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MK > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Gas exchange in COPD. What happens?

A

PaO2 is near normal until FEV1 is decreased to 50% of predicted
Elevation of PaCO2 is not expected until FEV1 is

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2
Q

What is shunting? Causes?

A

VQ ratio is 0
Alveoli are perfused with blood as normal but ventilation fails to supply the perfused region.

Causes:
Alveoli filled with fluid - Pulmonary oedema
Pneumonia

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3
Q

Which drug improves survival in PAH?

A

Prostacyclin (Bosentan) - reduced pulmonary vascular resistance (wood units)

Inhaled Bosentan provides relief but does not improve survival

May be combined with Sildenafil
Amlodipine can be used

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4
Q

PAH is defined as?

A

PAP > 25 mmHg

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5
Q

What is the Tx of a primary spontaneous pneumothorax?

A

If 3 cm, thoracentesis and catheter in place with a closed stop lock for 6 hrs.
Re-CXR, if resolved then discharge home.

Chest tube placement recommended if thoracentesis in unsuccessful (persistent air aspiration after 4 L removed) suggesting a bronchpleural communication leak

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6
Q

Hypersensitivity pneumonitis. Presentation, Ix?

A

Dyspnoea, cough, wheezing, crackles
Febilre episodes, fatigue and weight loss
Symptoms appear or worsen after antigen exposure

Ix:
CT chest- ground glass opacities, reticular,nodular
BAL - lymphocytosis > 20% consistent with Dx
CD4:CD8 ratio

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7
Q

What is the most common cause of a variable extrathoracic obstruction (impaired inspiratory loop)?

A

Vocal cord dysfunction is amongst the most common cause

Others:
Adenoid hyperplasia
Tracheomalacia

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8
Q

Complication of IVIG?

A

IVIG associated haemolytic anaemia

  • +ve DAT
  • reduced serum haptoglobin
  • elevated reitculocytes
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9
Q

Treatment for asthma?

A
  1. Reliever PRN
  2. Inhaled glucocorticoid and PRN reliever
  3. ICS + LABA (LD) combined + Reliever PRN
  4. ICS + LABA (HD) + PRN releiver
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10
Q

Hepatopulmonary syndrome. Triad?

Mx?

A 
Triad:
Liver disease (usually portal HTN)
Hypoxaemia
- PaO2  15mmHg (or > 20 mmHg if age>65)
Intrapulmonary vascular dilatations (contrast echo)

Mx:
Supportive
Transplant referral

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11
Q

Platypnea and Orthodeoxia are highly suggestive of Hepatopulmonary syndrome. What are they?

A

Platypnea

  • increase in dyspnoea worse in the upright position and relieved by recumbancy.
  • Improved by moving back to supine postion.

Orthodeoxia
- fall in arterial Oxygen tension (fall in sats >5% or PaO2 > 4 mmHg) when pt moves from supine to upright position

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12
Q

What is the hypoxia in hepatopulmonary syndrome due to?

A

VQ mismatch
diffusion limitation
AV shunting

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13
Q

Well’s criteria. Scores for low, moderate and high probability.

A

Low 6

Clinical signs of DVT = 3
No alternative Dx = 3
HR>100 = 1.5
Immobilisation or Sx in previous 4 weeks = 1.5
Previous DVT = 1.5
Haemoptysis = 1
Malignancy = 1

A score of 4.0 and -ve D-dimer result may safely exclude a PE in a large proportion of patients with a suspected PE.

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14
Q

What is the major toxic effect of a benzo overdose? Mx

A

Respiratory depression

Mx:
Supportive care

Flumazenil is a competitive antagonist at benozodiazepine (GABA-A) receptors in the CNS.
Not much role for Mx of benzo overdose however indicated in the following:
- warranted in elderly or other patients with resp disease (COPD) where intubation should be avoided.
- Tx of CNS depression due to iatrogenic over Tx (e.g. procedural sedation)
- Benzo overdose resulting in compromised airway or breathing when intubation equipment/skills not available

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15
Q

Flumazenil.
MOA
Indication

A

Flumazenil is a competitive antagonist at benozodiazepine (GABA-A) receptors in the CNS.

