PULMONOLOGY Flashcards

1
Q

What are the causes of COPD?

A

Smoking
a-1 antitrypsin deficiency
Dust e.g. cadmium, coal, cotton, cement, grain

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2
Q

What are the symtoms of COPD?

A

Cough (productive)
Wheeze
Dyspnoea

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3
Q

What are the signs of COPD?

A
Tachypnoea
Accessory Muscles
Hyperinflation
Hyperresonence
Reduced expansion
Reduced breath sounds e.g. over bullae 
Reduced corticosternal distance 
Cyanosis
Cor pulmonale (raised JVP)
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4
Q

What are the complications of COPD?

A
Acute exacerbations (+/- infection)
Respiratory failure
Polycythaemia abnormal increase in Hb
Pneumothorax due to ruptured bullae
Lung carcinoma
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5
Q

What are the stages of COPD?

A
FEV1
1 Mild >80%
2 Moderate 50-79%
3 Severe 30-49%
4 Very severe 30%
\+ post bronchodilator FEV1/FVC <0.7

BUT the patient must be experiencing symptoms to diagnose

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6
Q

What are the signs of COPD on CXR?

A

Hyperinflation
Bullae
Flat hemidiaphragm
Hyperlucent lung fields

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7
Q

What are the investigations for COPD?

A
  • Spirometry
  • FBC
  • CXR
  • BMI
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8
Q

How is COPD managed?

A
  1. Stop smokinh
  2. Flu vaccine (annual) and pneumococcal vaccine (one-off)
  3. SABA OR SAMA
  4. FEV1 > 50% LABA or LAMA
    FEV1 <50% LABA + ICS or LAMA
  5. Oral theophylline (reduce if giving macrolide or fluoroquinolone)

Persistant exacerbation/ breathlessness: LABA+ICS_LAMA

Mucolytics for productive cough

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9
Q

What can improve survivial in COPD?

A
  • Stop smoking
  • Lung volume reduction surgery
  • Long term O2 therapy
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10
Q

When should long-term O2 therapy be considered?

A
FEV1 <30% 
Cyanosis
Polycythaemia
Peripheral oedema
Raised JVP
PO2 <92% on room air
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11
Q

When should long-term O2 therapy be offered?

A

2 blood gasses, 3 weeks apart

pO2 < 7.3kPA or 7.3-.8kPA + 1 of…

  • Secondary polycythemia
  • Nocturna; hypoxaemia
  • Peripheral oedema
  • Pulmonary HTN
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12
Q

What microorganisms cause acute exacerbations of COPD?

A

H. Influenzae
S. Pneumoniae
Maroxella Catarrhalis
30% are viral

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13
Q

How are exacerbations of COPD managed?

A

Nebbed bronchodilator
7-14 days of prednisolone
Abx ONLY if sputum is purulent OR clinical signs of pneumonia

NIV when pH 7.25-35

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14
Q

What are ‘pink puffers’?

A

Primarily emphysema

Destruction in small airways leads to destruction of capillary beds so reduced O2 of Hb causing hyperventilation ‘puffers’ but with normal ABGs-less hypoxic so ‘pink’

TYPE 1 resp failure

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15
Q

What are ‘blue bloaters’?

A

Primarily chronic bronchitis

Redueced alveolar ventialtion so reduced O2 and reduced CO2

Cyanosed but not breathless (blue)

Chromic alveolar hypoxia leads to pulmonary HTN and R heart failure so oedematous (bloated)

Hypoxic drive maintains respiratory effor

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16
Q

What is Asthma?

A

TYPE I hypersensitivity (IgE) reaction causing CHRONIC INFLAMMATION OF THE AIRWAYS

REVERSIBLE BRONCHOSPASM (causing airway obstruction) due to:

  • Bronchial muscle contraction
  • Mucosal inflammation by mast cells and basophil degranualtion releasing inflammatory mediators
  • Increased mucous production
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17
Q

What are the risk factors for Asthma?

A
Atopy: eczema, hayfever
Not breast fed
Maternal smoking 
Very clean house
Multiple siblings
Hygiene
Aspirin
Occupational
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18
Q

How does asthma present?

A

Widespread Expiratory Polyphonic Wheeze
Hyperinflated chest-hyperresonnance
Obstruction
Nocturnal cough

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19
Q

What are the investigations for Asthma?

A

PEF
Spirometry
FEV1(reduced)/FVC(normal) <70%

Reversed when given SABA (improvement >12% and increase in volume >200ml

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20
Q

How is Asthma managed?

