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Medical School Finals > Core: Respiratory > Flashcards

Core: Respiratory Flashcards

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USMLE® Step 1 flashcards
1
Q

Patient - Kid, wheezy, worse at night, cough, worse when exercising etc, PMH of eczema and hayfever

A

Asthma

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2
Q

Asthma Aetiology

A
  • Hygiene hypothesis and Atopy
  • Genetics - IL3/4
  • Early exposure to allergens; smoking etc
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3
Q

Asthma Pathology

A
  • Bronchial hyper-reactivity (air trapping - reduced V/Q), airway inflammation (narrowed lumen), obstruction.
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4
Q

Asthma Presentation

A
  • Wheeze
  • SOB
  • PND (4-6am)
  • Nocturnal cough
  • Exercise bronchospasm
  • Chest tightness
  • General atopy
  • Acute presentation, unable to speak in full sentences, use of acc muscles.
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5
Q

Asthma Ix

A

1) PEFR - morning and before and after SABA. Comparison to personal best.
2) Spiro - FEV1 improvement after SABA - restrictive FEV1:FVC normal or high >70%
3) Exercise tests
4) Histamine or methacholine provocation test for hyper-responsiveness.
5) Steroid trial - improvement PO 30mg pred.
6) CXR
7) Allergen testing

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6
Q

Asthma Rx

A

1) Control trigger and educate
2) Adults
- Occasional Sx - SABA PRN
- Daily Sx - SABA + ICS
- Severe Sx - ICS + LABA
- Uncontrolled - ICS + LABA + LTRA or theophylline
- Still deteriorating - + Oral steds.
- PEFR <30% admit. Asthma attack.
3) Kids
- 1 = SABA
- 2 = SABA + ICS
- 3 = + LTRA
- 4 = SABA + ICS + LABA - Less than 5yo refer.

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7
Q

ASTHMA ATTACK RX

A
  • PEFR <30%, can’t speak in full sentences, increased WOB.
    1) Oxygen + serial PEF
    2) NEB salbutamol 10mg repeat if needed.
  • ABG, Bloods etc.
    3) NEB ipratropium
    4) IV hydrocortisone 200mg or PO pred
    5) IV MGSO4 or salbutamol
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8
Q

Patient - fat, old, claims they have asthma, smoking Hx, frequent chest infections.

A

COPD

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9
Q

COPD Aetiology

A
  • Long term exposure to toxins and smoking

- Alpha 1 antitrypsin

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10
Q

COPD Pathology

A
  • Increased mucus and goblet cells
  • Scarring and thickening of the walls of the airway
  • Emphysema - loss of elastic recoil and air trapping
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11
Q

COPD Presentation

A
  • Cough w/ clear sputum
  • SOB
  • Frequent exacerbation
  • Prolonged expiration
  • Increased WOB
  • Systemic = HTN, Osteoporosis, depression.
  • Pink puffer Vs blue bloater
  • PP sensitive to C02, SOB all the time but not cyanosed.
  • BB is insensitive to CO2 are cyanosed and oedematous however not SOB.
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12
Q

COPD Ix

A

1) Clinical
2) Spiro - obstructive (<70%) low PEF
3) CXR - often normal but rules out other patho.
4) Bloods - alpha 1 anti-trypsin + infection markers FBC - secondary polycythaemia+ raised MCV.
5) Sputum MC&S

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13
Q

COPD Rx

A

1) Lifestyle changes + monitoring regularly
2) SABA FOR Sx PRN
3) LABA + Anti-muscarinic (ipratropium)
4) + Steds
5) Rescue therapy - steds + ABx for those who need it.
6) Oxygen

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14
Q

Patient - Diagnosed CF, yellow sputum and failing lung function.

