Difference between revisions of "Lungs Circulatory - Pathology"

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==Hyperaemia==
 +
 +
*Localised of diffuse as part of acute inflammation
 +
 +
 +
==Congestion==
 +
 +
*Decreased outflow of venous blood
 +
*Most commonly caused by left-sided or bilateral cardiac failure
 +
**Stagnant blood in pulmonary vessels -> red blood cells move into alveoli and are phagocytosed -> [[General Pathology - Pigmentation and Calcification#Haemosiderin|haemosiderin in macrophages]] (heart failure cells)
 +
*One-sided in post-mortem hypostatic congestion
 +
*Acute pulmonary congestion is seen after barbiturate euthanasia
 +
*Leads to pulmonary oedema (below)
 +
 +
 +
==Pulmonary oedema==
 +
 +
*Excessive fluid in the lung
 +
*Normally, mechanisms are in place to protect the lung from the entry of circulatory fluid into alveolar spaces (See [[Respiratory System General Introduction - Pathology#Lungs|functional anatomy]])
 +
*Occurs when exudation of fluid from vessels into interstitium or alveoli exceeds the rate of alveolar or lymph removal
 +
*Generally a sequel to or part of congestion or inflammatory process
 +
*Generally begins as '''interstitial oedema''' characterised by expansion of perivascular and peribronchial and peribronchiolar fascia and distension of interstitial lymphatics
 +
*Only when this interstitial compartment is overwhelmed does fluid flood the airspaces causing '''alveolar oedema'''
 +
*Gross pathology:
 +
**Heavy wet lungs which do not properly collapse
 +
**Subpleural and interstitial tissue distended with fluid
 +
**Foamy fluid oozing from the cut surface and airways
 +
*Micro pathology:
 +
**Pinkish fluid in alveoli and airways in association with air bubbles, and also in dilated lymphatics of the interstitium
 +
**Colour of the fluid enhanced in cases where the endothelium is damaged - more protein present
 +
**In slowly developing cases, macrophages contain haemosiderin
 +
*The major causes of pulmonary oedema are:
 +
**Increased capillary or type I epithelial permeability caused by
 +
***Systemic toxins
 +
***Shock
 +
***Inhaled caustic gases
 +
**Increased capillary hydrostatic pressure ('''cardiogenic oedema''' - left-sided or biventricular heart failure, sympathetic stimulation in acute brain damage)
 +
**Decreased plasma oncotic pressure (hypoalbuminaemia)
 +
**Overloading in excessive fluid therapy
 +
**As part of inflammatory process
 +
 +
 +
==Pulmonary haemorrhage==
 +
[[Image:Pulmonary haemorrhage.jpg|right|thumb|100px|<small><center>Pulmonary haemorrhage (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]]
 +
*Potential sequel of septicaemias, bleeding disorders, disseminated intravascular coagulation, and severe congestion, severe acute inflammation, "back splashing" at slaughter (aspiration of blood)
 +
*[[Exercise induced pulmonary haemorrhage|'''Exercise-induced pulmonary hemorrhage''' (EIPH)]] occurs commonly in horses during racing or training
 +
**Shows as [[Respiratory System Clinical Signs - Pathology#Epistaxis|epistaxis]]
 +
**Undetected in many horses
 +
**Haemorrhage is dorsocaudal, large brown areas
 +
**Micro - alveolar haemorrhage, macrophages containing [[General Pathology - Pigmentation and Calcification#Haemosiderin|haemosiderin]], mild interstitial fibrosis
 +
 +
 +
 +
 +
 +
 +
 +
 +
==Embolism, thrombosis and infarction==
 +
[[Image:Pulmonary infarction.jpg|right|thumb|100px|<small><center>Pulmonary infarction (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]]
 +
[[Image:Segmental pulmonary infarction.jpg|right|thumb|100px|<small><center>Segmental pulmonary infarction (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]]
 +
 +
*Lungs are strategically situated to catch emboli carried in venous blood
 +
*Because the lung is supplied by both pulmonary and bronchial arteries and has extensive collateral channels, infarction usually does not follow embolism or thrombosis unless pulmonary circulation is already compromised
 +
*In animals, greatest risk comes from:
 +
**'''Tumor emboli'''
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***From e.g.: osteosarcoma and haemangiosarcoma in dogs, uterine carcinoma in cattle
 +
**'''Septic emboli''' 
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***From bacterial [[Endocardial - Pathology#Inflammatory-Endocarditis|endocarditis]], jugular thrombophlebitis, [[Liver - inflammatory#Hepatic abscessation|hepatic abscesses]] etc.
 +
***May cause unexpected death if in large numbers
 +
***May develop [[Lungs - inflammatory|suppurative pneumonia]] -> [[Lungs - inflammatory#Pulmonary abscesses|pulmonary abscesses]], [[Arterial Disease - Pathology#Inflammatory-Arteritis|arteritis]], [[General Pathology - Thrombosis|thrombosis]]
 +
*Pulmonary infarcts usually occur when there is embolisation or thrombosis during general circulatory collapse or passive congestion of heart failure
 +
*Pulmonary thromboembolism is a sequel to in cattle to large emboli from liver abscesses close to the vena cava
 +
**Death may ocur due to massive haemorrhaging into lung tissue
 +
*Parasites (e.g. [[Respiratory Parasitic Infections - Pathology#Dirofilaria immitis|''Dirofilaria immitis'']], [[Respiratory Parasitic Infections - Pathology#Angiostrongylus vasorum|''Angiostrongylus vasorum'']]) may be responsible
 +
*Long-term intravenous catheterisation may cuse thrombi pieces breaking off and lodging in pulmonary vessels
 +
 +
 +
 +
 +
 +
 +
 +
 +
 +
 +
 +
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==Pulmonary hypertension==
 +
 +
*Caused by '''left-to-right vascular shunts''' or increased resistance of the pulmonary vascular system
 +
 +
*In animals, it is most commonly a sequel of '''widespread fibrosis in the lung''' or [[Bronchi and Bronchioles Inflammatory - Pathology#Chronic bronchitis|chronic bronchitis or bronchiolitis]] which stimulates hypertrophy in the walls of small arteries
 +
*Severe prolonged pulmonary hypertension leads to [[Secondary Cardiac - Pathology|'''cor pulmonale''']], right-sided heart failure secondary to primary lung disease