Not much role for Mx of benzo overdose however indicated in the following:

  • warranted in elderly or other patients with resp disease (COPD) where intubation should be avoided.
  • Tx of CNS depression due to iatrogenic over Tx (e.g. procedural sedation)
  • Benzo overdose resulting in compromised airway or breathing when intubation equipment/skills not available
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16
Q

signs of opiod overdose? Tx

A

Depressed mental state
decreased resp rate and decreases tidal volume
decreased bowel sounds
miotic pupils

Tx:
Naloxone - mu opiod antagonsit
Goal of naloxone is adequate ventilation not normal GCS

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17
Q

RFTs. How is obstruction defined? The

A

Defined on spiro by FEV1/VC ratio

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18
Q

RFTs. How do you define restriction?

A

Defined on static lung volume measurements by TLC

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19
Q

RFTs. How you define a mixed restrictive and obstructive picture?

A

Meets both critera:

Obstructive
Defined on spiro by FEV1/VC ratio

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20
Q

NSCLCa. Staging and corresponding Tx.

A 
Staging:
Stage I:  7 cm or invading structures e.g. RLN, trachea, great vessels
Tx:
Need MDT to decide on Tx
Sx + adjuvant CTx OR
Chemoradiation OR
Palliative Rx

Stage IIIb:
N3 nodes (contrlateral mediastianal or hilar nodes, scalene nodes, or supraclavicular nodes)
Tumor with invasion of structures above + N2 nodes
Tx: Chemoradiation or palliative Rx

Stage IV
distant mets which include
- contrlaterla lung nodules
- PLEURAL noduels
- MALIGNANT PLEURAL OR PERICARDIAL EFFUSION
Tx:
Palliative RTx
However systemic Tx should be offered to all pts with ECOG 0-2
- Platinum doublet CTx e.g. cisplatin/gemcit 4-6 cycles. Prolongs OS and improves QOL.
- evidence that addition of bevacizumab to platinum doublet in non-squamous NSCLC results in improved RR, PFR, OS.

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21
Q

Pt with NSCLC, eGFR mutation with brain mets. Tx?

A

Still EGFR inhibitor, erlotinib.

MRI brain only performed if neurological symptoms. Not part of staging.

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22
Q

Pt with NSCLC and ALK mutation . Tx?

A

Crizotinib. On PBS now.

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23
Q

What does a +ve tuberculin skin test (TST) suggest?

A

TB acquisition (active or latent)
Non tuberculous mycobacterium (NTM)
BCG vaccine (if 1y 10% will have apositive TST)
Boosting (increased induration with each successive test)

False -ve

  • immunocompromised
  • recent aquisition, need to repeat test 8-12 weeks later
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24
Q 
Is IGRA (QF gold and T-spot) more sensitive or specific than TST?
What does a +ve result mean?
A

Equal or greater sensitivity, more specific than TST.
Measures T cell release found in MTB and some NTMs

Positive:
Latent or active Tb

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25
Q

Pt with +ve TST/QF, normal CXR and clinically well. Mx?

A

Tx with latent TB prophylaxis with isoniazid for 6-9 months or
CXR yrly for 2-3 years
Alternative Tx is Rifampacin for 4 months.

If compliant will reduce risk of reactivation by 90%

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26
Q

Pt with +ve TST/QF, CXR with Tb scar, clinically well. Mx?

A

CXR FU or Discharge

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27
Q

LTBI. What is the life time risk of active TB? RF?

A

10%

RF:
Most risky period is 2 years after acquisition
- should have repeat test 8-12 weeks later of 1st test -ve
Immunosuppression, esp T cell suppression

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28
Q

Who should you test for LTBI?

A

Those with recent acquisition
- should have repeat test 8-12 weeks later of 1st test -ve
Household contacts of TB
HCW exposed to active TB

Those at high risk of reactivation

  • any T cell problem: HIV infection, post tranplant immunosuppression, lymphoma, leukemia
  • Renal failure on dialysis
  • Tx with biologics
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29
Q

AE of Isoniazid?

A

Raised LFTs
- if >3 x ULN, stop Tx

Peripheral neuropathy
- take with pyridoxine 25 mg OD

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30
Q

Causes of HAGMA?

