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nicks phase 2a flaschards > respiratory > Flashcards

respiratory Flashcards

1
Q

what are the symptoms of COPD and all related conditions?

A

cough, sputum, dyspnoea and wheeze

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2
Q

what are the signs of COPD and all related conditions?

A

tachypnoea, use of accessory muscles of respiratory at rest, decreased expansion, cyanosis, cor pulmonale

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3
Q

how can COPD be diagnosed?

A
  • FBC- raised PCV
  • CXR- hyperinflation, flat hemidiaphragms, large pulmonary arteries
  • ABG- hypercapnia and decrease in PaO2
  • lung function tst- FEV1:FVC ratio less than 70%
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4
Q

how would a patent with COPD be treated?

A
  • smoking cessation
  • bronchodilators
  • short-acting antimuscarinic- ipratropium
  • inhaled tiotropium bromide
  • short acting beta2 agonist- salbutamol
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5
Q

how is severe COPD treated?

A

combination of long acting beta2 agonist and corticosteroids- e.g. budesonide and formoterol

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6
Q

how are acute exacerbations managed?

A
  • Controlled O2 given to maintain SaO2 >88-92% and PaO2 > 8kPa without increasing PaCO2- Low concentration oxygen given via Venturi mask, to prevent removing their hypoxic drive
  • Bronchodilators (salbutamol) given along with oral prednisolone
  • Abx given if there’s a history of more purulent sputum production or with CXR changes
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7
Q

what is Chronic bronchitis?

A

Chronic bronchitis is a clinical term defined as cough and sputum for 3 months in 2 consecutive years

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8
Q

how is chronic bronchitis characterised histologically

A

It is histologically characterised by a non-specific chronic inflammatory infiltrate within the walls of bronchi and bronchioles. This can be associated with the formation of bronchial-associated lymphoid tissue (BALT)

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9
Q

what is emphysema?

A

Emphysema is defined as an abnormal enlargement of alveolar airspaces distal to the terminal bronchiole. there is a loss of elastic recoil, resulting in expiratory airflow limitation and air trapping

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10
Q

what is asthma?

A

Asthma is defined as hyper-reactivity of the bronchial tree with paroxysmal narrowing of the small airways

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11
Q

what is asthma characterised by?

A

characterised by reversible small-airway obstruction characterised by bronchospasm, airway inflammation and oedema

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12
Q

how is asthma categorised?

A

A. Extrinsic (atopic)- allergens identified by positive skin prick reactions to common inhaled allergens such as dust mites, pollens and fungi
B. Intrinsic- usually occurs in middle age and no definite external cause can be identified

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13
Q

what environmental influences can cause asthma?

A

early childhood exposure to allergens, maternal smoking and childhood infections

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14
Q

describe the pathophysiology of asthma

A

During the inflammation process, mast cells and eosinophils migrate into the bronchial wall. Remodelling then occurs- the airway smooth muscle undergoes hyperplasia and hypertrophy. This results in a thickened airway wall, which damages the epithelium as ciliated columnar cells are lost into the lumen. Due to this loss of some epithelial cells, the epithelium undergoes metaplasia and increased the number of mucous secreting goblet cells

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15
Q

how do patients with asthma present clinically?

A

symptoms- dyspnoea, wheeze, cough, sputum

signs- tachypnoea, hyper inflated chest, air entry reduction, widespread polyphonic wheeze

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16
Q

how is asthma diagnosed?

A

Asthma can be diagnosed by the patient demonstrating a variable of greater than 15% airway limitation by measurement of PEF or FEV1. Skin prick tests can also be used to identify triggers and CXR is used during an acute attack to rule out pneumonia or pneumothorax

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17
Q

what is the first line of treatment in a patient with asthma?

A

lifestyle control- smoking cessation ,avoiding precipitants, checking inhaler technique

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18
Q

what is the pharmacological treatment pathway for asthma set out by the British Thoracic society guidelines?

A

1 .B2- agonist PRN- salbutamol
2. Inhaled steroid- beclomethasone
3/ Long acting B2-agonist- salmeterol
4. High doses of beclomethasome or modified-release theophylline
5. Oral prednisolone and refer to asthma clinic

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19
Q

what are the local effects of a primary lung tumour?

