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Belle Phase 2a > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Asthma

A

Chronic, inflammatory condition causing episodes of REVERSIBLE airway OBSTRUCTION due to bronchoconstriction and excessive secretion production

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2
Q

Aetiology of asthma

A

Hypersensitivity of the airways triggered by:

Cold air
Exercise
Cigarette smoke
Air pollution 
Allergens e.g. pollen, animals, mould
Time of day: early morning and night
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3
Q

Presentation of asthma

A

Episodes of wheeze (widespread, polyphonic)
Breathlessness
Chest tightness
Dry cough (often nocturnal)
Hyper resonant percussion (too much air)

Atopy (family or personal history)

Diurnal variability

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4
Q

Investigations for asthma

A

Spirometry:

  • bronchodilator reversible testing (>5 years)
  • obstructive pattern: FEV1 <80% predicted, FEV1/FVC ratio <0.7

Peak flow measurement (monitoring, not used for diagnosis)

Skin prick test + IgE

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5
Q

FEV1

A

Forced expiratory volume in one second

Obstructive: DECREASED
Restrictive: minimally decreased or normal

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6
Q

FVC

A

Forced vital capacity measures the amount of air you can breath out forcefully after taking a deep breath

Obstructive: decreased or normal
Restrictive: decreased

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7
Q

FEV1/FVC

A

Amount of air a person can forcefully exhale in ONE SECOND compared to the TOTAL amount they can exhale

= FEV1%

Normal: 85%
Obstructive: <80% (DECREASED: EXHALE disorder)
Restrictive: 85% (EQUALLY REDUCED)

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8
Q

Obstructive lung diseases

A

Difficulty EXHALING

Asthma
COPD

Wheezing, mucus production

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9
Q

Restrictive lung diseases

A

Difficulty INHALING

Pulmonary fibrosis

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10
Q

TLC

A

Total lung capacity = volume of air left in the lungs after exhalation (residual volume) + FVC

Obstructive: normal
Restrictive: DECREASED (INHALE disorder)

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11
Q

FEV1% predicted

A

FEV1% of the patient divided by the average FEV1% in the population for any person of similar age, sex, and body composition

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12
Q

Treatment of asthma

A

Avoid triggers
NICE guidelines: CHECK ADHERANCE AND INHALER TECHNIQUE BEFORE INCREASING DOSE OR ADDING NEW DRUG

1) SABA (salbutamol)
2) Add Low dose Inhaled corticosteroids (ICS; e.g. budesonide)
3) Add Leukotriene receptor antagonist (LRTA; e.g. montelukast)
4) Add LABA (salmeterol) (and stop LRTA)
5) Increase ICS dose

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13
Q

Indication for localised wheeze

A

Foreign body (not asthma)

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14
Q

COPD definition

A

NON-REVERSIBLE (i.e with bronchodilators) OBSTRUCTION in air flow through the lungs, caused by damage to lung tissue (almost always due to SMOKING)

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15
Q

Two main types of COPD

A

Chronic bronchitis: chronic inflammation of the bronchial wall > mucus hypersecretion > progressive narrowing

Emphysema: loss of elastic recoil of alveoli > keeps airways open during expiration

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16
Q

COPD presentation

A 
Long term smoker
Chronic shortness of breath
Cough
Sputum production (clear, white) 
Wheeze 
Recurrent respiratory infections (particularly in winter)

NO finger clubbing

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17
Q

Differential diagnosis in COPD

A

Lung cancer
Fibrosis
Heart failure

COPD does NOT cause Finger clubbing

Unusual:
Haemoptysis
Chest pain

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18
Q

MRC Dyspnoea scale

A
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19
Q

COPD risk factors

A

SMOKING
Age (usually presents between 40-60)
Secondhand smoke exposure
Occupational therapy exposure (mining, dust, asbestos)
Pollution
Genetics (alpha-1-antitrypsin deficiency can lead to earlier onset and increased severity as A1AT is protective)

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20
Q

COPD diagnosis

A

Clinical presentation and spirometry

LFT/Spirometry:

  • FEV1/FVC ratio <0.7
  • reversibility testing: no response

CXR: hyperinflated lungs

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21
Q

Severity of airflow obstruction using FEV1

A

Stage 1: FEV1 >80% predicted

Stage 2: FEV1 50-79% predicted

Stage 3: FEV1 30-49% predicted

Stage 4: FEV1 <30% predicted

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22
Q

Other investigations to support the diagnosis of COPD

A

Just know a few

Chest X-ray: exclude other pathology e.g. lung cancer

Full blood count: polycythaemia (high Hb; response to chronic hypoxia) or anaemia (low Hb)

BMI: weight monitoring for loss (cancer or severe COPD) or gain (steroids)

Sputum: chronic infection e.g. pseudomonas

ECG: cardiac function

Serum A1AT

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23
Q

Emphysema symptoms

A

‘PINK PUFFERS’

Dyspnoea/tachypnoea
Minimal cough 
Pink skin, pursed-lip breathing
Accessory muscle use 
Cachexia (muscle wasting, weight loss)
Hyperinflation (barrel chest)

