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| + | ==Hyperaemia== |
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| + | *Localised of diffuse as part of acute inflammation |
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| + | ==Congestion== |
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| + | *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) |
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| + | ==Pulmonary oedema== |
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| + | *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 |
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| + | ==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 |
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| + | ==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>]] |
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| + | *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''' |
| + | ***From e.g.: osteosarcoma and haemangiosarcoma in dogs, uterine carcinoma in cattle |
| + | **'''Septic emboli''' |
| + | ***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== |
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| + | *Caused by '''left-to-right vascular shunts''' or increased resistance of the pulmonary vascular system |
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| + | *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 |