Extra anions KIL U

A 
Extra anions KIL U
Ketones - DKA, EtOH, starvation
Ingestion - salicylates, methanol, glycols
Lactate - sepsis, dead gut, metformin
Uraemia
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31
Q

Causes of NAGMA?

A

Loss of HCO3 somewhere
GUT- diarrhoea (neGUTive urine AG)
Kidney e.g. RTA, renal failure (positive urine AG)

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32
Q

ETOH ketoacidosis. What will the ABG profile show?

A

Metabolic acidosis
High AG
NO HYPERGLYCAEMIA - Dx of EtOH ketoacidosis
If BSL raised than likely IGT/DM

33
Q

What will the ABG show in salicylate poisoning?

A

Primary Resp Alkalosis or

Mixed primary resp alkalosis- primary metabolic acidosis with HAG

34
Q

How is OSA Dx on PSG?

A

If Resp disturbance index (consist of apnoeas + hypopneas + reps effort related arousals) >5 with symptoms or complications (T2DM, HTN, AF, CCF)
OR
RDI>15 without symptoms/co-morbidities

35
Q 
Narcolepsy:
Presentation
Demographics
Pathophys
Dx
A

Tetrad of:
irresistable daytime sleepiness
cataplexy - sudden drop of muscle tone triggered by emotion esp laughter or anger
hypnagogoc hallucinations
sleep paralysis
Usually wakes refreshed and have refreshing naps

Demographics:
Usually in teens or early 20s

Patho:
Loss of orexin (= hypocretin) signalling which promotes and stabilises wakefulness

Dx:
PSG
- rule out other Dx. Should be normal.
- 40% wil have Periodic limb movement (PLMS)
- some have apnoea/hypopnea, sleep fragmentation
MSLT
- mean latency

36
Q

Idiopathic Hypersomnia:
Presentation
Dx

A 
Prolonged nocturnal sleep time
Prolonged but unrefreshing naps
Great difficulty awakening from sleep
Rare disease
Severe extensive day time sleepiness (EDS)

Dx:
3 of following:
- Daily period of irrepressible need to sleep or day time lapses into sleep for at leas t 3 months
- Cataplexy is absent
- MSLT - =660 minutes of 24 hr PSG
- Insufficient sleep ruled out
- no better explanation by another sleep disorder etc.

37
Q

What is Chylothorax?
Dx?
FBC abnormality associated with it?

A

Uncommon cause of a pleural effusion.
Caused by disruption or obstruction of thoracic duct or its tributaries that results in leakage of chyle (lymphatic fluid of intestinal origin) into the pleural space.

Dx:
Presence of chylomicrons and TG level > 110 mg/dL in pleural fluid

Lymphocytosis (lymphocyte predominant)

38
Q

How does caffeine affect RFTs?

A

Bronchodilation.
Belongs to a group pf chemical called methylxanthins along with bronchodilator drug theophylline.

Caffeine sig improved lung function measured in terms of FEV1 for up to 2 hours post ingestion.

39
Q

Formula for A-a gradient at sea level.

What is the normal A-a gradient?

A

= (150-1.25 x pCO2) - PaO2

Normal A-a

40
Q

Spiro changes indicative of following:
Gas trapping
Hyperinflation

A

FRC > 120% predited

41
Q

What is the normal sleep architecture in a young adult?

A

Sleep latency
Stage 1 - Light sleep 5%
Stage 2 - Deeper sleep 45%
Stage 3-4 - 25%. Deepest, non-REM sleep. Sleep walking, night terrors, bed wetting (slow wave sleep).
REM 25%
- Dreaming, loss of motor tone, possible a memory processing function, erections, Increase brain O2 use.
- REM sleep is like sex. Increase pulse, penile/clitoral etc. Decreases with age.

Serotonergic predominance of raphe nucleus key to initiating sleep.
Benzos reduce stage 4

42
Q

What changes in sleep architectures occur with aging?

A

Decreased slow wave sleep (stage 3 and 4) - MOST COMMON change
Decreased REM sleep
More frequent arousals
Reduced total sleep time

43
Q

At which lung volume is pulmonary vascular resistance at lowest?

