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Disease Profiles > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Sarcoidosis areas of effect

A

Multi system disorder, commonly lungs, lymph nodes, joints liver, skin and eyes

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2
Q

Sarcoidosis Overview

A

chronic granulatomous (type IV hypersensitivity) disorder of unknown origin.
Charecterised by granulomas associated with the accumulation of T cells and macrophages.
Chronic inflammation in lungs leads to fibrosis

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3
Q

Who gets sarcoidosis

A

Usually adults aged 20-40, non-smokers, more common in Afro-Caribbeans and women

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4
Q

Presentation of Sarcoidosis

A

Resp: dry cough, progressive shortness of breath, chest pain, reduced exercise tolerance
General: lymphadenopathy, poly arthritis, erythema nodosum
GI: Hepato-splenomegaly
Ophthalmological: conjunctivitis, dry eyes, glaucoma
Neurological: Bell’s palsy, neuropathy
Metabolic: hypercalcemia

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5
Q

Sarcoidosis investigations

A

Spirometry: normal restrictive pattern
CXR: bilateral hilar lymphadenopathy, fibrosis
Urine: increased calcium
DCLO: normal or reduced
Bloods: raised ESR, WCC, serum ACE, calcium

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6
Q

Sarcoidosis management

A

Most patients don’t need treatment, as the majority of cases will resolve after 2 years
Treatment indicated if symptoms include: interstitial lung disease, hypercalcemia, cardiac/neurological involvement, uveitis
Treatment plan: oral or inhaled steroids +/- immunosuppressants

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7
Q

Bronchiectasis overview

A

Chronic dilation of the airways, with increased mucus and decreased compliance due to scarring

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8
Q

Causes of bronchiectasis

A

Idiopathic, malignancy, chronic infection, immunodeficiency, genetic (cystic fibrosis), autoimmune (rheumatoid, ulcerative colitis), COPD/asthma, allergic lung inflammation, recurrent pulmonary aspiration, ciliary dyskinesia,

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9
Q

Presentation of Sarcoidosis

A

Increased mucus production, shortness of breath, fatigue, wheezing, chest pain, finger clubbing, haemoptysis, fever

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10
Q

Bronchiectasis investigations

A

Blood test for underlying cause (associated conditions, infection)
CXR or CT scan to show location and extent of respiratory damage/scarring (signet ring sign)
Spirometry should show restrictive curve
Sputum culture

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11
Q

Bronchiectasis management

A 
Postural drainage 
Salbutamol inhaler 
Long term antibiotics 
Nebuliser saline
(Carbocysteine)
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12
Q

Influenza overview

A

Viral infection caused by influenza A/B viruses

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13
Q

Presentation of influenza

A

Fever, malaise, exhaustion, myalgia, fever, cough, runny nose, vomiting and diarrhoea

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14
Q

Influenza management

A

Hydration and rest
Prescribe anti viral if in the midst of a recognised flu outbreak and the person part of an at risk group. Antivirals (oral oseltamivir and inhaled zanamivir) should only be started before 48 hours have passed since onset of symptoms
At risk groups and health care workers should get the annual flu vaccine

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15
Q

Upper respiratory tract infection overview

A

Usually a viral infection (rhinovirus, RSV, Coronavirus) or sometimes bacterial (Streptococcus pneumoniae, Staphylococcus aureus) or fungal (Aspergillus) in immunocompromised people), affecting the paranasal sinuses, nasal cavity, pharynx, and/or the larynx

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16
Q

Upper respiratory tract infection presentation

A

Rhinitis -> Runny nose/nasal congestion, sneezing
Rhinosinusitis -> Pain/pressure on face, change in voice (bunged up)
Pharyngitis -> Sore throat
Tonsillitis -> Pain/swelling, difficulty swallowing
Laryngitis-> Hoarse voice, dry cough
Epiglottitis -> Trouble breathing (EMERGENCY)
NO SYSTEMIC UPSET & CLEAR CHEST

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17
Q

Upper respiratory tract infection management

A

Rest and Hydration

Be careful as can progress to lower respiratory illness

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18
Q

Bronchiolitis overview

A

Inflammation of the small airways of the lungs (bronchioles), usually a result of an infection from the respiratory syncytial virus (RSV), mostly affecting young children, most children will be infected at least once.
RSV causes the the lining cells of the airway to merge into large multinucleated cells called syncytia

