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Med Sci Yr 2 > Module 2.02 > Flashcards

Module 2.02 Flashcards

1
Q

what is the physiology of breathlessness?

A

breathlessness is when the instructions sent by the respiratory centre in the medulla do not match the sensory feedback from the thorax. (severity of breathlessness is highly subjective)

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2
Q

define acute dyspnoea?

A
  • a new onset or abruptly worsening breathlessness
    (can be life threatening when accompanied by severe hypoxaemia, hypercapnia, exhaustion or low GCS)
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3
Q

what are the causes of acute dyspnoea which involve an upper airway obstruction?

A
  • inhaled foreign body
  • anaphylaxis
  • epiglottis
  • extrinsic compression (e.g. rapidly expanding haematoma)
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4
Q

what are the lower airway diseases which cause acute dyspnoea?

A
  • acute bronchitis
  • asthma
  • acute exacerbation of COPD
  • acute exacerbation of bronchiectasis
  • anaphylaxis
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5
Q

what are examples of parenchymal lung disease which lead to acute dyspnoea?

A
  • pneumonia
  • lobar collapse
  • acute respiratory distress syndrome (ARDS)
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6
Q

what are ‘other’ respiratory causes of acute dyspnoea?

A
  • pneumothorax
  • pleural effusion
  • pulmonary embolism
  • acute chest wall injury
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7
Q

what are the cardiovascular causes of acute dyspnoea?

A
  • acute cardiogenic pulmonary oedema
  • acute coronary syndrome
  • cardiac tamponade
  • arrhythmia
  • acute valvular heart disease
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8
Q

define chronic dyspnoea

A
  • breathlessness which persists for 2 weeks or longer
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9
Q

what are examples of respiratory causes of chronic dyspnoea?

A
  • asthma
  • COPD
  • pleural effusion
    -lung cancer
  • ILD (interstitial lung disease)
  • chronic pulmonary embolism
  • bronchiectasis
  • cystic fibrosis
  • pulmonary hypertension
  • pulmonary vasculitis
  • TB
  • laryngeal/tracheal stenosis (e.g. extrinsic compression, malignancy)
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10
Q

what are examples of cardiovascular causes of chronic dyspnoea?

A
  • chronic heart failure
  • coronary heart disease
  • valvular heart disease
  • paroxysmal arrythmia
  • constrictive pericarditis
  • pericardial effusion
  • cyanotic congenital heart disease
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11
Q

what are other (non cardiac or respiratory) causes of chronic dyspnoea?

A
  • severe anemia
  • obesity
    -chest wall disease
  • physical deconditioning
  • diaphragmatic paralysis
  • psychogenic hyperventillation
  • neuromuscular disorder
  • cirrhosis
  • tense ascites
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12
Q

what causes for dyspnoea need immediate correction if identified?

A
  • airway obsruction
  • tension pneumothorax
  • anaphylaxis
  • arrythmia with cardiac compromise
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13
Q

how is RDOS (respiratory distress observation scale) used to measure a patients dyspnoea?

A
  • heart rate per min
  • respiratory rate per min
  • restlessness
  • use of accsessory muscles to breath
  • pattern of breathing
  • nostril flare when breathing
  • grunting on expiration
  • look of fear
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14
Q

whats drugs can be used to relive dyspnoea?

A

opiods e.g. morphine

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15
Q

when is ABG analysis required in a patient with dyspnoea?

A
  • if they need ventillatory or airway support
  • signs of hypercapnia : drowsiness, confusion
  • SpO2 <92%, central cyanosis or high O2 requirments
  • severe, prolonged or worsening respiratory distress
  • background of COPD
  • chronic type 2 respiratory failure
  • suspected metabolic acidosis or primary hyperventilation.
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16
Q

What is partial pressure of arterial oxygen (PaO2)?

A
  • it measures the amount of oxygen in the arterial blood
  • perfect reading would be 104
  • a reading between 60-79 is considered mild hypoxaemia
  • 60 is the baseline value we want to maintain, if levels drop below 60, supplemental oxygen is required
  • PaO2 is only able to be measured through an ABG
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17
Q

What is oxygen saturation (SpO2)?