A
SABA (Salbutamol)
\+
ICS (Beclamethasone dipropionate or Fluicasone Proprionate) 100mch 2x2
\+
LEUKOTRIENE RECEPTOR ANTAGONIST
(Oral monteleukast) 
\+
LABA (Salmeterol) (review LTRA)
\+
Convert ICS and LABA to MART regimen (combined inhaler) with low maintenance ICS dose
\+ 
Convert ICS to moderate dose 200mcg 2x2
\+
Increase ICS to high dose 
or Trial LAMA or THEOPHYLLINE
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21
Q

How is acute asthma classified?

A

Moderate:

  • Worsening symptoms
  • PEF <75% best/predicted
  • No features of acute severe

Severe: any of

  • PEF 33-50%
  • RR >25
  • HR >110
  • Can’t complete sentances

Life-threatening: any of

  • PEF <33%
  • O2 <92% <8kPa
  • Cyanosis
  • CO2 normal
  • Silent chest
  • Poor respiratory effort and exhaustion
  • Arrhythmias
  • Hypotension
  • Altered consciousnes

Near-fatal:

  • Raised CO2
  • Any need for ventilation assistance (low pH)
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22
Q

How is acute asthma managed?

A

Nebulise 5mg salbutamol through oxygen
Teotropium Bromide
Oral prednsiolone (continue 40-50mg 5 days after) or IV hydrocortisone
Magnesium sulphate IV

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23
Q

What is Pneumonia?

A

Inflammation of the alveoli in a lobar pattern

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24
Q

How is Pneumonia classified?

A

CAP v HAP

Acute v Chronic

Causative organism: bacterial v viral v fungal

Lung pathology:
- Lobar- S. Pneumoniae
Alveoli fill with plasma exudate and neutrophils-consolidation on CXR
- Broncho-patchy consolidation of different lobes
- Interstitial- H. Influenze
Accumulates of infiltrates into the alveolar walls, walls thicken, increased diffusion distance and irritated walls cause dry cough

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25
Q

What are the causative organisms of Pneumonia?

A

Streptococcus Pneumoniae
Staphylococcus Aureus
Haemophilus Influenzae
Klebisiella Pneumoniae

Atypical:
Mycoplasma pneumonia
Legionella pneumophillia
Chlamydia Psittaci

Fungal:
Pneumocystis jiroveci

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26
Q

What are the non-infective causes of Pneumonia?

A
  • Aspiration Pneumonia

- Idiopathic interstitial Pneumonia

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27
Q

What is Streptococcal Pneumoniae Pneumonia?

A

Majority of cases

High fever
Rapid onset
Rusty sputum
>60 y/o

Associated with herpes virus

Vaccine available

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28
Q

What is Staphylococcal Pneumoniae Pneumonia?

A

After recent flu

IVDU

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29
Q

What is Haemophilus Influenzae Pneumonia?

A

COPD

Dry cough

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30
Q

What is Klebisiella Pneumoniae Pneumonia?

A

Alcoholics
Diabetics

‘Red-current jelly’ sputum
Upper lobes

Aspiration

Causes lung abscesses and empyema

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31
Q

How are the typical pneumonias treated?

A

Amoxicillin for 5 days
(Macrolide if penicillin allergic: doxycycline, Erythromycin or Clarithromycin)

If severe then add a macrolide for 7 days
Co-amoxiclav + clarithromycin/doxycycline/ceftriaxone/piptaz

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32
Q

What is Mycoplasma Pneumonia?

A

Atypical-won’t respond to penicillins as no peptidoglycan wall
Younger patients

Dry cough
Flu-like symptoms

Deranged LFTs
Bilateral CXR consolidation

Treat with macrolides e.g. Clarithromycin or Erythromycin

or Tetracyclines e.g. Doxycycline

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33
Q

What are the complications of Mycoplasma Pneumonia?

A
Complications:
Cold agglutinins (IgM) cause (+ve test):
Autoimmune haemolytic anaemia
Thrombocytopenia
Erythema multiforme
Meningoencephalitis
Guilla-Barre
Peri/myocarditis
Bullous myringitis (painful vesicles on tympanic emembrane-inflamed)
Hepatitis 
Pancreatitis
Acute gomerulonephritis
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34
Q

What is Legionella pneumophillia

A

legionnaire’s
Water tanks so air-conditioning

Flu-like fever
Dry cough
Bradycardia 
Confusion
Pleural Effusion 

Lymphopaenia
Hyponatreamia
Deranged LFTS

Macrolides Erythromycin or Clarithromycin

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35
Q

What is Chlamydia Psittacosis Pneumonia?

A

Parrots, poultry and sheep
Human to Human

Tetracyclines

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36
Q

What is Pneumocystis jiroveci Pneumonia?

