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CP1 revision > Deck 2 > Flashcards

Deck 2 Flashcards

1
Q

Define Asthma

A

Reversible, obstructive due to exercise/allergens/stress or idiopathic.
Key symptoms are expiratory wheeze, diurnal dyspnoea, chest tightness which VARY
Histologically, bronchial inflammation and eosinophils

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2
Q

Acute asthma phase vs late phase

A

Early is bronchospasm (histamine, PD2, leukotrienes)

Late phase has cellular infiltrates and oedema (narrows), also hyperreactive

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3
Q

Chronic asthma features

A

Bronchoconstriction, mucusal oedema, carcot leyden crystals (eosinophil granules), Curschman spirals, pulmonary HTN

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4
Q

Diagnosis of Asthma

A

If under 5, Tx based on obs/clinical judgement and objective testing ASAP
5-16, use spirometry (look for reversibility), if not then FeNO test
17+ uses spirometry, FeNO, peak flow variability. Also use airway hyperreactivity (histamine or methacholine challenge)

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5
Q

Tx for asthma

A

SABA
Add ICS
Add LRTA
LABA+ICS+SABA

MART is LABA+steroid as reliever and preventer

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6
Q

Moderate acute asthma

A

PEFR 50-75%, increasing symptoms, no acute asmtha features

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7
Q

Acute severe asthma

A

PEF 33-50%, RR>25, HR>110, inability to complete sentences in 1 breath

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8
Q

Life threatening asthma

A

SpO2 <92%, PEFR <33%, silent chest, poor respiratory effort, cyanosis, altered consciousness

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9
Q

COPD definition

A

progressive airflow obstruction but not fully reversible.
See mucus hypersecretion, ciliary dysfunction, airflow limitation, hyperinflation, impaired gas exchane and pulmonary HT (hypoxaemia induced vasoconstriction)

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10
Q

COPD RF

A

Smoking, indoor pollution, occupational toxin, genetic factor, infection, socioeconomic factors

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11
Q

COPD symptoms

A

Start as asymptomatic apart from exertion, then chronic cough, progressive dyspnoea, regular sputum, whzeeze, fatigue, weight loss, anorexia, cough syncope, depression

Haemoptysis is not common feature, so consider ddx (lung cancer, bronchiectasis, TB)

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12
Q

COPD examination

A

Hyperinflated chest, wheeze, quiet breath sounds, pursed lip breathing, accessor muscles, paradoxical movement of lower ribs, peripheral oedema, cyanoses, raised JVP, cachexia

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13
Q

COPD spirometry + other investigations

A 
FEV1<80%
FVC >80% (although may be reduced)
FEV1/FVC <0.7
DLCA reduced in emphysema
ECG may show cor pulmonale
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14
Q

COPD management

A 
SABA/SAMA
Add LAMA (tiotropium)
Steroids can be added
Mucolytics 
Smoking cessation
Rescue Abx
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15
Q

Chronic bronchitis

A

productive sputum on most days for 3 months of at least 2 successive years.
Does not imply airway inflammation.
Caused by chronic irritation stimulating mucus (increase goblet cells).
Sputum increases infection risk.
Proximal airspace disease.
Reid index shows ratio of gland: all thickness (increased)
Typically 40s, mild or late dysponoea, copious sputum, recurrent infection, repeated resp failure and increased airway resistance. on CXR, prominent vessels and large heart

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16
Q

Emphysema

A

Distal airspace disease with increased terminal bronchiole size and reduced gas exchange.
No fibrosis.
Caused by protease/antiprotease imbalance.
Centrobular is most common (smoking association). Panaacinar is whole lobule, alpha 1 antitrypsin.
Typically 50s-75, severe early dyspnoea, scant sputum, occasional infections. Resp failure at terminal phase. Relatively normal airway resistance but low recoil. Small heart and hyperinflation on CXR.

