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| − | {{review}}
| + | #REDIRECT[[:Category:Lungs - Circulatory Pathology]] |
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| − | {{toplink
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| − | |backcolour = D1EEEE
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| − | |linkpage =Cardiorespiratory System - Pathology
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| − | |linktext =Cardiorespiratory System
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| − | |maplink = Cardiorespiratory System (Content Map) - Pathology
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| − | |pagetype =Pathology
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| − | |sublink1=Lungs Degenerative - Pathology
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| − | |subtext1=LUNGS DEGENERATIVE
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| − | }}
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| − | <br>
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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
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| − | *Most commonly caused by left-sided or bilateral cardiac failure
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| − | **Stagnant blood in pulmonary vessels -> red blood cells move into alveoli and are phagocytosed -> [[Pigmentation and Calcification - Pathology#Haemosiderin|haemosiderin in macrophages]] (heart failure cells)
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| − | *One-sided in post-mortem hypostatic congestion
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| − | *Acute pulmonary congestion is seen after barbiturate euthanasia
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| − | *Leads to pulmonary oedema (below)
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| − | ==Pulmonary oedema==
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| − | *Excessive fluid in the lung
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| − | *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]])
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| − | *Occurs when exudation of fluid from vessels into interstitium or alveoli exceeds the rate of alveolar or lymph removal
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| − | *Generally a sequel to or part of congestion or inflammatory process
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| − | *Generally begins as '''interstitial oedema''' characterised by expansion of perivascular and peribronchial and peribronchiolar fascia and distension of interstitial lymphatics
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| − | *Only when this interstitial compartment is overwhelmed does fluid flood the airspaces causing '''alveolar oedema'''
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| − | *Gross pathology:
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| − | **Heavy wet lungs which do not properly collapse
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| − | **Subpleural and interstitial tissue distended with fluid
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| − | **Foamy fluid oozing from the cut surface and airways
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| − | *Micro pathology:
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| − | **Pinkish fluid in alveoli and airways in association with air bubbles, and also in dilated lymphatics of the interstitium
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| − | **Colour of the fluid enhanced in cases where the endothelium is damaged - more protein present
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| − | **In slowly developing cases, macrophages contain haemosiderin
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| − | *The major causes of pulmonary oedema are:
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| − | **Increased capillary or type I epithelial permeability caused by
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| − | ***Systemic toxins
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| − | ***Shock
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| − | ***Inhaled caustic gases
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| − | **Increased capillary hydrostatic pressure ('''cardiogenic oedema''' - left-sided or biventricular heart failure, sympathetic stimulation in acute brain damage)
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| − | **Decreased plasma oncotic pressure (hypoalbuminaemia)
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| − | **Overloading in excessive fluid therapy
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| − | **As part of inflammatory process
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| − | ==Pulmonary haemorrhage==
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| − | [[Image:Pulmonary haemorrhage.jpg|right|thumb|100px|<small><center>Pulmonary haemorrhage (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]]
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| − | *Potential sequel of septicaemias, bleeding disorders, disseminated intravascular coagulation, and severe congestion, severe acute inflammation, "back splashing" at slaughter (aspiration of blood)
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| − | *[[Exercise Induced Pulmonary Haemorrhage|'''Exercise-induced pulmonary hemorrhage''' (EIPH)]]
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| − | ==Embolism, thrombosis and infarction==
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| − | [[Image:Pulmonary infarction.jpg|right|thumb|100px|<small><center>Pulmonary infarction (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]]
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| − | [[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
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| − | *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
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| − | *In animals, greatest risk comes from:
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| − | **'''Tumor emboli'''
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| − | ***From e.g.: osteosarcoma and haemangiosarcoma in dogs, uterine carcinoma in cattle
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| − | **'''Septic emboli'''
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| − | ***From bacterial [[Endocarditis|endocarditis]], jugular thrombophlebitis, [[Hepatic Abscessation|hepatic abscesses]] etc.
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| − | ***May cause unexpected death if in large numbers
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| − | ***May develop [[Lungs Inflammatory - Pathology|suppurative pneumonia]] -> [[Lungs Inflammatory - Pathology#Pulmonary abscesses|pulmonary abscesses]], [[Arteritis|arteritis]], [[Thrombosis - Pathology|thrombosis]]
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| − | *Pulmonary infarcts usually occur when there is embolisation or thrombosis during general circulatory collapse or passive congestion of heart failure
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| − | *Pulmonary thromboembolism is a sequel to in cattle to large emboli from liver abscesses close to the vena cava
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| − | **Death may ocur due to massive haemorrhaging into lung tissue
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| − | *Parasites (e.g. [[Respiratory Parasitic Infections - Pathology#Dirofilaria immitis|''Dirofilaria immitis'']], [[Respiratory Parasitic Infections - Pathology#Angiostrongylus vasorum|''Angiostrongylus vasorum'']]) may be responsible
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| − | *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
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| − | *Severe prolonged pulmonary hypertension leads to [[Cor Pulmonale|'''cor pulmonale''']], right-sided heart failure secondary to primary lung disease
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