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first year revision > respiratory > Flashcards

respiratory Flashcards

1
Q

3 factors characterizing asthma

A

reversible airway inflammation
airway hyper responsiveness
inflammation of bronchi

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2
Q

causes of asthma

A 
atrophy 
hygiene hypothesis 
aspirin induced 
occupational 
exercise induced
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3
Q

describe atrophy and related conditions

A

genetic predisposition to IgE mediated allergen sensitivity

allergic asthma, atopic dermatitis, allergic rhinitis

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4
Q

what are the 3 phases of asthma

A

early phase
late phase
chronicity

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5
Q

describe early phase of asthma

A

type 1 hypersensitivity->IgE release activating mast cells

mast cells degranulate w/ histamine

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6
Q

what role does histamine play in early phase of asthma

A

smooth muscle contraction + bronchoconstriction

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7
Q

describe late phase of asthma

A

recurrence of inflammatory cells such as polymorphonuclear/ T cells
beta agonist cannot accomplish complete reversal

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8
Q

describe chronic phase of asthma

A 
airway remodelling (non reversible)
persistent inflammation w/ airways filled with fibrous tissue
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9
Q

diagnostic of asthma

A

spirometry: obstructive pattern
FeNO: eospinopilic airway inflammation is raised
peak flow tests daily recorded

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10
Q

obstructive vs restrictive pattern spirometry

A

obstructive:
FVC: normal/ reduced, FEV1: reduced
FEV1/FVC: <70%

restrictive:
both decreased, ratio is normal %

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11
Q

treatment of asthma

A

SABA
SABA+ low dose ICS
low dose ICS+ LABA
higher ICS+ LABA

(move to second stage when there is uncontrolled symptoms)

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12
Q

acute attacks of asthma

A

salbutamol (SABA)
oxygen (94-98%)
steroids (prednisolone/ IV hydrocortisone)
ipratropium bromide

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13
Q

mode of action: ipratropium bromide

A

SAMA: muscarinic antagonist

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14
Q

mode of action: adrenaline

A

alpha agonist

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15
Q

define COPD

A

non reversible long term blockage in air flow to lung tissue damage: smoking, alpha 1 antitrypsin deficiency

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16
Q

COPD vs ASTHMA

A

COPD not reversible w/ bronchodilators, symptoms will exacerbate during lung infections

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17
Q

describe COPD: chronic bronchitis

A
  1. chronic inflammation of bronchi with neutrophilic, CD8+ t lymphocytes and macorphages infiltration
  2. chronic productive cough for 3 months over 2 consecutive years
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18
Q

pathological changes in chronic bronchitis

A

goblet cell hyperplasia
mucus hypersecretion
narrowing of small airways

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19
Q

describe COPD: emphysema

A

abnormal air sac enlargement distal to terminal bronchioles causing reduced area for gas exchange->chronic hypoxia

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20
Q

what causes alveoli destruction in emphysema

A

^proteases due to neutrophils and macrophages-> protease elastase cause decrease elastin-> collapse/ dilation and bullae formation

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21
Q

COPD symptoms

A

productive cough, SOB, wheeze, recurrent respiratory infections

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22
Q

diagnosis of COPD

A

spirometry

CXR, FBC, BMI

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23
Q

COPD: long term management

A

smoking cessation+ flu vaccines

  1. SABA/ SAMA
  2. LABA/LAMA
  3. LABA + ICS
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24
Q

when is long term oxygen therapy used in COPD

A

PaO2< 7.3 kPa
or
PaO2< 8 kPa with:
pulmonary hypertension, peripheral oedema

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25
Q

symptoms of COPD exacerbation

A

pyrexia, SOB, sputum
CO2 retention-> flapping tremor/ confusion
cracked wheeze on auscultation

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26
Q

define type 1 respiratory failure

A

normal pCO2 and low pO2

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27
Q

define type 2 respiratory failure

A

raised pCO2 and low pO2

ie, COPD

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28
Q

effect of CO2 and HCO in lungs

A

^CO2= acidic (low pH)

^ HCO= basic (high pH)

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29
Q

2 rules for oxygen saturations in COPD

A
  1. if retaining CO2: aim for O2 at 88-92% with Venturi mask

2. not retaining CO2 + bicarbonate is normal: aim for oxygen sat 94% +

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30
Q

at home COPD exacerbation treatment

A

prednisolone
inhalers or nebulizers
antibiotics for infections

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31
Q

in hospital non severe COPD exacerbation treatment

A

nebulised bronchodilators
steroids
antibiotics for infection
physiotherapy for sputum

