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Phase 2A revision > respiratory to work on COPY > Flashcards

respiratory to work on COPY Flashcards

1
Q

Name 3 pathogens that can cause hospital acquired pneumonia (HAP)

A

mainly gram negative

  1. Pseudomonas aeruginosa
  2. E.coli
  3. Klebsiella penumoniae
  4. Staphylococcus aureus
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2
Q

What signs might you see in someone with pneumonia?

A
  • increased resp rate and HR
  • hypotension
  • decreased O2 saturation
  • dull to percuss
  • increased tactile fremitus
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3
Q

What is the treatment for someone with Legionella pneumoniae?

A

Fluoroquinolone + clarithromycin

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4
Q

What is the treatment for someone with Pseudomonas aeruginosa pneumonia?

A

IV ceftazidime + gentamicin

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5
Q

Give 3 potential complications of pneumonia

A
  1. Respiratory failure
  2. Hypotension
  3. Empyema
  4. Lung abscess
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6
Q

What can cause bronchiectasis?

A
  1. Congenital = Cystic fibrosis
  2. Idiopathic (50%)
  3. Post infection - (most common)
    • pneumonia,
    • TB,
    • whopping cough
  4. Bronchial obstruction
  5. RA
  6. Hypogammaglobulinaemia
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7
Q

Which bacteria might cause bronchiectasis?

A
  1. Haemophilus influenza (children)
  2. Pseudomonas aeruginosa (adults)
  3. Staphylococcus aureus (neonates often)
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8
Q

Give 3 signs of bronchiectasis

A
  1. Finger clubbing
  2. Coarse inspiratory crepitate (crackles)
  3. Wheeze
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9
Q

What investigations might you do on someone to determine whether they have bronchiectasis?

A

CXR = kerley B lines, dilated bronchi with thickened walls, multiple cysts containing fluid

High resolution CT = bronchial wall dilation

Spirometry = obstructive lung disease

Sputum culture - h.influenzae is most common

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10
Q

Describe the treatment for bronchiectasis

A
  1. Antibiotics
  2. Anti-inflammatories (azithromycin)
  3. Bronchodilators (nebulised salbutamol)
  4. Chest physio - physical training
  5. Surgery = lung resection or transplant
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11
Q

What are 3 possible respiratory complications of CF?

A
  1. Pneumothorax
  2. Respiratory failure
  3. Cor pulmonale
  4. Bronchiectasis
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12
Q

Name 3 associated conditions with CF

A
  1. Osteoporosis
  2. Arthritis
  3. Vasculitis
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13
Q

what are the risk factors of lung cancer

A
  1. Smoking = main cause
  2. Asbestos
  3. Radon exposure
  4. Coal products
  5. pulmonary fibrosis
  6. HIV
  7. genetic factors
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14
Q

Name 3 differential diagnosis’s of lung cancer

A
  1. Oesophageal varices
  2. COPD
  3. Asthma
  4. Pneumonia
  5. Bronchiectasis
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15
Q

Give 4 possible complications of lung cancer

A
  1. SVC obstruction
  2. ADH secretion –> SIADH
  3. ACTH secretion –> Cushing’s
  4. Serotonin secretion –> carcinoid
  5. Peripheral neuropathy
  6. Pathological fractures
  7. Hepatic failure
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16
Q

What are the 3 characteristic features of asthma?

A
  • Airflow limitation - usually reversible spontaneously or with treatment
  • Airway hyper-responsiveness
  • Bronchial inflammation with T lymphocytes, mast cells, eosinophils with associated plasma exudation
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17
Q

Describe neurogenic infalmmation

A

Sensory nerve activation initiates impulses which stimulates CGRP (pro-inflammatory)
this activates mast cells and innervates goblet cells

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18
Q

Describe the process of airway remodelling in asthma

A
  1. Hypertrophy and hyperplasia of smooth muscle cells narrow the airway lumen
  2. Deposition of collagen below the BM thickens the airway wall
  3. metaplasia occurs with an increase in number of mucus-secreting goblet cells
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19
Q

What are the signs of asthma?

A
  1. Tachypnoea - rapid breathing
  2. Audible wheeze
  3. Widespread polyphonic wheeze
  4. Cough
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20
Q

What are the signs of a life threatening asthma attack?

