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YEAR 2 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

In which lung is an aspiration more likely to happen?

A

Right lower lung
The right bronchus is more vertical and wider so a foreign object is likely to fall down this path over the left bronchus

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2
Q

What cells are involved in the mucociliary apparatus?

A

Goblet cells - secrete mucus to trap pathogens
Ciliated columnar cells - move mucus towards main bronchi and trachea to be expelled by coughing or swallowed

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3
Q

How does the innate immune system act as a defence mechanism for the respiratory tract against inhaled pathogens?

A

Alveolar Macrophages - recognise microbes via surface receptors - immobilise + destroy bacteria

Type II alveolar cells - secrete surfactant proteins to enhance phagocytosis and agglutination of gram-positive bacteria

Neutrophils - chemoattraction to alveolar space - phagocytose bacteria and kill via respiratory burst

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4
Q

What are neuraminidase and haemaglutinin and is their function?

A

Glycoproteins on influenza membranes

Haemaglutinin binds to sialic acid receptors on host respiratory epithelial cells for fusion and neuraminidase cleaves sialic acid residues to promote release and spread of viruses

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5
Q

What is the role of spike proteins on coronavirus?

A

A glycoprotein that facilitates the fusion and penetration of host cell by binding to ACE2 along our airways

S1 - recognise and bind to receptors on the host cell
S2 - fuses envelope of the virus with the host cell membrane

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6
Q

What is Antigenic Drift?

A

Small changes or mutations in the genes of influenza virus that can lead to changes in the surface proteins of the virus - HA, NA

Loss or reduction in protection from existing antibodies and vaccines - susceptible to the flu again

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7
Q

What is Antigenic Shift?

A

A major change where 2 or more strains combine to form new subtypes of HA, NA glycoproteins
e.g. When an zoonotic virus gains the ability to infect humans
Normally would result in a pandemic, no previous immunity, occurs infrequently

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8
Q

How can soap kill corona virus?

A

Tear apart the lipid shell surrounding the virus to make the inside susceptible to our immune system

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9
Q

What is the role of furin in viruses?

A

A protease released by the golgi apparatus

Cleaves glycoproteins once bound to host cell to allow for fusion and penetration into membrane

Increasing infectious and pathogenic nature of virus

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10
Q

What are common pathogens that cause a sore throat?

A

Influenza, Rhinovirus, Coronavirus
Adenovirus
EBV
CMV
Strep A

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11
Q

What are infections of the URT?

A

Common cold
Tonsilitis
Laryngitis
Pharyngitis
Sinusitis
Otitis Media

Mainly viral pathogens as causative agent

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12
Q

What are infections of the LRT?

A

Pneumonia
Tuberculosis
Lung abscess
Bronchiolitis

Mainly bacteria pathogens as causative agent

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13
Q

How can you distinguish between URT and LRT infections?

A

URTI - normal chest x-ray and breath sounds on auscultation
Symptoms - runny nose, dry cough, headache, sore throat, sneezing, myalgia

LRTI - changes/consolidation on x-ray and coarse crackles on auscultation
Symptoms - productive cough, SOB, breathlessness, wheezing, tight chest

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14
Q

What is the most common infective cause of COPD exacerbations?

A

Haemophilus Influenzae

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15
Q

What is the common causative bacteria of Pneumonia in HIV?

A

Pneumocystis jiroveci - PCP

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16
Q

What is the common causative bacteria of Pneumonia in alcoholics and diabetics?

A

Klebsiella pneumoniae

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17
Q

What type of bacteria are asplenic patients more susceptible to and why? Give 3 examples.

A

Insufficient splenic macrophages to opsonise and phagocytose encapsulated bacteria

Streptococcus pneumoniae
Haemophilus influenzae
Neisseria meningitis

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18
Q

What is the common causative bacteria of Pneumonia in someone recently exposed to air con and hot tubs?

A

Legionella pneumophilia

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19
Q

What is the difference between tuberculosis and sarcoidosis?

A

TB - caseating granuloma
Sarcoidosis - non-caseating granuloma

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20
Q

What are similarities in tuberculosis and sarcoidosis?

A

Granulomatous disease
Erythema nodosum
Hilar lymphadenopathy
Arthralgia
Systemic symptoms - fever, malaise, weight loss
Affect upper lobes of lungs

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21
Q

What is the management of active TB?

A

Isoniazid, rifampicin, ethambutol, and pyrazinamide
for 2 months

Isoniazid and rifampicin for a further 6 months

Longer courses if extra-pulmonary TB, HIV, immunosuppressed

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22
Q

What is the pathophysiology of the primary infection in TB?

A

M.tuberculosis inhaled as aerosolized droplets

M.T lodge in the alveoli and engulfed by macrophages

M.T continues proliferating intracellulary

AM travels to lymph nodes = hilar lymphadenopathy

Granuloma forms with caseous necrosis (TNF-alpha and IFN-Gamma activate to mature macrophages) = ghon focus

If healthy patient - heals by fibrosis and disease becomes latent

Ranke complex once Ghon focus calcified

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23
Q

What is a Ghon complex?

A

Primary lesion/ghon focus in the lungs and hilar lymphadenopathy

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24
Q

What is secondary and miliary TB?

A

Secondary - reactivation of TB - cavitating lesions of upper lobes of lung + systemic symptoms (Weight loss, fever, haemoptysis)

Miliary - haematogenous spread of TB (Potts disease - in spinal cord, meninges, kidneys, hepititis)

Mainly in immunocompromised

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25
Q

How can TB be diagnosed?

A

Sputum Smear - 3 specimens on 3 different days - Ziehl-Neelsen - stain red

Sputum Culture - Lowenstein-Jensen media

Tuberculin/Mantoux Test - Purified Protein Deviate injected into skin - reaction if immune recognition of TB(positive in those who have had BCG)

IFN-Gamma Release Assay - measure response - can’t tell difference between latent or active TB

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26
Q

Which drug class is contra-indicated in TB and why?

A

TNF-alpha inhibitors

Disrupt granuloma formation and can reactivate TB

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27
Q

What is the common causative bacteria of Pneumonia?

A

Streptococcus pneumoniae

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28
Q

What is the criteria for CURB 65?

A

C - confusion
Urea >7 mol
RR > 30/min
BP < 90/60

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29
Q

What result of CURB 65 would warrant consideration for hospital admission?

A

2+

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30
Q

What is the time frame for HAP?

A

Pneumonia occurring 48 hours or more after admission

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31
Q

What is the treatment for low severity CAP?

