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Medicine > Respiratory > Flashcards

Respiratory Flashcards

1
Q

all pts are advised not to fly up to __ ___ after successful treatment of a pneumothorax

A

2 weeks

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2
Q

Signs/Symptoms of Haemothorax (<1500ml blood loss, blood can come from chest wall or lung tissue)

A
  • respiratory distress
  • shock
  • decreased breath sounds
  • SOB, pleuritic chest pain
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3
Q

Signs/Symptoms of a tension pnemothorax

A
  • as for px: reduced breath sounds, pleuritic chest pain, breathlessness
  • mediastinal shift impedes venous return –> shock (hypotension)
  • tracheal deviation
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4
Q

What is flail chest and when does it happen? What is paradoxical motion?

A
  • a section of the chest wall that is moving independently to the rest of the thoracic cage
  • occurs when multiple adjacent ribs are broken in multiple sites
  • paradoxical motion when a section of chest moves in a opposite direction to most of chest on breathing
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5
Q

2 symptoms of flail chest? What is often underlying a flail chest along with multiple fractures? Mainstay of rx?

A
  • chest pain + SOB
  • pulmonary contusion
  • positive pressure ventilation
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6
Q

Cardiac tamponade signs/symptoms, dx made how, blood released how?

A
  • as blood fills pericardium –> haemodynamic shock
  • loss of consciousness
  • bedside echo
  • surgery to stop bleeding
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7
Q

A massive haemothorax is defined as

(likely to need thoracic surgery)

A

> 1500ml blood drainage

-continuous bleeding at 200ml/hr for at least 4hrs

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8
Q

What are the 3 most common types of lung cancer?

A
  • adenocarcinoma (present peripherally in lung)
  • squamous carcinoma (present centrally, more haemoptysis)
  • small cell cancer (more centrally)
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9
Q

diagnostic tests for lung cancer? from presentation to staging

A
  • CXR initial ix
  • CT guided biopsy, bronchoscopy, aspiration lymph node
  • PET scan to stage
  • lung function
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10
Q

EGFR mutations (common in non-smoker lung cancer -10%), lead to which class of medications being useful to treat? an example is osimertinib

A

-Tyrosine kinase inhibitors

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11
Q

PDL1 positive status translates to what in lung cancer? What medication is used to block this? This type of med is referred to as what?

A
  • PDL1 expression tricks immune system that cancer cells are friendly
  • Mab e.g. pembrolizumab blocks this so immune system can recognise the cancer cells and NK cells can kill the cancer, these are an example of “checkpoint inhibitors”
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12
Q

for lung cancer pts with no specific targetable mutation, what type of chemo is administered?

A

-doublet platinum based chemo

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13
Q

Normal mean pulmonary artery pressure (PAP) at rest is 10-14mmHg. Pulmonary hypertension is > at rest or > at exercise. It is often secondary to _ __ failure

A

> 25mmHg rest
30mmHg exercise
-right ventricular failure

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14
Q

What causes pulmonary hypertension? (one sentence hypothesis aetiology)

A

-increase in pulmonary vascular resistance or increase in pulmonary blood flow

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15
Q

Give 5 clinical fts of pulmonary hypertension:

A
  • exertional SOB
  • lethargy/fatigue (inability to increase CO on excercise)
  • peripheral oedema
  • abdo pain from hepatic congestion
  • loud pulmonary second sound on examination
  • right parasternal heave (from RV hypertrophy)
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16
Q

Name 3 signs of Right Heart Failure (cor pulmonale)

A
  • elevated JVP with a prominent V wave if tricuspid regurg present
  • hepatomegaly
  • a pulsatile liver
  • peripheral oedema
  • ascites
  • pleural effusion
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17
Q

Name 5 causes of pulmonary ARTERIAL hypertension (WHO grade I)

A
  • idiopathic esp. in young women
  • autoimmune rheumatic disease e.g. systemic sclerosis, RA, lupus
  • congenital HD e.g. ASD, VSD
  • portal hypertension
  • Drugs: cocaine, amphetamine long term
  • HIV
  • Schistosomiasis
  • Chronic haemolytic anaemia
  • Pulmonary veno-occlusive disease
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18
Q

Pulmonary hypertension can be secondary to many conditions. WHO class splits these into grades, give eg.s

2) sec to left HF e.g. ____
3) related to lung disease e.g ___
4) related to PE
5) sec to m___, gl____, chronic ___ failure

A

2) valvular, systolic dysfunction, diastolic dysfunction
3) COPD, OSA, pulmonary fibrosis
4) VTE occlusion of pulmonary vasculature
5) myeleoprolif. disoders, glycogen storage disease, chronic renal failure…

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19
Q

Suggest investigations and their findings of pulmonary hypertension? NB: any may also show cause e.g calcified mitral valve, emphysema, intracardiac shunt..