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32
Q

in hospital severe COPD exacerbation cases treatment

A

IV aminophylline
non-invasive ventilation, intubation
Doxapram

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33
Q

define pneumonia

A

inflammation of the lung parenchyma where normal air-filled lungs is filled with infective liquid known as consolidation

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34
Q

what are the three route for bacteria to reach the lungs

A

inhalation
aspiration
hematogenous

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35
Q

name the organisms involved in CAP: typical pneumonia

A

streptococcus pneumonia

haemophilus influenza

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36
Q

name the organisms involved in CAP: atypical pneumonia

A 
mycoplasma pneumoniae
coxiella burnetti (Q fever)
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37
Q

presentation of streptococcus pneumoniae

A

cough, pleuritic pain, pyrexia

leukocytosis and raised CRP

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38
Q

describe mycoplasma pneumoniae (type, patient type, symptoms, diagnostic)

A

rod shaped bacterium, no cell wall
young ppl
arthralgia, haemolytic anaemia
serology

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39
Q

define hospital acquired pneumonia

A

pneumonia contracted> 48 hours after hospital admission

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40
Q

organisms in hospital acquired pneumonia

A

gram negative bacteria:
pseudomonas aeruginosa
staphylococcus aureus
legionella pneumophila

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41
Q

describe pseudomonas aeruginosa (type, risk factor, sputum)

A

gram negative bacillus
immunosuppressed patients (ie, bronchiectasis due to cystic fibrosis)
green sputum

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42
Q

pseudomonas aeruginosa treatment

A

cephalosporin, amino glycoside

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43
Q

define aspiration pneumonia

A

inhalation of oropharyngeal or gastric contents

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44
Q

what type of patient may get aspiration pneumonia

A

neuro/muscular problems
oesophageal conditions
mechanical interventions like endotracheal tubes

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45
Q

complications of pneumonia

A

pulmonary effusion, pneumothorax

sepsis, AF

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46
Q

what does CURB-65 measure for

A

mortality risk of pneumonia

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47
Q

what does CURB-65 stand for

A 
C: confusion 
U: urea>7
R: respiratory rate> 30
B: blood pressure < 90/60
65 years of age or older
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48
Q

what does CURB-65 score mean

A

0-1=low risk/ mild
2= intermediate risk / moderate
3-5= high risk / severe

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49
Q

CAP treatment

A

mild: amoxicillin (use clarithromycin/ doxycycline instead for allergy)
moderate: amoxicillin + clarithromycin
severe: IV co-amoxiclav and clarithromycin

50
Q

2 types of lung cancer

A

small cell
non small cell (adenocarcinoma, squamous cell, large cell)

(also mesothelioma: asbestos)

51
Q

adenocarcinoma vs squamous cell

A

Adeno: non-smoker, lung peripheries
squamous: smoker, PTHcentral part of lungs (bronchus)

52
Q

unique features of small cell lung cancer

A

poor prognosis, fast doubling time
cancer of APUD (neuroendocrine) cell find in lungs
smokers

53
Q

symptoms that may present with small cell carcinoma

A

ectopic ADH/ACTH production (Cushing’s syndrome=^ cortisole)

weight gain, easy bruising and hyperpigmentation

54
Q

lung cancer: signs of pleural effusion

A

exudative
dull/ stony percussion
reduced vocal resoncance/ breath sound

55
Q

when should CXR be ordered for lung cancer

A

patient over 40 + concerning symptoms:

weightloss, hemoptysis

56
Q

diagnosis of lung cancer

A

CXR: focal lesion, pleural effusion , widen mediastinum

CT for suggestive CXR, include neck and upper abdomen for staging

57
Q

T in TNM staging

A

T0 - tumour not visible but found in sputum culture / bronchial fluids
T1 - 3cm or less
T2 - 3 < x

58
Q

N in TNM staging

A

N0 - no lymph node metastases
N1 - ipsilateral hilar lymph node
N2 - ipsilateral mediastinal or subcarinal lymph nodes
N3 - contralateral mediastinal or hilar lymph nodes

