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Medicine Year 2 (Bear) > Week 219 - Haemoptysis 2 (pulmonary circulation) > Flashcards

Week 219 - Haemoptysis 2 (pulmonary circulation) Flashcards

1
Q

Week 219

Define “Bronchopulmonary Segment”

A

This refers to one of ten segments in the right lung, and eight segments in the left lung. Each segment is a discrete anatomical and functional unit separated from the others by a layer of connective tissue.

  • “The Right Honourable 3’s stuck 2 middle fingers up to the 5 insiders.”*
  • “The left is fair, 4 up, 4 down”*
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2
Q

Week 219

Which arteries supply the lung parenchyma?

A

The Lung Parenchyma is supplied by the Bronchial arteries.

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3
Q

Week 219

Bronchial arteries drain into either ___ or _____.

A

Bronchial arteries drain into either bronchial or pulmonary veins. Thrombosis in these vessels can be associated with massive haemoptysis.

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4
Q

Week 219

Which branch of the major arterial vessels supplies the right lung?

A

One artery arising from the third right posterior intercostal artery, a branch of the aorta.

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5
Q

Week 219

Which branches of the major arterial vessels supplies the left lung?

A

Two Arteries

  • Superior arises from antero-medial surface of the aortic arch just lateral to the carina and posterior to the left main bronchus.
  • Inferior arises from aorta parallel to its superior counterpart, but at a point that is inferior to the left main bronchus.
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6
Q

Week 219

From where does the pulmonary trunk arise?

A

The right ventricle.

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7
Q

Week 219

The pulmonary circulation differs from the systemic circulation in which way?

A

Arteries - carry deoxygenated blood

Veins - Carry oxygenated blood.

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8
Q
A
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9
Q

Week 219

Label the image. Which lung is this?

A

This is the hilum of the left lung.

  • A PULMONARY ARTERY
  • B BRONCHIAL ARTERIES
  • C PRIMARY BRONCHUS
  • D SUPERIOR AND INFERIOR LOBAR BRONCHI
  • E BRONCHOPULMONARY LYMPH NODES
  • F SUPERIOR AND INFERIOR PULMONARY VEINS
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10
Q

Week 219

Label the image. Which lung is this?

A

This is the Hilum of the right lung.

  • A SUPERIOR LOBAR BRONCHUS
  • B PULMONARY ARTERY
  • C BRONCHUS INTERMEDIUS
  • D BRONCHIAL ARTERIES
  • E BRONCHOPULMONARY LYMPH NODES
  • F SUPERIOR AND INFERIOR PULMONARY VEINS
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11
Q

Week 219

What is the Ligamentum arteriosum?

A

This is a tiny ligament, that connects the arch of the aorta to the left pulmonary artery. Good in spotters.

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12
Q

Week 219

Which nerve hooks around the ligamentum arteriosum?

A

The Recurrent laryngeal nerve.

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13
Q

Week 219

The Ligamentum arteriosum represents the remnant of which foetal structure?

A

The foetal ductus arteriosus. A Patent ductus arteriosus (PDA) represents 5-10% of all congenital cardiac abnormalities.

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14
Q

Week 219

What are the main differences between venous and arterial blood gas results?

A
  1. SAO2 and PO2Is higher in arterial.
  2. CO2 levels are a little higher in venous blood.
  3. Other results are pretty much the same.
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15
Q

Week 219

What is Virchow’s triad?

A

Thrombosis may follow an alteration in:

  1. Blood flow
  2. Blood constituents
  3. Endothelium (due to injury)
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16
Q

Week 219

Peripheral venous emboli in the lung are what shape?

A

Wedge shaped.

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17
Q

Week 219

What are the sources of **venous emoblism, **and which two major pathologies could they cause?

A

Pulmonary Embolism:

  • **DVT ** in leg, pelvic veins or prostatic venous plexus.

Stroke Risk:

  • **Paradoxical emboli **cross from right heart to left through shunts, e.g. Atrial Septal Defect, Ventricular Septal Defect, Patent Foramen Ovale.
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18
Q

Week 219

Which three coagulopathies are the most common causes of thrombophilic pulmonary thrombo-embolism (PE)?

A
  • Factor V Leiden
  • Prothrombin mutation
  • Deficiencies of protein S and C, and antithrombin III
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19
Q

Week 219

What are the signs and symptoms of Deep vein thrombosis?

