Disturbances of Circulation. Histopathology Lab #2 (Web)

Transcription

1 Disturbances of Circulation Histopathology Lab #2 (Web) Paul Hanna Winter 2015

2 Slide #96 History: pig was fine in the morning & found dead in the afternoon there was ~100 mls of clear fluid in the pericardial sac patchy red areas evident on the epicardium & throughout the ventricular myocardium the lungs were red, heavy and wet

3 Questions from the history? What is the term used to indicate a clear fluid (ie non-inflammatory transudate) within the pericardial sac? Hydropericardium What is indicated by the lungs being red, heavy and wet? Pulmonary congestion and edema

4 Appearance of heart Note the ecchymotic to suffusive hemorrhages on the epicardial surface of the heart. Also note on the cut surface of the ventricle, the multifocal to coalescing hemorrhage within the myocardium.

5 Slide #96 Low power magnification is not very exciting. You might be able to determine that this is heart and that there are hypereosinophilic areas.

6 Slide #96

7 Slide #96 At medium magnification you can start to appreciate the congestion, hemorrhage and slight separation of the myofibers by edema.

8 Slide #96 At medium magnification you can start to appreciate the congestion, hemorrhage and slight separation of the myofibers by edema. Also note apparent fibrin thrombi within some of the small vessels

9 At high magnification you can clearly see the blood outside the capillaries (ie hemorrhage) and the swelling, acidophilia, loss of striation and karyolysis of the cardialc myofibers (ie necrosis).

10 PAS stain note fibrin thrombi within capillaries

11 Description: multiple areas of congestion & hemorrhage are scattered throughout the myocardium in some areas cardiac myofibres show karyolytic / pyknotic / karyorrhectic nuclei and have hypereosinophilic cytoplasm (ie indicative of coagulative necrosis) the interstitium is mildly edematous fibrin thrombi are present within many capillaries (seen best with PAS stain)

12 Slide #96 Morph Dx: 1) Myocardial congestion & hemorrhage, multifocal to coalescing, severe with microvascular thrombosis 2) Myocardial degeneration and necrosis, multifocal, acute, severe Comment: the findings in this case are characteristic of Mulberry Heart Disease (note, similar gross lesions can be seen with certain bacterial infections, esp Strep. suis infection) MHD is associated with a deficiency of Vit E (and sometimes selenium) some other diseases in swine associated with deficiencies of Vit E & Selenium, and can occur separately or in conjunction with MHD, include: Nutritional myopathy (white muscle disease) Hepatosis dietetica (see massive hepatic necrosis) Nutritional fat necrosis (aka steatitis or yellow fat disease ) This is a Mulberry!

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14 Slide #39 History: a 4-year-old Standardbred horse with a history of going around the race track twice and then losing control of its hind limbs hind limbs were cold to the touch & weak pulse felt in femoral artery at necropsy a thrombus / thromboembolus was present at the bifurcation ( quadrifurcation ) of the abdominal aorta

15 Fig (Dyce) Branches of the abdominal aorta, horse; 1, Aorta; 10, external iliac a.; 11, internal iliac a.; Fig (Evans & de Lahunta) Branches of the abdominal aorta, ventral aspect, dog.

16 Aortic-iliac thrombosis is occasionally seen in horses & causes exercise intolerance & hind-leg lamness. The underlying cause is usually not identified, but speculation about strongyle-related thromboemboli or hypercoagulability syndromes associated with sepsis / endotoxemia have been suggested.

