A. Questions for practical exam from autopsy 1.

External inspection A general description of the body as regards ethnicity, sex, age, hair color and length, eye color and other distinguishing features (birthmarks, old scar tissue, moles, etc) is then made. 2. Death and post mortal changes Many physico-chemical changes begin to take place in the body immediately or shortly after death and progress in a fairly orderly fashion until the body disintegrates. Each change has its own time factor or rate. Unfortunately, these rates of development of post mortem changes are strongly influenced by unpredictable endogenous and environmental factors.
- ALGOR MORTIS (body cooling) - RIGOR MORTIS

Ordinarily, death is followed immediately by total muscular relaxation primary muscular flaccidity - succeeded in turn by generalized muscular stiffening - rigor mortis. After a variable period of time rigor mortis passes off spontaneously to be followed by secondary muscular flaccidity. Rigor mortis results from a physicochemical change in muscle protein, the precise nature of which is unknown. When the muscle tissue becomes anoxic and all oxygen dependent processes cease to function, then the level of ATP is maintained by anaerobic glycolysis which results in increasing levels of pyruvic and lactic acids. Eventually, the muscle glycogen is depleted, the cellular pH falls to around 6, and the level of ATP falls below a critical level beyond which rigor rapidly develops.
- LIVOR MORTIS (HYPOSTASIS, POST MORTEM LIVIDITY, POSTMORTEM SUGGILLATIONS)

Lividity is a dark purple discolouration of the skin resulting from the gravitational pooling of blood in the veins and capillary beds of the dependent parts of the body following cessation of the circulation. The process begins immediately after the circulation stops, and in a person dying slowly with circulatory failure, it may be pronounced very shortly after death. Lividity is present in all bodies, although it may be inconspicuous in some and thus escape notice.
- POSTMORTEM DECOMPOSITION (PUTREFACTION)

Putrefaction is the post mortem destruction of the soft tissues of the body by the action of bacteria and enzymes (both bacterial and endogenous). Tissue breakdown resulting from the action of endogenous enzymes alone is known as autolysis. Putrefaction results in the gradual dissolution of the tissues into gases, liquids and salts. The main changes which can be recognized in the tissues

undergoing putrefaction are changes in colour, the evolution of gases, and liquefaction. - Adipocere or grave wax or mortuary wax is a water-insoluble material consisting mostly of saturated fatty acids. It is formed by the slow hydrolysis of fats in decomposing material such as a human cadaver by action of anaerobic bacteria. 3. Internal inspection - basis of macroscopic description of dissected tissues and organs A plastic or rubber brick called a "body block" is placed under the back of the body, causing the arms and neck to fall backward whilst stretching and pushing the chest upward to make it easier to cut open. This gives the pathologist maximum exposure to the trunk. After this is done, the internal examination begins. The internal examination consists of inspecting the internal organs of the body for evidence of trauma or other indications of the cause of death. A single vertical cut is made from the middle of the neck (in the region of the 'Adams apple' on a male body) The cut then extends all the way down to the pubic bone (making a deviation to the left side of the navel). Bleeding from the cuts is minimal, or non-existent, due to the fact that the pull of gravity is producing the only blood pressure at this point, related directly to the complete lack of cardiac functionality. However, in certain cases there is anecdotal evidence to prove that bleeding can be quite profuse, especially in cases of drowning. Scalpel blades are used to open the chest cavity. The pathologist uses the tool to cut through the ribs on the lateral sides of the chest cavity to allow the sternum and attached ribs to be lifted as one chest plate; this is done so that the heart and lungs can be seen in situ and that the heart, in particular the pericardial sac is not damaged or disturbed from opening. A scalpel is used to remove any soft tissue that is still attached to the posterior side of the chest plate. Now the lungs and the heart are exposed. The chest plate is set aside and will be eventually replaced at the end of the autopsy. At this stage the organs are exposed. Usually, the organs are removed in a systematic fashion. Making a decision as to what order the organs are to be removed will depend highly on the case in question. Organs can be removed in several ways: all the organs are removed as one large mass or they are divided into 4 groups.

The pericardial sac is opened to view the heart. Blood for chemical analysis may be removed from the inferior vena cava or the pulmonary veins. Before removing the heart, the pulmonary artery is opened in order to search for a blood clot. The heart can then be removed by cutting the inferior vena cava, the pulmonary veins, the aorta and pulmonary artery, and the superior vena cava. The left lung is then easily accessible and can be removed by cutting the bronchus, artery, and vein at the hilum. The right lung can then be similarly removed. The abdominal organs can be removed one by one after first examining their relationships and vessels. The various organs are examined, weighed and tissue samples in the form of slices are taken. Even major blood vessels are cut open and inspected at this stage. Next the stomach and intestinal contents are examined and weighed. This could be useful to find the cause and time of death, due to the natural passage of food through the bowel during digestion. The more area empty, the longer the deceased had gone without a meal before death. The body block that was used earlier to elevate the chest cavity is now used to elevate the head. To examine the brain, an incision is made from behind one ear, over the crown of the head, to a point behind the other ear. When the autopsy is completed, the incision can be neatly sewn up and is not noticed when the head is resting on a pillow in an open casket funeral. The scalp is pulled away from the skull in two flaps with the front flap going over the face and the rear flap over the back of the neck. The brain is then observed in situ. Then the brain's connection to the cranial nerves and spinal cord are severed, and the brain is then lifted out of the skull for further examination. If the brain needs to be preserved before being inspected, it is contained in a large container of formalin (15 percent solution of formaldehyde gas in buffered water) for at least two but preferably four weeks. This not only preserves the brain, but also makes it firmer allowing easier handling without corrupting the tissue. 4. Arrangement of diagnoses

5. Ischemic changes of brain - macroscopic description A. Infarction : its characterized by liquefactive necrosis leading to cyst formation.

- Thrombosis, Mostly caused by atherosclerosis. Arterial Obstruction of the internal and external carotid arteries at origin in the neck and middle cerebral artery are the most frequent sites of thrombotic occlusion. - Embolism, from cardiac mural thrombi, valvular vegetations, fat emboli. Middle cerebral artery is the most frequent site of embolic occlusion. Embolism is less common that thrombosis.
B.Hemorrhage

6. Brain hemorrhage - macroscopic description A. Intracerebral Hemorrhage consists of bleeding into the brain substance. - Most frequently, the cause is hypertension, which is often complicated by minute dilations at small artery bifurcation. These Charcot- Bouchard aneurysms may be sites of hemorrhagic rupture. - Most often, it occurs in the basal ganglia/ thalamus; other favored sites include the Pons, cerebellum, and frontal lobe white matter.
B. Subarachnoid Hemorrhage consists of bleeding into the subarachnoid space.

