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Year 2 > Resp: Sarcoidosis, Pulmonary Hypertension, Pleural Effusion, > Flashcards

Resp: Sarcoidosis, Pulmonary Hypertension, Pleural Effusion, Flashcards

1
Q

What is Sarcoidosis

A
  1. Collection of granulomas depositing in the lung distal to the terminal bronchiole (alveolar and capillary interface)
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2
Q

Where does sarcoidosis begin

A

Lungs

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3
Q

Where does sarcoidosis commonly spread

A
  1. Eyes
  2. Liver
  3. Heart
  4. Brain
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4
Q

General clinical Presentation of sarcoidosis

A
  1. Fatigue
  2. Lack of energy
  3. Weight loss
  4. Arthralgia
  5. Arthritis
  6. Dry Eyes
  7. Swelling of the knees
  8. Shortness of breath
  9. Dry cough
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5
Q

What syndrome is seen in sarcoidosis

A

Löfgren syndrome

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6
Q

What is lofgren syndrome

A

Acute sarcoidosis with:

  1. Erythema nodosum
  2. Bilateral hilar lymphadenopathy
  3. Joint pain
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7
Q

Sarcoidosis in the lungs

A

Stage I: Bilateral hilar lymphadenopathy
Stage II: BHL with pulmonary infiltrates
Stage III: Pulmonary infiltrates without BHL
Stage IV: Fibrosis

LYMPHADENOPATHY is common in INTRATHORACIC nodes

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8
Q

Sarcoidosis in the skin

A

Erythema nodosum
Maculopapular eruptions
Lupus pernio

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9
Q

Sarcoidosis in the heart

A
  1. Ventricular arythmias
  2. Conduction abnormalities (complete heart block)
  3. Causes fluid accumulation in the heart interstitium
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10
Q

Sarcoidosis in the eye

A
  1. Uveitis!!

2. Retinal inflammaation (blindness)

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11
Q

What is Heerfordt syndrome

A
  1. Anterior uveitis
  2. Parotitis
  3. VII cranial nerve paralysis
  4. Fever

Caused from sarcoidosis

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12
Q

Sarcoidosis in the CNS

A

CRANIAL NERVES effected

  1. Bilateral Peripheral facial nerve palsy (most common)
  2. Papilloedema
  3. Optic nerve dysfunction
  4. MYELOPATHY
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13
Q

Sarcoidosis in endocrine system

A
  1. HYPERPROLACTINEMIA (which lead stop amenorrhea, galactorrhea int omen)
  2. Causes increases in 1,25 (OH)2D (hydroxylation occurs in immune cells of granulomas not the kidneys) - HYPERCALCAEMIA
  3. Parotid enlargement
  4. Dry Mouth
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14
Q

Sarcoidosis in GI

A
  1. Mimimcs crohn’s disease
  2. Nephrocalciniosis
  3. Hepatomegaly/splenomegaly
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15
Q

Sarcoidosis in the blood

A
  1. LYMPHOPENIA
  2. ANAEMIA
  3. Lymphadenopathy in INTRATHORACIC NODES
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16
Q

What is lymphopenia

A

Low levels of lymphocytes in the blood

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17
Q

Sarcoidosis in MSK

A

lofgren syndrome! (Arthralgia comes with bilateral hilar lymphadenopathy and erythema nodosum)

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18
Q

Where does arthritis of Sarcoidosis occur

A

Ankles

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19
Q

What do sarcoid granulomas consist of

A
  1. Focal accumulations of epithelial cells, macrophages and lymphocytes
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20
Q

What people are effected by sarcoidosis

A
  1. African-caribbeans
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21
Q

What gender is effected by sarcoidosis

A

Women

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22
Q

Age of people with sarcoidosis

A
  1. 20-40
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23
Q

What is lupus pernio

A

Blueish red and purple nodules over the nose

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24
Q

Differential diagnosis of sarcoidosis

A
  1. RA
  2. Lymphoma
  3. TB
  4. SLE
  5. Multiple myeloma
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25
Q

