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REsp Flashcards

1
Q

Hospital acquired pneumonia - antibiotics to use

A

Ceftriaxone (low risk: HA from ward)

High risk: from ICU, ventilator etc (concern about pseudomonas)
Tazosin = piperacillin/tazobactram

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2
Q

Common causes of HA pneumonia

A

Gram neg: klebsiella, E coli, pseudomonas, bacteroides

MRSA

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3
Q

Common causes of community acquired pneumonia (typical)

A

Strep pneumonia (90% cases)
H influenzae
Moraxella
Staph aureus

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4
Q

Common causes of community acquired pneumonia (atypical)

A

Mycoplasma pneumonia
Chlamydia pneumoniae
Legionella

Pneumocystis Jiroveci

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5
Q

What is COPD characterised by?

A

airway inflammation and limitation that IS NOT FULLY reversible (asthma is fully reversible so is not COPD)

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6
Q

What medical conditions does COPD include? Define them

A

Emphysema - dilation and destruction of lung tissue distal to terminal bronchiole (alveolar wall destruction and overinflation)

Chronic bronchitis - persistent PRODUCTIVE cough for at least 3 consecutive months in at least 2 consecutive years (airway inflammation)

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7
Q

Risk factors/causes of COPD

A 
Cigarette smoking 
Air pollution
Occupational exposure 
Alpha1 antitrypsin deficiency 
Recurrent RTIs in childhood
Genetics
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8
Q

What pattern would you see on respiratory function test with COPD?

A

Restrictive lung disease.
Forced expiratory ratio (FEV1/FVC) <70% indicating airflow obstruction.
FEV1 is reduced but FVC normal.

With no improvement with bronchodilator (ventolin).

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9
Q

Pathophysiology of emphysema

A

Noxious agent causes release of destructive cytokines and neutrophils, macrophages and CD8+ T cells which cause ongoing destruction of lung parenchyma - destruction of elastin and alveolar membranes -> reduced elastic coil - air trapping during expiration

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10
Q

Pathophysiology of chronic bronchitis

A

Noxious agent causes release of destructive cytokines and neutrophils, macrophages and CD8+ T cells which cause ongoing destruction of lung parenchyma and airway inflammation and remodelling

-> enlarged mucus secreting glands, goblet cell metaplasia, bronchial wall fibrosis, hyper secretion of mucus, inflammation

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11
Q

Clinical features of COPD

A

Chronic productive cough
Wheeze
SOB

HX smoking

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12
Q

What will you find on chest examination for COPD (Non-examination)

A 
Auscultation - breath sounds reduced with prolonged expiratory phase, wheeze 
Percussion - normal/hyper-resonance
Vocal resonance - normal or reduced
Hyperinflation (barrel chest)
Decr expansion
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13
Q

Classic CXR findings for COPD

A

hyperinflation (>6 ribs anterior ribs above diaphragm in mid-clavicular line)
Flat hemidiaphragms
Large central pulmonary arteries
Decr peripheral vascular markings

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14
Q

Management plan for COPD

A

CONFIRM diagnosis w pulmonary function tests

  • smoking cessation
  • influenza and pneumococcus vaccine (reduces risk of exacerbations)
  • pulmonary rehab
  • medications (depend on stage of disease)
  • Long-term o2 therapy if chronic resp failure (Stage 4) - must be non-smokers
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15
Q

Pharmacological treatment of COPD

A

Stage 1: Short acting bronchodilators when needed

  • Short acting beta 2 agonists (Salbutamol/Ventolin)
  • SAMAR (ipratropium)

Stage 2: regular treatment with one or more long acting bronchodilators

  • LABAs (Salmeterol/Serevent)
  • LAMAR (Tiotropium/Spiriva)

Stage 3/4: Inhaled glucocorticosteroids if repeated exacerbations

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16
Q

Complications of COPD

A

CHRONIC BRONCHITIS COMPLICAITONS:

  • SCC of lung resulting from squamous metaplasia
  • Infective exacerbations
  • Hypoxia -> pulmonary HTN -> cor pulmonale

EMPHESEMA COMPLCIATIONS

  • Loss of diffusion capacity
  • pneumothorax
  • hypoxia -> pulmonary HTN -> cor pulmonale
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17
Q

Management of exacerbation of COPD

A

Give O2

Bronchodilators

Corticosteroids

Antibiotics

Mobilisation

Non-invasive ventilation - BiPap, VPAP

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18
Q

Why don’t you give high flow O2 with COPD?