A

HIV (most common opportunistic infection in AIDS) CD4+ <200

Dry cough
Dyspnoea
Fever
Exercise-induced desaturation
Absence of chest signs
Bronchoalveolar lavage-silver stain shows cysts (sputum often fails to show PCP)
CXR: Bilateral interstitial pulmonary infiltrates
Ground glass opacity
Pneumothorax is a common complication

Extrapulmonary (rare)
Hepatosplenomegaly
Lymphadenopathy
Choroid lesions

Co-trimoxazole
IV pentamidine
Steroids if hypoxic

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37
Q

What is Aspiration Pneumonia?

A

Foreign materials (e.g. saliva or food) entering the bronchiole tree
Risk factors:
- Incompetent swallowing
- Neurological diseases e.g. stroke and MS
- Intoxication
- Poor dental hygiene
- Impaired consciousness
- Impaired mucociliary clearance
- Prolonged hospitalisation/surgical procedures e.g. intubation

Chemical: acidic pneumonitis

Bacterial pathogens S. Pneumoniae, S. Aureus. H. Influenzae, Pseudomonas aeruginosa

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38
Q

What is Idiopathic Interstitial Pneumonia?

A

Non-infective pneumonia e.g. Cryptogenic organising pneumonia (bronchiolitis due to RA or amiodarone) can cause ground-glass opacity

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39
Q

What is Viral Pneumonia?

A

Damage to cells lining the airways/alveoli, alveoli fill with fluid impairing gas exchange
Severe viral pneumonia results in necrosis/haemorrhage into the lung parenchyma and presents like ARDS
Ground glass opacity (diffuse or patchy) on CXR

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40
Q

What are the risk factors for Lung Cancer?

A

SMOKING (x10)
Asbestos (x5)

(Arsenic, Radon, Nickle, Chromate)

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41
Q

What are the types of Lung Cancers?

A

Small Cell 15%

Non-Small cell:

  • Squamous 35%
  • Adenocarcinoma 30%
  • Large-cell 10%
  • Bronchial adenoma
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42
Q

How are Lung Cancers investigated?

A
  1. Contrast CT
  2. CXR (10% are reported as normal)
    - Peripheral nodule
    - Hilar enlargement
    - Consolidation
    - Lung collapse
    - Pleural effusion
    - Boney secondaries
  3. Bronchoscopy to biopsy
  4. PET scan for Non-Small Cell to establish eligibility for treatment
  5. Cytology
    - Sputum
    - Pleural fluid
  6. Lung function tests
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43
Q

How do Lung Cancers Present?

A
Cough
Haemoptysis
Dyspnoea 
Chest pain
Slow resolving/recurrent pneumonia
Cachexia
Anaemia
Clubbing 
Supraclavicular or axillary lymph nodes 
Hypertrophic Pulmonary Osteoarthropathy (wrist pain)
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44
Q

What are the paraneoplastic syndromes and complications for Small-Cell Lung Cancer?

A
  • ADH (SIADH) hyponatreamia
  • ACTH cushing’s
  • Lambert-Eaton syndrome is like myesthenia
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45
Q

How is Small-Cell Lung cancer managed?

A

Nearly always disseminated (only ~20% are suitable for surgery)

May respond to radio and chemo-mostly used for palliation (reduce bronchiole obstruction)

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46
Q

What are the features, paraneoplastic syndromes and complications of squamous cell lung cancers?

A

Central, cavitating tumours
Finger clubbing

PTH-rp -> hypercalcaemia

TSH -> hyperthyroid

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47
Q

What are the features of Adenocarcinomas?

A

Typically peripheral

Most common in non-smokers

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48
Q

What are the features and paraneoplastic syndromes of Large-cell lung cancers?

A

Typically peripheral
Anaplastic, poor differentiation and poor prognosis
Secrete B-HCG

Gynaecomastia

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49
Q

How are Non-Small Cell Lung Cancers managed?

A

Excision if:

  • SVC occluded
  • FEV <1.5
  • Malignant pleural effusion
  • Vocal cord paralysis

Radiotherapy can be curatice

Add platinum-based chemo if advanced disease

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50
Q

What are the paraneoplastic syndromes/complications of Lung masses?

A
  • Recurrent laryngeal nerve palsy
  • Horner’s syndrome
  • Phrenic nerve palsy
  • Pericarditis
  • SVC obstruction
  • P.E (all malignancies)
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51
Q

What is Horner’s syndrome?

A

Damage to the sympathetic trunk (arises in spinal cord and ascends to head and neck), due to the presence of a Pancoast tumour in the apex of the lung. symptoms appear on the same side

  • Miosis (constricted pupil. Light reflex is still present as this is parasympathetic)
  • Partial ptosis (drooped eyelid or lower eyelid raised due to inactivated superior tarsal muscle)
  • Anhidrosis (reduced sweating)
    Flusging
  • Psuedoenopthalmos (inset eyeball)
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52
Q

What is Pulmonary Fibrosis (ILD)?

A

Scarring of the lung interstitium?

