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Kofi: Pure clinical conditions 2 > Respiration > Flashcards

Respiration Flashcards

1
Q

What is Asthma?

A

A chronic inflammatory disorder of the airways

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2
Q

What are the defining characteristics of asthma?

A 
Susceptibility
Variable airflow obstruction 
Chronic inflammatory process
Reversibility
Airway-hyperreposniveness
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3
Q

What are the symptoms of asthma?

A 
Expiratory wheeze
Cough
Difficulty breathing
Chest tightness
Exercise induced wheeze
Atopic history - allergies
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4
Q

What differentiates asthma and COPD?

A
  • Airway obstruction in asthma is often reversible with bronchodilators(>15% improvement with treatment)
  • Airway obstruction in COPD is not fully reversible (<15% improvement with treatment)
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5
Q

What should an asthma diagnoses be made on?

A
  • History of characteristic symptom patterns

- Evidence of variable airflow limitation, from bronchodilator reversibility testing or other tests

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6
Q

What present with a severe asthma exacerbation?

A

Silent chest

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7
Q

What is the frequent finding on physical examination of asthmatic patient?

A
  • Often normal

- Wheezing may be absent during severe asthma exacerbation

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8
Q

What are common triggers for asthma?

A
  • Allergens
  • Cold air
  • Exercise
  • Fumes
  • Cigarette smoke
  • Perfumes
  • Chemicals
  • Drugs
  • Emotional distress
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9
Q

What cells primarily drive asthma?

A

TH2 cells

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10
Q

What are the main points in the pathophysiology of asthma?

A
  • Presentation of antigen to T lymphocytes
  • TH2 release cytokines which attract and activate inflammation cells including mast cells and eosinophils
  • Activation of B cells occurs as well which produce IgE
  • In a sensitised atopic asthmatic exposure to antigen results in a 2 phase response.
  • Immediate response and Late phase response
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11
Q

What is the immediate response for asthma pathophysiology?

A
  • Interaction of allergen and specific IgE antibodies

- Leads to mast cells

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12
Q

What is the late phase response?

A
  • Type 4 hypersensitivity
  • Involves inflammatory cells including eosinophils, mast cells, lymphocytes and neutrophils which release mediators and cytokines
  • This causes airway inflammation
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13
Q

What is the result inflammatory cells in asthma on the bronchioles?

A
  • Reduced airway calibre
  • Mucosal swelling (oedema) due to vascular leak
  • Thickening of bronchails wall due to inflammatory cell infiltration
  • Mucus overproduction (sticky, thick, tenacious)
  • Smooth muscle contraction
  • Epithelium shed and incorporated into thick mucus
  • Hyper responsiveness of the airway
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14
Q

What are the effect of long term poorly controlled asthma on the respiratory organs?

A
  • Hypertrophy and hyperplasia of smooth muscle
  • Hypertrophy of muccus glands
  • Thickening of the basement membrane
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15
Q

What type of respiratory failure normally occurs in severe asthma attacks?

A
  • Type 2 respiratory failure

- Hyperventilation cannot compensate due to extensive effect

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16
Q

What type of respiratory failure occurs in mild asthma?

A
  • Type 1 respiratory failure

- Compensation of hyperventilation

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17
Q

What test are used to assess the condition of a patient with suspected asthma?

A

Airflow limitation - FEV1/FVC reduced

Variation in lung function greater than normal

Spirometry

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18
Q

What does spirometry in asthmatic patient show?

A
  • FEV is reduced without the bronchodilator
  • FEV increases with bronchodilator
  • Scalloping reduces
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19
Q

How can eosinophilic inflammation be measured?

A
  • Induced sputum
  • Peripheral eosinophil count
  • FeNO
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20
Q

What are the principles of asthma treatment?

A
  • Patient education (SIMPLE)
  • Drug treatment involves brochodilators (beta2) and steroids such as prednisone . Inhalers are used to deliver in aerosol form.
  • Long acting reliever is prescribed with corticosteroid inhaler. B2 agonist is also given
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21
Q

How do we treat acute severe asthma?

A
  • Oxygen, high flow –aim to keep O2 94-98% sat
  • Nebulised salbutamol
  • Oral prednisolone
  • If moderate exacerbation not responding, or acute severe/life threatening, add nebulised ipratropium bromide
  • Consider iv magnesium and/or iv aminophylline if no improvement and life-threatening features not responding to above treatment (BEWARE if taking oral theophylline)
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22
Q

What are the characterises of acute severe asthma?

A
  • Respiratory rate >25
  • Heart rate >110/min
  • Inability to complete sentences in one breath
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23
Q

What are the features of life threatening asthma?

A
  • Altered conscious level
  • Exhaustion
  • Arrthymia
  • Hypotension
  • Cyanosis
  • Silent chest
  • Poor respiratory effort
  • PEF <33% best or predicted
  • SpO2 <92%
  • PaO2 <8 kPa
  • Normal PaCO2
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24
Q

What is COPD

A

A disease state characterised by airflow limitation that is not fully reversible. It encompasses both emphysema and chronic bronchitis.

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25
Q

What is the aetiology of COPD?

A
  • Tobacco(Smoking of 90% of cases
  • Air pollution
  • Occupational exposure
  • Alpha-1 antitrypsin deficiency
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26
Q

What are the pathological changes in COPD?

A
  • Enlargement of mucus-secreting glands of the central airways,
  • Increased number of goblet cells ( which replace ciliated respiratory epithelium)
  • Ciliary dysfunction
  • Breakdown of elastin leading to destruction of alveolar walls and structure, and loss of elastic recoil.
  • Formation of larger air spaces with reduction in total surface area available for gas exchange
  • Vascular bed changes leading to pulmonary hypertension.
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27
Q

What are the effects of the pathological changes in COPD?

A

-Progressive hypoxia leading to Cor Pulmonale

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28
Q

What is the pathophysiology of the COPD?

A
  • Host repose to to inhaled cigarette or other noxious substances
  • Chronic inflammation process and oxidative injury which affects central and peripheral airways, lung parenchyma, alveoli and pulmonary vasculature.
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29
Q

What are the symptoms of COPD?

A
  • Cough that is productive of sputum

- Shortness of breath initially on exertion but can progress to at rest

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30
Q

What are the sign of COPD on physical examination?

A
  • Tachypnoea
  • Use of accessory muscles of respiration
  • Barrel chest
  • Hyper resonance on percussion
  • Reduced intensity breath sounds
  • Wheezing may be present
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31
Q

What are some late features of COPD?

A
  • Central cyanosis
  • Flapping tremors
  • Signs of right sided heart failure second to pulmonary hypertension
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32
Q

What the specific features of emphysema?

A
  • Elastin breakdown
  • Loss of alveolar integrity
  • Permanent destructive enlargement of the airspaces distal to terminal bronchioles
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33
Q

What are the specific feature of chronic bronchitis?

A
  • Excessive mucus secretion
  • Impaired removal of section due to ciliary dysfunction
  • Chronic productive cough
  • Chronic respiratory infections
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34
Q

What are some lung function tests in COPD?

A
  • Spirometry (FEV1/FVC <70%)
  • Chest X-ray show hyper inflated lungs
  • Pulse oximetry
  • ABG analysis
  • Alpha-1 antitrypsin level checked
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35
Q

What is the management of COPD?

A
  • Smoking cassation
  • Bronochdilatos
  • Pulmonary rehabilitation
  • Long term oxygen management
  • Surgical interventions
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36
Q

What vaccinations are recommended for COPD patients?

A

Pneumococcal vaccinations

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37
Q

How are patient with acute exacerbations of COPD managed?

A
  • Montor for hypoxia and hypercapnia
  • Appropriate antibiotics to account for pneumococcus and haemophilia influenza
  • Nebulised bronchodilators
  • Oral steroids
  • 24 or 28% oxygen therapy
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38
Q

What are the complications of COPD?

A
  • Recurrent pneumonia
  • Peumothorax
  • Repsiraroy failre
  • Cor Pulmonale
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39
Q

What is bronchestaisis?

A

Bronchiectasis is the Chronic dilatation of one or more bronchi. The bronchi exhibit poor mucus clearance and there is predisposition to recurrent or chronic bacterial infection

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40
Q

What is the Gold standard diagnostic test for bronchiestasis?

A

High resolution CT

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41
Q

What are the symptoms of bronchiectasis?

A
  • Chronic cough
  • Daily sputum production
  • Breathless on exertion
  • Intermittent haemopytisis
  • Nasal symtoms
  • Chest pain
  • Fatigue
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42
Q

What is the pathophysiology of bronchiestasis?

A
  • Post infective
  • Immune deficiency
  • Genetic/Mucocilliary clearance defect
  • Obstruction
  • Toxic insult
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43
Q

What are the common organisms to cause bronchiestasis?

A
  • Haemophilus influenza
  • Pseudomonas aeruginosa
  • Moraxella catarrhalis
  • Stenotrophomonas maltophilia
  • Fungi (aspergillus, candida)
  • Non-tuberculous mycobacteria
  • Staph aureus (think about CF)
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44
Q

What is the management for bronchiestasis?

A
  • Treat underlying cause
  • Physiotherapy
  • Antibiotics according to sputum cultures
  • Supportive
  • Pulmonary rehabilitation
  • Management plan for infective exarcerbations
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45
Q

What is Cystic fibrosis?

A

CF is an autosomal recessive disease leading to mutations in the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR).

-No longer able to push chloride out of the cells

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46
Q

What is the pathophysiology and organs affected in Cystic fibrosis?

A
  • Chromosome 7 defect
  • Leads to Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) mutation
  • Leads to ineffective cell surface chloride transport
  • Leads to thick, dehydrated body fluids in organs which have CFTR (Mucus)
  • Affects Pancreas, Skin, GI tract, Vas deferens, Lungs, Reproductive Organs.
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47
Q

What are the presentations of CF?

A
  • Meconium Ileus (delay in passing first stool)
  • Intestinal malabsorption
  • Recurrent chest infections
  • Newborn screening
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48
Q

How is CF diagnosis made?

A

Or a history of CF in a sibling
Or a positive newborn screening test result

And
-An increased sweat chloride concentration
(> 60 mmol/l) – SWEAT TEST
-Or identification of two CF mutations – genotyping
-Or demonstration of abnormal nasal epithelial ion transport (nasal potential difference)

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49
Q

What is the management of CF?

A
  • Agressive therapy with respiratory infections with physic and antibiotics
  • Monitoring of body weight
  • Pancreatic enzyme supplements (Can present with distal intestinal obstruction syndrome)
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50
Q

How does distal intestinal obstruction syndrome present?