A
  • Bronchiectasis
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15
Q

Bronchiectasis Aetiology

A
  • CF
  • Immune deficiency
  • Kartagener’s syn
  • Bronchial obstruction - tumour
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16
Q

Bronchiectasis Pathology

A
  • Abnormal permanently dilated airways.
  • The bronchial walls become inflamed, thickened and damaged.
  • The mucus transport mechanisms are damaged.
  • Mucus stagnation
  • Infection; Pseudomonas, Haemophilus (most common), kleb.
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17
Q

Bronchiectasis Presentation

A
  • Productive cough
  • Developing SOB
  • Persistent SOB
  • Clubbing
  • Frequent exacerbations
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18
Q

Bronchiectasis Ix

A
  1. CXR/CT - dilated bronchi w/ thick walls
  2. MC&S of sputum
  3. Dx and test for CF
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19
Q

Bronchiectasis Rx

A
  1. Chest physio and mucus drainage.

2. ABx - cefaclor 500mg 3xdaily or cipro 500mg BD to shift infection and halt disease progression.

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20
Q

Patient - severe chest infection w/ XR changes

A
  • Pneumonia
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21
Q

Patient - develops new onset cough w/ sputum within 2 days of being admitted to hospital

A
  • HAP
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22
Q

Patient - Develops chest infection + XR changes following surgery, suspected aspiration of vomit

A
  • Aspiration pneumonia.
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23
Q

CAP causes

A
  • Bacteria = pneumococcus, mycoplasma, legionella, klebsiella (alcoholics)
  • Viral = influenza

RF’s = extremes of age, smoking, pre-existing resp conditions.

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24
Q

HAP causes

A
  • Bacteria = Pseudomonas, E.coli, Klebsiella, MRSA.
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25
Q

Immunocompromised pneumonia causes

A
  • Fungals - PCP, crytococcus, candida.
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26
Q

Pneumonia Presentation

A
  • Cough; often productive.
    Pneumococcal = rust coloured sputum.
  • SOB - as alveoli are full of pus and debris.
  • Fever
  • Pleuritic chest pain
  • Abdominal pain
  • Extrapulmonary = Myalgia, arthralgia, myo/pericarditis, erythema multiforme.
  • Mycoplasma can present w/ lots of extrapulmonary Sx.
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27
Q

Pneumonia Ix

A

1) ABCDE + CURB-65
2) Sputum MC&S
3) CXR
4) Bloods - FBC, U&E, LFT + culture.
5) ECG

28
Q

CURB-65

A 
C = Confusion <8/10 AMT 
U = Urea >7mmol/L 
R = RR >30/min 
B = BP <90mmHg 
65 = > 65yo
29
Q

Pneumonia Rx

A

1) ABCDE
2) General = Oxygen (keep SP02 between 94-98%), fluids, thromboprophylaxis, physio, nutrition, ABx
3) CURB - 65 1 or less –> Rx in the community w/ amoxicillin or clarithromycin + follow-up and safety netting.
4) CURB - 65 2 –> assess in hospital + CXR. Amoxicillin 500mg 3xdaily + clarithromycin 500mg BD.
5) CURB -65 3/4 –> Augmentin 1.2g IV 3xdaily + clarithromycin 500mg BD IV.

30
Q

Patient - Failure to thrive, failure/delay to pass a thick and viscous meconium. Guthrie test positive.

A
  • CF

- Immunoreactive trypsinogen on the Guthrie test.

31
Q

CF Aetiology

A
  • AR inherited

- Cystic fibrosis transmembrane conductance regulator - chloride channel.

32
Q

CF pathology

A
  • Decreased secretion of chloride into the airway.
  • Increased reabsorption of sodium and water
  • Thicker and more vicious mucus.
  • Colonising bacteria = Pseudomonas, S.aureus, aspergillus.
33
Q

CF Presentation

A

Resp = Increased infection leading to bronchiectasis.