Diagnostics for sarcoidosis

A
  1. CXR (staging 1,2,3,4)
  2. Blood tests
  3. Bronchoscopy
  4. ECG
  5. Lung function tests
  6. Tissue biopsy
  7. Bronchoalveolar lavage
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26
Q

FBC results for sarcoidosis

A
  1. Raised ESR
  2. Lymphopenia
  3. Raised LFT
  4. Raised Ca
  5. Raised immunoglobulins
  6. Serum ACE
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27
Q

Results of lung function test in sarcoidosis

A
  1. Reduced lung volumes
  2. Restrictive ventilatory defect
  3. Impaired gas transfer
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28
Q

What would a tissue biopsy show for sarcoidosis

A
  1. NON-CAVEATING GRANULOMATA
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29
Q

How is sarcoidosis treated

A

PATIENTS WITH stage I (bilateral hailer lymphadenopathy) will recover without treatment

DO NOT treat asymptomatic patients at stage 2 or 3

ACUTE:

  1. Bed rest
  2. NSAIDs
  3. Corticosteroids (oral prednioslone or IV methylprednisolone if severe)
  4. Transplantation
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30
Q

What is Idiopathic pulmonary fibrosis

A
  1. Distinct cellular infiltrates and extracellular matrix deposition in lung distal to terminal bronchiole

MOST COMMON CAUSE of interstitial lung disease + idiopathic pneumonias

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31
Q

What gender is affected by IPF

A
  1. Males
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32
Q

Pathophysiology of IPF

A
  1. Repetitive injury to alveolar epithelium caused by environmental stimuli
  2. Wound healing becomes uncontrolled (too many fibroblasts produced and deposition in interstitium with LITTLE INFLAMMATION
  3. Structural integrity of lung parenchyma is disrupted: loss of elasticity and ability to perform gas exchange is impaired leading to progressive resp failure
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33
Q

Risk factors of IPF

A
  1. Cigarette smoking
  2. CMV, HIV, EBV
  3. Occupational dust exposure (metals, woods)
  4. Srugs (methotrexate, imipramine)
  5. GORD
  6. Genetic predisposition
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34
Q

Clinical presentation of IPF

A
  1. Show USUAL INTERSTITIAL PNEUMONITIS (patchy with lower lobes affected)
  2. Infiltrates spread causing lung collapse and dilated spaces in fibrotic areas of lung (honeycombing)
  3. Dry cough with sputum
  4. Dyspneoa
  5. Malaise
  6. Arthralgia
  7. Cyanosis
  8. Finger clubbing
  9. Bilateral basal end-inspiratory crackles
  10. PNeumothorac, pulmonary embolism or intercurrent infection
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35
Q

Differential diagnosis of IPF

A
  1. COPD
  2. Asthma
  3. Bronchiectasis
  4. Heart failure (congestive)
  5. Atypical pneumonia
  6. Lung cancer
  7. Asbestosis
  8. Hypersensitivity pneumonitis
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36
Q

Diagnostics of IPF

A
  1. FBC
  2. CXR
  3. High-res CT
  4. Spirometry
  5. Lung biopsy
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37
Q

FBC results in IPF

A
  1. ABG: Low paO2 and high CO2 if severe
  2. Raised CRP
  3. Raised immunoglobulins
  4. ANA and RF to exclude RA and SLE
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38
Q

CXR results in IPF

A
  1. Small volume lungs with INCREASED RETICULAR SHADOWING at bases)
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39
Q

Ct results in IPF

A
  1. Basal distribution
  2. Subpleural reticulation in lung peripheries
  3. Traction bronchiectasis (fibrotic process pulls airways open)
  4. Honeycombing (basal layers of small, cystic airspaces with irregularly thickened walls composed of fibrous tissue)
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40
Q

Spirometry trace in IPF

A
  1. RESTRICTIVE pattern
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41
Q

