L19 Vascular disorders of the lung Flashcards

1
Q

What are the 2x routes by which lungs are supplied with blood?

A

Pulmonary artery- Pulmonary veins –> blood for O2 transfer @ alveoli, and supplies distal bronchioles

Bronchial artery from aorta –> blood supply to parenchyma, CT, bronchi

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2
Q

Contrast the flow and pressure of the pulmonary and bronchial arterial systems

A

Pulmonary high flow, Low pressure

Bronchial, low flow, high pressure

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3
Q

Describe the dual drainage of the lungs

A

Pulmonary veins drain capillary beds supplied by pulmonary artery to L heart

Azygous veins drain capillary beds supplied by bronchial artery to R heart

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4
Q

Describe the 2x sets of lymphatic drainage of the lungs

A

Superficial- drains CT of visceral pleura, interlobular septa

Deep- CT of distal bronchioles

*there are also anastomoses b/w both at interlobular septa

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5
Q

What are the blood-air barrier components from lumen outwards

A

Alveolar fluid + surfactant > epithelial cells (mostly Type1) > basement membrane > alveolar interstitial > monolayer capillary endothelial cells w/ basement membrane

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6
Q

Which cell type can actively resorb Na

A

Type II pneumocytes (Club) that have Na-K-ATPase pumps

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7
Q

According to Starling’s forces, some fluid will leave capillaries to enter alveoli, what prevents this fluid from flooding the alveoli?

A
  • Limited by interstitial oncotic pressure (albumin)
  • Type II pneumocutes passive Na channels
  • Clara cells of distal bronchioles also extract via osmosis
  • Rapid drainage b/c pressure becomes lower towards hilus of lungs
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8
Q

What are the 2x main mechanisms responsible for pulmonary oedema?

A

Inc hydrostatic pressure @ capillaries

Inc permeability of blood-alveolar barrier

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9
Q

Explain how INC hydrostatic pressure at the capillaries leads to pulmonary oedema

A

Inc hydrostatic pressure @ capillaries -> fluid leaks -> overloading of drainage system -> initial accumulation of oedema @ bronchovascular interstitium -> spillage into alveoli

oedma= low protein

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10
Q

Explain mechanisms how inc permeability of blood-alveolar barrier can lead to pulmonary oedema

A
  1. inflammation of lung parenchyma w/ inc vascular permeability, common in interstitial pneumonia
  2. direct damage to endothelium (e.g. uraemia)
  3. Direct damage to Type1 pneumocystis (e.g. ROS, NH3, H2S, smoke)
  4. Hypoalbuminaemia is less common (hepatic Dz)

High protein oedema

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11
Q

What special histo characteristic hints that pulmonary oedema might be due to increased permeability of the blood-alveolar barrier?

A

Hyaline membranes (intra alveolar fibrin strands)

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12
Q

Grossly, how will oedematous lungs appear?

A
wet 
heavy 
rubbery 
don't collapse w/ thorax opening 
distension of septa
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13
Q

Why might pulmonary congestion occur?

A

L sided heart failure (passive)

Prolonged recumbency (hypostatic congestion)

Lung lobe torsion

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14
Q

What might chronic passive congestion lead to?

A

fibrosis of alveolar septa

Accumulation haemosiderin by alveolar macrophagieaojsdnf

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15
Q

Under what circumstances would lungs experience active hyperaemia

A

Subacute lung injury & inflammation

Vasodilation
e.g. Red phase pneumonia

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16
Q

Grossly, how does pulmonary haemorrhage appear and how might it be distinguished from congestion?

A

Congestion is diffuse, haemorrhage Moore likely to be multifocal and patchy (petechia- massive)

17
Q

What is a common cause of pulmonary haemorrhage in hoses

A

EIPH

Rupture alveolar capillaries due to exercise induced inc in transmural pressure (pressure b/w lumen of capillary and alveolar space)

Exericse= marked inc in pulmonary arterial & alveolar capillary pressure (e.g. 25->90mmHg)

Marked decrease in -ve pressure

Dorsocaudal diaphragmatic lobes

18
Q

How might the histology compare with acute vs. chronic EIPH

A

Acute= blood @ trachea/ bronchi/ in macros @ BAL/ epistaxis

Chronic= alveolar interstitial fibrosis, siderophages, bronchiolitis, peribronchiolar fibrosis

19
Q

Why is there an increased chance of a horse suffering EIPH again after a first episode

A

pulmonary fibrosis reduces compliance @ interface b/w normal and affected lung

small airway obstruction –> weird shear stress

20
Q

how can pulmonary obstruction lead to cor pulmonale and what is a likely consequence

A

thrombi suddenly obstruction over 60% pulmonary arterial flow –> cariogenic shock/ cor pumonarle

21
Q

Why might pulmonary infarction occur?

A

obstruction of small/ medium arterial branch (any bigger & can go into shock/ cor pulmonale) might cause infarction if O2 supply to that area is already shit
e.g. congestion, atelectasis, pneumonia, anaemia

22
Q

What might cause a thrombis to be thrown into a pulmonary artery?

A

vegetative endocarditis of a valve

parasitism

DIC

prologned recumbency –> clot in leg

jugular, hepatic, CaVC vein thrombo

Pulmonary vasculitis

23
Q

Why is septic thrombo/embolism even shitter to get if you’re a lung

A

will set up a new infection

septic pulmonary infarcts > multifocal pulmonary abscessation > multifocal suppurative pneumonia/ interstitial pneumonia

24
Q

How might a lung twist ? Which is usually the culprit?

A

If you’re a deep chested dog ?? Predisposed by neoplasia, pneumonia, atelectasis, effusion, pneumothorax bla bla etc

Gen the R middle b/c long and narrow or left cranial lobe

25
Q

What are some causes of pulmonary vasculitis

A

parasitism
viral e.g. FiP , Hendra, EHV1, Nipah, BVD

i.e. septicaemia/ septic thrombi

26
Q

What might cause pulmonary hypertension?

A

Pulmonary Dz increasing pulmarony arterial blood flow (tumour, interstitial fibrosis, pnueonona, atelecstasissi etc)

heart worm @ pulmonary branch

Cardiac anomalies w/ L-R shunting (PDA, ASD, VSD)

27
Q

What is brisket Dz

A

oedematous swelling of briksein in cattle w/ R congestive heart failure due to failure of cardioresp system to adjust to hypoxia of high altitudes

hypoxia > sustained vasoconstriction of pulmonary arterioles > pulmonary hypertension > cor pulmonlae +/- RSCHF