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53
Q

What are the causes of Upper Zone Pulmonary Fibrosis?

A

Allergic Bronchopulmonary ASPERGILLOSIS
Alveolitis

TB
EXTRINSIC ALLERGIC ALVEOLITIS (fungal spores, avian proteins)
Ankylosing Spondylitis

Sarcoidosis
Histiocytosis
Occupational e.g. silicosis-egg shell calcification of hilar lymph nodes
Pneumoconiosis (dust)

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54
Q

What are the causes of Lower Zone Pulmonary Fibrosis?

A
Bronchiectasis
RA (others)
Asbestos
Drugs
- Amiodarone
- Methotrexate
- Sulfasalazine (anti-rheum drugs)
- Nitrofurantoin 
- Some dopamine receptor agonists

Idiopathic Interstitial

55
Q

What is Idiopathic Interstitial LD?

A

A.K.A CRYPTOGENIC FIBROSING ALVEOLITIS

50-60 y, M>f

ANA +ve in 30%
Rhuem factor 1%

Poor prognosis,, 50% 5 year

56
Q

What are the symptoms of Pulmonary Fibrosis?

A

Systemic:

  • Flu-like
  • Weight loss
  • Malaise

arthralgia

Cor Pulmonale 
- sacral oedema
- pitting oedema
Clubbing
Cyanosis
Chest pain

Dry Cough
Fine inspiratory crackles bibasal
Exerctional dyspnoea (high R.R)

57
Q

What are the investigations for Pulmonary Fibrosis?

A
Spriometry: restrictive
CT: Honeycombing
CXR: Ground glass opacity with lower lobe nodule shadows (reduced lung volume)
ABG Type 1 RF, Type 2 if severe
Biopsy: interstitial pneumonia
Reduced transfer factor
Broncho-alveolar Lavage: alveolitis
58
Q

How is Pulmonary Fibrosis managed?

A

Give O2
Pulmonary rehab
Palliation
Transplant

59
Q

What is Asbestosis?

A

Pleural plaques:

  • MC
  • 20-40 year latency
  • Benign, no malignant changes

Diffuse Pleural thickening

Asbestosis:

  • Severity is proportional to length of exposure
  • 15-30 year latency

Mesothelioma:

  • Malignant disease of the pleura
  • Progressive SOB, Chest pain, pleural effusion
  • Give palliative chemotherapy
60
Q

What is Extrinsic Allergic Alveolitis?

A

Inhalation of allergens e.g. fungal spores or avian proteins resulting in a HYPERSENSITIVITY REACTION

ACUTE: alveoli infiltrated with acute inflammatory cells
(Fevers, rigors, myalgia, cough, dyspnoea, crackles)

CHRONIC: granuloma formation and obliterative bronchiolitis
(Dyspnoea (exertional), weight loss, Type 1 resp failure, Cor Pulmonale)

FBC, Raised ESR, ABG
CXR: U. Zone motelling/consolidation
BAL: lymphocytes and mast cells

Remove allergens, give O2, Long-term prednisolone

61
Q

What is Allergic Bronchopulmonary Aspergillosis?

A

Allergy to aspergillus spores (RAST test)

Proximal BRONCHIECTASIS
EOSINOPHILIA- IgE
- Wheeze
- Cough
- Dyspnoea

CXR:

  • Tram track
  • Mass
  • Parahilar ring shadow
  • Central cystic/varicose

STEROIDS and ITRACONAZOLE

62
Q

What are the causes of Bilateral Hilar Lymphadenopathy?

A

SARCOIDOSIS
TB (mycoplasma)

Malignancy (lymphoma, carcinoma)
Pneumoconiosis
Extrinsic Allergic Alveolitis
Hystiocytosis

63
Q

What is Sarcoidosis?

A

MULTISYSTEM GRANULOMATOUS DISEASE

64
Q

What are the features of sarcoidosis?

A

Conjunctivitis and keratoconjunctivitis
Uveitis

Facial Nerve Palsy
Pituitary dysfunction

Upper Zone lung fibrosis with bilateral hilar lymphadenopathy

Hepatosplenomegaly

Raised Ca2+: renal stones

Erythema nodosum

Acute arthropathy

65
Q

What can be detected on investigation in Sarcoidosis?

A

Low Na+-ADH is produced ectopically

Raised serum ACE
Cytopenia = eosinophillia
Raised ESR
HyperCa2+

Lymphocytosis and lymphopaenia

Treat with Steroids and NSAIDS

66
Q

What is Pleural Effusion?

A

Build up of fluid in the pleural space

Can be Exudate >30g/L
or Transudate <30g/L of protein

67
Q

What are the features of Pleural Effusion?