A
  • chest XR: enlarged pulmonary arteries which taper distally
  • ECG: RV hypertrophy, P pulmonale-peaked, R axis
  • Echo: RV dilatation &/or hypertrophy, peak PAP w doppler
  • Right heart catheterisation can confirm elevated PAP, determine PWP, CO and assess for Pulmonary vascular resistance, can establish if any Left heart disease.
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20
Q

Pulmonary hypertension CXR finding of: enlarged pulmonary arteries that stay in the middle. so how does the periphery appear?

A

-‘pruning’ of the blood vessels, they stay in the middle enlarged, and the periphery is generally free of blood vessels (darker lung fields)

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21
Q

early pulmonary hypertension management

A
  • O2
  • warfarin
  • diuretics for oedema
  • CCBs as pulmonary vasodilators
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22
Q

When the RV tries to pump blood into the pulmonary outflow tract, is has to overcome the pressure of the pulmonary artery, in PHT, the ___ valve may not close fully –> __ __, so you get a __ __ jet, on echo you can measure its ___, this relates to the pressure in the RA.

A
  • tricuspid valve
  • TR
  • TRegurg. jet
  • velocity (w Doppler)
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23
Q

Pts with pulmonary hypertension are tested with _____ test e.g. give ___/___ see if Mean PAP drops by __, to less than 40mmHg. If positive pts can improve with __, but most are not so require advanced medications, such as__?

A
  • vasoreactivity test
  • NO/adenosine
  • > 10mmHg
  • if +, improve with CCBs
  • oral endothelin receptor antagonists, prostanoid analogues, epoprostenol, sildenafil, tedalafil
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24
Q

Give an eg of the following meds for pulmonary HT:

  • endothelin receptor antagonists
  • prostanoid analogues,
A
  • endothelin-R ant: bosentan, sitaxentan oral

- prostanoid: iloprost, treprostinil, beraprost inhaled

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25
Q

IV epoprostenol is a what agonist? These increase ___ leading to vaso___

A
  • prostacyclin agonist

- increase cAMP –> vasodilation

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26
Q

-endothelin-R ant: bosentan, sitaxentan oral are used to treat pulmonary HT, they block __ which is a potent ___

A

-blocks Endothelin 1 -receptor
-potent vasoconstrictor
(increases exercise tolerance and Q of L)

27
Q

sildenafil is a ___ inhibitor, action is

A

-PDE5 inhibitor
-c.GMP is broken down by phosphodiesterase, the sildenafil blocks this breakdown, so it builds up and stimulates an increase in the vasodilator NO
(don’t prescribe with other vasodilators like alpha blockers as risk of hypotensive falls etc)

28
Q

in primary pulmonary HT there is progressive downhill course…most pts ultimately need __ and __ ___

A

-heart and lung transplantation

29
Q

OSA is collapse of the ____ airway, apnoeic episodes are describes as

A
  • pharyngeal airway

- stopping breathing during sleep (can last few minutes) often noticed by partner

30
Q

RFs for OSA

A

-middle aged, male, obese, smoking, alcohol

31
Q

OSA may present with:

A
  • morning headache
  • daytime sleepiness
  • concenation problems
  • snoring
  • reduced O2 sats in the night
32
Q

If suspecting a dx of OSA, the key symptom to ask about is ___ ____ and you must ask what their ____ is because…

A
  • daytime sleepiness
  • their occupation (may need to be fully alert at work, if dangerous, will require an urgent referral +/- amended work duties)
33
Q

Severe cases of OSA/complications include:

A
  • hypertension
  • heart failure
  • MI
  • Stroke
34
Q

Management of OSA:

A
  • refer to ENT/sleep clinic
  • sleep studies
  • correct reversible RFs
  • continuous positive airway pressure (CPAP) helps keep airway open and not collapsing
  • surgery: often uvulopalatopharyngoplasty (UPPP)
35
Q

-sulphur dioxide, chorine, ammonia, oxides of nitrogen occupational exposure is linked to acute ___ and pulmonary ___

A

-acute bronchitis and pulmonary odema

36
Q

The most common occupational related lung disease is ___. Other lung-occupational related conditions include: hypersensitivity ____ and bronchial ____ due to ___, polycyclic hydrocarbons and ____ in mines.

