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(SG) condensed phase 2a > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Define Chronic Obstructive Pulmonary Disease (COPD)

A

Poorly reversible airflow limitation, usually progressive and persistent inflammatory response.

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2
Q

Define Asthma

A

Reversive obstruction of the airways.

Bronchospasm and excessive airway secretions.

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3
Q

Types of COPD

Types of asthma?

A

Blue Bloaters and Pink Puffers.

Extrinsic and intrinsic

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4
Q

How does COPD clinically present?

A

Respiratory: Chronic cough,

exertional breathlessness,

regular sputum production, wheeze.

Other: Abnormal posture (leans forward),

drowsiness/mental confusion,

underweight, ankle oedema.

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5
Q

How does Asthma clinically present?

A

Wheeze, dyspnoea, chest tightness, cough (particularly if after exercise/cold air/allergen).

Hx: FH of asthma, past hx of atopy, regular episodes.

Paroxysmal.

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6
Q

What does blue bloaters refer to?

Compensatory …….

A

Chronic bronchitis is underlying pathology.

Compensatory increase in cardiac output leads to hypoxia.

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7
Q

What does pink puffers refer to?

Compensatory.

A

Emphysema underlying pathology.

Compensatory hyperventilation prevents hypoxia.

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8
Q

What causes extrinsic asthma?

A

External factors.

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9
Q

What causes intrinsic asthma?

A

Idiopathic.

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10
Q

Cause of COPD

A

Chronic inflammation of the airways.

Usually by smoking, also occupational irritants.

This causes the mucous gland hypertrophy, and increase in neutrophils, macrophages and lymphocytes in airways

-> Increase in inflammatory mediators (recurrent cycle)

-> Breakdown of lung tissue.

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11
Q

Cause of Asthma

A

Largely unknown.

Two main categories: Atopy: IgE antibodies readily produced against common exposures.

Increased responsiveness of airways to inhaled stimuli: histamine and methacholine.

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12
Q

Diagnostic test for COPD

A

Spirometry, CXR: >6 ribs visible (hyperinflation).

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13
Q

Diagnostic test for Asthma

A

History and evidence of obstruction (PEF / Spirometry) during episodes.

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14
Q

Treatment of COPD

A

Stop smoking (slows deterioration).

1: SABA or short-acting antimuscarinic

2: +LABA / + long acting antimuscarinic

3: Inhaled glucocorticoid

4: Long-acting antimuscarinic + LABA + Inhaled steroid

5: + Long term oxygen therapy (care not to remove hypoxic drive in blue bloaters).

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15
Q

Treatment of Asthma

A

SABA

-> Corticosteroids

-> LABA

-> Increase dose of corticosteroids

-> prednisalone

-> hospital.

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16
Q

Complications of COPD

A

Respiratory failure.

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17
Q

Complications of Asthma

A

Pneumonia,

pneuomothorax.

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18
Q

Define Rhinitis

A

Sneezing attacks,

nasal discharge

or blockage for more than 1 hour most days.

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19
Q

Define Bronchiectasis

A

Permanent dilatation and thickening of the airways.

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20
Q

Types of Rhinitis

A

Seasonal.

Perennial.

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21
Q

How does seasonal rhinitis clinically present?

A

Seasonal sneezing attacks, in response to allergens.

Rhinorrhoea and nasal congestion.

Itchy eyes.

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22
Q

How does perennial rhinitis clinically present?

A

All year round sneezing attacks in response to allergens.

Rhinorrhoea and nasal congestion.

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23
Q

How does Bronchiectasis clinically present?

A

Variance: Intermittent episodes of expectoration and infection

—> persistent daily expectoration of purulent sputum.

Resp symptoms: chest pain, dyspnoea and haemoptysis.

May present as persistent asthma.

Signs: Coarse crackles, wheeze possible.

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24
Q

When does seasonal rhinitis occur?

A

Hay fever’ occurs during summer months.

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25
Q

When does perennial rhinitis occur?