  • Sinusitis and nasal polyps
  • SOB

GI = Pancreatic dysfunction leading to steatorrhea

  • Meconium ileus
  • Malabsorption of fats and fat soluble vitamins.
  • Rectal prolapse

Other =

  • Male infertility
  • DM more common
34
Q

CF Ix

A

1) Often via Guthrie test (immunoreactive trypsinogen)
2) Clinically diagnosed in adults: FHx, bronchiectasis.
3) Sweat testing showing a high level of sodium.
4) Genetic testing.

35
Q

CF Rx

A

1) General = no smoking and flu jabs etc.
2) BD postural chest drainage, deep breathing exercises and chest physio.
3) Prompt ABx if needed
4) SABA and ICS can help w/ Sx
5) NIV
6) Fat soluble vitamins and pancreatic enzymes w/ each meal.

36
Q

Patient - OMG, sudden onset chest pain, worse on breathing in, sudden SOB + haemoptysis. Swollen calf.

A

PE

37
Q

Virchow’s triad for thrombus formation

A
  1. Altered vessel wall
  2. Thrombophilia
  3. Abnormal blood flow.
38
Q

PE aetiology/pathology

A
  • Thrombus from the systemic veins or RHS heart dislodges and embolises to the lungs.
  • Downstream lung ischaemia from the embolus.
  • Lung tissue is ventilated but not perfused.
  • No gas exchange occurs.
  • After a few hours this lung area stops producing surfactant and it collapses.
39
Q

PE Presentation

A
  • Acute onset SOB, chest pain and haemoptysis.
  • In small emboli there may be no Sx.
  • Tachypnoea
  • Tachycardia
  • Massive PE may result in shock and circulatory collapse.
40
Q

PE Ix

A

1) Bloods; FBC, Clotting, D-dimer, U&E, ABG
2) ECG - tachycardia or signs of RHS heart strain RBBB
3) V/Q scan
4) CTPA
5) USS for clot source.
6) Well’s score.

41
Q

PE Rx

A

1) ABCDE
2) Anticoagulate w/ LMWH if not immediately thrombolysing.
3) Thrombolyse w/ streptokinase 250,000 units IV over 30 mins
4) Anticoagulate w/ warfarin or DOAC

42
Q

Pneumothorax Aetiology

A
  • Air in the pleural space
  • Spontaneous (rupture of pleural blebs; congenital defect in alveolar wall - linked to connective tissue disorders)
  • Traumatic
  • Secondary to resp disease.
  • Abscess breakdown and fistula formation.
43
Q

Tension Pneumothorax

A
  • valve mechanism
  • Air is sucked into the pleural space w/ inspiration and trapped as the valve closes in expiration.
  • Increasingly enlarging pneumothorax.
  • Mediastinal shift, and circulatory collapse due to the obstruction of great vessels.
44
Q

Pneumothorax Presentation

A
  • Unilateral pleuritic chest pain
  • Progressive SOB
  • Shock can develop if pneumothorax is large.
45
Q

Pneumothorax Ix

A

1) Clinical

2) XR to confirm however don’t delay Rx especially in tension pneumothorax as they will RIP.

46
Q

Pneumothorax Rx

A

1) ABCDE
2) Aspirate 2nd IC space midclav line with cannula.
2) Insert seldinger chest drain to prevent build up.
3) Talc or surgery may be required.
4) Manage underlying pathology.

Primary pneumothorax

  • If rim of air <2cm and patient is well - discharge.
  • If Sx then aspirate.
  • Aspiration fails - insert drain.

Secondary Pneumothorax

  • > 50yo and rim of air >2cm then chest drain.
  • Aspirate if rim of air between 1-2cm. If this fails - chest drain.
47
Q

Patient - Tall, thin, male, sudden onset chest pain w/ SOB. crashing vitals.

A

Pneumothorax

48
Q

Lung Ca aetiology

A
  • Smoking
  • Radon
  • Asbestos
  • Pulmonary fibrosis
  • Genetics.
49
Q

Lung Ca types

A
  • Bronchial carcinoma is most common.
  • Non-small cell - Squamous , adenocarcinoma
  • Small cell - Neuroendocrine cells.
50
Q

Lung Ca Presentation

A

Local effects;

  • Cough
  • SOB
  • Haemoptysis
  • Chest pain
  • Wheeze
  • Hoarse voice
  • Horner’s syndrome
  • Infections
  • Phrenic nerve invasion - paralysis of the diaphragm.