A
  1. Hypoxia = PaO2 <8 kPa, SaO2 <92%
  2. Silent chest
  3. Bradycardia
  4. Confusion
  5. PEFR < 33% predicted
  6. Cyanosis
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21
Q

Give 3 differential diagnosis’s of asthma

A
  1. COPD
  2. Bronchial obstruction
  3. Pulmonary oedema
  4. Pulmonary embolism
  5. Bronchiectasis
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22
Q

What is the long-term guideline mediation regime for asthma?

A
  1. SABA
  2. SABA + ICS
  3. SABA + ICS + LTRA
  4. SABA + ICS + LTRA/LABA + MART
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23
Q

Give 3 possible complications of asthma

A
  1. Exacerbation
  2. Pneumothorax
  3. Pneumonia
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24
Q

Describe the pathophysiology of chronic bronchitis

A

Airway inflammation –> fibrosis and luminal plugs –> decreased alveolar ventilation

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25
Q

Describe the pathophysiology of emphysema

A

Dilation and destruction of the lung tissue distal to the terminal bronchioles
Enlarged alveoli + loss of elastic recoil = increased alveolar ventilation

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26
Q

What can cause COPD?

A
  1. Genetic = alpha 1 antitrypsin deficiency
  2. Smoking = major cause
  3. Air pollution
  4. Occupational factors = dust, chemicals
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27
Q

Name 4 symptoms of COPD

A
  1. Dyspnoea
  2. Cough +/- sputum
  3. Expiratory wheeze
  4. Weight loss
  5. SOB
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28
Q

Give 4 signs of COPD

A
  1. Tachypnoea
  2. Barrel shaped chest
  3. Hyperinflantion
  4. Cyanosis
  5. Pulmonary hypertension
  6. Cor pulmonale
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29
Q

Give 3 differential diagnosis’s for COPD

A
  1. Asthma
  2. HF
  3. Pulmonary embolism
  4. Bronchiectasis
  5. Lung cancer
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30
Q

Give 3 factors that can be used to establish a diagnosis of COPD

A
  1. Progressive airflow obstruction
  2. FEV1/FVC ratio < 0.7
  3. Lack of reversibility
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31
Q

What are the treatments for COPD?

A

general:

  • stop smoking (refer to cessation services)
  • pneumococcal vaccine
  • annual flu vaccine

step 1:
- SABA (salbutamol or terbutaline) or SAMA (ipratropium bromide)

step 2:

  • If no asthmatic / steroid response:
    • LABA (salmeterol)
    • LAMA (tiotropium)
  • If asthmatic / steroid response:
    • LABA (i.e. salmeterol)
    • ICS (i.e. budesonide)

step 3:
- long term oxygen therapy

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32
Q

Give 3 advantages and 1 disadvantage of using ICS in the treatment of COPD?

A

Advantages

  1. Improve QOL
  2. Improve lung function
  3. Reduce the likelihood of exacerbations

Disadvantages:
1. There is an increased risk of pneumonia

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33
Q

Give 3 possible complications of COPD

A
  1. Exacerbations
  2. Infection
  3. Respiratory failure
  4. Cor pulmonale
  5. Pneumothorax
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34
Q

Give 2 potential consequences of exacerbations of COPD/asthma

A
  1. Worsened symptoms
  2. Decreased lung function
  3. Negative impact of QOL
  4. Increased mortality
  5. Huge economic cost
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35
Q

What is the treatment for an exacerbation of COPD?

A

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

Physiotherapy → sputum clearance

If severe:
IV aminophylline (bronchodilator),
NIV (CPAP / BIPAP)

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36
Q

What does the pleural fluid contain?

A

Protein - albumin, globulin, fibrinogen

Mesothelial cells, monocytes and lymphocytes

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37
Q

what are the causes of a transudate pleural effusion?