A

Occurs throughout the year.

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26
Q

Cause of seasonal rhinitis

A

Allergy to grass and tree pollen

and a variety of mould spores from cultivated plants.

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27
Q

Cause of perennial rhinitis

A

Allergens include house mites or domestic pets.

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28
Q

Cause of Bronchiectasis

A

Chronic inflammation of airways: large number of causative conditions;

Asthma, post-infection, immunodeficiency.

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29
Q

Diagnostic test for Rhinitis

A

Skin prick test with extensive medical history.

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30
Q

Diagnostic test for Bronchiectasis

A

HRCT: Bronchial wall dilation.

Thickening harder to define.

CXR: Exclude other causes.

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31
Q

Treatment of Rhinitis

A

Avoidance of allergens.

If practical; anti-histamines.

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32
Q

Treatment of Bronchiectasis

A

Prevent further deterioration.

Stop smoking.

Physiotherapy: Airway clearance.

Medication: Antibiotics, bronchodilators (if airflow obstruction).

Surgery: Lung resection.

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33
Q

Complications of Rhinitis

A

Reduced quality of life.

Sinusitis.

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34
Q

Complications of Bronchiectasis

A

Repeated infection,

respiratory failure,

pneumothorax (from coughing).

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35
Q

Sequelae of Rhinitis

A

Asthma.

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36
Q

Define Cystic fibrosis

A

Mutated CFTR Cl transport

-> Dysfunction of secretions

-> multiple organ dysfunction.

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37
Q

Define Sarcoidosis

A

Multisystem chronic inflammatory condition

  • formation of non-caseating epithelioid granulomata.
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38
Q

Types of Cystic fibrosis

A

Various mutations.

Most common DF508.

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39
Q

How does Cystic fibrosis clinically present?

A

Infancy: Recurrent resp infections, diarrhoea, failure to thrive,

rectal prolapse, nasal polyps, acute pancreatitis,

portal hypertension, variceal haemorrhage, steatorrhoea.

Adults: Recurrent resp infections, atypical asthma, bronchiectasis,

male infertility (congenital bilateral absence of vas deferens),

heat exhaustion, portal hypertension, steatorrhoea.

Signs: Finger clubbing, cough with purulent sputum, crackles,

wheezes, resp obstruction

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40
Q

How does Sarcoidosis clinically present?

A

50% of time, asymptomatic; incidental CXSR discovers.

Can affect any organ.

Tends towards lungs, eyes and skin.

Lung (>90% of cases): Dyspnoea, non-productive cough.

Skin: Erythema nodosum.

Eye: Granulomatous uveitis.

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41
Q

What is significant about cystic fibrosis?

A

Most common inherited condition.

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42
Q

What is sarcoidosis the most common cause of?

A

Lung granulomas.

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43
Q

Pathophysiology of Sarcoidosis

A

Non-caseating granulomata form at various sites in the body, particularly the thoracic cavity, skin and eyes.

Bilateral hilar lymphadenopathy and/or pulmonary infiltrations.

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44
Q

Cause of Cystic fibrosis

A

Autosomal recessive.

Various mutations.

Most common DF508.

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45
Q

Cause of Sarcoidosis

A

Unknown.

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46
Q

Diagnostic test for Cystic fibrosis

A

Sweat test (98% sensitive),

genetic testing,

sinus X ray (opacification of sinuses)

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47
Q

Diagnostic test for Sarcoidosis

A

CXR, High serum ACE.

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48
Q

Treatment of Cystic fibrosis

A

Resp: Chest physio 2qd, prophylactic antibiotics, bronchodilators

Nasal polyps: Steroids, poss. Polyopectomy

Endocrine: Pancreatic enzymes.

General: High protein intake, genetic counselling

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49
Q

Treatment of Sarcoidosis

A

If no pulmonary infiltration: No treatment; remits in 2/3s of cases in two years.

If pulmonary infiltration: prednisalone.