A

FRC

44
Q

In a shunt, what happens to the PaO2 with increased FiO2?

A

PaO2 will not rise

45
Q

When does diffusion impiarement occur?

A

Clinically uncommon.

Tends to occur during exercise only and even the not a major cause for hypoxia.

46
Q

In a PE, what happens to VQ?

A

VQ inequality + hypoxaemia

47
Q

What changes does pregnancy cause on RFTS?

A

Decreased in RVm therefore FRC.

Due to elevation of diaphram.

48
Q

What is the difference between a primary and secondary pneumothorax?

A

primary
- occurs without precipitating factor

Secondary
- underlying lung disease

49
Q

Mx of Pneumothorax.
Age > 50 and significant smoking Hx +
Evidence of underlying lung disease on exam or CXR.
next step?

A

Dx is a secondary pneumothorax
> 2cm or breathless
- chest drain 8-14 fr and admit

1-2 cm
- aspirate with 16-18G cannula
If size

50
Q

Mx of pneumothorax.

Age

A

Dx is a primary pneumothorax
Size> 2cm and or breathless
- aspirate 16-18G cannula
- aspirate

51
Q

Lung nodule > 8mm. Mx?

A

PET or sampling

If malignancy suggested -> surgical excision. If not, observe with serial CTs

52
Q

Mx of lung nodules 4-6 mm

>6-8 mm

A

No lung cancer RF:
4-6 mm
- FU CT at 12 months, if stable no further FU

> 6-8 mm

  • FU CT 6-12 m
  • if stable, FY 18-24 m
53
Q

Mx of lung nodules 4-6 mm

>6-8 mm

A

4-6 mm
- FU CT 6-12 months, if stable FU at 18-24 m

> 6-8 mm
- FU CT 3-6 m, 9-12 m and 24 m

54
Q

CI to NIPPV?

A 
Cardiac or resp arrest
Inability to co-operate, protect the airway
Severely impaired consciousness
Non resp organ failure
Facial Sx, trauma or deformity
High aspiration risk
Prolonged duration of mechanical ventilation anticipated
Recent oesophageal anastomosis
55
Q

What is the best way to monitos the need for NIPPV in a pt with GBS?
Which antibody is associated with RF for resp insufficiency?

A

Serial vital capacity measurements

Anti-GQ1b

56
Q

What are the indicators of mild, moderate and severe asthma?

A

Mild
SpO2 >95%
ABG not needed

Moderate
SpO2 90-95%
pCO2 40 mmHg

If no response within 2 hours of initial therapy with 
- ihnaled B agonist +/- anticholingeric
- systemic steroids
- Mg
and PEF
57
Q

What is the best predictor for a complicated course for a parapneumonic effusion?

A

Acidic pH,

58
Q

In COPD, what carries greatest risk pf death over the next 12 months.

A

BODE index - predictor of long term outcomes and mortality

BMI

59
Q

What is the most common cause of death in pts with mod to severe COPD?

A

Progressive respiratory failure

60
Q

What is the concern of taking azithromycin in reducing exacerbations?

A

Sudden cardiac death

61
Q

Which type of lung cancer is smoking most implicated in?

RR post smoking cessation is greatest for which lung cancer?

A

Small cell lung cancer most common in smokers

Smoking is a RF for all lung cancers.
RR is greatest for Small cell cancer and NSCLC. Less for adenocarcinoma.

62
Q

Sleep disordered breathing is rare in premenopausal women. Which hormone is responsible for this?

A

Progesterone increases ventilation.
Hyperventilation in pregnancy.
Luteal phase has highest ventilation, upper airway resistance at its lowest.

Oestrogen enhances progesterone effects. Increased OSA observed in women after menopause. Oestogen replacement improves OSA.

63
Q

How does testosterone affect the risk of OSA?

A

Excess testosterone decreases VR, increases risk of OSA

However men with OSA have lower testosterone levels, a paradox!

64
Q

What is sleep latency?

A

Time from lights out to sleep onset.

65
Q

What is the major contributor to falls is SpO2 during sleep in pt with COPD?

A

REM sleep related reduction in respiratory drive. Hypoventilation is the major contributor, VQ mismatch minor.

66
Q

What is the point of a maintenance wakefulness test?