-This is frequently associated with Berry aneurysm of the circle of Willis. - Cause includes arteriovenous malformations, trauma, or hemorrhagic diatheses. 7. Meningitis - macroscopic description Meningitis is inflammation of the protective membranes covering the brain and spinal cord, known collectively as the meninges. The inflammation may be caused by infection with viruses, bacteria, or other microorganisms, and less commonly by certain drugs. Meningitis can be diagnosed after death has occurred. The findings from a post mortem are usually a widespread inflammation of the pia mater and arachnoids layers of the meninges covering the brain and spinal cord. Neutrophil leucocytes tend to have migrated to the cerebrospinal fluid and the base of the brain, along with cranial nerves and the spinal cord, may be surrounded with pusas may the meningeal vessels. 8. Hydrocephalus - macroscopic description
Hydrocephalus is a term derived from the Greek words "hydro" meaning water,

and "cephalous" meaning head and this condition is sometimes known as "water on the brain". People with hydrocephalus have abnormal accumulation of cerebrospinal fluid (CSF) in the ventricles, or cavities, of the brain. This may cause

increased intracranial pressure inside the skull and progressive enlargement of the head, convulsion, and mental disability. Hydrocephalus is usually due to blockage of CSF outflow in the ventricles or in the subarachnoid space over the brain 9. Pleuritis - macroscopic description
Pleuritis is an inflammation of the pleura, the lining of the pleural cavity

surrounding the lungs. Among other things, infections are the most common cause of pleurisy. The inflamed pleural layers rub against each other every time the lungs expand to breathe in air. This can cause sharp pain with breathing (also called pleuritic chest pain).

10. Pericarditis - macroscopic description Pericarditis is an inflammation of the pericardium (the fibrous sac surrounding the heart).Its Caused by; A. Infectious Agents like viruses, pyogenic Bacteria, Tuberculosis, Fungi, and Parasites. B. Immunologically Mediated like Rheumatic fever, Postcardiotomy, Drug hypersensitivity reaction. Invasion of pericardial space by infective organism. It will have Exudates (Thin creamy Pus), Serosal Surfaces are reddened, Granular and coated with exudates. Sometimes the inflammatory process extends to surrounding structures. 11. Hydrothorax and hydro pericardium pathogenesis
A hydrothorax is a condition that results from serous fluid accumulating in the

pleural cavity. This specific condition can be related to cirrhosis with ascites in which ascitic fluid leaks into the pleural cavity. Hepatic hydrothorax is often difficult to manage in end-stage liver failure and often fails to respond to therapy. In similar pleural effusions, hemothorax this fluid is blood (as in major chest injuries), in pyothorax the fluid is pus (resulting from chest infections), and in chylothorax it is lymph fluid (resulting from rupture of the thoracic duct). 12. Emphysema pulmonum - macroscopic description

Emphysema is a chronic obstructive pulmonary disease (COPD, as it is otherwise

known, formerly termed a chronic obstructive lung disease). It is often caused by exposure to toxic chemicals, including long-term exposure to tobacco smoke. Emphysema is characterized by loss of elasticity (increased pulmonary compliance) of the lung tissue caused by destruction of structures feeding the alveoli, owing to the action of alpha 1 antitrypsin deficiency. This causes the small airways to collapse during exhalation, as alveolar collapsibility has increased. As a result airflow is impeded and air becomes trapped in the lungs, in the same way as other obstructive lung diseases. Symptoms include shortness of breath on exertion and later at rest, hyperventilation, and an expanded chest. 13. Oedema pulmonum - macroscopic description
Oedema is an abnormal accumulation of fluid beneath the skin, or in one or more

cavities of the body. Generally, the amount of interstitial fluid is determined by the balance of fluid homeostasis, and increased secretion of fluid into the interstitium or impaired removal of this fluid may cause oedema. Five factors can contribute to the formation of edema. It may be facilitated by increased hydrostatic pressure or reduced oncotic pressure within blood vessels, increased blood vessel wall permeability as in inflammation, obstruction of fluid clearance via the lymphatic or changes in the water retaining properties of the tissues themselves. Raised hydrostatic pressure often reflects retention of water and sodium by the kidney. Pulmonary edema occurs when the pressure in blood vessels in the lung is raised because of obstruction to removal of blood via the pulmonary veins. This is usually due to failure of the left ventricle of the heart. It can also occur in altitude sickness or on inhalation of toxic chemicals. Pulmonary edema produces shortness of breath. Pleural effusions may occur when fluid also accumulates in the pleural cavity. 14. Pneumonia - macroscopic description
Pneumonia is an inflammatory illness of the lung. Frequently, it is described as

lung parenchyma/alveolar inflammation and abnormal alveolar filling with fluid (consolidation and exudation).

The alveoli are microscopic air-filled sacs in the lungs responsible for absorbing oxygen. Pneumonia can result from a variety of causes, including infection with bacteria, viruses, fungi, or parasites, and chemical or physical injury to the lungs. Its cause may also be officially described as idiopathicthat is, unknownwhen infectious causes have been excluded.

Typical symptoms associated with pneumonia include cough, chest pain, fever, and difficulty in breathing.

15. Pneumothorax - macroscopic description A Pneumothorax , or collapsed lung , is caused by accumulation of air or gas in the pleural cavity. A pneumothorax can occur spontaneously, or as the result of disease or injury. It most commonly arises: - Spontaneously (most commonly in tall slim young males and in Marfan syndrome) - Following a penetrating chest wound - Following Barotrauma to the lungs It may also be due to: - Chronic lung pathologies including emphysema, asthma - Acute infections - Chronic infections, such as tuberculosis - Lung aggrevation caused by Cystic Fibrosis - Cancer 16. Tumors of the lung - macroscopic description
Lung cancer is a disease of uncontrolled cell growth in tissues of the lung. This

growth may lead to metastasis, which is the invasion of adjacent tissue and infiltration beyond the lungs. The vast majority of primary lung cancers are carcinomas of the lung, derived from epithelial cells. Lung cancer, the most common cause of cancer-related death in men and the second most common in women (after breast cancer). The most common symptoms are shortness of breath, coughing (including coughing up blood), and weight loss. The main types of lung cancer are small cell lung carcinoma and non-small cell lung carcinoma. The most common cause of lung cancer is long-term exposure to tobacco smoke. The occurrence of lung cancer in nonsmokers, who account for as many as 15% of cases, is often attributed to a combination of genetic factors.

Carcinomas of the lung begin as small mucosal lesions that are usually firm and gray-white. They may form intraluminal masses, invade the bronchial mucosa, or form large bulky masses pushing into adjacent lung parenchyma. Some large masses undergo cavitations caused by central necrosis or develop focal areas of hemorrhage. Finally, these tumors may extend to the pleura, invade the pleural cavity and chest wall, and spread to adjacent intrathoracic structures. More distant spread can occur via the lymphatics or the hematogenous routes.

17. Cor pulmonale - macroscopic description Cor pulmonale or pulmonary heart disease is a change in structure and function of the right ventricle of the heart as a result of a respiratory disorder. Right ventricular hypertrophy (RVH) is the predominant change in chronic cor pulmonale, whereas in acute cases, dilation dominates. Both hypertrophy and dilation are the result of increased right ventricular pressure. Left untreated, cor pulmonale can lead to right-heart failure and death. There are several mechanisms leading to cor pulmonale:

Pulmonary vasoconstriction Anatomic changes in vascularization Increased blood viscosity Idiopathic or primary pulmonary hypertension

18. Hypertension complications

Hypertension , also referred to as high blood pressure, HTN or HPN , is a

medical condition in which the blood pressure is chronically elevated. In current usage, the word "hypertension" without a qualifier normally refers to systemic, arterial hypertension.[1] Hypertension can be classified as either essential (primary) or secondary . Essential hypertension indicates that no specific medical cause can be found to explain a patient's condition. About 95% of hypertension is essential hypertension. Secondary hypertension indicates that the high blood pressure is a result of (i.e., secondary to) another condition, such as kidney disease or tumours (adrenal adenoma or pheochromocytoma). Persistent hypertension is one of the risk factors for strokes, heart attacks, heart failure and arterial aneurysm, and is a leading cause of chronic renal failure.
Distinguishing primary vs. secondary hypertension

Once the diagnosis of hypertension has been made it is important to attempt to exclude or identify reversible (secondary) causes.