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50
Q

Complications of Sarcoidosis

A

Respiratory failure and renal damage.

10% risk of death in black people.

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51
Q

Sequelae of Cystic fibrosis

A

Osteoporosis,

psych problems.

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52
Q

Define Idiopathic pulmonary fibrosis

A

Fibrosis of lung interstitium causing restrictive respiratory defect.

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53
Q

Define Pulmonary hypertension

A

Increase in mean pulmonary arterial pressure (>20mmHg).

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54
Q

How does Idiopathic pulmonary fibrosis clinically present?

A

Breathlessness, non-productive cough.

Finger clubbing (2/3) inspiratory basal crackles.

Eventually leading to: resp failure, pulmonary hypertension, cor pulmonale.

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55
Q

How does Pulmonary hypertension clinically present?

A

Exertional dyspnoea, lethargy and fatigue (inability to ^CO with exercise).

Once Rt Vent failure develops:

Peripheral oedema and abdominal pain (hepatic congestion).

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56
Q

Pathophysiology of Idiopathic pulmonary fibrosis

A

Patchy fibrosis of interstitium,

minimal or absent inflammation,

acute fibroblastic proliferation and collagen deposition.

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57
Q

Pathophysiology of Pulmonary hypertension

A

Depends on aetiology. Increase in pulmonary vascular resistance

-> Increase in mean pulmonary arterial pressure.

If chronic, this can cause damage to vasculature and further disease.

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58
Q

Cause of Idiopathic pulmonary fibrosis

A

Idiopathic.

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59
Q

Cause of Pulmonary hypertension

A

Various causative conditions

-> Increase in pulmonary vascular resistance.

Hereditary, idiopathic, SLE, HIV, Portal hypertension.

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60
Q

Diagnostic test for Idiopathic pulmonary fibrosis

A

CXR: Ground Glass appearance => honeycomb lung.

(CT :most sensitive).

ABG: hypoxia normal CO2.

Spirometry. ANA and RF Ab in 1/3.

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61
Q

Diagnostic test for Pulmonary hypertension

A

CXR: Enlarged pulmonary arteries.

ECG: Ventricular hypertrophy.

62
Q

Treatment of Idiopathic pulmonary fibrosis

A

High dose prednisolone (30mg).

Lung transplant.

63
Q

Treatment of Pulmonary hypertension

A

Oxygen, warfarin and diuretics for oedema, with oral CCB for pulmonary vasodilation.

Treat underlying cause.

64
Q

Complications of Pulmonary hypertension

A

Deteriorating Rt Heart function/failure (Cor pulmonale).

Pleural effusions.

Sudden cardiac death.

65
Q

Sequelae of Idiopathic pulmonary fibrosis

A

Median survival 5 years without transplant.

66
Q

Define pleural effusion

A

Pleural fluid is substantially higher volume than normal.

67
Q

Types of pleural effusion

A

Transudate.

Exudate.

Chylothorax.

68
Q

How does pleural effusion clinically present?

A

Asymptomatic, if small.

Otherwise dyspnoea.

Signs: Reduced chest wall movement,

dull ‘stony’ percussion,

absent breath sounds,

reduced vocal resonance.

69
Q

Cause of Transudate pleural effusion

A

Heart failure,

cirrhosis,

hypoalbuminaemia,

peritoneal dialysis.

70
Q

Cause of Exudate pleural effusion

A

Pneumonia,

malignancy,

pulmonary embolus with infarction.

71
Q

Cause of Chylothorax pleural effusion

A

Neoplasm,

trauma,

TB,

sarcoidosis,

cirrhosis.

72
Q

Diagnostic test for pleural effusion

A

CXR: Bilateral effusions indicate congestive cardiac failure.

Pleural aspiration: If clinical picture suggests transudate; avoid.

73
Q

Treatment of Transudate pleural effusion

A

Treat underlying cause.

Small effusions;

observation.

74
Q

Treatment of Exudate pleural effusion

A

Drained. If recurrent malignant;

possible pleurodesis following aspiration.