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17
Q

Lung cancer symptoms

A

Dry cough (over 3 weeks), haemoptysis, dyspnoea (esp exertional), chest pain (radiating to shoulder?), recurrent infections, clubbing, lymphadenopathy, B symptoms, thrombocytosis, bone pain, hoarseness, fever, dysphagia

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18
Q

Lung cancer investigation

A

CXR, then staging CT

Bronchoscopy can be used for histology, but only useful up to bronchioles.

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19
Q

Lung cancer types (general)

A

Small cell (15%) and NSC (85%)

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20
Q

Small cell lung cancer

A

OAT cell.Rare. Associated with smoking. Grow quickly and metastasise early, so poor prognosis.
Can cause cavitating lesions. Comes from bronchoepithelium but differentiates neuroendocrine. Associated with paraneoplastic syndromes (SIADH, Cushings - > rarely causes MG like syndrome (Eaten Lambert, but symptoms improve with use)
Has pulmonary carcinoid rare subtype which can be benign

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21
Q

Squamous cell lung cancer

A

NSC. 50% of lung cancers. Heavy smoking association. OFten central, near carina. Tend to have obstructive symptoms and may have overlying infection. Slow growth.
Can diagnose on sputum cytology. May secrete PTH and cause hypercalcaemia

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22
Q

Adenocarcinoma Lung cancer

A

20% of lung cancers. Equal gender. Less smoking association. Typically peripheral, but can be central. Can arise at scars.
Subtype is bronchoalveolar carcinoma (comes from alveoli and T2 pneumocytes -spreads along alveolar septa. Good prognossi if no mets)

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23
Q

Large cell anaplastic carcinoma (lung)

A

10% of lung cancers. Need EM to differentiate as often has squamous or adenocarcinoid features.

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24
Q

Metastases to lungs

A

Breast, kidney, testicular and bladder cancer

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25
Q

Primary lung cancer complications

A

SVC compression/obstruction, recurrent laryngeal nerve palsy, horner syndrome, distant mets to brain, bone, liver and adrenals

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26
Q 
Exudate:
Causes
Biochemistry
Typical precipitating factor
Associations
A

Alteration to formulation or absorption of pleural fluid
>30g/L (or >0.5 effusion:serum protein, effusion:serum LDH >0.6)
Seen in malignancy, infection, pulmonary embolism, pneumonia, TB, mesothelioma, RA, SLE, lymphoma

Often unilateral. If polymorphs in effusion then suggests PE, TB or asbestosis. Lymphocytes in effusion suggests malignancy or TB

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27
Q 
Transudate
Causes
Protein content
Typical precipitating factor
Associations
A

Caused by hydrostatic pressure alterations, pleural permeability and oncotic pressure
protein <30g/L, lower protein and lower LDH than exudates
Seen in ‘failures (HF, liver failure, peritoneal dialysis, nephrotic syndrome, (rarely) hypothyroidism or ovarian tumour (Meig’s syndrome)
Often bilateral.

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28
Q

Pleural effusion investigation

A

CXR (will only see once >250mL),

Chest tap and broncoscopy (esp if no known cause)

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29
Q

Empyema

A

Can form from stagnant effusion, esp exudate with high protein content

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30
Q

Pneumonia

A

Pulmonary parenchyma infection plus new shadow on CXR (separate from bronchitis)
In bacterial, inflammatory exudate in alveolar spaces gives consolidation.
In viral infections, alveoli often spared and interstitium affected (pneumonitis/interstitial pneumonia)

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31
Q

Bronchopneumonia

A

Primary infection around bronchi.
Spreads around lobules and can be multiple lobes. More common at age extremes (immobility and secretion retention.
Tends to affect bases

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32
Q

Lobar pneumonia

A

Distal airspace affected. Spreads over whole lobe. More common in adults

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33
Q

Pneumonia exam

A

Fever, productive cough, dyspnoea, tachypnoea, confusion, pleuritc chest pain (may refer). Coarse crackles. Dull to percussion. Pleural rub. Bronchial breathing. Increased vocal resonance (not in effusion, pneuothorax or collapse)