Over 91% of adult hypertension has no clear cause and is therefore called essential/primary hypertension . Often, it is part of the metabolic "syndrome X" in patients with insulin resistance: it occurs in combination with diabetes mellitus (type 2), combined hyperlipidemia and central obesity. Secondary hypertension is more common in preadolescent children, with most cases caused by renal disease. Primary or essential hypertension is more common in adolescents and has multiple risk factors, including obesity and a family history of hypertension.

19. Ischemic heart disease - macroscopic description Ischemic or ischemic heart disease (IHD), or myocardial ischemia , is a disease characterized by reduced blood supply to the heart muscle, usually due to coronary artery disease (atherosclerosis of the coronary arteries). Its risk increases with age, smoking, hypercholesterolemia (high cholesterol levels), diabetes, hypertension (high blood pressure) and is more common in men and those who have close relatives with ischemic heart disease. Ischemic heart disease may present with any of the following problems:

Angina pectoris Acute chest pain: acute coronary syndrome, unstable angina or myocardial infarction . Heart failure

20. Infarction of heart - complications The disease process underlying most ischemic heart disease is atherosclerosis of the coronary arteries. The arteries become "furred up" by fat-rich deposits in the vessel wall (plaques). Stable angina is due to inability to supply the myocardium (heart muscle) with sufficient blood in situations of increased demand for oxygen, such as exertion. Unstable angina, are attributed to "plaque rupture", where one of the plaques gets weakened, develops a tear, and forms an adherent blood clot that either obstructs blood flow or floats further down the blood vessel, causing obstruction there. 21. Atherosclerosis - complications

Atherosclerosis is a syndrome affecting arterial blood vessels. It is a chronic

inflammatory response in the walls of arteries, in large part due to the accumulation of macrophage white blood cells and promoted by low density (especially small particle) lipoproteins (plasma proteins that carry cholesterol and triglycerides) without adequate removal of fats and cholesterol from the macrophages by functional high density lipoproteins (HDL). It is commonly referred to as a hardening or furring of the arteries. It is caused by the formation of multiple plaques within the arteries.
Physiologic factors that increase risk

These can be divided into various categories: congenital vs. acquired, modifiable or not, classical or non-classical. Factors add to each other multiplicatively, with two factors increasing the risk of atherosclerosis fourfold. Hyperlipidemia, hypertension and cigarette smoking together increase the risk seven times.
Modifiable

Having diabetes or Impaired glucose tolerance (IGT) + Dyslipoproteinemia (unhealthy patterns of serum proteins carrying fats & cholesterol): + o High serum concentration of low-density lipoprotein and / or very low density lipoprotein o Low serum concentration of functioning high density lipoprotein o An LDL:HDL ratio greater than 3:1 Tobacco smoking , increases risk by 200% after several pack years Having high blood pressure +, on its own increasing risk by 60% Elevated serum C-reactive protein concentrations

Nonmodifiable

Advanced age Male sex Having close relatives who have had some complication of atherosclerosis (eg. coronary heart disease or stroke) Genetic abnormalities, e.g. familial hypercholesterolemia

Lesser or uncertain

The following factors are of relatively lesser importance, are uncertain or nonquantitated:

Being obese (in particular central obesity, also referred to as abdominal or male-type obesity) + A sedentary lifestyle Postmenopausal estrogen deficiency High carbohydrate intake Intake of trans fat Elevated serum levels of triglycerides +

22. Chronic venostasis -changes of liver - macroscopic description Venostasis is a condition of slow blood supply, usually to the limbs. A patient with venous stasis might be more vulnerable to the formation of blood clots due to long periods of immobility such as when driving for long distances. If you sit for long periods of time in one place, it is safe to say you may develop venostasis in your feet. I hope this helps you understand. Venostasis can predispose you to getting blood clots with more frequency than those that do not experience venostasis. That is why it is recommended when traveling over long distances, you need to get up and walk a little to get circulation stimulated in the legs. 23. Chronic venostasis -changes of lung - macroscopic description Venous stasis , or venostasis , is a condition of slow blood supply, usually to the limbs. A patient with venous stasis might be more vulnerable to the formation of blood clots due to long periods of immobility such as when driving for long distances.

24. Oedema - macroscopic description

Oedema is an abnormal accumulation of fluid beneath the skin, or in one or more

cavities of the body. Generally, the amount of interstitial fluid is determined by the balance of fluid homeostasis, and increased secretion of fluid into the interstitium or impaired removal of this fluid may cause oedema. Five factors can contribute to the formation of edema. It may be facilitated by increased hydrostatic pressure or reduced oncotic pressure within blood vessels, increased blood vessel wall permeability as in inflammation, obstruction of fluid clearance via the lymphatic or changes in the water retaining properties of the tissues themselves. Raised hydrostatic pressure often reflects retention of water and sodium by the kidney.

25. Cirrhosis hepatis - macroscopic description

Cirrhosis is a consequence of chronic liver disease characterized by replacement

of liver tissue by fibrous scar tissue as well as regenerative nodules (lumps that occur as a result of a process in which damaged tissue is regenerated), leading to progressive loss of liver function. Cirrhosis is most commonly caused by alcoholism, hepatitis B and C and fatty liver disease but has many other possible causes. Some cases are idiopathic, i.e., of unknown cause. Ascites (fluid retention in the abdominal cavity) is the most common complication of cirrhosis and is associated with a poor quality of life, increased risk of infection, and a poor long-term outcome. Other potentially life-threatening complications are hepatic encephalopathy (confusion and coma) and bleeding from esophageal varices. Cirrhosis is generally irreversible once it occurs, and treatment generally focuses on preventing progression and complications. In advanced stages of cirrhosis the only option is a liver transplant. Macroscopically, the liver may be initially enlarged, but with progression of the disease, it becomes smaller. Its surface is irregular, the consistency is firm and the color is often yellow (if associates steatosis). Depending on the size of the nodules there are three macroscopic types: micro nodular, macro nodular and mixed cirrhosis. In micro nodular form (Laennec's cirrhosis or portal cirrhosis) regenerating nodules are less than 3 mm. In macro nodular cirrhosis (postnecrotic cirrhosis), the nodules are larger than 3 mm. The mixed cirrhosis consists in a variety of nodules with different sizes. However, cirrhosis is defined by its pathological features on microscopy: (1) the presence of regenerating nodules of hepatocytes and (2) the presence of fibrosis, or the deposition of connective tissue between these nodules. The pattern of fibrosis seen can depend upon the underlying insult that led to cirrhosis; fibrosis can also proliferate even if the underlying process that caused it has resolved or ceased. The fibrosis in cirrhosis can lead to destruction of other normal tissues in the liver: including the sinusoids, the space of Disse, and other vascular structures, which leads to altered resistance to blood flow in the liver and portal hypertension. As cirrhosis can be caused by many different entities which injure the liver in different ways, different cause-specific patterns of cirrhosis, and other causespecific abnormalities can be seen in cirrhosis. For example, in chronic hepatitis B, there is infiltration of the liver parenchyma with lymphocytes; in cardiac cirrhosis there are erythrocytes and a greater amount of fibrosis in the tissue surrounding the hepatic veins; in primary biliary cirrhosis, there is fibrosis around the bile duct, the presence of granulomas and pooling of bile; and in alcoholic cirrhosis, there is infiltration of the liver with neutrophils.