A

Amoxicillin - 500mg TDS for 5 days

If Penicillin allergy
- Doxycycline - 200mg loading dose + 100mg OD - 5 days total
- Clarithromycin 500mg BD for 5 days

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32
Q

What is the management after pneumonia has been treated?

A

Repeat chest x-ray 6 weeks after clinical resolution to ensure consolidation has resolved and no underlying secondary abnormalities

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33
Q

What is the management for moderate-severe CAP?

A

Dual antibiotic therapy for 7-10 days

Moderate: Amoxicillin + Doxycycline/Clarithromycin

Severe: Co-amoxiclav/Benzylpenicillin/Vancomycin + Clarithromycin

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34
Q

What are features of sputum from different causative bacteria?

A

Strep pneumonia - rust coloured
Psuedomonas - green
Klebsiella - redcurrant jelly
Anaerobes - bad smell/bad taste

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35
Q

How is an infective exacerbation of COPD treated?

A

Amoxicillin PO 500mg TDS for 5 days

Doxycycline 200mg stat dose day 1 - 100mg 4 days OD - if penicllin allergy

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36
Q

What are features of Klebsiella?

A

Common in alcoholics and diabetics
Red-currant jelly sputum
Often affects upper lobes
Commonly causes lung abscess formation and empyema

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37
Q

What are features of PCP - pneumocystis jiroveci?

A

Typically seen in HIV patients
Dry cough, exercise-induced desaturations, absence of chest signs
Clear chest - may hear end inspiratory crackles

Treated with co-trimoxazole

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38
Q

In which patients are at risk of staphylococcal pneumonia?

A

Intravenous drug users
Elderly patients
Patients who already have an influenza infection

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39
Q

What are features of mycoplasma pneumonia?

A

Flu like symptoms - flu, arthralgia, myalgia, dry cough and headache
Auto-immune manifestation - erythema multiforme, hepatitis, cold autoimmune haemolytic anaemia

Primarily affects younger patients.

Associated with erythema multiforme, stevens-johnson syndrome, guillain-barre syndrome

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40
Q

How can Legionella pneumonia present in a patient and on labs?

A

Hyponataemia + Deranged LFTs, Raised CK

Diarrhoea, vomiting
Typically travel related - hot tubs and air con

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41
Q

How often is the pneumococcal vaccine given in at-risk individuals?

A

5 years

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42
Q

What bacteria can cause pneumonia in patients exposed to birds, parrots etc?

A

Chlamydophilia psittaci

Associated fevers, joint pain, nose bleeds

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43
Q

What is Q fever?

A

Disease caused by Coxiella burnetii

From exposure to sheep and goats

Q fever = fever, myalgia, headache, hepatitis - can present as pneumonia

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44
Q

What are the histological classifications of pneumonia?

A

Lobar - affects one or more lobes of the lungs

Bronchopneumonia - affects patches throughout both lungs

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45
Q

How is aspiration pneumonia treated?

A

Amoxicillin/Clarithromycin and Metronidazole

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46
Q

How is HAP treated?

A

1st line - co-amoxiclav 500/125mg TDS 5 days
2nd line - doxycyline

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47
Q

What test can identify the Legionella antigen?

A

Urinary antigen testing

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48
Q

How is severe HAP with sepsis/non-responsive treated?

A

IV tazocin - piperacillin/tazobactam

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49
Q

What is the pathophysiology of Pneumonia?

A

Infection leads to inflammatory response
Inflammatory response leads to exudate formation and alveoli oedema
Consolidation forms in lung tissue

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50
Q

What are typical features of atypical pneumonia?

A

Often fever, headache, sweating, myalgia

Moderate sputum production, often no consolidation on CXR, small increase in WCC

Less likely to present with typical ‘resp’ symptoms

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51
Q

What are common causative bacteria of aspiration pneumonia?

A

Streptococcus pneumoniae
Staphylococcus aureus
Haemophilus influenzae
Enterobacteriaceae
Pseudomonas

Anaerobic bacteria

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52
Q

What is the inheritance pattern of cystic fibrosis and what is the mutation?

A

Autosomal recessive disorder

Mutation in CFTR gene on chromosome 7 - DF508 mutation

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53
Q

What is the pathophysiology of cystic fibrosis?

A

CFTR protein - a channel that normally transports chloride ions out from mucus cells into mucus to attract water and make it less viscous

In CF - defective CFTR - chloride ions trapped in cell = mucus will be abnormally thick - builds up and obstructs organs. Chloride ions also stuck in sweat glands - unable to be reabsorbed - high chloride in sweat

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54
Q

What are symptoms of CF in a newborn?

A

Meconium ileus - rigid abdomen, green vomit, fever, can’t passed first stool

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55
Q

What are symptoms of CF in childhood?

A

Failure to thrive
Delayed puberty
Pancreatic insufficiency - pale stools, pancreatitis, gallstones
Chronic wet cough
Recurrent infections, pneumonia, bronchiectasis

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56
Q

What are symptoms of CF in adulthood?

A

Infertility
Amenorrhea
Clubbing
Diabetes

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57
Q

What are investigations for CF?

A

Heel prick test - screening at birth - detects IRT = pancreatic damage

Sweat test - chloride ion levels > 60

Genetic testing

Spirometry - obstructive disease - bronchiectasis

Faecal elastase
Sputum cultures
FBC

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58
Q

What can be seen on an x-ray in CF?

A

Bronchiectasis - tram-track lines
Hyperinflation
Soap bubbles
Ring shadows - clusters of cysts in upper lobes

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59
Q

What are common bacteria responsible for infections in CF?

A

Pseudomonas aeruginosa
Staphylococcus aureus
Haemophilus influenzae
Burkholderia cepacia
Aspergillus

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60
Q

How does Lumacaftor/Ivacaftor work to treat CF?

A

CFTR Modulators

Lumacaftor - increases the number of CFTR proteins on the cell surface

Ivacaftor - potentiator of CFTR to open channel and allow chloride ion to pass through

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61
Q

Which mucolytics are used in CF and how do they work?

A

Dornase alfa - Mucolytic peptide that cleaves DNA of mucus

Hypertonic saline - acts as a expectorant to increase airway surface fluid and improve clearance

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62
Q

What is Young Syndrome and what are the main differentials?

A

Characterised as…
- Male infertility
- Bronchiectasis
- Sinusitis

Differentials - CF, kartagener syndrome

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63
Q

What is Kartagener Syndrome?

A

Primary ciliary dyskinesia +
Situs inversus(or dextrocardia)
Bronchiectasis

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64
Q

What is the inheritance of primary ciliary dyskinesia?

