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Finals Studying - Condensed > Resp > Flashcards

Resp Flashcards

1
Q

vital capacity

A

the max change possible

IRV + TV + ERV

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2
Q

functional residual capacity

A

the volume in the lungs after a normal expiration

RV + ERV

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3
Q

FVC

A

total volume expired from max inspiration to max expiration

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4
Q

FEV1

A

max volume that can be expired in 1 sec

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5
Q

normal FEV1/FVC

A

> 70%

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6
Q

obstructive picture on spirometry

A

FEV1 reduced
FVC normal
FEV1/FVC ratio reduced

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7
Q

restrictive picture on spirometry

A

FEV1 reduced
FVC reduced
FEV1/FVC ratio normal or increased

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8
Q

presentation of SEVERE asthma attack

A

inability to complete sentences in 1 breath
PEF 33-50% of normal
HR > 110
RR > 25/min

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9
Q

presentation of LIFE THREATENING asthma attack

A 
silent chest
altered conscious level 
exhaustion/poor resp effort 
cyanosis 
PEF < 33% of predicated
normal PaCO2
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10
Q

presentation of NEAR FATAL asthma attack

A

raised PaCO2

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11
Q

Ix of asthma

A

spirometry and bronchodilator reversibility

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12
Q

why should NSAIDs be avoided in asthmatics

A

NSAIDs inhibit the COX pathway, which is involved in the production of prostaglandins

this induces overproduction by eosinophils, mast cells and macrophages - bronchospasm

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13
Q

Mx chronic asthma

A
  1. SABA
  2. SABA + ICS
  3. SABA + ICS + LTRA
  4. SABA + ICS + LABA +/- LTRA (stop if not working)
  5. SABA + MART(combo ICS + LABA)
  6. SABA + increase dose of MART
  7. SABA + increase dose of MART + refer
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14
Q

LTRA

A

montelukast

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15
Q

mnemonic for asthma attack Mx

A

OSHIT ME -

Oxygen

Salbutamol 5mg Neb

Hydrocortisone 100mg IV (or pred 40mg PO)

Ipratropium 500 mcg Neb

Theophylline (aminophylline infusion 1g in 1L saline (0.5ml/kg/h)

Magnesium sulphate 2g IV over 20min

Escalate care (intubate and ventilate)

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16
Q

how many nebs can be given /hr in asthma attack

A

can be given back to back - max 5-10mg/hr

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17
Q

how often can IV steroids be given in acute asthma attack

A

6hrly

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18
Q

where is theophylline usually given in asthma attack and why

A

ICU - needs to be monitored as it causes arrhythmias, seizures, GI upset

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19
Q

when is Mg sulphate given in asthma attack

A

before theophylline as a once off dose (theophylline can cause seizures)

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20
Q

chronic bronchitis

A

a cough productive of green sputum on most days for 3m of at least 2 successive years

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21
Q

emphysema

A

enlarged air spaces distal to terminal bronchioles with destruction of the alveolar wall. Causes loss of elastic recoil of the lungs and collapse on expiration.

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22
Q

Ix COPD

A

spirometry + bronchodilator reversibility
CXR to rule out lung ca
bloods (exclude secondary polycythaemia)

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23
Q

Mx COPD

A
  1. SABA or SAMA prn
  2. LABA + LAMA
  3. LABA + LAMA + ICS
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24
Q

should Abx always be given for exacerbation of COPD

A

no- only if increased sputum purulence

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25
Q

Abx for infective exacerbation COPD

A
  1. Amoxicillin 500mg tds for 5d

2. Doxycycline 200g on day 1 then 100mg OD for 5d

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26
Q

target sats for COPD

A

88-92%

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27
Q

CURB 65 score

A 
Confusion
Urea >7 
Resp Rate >30 
BP <90s, <60d
age >65

1 point for each
0-1: home Tx poss
2: hop Tx
3 or more: consider ITU

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28
Q

pneumonia signs on examination

A

signs of consolidation

  • reduced chest expansion
  • dull percussion note
  • increased tactile vocal fremitus
  • bronchial breathing
  • late inspiratory crackles
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29
Q

