G Slides - Cardio

Front 1

Back 1

1. Test tube: turbid specimen
When a tube of turbid plasma is left overnight in a refrigerator at 4OC, chylomicrons float on top of the plasma (form a supranate), since they have very little protein, while VLDL produces an infranate, since it contains more protein and is more dense than chylomicrons. This tube has both a supranate and an infranate (pinkish staining) indicating the presence of both chylomicrons and VLDL. This is type V hyperlipoproteinemia, which is commonly seen in diabetic ketoacidosis.

Front 2

Back 2

2. Test tubes
The tube on your left is clear, however the LDL fraction is markedly increased. LDL contains CH, which does not produce turbidity. The patient has a type II hyperlipoproteinemia. The tube on the right has a supranate (arrow) and clear infranate indicating the presence of chylomicrons. The most common cause of this is someone who did not fast and had a breakfast full of saturated fats. If this was a hyperlipoproteinemia, it would be a type I hyperlipoproteinemia.

Front 3

Back 3

Patient with xanthelasmas
Note the yellow, plaque-like lesions on the upper and lower eyelids in both eyes. These lesions are associated with hypercholesterolemia - e.g. familial hypercholesterolemia, obstructive jaundice, or hypothyroidism.

Front 4

Back 4

Vessel: hyaline arteriolosclerosis
Arteriosclerosis (hardening of the arteries) involves both small and large vessels. Hyaline arteriolosclerosis is a small vessel arteriosclerosis that is commonly found in diabetics and hypertensives.

Front 5

Back 5

Vessel: hyperplastic arteriolosclerosis: This is the other type of small vessel arteriosclerosis. It is predominantly seen in malignant hypertension and renal disease associated with polyarteritis nodosa and progressive systemic sclerosis. It is also characteristic of the arterioles in the spleen in patients with SLE. Note the "onion skin" appearance of the vessels. This is secondary to hyperplasia of the smooth muscle in the wall of the vessels.

Front 6

Back 6

Aorta: complicated atheromatous plaques
Note the raised yellow plaques and the fissures in between the plaques. Dystrophic calcification is likely present as well.

Front 7

Back 7

Aorta: aorta with complicated atheromatous plaques
Note the fissured-appearing endothelial surface and raised plaque-like structures from the surface. Red clot material is adherent to the plaques in multiple areas. These clots consist of platelets held together by fibrin strands. Aspirin would have prevented these clots from forming. The blotchy white areas represent dystrophic calcification. This is an example of advanced atherosclerosis. It is likely that this patient had an increase in LDL.

Front 8

Back 8

Patient: dry gangrene of the foot in a diabetic
Note the blackened big toe and little toe. Ulcers are present on the undersurface of the big toe and the metatarsophalangeal joint. These are called pressure ulcers and are primarily due to peripheral neuropathy and inability to feel any pain in areas of trauma. Ischemia and infection also play a role in their development. Coagulation necrosis is primarily operative in this patient. However, anaerobic infection commonly occurs leading to gas production, further ulceration of the foot, a malodorous exudate, and gas in the subcutaneous tissue. In this case, liquefactive necrosis would be the predominant type of infection, hence the term wet gangrene.

Front 9

Back 9

Ascending aorta: dissecting aortic aneurysm
The tear in the aorta is at the top of the screen. A toothpick extends through the opening. Blood dissected proximally and emptied into the pericardial sac. The small toothpick is where the pericardial reflection is located.

Front 10

Back 10

Aortic arch vessels: dissecting aortic aneurysm
This is a cross-section of two of the elastic arteries coming off the arch of the aorta. Note how the lumens of both vessels are compressed by clotted blood within the wall of the vessels. This is a type A proximal dissection, where blood entered an intimal tear and extended proximally and up into the arch vessels.

Front 11

Back 11

Aorta: dissecting aortic aneurysm
Note the two lumens in the aorta (double barreled aorta). The lumen on the top is a false lumen (clot has been removed) created by a more proximally located dissection. The false lumen represents the outer media and adventitia of the aorta. The lumen below the false lumen is the true lumen. This is a type B dissection.

Front 12

Back 12

Arch of aorta: syphilitic aneurysm
Note the large depression just below the ruler which represents the aneurysm. The aortic valve ring is stretched, which leads to the murmur of aortic regurgitation. The pathogenesis relates to a vasculitis of the vasa vasorum (endarteritis obliterans), which decreases blood flow to the tissue within the aorta. The weakened tissue begins to outpouch in response to the increased stroke volume.

Front 13

Back 13

Patient: varicose veins in the lower extremeties
Note the bulging and tortuous veins particularly in the left lower leg. There is some discoloration along the medial portion of the ankle, suggesting that the varicosities may be due to deep venous thrombosis and a backup of blood into the superficial saphenous system.