34
Q

Pneumonia RF

A

male, elderly, smoker, alcoholic, chronic disease, secondary to bronchial obstruction (e.g. cancer)

35
Q 
CAP 
Criteria
RF
Common organisms
Atypicals
A

CAP is in community or within 48h of admission. Peak age is 50-70, more in winter/spring.
Increase risk in COPD, diabetes, CVD and immunosuppression.
Common pathogens: S pneumonia (most common - lobar pneumonia and rusty sputum), H influenzae (COPD, <110) and moraxella catarrhalis.
S aureus more common after viral pneumonia
Atypicals are:
mycoplasma (more common in 17-44, longer illness, extra pulmonary features (rash, hepatitis, D&V, pericarditis, meningoencephalitis), legionella (classically smokers post holiday - often SIADH, CN palsy, proteinuria, haematuria, bilateral bases)
Chlamydia (LFT derangement and hyponatraemia)

Severity is CURB 65:
New confusion (MMT 8 or less)
Urea >7mmol/L
RR>30
BP <90 sys or <60 diastolic
65+
0-1 is low (community, 2 is mod (?hospital), 3 -5 is hospital
36
Q

HAP

A

LRTI +pneumonic change >48h admission or if admitted in last 7 days.
RF is increased hospital stay, poor mobility, reduced cough, over 70, underlying disease.
Most commo causes: enterobacteria, pseudomonas (60%), rest are s. pneumoniae, H influenzae and S aureus

37
Q

Aspiration pneumonia

A

May not show on CXR
Consider if low GCS and evidence of vomiting
Add metronidazole for anaerobic cover

38
Q

pneumonia stages

A

Congestion (24h, alveoli fill with fluid and bacteria)
Red hepatisation (airless, capillaries dilate, exudate in pleura)
Gray hepatisation (macrophages, neutrophils, fibrin)
Resolution (8-9 days without Abx)

39
Q

Pneumonia complications

A

Sepsis, lung abscess (mrore common in s aureus), empyema (more common with strep pneumoniae), carnification (scaring from resolution failure - reduces resp function), amylodiosis (amyloid deposit)

40
Q

TB infection

A

Drops lodge in alveoli.
80% of people eliminate, 20% have primary infection (can be asymptomatic). If elimination fails, TB in macrophages and multiplies and disseminates (more like in HIV) or cal form granulomatous lesion (heals by fibrosis, invades locally)
Can reactive during immunocompromise (RF are age, steroids, immunosuppressive drugs (esp ant TNF), diabetes, CKD, HIV.

41
Q

pulmonary TB symptoms

A

cough, haemoptysis, fever, B symptoms. clubbing (advanced), erythema nodosum

42
Q

TB investigation

A

Culture, sputum (AFB), histology (caseating granuloma), CXR primary: (Ghon focus, if lymphs then complex) - lobar/patchy consolidation, effusion, lymphadenopathy, miliary)
CXR latent may show nodules
CXR secondary shows necrosis, cavitation, consolidation, effusion, miliary TB
Mantoux test (>5mm is positive in immunosuppressed, prior TB or recent contact; >15 is positive in any individual)
PCR (can’t distinguish active/latent)
Culture is GSTD but takes 6 weeks on Lownstein Jensen medium

43
Q

Extrapulmonary TB and symptoms

A

Less common. Larynx, pleura, brain, kidneys, bone. Not infectious unless larynx.
Meningitis, painless lymphadenopathy, arthritis (Pott in spine), lupus vulgaris/erythema nodosum (cutaneous TB), chest pain (pericarditis)

44
Q

Bronchiectasis definition

A 
Structural pathology (subsegmental airways dilate (bronchi/bronchioles) - decreasing surface/volume ratio and allows mucus plugging. 
Cole's viscious circle with initial insult causing blockage, inflammatory infiltrate and elastase mediated parenchyma damage which distorts physiology. Mucus stasis gives risk of future insult
Overlap with COPD but COPD is functional/physiological and bronchiectasis is structural (see dilatation on CT)
45
Q

