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Year 2 semester 3 respiratory system > Session 11 > Flashcards

Session 11 Flashcards

1
Q

Name 4 resp conditions that affect the airways

A
  • Asthma
  • COPD
  • Bronchiectasis
  • Cystic Fibrosis
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2
Q

Name 3 resp conditions that affect the lung parenchyma

A
  • Pulmonary fibrosis

* Pneumonia • TB

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3
Q

Name a resp condition that affects the pulmonary circulation

A

• Pulmonary embolism

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4
Q

Name 2 resp conditions that affect the pleural space

A
  • Pneumothorax

* Pleural effusion

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5
Q

Name 2 conditions that affect the chest wall shape and neuromuscular

A

kyphoscoliosis, myasthenia gravis

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6
Q

Cardinal Signs and Symptoms of Respiratory Disease

A

Breathlessness, chest pain, coughing, haemoptysis, phlegm/sputum, sounds from respiratory system

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7
Q

What is dyspnoea?

A

Breathlessness (dyspnoea)
Subjective awareness of increased effort of breathing
• Symptom rather than a sign but may be objective evidence i.e. raised RR, accessory muscle use
• Very common (…variably described) - Common to all respiratory conditions but not specific to respiratory conditions - e.g. anaemia, heart failure, obesity, diabetic ketoacidosis
“Difficulty getting enough air”
“short of breath..”
“can’t catch my breath”
“chest feels tight
Important to consider:
Onset/timing/duration important -sudden/hours/months/years/intermittent/constant
Are there precipitating factors? Position/weather/pollen/grass/animals
Progression?
Severity? Speaking/exertion/can they leave the house

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8
Q

Chest pain causes

A

Mediastinal structures
• Acute coronary syndrome • Pericarditis • Oesophagitis/GORD • Aortic dissection

Pleura
• Infection (causing pleurisy) • Pneumothorax • Pulmonary embolism (not all)(causing infarct)

Chest wall
• Rib fracture • Costochondritis (inflammation of cartilage)• Shingles (varicella zoster)

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9
Q

How to look at chest pain

A

Determining a cause…consider Location, Character and Exacerbating/ Relieving Factors
• Central vs non-central
• Cardiac vs “pleuritic”?
Cardiac pain: central, dull (except pericarditis which will be sharp), poorly localised, may radiate to shoulder/jaw, coughing wont have an effect
Pleuritic pain (irritation of parietal pleura) pain felt in Thoracic wall or shoulder tip (referred - intercostal nerve / phrenic nerve(some areas innervated by phrenic nerve so pain will refer to the shoulder) - Sharp, well localised - Worse with coughing and breathing in (word sometimes used to describe MSK pain )

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10
Q

Cough

A

A short, explosive expulsion of air…
• Important protective mechanism
• Triggered by stimulation of mechano- and/or chemo-receptors within airway by any source of irritation e.g. inflammation, foreign body!
A cough occurs via contraction of internal intercostal and abdominal muscles increasing intra thoracic pressure with addiction of VCs followed by abduction of VCs
Important considerations
• Productive cough = sputum colour
• Character e.g. bovine or seal/barking (crook)
• Timing, seasonal/day/night
• Commonest cause is URTI
• But…can be a sign of more serious and/or chronic disease

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11
Q

Productive cough

A

Sputum and Haemoptysis
• Chronic bronchitis and COPD → clear sputum (no active infection)
• Yellow/green sputum (live/dead neutrophils)→ infection
• Large volumes (yellow/green) → could suggest bronchiectasis
• Haemoptysis (blood in sputum)…potential red flag

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12
Q

Cause of cough

A

• Any irritation of airways, lung parenchyma or pleura (acute or chronic)
Non-respiratory causes:
• LV heart failure (“pink frothy sputum”) • GORD • Drugs e.g. ACE-inhibitors

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13
Q

Wheeze and stridor

A

Abnormal breath sounds indicating narrowing within the airway causing turbulent air flow
• Wheeze: high pitched, “musical”
• Mostly on expiration
• Narrowing in intrathoracic airways – E.g. from bronchial smooth muscle contraction, oedema, mucous
• Narrowing exacerbated during expiration
• May only be audible with stethoscope

  • Stridor: high pitch, constant, loud
  • Mostly on inspiration
  • Indicates narrowing in extrathoracic airway - Supraglottis, glottis, infraglottis or trachea
  • Narrowing exacerbated during inspiration
  • Often audible without stethoscope!
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14
Q

Central or peripheral cyanosis

A

Bluish discolouration:
Peripheral (skin of feet, hands, nose and tips of ears) • Cold exposure and decreased cardiac output • Slowing of blood to peripheries (due to vasoconstriction) • Increased oxygen extraction • More deoxygenated blood present in that area
Central cyanosis: lips and tongue (mucous membranes) • Significant cardiac or respiratory cause • Caused by increase in amount of deoxygenated Hb in blood arriving at tissues [deoxygenated blood is leaving the heart]