A

Dullness on percussion
Reduced breath sounds and vocal resounnance
Reduced chest expansion

Non-productive cough
Dyspnoea
Pleuritic chest pain

68
Q

What are the causes of Transudate Pleural Effusion?

A

Increased venous pressure

HEART FAILURE
Hypoalbuminaemia
(Liver disease or nephrotic syndrome)
Hypothyroidism
Meig's syndomre:
- Ovarian tumour
- ascites
- Pleural effusion
69
Q

What are the causes of Exudate Pleural Effusion?

A

Increased capillary leakiness

INFECTION
(pneumonia, TB, Subphrenic abscess)
CT disease (RA, SLE)
Neoplasm (Lung cancer, mesothelioma, metastases)
Pancreatitis
PE
Dressler's syndrome
Yellow nail syndrome
70
Q

What is Light’s Criteria?

A

25-35g/L protein
Exudate likely if…

Pleural fluid protein/ serum >0.5

Pleural fluid LDH/ serum >0.6

Pleural fluid LDH >2/3 the upper limit of normal serum

71
Q

What else makes Exudative Pleural effusion more likely?

A

Low Glucose:

  • RA
  • TB

Raised Amylase:

  • Acute pancreatitis
  • Oesophageal perforation

Blood staining:

  • Mesothelioma
  • TB
  • PE
72
Q

What does imaging show in Pleural Effusion?

A

PA CXR

  • Small: Blunted costophrenic angles
  • Large: Concave border (unless pneumothorax too in which case flat border)

USS guided aspiration and detect seprations

Contrast CT to detect cause

73
Q

What is measured in Pleural Fluid analysis?

A
pH
Protein
LDH
Glucose
Cytology 
Microbiology
74
Q

How is Recurrent Pleural Effusion managed?

A
  • Aspirate
  • Pleurodesis: artificially obliterate the pleural space by adhering them together
  • Indwelling pleural catheter
  • Relieve symptoms
75
Q

What is Lambert-Eaton syndrome?

A

Small cell lung cancer

Reduced release of acetylcholine

Muscle weakness, depressed reflexes and autonomic dysfinction- postural BP drop

76
Q

What are the risk factors for a Pulmonary Embolism?

A
Sex-female
Pregnancy
Age
Surgery
Malignancy
Oestroge (OCP/HRT)
DVT (Prev PE)
Immobility
Colosal size (high BMI)
A
Lupus
77
Q

What is the pathophysiology of a Pulmonary Embolism?

A

Risk factors contribute to Virchow’s triad:

Venous throbosis in the:
Popliteal/Femoral/Iliac veins embolises and travels through the venous system -> RA -> RV -> occlude pulmonary a artery causing a:
Saddle embolism occluding central arteries or saddle embolus

  1. Clot reduces blood flow (V/Q mismatch)
    - Reduced CO2 delivery to lungs, builds up in blood, detected by medullary chemoreceptors increase R.R
    - Low O2 detecetd by aortic/carotid receptors increase R.R and H.R
  2. Saddle embolus causes PULMONARY HYPERTENSION -> back up of blood to heart -> RH strain
  3. Circulation to lung peripheries cut off leading to ischaemia and infarct (although infarct is rare due to lots of collaterals so only really occurs in patients with pre-existing poor flow to lungs e.g. COPD)
    - irritates somatic endings on parietal pleura causing adrenergic response increase H.R and pleuritic chest pain
    - ischaemic tissue becomes inflamed and adheres to pleura causing plueral rub and ARDS
78
Q

How does Pulmonary Embolism present?

A

Triad:

  • Dyspnoea/SOB
  • Haemoptysis
  • Pleuritic chest pain (focal and localised, with each breath)
Tachypnoea
Tachycardia
Cyanosis
Hypotension
Dizziness and syncope
Pyrexia
Signs of DVT
Pleural rub
Increased inflammatory cells -> increased vessel permeability -> ARDS
79
Q

What is Well’s score?

A
3 Signs and symptoms of DVT
3 Alternative diagnosis less likely
1.5 Tachycardia
1.5 Immobile >3days/ surgery <4 weeks ago
1.5 Previous DVT/PE
1 Haemoptysis
1 Malignancy 

> 4 means P.E is likely

80
Q

How are Pulmonary Embolisms investigated?

A
  1. Do a CXR to rule out other diagnoses
  2. If wellsscore >4 then immediately do CTPA (V/Q if renal failure/contrast allergy) Give LMWH if delayed
    If <4 do a D-Dimer and do above if +ve
  3. ECG
    - Tachycardia
    - RBBB+R axis deviation
    - S1Q3T3
    Large S in I Large Q and inverted T in III

(Pulmonary angiography is gold standard BUT high risk of complications)

81
Q

How are normal Pulmonary Embolisms managed?