A

-Palpable right iliac fossa mass

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51
Q

Examples of lifestyle advice for CF patients

A
  • No smoking
  • Avoid other CF patients
  • Avoid friends / relatives with colds / infections
  • Avoid Jacuzzis (pseudomonas)
  • Clean and dry nebulisers thoroughly
  • Avoid stables, compost or rotting vegetation – risk of aspergillus fumigatus inhalation
  • Annual influenza immunisation
  • Sodium chloride tablets in hot weather/vigorous exercise
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52
Q

What is the microbiology of mycobacterium tuberculosis?

A

Non-motile rod shaped bacteria
Obligate aerobe
Long chain fatty acids, complex waxes and glycolipids in cell wall
Slow growth compared to others

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53
Q

Where are the regions affected by extra-pulmonary TB?

A
  • Lymphadenitis (Scrofula, Cervical lymph nodes most commonly, Abscesses and sinuses)
  • Gastrointestinal (Swallowing of tubercles)
  • Peritoneal (Ascitis or adhesive)
  • Genitourinary (Slow progression to renal disease, Subsequent spreading to lower urinary tract)
  • Bone and joint (Haemotgenous spread, Spinal TB is most common, Potts disease)
  • Tuberculous meningitis (Chronic headache, fevers, CSF – markedly raised proteins, lymphocytosis)
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54
Q

What is military TB?

A

Bacilli is spread through the blood stream

  • Headaches suggest meningeal involvement
  • Pericardial, pleural effusions small
  • Ascites may be present
  • Retinal involvement (choroid tubercles seen)
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55
Q

What is the transmission of TB?

A
  • Spread by respiratory droplets –coughing, sneezing
  • Droplet nuclei
  • Suspended in air
  • Reach lower airway
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56
Q

How easy is it to catch TB?

A

Contagious but not easy to acquire infection. Prolonged exposure to active TB individuals facilitates transmission

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57
Q

What is the pathogenesis of TB?

A
  • Engulfed by alveolar macrophages
  • Unique structure allows the TB bacteria to evade destruction by macrophages. Can survive and multiply within the macrophage
  • TB bacilli from the macrophage can get carried to the lymph nodes during drainage
  • Formation Primary complex (Ghon’s focus + draining lymph nodes)
  • Minority (5%) – Can proceed to active disease after the primary complex. Primary TB develops
  • Majority of patient – latent infection (95%). Containment of the infection to prevent the bacilli from multiplying. Live organism in the site of infection and lymph node
  • Small number of latent infection patient can develop post primary. 2 years after the initial infection.
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58
Q

What is the effect of post primary TB?

A

Reactivation and hypersensitivity can occur. Massive destruction of the lung due to increased inflammatory response and bacterial damage. This can also occur with reexposure to the bacteria

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59
Q

What determine the formation of the primary complex?

A
  • The infectious dose
  • Strain of TB
  • Immune response to the TB bacilli which depends on T cells to decide fate of primary complex (HIV)
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60
Q

Compare Latent Tb and Active TB.

A

Latent TB

  • Inactive, contained tubercle bacilli in the body
  • TST or IFN gamma test results usually positive.differentiate
  • Chest X-ray usually normal
  • Sputum smears and cultures negative
  • No symptoms
  • Not infectious
  • Not a case of TB

Active TB

  • Active, multiplying tubercle bacilli in the body
  • TST or blood test results usually positive
  • Chest X-ray usually abnormal
  • Sputum smears and cultures may be positive
  • Symptoms such as cough, fever, weight loss
  • Often infectious before treatment
  • A case of TB
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61
Q

Why doest the TST or IFN test differentiate between latent and active TB?

A

Both Latent and Active have Primary Complex so doesn’t differentiate between the two.

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62
Q

What are the histological features of Tuberculosis?

A

-Caseting granuloma is lung parenchyma and/or mediastinal lymph nodes

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63
Q

Where are the features of TB on an X-ray?

A
  • Apex of the lung often involved
  • Ill-defined paths consolidation
  • Cavitatons usually develop with consolidation
  • Healing results in fibrosis
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64
Q

How is a TB diagnosis established through investigations?

A
  • Culture is the Gold standard technique
  • NAAT
  • Chromatography
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65
Q

How are antibiotics tested for effect on a micro-organism?

A

Drug sensitivity test

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66
Q

What are symptoms of TB?

A
  • Night sweats
  • Tiredness and malaise
  • Weight loss and anorexia
  • Fever
  • Cough
  • Haemoptysis occasionally
  • Breathlessness if pleural effusion
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67
Q

What are the signs seen on examination for TB?

A
  • Often no chest signs despite CXR abnormality
  • Maybe crackles in affected area

In extensive disease

  • Sings of cavitation
  • Fibrosis

-Pleural involvement: typical signs of effusion

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68
Q

What is important about the history of a TB patient?

A
  • Ethnicity
  • Recent arrival or travel to high TB burden countries
  • Contacts with TB
  • BCG vaccination
  • Specific clinical features
  • Fever
  • Weight loss
  • Malaise
  • Anorexia
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69
Q

What are the risk factors of TB?

A
  • Non-UK born/recent migrants (South Asia, Sub-Saharan Africa)
  • HIV – latent infections can reactivate due to the immune system being affected
  • People sustpected of TB are tested for HIV
  • Other immunocompromised states
  • Homeless
  • Drug users, prison
  • Close contacts
  • Young adults
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70
Q

How are People suspected of TB managed?

A
  • Early and adequate treatment
  • Close monitoring of compliance to treatment (Direct observed therapy, Video observed therapy)
  • Treatment for a long duration due to long duration of TB to multiply
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71
Q

What is the First line medication to treat TB?

A
  • Rifampicin (orange pee)
  • Isoniazid
  • Pyrazinamide
  • Ethambutol

2nd line
Quinolones

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72
Q

What is the BCG vaccination?

A
  • Live attenuated M bovis strain
  • Given to babies in high prevalence communities only (0-80% effectiveness)
  • Protection wanes
  • Little evidence in adults to work
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73
Q

Why is multi drug therapy used?

A
  • The drugs are given for a long time so likely for mutations to occur and resistant strains to develop. Less chance of survival against all drugs of resistant strains which can cause a lot of damage
  • Resistance can develop due to inadequate treatment or spontaneous mutation
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74
Q

How is TB transmission prevented?

A

Notification

  • Triggers contact tracing to detect and treat cases and contacts to prevent transmission
  • Provides surveillance data to detect outbreak and monitor epidemiological transmission
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75
Q

How is TB controlled in the population?

A
  • Treatment of index case

- Reduces susceptible contacts by vaccinating or addressing risk factors

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76
Q

What are the risk factors for reactivation of latent TB?

A
  • Infection with HIV
  • Substance abuse
  • Prolonged therapy with corticosteroids
  • Other immunosuppressive therapy
  • Organ transplant
  • Haematological malignancy
  • Severe kidney disease/haemodialysis
  • Diabetes mellitus
  • Silicosis
  • Tumour necrosis factor alpha antagonists
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77
Q

What is pneumonia?

A

Pneumonia is a general term denoting inflammation of the lung parenchyma due to infection.

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78
Q

What is lobar pneumonia?

A

Pneumonia localised to a particular lobe

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79
Q

What is bronchpneumonia?

A

Diffuse and patchy pneumonia

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80
Q

What are the common microbes that cause community acquired pneumonia?

A
  • Streptococus pneumoniae

- Haemophilus influenzae

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81
Q

What are atypical organisms causing community acquired pneumonia?

A
  • Legionella - contaminated water
  • Mycoplasma
  • Coxiella burnetti
  • Chlamydia psittaci – exposure to birds
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82
Q

What are the organisms causing hospital acquired pneumonia?

A
  • Haemophilus influenza
  • Staphylococcus aureus
  • Pseudomonas spp
  • Acinetobacter baumanii
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83
Q

What is the pathophysiology of viral pneumonia

A
  • Damage to cells lining the airways/alveoli by the virus and immune cells
  • Gas exchanged is hindered by fluid
  • Can be mild or severe
  • Sevre viral pneumonia can lead to necrosis and haemorrhage
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84
Q

What is the appliance o viral pneumonia on a chest X-ray?

A

-Patchy and diffuse ground glass opacity on the X-ray

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85
Q

What are the symptoms of pneumonia?

A
  • Malaise, Nausea and vomiting
  • Fever
  • Cough productive of sputum (purulent or rust coloured)
  • Pleuritic chest pain
  • Patients often feel breathless
  • Rigors
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86
Q

What are the features of pneumonia on clinical examination?

A
  • Tachycardia
  • Tachypnoea
  • Cyanosis
  • Dullness to percussion, tactile vocal fremitus
  • Bronchial breathing – Crackles
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87
Q

What are the investigations undertaken for patient suspected of pneumonia?

A
  • Full blood count
  • Urea and electrolytes
  • C-reactive protein
  • Arterial blood Gases
  • Chest X-ray

Microbiological
-Sputum / Induced sputum
-Blood culture
-Broncho Alveolar Lavage fluid (BAL)
Nose and Throat swabs or NPAs (viruses)
-Urine (antigen test for legionella / pneumococcus)
-Serum (antibody test) acute and convalescent sera (usually collected at presentation and 10-14 days later)

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88
Q

What is used to assess severity of asthma?

A

CURB-65

C – New mental confusion

U – Urea > 7 mmol/L

R – Respiratory rate > 30 per minute

B – blood pressure (systolic BP < 90 or DBP <60 mmHg)

Age > 65 years

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89
Q

What are the aetiological features of pneumonia?

A
  • Poor swallow (CVA, muscle weakness, alcohol)
  • Abnormal ciliary function (smoking, viral infection)
  • Abnormal mucus (cystic fibrosis)
  • Dilated airways: bronchiectasis
  • Defects in host immunity (HIV, Immunosuppression)
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90
Q

What are general measures for management of pneumonia?

A
  • Maintain a good oral fluid intake to avoid dehydration.
  • Anti-pyretic drugs- fever and malaise, together with stronger analgesics for pleural pain
  • More severe illness may require intravenous fluids and oxygen.
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91
Q

What are the treatment measures for community acquired pneumonia?

A
  • Target organism is Pneumococcus
  • Amoxicillin or Doxycycline for Mild/Moderate pneumonia
  • Co-amoxiclav and Doxycycline for Moderate/Severe
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92
Q

What is the treatment for hospital acquired pneumonia?

A

Hospital acquired pneumonia is more likely to be due to gram negative organisms
use antibiotics which would cover these organisms .

First line: IV Co-Amoxiclav

Second line: Meropenem

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93
Q

What drugs are used to treat atypical organism?

A

Erythromycin/clarithromycin) or tetracycline (doxycycline)

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94
Q

Why are people with TB checked for HIV?

A

Dysfunction in the immune system can result in the latent infection activating

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95
Q

What are preventative methods of pneumonia?