Why do we do a lung biopsy for IPF

A
  1. To check histology for Usual interstitial pneumonia
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42
Q

Treatment of IPF

A
  1. Serial lung function test
  2. Oxygen therapy
  3. Pulmonary rehabilitation
  4. Opiates
  5. Treat GORD to stop alveolar damage
  6. Treat cough
  7. Pirfenidone (antifibrotic agent to stop FVC decline)
  8. Lung transplants
  9. NO HIGH DOSE STEROIDS
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43
Q

Define pulmonary hypertension

A
  1. mPAP of above 25 mmHg
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44
Q

Pathophysiology of pulmonary hypertension

A
  1. Narrowing of blood vessels makes it harder for blood to be pumped through the lungs
  2. Blood vessels fibres and become stiffer and thicker
  3. Vasoconstriction and thrombosis occurs
  4. Vascular remodelling caused by inflammation occurs causing the blood vessels to become even stiffer and thicker
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45
Q

How does pulmonary hypertension affect the heart

A
  1. RV is not used to the higher pressure in the pulmonary artery causing int to hypertrophy to deal with high pressures - PRESERVES stroke volume of the heart

Eventually RV can’t get enough oxygen to meet its needs to RV HF occurs

  1. Left side of the heart receives les blood
  2. Becomes harder and harder for LV to pump to supply sufficient blood to tissues

LV can’t efificnetly pump so eventually blood moves back into the lungs causing pulmonary oedema and pleural effusions

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46
Q

What happens in pulmonary hypertension du etc lung disease or hypoxia

A

HYPOXIC PULMONARY VASOCONSTRICTION to stop too much blood flowing to areas that are damaged and have no oxygen - eventually increase in arterial pressure causes thickening of walls

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47
Q

What MSK conditions can cause Pulmonary hypertension

A
  1. Kyposcoliosis
  2. Poliomyelitis
  3. MG (causes muscle weakness)
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48
Q

Cardiac causes of pulmonary hypertension

A
  1. LV failure
  2. Left atria myxoma
  3. Congenital heart disease
  4. Mitral stenosis
  5. Appetite suppression drugs
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49
Q

Clinical presentation of pulmonary hypertension

A
  1. Shortness of breath
  2. Fatigue
  3. Chest pains
  4. Palpitations
  5. Right side of abdo pain
  6. Poor appetite
  7. Syncope
  8. Syncope
  9. Swelling of ankles
  10. Third heart sounds
  11. right Parasternal heave due to hypertrophies right atrium
  12. Loud pulmonary second sound

Signs of HF

  1. ASICTES
  2. Hepatojugular reflux
  3. Hepatomegaly
  4. Prominent V wave in tricuspid regurgitation
  5. Elevated jugular venous pressure
  6. Pleural effusion
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50
Q

Differential diagnosis of pulmonary hypertension

A
  1. Cor pulmonale
  2. Cardiomyopathies
  3. Primary RV HF
  4. Congestive cardiac failure
  5. Portal hypertension
51
Q

Diagnostics of pulmonary hypertension

A
  1. CXR
  2. ECG
  3. ECHO
  4. LFT for portal hypertension
  5. RIGHT HEART CATHETERISATION
  6. CT
52
Q

CXR results for pulmonary hypertension

A
  1. Enlarged proximal pulmonary arteries which taper distally
  2. Enlarged heart
  3. Emphysema or calcified mitral valve
53
Q

ECG results in pulmonary hypertension

A
  1. RV hypertrophy and Pulmonale (tall and peaked P waves)
54
Q

ECHO in pulmonary hypertension

A
  1. RV dilatation and hypertrophy

SHUNTS

55
Q

How is pulmonary hypertension treated

A
  1. OXYGEN
  2. Warfarin
    3, Diuretics
  3. Oral calcium channel blockers
  4. Endothelia receptor antagonist (bosenten)
  5. Phosphodiesterase-5 inhibitors
  6. Prostanoid (mediators of vasoconstriction) analogues - iloprost
  7. Heart-lung transplant
56
Q