A

Don’t give too much too quickly though, may be in chronic resp failure where their drive to breathe is low O2.
If you increase O2 then you decrease their drive to breathe which leads to hypercapnoea

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19
Q

Definition of bronchiectasis

A

Chronic infection of bronchi and bronchioles leads to permanent dilation of bronchi, as well as inflammatory changes in airway walls and neighbouring parenchyma

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20
Q

Pathophys of bronchiectasis

A

Recurrent inflammation of bronchial walls weakens walls

Fibrosis of surrounding parenchyma puts traction on and weakens walls, causes dilation

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21
Q

Symptoms of bronchiectasis

Signs

A

Cough
Copious purulent foul smelling sputum
intermittent haemoptysis

Signs:

  • Clubbing
  • Exp wheeze
  • Coarse insp crepitations
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22
Q

Causes of bronchiectasis

A

Obstructive

  • tumour
  • foreign body
  • thickened mucus (asthma)

Post-inflammation

  • pneumonia
  • Tb
  • measles etc

Weakened defences
-CF

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23
Q

Common causes of lung abscesses

A
  • Most commonly a complication of aspiration pneumonia (aspirated objects accompanied by bacteria -> inflammation secondary to inflammation -> localised consolidation)
  • Pulmonary infarct
  • malignancy
  • Penetrating trauma
  • Bronchial obstruction
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24
Q

Management of lung abscess

A

Empiracle antibiotics

If non-resolving, surgical intervention

+/- postural drainage
+/- chest physiotherapy

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25
Q

What is the histopath pattern of Tb?

A

Caseating granulomatous inflammation with epithelial cells, giant cells and lymphocytes and central caseating necrosis.

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26
Q

Tests for DIAGNOSIS OF Tb

A

Quantiferon GOLD test or Mantoux test

Ziel-nelson stain

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27
Q

When does primary vs progressive vs secondary occur?

A

Primary Tb is what occurs following first exposure to M. Tb

Progressive Tb occurs in less than 10% patients, mostly immunocompromised/malnourished. Rapid spread through lungs/body

Secondary: reactivation of a dormant focus of primary infection, often with immunosuppression (steroids and HIV)

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28
Q

Possible sequelae of progressive Tb

A

Caveatting fibrocaseous Tb (erosion of ghon complex into bronchiole)

Miliary Tb (haematogenous dissemination)

Tuberculous bronchopneumonia (infection spreads rapidly -> diffuse bronchopneumonia or lobar exudative consolidation)

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29
Q

Gohn complex vs focus in Tb

A

Occurs in primary Tb

GHON focus - small area of encapsulated granulomatous inflammation (central cassation)

GHON complex - involves adjacent lymphatics and lymph nodes

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30
Q

What area of lungs do Tb GHON focuses in primary Tb occur in?

A

Mid zone sub-pleural

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31
Q

At what stage in Tb do patients become symptomatic and what are those SX?

A

Primary Tb usually asymptomatic

Progressive- have pulmonary and systemic SX

Secondary Tb - systemic symptoms (cough, fever, malaise, weight loss)

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32
Q

What area of lungs does secondary tb affect?

A

Upper lobes

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33
Q

Causes of granulomatous inflammation in the lung

A 
Tb
Sarcoid (non-caseating)
Hypersensitivity pneumonitis
Wegener's granulomatosis vasculitis
Aspiration pneumonia 
Rheumatoid nodules
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34
Q

Treatment of Sarcoidosis

A

Immunosuppression

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35
Q

What is sarcoidosis?

A

Non-caseating granulomatous inflammation

  • affects lungs, skin
  • common in young adults 20-40
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36
Q

Asthma

A
  • 3 characteristics
    1. reversible airflow limitation
    2. airway hyperresponsiveness to a variety of stimuli
    3. bronchial inflammation (T lypmphocytes, mast cells, eosinophils)
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37
Q

Asthma symptoms

A

Wheeze (exp if mild; exp and insp if severe)
Cough
Chest tightness
SOB

Often worse at night

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38
Q

Why might asthma become associated with irreversible airflow limitation?