A
  • Flu vaccine (annually given)
  • Pneumococcal vaccine (5 yrs)
  • Chemoprophylaxis – oral penicillin/erythromycin to patients with higher risk of LRT infections
  • Smoking advice
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96
Q

What are some complications of pneumonia?

A
  • Pleural effusion
  • Empyema
  • Lung abscess formation
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97
Q

What are the links between immunosuppression and lower trespiratory tract infection?

A
  • HIV: PCP, TB, atypical mycobacteria
  • Neutropenia: fungi e.g. Aspergillus spp
  • Bone marrow transplant: CMV
  • Splenectomy: encapsulated organisms –e.g. S. pneumoniae, H. influenzae, malaria
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98
Q

What are common respiratory flora?

A
  • Viridans streptoccic
  • Neisseria spp
  • Anerobes
  • Candida sp

Less common

  • Streptococcus pneumoniae
  • Streptococcus pyogens
  • Haemophilus influenzae
  • Psedomonas
  • E.coli
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99
Q

What are muco-ciliary mechanisms for clearance of respiratory mucosa?

A
  • Nasal hairs, ciliated columnar epithelium of the respiratory tract
  • Cough and the sneezing reflex
  • Respiratory mucosal immune system. Lymphoid follicles of the pharynx and tonsils, alveolar macrophages, secretary IgA and IgG
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100
Q

What are common upper respiratory infections?

A
  • Rhinitis (common cold)
  • Pharyngitis
  • Epiglottis
  • Laryngitis
  • Tracheitis
  • Sinusitis
  • Otitis media
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101
Q

What are common viruses that infect the upper respiratory tract?

A
  • Rhinovirus
  • Coronavirus
  • Influenza
  • Parainfluenza Respiratory syncytial virus (RSV)
  • Bacterial super-infection common with sinusitis and otitis media –can lead to mastoiditis, meningitis, brain abscess
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102
Q

How does aspiration pneumonia occur and how is it treated?

A

-Aspiration of exogenous material or endogenous secretions into respiratory tract
-Common in patients with neurological dysphasgia (epilepsy, alcoholics, drowning, strokes)
-Risk groups (nursing home residents, drug overdose)
-Mixed infection (viridans streptococci, anaerobes
Treat with Co-amoxiclav)

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103
Q

What is ventilation?

A

The process of inspiration and expiration

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104
Q

What is the tidal volume?

A

The volume of air which enters and leaves the lungs with each breath

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105
Q

Can the lungs be emptied completely?

A

No. Residual volume will remain

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106
Q

What is the physiological dead space?

A

Air in alveoli which are not perfused or are damaged do not take part in gas exchange, and ventilation of these alveoli are wasted

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107
Q

What are the lung capacities defined by?

A

Maximum inspiration
Maximum expiration
End of a quiet expiration

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108
Q

What is the volume of the conducting airways termed as?

A

Anatomical dead space

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109
Q

What is the equation for the total dead space?

A

Anatomical dead space + Physiological dead space

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110
Q

What is the equation for tidal volume?

A

Anatomical dead space + alveolar ventilation

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111
Q

What is the equation for total pulmonary ventilation?

A

Tidal volume X respiratory rate

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112
Q

What is the equation for the alveolar ventilation?

A

(Tidal volume - Dead space) X Respiratory rate

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113
Q

What is the inward force acting on the lung at rest?

A

The lung’s elasticity and surface tension generate an inwardly directed force that favours small lung volumes

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114
Q

What is the outward force acting on the lung at rest?

A

The muscles and various connective tissues associated with the rib cage also have elasticity. At rest these elastic elements favour outward movement of the chest wall.

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115
Q

What is the result of the inward and out ward force acting on the lung at rest?

A

They balance each other and create a negative pressure within the intrapleural space relative to atmospheric pressure

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116
Q

How does inspiration occur?

A
  • Contraction of the diaphragm and the external intercostal muscles expands the thoracic cavity outward from equilibrium position
  • Pleural seal ensure that the lungs expand along with the thorax.
  • Lung volume increase so air pressure within the lungs fall below atmospheric pressure. Air flows into the lungs
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117
Q

What happens in (quiet) expiration?

A
  • Muscle contraction ceases
  • Elastic recoil of the lung results in the thoracic cavity and lung returning to the original position
  • Passive process
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118
Q

What ensures that the chest wall and lung move together?

A

-Surface tension due to fluid lining the pleural space which holds the outer surface of the lungs to the inner surface of the chest wall. This ensure that the chest wall and lungs move together.

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119
Q

What happens to the intrapleural pressure during inspiration?

A

The intrapleural pressure becomes more negative and returns to resting pressure at the end of quiet expiration

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120
Q

What are the muscle of quiet inspiration?

A
  • Diaphragm

- External Intercostal muscles

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121
Q

What muscles are involved in quiet expiration?

A

None!

Due to elastic recoil

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122
Q

Which muscles are involved in forced inspiration?

A

Accessory muscles of inspiration.

  • Sternocleidomastoid
  • Scalene
  • Serratus anterior
  • Pectoralis major
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123
Q

What muscles are used in forced expiration

A
  • Internal intercostal muscles

- Abdominal wall muscles

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124
Q

What is the stretchiness of the lung known as?

A

Compliance

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125
Q

What is compliance defined as?

A

Volume change per unit pressure change

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126
Q

What contributes to the elastic properties of the lung?

A
  • Elastic tissue in the lungs

- Surface tension forces of fluid lining the alveoli

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127
Q

What is contained in the alveolar lining fluid?

A

Surfactant

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128
Q

What is the purpose of surfactant?

A
  • Reduce surface tension thereby increasing lung compliance
  • Stabilise the lungs by preventing small alveoli collapsing into big ones
  • Prevents the surface tension in alveoli creating a suction force tending to cause transudation fluid from pulmonary
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129
Q

How does surfactant increase surface tension as the alveolus expands?

A

Surfactant molecules spread further apart making them less efficient

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130
Q

How does surfactant decrease the surface tension as the area of the alveolus decreases?

A

Surfactant molecules comes closer together increasing their concentration and act more efficiently thereby reducing the surface tension

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131
Q

What is the effect of the increase in concentration of surfactant in the smaller alveoli?

A

The force required to expand smaller alveoli is therefore less than that required to expand the large one

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132
Q

What would happen between the different sized alveoli if the surface tension was constant?

A

-Smaller alveoli would have a higher pressure within it.
-Therefore if two unequaled size alveoli were connected by an airway the smaller alveolus would empty into the larger alveolus due to having a higher pressure
Law of Laplace

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133
Q

What would happens to the surface area for gas exchange if the surface tension was a constant in the variable alveolus sizes?

A
  • The smaller alveoli would collapse into larger alveoli to from huge air filled spaces
  • Combined surface area of a few large bubbles would be much less than combined surface area of thousands of small alveoli
  • Surface area for gas exchange would decrease
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134
Q

What is the effect of surfactant on the alveoli as the size increases?

A

As the alveolus expands the surface tension and the radius increase as well.

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135
Q

What is the effect of surfactant on the alveolus as the size decreases?

A

As the alveolus shrinks

  • Radius decreases
  • Surface tension reduces
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136
Q

What is the overall effect of surfactant?

A

Different sized alveoli can have the same pressure within them. This stabilises the lungs preventing small alveoli collapsing into big ones.

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137
Q

What is respiratory distress syndrome of the newborn?

A

Condition usually seen in premature babies particularly those less than 30 weeks old due to lack of surfactant.
-Without surfactant, surface tension of alveolar sacs is high so increases tendency of the alveoli to collapse.

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138
Q

What is the treatment for RDS?

A
  • Surfactant replacement via endotracheal tube

- Supportive treatment with oxygen and assisted ventillation

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139
Q

What are the sign of RDS in the babies?

A
  • Cyanosis
  • Grunting
  • Intercostal and subcostal recessions
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140
Q

What is the question for the minute ventilation?

A

Tidal volume X Breaths per minute

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141
Q

How do you calculate the tidal volume entering the gas exchange region of the lung?

A

Resting tidal volume - Amount in anatomical deadspace

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142
Q

What is alveolar ventilation?

A

Respiratory frequency X volume available for gas exchange

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143
Q

Where in the bronchial tree is the main site of airways resistance?

A

The upper respiratory tract
-Although resistance increases sharply with lower radius the combined cross sectional area of the bronchioles is a lot bigger than the cross sectional area of the trachea.

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144
Q

What are different mechanism for increased airways resistance?

A
  • Increased mucus (Chronic bronchitis)
  • Hypertrophy of the smooth muscle, and/or oedema (Asthma)
  • Loss of radial traction (Emphysema)
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145
Q

What is the equation for resistance?

A

Pressure/Flow=Resistance

Resistance is also directly proportional to 1/r^4
Small change in r makes a big difference in resistance

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146
Q

Why do lungs collapse when air enter the pleural cavity?

A

Lack of negative pressure in the pleural cavity so the lungs aren’t held against the thoracic wall so they collapse

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147
Q

How can damage to the intercostal vessels and nerves be avoided during procedure requiring insertion into the pleural space?

A

The costal groove runs underneath each rib so inserting into the lower border of the intercostal space or inserting into superior border of the rib

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148
Q

Explain why lack of surfactant causes difficulty breathing?

A
  • Increased surface tension so alveolar walls held closer together
  • Smaller alveoli are not able to expand as well due to increased pressure
  • Bigger alveoli will expand
  • Higher volume in the thorax is need to lower the pressure in the alveoli
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149
Q

Why is there indrawing of intercostal spaces during respiration?

A
  • Active contraction of external intercostal muscle in order to pull the thoracic wall upwards which will increase volume.
  • Pressure decreases as result
  • Indrawing is the presence of the active contraction
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150
Q

How does fibrosis affect compliance?

A

Reduced compliance

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151
Q

How does emphysema affect compliance of the lungs?

A

Increased compliance

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152
Q

What is the ideal gas equation?

A

PV=nRT

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153
Q

What is Boyle’s law?

A

Pressure in a gas is inversely proportional to its volume

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154
Q

What is the total partial pressure exerted in a mixture of gases equal to?

A

The sum of the partial pressure of the individual gases

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155
Q

What is composition of atmospheric air?

A 
20.9% = Oxygen
78% = Nitrogen
0.03% = CO2
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156
Q

How do gases diffuse in the body?

A

Down the partial pressure gradient

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157
Q

What happens when gas molecules come into contact with body fluids?

A
  • Gas molecule will enter the fluid to dissolve

- The water molecules evaporate to enter air

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158
Q

What is the saturated vapour pressure at body temperature?

A

6.28 kPa

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159
Q

What happens to inhaled air in the upper respiratory tract?

A

Saturated with water

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160
Q

How does water vapour affect the partial pressure of other gases at 101 kPa?

A

101-6.28

The use the normal ratios

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161
Q

When is the equilibrium of gases established in a fluid?

