Path Pot Specimens Flashcards
No clinical details are available for this specimen.
This mounted specimen shows a bisected heart.
The pericardium is partly covered by a shaggy fibrinous exudate with associated congestion and hyperaemia of the underlying tissues.
This appearance is described by pathologists as a “bread and butter” pericarditis because it looks like the butter of a bread and butter sandwich that has been pulled apart!
Other features include some minor atherosclerosis. seen in the large blood vessels.
Microscopically, the myocardium revealed scattered focal lymphocytic collections and the pericardium was coated by a fibrinous exudate.
The pathology is consistent with a viral myocarditis and pericarditis.
The mounted specimen consists of the heart with the pericardial sac opened and reflected back to show a classic “bread and butter” pericarditis. Both the visceral and parietal pericardial surfaces are coated by a thick, yellow-white fibrino-purulent inflammatory exudate.
The specimen shows widespread involvement of the pericardial surface by shaggy, pale yellow-grey material that appears quite similar to a fibrinous exudate but histology confirmed this to be involvement of the pericardium by metastatic tumour similar to that identified in the neck mass.
The specimen shows a large infarct of the myocardium involving the apex, the lateral and posterior walls of the left ventricle and much of the interventricular septum. This is the distribution of the left anterior descending coronary artery.
There is a pericarditis overlying the infarct and the infarct is seen as an irregular, transmural, yellow necrotic zone surrounded by a hyperaemic margin.
There is severe coronary artery stenosis as a result of atherosclerosis.
The specimen shows a slice through the left and right ventricles.
A massive recent infarct is present in the anterior, septal and posterior regions of the left ventricle with a slight extension onto the posterior wall of the right ventricle. The necrotic muscle appears pale yellow-grey in colour and reactive hyperaemia is seen at the interface with the viable myocardium. This is the territory of the left anterior descending coronary artery.
A mural thrombus has formed on the anteroseptal infarcted zone.
The anterior and posterior descending coronary arteries can be seen in cross-section in the epicardial fat and they are severely stenosed by atherosclerosis.
Histological sections confirmed a recent infarct, only days old, with loss of cardiac muscle nuclei and intense hyperaemia bordering the infarct.
The postmortem also revealed numerous peripheral pulmonary emboli with an occasional associated infarct and a left calf deep venous thrombosis. A small recent infarct was also present in one kidney.
The mounted specimen shows two transverse slices through the heart. There is an extensive anteroseptal myocardial infarct. Geographic zones of pale yellow necrotic cardiac muscle (coagulative necrosis) are present edged by congested, translucent grey tissue (granulation tissue). This infarct involves the full thickness of the myocardium at the apex.
The visceral pericardium is intensely congested and covered by a fibrinous exudate, consistent with the friction rub detected clinically. Adherent apical mural thrombus is present. The left ventricle is also markedly hypertrophied.
The mounted specimen consists of a series of cardiac slices that show an extensive old anteroseptal infarct. In the area of the old infarct the muscle wall is slightly thinner and contains grey-white scar tissue and there is focal congestion related to the old scar suggestive of a more recent insult. There is also moderate hypertrophy of the uninvolved left ventricular muscle.
Examination of the anterior descending branch of the left coronary shows marked atherosclerotic stenosis but no thrombosis.
All vessels show some degree of atherosclerotic narrowing which, even for the right coronary artery, approaches 50% (see upper left slice).
The forensic postmortem revealed an extensive old antero-septal myocardial infarct and the complete occlusion of the anterior descending branch of the left coronary artery. The old infarct shows relative thinning of the ventricle wall, with grey-white scar tissue and some vascular congestion.
The vessels displayed in the upper corner show a recent thrombus and also a yellow atherosclerotic plaque in a smaller branch vessel.
Although no histological evidence of an acute infarct was found the recent thrombus in the coronary artery would suggest an acute infarct was the most likely reason for the accident. The changes of infarction take time to evolve and this man died before this process could occur. His mode of death would most likely have been a cardiac arrythmia precipitated by the myocardial ischaemia.
The left ventricular wall is markedly hypertrophied suggesting an underlying hypertensive condition.
The mounted specimen shows her heart with a large old healed antero-septal and apical myocardial infarct scar with bulging at the apex and the formation of a small cardiac aneurysm.
There is some mural thrombus on the endocardial aspect of the infarct and fibrous pericardial adhesions overlying it.
The left anterior descending coronary artery is narrowed by atherosclerosis and there is a recent occluding thrombus present(arrow).
The mounted specimen of the heart has been opened to show the left ventricle and aortic valve.