A

haemoptysis, bronchial obstruction, breathlessness, consolidation
tumour can also infiltrate the visceral pleura leading to pleural effusion

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20
Q

what are the most common sites that primary lung tumours will metastasise to?

A

lymph nodes, liver, pleura, adrenal glands, bone and brain

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21
Q

what are the risk factors of a pulmonary embolism?

A

recent surgery, thrombophilia, leg fracture, prolonged bed rest, malignancy, pregnancy or a previous PE

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22
Q

what symptoms will a patient with a PE present with?

A

acute breathlessness, pleuritic chest pain, haemoptysis and syncope

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23
Q

what clinical signs can be detected in a patient with a PE?

A

pyrexia, cyanosis, tachypnoea, tachycardia, hypotension, pleural rub and pleural effusion

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24
Q

what will the results of an ABG be in a patient with a PE?

A

low PaO2, Low PaCO2

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25
Q

How would you manage a patient with a PE?

A
  • Give oxygen if hypoxic
  • morphine and LMWH
  • if patient is still harm-dynamically unstable, consider thrombolysis or vasopressors
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26
Q

what causes the initial infection in TB?

A

mycobacterium tuberculosis

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27
Q

what are the systemic symptoms of TB?

A
  • Pulmonary TB- cough, sputum, malaise, weight loss, sweats, pleurisy, haemoptysis
  • Miliary TB- CXR shows nodular opacities
  • Genitourinary TB- dysuria, frequency, back pain, haematuria
  • Bone TB- vertebral collapse and Pott’s vertebra
  • Skin TB- jelly-like nodules on face and neck
  • Peritoneal TB- abdo pain, GI upset
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28
Q

how can TB be diagnosed?

A
  • CXR- consolidation, cavitation, calcification and fibrosis
  • sputum sample testing
  • PCR for mycobacterium tuberculosis
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29
Q

what is the treatment plan for a patient with TB?

A

6- month regimen- take rifampicin, isoniazid, pyrazinamide and ethambutol for 2 months then taking rifampicin and isoniazid for a further 4 months

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30
Q

which groups of people are most at risk of pneumonia?

A

infants, elderly, immunocompromised, nursing home residents and alcoholics

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31
Q

what are some differential diagnoses of asthma?

A

pulmonary oedema, COPD, large airway obstruction due to a tumour, SVC obstruction, pneumothorax, PE, bronchiectasis or obliterative bronchiolitis

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32
Q

what conditions can increase a patients’ chance of developing pneumonia?

A

COPD, diabetes and congestive heart disease

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33
Q

what are the symptoms of pneumonia?

A

fever, sweats, rigors, cough, sputum, SOB, pleuritic chest pain that is worse on deep breathing, systemic features and rash

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34
Q

what clinical signs can be seen in a patient with pneumonia?

A

raised heart and respiratory rate, low BP, fever and dehydration

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35
Q

in pneumonia, lung consolidation can occur- what can be heard on percussion and auscultation in patients with this?

A

dull to percussion, decreased air entry, bronchial breath sounds, crackles and increased vocal resonance

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36
Q

what investigations can be done on a patient with pneumonia?

A
  • CXR- multi lobar suggestive of S. pneumonia/ s.aureus, multiple abcesses or pneumatoceles of S. aureus
  • Full blood count
  • Biochemistry- urea, electrolytes and liver function tests
  • C- reactive protein
  • pulse oximetry
  • Microbiological tests
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37
Q

what is the CURB65?

A

used to predict the mortality of patients with pneumonia.
1 point is given for each of the criteria met:
-Confusion
-Urea ≥7mmol/L
-Respiratory rate≥ 30/min
-Blood pressure; low systolic < 90mm/Hg or diastolic ≤60mm/Hg
- Age ≥ 65

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

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38
Q

what is the treatment of mild community-acquired pneumonia?

A

oral amoxicillin/ erythromycin/ clarithromycin.

if no response in 48 hours- CXR and review treatment

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39
Q

what is the treatment of severe community- acquired pneumonia?

A
  • IV cefuroxime and IV clarithromycin

- flucloxacillin and sodium fusidate added if gram positive cocci are present

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40
Q

what viruses most commonly cause upper respiratory tract infections (URI’s)?

A

include rhinovirus, infleunza A, coronavirus, adenovirus, parainfluenza virus and respiratory syncytial viruses

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41
Q

what are the main complication of URI’s?