A
  • Increased swelling one or both legs
  • Pain and tenderness
  • Increased skin temperature and erythema
  • Dilated superficial veins
  • _But may be silent and inconspicuous _
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20
Q

Week 219

What are the differential diagnoses for a Deep Vein Thrombosis (DVT)?

A

Differential diagnoses include:

  • Superficial thrombophlebitis
  • Haematoma due to trauma or torn muscle
  • Cellulitis
  • Ruptured Baker’s cyst
  • Dependent oedema (cardiac failure, nephrotic syndrome, liver cirrhosis, lymphatic obstruction)
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21
Q

Week 219

What is this?

A

This is a Bakers Cyst.

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22
Q

Week 219

What is this?

A

This is Cellulitis.

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23
Q

Week 219

What are the risk factors for Deep Vein Thrombosis?

A
  • Prolonged immobilisation
  • Myocardial infarction and heart failure
  • Tissue damage in surgery, burns, fractures
  • Cancer esp pancreas
  • Nephrotic syndrome
  • Oral contraceptives
  • Smoking
  • Genetic factors
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24
Q

Week 219

Other than a thromboembolism, what (other) types of venous embolisation are there?

A
  • Fat embolism: in fractures. May cause rash, confusion, neurological signs, thrombocytopaenia, anaemia
  • Gas embolism from rapid ascent from scuba dives (either air or nitrogen) or knife injuries to head and neck
  • Amniotic fluid embolism: 1 in 50,000 deliveries
  • Tumour embolism: usually seen in lung.
  • Schistosomiasis; worms in pelvic veins and portal veins release eggs which are carried to the liver causing granulomatous scars resulting in portal hypertension
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25
Q

Week 219

What does this image show? Label it.

A

This is a (Tumour) Pulmonary Embolus.

  • A Wall of pulmonary artery
  • B Tumour Embolus
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26
Q

Week 219

What is this? What does the arrow point to?

A

This is an embolism caused by the egg of a Schistoma worm.

The arrow is pointing to a Schistoma ova (egg).

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27
Q

Week 219

What is this?

A

This is a fat embolism.

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28
Q

Week 219

Name Six (6) sources of arterial emboli.

A
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29
Q

Week 219

What are the four major causes of atheromatous plaques?

A
  • Hypertension
  • Hyperlipidaemia
  • Cigarette smoking
  • Diabetes mellitus
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30
Q

Week 219

What are the effect of altered flow on the development of atheromatous plaques?

A
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31
Q

Week 219

What is Polycythaemia rubra vera?

A

An increase in all cell types. Can lead to thrombosis.

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32
Q

Week 219

Name some causes of secondary polycythaemia.

A
  • Altitude
  • COPD
  • Cardiac shunts
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33
Q

Week 219

There are five physiological outcomes of thrombosis - what are they?

A
  • Resolution: thrombus may be dissolved by endogenous fibrinolytic proteins or administration of Streptokinase
  • Organisation: macrophages remove fibrin clot which is replaced by fibrous scar tissue
  • Recanalisation: new channels may form within the organising thrombus
  • Embolism: detachment from wall. The fragment/s float away until they lodge in a smaller vessel
  • Propagation: extension of thrombus along the vessel as seen in DVT
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34
Q

What does this image show?

A

This is a recanalised thrombus.

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35
Q

Week 219

What is this?

A

Right pleural effusion

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36
Q

Week 219

What is this?

A

Left pneumothorax

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37
Q

Week 219

What is the best Investigation for suspected pulmonary embolism?

A

CTPA- best test generally. High sensitivity and specificity. Detects other pathology

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38
Q

Week 219

What are the arrows pointing to?

What type of imaging is this?

A

The arrows are pointing to Pulmonary Emboli. The imaging technique is CTPA.

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39
Q

Week 219

A Patient collapses with sudden chest pain. This is their CTPA. What can you see?

A

There are emboli here. This patient is having a P.E.

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40
Q

What can you see?

A

A Normal CXR!

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41
Q

What can you see?

A

PE

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42
Q

Week 219

What can you see?

A

PE

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43
Q

Week 219

Label this image.

A
44
Q

Week 219

Bronchiectasis is a cause of profuse ____.

A

Bronchiectasis is a cause of profuse haemoptysis .

45
Q

Week 219

A 56 YO bangladeshi man has a history of 6 months weight loss, and 3 weeks oa haemoptysis - clots of bright red blood.

Which tests should you perform?

A

It is likely that this man has TB. Test sputum for Acid Fast Bacili and do a CXR.

