Respiratory Medicine Flashcards
1
Q
Define TYPE 1 Respiratory Failure.
Explain the underlying pathology of this presentation and the most common causes.
A
Type 1 RF is characterised by hypoxemia (PaO2 < 60mmHg).
The underlying perfusion is inadequate oxygenation of blood as it moves through the lungs, due to impaired perfusion.
Common causes (IBASE): ✔️ I = interstitial lung disease ✔️ B = bacterial infection (e.g. pneumonia) ✔️ A = adult lung disease ✔️ S = shunt (cardiopulmonary) ✔️ E = emphysema / embolism
2
Q
Define TYPE 2 Respiratory Failure.
Explain the underlying pathology of this presentation and the most common causes.
A
Type 2 RF is characterised by hypercapnia (PaCO2 > 50mmHg).
The underlying pathology is either increased CO2 production or impaired CO2 excretion.
Common causes (COPD): ✔️ C = central causes (e.g. brain injury, meningitis, drugs and alcohol) ✔️ O = obstructive causes (e.g. foreign body inhalation, tumour) ✔️ P = pump disorder (e.g. GBS, MND, myopathy) ✔️ D = diaphragm involvement (e.g. obesity)
3
Q
Identify risk factors for COMMUNITY ACQUIRED PNEUMONIA (CAP).
A
✔️ extremes of age (very old or very young)
✔️ smoking
✔️ impaired ciliary function (e.g. cystic fibrosis)
✔️ impaired cough or gag reflex
✔️ factors that increase risk of aspiration (e.g. Parkinson’s Disease, MND, impaired consciousness, mechanical ventilation)
4
Q
Identify risk factors for ATYPICAL PNEUMONIA.
A
✔️ immunocompromised (e.g. chemotherapy, immunosuppression, transplant recipient, HIV patient, drugs / medications)
✔️ smoking
✔️ alcohol consumption
5
Q
Identify the three most common pathogens associated with COMMUNITY ACQUIRED PNEUMONIA.
A
- S. pneumonia
- H. influenza
- M. catarrhalis
6
Q
Identify the three most common pathogens associated with ATYPICAL PNEUMONIA.
A
- M. pneumoniae
- C. pneumoniae
- Legionella
7
Q
Identify two important organisms associated with pneumonia in the tropics.
A
- Burkholderia pseudomallei
2. Acintobactor baumanii
8
Q
Identify three important organisms associated with pneumonia in alcoholic patients.
A
- Klebsiella
- Enteric GNB
- Staph. aureus
- TB
9
Q
Outline the common clinical symptoms associated with pneumonia.
A
✔️ fatigue + lethargy ✔️ fever ✔️ cough --> begins as dry and progresses to productive ✔️ "rust" coloured sputum ✔️ dysponea ✔️ pleuritic chest pain ✔️ +/- haemoptysis
10
Q
Outline common clinical signs associated with pneumonia.
A
✔️ appears unwell
✔️ lethargic / perhaps reduced consciousness / drowsy
✔️ peripheral or central cyanosis
✔️ dry mucus membranes + poor hydration
✔️ febrile, tachycardia, tachyponea, hypotensive (if severe)
✔️ reduced CRT
✔️ reduced chest expansion asymmetrically
✔️ increased tactile and vocal fremetus
✔️ dullness on percussion over affected area
✔️ coarse inspiratory crackles on auscultation
✔️ bronchial breath sounds
11
Q
Identify the components that make up the SMART-COP score. Outline / describe how this is to be interpreted.
A
S = systolic blood pressure < 90mmHg M = multi-lobar involvement on X-Ray A = albumin < 3.5 R = respiratory rate > 25 T = tachycardia > 125 C = confusion (new onset) O = oxygen < 93% P = pH < 7.35
The SMARTCOP Score is a risk stratification tool that helps determine the risk of invasive ventilation in a patient with community acquired pneumonia.
0 to 2 - low risk
3 to 4 - moderate risk
5 to 6 - high risk
> 7 - significant / extreme risk
12
Q
Identify some factors that worsen the prognosis of pneumonia (red flags).
A
✔️ tachyponea > 22 bpm ✔️ tachycardia > 120bpm ✔️ systolic blood pressure < 90mmHg ✔️ oxygen < 93% ✔️ confusion (new onset) ✔️ blood lactate > 2.0 mmol / L
13
Q
Identify the components that make up the CURB-65 score. Outline / describe how this is to be interpreted.