what pneumonia do u get after influenza infection

A

staphylococcal

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30
Q

Mx staphylococcal pneumonia

A

cefotaxime or imipenem

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31
Q

who gets klebsiella pneumonia

A

alcoholics

diabetics

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32
Q

Mx klebsiella pneumonia

A

meropenem

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33
Q

who gets pseudomonas pneumonia

A

CF patients

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34
Q

Mx pseudomonas pneumonia

A

Ciprofloxacin

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35
Q

pneumonia associated with erythema nodosum

A

mycoplasma

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36
Q

presentation mycoplasma pneumonia

A

insidious onset
dry cough
flu-like symptoms

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37
Q

Ix mycoplasma pneumonia

A

serology

- cold agglutinins, can cause haemolytic anaemia

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38
Q

Mx mycoplasma pneumonia

A

macrolide - clarithromycin, azithromycin

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39
Q

Mx chlamydia psittaci pneumonia

A

doxycycline

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40
Q

who gets pneumocystis jirovecii pneumonia

A

HIV/AIDs patients

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41
Q

Ix pneumocystis jirovecii pneumonia

A

bronchoalveolar with lavage

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42
Q

Mx pneumocystis jirovecii pneumonia

A

high dose co-trimoxazole

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43
Q

most common cause of CAP

A

strep pneumoniae

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44
Q

Empirical Mx mild/mod CAP (0-2)

A

Amoxicillin 1g tds for 5d

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45
Q

Empirical Mx severe CAP (3-5)

A

co-amoxiclav IV + doxycycline PO for 7d

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46
Q

Empirical Mx severe CAP if in ICU/HDU or NBM

A

co-amoxiclav IV + clarithromycin IV

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47
Q

most common cause of HAP

A

strep pneumoniae

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48
Q

Mx non-severe HAP

A

Amoxicillin

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49
Q

Mx severe HAP

A

IV Amox + Gent

if allergic: IV co-trim + gent

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50
Q

Most common cause of aspiration pneumonia

A

strep pneumoniae, anaerobes

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51
Q

Mx non severe aspiration pneumonia

A

PO amoxicillin + metronidazole

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52
Q

Mx severe aspiration pneumonia

A

amox + met + gent

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53
Q

Ix lung ca

A
  1. CXR
  2. CT chest/abdo
  3. Pathological confirmation - either bronchoscopy or transthoracic needle biopsy
  4. staging: MRI (brain mets), PET-CT
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54
Q

small cell lung ca paraneoplastic syndromes

A

ADH production - SIADH, hyponatraemic

ACTH production - cushings syndrome

Lambert Eaton syndrome - antibodies to voltage gated ca channels

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55
Q

squamous cell lung ca paraneoplastic syndromes

A

PTH-rp production - hypercalcaemia

Finger clubbing

Hypertrophic pulmonary osteoarthropathy

56
Q

where do lung adenocarcinomas tend to be located

A

peripherally

57
Q

where do large cell lung cancers tend to be located

A

centrally

58
Q

adenocarcinoma paraneoplastic syndromes

A

gynaecomastia

hypertrophic pulmonary osteoarthropathy

59
Q

causes of pneumothorax

A

spontaneous - primary or secondary

secondary to trauma

either can be complicated by tension

60
Q

pathology of pneumothorax

A

communication develops between alveoli and pleural space, or the atmosphere and the pleural space.

gas then follows the pressure gradient into the pleural space.

61
Q

tracheal deviation in tension penumothorax

A

AWAY from affected side

62
Q

presentation spontaneous pneumothorax

A 
sudden onset SOB 
ipsilateral chest pain 
ipsilateral hyperinflation 
reduced chest expansion 
diminished breath sounds
hyper-resonance on percussion
63
Q

Mx primary spontaneous pneumothorax

A

< 2cm + asymptomatic = discharge.

> 2cm + symptomatic = admit for aspiration.
If this fails = chest drain.

64
Q

Mx secondary spontaneous pneumothorax

A

0-1cm + asymptomatic = oxygen & admit for 24h

1-2cm + asymptomatic = aspiration.
If this fails = chest drain.

> 2cm or symptomatic = chest drain.

