary:
Treat underlying cause

Supportive treatment for complications e.g. resp failure, arrhythmias and heart failure

88
Q

What is the prognosis for pulmonary hypertension”

A

30-40% 5yr survival rate

89
Q

What is pulmonary fibrosis?

A

thickening or scarring of the lung tissue, the most common interstitial lung disease

90
Q

What are the risk factors for pulmonary fibrosis?

A

Smoking
Occupational (e.g. dust)
Drugs (methotrexate)
Viruses (EBV, CMV)

91
Q

What are the key presentations of pulmonary fibrosis?

A

Exertional dyspnoea
Dry unproductive cough

92
Q

What are the investigations for pulmonary fibrosis?

A

Spirometry = restriction (FEV1:FVC >0.7) but FVC ↓ (<0.8 normal)
High res CT (chest) → ground glass lungs + traction bronchiectasis

93
Q

What is the management for pulmonary fibrosis?

A

Smoking cessation + vaccines
pirfenidone , nintedanib
Surgery (lung transplant)

94
Q

What is sarcoidosis?

A

Idiopathic granulomatous inflammatory disease

95
Q

What are the risk factors for sarcoidosis?

A

Female
20-40yrs
Afrocaribbean

96
Q

What is the pathophysiology of sarcoidosis?

A

Granulomas are nodules of inflammation full of macrophages which can occur in almost any organ in the body (most commonly lungs)
Symptoms vary dramatically from asymptomatic (up to 50%) to severe + life-threatening

97
Q

What are the key presentations of sarcoidosis?

A

fever , fatigue
Resp = dry cough; dyspnoea
Other = eye lesions (uveitis), lupus pernio (blue + red nodules on nose + cheeks)

98
Q

What is Lofgren’s syndrome?

A

A specific presentation of sarcoidosis characterised by: Erythema nodosum, lymphadenopathy, polyarthralgia

99
Q

What are the investigations for sarcoidosis?

A

CXR (staging 1-4) → bilateral hilar adenopathy + pulmonary infiltrates
GS: Lung biopsy → non-caseating granuloma
↑Serum Ca2+, ↑serum ACE, hypercalcaemia

100
Q

What are the differential diagnoses for sarcoidosis?

A

Tuberculosis, lymphoma, hypersensitivity pneumonitis, HIV, toxoplasmosis, histoplasmosis

101
Q

What is the management for sarcoidosis?

A

Early stages are self-resolving
Symptomatic patients → corticosteroids
2nd line options: methotrexate or azathioprine

102
Q

What is the prognosis for sarcoidosis?

A

60% spontaneously resolve in 6 months, can progress with pulmonary fibrosis and pulmonary hypertension potentially requiring a lung transplant

103
Q

WHat is hypersensitivity pneumonitis

A

Type III hypersensitivity reaction to an environmental allergen which causes parenchymal inflammation and destruction in people that are sensitive to that allergen

104
Q

What are some examples of hypersensitivity pneumonitis

A

Bird fancier’s lung - caused by proteins in bird feathers or droppings
Farmer’s lung - caused by mould which grows on hay, straw and grain
Hot tub lung - caused by bacteria in water vapour from hot tubs
Humidifier lung - caused by fungi and bacteria in humidifiers, heating and air con systems

105
Q

What is the aetiology of hypersensitivity pneumonitis?

A

Over 300 known causes including:
Bacteria
Moulds and fungi
Certain chemicals and metals
Animal and plant proteins

106
Q

What are the risk factors for hypersensitivity pneumonitis?

A

Occupation (e.g. farming), bird keeping
50-70 yrs

107
Q

What are the key presentations of acute hypersensitivity pneumonitis?

A

SOB
Dry cough
Chest tightness
Chills
Fatigue
Fever
Muscle aches

108
Q

What are the symptoms of chronic hypersensitivity pneumonitis?

A

SOB
Cough
Fatigue
Weight loss
Finger or toe clubbing

109
Q

WHat are the investigations for hypersensitvity pneumonitis?