A
C = confusion U = urea > 7mmol/l R = respiratory rate > 30 bpm B = blood pressure 65 = > 65 years of age
CURB-65 stratifies the likely risk of mortality in a patient with CAP. This helps to determine the most appropriate setting for treatment.
0 to 2 - outpatient
3 to 4 - consider inpatient admission
> 4 - requires inpatient admission
14
Q
Outline and justify appropriate investigations for PNEUMONIA.
A
Bedside Ix
✔️ ECG –> to evaluate chest pain
✔️ ABG –> to evaluate dyspnoea; measure blood pH and lactate levels
✔️ sputum MCS –> to isolate pathogen
Laboratory Ix
✔️ FBC + WCC
✔️ ESR + CRP –> to monitor response to treatment once commenced
✔️ UECs –> identify any electrolyte disturbances from reduced fluid intake
✔️ LFTs + albumin –> to stratify risk
✔️ blood culture –> to isolate organism if septic
Imaging Ix
✔️ CXR –> to isolate location of pneumonia
✔️ bronchoscopy –> diagnostic if malignancy is suspected
15
Q
Outline the appropriate treatment for MILD CAP.
A
Amoxicillin 1mg PO, 8-hourly for 5 to 7 days OR
Doxycycline 100mg PO, 12-hourly for 5 to 7 days
For all patients with mild CAP, mono therapy should be commenced unless the patient is unlikely to be reviewed within 48 hours.
16
Q
Outline the appropriate treatment for MODERATE CAP.
A
Benzylpenicilin 1.2g IV every 6 hours PLUS EITHER
Doxycycline 100mg PO, 12-hourly OR clarithromycin 500mg PO, 12-hourly
Once stabilised, patients with moderate CAP should be stepped down to dual oral therapy:
- amoxicillin PLUS
- doxycycline OR clarithromycin
Treatment should be continued for 5 to 7 days.
17
Q
Outline the appropriate treatment for SEVERE CAP.
A
Ceftriaxone 2g IV, daily.
Once stabilised, patients with moderate CAP should be stepped down to dual oral therapy:
- amoxicillin PLUS
- doxycycline OR clarithromycin
Treatment should be continued for 5 to 7 days.
18
Q
Describe some non-pharmacological treatment options for patients with pneumonia.
A
Patients who have experienced an episode of pneumonia are at increased risk of future events.
This risk can be minimised by:
✔️ smoking cessation
✔️ reduced alcohol consumption
✔️ Pneumococcal and influenza vaccination
✔️ exercise and BMI optimisation
✔️ reducing risk of aspiration in patients who experience this problem
19
Q
Identify the pathogen that causes MELIOIDOSIS.
A
Burkholderia pseudomallei.
This bacteria is a gram-negative bacilli found in soil.
20
Q
Outline some common risk factors for MELIOIDOSIS infection.
A
✔️ Aboriginal and Torres Strait Islander people ✔️ immunocompromised ✔️ chronic / severe alcoholism ✔️ cane farmers ✔️ chronic renal disease patients ✔️ patients who reside in the tropics
21
Q
Describe the clinical presentation of MELIOIDOSIS infection.
A
Melioidosis is characterised by widespread cavity and abscess formation throughout the body. This can manifest in areas such as: ✔️ skin ✔️ lungs ✔️ brain ✔️ prostate (males) ✔️ liver and spleen ✔️ skeletal muscle
The most common sites are skin (site of inoculation) and the lungs (giving rise to pulmonary symptoms).
22
Q
Outline appropriate investigations for MELIOIDOSIS.
A
Bedside Ix
✔️ ECG
✔️ ABG
✔️ sputum culture
Laboratory Ix ✔️ FBC + Inflammatory markers ✔️ ESR + CRP ✔️ UECs ✔️ blood culture ✔️ B. pseudomallei serology
Imaging Ix
✔️ CXR
✔️ Chest CT
✔️ US / CT abdomen –> to detect distant / metastatic seeding
Note that blood culture many be negative on numerous attempts. Often blood culture is NEGATIVE except in the case of severe septicaemia.
23
Q
Outline the appropriate antibiotic management of MELIOIDOSIS.