26. Steatosis hepatis - macroscopic description

Steatosis (also called fatty change, fatty degeneration or adipose degeneration) is

the process describing the abnormal retention of lipids within a cell. It reflects an impairment of the normal processes of synthesis and elimination of triglyceride fat. Excess lipid accumulates in vesicles that displace the cytoplasm. The risk factors associated with steatosis are varied, and include diabetes mellitus, protein malnutrition, hypertension cell toxins, obesity, and anoxia. As the liver is the primary organ of lipid metabolism it is most often associated with steatosis. Despite having multiple causes, fatty liver can be considered a single disease that occurs worldwide in those with excessive alcohol intake and those who are obese (with or without effects of insulin resistance). Fatty change is most commonly seen in the liver and the heart. Mild fatty change in the liver may not affect the gross appearance. With increasing accumulation, the organ enlarges and becomes progressively yellow until, in extreme cases, it may weigh 3 to 6 kg(1.5 3 times normal weight) and appear bright yellow, soft, and greasy.

27. Cholecystitis chronica - macroscopic description Cholecystitis is inflammation of the gall bladder. It may be acute, chronic, or acute superimposed on chronic, and almost always occurs in association with gallstones. Cholecystitis is often caused by cholelithiasis (the presence of choleliths, or gallstones, in the gallbladder), with choleliths most commonly blocking the cystic duct directly. This leads to inspissation (thickening) of bile, bile stasis, and secondary infection by gut organisms, predominantly E. coli and Bacteroides species. The gallbladder's wall becomes inflamed. Extreme cases may result in necrosis and rupture. Inflammation often spreads to its outer covering, thus irritating surrounding structures such as the diaphragm and bowel. Less commonly, in debilitated and trauma patients, the gallbladder may become inflamed and infected in the absence of cholelithiasis, and is known as acute acalculous cholecystitis. Stones in the gallbladder may cause obstruction and the accompanying acute attack. The patient might develop a chronic, low-level inflammation which leads to a chronic cholecystitis, where the gallbladder is fibrotic and calcified.

28. Icterus - macroscopic description

Jaundice , also known as icterus , is a yellowish discoloration of the skin, the

conjunctival membranes over the sclerae (whites of the eyes), and other mucous membranes caused by hyperbilirubinemia (increased levels of bilirubin in the blood). This hyperbilirubinemia subsequently causes increased levels of bilirubin in the extracellular fluids. Typically, the concentration of bilirubin in the plasma must exceed 1.5 mg/dL, three times the usual value of approximately 0.5mg/dL, for the coloration to be easily visible. One of the first tissues to change color as bilirubin levels rise in jaundice is the conjunctiva of the eye, a condition sometimes referred to as scleral icterus. However, the sclera themselves are not "icteric" (stained with bile pigment) but rather the conjunctival membranes that overlie them. The yellowing of the "white of the eye" is thus more properly conjunctival icterus.

Pre-hepatic: The pathology is occurring prior the liver. Hepatic: The pathology is located within the liver. Post-Hepatic: The pathology is located after the conjugation of bilirubin in the liver.

Pre-hepatic jaundice is caused by anything which causes an increased rate of

hemolysis (breakdown of red blood cells). In tropical countries, malaria can cause jaundice in this manner. Certain genetic diseases, such as sickle cell anemia, spherocytosis and glucose 6-phosphate dehydrogenase deficiency can lead to increased red cell lysis and therefore hemolytic jaundice. Commonly, diseases of the kidney, such as hemolytic uremic syndrome, can also lead to coloration. Defects in bilirubin metabolism also present as jaundice. Jaundice usually comes with high fevers.
Laboratory findings include:

Urine: no bilirubin present, urobilirubin > 2 units (except in infants where gut flora has not developed). Serum: increased unconjugated bilirubin.

Hepatic jaundice causes include acute hepatitis, hepatotoxicity and alcoholic liver

disease, whereby cell necrosis reduces the liver's ability to metabolise and excrete bilirubin leading to a buildup in the blood. Less common causes include primary biliary cirrhosis, Gilbert's syndrome (a genetic disorder of bilirubin metabolism which can result in mild jaundice, which is found in about 5% of the population), Crigler-Najjar syndrome, metastatic carcinoma and Niemann-Pick disease, type C. Jaundice seen in the newborn, known as neonatal jaundice, is common, occurring

in almost every newborn as hepatic machinery for the conjugation and excretion of bilirubin does not fully mature until approximately two weeks of age. Laboratory findings include:

Urine: Conjugated bilirubin present, urobilirubin > 2 units but variable (except in children).

Post-hepatic jaundice, also called obstructive jaundice, is caused by an

interruption to the drainage of bile in the biliary system. The most common causes are gallstones in the common bile duct, and pancreatic cancer in the head of the pancreas. Also, a group of parasites known as "liver flukes" live in the common bile duct, causing obstructive jaundice. Other causes include strictures of the common bile duct, biliary atresia, ductal carcinoma, pancreatitis and pancreatic pseudocysts. A rare cause of obstructive jaundice is Mirizzi's syndrome. The presence of pale stools and dark urine suggests an obstructive or post-hepatic cause as normal feces get their color from bile pigments. Patients also can present with elevated serum cholesterol, and often complain of severe itching.

29. Pancreatitis acuta haemmorhagica - macroscopic description Pancreatitis is the inflammation of the pancreas. Acute pancreatitis is a sudden inflammation of the pancreas. Depending on its severity, it can have severe complications and high mortality despite treatment. The acute pancreatitis (acute hemorrhagic pancreatic necrosis) is characterized by acute inflammation and necrosis of pancreas parenchyma, focal enzymic necrosis of pancreatic fat and vessels necrosis - hemorrhage. These are produced by intrapancreatic activation of pancreatic enzymes. Lipase activation produces the necrosis of fat tissue in pancreatic interstitium and peripancreatic spaces. Necrotic fat cells appear as shadows, contours of cells, lacking the nucleus, pink, finely granular cytoplasm. It is possible to find calcium precipitates (hematoxylinophilic). Digestion of vascular walls results in thrombosis and hemorrhage. Inflammatory infiltrate is rich in neutrophils. Macroscopically, the pancreas exhibits red-black hemorrhage interspersed with foci of yellow white, chalky fat necrosis. Fat necrosis can also occur in extra-pancreatic fat, including the omentum and bowel mesentery, and even outside the abdominal cavity ( e.g Subcutaneous fat). In most cases the peritoneum contains a serous,

slightly turbid, brown-tinged fluid with globules of fat. In the most severe form, hemorrhagic pancreatitis, extensive parenchymal necrosis is accompanied by diffuse hemorrhage. 30. Thrombosis - macroscopic description Thrombosis is the formation of a blood clot (thrombus) inside a blood vessel, obstructing the flow of blood through the circulatory system. When a blood vessel is injured, the body uses platelets and fibrin to form a blood clot, because the first step in repairing it (hemostasis) is to prevent loss of blood. If that mechanism causes too much clotting, and the clot breaks free, an embolus is formed. In classical terms, thrombosis is caused by abnormalities in one or more of the following (Virchow's triad):

The composition of the blood (hypercoagulability) Quality of the vessel wall (endothelial cell injury) Nature of the blood flow

There are 2 types of thrombosis: Venous and Arterial Thrombosis.