A
  • it is the percentage of oxygen you inhale that makes it to your arterial blood supply
  • anything above 95% is considered normal
  • is measured with a pulse oximeter
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18
Q

how do you assess for adequacy of oxygen?

A

Use the SpO 2 ± PaO 2

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19
Q

what does PaCO2 tell us about ventillation?

A

-PaCO2 is directly determined by alveolar ventilation – the volume of air transported between the alveoli and the outside world in any given time.
- therefore a high PaCO2 (hypercapnia) indicates ventillatory failure (type 2 respiratory failure)

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20
Q

what does ABG results tells us about oxygenation?

A
  • low PaO2 means an impairment of oxygenation, if this is accompanied by a normal PaCO2 this indicated a ventillation and perfusion mismatch- type 1 respiratory failure
  • however if PaCO2 is also low it indicates a ventillation issue- type 2 respiratory failure
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21
Q

If a patient is on supplemental oxygen how does it affect ABG analysis?

A
  • it makes the analysis of PaO2 more difficult as it is hard to know wether it is appropiate for the FiO2 (amount of oxygen being inspired)
  • A useful rule of thumb is that the difference between FiO 2 (%) and PaO 2 (in kPa) should be ≤10.
  • If slight impairment is suspected repeat ABG with room air
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22
Q

what is FiO2?

A

fraction of inspired oxygen
The fraction of inspired oxygen (FiO2) is the concentration of oxygen in the gas mixture. The gas mixture at room air has a fraction of inspired oxygen of 21%, meaning that the concentration of oxygen at room air is 21%

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23
Q

what does an ABG tell us about acid- base status?

A
  • if blood pH is lowered it is an acidosis, if blood pH increases it is an alkalosis
  • a high PaCO2 indicates acidosis and a low PaCO2 indicates alkalosis
  • there is both respiratory and metabollic pathways to control blood pH if one is failing the other takes over to try return to normal (metabollic pathway is much slower)
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24
Q

what tests can be done when a patient presents with breathlessness to differentiate between potential diagnosis?

A
  • chest xray
  • measure Peak expiratory flow rate (PEFR)
    -ECG
  • Evaluate for PE
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25
Q

what issues in the airways of the lungs could cause haemoptysis?

A
  • acute bronchitis
  • bronchiectasis
  • cancer: primary lung or metastatic to lung
  • inspiration of a foreign body
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26
Q

what issues involving pulmonary vasculature will cause haemoptysis?

A
  • pulmonary embolism
  • pulmonary AVM
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27
Q

What are important questions to ask when taking a history from a patient presenting w haemoptysis?

A
  • duration and volume of blood (although can be hard to measure)
  • presence of dyspnoea, fever, night sweats or weight loss
  • chronic lung disease
  • immunosuppression
  • smoking history
  • travel history
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28
Q

What investigations are carried out on a patient presenting with haemoptysis?

A
  • examination: cardiac and respiratory
  • Blood tests: FBC, aPTT (checks clotting), INR
  • chest Xray, chest CT
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29
Q

how do you differentiate between haemoptysis and haematemesis?

A
  • can suspect blood has been coughed up when : no GI symptoms, pink/red appearence, known lung disease, consistency is liquid/ clotted
  • can suspect blood have been vomited when: known GI symptoms, feelings of nausea, blood is dark red, brown or black and has consistency of coffee grounds
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30
Q

after a chest Xray and infection is presented, what elements of the patient history may help us make differential diagnosis?

A
  • if illness had an acute onset, fever and only mild haemoptysis, focal opacities on CXR. -> suspect bacterial pneumonia
  • if illness is more on the chronic side, weightloss, immunosupression or relevant travel history, cavitary/nodular lesions on CXR -> suspect myobacterial or fungal pneumonia, or TB
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31
Q

if a patient presents with haemoptysis but then has a normal chest Xray what should be considered?

A

check if history is suggestive of acute bronchitis:
-single, self limited episode of haemoptysis
- no systemic symptoms
- non smoker
–> chest CT can still be done as malignancies may not show up

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32
Q

what are the most common causes of haemoptysis?