A
Antibiotic management is divided into two phases:
- initiation phase –> usually lasts between 2 to 4 weeks
- eradication phase –> usually lasts up to 12 weeks
INITIATION PHASE
The two preferred antibiotics are:
1. ceftazidime IV for 14 days OR
2. meropenem IV for 14 days
ERADICATION THERAPY
- trimethoprim + sulfamethoxazole orally for 3 to 6 months PLUS
- folic acid supplementation
24
Q
Define CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD).
A
COPD is a term that encompasses two clinical phenotypes:
- emphysema (pink puffer)
- chronic bronchitis (blue bloater)
The term refers to chronic changes in the small airways that lead to non-reversible airway obstruction.
25
Identify risk factors for COPD.
✔️ tobacco smoking --> only 15% of smokers have COPD, however, 50% of cases with COPD are people with a smoking history
✔️ second-hand smoking
✔️ occupational exposure
✔️ household smoke exposure
✔️ childhood respiratory illness and asthma
✔️ premature birth
✔️ genetic susceptibility (e.g. alpha-1 AT deficiency)
26
Explain the pathophysiology of EMPHYSEMA.
Emphysema is typically associated with tobacco smoking.
Tobacco smoking increases the influx of neutrophils into the small / distal airways. Neutrophils release enzymes (e.g. protease and elastase) that break down collagen fibres that help to maintain elastic recoil. Consequently, elastic recoil is reduced.
Tobacco smoking also inhibits anti-protease enzymes such as alpha-1 AT. This contributes to greater loss of elastic recoil.
Emphysema is characterised by:
✔️ increased "dead space" and hyperinflation
✔️ pulmonary shunting
✔️ continuous breakdown of elastic tissue due to imbalance of oxidants and free radicals
27
Explain the pathophysiology of CHRONIC BRONCHITIS.
Chronic bronchitis is typically associated with chronic airway pollution exposure and / tobacco smoking.
The clinical diagnosis is a productive cough, most days of the week for three months minimum, for TWO consecutive years.
Chronic inflammation promotes Goblet cell proliferation, gland hypertrophy, increased mucus secretion and impaired ciliary functioning.
Smooth muscle fibres also undergo hypertrophy, leading to bronchoconstriction. This can contribute to pulmonary hypertension and cor pulmonale.
28
Define REID INDEX.
The Reid Index is the ratio of depth in the submucosal mucus-secreting glands compared to the epithelium and cartilage of the bronchial tree. In chronic bronchitis, this thickness is > 0.5.
29
Define ACUTE EXACERBATION OF COPD.
```
Acute Exacerbation (AE) of COPD is defined as a worsening in intensity / severity of symptoms greater than usual day to day variation, for a period of ~48 hours, as demonstrated by:
✔️ increased dysponea
✔️ increased cyanosis
✔️ tachyponea
✔️ tachycardia
✔️ worsening or more productive cough
✔️fever
```
30
Identify some common triggers for AECOPD.
```
✔️ non-adherence to medications
✔️ viral infection (e.g. URTI)
✔️ change in weather / air conditions
✔️ pulmonary embolism
✔️ exacerbation of heart failure
✔️ systemic illness
```
31
Outline the appropriate management for AECOPD.
1. Primary survey --> A, B, C, D, E
2. Consult a senior doctor / registrar
3. Commence O2 via face mask if sats < 82% (aim for between 88 to 92%)
4. Bronchodilator therapy (e.g salbutamol, ipatropium bromide) inhaled / nebulised
5. Oral corticosteroids for 5 to 7 days (e.g. prednisolone 30 to 50mg, PO)
6. Consider antibiotics (e.g. amoxicillin)
32
Outline the criteria used to determine if antibiotic therapy is appropriate in AECOPD.
1. fever
2. increased sputum production
3. increased purulence of sputum
33
Describe appropriate management considerations for post-acute management of COPD.
✔️ medication review, check adherence, spacer technique etc.
✔️ check COPD Management Plan is up to date and accurate
✔️ referral to physiotherapy for chest rehabilitation
✔️ discharge summary to GP
34
Describe the appropriate drug therapy for long-term management of COPD.
1. SABA (e.g. salbutamol) --> mild disease
2. LABA (e.g. salmeterol) --> moderate disease
3. LABA + LAMA --> moderate disease
4. LABA + LAMA + ICS (e.g. trelegy)
35
Outline appropriate ways to prevent deterioration in a patient with COPD.