A

Autosomal recessive disease producing defective cilia

= recurrent infections, sinusitis, otitis media, subfertily, bronchiectasis

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65
Q

What are symptoms related to the different URTI?

(rhinosinusitis, pharyngitis, tonsillitis, laryngitis, epiglottis, bronchitis, croup)

A

Rhinosinusitis - pain/pressure on face
Pharyngitis - sore throat
Tonsillitis - pain swallowing
Laryngitis - hoarse voice and dry cough
Epiglottitis - trouble breathing
Bronchitis - productive cough for up to 3 weeks, chest tightness, wheeze
Croup - harsh barking cough, stridor

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66
Q

What guides antibiotic treatment for acute bronchitis and what is the criteria?

A

CRP
20-100 - offer delayed prescription of doxycycline
>100 - prescribe doxycycline 5 days

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67
Q

How long do URTIs last?

A

Acute otitis media: 4 days

Acute sore throat/acute pharyngitis/acute tonsillitis: 1 week

Common cold: 1+1/2 weeks

Acute rhinosinusitis: 2+1/2 weeks

Acute cough/acute bronchitis: 3 weeks

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68
Q

What is part of the centor criteria that helps guide the decision of whether to prescribe abx in URTIs?

A

Presence of tonsillar exudate
Tender anterior cervical lymph nodes/ Lymphadenopathy or lymphadenitis
History of fever
Absence of cough

(3+ indicates to prescribe abx, also high chance strep A is causing sore throat)

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69
Q

When should immediate abx be prescribed in an URTI?

A

Systemically very unwell
Symptoms suggestive of serious illness
High risk complications due to co-morbidities
Children<2 with bilateral otitis media
Centor criteria 3+
>65 with acute cough + 2 of … hospitalisation in previous year, diabetes, CHF, steroid use
>80 with acute cough + 1 of … hospitalisation in previous year, diabetes, CHF, steroid use

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70
Q

What fibres in epithelial cells are involved in the cough reflex?

A

C fibres - chemical driven, inflammation
RAR - mechanically driven
SAR - mechanically driven

Send signals down vagus nerve

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71
Q

What is the mechanism behind the cough?

A

C fibres/RAR/SAR in respiratory epithelial cells stimulated - send signals down vagus nerve - reach tractus solitarus in the brainstem - goes to cough and respiratory pattern generator = synapse with efferent nerve fibres - output of cough

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71
Q

What can activate the tractus solitarus to stimulate a cough?

A

Vagus nerve - from respiratory epithelium

Ear, Heart, Oesophagus, Stomach

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72
Q

How do ACEi cause a dry cough as a side effect?

A

ACEi prevent the inactivation of bradykinin and cause it to accumulate in the respiratory tract.

Accumulation of bradykinins, substance P and prostaglandins act as chemical irritants of the c-fibres of the respiratory tract which induces the cough reflex

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73
Q

What are the 3 phases of the cough reflex?

A

Inspiratory phase
- glottis opens wide, diaphragm and external intercostal muscle contract, big breath in, increase pressure inside the lungs

Compress phase
- glottis closes, increase pressure in the lungs

Expiratory phase
- abdominal and internal intercostal muscles contract, glottis opens - air pushed out due to high pressure in the lungs = cough

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74
Q

Differentials for acute, sub-acute, chronic cough?

A

Acute < 3 weeks
- URTI
- Allergens
- PE

Sub-acute 3-8 weeks
- Post-infectious - covid, bronchitis
- ACEi

Chronic > 8 weeks
- COPD
- Asthma
- GORD
- Lung cancer
- TB

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75
Q

Causes of bronchiectasis?

A

Post-Infection: Tuberculosis; HIV; Measles; Pertussis; Pneumonia

Bronchial Pathology: Obstruction by foreign body or tumour

Allergic Bronchopulmonary aspergillosis (ABPA)

Congenital: Cystic fibrosis; Kartagener’s syndrome; Primary ciliary dyskinesia; Young syndrome

Hypogammaglobulinaemia

Idiopathic

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76
Q

Features of bronchiectasis?

A

Productive cough - large amounts of purulent sputum
Dyspnoea
Haemoptysis
Halitosis

Coarse crackles
Wheeze
Clubbing

Spirometry - obstructive pattern
X-ray - thickened, dilated airways - tramtrack sign, ring shadows
CT scan - thickened, dilated airways, signet ring

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77
Q

What is the most common bacteria found in bronchiectasis?

A

Haemophilus influenzae

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78
Q

What is bronchiectasis?

A

Permanent dilation of bronchi due to irreversible destruction of the elastic and muscular components of the bronchial wall, causing them to dilate and thicken

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79
Q

What is the management of bronchiectasis?

A

Smoking cessation
Treat underlying disease
Chest physiotherapy
Postural drainage
Patient education
Antibiotics - 10-14 days - amoxicillin or ciprofloxacin
Bronchodilators
Immunisations
Surgery for localised disease
Carbocysteine

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80
Q

What is the pathophysiology behind asthma?

A

1.Dendritic cells pick up allergens from environmental triggers and present them to T helper 2 cells.

  1. TH2 cells produce IL-4 and IL-5.
  2. IL-4 + IL-13 leads to the production of IgE antibodies which stimulate the release of granules from mast cells. Histamine, leukotrienes and prostaglandins released in this type 1 hypersensitivity reaction to give the common symptoms known as allergies.
  3. IL-5 activate eosinophils which release more cytokines and leukotriene
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81
Q

What drugs can trigger asthma?

A

Beta blockers
NSAIDs
Aspirin

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82
Q

What is Samter’s triad?

A

Asthma
Nasal polyps
Aspirin sensitivity

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83
Q

What is the spirometry reading in asthma?

A

FEV1/FVC < 70%
FEV1 < 80%

Bronchodilator reversibility - FEV1 > 12% and 200ml after 20 min use with SABA

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84
Q

What other investigations are done in asthma after spirometry?

A

Peak flow - 20% variability QDS for 2-4 weeks
FeNO - 40ppm
Eosinophils > 0.15
Methocholine < 8mg/ml
Skin prick allergy test
IgE in blood

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85
Q

What is the step up for asthma treatment?

A

SABA

SABA + Low dose ICS

SABA + Low dose ICS + LABA

SABA + Medium dose ICS + LABA

SABA + Medium dose ICS + LABA + LTRA

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86
Q

What is the treatment for an acute exacerbation of asthma?