A

Useful for assessing effectiveness of therapy, safety to drive.
Pt placed in a quiet darkened room and instructed to stay awake.

67
Q

Obesity Hypoventilation Syndrome (OHS)
Dx
Tx

A
  • Dx
    • daytime hypercapnoea, PCO2 > 45 mmHg, is a cardinal sign of OHS
    • reflects reduced ventilation during wakefulness as well as sleep which is believed to result from a combination of mechanical load imposed by obesity and attenuation of both hypoxic and hypercapnic ventilatory drive
    • high rates of biventricular failure and pulmonary HT
    • OSA co-exist with OHS
  • Tx
    • CPAP
    • weight loss
68
Q 
High Altitude related illness
What
Clinical
Patho
Tx
A

If you ascend to elevations >7500 m (25, 000 feet), High altitude periodic breathing (HAPB) will occur characterised by cyclic central apnoeas and hyperapneas associated with repetitive arousals from sleep and paroxysm of dyspnoea.

Clinical

  • HAPB will occur on the first night of elevation
  • Symptoms do not usually occur below 2500 m

Patho

  • Exaggerated ventilatory response to there reduced ambient partial pressure of inspired O2 (known as hypbaric hypoxia) leading to hypocapnia and ventilatory instability

Tx

  • Prevention by acclimatisation
  • Acetazolamide can be used prophylactically, accelerates acclimatisation process
69
Q

Interstitial Lung Disease.

Classification

A 
Idiopathic interstitial pneumonitis
- Idiopathic pulmonary fibrosis/Usual interstitial pneumonia (UIP) - most common
- Non specific interstitial pneumonia (NSIP) - most common
Drug induced lung disease
Granulomatous lung disease
Other
- pLAM
- histiocytosis X
- Sarcoid
70
Q

Idiopathic pulmonary fibrosis/Usual interstitial pneumonia (UIP).
Features

A
  • no age distribution
  • lower zone and sub pleural dominance
  • maximal posteriorly at the bases, increasingly anterior in the upper lung
  • reticular pattern with associated honey combing in 95%
  • traction bronchiectasis and architectural distortion
71
Q

Non specific interstitial pneumonia (NSIP).

Features

A
  • affects middle age adults 40-50 y
  • bilateral patchy and sub pleural areas of ground glass, lower zone distrinution
  • areas of irregular linear opacity
  • 50% features suggesting fibrosis
    • bronchila dilatatin
    • traction bronchiectasis
  • absence of honey combing
72
Q

Cryptogenic orgnaising pneumonia (COP aka BOOP).

features

A
  • typically 55-60 y
  • non productive cough
  • consolidation, subpleural and lower zones
  • ground glass
  • pulmonary nodules
  • pleural tags and thickening
  • raised inflammatory markers
  • involvement of bronchioles
  • Histo
    • buds of granulation tissue in terminal bronchiole/alveoli
    • finrin exudates and collagen
    • HRCT - consolidation , nodules, reverse halo sign
73
Q

Interstitial Lung Disease (ILD). When to Bx?

A
  • Differentiate between UIP and NSIP

- Dx uncertain, radiology or clinical pattern unusual

74
Q

Interstitial Lung Disease (ILD). When to refer fro transplant?

A
  • advanced disease TLCO
75
Q

Which stage of sleep does parasomnia (abnormal behaviors or experiences) and night terrors occur?

A

Slow wave sleep

76
Q

How do you distinguish from Pulmonary arterial HTN and pulmonary venous HTN (HF)?

A

Right heart catheter confirms diagnosis of Pul HTN and distinguishes between the two.
Pulmonary arterial HT
- pul arterial pressure > 25 mmHG (10-20)
- pul artery capillary wedge pressure 15, then the cause is elevated pulmonary venous pressure e.g. HF
Common in HF with preserved ejection fraction

77
Q

treatment of pt with pneumonia from NH?

A 
2 agents for MDR Anti-pseudo
- Cefepime, Tazocin or mero
AND
MDR Staph aureaus
- Vanc
78
Q

How do you Dx ABPA?

A

Skin prick test to aspergillus

Aspergillus abx >1000U/ml another test

MK (28 decks)

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