Front 14

Back 14

Superficial saphenous veins: primary varicosities involving the superficial saphenous veins
Note the marked tortuosity and dilatation of the vessels. Usually there is absence of the sentinel valve in the femoral vein.

Front 15

Back 15

Patient: superior vena caval syndrome:
This patient has a small cell cancer of the lung that has blocked off the superior vena cava. Note the congestion of the head and neck due to the backup of venous blood.

Front 16

Back 16

Patient: lymphedema of the arm post-modified radical mastectomy and radiation
Note the marked enlargement of the extremity. Lymphedema is non-pitting.

Front 17

Back 17

X-ray study: Takayasu's arteritis
The arrows point to numerous areas of constriction in the subclavian arteries. The patient most likely had weak to absent pulses in both upper extremities.

Front 18

Back 18

Arteriole: fibrinoid necrosis (leukocytoclastic vasculitis):
Note the pink staining material (fibrinoid necrosis) in multifocal areas of the thickened wall of the venule. The material represents protein derived from the plasma that has deposited in the vessel wall owing to an increase in vessel permeability from the inflammatory process. It is called fibrinoid because it looks like fibrin in a clot but it is really protein. Small vessel vasculitis is usually due to immune complex (IC) disease (type III hypersensitivity). ICs are deposited in the vessel wall and then activate the complement system. C5a, a chemotactic factor, attracts neutrophils (only a few are visible at around 7 o'clock). Neutrophils are responsible for the vessel injury.

Front 19

Back 19

Patient's lower legs: palpable purpura
Note the red-blotchy areas scattered randomly over the skin surface. These lesions would be palpable, hence the term palpable purpura. Palpable purpura is due to a small vessel vasculitis with destruction of the vessel leading to an extravasation of blood into the subcutaneous tissue. The inflammation around the vessel (tumor of inflammation) makes the lesion palpable. This patient had Henoch-Schoenlein�s purpura.

Front 20

Back 20

Patient: temporal arteritis
Note the prominent temporal artery. A biopsy of the artery reveals multinucleated giant cells (granulomatous vasculitis, see arrow).

Front 21

Back 21

Patient: thromboangiitis obliterans (Buerger's disease)
Note the blackened digits (coagulation necrosis). Autoamputation of the digits is likely to occur in this patient.

Back 22

Child: swelling of the hand in Kawasaki's disease
The patient had all the findings of this disease including chest pain (coronary artery vasculitis), erythema of mucous membranes and swelling of the dorsum of the hands. Desquamation of skin has not yet occurred.

Front 23

Back 23

Child: swelling of the hand in Kawasaki's disease
The patient had all the findings of this disease including chest pain (coronary artery vasculitis), erythema of mucous membranes and swelling of the dorsum of the hands. Desquamation of skin has not yet occurred.

Front 24

Back 24

Patient: saddle nose of Wegener's granulomatosis
Note the flattened nose in this patient owing to destruction of the nasal septum by granulomatous inflammation. Congenital syphilis can also produce the saddle nose deformity.

Front 25

Back 25

Patient: Raynaudï's phenomenon
Note the white discoloration of some of the digits owing to spasm of the digital vessels.

Front 26

Back 26

Vessel: Mucormycosis
Vasculitis may be secondary to fungi that invade vessel walls. Note the non-septate hyphae and wide-angled branches of Mucor. Candida and Aspergillus can also invade vessels.

Front 27

Back 27

Stomach: hereditary telangiectasia (Osler-Weber-Rendu disease)
The stomach close-up reveals a vessel dilatation in the submucosa. A histologic section of the lesion exhibits dilated vascular channels. These lesions bleed causing the loss of blood in the stool. Similar lesions occur on the skin and mucous membranes of the mouth.

Front 28

Back 28

Patient: spider angiomata
Note the tentacle-like appearance of this lesion. Compression of the central portion of this lesion causes the tentacles to disappear, hence this lesion is an arteriovenous fistula. They are secondary to hyperestrinism (pregnancy, cirrhosis of the liver).

Front 29

Back 29

Child: capillary hemangioma on the nose
These benign lesions that present at birth invariably disappear with increasing age in the patient. Most pediatricians recommend that they be left alone.

Front 30

Back 30

nt: Kaposi's sarcoma:
Note the raised, elongated red lesion on the neck. This patient is HIV positive and has Kaposi's sarcoma, which is due to HSV-8. Kaposi's sarcoma is an AIDS-defining lesion.

Front 31

Back 31

Renal angiogram: bilateral fibromuscular hyperplasia of the renal arteries
Note the "beaded" appearance in the right renal artery. This is due to fibromuscular hyperplasia in the wall of the renal artery (narrow lumen) alternating with a normal sized lumen.