A

OSHITME

  • Oxygen - 94-98%
  • Salbutamol - 5mg nebs - driven by oxygen
  • Hydrocortisone - give oral steroids if can swallow or IV if not, minimum 5 days
  • Ipratropium - 500 micrograms nebs
    CALL FOR SENIOR
  • Theophylline - give aminophylline IV bolus plus IV - specialist give only
  • Magnesium - 1.2-2g IV infusion 20 minutes
  • Escalate - need ITU if still unwell for non-invasive ventilation/mechanical
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87
Q

What is the discharge criteria following an acute exacerbation of asthma?

A

Stable on discharge meds for 12 - 24 hours with no nebulisers or oxygen

PEFR > 75% with diurnal variability of < 20%

Inhaler technique checked and recorded

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88
Q

What are features of a moderate asthma attack?

A

PEFR 50-75% best or predicted

Increasing symptoms

RR > 25 / min

Pulse > 110 bpm

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89
Q

What are features of a severe asthma attack?

A

PEFR 33 - 50% best or predicted

Can’t complete sentences

RR > 25/min

Pulse > 110 bpm

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90
Q

What are features of a life-threatening asthma attack?

A

PEFR < 33% best or predicted

Oxygen sats < 92%

Silent chest, cyanosis or feeble respiratory effort

Bradycardia, dysrhythmia or hypotension

Exhaustion, confusion or coma

Normal pCO2 - indicates exhaustion

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91
Q

What are features of a near fatal asthma attack?

A

Raised pCO2

Requiring mechanical ventilation with raised inflation pressures

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92
Q

Differentials for asthma?

A

ABPA
GORD
Churg-strauss syndrome
COPD
CF

93
Q

What is a complication of a mucus plug in asthma?

A

Lobar collapse

94
Q

What are the classifications of COPD?

A

Stage 1 - Mild - FEV > 80%
Stage 2 - Moderate - FEV 50-79%
Stage 3 - Severe - FEV 30-49%
Stage 4 - Very Severe - FEV <30%

95
Q

What is the pathophysiology of emphysema in COPD?

A

Imbalance between antiprotease < protease activity

Activate Protease -> Smoking stimulates macrophages and neutrophils which stimulate release of elastase that destroys elastin in alveolar wall
Inactivate anti-protease -> Free radicals from smoking/pollutants inhibit alpha1-antitrypsin

Results in destruction of alveolar wall - unable to recoil so collapses during expiration and traps air

96
Q

What is the criteria for chronic bronchitis in COPD?

A

Productive cough for more than 3 months each year for 2+ consecutive years

97
Q

What is the role of alpha-1 antitrypsin?

A

An anti-protease synthesised in the liver that inhibits neutrophil elastase to protect cells.

In deficiency - causes liver cirrhosis and allows build up neutrophil elastase in lungs(destroys elastin-leads to emphysema in lower lobes-loss of recoil in alveoli)

98
Q

Complications of COPD?

A

Secondary polycythaemia - due to hypoxemia
Pulmonary hypertension
Cor pulmonale
Pneumothorax

99
Q

What are examination findings in COPD?

A

Anteroposterior diameter of chest upwards - hyperinflation
Reduction of the cricosternal distance
Percussion - hyperresonance
Auscultation - expiratory wheeze
Reduced chest expansion
Decreased/quiet breath sounds
Cyanosis
Cor pulmonale

100
Q

What is the spirometry results in COPD?

A

Obstructive
FEV1/FVC < 70%
FEV1 <80%

No bronchodilator reversibility

101
Q

What is seen on a chest x-ray in COPD?

A

Hyperinflated chest (>6 anterior ribs)

Bullae

Decreased peripheral vascular markings

Flattened hemidiaphragms

102
Q

Patients with what should be assessed for LTOT in COPD?

A

Very severe airflow obstruction (FEV1 < 30% predicted). Assessment should be ‘considered’ for patients with severe airflow obstruction (FEV1 30-49% predicted)
Cyanosis
Polycythaemia
Peripheral oedema
Raised jugular venous pressure
Oxygen saturations less than or equal to 92% on room air

103
Q

Who should be offered LTOT in COPD?

A

pO2 of < 7.3 kPa

pO2 of 7.3 - 8 kPa and one of the following:
secondary polycythaemia
peripheral oedema
pulmonary hypertension

(measurements taken on 2 occasions at 3 weeks apart, NON smokers)

104
Q

What is the pharmacological management of chronic COPD?

A

SABA/SAMA

Asthmatic Features: LABA + ICS -> + LAMA
NO Asthmatic Features: LABA + LAMA

Mucolytics
Prophylactic azithromycin
DIuretics if cor pulmonale

105
Q

What are asthmatic features that can suggest steroid responsiveness in COPD?

A

Previous diagnosis of asthma or atopy
High blood eosinophil count
Variation in FEV1
Diurnal variation in peak flow >20%

106
Q

What are factors contributing to ‘difficult to treat’ asthma?

A

Non adherence
- Unintentional
- Lack of knowledge about necessity
- Concerns of adverse effects
- Regimen burden
- Cost of medicines
Poor inhaler technique
Medications - NSAIDs, beta-blockers, aspirin
Smoking or second-hand smoking
Exposure to asthma triggers - allergy/environment
Female hormones - symptoms can worsen around periods, menopause, pregnancy
Co-morbidities
- Acid reflux/GORD
- Anxiety and depression
- COPD
- Rhinosinusitis
- Rhinitis
- Overweight
- ABPA

107
Q

What is the management in acute exacerbation of COPD?

A

Oxygen - 88-92% target
Salbutamol - 5mg nebs driven by oxygen
Hydrocortisone - oral steroids if can swallow, if not give IV
Ipratropium - 500 microgram nebs
- CALL FOR SENIOR
Theophylline - give aminophylline IV
Escalate - need ITU if unwell not ventilation, pH<7.35

108
Q

What is acute respiratory distress syndrome?

A

Non-cardiogenic pulmonary oedema and diffuse lung inflammation - secondary to underlying illness

109
Q

What is the pathophysiology behind acute respiratory distress syndrome?

A

Inflammation results in diffuse bilateral alveolar injury mediated by TNF-alpha, IL-1, IL-8

Endothelial injury activates neutrophils in the pulmonary capillaries releasing ROS and proteases that damage the alveolar endothelium and type 2 alveolar cells

Increased permeability of alveolar capillaries leading to fluid accumulation in the alveoli = non-cardiogenic pulmonary oedema + hypoxemia

Deficiency in surfactant in alveoli = alveoli collapse

110
Q

What are causes of ARDS?