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15
Q

Pursed lip breathing

A

Breathing out slowly through mouth with pursed lips
• Commonly seen in COPD
• Pursing lips increases resistance to outflow on expiration
• Maintains intrathoracic airway pressures allowing for small
airways to remain open for longer• prolonging period for gas exchange to occur • and to allowing more air to empty (rather than trap)

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16
Q

Barrel Shaped Chest

A

Increased A-P diameter
• Associated with lung hyperinflation • Seen in severe COPD (especially emphysema)
• AP diameter > lateral diameter
• Chronic over-inflation of lungs (due to air trapping)
• Hyperexpands the chest wall over time

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17
Q

Clinical Examination Palpation

A
  • Tracheal position (pleural effusion, malignancy, pulmonary fibrosis, tension pneumothorax, lobectomy)
  • Chest expansion - Symmetrical?
18
Q

Clinical Examination Percussion

A
  • Resonant? - Normal
  • Hyper-resonant - Increased air
  • Dull - Consolidation
  • Stony-dull -
19
Q

Clinical Examination Auscultation

A
  • Normal (vesicular) - ‘Rustling leaves’ - Inspiration and first part of expiration - No gap between inspiratory and expiratory components
  • Bronchial - ‘Blowing’ harsh sound - Inspiration and expiration - Gap between
  • Reduced or absent
  • Added sounds:
  • Wheeze or stridor
  • Crackles - Snapping open of alveoli/small bronchi - Fine → pulmonary fibrosis - Course → COPD, bronchiectasis (air bubbling through mucous secretions)
  • Pleural rub (hand over ear and scratch your hand is what it sounds like)- Scratching, coarse sound - Inflammation of pleura e.g. pleurisy
20
Q

Order of chest examination

A

Inspection
Palpation
Percussion
Auscultation

21
Q

Table

A

end of lec 1

22
Q

Clinical examination:inspection

A

raised RR, clubbing, accessory muscles, chest shape, symmetry? Cyanosis

23
Q

What is an embolism

A

• Obstruction of a blood vessel by a foreign substance or a blood clot that travels through the bloodstream, lodging in a blood vessel, plugging the vessel • The material may or may not be derived from the circulation itself. Pulmonary embolism means that the material passes through the right side of the heart and lodges in the pulmonary arteries

24
Q

What can embolise

A
  • Thrombus - Tumour - Air - Fat - Amniotic fluid - Bullet
25
Q

Describe a CXR of someone with an embolism

A

Diffuse air space opacities/infiltrates bilaterally
Clinical signs may Include petechial rash, tachycardia, fever, hypoxaemia – may be refractory to O2
May have CNS Effects –HOW?? Triad of lung, brain and skin = FES – Fat Embolism Syndrome
Donut Sign - Peri-bronchial cuffing

26
Q

Why might someone get an air embolism?

A

Cerebral Air Embolism- usually iatrogenic occurring especially in patients in ICU setting
Air entry through central venous cannulae, pulmonary artery catheters or haemodialyis catheters

27
Q

Risk factors within the context of pathophysiology of thromboembolism

A 
Virchow triad:
• Endothelial injury
• Stasis or turbulence of blood flow
• Blood hypercoagulability
Risk factors in order of importance:
• Pregnancy • Prolonged immobilisation  • Previous VTE  • Contraceptive pill • Long haul travel (> 4 hrs) • Cancer • Heart failure  • Obesity  • Surgery > 30 mins  • HRT  • Thrombophilia
28
Q

Pathology of deep VENOUS thrombosis

A

use slide 7

29
Q

Hypercoagulable Conditions

A

• Antithrombin III deficiency • Protein C or protein S deficiency or resistance – Factor V Leiden mutation causing resistance to activated protein C is the most common risk factor for DVT/PE in younger people (3-8% European people have only one version of thee gene) • Lupus anticoagulant • Homocystinuria • Occult neoplasm • Connective tissue disorders such as RA

30
Q

Pathophysiology of clinical outcomes in PE

A
  1. Acute right ventricular overload • Pulmonary artery pressure increases if more than 30% of the total cross section of the pulmonary arterial bed is occluded. • This leads to acute right ventricular dilatation and strain • Also inotropes are released by the body in an attempt to maintain systemic BP : these cause pulmonary artery vasoconstriction that further exacerbates the situation. • The main cause of death in PE is acute right sided heart failure leading to cardiogenic shock with circulatory failure and/or cardiac arrest secondary to arrythmias.
  2. Respiratory failure • Due to areas of ventilation perfusion mismatch • Low right ventricle output due to venous congestion due to embolism. Shunt with patent foramen ovale allows blood from right to left side of heart. May lead to severe hypoxaemia and an increased risk of paradoxical embolization and stroke
  3. Pulmonary infarction
    • Small distal emboli may create areas of alveolar haemorrhage resulting in haemoptysis, pleuritis, and small pleural effusion. This clinical presentation is known as pulmonary infarction • Relatively uncommon – approx. 10-20% cases – may be visible on CXR as wedge shape
31
Q

Symptoms of pulmonary embolism

A

From most common to least:• Dyspnea • Pleuritic chest pain • Substernal chest pain • Cough • Haemoptysis • Syncope • Unilateral leg pain • Fever of less than 39°C (102.2ºF) may be present in 10-15% of patients; however, temperature higher than 39.5°C typically not from pulmonary embolism • Chest wall tenderness upon palpation, without a history of trauma, may be the sole physical finding in rare cases.