```
✔️ smoking cessation
✔️ immunisation (e.g. pneumococcal, influenza)
✔️ weight optimisation
✔️ physical activity
✔️ chest physiotherapy
✔️ optimise nutrition
```
36
Outline the diagnostic criteria for COPD.
COPD is diagnosed on spirometry when FEV1 / FVC ratio < 70%. COPD does NOT show reversibility.
Mild disease - 60 to 80%
Moderate disease - 40 to 60%
Severe disease - FEV1 < 40%
37
Identify situations in which it would be appropriate to consider hospitalisation for COPD.
✔️ marked intensity in severity of symptoms
✔️ onset of new physical signs (e.g. cyanosis, peripheral oedema)
✔️ failure to respond to medication
✔️ history of frequent exacerbations
✔️ older age
✔️ insufficient home support
38
Complications for COPD?
✔️ polycythemia
✔️ right-sided heart failure
✔️ pulmonary hypertension
✔️ pneumothorax secondary to bulli rupture
39
Define ACUTE ASTHMA. Identify common triggers.
Acute asthma, also known as acute exacerbation of asthma, is characterised by acute onset worsening of respiratory symptoms, specifically dyspnoea, chest tightness, cough and wheeze.
```
Common triggers include:
✔️ viral URTI
✔️ systemic illness
✔️ pollen, pollution, medication
✔️ non-adherence to medication
```
40
Outline key features used to assess the severity of an acute asthma attack.
MILD
✔️ able to speak in full sentences
✔️ oxygen saturation > 94%
```
MODERATE
✔️ unable to speak in full sentences
✔️ increased work of breathing and accessory muscle use
✔️ obvious respiratory distress
✔️ oxygen saturation 90 to 94%
```
```
SEVERE
✔️ significant work of breathing
✔️ reduced consciousness
✔️ silent chest
✔️ collapse
✔️ pulses paradoxus (>20mmHg)
✔️ cyanosis
```
41
Outline key investigations used to diagnose acute exacerbation of asthma.
Acute exacerbation of asthma is predominately a clinical diagnosis. Investigations that may aid diagnosis include:
✔️ ECG
✔️ ABG
✔️ FBC + WCC
✔️ Inflammatory markers
✔️ UECs --> hypokalaemia is associated with ongoing salbutamol use
✔️ CXR
✔️ Spirometry --> not to be used in the acute setting
42
Describe the spirometric diagnosis of asthma.
FEV1/FVC < 70% with reversibility of > 200mL or 12% following bronchodilators therapy.
43
Describe ASTHMA FIRST AID for an acute exacerbation of asthma.
4 puffs of reliever puffer (e.g. SABA) via a spacer with 4 breaths per puff.
This is to be repeated every 4 minutes if symptoms do not improve until an ambulance / first aid arrives.
44
Outline the hospital / emergency management of acute exacerbation of asthma.
1. Primary survey --> A, B, C, D, E
2. Consult senior doctor / registrar
3. Remove trigger
4. Bronchodilator therapy (e.g. salbutamol, ipatropium bromide BURST THERAPY)
✔️ salbutamol 100microg via face mask (6 puffs if < 6 years of age; 12 puffs if > 6 years of age every 20 minutes)
✔️ ipatropium bromide 21microg via face mask (4 puffs if < 6 years of age; 8 puffs if > 6 years of age)
N.B. Consider nebulised SABA if unreponsive to face mask
5. Oxygen via face mask if < 94%
6. Oral / IV corticosteroids
✔️ prednisolone 30 to 50mg PO, continue for 5 to 7 days
✔️ dexamethasone
✔️ hydrocortisone IV (if unable to tolerate oral medications)
7. Consider IM adrenaline if symptoms not responsive to SABA therapy
45
Outline the long-term management of ASTHMA.
1. SABA (e.g. salbutamol) PRN
2. Introduce ICS (e.g. fluticasone) daily + SABA
3. ICS + LABA / LAMA (low dose)
4. ICS + LABA / LAMA (high dose)
5. Referral to asthma / respiratory specialist
46
What are some indicators for GOOD asthma control?