CT results in pulmonary hypertension

A
  1. Enlargement of the pulmonary trunk

2. Mural calcification (patients with eisenmenger’s syndrome)

57
Q

What is pleural effusion

A
  1. Excessive accumulation of fluid in pleural space
58
Q

Functions of th epleura

A
  1. Allows movement of lung against chest wall
  2. Coupling system between lungs and chest wall
  3. Clearing fluid from pulmonary interstitium
59
Q

What is contained in pleural fluids

A
  1. Proteins - albumin, globulin and fibrinogen

2. Mesothelial cells, monocytes and lymphocytes

60
Q

Where is pleural fluid produced

A

Parietal pleura (lymphatic stoma)

61
Q

How is pleural fluid drained

A

Lymphatic pump (contractions of smooth muscles in lymphatic walls)

62
Q

What condition has recurrent pleural effusions

A
  1. Malignant mesothelioma
63
Q

Risk factors for pleural effusions

A
  1. Previous lung damage

2. Asbestos exposure

64
Q

Transudative cause of pleural effusion

A
  1. HEART FAILURE, CIRRHOSIS and NEPHROTIC SYNDROME
  2. Cause loss in albumin and reduced colloid osmotic pressure
3. Occurs when there is high venous pressure:
Heart failure
Constrictive pericarditis 
Fluid overload
Hvpoporteinaemia  
Peritoneal dialysis 
Hypothyroidism
65
Q

What is exudate pleural effusion

A

Pleural fluid protein is more than 30g/L since endothelial cells of vessels are more apart meaning fluid and protein is able to leak out

Occurs due to increased permeability and thus leakiness of pleural space and capillaries due to inflammation, infection or malignancy

66
Q

What conditions cause exudate pleural effusion

A
  1. Pneumonia
  2. Malignancy
  3. TB
  4. Pulmonary infarction
  5. Lymphoma
  6. Mesthothelioma
  7. MI
67
Q

Other than exudate and transudate pleural effusions what else can cause them

A
  1. Haemothorax
  2. Empyema
  3. Lymph fluid (chylotorax - caused by leakage of lymph from thoracic duct as a result of trauma or infiltration by carcinoma)

Build up of fluid results in pressure increase on lungs - breathing difficulty

68
Q

Clinical presentation of pleural effusions

A

CXR
1. NORMALLY space between visceral and parietal pleura is not seen, you can see it in lower portions of the lungs
2. Effusions reduce costophrenic angles
3. Water-dense shadows with concave upper borders in larger
4. Completely flat horizontal upper border implies PNEUMOTHORAX co-infection
Ultrasound
Diagnostic aspiration
Biopsy

69
Q

What is seen in ultrasound for pleural effusions

A
  1. Identifying presence of pleural fluid and diagnosing therapeutic aspiration
70
Q

What is seen in diagnostics aspiration

A
  1. Pus effusion (prurient in empyema)
  2. Turbid (cloudy) in infections
  3. Milky in chylothorax

Sample sent for pH (acidity = infection), cytology (WCC) and microbiology (gram stain and culture)

71
Q

Treatment of pleural effusions

A
  1. Exudates are DRAINED
  2. Transudates are treated by treating underlying caused
  3. Malignant effusion reaccumualte after drainage
  4. Pleurodesis
  5. Surgery to stop increasing pleural thickness
72
Q

What is pleurodesis

A
  1. Injection that causes adhesion of visceral and parietal pleura to help prevent accumulation of the effusion (tetracycline)
73
Q

Three forms of Parapneumonic effusion

A
  1. Simple (non-infected) - will resolve on its own
  2. Complicated (infected) - DRAINAGE
  3. Empyema - requires drainage
74
Q