17 You can see why they are called saddle thrombi Saddle thrombi are also occasional seen in dogs, esp those with hypercoagulability states (eg loss of antithrombin 3 with glomerular disease) Saddle thromboemboli are most often seen in cats which have cardiomyopathy with dilation and turbulence in the left atrium (ie thrombi form in the left atrium and then travel / impact at the bifrucation of the abdominal aorta)

18 Slide #39 note thrombus obstructing most of the lumen of this large artery; also note crescent shaped area of palor (ie area of organization) at the bottom segment of the lumen

19 note area of organization with a few recanalized vessels note thrombus composed of fibrin and entrapped cells & basophilic debris

20 note area of organization with a few recanalized vessels

21 Slide #39 at this magnification you can see that the area of organization is composed of fibrous connective tissue with a few newly formed recanalized vessels

22 Slide #39 at this magnification you are starting to see the macrophages that contain pigments from erythrocyte breakdown; the dark brown granular pigment (ie hemosiderin which is from iron storage) and the bright yellow pigment (ie hematoidin which is from bilirubin accumulation)

23 Slide #39 at this magnification you are starting to see the macrophages that contain pigments from erythrocyte breakdown; the dark brown granular pigment (ie hemosiderin which is from iron storage) and the bright yellow pigment (ie hematoidin which is from bilirubin accumulation)

24 Slide #39 At this magnification you can clearly see the macrophages with the hemosiderin & hematoidin embedded in abundant fibrous connective tissue

25 Slide #39 Description: this is a section of a large, muscular artery. the lumen is nearly completely occluded by a thrombus. at one margin there is a crescent shaped area of organization where there has been removal of the thrombotic material (as evidenced by macrophages containing hemosiderin and hematoidin pigment, derived from phagocytosed rbc s that were trapped in the thrombus) and replacement with fibrous connective tissue. note the recanalized areas within the area of organization. Morphologic Diagnosis: Arterial organizing thrombus, chronic, severe Comment: the clinical signs can be accounted for by ischemia to the rear legs resulting from the thrombus, ie cold temperature, lack of arterial pulse & muscle weakness. there is not complete ischemia and infarction of the hindlimbs because of collateral circulation and this also accounts for the loss of function only showing up during exercise

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27 Slide #91 Clinical History: a necropsy was performed on an aged cat. the gross pathological changes included: widespread subcutaneous edema, ascites, hydrothorax, multiple, pale, wedge-shaped lesions in kidneys Well demarcated pale wedge shaped lesion in renal cortex; with base of the wedge near the capsule and apex near cortico-medullary junction.

28 Normal kidney, gross sagittal section, cat (above left) and normal histology of the kidney

29 Well demarcated pale wedge shaped lesion in renal cortex; with base of the wedge near the capsule and apex near corticomedullary junction.

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31 Slide #91 note within the affected area the basic architectural arrangement of the glomeruli and tubules is apparent however the cells resemble eosinophilic shadow (ghostlike remnant) of the original cells. Note surrounding layer of inflammatory cell debris.

32 note within the affected area the basic architectural arrangement of the glomeruli and tubules is apparent however the cells resemble eosinophilic shadows (ghost-like remnants) of the original cells Note surrounding layer of inflammatory cell debris

33 note within the affected area the basic architectural arrangement of the glomeruli and tubules is apparent however the cells resemble eosinophilic shadows (ghost-like remnants) of the original cells. Most nuclei are inapparent (ie karyolysis) Note surrounding layer of inflammatory cell debris.

34 note within the affected area the basic architectural arrangement of the glomeruli and tubules is apparent however the cells resemble eosinophilic shadows (ghost-like remnants) of the original cells. Most nuclei are inapparent (ie karyolysis)

35 Slide #91 Description: on low-power this section of kidney contains an irregular, wedge-shaped pale eosinophilic area which has a basophilic border. the apex of this triangular area is within the medulla, while the base is approximately 1-2 mm from the capsular surface. the inner material is composed of ghost-like remnants of the renal parenchyma (coagulation necrosis of tubules, glomeruli, etc) and the whole area is surrounded by a thick layer of inflammatory cell debris. there is an increase of fibrous connective tissue and some inflammatory cells within the interstitium of the remainder of the renal cortex (pre-existing nephritis). Morphologic Diagnosis: Renal infarct

36 Slide #91 Comment: an interlobar artery was obstructed by a thrombus or thromboembolus resulting in ischemia to the renal parenchyma and subsequently coagulation necrosis.

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