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19
Q

Bronchiolitis presentation

A

Initially congestion, sore throat, cough
Progressing into difficulty breathing, wheezing, fever
Hypoxia can cause increased heart and resp rate, leading to exhaustion and hospitalisation
Infants can exhibit central apnea (periods of no breathing)

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20
Q

Bronchiolitis risk factors

A

Time of year, age, not breastfed, born prematurely, neuromuscular disorders

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21
Q

Bronchiolitis management

A

Rest and hydration
Supplementary Oxygen if required
Those at particular risk (premature or have significant pulmonary disease) can receive monthly antibody injections (Palivizumab)

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22
Q

Epiglottitis overview

A

Inflammation of the epiglottis, usually bacterial! (Haemophilus influenzae, group A streptococcus). Can be deadly due to blockage of airflow

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23
Q

Epiglottitis presentation

A

Fevers, difficulty breathing, stridor, retractions (ribs emphasised on inhalation), trpodding, hot potato voice

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24
Q

Epiglottis investigations

A

X-ray: swollen epiglottis & aryepiglottic folds
CT: Narrowed airway (NOT RECOMMENDED)
Endoscope: epiglottis red and swollen

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25
Q

Epiglottitis management

A

Supplemental oxygen or even intubation or cricothyroidotomy if very severe
Relevant antibiotics
IV steroids to reduce immune response
H. Influenzae vaccine to prevent epiglottitis

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26
Q

Croup overview

A

Acute respiratory condition characterised by laryngotracheitis, also known as laryngotracheobronchitis. Usually caused by viral vectors (RSV, parainfluenza, adenoviruses, could be bacterial (C. diphtheriae) if unvaccinated. Most common in children under 6 y/o

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27
Q

Croup presentation

A

Sore throat, hoarse voice, ‘barking’ cough, tachypnea, grunting, inspiratory stridor
Severe: HYPOXIA, RESP. FAILURE, PULSUS PARADOXUS (decrease of systolic arterial pressure > 10mmHg on inspiration)

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28
Q

Croup investigations

A

X-ray: ‘steeple’ sign (airways marrow to a point towards epiglottis)

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29
Q

Croup management

A

Rest and Hydration
Single dose of dexamethasone or prednisilone to reduce swelling in throat
Nebuliser epinephrine and humidified supplemental oxygen if patient is struggling to breath

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30
Q

Acute bronchitis overview

A

UTRI has progressed down into chest to cause a lower respiratory tract infection. Characterised by inflammation of the bronchi.

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31
Q

Acute bronchitis presentation

A

Recent URTI/current URTI
Productive cough, aches and pains, tiredness
Sore chest and stomach muscles, shortness of breath

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32
Q

Acute bronchitis management

A

Usually clears by itself in 3 weeks
Rest and hydration
Antibiotics (amoxicillin or doxycycline) can be discovered if >65 or has other co-morbidities like COPD

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33
Q

Cystic fibrosis overview

A

Autosomal Recessive deltaF508 mutation in the Cystic Fibrosis Transmembrane conductance Regulator (CFTR) Gene
Prevents the pumping of chlorine ions into secretions, leading to the secretions being dry

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34
Q

Cystic fibrosis areas of effect

A

Sinuses, lungs, pancreas, intestines, gall bladder, heart, liver,

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35
Q

Who gets diagnosed with cystic fibrosis?

A

Children and young adults, usually of Northern European descent
1/25 people in the UK carry the gene
Both parents carry mutation/family members already have condition

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36
Q

Presentation of cystic fibrosis

A

History of delayed meconium or meconium ileus
Poor weight gain and failure to thrive, due to pancreatic insufficiency, steatorrhea - fat containing stools, pancreatitis, diabetes
Defective cilia lead to bacterial recurrent infection, CF exacerbation (cough, fever, pneumonia), bronchiectasis, haemoptysis, pulmonary fibrosis
Infertility in men (no vas deferens), digital clubbing, nasal polyps

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37
Q

Cystic fibrosis investigations

A

New born screening for immunoreactive trypsinogen (IRT), found in the blood in the case of pancreatic damage
Sweat test shows high levels of chloride (>60mmol)
Genetic testing

38
Q

Cystic fibrosis management

A

Chest physiotherapy (postural drainage), mucolytics
Pulmonary lung function tests to track deterioration (obstructive)
Prophylactic antibiotics
Fat soluble vitamins, extra calories, replacement pancreatic enzymes
Ivecaftor used in G551D mutation, CFTR in membrane but not activated
Lung transplant