A

Pneumonia
Sepsis
Aspiration
Acute pancreatitis
Transfusion reactions
Trauma and fractures
Fat embolism
COVID-19
Smoke inhalation

111
Q

What is the presentation of ARDS?

A

Dyspnoea - severe SOB
Elevated respiratory rate - fast, shallow breathing
Bilateral lung crackles - rails
Low oxygen saturations - fails to improve with oxygen
Cyanosis
Feeling faint, Tiredness, drowsiness, confusion
Fever, cough, pleuritic chest pain

112
Q

What does ARDS look like on an x-ray?

A

Bilateral alveolar infiltrates on chest x-ray
NO features of heart failure

113
Q

What are differentials of ARDS?

A

COVID-10
Acute heart failure
Bilateral pneumonia
Hypersensitivity pneumonitis
Acute interstitial pneumonia

114
Q

What are respiratory causes of chronic breathlessness?

A

Asthma
COPD
Lung cancer
Interstitial lung diseases
TB
Sarcoidosis
Pulmonary hypertension

115
Q

What are non-respiratory causes of breathlessness?

A

Anaemia
Obesity
Anxiety
IHD
Cardiac arrhythmias
CHF

116
Q

Is wheeze normally heard on expiration or inspiration?

A

Expiration

117
Q

What are the two types of wheeze sounds?

A

Polyphonic - widespread airflow obstruction - asthmatics

Monophonic - single airway partially obstructed - tumour, mucus plug

118
Q

What are key differentials for wheeze?

A

Asthma
COPD
Pulmonary oedema
Bronchial spasm
CF
Allergies
Resp tract infections
Excessive secretions

119
Q

What is the difference between a high or low pitched wheeze

A

High pitched - narrowing of smaller bronchi
Low pitched - narrowing of large bronchi - rhonchi

120
Q

What is the difference between stridor and wheeze?

A

Wheeze - typically high-pitched music sound during expiration - indicating smaller lower airway obstruction

Stridor - typically harsh monophonic sound during inspiration - indicating large upper airway obstruction

121
Q

What is allergic bronchopulmonary aspergillosis?

A

Hypersensitivity reaction of IgG and IgE to the fungus aspergillus which leads to a lung disease

More common in asthmatics and CF patients

122
Q

What are features of ABPA?

A

Frequent productive cough
Lots of mucus - brown mucus plugs, blood
Wheezing
SOB
Chest pain or tightness
Bronchiectasis

Chest x-ray - infiltrates, aspergilloma
High levels of IgE and eosinophils
Skin testing of aspergillus

123
Q

How is ABPA treated?

A

Oral steroids
Anti-fungals - itraconazole
Optimizing underlying condition - asthma, CF

124
Q

What is the most dangerous type of asbestos?

A

Blue asbestos - Crocidolite

Extremely fine sharp fibers - greatest ability to inhale and reach alveoli

125
Q

What are common features of asbestosis?

A

SOB and reduced exercise tolerance
Cough
Clubbing

Typically 15-30 years after asbestos exposure

126
Q

What is found on investigations in asbestosis and idiopathic pulmonary fibrosis - spirometry, auscultation, x-ray, CT

A

Spirometry - restrictive pattern with reduce gas transfer
Auscultation - bilateral basal fine end-inspiratory crackles
X-ray - Reticular shadowing - basal predominance
CT - honeycombing, traction bronchiectasis, reticular scarring

127
Q

How does asbestosis occur?

A

Inhalation of asbestos fibres
Remain in alveoli indefinitely, can not be degraded - become coated in iron to form asbestos bodies - cause fibrosis and disease

128
Q

What is the management of asbestosis, coal workers pneumoconiosis?

A

Removal of triggers
Smoking cessation
Oxygen therapy
Treatment of symptoms
Lung transplant

Industrial compensation

129
Q

What is the benign change that can happen from asbestos exposure?

A

Pleural plaques

Benign and do not undergo malignant change - no follow ups necessary

130
Q

Which lung diseases form granulomas and are they caseating/ non-caseating?

A

Caseating - Tuberculosis

Non-caseating - Sarcoidosis + Hypersensitivity pneumonitis

131
Q

What is the pattern seen on spirometry for interstitial lung diseases?

A

Restrictive pattern with reduced transfer factor

132
Q

What is the immunology pathophysiology behind hypersensitivity pneumonitis?

A

Type III hypersensitivity(acute) and Type IV hypersensitivity(chronic), reaction to inhaled organic particles causing lung damage

Inflammation leads to (non-caseating) granuloma formation(acute) and fibrosis(from chronic exposure)

133
Q

How is hypersensitivity pneumonitis treated?

A

Removal of trigger
Steroids

134
Q

What can increase the transfer factor(TLCO)?

A

Asthma
Pulmonary haemorrhage (Wegener’s, Goodpasture’s)
Left-to-right cardiac shunts
Polycythaemia
Hyperkinetic states
Male gender, exercise

135
Q

What can lower the transfer factor (TLCO)?

A

Pulmonary fibrosis
Pneumonia
Pulmonary emboli
Pulmonary oedema
Emphysema
Anaemia
Low cardiac output

136
Q

What are features of hypersensitivity pneumonitis?

A

Acute - SOB, dry cough, fever

Chronic - lethargy, productive cough, SOB

Diffuse crackles, wheeze, squeaks

137
Q

Which lung diseases show predominantly as upper lung fibrosis?

A

CHARTS

Coal workers pneumoconiosis
Hypersensitivity pneumonitis
Ankylosing spondylitis
Radiotherapy
Tuberculosis
Silicosis and sarcoidosis

138
Q

What are extra-pulmonary causes of a restrictive lung breathing pattern?

A

Neuromuscular - muscular dystrophies, guillain-barre, myasthenia gravis

Musculoskeletal - kyphoscoliosis, obesity, anky spon

139
Q

What does hypersensitivity pneumonitis show on x-ray and CT?

A

X-ray = reticular shadowings, micronodular changes

CT = ground glass, mosaicism

Apical dominance

140
Q

What drugs are given in idiopathic pulmonary fibrosis?

A

Anti-fibrotic drugs - when FVC 50-80%
- Pirfenidone - S/E: nausea, photosensitivity rash
- Nintedanib - S/E: diarrhoea

141
Q

What is the histological features of asbestosis?

A

Asbestosis bodies and fibrosis

142
Q

What is the histological features of hypersensitivity pneumonitis?

A

Non-caseating granuloma
Honeycomb - alveolar space

143
Q

What is the histological features of idiopathic pulmonary fibrosis?

A

Collagen deposition and fibrosis in the alveolar interstitium

144
Q

What are features of malignant mesothelioma?