Most of the distal antero-septal left ventricular wall has been replaced by white scar tissue that bulges outward to form a cardiac aneurysm.
Dense white scar tissue is seen lining the endocardial surface and only a thin ribbon of brown viable myocardium is visible in the aneurysmal wall. There is also extensive scarring and some degree of thinning of the lateral aspect of the left ventricle wall.
There is severe atherosclerosis with stenosis of the left anterior descending (red arrow) and left circumflex coronary arteries.
The heart shows a thinned aneurysmal dilatation of the postero-lateral aspect of the left ventricle. The myocardium of this “blown out” portion is haemorrhagic and shows a small perforation.
The circumflex branch of the left coronary artery is completely occluded by thrombus.
Ventricular rupture is a complication of myocardial infarction. It occurs in 1-2% of transmural infarcts usually in the first 4-5 days. Pericardial tamponade results if it is the free wall of the left ventricle that ruptures. If the septum ruptures then there is a left to right shunting of blood.
In the mounted specimen of the heart the lateral wall of the left ventricle has been cut away to reveal the large mural thrombus overlying an old healed myocardial infarct of the anteroseptal region which is bulging anteriorly to form a cardiac aneurysm.
The pericardium overlying the thinned infarct scar is thickened and fibrous with adhesion of the parietal and visceral layers.
The left coronary artery branches are narrowed by atherosclerosis and the anterior descending branch is occluded by a recent thrombus.
The heart shows the very marked thinning of the greater part of the anterior, apical and septal parts of the left ventricle. Most of the ventricular muscle has been replaced by a thin fibrous scar a few millimetres in thickness.
The scarred area bulges slightly outward and there is a large layered mural thrombus filling the space of the bulge.
The origin of the anterior descending branch of the left coronary artery is seen to be occluded by gelatinous-looking fibrous tissue which represents an old organised thrombus.
The specimen comprises two horizontal slices through the heart. The smaller slice is from close to the apex of the heart.
There is a large old antero-septal infarct of the left ventricle.
The anterior and septal parts of the wall of the left ventricle show loss of the normal tan muscle tissue and replacement by a much thinner layer of variegated pale grey-brown and grey-white tissue that represents the scar of an old healed myocardial infarct.
Adherent to this scarred myocardium is a large layered mural thrombus.
The fibrous tissue scar also extends around into the posterior wall of the left ventricle towards the apex. (smaller slice)
The mounted specimen of his heart has been bisected longitudinally and an arrow points to rupture of the myocardium over the infarct.
Ventricular rupture is a complication of myocardial infarction. It occurs in 1-2% of transmural infarcts usually in the first 4-5 days.
On the cut surface the recent haemorrhagic infarct can be seen in the posterolateral wall of the left ventricle.
There is also an extensive scar resulting from the previous episodes of ischaemic necrosis of the myocardium.
The coronary arteries are narrowed by atherosclerosis.
The mounted specimen shows a bicuspid aortic valve with a narrow slit-like opening between the two leaflets. One leaflet has a central raphe (the conjoined leaflet). This raphe is thickened and calcified along with the rest of the valve. Nodular calcified deposits can be seen in the valve sinuses and along the leaflet margins.
The bicuspid aortic valve is the most common congenital anomaly of the heart, first described by Sir William Osler. It may be associated with coarctation of the aorta. There is increasing evidence for an autosomal-dominant inheritance pattern with variable penetrance.
About 30% of patients are symptomatic. The defective valve may be incompetent or stenotic. Sclerosis of the bicuspid valve usually begins in the second decade of life. About 50% of adults with severe aortic stenosis have a bicuspid valve. There is a 10-30% life-time risk of infective endocarditis.
The mounted specimen shows a congenitally bicuspid valve with the conjoined leaflet showing partial fusion at its centre (a raphe).
Nodular masses of calcium are seen heaped up in the sinuses of Valsalva and along the raphe associated with thickening of the aortic valve leaflets.
There is a very severely stenosed slit-like opening in the valve.
The bicuspid aortic valve is the most common congenital anomaly of the heart, first described by Sir William Osler. It may be associated with coarctation of the aorta. There is increasing evidence for an autosomal-dominant inheritance pattern with variable penetrance.
About 30% of patients are symptomatic. The defective valve may be incompetent or stenotic. Sclerosis of the bicuspid valve usually begins in the second decade of life. About 50% of adults with severe aortic stenosis have a bicuspid valve. There is a 10-30% life-time risk of infective endocarditis.
The mounted specimen shows a large friable and polypoid vegetation on the posterior cusp of the aortic valve which has eroded through into both atria and has also involved both mitral and tricuspid valves. This vegetation would have been the source of the infective emboli to her right kidney and also the subclavian artery.