75
Q

Treatment of Chylothorax pleural effusion

A

Depends on cause.

Trauma; surgical repair and drain.

Malignant; possible pleurodesis following aspiration.

76
Q

Complications of Transudate pleural effusion

A

Depends on cause.

Unilateral heart failure

-> congestive heart failure.

77
Q

Complications of pleural and chylothorax pleural effusion

A

If caused by malignancy; poor prognosis.

78
Q

Define Pneumothorax

A

Collection of air in the pleural cavity

-> collapse of lung.

79
Q

Types of Pneumothorax

A

Primary Spontaneous (PSP).

Secondary.

Tension pneumothorax.

80
Q

How does PSP and Secondary pneumothroax clinically present?

A

Sudden onset of pain.

Shortness of breath.

81
Q

How does tension pneumothorax clinically present?

A

Sudden onset of pain.

Shortness of breath.

Severe respiratory distress.

82
Q

Pathophysiology of PSP and Secondary pneumothorax?

A

Pocket of air in the pleural cavity

-> Partial/complete collapse of the lung on affected side.

83
Q

Pathophysiology of tension pneumothorax

A

Pleural tear acts as a one-way valve.

Allows air into the cavity but not out. Increasing unilateral pressure

-> Severe respiratory distress,

shock and cardio-respiratory arrest.

84
Q

Cause of primary spontaneous pneumothorax

A

Thought to be a congenital issue

-> Rupture of the pleural bleb.

Can be trauma.

85
Q

Cause of secondary pneumothorax

A

Depends on underlying disease.

Associated with COPD.

Can be due to trauma.

86
Q

Cause of tension pneumothorax

A

Rare, can be iatrogenic from mechanical ventilation/chest drains.

Can be trauma.

87
Q

Diagnostic test for PSP and Secondary pneumothorax

A

CXR.

88
Q

Diagnostic test for tension pneumothorax

A

Skip - immediate action.

89
Q

Treatment of pneumothorax

A

Aspiration and oxygen.

Stop smoking to prevent recurrence.

Pleurodesis.

90
Q

Complications of PSP and Secondary pneumothorax

A

Recurrence.

91
Q

Complications of tension pneumothorax

A

Imminent death.

92
Q

Define Mesothelioma

A

Cancer of the mesothelial cells.

93
Q

Define carcinoma of the lung

A

Cancer of a lung cell

(95% of the time bronchial).

94
Q

Types of lung cancer -

A

Non-small: Squamous.

Non-small: Large cell.

Non-small: Adenocarcinoma.

Small cell.

95
Q

How does mesothelioma clinically present?

A

Shortness of breath,

dull diffuse chest pain (occasionally pleuritic),

weight loss, lethargy.

Pleural effusion.

History of asbestos exposure, sometimes.

Potentially a palpable chest wall mass.

96
Q

How does carcinoma of the lung clinically present?

A

Local effects: Cough, chest pain, haemoptysis and breathlessness.

Spread within chest: Involve pleura/ribs -> pain and fractures.

Spread to brachial plexus causes pain in shoulder and arm.

Spread to sympathetic ganglion -> Horner’s syndrome.

Spread to left recurrent laryngeal nerve -> hoarseness of voice.

Metastases: Bone and brain

Other: Weight loss and finger clubbing.

97
Q

Mesothelioma - note

A

Rarely metastasises to distant sites.

Associated with asbestos.

98
Q

Non-small: Adenocarcinoma (lung cancer) - note

A

Most common lung cancer in non-smokers.

99
Q

Pathophysiology of Non-small: Squamous (lung cancer) clinically present?

A

Most present as obstructive lesion -> infection.

Occasionally cavitates.

Commonly has local spread.

Widespread metastases.

100
Q

Cause of mesothelioma

A

Strong association with asbestos inhalation (80% of cases attributable).

Genetic risk.