59
Q

M in TNM staging

A

M0 - no distant metastases

M1 - distant metastases

60
Q

cause and spread of TB

A

caused by mycobacterium spread via aerosolized droplets

61
Q

characteristics of mycobacterium

A

aerobes
facultative intracellular
acid fast bacilli

62
Q

primary vs progressive primary vs latent TB

A

prim: initial infection, suppressed in majority of individuals
1a. latent: non infectious state after primary infection
1b. progress: primary infection not suppressed, prolonged infection

63
Q

what is the ghon complex

A

lesion seen in children w/ TB

ghon focus+ ipsilateral mediastinal lymph node

64
Q

symptoms of TB

A

fever, weightless, malaise

65
Q

diagnosis of TB

A

Active: CXR, Ziehl-Neelson stain(AFB, langhans type giant cells)
Latent: Tuberculin skin test

66
Q

CXR findings in TB

A

Ghon focus
Bilateral hilar lymphadenopathy
Miliary shadowing

67
Q

active TB treatment

A
  • Rifampicin, Isoniazid, Pyrazinamide and Ethambutol for 4 months
  • Rifampicin and Isoniazid for a further 2 month
68
Q

latent TB treatment

A

Rifampicin and Isoniazid for 3 months
OR
Isoniazid for 6 months

69
Q

side effects of TB drugs

A

Rifampicin: hepatitis, orange urine/sweat
Isoniazid: peripheral neuropathy
Pyrazinamide: ^ uric acid, gout
Ethambutol: optic neuritis

70
Q

define pneumothorax

A

air in intrapleural cavity (between visceral pleura and parietal pleura)

71
Q

what are the 2 types of pneumothorax

A

spontaneous (no trauma)

traumatic (yes trauma)

72
Q

2 types of spontaneous pneumothorax and their risk groups

A

primary: no pathophysiological lungs (tall/thin male)
secondary: pathological lungs (50+ and COPD/ asthmatic patients)

73
Q

symptoms of spontaneous pneumothorax

A

sudden onset dyspnoea and chest pain
hyper resonance on percussions
decrease air entry

74
Q

what is tension pneumothorax

A

spontaneous pneumothorax patients who are hemodynamically (abnormal bp, arrhythmias) unstable

75
Q

tension pneumothorax treatment

A

urgent needle decompression inserted through 2nd intercostal space midclavicular line

76
Q

procedure for haem stable patients w/ spontaneous pneumothorax

A

send for CXR

77
Q

treatment for primary pneumothorax patients

A

large (>2cm) or breathless: needle aspiration (14-16G)

small (<2cm) and asymptomatic: outpatient followup

78
Q

treatment for secondary pneumothorax

A

(>2cm) or breathless: chest drain
(1-2) : needle aspiration (14-16G)
< 1cm: observe for at least 24h

79
Q

symptoms of traumatic pneumothorax

A

hypotension + tachycardia

chest pain + hypoxaemia

80
Q

treatment of traumatic pneumothorax

A

immediate needle decompression

81
Q

define bronchiectasis

A

irreversible + abndomal dilatation of airways

commonly secondary to cystic fibrosis

82
Q

what is the predominant inherited cause of bronchiectasis

A

primary ciliary dyskinesia

83
Q

symptoms of bronchiectasis

A

persistent sputum production and cough over years

may have immune disorders/ COPD

84
Q

diagnostic of bronchiectasis

A

high resolution CT scan

85
Q

what is bronchiectasis exacerbation

A

infections cause worsening symptoms

H. influenzae, S. aureus, P. aeruginosa, and S. pneumoniae.

86
Q

define cystic fibrosis

A

autosomal recessive mutations to the CFTR gene on the long-arm of chromosome 7

87
Q

when and what test is used to screen CF

A

day 5 after birth

newborn heel prick test (measure Immuno-reactive trypsin)

88
Q

what are some confirmatory testings for CF

A

Sweat test: sweat chloride > 60mmol/L = +++

Genetic testing: screen for common mutations or entire CFTR gene

89
Q

define pleural effusion

A

abnormal collection of fluid in pleural cavity (between visceral pleura and parietal pleura)

90
Q

what are the 3 serous membranes that line the lung

A

Visceral pleura: inner layer. Covers the lungs, blood vessels and bronchi
Pleural space: Contains ~10 mL of fluid
Parietal pleura: outer layer. Attaches to the chest wall

91
Q

function of pleural cavity fluid

A

Lubricates: easier for the layers to slide over one another during respiration
Generates surface tension: pulls the two layers (parietal and visceral) adjacent to one another

92
Q

where does the pleural cavity get the liquid from?