A
  • occupational asthma
  • hypersensitivity pneumonitis
  • bronchial carcinoma due to asbestos… and radon in mines
37
Q

Coal workers pneumoconiosis, occurs as small coal particles escape the normal clearance mechanisms to reach the acinus and initiate an ____ ___ and subsequent ____. On CXR may see ___. With continued exposure may progress to __ ___ __ (PMF) characterised by large ___ ___ , mostly in the ____ lobes. Symptoms:

A
  • inflammatory reaction, subsequent fibrosis
  • CXR: small pulmonary nodules
  • PMF=progressive massive fibrosis, large fibrotic masses up to 10cm, mostly in upper lobes
  • symptoms: SOB, cough w black sputum –> resp failure
38
Q

Coal workers pneumoconiosis treatment:

A
  • no specific rx available
  • must limit further exposure
  • PMF pts may be eligible for disability benefit in UK
39
Q

The pathophys of Coal workers pneumoconiosis aka (______ ) is the same of asbestosis, aluminosis, silicosis/Potter’s rot/grinder’s disease, bauxite fibrosis, siderosis (caused by iron), berylliosis, byssinosis (cotton fibres), stannosis (tin oxide)

A

-miner’s lung, black lung, anthracosis

40
Q

Contact with dust particles are the occupational RFs for lung disease name 3 at risk occupations:

A
  • plumbing, roofing, building
  • coal mining
  • textile workers
  • risk higher with higher concentrations, lack of PPE (respirators), and longer exposure over yrs
41
Q

Asbestos lung-related disease have a ___latency period from exposure to disease, diagnose with __ and typical ___ appearances.

A
  • 20-40yrs+
  • history of exposure
  • chest XR
42
Q

Asbestos lung-related disease includes many pathologies name 2 non-malignant and their symptoms:

A
  • pleural plaques: fibrotic, on parietal and diaphragmatic pleura, asymptomatic
  • pleural effusion: pleural biopsy to differentiate from malignant effusion, pleuritic pain and SOB
  • diffuse pleural thickening: of parietal and visceral pleura, SOBOE and restrictive ventilatory defect
43
Q

Mesothelioma arises from mesothelial cells of p__, p____ and p____, often presents with dull, diffuse progressive __ __ and a ___ ___, rx with __ or __ procedures, prognosis is ___

A
  • pleura, pericardium, peritoneum
  • chest pain and pleural effusion
  • chemo or debulking
  • poor prognosis
44
Q

Asbestosis presents with -

and pulmonary function tests show:

A
  • SOB, finger clubbing, bilat inspiratory crackles

- restrictive ventilatory defect

45
Q 
Sarcoidosis presentation 
(NB: >50% cases are incidental findings on CXR)
A
  • bilat hilar lymphadenopathy
  • pulmonary infiltrations
  • skin or eye lesions
46
Q

Sarcoidosis epidemiology to note:

A
  • more common in females
  • more common in northern Europe
  • disease course more severe in black ethnicities
47
Q

Typical non-caesating sarcoid granuloma consists of a focal accumulation of ___ cells, __ and lymphocytes-mainly __ cells, what does this lead to as a result of the sequestration in lung?

A
  • epitheliod cells, MO, -T cells

- overall lymphopenia with low circulating T cells (slightly increased B cells)

48
Q

What will transbronchial biopsies show in sarcoidosis before granuloma formation?