A

sinusitis, pharyngitis, otitis media, bronchitis and pneumonia

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42
Q

what virus causes the common cold (acute coryza)?

A

rhinovirus infection

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43
Q

what are the symptoms of acute coryza?

A
  • Malaise
  • Slight pyrexia
  • Sore throat
  • Watery nasal discharge – becomes mucopurulent after a few days
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44
Q

what is sinusitis?

A

infection of the paranasal sinuses

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45
Q

what organisms most commonly cause sinusitis?

A

Strep pneumonia or H influenzae

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46
Q

what are the symptoms of sinusitis?

A

Frontal headache
Facial pain and tenderness
Nasal discharge

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47
Q

how is sinusitis treated?

A
  • Broad-spectrum abx (e.g. co-amoxiclav)
  • Topical corticosteroids – e.g. fluticasone propionate nasal spray to reduce local mucosal swelling
  • Steam inhalations
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48
Q

what is rhinitis?

A

•Sneezing attacks, nasal discharge or blockage occurring for more than 1h for most days:
oFor a limited period of the year (seasonal rhinitis)- e.g. hay fever
o Throughout the whole year (perennial or persistent rhinitis)

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49
Q

how is perennial rhinitis categorised?

A

allergic

non-allergic- triggered by cold air, smoke and perfume

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50
Q

how is rhinitis managed?

A
  • Avoid allergens
  • Antihistamines e.g. cetirizine
  • Decongestant topical steroids e.g. beclometasone spray twice daily
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51
Q

what virus must commonly causes acute pharyngitis?

A

adenoviruses

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52
Q

if acute pharyngitis is more persistent what does this imply?

A

bacterial infection caused by

haemolytic Strep, Haemophilus influenza, staphylococcus aureus

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53
Q

what are the symptoms of acute pharyngitis?

A

sore throat and fever

54
Q

how is acute pharyngitis treated?

A

penicillin V four times a day for 10d

if allergic to penicillin use erythromycin

55
Q

what is acute laryngotracheobronchitis (croup)?

A

infection with a parainfluenza virus or measles virus

56
Q

when doe symptoms of acute laryngotracheobronchitis most commonly present?

A

when the patient is under 3 years old

57
Q

what are the symptoms of acute laryngotracheobronchitis?

A

hoarse voice, barking cough (croup) and stridor

symptoms caused by inflammatory oedema

58
Q

how is acute laryngotracheobronchitis treated?

A

O2 therapy
oral/ IM corticosteroids
nebuliser adrenaline

59
Q

what is the pathophysiology of influenza?

A
  • Two main forms of the influenza virus = A and B
  • Surface of virion is coated with haemagglutinin (H) and neuraminidase (N) – both are necessary for attachment to the host respiratory epithelium
  • Human immunity develops against the H and N antigens
  • Influenza A has the capacity to undergo antigenic ‘shift’ and major changes in the H and N antigens are associated with pandemic infections
  • Minor antigenic ‘drifts’ are associated with less severe epidemics
60
Q

what are the clinical features a patient with influenza would present with?

A
  • Incubation periods = 1-3d
  • Abrupt onset of fever
  • Generalized aching of limbs
  • Severe headache
  • Sore throat and dry cough
  • May last several weeks
  • Flu symptoms are a lot worse than common cold
  • Fever, generalized aching and dry cough = flu
  • Runny and stuffy nose = common cold
61
Q

how is influenza diagnosed?

A
  • serology shows rise in antibody titre

- virus demonstrated in throat and nasal secretions

62
Q

how is influenza managed?

A
  • Symptomatic treatment – paracetamol, bed rest, maintenance of fluid intake
  • Antibiotics to prevent secondary infection
  • In a pandemic, neuraminidase inhibitors (e.g. zanamivir and oseltamivir) are offered to all with suspicious symptoms
63
Q

what is the main complication of influenza?

A

pneumonia

64
Q

what is pulmonary fibrosis?

A

Pulmonary fibrosis is a type of idiopathic interstitial pneumonia. Patients typically present late in their 60’s and are commonly male

65
Q

what are the symptoms of pulmonary fibrosis?

A

a dry cough, exertional dyspnoea, malaise, weight loss and arthralgia

66
Q

what are the clinical signs seen in a patient with pulmonary fibrosis?