A

Chronic inflammation leading to airway remodeling (smooth and goblet cell hyperplasia with incr mucus secretion) in chronic asthma patients (60-70)

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39
Q

Triggers for asthma

A 
Cold
Exercise
Pollen, dust, pollution
Tobacco smoke
Animals - cat, dog, birds
URTI
Medications (NSAIDs, beta blocers)
Emotion, stress
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40
Q

Investigations for asthma

A

CXR and ABG

Lung function tests (forced peak expiratory flow) - decr

Spirometry - >15% improvement in FEV1 or peak exp flow rate following bronchodilator

Blood or sputum test - large eosinophil titre and IgA/IgE levels

Skin prick tests to help identify allergic causes

Histamine or methacholine bronchial provocation testing (measures airway hyperresponsiveness). Note: can provoke resp arrest so dont do in individuals w FEV1<1.5L or w brittle asthma

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41
Q

Management of chronic asthma

A

Intermittent asthma
§ Inhaled SABA (beta 2 agonist) as needed

Mild persistent
§ Use low potency inhaled GC

Moderate persistent
§ Mild dose of inhaled GC + LABA (or leukotriene antagonist)
§ OR moderate dose of inhaled GC

Severe persistent
§ Med-high dose of inhaled GC + LABA +/- leukotriene antagonist

+ SABA as needed Salbutamol

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42
Q

Management of acute asthma attack (in ED) = status asthmaticus

A

O2
Nebulise bronchodilators on O2, not air
CXR

Large dose oral prednisilone or IV hydrocortisone

+/- IV Mg (vasodilator/dilates airway)

ICU assessment if no improvement in 1 hour

DO NOT give IV beta agonists - toxic.

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43
Q

Medications used for asthma

A

Beta 2 agonists - SABA Salbutamol; LABA Salmeterol (SX relief)

Inhaled corticosteroids -fluticasone (preventer)

Oral coritcosteroids in ED only

Combination inhaleds - Seretide (ICS/LABA = fluticasone/salmeterol)

Leukotriene R antagonists (oral montelukast)

Anti IgE (omalizumab) - SC inj every 2-4 weeks w persistent allergic asthma

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44
Q

SE of Inhaled corticosteroids in treatment of asthma

A

Thrush, hoarse voice

Cushingoid syndrome w v high doses

45
Q

Features of life threatening asthma (status asthmaticus)

A 
silent chest
cyanosis
feeble resp effort
exhaustion, confusion, coma
bradycardia or hypotension
peak exp flow rate <30% of predicted normal

hypercalaemia, hypoxaemia
Low/falling arterial pH

46
Q

Treatment of pulmonary oedema

A

LMNOPP

Lasix (frusemide)
Morphine 
Nitroglycerin (GTN)
O2 (hypoxemic)
Position (sit upright)
Positive airway (CPAP, BiPAP)
47
Q

Causes of viral pneumonia . is this a typical or atypical pneumonia ?

A

Influenza
Parainfluenza
RSV

Atypical presentation

48
Q

Atypical vs typical pneumonia

Who does it affect?
Time course
Pattern
Degree of rise - WCC
SX
A

Typical (bacterial):

  • Older people
  • Sudden onset, lasts 7-10days
  • Lobar consolidation
  • High rise WCC
  • Fatigue, high fever, productive cough (resp Sx only)

Atypical:

  • Younger people
  • Gradual onset over 2-3 weeks
  • Diffuse, bilateral
  • No consolidation; mild incr WCC
  • SX not as severe - cough w minimal sputum; low grade fever + extrapulm SX (muscle aches, headache, nausea, vomiting diarrhoea, abdo pain)
49
Q

Acute bronchopneumonia vs acute lobar pneumonia

A

Acute bronchopneumonia

  • Patchy bilateral distribution involving multiple lobes, multiple foci of inflammation
  • Bug w low virulence

Acute lobar pneumonia
-Inflammation of an entire lobe w no part spared
-Bug w high virulence
+Pleural pain (inflame of pleura)

50
Q

Consolidation - findings on chest examination

A 
Decr expansion
Dull percussion note
Incr vocal resonance 
Bronchial breathing
Pleural rub
51
Q

Investigations for suspected pneumonia

A

Bloods: FBE, U&E (renal baseline), CRP, blood culture

CXR
Pulse oximetry
Sputum sample for MCS

If suspected atypical infection:
Urine test - legionella and pneumococcal Ag
Viral serology
Nasopharyngeal swab for influenza PCR

52
Q

Treatment for CA atypical pneumonia

A

Doxycycline + macrolide

53
Q

Treatment CA typical pneumonia

A

Augmentin (Strep)
Azithromycin (H infl, moraxella)
Doxycycline (H infl)

54
Q

What agents, in what context, might cause lung abscess

A

Strep pygenes, staph aureus, Klebsiella

Secondary to bacterial pneumonia

55
Q

Complications of pneumonia

A 
Empyema
Pleural effusion
Lung abscess
Respiratory failure 
Sepsis
56
Q

What is cor pulmonale?