A

Rate of gas molecules entering water = rate of gas molecules leaving the water

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162
Q

What is occurring at equilibrium of gas in fluid?

A

Partial pressure of the gas in the liquid = partial pressure gas in the air above it

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163
Q

Partial pressure is the same as the amount of dissolved gas. True/False. Why?

A

False

Amount of gas dissolved = Partial pressure X solubility coefficient of gas

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164
Q

When is partial pressure established if there is a component of liquid that the gas reacts with?

A

Partial pressure is established after the gas reacts with component

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165
Q

What happens when oxygen encounters plasma?

A
  • Enters plasma and dissolves in it
  • Dissolved oxygen enter red blood cells to bind to Hb
  • Process continues till Hb fully saturated
  • After Hb is fully saturated, oxygen continues to dissolve until the equilibrium is established
  • At equilibrium pO2 of plasma=pO2 of alveolar air
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166
Q

What happens to the dissolved oxygen in plasma when it encounters tissues?

A

It is available to diffuse into tissues and is replaced by the oxygen bound to haemoglobin

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167
Q

Why does alveolar air equilibrate with the blood air?

A

There is constantly gas moving out and into the alveolus. Oxygen move into the blood stream constantly .

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168
Q

What happens to the atmospheric pressure and gases at high altitudes?

A
  • The atmospheric pressure is lower

- There are fewer molecules of gas.

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169
Q

What happens to pressure as you dive further into the sea?

A

The pressure increase dramatically

Pressure below sea level = Atmospheric pressure+weight of water

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170
Q

What is decompression sickness in divers?

A
  • Nitrogen moves from high pressure in the lungs into the blood during a dive
  • A slow return to the surface lets the nitrogen return to the lungs where it is breathed out
  • A quick return doesn’t give the nitrogen enough time to leave the blood so instead it can form painful bubbles
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171
Q

What are the features of oxygen binding?

A
  • Reaction has to be reversible
  • Oxygen must dissociate at the tissue to supply them
  • Oxygen combines reversibly
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172
Q

What are 2 examples of oxygen binding pigments?

A
  • Haemoglobin: Tetramer to bind 4 oxygen molecules

- Myoglobin: binds 1 oxygen molecule

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173
Q

What is myoglobin?

A
  • Pigment found in muscles

- Contains 1 subunit of haem

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174
Q

Why is myoglobin not a good carrier of oxygen?

A

It will not give up oxygen at the tissues due having a high affinity for oxygen even at low partial pressure. It acts as a storage molecule that will give up oxygen if the oxygen in the tissue gets very low. Also acts as a pigment for the muscle giving it the red appearance

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175
Q

What is the structure of haemoglobin?

A
  • Tetramer consisting of 2 alpha and 2 beta subunits
  • Each subunit has a haem group and a globin group
  • 4 oxygen molecules bind to each molecule of haemoglobin
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176
Q

What are the forms of haemoglobin?

A
  • Low affinity T state

- High affinity R state

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177
Q

What happens to haemoglobin when the pO2 is low?

A

The haemoglobin shift to the low affinity T state so it is harder for the first O2 molecule to bind

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178
Q

What happens as each O2 molecules bind to the haemoglobin?

A

The molecule becomes more relaxed and the binding of the next O2 molecule is easier

179
Q

What is the shape of the haemoglobin dissociation curve?

A

Sigmoidal curve

180
Q

What are the features of the haemoglobin dissociation curve?

A
  • Saturation changes greatly over a narrow range

- Reaction is highly reversible and depends on pO2 levels

181
Q

What happens to the oxygen content and pO2 if the patient is anaemic?

A
  • pO2 is normal

- Oxygen content is much lower

182
Q

What is the oxygen content of blood when the haemoglobin is saturated (13.3 kPa)?

How would you work out the amount of oxygen given up?

A

-2.2 mmol/l if the Hb concentration is normal

Each haemoglobin bind 4 oxygen molecules
2.2X4 = 8.8 mmol/l

Amount of oxygen given up = ((100 - Saturation at Partial pressure in the site)/100) X 8.8

183
Q

What happens to the dissociating at tissue with a lower pO2 and the result of this on venous blood?

A
  • Increased dissociation

- Lower saturation of venous blood

184
Q

What is the saturation of haemoglobin in venous blood?

A

-Over half the oxygen is still bound

185
Q

What is the adaptation of very metabolically active tissue to allow them to receive sfficnet oxygen?

A

Very high capillary density so that pO2 will fall lower due to decreased diffusion distance

186
Q

What is the Bohr effect?

A
  • pH affects the affinity of haemoglobin
  • Acid condition shifts dissociation curve to the tight
  • Lower pH promotes gift to the T state and higher ph promotes a shift to the R state
187
Q

Why is the Bohr effect beneficial to the metabolically active tissues?

A

-pH is lower in most metabolically active tissue so extra O2 is given up

188
Q

What is maximum unloading of oxygen?

A
  • Occurs in tissues where pO2 can fall to a low level
  • In conditions where increased metabolic activity results in more acidic environment and higher temperature
  • Under these conditions about 70% bound oxygen can be given up
189
Q

In extreme exercise , metabolism can increase 10x but the cardiac output only goes up by 5x. What supplies the tissues with oxygen?

A

Tissues have improved extraction of oxygen.

This is due to a number of factors

190
Q

What is the function of 2,3 BPG?

A

Increased 2,3-BPG shift the Hb dissociation curve for O2 to the right
This allows more O2 to be given up to tissues because of a shift in the curve

191
Q

What is the result of carbon monoxide poisoning?

A
  • Reacts with Hb to form COHb
  • Increased affinity for unaffected subunits for O2
  • Therefore O2 is not given up at tissues
  • This is fatal if the HbCO is greater than 50%
192
Q

What is hypoxaemia?

A

Low pO2 in arterial blood

193
Q

What is hypoxia?

A

Low oxygen levels in the body and tissues

194
Q

What is cyanosis?

A
  • Bluish coloration due to unsaturated haemoglobin

- Can be peripheral due to poor local circulation or systemic due poorly saturated blood in systemic circulation

195
Q

Why is cyanosis difficult to detect sometimes?

A
  • Poor lighting

- Skin colouration

196
Q

What is pulse oximetry?

A
  • Detection of level of Hb saturation by detection of difference in absorption of light between oxygenated and deoxygenated Hb
  • It only detect the pulsatile arterial blood
  • Venous blood and blood in tissues is ignored
197
Q

What is the limitation of pulse oximetry?

A
  • It doesn’t say how much haemoglobin is present

- It will not detect anaemia but just how well saturated a person blood is

198
Q

Why does cyanosis appear blue?

A

-Deoxygentated haemoglobin is less red that oxygenated haemoglobin

199
Q

What are the features of carbon dioxide when compared with oxygen?

A

It is more soluble
It reacts chemically with water
React with haemoglobin as well at a different site
2.5 times as much in arterial blood

200
Q

CO2 control is more important for pH than for transporting it from the tissues to the lungs. True/False

A

True

201
Q

What is the pH range that arterial blood must be kept in?

A

7.35-7.45

202
Q

How does CO2 interact with arterial blood?

A

Reacts with water in plasma and red blood cells. It is not there as a waste product

203
Q

What does dissolved CO2 form in blood?

A

Reacts with water to form carbonic acid

204
Q

Why is does the amount of carbonic acid need to be controlled?

A

Dissociates quickly to hydrogen ions and hydrogen carbonate ions.

205
Q

The reaction that form carbonic acid from CO2 and water is irreversible. True/False

A

False. It reversible and rate of reaction depends on amount of reactants and products

206
Q

What does the pH of plasma depend on?

A

-Depends on how much CO2 reacts to form H+ (dissolved CO2 pushes the reaction to the right and HCO3- pushes the reaction to the left)
This depends on dissolved CO2 and concentration of hydrogen carbonate

207
Q

What determines how much CO2 dissolved in the plasma?

A

-Partial pressure of CO2

208
Q

What happens to plasma pH when pCO2 rises?

A

Becomes more acidic

209
Q

What happens to the plasma pH when the pCO2 falls?

A

It will become more alkaline

210
Q

What is the determining factors for dissolved CO2?

A

pCO2 of alveoli which is controlled by rate of breathing

211
Q

What does high HCO3- prevent from happening in the blood?

A

Prevent nearly all dissolved CO2 from reacting by shifting the equilibrium

212
Q

What determines the pH of arterial blood?

A

Ratio of HCO3- and pCO2.

213
Q

What is the Henderson-Hasselbalch equation?

A

pH=pK+log([HCO3-])/(pCO2 X 0.23))

214
Q

What enzyme speeds up the reaction that speeds up hydrogen carbonate production in red blood cells?

A

Carbonic anhydrase

215
Q

How do the red blood cells produce hydrogen carbonate?

A
  • H+ ions bind to the negatively charged Hb inside the red blood cells
  • Chloride-bicarbonate exchanger transports HCO3- out of red blood cells which is left front he reaction between CO2 and H2O.
216
Q

Eythrocytes control concentration of HCO3- in plasma. True/False

A

False. They merely produce HCO3-.

217
Q

What determine the amount of HCO3- that is produced by the erythrocytes?

A

Binding of H+ to haemoglobin

218
Q

What is the main determant of plasma hydrogen carbonate? pCO2 or erythrocytes ?

A

Most of the HCO3- comes from the red blood cells

219
Q

What is the role of the kidney in controlling HCO3-?

A

The kidney controls the amount of HCO3- by varying the excretion of bicarbonate. Concentration present in blood is controlled by the kidneys

220
Q

How does hydrogen carbonate buffer extra acid?

A

Acids react with HCO3- to produce CO2. Therefore the bicarbonate decreases.
CO2 produced is removed by breathing and pH changes are minimised

221
Q

What determine arterial pCO2?

A

Alveolar pCO2 which determine how much CO2 is dissolved. This therefore affects pH.

222
Q

pCO2 is higher in venous blood than arterial blood. True/false

A

True. It is returning from metabolically active tissue so more CO2 is dissolved

223
Q

What does the buffering of H+ by the haemoglobin depend on?

A

Level of oxygenation

224
Q

What happens to the amount of H+ ions that can bind to Hb as more O2 binds to Hb?

A

The haemoglobin switches into the R state

-Less H+ ions bind as a result

225
Q

What happens to the amount of H+ ions that can bind to Hb as less O2 binds to Hb?

A

The haemoglobin switches to the T state

-More H+ ions bind

226
Q

How does the amount of CO2 increase in plasma in the venous system?

How does this affect the pH?

A
  • Less O2 bound to Hb so haemoglobin switches to the T state
  • More H+ ions bind to Hb
  • More HCO3- can be produced and is exported to the plasma
  • Therefore more CO2 is present in plasma in venous system.

-More HCO3- is also present so therefore ratio is similar. Small change in plasma pH as both CO2 and HCO3- have increased

227
Q

What happens when venous blood arrives at the lungs?