The mounted specimen consists of part of the heart. The left ventricle has been opened and mounted to display both the inflow and outflow tracts.
The mitral valve shows no abnormality.
The aortic valve is abnormal with irregular pale yellow small vegetations attached to the free edges of all three cusps, but predominantly involving the R and L cusps. The underlying valve shows no evidence of pre-existing disease. In particular, the valve is tricuspid; there is no commissural fusion and no calcifications within the valve sinus. The vegetations are not associated with any destructive change within the valve cusps.
Early atheromatous change is seen in the aortic root immediately above the aortic valve.
The L ventricle is thick-walled indicative of left ventricular hypertrophy.
Microscopically the vegetations consist of an inflammatory exudate with fibrin, neutrophils, cellular debris and colonies of moderate to low virulence bacteria.
The mounted specimen consists of the upper part of the left ventricle and the aortic root which has been opened to display the aortic valve.
The aortic valve cusps are distorted by the presence of pale yellow-grey vegetations on the free edge of all three cusps. One of the commissures appears partly fused and vegetations are seen at the point of fusion. In another area, the vegetations extend onto the ventricular endocardium. These large vegetations are typical of infective endocarditis.
Physical examination revealed a BP of 150/80 with absent femoral pulses.
The mounted specimen consists of a 1cm length of aorta that shows a greatly reduced luminal diameter with only a pin-hole sized lumen.
Coarctation of the aorta is more common in males. It occurs as an isolated defect in 50% of cases.
This is the ‘post-ductal’ (adult) form. The effects depend on ductus arteriosus patency. If the ductus is closed flow around the obstruction occurs via the internal mammary and axillary artery collaterals and this may result in rib notching that can be seen on X-ray. If the ductus is patent then right to left shunting results in lower body cyanosis.
At necropsy an adult type coarctation of the aorta was found complicated by a dissecting aneurysm which had ruptured into the pericardium causing pericardial tamponade.
The reverse of the mounted specimen shows the coarctation at the attachment of the ligamentum arteriosum. Proximal to the coarctation the aorta is dilated.
When viewed from the front a small longitudinal tear 1.5cm in length is seen just above the aortic valve. This tear involves the inner part of the media.
From this tear the aorta has dissected proximally to the pericardium and distally to the coarctation and involves the origins of the innominate, left common carotid and left subclavian arteries, tonly he last two being shown in the specimen.
The mounted specimen shows a typical ‘adult type’ coarctation of the aorta, just distal to the attachment of the ligamentum arteriosum.
Proximally there is an obviously dilated segment of aorta, with dilated innominate and left subclavian branches.
Beyond the coarctation the aorta is smaller than normal, but the first two intercostal branches are enlarged. Flow around the obstruction also occurs via the internal mammary and axillary artery collaterals and this may result in rib notching that can be seen on X-ray.
The aortic valve is bicuspid and the valve leaflets are markedly thickened, nodular and clalcified with only a slit-like stenosed opening.
The mounted specimen shows the heart and thoracic aorta.
There are two transverse tears in the arch of the aorta. These represent the origin of the dissecting aneurysm. The blood has dissected the outer media and adventitia from the inner media creating a false channel within the wall of the aorta. The dissection has extended proximally to the root of the aorta resulting in a haemopericardium (the blood in the pericardial sac has been washed from the specimen) and the dissection has extended distally involving the entire thoracic aorta.
Dissection typically occurs in older patients, usually men, with hypertension and in younger patients with connective tissue defects eg Marfan’s syndrome. The common factor is degeneration of the media of the vessel wall. with loss of normal extra-cellular matrix synthesis and an increase in amorphous ground substance, cystic medial degeneration.
The mounted specimen shows the lower thoracic and abdominal aorta with a number of uncomplicated lipid (yellow) and fibrous (white) atherosclerotic plaques.
Atherosclerosis is a chronic inflammatory and healing response that occurs in the arterial wall in response to endothelial cell injury.
The complications of atherosclerosis produce the clinical symptoms and signs. These include stenosis of the arteries, vasoconstriction of the arteries, acute changes in the athersclerotic plaques, thrombus formation over the plaques and weakening of the vessel wall with aneurysm formation.
The mounted specimen of the abdominal aorta shows extensive severe and almost confluent atherosclerosis .
There is focal ulceration of plaques and calcification involving most of the specimen.
Atherosclerosis is a chronic inflammatory and healing response that occurs in the arterial wall in response to endothelial cell injury.
