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Year 2 > Resp: Lung Cancer metastases, Mestholeioma, Goodpasture's Syndrome, Wegener's granulomatosis, Pulmonary thromboembolism, Upper Respiratory Tract Infections, Pharyngitis/Tonsilitis, Epiglottis > Flashcards

Resp: Lung Cancer metastases, Mestholeioma, Goodpasture's Syndrome, Wegener's granulomatosis, Pulmonary thromboembolism, Upper Respiratory Tract Infections, Pharyngitis/Tonsilitis, Epiglottis Flashcards

1
Q

What macrophages tend to be involved in pneumoconiosis and out immune-mediated lung problems

A
  1. ALVEOLAR macrophage

2. INTERSTITIAL macrophages (which live in the lung parenchyma)

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2
Q

What is Caplan’s Syndrome

A

Caused in all types of pneumoconiosis:

  1. Rheumatoid Arthritis
  2. Pneumoconiosis

basically a person with RA has a bigger risk of developing pneumoconiosis, asbestosis, silicosis etc.

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3
Q

What particles size are most dangerous in pneumoconiosis and why

A

1-5 micrometers

This is because 5-10 won’t make it to the alveoli and less than 1 micrometers can be inhaled back out without causing difficulties

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4
Q

Sites of metastatic spread form lung cancer

A
  1. Liver (anorexia, nausea, weight loss, right upper quadrant pain)
  2. Bone (bony pain)
  3. Adrenal Glands
  4. Brain (space occupying lesions)
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5
Q

What cancers spread tot helpings

A
  1. Breast cancer
  2. Bowel cancer
  3. RENAL CELL CARCINOMA
  4. Bladder cancer
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6
Q

Clinical presentation of lung cancer

A
  1. Cough
  2. Breathlessness
  3. Haemoptysis
  4. Chest pain
  5. Wheeze
  6. Clubbing
  7. Recurrent pneumonia
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7
Q

Symptoms of metastictic disease

A
  1. Bone pain
  2. headaches
  3. Seizures
  4. Neurological deficit
  5. Hepatic pain
  6. Abdo pain
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8
Q

Factors of paraneoplastic changes in the lung

A
  1. PTH secretion
  2. Inappropriate ADH secretion
  3. Secretion of ACTH
  4. Hypertrophic pulmonary osteo-arthropathy
  5. Finger clubbing
  6. Non-infective endocarditis
  7. DIC
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9
Q

What is T1

A

< 3cm

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10
Q

What is T2

A

> 3 cm

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11
Q

What is T 3

A

Invades chest wall , diaphragm and mediastinum

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12
Q

What is T4

A

Invades mediastinum, heart, great vessels, teaches, oesophagus, vertebra, carina (bifurcation of the bronchi)

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13
Q

What is N0

A

No Nodes
N1 - hilar nodes
N2 - Same side as mediastinal nodes
N3 - Contralateral mediastinum effected

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14
Q

What is m1a

A

Tumour on same side

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15
Q

What is m1b

A

Tumour is elsewhere

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16
Q

Diagnosis of lung cancer

A
  1. CXR
  2. CT
  3. Bronchoscopy
  4. Cytology
  5. FBC
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17
Q

Appearance of lung cancer on CXR

A
  1. ROUND SHADOWS with spikes edges
  2. Hilar enlargement
  3. Lung collapse
  4. Pleural effusion
  5. Consolidation
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18
Q

Why is a CT used in lung cancer

A

STAGING

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19
Q

Role of bronchoscopy and endobronchial ultrasound for lung cancer

A

Histology and assess operability

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20
Q

Role of cytology in lung cancer

A

Sputum and pleural fluid analysis

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21
Q

How is non-small cell lung cancer treated

A
  1. SURGICAL EXCISISON
  2. Curative radiotherapy if pneumonitis and fibrosis is seen
  3. Chemotherapy and radiotherapy (CETUXIMAB)
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22
Q

How is small cell lung tumours treated

A 
1. CHEMO AND RADIO 
Usually results in relapses
2. Palliation to relief symptoms 
3. Superior vena cava stent + radiotherapy and dexamethasone to treat obstruction
4. Endobronchial therapy 
5. Pleural drainage
6. Drugs
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23
Q