65
Q

chest drain insertion site

A

5th IC space mid axillary line in the ‘safe triangle’

66
Q

borders of ‘the safe triangle’ for chest drain insertion

A

base of axilla

lateral edge of pectoralis major
lateral edge of lat dorsi

5th IC space

67
Q

Mx tension pneumothorax

A
  1. large bore needle with syringe partially filled with saline into 2nd IC space, mid-clavicular line
  2. then CXR
  3. then chest drain
68
Q

presentation PE

A 
SOB
pleuritic chest pain 
dizziness
syncope 
haemoptysis
69
Q

clinical assessment of PE - scoring systems

A

wells score

Geneva score

70
Q

1st Ix if PE unlikely

A

D-dimers

if normal = exclude PE
if raised = CTPA

71
Q

1st Ix if PE likely

A

CTPA

72
Q

Ix if CTPA contraindicated

A

V/Q scan

73
Q

ECG appearance in PE

A

sinus tachy (most common)

S1Q3T3 pattern (uncommon)

74
Q

CXR appearance in PE

A

wedge-shaped opacities

75
Q

Mx PE if haemodynamically unstable

A

thrombolysis (alteplase) - NOT if there is a bleeding risk tho!

76
Q

Initial Mx PE

A

LMWH or Fondaparinux

then once Dx has been confirmed, put on Warfarin (or NOAC).
The heparin can be stopped when anticoagulation with the warfarin has been established (usually 6-10d) or INR >2.0

77
Q

how long should warfarin (or NOAC) be continued in a provoked PE

A

3m

78
Q

how long should warfarin (or NOAC) be continued in an unprovoked PE

A

6m

79
Q

long term anticoagulation in malignant PE

A

LMWH for 6m

80
Q

transudative pleural effusion protein content

A

<30g/L

81
Q

causes of a transudative pleural effusion

A

SYSTEMIC FACTORS:
- increased venous pressure (HF, constrictive pericarditis, fluid overload)

  • hypoalbuminaemia (cirrhosis, nephrotic synd)
  • hypothyroidism
  • meigs syndrome
82
Q

exudative pleural effusion protein content

A

> 30gL

83
Q

causes of an exudative pleural effusion

A

LOCAL FACTORS:

i. e. inflammation of the lung or pleura, causing capillary leakage into the pleural space
- pneumonia
- TB
- SLE
- malignant mets

84
Q

when is light’s criteria applied to a pleural effusion

A

when protein content is between 25-35 g/L

85
Q

light’s criteria

A

exudative is likely if:

  • pleural fluid protein / serum protein > 0.5
  • pleural fluid LDH / serum LDH > 0.6
  • pleural fluid LDH >2/3 serum LDH upper limit of normal
86
Q

presentation of pleural effusion

A 
SOB 
non-productive cough 
pleuritic chest pain 
stony dull to percuss 
reduced breath sounds
reduced chest expansion
87
Q

stony dull to percuss

A

pleural effusion

88
Q

Ix pleural effusion

A
  1. CXR - blunting of costophrenic angles
  2. pleural USS
  3. pleural aspiration
89
Q

where is needle inserted for draining pleural effusion

A

on the upper border of the rub (so to miss nerves)

90
Q

reason for doing pleural USS before aspiration

A

to increase likelihood of success (know the exact location)

91
Q

pathology of primary TB

A

infection inhaled by droplets.
most people clear the infection, or it sits dormant as latent TB.
in some, they develop a primary infection of the lung.

92
Q

ghon focus

A

tubercle-laden macrophages in primary TB,

the lung lesion is walled off by macrophages and the cells inside die (caseating necrosis)

93
Q

ghon complex

A

ghon focus + hilar lymph nodes

94
Q

where does secondary TB occur in the lung

A

apex

95
Q

TB in the vertebral bodies

A

pott’s disease

96
Q

presentation TB

A 
cough
haemoptysis 
night sweats
wt loss
malaise 
pleural effusion 
clubbing 
erythema nodosum
97
Q

latent TB

A

pt has no symptoms

98
Q

Ix for latent TB

A

screening tests

  • tuberculin skin test
  • interferon-gamma test

if either are +ve, do CXR

99
Q

Ix for active TB

A

CXR

sputum sample for NAAT and ziehl-neelson staining

100
Q

Ix for active TB if pt unable to provide sputum samples

A

bronchoalveolar with lavage

101
Q

ziel-neelson staining in TB

A

acid fast bacilli

102
Q

Mx TB

A

“4 for 2 and 2 for 4”
- 4 drugs for 8w, then 2 drugs for 16w

  • Rifampicin
  • Isoniazid
  • Pyrazinamde
  • Ethambutol

(Rifampicin and Isoniazid for 16w)