A

fluid movement (systemic causes)

  1. Heart failure
  2. fluid overload
  3. Peritoneal dialysis
  4. Constrictive pericarditis
  5. hypoproteinaemia
    • cirrhosis
    • hypoaluminaemia
    • nephrotic syndrome
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38
Q

Name 3 causes of a exudate pleural effusion

A

inflammatory (local causes)

  1. Pneumonia
  2. Malignancy
  3. TB
  4. pulmonary infarction
  5. lymphoma
  6. mesothelioma
  7. asbestos exposure
  8. MI
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39
Q

How does a pleural effusion present?

A
  • SOB especially on exertion
  • Dyspnoea
  • Pleuritic chest pain
  • cough
  • Loss of weight (malignancy)
  • Chest expansion reduced on side of effusion
  • In large effusion the trachea may be deviated away from effusion
  • Stony dull percussion note on affected side
  • Diminished breath sounds on affected side
  • Decreased tactile vocal fremitus (vibration of chest wall when speaking)
  • Loss of vocal resonance
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40
Q

How might you diagnose a pleural effusion?

A

1st line: CXR =
blunt costophrenic angles, fluid in lung fissures, meniscus, tracheal and mediastinal deviation

USS - identify pleural fluid

aspiration (thoracentesis/pleural tap)

  • purulent = empyema (pus)
  • turbid (cloudy) = infected
  • milky = chylothorax
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41
Q

How would you treat a pleural effusion?

A

Dependent on cause
Fluid overload or congestive HF - diuretic
Infective - antibiotics
Large effusions often need aspiration or drainage

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42
Q

How can pneumothorax be classified?

A 
Spontaneous pneumothorax
Traumatic pneumothorax
Iatrogenic pneumothorax
Lung Pathology
Tension pneumothorax
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43
Q

How does a pneumothorax present?

A
  • Sudden onset dyspnoea and pleuritic chest pain
  • as the pneumothorax enlarges the patient becomes more breathless and may develop pallor and tachycardia
  • Reduced expansion
  • Hyper-resonant percussion
  • Diminished breath sounds
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44
Q

What investigation might you do in someone you suspect to have a pneumothorax?

A

CXR = translucency and collapse

ABG = in dyspnoeic patients check for hypoxia

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45
Q

Name a possible complication of a pneumothorax

A

Tension pneumothorax

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46
Q

What are 5 major categories of interstitial lung disease

A
  1. Associated with systemic disease - rheumatological
  2. Environmental aetiology - fungal, dusts
  3. Granulomatous disease - sarcoidosis
  4. Idiopathic - idiopathic pulmonary fibrosis
  5. Other
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47
Q

What are the 4 major features of interstitial lung disease?

A
  1. Cough
  2. Dyspnoea
  3. Restirictve spirometry
  4. Abnormal CXR/CT
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48
Q

Give 3 pulmonary symptoms of sarcoidosis

A
  1. Dry cough
  2. Progressive SOB
  3. Wheeze
  4. Chest pain
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49
Q

What investigations might you do in someone who you suspect to have sarcoidosis?

A

CXR = hilar and/or paratracheal adenopathy with upper lobe predominant, bilateral infiltrates; pleural effusions

Bloods = increase ESR, lymphopenia, increase CAE, raised LFTs

Bronchoalveolar lavage = increased lymphocytes

Lung tissue biopsy = diagnostic = non-caseating granulomata (increased lymphocytes in active disease and increased neutrophils in pulmonary fibrosis)

CXR = staging

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50
Q

How can you stage sarcoidosis?

A

Using CXR
Stage 1 = bilateral hilar lymphadenopathy (BHL)
Stage 2 = pulmonary infiltrates with BHL
Stage 3 = pulmonary infiltrates without BHL
Stage 4 = progressive pulmonary fibrosis, bulla formation and bronchiectasis

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51
Q

How do you treat acute sarcoidosis?

A

NSAIDs and bed rest

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52
Q

How do you treat sarcoidosis?

A

do not treat symptomatic stage 1, and asymptomatic stage 2 or 3
patients with BHL do not need treatment - most recover spontaneously

acute = bed rest and NSAIDs

prednisolone orally
if severe = IV methylprednisolone
if steroid resistant = methotrexate (requires close monitoring)

lung transplant in severe cases

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53
Q

Give 2 possible differential diagnosis’s for sarcoidosis

A
  1. Lymphoma

2. Pulmonary TB

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54
Q

Describe the pathophysiology of idiopathic pulmonary fibrosis

A

repetitive injury to the alveoli epithelium causes wound healing mechanisms to become uncontrolled

this leads to fibroblast over-production and increased fibrosis

this leads to a loss of elasticity and ability to perform gas exchange is impaired -> restrictive lung disease and progressive respiratory failure

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55
Q

what are the risk factors of idiopathic pulmonary fibrosis?

