Practical 4 Cardivascular and Hepatobiliary System

8/18/2019 Practical 4 Cardivascular and Hepatobiliary System

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UTAR UDDD 2124

ESSENTIAL PATHOLOGY

Year 2 Sem 1

Practical 4

GASTROINTESTINAL TRACT CARDIOVASCULAR SYSTEM

Atherosclerosis

General gross description

- lesions in childhood appear as fatty streaks

- adults plaques are discrete, yellow white random elevations, more prominent around ostia

of large branches, abdominal aorta and coronary, internal carotid and cerebral arteries

- plaque may have sclerotic firm surfaces, or ulcerate with soft exposed material

-

plaques may become confluent with thrombosis- severity increases with age, into very old age

General Microscopic Description

- an intimal lesion, made up of a deposition of fats, cholesterol`l esters, necrotic debris and

foam cells with a variable chronic fibrotic inflammatory response forming a superficial

fibrous cap containing smooth muscle and foam cells and lymphocytes

- complications are ulcers with ulcers with thrombi, bleeding into plaque, embolization of

thrombi and/or atheroma, calcifications and atrophy of media with formation of aneurysm

Ruptured

plaque

Lumen

thickening of

intima layer



Advanced plaque

- note the discrete intimal nodulae thickening the arterial wall, obstruction of lumen and

ruptures of atheromatous plaque

- the increased cellularity is made up of both fibroblasts and smooth muscle cells

-

the proliferation of these cells is a major component of the genesis of the atherosclerotic plaque

field shows atheromatous plaque in intima layer

The more deeply pinker staining right upper portion of the field is the sclerotic fibrous

cap. the lighter stain elsewhere is due to deposition of neutral fats which are washed out

by the tissue processing for slide preparation

note the slit like clear spaces which were occupied by washed out cholesterol esters

crystals before processing

the fine blue stipples throughout are calcific spherules

the high magnification the atheroma shows numerous foam cells and an occationalcholesterol cleft. a few dark blue inflammatory cells are scatter within the atheroma.

Foam cells filled with lipid appear as large, pale staining cells very vacuolated cytoplasm.

These cells may derive form myointimal cells or macrophage. As the lesion progress

some of the foam cells break down and liberate free lipid into the intima where it is

represented by non staining angular clefts.

Question

1. Draw and describe the histopathological changes of the given slide

2.

Explain the pathogenesis of atheroma formation

3. Discuss the sequelae of atherosclerosis



Myocardial Infarct

General Gross Description

- lesions not visible before 18 – 24 hours after onset

- size variable up to entire transverse sectional area

- may involve partial (subendocardial) or full (transmural) thickness of left ventricular wall

- Earliest change is a poorly defines pale area some with hemorrhagic changes. Area

defines better with time turning yellow with a pink margin of organizing tissue and

finally a discrete scar.


- Earliest changes at 4 to 12 hours, shows feature of acute inflammation processes; nuclear

necrosis, muscle coagulative necrosis at 24-72 hours, loss of fiber nuclei and heavy

neutrophilic infiltrate

- Macrophage phagocytic activity and early organization at 3 to 7 days; healed scar by 7

weeks.

early acute MI

- note the copious exudates of neutrophils (PMN) between the muscle fibers

- note the absence of nuclei in the myocardial fibers indicating necrosis, eg infarction

- PMN’s have a life span of 24 hours and then undergo karyorrhexis which is not seen here

suggesting that this lesion is less than 2 days old.

http://www.wikidoc.org/index.php/File:Myocardial_infarct_emmolition_phase_histopathology.jpg



Healing acute MI

- capillaries, elongate fibroblast nuclei, collagen fibrils and macrophages all typical

components of granulation tissue can be seen

- macrophages can be seen containing a dark pigment which is probably hemosiderin

because of the color and variation in particle size

- the rest, wave fibers are collagen and represent the scar tissue that will ultimately replace

the dead myocardium



Healed old myocardial infarct

- this is a myocardial infarct perhaps hypertrophic fibers

- the extra cellular matrix appears sparsely cellular and densely collagenized indicating that

this is an old lesions from a few months to years old

Questions

1. Draw and describe the histopathological changes of the given slide

2. Identify the stage of infarction.

Cirrhosis of liver

Cirrhosis is the end result of continued damage to liver cells from a great many causes. It is

characterized by wholesale disruption of the liver architecture and the formation of nodules of

regenerating liver cells separated by fibrous band. There are two main effects of this altered liver

architecture and cellular damage namely disturbance of blood flow through the liver from portal

vein to hepatic vein. The classification of cirrhosis is based on the disease which causes theunderlying liver damage. The most important causes are chronic alchol abuse, chronic hepatitis

and biliary cirrhosis. In small percentage of cases no underlying disease can be found: this is

known as cryptogenic cirrhosis.




Macronodular Cirrhosis: Larger nodules

separated by wider scars and irregularly

distributed throughout the liver usually due

to an infectious agent such as viral hepatitis

which does not diffuse uniformly throughout

the liver.

Microndular Cirrhosis: Small rather

uniform• 2m nodules seperated by thin

fibroussepta usually due to a chemicalagent

as alcohol which diffuseuniformly throught

the liver.


Alcoholic cirrhosis

- broad fibrous bands connecting portal areas and intervening nodules of liver cells

-

marked fatty changes



Cryptogenic cirrhosis

- bands of fibrous tissue disrupting the lobular architecture

- no inflammation, fatty changes or specific features

Cirrhosis due to progressive chronic hepatitis

- the portal tracts contain large number of chronic inflammatory cells and in some area

these inflammatory cells spill over the limiting plate into nodules of hepatocytes

-

fibrous bands containing inflammatory cells found

1. Identify the type of liver cirrhosis and describe the features.



Metastatic carcinoma of liver

Though most any type of cancer may metastasize to the liver, some are more likely to do so than

others. Breast, lung, colorectal, stomach, pancreas, and small intestine tumors are among those

that are most closely associated with the liver. The prognosis of an individual with metastases in

the liver is to some extent related to the site of the primary cancer.


- Separate lesions (not clustered)

- Necrotic tissue


Liver-Metastatic pulmonary small cell carcinoma.

nests of small primitive appearing epithelial cells with hyperchromatic nuclei and high nuclear

to cytoplasmic ratio



Liver-Metastatic adenocarcinoma of stomach

Glandular type carcinoma can be found with hyperchromatic nuclei and high nuclear to

cytoplasmic ratio

1. Identify the type of metastatic carcinoma in liver and describe the features.

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Practical 4 Cardivascular and Hepatobiliary System