Venous thrombosis

Venous thrombosis is the formation of a thrombus (blood clot) within a vein. There are several diseases which can be classified under this category:
Deep vein thrombosis

Deep vein thrombosis (DVT) is the formation of a blood clot within a deep vein. It most commonly affects leg veins, such as the femoral vein. Three factors are important in the formation of a blood clot within a deep veinthese are the rate of blood flow, the thickness of the blood and qualities of the vessel wall. Classical signs of DVT include swelling, pain and redness of the affected area.
Portal vein thrombosis

Portal vein thrombosis is a form of venous thrombosis affecting the hepatic portal vein, which can lead to portal hypertension and reduction of the blood supply to the liver. It usually has a pathological cause such as pancreatitis, cirrhosis, diverticulitis or cholangiocarcinoma.
Renal vein thrombosis

Renal vein thrombosis is the obstruction of the renal vein by a thrombus. This tends to lead to reduced drainage from the kidney. Anticoagulation therapy is the treatment of choice.

Jugular Vein Thrombosis

Jugular Vein Thrombosis is a condition that may occur due to infection, intravenous drug use or malignancy. Jugular Vein Thrombosis can have a varying list of complications, including: systemic sepsis, pulmonary embolism, and papilledema. Characterized by a sharp pain at the site of the vein, it's difficult to diagnose, because it can occur at random.
Budd - Chiari syndrome

Budd-Chiari syndrome is the blockage of the hepatic vein or the inferior vena cava. This form of thrombosis presents with abdominal pain, ascites and hepatomegaly. Treatment varies between drug therapy and surgical intervention by the use of shunts.
Paget - Schroetter disease

Paget-Schroetter disease is the obstruction of an upper extremity vein (such as the axillary vein or subclavian vein) by a thrombus. The condition usually comes to light after vigorous exercise and usually presents in younger, otherwise healthy people. Men are affected more than women.
Cerebral venous sinus thrombosis

Cerebral venous sinus thrombosis (CVST) is a rare form of stroke which results from the blockage of the dural venous sinuses by a thrombus. Symptoms may include headache, abnormal vision, any of the symptoms of stroke such as weakness of the face and limbs on one side of the body and seizures. The diagnosis is usually made with a CT or MRI scan. The majority of persons affected make a full recovery. The mortality rate is 4.3%.
Arterial thrombosis

Arterial thrombosis is the formation of a thrombus within an artery. In most cases, arterial thrombosis follows rupture of atheroma, and is therefore referred to as atherothrombosis. There are two diseases which can be classified under this category:
Stroke

A stroke is the rapid decline of brain function due to a disturbance in the supply of blood to the brain. This can be due to ischemia, thrombus, embolus (a lodged particle) or hemorrhage (a bleed). In thrombotic stroke, a thrombus (blood clot) usually forms around atherosclerotic plaques. Since blockage of the artery is gradual, onset of symptomatic thrombotic strokes is slower. Thrombotic stroke can

be divided into two categorieslarge vessel disease and small vessel disease. The former affects vessels such as the internal carotids, vertebral and the circle of Willis. The latter can affect smaller vessels such as the branches of the circle of Willis.
Myocardial infarction

Myocardial infarction (MI) is caused by an infarct (death of tissue due to ischemia), often due to the obstruction of the coronary artery by a thrombus. MI can quickly become fatal if emergency medical treatment is not received promptly. If diagnosed within 12 hours of the initial episode (attack) then thrombolytic therapy is initiated.

31. Embolism - macroscopic description An embolism occurs when an object migrates from one part of the body (through circulation) and causes a blockage (occlusion) of a blood vessel in another part of the body. This is in contrast with a thrombus, or clot, which forms at the blockage point within a blood vessel and is not carried from somewhere else. There are different types of emboli.
Material

They can be classified based on the embolic material:

Thromboembolism embolism of thrombus or blood clot.

Cholesterol embolism - embolism of cholesterol, often from atherosclerotic plaque inside a vessel. Fat embolism embolism of fat droplets. Air embolism (also known as a gas embolism) embolism of air bubbles. Septic embolism embolism of pus-containing bacteria. Tissue embolism embolism of small fragments of tissue. Foreign body embolism embolism of foreign materials such as talc and other small objects. Amniotic fluid embolism embolism of amniotic fluid, foetal cells, hair, or other debris that enters the mother's bloodstream via the placental bed of the uterus and triggers an allergic reaction.

In thromboembolism , the thrombus (blood clot) from a blood vessel is completely or partially detached from the site of thrombosis (clot). The blood flow will then carry the embolus (via blood vessels) to various parts of the body where it can block the lumen (vessel cavity) and cause vessel obstruction or occlusion. Note that the free-moving thrombus is called an embolus. A thrombus is always

attached to the vessel wall and is never freely moving in the blood circulation. This is also the key difference for pathologists to determine the cause of a blood clot, either by thrombosis or by post-mortem blood clot. Vessel obstruction will then lead to different pathological issues such as blood stasis and ischemia. However, not only thromboembolism will cause the obstruction of blood flow in vessels, but also any kind of embolism is capable of causing the same problem.
Fat embolism usually occurs when endogenous (from sources within the

organism) fat tissue escapes into the blood circulation. The usual cause of fat embolism is therefore the fracture of tubular bones (such as the femur), which will lead to the leakage of fat tissue within the bone marrow into ruptured vessels. There are also exogenous (from sources of external origin) causes such as intravenous injection of emulsions. An air embolism , on the other hand, is usually always caused by exogenic factors. This can be the rupture of alveoli, and inhaled air can be leaked into the blood vessels. Other more-common causes include the puncture of the subclavian vein by accident or during operation where there is negative pressure. Air is then sucked into the veins by the negative pressure caused by thoracic expansion during the inhalation phase of respiration. Air embolism can also happen during intravenous therapy, when air is leaked into the system (however this iatrogenic error in modern medicine is extremely rare). 32. Peritonitis - macroscopic description Peritonitis is defined as inflammation of the peritoneum (the serous membrane which lines part of the abdominal cavity and some of the viscera it contains). It may be localised or generalised, generally has an acute course, and may depend on either infection (often due to rupture of a hollow organ as may occur in abdominal trauma) or on a non-infectious process. The peritoneum normally appears greyish and glistening; it becomes dull 24 hours after the onset of peritonitis, initially with scarce serous or slightly turbid fluid. Later on, the exudate becomes creamy and evidently suppurative; in dehydrated patients, it also becomes very inspissated. The quantity of accumulated exudate varies widely. It may be spread to the whole peritoneum, or be walled off by the omentum and viscera. Inflammation features infiltration by neutrophils with fibrino-purulent exudation. 33. Ileus - macroscopic description Ileus is a disruption of the normal propulsive gastrointestinal motor activity from non-mechanical mechanisms. Motility disorders that result from structural abnormalities are termed mechanical bowel obstruction. Some mechanical