A

cyanosis, finger clubbing and fine-end inspiratory crepitations

67
Q

how is pulmonary fibrosis diagnosed?

A
  • bloods- raised CRP and ANA
  • ABG- low PAo2
  • CXR- decreased lung volume and bilateral lower zone reticulonodular shadows- honeycomb appearance
68
Q

how is pulmonary fibrosis treated?

A

oxygen therapy, pulmonary rehabilitation, opiates and supportive care of the patient

69
Q

what is sarcoidosis?

A

Sarcoidosis is a multisystem granulomatous disorder, of which the cause is unknown

70
Q

how is sarcoidosis diagnosed?

A

usually found incidentally on a CXR- bloods showing raised ESR, LFT and serum ACE can confirm diagnosis.
an US can also be done which will show hepatosplenomegaly

71
Q

what are the symptoms of sarcoidosis?

A

fever, erythema nodosum and bilateral hilar lymphadenopathy

72
Q

what are the non-pulmonary signs of sarcoidosis?

A

hepatosplenomegaly, uveitis, glaucoma and conjunctivitis

73
Q

how is sarcoidosis treated?

A
  • most recover spontaneously

- bed rest and NSAIDs

74
Q

what is bronchiectasis?

A

Bronchiectasis is chronic inflammation of the bronchi and bronchioles leading to permanent dilatation and thinning of these airway

75
Q

what organisms most commonly cause bronchiectasis?

A

h. influenzae, strep. Pneumoniae, staph. Aureus and pseudomonas aeruginosa

76
Q

apart from viral causes what else can cause bronchiectasis?

A

cystic fibrosis, bronchial obstruction, allergic bronchopulmonary aspergillosis and rheumatoid arthritis

77
Q

what signs and symptoms will a patient with bronchiectasis present with?

A

symptoms- persistent cough and sputum

signs- finger clubbing, coarse inspiratory crepitations and wheeze

78
Q

how is bronchiectasis diagnosed?

A

through either a sputum culture, a CXR showing cystic shadows and thickened bronchial walls, spirometry showing an obstructive pattern or bronchoscopy to locate the site of haemoptysis

79
Q

how can a patient with bronchiectasis be diagnosed?

A
  • airway clearance techniques

- antibiotics

80
Q

what is cystic fibrosis?

A

Cystic fibrosis is an autosomal recessive condition caused by mutations in a gene on chromosome 7

81
Q

what is the pathophysiology of cystic fibrosis?

A

a deletive mutation results in a reduction in the numbers of a type of chloride channel found in the lungs, pancreas, GI and reproductive tract. This results in decreased chloride secretion and increased sodium absorption across the airway epithelium, therefore the mucous produced is very viscous

82
Q

what symptoms will a neonate with cystic fibrosis present with?

A

failure to thrive and rectal prolapse

83
Q

what systemic symptoms will children and adults with cystic fibrosis present with?

A
  • Respiratory- wheeze, cough, infections, bronchiectasis, pneumothorax, haemoptysis, respiratory failure and cor pulmonale
  • GI- pancreatic insufficiency, gallstones and cirrhosis
  • Other- male infertility, osteoporosis, arthritis, vasculitis, sinusitis
  • General signs such as cyanosis, finger clubbing and bilateral coarse crackles.
84
Q

how is cystic fibrosis diagnosed?

A
  • genetic testic
  • sweat test- greater Cl concentration that Na
  • sputum culture
  • CXR- lung hyperinflation and bronchiectasis
  • spirometry- obstructive defect
85
Q

how can cystic fibrosis be treated?

A

chest physiotherapy, postural drainage, antibiotics for infective exacerbations and mucolytics.
Systems also need to be treated- e.g. pancreatic enzyme replacement

86
Q

what is pulmonary hypertension associated with?

A

development of cor pulmonale- right ventricular hypertrophy

87
Q

what is the aetiology of pulmonary hypertension?

A
  • Pre-capillary affects- pulmonary emboli, left-to-right shunts (cardiac septal defects) and primary pulmonary hypertension (unknown cause)
  • Capillary defects- severe reduction in the vascular bed- e.g. in emphysema
  • Post-capillary defects- high pressure in the pulmonary venous system resulting in secondary back pressure into the arterial tree. Examples of this include mitral stenosis and left ventricular failure
88
Q

how does a patient with pulmonary hypertension present clinically?