Complication: pneumothorax (in bullous emphysema/vanishing lung syndrome)

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24
Q

Chronic bronchitis symptoms

A

‘BLUE BLOATERS’

Chronic productive cough (purulent sputum)
Dyspnoea
Cyanosis (hypoxaemia): secondary polycythaemia, pulmonary HT (reactive vasoconstriction)
Peripheral oedema
Obesity
Haemoptysis

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25
Q

Management of COPD

A

General:
SMOKING CESSATION
Vaccine regime (pneumococcal, annual flu)

Step 1 (stable): SABA or SAMA

Step 2 (no asthmatic responsive features): LABA plus LAMA

Step 2: (asthmatic response): LABA plus ICS

Severe COPD: long term oxygen therapy (note: chronic COPD causes CO2 insensitivity so the system is dependent on hypoxia, 100% oxygen removes the respiratory drive)

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26
Q

SAMA

A

Short acting muscarinic antagonist

Ipratropium bromide

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27
Q

LAMA

A

Long acting muscarinic antagonist

Tiotropium

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28
Q

ICS

A

Inhaled corticosteroid

Budesonide

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29
Q

Management of exacerbated COPD (IE)

A

Usually triggered by infection (IE)
Acute worsening of symptoms i.e. SoB, sputum, wheeze

ABG:

  • Co2 retention = acidosis
  • normal pCO2 + low pO2 = T1RF
  • high pCO2 + low pO2 = T2RF

CXR, sputum culture + sensitivities for AB therapy, FBC, U&Es

Steroids (hydrocortisone/prednisolone) + nebulised bronchodilators (salbutamol/ipratropium bromide) + ABs

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30
Q

Alpha 1 antitrypsin deficiency

A

A1AT is a protease inhibitor produced by the liver which acts protectively by inhibiting neutrophil elastase (an enzyme that digests connective tissue)

An autosomal recessive defect causes a deficiency in this enzyme causes:

  • EARLY ONSET COPD (emphysema) and bronchiectasis (after 30 years old)
  • cirrhosis of the liver (after 50 years old)
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31
Q

A1AT deficiency presentation (specific to liver pathology)

A 
Fatigue 
Loss of appetite 
Weight loss
Oedema 
Jaundice 
Haematemesis/blood in stools
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32
Q

A1AT deficiency presentation (specific to lung pathology)

A 
Shortness of breath
Excessive cough with sputum production
Wheeze 
Decreased exercise capacity, persistent fatigue
Chest pain (worse on inhalation)
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33
Q

Diagnosis of A1AT deficiency

A

Gold standard: low serum A1AT

Liver biopsy: cirrhosis, acid-Schiff-positive staining globules (mutant A1AT proteins) in hepatocytes

Genetic testing: A1AT gene

CT thorax: diagnose bronchiectasis and emphysema

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34
Q

Management of A1AT deficiency

A

Smoking cessation
Supportive treatment: inhalers, oxygen therapy
Organ transplant for end stage liver/lung disease
Monitoring: hepatocellular carcinoma

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35
Q

Interstitial lung disease

A

Umbrella term to describe conditions that affect the lung parenchyma causing inflammation and fibrosis

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36
Q

Types of interstitial lung disease

A

Idiopathic pulmonary fibrosis (IPF)

Occupational: silicosis, asbestosis, hypersensitivity pneumonitis

Systemic: granulomatosis with polyangiitis, Goodpasture’s

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37
Q

Idiopathic pulmonary fibrosis

A

Formation of scar tissue in the lungs with no known cause

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38
Q

IPF epidemiology

A

The most common interstitial lung disease

2/3 of patients are >60 at presentation

M > F

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39
Q

Presentation of IPF

A

Ds!!

Dyspnoea
Dry cough (> 3 months)
Diffuse bibasal inspirations crackles
Digits (Finger clubbing)

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40
Q

Diagnosis of IPF

A

High resolution CT thorax: ground glass appearance

Bloods: increased CRP

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41
Q

Treatment of IPF

A

No real cure

Pharmacological:

  • Pirdenidone (antifibrotic)
  • Nintedanib (monoclonal)

Non-pharmacological:
Smoking cessation, physiotherapy, vaccination schedule

Poor prognosis

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42
Q

Asbestosis presentation

A

Dyspnoea on exertion
Dry cough
Onset >10 years after initial exposure
Bibasal inspiration crackles

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43
Q

Investigations of asbestosis and silicosis

A

CXR
Spirometry (restrictive)
HRCT

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44
Q

Treatment of asbestosis and silicosis

A

Remove exposure
Smoking cessation
Symptom treatment

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45
Q

Complications of asbestosis

A

Mesothelioma
Adenocarcinoma
Pleural thickening

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46
Q

Symptoms: Acute renal failure and Haemoptysis

Differential diagnosis?