Why is radiotherapy use din lung cancer

A
  1. Bronchial obstruction
  2. Haemoptysis
  3. Bone Pain
  4. Cerebral metastases
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24
Q

What is endobronchial therapy

A
  1. Tracheal stunting
  2. Cryotherapy
  3. Brachytherapy (radioactive source is placed close to tumour)
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25
Q

What drugs are given in lung cancer

A
  1. Analgesics
  2. Steroids
  3. Antiemetics
  4. Codeine
  5. Bronchodilators
  6. Antidepressants
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26
Q

What is mesothelioma

A
  1. Tumorus of mesothelial cells of the pleura
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27
Q

Where are mesothelial cells found other than lung pleura

A
  1. Peritoneum
  2. Pericardium
  3. Testes
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28
Q

At what age does mesothelia present

A
  1. 40-70 years
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29
Q

What causes mesothelioma

A

ASBESTOS

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30
Q

What is th latent period of mesothelioma

A

UP to 45 years

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31
Q

Pathophysiology of mesothelioma

A
  1. Tumour begins as nodules in pleura which extend to surrounding lung and fissures
  2. Chest wall invaded and infiltrate intercostal nerves = SEVERE PAIN
  3. Invasion of lymphatics - hilar node metastases
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32
Q

Clinical presentation of mesothelioma

A
  1. Chest pain
  2. Dyspnoea
  3. Weight loss
  4. Finger clubbing
  5. Recurrent pleural effusions
  6. Breathlessness
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33
Q

Signs of mesothelioma metastases

A
  1. Lymphadenopathy
  2. Hepatomegaly
  3. Bone pain
  4. Abdo pain
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34
Q

Diagnostics of mesothelioma

A
  1. CXR + CT
  2. Bloody pleural fluid
  3. Pleural biopsy
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35
Q

Role of CXR and CT in mesothelioma

A
  1. Unilateral pleural effusion

2. Pleural thickening

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36
Q

Treatment of mesothelioma

A
  1. Surgery excision

2. RESISTANT to chemotherapy and radiotherapy

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37
Q

What is the average diagnosis to death in mesothelioma

A

8 months

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38
Q

Why are conducting airways (bronchi) in the lungs worse for drug delivery than respiratory regions (alveoli etc)

A

Have a smaller surface area and lower regional blood flow

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39
Q

What makes an effective drug

A
  1. RAPID ABSORPTION (small hydrophobic molecules)
  2. PARTICLE SIZE (not too small as they will be exhaled or too big as they will deposit in th upper airways)
  3. Inhalation technique
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40
Q

Advantage of a spacer

A
  1. Slows down particles of the drug and allow more time for evaporation of the propellant so more of the drug can be inhaled
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41
Q

What is the inhaler’s full name

A

PRESSURISED METERED-DOSE INHALERS

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42
Q

What are dry powder inhaler

A
  1. The device releases a small amount of drug in powder form which is inhaled (must have high inspiratory effort)
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43
Q

Pro of nebulisers

A

No coordination required by user

High dose delivery

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44
Q

Why do inhaled medications have to be done multiple times a day

A

They are absorbed and cleared from th blood very fast

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45
Q

What characteristics of inhaled drugs allow them to stay in th body for a long time

A
  1. SOLUBILITY
  2. Charge and tissue retention can increase half-life
  3. Encnapsulation
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46
Q

Advantages of inhaled drugs

A
  1. RAPID ABSORPTION
  2. LARGE SA
  3. NON-INVASIVE
  4. FEW METABOLISING ENZYMES
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47
Q

How do B2 adrenoceptor agonists work (2)

A
  1. Smooth muscle relaxation

2. Inhibit histamine release by mast cells

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48
Q

What drug is given when bronchoconstriction is being caused by parasympathetic nerve stimulation

A

ATROPINE

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49
Q

In what conditions are glucocorticoids (corticosteroids) not given and why

A

INEFFICIENT: COPD. CF and IPF

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50
Q

What ICS is commonly used

A

BECLOMETASONE DIPROPIONATE

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51
Q

Why are SABAs given alongside ICS

A
  1. ICS increases transcription of B2 receptors and B2 agonists increase translocation of GR from cytoplasm to nucleus
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52
Q

What condition is bronchiectasis associated with

A

CF

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53
Q

What antifriobtic medication is given in IPF

A
  1. PIRFENIDONE

2. NINTEDANIB

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54
Q

How does PIRFENIDONE work

A

REDUCES:

  1. Fibroblast proliferation
  2. Collagen production
  3. Production of fibrogenic mediators
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55
Q

How is Pirfenidone taken

A

Orally

56
Q

What is NINTEDANIB

A

Tyrosine Kinase inhibitor

57
Q

How do Tyrosine Kinsase inhibitors work

A
  1. Inhibit VEGFR)
58
Q

How is NINTEDANIB taken

A

Orally

59
Q

What cause type I respiratory failure

A
  1. AIRWAY AND PERFUSION problems
60
Q

What causes type II respiratory failure

A

Failure of ventiltion

61
Q

Clinical presnetation of airflow obstruction

A
  1. Obstructive sleep apnoea
  2. Relaxation of the pharynx during sleep
  3. Occlusion causes waking
62
Q

What causes continuous positive airways pressure

A
  1. Pulmonary oedema

2. Obstructive sleep apnoea

63
Q

What respiratory failure is caused in Bi-level positive airway pressure

A

TYPE II

64
Q

What causes Bi-level positive airway pressure

A
  1. COPD exacerbation

2. MND

65
Q

What is good pasture’s syndrome

A
  1. Co-existence of acute glomerulonephritis and pulmonary alveolar haemorrhage due to the presence of antibodies directed against antigens of the basement membrane of the kidney addling
66
Q

When is good pasture’s syndrome common

A

Over 16 in men

67
Q

Type hypersensitivity in good pasture’s

A

Type II

68
Q

Clinical presentation of good pasture’s syndrome

A
  1. Upper resp infection (sneezing, nasal discharge, runny nose and fever)
  2. Cough
  3. Intermittent haemoptysis
  4. Tiredness
  5. Anaemia
  6. Acute glomerulonephritis
69
Q

Differential diagnosis of good pasture’s syndorme

A

Idiopathic pulmonary hemaosiderosis
SLE
RA

70
Q

How is good pasture’s diagnosed

A
  1. Anti-basement membrane antibodies in the blood
  2. CXR (shows shadows due to haemorrhage in lower zones)
  3. Kidney biopsy (crescentic glomerulonephritis)
71
Q

How is good pasture’s treated

A
  1. Some improve
  2. Treat shock and renal failure
  3. IMMUNOSPRESSION (PREDNISOLONE AND PLASMAPHERESIS)
72
Q

What is plasmapheresis

A

Remove blood and clean to remove offending antibodies before inserting it back

73
Q

What is WEGENER’s GRANULOMATOSIS

A
  1. ANCA-associated vasculitis

Multisystem disorder of unknown origin where there are necrotising granulomatous inflammation and vasculitis of small and medium sized vessels

74
Q

What does ANCA stand for

A

Anti-neutrophil cytoplasmic antibody

75
Q

What causes vasculitis in WGENER’s

A

GRANULOMAS

76
Q

Pathophysiology of WGeNER’s

A

As neutrophil rolls along blood vessel before emigrating into tissues, autoantibodies bind to it and activate neutrophils inappropriately causing more recruitment when there is no infection
2. Production of reactive oxygen species and neutrophil degranulation
3.
Microabcessess, recruiting of monocytes, macrophages and lymphocytes

77
Q

Clinical presentation of WEGENER’s

A
  1. Leisons of URT, Lnugs and kidneys
  2. SEVERE RHINORRHEA
  3. Casal mucosal ulceration due to rihnorhhea- CHARACTERISTIC ‘saddle-nose deformity’
  4. Cough
  5. Pleuritic chest pain
  6. Haemoptysis
  7. Renal disease
  8. Skin purport or nodules, peripheral neuropathy and arthritis
78
Q

Differential diagnosis of wagerer’s

A

CHURG-STRAUSS syndrome

79
Q

What is Churg-strauss syndrorme

A

Small arteries effected but causes asthma and eosinophilia

80
Q

Diagnosis of WEGENER’s

A

1, FBC (c-ANCA is positive, elevated PR3 antibodies, raised ESR and CRP)

  1. CXR (nodular masses and pneumonic infiltrates with cavitation)
  2. CT (diffuse alveolar haemorrhage)
  3. Urinalysis (Proteinuria and haematuria - follow with biopsy)
81
Q

