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Thoracics > Thoracics > Flashcards

Thoracics Flashcards

0
Q

Causes of reduced DLCO

A 
Anaemia
Pulmonary hypertension 
Pulmonary fibrosis 
COPD
Diffuse pneumonia
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1
Q

Causes of high DLCO

A

Pulmonary haemorrhage

Asthma-increased lung vol and inflammation

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2
Q

Cxr upper lung distribution opacities

A

Sarcoidosis
Silicosis
Langerhan cell histiocytosis
Reactivated TB

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3
Q

Lower zone opacities on plain film

A

Heart failure
Pulmonary fibrosis
Asbestosis
Pneumonia

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4
Q

FDG in pet stands for

A

18 fluorodeoxyglucose

Taken up by metabolically active malignant cells and trapped

Sensitivities 95% mediastinal LN malignancy
Spec 80%

False neg in low grade tumours like adenocarcinoma in situ, less than 1cm, carcinoid

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5
Q

What is the role of PET-CT in lung Ca

?

A

Known or suspected lung cancer staging evaluation
Simultaneously acquired pet and ct images
Higher spec and sens than either alone
Expensive
Radiation
Detects 10-20 percent of patients with known or suspected lung cancer who was otherwise thought to be a candidate for surgery
Still need a tissue diagnosis if positive pet

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6
Q

Role of exhaled nitric oxide levels in asthma?

A

Noninvasive
Reflects active airway inflammation
Correlates with airway eosinophilia
Assess adherence to therapy

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7
Q

ABPA is from sensitisation to

A

Aspergillus fumigatus

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8
Q

Diagnose ABPA with-

A

Elevated serum total and specific aspergillus IgE
Positive skin test to aspergillus fumigatus
Eosinophilia

Also see proximal bronchiectasis
Mucus plugging –> atelectasis
Long term get pulm fibrosis if not controlled

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9
Q

Mechanism of leukotriene modifying drugs eg minteleukast

A

Modest anti inflammatory and bronchodilator effect
Block receptors or production by inhibiting 5-lip oxygenase

Can cause mood and psych side effects

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10
Q

Causes of increased DLCO

A

Polycythemia
Asthma
Pulmonary haemorrhage
Left to right shunt

Useful to differentiate asthma from emphysema, evaluate restrictive, early stages pulm hypertension
DLCO USUALLY NORMAL IN CHRONIC BRONCHITIS and TLC NORMAL compared with emphysema where increased

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11
Q

What is a better predictor of survival in copd? Hyperinflation or FEV1?

A

Hyperinflation

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12
Q

Workup for ILD

A

ANA, RF
ANCA if suspect vasculitis
Anti-GBM antibodies if suspect
ECG-? pulmonary hypertension suspected

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13
Q

Upper zone predilection ILD

A 
sarcoid
pulmonary langerhan cell histiocytosis
hypersensitivity pneumonitis
silicosis
berylliosis
RA (necrobiotic nodular form)
Ank spond
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14
Q

BAL findings in sarcoidosis

A

lymphocytosis; CD4:CD8 ratio over 3.5 most specific of diagnosis

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15
Q

COP BAL findings

A

foamy macrophages

decreased CD4:CD8 ratio

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16
Q

Respiratory disease in RA

A

pleurisy
+/- effusion
ILD
necrobiotic nodules (non pneumoconiotic intrapulmonary rheumatoid nodules)
Caplan’s syndrome (rheumatoid pneumoconiosis)
pulmonary hypertension secondary to rheumatoid pulmonary vasculitis
organised pneumonia
upper airway obstruction due to crico-arytenoid arthritis

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17
Q

Lung involvement in SLE

A

-pleuritis +/- pleurisy most common
-atelectasis
pulmonary vascular disease
pulmonary haemorrhage
uraemic pulmonary oede,a
infectious pneumonia
chronic progressive ILD uncommon

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18
Q

lungs in polymyositis/dermatomyositis

A

ILD in 10% of all these patients

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19
Q

Lung involvement in Sjogren’s

A 
general dryness and lack of airway secretion-->cough and hoarseness
Lymphocytic interstitial pneumonia
Lymphoma
Bronchitis
Bronchiolitis obliterans
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20
Q

LAM has what picture on PFTS

A

obstructive

21
Q

Upper zone fibrosis predominant

A 
Extrinsic allergic alveolitis
Silicosis
Sarcoidosis
Coal workers pneumconiosis
Histiocytosis
TB
Ank spond
22
Q

Lower zone fibrosis

A

IPF
Most CT disorders not ank spond
drug induced: amiodarone, bleomycin, methotrexate
asbestosis

23
Q

CXR staging of sarcoidosis- 1 to 4… GO!

A
  1. BHL
  2. BHL + infiltrates
  3. Infiltrates
  4. Fibrosis
ACE sens 60 spec 70
Hypercalcaemia in 10%
May have an ACE role in monitoring disease activity
Spirometry: restrictive
Biopsy: noncaseating granulomas
24
Q

Hyperkalaemia- quick run through causes including drug causes.

A 
AKI
Drugs: K sparing diuretics, BETA BLOCKERS, ACE, ARB, spiro, ciclosporine, heparin (inhibit aldosterone secretion)
Metabolic acidosis
Addisons
Rhabdo
massive blood transfusion
25
Q

IPF negative prognostic markers

A 
Male
age over 50
mod-severe spirometry and DLCO
extensive smoking history
neutrophilia on BAL
extensive honeycomb on HRCT
mod-sev dyspnoea on exertion
desaturation to below 88% on 6mwt
26
Q

What is the most powerful tool for reducing cigarette consumption?