A
  • acute bronchitis
  • bronchiectasis
  • lung cancer
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33
Q

what are the serious pathologies we want to exclude when a patient has haemoptysis?

A
  • lung cancer
  • TB
  • pulmonary embolism (PE)
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34
Q

what signs and symptoms may make you suspect lung tumor in a patient presenting with haemoptysis?

A
  • acute onset of cough, weightloss, finger clubbing and swollen lymph nodes
  • chest Xray mat show some abnormalities, however may appear normal
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35
Q

what abnormalities may be seen on a chest Xray of a patient with suspected lung tumour?

A
  • a discrete mass or cavitating lesions
  • collapse of a lobe or tumour obstruction
  • unilateral hilar enlargment or pleural effusion
  • consolidation that fails to resolve
  • chest xrays may sometimes appear normal despite there being a lung tumour (normal CXR does not rule out a tumour)
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36
Q

what are the signs and symptoms for pulmonary embolism?

A
  • frank haemoptysis due to pulmonary infarction
  • sudden onset dyspnoea and pleurtic chest pain
  • in a minority of cases signs of deep vein thrombosis (DVT) is present
  • chest Xray may show a wedge shaped peripheral opacity or pleural effusion, but is most often normal
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37
Q

what are the signs and symptoms for bronchiectasis?

A
  • typically a background of chronic cough with copious foul-smelling purluent sputum
  • finger clubbing and coarse inspiratory crackles upon examination
38
Q

what bacteria causes TB (in humans)?

A

it is caused by myobacterium tuberculosis (MTB):
- M. tuberculosis – by far the most common type
- M. bovis (bovine TB)
- M. africanum

39
Q

what happens when the immune system encounters TB?

A
  • granulomas are formed
  • the main site for these is the lungs however they can move all around the body via the lymphatics
  • in most cases these granulomas heal and the infection is cured
  • in majority of the remaining cases the infection stays in the lungs and under control in granulomas of the host immune system. This is latent TB and only becomes known later in life or if the immune system becomes supressed (thus becoming active TB)
40
Q

how does testing differ for active TB and latent TB?

A

Latent TB: interferon gamma release assay (IGRA) or Tuberculin skin testing (TST)
Active TB: CXR and microbiology (usually sputum) for acid fast bacilli

41
Q

how is TB transmitted?

A
  • Via droplets - only pulmonary type is infectious
  • Usually need sustained close contact with an infectious case
42
Q

what are risk factors for catching TB?

A
  • HIV
  • someone in the household being infected (1/3 chance of spreading with in a household)
  • homelessness
  • IV drug use
  • malnutrition
  • chronic lung disease
  • immunosuppression
43
Q

describe the pathogenesis of TB?

A
  • MBT is engulfed by macrophages in the lung alveolus, and replicates with in them (in most cases the infection stays under control here)
  • the lymphocytes and fibroblasts surround the macrophages and forms granulomas
  • stops the spread of the bacteria
  • inside these lesions the cells will then die
  • the infection will either fully clear or remain as LTBI (latent tuberculosis infection)
  • if there is a failure of the above mechanism MTB may enter the blood stream and cause extra-pulmonary TB
44
Q

how does primary progressive TB occur in immunosuppressed ppl?

A
  • granulomas are able to form but then the necrotic tissue becomes liquid and the fibrous walls breakdown
  • the necrotic liquid then drains into the bronchi and is able to be coughed up (so able to infect others)
  • or the necrotic material is able to makes its way into the blood stream and cause extra-pulmonary TB
45
Q

what are the pulmonary clinical features of TB? (90% of cases only have pulmonary features)

A
  • haemoptysis
  • shortness of breath
  • cough
46
Q

what is a carcinoma?

A

carcinoma – this cancer begins in the skin or in tissues that line or cover internal organs.

47
Q

what are some of the most common differential diagnosis of a patient w TB?

A
  • carcinomas
  • pneumonia
  • PUO (sustained fever with unknown cause)
  • lymphoma
  • fibrotis lung disease
48
Q

what signs might you see on a chest Xray that will indicate TB?