101
Q

Cause of all 3 non-small lung cancers

A

Smoking, urban areas and asbestos exposure.

Probably a genetic risk.

102
Q

Cause of small cell lung cancer

A

Smoking, urban areas and asbestos exposure.

Probably a genetic risk.

103
Q

Diagnostic test for mesothelioma

A

CXR: Pleural effusion.

Potentially rib destruction.

Pleural aspiration: Straw coloured or blood stained.

Pleural biopsy: Gold standard.

104
Q

Diagnostic test for carcinoma of the lung (all types)

A

CXR: Round fluffy/spiking shadow

Sputum/Bronchoscope biopsy: Determine cell type.

105
Q

Treatment of mesothelioma

A

Surgical: Ressection (pleurectomy and decortication may relieve pain and effusions)

Chemo: Improves survival of patients with unressectable mesothelioma.

Radio: Mostly for pain control if at all.

106
Q

Treatment of all 3 non-small lung cancers

A

Surgery can be curative.

Chemo can downstage tumours to render them operable.

Radio: Large doses can help localised squamous cancers (can cause fibrosis).

107
Q

Treatment of small cell lung cancer

A

Limited disease (single anatomical or radiation field):

Chemo- Radio- combination.

Extensive disease: Chemotherapy.

108
Q

Complications of mesothelioma

A

Poor prognosis.

109
Q

Complications of carcinomas of the lung (all types)

A

Local: Nerve palsy (recurrent laryngeal, Horner’s syndrome)

Metastatic: Brain; confusion, fits, neuro deficit

Bone; pain, hypercalcaemia

Liver; Hepatomegaly

Non-metastatic: Endocrine; IADHS, Cushings, hyperthyroidism.

Skeletal; clubbing.

110
Q

Define Pulmonary thromboembolus and infarct

A

Thromboembolus blocks right ventricular outflow, pulmonary arteries, branches.

111
Q

Types of Pulmonary thromboembolus and infarct

A

Small-medium.

Massive - (medical emergency).

112
Q

How does a small-medium pulmonary thromboembolus and infarct clinically present?

A

Breathlessness,

pleuritic chest pain,

haemoptysis if infarction.

Tachypnoea, pleural rub, exudative pleural effusion.

113
Q

How does a massive pulmonary thromboembolus and infarct clinically present?

A

Severe central chest pain,

shock,

pale,

sweaty,

tachypnoea,

tachycardia,

cyanosis,

^JVP, RV heave and ^2nd heart sound + gallop.

114
Q

Small-medium pulmonary thromboembolus and infarct - note

A

Can be clinically silent.

115
Q

Cause of pulmonary thromboembolus and infarct

A

Risk factors for DVT (see heamotology).

Long periods of immobility (usually sat down) such as a long flight or surgery.

116
Q

Diagnostic test for pulmonary thromboembolus and infarct

A

Revised Geneva score to predict probability of PE.

CXR (decreased vascular markings, raised hemi diaphragm).

ECG may exclude differentials eg MI. D-dimers, spiral CT.

ECHO diagnostic and can be performed at bedside, good for massive.

117
Q

Treatment of pulmonary thromboembolus and infarct

A

Initial therapy: Oxygen.

Thrombolysis, LMWH, warfarin.

High risk of recurrence: Vena cava filter.

118
Q

Complications of massive pulmonary thromboembolus and infarct

A

Acute right heart failure,

syncope and death follow rapidly.

119
Q

Define Acute coryza

A

Common cold - infection by rhinovirus.

120
Q

Define Influenza

A

Infection by influenza virus.

121
Q

Types of Influenza

A

Serotype A

Serotype B

Serotype C

122
Q

How does Acute coryza clinically present?

A

Incubation period of 12hrs - 5 days.

Then, malaise, mild pyrexia, sore throat and watery nasal discharge.

123
Q

How does Influenza clinically present?

A

Incubation period of 1-3 days.

Abrupt fever, aching in limbs, sore throat and dry cough.

