Laboratory Worksheet

Subject:______________
Name of student:__________________________________ Date:
Class no.______ Signature:_______________ activity no.
Instructor/s-in-charge: Dr. Marilag
Activity title:___________________________________________________________________
____________________________________________________________________________
____________________________________________________________________________

Figure 1.1 Pulmonary edema, microscopic

The alveoli on the left are filled with a smooth to slightly floccular pink material ( ) characteristic of pulmonary edema.
Capillaries within alveolar walls are congested, filled with many red blood cells (RBCs). Pulmonary congestion with edema is
common in patients with heart failure and in areas of inflammation of the lung. On the right is more marked pulmonary
congestion with dilated capillaries and leakage of blood into alveolar spaces, leading to the appearance of hemosiderin-laden
macrophages (“heart failure cells”) containing brown cytoplasmic hemosiderin granules ( ) from breakdown of RBCs.

1. Differentiate exudate and transudate

2. Most common cause of pulmonary edema

Figure 1.2 Pulmonary infarct, gross
Medium-sized thromboemboli (blocking a pulmonary artery to a lobule or set of lobules) can produce a hemorrhagic pulmonary
infarction ( ) because the patient survives. The infarct is wedge shaped and based on the pleura. These
infarcts become hemorrhagic because, although the pulmonary artery carrying most of the blood is cut off, the bronchial arteries
from the systemic circulation (supplying about 1% of the blood to the lungs) are not cut off. It is also possible to have multiple
small pulmonary thromboemboli that do not cause sudden death and do not occlude a large enough branch of pulmonary artery to
cause infarction. Clinical findings include chest pain and hemoptysis.
Figure 2.1 Pulmonary embolism, microscopic
Within this pulmonary artery are interdigitating areas of pale pink and red that form the lines of Zahn ( ) characteristic of a
thrombus. These lines represent layers of RBCs, platelets, and fibrin that are laid down as the thrombus forms within a vein. Here
the thrombus has become a thromboembolus that has traveled up the inferior vena cava and the right side of the heart to become
packed into a pulmonary artery branch. Over time, if the patient survives, the thromboembolus can undergo organization and
dissolution

Figure 2.2 Pulmonary embolism, microscopic

Here is a small peripheral pulmonary artery thromboembolus in the region of a hemorrhagic infarct, marked by many RBCs
within alveolar spaces. There is partial recanalization ( ) of this blocked artery. Such a small embolus probably
would not cause dyspnea or pain, unless there were many emboli and they were showered into the lungs over time. They could
collectively block enough small arteries to produce secondary pulmonary hypertension with cor pulmonale
 1. Common sources of pulmonary thromboemboli

2. What is paradoxical embolism?

Figure 3.1 Coronary thrombosis, gross

One of the severe complications of coronar yatherosclerosis, shown here with thickened arterial walls with yellow-tan plaques
that narrow the arterial lumen, is thrombosis. The dark red thrombus ( ) occludes this anterior descending coronary artery, opened
longitudinally. The thrombotic occlusion leads to ischemia or infarction of the myocardium supplied by the artery. One possible
outcome of coronary thrombosis is sudden death. Other complications include ongoing arrhythmias and congestive heart failure.

1. Risk factors for the development of atherosclerosis

2. What characteristic of atherosclerotic plaque is associated with greatest risk of rupture?

Figure 3.2 Coronary thrombosis, microscopic
The recent thrombus shown here nearly occludes the remaining small lumen of this coronary artery already narrowed from severe
atherosclerosis. Note the fibrointimal proliferation ( ) with cholesterol clefts. Endothelial damage with platelet activation
promotes thrombosis. A small dose of aspirin taken each day helps reduce platelet function, making the platelets less sticky and
less prone to participate in thrombotic events.

Figure 4.1 Centrilobular congestion, gross

This is a nutmeg liver with chronic passive congestion. Note the dark-red congested regions that represent accumulation of red
blood cells within centrilobular regions. The nutmeg pattern results from congestion around the central veins, usually from right-
sided heart failure. If the passive congestion is pronounced and heart failure
leads to ischemia, there can be centrilobular necrosis because the oxygenation in zone 3 of the hepatic lobule is diminished, and
the AST and ALT increase. Rarely, chronic passive congestion leads to fibrosis extending between central veins—a “cardiac
cirrhosis.” Extensive hepatic congestion can accompany disseminated intravascular coagulation and hemoglobinopathies such as
sickle cell disease
Figure 5.1 Renal infarct, gross
Note the wedge shape of this acute infarct ( ), with the pale zone of coagulative necrosis resulting from loss of blood supply with
resultant tissue ischemia that progresses to infarction. The small amount of blood from the capsular arteries supplies the
immediate subcortical zone, which is spared. The remaining cortex is congested, as is the medulla. Renal infarcts most often
occur with emboli that originate from cardiac diseases, such as endocarditis, rheumatic mitral stenosis with left atrial dilation and
mural thrombosis, or ischemic heart disease with ventriculomegaly and mural thrombosis. Patients may be asymptomatic or may
have costovertebral angle tenderness and hematuria.

Figure 5.2 Renal infarct, microscopic

On the right is normal kidney; to the left of that, hyperemic parenchyma ( ) is becoming necrotic ( ); to the far left is pale pink
infarcted kidney, in which tubules and glomeruli have undergone coagulative necrosis, leaving just the cellular outlines of tubules
and glomeruli. Renal infarction is most likely a consequence of embolization, although arterial or arteriolar vasculitis may also
lead to focal smaller areas of infarction. The renal parenchyma is at increased risk for ischemic injury because there is no
collateral blood flow. Infarcts may cause pain and hematuria, but less likely renal failure as a result of their focality.
Figure 5.3 Atheroembolic renal disease, Microscopic
Shown here in a renal artery branch are cholesterol clefts (▶) characteristic of such an embolus filling the lumen. This patient had
severe ulcerative, friable aortic atheromatous plaques and had undergone angiography, which increases the risk for such emboli.
Large numbers of these emboli can produce focal ischemia and compromise renal function. Multiple atheroemboli are most likely
to be a cause of renal failure in patients with preexisting renal disease.

1. Causes of atheromatous emboli

2. What factors accelerate atherosclerosis?