Mets;

  • Liver - RUQ pain, anorexia, weight loss and nausea
  • Bone - bony pain, fractures, SCC, raised ALP
  • Brain - Raised ICP and mass effect, seizures
  • Malignant plural effusion.
51
Q

Type 1 Respiratory failure

  1. Define
  2. Causes
A
  1. PaO2 is decreased
    - PaCO2 may decrease or remain normal.
    - Patients often increase RR to remove excess CO2 but can’t increase oxygen.
  2. Pneumonia
    - PE
    - Pulmonary oedema
    - Acute Asthma
    - ARDS
    - Pulmonary fibrosis.
52
Q

Type 2 Respiratory

  1. Define
  2. Causes
A
  1. PaO2 is decreased
    - PaCO2 is increased.
    - The patient fails to blow off the excess CO2 and can’t get adequate oxygen.
  2. Chronic asthma
    - COPD
    - Pneumonia
    - Sleep apnoea
    - Reduced resp drive w/ drugs etc.
    - Flail chest.
53
Q

How to read an ABG

Easily because I’m basic.

A
  1. How is the patient? well or not well
  2. Is the patient hypoxic - the PaO2 on air should be >10kPa.
  3. Is the patient acidotic (pH <7.35) or alkalotic (pH >7.45)
  4. Resp component -
    - PaCO2 high –> suggests a respiratory acidosis or a respiratory compensation for a metabolic acidosis.
    - PaCO2 low –> suggests a respiratory alkalosis or a respiratory compensation for a metabolic acidosis.
  5. Metabolic component -
    - Bicarbonate <22mmol/L (or a BE < -2mmol/L) suggests a metabolic acidosis or a renal compensation for a respiratory alkalosis.
    - Bicarbonate >26mmol/L (or a BE >2mmol/L) suggests a metabolic alkalosis or a renal compensation for a respiratory acidosis

ROME
Respiratory = opposite
- Low pH + High PaCO2 = acidotic.
- High pH + Low PaCO2 = Alkalosis

Metabolic = Equal

  • Low pH + Low bicarbonate = acidosis
  • High pH + high bicarbonate = Alkalosis.
54
Q

Stable COPD Management

A

1) SABA or SAMA
2) If FEV1 is >50% predicted offer LAMA or LABA
3) If FEV1 <50% predicted offer LAMA or combo LABA+ICS
4) If still SOB - triple therapy = LABA + ICS + LAMA

55
Q

Cannon ball metastases

A
  • Multiple well circumscribed masses in both lungs.

- From RCC or endometrial carcinoma.

56
Q

Asthma management

A
  1. SABA
  2. SABA +ICS
  3. SABA + ICS + LTRA
  4. SABA + ICS + LABA (+LTRA)
  5. SABA (+/-LTRA) + Maintenance reliever therapy
  6. SABA (+/- LTRA) + MART
  7. SABA (+/- LTRA) + ICS/LAMA/Secondary care.
57
Q

Bilateral hilar lymphadenopathy causes

A
  • TB
  • Sarcoidosis
  • Lymphoma
58
Q

Sarcoidosis

  1. Causes
  2. Presentation
  3. Ix
  4. Rx
A
  1. Multisystem disorder of UK aetiology.
    - Non-caseating granuloma.
    - Black people.
  2. Erythema nodosum
    - Bilateral hilar lymphadenopathy
    - Swinging fever
    - Polyarthralgia
    - SOB
    - Malaise
    - Weight loss
    - Hypercalcaemia.
  3. Clinical
    - Serum ACE (kinda works)
    - Bloods may show hypercalcaemia or raised ESR.
    - CXR
    - Spiro - restrictive pattern.
  4. Steroids; w/ stage 2/3 XR disease or severe progressive Sx or hypercalcaemia or heart/neuro involvement.
59
Q