A
  • Hb picks up O2 and goes into R-state
  • Causes Hb to give up the extra H+ it took on at the tissues
  • H+ reacts with HCO3- to form CO2
  • CO2 is breathed out
228
Q

How are carbamino compounds formed?

A
  • CO2 binds directly to amine groups on the globulin on Hb.
  • This contribute to the CO2 transport but it is not part of the acid base balance
  • This is CO2 given up at the lungs
229
Q

Why are more carbamino compounds formed at the tissues?

A

-The pCO2 is higher and unloading of oxygen facilitates binding of CO2 to haemoglobin

230
Q

What are the forms that CO2 is transported in?

A
  • Dissolved CO2
  • Hydrogen carbonate
  • Carbamino compounds
231
Q

What is the main role of CO2 in blood?

A

-Acts as part of the pH buffering system

Only 8% of the total CO2 is transported

232
Q

What is hypercapnia?

A

Rise in pCO2

233
Q

What is hypocapnia?

A

Fall in pCO2

234
Q

What is hypoxia?

A

Fall in pO2

235
Q

How does exercise affect the partial pressure of CO2 and O2?

A
  • pO2 drops and pCO2 rises

- Breathing more will restore both

236
Q

What is hyperventilation?

A

Ventilation increase without change in metabolsim

237
Q

What is hypoventilation?

A

-Ventilation decrease without change in metabolism

238
Q

What happens to pCO2 and pO2 in hyperventilation?

A
  • pO2 will rise

- pCO2 will fall

239
Q

What happens to pCO2 and pO2 in hypoventilation?

A
  • pO2 will fall

- pCO2 will rise

240
Q

What happens if the pO2 changes without a change in CO2?

A

Correction of the pO2 will cause the pCO2 to drop

This leads to hypocapnia

241
Q

Control system are in place to prevent marked hypoxia. True/False

A

True

242
Q

What is the effect of CO2 on plasma pH if bicarbonate remains unchanged?

A
  • If pCO2 increase then pH falls
  • If pCO2 decreases then pH rises

Small changes in pCO2 lead to large changes in pH.

243
Q

What are the effects of pH falling and pH rising?

A
  • If pH falls below 7.0 then enzymes become denatured

- If pH rises above 7.6 free calcium concentration drops leading to tetany

244
Q

What are the effects of hypercapnia on plasma pH?

A

-Respiratory acidosis due to fall in plasma pH

245
Q

What are the effects of hypocapnia on plasma pH?

A

-Respiratory alkalosis due to rise in plasma pH

246
Q

How does the kidney compensate for respiratory acidosis?

A
  • Kidneys increase reabsorption of HCO3-
  • This compensate for the the increase in pCO2

(can take 2-3 days)

247
Q

How does the kidney compensate for respiratory alkalosis?

A
  • Kidneys decrease reabsorption of HCO3-
  • This compensates for the decrease in pCO2

(can take 2-3 days)

248
Q

How does metabolic acidosis occur?

A
  • If tissues produce acid, this reacts with HCO3-
  • Fall in [HCO3-] leads to fall in pH
  • This causes metabolic acidosis
249
Q

How is metabolic acidosis compensated for?

A
  • Compensated for by changing ventilation
  • Increased ventilation lowers pCO2
  • Restores pH towards normal
250
Q

How does metabolic alkalosis occur?

A
  • If the plasma HCO3- rises
  • Plasma pH rises
  • Causes metabolic alkalosis
251
Q

How is metabolic alkalosis compensated for?

A

-Decreasing ventilation so that pO2 falls and pCO2 increases

252
Q

How are the respiratory pathways controlled?

A
  • Sensors located in CNS and the periphery feed information back to the control centre for processing
  • Ventilation is adjusted as necessary
253
Q

What are the examples of peripheral chemoreceptors?

A

Carotid and aortic bodies

254
Q

What stimulates the peripheral chemoreceptors and what does it lead to?

A

Large falls in pO2 stimulate the peripheral chemoreceptors. This leads to

  • Increased breathing
  • Changes in the heart rate
  • Changes in blood flow distribution which increases the flow to the brain and kidneys
255
Q

What is the sensitivity of the peripheral chemoreceptors to the pCO2?

A

Relatively insensitive to pCO2

256
Q

What is the sensitivity of the central chemoreceptors to the pCO2?

A

Sensitive to the pCO2

257
Q

Where are the central chemoreceptors found?

A

Medulla of the brain

258
Q

Why isn’t the central chemoreceptor affected by bicarbonate ions and H+ but it is affected by CO2?

A
  • The ECF and CSF is impermeable to HCO3- and H+ due to the blood brain barrier
  • The blood brain barrier is selective permeable to CO2 however
259
Q

How do the central chemoreceptors work?

A
  • Respond to changes in the pH of cerebrospinal-spinal fluid
  • CSF is operated from blood by the blood brain barrier
  • CSF [HCO3-] is controlled by choroid plexus cells
  • CSF pCO2 is determined by arterial pCO2
260
Q

How is CSF pH determined?

A
  • Determined by ratio of [HCO3-] to pCO2
  • [HCO3-] fixed in the short term as the blood brain barrier is impermeable to HCO3-
  • Falls in pCO2 lead to rise in CSF pH
  • Rises in pCO2 lead to falls in CSF pH
  • Persisting changes in pH corrected by choroid plexus cells which change the [HCO3-]
261
Q

How do the central chemoreceptors counteract an increase in the pCO2?

A
  • Elevated pCO2 drives the CO2 into the CSF across the blood brain barrier
  • CSF [HCO3-] is initially constant
  • CSF pH falls
  • Fall in CSF pH detected by central chemoreceptors
  • Drives increased ventilation
  • This lowers the pCO2 to restore the CSF pH
262
Q

What is the action of the choroid plexus?

A
  • Determine what is normal
  • CSF [HCO3-] determine which pCO2 is associated with normal CSF pH.
  • CSF [HCO3-] therefore sets the control system to a particular pCO2
  • Can be reset by changing CSF [HCO3-] with persistent hypercapnia
263
Q

How does persisting hypoxia affect the central chemoreceptors?

A
  • Hypoxia is detected by the peripheral chemoreceptors which will trigger increase in ventilation
  • pCO2 will fall further and this causes decrease in ventilation
  • CSF composition compensates for the altered pCO2
  • Choroid plexus cells selectively add H+ or HCO3- into the CSF
  • Central chemoreceptors accept the pCO2 as normal
264
Q

How does persisting hypoxia and hypercapnia affect the central chemoreceptors?

A
  • Hypoxia and hypercapnia lead to respiratory acidosis
  • Decreased pH of CSF
  • Peripheral and central chemoreceptors stimulate breathing
  • CO2 diffuses into CSF and CSF pH drops
  • Persistently CSF acidity harmful to neurons
  • Low CSF pH corrected by choroid plexus cells which secrete HCO3- in to CSF

  • The CSF pH returns to normal; central chemoreceptors no longer stimulated
  • pCO2 in the blood is still high but central chemoreceptors now unresponsive to this pCO2 i.e. Central chemoreceptors have ‘reset’ to a new higher CO2 level
  • The persistent hypoxia stimulates peripheral chemoreceptors

  • Respiratory drive is now driven by hypoxia (via peripheral chemoreceptors)
265
Q

What is alkalaemia and acidaemia?

A 
Alkalaemia = >7.45
Acidaemia = <7.35
266
Q

What is the effect of alkalaemia?

A
  • Lower free calcium by causing Ca2+ t come out of solution
  • This increase neuronal excitability
  • Can lead to paraesthesia and tetany

Higher mortality compared to acidaemia

267
Q

What is the effect of acidaemia?

A
  • Causes an increase plasma potassium ion concentration affects excitability particularly in heart muscle and can cause arrhythmia
  • Can denature enzymes high can affect muscle contractility, glycolysis and hepatic function
  • Severe effect below 7.1 and life threatening below 7
268
Q

How are pCO2 and HCO3- disturbed ?

A

pCO2 is disturbed by respiratory disease

HCO3- is disturbed by metabolic and renal disease

269
Q

Why doesn’t acid produced by metabolism deplete HCO3-?

A
  • Kidney recovers all filtered HCO3-
  • Proximal tubule make HCO3- from amino acids, putting NH4+ in the urine
  • Distal tubule makes HCO3- from CO2 and H2O. The H+ is buffered by phosphate and ammonia in the urine when excreted
270
Q

What is the process for recovery of HCO3-?

A
  • HCO3- filtered at the glomerulus
  • Mostly recovered in PCT
  • H+ excretion is linked to Na+ entry in PCT
  • H+ react with HCO3- in the lumen to form CO2 which enters the cell
  • CO2 converted back to HCO3- which enters the ECF
271
Q

Describe the creation of HCO3- in the proximal tubule.

A
  • Glutamine is convert to alpha ketoglutarate
  • Produces HCO3- and ammonium
  • HCO3- enters the ECF
  • NH4+ enters lumen
272
Q

Describe the formation of HCO3- in the distal tubule

A
  • Distal tubule and collecting ducts also secrete H+ produced from reaction of CO2 with water
  • H+ ions are actively secreted
  • H+ buffered by ammonia and phosphate. NH4+ and H2PO4- created
  • No CO2 is formed to re-enter the cell
  • Allows HCO3- to enter plasma
273
Q

What is the kidney response to an increased acid load in an individual?

A
  • Ammonium generation from glutamine in proximal tubule can be increased in response to low pH
  • Ammonium splits to form NH3
  • NH3 moves into lumen and throughout the interstitum
  • H+ actively pumped into lumen in DCT and CT
  • H+ combines with NH3 to form NH4+. This is trapped in lumen
  • Ammonium can’t move back into the cell
  • Increased excretion of ammonium as a result

-NH4+ can also be taken up in TAL and transported to interstitum and dissociated to H+ and NH3. This moves into the lumen of collecting ducts

274
Q

What are the features of urine in terms of cations and anions?

A
  • Minimum pH is 4.5
  • No HCO3-
  • Some H+ is buffered by phosphate
  • Some H+ has reacted with ammonia to form ammonium
275
Q

What is the effect of acidosis on potassium?

A
  • Potassium ions move out of cells
  • Decreased potassium excretion in distal nephron
  • Hyperkalaemia
276
Q

What is the effect of alkalosis on potassium?

A
  • Potassium ions move into cells
  • Enhanced excretion of potassium in distal nephron
  • Hypokalaemia
277
Q

What is the effect of hypokalaemia on intracellular pH of tubular cells?

A
  • H+ move into the cells
  • Favours K+ excretion and HCO3- recovery
  • Metabolic alkalosis
278
Q

What is the effect of hyperkalaemia on intracellular pH of tubular cells?

