Case #1

Clinical Summary
65-year-old man was delivered to emergency department
complaining of squeezing, burning chest pain. Patient was
treated in cardiology department 5 years ago.
After coronography blood pressure suddenly dropped and
patient died.
Autopsy findings:
Scars in the anterior wall of left ventricle;
Anterior interventricular artery stenosis (90%) with lumen
thrombosis;
Yellow plaques in aorta with focal ulceration.

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 Questions
1. Name histologic changes in myocardium
and artery (SLIDES 1-5). Describe the
pathogenesis of morphologic changes.
2. Describe this process.
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 Answers
1. The intensely pink region in myocardium results
from loss of nuclei but preserved cell outlines,
typical for coagulative necrosis as a
consequence of tissue hypoxia (due to arterial
stenosis (atherosclerosis) and thrombosis) and
cell death.
2. Necrosis is a form of cell injury which results in
the premature death of cells in living tissue.
 Diagnosis:
Myocardial infarction
Case #2
 Clinical Summary
37-year-old woman with a history of rheumatic mitral
stenosis had a mechanical prosthetic valve implanted 2 years
ago. The patient experienced sudden onset of a fever of an
unkown origin. The patient's condition deteriorated,
antibiotic therapy was unsuccessful and she died.
Autopsy findings:
The mechanical valve and aortic valve showed some
light brown vegetation;
An area of the brain tissue dissolution in the right
hemisphere.

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 Questions
1. What are the microscopic features shown
(SLIDES 1-3)?
2. Describe the pathogenesis of morphologic
changes.
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 Answers
1. The loss of brain parenchyma and macrophages
which have phagocytosed the dead brain tissue.
2. A scarred rheumatic valve is more susceptible to
endocarditis; subsequent embolization on an
infected vegetation produce a septic infarct.
 Diagnosis:
Brain Infarction
Case #3
 Clinical Summary
60-year-old man was admitted to the hospital with a history of periodic
diarrhea, general malaise, all of approximately 7 years duration. Recently
subfebrile fever (37,5C) , diarrhea, nausea, dry cough evolved.
The patient progressively deteriorated and died due to progressive
cardiopulmonary failure.
Autopsy findings:
Disseminated small (2 mm) white/yellow nodules in the lungs.
A grey/black nodule (2 cm) in the apex of the right lung;
Enlarged mediastinal lymph nodes.

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 Questions
1. Describe changes in lungs (SLIDES 1-7).
2. What disease could be suspected?
3. What is relation between new symptom
occurence and changes in the lungs?
4. What is the cause of long standing complains?
5. What tests could help in diagnosis?
6. What would be appropriate treatment in this
condition?
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 Answers
1. Granulomas with a necrotic center and a rim of
epithelioid hystiocytes, and occasional
multinucleated Langhans giant cells at the
periphery.
2. Disseminated tuberculosis.
3. Reactivation and dissemination of the
infection.
4. Damage to the lungs an gastrointestinal tract.
5. Sputum smears and cultures, radiography.
6. Long-term antibiotic therapy.
 Diagnosis:
Tuberculosis
Caseous necrosis is encountered most often in foci of tuberculous
infection.
Tuberculosis is a serious chronic pulmonary and systemic disease
caused most often by M. Tuberculosis (rarely M. bovis).
Histologicaly characteristic granulomatous infalmmation:
caseous necrosis enclosed within epithelioid and multinucleate
giant cells (Langhans type), fibroblastic rim punctuated by
lymphocytes. Systemic miliary tuberculosis occurs when bacteria
disseminate through the systemic arterial system and is most
prominent in the liver, bone marrow, spleen, adrenals, meninges,
kidneys, fallopian tubes and epididymis, but could involve any
organ.
Case #5
 Clinical Summary
50-year-old overweight man was hospitalised after his
birthday party. The patient was complaining of severe
abdominal pain. Inspection: pallor of the skin, excessive
sweating, relief of pain by sitting up and bending forward.
After few hours: sudden drop of blood pressure
(80/40mmHg), arrhythmia; clinical death occured;
reanimation with no effect.
Autopsy: confluent white/yellow masses in pancreatic
parenchyma, peritoneum and mesenteric fat tissue.

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 Questions
1. Explain the changes seen in the slides.
2. What pathologic process could be identified in
a fat tissue?
3. What caused this pathologic process?
4. Is this distinctive type of necrosis?
5. What could be the consequences after release
of toxic enzymes, cytokines, and other
mediators into the circulation and tissues.
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 Answers
1. Fat necrosis (Steatonecrosis).
2. Release of activated pancreatic lipases into the substance
of the pancreas, peripancreatic adipose tissue and the
peritoneal cavity.
3. Its type of coagulative necrosis with visually distinctive
pattern. Mechanism of formation similar to liquefactive
necrosis.
4. Explosive activation of a systemic inflammatory response,
resulting in leukocytosis, disseminated intravascular
coagulation (DIC), edema, and acute respiratory distress
syndrome. Shock due to the systemic inflammatory
response syndrome and acute renal tubular necrosis may
occur.
Diagnosis:
Necrosis
Case #5
 Clinical Summary
30-years-old woman was complaining of morning stiffness
and swelling in finger joints of both hands.
Recently stiff nodules of 1 cm diameter appeared in elbow
region. Tumor was suspected complete resection and
histologic evaluation was performed.
 Questions
1. Name histologic changes in nodules
(SLIDES 1-2).
2. What disease could be suspected?
3. What would help to establish diagnosis?
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 Answers
1. Fibrinoid necrosis is surrounded by rim of
epithelioid histiocytes, lymphocytes, and
plasma cells.
2. Rheumatoid arthritis.
3. Radiographs of the involved joints, RF,
anti-CCP in blood serum.
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 Diagnosis:
Rheumatoid arthritis
Rheumatoid arthritis(RA) is a chronic inflammatory disorder of autoimmune origin that may
affect many tissues and organs but principally attacks the joints, producing a nonsuppurative
proliferative and inflammatory synovitis. RA often progresses to destruction of the articular
cartilage and ankylosis of the joints.
Extraarticular lesions may involve skin, heart, blood vessels and lungs. The pathologic changes
are mediated by antibodies against self-antigens and cytokine-mediated inflammation,
predominantly secreted by CD4+ T-cells.
Rheumatoid subcutaneous nodules are the most common cutaneous lesions. They occur in
approximately 25% of affected individuals, usually those with severe disease, and arise in regions
of the skin that are subjected to pressure, including the ulnar aspect of the forearm, elbows,
occiput, and lumbosacral area.
Diagnostic criteria:
Inflammatory arthritis involving three or more joints.
Positive rheumatoid factor (RF) and/or anti-citrullinated peptide/protein antibody (such as anti-cyclic
citrullinated peptide [CCP])) testing.
Elevated levels of C-reactive protein (CRP) or the erythrocyte sedimentation rate (ESR).
The duration of symptoms is more than six weeks.
Diseases with similar clinical features have been excluded, particularly psoriatic arthritis, acute viral
polyarthritis, polyarticular gout or calcium pyrophosphate deposition disease, and systemic lupus
erythematosus (SLE).