Sarcoidosis XR changes Staging

A 
0 = normal 
1 = BHL 
2 = BHL + interstitial infiltrates 
3 = diffuse infiltrates only 
4 = diffuse fibrosis
60
Q

Acute respiratory distress syndrome

  1. Causes
  2. Presentation
  3. Ix
  4. Rx
A
  1. Acute condition w/ BL pulmonary infiltrates and severe hypoxia in the absence of cardiogenic or pulmonary pathology.
    - Sepsis
    - Direct lung injury
    - Acute pancreatitis
    - Long bone ### via fat embolus.
    - Head injury.
  2. Acute SOB and hypoxia
    - Multi organ failure
    - Rising ventilation requirements
  3. Clinical
    - CXR
  4. Rx underlying cause
    - ABx
    - Diuretics
    - Use PEEP and prone ventilation
61
Q

Kartagener syndrome

  1. Causes
  2. Presentation
  3. Ix
  4. Rx
A
  1. Primary ciliary dyskinesia
    - Dynein arm defect - immotile cilia.
  2. Dextrocardia + complete situs inversus
    - Bronchiectasis
    - Recurrent sinusitis
    - Subfertility
  3. CXR - dextrocardia
    CT - signs of bronchiectasis
    - Transmission electron microscopy of cilia from airway biopsy.
    - Lung function tests - obstructive pattern.
    • ABx to treat airway infection
    • Rx lung disease as COPD etc.
62
Q

PE ECG changes

A
  1. Tachycardia

2. S1Q3T3 - S waves in lead 1, Q waves and inverted T waves in lead 3.

63
Q

Wells score for PE

A

DVT = 3 points
Alternative diagnosis less likely than PE = 3
HR >100 = 1.5
Immobilisation for more than 3 days or surgery in the previous 4 weeks = 1.5
Previous DVT/PE = 1.5
Haemoptysis = 1
Malignancy = 1

PE likely = more than 4 points

64
Q

Idiopathic pulmonary fibrosis

  1. Causes
  2. Presentation
  3. Ix
  4. Rx
A
  1. Progressive fibrosis of the lung interstitium.
    - Many causes; meds, CTD, asbestos.
    - IPF is when no cause is found.
  2. Patients aged 50-70 men.
    - SOBOE
    - Bibasal fine end inspiratory creps
    - Dry cough - Clubbing
  3. Spiro - restrictive (FEV1 normal decreased, FVC decreased. Ratio increased)
    - Impaired gas exchange - reduced transfer factor.
    - CXR - BL ground glass progressing to honeycombing.
    - CT is gold standard.
  4. Pulmonary rehab.
    - Most require oxygen and transplant.
65
Q

Lung Ca management

A
  • Usually metastatic at diagnosis
  • Patients with very early disease T1,N0,M0 can be considered for surgery.
  • Most receive a combo of chemo/radio.
66
Q

Klebsiella pneumonia

A
  • Gram neg bacilli
  • More common in alcoholics and diabetics.
  • Aspiration
  • Red current sputum
  • Affects upper lobes
  • Causes lung abscess and empyema.
67
Q

Pulmonary fibrosis

  1. Causes
  2. Presentation
  3. Ix
  4. Rx
A
  1. Idiopathic
    - Progressive fibrosis of the lung interstitium.
    - Medications (amioderone)
    - CTD
  2. Men 50-70
    - SOBOE
    - Bibasal crep
    - Dry cough
    - Clubbing
  3. Spiro - restrictive.
    - Impaired gas exchange (TLCO)
    - Bilateral interstitial shadowing ground glass appearance on CXR
    - Hig resolution CT is best
    - ANA positive
  4. Pulmonary rehab
    - Very few medications - pirfenidone (antifibortic)
    - Tx

Medical School Finals (24 decks)

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