A

Bronchoscopy + broncheolar lavage (shows lymphocytes and mast cells)
Allergy blood tests
Imaging (CXR, CT)
Lung function tests

110
Q

What is the management for hypersensitivity pneumonitis?

A

Remove allergen, give oxygen and steroids
Anti-fibrotic drugs (slow lung scarring)
Oxygen therapy
Pulmonary rehabilitation
Lung transplant

111
Q

What is pharyngitis?

A

Inflammation of the pharynx +/- exudate

112
Q

What is the aetiology of pharyngitis?

A

Viral (EBV, adenoviruses) - 70-80%
Bacterial (group A B-haemolytic strep (GAS); S. pyogenes)
Fungal

113
Q

What are the key presentations of pharyngitis?

A

Sore throat
Fever
Viral = + cough + nasal congestion
Bacterial = + exudate
headache

114
Q

What are the investigations for pharyngitis?

A

Rapid antigen test for group A strep
Nucleic acid amplification for group A strep

115
Q

What is the management for pharyngitis?

A

generally self-limiting
analgesia
OTC medications
antibiotics for bacterial

116
Q

What is sinusitis? and what are the 4 types

A

Inflamed mucosa of nasal cavity and nasal sinuses
Acute ≤4 weeks
Subacute 4-12 weeks
Chronic ≥12 weeks
Recurrent acute ≥4 episodes per year

117
Q

What is the aetiology of sinusitis?

A

Mostly viral (<10 days, non purulent discharge)
Sometime bacterial - S.pneumococcus (40%), H. influenzae (30%)

118
Q

What are the risk factors for sinusitis?

A

viral URTI
allergic rhinitis

119
Q

WHat is the pathophysiology of sinusitis?

A

Most likely to be caused by the interaction of a predisposing condition (e.g. environmental triggers), a viral infection, and a consequent inflammatory response with the sinonasal mucosa

With increased oedema and mucus production, the sinus ostium is obstructed, blocking normal ventilation and drainage of the sinus.

With decreased mucociliary clearance, stasis of secretions occurs and a secondary bacterial infection can take place

120
Q

What are the key presentations of sinusitis?

A

Purulent nasal discharge
Nasal obstruction
Facial pain/pressure

121
Q

What are some other symptoms of sinusitis?

A

Cough
Myalgia
Sore throat
Hyposmia
Oedematous turbinate
Fever

122
Q

What is the management for sinusitis?

A

Generally self-limiting
Treatment is primarily symptomatic

123
Q

What is otitis media?

A

Infection involving the middle ear space which is a common complication of viral respiratory illnesses

124
Q

What are the risk factors for otitis media?

A

Young age
FHx
Native american or native alaskan
Lower socioeconomic status
Craniofacial anomaly
Immunological deficiency

125
Q

What is the pathophysiology of otitis media?

A

Upper respiratory viruses can infect the nasal passages, eustachian tube and middle ear, causing inflammation and impairing the mucociliary action and ventilatory function of the eustachian tube → development of OM

Middle ear effusion develops and nasopharyngeal bacteria contaminate the effusion

Suppuration and subsequent pressure against the tympanic membrane lead to pain and fever, which are typical symptoms of OM

126
Q

What are the key presentations of OM

A

Otalgia (ear pain)
Preceding upper resp symptoms
Bulging tympanic membrane
Myringitis

127
Q

What are some other symptoms of OM?

A

Irritability
Sleep disturbance
Fever
Decreased appetite

128
Q

What is the management of OM?

A

Analgesia
Some patients may require antibiotic therapy

129
Q

What is acute epiglottitis?

A

Infection of the supraglottis which can result in airway compromise

130
Q

What is the aetiology of acute epiglottitis?

A

infection of the supraglottis which can result in airway compromise

131
Q

What are the causes of epiglottitis>

A

Most common: H.influenzae
Also Strep penumoniae, S. aureus, MRSA

132
Q

What is the pathophysiology of acute epiglottitis?