39
Q

Acute respiratory distress syndrome overview

A

Non cardio genie pulmonary oedema caused by widespread inflammation of the lungs.
Juice in alveoli

40
Q

Causes of acute respiratory distress syndrome

A

Cytokines (TNF-alpha, Interleukin 1) present in blood are taken up from blood stream. Inflammation causes blood clots, endothelium becomes leaky, pneumocytes die and form hyaline membrane.
Shock, trauma and burns, infection (sepsis,malaria), drugs (aspirin, heroin), GI (acute liver failure, pancreatitis), Obstetric (eclampsia, amniotic fluid embolus), Resp (pneumonia, inhalation injuries, vasculitis)

41
Q

Presentation of acute respiratory distress syndrome

A

Shortness of breath + tachypnoea hours-days after initial injury
Rapidly deteriorates into resp. failure
Cyanosis, bilateral crepitations, tachycardia, peripheral vasodilation

42
Q

Investigations for acute respiratory distress syndrome

A

CXR: opacity/white out across both lungs
PF ratio: PaO2/FiO2 < 300mmHg
Pulmonary artery catheter: capillary wedge pressure = normal

43
Q

Management of acute respiratory distress syndrome

A

Supplemental oxygen or mechanical ventilation (positive-end expiratory pressure prevents alveolar collapse)
Treat underlying cause
Treat any persistent lung damage appropriately

44
Q

Idiopathic pulmonary fibrosis

A

Pulmonary fibrosis of unknown cause
Chronic process causing progressing loss of lung tissue
Over production of collagen by myofibroblasts

45
Q

Who gets idiopathic pulmonary fibrosis

A

Old people
Men
Smokers

46
Q

Presentation of idiopathic pulmonary fibrosis

A

History of dry cough, shortness of breath, malaise, weight loss and fatigue
Digital clubbing, bibasal inspiratory crackles, and cyanosis
Respiratory failure

47
Q

Investigations for idiopathic pulmonary fibrosis

A

CXR: lower zone fibrosis
CT: honeycombing and interstitial thickening
Spirometry: decreased totally lung capacity, decreased FVC, decreased FEV1, normal FEV1/FVC. Restrictive pattern
ABG: reduced PaO2/increased PaCO2
DCLO: reduced

48
Q

Treatment of idiopathic pulmonary fibrosis

A

50% 5 year mortality rate
Smoking cessation and anti fibrotic (perfenidone)
Supplemental oxygen
Lung transplant

49
Q

Tuberculosis overview

A

An infection caused by mycobacterium tuberculosis
Can effect all organs but primarily affects the lungs
Usually contracted by inhalation of contaminated droplets

50
Q

Tuberculosis primary infection

A

Bacterium reaches alveoli (usually in upper lung)
Macrophage and T cell immune response results in the formation of a caseating granuloma called the ghon focus, lymph node involvement vghon complex, calcification = ranke complex
3 outcomes: 50% result in spontaneous resolution, primary TB induced (symptomatic), or bacteria becomes dormant in granuloma (latent infection)

51
Q

Tuberculosis latent infection

A

Bacteria lays dormant in patient and is asymptomatic

Bacteria can be reactivated due to changes like: diabetes, homelessness or drug abuse, steroids and HIV

52
Q

Miliary tuberculosis

A

Occurs due to dissemination due to entry into blood stream

Assman focus: secondary pulmonary lesions that have spread from the initial site, usually small and numerous

53
Q

Who gets tuberculosis

A

Deprived people

People originating from or have traveled to: Indian subcontinent, SE Asia, and Africa

54
Q

Presentation of Tuberculosis

A

History of malaise, fever, night sweats, productive cough, SOB, chest pain, hoarseness, haemoptysis, and bone pain
Erythema nodossum, lymphadenopathy, vertebral collapse, erythema nodossum, and meningitis

55
Q

Tuberculosis investigations

A

CXR: pneumonia, cavitating upper lobe lesions, lymphadenopathy, fibrosis/calcified lesions
Skin: Purified protein derivative intradermal skin test/manors test, shows exposure (past or present) to TB or BCG vaccine
Blood: Interferon Gamma Release Assay (IGRA)
Sputum: PCR and Zhiel Nielsen stain shows up red

56
Q

Tuberculosis management

A

Active TB:
Rifampicin, Isoniazid, Pyrazinamide, Ethambutol for 2 months, AND rifampicin and isoniazid for a further 4 months
Latent TB:
Rifampicin and isoniazid for 3 months OR isoniazid for 6 months
Compliance is very important as it reduces infectiousness

