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Module 103, Theme 4: Physiology of the lungs and gaseous exchange. Pulmonary disorders and principles of their treatment. > PE, sarcoidosis and cystic fibrosis > Flashcards

PE, sarcoidosis and cystic fibrosis Flashcards

1
Q

Pulmonary embolism

A

A thrombus that dislodged from a deep vein to form an embolus: Leg, arms, pelvis

This blocks the pulmonary artery.

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2
Q

Signs and symptoms of PE

A

Dyspnoea

Syncope

Pleuritic chest pain

Calf pain and swelling

Haemoptysis

Cough

Hypoxaemia

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3
Q

Risk factors of PE

A

Hypercoagulability: OCP, genetic conditions, pregnancy, malignancies.

Vascular damage: Smoking, surgery (iatrogenic), hypertension.

Circulatory stasis:
Prolonged immobility, pregnancy

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4
Q

D-dimer test

A

Used to diagnosis PE.

D-dimers are created when clots are broken down.

This test screens the blood and rules out the presence of inappropriate blood clots when negative.

Excludes thromboembolic disease when probability is low

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5
Q

Duplex ultrasound

A

Ultrasound that looks into the blood vessels and calculates the velocity of blood moving.

Used in investigating PE.

The ultrasound will show the blood clot and also the blood being occluded.

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6
Q

CT pulmonary angiography

A

CT scan that images of the pulmonary arteries. The blood vessels are filled with contrast which will appear.

It is used to diagnose PE- it will show dark masses in the arteries.

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7
Q

V/Q scan

A

Medical imaging that uses isotopes to analyse the circulation of air and blood in the lungs.

Ventilation= looks at air flow
Perfusion= looks at blood flow.

Each scan done separately to calculate a V/Q ratio.

Mismatch is seen in patients with PE BUT does not exclude other underlying pulmonary diseases.

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8
Q

Diagnostic tests used to diagnose PE

A

CT pulmonary angiogram.

Duplex ultrasound.

V/Q scan

CXR

D-dimer test

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9
Q

Well’s criteria

A

Used to assess the likelihood of PE.

Certain signs observed are assigned to ‘points’.

If the sum of the points >4, definitive testing is carried out.

If the sum <4, D-dimer test is carried out.

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10
Q

Typical ABG result of PE

A

Hypoxaemia- O2 will be below 95%.
PAO2= low, lot less than 14/15 kPa / 95 mm Hg.

There is an increase in PAO2 due to hyperventilation= 15 kPa

Decrease in PaO2 due to perfusion obstruction- 11.3 kPa

Causes the A-a gradient increases.

Hypoxic pulmonary vasoconstriction does not happen- it is dysregulated by inflammation.

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11
Q

Blood pH in PE

A

Alkalemia: pH will be 7.49

Due to hyperventilation, there is depletion in CO2, causing hypocapnia.

CO2 levels: 30 mm Hg/ 4 kPa

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12
Q

Normal CO2 levels vs PE CO2 levels in blood.

A

Normal: 5kPa/ 40 mm Hg

PE: 4 kPa/ 30 mm Hg.

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13
Q

Anticoagulants used to treat PE

A

Warfarin

Heparin

DOACs: Dabigatran (direct thrombin inhibitor), Rivaroxaban ( direct Xa inhibitor)

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14
Q

Non- pharmacological treatment of PE

A

Removable inferior vena cava filter

Screening for pro-coagulable conditions

Screening for cancers in certain patients.

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15
Q

Sarcoidosis

A

Inflammatory pulmonary disease that has heterogeneity. It causes both restriction and obstruction.

Granulomas primarily form in the lungs but the condition spreads to the skin and lymph nodes, as well as the eyes, liver, heart and brain.

The clinical course is variable but most patients go into remission.

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16
Q

Pathogenesis of sarcoidosis

A

Unidentified antigen in inhaled and presented by APCs.

This activates CD4+ T cells causing them to release cytokines- IFN-g, IL-2, IL-12.

Macrophages also release TNF-alpha and form granulomas.

Granulomas are sterile as inflammation is not triggered by pathogens- therefore the granuloma has to be biopsied.

17
Q

Chronic sarcoidosis

A

This occurs when chronic inflammation of the lungs turn into fibrosis.

18
Q

Symptoms of sarcoidosis

A

Can be asymptomatic in some cases.

Cough, Dyspnoea

Systemic symptoms- fatigue, weight loss, fever.

19
Q

Imaging of sarcoidosis in CXR

A

Lymphadenopathy.
Triad of adenopathy: swollen lymph nodes in three locations.
Bilateral hilar
Right paratracheal

Lung nodules: grow in size during progression.

Fibrosis: mainly in the airways.

20
Q

Pharmacological management of sarcoidosis

A

Corticosteroids- immunosuppressants

21
Q

Non-pharmacological management of sarcoidosis

A

Screening for multiorgan diseases: eye exam, ECG, blood tests for liver, kidney function.

Baseline PFT data

22
Q

Example of corticosteroid used to treat sarcoidosis

A

Prednisolone- immunosuppressant drug.

23
Q

Cystic fibrosis

A

Autosomal recessive disorder caused by a deletion of a nucleotide in CFTR protein.

This prevents transportation of chloride and thiocyanate ions across cell membranes.

Hence, fluid transport is disrupted and there is an excess production of thickened mucus that obstruct exocrine glands.

24
Q

CFTR

A

Cystic fibrosis transmembrane conductance regulator- 1480 amino acids

Protein channel in epithelial membranes that allows conductance of Cl- and thiocyanate ions.

In CF, this protein is dysfunctional.

25
Q

Most common gene alteration in CF

A

Delta-F508

Loss of phenylalanine

26
Q

Systems affected by CF

A

Lungs

Pancreas- enzyme secretion inhibited.

Intestines- causes malnourishment, nutrients not absorbed.

Meconium Ileus- when newborn faeces is obstructed and thickened.

Male infertility

Osteoporosis: more intake of vitamin D from diet.

27
Q

Diagnosis of CF

A

Screening- genetic screening. Finding the mutation.

Sweat test- will show increase Na+ and Cl- because Cl- is not excreted into the dermis.

28
Q

Signs of CF

A

Wheezing

Haemoptysis

Rhonchi- low rumbling noise in lungs, like snoring. Heard when large airway is obstructed.

29
Q

Imaging of CF

A

Bronchiectasis- both CT and CXR

Opacities- mucous plugging

Hyperinflation

Shrunken, fibrotic lungs

30
Q

Acute infections in CF

A

Infections by:

Pseudomonas aeruginosa

MRSA

Normal flora changes to resistant gram negatives with age.

31
Q

Chronic infections in CF

A

Pseudomonas

B cepacia- gram negative species of bacteria

Allergic bronchopulmonary aspergillosis (ABPA)- hypersensitive reaction of the immune system to fungus.

32
Q

Complications of CF

A

Acute and chronic infections

Haemoptysis- due to inflamed BVs in bronchiectasis

Respiratory failure

Social restrictions

33
Q

Treatment of CF

A

Bronchodilators

Airway clearance techniques

Mucus thinners

Corticosteroids

Antibiotics

CFTR potentiators

Lung transplant

Pancreatic enzyme replacement.

34
Q

Airway clearance techniques

A

Postural drainage

Chest physical therapy

35
Q

Mucus thinners for CF

A

Hypertonic nebuliser

Module 103, Theme 4: Physiology of the lungs and gaseous exchange. Pulmonary disorders and principles of their treatment. (16 decks)

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