103
Q

Mx latent TB

A

3m - Isoniazid (with pyroxidine) and Rifampicin

or

6m - Isoniazid (with pyroxidine)

104
Q

s/e of Rifampicin

A

orange discolouration of urine and tears
raised LFTs
reduced platelets
inactivation of the pill

105
Q

s/e of Isoniazid

A

raised LFTs
reduced WCC
neuropathy (stop and give pyroxidine)

106
Q

s/e of Pyrazinamide

A

hepatitis

arthralgia - gout

107
Q

s/e of Ethambutol

A

optic neuritis

108
Q

what are ILD characterised by

A

fibrosis of the lung, causing a restrictive pattern on spirometry

109
Q

presentation of the interstitial lung diseases

A

dry cough
SOB on exertion
finger clubbing
bi-basal inspiratory crackles

110
Q

farmer’s lung

A

hypersensitivity pneumonitis

caused by an allergic reaction to spores in mouldy hay

111
Q

bird fancier’s lung

A

hypersensitivity pneumonitis

caused by reaction to avian proteins in dry droppings

112
Q

occupations causing asbestosis

A

asbestos
ship building
power stations

113
Q

what type of asbestos is the most and least dangerous

A

most - blue

least - white

114
Q

industry causing berylliosis

A

aerospace industry

115
Q

industries causing silicosis

A

stonemasons

pottery workers

116
Q

egg shell calcification of hilar nodes

A

silcicosis

117
Q

miners lung a.ka. ?

A

coal workers pneumoconiosis

118
Q

presentation of CWP on CXR

A

small round opacities in the upper zones

119
Q

what can CWP lead to

A

Progressive Massive Fibrosis

  • large round opacities
  • emphysema
  • black sputum

leading to pulmonary HTN and cor pulmonale

120
Q

systemic causes of ILD

A 
RA
sarcoidosis 
SLE 
systemic sclerosis 
ank spond
psoriasis
121
Q

drug causes of ILD

A

nitrofurantoin
amiodarone
sulfasalazine

122
Q

idiopathic pulmonary fibrosis - area of lung usually affected

A

lower zones

123
Q

CXR appearance IPF

A

ground glass / honeycomb appearance

124
Q

Caplan’s syndrome

A

RA
Pneumoconiosis
Pulmonary rheumatoid nodules

125
Q

Mx ILD

A

remove causative factor

steroids +/- immunosuppression

126
Q

presentation of sarcoidosis

A

very non-specific

acute: erythema nodosum, bilateral hilar lymphadenopathy, swinging fever, polyarthralgia
insidious: SOB, non-productive cough, malaise, wt loss
skin: lupus pernio

hypercalcaemia

127
Q

Mx sarcoidosis

A

Asymptomatic + stable stage 2 or 3: no Tx

Stage 2 0r 3 with symptoms: oral steroids

128
Q

CXR stages of sarcoidosis

A 
0 = normal 
1 = BHL 
2 = BHL + interstitial infiltrates
3 = diffuse interstitial infiltrates
4 = fibrosis
129
Q

causes of bronchiectasis

A

GENETIC:
CF
alpha-1-antitrypsin deficiency

POST-INFECTION:
childhood viral infections (haemophilus most common)

CTD:
RA, sjogren’s

130
Q

presentation bronchiectasis

A 
persistent cough 
copious sputum 
finger clubbing 
course crackles 
wheeze
131
Q

Ix bronchiectasis

A

CT - signet ring bronchi

132
Q

Mx bronchiectasis

A 
inspiratory muscle training 
postural drainage 
Abx for exacerbations 
bronchodilators
surgery - focal disease
133
Q

inheritance of CF

A

autosomal recessive

134
Q

Ix CF

A

sweat test - positive if > 60mmol/L
(normal <30)
if in between - do genetic testing

135
Q

most common bacteria to colonise CF pts

A

pseudomonas

136
Q

Mx CF

A

2x daily postural drainage and chest physio

high calorie diet, high fat intake

minimise contact with other CF pts

vit supplements, pancreatic enzymes

Finals Studying - Condensed (22 decks)

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