A
  • H+ ions move out of the cells
  • This favours HCO3- excretion
  • Metabolic acidosis
279
Q

What are the characteristics of uncompensated respiratory acidosis?

A
  • High CO2
  • Normal HCO3-
  • Low pH
280
Q

What are the characteristics of uncompensated respiratory alkalosis?

A
  • Low pCO2
  • Normal HCO3-
  • Raised pH
281
Q

What are the characteristics of compensated respiratory acidosis?

A
  • High pCO2
  • Raised HCO3-
  • Relatively normal pH
282
Q

What are the characteristics of compensated respiratory alkalosis?

A
  • Low pCO2
  • Lowered HCO3-
  • Relatively normal pH
283
Q

What is the anion gap?

A
  • Difference in measured anions and cations

- Normally 10-18 mmol/l

284
Q

When is the anion gap increased?

A
  • If HCO3- is replaced by other anions

- If a metabolic acid reacts with HCO3-, the anion of the acid replaces HCO3-

285
Q

What is the effect of Renal causes of acidosis on the anion gap?

A
  • In renal causes of acidosis anion gap will be unchanged

- Not making enough HCO3- but it is replaced by Cl-

286
Q

What are the features of uncompensated metabolic acidosis?

A
  • Normal pCO2
  • Low HCO3-
  • Low pH
  • Increased anion gap if HCO3- is replaced by another organic anion from an acid
  • Normal anion gap if HCO3- is replaced by Cl-
287
Q

What are the characteristics of compensated metabolic acidosis?

A
  • Low HCO3-
  • Lowered pCO2
  • Nearer normal pH
288
Q

What are the characteristics of uncompensated metabolic alkalosis?

A
  • Normal pCO2
  • Raised HCO3-
  • Increased pH
289
Q

What is type 2 respiratory failure?

A
  • Low pO2 and High pCO2

- Alveoli cannot be properly ventilated

290
Q

What are causes of type 2 respiratory failure?

A
  • Severe COPD
  • Severe asthma
  • Drug overdose
  • Neuromuscular disease
291
Q

How can type 2 respiratory failure be compensated for?

A

Increase in HCO3-

-Chronic conditions can be well compensated to the near normal

292
Q

What are conditions that can cause respiratory alkalosis?

A

Hyperventilation caused by Anxiety/panic attacks (acute setting)

Hyper ventilation in response to long-term hypoxia (type 1 respiratory failure)

293
Q

What are conditions that cause metabolic acidosis?

A
  • Keto acidosis in diabetes
  • Lactic acidosis (exercising to exhaustion, poor tissue perfusion)
  • Uraemic acidosis (advanced renal failure)
294
Q

What are conditions leading to metabolic acidosis with a normal anion gap?

A
  • Renal tubular acidosis. Problems with transport mechanism in the tubules
  • Severe persistent diarrhoea which can lead to metabolic acidosis due to loss of HCO3-. Replaced by Cl-
295
Q

What happens in diabetic acidosis to potassium?

A
  • K+ moves out of cells
  • Osmotic diuresis means K+ is lost in urine
  • Total body depletion of K+
296
Q

What are conditions leading to metabolic alkalosis?

A
  • Severe prolonged vomiting or mechanical drainage of the the stomach leads to loss of H+. Stomach secretes more H+ and produces HCO3- in this process.
  • Potassium depletion/mineralcoritcoid excess
  • Certain diuretics
297
Q

How is metabolic alkalosis corrected?

A
  • Rise in pH of tubular cells leads to fall in H+ excretion and reduction in HCO3- recovery
  • Problems can occur is there is also volume depletion
298
Q

Why can problems occur with correction of metabolic alkalosis if there is volume depletion?

A
  • High Na+ recovery rate so capacity to loss HCO3- is reduced
  • Recovering Na+ favours H+ excretion and HCO3- recovery
299
Q

How can vital capacity be calculated?

A

Inspiratory capacity + expiratory reserve volume

300
Q

What are the features of an obstructive disorder?

A
  • FEV1 is reduced
  • FVC may be reduced
  • FEV1/FVC is reduced
  • Shark peak peak flow
  • Scoopiness/Scalloped
301
Q

What are the features of a restrictive disorder on spirogram?

A
  • FEV1 appropriate for FVC
  • FVC reduced
  • FEV1/FVC is normal
  • No Scoopiness/Scalloped
  • Straight
302
Q

What are some quality control and practical aspects of spirometry?

A
  • Demostration and carful explanation
  • Person making the recordings is every bit as important as spirometer
  • Use of incentive spirometry
  • Observe the subject
  • Inspect raw data
303
Q

When is extrathoracic abnormality evident?

A

On Inspiration

304
Q

When is intrathoracic abnormality evident?

A

On Expiration

305
Q

What is an embolism?

A

Movement of material from one part of circulation to another. Can be

  • Thrombus
  • Tumour
  • Air
  • Fat
  • Amniotic fluid
  • Bullet
306
Q

What is the aetiology of a pulmonary embolism?

A
  • Thrombus entering the right side of the heart and pulmonary arteries in most cases
  • 90% arise form a DVT in the legs particularly in the popliteal vein and more proximal veins such as pelvic veins
  • However only 25% of patients with a PE have symptoms or signs of a DVT
307
Q

What is the epidemiology of pulmonary embolism?

A
  • Third commoners cause of vascular death after myocardial infarction and stroke
  • Commonest cause of preventable death in hospital patient
  • Risk facts are age and incidence increase past 40
308
Q

What are some risk factors for thromboembolism?

A
  • Surgery
  • Obesity
  • Cancer
  • Prolonged immobilisation
  • Previous thromboembolism
  • Heart failure
  • Contraceptive pill
  • Pregnancy
  • HRT
  • Long haul travel (>4hrs)
  • Thrombophilia
309
Q

What are the outcomes of PE?

A
  • Sudden death

- Asymptomatic

310
Q

What is the pathophysiology of a PE?

A
  • Right ventricular overload
  • Respiratory failure
  • Pulmonary infarction
311
Q

How does right ventricular overload occur in PE?

A
  • Pulmonary artery pressure increase if more than 30% of total cross sectional area of peulmary arterial bed occluded.
  • Lead to right ventricle dilatation and strain
  • Inotropes released in attempt to maintain systemic BP which causes pulmonary vasoconstriction that further exacerbates the situation
  • This all leads to Right ventricular overload

-Right to left shunting through patent foramen ovale is present in 1/3 of patient and may lead to severe hypoxaemia and paradoxical embolisation and stroke

312
Q

How does respiratory failure occur in PE?

A

-Due to areas of ventilation perfusion mismatch and low right ventricle output

313
Q

How does pulmonary infarction occur in PE?

A
  • Small distal emboli may create areas of alveolar haemorrhage resulting in haemoptysis, pleuritis and small pleural effusion
  • Pleuritic pain is worse on inspiration
314
Q

What are physical signs of PE?

A
  • Pleural rub in cases of pulmonary infarction

- Raised JVP

315
Q

What are symptoms of PE?

A
  • Pleuritic chest pain
  • Haemoptysis
  • Dyspneoa
  • Cough
  • Fever
  • Syncope
  • Unilateral leg pain
  • Substernal chest pain
316
Q

What are investigations undertake for Pulmonary embolism?

A

CXR - Not useful as a primary diagnostic tool. Used to rule out other diagnoses

ECG - Right ventricular strain. S1 Q3 T3

Blood gas - Show hypoxaemia and hypocapcnia due to hyperventilation

D-dimer - Normal D-dimer rules out PE in those at low likelihood of having a PE. In those with high likelihood, the negative predictive value of D-dimer is too low to use

317
Q

What are D-dimers?

A
  • Fibrin degradation product.
  • Small protein fragment released into the blood when a thrombus is degraded by fibrinolysis.
  • Normally not present unless coagulation system has been activated
318
Q

What is the gold standard imaging technique for a PE?

A

-CT pulmonary angiography

319
Q

How is a pulmonary embolism treated?

A

-Immediate heparinisation

320
Q

How does immediate heparinaistion reduce mortality in a PE?

A
  • Stops thrombus propagation in the pulmonary and allows the body’s fibrinolytic system to lyse the thrombus
  • Stop thrombus propagation at the embolic source and reduced the frequency of further pulmonary embolism
321
Q

How are high risk PE patients treated?

A
  • Haemodynamic support
  • Respiratory support
  • Exogenous fibrinolytic (peripheral IV, delivered directly via percutaneous catheter into pulmonary arteries)
  • Percutaneous catheter directed thrombectomy
  • Surgical pulmonary embolectomy
322
Q

What happens after the initial heparinisation of the patients?

A

-Oral anticoagulants

3 mouths if identifiable temporary risk factor
Indefinitely if cancer or no identifiable risk factor

323
Q

What are causes of hypoxia?

A
  • Low inspired pO2
  • Hypoventilation – (respiratory pump failure)
  • Ventilation/Perfusion mismatch
  • Diffusion defect – problems of the alveolar capillary membrane
  • Right to left shunt (eg. Cyanotic heart disease)
324
Q

How does hypoventilation lead to type 2 respiratory failure?

A
  • Alveolar ventilation is decreased
  • Amount of O2 entering the blood and CO2 leaving the blood remains unchanged at the start
  • Alveolar pO2 falls so arterial pO2 falls which leads to hypoxaemia
  • Alveolar pCO2 rises so arterial pCO2 increases which leads to hypercapnia
325
Q

What is the difference in treatment for acute and chronic hypoventilation ?

A

Acute (Opiates, Head injury, Very severe acute asthma)
-Need urgent treatment
+/- artificial ventilation

Chronic (Severe COPD)

  • Chronic hypoxia and Chronic hypercapnia
  • Slow onset and progression

  • Time for compensation
  • Therefore better tolerated
326
Q

What are causes of hypoventilation?

A
  • Brainstem (Opiates, Head injury)
  • Spinal cord (Trauma)
  • Phrenic and intercostal nerves (Guilain Barre syndrome)
  • Muscle of respiration (myopathy)
  • Neuromuscular junction (Myasthenia Gravis)
  • Chest wall (Severe Obesity, Kyphoscoliosis)
  • Pleural cavity (Pneumothorax, Large pleural effusions)
  • Poor lung compliance (Respiratory distress of newborn)
  • High airway resistance (very severe acute asthma, late stages of COPD)
  • Upper airway obstruction (Laryngeal oedema, Foreign body)
327
Q

What are the effects of hypercapnia?

A
  • Respiratory acidosis
  • Impaired CNS function: drowsiness, confusion, coma, flapping 
tremors
  • Peripheral vasodilatation –warm hands, bounding pulse
  • Cerebral vasodilation – headache
328
Q

How is chronic hypercapnia compensated ?

A

Retention of HCO3- compensates for the respiratory acidosis

329
Q

How can treatment of hypoxia worsen hypercapnia?