A

Inflammatory pathways lead to localised oedema of the airway, exponentially increasing airway resistance while narrowing the effective supraglottic aperture
The glottis is usually not inflamed or affected as the process affects the supraglottic structures

133
Q

What are the key presentations of acute epiglottitis?

A

tripoding (leant forard, mouth open + tongue out = max air in)
sore throat
SOB
dysphagia
acute distress
fever

134
Q

What are the investigations for acute epiglottitis?

A

GS: Laryngoscopy
Lateral XR radiograph (thumbprint sign), FBC, cultures of blood/supraglottis

135
Q

What is the management for acute epiglottitis?

A

ABC - secure airway
Oxygen
Intravenous antibiotics
Corticosteroids if needed

136
Q

What is croup?

A

Complication of upper respiratory tract infection characterised by sudden onset barking cough

137
Q

What is the aetiology of croup?

A

Due to viral infection
Often accompanies parainfluenza/measles infection

138
Q

What are the risk factors for croup?

A

Children 6 months-6years
Male
Prior intubation

139
Q

What is the pathophysiology of croup?

A

Symptoms result from upper-airway obstruction due to generalised inflammation and oedema of the airways.

At the cellular level this progresses to necrosis and shedding of the epithelium

Narrowed subglottic region is responsible for the symptoms of seal-like barky cough, stridor (from increased airflow turbulence), and sternal/intercostal indrawing

If the upper airway obstruction worsens, respiratory failure can result, leading to asynchronous chest and abdominal wall motion, fatigue, hypoxia, and hypercapnia

140
Q

What are the key presentations of croup?

A

Hoarse voice
Barking cough
Stridor
Abrupt onset of symptoms
Respiratory distress
Fatigue
Signs of hypoxia/hypercapnia in severe cases

141
Q

What is the management for croup?

A

Single dose of dexamethasone
Supportive care

142
Q

What is whooping cough?

A

Chronic cough caused by Bordetella pertussis (gram -ve bacillus)

143
Q

What are the risk factors for whooping cough?

A

unvaccinated/under-vaccinated
<5y/o
close contact with infected person

144
Q

What is the pathophysiology of whooping cough?

A

bordatella ↑↑virulence
- haemaglutinin + fimbriae adhere to URT
- adenylate cyclase toxin inhibits phagocyte chemotaxis
- pertussis toxin inhibits alveolar macrphages

145
Q

What are the key presentations of whooping cough?

A

Pertussis typically starts with mild coryzal symptoms (low grade fever and mild, dry cough)
Paroxysmal cough starts after a week + (sudden and recurring attacks of coughing)
Loud inspiratory whooping sound between coughs (forceful sucking in of air)
Patient can cough so hard they faint, vomit or even develop pneumothorax
Can present with apnoeas rather than cough

146
Q

What are the investigations for whooping cough?

A

Nasopharyngeal or nasal swab with PCR testing or bacterial culture can confirm the diagnosis within 2 to 3 weeks of symptom onset
If cough present for 2+ weeks - anti-pertussis toxin immunoglobulin G

147
Q

What is the management for whooping cough?

A

supportive care
macrolide antibiotics (azithromycin, erythromycin, clarithromycin)

148
Q

What are the primary metastasis sites of lung cancer?

A

bone, liver, adrenals, brain, lymph nodes

149
Q

What are the types of non-small cell cancer affecting the lung parenchyma?

A

squamous, adenocarcinoma, carcinoid, large cell

150
Q

What is mesothelioma?

A

malignancy affecting the mesothelial cells of the pleura which is strongly linked to asbestos inhalation

151
Q

What are the risk factors for mesothelioma?

A

male
50-80 yrs
asbestos exposure
radiation exposure
genetic predisposition

152
Q

What is the pathophysiology of mesothelioma?