A

Goodpasture syndrome: anti-GBM antibodies

Granulomatosis with polyangiitis: c-ANCA antibodies, saddle-shaped nose

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47
Q

Goodpastures syndrome

A

Autoimmune anti-glomerular basement membrane (anti-GBM) disease

Anti-GMB antibodies attack glomerulus and alveoli basement membranes (Type IV collagen)

Glomerulonephritis and pulmonary haemorrhage

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48
Q

Presentation of Goodpasture syndrome

A 
Haemoptysis 
Haematuria 
Dyspnoea 
Glomerulonephritis 
Oedema 
Reduced urine output 
Chest pain
Fever
Fatigue
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49
Q

Investigations for Goodpasture syndrome

A

Anti-GBM antibodies

Lung and kidney biopsy

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50
Q

Treatment for Goodpasture syndrome

A

Supportive
Corticosteroids (prednisolone)
Immunosuppressant (cyclophosphamide)
Plasmapheresis (removal of plasma)

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51
Q

Hypersensitivity pneumonitis

A

“Extrinsic allergic alveolitis”

Type 3 Hypersensitivity reaction to an inhaled allergen

Causes alveolar and bronchial inflammation

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52
Q

Examples of specific causes of hypersensitivity pneumonitis

A

Bird-fanciers lung: bird droppings

Farmers lung: mouldy spores in hay

Mushroom workers lung: specific mushroom antigens

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53
Q

Presentation of hypersensitivity pneumonitis

A 
Dyspnoea 
Cough
Fever
Malaise
Weight loss
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54
Q

Investigations for hypersensitivity pneumonitis

A

Bronchoalveolar lavage during bronchoscopy:

  • raised lymphocytes
  • mast cells

CXR

  • acute: patchy reticulonodular infiltrates
  • chronic: fibrosis
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55
Q

Treatment for hypersensitivity pneumonitis

A

Remove allergen

Steroids

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56
Q

Granulomatosis with polyangiitis

A

Wegener’s granulomatosis

Systemic vasculitis involving small and medium vessels

ENT, lung and kidney involvement (ELK)

Associated with c-ANCA antibodies

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57
Q

Presentation of granulomatosis with polyangiitis

A 
ENT:
Epistaxis 
Crusty nasal secretions
Hearing loss
Sinusitis 
Saddle shaped nose (perforated septum)

Lungs: Cough, wheeze, haemoptysis

Kidneys: Rapidly progressing glomerulonephritis (haematuria)

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58
Q

Investigations for granulomatosis polyangiitis

A

c-ANCA (anti-neutrophil cytoplasmic antibodies)
Urinalysis
CT chest

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59
Q

Treatment for granulomatosis polyangiitis

A

Corticosteroids (methylprednisolone, prednisolone)
Immunosuppression (rituximab, methotrexate)
Prophylactic ABx

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60
Q

Clinical presentation of lung cancer

A 
Local disease:
Persistent cough
Shortness of breath
Haemoptysis 
Weight loss
Chest pain, wheeze, recurrent infections 
Metastatic disease:
Bone pain
Horners syndrome (ptosis, anhydrosis, miosis)
Headache, seizures, neurological deficit
Abdominal pain 
Paraneoplastic changes:
Increased PTH (hyperparathyroidism)
Increased ADH (SIADH)
Increased ACTH (Cushing’s)
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61
Q

Two main types of lung cancer

A

Small cell lung carcinoma (SCLC) - 20%

Non-small cell carcinoma - 80%

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62
Q

Types of non-small cell carcinoma

A

Adenocarcinoma (40%)
Squamous cell carcinoma (20%)
Large cell and differentiated carcinoma (10%)
Other including carcinoid tumours (10%)

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63
Q

Risk factors for lung cancer

A 
Cigarette smoking (biggest cause) 
Asbestos
Coal
Radon exposure
Pulmonary fibrosis 
HIV
Genetic factors
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64
Q

Why is small cell lung cancer responsible for paraneoplastic syndromes

A

SCLC cells contain neurosecretory granules that can release neuroendocrine hormones

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65
Q

Investigations for lung cancer

A

First line: Chest X-ray (central mass, hilar lymphadenopathy, pleural effusion) but a negative CXR doesn’t rule out cancer

CT thorax: staging of cancer

Sputum cytology: malignant cells (high specificity, low sensitivity)

Diagnosis: biopsy + histology

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66
Q

SCLC

A

Strongly associated with cigarette smoking

Arises from ENDOCRINE cells (kulchitsky cells) typically in the central bronchus

Secretes polypeptide hormones which act as hormones and neurotransmitters

Treatment: chemotherapy

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67
Q

Squamous cell carcinoma

A

Most strongly associated with cigarette smoking

Arises from EPITHELIAL cells (cells that line the airways) typically in the central bronchus

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68
Q

Adenocarcinoma lung cancer

A

Most common cell type in non-smokers

Strongest association with asbestos exposure

Originate from mucus-secreting glandular cells

Metastasises to: pleura, lymph nodes, brain, bone, adrenal glands

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69
Q

Sites of metastatic spread TO lung

A 
Breast
Colon
Prostate
Sarcoma 
Bladder

Cancer metastasising from elsewhere is more common than a primary lung tumour!