Revision as of 21:20, 6 August 2008

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()Map CARDIORESPIRATORY SYSTEM (Map)
LUNGS DEGENERATIVE



Hyperaemia

  • Localised of diffuse as part of acute inflammation


Congestion

  • Decreased outflow of venous blood
  • Most commonly caused by left-sided or bilateral cardiac failure
    • Stagnant blood in pulmonary vessels -> red blood cells move into alveoli and are phagocytosed -> haemosiderin in macrophages (heart failure cells)
  • One-sided in post-mortem hypostatic congestion
  • Acute pulmonary congestion is seen after barbiturate euthanasia
  • Leads to pulmonary oedema (below)


Pulmonary oedema

  • Excessive fluid in the lung
  • Normally, mechanisms are in place to protect the lung from the entry of circulatory fluid into alveolar spaces (See functional anatomy)
  • Occurs when exudation of fluid from vessels into interstitium or alveoli exceeds the rate of alveolar or lymph removal
  • Generally a sequel to or part of congestion or inflammatory process
  • Generally begins as interstitial oedema characterised by expansion of perivascular and peribronchial and peribronchiolar fascia and distension of interstitial lymphatics
  • Only when this interstitial compartment is overwhelmed does fluid flood the airspaces causing alveolar oedema
  • Gross pathology:
    • Heavy wet lungs which do not properly collapse
    • Subpleural and interstitial tissue distended with fluid
    • Foamy fluid oozing from the cut surface and airways
  • Micro pathology:
    • Pinkish fluid in alveoli and airways in association with air bubbles, and also in dilated lymphatics of the interstitium
    • Colour of the fluid enhanced in cases where the endothelium is damaged - more protein present
    • In slowly developing cases, macrophages contain haemosiderin
  • The major causes of pulmonary oedema are:
    • Increased capillary or type I epithelial permeability caused by
      • Systemic toxins
      • Shock
      • Inhaled caustic gases
    • Increased capillary hydrostatic pressure (cardiogenic oedema - left-sided or biventricular heart failure, sympathetic stimulation in acute brain damage)
    • Decreased plasma oncotic pressure (hypoalbuminaemia)
    • Overloading in excessive fluid therapy
    • As part of inflammatory process


Pulmonary haemorrhage

Pulmonary haemorrhage (Image sourced from Bristol Biomed Image Archive with permission)
  • Potential sequel of septicaemias, bleeding disorders, disseminated intravascular coagulation, and severe congestion, severe acute inflammation, "back splashing" at slaughter (aspiration of blood)
  • Exercise-induced pulmonary hemorrhage (EIPH) occurs commonly in horses during racing or training
    • Shows as epistaxis
    • Undetected in many horses
    • Haemorrhage is dorsocaudal, large brown areas
    • Micro - alveolar haemorrhage, macrophages containing haemosiderin, mild interstitial fibrosis





Embolism, thrombosis and infarction

Pulmonary infarction (Image sourced from Bristol Biomed Image Archive with permission)
Segmental pulmonary infarction (Image sourced from Bristol Biomed Image Archive with permission)
  • Lungs are strategically situated to catch emboli carried in venous blood
  • Because the lung is supplied by both pulmonary and bronchial arteries and has extensive collateral channels, infarction usually does not follow embolism or thrombosis unless pulmonary circulation is already compromised
  • In animals, greatest risk comes from:
  • Pulmonary infarcts usually occur when there is embolisation or thrombosis during general circulatory collapse or passive congestion of heart failure
  • Pulmonary thromboembolism is a sequel to in cattle to large emboli from liver abscesses close to the vena cava
    • Death may ocur due to massive haemorrhaging into lung tissue
  • Parasites (e.g. Dirofilaria immitis, Angiostrongylus vasorum) may be responsible
  • Long-term intravenous catheterisation may cuse thrombi pieces breaking off and lodging in pulmonary vessels







Pulmonary hypertension

  • Caused by left-to-right vascular shunts or increased resistance of the pulmonary vascular system
  • In animals, it is most commonly a sequel of widespread fibrosis in the lung or chronic bronchitis or bronchiolitis which stimulates hypertrophy in the walls of small arteries
  • Severe prolonged pulmonary hypertension leads to cor pulmonale, right-sided heart failure secondary to primary lung disease
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