A

vessels at the parietal and visceral pleura

93
Q

define hydrostatic pressure and the role it has on pleural cavity fluid

A

Hydrostatic: pressure exerted by a fluid against a membrane, Increases lead to fluid leaking from blood vessels

94
Q

define oncotic pressure and the role it has on pleural cavity fluid

A

Oncotic pressure: osmotic pressure produced by large macromolecules (e.g. proteins). Exerts a ‘pulling power’ on fluid

95
Q

define lymphatic drainage and the role it has on pleural cavity fluid

A

Lymphatic drainage: drains body fluid and returns it to the systemic circulation. Can alter the hydrostatic pressure

96
Q

3 reasons that increase fluid entry to pleural cavity

A

Increased vasculature permeability
Increased microvascular pressure
Decreased plasma oncotic pressure

97
Q

what causes Increased vasculature permeability

A

infection, malignancy: loss of fluid and macromolecules from ‘leaky’ vessels

98
Q

what causes increase microvascular pressure

A

heart failure: increased venous pressure affects hydrostatic pressure forcing fluid out

99
Q

what causes decreased plasma oncotic pressure

A

cirrhosis: leading fluid accumulation

100
Q

transudative vs exudative pleural effusion

A

Transudate: no protein/ cellular content, due to change in hydrostatic and oncotic pressure (HF, cirrhosis)

Exudate: high protein/ cellular content, from inflammatory conditions that affect vessel permeability /lymphatic drainage. (infection/ malignancy)

101
Q

symptoms of pleural effusion

A

reduced vocal resonance/ breath sounds
stony dull percussion
SOB + non productive cough

102
Q

diagnostic of pleural effusion

A

CXR

103
Q

symptoms of pulmonary embolism

A

SOB, pleuritic chest pain, pleural rub,

sinus tachycardia, DVT symptoms

104
Q

diagnostic of PE

A

well’s score 4+: CTPA, not available-> anticoagulation if safe.
well’s score ≤ 4: d-dimer . positive= send for CTPA

105
Q

what is d-dimer

A

fibrin-degradation product, produced when blood clots are broken down by fibrinolytic system

106
Q

management for PE/ DVT initial and long term

A

initial: apixaban or rivaroxaban-> LMWH-> thrombolysis

long term: warfarin, a DOAC or LMWH

107
Q

key features of sarcoidosis

A

mostly black
CXR: Bilateral hilar lymphadenopathy
red lesions/ erythema nodusum

108
Q

key features of pulmonary fibrosis/ interstitial lung disease

A

chronic exertion dyspnea
honeycombing (clusters of cystic air spaces)
reticular opacities

109
Q

TLC formula

A

VC+ RV

vital capacity + residual volume

110
Q

describe type 1 pneumocytes

A

thin squamous cell covering 97% of alveolar surface

111
Q

describe type 2 pneumocytes

A

cuboidal cells, secret surfactant

may not produce enough until 35 weeks causing premature babies being prone to respiratory distress

112
Q

law of Laplace+ example

A

tension/ pressure exerted on spherical wall, is inversely proportional to sphere’s thickness (thin wall=more pressure/tension)
ie, alveoli are prone to collapse due to alveolar surface tension and surfactant increase alveolar thickness reducing surface tension

113
Q

describe coup symptoms and treatment

A

inspiratory stridor, cough, and hoarseness

dexamethasone and supportive care

114
Q

What does wells score PE look for

A 
Clinical signs of DVT 
PE is likely 
Tachycardia > 100
Surgery in the past Monet 
Prior DVT/PE
Haemoptysis
Malignancy
115
Q

Treatment for HAP

A

Amoxicillin and metronidazole

If sevré give in IV form

116
Q

Acute exacerbation of asthma treatment

A 
oxygen (94-98%)
salbutamol (neb)
Hydrocortisone (IV) OR oral prednisolone
Ipratropium (neb)
Theophylline (oral)
Magnesium sulphate (IV)
An anesthetist (to intubate)
117
Q

Acute exacerbation of COPD treatment

A 
Ipratropium
Salbutamol
oxygen (target 88-92%)
Amoxicillin (/doxycycline)
Prednisolone
118
Q

Define tidal vs vital volume

A

Tidal: normal passive air intake and out
Vital: force inspiration and expiration

119
Q

Sevré asthma symptoms

A
120
Q

Life threatening asthma symptoms

A

first year revision (5 decks)

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