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70
Q

Tuberculosis epidemiology

A

Majority of cases in Africa and Asia (India and China)

Cause of death for most people with HIV

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71
Q

Pathophysiology of TB

A

Mycobacterium TB spreads via respiratory droplets (airborne)

1) alveolar macrophages ingest bacteria and the rods proliferate inside
2) hilar lymph nodes > present antigen to T-cells > cellular immune response
3) delayed hypersensitivity reaction > tissue necrosis and CASEATING granuloma formation (central necrosis and cheese like) - primary TB
4) necrotic zone disintegrates (e.g. in immunocompromised) and TB spreads (secondary TB)

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72
Q

Systemic symptoms of TB

A 
WEIGHT LOSS
Low grade fever
Anorexia
Drenching NIGHT SWEATS 
Malaise
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73
Q

Pulmonary symptoms of TB

A 
Productive cough
HAEMOPTYSIS  
Cough >3 weeks (dry or productive) 
Breathlessness 
Chest pain (sometimes)
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74
Q

Signs of TB

A 
Bronchial breathing
Dullness on percussion
Decreased breathing 
FEVER 
Cackles

RECENT TRAVEL

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75
Q

TB investigations

A

CXR:

  • Ghon complex (primary TB lesion alongside ipsilateral mediastinal lymphadenopathy) - dense homogenous fibronodular opacities on upper lobes (caseating granuloma)
  • hilar lymphadenopathy

Sputum culture (3 x samples): Ziehl-Neelsen stain on Lowenstein-Jensen agar = acid-fast bacilli

Lymph node aspiration or biopsy: caseating granuloma

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76
Q

Diagnosing latent TB

A

Mantoux skin test: TB injected intradermally; 72 hours later, positive test = induration of >5mm (offered to young people in close contact with TB and new entrants to UK from TB prevalent countries)

Positive Mantoux test but no features of active TB:
Interferon gamma release assay: sample of blood mixed with TB antigens; previous TB contact = WBCs will be sensitised and release IFN-y = positive for latent TB

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77
Q

Treatment for ACUTE active TB

A

RIPE

Rifampicin
Isoniazid
Pyrazinamide
Ethambutol

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78
Q

Rifampicin

Course, MOA, side effects

A

6 months
MOA: Bactericidal (blocks protein synthesis)
SE: red urine, sweats, hepatitis

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79
Q

Isoniazid

Course, MOA, side effects

A

6 months
MOA: Bactericidal (blocks cell wall synthesis)
SE: neuropathy, hepatitis

Pyridoxine (Vit B6) is co-prescribed prophylactically for peripheral neuropathy SE

“I’m-so-numb-azid”

80
Q

PYRAzinaMIDe

Course, MOA, side effects

A

2 months
MOA: Bactericidal initially, less effective later
SE: hyperuricaemia resulting in GOUT, hepatitis

81
Q

Ethambutol

Course, MOA, side effects

A

2 months
MOA: Bacteriostatic (blocks cell wall synthesis)
SE: optic neuritis

“Eye-thambutol”

82
Q

Miliary TB

A

immune system is unable to control the disease

disseminated + severe disease

83
Q

Extrapulmonary TB

A

Lymph nodes: “cold abscess” in neck without the inflammation, redness and pain from an acutely infected abscess

Cutaneous TB

CNS, GI, GU system

84
Q

Pneumonia

A

Inflammation of the lung tissue
Acute lower respiratory tract infection (alveoli and terminal bronchioles)

Note: lower airways should always be sterile in a healthy person

85
Q

Aetiology of pneumonia

A

Typically caused by a bacterial infection of the distal airways and alveoli
Two most common causes: Streptococcus pneumoniae (50%), Haemophilus influenzae (20%), mycoplasma pneumoniae

Can also be caused by viruses and fungi or atypical pneumonia e.g. Legionella pneumophila (AIR CONDITIONING IN A FOREIGN COUNTRY)

86
Q

Types of pneumonia

A 
Community acquired (CAP): develops outside of hospital 
Hospital acquired (HAP): develops more than 48h after admission

Other:
Atypical: caused by atypical organisms not detected on gram stain
Pneumocystis jirovecii: fungi

87
Q

Pathophysiology of pneumonia

A

Invasion and overgrowth of a pathogen in lung parenchyma
Overwhelming of host immune defences
Production of intra-alveolar exudates

88
Q

Clinical presentation of pneumonia

A 
Fever
Productive cough 
Shortness of breath 
Pleuritic chest pain
Delirium

Sepsis secondary to pneumonia:
Basic Observations - Increased RR and HR, Low BP, Hypoxia

89
Q

Characteristic chest signs of pneumonia

A

Bronchial breath sounds (harsh sounds equally loud on inspiration and expiration)
Focal coarse crackles (air passing through sputum)
Dullness to percussion (lung tissue collapse and consolidation)

90
Q

Severity assessment of pneumonia

A 
CURB-65 
Confusion
Urea >7 
Respiratory rate >30 
Blood pressure <90 systolic <60 diastolic 
65 (Age)
91
Q

Diagnosis of pneumonia

A 
CXR: consolidation, multi-lobar (strep. pneumoniae, s. aureus), multiple abscesses (s. aureus)
FBC: raised WBC
CRP (useful for monitoring)
Sputum culture
U&Es (urea)
92
Q