Front 32

Back 32

Kidney: benign nephrosclerosis (BNS)
Note the cobblestoned surface of this kidney in a patient with long-standing essential hypertension. BNS is the kidney of hypertension. The cortical effect is secondary to hyaline arteriolosclerosis (Slide 4) of the arterioles in the cortex with subsequent tubular atrophy and glomerular fibrosis.

Front 33

Back 33

Retina: grade I hypertensive retinopathy
Note the narrow caliber of the retinal vessels. There is very mild AV nicking (slightly to your left of the red line going down the slide) where the large vessel at the top of the screen crosses a small venule.

Front 34

Back 34

Retina: grade III hypertensive retinopathy Note the flame hemorrhage (ruptured microaneurysm) directly superior to the optic disc (pale area at 5 o'clock). The white lesions (arrow) are well demarcated and represent hard exudates (increased vessel permeability). There is no papilledema.

Front 35

Back 35

Retina: grade IV hypertensive retinopathy
Note the obliteration of the optic disc (papilledema, arrow to center of the slide), flame hemorrhages, soft exudates (white exudates with a fuzzy margin like cotton [cotton wool exudates, arrow at 9 o'clock] representing microinfarctions, hard exudates (white patch that is well demarcated [arrow along the periphery of the slide at 3 o'clock] indicating increased vessel permeability.

Front 36

Back 36

Hearts: normal heart on the left; concentric hypertrophy on the right
Recall that concentric hypertrophy is due to an increase in afterload (e.g., essential hypertension, aortic stenosis).

Front 37

Back 37

Heart: right and left ventricular hypertrophy
The left ventricle is on your left and the right ventricle on your right. Note that both ventricles are thickened. One possible explanation for RV hypertrophy is pulmonary artery hypertension, which imposes an increased afterload against the RV.

Back 38

Lungs: microscopic of pulmonary edema
Note the pink staining fluid (transudate) filling the alveoli. Pulmonary edema occurs in left heart failure.

Front 39

Back 39

Lungs: microscopic of pulmonary edema
Note the pink staining fluid (transudate) filling the alveoli. Pulmonary edema occurs in left heart failure.

Front 40

Back 40

Liver: congestive hepatomegaly ("nutmeg" liver)
Note the red dots scattered throughout the liver parenchyma. These represent blood backed up into the terminal hepatic venules (central vein) in a patient with right heart failure. Recall the terminal hepatic venules eventually coalesce to form the hepatic vein, which empties into the vena cava, which empties into the right heart. Hence an increase in systemic venous pressure transmits back into the liver.

Front 41

Back 41

Aorta: postductal coarctation of the aorta
Note the area of constriction just distal to the ligamentum arteriosum (arrow) extending off the transected pulmonary artery. The proximal aorta is dilated and the posterior wall of the aorta hit by the jet-stream of blood going through the narrow opening is also aneurysmally dilated. You can trace a figure 3 lying on its side.

Front 42

Back 42

Children: cyanotic congenital heart disease
Note the blue discoloration of the lips in these two children, both of which have tetralogy of Fallot. Refer to course notes for why these patients squat to relieve cyanosis.

Front 43

Back 43

Right coronary artery angiogram
RCA stenosis secondary to atherosclerosis. Note the area of constriction (arrow) in the mid-portion of the coronary artery.

Front 44

Back 44

Heart: heart with coronary artery bypasses using saphenous vein grafts
Note the 2 veins, one bypassing the LAD coronary artery (arrow) and the other the RCA.

Front 45

Back 45

Heart: coagulation necrosis of cardiac muscle in an AMI
Note the eosinophilic staining cells with no cross striations or nuclei.

Front 46

Back 46

Heart: cardiac tamponade secondary to rupture of the left ventricle in a patient with an AMI
At the apex of the heart, there is a rupture site in the area of a transmural AMI. Blood fills the pericardial sac and encircles the heart.

Front 47

Back 47

Heart: posteromedial papillary muscle rupture in a patient with a right coronary artery thrombosis
A portion of papillary muscle hangs from the chordae tendineae of the mitral valve. A biopsy of the muscle shows coagulation necrosis. Recall that the right coronary artery supplies this muscle.

Front 48

Back 48

rt: mural thrombus on anterior wall of the ventricle
Note the large thrombus occupying most of the lumen of the left ventricle. A pale infarct overlies the thrombus. It is a mixed clot with the part attached to the endocardium representing a platelet thrombus and the part projecting into the lumen a "venous" type clot.

Front 49

Back 49

Heart: ventricular aneurysm
Note the thin aneurysmal sac extending from the anterior portion of the left ventricle. Very little functional muscle tissue is left in the ventricle. These are late complications and present with a precordial bulge of the anterior chest with each systolic contraction. Rupture is uncommon, since the tissue is scar tissue. Most patients die of heart failure.