A
  • cigarette smoking
  • infectious agents - CMV, Hep C, EBV
  • occupational dust exposure
  • drugs - methotrexate, imipramine
  • GORD
  • genetic predisposition
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56
Q

what are the clinical features of idiopathic pulmonary fibrosis

A
  1. Dry cough
  2. SOB on exertion
  3. Systemic = malaise, weight loss, arthralgia
  4. Cyanosis
  5. Finger clubbing
  6. bibasal crackles (Inspiratory crackles/crepitus)
  7. dyspnoea
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57
Q

What investigations might you do in someone you suspect to have idiopathic pulmonary fibrosis?

A

ABG = type 1 respiratory failure

Bloods = raised CRP, immunoglobulins and check autoantibodies

CXR/CT = degreased lung volume + honeycomb lung

High resolution CT = ground glass appearance

Spirometry = restrictive

Lung biopsy = confirmation

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58
Q

What is the treatment for idiopathic pulmonary fibrosis?

A

Pharmacological: Pirfenidone, nintedanib - antifibrotic

Non pharmacological: Smoking cessation, physiotherapy, vaccines up to date

Lung transplantation last resort

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59
Q

what are the possible complications of idiopathic pulmonary fibrosis

A
  1. Respiratory failure

2. Cor pulmonale

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60
Q

Define pulmonary hypertension

A

A disease of the small pulmonary arteries characterised by vascular proliferation and remodelling. It results in a progressive increase in pulmonary vascular resistance (PVR)

Increase in mean pulmonary arterial pressure >25 mmHg and secondary right ventricular failure

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61
Q

What can cause an increase in mPAP?

A

Increase resistance to flow

Increased flow rate

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62
Q

what are the causes of pulmonary hypertension

A
  • pre-capillary
    • multiple small PE’s
    • left-to-right shunts
    • primary
  • capillary
    • emphysema
    • COPD
  • Post-capillary
    • backlog of blood causes secondary hypertension
    • LV failure
  • chronic hypoxaemia
    • living at high altitude
    • COPD
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63
Q

what is the clinical presenation of pulmonary hypertension

A

initial features - due to an inability to increase cardiac output

  • exertional dyspnoea
  • lethargy and fatigue
  • ankle swelling
  • Accentuated pulmonic component to the 2nd heart sound
  • Tricuspid regurgitation murmur
  • peripheral oedema, cyanosis
  • cor pulmonale
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64
Q

What investigations might you do in someone to determine whether they have pulmonary hypertension?

A

Initial tests:
- CXR - Enlarged main pulmonary artery, enlarged hilar vessels and pruning.

  • ECG - right ventricular hypertrophy,right axis deviation, right atrial enlargement. (A normal ECG does not rule out the presence of significant pulmonary hypertension)
  • TTE - (trans-thoracic echocardiogram)

Diagnostic test: Right heart catheterisation

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65
Q

Describe the treatment of pulmonary hypertension

A 
General supportive therapy:
       Treat underlying cause
       - Oral anticoagulants - WARFARIN
       - diuretics for oedema
       - oxygen 
       - oral CCBs
       - Supervised exercise training
       Avoiding pregnancy

In treatment-resistant patients:
Balloon atrial septostomy - produces right-to-left shunting that decompresses the right atrium and right ventricle, increases systemic cardiac output, and decreases systemic arterial oxygen saturation
Lung transplantation

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66
Q

Describe pulmonary infection of TB

A

Bacilli settle in lung apex

Macrophages and lymphocytes mount an effective immune response that encapsulate and contains the organism forever

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67
Q

Describe the pathogenesis of pulmonary TB disease

A

TB spread via respiratory droplets as it is an airborne infection
1. Alveolar macrophages ingest bacteria and the rods proliferate inside.