General management of pneumonia

A

Maintain O2 sats 94-98% (COPD: 88-92%)
Analgesia: paracetamol or NSAIDs
IV fluids

93
Q

CURB-65 guided treatment for pneumonia

A

0-1: oral amoxicillin in the community
2: hospital: oral amoxicillin + macrolide (clarithromycin)
3+: consider ITU, IV co-amoxiclav + macrolide (clarithryomycin)

94
Q

Complications of pneumonia

A 
Sepsis
Pleural effusion 
Emphysema 
Lung abscess 
Death
95
Q

Community acquired pneumonia

A

Commoner in the age extremities

Commonest cause: Streptococcus pneumoniae

Other: Legionella, Haemophilus influenzae

Antibiotic: Amoxicillin and Clarithromycin

96
Q

Type of sputum characteristic of strep pneumoniae

A

Rusty sputum

97
Q

What organisms are hospital acquired pneumonia caused by?

A

Most cases caused by aerobic gram-negative bacilli:

After 4 days admission

  • Staph aureus
  • Strep pneumoniae

After 5 days admission

  • Pseudomonas aeruginosa
  • MRSA
98
Q

Atypical pneumonia

A

Bacterial pneumonia caused by atypical organisms not detectable by standard methods e.g. legionella pneumophila

Characteristic symptoms: headache + low grade fever + cough
Legionnaires disease = pneumonia + hyponatraemia + recent hotel stay with poor air conditioning

99
Q

Pleural effusion

A

Collection of fluid in the pleural cavity (between the parietal and visceral pleural surfaces)

100
Q

Pathophysiology of pleural effusion

A

Rate of fluid formation > Rate of fluid removal

101
Q

Exudative pleural effusion

A

Inflammation causes PROTEIN to leak out into the pleural space (ex = moving out)

Local factors

Causes: (think inflammation) 
Lung cancer
Pneumonia
Rheumatoid arthritis 
SLE
TB
102
Q

Transudative pleural effusion

A

Fluid moving across into the pleural space (trans = moving across)

Systemic factors e.g. elevated pressure

Causes: (think fluid shifting)
Congestive HF
Hypoalbuminaemia
Hypothyroidism

103
Q

Presentation of pleural effusion

A

DYSPNOEA (decreased lung volume)
Dullness to percussion over the fluid-filled effusion
Reduced breath sounds
Tracheal deviation if the effusion is massive

104
Q

Investigations of pleural effusion

A

1st line: CXR

  • blunting of the costophrenic angle
  • fluid in the lung fissures
  • meniscus
  • tracheal deviation

Pleural ultrasound

Thoracocentesis identifies and diagnoses underlying cause

105
Q

Treatment of pleural effusion

A

Dependent on cause:

Congestive HF: Loop diuretics
Infective: AB
Malignant: Thoracentesis (pleural aspiration)

106
Q

What is a pulmonary embolism?

A

Type of venous thromboembolism

A thrombus (usually from DVT) passes through the IVC and RA/RV to reach the pulmonary circulation

Causes: FATBAT (fat, air (travel), thrombosis (venous), bacteria, amniotic fluid, tumour)

107
Q

Risk factors for pulmonary embolism

A 
Increased age 
Immobility e.g. post surgery 
Pregnancy 
Active malignancy 
DVT
Family history of VTE
Hormone therapy with oestrogen
108
Q

Pathophysiology of venous thromboembolism formation

A

Virchow’s triad:
Vessel wall damage (e.g. surgery)
Venous stasis (e.g. long haul flight)
Hyper-coagulability

= Intrapulmonary dead space
= Decrease in CO

109
Q

Clinical presentation of pulmonary embolism

A

Risk factors may give more of a clue than symptom presentation e.g. immobility/surgery

Acute onset dyspnoea
Pleuritic chest pain (increases on inhale, worse on lying down)
Cough or haemoptysis

Features of DVT e.g. unilateral leg swelling and tenderness
Hypoxia e.g. tachypnoea, tachycardia
Crepitations on auscultation

110
Q

Wells score

A

Predicts the risk of a patient presenting with symptoms actually having a DVT or PE

Takes into account RF such as recent surgery and clinical findings such as tachycardia (>100) and haemoptysis

<4 = PE unlikely 
>4 = PE likely
111
Q

Pulmonary embolism investigations

A

Wells score >4 likely PE: immediate CT pulmonary angiogram

Wells score <4 unlikely PE: D-dimer and if positive, perform CTPA

Haemodynamically unstable: echocardiogram

112
Q

PE investigation where CTPA is contraindicated

A

E.g. renal impairment, contract allergy or at risk from radiation

Ventilation-perfusion (VQ) scan

113
Q

Two main causes of a respiratory ALKALOSIS

A

Pulmonary embolism
Hyperventilation syndrome

High respiratory rate causes CO2 to be expired

Differential: PE = low pO2, HS = high pO2

114
Q

Initial management of PE

A

Anticoagulation: start immediately before confirming diagnosis

1) DOAC: Apixaban or Rivaroxaban
2) LMWH e.g. enoxaparin and dalteparin

115
Q

Haemodynamic instability in PE

A

Patients presenting with hypotension + raised JVP + shock

Treatment: continuous unfractioned heparin and thrombolysis e.g. alteplase

Other options: surgical embolectomy, vena cava filter

116
Q

Differential diagnosis in PE

A 
Unstable angina
MI
Pneumonia
Acute bronchitis 
Pneumothorax
117
Q

Long term anti coagulation options for PE

A

Warfarin
DOAC e.g. apixaban, dabigatran, rivaroxaban
LMWH (1st line in pregnancy or cancer)