Define pneumothorax

A

Air in the pleural space leading to partial or complete collapse of the lung

75
Q

What causes pneumothorax

A

Divided into primary and secondary spontaneous pneumothorax

76
Q

What causes primary spontaneous pneumothorax

A
  1. Occurs in absence of known lung disease

Decompression sickness when divers scuba dive

77
Q

What causes secondary spontaneous pneumothorax

A
  1. COPD
  2. TB
  3. Connective tissue diseases - RA, ankylosing spondylitis and polymyositis
  4. Lung cancer
  5. Trauma
78
Q

What hereditary syndrome causes pneumothorax

A
  1. alpha 1-antitrypsin deficiency
  2. Ehlers-Dalos syndorme
  3. Marfan syndrome
79
Q

Pathophysiology of pneumothorax

A
  1. Normall presspur ein pleural space is negative but is lost when there is communication with atmospheric pressure + elastic recoil of lungs causes it to deflate partially
  2. Communication between airways and pleural space remains open causing bronchopleural fistula to form
  3. Once communication between the lung and pleural space is closed, air is reabsorbed slowly
80
Q

What patients are commonly affected by spontaneous pneumothorax

A

MALES YOUNG

Tall and thin

81
Q

What is tension pneumothorax

A
  1. When opening that allows air to enter pleural space functions as a one way valve - AIR CANNOT ESCAPE
  2. Body compensates by increasing resp rate and tidal volume which worsens the problem
  3. Hypoxia and respiratory arrest follows
82
Q

What patients tend to get tension pneumothorax

A
  1. On ventilation
  2. On Resus
  3. Trauma
  4. Lung disease
83
Q

Clinical presentation of tension pneumothorax

A
  1. Tachycardia
  2. Tachypnoea
  3. Low O2
  4. Low BP
  5. Trachea deviated away from the affected side
84
Q

Clinical presentation of pneumothorax

A
  1. YOUNG MALE
  2. Chest pains
  3. Breathlessness
  4. Hypoxia (cyanosis)
  5. Hypercapnia (causes confusion and drowsiness, flapping tremors)
  6. Mechanically ventilated patients will present with hypoxia
  7. Reduced expansion, hyper-resonance to percussion and diminished breath sounds of affected lung
  8. UNILATERAL pleuritic chest pain
85
Q

Differential diagnosis of pneumothorax

A
  1. Pleural effusion
  2. Chest pains
  3. Pulmonary embolism
86
Q

Diagnostics of pneumothorax

A
  1. CXR (not needed in tension pneumothorax - wastes time)

2. ABG

87
Q

CXR result for pneumothorax

A
  1. Look for area devoid of lung markings, peripheral to the edge of the collapsed lung
88
Q

How is pneumothorax treated

A
  1. CHEST DAIN if due to trauma, haemothorax or mechanical ventilation
  2. Needle aspiration then chest drain for tension pneumothorax
  3. Observation
  4. Oxygen for hypoxia
  5. Surgery for persistent pneumothorax
  6. Smoking cessation
89
Q

What is needle aspiration needed for in pneumothorax

A

Removes excess air

90
Q

Risk factors of bronchial carcinoma

A
  1. Cigarette smoking
  2. Occupational jobs:
    Asbestos
    Coal
    Chromium
    Arsenic
    Nickel
    Petroleum products
    Iron Oxide
  3. Environmental:
    Radon exposure
    Ionising radiation
  4. Host factors:
    Pre-existing lung disease such as pulmonary fibrosis
    HIV infection
    Genetic factors
91
Q

What main types of bronchial cancer are there

A
  1. Small cell lung carcinoma
  2. Squamous carcinoma
  3. Adenocarcinoma
  4. Large cell and differentiated carncioma
92
Q

Why is small cell lung carcinoma dangerous

A
  1. Spreads by the time clinical presentations arise (metastases is early)
93
Q

Where is small ell lung carcinoma seen

A
  1. Central bronchus
94
Q

What can does small cell lung carcinoma arise from

A
  1. Arises from endocrine cell so the tumours secretes polypeptide hormones
95
Q