A
  1. LMWH or FONDAPURINUX until INR >2.0 (3.5 in recurrent P.Es) or for 5 days (6 mo in CA patients)
  2. Warfarin within 24 hours for at least 3 months (definitely >3 mo if PE unprovoked)
82
Q

How are Massive Pulmonary Embolism with Circulatory Failure managed?

A

THROMBOLYSIS

83
Q

What is Homan’s sign?

A

Tender calf muscle when leg dorsiflexed

84
Q

How are Pulmonary Embolisms prevented?

A

Give heparin e.g. deltaparin/Enoxiparin to all immobile patients

Stop oestrogen 4 weeks prior to surgery

85
Q

What are the causes of Bronchiectasis?

A

Post-infective

  • HIV TB
  • Measles
  • Pertussis
  • Pneumonia

Cystic fibrosis

Bronchiole obstruction

  • Cancer
  • Foreign body

Immune deficiency
- Selective IgA

Allergic Bronchopulmonary Aspergillosis

Cilliary Dyskinesia

  • Kartagener’s
  • Young’s

RA
UC
Idiopathic

Yellow nail syndrome

86
Q

What is the pathophysiology of Bronchiectasis?

A

Inflammation
Neutrophils, Cytokines
NO and O. radicals accumulate

Bronchial and prebronchial destruction

Elastic tissue lost

BRONCHIOLES PERMANENTLY DILATED (would usually taper)

87
Q

What are the features of Bronchiectasis?

A

OBSTRUCTIVE PATTERN

  • Persistent cough
  • Purulent sputum
  • Intermittent haemoptysis
  • Clubbing
  • Wheeze
  • Coarse insipiratory crepitus
88
Q

What are the complications of Bronchiectasis?

A

Pneumonia

Plueral effusion

Pneumothorax

Cerebral abscess

Amyloidosis

89
Q

What is seen on CT in Bronchiectasis?

A

Signet rings where the artery looks much denser next to the airy bronchi

Clusters of grapes: appear to crowded together

Bronchi seen within 1cm of pleura as dilation makes them more visible

90
Q

What is seen on CXR in Bronchiectasis?

A

Tram tracking: outlining of dilated and thickened bronchi

Cystic shadows

91
Q

How is Bronchiectasis managed?

A
  • Physical training
  • Postural drainage BD
  • Abx when axacerbated
    (
  • Sometimes bronchodilators
  • Immunisations
  • Surgery if localised
92
Q

What is Kartagener’s syndrome?

A

Primary CILLIARY DYSKINESIA-immobility

Associated with DEXTROCARDIA and SINUS INVERSUS

Causes recurrent SINUSITIS and INFERTILITY

93
Q

What are the causes of ARDS?

A

Infection:

  • Sepsis
  • Pneumonia

Trauma

Smoking

Pancreatitis:
- Liver failure

Massive blood transfusions

Cardio-pulmonary bypass

94
Q

What is the pathophysiology of ARDS?

A

Lung damage releases inflammatory mediatorys which increases permeability of alveolar capillaries causing fluid to accumulate in the alveoli = NON-CARDIOGENIC PULMONARY OEDEMA

95
Q

What are the features of ARDS?

A
Dyspnoea
Tachypnoea
Tachycardia
Peripheral vasodilation
Cyanosis 
Bilateral FINE INSPIRATORY LING CRACKLES (pulmonary oedema)
96
Q

How is ARDS investigated?

A
  • CXR shows bilateral lung infilitration
  • ABG shows low O2
  • Pulmonary artery catheter measures pulmonary capillary wedge pressure which gives an idea of L atrial pressure, if >20mmHg then pulmonary oedema caused by cardiogenic issues
97
Q

What are the diagnostic criteria for ARDS?

A

Acute Onset (<1 week)
CXR shows pulmonary oedema (bilateral infiltration)
Non-cardiogenic pulmonary oedema PCWP <19mmHg or NO CONGESTIVE HF
Refractory hypoxaemia

98
Q

How is ARDS managed?

A

ITU
Respiratory support: oxygenate/ventilate with CPAP
Circulatory support
Treat sepsis

99
Q

What is Pulmonary Oedema?

A

FLUID accumulates in the TISSUE and AIRSPACE of the lung resulting in impaired gas exchange and RESPIRATORY FAILURE

CXR is same as in HF

100
Q

What are the causes of Pulmonary Oedema?

A

CARDIOGENIC: L ventricle fails to remove blood from pulmonary circulation
e.g. HEART FAILURE

NON-CARDIOGENIC: initial and rapid increase in PUMONARY VASCULAR PRESSURE due to vasoconstriction or blood flow causing parenchyma and vacular injury = LEAKY CAPILLARIES

  • ARDS
  • Drowning
  • Fluid overload
  • Aspiration
  • Neurogenic
  • Allergic
  • Acute glomerulonephritis
101
Q

What is Idiopathic Pulmonary Arterial Hypertension?