Front 50

Back 50

Heart: scar tissue in an old anterior AMI
Note the completely calcified LAD coronary artery buried in the epicardial fat. The white patchy area in the anterior wall is fibrous tissue.

Front 51

Back 51

Patient: erythema marginatum in a patient with acute rheumatic fever
This skin rash is one of the five Jone's criteria for diagnosing acute rheumatic fever. Note the erythematous circular lesions with central areas of pallor.

Front 52

Back 52

Heart: mitral stenosis
You are looking down from the enlarged left atrium into the orifice of the mitral valve. Note that it has a fish-mouth appearance. This patient probably had a significant component of mitral insufficiency as well as stenosis.

Back 53

Heart: mitral valve prolapse
Note the baggy-appearing mitral valve leaflets. When blood collects beneath these voluminous valves, it projects them into the left atrium like a parachute. When the chordae abruptly stop the valves from moving any further, a systolic click is heard followed by a murmur of mitral insufficiency.

Front 54

Back 54

Heart: mitral valve prolapse
Note the baggy-appearing mitral valve leaflets. When blood collects beneath these voluminous valves, it projects them into the left atrium like a parachute. When the chordae abruptly stop the valves from moving any further, a systolic click is heard followed by a murmur of mitral insufficiency.

Front 55

Back 55

Heart: mitral valve prolapse
Note the parachute-like redundancy of the mitral valve and how it has prolapsed into the left atrium. A close-up of the valve shows that one of the chordae has ruptured causing the patient to develop acute mitral regurgitation, and, in this case, death.

Front 56

Back 56

Heart: aortic stenosis with left ventricular hypertrophy
The left atrium is at the bottom of the screen and the left ventricle lumen is markedly diminished owing to LVH. The aortic valve just above the left atrium is markedly calcified.

Front 57

Back 57

Heart: aortic insufficiency secondary to old rheumatic heart disease
Note that the aortic valve is fibrotic and plastered against the aorta, hence leaving an expanded AV orifice (blood will leak back into the LV during diastole). As expected, the LV was volume overloaded and exhibits both dilatation and hypertrophy.

Front 58

Back 58

Aortic valve: infective endocarditis complicating a ventricular septal defect
A metal probe exits one of the two holes in the membranous portion of the IVS. This represents a VSD. Small vegetations line the valve cusps and the thread extends through a hole in the valve that developed from the infection. The edge of the other valve cusp looks half eaten away. This underscores the increased incidence of infective endocarditis in patients with an underlying congenital defect.

Front 59

Back 59

Mitral Valve: acute infective endocarditis
The vegetations are on the atrial side of the valve leaflets. Note the bulky vegetations and chordae tendineae that has been ruptured. Staphylococcus aureus grew out in the blood culture.

Front 60

Back 60

Patient: splinter hemorrhages on your left and Osler's nodes on your right
This patient has acute infective endocarditis. Recall that these lesions are an example of immunocomplex vasculitis (type III hypersensitivity).

Front 61

Back 61

Retina: Roth's spot in a patient with acute infective endocarditis
Note the red lesion with a pale center (arrow). This represents an immunocomplex vasculitis with hemorrhage.

Front 62

Back 62

Heart: congestive cardiomyopathy
Note the extreme dilatation of both the left (on your right) and right ventricular chambers (on your left). The patient had a previous history of a coxsackie myocarditis.

Front 63

Back 63

Heart: restrictive cardiomyopathy secondary to amyloidosis
Note the thickened myocardial tissue and the blotchy-white deposits of amyloid in the muscle. The special stain on the right demonstrates the blue-green staining amyloid encasing and destroying the myocardial fibers.

Front 64

Back 64

Heart: fibrinous pericarditis
This is a classic example of fibrinous inflammation involving the visceral pericardium ("bread and butter" pericarditis). Fibrinous inflammation is due to increased vessel permeability leading to the leakage of a sterile exudate with fibrin on to the surface of the heart. The patient would likely have had a pericardial friction rub. This particular patient had SLE.

Front 65

Back 65

Chest x-ray: pericardial effusion
Note the "water bottle" configuration of the heart owing to a collection of fluid in the pericardial sac. The patient had a coxsackie myocarditis and pericarditis.

Front 66

Back 66

Heart and Pericardium: constrictive pericarditis secondary to TB
Note the caseous necrosis in the hilar lymph nodes directly above the heart. The pericardium is markedly thickened and has chalky white area most likely representing dystrophic calcification. Note what little room the heart has to expand with blood and why a pericardial knock would likely be heard when the ventricle hit the thickened parietal pericardium during diastole.