  1. Drain into hilar lymph nodes 🡪 present antigen to T lymphocytes 🡪 cellular immune response.
  2. Delayed hypersensitivity reaction 🡪 tissue necrosis and granuloma formation: caseating.
    • Primary Ghon Focus
    • Ghon Complex – Ghon focus + lymph nodes
68
Q

Give 3 risk factors for TB

A
  1. Living in a high prevalence area
  2. IVDU
  3. Homeless
  4. Alcohol
  5. HIV +ve
69
Q

What systemic symptoms might you see as a result of TB?

A
  1. Weight loss
  2. Night sweats
  3. Anorexia
  4. Malaise
  5. low grade fever
70
Q

What pulmonary symptoms might you see as a result of TB?

A 
Productive cough
Haemoptysis
Cough >3 weeks (dry or productive)
Breathlessness
Sometimes chest pain
71
Q

Name 3 places where TB might spread to?

A
  1. Bone and joint = pain and swelling
  2. Lymph nodes = pain and discharge
  3. CNS = TB meningitis
  4. Biliary TB = disseminated
  5. Abdominal TB = ascites, malabsorption
  6. GU TB = sterile pyuria, WBC in GU tract
72
Q

What investigations might you do to determine whether someone has TB?

A

Inflammatory markers = raised CRP, hyperalbuminaemia, thromobocytosis, high B cell count
CXR = consolidation, collapse, pleural effusion
Microbiology - sputum/biopsy = Ziehl-Neelson stain and culture

73
Q

Give 2 potential side effects of Rifampicin

A
  1. Red urine
  2. Hepatitis
  3. Drug interaction - it’s an enzyme inducer
74
Q

Give 2 potential side effects of Isoniazid

A
  1. Hepatitis

2. Neuropathy

75
Q

Give 2 potential side effects of Pyrazinamide

A
  1. Hepatitis
  2. Gout
  3. Neuropathy
76
Q

Give a potential side effect of Ethambutol

A

Optic neuritis

77
Q

Give 2 factors that can increase the risk of drug resistance in TB

A
  1. If the patient has had previous treatment
  2. If they live in a high risk area
  3. If they have contact with resistant TB
  4. If they have a poor response to therapy
78
Q

Describe the disease course of whooping cough

A

7-10 day incubation –> 1-2 week catarrhal stage –> 1-6 week paroxysmal stage

79
Q

What is the treatment of whooping cough?

A

Clarithromycin - in catarrhal or early paroxysmal stages

  • have little effect on disease course in paroxysmal stage
80
Q

Give 2 possible complications of whooping cough

A
  1. Pneumonia
  2. Encephalopathy
  3. Sub-conjunctival haemorrhage
81
Q

what is the clinical presentation of the alimentary effects of cystic fibrosis?

A

• Thick secretions
• Reduced pancreatic enzymes (due to mucus blocking pancreatic duct)
• Pancreatic insufficiency (diabetes mellitus & steatorrhoea (fatty stools
since enzymes not released to digest fat)
• Distal intestinal obstruction syndrome - bowel obstruction (equivalent of
meconium ileus) resulting in reduced GI motility
• Reduced bicarbonate (HCO3-)
• Maldigestion & malabsorption thus poor nutrition (associated with
pulmonary sepsis)
• Cholesterol Gallstones (in increased frequency) & cirrhosis
• Increased incidence of peptic ulcers & malignancy

82
Q

what are the risk factors for pleural effusion?

A
  • Previous lung damage

- Asbestos exposure

83
Q

what are the risk factors for pneumothorax?

A 
Smoking
Family history
Male
Tall and slender build
Young age 
Presence of underlying lung disease
84
Q

what is the pathophysiology of pneumothorax?

A

Normally intrapleural pressure is negative

When there is a bridge between alveoli and pleural space or atmosphere and pleural space

Flow of air in until communication closed or gradient closed.

85
Q

what is the clinical presentation of a tension pneumothorax?

A 
Cardiopulmonary deterioration:
Hypotension – imminent cardiac arrest
Respiratory distress
Low sats
Tachycardia
Shock
Severe chest Pain
86
Q

what are the clinical features of a tension pneumothorax?