A

symptoms- exertional dyspnoea, lethargy, fatigue, peripheral oedema and abdominal pain due to hepatic congestion

signs- loud pulmonary second sound, elevated JVP, hepatomegaly and a pulsatile liver

89
Q

how is pulmonary hypertension diagnosed?

A

depends on the cause- a CXR can show enlarged proximal pulmonary arteries, and ECG will indicate RVH and cor pulmonale and an echocardiogram will show right ventricular dilation/ hypertrophy

90
Q

what are the treatment options for a patient with pulmonary hypertension?

A

oxygen therapy, warfarin, diuretics to treat the oedema, oral CCBs as well as treating the underyling cause

91
Q

what is the aetiology of Hypersensitivity pneumonitis/ extrinsic allergic alveolitits?

A

This is caused by inhalation of allergens provoking a hypersensitivity reaction- e.g. farmers lung, bird-fanciers lung, malt workers lung

92
Q

what is the key difference between acute and chronic Hypersensitivity pneumonitis/ extrinsic allergic alveolitits?

A

acute- alveoli are infiltrated with acute inflammatory cells

chronic- granuloma formation and obliterative broncholitis

93
Q

how would a patient with Hypersensitivity pneumonitis/ extrinsic allergic alveolitits present clinically?

A

acute- fever, rigors, myalgia, dry cough

chronic- weight loss, exertion dyspnoea, type 1 respiratory failure and cor pulmonale

94
Q

how are both acute and chronic hypersensitivity pneumonitis/ extrinsic allergic alveolitits diagnosed?

A

acute- bloods indicating neutrophilia, CXR and lung function tests showing a reversible restrictive effect

chronic- persistent changes on lung function tests

95
Q

how are acute and chronic hypersensitivity pneumonitis/ extrinsic allergic alveolitits treated?

A

acute- oral prednisolone

chronic- avoiding exposure and long-term steroids

96
Q

what is the pathophysiology of coal-workers pneumoconiosis?

A
  • Coal is ingested by alveolar macrophages
  • These aggregate around bronchioles
  • Anthracosis- presence of coal dust pigment in the lung
97
Q

what is silicosis?

A

fibres can be toxic to macrophages- this leads to their death with the release of proteolytic enzymes

98
Q

how does a patient with silicosis present clinically?

A

present with progressive dyspnoea and a CXR showing military or nodular pattern

99
Q

what can asbestos disease lead to?

A

diffuse pulmonary fibrosis, diffuse pleural fibrosis, lung cancer or mesothelioma

100
Q

how do patients with asbestos disease present clinically?

A

progressive dyspnoea, clubbing, pleural plaques and fine end-inspiratory crackles

101
Q

what are examples of extrinsic allergic alveolitis?

A

bird fancier’s lung or farmer’s lung, type 3 hypersensitivity

102
Q

what is byssinosis?

A

common in cotton mill workers

-Symptoms begin once returning to work (Monday) and get better during working week

103
Q

what are the symptoms of byssinosis?

A

tight chest, cough and breathlessness

104
Q

what is berylliosis?

A

beryllium is a copper alloy used in the aerospace industry. Beryllium is inhaled and causes a systemic illness that causes progressive dyspnoea and pulmonary fibrosis

105
Q

what is good pastures syndrome?

A

a pulmonary-renal syndrome that presents with acute glomerulonephritis and lung symptoms

106
Q

what is the aetiology of good-pastures syndrome?

A

Caused by anti-glomerular basement membrane antibodies – bind kidney basement membrane and alveolar membrane

107
Q

how is good pastures syndrome diagnosed?

A
  • CXR – infiltrates due to pulmonary haemorrhage, often in lower zones
  • Kidney biopsy – crescenteric glomerulonephritis
108
Q

how is good pastures treated?

A

Vigorous immunosuppressive treatment and plasma pharesis

109
Q

what is Wegener’s granulomatosis?

A

This is a multisystem disorder of unkown cause that is characterised by necrotizing granulomatous inflammation and vasculitis of small and medium vessels. This affects the respiratory tract, lungs and kidneys.

110
Q

how does Wegener’s granulomatosis present clinically?