124
Q

Influenza - Serotype A - note

A

More frequent and cause of major outbreaks.

Further categorised by surface antigens: H (haemagglutinin) and N (neuraminidase).

125
Q

Influenza - Serotype B - note

A

Tends to circulate with A in yearly outbreaks.

Not as severe.

126
Q

Influenza - Serotype C - note

A

Mild/asymptomatic illness akin to the common cold.

127
Q

Pathophysiology of Acute coryza

A

Virus binds to ICAM-1 receptors

-> releases inflammatory mediators by unknown mechanism.

128
Q

Cause of Acute coryza

A

Infection by rhinovirus:

spread by droplets and close personal contact.

129
Q

Cause of Influenza

A

Infection by influenzae virus.

Transmission by droplet or direct nasal or eye contact with hands carrying virus.

130
Q

Diagnostic test for Influenza

A

Not needed.

Serology shows four fold increase in antibody titre over a 2 week period.

131
Q

Treatment of Acute coryza

A

Symptomatic.

Nasal decongestants, ibuprofen for malaise.

132
Q

Treatment of Influenza

A

Symptomatic.

Paracetamol, bed rest, fluids.

133
Q

Complications of Influenza

A

Pneumonia, either viral or bacterial.

134
Q

Define Pneumonia

A

Acute inflammation,

with intense infiltration of neutrophils in and around alveoli and terminal bronchioles.

135
Q

Define Tuberculosis

A

Infection by Mycobacterium tuberculosis.

136
Q

Types of Pneumonia

A

Location.

Causative agent.

137
Q

Types of Tuberculosis

A

Primary TB.

Milliary TB.

Secondary TB.

138
Q

Primary TB - note

A

Dormant infection within calcified caeseating granulomatous lesions.

139
Q

Milliary TB - note

A

Initial infection is not successfully controlled by caeseating granulomas.

140
Q

Secondary TB - note

A

Occurs when semi dormant TB is activated by impaired immune function,

as in AIDS, malnutrition or immunosuppressive therapy.

141
Q

How does Pneumonia clinically present?

A

Vary depending on infecting agent.

Most commonly; pyrexia, cough, sputum, pleurisy, dyspnoea, pleural effusion, pleural rub.

142
Q

How does Primary TB clinically present?

A

Asymptomatic.

143
Q

How does Milliary and Secondary TB clinically present?

A

Fatigue, malaise, fever, weight loss, anorexia, failure to thrive, pyrexia.

144
Q

Pathophysiology of TB

A

Initial infection: bacteria is engulfed by macrophages in the lung and stored in granulomas.

Leaves granulomatous lesions (caseating centres, surrounded by epithelial cells).

Can lay dormant around the body; moved by lymph.

Reactivated by being immunocompromised.

145
Q

Cause of Pneumonia

A

Various causative agents; S. aureus, L. pneumophila, M. pneumoniae.

Can be iatrogenic.

Community Acquired, due to atypical pathogens, or occur in the immunocompromised.

146
Q

Cause of TB

A

Commonly spread by inhalation of droplets.

Infection with TB.

147
Q

Diagnostic test for Pneumonia

A

CXR: Consolidation.

FBC and sputum culture.

CURB 65.

148
Q

Diagnostic test for Primary TB

A

Tuberculin test positive.

Normal CXR.

149
Q

Diagnostic test for Milliary and Secondary TB

A

CXR: pleural effusion.

Typical; patchy or nodular shadow.

Microbio samples: Culture of sputum

150
Q

Treatment of Primary TB

A

As with Active TB,

in patients identified as being at risk.

151
Q

Treatment of Milliary and Secondary TB

A

6 month drug treatment: Isoniazid,

rifampicin (first two months; pyrazinamide and ethambutol).

152
Q

Treatment of Milliary and Secondary TB

A

6-month drug treatment: Isoniazid,

rifampicin (first two months; pyrazinamide and ethambutol).

(SG) condensed phase 2a (9 decks)

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