Continue for 3 months if there is an obvious reversible cause
Beyond 3 months if the cause is unclear

118
Q

Pulmonary hypertension

A

> 25mmHg

Increased resistance and pressure of blood in the small pulmonary arteries characterised by vasoconstriction, smooth muscle cell and endothelial cell proliferation and thrombosis

Progressive increase in pulmonary vascular resistance (PVR)

Causes strain on the right side of the heart and back pressure into the systemic venous system

119
Q

Four causes of pulmonary hypertension

A

Increased PVR:

1) Primary pulmonary hypertension (pre-capillary)
2) LV failure (post-capillary)
3) COPD/emphysema (capillary)
4) PE (pre-capillary)

120
Q

Main presenting symptoms of pulmonary hypertension

A

Exertional dyspnoea
Lethargy and fatigue

(Due to inability to increase CO)

121
Q

Other signs and symptoms of pulmonary hypertension

A

As RV failure develops, there will be peripheral oedema, abdominal pain, and cyanosis
Raised JVP
Accentuated pulmonic component on 2nd heart sound
Tricuspid regurgitation murmur

122
Q

Investigations pulmonary hypertension

A 
Initial:
CXR: enlargement of pulmonary arteries, enlarged right atrium
ECG
trans-thoracic echocardiogram
raised NT-proBNP for RVF

Diagnostic: right heart catheterisation

123
Q

ECG changes seen with right sided heart strain (in PHT)

A

Right ventricular hypertrophy (R waves on V1-V3 (right side) and S waves on V4-V6 (left side))
Right axis deviation
Right BBB

124
Q

CXR changes seen in PHT

A

Dilated pulmonary arteries

Right ventricular hypertrophy

125
Q

Pulmonary hypertension management

A

General supportive therapy: oral anticoagulants, diuretics for fluid retention

Primary: IV prostanoids, endothelial receptor antagonists, phosphodiesterase-5 inhibitors

Secondary: treat underlying cause

126
Q

Pneumothorax

A

Air in the pleural space

127
Q

Causes of pneumothorax

A

Spontaneous
Traumatic
Iatrogenic
Lung pathology

128
Q

Risk factors for pneumothorax

A 
Smoking
Family history
Trauma
TALL, THIN, MALE (basketball player) 
Young 
Underlying lung disease
Previous PTX
129
Q

Pathophysiology pneumothorax

A

Intrapleural pressure should be negative

Pneumothorax = Air enters the pleural space = Intrapleural pressure increases = lung volume decreases

130
Q

Clinical presentation of pneumothorax

A

Stable patient
Sudden onset PLEURITIC CHEST PAIN, DYSPNOEA or cough

On examination:
Look for evidence of trauma

131
Q

Diagnosis of pneumothorax

A

1st line: Erect CXR

- reduced/absent lung markings between lung margin and chest wall + visible rim

132
Q

Management of pneumothorax

A

Small primary spontaneous PTX (visible rim <2cm) and no SOB = will spontaneously resolve

Large primary spontaneous PTX (visible rim >2cm) and/or SOB = needle aspiration

Chest drain if >2cm on reassessment

133
Q

Tension pneumothorax

A

MEDICAL EMERGENCY

Trauma to chest wall creates a one way valve mechanism: air enters pleural space but cannot exit (i.e. more air gets trapped with each breath causing increased positive pressure)

TRACHEAL DEVIATION: Pushes the mediastinum across, compressing the trachea, heart and other structures and causing cardiorespiratory arrest and collapse of the ipsilateral lung

134
Q

Clinical presentation of tension pneumothorax

A 
Cardiopulmonary deterioration:
Hypotension
Tachycardia
Low sats
Respiratory distress

Severe chest pain

135
Q

Physical examination of tension pneumothorax

A

Tracheal deviation away from side of pneumothorax (contralateral)

Hypoxia

136
Q

Management of tension pneumothorax

A

MEDICAL EMERGENCY

High flow oxygen

1st line: “Insert a large bore cannula into the second intercostal space in the midclavicular line” same side as the PTX

Chest drain

137
Q

Whooping cough

A

UPPER respiratory tract infection caused by Bordetella pertussis (gram negative)

Whooping = loud inspiratory whoop when the coughing ends

Notifiable disease

138
Q

Diagnostic test for whooping cough

A

<2 weeks: Nasopharyngeal PCR or bacterial culture

> 2 weeks: Anti-pertussis toxin IgG

139
Q

Mesothelioma summary

A

Cancer of the LINING of the lungs (pleura)