A

-Patchy nodal shadows in the upper zones
-Cavitating lesions
-Fibrous contractions
-Air space consolidation
-Typically apical lesions
-Milliary TB – multiple 1-10mm nodules throughout the lungs
- hard to distguish between latent and active on CXR

49
Q

what samples can be taken to diagnose TB?

A
  • 3 seperate sputum samples (one from the morning)
  • broncoscopy
  • Ziehl-Neelsen (ZN) stain - test for AFB , acid-fast bacilli
  • Löwenstein-Jensen culture (takes 4-8 weeks due to slow bacterial growth and sensitivities take a 3-4 weeks more)
50
Q

what is the Mantoux tuberculin skin test (TST)?

A
  • identifies latent TB
  • tuberculin is injected into the dermis and then re-assessed in 48-72 hrs
  • the level of inflammation indicates the likelihood of them having TB
  • result is inconsideration with other risk factors for TB
  • false positive if you have had vaccination, also may be no inflammation even if the patient does have TB if they have certain diseases
51
Q

how is Interferon gamma release assays (IGRA) able to test for TB?

A
  • results are not affected by previous TB vaccine
  • checks if the immune system recognises TB antigens, suggesting a previous latent or active TB infection
  • further tests need to be done to differentiate wether it was latent or active
52
Q

how are antibiotics used in the treatment of TB?

A
  • multi drug regime, ( isoniazid and rifampicin, pyrazinamide and ethambutol) -> all 4 for 2 months
  • single antibiotic use for latent TB
  • MDR-TB (TB which is resistant to at least isoniazid and rifampin), this should be treated with 4 effective antibiotics for 18 to 24 months
53
Q

what antibiotics are used in treatment for TB? (RIPE)

A
  • Rifamycins (inhibits DNA transcription)
  • Isoniazid (inhibits synthesis of cell wall)
  • Pyrazinamide (Lowers intracellular pH, disrupting synthesis of fatty acids)
  • Ethambutol (Interferes with cell wall synthesis)
54
Q

what does it mean if bacteria is acid fast?

A
  • it doesnt stain using normal staining techniques. The name refers to the fact they can’t be stained by normal acid (ethanol) staining techniques. These bacteria are often particularly difficult to culture and identify; e.g. TB takes around 6-8 weeks
55
Q

what is pneumonia?

A
  • infection of the lung tissue, causing inflammation
  • causes sputum to fill the airways and alveoli
  • can be seen as consolidation on chest Xrays
56
Q

what are 3 different classifications of pneumonia?

A
  • community accquired pneumonia
  • hospital accquired pneumonia - infection after 48hrs of being on hospital
  • aspiration pneumonia- a result of inspiring a foreign body
57
Q

what is the symptoms of pneumonia?

A

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

58
Q

what are the signs of pneumonia?

A
  • tachypnoea (raised resp rate)
  • tachycardia
  • fever
  • confused
  • hypoxia
  • hypotension (shock)
59
Q

what chest sounds are characteristic of pneumonia?

A

focal coarse crackles - due to sputum
bronchiole breath sounds-as loud on inspiration and expiration due to consolidation around airways
dullness to percussion- due to consolidation or lung collapse

60
Q

how is the severity of pneumonia assessed?

A
  • CURB-65 in hospital and CRB-65 out of hospital
    Confusion (new disorientation)
    Urea ( above 7)
    Resp rate (above 30)
    Blood pressure (< 90 systolic or ≤ 60 diastolic)
    Age (over 65)
    -> anything above 1 consider admission
61
Q

what bacteria can cause pneumonia?

A

most common: Streptococcus pneumoniae (50%),
Haemophilus influenzae (20%)

other causes:
-Moraxella catarrhalis in immunocompromised patients or those with chronic pulmonary disease
-Pseudomonas aeruginosa in patients with cystic fibrosis or bronchiectasis
-Staphylococcus aureus in patients with cystic fibrosis

62
Q

define what atypical pneumonia is?