A

Price - in large increments ie 10%

27
Q

Criteria for diagnosis ABPA- need 6 or more? (8)-

A 
Asthma
Fleeting pulmonary shadows
Aspergillus precipitans
IgE over 1000
RAST for aspergillus
Positive skin prick test (type 1)
Eosinophilia
Central bronchiectasis

Minor criteria are:

  • Aspergillus in sputum (DO NOT NEED TO CONFIRM DIAGNOSIS)
  • Expectoration black/brown mucus plugs
  • Delayed skin reaction to aspergillus Ag (type 3 reaction)
28
Q

What is a normal residual volume?

A

About 25% of TLC

If see reduced FVC, could be due to restrictive defect, or could also be due to hyperinflation causing increased residual volume.

29
Q

What effect does Carboxyhaemoglobin or pCO2 alveolar have on DLCO/

A

CO will reduce because reduction in diffusion gradient

increase CO2 in alveolus will increase TLCO because reduce PaO2- less competition for binding sites

30
Q

Classes of CFTR mutation and which one is DF506 and which is G551D?

A

I - no synthesis CFTR

2- Defective maturation and premature degradation and what is there does not work well- delta F 508

3- Abnormal ion channel regulation eg ATP binding- channels there but not working eg G551D

4- Defective conduction of chloride- some chloride still gets through

5- reduce number of transcripts but the ones there are working

6-accelerated turnover

31
Q

When can you use Ivacaftor?

A

For G551D mutation (class 3)- corrects the defect in the existing channel

IMproves FEV1, reduces exacerbation risk, causes weight gain

32
Q

Which to bugs if colonised in CF cause worse transplant outcomes?

A 
Burkholderia ceppacia
Mycobacterium abscessus (not MAC)
33
Q

What are some different BAL cell patterns? What is normal?

A

Normal is over 95% alveolar macrophages
CD4/8 over 3.5–>sarcoid
CD4/CD8 under 1 –>hypersensitivity pneumonitis
Eosinophils over 25% in eosinophilic pneumonia, fungal/parasitic
Neuts +++–>in IPF
Lymphocyte predom –>sarcoid, hypersens pneumonitis
Foamy Macrophages, mixed pattern increased cells and ratio under 1–> COP

34
Q

Primary offender in lung destruction in COPD?

A

Human leukocyte elastase

Also proteinase 3, macrophage derived matrix metalloproteinases, plasminogen activator, cigarette smoke free radicals

35
Q

What is the significant of microalbuminuria in COPD?

A

associated with hypoxaemia independent of other risk factors

36
Q

What is the significance of centri-acinar, panacinar, distal acinar/paraseptal patterns of emphysema?

A

Centri- cig smoking with upper lobe predom
Panacinar with homozygoous alpha 1 AT- lower lobe predom
Distal/paraseptal- bullae formation but no obstruction

37
Q

In mild vs mode to severe emphysema, what is the predominant pathological mechanism?

A

Mild- bronchiolar disease

Mod-Sev- loss elastic recoil

38
Q

What predict survival in COPD better- hyperinflation or FEV1?

A

Hyperinflation

39
Q

What should be the first step in asthmatics being evaluated for ABPA?

A

Skin prick test- if neg excludes.

if positive, check IgE and aspergillus precipitins
If positive then do aspergillus specific IgE and G

40
Q

Why is REM so hard in OSA?

A

Because lose muscle tone–>collapse airways even more!!

41
Q

Complications of OSA?

A 
MVA
Stroke
Hypertension
Pulmonary hypertension
CAD, arrhythmias, HF
Insulin resistance and diabetes
TAG up
All cause mortality  increase 2-3 times if AHI over 30 INDEPENDENTLY of other RF
Depression
42
Q

Where is the respiratory centre located?

A

Bilaterally in the ventrolateral medulla at the caudal fourth ventricle

43
Q

Causes of central sleep apnoea?

A

Basically these patients hyperventilate to drive the CO2 down so that there is no stimulus for sleeping ventilationany more:
Hence oximetry not useful

opioids
CCF
AF
Stroke
CKD
high altitude
treated OSA

**If the CO2 is HIGH it is NOT central apneoa- it is sleep related hypoventilation syndrome. See SUSTAINED hypoxaemia - usually 30% total sleep time

44
Q

When would you need supplemental oxygen while flying?

A

If sats 88-95% on room air at sea level, may need
Pressure is equivalent of 2500m altitude equivalent, as if breathing 15% oxygen at sea level- gives normal people paO2 53-64% and sats of 85-91%

Remember that A-a is NORMAL in healthy adults at high altitude.

45
Q

What is COPD diagnosis based on?

A

History of exposure to smoke or other noxious agents
or
FEV1/FVC

46
Q

What factors correlate with COPD mortality?

A

Degree of hyperinflation reflected by IC/TLC
Poor 6MWT
VO2max
BMI
MMRC dyspnoea scale
BODE score (BMI, degree obstruction, dyspnoea score, exercise score on 6MWT)
Hypoxaemic resp failure

All better than FEV1

47
Q

When is IGRA unreliable in HIV?

A

CD4 under 100

48
Q

What is the worst risk of TB reactivation? Adalimumab, Infliximab, Ertanacept or DMARDS?

A

Adalimumab worst.

DMARDS not really increase, Tocilizumab (anti IL-6), Abatacept (CD80/86), Anakinra (IL-1) no increase over DMARDs

So just the TNF aplhas really.

49
Q

Which of the TB bugs are the Isoniazid and Rifampicin most important for?

A

Isoniazid- first two months for the rapidly multiplying
Pyrazinamide for the slowly multiplying
Rifampicin for the sporadically multiplying

50
Q

Why should you never add a single drug to a failing TB regiment?

A

Selects out the resistant clone and makes more resistant.

Thoracics (16 decks)

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