A

Dyspnoea, weight loss, chest wall pain
Clubbing
Pleural effusion - 30% present as painless pleural effusions
Asbestosis - 20%

145
Q

Is mesothelioma or asbestosis linked to length of exposure of asbestos ?

A

Asbestosis severity related to length of exposure

Mesothelioma - even limited exposure can cause disease

146
Q

What are types of coal worker’s pneumoconiosis ?

A

Simple - typically asymptomatic

Progressive massive fibrosis
- Features: Breathlessness, Cough, Black sputum
- X-ray: fibrotic masses in upper lobes

147
Q

What is caplan syndrome?

A

Combination of RA and pneumoconiosis with nodules

148
Q

What is the pathophysiology of coal workers pneumoconiosis?

A

Coal dust reaches terminal bronchioles - engulfed by alveolar macrophages - overwhelmed, unable to clear the coal - macrophages accumulate and settle on alveoli lining - aggregates into fibrotic masses - can cavitate and necrose

149
Q

Which interstitial lung disease increases your risk for TB?

A

Silicosis

Silica impairs the formation of phagolysosome and so more susceptible to tuberculosis

150
Q

What does silicosis look like on an x-ray?

A

Upper zone fibrotic opacities
Egg shell calcification of hilar lymph nodes

151
Q

What is Lofgren syndrome characterised by?

A

Acute sarcoidosis
- Fever
- Hilar lymphadenopathy
- Erythema nodosum
- Polyarthralgia

152
Q

What are the 1-4 stages of sarcoidosis via x-ray?

A

Stage 1 - Bilateral hilar lymphadenopathy (BHL)
Stage 2 - BHL with interstitial infiltrates
Stage 3 - Diffuse interstitial infiltrates only
Stage 4 - Diffuse fibrosis

153
Q

What findings would you see in investigations for sarcoidosis?

A

Hypercalcaemia
Increased ACE levels
High ESR
Non-caseating granuloma - biopsy

154
Q

What features would you see in sarcoidosis?

A

Pulmonary - dry cough, SOB
Skin - lupus pernio, erythema nodosum
Eyes - uveitis
Abdominal - hepatosplenomegaly, renal stones
Constitutional - fever, weight loss, arthralgia, fever, lymphadenopathy
Neurological - meningitis, peripheral neuropathy, bell’s palsy, seizures
Heart - arrhythmias

155
Q

When do you use steroids to treat sarcoidosis?

A

Hypercalcaemia
Eye, heart or neuro involvement
Evidence of fibrosis on x-ray - stage 2+

156
Q

What is the 4 criteria for diagnosis of ARDS?

A
  1. Acute presentation
  2. Chest x-ray/CT - white out in both lungs
  3. PF ratio <300mmHg
  4. NOT due to cardiac causes
157
Q

Why are tall, slender men at an increased risk of a pneumothorax?

A

More negative pressure at the apex of the lung compared to the base

More likely to have pleural blebs (these burst and let air in)

158
Q

How does a tension pneumothorax occur?

A

A one-way valve is created in which air can enter the pleural cavity but is unable to leave - progressive accumulation of air in the pleural cavity - mediastinal shift and compromise of cardiovascular system

Tracheal deviation
Low blood pressure
High heart rate

159
Q

What is the management of a primary pneumothorax?

A

<2cm + clinically well = send home, review in 2-4 weeks + safety net - resolves without intervention

> 2 cm or unwell = aspirate - safe triangle, measure success - if still not better = needs chest drain

160
Q

What is the management of a secondary pneumothorax?

A

<1cm and symptomless - admitted for observation for 24 hours + oxygen PRN

1-2cm - aspiration 16-18 gauge cannula

> 2cm intercostal chest drain

161
Q

What is the management of a tension pneumothorax and where should it be inserted?

A

Immediate needle decompression using 16 gauge cannula

Second intercostal space - just above third rib, mid-clavicular line

162
Q

Lifestyle advice following a pneumothorax?

A

Smoking cessation

No flying for a week after a clear x-ray

Can never scuba dive

163
Q

Where should a chest drain be inserted?

A

5th intercostal space

Safe triangle:
Anterior - lat border of pec major
Inferior - line of 5th ICS - along nipple line
Lateral - anterior edge of lat dorsi
Superior - base of axilla

164
Q

What is found on examination on a chest with a pneumothorax?

A

Reduced chest expansion of affected side.

Hyper-resonant percussion note on affected side.

Reduced or absent breath sounds on affected side, with no added sounds.

Vocal resonance reduced on the affected side

165
Q

What are exudative causes of a pleural effusion?

A

Inflammation of pulmonary capillaries - increase capillary permeability

Infections - pneumonia, TB
Malignancy - bronchial carcinoma, mesothelioma, or lung metastases.
Inflammatory conditions - RA, SLE, acute pancreatitis.
Pulmonary infarct (for example secondary to a pulmonary embolism) and trauma.

166
Q

What are transudative causes of pleural effusion?

A

Increase hydrostatic pressure, decrease oncotic pressure

Heart failure
Liver cirrhosis
CKD
Coeliac disease
Hypothyroidism
Meigs syndrome

167
Q

What is the difference between exudative and transudative pleural effusions?

A

Exudative - typically unilateral, high protein content >30g/L - cloudy liquid

Transudative - typically bilateral - low protein content <30g/L - clear liquid

168
Q

What is Light’s criteria for exudative pleural effusion

A

Pleural protein/Serum protein > 0.5

Pleural lactate dehydrogenase (LDH)/serum LDH >0.6

Pleural LDH > than two-thirds of upper limit of normal for serum

169
Q

What is meigs syndrome?

A

Triad of…
1. Benign ovarian tumour
2. Ascites
3. Pleural effusion - transudate

170
Q

What is found on examination of the chest in a pleural effusion?

A

Trachea central or deviated away from affected side

Stony dullness when percuss over effusion

Reduced chest expansion

Vocal resonance reduced over effusion

Reduced or Absent breath sounds

Bronchial breathing at upper border of pleural effusion

171
Q

What is the criteria for an empyema?

A

Pleural liquid - pH < 7.2

172
Q

What other substances can be seen in the pleural fluid findings?

A

Low glucose - RA, TB
Raised amylase - pancreatitis, oesophageal perforation
Blood staining - mesothelioma, PE, TB

173
Q

How is a pleural effusion treated?

A

Ultrasound-guided pleural aspiration
Intercostal drain - if large effusion or empyema
Treating underlying factor

Pleurodesis if recurrent

174
Q

What is a chylothorax?