```
✔️ daytime symptoms < 4 times per week
✔️ nighttime symptoms < 1 time per week
✔️ physical activity levels normal
✔️ exacerbations mild and infrequent
✔️ no asthma-related absence from school / work
✔️ beta-agonist therapy < 4 times per week
✔️ FEV1 > 90% of personal best
✔️ diurnal variation of 10 to 15%
```
47
Identify some risk factors for SEVERE ASTHMA.
✔️ hospital admission in last 12 months
✔️ previous severe asthma attack
✔️ previous hospital admission, including to ICU
✔️ long-term corticosteroid treatment
✔️ carelessness whilst taking medications
✔️ nighttime attacks, particularly with severe chest tightness
✔️ recent emotional problems
✔️ frequent SABA use
48
Identify RED FLAGs in an asthma attach.
```
✔️ pulsus paradoxus (>20mmHg)
✔️ cyanosis
✔️ inability to speak in full sentences
✔️ exhaustion
✔️ tachycardia
✔️ drowsiness due to hypercapnia
✔️ appearance of fear
✔️ silent chest
```
49
What is VIRCHOW'S TRIAD for VTE (DVT/PE)?
1. hypercoaguable state
2. trauma
3. immobility
50
Identify common risk factors for VTE (DVT/PE).
✔️ recent trauma
✔️ recent surgery
✔️ recent immobility (e.g. hospitalisation, long-haul travel)
✔️ active / recent malignancy (treated within 6 months)
✔️ unopposed oestrogen therapy (e.g. HRT)
✔️ obesity
✔️ history of previous unprovoked DVT / PE
✔️ increasing age
51
Describe common clinical sypmtoms and signs for PULMONARY EMBOLISM.
```
CLINICAL SYMPTOMS
✔️ sudden onset dysponea
✔️ sudden onset pleuritic chest pain (worse with inspiration)
✔️ haemoptysis
✔️ syncope / dizziness
✔️ palpitations
✔️ unilateral calf pain / tenderness
✔️ low-grade fever
```
CLINICAL SIGNS
✔️ tachycardia, tachyponea, reduced O2 %age, hypotension
✔️ reduced chest wall expansion unilaterally
✔️ reduced breath sounds unilaterally
✔️ splitting P2 heart sound
✔️ right ventricular heave
✔️ elevated JVP (>3cm)
✔️ pleural rub
✔️ signs of DVT (e.g. unilateral calf tenderness, swelling, oedema, Homan's Sign +ve)
52
Outline the components of the WELLS' CRITERIA and discuss how this is to be interpreted.
Well's Criteria is used to judge the likelihood that a clinical presentation is PE --> determines the most appropriate management options.
Clinical Judgement:
✔️ PE most likely diagnosis (+3 points)
Risk Factors
✔️ recent surgery (+1.5 points)
✔️ previous DVT / PE (+1.5 points)
✔️ active or recently treated malignancy (+1.5 points)
Clinical Symptoms
✔️ haemoptysis (+1 point)
Clinical Signs
✔️ tachycardia (+1.5 points)
✔️ clinical signs / evidence of DVT (+3 points)
If Well's Criteria > 4 --> CTPA
If Well's Criteria < 4 --> PERC + D Dimer
53
Outline appropriate investigations for PE.
Bedside Ix
✔️ ECG --> sinus tachycardia, RVH +/- strain, RBBB, right atrial abnormality, S1Q3T3 pattern
✔️ pulse oximetry
✔️ ABG --> to evaluate breathlessness
```
Laboratory Ix
✔️ FBC + WCC
✔️ Inflammatory markers
✔️ UECs + eLFTs
✔️ coags
✔️ D-Dimer
✔️ CK and troponin (if chest pain present)
```
```
Imaging Ix
✔️ CTPA --> if Well's Criteria > 4
✔️CXR
✔️ Doppler USS of calf
✔️ V/Q perfusion score (if CTPA contraindicated)
```
54
Identify THREE contraindications for CTPA.
✔️ pregnancy
✔️ renal disease
✔️ allergy to contrast agent
55
Outline the emergency management for PE.
The emergency management of PE depends on whether the patient is haemodynamically stable (SBP > 90mmHg) or haemodynamically unstable (SBP < 90mmHG).
