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#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 - Pathology|'''Exercise-induced pulmonary hemorrhage''' (EIPH)]] occurs commonly in horses during racing or training
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**Shows as [[Respiratory System Clinical Signs - Pathology#Epistaxis|epistaxis]]
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**Undetected in many horses
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**Haemorrhage is dorsocaudal, large brown areas
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**Micro - alveolar haemorrhage, macrophages containing [[Pigmentation and Calcification - Pathology#Haemosiderin|haemosiderin]], mild interstitial fibrosis
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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 [[Endocardial - Pathology#Inflammatory-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]], [[Arterial Disease - Pathology#Inflammatory-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 [[Secondary Cardiac - Pathology|'''cor pulmonale''']], right-sided heart failure secondary to primary lung disease
 
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