A
  • O2 removes stimulus for the hypoxic respiratory drive

  • Alveolar Ventilation drops which causes worsening hypercapnia
  • Correction of hypoxia removes pulmonary hypoxic vasoconstriction which leads to increased perfusion of poorly ventilated alveoli, diverting blood away from better ventilated alveoli.
330
Q

What are the adjustments made to treat patients with severe COPD?

A
  • pO2 given but pCO2 needs to be monitored
  • Controlled oxygen therapy with a target saturation of 88-92%
  • If oxygen therapy causes rise in pCO2 - need ventilator support
331
Q

What are the effects of hypoxaemia?

A
  • Impaired CNS function, confusion, irritability
  • Cyanosis
  • Cardiac arrhythmia
  • Hypoxic vasoconstriction
332
Q

How is chronic hypoxaemia compensated?

A
  • Increased EPO secreted by kidney so raised Hb (Polycythaemia)
  • Increased 2,3, DPG to increase oxygen dissociation 

333
Q

What are the effects of chronic hypoxaemia?

A

Chronic hypoxic vasoconstriction of pulmonary vessels results in

  • Pulmonary hypertension
  • Right heart failure

  • Cor pulmonale
334
Q

What is the optimal V/Q ratio?

A

1

335
Q

What happens when V/Q ratio is <1?

A

-Alveolar pO2 falls and pCO2 rises

336
Q

What happens when pathology impairs ventilation in an area of the lung?

A
  • V/Q < 1 in these alveoli
  • Hypoxic vasoconstriction occurs so this diverts some (but not all) blood to better ventilated areas
  • Blood from these alveoli will have low pO2 and high pCO2 mixed in the left atrium
  • Central and peripheral chemoreceptors are stimulated which causes hyperventilation
  • Affected area are still poorly ventilated due to the pathology
337
Q

What is effect on an unaffected area of the lung when a pathology affects a region of the lungs?

A
  • Unaffected segments have increased ventilation. V/Q > 1
  • pO2 rises and pCO2 falls
  • Rise in pO2 leads to increased dissolved oxygen (very small amount)
  • But Hb is fully saturated above 10 kPa
  • Further increases in pO2 has no effect on Hb.
  • O2 content not significantly increased (only tiny amount of extra dissolved O2
  • Insufficient to compensate for low pO2 from segments with V/Q <1
  • Drop in pCO2 accompanied by reduction in total CO2 content in blood
  • Sufficient to compensate for CO2 retention from segments with V/Q <1
  • Final result: low pO2 with normal (or low) pCO2
  • Type 1 respiratory failure
338
Q

How does a pulmonary embolus cause type 1 respiratory failure?

A
  • The embolus results in redistribution of pulmonary blood flow
  • The blood is diverted to unaffected areas of the pulmonary circulation 

  • Leads to V/Q ratio < 1 if hyperventilation cannot match the increased perfusion which causes hypoxaemia.
  • Hyperventilation sufficient to get rid of CO2 

339
Q

How can a diffusion defect lead to type 1 respiratory failure?

A
  • CO2 is more soluble
  • CO2 diffusion less affected than diffusion of O2 affected
  • pO2 low pCO2 normal or low Type 1 respiratory failure
340
Q

What are the causes of diffuse lung fibrosis?

A
  • Idiopathic fibrosing alveolitits
  • Asbestosis
  • Extrinsic allergic alveolitis
  • Pneumoconiosis
341
Q

What are the 6 cardinal signs of respiratory disease?

A
  • Breathlessness (dyspnoea)
  • Cough
  • Chest pain
  • Wheeze/stridor
  • Sputum
  • Haemoptysis
342
Q

What are the causes of dyspnoea?

A
  • Asthma
  • COPD
  • Idiopathic pulmonary fibrosis
  • Myocardial dysfunction
  • Anaemia
  • Obesity
  • Deconditioning
343
Q

What are possible causes of instantaneous breathlessness?

A
  • Pulmonary embolism

- Pneumothorax

344
Q

What are possible causes of acute breathlessness?

A
  • Asthma
  • Pulmonary embolism
  • Pneumonia
  • LVF/MI
  • Hyperventilation syndrome
345
Q

What are causes of gradual breathlessness?

A
  • Lobar collapse (e.g. lung cancer)

- Pleural effusion

346
Q

What are causes of chronic breathlessness?

A
  • COPD
  • Idiopathic pulmonary fibrosis
  • Bronchiectasis
347
Q

What are causes of chest pain?

A
  • Cardiac
  • Pericarditis (relieved by sitting forward)
  • Oesophageal pain – reflux which is a burning pain. Nut cracker oesophagus (oesophagus goes into spasm)
  • Chest wall (costochondritis, rib fracture, spinal osteoarthritis, Herpes zoster)
  • Pleuritic chest pain (viral, bacterial, pulmonary embolism, pneumothorax, pericarditis)
348
Q

What is cough?

A

A reflex arc initiated by mechano- and/or chemoreceptors receptors in the:

  • Respiratory epithelium
  • Oesophagus (reflux oesophagitis leads to chronic cough. Fluid comes up to the mouth and into the trachea)
  • Diaphragm
349
Q

What are causes of cough?

A
  • Respiratory (Acute infection, Chronic infection, Nasal/sinus disease, Airways disease, Parenchymal disease, Irritant, Pleural disease)
  • Cardiovascular (LVF due to orthopnoea)
  • Gastrointestinal (Gastro-oesophageal reflux)
  • Drugs (ACE inhibitor, Inhaled drugs)
350
Q

What are causes of stridor?

A
  • Epiglottitis
  • Croup
  • Diptheria
  • Aspirated foreign bodies
  • Extrinsic compression e.g. large goitre
351
Q

What is stridor?

A

Stridor describes a coarse inspiratory wheeze.

352
Q

What are cause of increased sputum production?

A
  • Smoking/smoke pollution
  • COPD
  • Acute viral or bacterial bronchitis
  • Pneumonia
  • Bronchiectasis (maybe foul-smelling sputum) – anaerobic infection
  • Lung abscess
  • Acute asthma
  • Lung cancer
  • LVF (pink-tinged frothy sputum)
353
Q

How does asthma causes a wheeze?

A

Positive intrapulmonary pressure during expiration will exacerbate any narrowing of intrathoracic airways.

354
Q

What is a wheeze?

A

Wheeze refers to a noisy musical sound produced by turbulent flow through narrow small airways. It is mostly expiratory.

Underlying pathophysiology is bronchial smooth muscle contraction, oedema and mucus production

355
Q

What are the causes of wheeze?

A
  • Asthma
  • COPD
  • Bronchiolitis
  • Sometimes seen in LVF – fluid in the airway causes wheezing
356
Q

Why is a silent chest concerning in asthma attacks?

A

Absent wheeze during a severe asthma attack (‘silent chest’) is a medical emergency

357
Q

What are the conditions associated with a nocturnal wheeze?

A
  • Asthma (PNS is more active at rest so constriction of the airways)
  • LVF (so-called ‘cardiac asthma’. Fluid in lung. Legs are up so more strain on heart)
358
Q

What are causes of central cyanosis?

A
  • Congenital cardiac disease with right to left shunt and severe heart failure.
  • Severe respiratory diseases including COPD
  • Severe pneumonia
  • Severe bronchospasm (including acute asthma
359
Q

Where can central cyanosis be seen?

A
  • Lips

- Tongue

360
Q

What are the causes of peripheral cyanosis?

A
  • Cold exposure
  • Raynaud’s disease.

Present if central is present.

361
Q

What are respiratory causes of clubbing?

A
  • Lung cancer
  • Mesothelioma
  • Bronchiectasis, including cystic fibrosis
  • Empyema
  • Idiopathic pulmonary fibrosis
362
Q

When are accessory muscle of inspiration used?

A
  • Advanced emphysema – need the accessory to take in breath with already inflated lungs
  • Attack of severe asthma
  • Stridor due to laryngeal or tracheal obstruction
363
Q

When are accessory muscle of expiration used?

A
  • Some patients with emphysema
  • Some cases of chronic bronchitis
  • Asthma

Some patients with expiratory obstruction will stand and grasp a table so that they fix the shoulder girdle and use latissimus dorsi to augment the expiratory effort

364
Q

What is the purpose of pursed lip breathing?

A
  • La Places law
  • Trouble breathing in with COPD
  • Stop the alveoli getting too small to prevent difficulty in taking the next breath
365
Q

What is barrel chest?

A
  • Fight between the ribs and lungs. The ribs want to expand but the elastic recoil of the chest prevent it from expanding normally.
  • Loss of elastin in lungs so therefore less elastic recoil
366
Q

Where are the upper and lower lobes percussed?

A

Upper lobes are mainly percussed in the front

Lower lobes are mainly percussed in the back

367
Q

When does tracheal deviation away from affected side occur?

A
  • Tension pneumothorax – pressure in the pleural cavity shifts the mediastinum
  • Large pleural effusion
368
Q

When does tracheal deviation towards the affected side occur?

A
  • Lung or lobar collapse (Common and occurs following obstruction of bronchus. Gas is resorbed from lung parenchyma distal to the obstruction resulting in collapse of the lung, with volume reduction and negative mass effect)
  • Pulmonary fibrosis, particularly upper lobe (fibrosis pulls the lobe)
369
Q

What is lung consolidation?

A

This means a solidification of lung tissue due to the filling of the lungs with liquid and solid material. These liquids replace the air normally
present in alveoli. By far the commonest cause is pneumonia

370
Q

How is the nasal cavity divided?

A

By the medial nasal septum

371
Q

What are the paranasal sinuses?

A
  • 4 air containing cavities named for the skull bones within which they are situated.
  • Lined by respiratory epithelium and open into spaces below the turbinates in the nasal cavity
372
Q

What can be found the lateral wall of each nasal cavity?

A

3 bony projections known as turbinates

373
Q

What do the vascular mucosa do?

A
  • Lined large surface area presented by turbinates and paranasal sinuses
  • Allow inhaled air to be warmed and humidified
374
Q

How does turbulence caused by the turbinates affect airflow?

A
  • Slows down airflow

- Increases the time available for warming and humidification. Air is heated to approximately room temperature

375
Q

How is humidification achieved?

A
  • Transudation of fluid through the epithelium

- By mucus secretion although lesser extent

376
Q

How are nostril equipped to trap particles inhaled in air?

A
  • Coarse hairs

- Mucus secretion by the goblet cells traps particles and are wafted by cilia to oropharynx where it is swallowed

377
Q

What is the common passage for air and food?

A

-Parts of the pharynx

378
Q

What is the purpose of the larynx?

A
  • Links the pharynx to the trachea

- Contains vocal chords which guard the entrance to the trachea

379
Q

What is the glottis?

