RESP ashtma Flashcards

1
Q

what are three characteristics of asthma?

A
  1. airflow limitation
  2. airway hyper-responsiveness
  3. Bronchial inflammation
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2
Q

what causes inflammation in airways?

A
  • Increase in mast cell mediated release of histamine, tryptase, PGD2 and cytokines
  • increase eosinophils in the bronchial wall releasing LTC4
  • Increase CD4
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3
Q

what are the results of lung function tests in asthma?

A
  • peak expiratory flow rate before and after using a bronchodilator
  • spirometry will show an obstructive condition
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4
Q

what is the step wise management of asthma?

A
  1. SABA
    • Low dose corticosteroids
  2. +LABA
  3. +high dose inhaled corticosteroids and regular bronchodilator
    • oral corticosteroid
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5
Q

how are SABAS used in asthma?

A

Salbutamol 100mg. Can be used in any step

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6
Q

when are inhaled low dose corticosteroids used in asthma treatment?

A

From step 2 (with SABA)

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7
Q

what are unwanted effects of inhaled corticosteroids?

A

oral candidiasis

hoarseness

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8
Q

What are signs of an asthma attack?

A
  • inability to complete a sentence in one breath
  • RR>25
  • tachycardia >110
  • PEFR<50%
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9
Q

what is management of an asthma attack?

A

Nebulised SABA
CXR to exclude causes
oral prednisolone

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10
Q

how does SABA work?

A

A beta 2 agonist

smooth muscle relaxation on the bronchi

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11
Q

what are the major side effects of SABA?

A
tachycardia
fight or flight effects
- palpitations
- anxiety
-tremor
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12
Q

how do leukotriene antagonists work?

A
  • bronchodilator and anti inflammatory effect

- stop the formation of LTC4,LTD4,LTR4 which are all pro inflammatory

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13
Q

what drug should you not give an asthmatics?

A

NSAIDS especially COX 1 specific

Beta blockers (bronchoconstriction)

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14
Q

what is the emergency management for life threatening asthma?

A

Nebulised oxygen and salbutamol Hydrocortisone
Ipratropium
Magnesium sulphate if they get resp acidosis

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15
Q

what is the role of NIV in the management of acute asthma?

A

It has no place here

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16
Q

what are features of severe asthma?

A
  • peak flow 33-50% of predicted
  • RR>25
    HR >110
  • Can’t complete sentences
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17
Q

what are features of life threatening asthma?

A
  • peak flow <33% predicted
  • oxygen sats <92%
  • hypoxic
  • silent chest cyanosis
  • bradycardia
  • hypotension
  • exhaustion
  • confusion
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18
Q

what is the emergency management of asthma for someone coming into A and E?

A
O- nebulised oxygen
S-salbutamol
H- hydrocortisone
I- ipratropium
M- magnesium sulphate if they get resp acidosis
T-theophiline
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19
Q

what symptoms are experienced by people with COPD?

A
  • COB
  • productive cough
  • increased sputum
  • frequent bronchitis
  • pursed lipped breathing
  • red faced
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20
Q

what are the systemic symptoms of COPD?

A
  • cachexia
  • increased CRP leading to increased CVS risk
  • normochromic normocytic anaemia
  • systemic inflammation
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21
Q

what clinical signs are found in people with COPD?

A
  • nicotine stained fingers due to heavy smoking
  • pursed lip breathing
  • breathing with accessory muscles
  • barrel chested
  • reduced expansion
  • crackles
  • soft heart sounds
  • hypercapnia
  • hyperinflation
  • liver problems if there is an AAT deficiency.
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22
Q

what anatomical changes are involved in the pathophys of COPD?

A

Proximal airways:
- trachea and cartilagenous airways become enlarged >2mm due to submucosal bronchial enlargment, squamous metaplasia of the airway epithelium and increased smooth muscle

The peripheral airways become <2mm as there is increased macrophages ND FIBROBLASTS.

  • alveolour wall destruction and emphysema
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23
Q

where is centrilobular emphysema?

A

Main in the upper lobes associated with smokers.

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24
Q

what is panacinar emphysema?

A

Destruction of the acinus seen in AAT deficiency. affects the lower zomes

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25
Q

what are the three main processes in COPD development?