A

Cor pulmonale is RV enlargement and eventually failure secondary to a lung disorder that causes pulmonary artery hypertension.

57
Q

Causes of pulmonary HTN

A

Primary pull artery HTN

Increased LA pressure

  • Mitral Stenosis
  • LV failure
  • Diastolic dysfunction

Increased pulmonary blood flow

  • L-R shunts
  • high flow states
  • Fluids overload

Increased pulmonary vascular resistance

  • Vasoconstriction secondary to hypoxia (COPD, bronchiectasis)
  • Obstruction (PE)
  • Obliteration (emphysema, pulmonary fibrosis, arteritis)
58
Q

Signs of pulmonary HTN (without R heart failure)

A

RV (L parasternal) heave
Prominent “v” wave in JVP
Cyanosis, tachypnoea

59
Q

How does pulm HTN lead to RV hypertrophy (what sort) and Cor pulmonale?

A

Pulmonary HTN leads to incr afterload on R ventricle -> R ventricular concentric hypertrophy

- >  decr CO -> RH failure 
- > incr systemic venous pressure -> extravasation of fluid into interstitial tissues and peritoneal and/or pleural spaces
60
Q

Type 1 vs Type 2 resp failure

A

Type 1: Hypoxaemia WITHOUT Co2 in blood. caused by VQ mismatch (failure of blood oxygenation)

Type 2: Hypoxaemia WITH hypercapnoea; low pH . caused by inadequate alveolar ventilation or high inspired CO2 or high CO2 production (fever, sepsis, acidosis etc)

61
Q

What is Mesothelioma strongly associated with, in terms of social history?

A

Asbestos

Workers: miners, dockers, masons, plumbers, welders, installation

62
Q

What is the most frequent initial presentation of mesothelioma?

A

Pleural effusion

63
Q

What is mesothelioma?

What is the life expectancy?

A

Primary malignancy of pleura, usually occurring 20-30 years after asbestos exposure
<1 year after symptom onset

64
Q

Investigations/diagnosis of mesothelioma

A

CXR/chest CT

Biopsy of pleura with histological confirmation and biomarker staining

65
Q

What are benign manifestations of asbestos exposure?

A 
Pleural plaques (asymptomatic radiological finding)
Pleural effusion - Self-resolving and exudative
66
Q

How do you characterise pleural effusions are what are possible causes under each category?

A
  1. Transudative:
    - High hydrostatic pressures or low oncotic pressure
    - Low protein content)
  • CCF, cirrhosis, renal failure
  • Hypoproteinemia (nephrotic syndrome, cirrhosis, malabsorption)
  1. Exudative:
    - Incr vasc permeability/damage to vessels
    - High protein content
  • Infectious: Pneumonia, Tb
  • Malignant: Primary cancer, mets
  • Inflammatory: RA, SLE, PE-> Pulm Infarct
  1. Haemothorax (blood, traumatic )
  2. Chylous effusion (lymph in pleural space)
  3. Empyema (pus)
67
Q

Signs of a pleural effusion on chest examination

A

Chest expansion: decr
Percussion: stony dull
Vocal resonance: decr
Breath sounds: decr

If severe, tracheal deviation away from effusion

68
Q

Investigations for pleural effusion

A

CXR (blunting of costophenic angle +/- meniscus)

Pleural tap (diagnostic or therapeutic)
-> Protein and LDH
-> MCS
-> Tb stain
-> Cytology
-> Immunology if indicated (Rh factor; ANA, C’ for SLE)
+/- biopsy (if malignancy, Tb suspected)

+/- US (locate pleural fluid and guide diagnostic or therapeutic aspiration)

69
Q

Management of pleural effusion

A

Pleural tap to drain the effusion if symptomatic

PLeurodesis for recurrent effusions

70
Q

What is an empyema?

A

Pus in pleural space or pleural effusion with purulent bacteria seen on Gram stain or culture

71
Q

Causes of empyema?