A

No known underlying cause

Risk factors:
- Female
- 20-40
- FHx (10% A.D)
Cocaine
102
Q

What are the features of Idiopathic Pulmonary Arterial Hypertension?

A

Increased pulmonary artery pressure >25mmHg at rest and >30mmHg on exercise

Progressive SOB

Cyanosis

Tricuspid regurgitation on ECHO

Raised JVP with prominent A wave

Loud O2

R ventricular heave

RHF

103
Q

How is What Idiopathic Pulmonary Arterial Hypertension managed?

A
  • Diuretics in RHF
  • Anticoagulation
  • Heart-lung transplant
  • Vasodilator therapy
104
Q

What is the gene mutation in Cystic Fibrosis?

A

A.R mutation of DELTAF508 on CHROMOSOME 7
(CF Transmembrane Conductance Regulator (CFTR))

1/25 people are carriers

105
Q

What is the pathophysiology of Cystic Fibrosis?

A

Dysfunction of the CFTR protein (which is the Cl- ion channel in exocrine glands) means that less Cl- diffuses into secretions from the duct epithelial cells.

This reduces the H2O content of the peri-cilliary mucous (reduced osmotic gradient) leading to THICK and STICKY mucous (increased viscosity)

Reduced clearance of mucous means it accumulates and obstructs the secretory passageways in the GI, Resp and Genito-urinary tracts

This also reduces Cl- ABSORPTION in sweat glands so there is more Cl- in sweat (salty babies)

106
Q

What are the GI tract features of Cystic Fibrosis?

A

BILIARY TREE-delayed passage of BILE causing LIVER INFLAMMATION resulting in

  • GALLSTONES
  • CIRRHOSIS
  • PORTAL HTN

GI TRACT- reduced movement of INTESTINAL contents

  • CHILDREN/ADULTS this causes DISTAL ILEAL OBSTRUCTION SYNDROME (DIOS)
  • Neonates causes MECONIUM ILEUS (meconium is retained) resulting in JAUNDICE and RECTAL PROLAPSE

PANCREAS-can’t secrete DIGESTIVE ENZYMES
- STEATORRHOEA
- reduced FAT and PROTEIN absorption resulting in FAILURE TO THRIVE and reduced ADEK vitamin absorption
- OSTEOPOROSIS due to reduce VIT D
the enzymes DEGRADE the pancreas causing scarring and inflammation eventually resulting in
- DMT2

107
Q

What are the Respiratory tract features of Cystic Fibrosis?

A

URT:

  • Nasal polyps
  • Sinusitis due to retained secretions
LRT:
Resp failure causing Hypoxia
- Cyanosis
- Clubbing
Cor Pulmonale
Pneumothorax
Haemoptysis
Obstructive Lung disease: hyperinflation and abnormal spirometry
Retention of secretions: BRONCHIECTASIS
Chronic Productive Cough
Bilateral Coarse Crackles
Recurrent Chest infections
108
Q

What are the Genito-urinary tract features of Cystic Fibrosis?

A

Vas deferens issues in utero leading to male infertility

Female subfertility

109
Q

What are the common organisms in Cystic Fibrosis related chest infections?

A
  • Staph Aureus
  • Psuedomonas Aeruginosa
  • Aspergillus
  • Burkholderia cepacia
110
Q

What are the investigations for Cystic Fibrosis?

A
  • genetic screening
  • Cl- IN SWEAT > 60MMO/L (Cl>Na)
  • Faecal elastase
  • Annual Glucose Tolerance Test
111
Q

How is Cystic Fibrosis managed?

A
  • Ursodeoxycholic acid in liver inflammation
  • Pancreatic enzyme supplements
  • Supplements (high fat and calorie diet)
  • Chest physio BD
  • Antibiotics
  • Vaccinations
112
Q

What is a Pneumothorax?

A

Presence of gas in the pleural space

113
Q

What are the types of Pneumothorax?

A

Primary: no underlying lung pathology
Secondary: underlying lung disease

Closed: Pleuritic cavity pressure < atmospheric pressure

Open: Air can enter the chest from the outside

Tension: Pleuritic cavity pressure > atmospheric pressure

  • One way valve formed between damaged tissue so gas continues to enter
  • this significantly impairs respiration and/or blood circulation by putting pressure on the mediastinal/thoracic structures
114
Q

What are the features of Pneumothorax?

A
  • Chest pain
  • Shortness of breath
  • Reduced breath sounds on that side
  • Hyperresonance
  • Reduced vocal resonance and tactile fremitus ‘99’
115
Q

How are Pneumothoraces managed?