A
  1. inflammation
  2. protease and anti-protease imbalance
  3. oxidant and anti oxidant imbalance
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26
Q

what is the inflammation seen in COPD?

A
  1. cigarrete smoke activates macrophages and epithelial cells
  2. release of chemotactic factors
  3. recruitment of neutrophils and CD8 (CD8>CD4)
  4. activation of fibroblasts
  5. abnormal repair and bronchiolar fibrosis
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27
Q

What is the problem of the increased protease activity in COPD?

A

they lead to increased alveolour wall destruction and cause mucous release

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28
Q

what proteases are released from neutrophils in COPD?

A

elastase, cathepsin G, protease 3

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29
Q

what proteases come from macrophages in COPD?

A

cysteine protease

cathepsins EALS

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30
Q

what are the main ant proteases that you lack in COPD?

A

AAT#secretory leucoprotease inhibitor

tissue inhibitor of MMP

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31
Q

what causes the increased oxidative stress in COPD?

A

activation of antiproteases, stimulation of mucous production
oxidants come from cigRETTE SMOKE.

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32
Q

what are some causes of COPD?

A
AAT1 deficiency
smoking
ashtma/ airway hyperactivity 
recurrent infections
dust mining
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33
Q

what spirometry figures are for mild airflow obstruction in COPD?

A

FEV 50-80%

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34
Q

what spirometry figures are for moderate airway obstruction in COPD?

A

FEV: 30-49%

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35
Q

what spirometry figures are for severe airway obstruction in COPD?

A

FEV <30%

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36
Q

what may be seen in a chest xray of a COPD patient?

A

hyperinflation of the lungs
flattening of the diaphragm
bullae
large proximal vessels

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37
Q

what can be seen in the ECG of a COPD patient?

A

RVH
right axis deviation
big P waves

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38
Q

what main drugs are used in smoking cessation?

A

bupropion/zyban
varenicline/ chantix
Cytisine

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39
Q

what is bupropion?

A

Used for smoking cessatation and reduces cravings

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40
Q

what are side effects of bupropion?

A

dry mouth
problems sleeping
behaviour changes

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41
Q

who shouldn’t take bupropion?

A

pregnant

under 18

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42
Q

what is varenicline?

A

Oral partial agonist of nicotonic Ach receptor to reduce withdrawal and craving.

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43
Q

what are types of bronchodilators?

A

Beta agonists

Anti cholinergics

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44
Q

what are examples of SABA used in COPD?

A

anti cholinergic: ipratropium

Beta 2: albuterol

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45
Q

why are corticosteroids used in COPD?

A

to improves symptoms, lung function and aid chronic inflammation

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46
Q

what is the problem of giving corticosteroids in COPD?

A

increased risk of pneumonia

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47
Q

what is theophyline?

A

A bronchodilator that blocks conversion of Camp.

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48
Q

what are adverse effects of theophylline?

A
nausea
hypokalaemia
abdominal pain
headache
diarrhoea
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49
Q

what are complications of COPD?

A
Cor pulmonale 
Depress
Resp failure
Increased infections
Polycythaemia
Pulmonary hypertension
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50
Q

what causes cor pulmonale in COPD?

A

Pulmonary hypertension due to peripheral vascular constriction. this leads to right ventricular hypertrophy.

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51
Q

what is the main organism respinsible for infection in COPD?

A

haemophillus influenzae B

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52
Q

why can COPD patients get polycythaemia?

A

COPD causes hypoxia causes excess EPO leading to increased red blood cells

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53
Q

what is the emergancy maanagement in a patient presenting with IECOPD?

A
  1. sit up
  2. stop any sedatives
  3. salbutamol (bronchodilator)
  4. ipratropium
  5. antibiotics
  6. corticosteroids
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54
Q

what is the oxygen target in COPD?

A

88-92%

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55
Q

what organisms are common in COPD patients?

A

haemophilus influenzae B
Strep pneumonia
moraxella catarhallis

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56
Q

what are the consequences of hypoxia?

A
Polycythaemia
cerebral ischaemia
myocardial ischaemia
tumour angiogenesis
pulmonary vasoconstriction
Peripheral vessel vasodilation
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57
Q

what are the consequences of hypercapnia?