A
  • pneumonia which cannot be cultured and cannot be identified with gram staining
  • They don’t respond to penicillins and can be treated with macrolides (e.g. clarithomycin), fluoroquinolones (e.g. levofloxacin) or tetracyclines (e.g. doxycycline)
63
Q

which atypical pneumonia can be caused by infected air conditioning and water supplies?

A

Legionella pneumophila (Legionnaires’ disease).

64
Q

which atypical pneumonia can cause neurological symptoms in younger patients, and rash? (explain the type of rash)

A

Mycoplasma pneumoniae.
-This causes a milder pneumonia and can cause a rash called erythema multiforme characterised by varying sized “target lesions” formed by pink rings with pale centres.
-It can also cause neurological symptoms in young patient in the exams.

65
Q

which atypical pneumonia may be suspected in a school aged child with a mild to moderate chronic cough and a wheeze?

A
  • Chlamydophila pneumoniae.
  • Be cautious though as this presentation is very common without chlamydophilia pneumoniae infection.
66
Q

which atypical pneumonia presents with a fever and usually is related to exposure to animals and their bodily fluids?

A

Coxiella burnetii AKA “Q fever

67
Q

which atypical pneumonia is contracted from contact with birds?

A

Chlamydia psittaci.

68
Q

name the 5 causes of atypical pneumonia using Legions of psittaci MCQs”

A

M – mycoplasma pneumoniae
C – chlamydydophila pneumoniae
Qs – Q fever (coxiella burnetii)

69
Q

what are the charcateristics of fungal pneumonia?

A
  • Pneumocystis jiroveci (PCP) pneumonia
  • more common in immunosupressed patients
  • presents with a dry cough and night sweats and SOB on exertion
  • treatment is with co-trimoxazole
  • Patients with low CD4 counts are prescribed prophylactic oral co-trimoxazole to protect against PCP
70
Q

what investigations are carried out on patients in hospital with pneumonia?

A

-Chest xray
-FBC (raised white cells)
-U&Es (for urea)
-CRP (raised in inflammation and infection)
In more severe cases:
- Sputum cultures
-Blood cultures
-Legionella and pneumococcal urinary antigens (send a urine sample for antigen testing)

71
Q

how are antibiotics used to manage pneumonia?

A
  • should look at local guidlines
  • Mild CAP: 5 day course of oral antibiotics (amoxicillin or macrolide)
    -Moderate to severe CAP: 7-10 day course of dual antibiotics (amoxicillin and macrolide)
72
Q

what complications can occur in patients with pneumonia?

A

-Sepsis
-Pleural effusion
-Empyema
-Lung abscess
-Death

73
Q

define what COPD is

A

chronic obstructive pulmonary disease, is a disruption of airflow in and out of the lungs caused by damaged tissue. nearly always caused by smoking.
- thus making it more diffucult to ventillate the lungs and making them more prone to infections

74
Q

how does COPD present?

A
  • SOB
  • productive cough with sputum
  • wheeze
  • recurrent chest infections (particularly in winter)
  • does NOT cause clubbing and unusual to cause haemoptysis -> in these cases consider something else
75
Q

what is the MRC (Medical Research Council) Dyspnoea Scale, a 5 point scale that NICE recommend for assessing the impact of their breathlessness?

A

Grade 1 – Breathless on strenuous exercise
Grade 2 – Breathless on walking up hill
Grade 3 – Breathless that slows walking on the flat
Grade 4 – Stop to catch their breath after walking 100 meters on the flat
Grade 5 – Unable to leave the house due to breathlessness

76
Q

what will spirometery show in a patient with COPD?

A
  • overall lung capacity is not as bad as their ability to blow air out quickly
  • lung capacity is measured by FVC (forced vital capacity)
  • ability blow air out is measured by FEV1 (forced expiratory volume in 1 second)
  • In COPD patients: FEV1/FVC ratio <0.7
77
Q

what is reversibility testing during spirometery?

A
  • reversibility testing is where a beta-2 antagonist such as salbutamol is given during spirometery testing
    -If this helps asthma will need to be considered rather than COPD
78
Q

how can airflow obstruction severity be measured?

