Pulmonary Vascular Disease Flashcards

1
Q

Pulmonary Embolism Causes

A

Venous thrombosis (lower extremities or pelvis),
fat, amniotic fluid, clumps of tumour cells or bone marrow

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2
Q

Pulmonary Embolism Risk factors

A

Stasis of blood flow (prolonged bed rest or
immobilisation), hypercoagulable states, use of oral
contraceptives

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3
Q

Saddle embolus

A

Large emboli → Major vessels

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4
Q

Clinical finding of Saddle embolus

A

Sudden increase in Pulmonary Artery pressure
Acute right ventricular strain → Sudden death

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5
Q

Clinical findings of Pulmonary infarction

A

Sudden onset of dyspnoea and tachypnoea
Pleuritic chest pain
Friction rub
Effusion
Expiratory wheezing

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6
Q

Laboratory Findings of pulmonary embolism

A

Respiratory alkalosis (arterial PCO2 <33 mmHg)
PaO2 <80 mmHg (90% of cases)
Increase in Alveolar - arterial gradient (100% of cases)
Increase in D-dimers
✓Positive D-dimers

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7
Q

Chest X-ray of pulmonary embolism

A

Elevation of ipsilateral hemi-diaphragm
Pleural effusion (haemorrhagic)
Westermark’s sign of peripheral oligaemia
Fleischner’s sign of “amputated” pulmonary artery
Hampton hump (wedge-shaped area of
consolidation)

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8
Q

Ventilation scan will be _______ in pulmonary embolism

A

Normal

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9
Q

Perfusion Radionuclide Scan

A

Abnormal

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10
Q

What is the Gold standard
confirmatory test of pulmonary embolism?

A

Pulmonary angiogram

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11
Q

Macro-/Microscopic finding in pulmonary embolism

A

Red-blue raised wedge-shaped area that extends to
the pleural surface
Majority are located in the lower lobes (Perfusion >
Ventilation)
Fibrinous exudate on pleural surface
Haemorrhagic pleural effusion

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12
Q

Mean pulmonary artery pressure >25mmHg
at rest (normal: 15 mmHg) >30mmHg
with exercise (normal: 20 mmHg)

A

Pulmonary Hypertension

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13
Q

Histologic picture of pulmonary hypertension

A

Characteristic plexiform lesions

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14
Q

Which form of pulmonary hypertension is more common?

A

Secondary pulmonary hypertension

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15
Q

Pathogenesis of 2nd pulmonary hypertension

A

Endothelial cell dysfunction ->Loss of vasodilators (e.g. NO) -> Increase in vasoconstrictors (e.g. Endothelin)
Hypoxaemia & Respiratory Acidosis → Pulmonary
arteries vasoconstriction → Smooth muscle
hyperplasia and hypertrophy

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16
Q

Causes of 2nd pulmonary hypertension

A

Chronic hypoxaemia (e.g. Chronic lung disease)
Chronic respiratory acidosis (e.g. Chronic bronchitis)
Loss of pulmonary vasculature → Workload for
remaining vessels (e.g. Emphysema, recurrent
pulmonary emboli)
Left-to-right cardiac shunts → Volume overloading
pulmonary vasculature
Left-sided valvular disease (e.g. Mitral stenosis) →
Backup of blood into pulmonary veins → Venous
hypertension

17
Q

Histologic picture of 2nd pulmonary hypertension

A

Atherosclerotic changes of main pulmonary
arteries (Result of ↑ pressure to endothelium →
Endothelial injury)
Proliferation of myo-intimal and smooth muscle
cells

18
Q

Intra-alveolar accumulation of fluid

A

Pulmonary Oedema

19
Q

Pathogenesis of pulmonary oedema

A

Due to alterations in Starling forces (transudate)
Due to micro-vascular or alveolar injury (exudate)
Increased alveolar capillary permeability

20
Q

Causes of Adult Respiratory Distress Syndrome

A

Shock, sepsis, trauma, uraemia, aspiration of
gastric contents, acute pancreatitis, inhalation of chemical irritants, oxygen toxicity, heroin, bleomycin

21
Q

Pathogenesis of Adult Respiratory Distress Syndrome

A

Damage to alveolar capillary endothelium and alveolar epithelium (Diffuse alveolar
damage) → ↑ in alveolar capillary permeability →
Leakage of protein-rich fluid into alveoli

22
Q

Pathogenic factors of Adult Respiratory Distress Syndrome

A

Neutrophils → Release of substances, toxic to
alveolar wall
Activation of coagulation cascade → Micro-emboli
Oxygen-derived free radicals → Oxygen toxicity

23
Q

ARDS can be a manifestation of

A

Severe Acute Respiratory Syndrome

24
Q

SARS Coronavirus destroys

A

type II pneumocytes and causes diffuse alveolar damage

25
Q

Clinical Features of ARDS

A

Impairment of respiratory gas exchange → Severe hypoxia

26
Q

Histopathological features of ARDS

A

Formation of intra-alveolar hyaline membranes (fibrin and cellular debris)

27
Q

Hyaline Membrane Disease

A

Neonatal Respiratory Distress Syndrome

28
Q

Most common cause of respiratory failure in newborns
Most common cause of death in premature infants

A

Neonatal Respiratory Distress Syndrome

29
Q

Cause of Neonatal Respiratory Distress Syndrome

A

Deficiency of surfactant, due to immaturity

30
Q

Clinical Features of NRDS

A

Dyspnoea
Cyanosis
Tachypnoea

31
Q

What secretes surfactant?

A

Type II pneumocytes

32
Q

What does surfactant do?

A

Reduces surface tension within the lung →
Facilitates expansion during inspiration and
prevents atelectasis during expiration

33
Q

Predisposing factors of NRDS

A

Prematurity
Maternal Diabetes Mellitus
Birth by caesarian section

34
Q

Macro\Micro of NRDS

A

Heavy lungs, with alternating areas of atelectasis
and alveolar or alveolar-ductal dilatation
Engorgement of small pulmonary vessels
Leakage of blood products into the alveoli →
Formation of intra-alveolar hyaline membranes
(fibrin and cellular debris)

35
Q

Complications of NRDS

A

Broncho-Pulmonary Dysplasia: Result of treatment
with high-concentration oxygen and mechanical
ventilation
Patent ductus arteriosus: Due to immaturity and
hypoxia
Intra-ventricular brain haemorrhage
Necrotising Enterocolitis: Fulminant inflammation of
the small and large intestines