A
acidosis
cerebral vasodilation
hypoxia
mild: increased RR
severe: decreased RR
58
Q

what is type 1 resp failure?

A

oxygen below 8kpa

59
Q

what is type 2 resp failure?

A

oxygen below 8

carbon dioxide above 6

60
Q

what are the three areas of the brain that control breathing?

A
  1. inspiratory centre
  2. pneumotaxic centre
  3. expiratory centre
61
Q

what are symptoms and signs of pulmonary TB?

A
long term cough
pleurisy
haemoptysis
pleural effusion
systemic symptoms
62
Q

what is the microbiology of TB?

A

ziehl neelsen or auramine rhodamine staining

nucleic acid amplification

63
Q

what is the pathophys of pulmonary TB?

A

inhalation of the bacteria
ingestion of the bacteria by alveolour macrophages
bacteria will proliferate in the macrophages
release of neutrophil chemoattractants and cytokines
inflammatory cell infiltrate will reach the lung and hilar lypmh nodes
macrophages present to T cells
cellular response of a delayed hypersensitivity reaction
tissue necrosis and granuloma formation

64
Q

what is a granuloma lesion in TB?

A

there is a central necrotic caseation surrounded by epitheliod cells and langhans giant cells both from macrophages

65
Q

how do you investigate TB?

A
  • ziehl nelson stainin
  • culture
  • nucleic acid amplification
  • CXR
  • sputum smear for acid fast bacilli
  • mantoux testing
66
Q

what is the size needed of the mantoux testing area for TB?

A

> 5mm if there are risk factors

>15mm if there are no risk factors

67
Q

what drugs are used to treat TB?

A

Rifampicin
Isoniazid
Pyrazinamide
Ethambutol

68
Q

how is rifampicin given for TB?

A

2 months intensive and 4 months continuation

69
Q

when should rifampicin be stopped?

A

when it causes more than 3x elevation of bilirubin or transferases

70
Q

what are side effects of isoiazid?

A
  • polyneuropathy if causing a B6 deficiency

- hepaitits so give with pyridoxine

71
Q

when should you change the dose of pyrazinamide?

A

GFR <30

72
Q

what are effects of ethambutol?

A

retrobulbar neuritis
colour blindness
change in visual acuity

73
Q

what is primary TB?

A

the first infection with the myobacterium.

74
Q

what factors are involved in the reactivation of latent TB?

A

HIV, immunosuppresion, diabetes, end stage CKD, malnutrition, ageing.

75
Q

what is the mantoux test?

A

A screening test for TB

if positive will cause a delayed hypersensitivity reaction and raised skin lesion

76
Q

why does a positive mantoux test cause a raised skin lesion?

A

Previous infection means T cells are sensitised and will be recruited to the injection site.
T cells will cause release of lymphokines which cause vasodilation, oedema, fibrin deposition and recruitment

77
Q

what are indications for the BCG vaccine?

A
  • all infants where the annual incidence is greater than 40/100,000
  • all infants with a parent or grandparent born in a country where the risk is greater than 40/100,000
  • occupational risk
  • travel risk
78
Q

what are features of a tension pneumothorax?

A
  • sudden onset unilateral -pleuritic chest pain
  • SOB
  • chest tightness
  • hypotension
  • tachycardia
  • distended neck veins
  • tracheal deviation
79
Q

what is the emergency management of a tension pneumothorax?

A
  • rapid decompression in the 2nd intercostal mid clavicular line
  • thoracostomy in the 5th intercostal space mid auxillary line
80
Q

what are causes of a pneumothorax?

A
  • trauma
  • spontaneous in tall, thin people
  • ashtma
  • COPD
  • cystic fibrosis
  • carcinomas
  • connective tissue disorders
81
Q

what investigations should be done for a pneumothorax?

A
  • CXR
  • reduced breath sounds
  • hyperesonant on percussion
  • ABG
82
Q

what is the management of a pneumothorax?

A
  • no SOB and <2cm = conservative watch and wait
  • SOB and air space >2cm–> needle aspiration in the 2nd intercostal space mid clavicular line

chest drain if unsuccessful

83
Q

what are signs of pneumonia?