A

When the thoracic duct is obstructed by tumours or surgery and lymphatic fluid accumulates in the pleural space = lymphatic pleural effusion

175
Q

What is the difference between atelectasis and pleural effusion on an x-ray?

A

Similar - white out

Different
- Pleural effusion - Mediastinum shifted to opposite side
- Atelectasis - Mediastinum pulled to same side

176
Q

What are causes of atelectasis?

A

Obstruction - mucus plugs, tumours, foreign objects

Lack of surfactant - neonatal respiratory distress syndrome, ARDS

Compressive - Pleural effusion, pneumothorax

Contraction - scarring - sarcoidosis, ILD

Anaesthesia
Respiratory depression

177
Q

What are common contra-indications for surgery in lung cancer?

A

Tumour near the hilum
Vocal cord paralysis
SVC obstruction
Stage IIIb + (mets present)
FEV <1.5 litres
Malignant pleural effusion
Poor general health

178
Q

In which cancer can cavitary lesions be seen on an x-ray?

A

squamous cell carcinoma

179
Q

What is a specific presentation for bronchoalveolar carcinoma?

A

Lots of mucus production - golden brown colour

180
Q

What are paraneoplastic features of small cell lung cancer?

A

ACTH - increase cortisol - cushings syndrome

SIADH - increases water reabsorption = high BP, hyponatraemia, oedema, concentrated urine

Lambert-Eaton Syndrome - antibodies against voltage gated calcium channels = muscle weakness, double vision, drooping eyelids, difficulty swallowing

181
Q

Which cancer has the worst prognosis where surgery is not normally an option and why?

A

Small cell lung cancer
Very aggressive - frequently metastasized to mediastinal lymph nodes and normally disseminated on presentation

182
Q

Where does small cell lung cancer typically grow and from what cell does it develop from?

A

Develops centrally near a main bronchus

Arise from endocrine cells - Kulchitsky cells

183
Q

What cancer is common in non-smokers?

A

Adenocarcinoma

184
Q

What are some non-respiratory symptoms associated with bronchial carcinoid tumours and how?

A

Serotonin secretion = increase peristalsis - diarrhoea, facial flushing, wheeze

185
Q

What are paraneoplastic syndromes associated with adenocarcinomas?

A

HPOA - clubbing
Gynaecomastia

186
Q

What are paraneoplastic syndromes associated with squamous cell carcinomas?

A

PTHrp - bone resorption - high calcium
HPOA - clubbing

187
Q

Where does lung cancer typically metastasize to?

A

BALLS

Brain
Adrenal glands
Liver
Lung
Skeleton

188
Q

How does horner’s syndrome present and why?

A

Ptosis, meiosis, anhydrosis

Pancoast tumour in apical region - pressing on sympathetic trunk

189
Q

What does mesothelioma express?

A

Calciretinin

190
Q

What can compression of the recurrent laryngeal nerve present as?

A

Hoarseness of voice

191
Q

What can compression of the phrenic nerve present as?

A

Difficulty breathing

192
Q

How does SVC obstruction present?

A

Swollen, flushed face and upper body
Shortness of breath
Swollen veins in chest or neck

193
Q

When do you refer people for the 2WW suspected lung cancer?

A

Have chest x-ray findings that suggest lung cancer
Aged 40 and over with unexplained haemoptysis
SVC obstruction
Neck nodes in smokers
Symptoms suggestive lung cancer

194
Q

Where does squamous cell typically develop and what do they produce?

A

Develops centrally

Produce keratin

195
Q

Where do adenocarcinomas typically develop in the chest?

A

Develop peripherally - of the bronchial or alveoli wall

196
Q

Where is large cell lung cancer more common in the lungs?

A

More common in periphery but found throughout

197
Q

From where does cannonball mets seen in the lung metastasize from?

A

Renal cell carcinoma

198
Q

Who should be referred for an urgent x-ray when suspecting cancer?

A

Persistent unexplained haemoptysis
Chest or shoulder pain
Hoarseness
Cough>3 weeks
SOB
Weight loss

199
Q

What are the 2 features to look at when deciding whether to do surgery in lung cancer?

A
  • Resectability - ability to completely excise the tumour at surgery - disease features
  • Operability - risk of morbidity/mortality - patient features
200
Q

What is Type I Respiratory Failure and how do you treat?

A

Low oxygen with normal or low carbon dioxide
Typically due to V/Q Mismatch

Once optimum medical management reached and still symptomatic - NIV - CPAP

201
Q

What is Type II Respiratory Failure and how do you treat?

A

Low oxygen with high carbon dioxide
Can be acute or chronic - distinguish on ABG by metabolic compensation

Once optimum medical management reached and still symptomatic - NIV -BiPAP

202
Q

Symptoms of hypoxia?

A

Dyspnoea
Restlessness and agitation
Confusion
Cyanosis

203
Q

Symptoms and signs of hypercapnia?

A

Headaches
Drowsiness
Confusion
Tachycardia with bounding pulse
CO2 retention hand flap
Peripheral vasodilation
Papilloedema

204
Q

Risk factors for obstructive sleep apnoea?

A
  • More common with increasing age
  • Obesity
  • Male
  • Maxillomandibular anomalies - micrognathia, retrognathia
  • Macroglossia
  • Large neck circumference
  • Family history of OSA
  • Tobacco smoking
  • Hypothyroidism
  • Down’s syndrome
  • Marfans
  • Post-menopausal women
  • Increased volume of soft tissues
205
Q

When does REM and non-REM sleep occur whilst we sleep and what is the differences between the two?

A

Non-REM Sleep - first half of sleep
- N1 - light sleep
- N2 - slightly deeper slee
- N3 - deep sleep - to make ourselves feel refreshed
- Breathing is normal, muscles has tone

REM(rapid eye movement) sleep - 2nd half of sleep
- After 3/4am
- Dreaming
- Muscles are atonic except diaphragm, erratic breathing

206
Q

What is the pathology for obstructive sleep apnoea?

A

Recurrent episodes of partial or complete upper airway obstruction during sleep, leading to intermittent hypoxia and arousals from sleep

  • On inspiration upper-airway pressure becomes negative, but airway patency is maintained by upper-airway muscle tone. During deep sleep, these muscles relax causing narrowing of the upper airways as the norm. If the airway is already narrowed, the airway collapses and OSA results.
207
Q

Features of obstructive sleep apnoea?