A

Suggested that exposure to asbestos fibres results in recruitment and activation of alveolar macrophage and neutrophils with subsequent generation of reactive oxygen and nitrogen species
Chronic inflammation and oxidative stress may culminate in DNA damage alterations in gene expression, and eventually malignant transformation

153
Q

What are the key presentations of mesothelioma?

A

Cancer symptoms: weight loss, night pain, fatigue
SOB
Cough
Pleuritic chest pain
Haemoptysis
Finger clubbing
Recurrent pneumonia
Lymphadenopathy

154
Q

What are the investigations for mesothelioma?

A

CXR + CT (pleural thickening), CA-125 (non-specifically raised in many tumours, sensitive but not specific)
GS: lung biopsy

155
Q

What is the management for mesothelioma?

A

Very aggressive tumour so tx normally palliative
If found early can try surgery + chemotherapy (but generally resistant)

156
Q

What occurs in restrictive lung diseases?

A

Expansion of the lung is reduced due to:
1. altered lung parenchyma
2. pleural disease
3. neuromuscular disease
4. chest wall disease

157
Q

What are the common obstructive ventilatory disorders or “airways diseases”?

A

COPD
Asthma
Bronchiectasis
Cystic fibrosis

158
Q

What is dyspnoea?

A

shortness of breath or breathlessness

159
Q

What is the MRC dyspnoea scale?

A

Assessment tool for degree of baseline functional disability due to dyspnoea

160
Q

What are the categories in the MRC dyspnoea scale?

A

0 - no breathlessness except with strenuous exercise
1 - shortness of breath when hurrying on the level or walking up a slight hill
2 - walks slower than people of the same age on the level because of breathlessness or has to stop for breath when walking at own pace on the level
3 - stops for breath after walking about 100m or after few minutes on the level
4 - too breathless to leave the house or breathless when dressing or undressing

161
Q

What are the common causes of dyspnoea?

A

asthma
heart failure
myocardial ischaemia
COPD
interstitial lung disease
pneumonia
psychogenic disorders

162
Q

What is type 1 respiratory failure?

A

associated with damage to lung tissue which prevents adequate oxygenation of the blood (hypoxaemia) but the remaining normal lung is still sufficient to excrete CO2.
=> low O2, normal or low CO2, PaO2 <8kPa (low) and normal or low PaCO2

163
Q

WHat is type 2 respiratory failure?

A

when alveolar ventilation is insufficient to excrete the CO2 being produced. Inadequate ventilation is due to reduced ventilatory effort or inability to overcome increased resistance to ventilation. It affects the lung as a whole and therefore CO2 accumulates
=> low or normal PaO2 and PaCO2 >6.0kPa (hypercapnia)

164
Q

What are the signs and symptoms specific to type 1 respiratory failure (hypoxaemia)?

A

dyspnoea, irritability
confusion, somnolence, fits
tachycardia, arrythmia
tachypnoea
cyanosis

165
Q

What are the signs and symptoms specific to type 2 respiratory failure?

A

headache
change of behaviour
coma
papilloedema
warm extremities

166
Q

Which respiratory conditions cause T1 respiratory failure?

A

pulmonary oedema
pneumonia
COPD
asthma
acute respiratory distress syndrome
chronic pulmonary fibrosis
pneumothorax
pulmonary embolism
pulmonary hypertension

167
Q

Which conditions cause T2 respiratory failure

A

COPD (mc)
chest-wall deformities, respiratory muscle weakness
CNS depression
severe asthma
myasthenia gravis
muscle disorders
obesity
hypothyroidism
adult respiratory syndrome

168
Q

What is COPD?

A

Chronic obstructive pulmonary disease
= progressively worsening, irreversible airflow limitation

169
Q

What are the types of COPD?

A

chronic bronchitis
emphysema
A1AT deficiency

170
Q

What are the causes of COPD?

A

almost always due to smoking
patients are susceptible to exacerbations during which there is worsening of their lung function
exacerbations are often triggered by infections

171
Q

What are the risk factors for COPD?

A

SMOKING
air pollution
genetics
occupational exposure
age

172
Q

What is the pathophysiology of chronic bronchitis?