A
fever, chills
increased sputum production, SOB, pleuritic pain
-crackles
- cyanosis
- dull percussion
- pleuritic chest pain
- myalgia
84
Q

what pneumonia causes rust coloured sputum?

A

pneumococcal

85
Q

what are risk factors for CAP?

A
  • aged under 16 or over 65
  • Co morbidities such as D.M, CKD, malnutrition
  • respiratory conditions
  • smoking, alcohol, IV drugs
  • immunosuppresed
86
Q

what are the main causes of pneumonia CAP?

A
  • strep pneumoniae
  • haemophillus
  • staph aureus
87
Q

what are the main causes of HAP?

A
  • gram negatives

- staph aureus

88
Q

what causes atypical lower resp infections?

A
  • chlamydia pneumoniae
  • mycoplasma pneumoniae
  • legionella pneumoniae
89
Q

what signs suggest an atypical is responsible for pneumonia?

A
  • symptoms emerge slower
  • low grade fever
  • dryer cough
  • more mild
90
Q

how do you determine the severity of pneumonia?

A

CURB 65?

91
Q

what is CURB 65?

A
  1. confusion using AMTS score
  2. urea >7
  3. resp rate >30
  4. BP <90/60
  5. aged 65 or over
92
Q

what do different CURB 65 scores mean?

A
0-1 = outpatient treatment
2= admit to hospital 
3= consider intensive care
93
Q

why can a urine sample be helpful in pneumonia diagnosis?

A

check for legionella and pneumococcal antigens

94
Q

what antibiotics are effective against strep pneumoniae?

A

penicillin

erythromycin

95
Q

what antibiotic is helpful in aspiration pneumonia?

A

metronidazole

96
Q

what antibiotics are often used for HAP?

A
  • aminoglycoside with penicillin/ 3rd gen cephalosporin
97
Q

what antibiotics are often used for legionella?

A

fluoroquinolone with rifampicin or clari

98
Q

what antibiotics is often given for chlamydiophilia pneumoniae?

A

tetracycline

99
Q

who should get the pneumococcal vaccine?

A

All adults over 65
chonic heart, liver or renal conditions
- DM
- immunosupresion

100
Q

what are signs and symptoms of a DVT?

A
  • asymptomatic
  • PE features
  • calf pain
  • warmth on the site
  • homans sign
  • mild fever
  • pitting oedema
101
Q

what are risk factors for DVT/PE?

A
  • malignancy or treatment
  • age >60 years
  • long distance flight
  • known thrombophilia
  • BMI>30
  • Personal history/ family history of VTE
  • varicose veins with phlebitis
  • pregnancy and childbirths
  • COCP
102
Q

what is in wells score?

A

1, active cancer or treatment within the last 6 months

  1. Paralysis, paresis or immobilisation of the leg.
  2. Recently bedridden for over 3 days or major surgery in the last 12 weeks
  3. Local tenderness along distribution of leg venous system
  4. Entire leg swollen
  5. Calf swelling >3cm compared with asymptomatic leg
  6. Pitting oedema
  7. Collateral superficial veins
  8. Previously documented DVT
  9. The alternative diagnosis is at least as likely as DVT
103
Q

what investigations do you do for a suspected DVT?

A

D dimer
doppler ultrasound
- venogram

104
Q

what is the MOA of LMWH?

A

inhibits thrombin and factor X

105
Q

what is the MAO of warfarin?

A

inhibits hepetic production of vitamin K dependant clotting factors

106
Q

what makes a patient moderate risk for DVT/PE for travel?

A
  • previous history of DVT/PE
  • surgery in the past 2 months but not in the past 4 weeks
  • pregnant/postpartum
  • cardiac disease
  • HRT/COCP
  • BMI >30
  • Varicose veins with phlebitis
  • first degree relative with a thromboembolism history
  • polycythaemia
  • ## lower limb fracture in plaster
107
Q

what advise is given to people travelling at moderate risk of DVT/PE?

A
  • General advise

- compression stockers

108
Q

what puts patients at high risk of a DVT/PE when travelling?

A
  • surgery in the past four week
  • known thrombophilia
  • cancer
109
Q

what adive is given to high risk patients of DVT/PE when travelling?