A

PRIMARY:
Small <2cm: Monitor
Large: Syringe and Chest drain into 2nd intercostal space mid clavicular line

SECONDARY:
Small: Syringe and Chest drain
Surgery: Pleurodesis- stick pleura together or Pleurectomy-remove the pleural membranse

Will fail to inflate if there is an injury to a right main bronchus

116
Q

What is Atelectasis?

A

BLOCKAGE or INCREASED PRESSURE in or around BRONCHIOLES
BASAL ALVEOLAR COLLAPSE causing COLLAPSE OF 1 or MORE LOBES
RESPIRATORY DIFFICULTY (Tachypnoea and Pleural Effusion)
AIRWAYS OBSTRUCTED BY BRONCHIAL SECRETIONS with REDUCED OR ABSENT GAS EXCHANGE
AIR IS TRAPPED

Causes by:

  • TB
  • Post-op
  • Lack of surfactant in infants
117
Q

What are the features of Tension Pneumothorax?

A
  • Respiratory distress
  • Tachycardia
  • Cyanosis
  • Reduced consciousness

Displacement of Apex HB
Resonance on tapping the sternum
Trachea displaced away from the collapse
JVP

118
Q

What are the features of an Obstructive respiratory disease pattern?

A

Reduced FEV1
FVC normal or a bit reduced

FEV1/FVC= REDUCED

e.g. Asthma, COPD, Bronchiectasis

119
Q

What is Bronchiolitis Obliterans?

A

Popcorn lung

Obstruction of smallest airways due to inflammation

120
Q

What are the feature of a Restrictive respiratory disease pattern?

A

Reduced FEV1
Reduced FVC
equally

FEV1/FVC= NORMAL OR RAISED

e.g. Fibrosis (aspestosis, sarcoidosis), ARDS
Neuromusclar and Kyphoscoliosis

121
Q

What are the causative organisms for TB?

A

MYCOBACTERIUM

TUBERCULOSIS

Bovis
Africanum

Non-mobile, rod bacili, obligate aerobe

122
Q

What is the pathophysiology of TB?

A

Mycobacterium ENGULFED by ALVEOLAR MACROPHAGES but can’t kill so continue to multiply

Primary complex of TUBERCLE LADEN MACROPHAGES
CASEATING GRANULOMA
Local drainage into HILAR LYMPH NODES
Lymphocytes and epitheloid + LANGHERHAN’S GIANT CELLS

GHON COMPLEX: INFECTION IS CONTAINED

123
Q

What are the features of Primary and Milliary TB?

A
Immune destruction of the lung
- Fever
- Cough: haemoptysis
- Night sweats
- Weight loss
- Malaise
- Breathlessness
- Crackles
- Pleural Effusion
- Cavitation and fibrosis
Seen on CXR
124
Q

What conditions can reactivate TB?

A
  • Diabetes
  • CKD
  • Haem malignancy
  • Organ transplant
  • Tumour necrosis
  • Silicosis
  • Low body weight
  • HIV
  • Substance abuse and IVDU
  • Immunosupression i.e. STEROIDS
125
Q

What are the extra-pulmonary features of Secondary TB?

A
  • Larynx
  • Lymph nodes -> cervical SCROFULODERMA
  • CNS -> TB meningitis
  • Renal spread to LUT
  • GI due to swallowing
  • Bones and Joints -> Vertebral bodies -> Pott’s
126
Q

What is Pott’s (TB)?

A

In the spine

127
Q

How is TB managed?

A

Rifampicin
Isonazid
Pyroxidine
Ethambutol

3 or 4 for 2/12
18/12 if CNS

128
Q

What are the diagnostic tests for TB?

A
  • NAAT and chromotography
  • ACID FAST
  • ZIEHL NEILSEN stain
  • Auramine stain
  • Culture is gold standard
  • Tuberculin Sensitivity Test on skin (delayed-type hypersensitivity reaction)
  • Gastric aspirates in children
129
Q

Define: stridor

A

narrow or obstructed upper airways, sounf od turbulent airflow through larynx or bronchial tree

130
Q

What is Obstructive Sleep Apnoea?

A

Throat muscles intermittently relax in sleep blocking airways, breathing repeatedly stops and starts

131
Q

What are the predisposing factors for Obstructive Sleep Apnoea?

A
  • MARFAN’S
  • large tonsils
  • Obesity -> loswe weight
  • Macroglossia e.g. in Acromegaly, Hypothyroidism, Amyloidosis -> Can manage with intraoral devices
132
Q

What are the consequnces of Obstructive Sleep Apnoea?

A

Daytime sleeping: EPWORTH sleepiness scale, multi-sleep latency test

Reduced arousal response in REM

HTN

Compensated RESPIRATORY ACIDOSIS

133
Q

What is Thoracoabdominal movement paradox?

A

Reverses inspiration/expiration chest contractions: abdomen moves weirdly