46
Q

Week 219

Define the term “Bronchiectasis”.

A

Bronchiectasis is an abnormal and permanent (chronic) dilatation of one or more of the bronchi.

47
Q

Week 219

Name the inherited causes of bronchiectasis.

A

Cystic fibrosis, Immotile cilia syndromes, e.g. Kartagener’s syndrome

48
Q

Week 219

What are the Acquired causes of bronchiectasis?

A
  • Childhood pneumonia (Pertussis, measles, TB)
  • Chronic bronchial obstruction (Inhaled foreign body, benign tumours) • Chronic aspiration
  • Allergic Bronchopulmonary Aspergillosis (ABPA)
  • Immunoglobulin deficiency (usually IgG or lymphoproliferative disease) & HIV

• Associations with RA, Ulcerative colitis

49
Q

Week 219

What are the physical signs of bronchiectasis?

A
  • Breathlessness
  • Polyphonic Wheeze
  • Finger clubbing
  • Coarse, mid inspiratory crackles (may be focal)
  • Respiratory failure
50
Q

Week 219

What is the commonest cause of maternal death in the UK?

A

PE

51
Q

Week 219

What is Homans’ sign?

A

This is pain in the calf on dorsiflexion of the foot.

52
Q

Week 219

What is a D-Dimer?

A

– A breakdown product of cross-linked fibrin elevated in thromboembolism (NB Also elevated post surgery / trauma / liver, renal disease, pregnancy, cancer, heart disease etc)

– A negative test in ‘low risk’ patients ‘virtually’ excludes DVT

53
Q
A
54
Q

Week 219

What is the definition of haemoptysis?

A

The Coughing up of blood or bloody sputum from the respiratory tract below the larynx.

55
Q

Week 219

Acute or Chronic bronchitis is a common cause of which symptom?

A

Haemoptysis.

56
Q

Week 219

What is the most common cause of massive haemoptysis? (>100ml)

A

Bronchiectasis.

57
Q

Week 219

Which component of the clotting cascade does Tranexamic acid act?

A

Tranexamic acids inhibits the formation of plasmin from plasminogen.

58
Q

Week 219

What is the action of Plasmin?

A

Plasmin is a molecule essential for the degradation of Fibrin clots.

59
Q

Week 219

What is being measured in the “Wells’ Score”?

A

This is a measurement of a patients likelyhood of suffering a DVT.

60
Q

Week 219

What is the imaging technique most commobly used to assess DVT?

A

Doppler Ultrasound.

61
Q

Week 219

What happens to D-Dimer in thromboembolism?

A

D-dimer is a breakdown product of cross-linked fibrin, elevated in thromboembolism.

62
Q

Week 219

How do you treat Deep Vein Thrombosis?

A

Until the diagnosis is confirmed, treat with sub-cut, low molecular weight Heparin. If confirmed, continue heparin until INR is around 2.5. Trial warfarin for 3 months, before re-assessing.

63
Q

Week 219

What is meant by the term “Pulmonary infarction”?

A

Necrosis of lung parenchyma resulting from interference of blood supply. NB: There is dual circulation to the lung parenchyma, from pulmonary and bronchial circulation - so this is not necessarily directly related to PE.

64
Q

Week 219

What is the difference between Classification I and classfication II Pumonary Embolism?

A

I - This is ACUTE, often following recent surgery or immobility. It can be massive or minor.

II - This is CHRONIC, and is usually progressive, originating from many smaller clots.

65
Q

Week 219

What are the typical symptoms of PE?

A
  • Acute / sub-acute SOB
  • Pleuritic chest pain
  • Haemoptysis (usually small)
  • Dizziness
  • Syncope
  • Restlessness / anxiety
66
Q

Week 219

What are the clinical **signs ** of Pulmonary embolism?

A

Cardinal: Dyspnoea, tachypnoea, pleuritic pain

Others: – Tachycardia Loud/widely split P2 – Cyanosis JVP – Pyrexia hypotension – AF pleural rub – signs of DVT or scar from recent surgery

67
Q

Week 219

What findings do you expect on an arterial blood gas taken from a patient suffering from a pulmonary embolism ON AIR?

A

hyperventilation (low CO2 and high pH) with hypoxia

68
Q

Week 219

What is the most common first line imagint echnique for suspected PE?

A

CT Pulmonary Angiogram (CTPE)

69
Q

Week 219

What are Apixaban and rivoroxaban?