obstructions are misnomers, such as gallstone ileus and meconium ileus, and are not true examples of ileus by the classic definition. 34. Pyelonephritis acuta - macroscopic description Pyelonephritis is an ascending urinary tract infection that has reached the pyelum (pelvis) of the kidney. If the infection is severe, the term "urosepsis " is used interchangeably (sepsis being a systemic inflammatory response syndrome due to infection). It requires antibiotics as therapy, and treatment of any underlying causes to prevent recurrence. It is a form of nephritis. It can also be called pyelitis. It presents with dysuria (painful voiding of urine), abdominal pain (radiating to the back on the affected side) and tenderness of the bladder area and the side of the involved kidney ("renal angle tenderness") which may be elicited by performing the kidney punch. In many cases there are systemic symptoms in the form of fever, rigors (violent shivering while the temperature rises), headache and vomiting. In severe cases, delirium may be present. Acute pyelonephritis is an exudative purulent localized inflammation of the renal pelvis (collecting system) and kidney. The renal parenchyma presents in the interstitium abscesses (suppurative necrosis), consisting in purulent exudate (pus): neutrophils, fibrin, cell debris and central germ colonies (hematoxylinophils). Tubules are damaged by exudate and may contain neutrophil casts. In the early stages, glomeruli and vessels are normal. Gross pathology often reveals pathognomonic radiations of hemorrhage and suppuration through the renal pelvis to the renal cortex. Chronic infections can result in fibrosis and scarring. 35. Pyelonephritis chronica - macroscopic description Pyelonephritis is an ascending urinary tract infection that has reached the pyelum (pelvis) of the kidney (nephros in Greek). If the infection is severe, the term "urosepsis" is used interchangeably (sepsis being a systemic inflammatory response syndrome due to infection). It requires antibiotics as therapy, and treatment of any underlying causes to prevent recurrence. It is a form of nephritis. It can also be called pyelitis. Acute pyelonephritis is an exudative purulent localized inflammation of the renal pelvis (collecting system) and kidney. The renal parenchyma presents in the interstitium abscesses (suppurative necrosis), consisting in purulent exudate (pus): neutrophils, fibrin, cell debris and central germ colonies (hematoxylinophils). Tubules are damaged by exudate and may contain neutrophil casts. In the early stages, glomeruli and vessels are normal. Gross pathology often reveals pathognomonic radiations of hemorrhage and suppuration through the renal pelvis to the renal cortex. Chronic infections can result in fibrosis and scarring.

36. Urolithiasis - macroscopic description

Urolithiasis is the condition where urinary calculi are formed at any level in the

urinary collecting system, but most often the calculi arise in the kidney. They occur frequently, as is evidenced by the finding of stones in about 1% of all autopsies. The term kidney stone (or "renal calculus") is sometimes used to refer to urolithiasis in any part of the urinary tract. However, the term "kidney stone" is more properly reserved for stones that are actually in the collecting duct of the kidney itself. The term nephrolithiasis can be used to describe the condition of having kidney stones, ureterolithiasis can be used to describe the condition of having stones in the ureter. Obstruction of the ureter by the kidney stones causes a renal colic attack which is why intense pain is felt in groin and back. The term bladder stone is more frequently associated with veterinary science. 37. Tumors of the kidney - macroscopic description Kidney cancer is any cancer that originates in a kidney. The two most common types of kidney cancer, reflecting their location within the kidney, are renal cell carcinoma and renal pelvis carcinoma.
Renal cell carcinoma (RCC) is a kidney cancer that originates in the lining of the

proximal renal tubule, the very small tubes in the kidney that filter the blood and remove waste products. RCC is the most common type of kidney cancer, and the most common type in adults, responsible for approximately 80% of cases. Macroscopic examination shows a yellowish, multilobulated tumor in the renal cortex, which frequently contains zones of necrosis, hemorrhage and scarring. Light microscopy shows tumor cells forming cords, papillae, tubules or nests, and are atypical, polygonal and large. Because these cells accumulate glycogen and lipids, their cytoplasm appear "clear", lipid-laden, the nuclei remain in the middle of the cells, and the cellular membrane is evident. Some cells may be smaller, with eosinophilic cytoplasm, resembling normal tubular cells. The stroma is reduced, but well vascularized. The tumor compresses the surrounding parenchyma, producing a pseudocapsule.

Secretion of vasoactive substances (e.g. renin) may cause arterial hypertension, and release of erythropoietin may cause erythrocytosis (increased production of red blood cells). 38. Hyperplasia of the prostate - macroscopic description Hyperplasia (or "hypergenesis") is a general term referring to the proliferation of cells within an organ or tissue beyond that which is ordinarily seen (e.g. constantly dividing cells). Hyperplasia may result in the gross enlargement of an organ, the formation of a benign tumor. Hyperplasia is different from hypertrophy that the adaptive cell change in hypertrophy is by increased cellular size only unlike in hyperplasia by increased cellular number. Benign prostatic hyperplasia (BPH) occurs in older men; the prostate often enlarges to the point where urination becomes difficult. Benign prostatic hyperplasia (BPH) refers to the increase in size of the prostate in middle-aged and elderly men. It is characterized by hyperplasia of prostatic stromal and epithelial cells, resulting in the formation of large, fairly discrete nodules in the periurethral region of the prostate. When sufficiently large, the nodules compress the urethral canal to cause partial, or sometimes virtually complete, obstruction of the urethra, which interferes the normal flow of urine. It leads to symptoms of urinary hesitancy, frequent urination, dysuria (painful urination), increased risk of urinary tract infections and urinary retention. Although prostate specific antigen levels may be elevated in these patients because of increased organ volume and inflammation due to urinary tract infections, BPH is not considered to be a premalignant lesion... The affected prostate is enlarged, with weights in excess of 300gm reported in severe cases. The cut surface contains many fairly well-circumscribed nodules that bulge from the cut surface. This nodularity may be present throughout the prostate, but it is usually most pronounced in the inner region. The nodules may have a solid appearance or may contain cystic spaces, the latter corresponding to dilated glandular elements seen in histologic section. 39. Myoma uteri - macroscopic description

40. Acute myeloic leukemia - macroscopic description

Acute myeloid leukemia (AML ), is a cancer of the myeloid line of cells,

characterized by the rapid proliferation of abnormal cells which accumulate in the

bone marrow and interfere with the production of normal blood cells. AML is the most common acute leukemia affecting adults, and its incidence increases with age. Although AML is a relatively rare disease. The symptoms of AML are caused by replacement of normal bone marrow with leukemic cells, resulting in a drop in red blood cells, platelets, and normal white blood cells. These symptoms include fatigue, shortness of breath, easy bruising and bleeding, and increased risk of infection. Although several risk factors for AML have been identified, the specific cause of AML remains unclear. Acute myeloid leukemia is a potentially curable disease; but only a minority of patients are cured with current therapy. AML is treated initially with chemotherapy aimed at inducing a remission. Distinctive red-staining rod-like structures (Auer rods) may be present in myeloblasts or more differentiated cells. 41. Acute lymphatic leukemia - macroscopic description
Acute lymphoblastic leukemia (ALL), is a form of leukemia, or cancer of the

white blood cells characterized by excess lymphoblasts. Malignant, immature white blood cells continuously multiply and are overproduced in the bone marrow. ALL causes damage and death by crowding out normal cells in the bone marrow, and by spreading (metastasizing) to other organs. ALL is most common in childhood with a peak incidence at 4-5 years of age, and another peak in old age. The overall cure rate in children is 85%, and about 50% of adults have long-term disease-free survival. 'Acute' refers to the undifferentiated, immature state of the circulating lymphocytes ("blasts"), and to the rapid progression of disease, which can be fatal in weeks to months if left untreated.