Treatment of WEGENER’s

A
  1. CORTICOSTEROIDS

2. AZATHIOPRINE and METHOTREXATE as maintenance

82
Q

What does the thoracic aorta branch into

A

Internal thoracic artery -> superior epigastric artery

83
Q

Where does bronchial circulation originate from

A

Aorta

84
Q

When do we suspect pulmonary embolism

A

Sudden collapse following 1-2 weeks after surgery

85
Q

Describe the production of pulmonary thromboembolus

A
  1. Clots break off and pas through veins to the IVC then to the right side of the heart before lodging in the pulmonary circulation
86
Q

Where do most pulmonary emboli come from

A
  1. Pelvic and abdominal veins
  2. Femoral DVT
  3. Axillary thrombosis
87
Q

Rar causes of pulmonary embolisms

A
  1. Fat embolism
  2. Septic emboli (right sided endocarditis)
  3. Fat embolism
  4. Air embolism
  5. Amniotic fluid embolism
  6. Neoplastic cells
  7. Parasites
  8. Foreign material during IV drug misuse
88
Q

Risk factors for pulmonary embolisms

A

Change in blood flow:

  • Immobility
  • Obesity
  • Pregnancy

Change in blood vessel:

  • Smoking
  • Hypertension

Changes in blood constituents

  • Dehydration
  • Malignancy
  • High oestrogen (combined oral contraceptive pill)
  • Polycythaemia
  • Nephrotic syndrome
  • Protein C/S deficiency or Factor V leiden

Recent surgery (hip/knee replacement)
Leg fracture
Age over 60

89
Q

What three main factors predispose you to a lot

A
  1. Circulatory stasis
  2. Endothelial injury
  3. Hypercoagulable state
90
Q

Where do pulmonary embolisms get lodged

A

Alveoli

91
Q

How is V/Q effected in the lungs

A
  1. Lung tissue ventilated and NOT PERFUSED resulting in dead space + impaired gas exchange
92
Q

What happens to the non-perfused alveoli after a while

A

Surfactant production stops = alveolar collapse and hypoxia

93
Q

How does PE affect pulmonary pressure

A
  1. Increases

Reduction in CO

94
Q

How can right Ventricular ischaemia be detected

A

Elevation of troponin and creatine kinase

95
Q

Clinical presentation of pulmonary embolisms

A
  1. Pleuritic chest pain
  2. Dizziness
  3. Haemoptysis (infarction)
  4. Past history
  5. Pyrexia
  6. Tachypnoea
  7. tachycardia
  8. Raised jugular venous pressure
  9. Pleural rub
  10. Pleural effusion
96
Q

What is pleural rub

A

Rubbing together of the pleural lining (they inflame

97
Q

Differential diagnosis of central chest pain

A
  1. Asthma
  2. COPD
  3. MI
  4. Pneumonia
  5. Heart Failure
98
Q

How’s PE diagnosed

A
  1. CXR
  2. ECG
  3. ABG
  4. Plasma D-dimer
  5. Ultrasound
  6. CT pulmonary angiography (GOLD STANDARD)
99
Q

What is seen on a CXR for PE

A
  1. NORMAL
  2. Decreased vascular markings
  3. Blunting of costophrenic angles (small effusion)
  4. Wedge-shaped areas of infarction
  5. Pulmonary oligaemia (reduction in blood perfusion) in massive embolism
  6. MI or pneumothorax
100
Q

ECG in PE

A
  1. Sinus tachicardia
  2. RA dilation with tall-peaked P waves in lead II
  3. Right bundle branch block
  4. Right ventricular strain (inverted T waves V1- V4)
101
Q

Ultrasound for PE

A

Leg and pelvic clots

102
Q

How is PE treated

A
  1. High flow Oxygen (60-100%)
  2. Anticoagulant with low molecular weight heparin
  3. IV fluids and inotropic agents
  4. Thrombolysis
  5. Surgical embolectomy
  6. Vena cava filter
103
Q

Preventative treatment of DVT

A
  1. Patients mobilised
  2. TED stockings
  3. Warfarin for 3-6 months (2-3 INR)
104
Q

How does Warfarin work

A

Stops Vit K being used by liver to produce 2,7,9,10 factors

105
Q

How is emergency PE treated

A
  1. OXYGEN THERAPY
  2. MOrphine with anti-emetic
  3. Immediate thrombolysis with alteplase
  4. IV heparin
106
Q