A

Tracheal deviation to contralateral side

Ipsilateral reduced breath sounds
Hyperresonance on percussion

Hypoxia

87
Q

what are the causes of pneumothorax?

A
  • In patients over 40 years of age the usual cause is underlying COPD
  • Other/rarer causes include:
    • Bronchial asthma
    • Carcinoma
    • Breakdown of a lung abscess leading to bronchopleural fistula
    • Severe pulmonary fibrosis with cyst formation
    • TB
    • Pneumonia
    • Cystic fibrosis
    • Trauma (penetrating or rib fracture)
    • Iatrogenic e.g. pacemakers or central lines
88
Q

what is the catarrhal phase of whooping cough?

A
  • Patient highly infectious
  • Cultures from respiratory cultures are positive in 90% of cases
  • Malaise
  • Anorexia
  • Rhinorhoea (nasal cavity congested with significant amount of mucus)
  • Conjunctivitis
89
Q

what are the investigations for whooping cough?

A
  • Chronic cough and one clinical feature indicated pertussis
  • Chronic cough and history of contact or microbiological diagnosis is used to confirm pertussis
  • Suggested clinically by the characteristic whoop and history of contact with an infected individual
  • PCR test
  • But culture of a nasopharyngeal swab = definitive diagnosis
90
Q

what are the signs of TB?

A 
Signs of bronchial breathing
Dullness to percuss
Decreased breathing
fever
crackles
91
Q

what is the treatment for pneumonia?

A

Maintaining O2 Sats between 94-98%
In COPD patients: maintain O2 sats between 88-92%
Analgesia: paracetamol or NSAIDs
IV fluids

92
Q

what are the common organisms that cause atypical pneumonia?

A

Mycoplasma pneumoniae,
Chlamydophila pneumoniae,
Legionella pneumophila
coxiella burnetii

93
Q

what is the mechanism of action for rifampicin for TB?

A

bactericidal - blocks protein synthesis

94
Q

what is the mechanism of action of isoniazid for TB?

A

bactericidal - blocks cell wall synthesis

95
Q

what is the mechanism of action for pyrazinamide for TB?

A

bactericidal initially, less effective later

96
Q

what is the mechanism of action for ethambutol

A

bacteriostatic - blocks cell wall synthesis

97
Q

what antibiotics are used for bronchiectasis?

A
  • pseudomonas aeruginosa = oral ciprofloxacin
  • h.influenzae = oral amoxycillin, co-amoxyclav or doxycycline
  • staph aureus = flucloxacillin
98
Q

what is the characteristic presentation of COPD?

A 
productive cough
white or clear sputum
wheeze
SOB
following many years of smoking
99
Q

what are the systemic effects of COPD?

A 
hypertension
osteoporosis
depression
weight loss
reduced muscle mass with general weakness
100
Q

what is the pathophysiology of pulmonary hypertension?

A

The main vascular changes are:
Vasoconstriction
Smooth-muscle cell and endothelial cell proliferation
Thrombosis

101
Q

what are the signs of emphysema?

A 
Dyspnoea / Tachypnoea
Minimal cough
Pink skin, pursed-lip breathing
Accessory muscle use
Cachexia
Hyperinflation (barrel chest)
Weight loss (due to increased work of breathing and cachexia)
102
Q

what are the investigations for IE COPD?

A

ABG

  • CO2 retention → acidosis
  • Raised pCO2 + low pO2 = T2RF

Chest X-Ray, sputum culture + sensitivities for antibiotic therapy, FBC + U&E

103
Q

what is intrinsic allergic asthma?

A
  • Often starts in middle-aged and attacks are usually triggered by respiratory infections
104
Q

what are the genetic factors for asthma?

A
  • Genes controlling the production of cytokines IL-3,-4,-5,-9 & -13
  • ADAM33 is associated with airway hyper-responsiveness and tissue remodelling
105
Q

what are the risk factors for developing asthma

A
  • Personal history of atopy
  • Family history of asthma or atopy
  • Obesity
  • Inner-city environment
  • Premature birth (low birth weight, not breast-fed)
  • Socio-economic deprivation
  • exposure to allergens
106
Q

which drugs can trigger asthma attacks?