Primary treatment for small cell lung carcinoma

A
  1. CHEMOTHERAPY
96
Q

What causes non-small cell lung carcnioma

A

CIGARETTE SMOKING

97
Q

Why is non-small cell lung carcinoma dangerous

A

May have metastasised by the time of diagnosis

98
Q

How is non-small cell lung carcinoma treated

A

Surgical oblation with lymph node sampling

CHEMOTHERAPY and RADIOTHERAPY as follow-up

99
Q

Where do squamous cell carcinomas arise

A

Tumours are central in location and capitate with central necrosis

100
Q

What do swaumous cell lung carcinomas secrete

A

Keratin

101
Q

Problems of squamous cell carcinoma in the lungs

A

Causes obstructive lesions of the bronchus with post-obstructive infection

102
Q

At what stage of the disease does squamous cell carcinoma metastases occur

A

Relatively late

103
Q

What is the most common type of non-small cell lung carcinoma

A
  1. ADENOCARCINOMA
104
Q

What are adenocarcinomas of th lung

A

Single lesions that arise in multifocal pattern (bilateral)

105
Q

Where do adenocarcinomas of the lung originate

A
  1. Mucus-secreting glandular cells
106
Q

What is seen on CXR and CT for adenocarcinomas of th lung

A
  1. Peripheral lesions
107
Q

Where does adenocarcinomas metastases

A
  1. Pleura
  2. Lymph node
  3. Brain
  4. Bones
  5. Adrenal glands
108
Q

What is lung adenocarcinoma associated with

A

ASBESTOS

109
Q

Where do lung carcinoid tumours arise

A

Middle age

110
Q

What do carcinoid tumours secrete

A

Neuroendocrine secreting cells

111
Q

Why does it take time for carcinoid tumours to grow

A
  1. Low rate of invasion but still malignant
112
Q

What i the main lung lymphoma called

A

BALTOMA (Bronchus Associated Tissue Lymphoma) - B cell lymphoma

113
Q

What is a common benign tumour of the lung

A

HAMARTOMAS

114
Q

What are hamartomas

A
  1. Irregular proliferations of benign/normal tissues that are not normally found within the lung s
115
Q

What i the most common type of hamargtoma

A

Chondroid hamartoma (Incorporates cartilage glandular tissue, fat, fibrous tissue and blood vessels)

116
Q

Where do small cell carcinomas grow

A

Main Bronchi

117
Q

What do small cell carcinomas secrete

A

Adrenocorticotropic hormones

Excess cortisol - Cushing’s

OR autoantibodies against neurones:
Lambert-Eaton Myasthenic Syndrome

118
Q

Where do adenocarcinomas and squamous cell carcinomas occur

A

Adeno - peripheries (alveoli)

Squamous - Bronchi

119
Q

Pathophysiology of adenocarcinomas and sqamous carcinomas

A

Form pancoast tumours at the top of the lungs (compress blood vessels and brachial plexus + cervical sympathetic nerve)

Horner’s syndrome caused by cervixal sympathetic nerve

120
Q

What is Horner’s syndrome

A

Constricted pupils
Drooping Eyelid
Can’t sweat on same side as damage

121
Q

Clinical Presentation of squamous cell carcinoma

A 
Secretes keratin (obstructive lesions)
Produces PTH (osteoporosis)
122
Q

Bronchial carcinoma secretions

A

Secretes serotonin

123
Q

Clinical Presentation of bronchial carcinoid tumour

A

Serotonin:
Diarrhoea due to increased peristalsis

Bronchoconstriction: Asthma

124
Q

Clinical Presentation of lung cancer

A

Weight, Fever, Night Sweats

Obstructive:
Pneumonia
Shortness of breath
Cough

Compression of phrenic nerve: difficulty breathing
Compression of recurrent laryngeal: change in voice

Compression of blood vessels (superior vena cava) - face swelling and shortness of breath

Year 2 (155 decks)

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