What is given is systolic BP is less than 90 mmHg

A

Start colloid infusion
Then dobutamine
Then IV noradrenaline
Then Thrombolysis

107
Q

How is systolic BP of more than 90mmHg treated

A

Warfarin

108
Q

What is the upper respiratory tract

A

Nose to larynx

109
Q

What microbes colonise the upper respiratory tract

A

Staphylococcus aureus

Streptococcus pneumoniae

110
Q

What protects against upper respiratory tract infections

A
  1. Mucosal defences:
    Cough reflex
  2. Mucus barrier + respiratory cilia
  3. Surface secretions (defensives and complement)

Innate immune defences
Macrophages
Neutrophils

Adaptive immune defences

111
Q

What conditions are caused by rhinovirus

A

Common cold

112
Q

What commonly causes sore throat

A

Adenvirus

Epstein-Barr virus

113
Q

What causes bronchitis

A

Adenvirus - acute

Rhinovirus - Chronic

114
Q

Conditions caused by adenovirus

A
  1. Upper respiratory tract infection
  2. Pharyngitis
  3. Bronchitis
  4. Pneumonia
115
Q

What is Severe Acute respiratory syndrome

A
  1. Severe respirartoy illness and failure
116
Q

What virus causes SARS

A

Coronavirus

117
Q

What is the new form of influenza virus called

A

Avia influenza

118
Q

How is avian influenza spread

A

Poultry

119
Q

Tonsilitis vs pharyngitis

A

Tonsils

Throat

120
Q

What virus commonly causes pharyngitis

A

Adenovirus!!

Rhinovirus
EBV
HIV

121
Q

Bacterial causes of pharyngitis

A
  1. Lancefield Group A Beta-haemolytic streptococci (strep pyogenes)
122
Q

Clinical presentation of tonsillitis and pharyngitis

A
  1. Tender glands in neck
  2. Temperature = 38.5
  3. Vital signs stable
  4. Large tonsils with exudates
  5. Tender anterior cervical lymph nodes
123
Q

How is pharyngitis and tonsillitis treated

A
  1. ONLY if persistent = phenoxylmethypenicillin or cefaclor
124
Q

Diagnosis of pharyngitis and tonsillitis

A
  1. Sore throat
  2. fever
  3. Oropharynx and soft palate are red
  4. Tonsils inflamed and swollen
  5. Tonsils lymph node enlarge in 1-2 days
125
Q

Define sinusitis

A
  1. Infection of paranasal sinuses
126
Q

What causes sinusitis

A
  1. Strep. pneumoniae

2. Haemophilus influenza

127
Q

Clinical presentation of sinusitis

A
  1. Fever (sometimes present)
  2. Facial pain
  3. Prurient nasal discharge
  4. Pain in left ear into teeth and no fever
  5. No dental problems
  6. Cold for 10 days and facial pain for same duration
  7. Allergic rhinitis past history
128
Q

Diagnosis of sinusitis

A
  1. Forntal headache
  2. Prurulent rhinorrhoea (mucus fluid in nasal cavity)
  3. Bacterial sinusitis (unilateral pain and discharge with or without fever for 10 days)
  4. Facial pain with tenderness
  5. Fever
129
Q

Treatment of sinusitis

A
  1. Nasal decongestants (xylometazoline)
  2. CO-amoxiclav
    3
130
Q

Complications of sinusitis

A
  1. Brian abscess
  2. Sinus vein thrombosis
  3. Orbital cellulitis
131
Q

Define acute epiglottitis

A

Inflammation of the epiglottis

132
Q

What people are effects day epiglottis

A
  1. Children under 5 years of age
133
Q

Clinical presentation of epiglottis

A
  1. Sore throat
  2. Odynopahgia
  3. Febrile
  4. Inspiratory stridor (high pitched wheezing on breathing in)
  5. Unwell for 6 months
  6. Fatigue
  7. Weight loss
  8. Diarrhoea
  9. Oral thrush

Severe airflow obstruction
Meningitis
Septic arthritis
Osteomyelitis

134
Q

What causes epiglottis

A

Haemophilus influenza type B

135
Q

How is epiglottis treated

A
  1. Endotracheal intubation

2. IV antibiotics (ceftazidime

Year 2 (155 decks)

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