A

Complication of pneumonia (contiguous spread)

Infection through chest wall (trauma, surgery)

72
Q

definition of Sarcoidosis

A

Multisystem granulomatous disease of unknown cause, commonly affecting lungs, and skin (but also lymph nodes, liver, spleen, eyes, heart, brain)

73
Q

Diagnosis of Sarcoidosis

A

Tissue Biopsy showing non-caseating granulomatous inflammation (lung, liver, lymph nodes, skin nodules, lacrimal glands)

Bloods: raised serum ACE (60%), +/- hypercalcaemia, raised ESR, incr LFTs

CXR: 90% peripheral pulmonary infiltrates +/- bilatera hilar lymphadenopathy

74
Q

Management of Sarcoidosis

A
  1. Bilateral hilar lymphadenopathy alone: no treatment, spontaneous recovery
  2. Acute sarcoidosis: bed rest and NSAIDS
  3. Pulmonary disease, uveitis, hypercalcaemia, cardiac or neuro involvement
    - Oral prednisilone
    - IV steroids or immunosuppressants if severe
    - Anti TNF alpha or lung transplant if refractory
75
Q

What are the presenting features of acute sarcoidosis?

Treatment?

A

Erythema Nodosum
+/- polyarthralgia

Treatment: bed rest and NSAIDs

76
Q

What is Cystic Fibrosis? and how does it present?

A

Autosomal recessive condition (mutation in Cl channel)

Chloride transport dysfunction
-> defective Cl secretion and increased Na absorption across airway epithelium.

This Cl channel involved in fluid production
In lungs -> leads to thicker secretions of airway mucus which clogs airways and predisposes to pulm infection and bronchiectasis

Also affects pancreas, skin, reproductive organs

77
Q

How does CF usually present?

What else happens w time?

A

Presenting in childhood with recurrent lung infections that become persistent and chronic.

Results in

  • severe lung disease
  • pancreatic insufficiency
  • diabetes
  • azoospermia
78
Q

Signs on examination of CF (lung disease)

A

Clubbing
Bilateral coarse crackles
Cyanosis

79
Q

How do you diagnose CF?

A

Sweat chloride test (incr [NaCl and K in sweat)

Pulmonary function tests (reduced FEV1 - obstructive pattern)

ABGs - hypoxaemia, w hypercapnoea later on

CXR: hyperinflation, incr pulmonary markings

80
Q

What diseases are associated with industrial dust

A

Coal Worker’s Pneumoconiosis (inhalation of coal dust), can progress to ‘Progressive Massive Fibrosis’

Silicosis (inhalation of silica which is fibrogenic)

Asbestosis (inhalation of asbestos which is fibrogenic), assoc w Mesothelioma

Mesothelioma

81
Q

Definition of Interstitial Lung Disease

A

Inflammatory and/or fibrosing process in the alveolar walls causing distortion and destruction of normal alveoli and microvasculature . Generally BILATERAL.

82
Q

Common causes of interstitial lung disease

A

Rheumatic
- RA, SLE, Scleroderma

Drugs
-Methotrexate, amiodarone, bleomycin, nitrofurantoin

Radiation

Environmental/Occupational
- Silicosis, asbestosis, coal worker’s pneumoconiosis

Pulmonary Vasculitis

Inherited

Sarcoidosis

83
Q

What pattern do you get on spirometry w ILD?

A

Restrictive due to decr lung compliance (TLC and VC reduced; FEV1/FVC incr/normal)

84
Q

Common causes of acute bronchitis

A

Mostly viral.

Influenza when + fever.

85
Q

Definition of acute bronchitis

A

Acute bronchitis is suggested by the persistence of cough for more than five days.

Cough generally persists two to three weeks, and airway hyperreactivity may last five to six weeks.

Fever uncommon and suggests influenza or pneumonia.

86
Q

What are the indications for CXR in patients w acute cough?

A

To exclude pneumonia:

Tachypnoea
Tachycardia
Fever

Chest exam: signs of consolidation, rales

Hypoxaemia (pulse oximetry)

Altered mental state

87
Q

Treatment of acute bronchitis

A

Reassurance and symptomatic treatment (NSAIDs, aspirin and/or ipratropium)

NOT ANTIBIOTICS.

88
Q

Classifying lung tumours

A

Benign or malignant

Primary or secondary

Endobronchial or parencymal

89
Q

What is the most common type of primary lung tumour?

A

Bronchogenic carcinoma

  • small cell
  • non-small cell (SCC, adenocarcinoma, large cell undifferentiated)

-Adenocarcinoma the most common overall

90
Q

Which type of lung cancer is most common in NON SMOKERS

A

non small cell adenocarcinoma

91
Q

Where are bronchogenic non small cell SCCs found in lungs

A

centrally

92
Q

Where are bronchogenic small cell carcinomas found?