57
Q

Pleural effusion overview

A

Excess fluid present in the pleural space

Comes in 3 flavours transudative, exudative, and lymphatic

58
Q

Exudate effusion explanation and causes

A

Pleural effusion that contains >30g/l of protein
This is caused by anything that causes an inflammation of pulmonary capillaries like: trauma, malignancy, infection, autoimmune diseases

59
Q

Transudate effusion explanation and causes

A

Effusion with a protein content of <30g/l
This is caused by an increase in hydrostatic pressure within the blood pulmonary arteries (heart failure) or a decrease in osmotic pressure within the pulmonary capillaries (cirrhosis of the liver or nephrotic syndrome)

60
Q

Presentation of pleural effusion

A

Can be asymptomatic
History of shortness of breath and pleuritic chest pain
Stony dull to percussion and reduced breath sounds in the area effected

61
Q

Investigations for pleural effusion

A

CXR: blunting of the costophrenic angle, dense shadows with meniscus
Thoracentesis (chest drain): yellow=parapneumonic, neutrophils=parapneumonic or PE, Lymphocytes=malignancy or TB or autoimmune, mesothelial cells=PE, abnormal mesothelial cells=mesothelioma

62
Q

Management of a pleural effusion

A

Thoracentesis = hollow needle inserted just above a rib in order to remove the fluid
Treat underlying cause
Plurodesis (the binding of the two pleural walls) if pleural effusion is recurrent

63
Q

Pneumothorax overview

A

Presence of air within the pleural space

64
Q

Tension pneumothorax

A

Presence of air in the pleural space that is at high pressure due to the entry hole acting as a one way valve
High pressure can cause deviation of structures: lungs, heart, trachea

65
Q

What causes a pneumothorax

A

Spontaneous: bullae (air pocket) forms in lung due to small leak in alveoli, this air pocket breaks
Trauma
Iatrogenic: mechanical ventilation, GVP line placement

66
Q

Who gets a pneumothorax

A

Primary: thin, tall, adolescent, male with a history of holding their breath, no underlying cause
Secondary: underlying health cause (CF, carcinoma, asthma, emphysema, marfans)

67
Q

Presentation of pneumothorax

A

History of shortness of breath and pleuritic chest pain

Reduced expansion, hyper resonance and reduced breath sounds over effected area, hypoxia

68
Q

Investigations for pneumothorax

A

CXR: peripheral loss of lung markings

69
Q

Primary spontaneous pneumothorax management

A

If <2cm and asymptomatic there is no need for treatment
If >2cm or symptomatic attempt aspiration up to two times, if not possible, insert a chest drain
Aspiration = insertion of a 16g cannula into the 2nd intercostal space, on the midclavicular line
?pleurodesis if recurrent

70
Q

Secondary spontaneous pneumothorax management

A

0-1cm and asymptomatic: oxygen and admit for observation for 24 hours
1-2cm and asymptomatic: attempt aspiration, if this fails, insert chest drain
> 2cm or symptomatic: insert chest drain

71
Q

Tension pneumothorax management

A

If suspected, do not delay for results of CXR

Proceed with immediate aspiration, followed by a chest drain

72
Q

Pulmonary embolism overview

A

Blockage in within the pulmonary arteries

Usually caused by a thrombus originating within the deep veins of the leg

73
Q

Pulmonary embolism risk factors

A

Wirchow’s triad

  1. Slowed blood flow (stasis) - turbulent blood flow, bed rest, prolonged travel, pregnancy
  2. Hypercoagulation - genetics, surgery/trauma, medications (birth control)
  3. Damage to endothelium - infections, chronic inflammation, toxins (tobacco smoke
74
Q

Pulmonary embolism presentation

A

History of leg pain/swelling, shortness of breath, chest pain, haemoptysis, syncope/sudden death (-> occlusion of pulmonary saddle)
Tachycardia, tachypnoea, cyanosis, fever, low BP, crackles and dullness (effusion), rub

75
Q

Pulmonary embolism investigations

A

ABG: decreased PaO2, decreased SaO2, normal or low PaCO2 (type 1 respiratory failure
CXR: normal before infarction, progress to basal atelectasis, consolidation, pleural effusion
D-dimmer: raised
ECG: acute right heart strain pattern (S1Q3T3, T inversion in V1-V3)
Troponin and BNP: raised