In both situations, begin management with:
1. primary survey --> ABCDE
2. oxygen if < 92%
3. two large bore IVC insertion
4. IV fluid resuscitation (250mL crystalloids) if SBP < 90mmHg
5. analgesia, as appropriate
If patient is STABLE (SBP > 90mmHg), treatment is via oral LMWH (e.g. enoxaparin).
If patient is UNSTABLE (SBP < 90mmHg), treatment is via IV heparin and IV alteplase 10mg bolus stat, followed by 90mg infusion over 2 hours.
56
Outline the protocol for ongoing management of PE following discharge.
All patients with PE require minimum THREE MONTHS anticoagulation therapy.
There are three drugs classes that can be used:
1. NOACs (e.g. rivaroxaban) --> appropriate for PE not associated with malignancy
2. LMWH (e.g. enoxaparin) --> appropriate for PE associated with malignancy
3. warfarin --> appropriate for patients in which NOACs are not suitable; INR between 2.0 and 3.0
All patients should be re-evaluated at THREE months to determine the appropriateness of ongoing treatment.
Distal DVT --> cease therapy
Provoked proximal DVT / PE (reversible risk factors) --> ceased therapy
Unprovoked DVT / PE --> cease therapy and test D-Dimer in one month; if positive, continue indefinite therapy; if negative, cease therapy
Cancer related DVT / PE --> lifelong therapy required
57
Identify risk factors for recurrent PE / DVT.
```
✔️ male gender
✔️ previous unprovoked DVT / PE
✔️ active / recent malignancy
✔️ exogenous hormone use
✔️ hypercoaguable state (e.g. Protein C / S deficiency)
```
58
Define PNEUMOTHORAX.
Pneumothorax is the accumulation of air between the parietal and visceral pleura.
Pneumothorax can be of two types:
1. spontaneous --> primary or secondary
2. traumatic --> communicating or tension
59
Describe the clinical signs and symptoms associated with pneumothorax.
```
CLINICAL SYMPTOMS
✔️ acute onset dysponea
✔️ acute onset pleuritic chest pain
✔️ fear / restlessness
✔️ haemoptysis
```
```
CLINICAL SIGNS
✔️ tachycardia, tachypnoea, hypotension
✔️ reduced chest expansion unilaterally
✔️ reduced air entry unilaterally
✔️ hyper resonance on percussion unilaterally
```
60
Descibe clinical findings of TENSION PNEUMOTHORAX.
```
Signs of haemodynamic instability:
✔️ tachycardia
✔️ tachypnoea
✔️ hypotension
✔️ reduced O2
```
Tracheal tug
Distended neck veins
Cyanosis, restlessness and dysponea
61
Outline appropriate investigations for PNEUMOTHORAX.
Bedside Ix
✔️ ECG
✔️ ABG
✔️ Pulse oximetry
```
Laboratory Ix
✔️ FBC + WCC
✔️ Inflammatory markers
✔️ UECs
✔️ D-Dimer (if PE suspected)
✔️ troponin and CK (if ACS suspected)
```
Imaging Ix
✔️ CXR
✔️ CTPA (if PE suspected)
✔️ Chest CT
62
Describe the appropriate management of PNEUMOTHORAX.
1. Primary spontaneous pneumothorax confirmed on CXR or CT.
2. Look for signs of haemodynamic compromise (e.g. ↑HR, ↑RR, ↓BP, pulsus paradoxus, unable to mobilise due to severe pain).
3. If NO compromise evident, observe for 4 hours. If remains clinically stable, discharge with planned F/U with GP; ongoing CXR every 2 weeks until resolved; follow up with specialist if not resolved after 8 weeks.
4. If compromise evident OR patient deteriorates, insert intercostal catheter.
Intercostal catheter should be inserted in the fifth ICS, mid-axillary line using 5 to 10mL 1% lidocaine.
63
Define PLEURAL EFFUSION.
A pleural effusion is the accumulation of fluid between the parietal and visceral layers of the pleura.
```
There are numerous types of pleural effusions including:
✔️ transudate
✔️ exudate
✔️ hemothorax
✔️ chylothorax
✔️ empyema
```
64
Define TRANSUDATE PLEURAL EFFUSION. Identify common causes.
Transudate is a pleural effusion that occurs when fluid accumulates within the pleural space through in-tact blood vessels.