A
  1. hypertrophy and hyperplasia of mucous glands in response to toxic or infectious stimuli
  2. chronic inflammation cells infiltrate bronchi + bronchioles –> luminal narrowing
  3. mucous hypersecretion, ciliary dysfunction, narrowed lumen –> infection risk + airway trapping
173
Q

What is the pathophysiology of emphysema?

A
  1. destruction of the elastin layer in alveolar ducts/sacs/respiratory bronchioles
  2. elastin keeps the walls open during expiration (Bemouli principle)
  3. decreased elastin –> air trapping distal to blockage
174
Q

What are the different types of emphysema?

A

centriacinar (respiratory bronchioles affected only)
panacinar (rib, alveoli, alveolar sacs)
distal acinar
irregular

175
Q

What is the pathophysiology of A1AT deficiency COPD?

A

Autosomal dominant inheritance
- A1AT normally degrades neutrophil elastase (NE) and protects excess damage to elastin layer in lungs especially
- deficiency results in increased NE which causes panacinar emphysema and liver issues

176
Q

What are the clinical manifestations of COPD?

A

Chronic cough with often purulent sputum (infection risk due to mucus hypersecretion + stasis)
Blue bloater (chronic bronchitis) - chronic purulent cough, dyspnoea, cyanosis, obesity
Pink puffer (emphysema) - mimics cough, pursed lip breathing, cachectic (muscle wasting), barrel chest, hyperresonant, percussion
Most patients a mix of BB/PP

177
Q

What are the investigations for COPD?

A

clinical exam/history
GS: spirometry (FEV1/FVC ratio <0.7)
reversibility testing with B-2 agonists like salbutamol during spirometry testing, CXR, FBC sputum, ECG/echo, serum A1AT

178
Q

What are the differential diagnoses for COPD?

A

lung cancer, fibrosis, heart failure, asthma

179
Q

What is the management for COPD

A

first smoking cessation + vaccines for flu + pneumococcal
1. short acting bronchodilators - B-2 agonists (SABA) (salbutamol/terbutaline) or short acting antimuscarinics (ipatropium bromide)
2. Long acting beta agonist (LABA) + long acting muscarinic antagonist (LAMA)

for more severe cases:
+ nebulisers, oral theophylline, oral mucolytic therapy
+ long term oxygen therapy is used for severe COPD

180
Q

What is asthma?

A

chronic reversible airway disease characterised by airway obstruction, airway hyperresponsiveness, inflamed bronchioles +mucous hypersecretion

181
Q

What are the types of asthma and their causes?

A

allergic (70%) - IgE mediated, extrinsic, T1 hypersensitivity
- triggered by pollen, smoke dust, mould, antigens

non-allergic (30%) - non-IgE mediated, intrinsic
- may present later, harder to treat, associated with smoking (like COPD)

182
Q

What are the risk factors for asthma?

A

Family History
allergies
atopic dermatitis
hay fever
obesity
smoking
occupational exposure
nasal polyps, aspirin sensitivity (+ asthma = Samter’s triad)

183
Q

What is the pathophysiology of asthma?

A

TH2 cells are overexpressed in airways and when exposed to trigger release cytokines (IL-3,4,5,13), produce IgE antibodies and recruit eosinophils
IgE stimulates mast cell degranulation which leads to histamine, leukotriene and tryptase release
eosinophilia leads to release of toxic proteins
this causes bronchoconstriction, mucous hypersecretion

184
Q

What are the key presentations of asthma?

A

Wheeze, cough (typically dry), chest tightness, SOB
*typically episodic with triggers and diurnal variation
* episodes can be classed as moderate (PEF 50-75%), severe (PEF 33-50% - can’t finish sentences), life threatening (PEF <33% - decreased consciousness, fatal (hypercapnic pKa>6)

185
Q

What are the investigations for asthma?