A

The vocal cords + aperture between the cords

380
Q

What happens to the entrance to the trachea when swallowing?

A
  • Laryngeal inlet becomes narrowed
  • The epiglottis folds downwards over laryngeal inlet
  • The vocal cords come together to act as a sphincter closing off the entrance to the trachea
381
Q

Which muscles cause movement of the vocal cords?

A

Intrinsic laryngeal muscles

382
Q

What nerve supplies the intrinsic laryngeal muscles ( except the cricothyroid muscle)?

A

Recurrent laryngeal nerve

383
Q

What can intra-thoracic disease lead to?

A

Compression of the recurrent laryngeal nerve on the left side which can result in a hoarse voice due to paralysis of the left vocal cord

384
Q

Why is the left side of the recurrent laryngeal nerve at risk?

A

It has a long course part of which is inside the thoracic cavity

385
Q

If the larynx and vocal cords are dysfunctional, what can the effect of this be?

A

Trachea may not be properly closed off during swallowing hence there is a risk of inhalation of food/liquid.

386
Q

What is the purpose of the cough reflex?

A

Protective mechanism to expel inhaled particles and also serves as a clearance mechanism for disposing of excessive secretions from the airways.

387
Q

What can the opening between the vocal cords present as?

A

Airway obstruction and difficulty in breathing which can be an emergency

388
Q

What is the first sign of the intra-thoracic disease?

A

Voice change

389
Q

What is the bronchopulmonary segment?

A

Area of lung supplied by segmental bronchus and the accompanying segmental branch of the pulmonary artery. It is drained by segmental pulmonary vein.

Pyramid shaped with its apex facing towards segmental bronchus and base toward lung surface

390
Q

What is the blood supply for the lungs?

A

Bronchial arteries and pulmonary arteries.

391
Q

What is the purpose of the bronchial arteries?

A

Supply the bronchial tree and visceral pleura with oxygenated blood.

392
Q

How is most of the blood supplied to the bronchial tree and visceral pleura returned to the heart?

A

Pulmonary veins

393
Q

How many pulmonary veins leave each hilum?

A

2

394
Q

What is the lymphatic drainage of the lungs?

A
  • Hilar nodes (bronchopulmonary nodes)

- Tracheobronchial nodes (efferents from bronchopulmonary nodes)

395
Q

How is the lung innervated?

A

Right and Left vagus nerves and the sympathetic trunk

396
Q

How is the bronchial smooth muscle innervated?

A

Parasympathetic efferents from the vagus are motor to the bronchial smooth muscle

397
Q

How are the mucous glands innervated?

A

Secretomotor nerves

398
Q

How is the diaphragm shaped?

A

Dome shaped

  • Right dome lies at the left of the 5th rib
  • Left at the level of the 5th intercostal space
399
Q

Where does the apex of the lung extend to?

A

Root of the neck

400
Q

What are the local effects of apical lung cancers?

A

Involve

  • Subclavian artery: affects blood supply
  • Subclavian vein: affects blood supply
  • Brachial plexus: Neurological problems
  • Sympathetic chain: affect sympathetic innervation of head and can cause Horner’s
  • Laryngeal nerve: hoarse voice
  • Phrenic nerve: loss of Diaphragm innervation
401
Q

What are some example causes of puncture in the lungs?

A

Stab wounds of the lower neck and cannulation of the subclavian vein

402
Q

What is the effect of punctures to the lung?

A
  • Pneumothorax (air in pleural cavity)

- Haemothorax (blood in pleural cavity)

403
Q

What occurs in pleural effusion?

A

Fluid collects in costo-diaphragmatic space In the upright position

404
Q

Why is the right lung more likely to be the location of foreign bodies?

A

The right bronchus has a wider shaped and is more vertically aligned when compared to the left bronchus

405
Q

Which vertebral levels do these structure pass through the diaphragm?

A)Vena Cava
B)Oesophagus
C)Aortic Hiatus

A

A) T8
B) T10
C) T12

406
Q

What is the importance of the azygos veins?

A

They collect blood from the intercostal spaces and drain it into the vena cava.

407
Q

What is the structure of the right and left lobe of the lung?

A
  • The left lobe has a superior and inferior lobe.The left lobe has an indentation as a result of the heart.
  • The right lobe has superior, inferior and middle lobe most of the time.
408
Q

What is the pathway for the movement of air into the lungs?

A
  • Trachea
  • PRimary bronchi
  • Secondary bronchi
  • Tertiary bronchi
  • Terminal bronchioles
  • Respiratory bronchioles
  • Alveoli
409
Q

How does the respiratory system develop?

A

Develops as a diverticulum from the pharynx

410
Q

What is the purpose of the nasal cavity?

A
  • Induce turbulent flow
  • Warm and moisten inspired air
  • Recover water from expired air
  • Speech production
  • Olfaction (sense of smell)
411
Q

What is the role of turbinates?

A
  • Increase in surface area of contact between air and mucosa

- Induces turbulence of air so increase efficiency for exchange

412
Q

Which arteries supply the lung tissue itself with oxygen in the event of a pulmonary embolism?

A

Bronchial arteries

413
Q

How many fissures are on the left and right lungs?

A

Left lung: Oblique fissure

Right lung: Horizontal Fissure and Oblique Fissure

414
Q

Which sits more posteriorly? Oesophagus or trachea

A

Oesaphagus

415
Q

What is special about the articulation of Ribs 11 and 12?

A

They do not articulate with their cartilages

416
Q

What are the features of vesicular breath sounds?

A 
Long inspiratory phase
Short expiratory phase
Softer sounds
Low pitch
Continuous
417
Q

What are the features of bronchial breath sounds?

A
  • Shorter inspiratory
  • Longer expiratory phase
  • Gap between the expiratory and inspiratory phase
  • Higher pitch
  • Loud, less harsh and hollow
418
Q

What is the classic finding in breath sounds during consolidation?

A

-Bronchial breath sounds heard over lung fields where it is normal to hear vesicular breath sounds.

419
Q

Why are bronchial breath heard over lung fields in consolidation?

A

Bronchial breath sounds heard over the lung field is due to due to more solid material so conduction is better

420
Q

Does a pneumothorax always result in a mediastinal shift?

A

No.

Tension pneumothorax causes a mediastinal shift

421
Q

When are crackles heard?

A

Fine crackles

  • Idiopathic pulmonary fibrosis
  • Consolidation
  • LVF

Coarse crackles

  • Early and coarse in COPD
  • Bronchiectasis. Due to viscid secretions and may reduce after coughing
422
Q

When is a pleural friction rub heard?

A
  • Pleurisy

- Pulmonary infarction due to PE

423
Q

Describe the incidence of lung cancer

A
  • 35 000 cases a year. Most deaths per year
  • Higher among lower socioeconomic groups
  • Higher with older people
424
Q

What are the aetiological factors of lung cancer?

A
  • Smoking
  • Passive smoking
  • Asbestos
  • Radon (Cornwall)
  • Occupational carcinogens (chromium, nickel, arsenic)
  • Genetic/familial factors
425
Q

Describe the symptoms of primary lung tumour

A
  • Asymptomatic
  • Persistent cough
  • Dyspnoea
  • Wheezing
  • Haemoptysis
  • Lung infection
  • Chest/shoulder pain
  • Weight loss
  • Lethargy/Malaise
426
Q

What are the symptoms of a regional metastases?

A
  • Bloated face
  • Hoarseness
  • Dyspnoea
  • Dysphagia
  • Chest pain
427
Q

What are the symptoms of distant metastases?

A
  • Bone pain/fracture

- CNS symptoms (headache, double vision, confusion)

428
Q

What are signs of lung cancer?

A
  • Cachexia
  • Pale conjunctiva
  • Cervical lymphadenopathy
  • Horner’s syndrome
  • Consolidation
  • Sign of pleural effusion
  • Muffled heart sounds
  • Liver enlargement
  • Skin metastases
  • Neurological long tract signs
  • Asymptomatic
429
Q

Give an overview of the T stage in lung cancer.

A
  • Describes size of tumour
  • The location of the tumour
  • Multiple tumours (number)
430
Q

Give an overview of the N stage in lung cancer.

A

Describes the locationof the metastasis to the node. Same side is N1-N2. Contralateral side is contralateral side

431
Q

Give an overview of the M stage in lung cancer.

A

How far it has spread outside the region or in the region. M3 is sprading outside the region to many

432
Q

What are the implications of staging on the treatment in lung cancer?

A

2B and below can be operable with radical treatment

3A – Non operable. Can sometime be cured with non adjuvant treatment

3B and above – considered for palliative care

433
Q

What are the methods of biopsy in lung cancer?

A
  • Bronchoscopy
  • Cervical lymph node fine needle aspiration (FNA)
  • Pleural fluid aspiration (thoracentesis)
  • USS – Neck node. Node can give you an idea of the staging if positive
  • CT biopsy
  • Thoroscopy
  • Surgical
  • Adrenal biopsy
  • Skin, Bone, Brain Biopsy
  • Lymph node biopsieis
434
Q

What are the imaging techniques used in all investigations of lung cancer?

A
  • Chest X-ray
  • CT scan

For some:
(PET scan, MRI, USS, Bone Scan, ECHO. Thee test depend on the stage)

435
Q

What is the most common histological type in lung cancer?

A

Non-Small cell lung cancer (80%)

  • Squamous cell carcinoma (40%)
  • Adenocarcinoma (35%)
  • Large cell carcinoma (5%)
436
Q

What are the other type of histological types in lung carcinoma?

A
  • Small cell carcinoma

- Rare tumours (e.g. carcinoid tumours)

437
Q

What are the common treatment methods used for lung cancer?

A
  • Surgery
  • Radiotherapy
  • Combination chemotherapy
  • Combination therapy
  • Biological therapies
  • Palliative care and other treatments
438
Q

What are metabolic symptoms of lung cancer?

A

Thirst (hypercalcaemia)
Constipation (hypercalcaemia)
Seizure (hyponatraemia – SIADH, small cell)

439
Q

What is surgery used to treat in lung cancer?

A

Non small cell carcinoma

20-25% curable

440
Q

Describe the principles of radiotherapy treatment used in lung cancer?

A
  • Radical with a curative intent

- Palliative with intent of symptom control

441
Q

Describe the use of combination chemotherapy in the treatment of lung cancer.

A
  • Small cell carcinoma is curative
  • Non-small cell modest survival increase and symptoms control
  • Neo advent therapy before surgery
  • Adjuvant chemotherapy after surgery
442
Q

Describe the principles of combination therapy

A

-Combination chemo-radiotherapy which is potentially curative

443
Q

Describe the principles of biological therapies

A

Based on mutational analysis

444
Q

Describe the principles of palliative care and other treatments.

A

Active symptoms control eg analgesia, radiotherapy, airway stents

Kofi: Pure clinical conditions 2 (5 decks)

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