76
Q

Circumstantial pulmonary embolism investigations

A

If unwell with suspected intermediate to high risk PE: CT pulmonary angiogram to look for artery filling defect
In the ambulatory setting with suspected low risk PE: V/Q scan or CTPA
Pregnant: ultrasound on legs -> positive findings -> presume PE and treat accordingly OR just perfusion scan. Disregard damage to baby if mother is in danger

77
Q

Investigations for cause of ?PE

A

Thrombophillia screening
Cancer screening
Autoantibodies (SLE)

78
Q

Anticoagulant management following Pulmonary evidence

A

Anticoagulants: therapeutic dose of s/c low molecular weight heparin (dalteparin/fragmin), rarely IV heparin.
Begin this immediate if high suspicion of PE, if low suspicion, wait for test results
Start warfarin simultaneously
Stop heparin when INR>2 (3-5 days)
Alternatively: solely use DOACs -> direct oral thrombin inhibitor (dabigatran) or factor X inhibitor (rivaroxaban/apixaban)

79
Q

Target INR ranges for pulmonary embolism

A

First event: 2-3
Recurrent PE: 3 or more
Recurrent PE whilst on warfarin: 3.5
Warfarin interactions: alcohol, antibiotics, amiodarone, cimetidine, grapefruit… BE CAREFUL

80
Q

Thrombolysis management following a Pulmonary embolism

A

In case of life-threatening massive/sub-massive PE (low BP (<90mmHg systolic for 15 mins), severe hypoxia, imminent or actual cardiopulmonary arrest)
IV tissue plasminogen activator (tPA) - tenecteplase
Contraindications: haemorrhagic stroke are any time, ischaemic stroke within last 6 months, recent major trauma/surgery, current haemorrhage
Relative contraindications: pregnancy/post-partum, TIA in last 6 months, peptic ulcers, refractory resuscitation/hypertension, advanced liver disease

81
Q

Extra management of pulmonary embolism

A

IVC filter to prevent further embolisation of recurrent clots
Intra-catheter directed thrombolysis
Thrombo-embolectomy (v. rare)

82
Q

Duration of anti-coagulant treatment following a pulmonary embolism

A

Unprovoked 1st PE -> 6 months
Provoked PE/temporary risk factor -> 3 months
Unprovoked low risk distal DVT -> 3 months
High risk proximal DVT -> 6 months
Recurrent DVT/PE -> life long

83
Q

Extrinsic allergic alveolitis overview

A

Type 3 hypersensitivity (IgG driven) caused by the inhalation of an allergen
Can present both acutely and chronically

84
Q

Extrinsic allergic alveolitis causes

A

Spores from hay: farmer’s lung
Protein in bird poo: pigeon fancier’s lung
Aspergillus from malt: malt worker’s lung
No cause is discovered in 30% of cases

85
Q

Presentation of extrinsic allergic alveolitis

A

Acute (4-6 hours after exposure): flu like symptoms (fever, rigor, myalgia, dry cough, shortness of breath, crepitations)
Chronic (repeated low dose exposure): fibrosis of the lungs due to chronic inflammation, progressive shortness of breath, weight loss, type 1 respiratory failure, cor pulmonale

86
Q

Acute presentation of extrinsic allergic aalveolitis investigations

A

Bloods: neutrophilia, increased erythrocyte sedimentation rate
CXR: upper zone consolidation
Spirometry: reversible restrictive pattern

87
Q

Chronic presentation of extrinsic allergic aalveolitis investigations

A

Blood: positive serum precipitins
CXR: upper lobe fibrosis (honeycomb lung)
Spirometry: restrictive pattern
DCLO: reduced

88
Q

Management of extrinsic allergic alveolitis

A

Acute: remove allergen, supplementary oxygen, tapered dose of oral steroids
Chronic: allergen avoidance, long term steroids

89
Q

Coal Miner’s Pneumoconiosis

A

Interstitial lung disease caused by inhalation of coal dust
Initially asymptomatic, but later presents with progressive massive fibrosis in the mid lung
Callan syndrome = the association between rheumatoid, pulmonary rheumatoid nodules and coal miners pneumoconiosis

90
Q

Silicosis

A

Interstitial lung disease caused by inhalation of silicone
Seen in glass worker’s, metal miners, and stone quarries
Presents with progressive shortness of breath
CXR = upper lobe fibrosis, egg shell calcification at the hilar nodes

91
Q

Asbestosis

A

Interstitial lung disease associated with inhalation of asbestosis
As well as ILD, asbestos can also cause pleural disease: benign pleural plaques, pleural thickening, mesothelioma

Disease Profiles (3 decks)

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