A

recommend delaying/ cancelling

  • general advise
  • compression stockings
  • LMWH
110
Q

what are symptoms/signs of a PE?

A
  • sudden SOB
  • tachycardia
  • elevated JVP
  • pleuritic chest pain
  • haemoptysis
  • syncope
  • hypotension
  • gallop rhythm
111
Q

what imaging is helpful in suspected PE?

A
  • V/Q scanning

- CTPA

112
Q

what are the clinical featuers of a massive PE?

A
severe central chest pain
shocked, pale and sweating
syncope
raised JVP
right ventricular heave
113
Q

what is the management of PE?

A
  • high flow oxygen
  • anticoagulation with fondaparinux or LMWH
  • thrombolysis with alteplase
114
Q

what is the clinical definition of COPD?

A

progressive airway obstruction which doesn’t change over months, persistant and poorly reversible

115
Q

what is the definition of chronic bronchitis?

A

cough productive of sputum for 3 consecutive months for 2 consecutive years with no other cause

116
Q

what is emphysema?

A

permanent dilatation of the airways distal to the terminal bronchiole, dilations due to destruction of alveolour walls

117
Q

how does smoking effect the bronchi?

A

hyperplasia of mucus producing glands in the submucosa and hyperplasia of goblet cells on the surface epithelium meaning increased sputum production

118
Q

how does smoking affect smaller airways?

A

chronic inflammation leads to fibrosis healing causing stenosis

119
Q

in COPD there is destruction of alveolour walls, what are the two main effects of this destruction?

A
  • loss of pulmonary surface area leading to hypoxia

- loss of elastic tissue in the terminal airways leading to a loss of natural recoil meaning reduction in airflow

120
Q

what are causes of acute exacerbations fo COPD?

A
  • infection
  • pneumothorax
  • PE
    = LVF
  • lung carcinoma
121
Q

what are the common causes of infective exacarbations of COPD?

A

h. influenzae
M. catarrhalis
S pneumonia
virus

122
Q

why can COPD cause pulmonary hypertension?

A
  • emphysema
  • hypoxia causes pulmonary vasoconstriction
  • increased EPO MEANING INCREASED BLOOD VISCOSITY
123
Q

what is pulmonary hypertension?

A

an increase in blood pressure in the pulmonary vasculature above 25

124
Q

what is pneumonia?

A

inflammation of the lung parenchyma due to infection

125
Q

what is bronchopneumonia?

A

widespread patchy inflammation centred on the airways often bilateral

126
Q

what is lobar pneumonia?

A

diffuse inflammation affecting the entire lobes or lobe.

127
Q

what is the most common cause of mild CAP?

A

s.pneumoniae

128
Q

what are important causes of severe CAP?

A

s.pneumoniae
legionella
s.aures

129
Q

what are diffuse parenchymal lung disease?

A

conditions characterised by inflammation centres on the interstitum of alveolour walls

130
Q

Pneumoconioses are a cause of DLPD what does this mean?

A

That it is caused by inhaled inorganic dusts often mineral for example coal dust, silica or asbestosis

131
Q

extrinsic allergic alveolitis are a cause of DLPD what does this mean?

A

inhaled organic particles are to blame for example pigeon poo or farmers lung

132
Q

what multisystem diseases can cause DLPD?

A

Sarcoid, SLE,RA, scleroderma, sjogrens, polymyositis, dermatomyositis

133
Q

how do you diagnose DPLD?

A
  • CXR
  • CT shows reticulation
  • lung biopsy
134
Q

what are long term complications of DLPD?

A

cor pulmonale

pulmonary heart failure

135
Q

what are the majority of lung cancers?

A

Adenocarcinoma

136
Q

what is the most common sit of metastatic caner?

A

The lung

137
Q

what lung cancers have a strong association with smoking?

A
Small cell (strongest association)
squamous cell
138
Q

where dpes squamous cell carcinoma tend to arise?

A

larger airways near the hilum

139
Q

what is the most common type of lung cancer in non smokers?

A

adenocarcinoma

140
Q

what gene can adenocarcinomas be assoicated with?

A

EGFR

141
Q

where do adenocarcinomas tend to arise?

A

peripheral smaller airways

142
Q

where do small cell carcinomas tend to arise?

A

centrally