Main cause: asbestos (80%)

Gold standard diagnosis: pleural biopsy

CXR
Pleural aspiration

140
Q

Bronchiectasis

A

Irreversible dilation of the bronchioles due to recurrent damage and inflammation (they become scarred, dilated, with loss of cilia)

Excess secretion of mucus but less clearance of it due to loss of cilia

Build up of mucus: stagnant bacteria cause increased chance of infection

141
Q

Causes of bronchiectasis

A

Cystic fibrosis
COPD

Post-infectious bronchial damage: H. Influenzae, S. pneumoniae, S. aureus, TB

Immunodeficiency

Bronchiogenic carcinoma

142
Q

Bronchiectasis investigations

A

Gold standard: HRCT: dilated bronchi (SIGNET RING sign = prominently dilated airway compared to accompanying vessel)

Sputum culture: look for infectious agents

CXR

143
Q

Treatment of bronchiectasis

A

Can’t be cured!
Symptom control:
Non-pharm: Stop smoking, healthy diet, exercise
Pharm: Bronchodilators, steroids, antibiotics (dependent on cause e.g. pseudomonas = ciprofloxacin)

144
Q

Cystic fibrosis

A

Autosomal recessive genetic condition

Defect in CFTR chloride channel protein on chromosome 7

  • Transmembrane conductance regulator gene
  • water follows salt = less water in mucus = thickened

Affects all ducts that produce mucus in the body (pancreas, airways, GI tract etc)

Presents in childhood

145
Q

Three key consequences of cystic fibrosis

A

Thick pancreatic and biliary secretions that cause blockage of the ducts resulting in a lack of digestive enzymes e.g. pancreatic lipase

Low volume thick airway secretions that reduce airway clearance, resulting in infection susceptibility

Congenital bilateral absence of the vas deferens in males

146
Q

Signs and symptoms of cystic fibrosis

A

Symptoms:
HEAVY MUCUS PRODUCTION
Chronic COUGH

Signs:
Steatorrhea due to lack of lipase 
Failure to thrive in children 
Finger clubbing 
Crackles and WHEEZE on aus
Rectal prolapse 
Cyanosis
147
Q

Key diagnostic methods for CF

A

Gold standard: sweat test (NaCl) for chloride concentration

Genetic testing for CFTR gene during pregnant or after birth

Faecal elastase (pancreatic insufficiency)

Newborn blood spot testing

148
Q

First sign of CF in babies

A

Meconium ileus (not passing meconium within 24 hours, abdominal distention and vomiting)

149
Q

Two key bacteria that cause infections in CF

A 
Staphylococcus aureus 
Pseudomonas aeruginosa (very difficult to get rid of and increases CF mortality)

Patients take prophylactic Flucloxacillin to prevent S. aureus

150
Q

Management of CF

A

No cure, symptomatic management
Chest physiotherapy
Antibiotics, anti-mucinolytics, bronchodilators, enzymes, insulin, bisphosophonates
Lung transplantation in end stage respiratory failure

151
Q

Complications of CF

A

Respiratory tract infections

Bronchiectasis

Most males are infertile due to absent van deferens

90% develop pancreatic insufficiency

50% develop CF-related diabetes and require insulin

30% develop liver disease

152
Q

Sarcoidosis

A

Multi system inflammatory disorder
Mostly in the lungs and mediastinal lymph nodes

African American women <50

Non-caseating granulomas form due to CD4 interactions (Type 4 hypersensitivity)

Signs: bilateral hilar lymphadenopathy, erythema nodosum, polyarthritis, uvietis

Investigation: tissue biopsy for non-caseating granulomas; serum ACE levels (secreted from nodules)

Complications: interstitial lung disease

153
Q

Type 1 respiratory failure

A

V/Q mismatch/problem with gas exchange

Low Oxygen
Low or normal CO2

Causes: 
COPD
Pneumonia 
Asthma
Pulmonary fibrosis 
Pneumothorax
154
Q

Type 2 respiratory failure

A

Inadequate ventilation

Low oxygen
High CO2

Increased resistance (COPD)
Respiratory centres (Drug overdose)
Neuromuscular problems (Guillain Barre/MND)
Reduced compliance (Pneumonia)
Severe asthma
155
Q

Respiratory centres

A

Medulla oblongata
Pons
Carotid bodies/Aortic arch

156
Q

Croup

A

Parainfluenza virus (HPIV)

Barking cough

157
Q

Eosinophilic asthma

A

Allergic asthma

158
Q

Non-eosinophilic asthma

A

Exercise, cold air, stress, smoking, obesity

159
Q

Main cells involved in asthma

A

Eosinophils

Mast cells

160
Q

Three characteristic pathological features of asthma

A

Airway obstruction (narrowing):

  • Smooth muscle bronchial contraction leading to bronchoconstriction
  • Mucosal inflammation (thickening of the airway) - mast cells + basophils
  • Presence of mucosal secretions in the lumen
161
Q

Severity of acute asthma

A

PEFR:
>50% = moderate
33-50% = severe
<33% = life threatening (silent chest)

162
Q

Why does age matter in the history of asbestosis?