A
  • severity of airflow obstruction can be graded using FEV1
    Stage 1: FEV1 >80% of predicted
    Stage 2: FEV1 50-79% of predicted
    Stage 3: FEV1 30-49% of predicted
    Stage 4: FEV1 <30% of predicted
79
Q

what other investigations are done to diagnose COPD and rule out other conditions?

A
  • chest Xray, rule out any malignancies
  • FBC, for polycythaemia or anaemia.
  • sputum culture to check for infections
  • ECG and echocardiogram to check heart function
  • chest CT, check for fibrosis or bronchiectasis or cancer
  • Serum alpha-1 antitrypsin to look for alpha-1 antitrypsin deficiency. Deficiency leads to early onset and more severe disease.
    -Transfer factor for carbon monoxide (TLCO) is decreased in COPD
80
Q

define chronic bronchitis and emphysema in terms of COPD?

A
  • chronic bronchitis: chronic productive cough that lasts for 3 months over 2 years, alternative explanation should be ruled out
  • emphysema: creates larger airspaces in alveolus, due to alveoli destruction
81
Q

how does alpha-trypsin 1 deficency play a role in causing emphysema?

A
  • emphysema is caused by the breakdown of elastin
  • elastase causes the breadown of elastin
  • Alpha-1 antitrypsin is a natural inhibitor of neutrophil elastase, which is reduced or absent in alpha-1 antitrypsin deficiency, which predisposes to COPD.
82
Q

what is the pathophysiology of chronic bronchitis causing COPD?

A
  • chronic inflammattion of bronchi with neutrophillic infiltration, CDT8+ T lymphocytes and macrophages
  • leads to: goblet cell hyperplasia, mucus hypersecretion, narrowing of airways and chronic inflammation and fibrosis
83
Q

what is the pathophysiology of emphysema causing COPD?

A
  • an inflammatory process leads to the production of protease from inflammatory cells such as macrphages.
  • the protease elastase breaks down elastin in the alveoli
  • this breakdown of elastin causes: alveoli prone to collapse, and cause alveoli to dilate and form bullae where multiple alveoli join together
84
Q

what is cor pulmonae?

A
  • right ventricular impairment secondary to pulmonary disease
  • chronic hypoxia causes vasoconstriction of pulmonary arteries and causes a build up of pulmonary arterial pressure and lead to right sided heart failure.
85
Q

what are the signs of COPD?

A
  • purse lip breathing
  • coarse crackles
  • loss of cardiac dullness
  • signs of CO2 retention
86
Q

what is the MOA of a beta- receptor antagonist?

A

bind to beta receptors of the sympathetic nervous system. Causes relaxation of airway smooth muscle and subsequent bronchodilation. May be short or long-acting.

87
Q

what is the MOA of Muscarinic receptor antagonists?

A

these drugs prevent the activation of muscarinic receptors by acetylcholine. This prevents airway smooth muscle contraction and causes bronchodilation. Can be short or long-acting.

88
Q

what is the MOA of cortico steriods?

A

inhaled corticosteroids work by reducing inflammation within the lungs. They are thought to reduce the number of exacerbations, improve the efficacy of bronchodilators and decrease dyspnoea in stable COPD

89
Q

what are the different inhaler types?

A
  • Short-acting beta-agonists (SABA)
  • Long-acting beta-agonists (LABA)
  • Short-acting muscarinic antagonists (SAMA)
  • Long-acting muscarinic antagonists (LAMA)
  • Inhaled corticosteroid (ICS)
  • LABA-ICS
  • LABA-LAMA
  • LABA-LAMA-ICS
90
Q

what is Atopy?

A

Atopy is a genetic predisposition to IgE-mediated allergen sensitivity.
- predisposed to asthma, eczma and hayfever

91
Q

what is aspirin induced asthma?

A
  • a small set of patients have asthma and are affected by a sensitivity to aspirin
  • they experience: samters triad: Asthma, Aspirin sensitivity, Nasal polyps

Med Sci Yr 2 (2 decks)

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