A

Spirometry - ↑FeNO + spirometry showing obstruction (FEV1/FVC<0.7), FEV1 >12%

186
Q

What is the chronic asthma treatment algorithm

A
  1. SABA
  2. SABA + ICS
  3. SABA + ICS + LTRA (leukotriene receptor antagonist like montelukast)
  4. SABA + ICS + LABA +/- LTRA
  5. Increases ICS dose
187
Q

What is the management for asthma exacerbations?

A

O2
Nebulisers SABA
ICS hydrocortisone
IV MgSO4
IV theophylline
CPAP/BiPAP
+/- Abx if infection present

188
Q

What are the 4 types of non-small cell lung cancers?

A

Adenocarcinoma (45% of NSCLC)
Squamous cell carcinoma
Carcinoid Tumour
Large cell carcinoma

189
Q

What is adenocarcinoma?

A

Malignant tumour formed from the mucous-producing glandular epithelial cells lining the outside of the lungs
- commonly caused by asbestos
- mets common –> bone, brain, adrenals, lymph nodes, liver

190
Q

What is squamous cell carcinoma?

A

malignant tumour arising from lung epithelium which forms lesions with central necrosis and may secrete PTHrP–> hypercalcaemia
- mostly smokers
- late mets, mostly locally spread

191
Q

What are carcinoid tumours?

A

serotonin-secreting neuroendocrine tumours which mostly arise in the GIT and sometimes the lungs
- associated with genetics, MEN1 mutations and neurofibromatosis

192
Q

What is large cell carcinoma?

A

lung cancer in which the cells are large and look abnormal when viewed under microscope
- fast growing, aggressive type of cancer

193
Q

What are the risk factors for NSCLC?

A

Smoking
Asbestos
Coal
Ionising radiation
Lung disease already present
COPD
Older age

194
Q

What are the key presentations of NSCLC?

A

Chest pain (+/- shoulder pain)
Cough + haemoptysis
Cancer symptoms; weight loss, nausea, fatigue
Signs of mets (e.g. hoarse voice Permberton sign, Homer’s syndrome)

195
Q

What are the investigations for NSCLC?

A

Imaging - CXR, CT
GS: Bronchoscopy + biopsy
MRI - staging (TNM)

196
Q

What is the management for NSCLC?

A

If caught early ⇒ surgical excision
Metastasised ⇒ chemo +/- radio e.g. mAB therapy cetuximab

197
Q

WHat is small cell carcinoma?

A

Malignant epithelial tumour arising from cells lining the lower respiratory tract

198
Q

What are the risk factors for SCC?

A

Cigarette smoking
Environmental tobacco exposure
Radon gas exposure
Asbestos exposure
Aged 65 to 70
Male

199
Q

What is the appearance of SCC on microscopy?

A

The tumour cells and small and densely packed, with scant cytoplasm, finely granular nuclear chromatin, and absence of nucleoli

200
Q

What are the key presentations of SCC?

A

Cough
Dyspnoea
Haemoptysis
Chest pain
Weight loss
Fatigue
Hoarseness
Nausea

201
Q

What are the investigations for SCC?

A

CXR, CT
Bronchoscopy and biopsy
MRI - staging (TNM)

202
Q

What is the management for SCC?

A

Most patients present with advanced disease so surgery usually not an option
1st line: chemotherapy +/- radio (often unsuccessful)
Metastasised ⇒ palliative

203
Q

What are the indicators of severity in respiratory infections?

A

pro-inflammatory cytokines
vasodilation
impaired
cardiac contractility
reduced blood pressure
impaired organ perfusion
tissue hypoxaemia

204
Q

What are the signs of sepsis?

A

delerium
renal impairment - raised urea
increased oxygen demand
- high resp rate
lactic acid production from anaerobic respiration
systolic diastolic BP drop

205
Q

Why is the respiratory tract so susceptible to infection?

A

in the lungs a very thin membrane for gas transfer is needed which also means there is not much space for barriers, immune defence or commensals like in other parts of the body.

Phase 2A (18 decks)

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