A

NSAIDs and aspirin

beta blockers - results in bronchoconstriction which results in airflow limitation and potential attack

107
Q

what is the acute management of asthma?

A
  1. oxygen
  2. salbutamol nebuliser
  3. ipratropium bromide nebuliser
  4. hydrocortisone IV or oral prednisolone
  5. IV magnesium sulfate
  6. aminophylline / IV salbutamol
108
Q

give 2 examples of LABAs

A
  • salmeterol

- formoterol (full agonist)

109
Q

give an example of a SAMA

A

ipratropium

110
Q

give an example of a LAMA

A

tiotropium

111
Q

what is the mechanism of action for ICS?

A
  • They reduce the number of inflammatory cells in the airways
  • Suppress production of chemotactic mediators
  • Reduce adhesion molecular expression
  • Inhibit inflammatory cell survival in the airway
  • Suppress inflammatory gene expression in airway epithelial cells
112
Q

what are the side effects of ICS?

A

Loss of bone density
Adrenal suppression
Cataracts
Glaucoma

113
Q

what are the advantages of inhaled drugs?

A
  • lungs are robust -> can handle repeated exposure
  • very rapid absorption
  • large SA
  • fewer drug metabolising enzymes
  • non-invasive port of entry
  • fewer systemic side effects
114
Q

what are the risk factors for developing pneumonia?

A
  • under 16 or over 65
  • HIV infection
  • DM
  • CF
  • COPD
  • smoking
  • excess alcohol
  • IVDU
  • immunosuppressant therapy
115
Q

what are the extra-pulmonary manifestations of lung cancer?

A

Recurrent laryngeal nerve palsy - hoarse voice

Superior vena cava obstruction - facial swelling, distended veins in neck and upper chest, Pemberton’s sign

Horner’s syndrome - ptosis, miosis, anhidrosis

116
Q

what is the management for PE?

A
  • if investigations are delayed start anticoagulation

1st line = apixaban/rivaroxaban

LMWH for 5 days followed by dabigatran
3 months for provoked
>3 months for unprovoked

IVC filter

117
Q

what is the management for haemodynamic instability caused by a PE?

A
  • IV thrombolysis - alteplase
  • catheter directed thrombolysis
  • embolectomy
118
Q

what are the most common causes of pharyngitis?

A

group A strep = most common

EBV

119
Q

what are the clincial features of pharyngitis that suggest a viral cause?

A

runny nose, blocked nose, sneezing, cough

120
Q

what are the clinical features of pharyngitis that suggest a bacterial cause?

A

fever, pharyngeal exudate, cervical lymphadenopathy, absence of cough + runny nose

121
Q

what is the management for pharnygitis?

A

group A strep = phenoxymethylpenicillin (clarithromycin if allergic to penicillin)

viral = self resolving, supportive care

122
Q

what are the most common causes of sinusitis?

A

Common infectious agents:
Streptococcus pneumoniae
Haemophilus influenzae
Rhinoviruses

123
Q

what are the risk factors for sinusitis?

A

nasal pathology e.g. septal deviation or nasal polyps
recent local infection e.g. rhinitis or dental extraction
swimming/diving
smoking

124
Q

what is the clinical presentation of sinusitis caused by bacteria?

A 
symptoms > 10 days
purulent nasal discharge
nasal obstruction
dental/facial pain
headache
125
Q

what is the management for sinusitis?

A

Symptom management with analgesia and intranasal decongestants

intranasal corticosteroids considered if symptoms have been present for >10 days

Antibiotic therapy not normally required but may be given for severe presentations (phenoxymethylpenicillin first-line)

126
Q

what is the clinical diagnosis of chronic bronchitis?

A

cough/sputum for more than 3 months in 2 consecutive years

127
Q

what are the signs of COPD on CXR?

A

hyperinflation
bullae
flat hemidiaphragm

128
Q

what are the signs that long term oxygen therapy is required in COPD?

A
  • FEV1 < 30% predicted value
  • cyanosis
  • polycythaemia
  • peripheral oedema
  • raised JVP
  • O2 less than or equal to 92% on room air
129
Q

what is the treatment for latent TB?