A

centrally

93
Q

Where are bronchogenic non-small cell adenocarcinomas found?

A

Peripherally

94
Q

Which type of lung cancer is most aggressive?

A

Small cell - disseminated at presentation.

95
Q

What are the histological features of :
SCC
adenocarcinoma

A

SCC: keratin pearls and intercellular bridges

Adenocarcinoma: glandular, mucin-producing

96
Q

What are apical lung tumours called and what are common SX?

A

Pan coast tumour .

Horner Syndrome
Brachial plexus palsy (C8, T1 nerve roots -> weak intrinsic hand muscles)

97
Q

What are distant met sites for lung cancer?

A

Brain
Bone
Liver

98
Q

What are local sites of spread/obstruction for lung cancer?

A 
Hilum, mediastinum, pleura
Pericardium
Oesophagus
Phrenic nerve 
Recurrent laryngeal nerve
SVC
Rib and vertebrae
99
Q

Investigations for lung cancer

A

Bloods: UEC, LFTs, Ca

CXR, CT chest and abdo

+/- PET and bone scan

Sputum sample cytology

Bronchoscopy -> biopsy

100
Q

Horner’s syndrome

A

Mitosis
ANhydrosis
Ptosis

101
Q

Treatment for lung cancer

A

Combination treatment

surgery (not for small cell and CI with spread to lymph nodes or distant sites or poor pulm function)

radiotherapy
chemotherapy
palliation

102
Q

Causes of pneumothorax

A
  1. Traumatic - penetrating or non-penetrating injuries
  2. Iatrogenic
  3. Spontaneous (no HX trauma)
    ○ Primary (no underlying lung disease)
    § Generally due to spontaneous rupture of subpleural bleb of lung into pleural space
    § Common in tall, healthy young males

○ Secondary (underlying lung disease)
§ Rupture of subpleural bleb
§ Necrosis of lung tissue adjacent to pleural space (Often w pneumonia, abscess, PCP, lung CA, emphysema )

103
Q

Treatment for pneumothorax

A

○ Give 100% O2 in all cases

Small pneumothoraxes (haem stable) resolve spontaneously

Small intercostal tube for spontaneous pneumothoraces

Large pneumothoraces or those w secondary causes
○ Chest tube connected to underwater seal +/- suction
○ Treat underlying causes (ex: antibiotic for PCP)

104
Q

Signs on examination of pneumothorax

A
  • Tracheal deviation (if tension -> deviates AWAY from pneumothorax)
  • Unilateral reduced chest expansion
  • Decr vocal/tactile fremitus
  • Hyper-resonant
  • Unilateral reduced breath sounds
105
Q

What signs make you think that a person might have a tension pneumothorax rather than a simple one and how does this change your management?

A
  • Severe resp distress
  • Tracheal deviation away from affected lung
  • Distended neck veins (incr JVP)
  • Hypotension

In this case, do NOT perform CXR -> needs immediate MX

106
Q

Treatment for resp failure.. what investigations would you do?

A

Investigations: serial ABGs, CXR, chest CT (for underlying cause)

  1. Give O2
  2. Positive pressure ventilation: BiPAP, CPAP
  3. Reverse/manage underlying pathology and/or exacerbators

NOTE: in COPD patients w chronic hypercapnoea, give low-flow O2 to achieve target SaO2 of 88-92%

107
Q

What is the different in definition between OSA and central sleep apnea?

A

OSA: Transient, episodic obstruction of upper airway with reduced or absent airflow despite persistent respiratory effort.

CSA: Transient, episodic decreases in CNS drive to breathe with no airflow because no resp effort.

108
Q

Signs and symptoms of sleep apnea

A 
• Due to fragmented sleep:
	○ Daytime somnolence
	○ Personality and cognitive changes
	○ Snoring 
• Due to hypoxemia and hypercapnia
	○ Morning headache
	○ Polycythemia 
	○ Pulmonary/systemic HTN
	○ Cor pulmonale/CHF 
	○ Nocturnal angina
	○ Arrhythmias
109
Q

Investigations and treatment for OSA

A

Investigate w sleep study

Treatment

  • manage risk factors (weight loss, decr alch and sedatives, nasal decongestion, treat underlying medical conditions)
  • nasal CPAP
  • no supine sleeping
  • dental appliance
  • surgery (tonsillectomy. uvulopalatopharyngoplasty)

MD2 (16 decks)

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