```
Common causes include:
✔️ left sided heart failure
✔️ congestive cardiac failure
✔️ hypoalbuminemia (e.g. nephrotic syndrome, chronic liver disease)
✔️ hypothyroidism
```
65
Define EXUDATE PLEURAL EFFUSION. Identify common causes.
Exudate is a pleural effusion that occurs when fluid accumulates in the pleural space through damaged blood vessels (i.e. increased permeability).
```
Common causes include:
✔️ pneumonia
✔️ sepsis
✔️ tuberculosis
✔️ subphrenic abscess
```
66
Identify the most common causes for an empyema.
```
✔️ pneumonia / lower respiratory tract infection
✔️ lung abscess
✔️ bronchiectasis
✔️ tuberculosis
✔️ penetrating chest wound
```
67
Describe SYMPTOMS and SIGNS of pleural effusion.
```
CLINICAL SYMPTOMS
✔️ dyspnoea
✔️ pleuritic chest pain
✔️ cough
✔️ symptoms of underlying disease process (e.g. cachexia, fever, orthopnea and PND)
```
CLINICAL SIGNS
✔️ displaced trachea (away from the massive effusion)
✔️ reduced chest wall expansion on the affected side
✔️ reduced tactile and vocal fremitus (due to pleural fluid blocking the transmission of sound)
✔️ stony dullness on percussion
✔️ reduced breath sounds over the affected area
✔️ bronchial breath sounds above the affected area --> due to compression of lung tissue
NOTE that patients with a pleural effusion < 300mL may be asymptomatic.
68
Define LIGHT'S CRITERIA.
Light's Criteria is used to determine the likelihood of pleural effusion being EXUDATE.
ONE of the following THREE must be met:
1. pleural protein divided by serum protein > 0.5
2. pleural LDH divided by serum LDH > 0.6
3. pleural LDH > two-thirds the upper limit of "normal" serum LDH
69
Outline the appropriate tests to be performed on pleural fluid.
```
Biochemistry
✔️ LDH
✔️ glucose
✔️ protein
✔️ pH
```
MCS
Gross fluid analysis
✔️ blood
✔️ pus
✔️ clear versus cloudy
70
Identify indications for drainage of a para-pneumonic effusion.
✔️ large diameter
✔️ ongoing fever and systemic signs, despite antibiotic therapy
✔️ locaulated pleural effusion
Empyema ALWAYS requires drainage.
71
Define OBSTRUCTIVE SLEEP APONEA (OSA).
Obstructive sleep apnea (OSA) is a pathological condition characterised by multiple aponeic / hypoaponeic events during sleep, resulting in reduced restfulness of sleep, daytime tiredness and increased cardiovascular risk.
72
Identify risk factors for OSA.
```
✔️ male gender
✔️ increasing age
✔️ overweight / obese BMI
✔️ thick neck
✔️ alcohol and tobacco consumption
✔️ abnormal respiratory / airway anatomy (e.g. high-arched palate)
```
73
Explain the pathophysiology of OSA and how it contributes to increased cardiovascular risk.
1. Nighttime airway obstruction is due to loss of tone in the airways whilst asleep. This leads to multiple events of apnea throughout the night.
2. Apnea stimulates hypoxic pulmonary vasoconstriction, which contributes to pulmonary hypertension and cor pulmonale.
3. Increased sympathetic activity secondary to hypoxic events contributes to systemic hypertension.
4. Respiratory acidosis triggers renal compensation --> increased HCO3 and decreased chloride retention (to maintain anion gap).
74
Outline symptoms associated with OSA.
```
✔️ snoring
✔️ witnessed apnea events (e.g. witnessed by partner)
✔️ frequently wakes throughout night
✔️ nocturia
✔️ fatigue upon waking / feeling of being unrefreshed
✔️ daytime sleepiness and irritability
✔️ poor concentration throughout the day
✔️ morning time headache
✔️ GORD
✔️ erectile dysfunction
```
75
How is OSA diagnosed?
Gold standard for diagnosis of OSA is an overnight sleep study.
Significant symptoms are indicated by > 5 events per hour.
Severe symptoms are indicated by > 30 events per hour.
A patient can be referred for a sleep study when they score:
> 8 Epworth Sleepiness Score
> 4 STOPBANG Score
> 5 OSA50 Score
76
Outline the management for OSA.