A

rifampicin
isoniazid

RI for 6 months
I for 3 months

130
Q

what is the name of the lung disorder that reflects inhaled dust/toxins?

A

pneumoconiosis

131
Q

what happens to FEV1, FVC and FEV1/FVC ratio in obstructive disease?

A

FVC < 80%
FVC = normal
FEV1/FVC < 0.7

132
Q

what happens to FEV1, FVC and FEV1/FVC ratio in restrictive disease?

A

FVC reduced

FEV1/FVC normal

133
Q

define inspiratory reserve volume (IRV)

A

additional volume of air that can be forcibly inhaled after tidal volume inhalation

134
Q

define expiratory reserve volume (ERV)

A

additional air that can be forcibly exhaled after tidal volume expiration

135
Q

what is forced vital capacity (FVC)

A

maximum air that can be forcibly exhaled after maximal inhalation

136
Q

defiine total lung capacity

A

vital capacity plus residual volume

maximum amount the lungs can hold

137
Q

define residual volume (RV)

A

volume remaining in the lungs after maximal exhalation

138
Q

define functional residual capacity

A

volume of air remaining in lungs after tidal volume exhalation

139
Q

define tidal volume

A

volume of air moved in and out of lungs during normal breath

140
Q

define FEV1

A

volume of air forcibly exhaled during 1 second

141
Q

give 2 equations to work out TLC

A 
TLC = VC + RV
TLC = TV + FRC + IRV
142
Q

what is normal tidal volume?

143
Q

givee the equation for FRC

A

FRC = ERV + RV

144
Q

define peak expiratory flow (PEF)

A

greatest rate of airflow tjat can be obtained during forced expiration

145
Q

what is the transfer co-efficient?

A

ability of O2 to diffuse across alveolar membrane

146
Q

how can you find transfer coefficient?

A

low dose CO is inspired, patient asked to hold breath for 10s at TLC
amount of gas transferred is measured

147
Q

what is bronchiolitis?

A

airway obstruction caused by inflammation of broncholes

caused by RSV

148
Q

what is bronchiolitis caused by?

149
Q

what is the difference between bronchitis and bronchiolitis?

A 
bronchiolitis = inflammation of bronchioles - due to RSV
bronchitis = inflammation of bronchi - due to irritants and chemicals
150
Q

what is Centor criteria used for?

A

determines likelihood a sore throat is bacterial

151
Q

what causes croup?

A

parainfluenza virus

152
Q

give 5 side effects of radiotherapy

A 
fatigue
anorexia
cough
oesophagitis
systemic sypmtoms
153
Q

give 4 side effects of chemotherapy

A

alopecia
nausea/vomiting
peripherral neuropathy
constipation or diarrhoea

154
Q

what is type 1 respitatory failure

155
Q

what is type 2 respiratory failure?

A

hypoxia and hypercapnia

156
Q

give 3 signs of hypercapnia

A

bounding pulse
flapping tremor
confusion

157
Q

what can cause type 1 respiratory failure

A

airway obstruction - COPD, asthma
failure of diffusion - emphysema, ILD
V/Q mismatch - dead space, shunt, HF
alveolar hypoventilation - opiates, emphysema

158
Q

what can cause type 2 respiratory failure

A

alveolar hypoventilation

159
Q

which diseases can result in type 1 respiratory failure?

A

COPD
sleep apnoea
asthma

160
Q

is TLC increased or decreased in restrictive lung disease?

161
Q

is TLC increased or decreased in obstructive lung disease?

162
Q

name 6 places TB can spread to?

A 
bones and joints = swelling and pain
lymph nodes = swelling and discharge
CNS = TB meningitis
abdominal TB = ascites, malabsorption
GU = sterile pyuria, WBC in GU tract
163
Q

what might you see on CXR of someone with TB?

A

consolidation
collapse
pleural effusion

164
Q

what treatments are given for V/Q mismatch?

A

ventilation support - CPAP, BIPAP

165
Q

what are the signs of asthma?

A

decreased air entry
hyper-inflated chest
hyper-resonant percussion
tachypnoea

166
Q

what are the atypical causes of pneumonia?

A
  • Mycoplasma pneumoniae

- Chlamydophila pneumoniae

Phase 2A revision (38 decks)

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