42. Chronic myeloic leukemia - macroscopic description Chronic myelogenous (or myeloid) leukemia (CML), is a form of leukemia characterized by the increased and unregulated growth of predominantly myeloid cells in the bone marrow and the accumulation of these cells in the blood. CML is a clonal bone marrow stem cell disorder in which proliferation of mature granulocytes (neutrophils, eosinophils, and basophils) and their precursors is the main finding. It is a type of myeloproliferative disease associated with a characteristic chromosomal translocation called the Philadelphia chromosome. The bone marrow is hypercellular as a result of a hyperplasia of granulocytics and megakaryocytic precursors. Myeloblasts are usually only slightly increased, and there is frequently an increase in the number of phagocytes. The red pulp of the

enlarged spleen has an appearance that resembles bone marrow because of the extensive extramedullary hematopoiesis. This mass of cell affects the local blood supply, leading to splenic infarcts. 43. Chronic lymphatic leukemia - macroscopic description B-cell chronic lymphocytic leukemia (also known as "chronic lymphoid leukemia " or "CLL "), is a type of leukemia, or cancer of the white blood cells (lymphocytes). CLL affects a particular lymphocyte, the B cell, which originates in the bone marrow, develops in the lymph nodes, and normally fights infection. In CLL, the DNA of a B cell is damaged, so that it can't fight infection, but it grows out of control and crowds out the healthy blood cells that can fight infection. CLL is an abnormal neoplastic proliferation of B cells. The cells accumulate mainly in the bone marrow and blood. Although not originally appreciated, CLL is now felt to be identical to a disease called small lymphocytic lymphoma (SLL), a type of non-Hodgkin's lymphoma which presents primarily in the lymph nodes. CLL is a disease of adults. Most (>75%) people newly diagnosed with CLL are over the age 50, and the majority are men. Most people are diagnosed without symptoms as the result of a routine blood test that returns a high white blood cell count, but as it advances CLL results in swollen lymph nodes, spleen, and liver, and eventually anemia and infections. Early CLL is not treated, and late CLL is treated with chemotherapy and monoclonal antibodies. In CLL, sheets of small round lymphocytes and scattered ill-defined foci of larger, actively dividing cells diffusely efface involved lymph nodes. The predominant cells are compact, small, resting lymphocytes with dark-staining round nuclei, scanty cytoplasm, and little variation in size.

44. Ulcus ventriculi - macroscopic description A peptic ulcer or Ulcus venticuli , is an ulcer (defined as mucosal erosions equal to or greater than 0.5 cm) of an area of the gastrointestinal tract that is usually acidic and thus extremely painful. As many as 80% of ulcers are associated with Helicobacter pylori, a spiral-shaped bacterium that lives in the acidic environment of the stomach.Ulcers can also be caused or worsened by drugs such as aspirin and other NSAIDs. All peptic ulcers, whether gastric or duodenal, have an identical gross and microscopic appearance. By definition, they are defects in the mucosa that

penetrate at least into the submucosa, and often into the muscularis propria or deeper. Most are round, sharply punched-out craters 2 to 4 cm in diameter. Contrary to general belief, more peptic ulcers arise in the duodenum (first part of the small intestine, just after the stomach) than in the stomach. About 4% of stomach ulcers are caused by a malignant tumor, so multiple biopsies are needed to exclude cancer. Duodenal ulcers are generally benign. A peptic ulcer may arise at various locations:

Stomach (called gastric ulcer ) Duodenum (called duodenal ulcer ) Oesophagus (called Oesophageal ulcer ) Meckel's Diverticulum (called Meckel's Diverticulum ulcer )

Types of peptic ulcers:

Type I: Ulcer along the lesser curve of stomach Type II: Two ulcers present - one gastric, one duodenal Type III: Prepyloric ulcer Type IV: Proximal gastroesophageal ulcer Type V: Anywhere along gastric body, NSAID induced

Gastric ulcers are most often localized on the lesser curvature of the stomach. The ulcer is a round to oval parietal defect ("hole"), 2 to 4 cm diameter, with a smooth base and perpendicular borders. These borders are not elevated or irregular in the acute form of peptic ulcer, regular but with elevated borders and inflammatory surrounding in the chronic form. In the ulcerative form of gastric cancer the borders are irregular. Surrounding mucosa may present radial folds, as a consequence of the parietal scarring.
Gastrointestinal bleeding is the most common complication. Sudden large

bleeding can be life-threatening. It occurs when the ulcer erodes one of the blood vessels. Perforation (a hole in the wall) often leads to catastrophic consequences. Erosion of the gastro-intestinal wall by the ulcer leads to spillage of stomach or intestinal content into the abdominal cavity. Perforation at the anterior surface of the stomach leads to acute peritonitis, initially chemical and later bacterial peritonitis. The first sign is often sudden intense abdominal pain. Posterior wall perforation leads to pancreatitis; pain in this situation often radiates to the back. Penetration is when the ulcer continues into adjacent organs such as the liver and pancreas.

Scarring and swelling due to ulcers causes narrowing in the duodenum and gastric outlet obstruction . Patient often presents with severe vomiting. Pyloric stenosis

45. Ulcus duodemi - macroscopic description All peptic ulcers, whether gastric or duodenal, have an identical gross and microscopic appearance. By definition, they are defects in the mucosa that penetrate at least into the submucosa, and often into the muscularis propria or deeper. Most are round, sharply punched-out craters 2 to 4 cm in diameter; those in the duodenum tend to be smalle, and occasional gastric lesions are significantly larger. Favoured sites are the anterior and posterior walls of the first portion of the duodenum and the lesser curvature of the stomach. See Question 44 for more info. 46. Tumors of the bowel - macroscopic description Bowel Tumor or Colorectal cancer , also called colon cancer or large bowel cancer , includes cancerous growths in the colon, rectum and appendix. With 655,000 deaths worldwide per year, it is the third most common form of cancer and the second leading cause of cancer-related death in the Western world. Many colorectal cancers are thought to arise from adenomatous polyps in the colon. These mushroom-like growths are usually benign, but some may develop into cancer over time. The pathology of the tumor is usually reported from the analysis of tissue taken from a biopsy. The most common colon cancer cell type is adenocarcinoma. Other, rarer types include lymphoma and squamous cell carcinoma. Cancer on the right side (ascending colon and cecum) tends to be exophytic, that is, the tumour grows outwards from one location in the bowel wall. This very rarely causes obstruction of feces, and presents with symptoms such as anemia. Left-sided tumours tend to be circumferential, and can obstruct the bowel much like a napkin ring. Adenocarcinoma is a malignant epithelial tumor, originating from glandular epithelium of the colorectal mucosa. It invades the wall, infiltrating the muscularis mucosae, the submucosa and thence the muscularis propria. Tumor cells describe irregular tubular structures, harboring pluristratification, multiple lumens, reduced stroma ("back to back" aspect). Sometimes, tumor cells are discohesive and