The complications of atherosclerosis produce the clinical symptoms and signs. These include stenosis of the arteries, vasoconstriction of the arteries, acute changes in the athersclerotic plaques, thrombus formation over the plaques and weakening of the vessel wall with aneurysm formation.
The mounted specimen shows the two halves of the slightly tortuous and midly dilated abdominal aorta in which there is severe extensive, complicated atherosclerosis with intimal ulceration,calcification and a number of mural thrombi.
Atherosclerosis is a chronic inflammatory and healing response that occurs in the arterial wall in response to endothelial cell injury.
The complications of atherosclerosis produce the clinical symptoms and signs. These include stenosis of the arteries, vasoconstriction of the arteries, acute changes in the athersclerotic plaques, thrombus formation over the plaques and weakening of the vessel wall with aneurysm formation.
The mounted specimen shows the abdominal aorta. In the lower part there is a saccular aneurysm 4 cm. in diameter which projects forward and to the left side. The unruptured aneurysm and nearby aorta has been opened to display a layered mural thrombus occupying the dome of the aneurysmal sac.
Atherosclerosis is a chronic inflammatory and healing response that occurs in the arterial wall in response to endothelial cell injury.
The complications of atherosclerosis produce the clinical symptoms and signs. These include stenosis of the arteries, vasoconstriction of the arteries, acute changes in the athersclerotic plaques, thrombus formation over the plaques and weakening of the vessel wall with aneurysm formation.
The mounted specimen consists of the abdominal aorta and its bifurcation into right and left common iliac arteries.
The vessels have been opened to reveal several large complicated, ulcerated plaques of atheroma and a fusiform atheromatous aneurysm of the aorta.
The aneurysm is filled by laminated thrombus which has almost completely occluded the lumen of the aorta.
Atherosclerosis is a chronic inflammatory and healing response that occurs in the arterial wall in response to endothelial cell injury.
The complications of atherosclerosis produce the clinical symptoms and signs. These include stenosis of the arteries, vasoconstriction of the arteries, acute changes in the athersclerotic plaques, thrombus formation over the plaques and weakening of the vessel wall with aneurysm formation.
The mounted specimen of the lower aorta and iliac arteries shows an aneurysm extending from several centimetres below the renal arteries to just above the bifurcation. There is also some aneurysmal dilatation of the left iliac artery. The aneurysm is partially filled with thrombus and on its posterior aspect towards the left side there is a jagged tear about 3cm in length.
A few remnants of the massive retroperitoneal haemorrhage extended from the diaghragm into the pelvis and forward into the mesentery and laterally around the left kidney.
The mounted specimen shows a large fusiform abdominal aortic aneurysm which commences just below the renal vessels and extends to involve the beginning of the common iliac arteries.
The fibrofatty plaques of atherosclerosis are seen in the aorta and there is definite dilation and possibly early aneurysm formation of the right common iliac artery too. Atherosclerosis is the commonest cause of abdominal aortic aneurysms. A very large mural thrombus is evident within the aneurysm.
The aneurysm has ruptured resulting in the extensive haemorrhage visible in the surrounding retroperitoneal tissue. The risk of rupture of these aneurysms increases with their size.
Both kidneys have been removed along with the inferior vena cava, however both adrenal glands are present on the uppermost cut surface.
The mounted specimen is a slice of lung showing a large embolus impacted in the pulmonary artery with congestion and oedema of the lung.
The mounted specimen is the posterior half of the left lung. In the proximal part of the pulmonary artery is a large, pale, laminated embolus.
The mounted specimen is the right lung sliced to show the pulmonary arteries occluded by a massive embolus which has originated in the right femoral vein.
The specimen shows the bifurcations of both common carotid arteries seen from behind.
The origin of the right internal carotid artery is very severely stenosed by atherosclerosis with associated intimal haemorrhage.
The left internal carotid artery origin is virtually occluded by a similar lesion with a recent thrombus almost completing the occlusion.
The mounted specimen consists of the distal portion of the abdominal aorta, the aortic bifurcation and both common iliac arteries.
The common iliac arteries have been opened to show extensive , complicated atherosclerosis with fusiform dilatation of the vessel walls.
Laminated thrombus is present within the aneurysm of the right common iliac artery.
The atherosclrotic plaques in both vessels are partially calcified.
Atherosclerosis is a chronic inflammatory and healing response that occurs in the arterial wall in response to endothelial cell injury.
The complications of atherosclerosis produce the clinical symptoms and signs. These include stenosis of the arteries, vasoconstriction of the arteries, acute changes in the athersclerotic plaques, thrombus formation over the plaques and weakening of the vessel wall with aneurysm formation.