Cylindrical bronciectasis

A

Most common, airways widen but structure remains

46
Q

Varicose bronchiectasis

A

Tortuous

47
Q

Cystic bronchiectasis

A

Rare, sever, outpouchings. Associated with CF

48
Q

Bronchiectasis RF

A

CF, primary ciliary dyskinesia, infection, obstruction (COPD, tumour, aspergillosis, irritants), idiopathic. Can be tertiary due to primary disease (hypogammaglobulinaemia (immune deficiency) or RA)

49
Q

Bronchiectasis S+S

A

SOB, cupfuls of sputum (often green+/- blood), fatigue, PMHx of lung insult.
Can have dry bronchiectasis with no cupfuls of sputum
Clubbing, coarse inspiratory crackles, wheeze, low body habitus due to demands

50
Q

Bronchiectasis complications

A

Mixed obstructive/restrictive condition
Recurent pneumonia
Pleural effusion (transudate)
Larger blood vessels erode (massive haemoptysis)
Increased pulmonary resistance (RHF)
Cerebral abscess if bacteria spread
Amyloidosis (autoimmune response to chronic inflammation

51
Q

Bronchiectasis investigations

A

FBC, U&E, coag screen, CRP, sputum microscopy (H influenzae, S pneumoniae, P aeruginosa most common - consider fungal)
CXR (pneumonia, effusion, bronchial thickening
Spirometry (obstructive) - note peek flow not appropriate)
CT scan (signet ring pattern, widening around inflammed bronchiole)
Igs, functional antibodies, aspergillus serology

52
Q

Restrictive lung disease

A

Get reduced max lung volume (e.g. fibrosis), increase in dead space (effusion/pus)
FEV1 reduced, reduced FVC but FEV1/FVC may be normal or increased

53
Q

Restrictive lung causes

A

Fibrosis, occupational lung disease, oedema, lobectomy, bronchiectasis, kyphoscoliosis, neuromuscular disease affecting diaphragm, obesity, pregnancy, sarcoidosis, RA, SLE

54
Q

Pulmonary fibrosis symptoms and signs

A

ronchi, SOB, Wheeze, chest pain, fatigue, anxiety, depression, cyanosis, clubbing, fine crackles

55
Q

Pulmonary fibrosis:

Focal, interstitial or replacement disease

A

Focal is generally occupation link and affects lymphoid tissue (can be triggered by local inflammation)
Interstitial is more diffuse (think extrinsic allergic alveolitis (T3HS)
Replacement is seen in RA, TB and CT disease where tissue damage has been

56
Q

Apical fibrosis causes

A 
Aspergillosis
TB
Extrinsic allergic alveolitis
Ankylosing spondylitis
Sarcoid
Histiocytosis
Occupational (beryllosis/silicosis)
57
Q

Basal fibrosis causes

A 
Drug induced (amiodarone, bleomycin, busulfan, methotrexate, vincristine, nitrofurantoin)
RA
CT disease
Idiopathic pulmonary fibrosis
Asbestosis
58
Q

Extrinsic allergic alveolitis

A

T3HS. Tertiary fibrosis. Can be bird droppings, hay mould, hops, M avium from hot top, fungi from musical instrument

59
Q

Fibrosis investigations and prognosis

A 
ABG, CPR, ANA/Rh factor for CT disease
CXR/CT (honeycomb)
FEV1>80, FVC<80, FEV1/FVC>0.7
Reduced gas exchange
Lung biopsy

Poor prognosis, tx is slowing progression.
Pirfenidone downregulates procollagens. Nintedanib is TK inhibitor
Alternative is lung transplant

60
Q

Mesothelioma O/E

O/I

A

Diminished breath sounds (effusion, trapped lung, bronchial obstruction), dull to percusion
CXR (effusion, pleural thickening, reduced lung volume, calcification/fibrosis)
CT nodular thickening (but can be benign)
Effusion tap can allow differentiation of transudate and exudate, but cytology not useful.