A

These are new oral anticoagulants (Factor Xa (FXa) inhibitors), that do not require monitoring.

70
Q

Week 219

What is Dabigatran?

A

This is a direct thrombin inhibitor (a new class of anticoagulants), used only in the treatment of AF.

71
Q
A
72
Q

Week 219

What are the differential diagnoses for a cavitating lung mass?

A
  • Carcinoma (usually squamous cell)
  • Lung abcess
  • Rheumatoid nodule
  • Embolus (septic - usually iv drug abuser)
  • Vasculitis with granulomatosis (Wegener’s)
  • Bronchogenic cyst
  • Hydatid cyst
73
Q

Week 219

What is Pulmonary Arterial Hypertension (PAH)?

A

Hypertension of the pulmonary ARTERIAL vasculature

  • Usually Idiopathic or Familial
  • Associated with collagen vascular disease, congenital disorders, portal hypertension, HIV, and drug use (and a bunch of other things)!
74
Q

What is the obvioius clinical feature of this CT?

A

This is a CAVITATING MASS (R side).

75
Q

Week 219

What is Persistent pulmonary hypertension of the Newborn?

A

Defined as the failure of the normal circulatory transition that occurs after birth.

It is a syndrome characterized by marked pulmonary hypertension that causes hypoxemia and right-to-left intracardiac shunting of blood.

76
Q

Week 219

What are the causes of Pulmonary Venous Hypertension?

A
  • Left-sided atrial or ventricular heart disease
  • Left-sided valvular heart disease
77
Q

Week 219

Which chronic disease is associated with Pulmonary Hypertension associated with hypoxemia?

A

Chronic obstructive pulmonary disease (COPD)

78
Q

Week 219

Other than COPD, which conditions can cause Pulmonary Hypertension associated with Hypoxaemia?

A

Interstitial lung disease
• Sleep-disordered breathing
• Alveolar hypoventilation disorders
• Chronic exposure to high altitude (Mountaineers, for example)
• Developmental abnormalities

79
Q

Week 219

What causes Pulmonary Hypertension of Chronic thrombotic disease?

A
  • Thromboembolic obstruction of proximal pulmonary arteries
  • Thromboembolic obstruction of distal pulmonary arteries
  • Non-thrombotic pulmonary embolism (tumor, parasites, foreign material)
80
Q

Name THREE Miscellaneous causes of Pulmonary Hypertension

A
  • Sarcoidosis
  • Histiocytosis X
  • Lymphangiomatosis
81
Q

Week 219

Define Pulmonary Arterial Hypertension

A

• This is a pathology of ** Haemodynamics**
– Mean PAP (pulmonary arterial pressure) >25mmHg at rest

+ Pulmonary capillary wedge <=15mmHg (That’s where they stick a baloon into a pulmonary artery to measure the pressure)
+ Pulmonary Vascular Resistance >= 3 Wood Units (this is just a measure of pressure - it can be converted)!

• Needs R+LHC to confirm (Heart chamber catheterisation)

82
Q

Week 219

How is Pulmonary Arterial Hypertension diagnosed?

A

This is a diagnosis of exclusion, identified by ruling out other causes of pulmonary hypertension, particuarly left sided heart disease.

83
Q

Week 219

What are the symptoms of pulmonary arterial hypertension?

A

Usually silent until right heart fails
– Progressive Dyspnoea
– Fatigue
– Palpitations
– Chest pain
– Cough / Haemoptysis
– Presyncope / Syncope

84
Q

Week 219

Describe the pathophysiology of pulmonary arterial Hypertension

A
  1. Endothelial Dysfunction - Vasoconstriction
  2. Vascular remodelling - Muscle cell proliferation - hypertrophy
  3. Thrombosis - < platelet activation

These all lead to R sided ventricular strain and dysfunction.

85
Q

Week 219

Describe the major therapies utilised in the treatment of pulmonary arterial hypertension.

A
  • Vasodilators (Oxygen, Ca2+ blockers, natriuretic peptide) - These act on SMOOTH MUSCLE CELLS to reduce proliferation.
  • Antiinflammatory (NO Donors, statins, prostacyclin analogues) - These act on Leukocytes and complement pathways
  • Antiplatelet therapies (NO donors, prostacyclin) - These aim to prevent clot formation
  • **Anticoagulant **(Warfarin, LMW Heparin) - act on clotting cascade to prevent formation of fibrin - prevents clots
  • Remodelling therapies (NO donors, Endothelin-receptor antags) - aim is to prevent vasculature remodelling/fibrosis
  • Inhalation therapies (Oxygen, NO donors, ethyl nitrate)

Think “Treating PAH is VAAARI hard”!