32
Q

Physical signs in pulmonary embolism

A

Physical signs of pulmonary embolism include the following:
• Tachypnea (respiratory rate >16/min): ~90-96%
• Rales or decreased breath sounds: ~50 %
• Accentuated second heart sound: ~50 -55% (loud P2)
• Tachycardia (heart rate >100/min): ~44 – 50 %
• Fever (temperature >37.8°C ): ~30-45%
• Diaphoresis: ~30-35%
• Clinical signs and symptoms suggesting thrombophlebitis: ~30% • Lower extremity oedema: ~25% • Cardiac murmur: ~20% • Cyanosis: ~15-20%

33
Q

Main differential diagnoses for pulmonary embolism

A

• Pneumothorax • Pneumonia • Myocardial infarction • Pericarditis • Pleurisy • Musculo-skeletal chest pain

34
Q

Investigation

A

• Blood gases – May show hypoxaemia and hypocapnia(respiratory alkalosis) due to hyperventilation – Undertaken if evidence of hypoxia requiring oxygen – In a small proportion of patients arterial PaO2 may be normal • CXR – By far the commonest finding in PE is a normalCXR. – May be done to exclude other diagnoses.
•ECG –May show signs of right ventricular strain T wave inversion in the right precordial leads (V1 - V4 and the inferior leads, II, III and aVF). –The ‘classic’ finding is SI QIII TIII - deep S wave in lead I, Q wave in III, inverted T wave in III – only found 20% patients with PE –People who have had a PE are also acutely prone to supraventricular tachyarrhythmias
–Not useful as a primary diagnostic tool
• D-dimer: – D-dimer is a fibrin degradation product, a small protein fragment released into the blood when a thrombus is degraded by fibrinolysis.
– A normal D-dimer effectively rules out PE in those at low likelihood of having a PE.
– In those at high likelihood the negative predictive value of D dimer is too low to use – need further imaging tests
Likelihood determined by

35
Q

Imaging for PE

A

CT Pulmonary Angiography (CTPA)

36
Q

Treatment of PE

A

Treatment of high and low risk patients
• Immediate heparinisation. • This reduces mortality
• IV heparin now superseded by Subcutaneous Low Molecular Weight Heparin

Treatment of high risk patients:
• Haemodynamic support • Respiratory support • Exogenous fibrinolytics (streptokinase/tPA) – Peripheral intravenous – Delivered directly via a percutaneous catheter into the pulmonary arteries • Percutaneous catheter directed thrombectomy • Surgical pulmonary embolectomy

37
Q

How does heparinisation reduce mortality?

A
  1. Stops thrombus propagation in the pulmonary arteries and allows the body’s fibrinolytic system to lyse the thrombus 2. Stops thrombus propagation at the embolic source and reduces the frequency of further pulmonary embolism 3. It does NOT dissolve the clot – the body does that
38
Q

What is heparin-induced thrombocytopenia?

A
  • Body produces antibodies to a portion ofheparin that also recognize heparin-platelet complexes – binding of the antibody to the platelets activates them, platelet clumps are formed leading to thrombi • LOW platelet count, but paradoxically increased risk thromboses • Thromboembolic complications can be venous, arterial, or both and include deep venous thrombosis, pulmonary embolism, myocardial infarction, thrombotic stroke and occlusion of limb arteries
  • Treatment - immediate cessation of all formulations of heparin , but may not stop continuing thrombin generation nor avoid subsequent thrombotic events (~40% pts) - need to use non-heparin based anticoagulants
39
Q

What happens after initial heparinisation

A
  • Patients are started on an oral anticoagulant (e.g warfarin*): – For 3 months if there is an identifiable ‘temporary’ risk factor (50%) – Indefinitely if cancer or no identifiable risk factor (50%)
  • What about those patients who cannot be safely anticoagulated? (e.g have oesophageal varices, previous haemorrhagic stroke, severe thrombocytopenia)
    • ‘Direct Oral Anti Coagulant – DOAC-’ e.g. rivaroxaban now increasingly prescribed- lower risk bleeding
40
Q

What if no form of anti-coagulation can be used for pulmonary embolism risk patients?

A

Inferior vena cava filter

41
Q

Prevention DVT/PE

A
  • Outpatient – recognise and address risk factors – – Should an obese women who smokes be placed on OCPs or HRT? No – Advice for people with thrombophilia who travel > 4 hours
  • Inpatient – DVT prophylaxis after surgery – DVT prophylaxis for patients with malignancy

Year 2 semester 3 respiratory system (13 decks)

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