A

presents with nasal obstruction, glomerulonephritis, haematuria, cough, haemoptysis, pleuritis, peripheral neuropathy, arthritis and ocular involvement (keratitis, conjunctivitis, scleritis, episcleritis and uveitis)

111
Q

how is Wegener’s granulomatosis diagnosed?

A
  • bloods- raised cANCA, ESR, CRP
  • urinanalysis- proteinuria and haematuria
  • CXR- nodules
  • CT- diffuse alveolar haemorrhage
112
Q

how is Wegener’s granulomatosis treated?

A

azathioprine and methotrexate

113
Q

what is a mesothelioma?

A

A mesothelioma is a tumour of the mesothelial cells that occurs in the pleura

114
Q

what is the most common cause of mesothelioma?

A

asbestos

115
Q

how does a patient with mesothelioma present clinically?

A

chest pain, dyspnoea, weight loss, finger clubbing, recurrent pleural effusions, lymphadenopathy, hepatomegaly and abdominal pain

116
Q

how is a mesothelioma diagnosed?

A
  • CXR- pleural thickening
117
Q

how is a mesothelioma treated?

A

pemetrexed and cisplatin chemotherapy

118
Q

what conditions does COPD cover?

A

chronic bronchitis and emphysema

119
Q

what is the genetic influence on asthma?

A

IL-4 gene cluster on chromosome 5, controls production of IL-3, -4, -5 and -13 – affects mast and eosinophil cell development and longevity, and IgE production

120
Q

what is a pneumothorax?

A

Air in the pleural space leading to partial or complete collapse of the lung

121
Q

what is a tension pneumothorax?

A

Tension pneumothorax (rare, unless px is on mechanical ventilation) – pleural tear acts as a one way valve – air passes through during inspiration but is unable to exit during expiration

122
Q

what is the aetiology of a pneumothorax?

A
  • spontaneous
  • chest trauma
  • asthma
  • COPD
  • TB
  • pneumonia
123
Q

how does a pneumothorax present clinically?

A

symptoms- sudden onset pleuritic chest pain

signs- reduced expansion, diminished breath sounds on affected side

124
Q

how is a pneumothorax diagnosed?

A

CXR

125
Q

how is a pneumothorax treated?

A
  • if due to trauma- chest drain

- aspiration

126
Q

how is a tension pneumothorax treated?

A
  • large-bore needle inserted into 2nd intercostal space in mid-clavicular line
127
Q

what is the pathophysiology of a tension pneumothorax?

A
  • Air drawn into pleural space with each inspiration has no escape during expiration
  • Mediastinum is pushed over into the contralateral hemithorax – kinking and compressing the great veins
  • Unless air is rapidly removed, cardiorespiratory arrest will occur
128
Q

how are primary bronchial tumours staged?

A

TNM staging
Primary tumour
• T0 = none evident
• T1 = <3cm in lobar, or more distal airway
• T2 = >3cm and >2cm distal to carina or any size if pleural involvement or obstructive pneumonitis extending to hilum
• T3 = involves chest wall, diaphragm, mediastinal pleura, pericardium or <2cm from carina. T >7cm and nodules in same lobe.
• T4 = involves mediastinum, heart, great vessels, trachea, oesophagus vertebral body, carina, malignant effusion, or nodules in another lobe

Regional nodes
• N0 = none involved
• N1 = peribronchial and/or ipsilateral hilum
• N2 = ipsilateral mediastinum or subcarinal
• N3 = contralateral mediastinum or hilum, scalene or supraclavicular

Distant Metastases
• M0 = none
• M1 = (a) nodule in other lung, pleural lesions or malignant effusion; (b) distant metastases present

129
Q

what are some risk factors of bronchial carcinoma?

A
  • smoking
  • asbestos
  • chromium
  • arsenic
  • radiation
130
Q

how does a bronchial carcinoma present clinically?

A
  • cough
  • haemoptysis
  • dyspnoea
  • chest pain
  • lethargy
  • anorexia
  • weight loss
131
Q

how can a bronchial carcinoma be diagnosed?

A
  • CXR- consolidation, pleural effusions, lung collapse
  • fine needle biopsy
  • CT- tumour staging
132
Q

how is bronchiectasis managed?

A
  • airway clearance techniques alongside antibiotics

- nebulised salbutamol can also be used if patient is asthmatic

nicks phase 2a flaschards (15 decks)

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