Lifestyle Management
✔️ weight reduction
✔️ smoking cessation
✔️ reduced alcohol consumption, particularly before bed
✔️ improved sleep hygiene
✔️ intranasal corticosteroid spray to reduce nasal resistance
Medical Therapy
✔️ CPAP
77
Identify complications of OSA.
✔️ hypertension
✔️ atrial fibrillation
✔️ right sided heart failure (e.g. cor pulmonale)
✔️ pulmonary hypertension
✔️ obesity hypoventilation syndrome (OHS)
78
Outline key features of SMALL CELL LUNG CANCER (SCLC).
✔️ accounts for ~ 10 to 50% of lung cancers
✔️ strong correlation with smoking
✔️ centrally located
✔️ histology --> "oat cells"
✔️ neuroendocrine / paraneoplastic syndromes are COMON
✔️ disseminated at presentation
✔️ poorest prognosis (5-year-survival rate 1%)
79
Outline key features of ADENOCARCINOMA.
✔️ accounts for 35 to 40% of lung cancers
✔️ poor correlation with smoking; more common in females
✔️ peripherally located
✔️ histology --> glandular cells; mucin-producing
✔️ early metastasis
✔️ poor prognosis (5-year-survival rate 12%)
80
Outline key features of SQUAMOUS CELL CARCINOMA.
✔️ accounts for ~30% of all lung cancers
✔️ strong correlation to smoking
✔️ centrally located
✔️ histology --> keratin pearl cells with "onion skin" appearance
✔️ early local metastases with cavitation
✔️ prognosis is 25% 5-year-survival rate
81
Describe the key clinical symptoms of LUNG CANCER.
```
✔️ cough --> persistent; change from previously "normal" cough
✔️haemoptysis
✔️ dysponea
✔️ pleuritic chest pain
✔️ weight loss, fever, night sweats
✔️ lymphadenopathy
```
82
What are some differential diagnoses for HAEMOPTYSIS?
1. pneumonia / infective cause
2. bronchiectasis
3. tuberculosis
4. lung cancer
83
Define PARANEOPLASTIC SYNDROME. What subtype of lung cancer are these syndromes most commonly associated with?
"Paraneoplastic syndrome" pertains to a group of syndromes that are associated with malignant disease but not related to the physical effects of the tumour itself; these symptoms manifest from hormones that are secreted from tumours.
Most commonly associated with SCLC.
84
Define CYSTIC FIBROSIS. What is the most common genetic mutation in this condition? How is it inherited?
Cystic Fibrosis is an AUTOSOMAL RECESSIVE condition caused by mutation to the CFTR gene, which regulates the transport of chloride across cell membranes.
There are > 100 different mutations that can give rise to CF, with the most common being the △F508 mutation.
In order for a patient to present with CF, both parents must be carriers for the gene; the child must inherit both defective genes and be homozygous for the mutation.
1/25 Australian adults are carriers of the defective CFTR gene.
85
Describe the clinical presentation of CYSTIC FIBROSIS.
RECURRENT RESPIRATORY TRACT INFECTIONS
✔️ initially H. influenza and S. aureus infections --> progress to Pseudomonas infections (difficult to treat)
✔️ opportunities inspiratory tract infections
✔️ bronchiectasis of the upper lobes
PANCREATIC INSUFFICIENCY
✔️ malabsorption --> poor growth
✔️ secondary diabetes mellitus
```
GASTROINTESTINAL COMPLICATIONS
✔️ meconium ileus in infants
✔️ distal ileac obstruction in adults
✔️ steatorrhea
✔️ liver disease
```
FERTILITY COMPLICATIONS
✔️ azoospermia in males
86
Identify how CF is diagnosed.
The Gold Standard for diagnosis is the Sweat Chloride Test (>60mmol/L is diagnostic in children).
Other means of diagnosis include:
✔️ spirometry --> mixed obstructive and restrictive disease
✔️ ABG --> Type 1 or Type 2 respiratory failure
87
Describe some complications of CYSTIC FIBROSIS.
```
✔️ recurrent respiratory tract infections
✔️ bronchiectasis
✔️ cor pulmonale
✔️ respiratory failure
✔️ reduced life expectancy
```
88
What antibiotic is commonly used to treat CF infections?
Tobromycin 14 days IV (for Pseudomonas aeruginoa infection).