A

-infiltration of alveolar walls and interstitial spaces with mononuclear cells

49
Q

Sarcoidosis lung disease symptoms include:
Some pts have pulmonary infiltration -> progressive fibrosis w symptoms of:
Chest exam=normal or __ ___ esp anteriorly

A
  • non-productive cough, SOB, +/- wheeze
  • worsening SOB, cor pulmonale, death
  • fine crackles

NB: fatigue is main big problem for pts

50
Q

Extra-pulmonary fts of sarcoidosis, give e.g of each: derm, eye, MSK, metabolic, liver, neuro and cardiac:

A

derm: erythema nodosum-tender, waxy macpap lesions, lupus pernio (red/blue nose), granuloma in scar tissue
eye: ant/post uveitis, conjunctival nodules, lacrimal gland enlargement, parotid enlargement, facial nerve palsy
MSK: arthralgia, arthrits, myopathy bone cysts
metabolic: hypercalcaemia can –> kidney stones and nephrocalcinosis (sarcoid MOs produce vit D)
liver: granulomatous hepatitis, hepatospenomegaly, cholestasis, cirrhosis
neuro: meningeal inflamm, seizures, mass lesions, pituitary infiltration -> diabetes insipidus
cardiac: vent. arrhythmias, conduction defects, HF

51
Q

Lofgren’s syndrome triad of sarcoidosis

A
  • erythema nodosum
  • bilat hilar lymphadenopathy
  • polyarthalgia
52
Q

give 3 ddx of sarcoidosis:

A
  • TB
  • lymphoma
  • hypersensitvity pneumonitis
  • HIV
  • toxoplasmosis, histoplasmosis
53
Q

Sarcoid investigations on blood test, name 3:

A
  • serum ACE - raised in 75% cases
  • serum Ca2+ may be high
  • soluble IL-2 receptors may be high
  • CRP may be high
54
Q

Sarcoid investigations on imaging:

A
  • chest XR: for staging
  • high res CT for assessing pulmonary involvement and identifies abnormal nodes for biopsy
  • MRI for CNS involvement
  • PET scan for active areas of inflammation
55
Q

Gold standard for sarcoid diagnosis? Finding?

A
  • histology from biopsy e.g. of mediastinal nodes with US-guided bronchoscopy, biopsy of skin lesions
  • non caseating granulomas with epitheliod cells on histology
56
Q

In sarcoidosis with pulmonary infiltration, what will pulmonary function tests show?

A

-restrictive lung defect with a decrease in total lung capacity, FEV1, FVC and gas transfer

57
Q 
Sarcoidosis treatment:
-
-
-
-
A
  • none if no/mild sx as may self-resolve in 2yrs for majority
  • oral steroids (30mg prednis 6weeks then 15mg alternate daily) for 6-12months therefore also give bisphosphonates for bone protection
  • steroid sparing immunosuppressants: methotrexate, azathioprine, cyclophosphamide for long term
  • lung transplant
58
Q

Exam findings of lung examination on side with a pleural effusion (3)

A
  • reduced chest wall movement
  • stony dull to percussion
  • absent breath sounds
  • decreased vocal resonance
  • mediastinum shifted away
59
Q

What are chylous effusions of lung caused by and how to differentiate?

A
  • leakage of lymph from the thoracic duct as result of trauma or infiltration by a carcinoma
  • chylothorax is milky and high in TGs lower in cholesterol
  • pseudoschylothorax is milky and lower in TGs, higher in cholesterol +/- crystals as is a chronic phenomenon
60
Q

How are large pleural effusions causing breathlessness initially managed? What do you send fluid for?

A

Large volume thoracocentisis (1L)

  • for diagnostic and therapeutic purposes
  • protein, LDH, glucose, pH (<7.3 - infection)
  • cytology (WCC, malignant cells)
  • microbiology (gram stain, culture, AFB)
61
Q

What initial plural fluid measurement can distinguish exudate from transudate?

A

Protein

  • > 30g/L = exudate
  • <30g/L = transudate
62
Q

If pleural protein is ~25-30g/L what are the criteria to establish type?
There are 3 points and if any 1 is present that is satisfactory.

A

Exudate in following:

  • Pleural fluid protein : s protein > 0.5
  • pleural fluid LDH : s LDH >0.6
  • Pleural LDH > 2/3rd upper limit normal
63
Q

Name 3 common exudate causes and 3 transudate

A

Exudate: infection (TB, empyema, parapneumonic), malignancy, PE, CT disease, chylothorax, methotrexate, amiodarone

Transudate: HF, low albumin (nephrotic s,, cirrhosis), constrictive pericarditis, hypothyroidism, ovarian fibroma (meig’s s)

64
Q

What lab values suggest exudate of following:

  • glucose
  • specific gravity
  • cholesterol
  • protein
  • pH
A
  • glucose <60
  • specific gravity >1.016
  • cholesterol >60
  • protein >30
  • pH <7.3

Medicine (10 decks)

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