86
Q

Week 219

What action does Nitric Oxide have on Vascular tone?

A

NO is a selective pulmonary vasodilator, produced by the epithelium, that plays an important role in the regulation of blood pressure, inflammatory processes and neurotrnasmission.

87
Q

Week 219

What role do prostaglandins play in the regulation of vascular tone?

A

Prostacyclin, produced mainly by epithelial cells, is a
potent vasodilator and inhibitor of platelet aggregation. It
has cytoprotective and anti-proliferative activities

88
Q

What role does Endothelin-1 play in the regulation of vascular tone?

A

Produced by vascular endothelial cells, it is a potent and
long-acting vasoconstrictorandstimulates proliferation of
pulmonary artery smooth muscle cells.

It is also associated with fibrosis, vascular cell hypertrophy, inflammation and neurohormonal activation (mediated through binding to two types of receptor ETa and ETb).

89
Q

Week 219

Which receptor type is seen in 50% of familial cases of pulmonary arterial hypertension?

A

Bone morphogenic protein receptor type-2 (BMPR2)

90
Q

Week 219

Describe the WHO classification of Pulmonary Arterial Hypertension functional status.

A

I No limitation of usual physical activity

II Mild limitation of physical activity.

III Marked limitation of physical activity, but there is no discomfort at
rest

IV Unable to perform any physical activity at rest and may have
signs of right ventricular failure. Dyspnoea and/or fatigue may be
present at rest and symptoms are increased by almost any physical
activity

91
Q

Week 219

Pulmonary arterial hypertension is related to (found in conjunction with) which group of diseases?

A

Connective tissue diseases

(Scleroderma, SLE, Mixed, Antiphospholipid syndrome, RA)

92
Q

Week 219

What are epoprostenol and trepostinil?

A

These are prostaglandin analogues.

93
Q

Week 219

Name a PDE5 inhibitor

A

Sildenafil

94
Q

Week 219

Name an Endothelin R Antagonist.

A

Bosentan

95
Q
A
96
Q

Week 219

What makes up Wegener’s triad?

A
  1. Vasculitis affecting arteries and veins
  2. Focal necrotising glomerulonephritis
  3. Varying systemic vasculitis
97
Q

How long would you have to take Warfarin if you had had a DVT following a Long-Haul flight?

A

Three months minimum.

98
Q

Week 219

How long would you want to take warfarin if you had a massive PE?

A

This has probably not been caused by a major event, and was preceded by several smaller clot formations. For this reason, it is likely that long-term therapy on warfarin will be conducted.

99
Q

Week 219

Which test would identify idiopathic pulmonary haemosiderosis?

A

Perl’s stain (Shows Haemosiderin-laden macrophages).

100
Q

Week 219

What are the signs and symptoms of persistent newborn pulmonary hypertension?

A
  • Asphyxia
  • Tachypnea
  • Loud, single heart sound, or a harsh systolic murmur
  • Low APGAR score
  • Systemic hypotension
  • Symptoms of shock
101
Q
A
102
Q

Week 219

What is bronchiectasis?

A

Abnormal and persistent dilation of the proximal bronchioles due to inflammation.

103
Q

Week 219

What drug types would be most useful in the treatment of the symptoms of bronchiectasis and cystic fibrosis?

A
  • Bronchodilators (anticholinergics, B2 agonists)
  • Mucolytics
    *
104
Q

Week 218

What is the CFTR protein, and in which condition is it produced?

A

CFTR:

Cystic fibrosis transmembrane conductance regulator - cystic fibrosis.

105
Q

Week 218

How could cystic fibrosis cause malabsorbtion?

A

faulty CFTR gene means that Cl- gets pumped out of cells, and NA+ follows. This creates an osmotic gradient that causes water to leave cells, resultiong in thick mucous secretions. subsequently, the pancreatic duct becomes blocked, leading to poor digestion and absorbtion of fats, and vitamin B12.

106
Q

Week 218

A PE will result in R ventricular strain. What would this look like on an ECG?

A

Rt Axis deviation, Tall R waves and T wave inversion in R sided leads (V1-3, 2 and AVF)

107
Q
A

Medicine Year 2 (Bear) (30 decks)

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