A
  • Snoring
  • Witnessed apnoea
  • Excessive day time sleepiness
  • Restless sleep
  • Insomnia
  • Nocturia - increased frequency to pass urine at night > 4 times
  • Unrefreshed sleep
  • Morning headaches
  • Dry throat
  • Mood swings
  • Loss of libido
  • Difficulty concentrating
208
Q

What is the score of Epsworth Sleepiness Scale that is pathological for OSA and what are the negatives of this scale?

A

> 11/24 = pathological

Shows excessive sleepiness but not the score
Limitations - not telling the truth, exaggerations

209
Q

What is the definition of apnoea?

A

Cessation of breathing for 10 seconds or more for 15+ episodes - usually scored with >4% desaturation SpO2 - diagnostic

210
Q

What is the definition of hypopnea?

A

Reduction in the airflow (nasal flow) by 50% or more. May not cause O2 desaturations

211
Q

What is the difference between OSA Syndrome and OSA?

A

OSA syndrome = abnormal sleep study and excessive day time sleepiness

OSA = abnormal sleep study and no excessive day time sleepiness

212
Q

What is the criteria for categorising OSA?

A

Desaturation Index > 4%

Apnoea Hyponoea Index /hour
- Normal: <5
- Mild OSA: 5-15
- Moderate OSA: 15-30
- Severe OSA: >30

213
Q

What are driving regulations in OSA?

A
  • Declare to DVLA of diagnosis or receiving treatment
  • CPAP compliance > 4 hours a night
  • HGV/Bus/Taxi drivers - declare to employer
214
Q

What is the management of mild-moderate OSA?

A

Lifestyle modifications
Weight reduction
Sleep hygiene
- Reduction of caffeine
- 8 hours a night
- Avoiding alcohol
Positional training
Mandibular advancement device
- Gum shield device to create more room at the back of the throat to breathe
- Fitted by dental practitioner

215
Q

What is the management of moderate-severe OSA?

A

CPAP
- Blows continuous air into lungs to keep them expanded
- Minimum 4 hours a night

216
Q

Features of Obesity Hypoventilation Syndrome?

A
  • Morbid Obesity: BMI > 35kg/m2
  • Mean SpO2 < 90% in sleep study, hyperventilate at night
  • Time spent < 90% SpO2 in sleep study
  • Daytime CO2 retention and/or elevated HCO3 > 27mmol/L
  • TX: Weight loss, Non-invasive ventilation
217
Q

What is the gold standard investigation for OSA?

A

Polysomnography

218
Q

Possible complications from OSA?

A

Accidents related to excessive daytime sleepiness
Systemic hypertension, MI, CVD, stroke
Psychological consequences - depression, stress
Pulmonary arterial hypertension
Impaired glucose metabolism - diabetes
Associated with increase in all cause mortality

219
Q

Associated symptoms with chest pain and differentials?

A
  • Autonomic disturbance - sweating, nausea, vomiting - aortic dissection, PE, MI
  • Breathlessness, cough, wheeze - respiratory causes
  • Prodromal viral illness - myocarditis or pericarditis
  • Throat tightness, perioral tingling, emotional distress - anxiety
220
Q

Different onset types of chest pain with differentials?

A
  • During exertion - angina, musculoskeletal or psychological in origin
  • Sudden - aortic dissection, PE, pneumothorax
  • Several minutes - MI
  • Worse after eating and in supine position, regurgitation, dysphagia - GERD
221
Q

Characteristics of chest pain with differentials?

A
  • Sharp - catching chest pain aggravated by deep breathing - respiratory pathology
  • Sharp catching pain during inspiration, coughing, lying flat - myocarditis, pericarditis
  • Dull, constricting, choking, squeezing, crushing, burning, aching - MI
  • During exertion and relieved by rest, exacerbated by cold weather, emotion - angina, asthma
222
Q

What are risk factors for pulmonary hypertension?

A
  • Systemic sclerosis + other connective disease
  • Heart failure
  • Lung disease - COPD, ILD
  • Drugs - amphetamines, leflunomide, fenfluramine, SJW
  • History of clots
  • Group 1 - Family history - mutation in BMPR2 - member of TGF-Beta superfamily
  • Schistosomiasis
  • Female for group 1
223
Q

What are the 5 different classifications of pulmonary hypertension?

A
  1. Pulmonary arterial hypertension - drugs, HIV, geneS, CTD
  2. PH due to left heart disease
  3. PH due to lung disease
  4. CTEPH - recurrent clots increasing pressure
  5. Unclear and multifactoral mechanisms
224
Q

What is the criteria for pulmonary arterial hypertension diagnosis and what is the gold standard diagnostic investigation?

A

> 25mmHg at rest or
30mmHg on exercise

Right heart catheterisation (only when high suspicion for diagnosis and all other tests done to rule out differentials)

225
Q

What is the main complication of pulmonary hypertension?

A

Cor Pulmonale
- Peripheral oedema
- Ascites
- Elevated JVP
- Cyanosis
- Hepatomegaly
- Parasternal heave - right ventricular enlargement

Arrhythmias - AF or atrial flutter
Haemoptysis
Compression of recurrent laryngeal nerve - hoarseness

226
Q

What is an heritable gene mutation in Pulmonary Arterial Hypertension

A

Mutation in BMPR2 gene = excessive proliferation of smooth muscle cells in blood vessels = narrowing vessel = hypertension

227
Q

What are investigations done in pulmonary hypertension - not diagnostic?

A

Chest x-ray - enlarged pulmonary arteries
Echo - enlarged right ventricle, increased arterial pressure
Spirometry - underlying causative lung disease
V/Q Perfusion Scan - rule out chronic thrombus
Antibody screen - rule out autoimmune diseases

228
Q

What are signs of pulmonary hypertension on an ECG?

A

Right ventricular hypertrophy
- right axis deviation
- T inversion in anterior leads
- persistent s wave
- RBBB

229
Q

What is the functional classification in pulmonary hypertension?

A

Class I - comfortable at rest and exertion
Class II - comfortable at rest, slight limitation of activity on exertion
Class III - comfortable at rest, marked limitation of physical activity even on mild exertion
Class IV - symptoms at rest and severe on exertion

230
Q

What is the pathophysiology behind pulmonary arterial hypertension

A

Disruption in major signalling pathways = increases pulmonary vascular resistance
1. Nitric oxide and prostacyclin pathway disrupted = impaired vasodilation
2. Disrupted endothelin pathway = increased vasoconstriction

231
Q

What are supportive therapies in pulmonary hypertension?

A
  • Diuretic therapy
  • Anticoagulants - increased risk clots
  • Long term oxygen therapy
  • Vaccinations

YEAR 2 (8 decks)

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