61
Q

methothelioma types and mets

A

Epitheloid is more favourable
Sarcoimoid and mixed are unfavourable

Often mets to contralateral lung, liver, adrenal gland, kidney, potentially bone
90% are pleural, 5-10% peritoneal, but can get pericardial and testicular

62
Q

Air cannulae %

A

on air, 21%.

1L = 25%, 2L=28%, 3L= 32%, 4L=36%

63
Q

Base excess

A

Amount of acid required to normalise pH.

Negative means metabolic acidosis, positive is metabolic alklaosis.

64
Q

pH and oxygen binding

A

In acidotic blood, oxygen more tightly bound.

In alkalosis, oxygen dissociates more readily

65
Q

Lung cancer referral and investigations

A

40+ with 2+ symptoms (or 1+ if smoker) then urgent CXR and referral
CR scan for staging (liver and neck)
PET-CT if aiming for cure (may have problems in renal impairment).
If PET CT is positive nodes, then EBUS TBNA needed

Bone scintigraphy can be used for bone mets (not needed if PET-CT negative)
CR/MRI for ?brain mets

66
Q

LUL collapse

A

Veil sign

67
Q

LLL collapse

A

Sail sign

68
Q

RUL collapse

A

Reverse S sign of Golden (?mass) -see horizontal fissure displacement

69
Q

RML collapse

A

Loss of R heart silhouette

70
Q

RLL collapse

A

Loss of R hemidraphram silouhette. May see rib crowding due to volume loss

71
Q

Superior sulcus tumour

A

Pancoast tumour. T3. MRI recommended (although CT may be useful)

72
Q

Visceral/parietal pleural extensions

A

Visceral goes to 6th rib in MCL, 8th in MAL and 10th in MSL.

Parietal goes to 8th, 10th and 12

73
Q

Kco vs TLCO

A

diffusion capacity per unit area vsDiffusion capacity for total lung
Decrease means gas exchange problem, not a chest wall deformity.

74
Q

smoking cessation

A

NRT or bupropion if >10day

75
Q

Empyema organisms

A

Streptococcus pneumoniae, H influenzae, Klebsiella, pseudomonas
cAN BE VIRAL (COXSACKIE, ADENOVIRUS, ECHOVIRUS)
cAN GIVE FIBROUS PLEURAL ADHESIONS AND CALCIFICATION

76
Q

Causes of resp acidodis and symptoms

A

poor ventilation, airway obstruction, emphysema, neuromuscular obesity
Gives headache, tachycardia, bounding pulse, CO2 flap, papilledema, Kussmaul respiration, Potassium derangement (hypokalaemia, or hyperkalaemia if renal function impaired)

77
Q

Causes of resp alkalosis

A

Can be CNS (pain/anxiety/meningitis, trauma, psychosis, fever), hypoxaemia (pneumonia, pulmonary oedema, severe anaemia, high altitude), salicates, progesterone, pregnancy, haemothorax, flail chest, PE, HF, heat exposure, septicaemia

78
Q

Metabolic acidosis

A

Either too much acid or not enough H+ excretion. Normal anion gap then bicarb is lost (GI/renal loss), renal acidosis, potassium sparing diuretics, ACEi/NSAID, bicarbonate secreting villous adenoma
Large anion gap in increased acid (DKA, lactic, urate, ingested acid/aspirin)

79
Q

Anion gap

A

Note that bases (cations) are positive, and acids (anions) negative.
So a large anion gap means extra acid.

80
Q

Metabolic alklaosis

A

Can be H+ loss (vomiting) or from direct increase in bicarb (retention, alkali ingestion - Milk alkali syndrome, villous adenoma if chloride secreting, hypercalcaemia, aldosteronism, steroids, Cushings

CP1 revision (16 decks)

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