secrete mucus, which invades the interstitium producing large pools of mucus/colloid (optically "empty" spaces) - mucinous (colloid) adenocarcinoma, poorly differentiated. If the mucus remains inside the tumor cell, it pushes the nucleus at the periphery - "signet-ring cell." Depending on glandular architecture, cellular pleomorphism, and mucosecretion of the predominant pattern, adenocarcinoma may present three degrees of differentiation: well, moderately, and poorly differentiated. 47. Tumors of the stomach - macroscopic description Stomach or gastric cancer can develop in any part of the stomach and may spread throughout the stomach and to other organs; particularly the esophagus, lungs and the liver. The macroscopic appearance of advanced cancer is of great importance in distinguishing carcinomas from benign lesions and assessing the degree of spread. Advanced gastric cancers are divided into 3 major macroscopic types: - Polypoid (fungating) adenocarcinoma accounts for 1/3 of advanced cancers. The tumor is a solid mass, often several cm in diameter, that projects into the stomach lumen. The surface may be party ulcerated, and deeper tissues may or may not be infiltrated. - Ulcerating adenocarcinoma comprises another 1/3 of gastric cancers. The have shallow ulcers of variable size. Surrounding tissues are firm, raised and nodular. Characteristically, the lateral margins of the ulcers are irregular and the base is ragged. This appearance stands in contrast to that of the usual benign peptide ulcer, which exhibits punched out margins and a smooth base. - Diffuse or infiltrating adenocarcinoma accounts for 1/10 of all stomach cancers. No true tumor mass is seen; instead, the wall of the stomach is thickened and firm. If the entire stomach is involved, it is called Linitis plastica. In the diffuse type of gastric carcinoma, invading tumor cells induce extensive fibrosis in the submucosa and muscularis. Thus, the wall is stiff and may be more than 2 cm thick. 48. Tumors of the pancreas - macroscopic description
Pancreatic cancer is a malignant neoplasm of the pancreas. About 95% of

exocrine pancreatic cancers are adenocarcinomas. The remaining 5% include adenosquamous carcinomas, squamous cell carcinomas, and giant cell carcinomas. Exocrine pancreatic cancers are far more common than endocrine pancreatic cancers (islet cell carcinomas). Approximately 60% of pancreatic cancers arise in the head of the gland, 15% in the body, and 5% in the tail; in 20%, the neoplasm diffusely involves the entire organ. Carcinomas of the pancreas are usually hard, stellate, gray-white, poorly defined masses. The vast majority of carcinomas are ductal adenocarcinomas

recapitulating to some degree and the normal duct epithelium by forming glands and secreting mucin. Two features are characteristic of pancreatic cancer; it is highly invasive, and it elicits an intense non-neoplastic host reaction composed of fibroblasts, lymphocytes, and extracellulr matrix. Most carcinomas of the head of the pancreas obstruct the distal common bile duct as it courses through the head of the pancreas. In 50% of such cases, there is marked distention of the biliary tree, and patients typically exhibit jaundice. Pancreatic cancers often extend through the retroperitoneal space, entrapping adjacent nerves, and occasionally invade the spleen, adrenals, vertebral column, transverse colon, and stomach. Peripancreatic, gastric, mesenteric, omental, and portahepatic lymph nodes are frequently involved, and the liver is often enlarged because of metastatic deposits. Distant metastases occur, principally to the lungs and bones. 49. Metastasis - macroscopic description
Metastasis (Greek: displacement, =next + =placement, plural: metastases), or Metastatic disease , is the spread of a disease from one organ or

part to another non-adjacent organ or part. Only malignant tumor cells and infections have the established capacity to metastasize ;

Cancer cells can "break away", "leak", or "spill" from a primary tumor, enter lymphatic and blood vessels, circulate through the bloodstream, and settle down to grow within normal tissues elsewhere in the body. Metastasis is one of three hallmarks of malignancy (contrast benign tumors). Most tumors and other neoplasms can metastasize, although in varying degrees (e.g., glioma and basal cell carcinoma rarely metastasize). When tumor cells metastasize, the new tumor is called a secondary or metastatic tumor, and its cells are like those in the original tumor. This means, for example, that, if breast cancer metastasizes to the lungs, the secondary tumor is made up of abnormal breast cells, not of abnormal lung cells. The tumor in the lung is then called metastatic breast cancer, not lung cancer.

50. Portal hypertension - macroscopic description In medicine, portal hypertension is hypertension (high blood pressure) in the portal vein and its tributaries. It is often defined as a portal pressure gradient (the difference in pressure between the portal vein and the hepatic veins) of 5 mm Hg or greater.

Portal hypertension is abnormally high blood pressure in branches of the portal vein, the large vein that brings blood from the intestine to the liver.

Cirrhosis is the most common cause in Western countries. The effects of portal hypertension can lead to an enlarged abdomen, abdominal discomfort, confusion, and internal bleeding.

Two factors can increase blood pressure in the portal blood vessels:

Increased volume of blood flowing through the vessels Increased resistance to the blood flow through the liver

In Western countries, the most common cause of portal hypertension is increased resistance to blood flow caused by extensive scarring of the liver in cirrhosis, which is most often due to chronic excessive alcohol intake. Portal hypertension leads to the development of new veins (called collateral vessels) that directly connect the portal blood vessels to the general circulation, bypassing the liver. Because of this bypass, substances (such as toxins) that are normally removed from the blood by the liver can pass into the general circulation. Collateral vessels develop at specific places. The most important are located at the lower end of the esophagus and at the upper part of the stomach. Here, the vessels become engorged and full of twists and turnsthat is, they become varicose veins of the esophagus (esophageal varices) or stomach (gastric varices). These engorged vessels are fragile and prone to bleeding, sometimes seriously and occasionally with fatal results. Other collateral vessels may develop on the abdominal wall and at the rectum. Portal hypertension often causes the spleen to enlarge because the pressure interferes with blood flow from the spleen into the portal blood vessels. Pressure in the portal blood vessels may cause protein-containing (ascitic) fluid from the surface of the liver and intestine to leak into the abdominal cavity. This condition is called ascites.

51. Autopsy of pediatric patients - macroscopic description

52. Macroreactions

53. Dissection of brain and spinal cord The skull vault is opened using two saw cuts, one in front, and one in back. These will not show through the scalp when it is sewed back together. The top of the skull is removed, the brain is then observed in situ. Then the brain's connection to the cranial nerves and spinal cord are severed, and the brain is then lifted out of the skull for further examination. Inspecting the brain often reveals surprises. A good pathologist takes some time to do this. 54. Dissection of neck and chest organs A single vertical cut is made from the middle of the neck (in the region of the 'adam's apple' on a male body) and extends all the way down to the pubic bone (making a deviation to the left side of the navel). Bleeding from the cuts is minimal, or non-existent, due to the fact that the pull of gravity is producing the only blood pressure at this point, related directly to the complete lack of cardiac functionality. A pathologist cuts the cartilages that join the ribs to the breastbone, in order to be able to enter the chest cavity. This can be done using a scalpel, a saw, or a special knife, depending on the pathologist's preferences and whether the cartilages have begun to turn into bone, as they often do in older folks. Then the pathologist must decide in what order to perform the rest of the autopsy. The choice will be based on a variety of considerations. The pathologist removes the neck organs, large airways, and lungs in one piece. This requires careful dissection. The pathologist always examines the neck very carefully. The lungs are almost never normal at autopsy. Normal lungs are pink, if the person was a non-smoker. The pathologist will inspect and feel them for areas of pneumonia and other abnormalities. Dissecting the lungs can be done in any of several ways. All methods reveal the surfaces of the large airways, and the great arteries of the lungs. Most pathologists use the long knife again while studying the lungs. The air spaces of the lungs will be evaluated based on their texture and appearance. The pathologist examines the heart, and generally the first step following its removal is sectioning the coronary arteries that supply the heart with blood. There

is often disease here, even in people who believed their hearts were normal. After any organ is removed, the pathologist will save a section in preservative solution. 55. Dissection of liver and urogenital complex Liver is removed and observed. The size, shape, colour and weight are noticed. The liver is cut at intervals of about a centimeter, using a long knife. This enables the pathologist to examine its inner structure. 56. Signs of maturity