A

Many buildings built before the 80s contained asbestos

163
Q

Horners syndrome symptoms

A

Ptosis
Miosis
Anhydrosis

164
Q

Pancoast tumour

A

tumour of the apex of the lung

Invades the apical chest wall
Affects nearby structures including intercostal nerves, brachial plexus (shoulder pain, arm weakness), sympathetic chain (HORNERS SYNDROME)

Diagnosed based on clinical picture, imaging and biopsy

165
Q

Sites of metastatic spread FROM lung cancer

A

Bone
Brain
Adrenal glands

166
Q

Bilateral hilar lymphadenopathy on x-ray

Differential diagnoses

A

Sarcoidosis

Infection: TB

Malignancy: lymphoma (Hodgkin)

Occupational: silicosis

167
Q

Signs of bronchiectasis on examination

A

Coarse crackles in early inspiration and often in the lower zones

Large airway ronchi (low-pitched snore like sounds)

Wheeze

168
Q

Complications of bronchiectasis

A 
Repeated infection and deteriorating lung function
Empyema 
Lung abscess 
Pneumothorax (repeated coughing)
Respiratory failure
169
Q

Differential diagnosis of COPD

A

Asthma
A1AT deficiency
Bronchiectasis
Cystic fibrosis

170
Q

COPD complications

A

Respiratory infections
Lung cancer
Cardiovascular

171
Q

Small gram-negative coccobacillus

Symptoms: malaise, coughing up green phlegm in the COMMUNITY

RF: elderly

Causative organism + Ab?

A

Causative organism: Haemophilus influenzae

Antibiotic: Co-amoxiclav

172
Q

Differential diagnoses for a COPD exacerbation

A 
Pneumonia
Pneumothorax
Congestive HF
Pulmonary oedema 
Pleural effusion
173
Q

Groups of patients most at risk of respiratory infections

A

Extremities of age
COPD
Immunocompromised

174
Q

D-dimer test

A

Pulmonary embolism

High sensitivity, low specificity

175
Q

Pneumothorax vs pleural effusion differentiated:

1) Respiratory examination
2) History

A

1)
Pleural effusion = dullness on percussion
PTX = hyper-resonant on percussion

2)
Pleural effusion = slower onset, PMH of CHF, cancer, pneumonia
PTX = rapid onset, history of trauma, PTX FH, smoking

176
Q

CT angiogram polo mint sign

A

Pulmonary embolism

Partial filling defect in blood vessel surrounded by a rim contrast material

177
Q

Hyperexpansion of the chest

Type of lung disease

A

Obstructive

178
Q

Patients most likely to develop a spontaneous PTX

A

Young males with low BMI

179
Q

Clinical features of bronchiectasis

A 
Persistent cough
Clubbing
Dyspnoea 
No history of smoking + young age of onset 
Haemoptysis
180
Q

Most commonly affected sinus in sinusitis

A

Maxillary: drains down to the bottom

181
Q

Beclomethasone inhaler MOA

A 
STEROID ACTIONS e.g.
Decrease formation of cytokines
Inhibit influx of eosinophils 
Reduce bronchial hyper responsiveness 
Decrease microvascular permeability
182
Q

Walls of the bronchIOLEs lack

A

Hyaline cartilage

183
Q

Kyphoscoliosis

A

Causes a restrictive lung disease

184
Q

Respiratory symptoms are most likely caused by which bacteria

A

Haemophilus inFLUenzae

185
Q

Aspiration pneumonia

A

Infection of the lungs caused by inhaling saliva, food, liquid, vomit and small foreign objects

More likely to go down right side in bottom two lobes

186
Q

Atypical pneumonia: Chlamydia psittaci

A

Contracted from infected birds - patient often owns a parrot

187
Q

Atypical pneumonia: Coxiella burnetii

A

‘Q fever’ - associated with contact with animals

188
Q

Mycobacterium avium complex

A

AIDS defining illness

Presents similarly to pulmonary TB

189
Q

Two most common causes of pneumonia

A 
Streptococcus pneumoniae (50%)
Haemophilus influenzae (20%)
190
Q

Crepitations indication

A

Pneumothorax

191
Q

Most likely cause for consolidation X-Ray

A

Lobar pneumonia

Consolidation = indicates filling of the alveoli and bronchioles in the lung with pus (pneumonia), fluid (pulmonary oedema), blood or neoplastic cells

192
Q

Hyper-resonance indication

A

Hyperinflation with air i.e. COPD

193
Q

Dullness on percussion indication

A

FLUID or solid replaces alveoli e.g. pneumonia or pleural effusion

194
Q

Severe asthma Tx

A

Salbutamol on OXYGEN + steroids

195
Q

Empyema

A

Infected pleural effusion (pus)

196
Q

Prophylactic treatment for a pulmonary embolism

A

LMWH e.g. enoxaparin

197
Q

Which respiratory disease do you typically see high bicarbonate with respiratory acidosis?

A

COPD - chronically high CO2 causes the kidneys to COMPENSATE by releasing bicarbonate

Belle Phase 2a (14 decks)

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