Goljan lecture slides download

If you have 5 gm of Hb, there is not a whole lot of O2 that gets to tissue, therefore get tissue hypoxia and the patient has exertional dyspnea with anemia, exercise intolerance. Carbon monoxide CO : classic — heater in winter; in a closed space with a heater heater have many combustable materials; automobile exhaust and house fire. When theres heat, cyanide gas is given off; therefore pts from house fires commonly have CO and cyanide poisoning. Clue was that O2 did not correct the cyanosis.

Most recent drug, Dapsone used to Rx leprosy is a sulfa and nitryl drug. Therefore does two things: 1 produce methemoglobin and 2 have potential in producing hemolytic anemia in glucose 6 phosphate dehydrogenase deficiencies. Therefore, hemolysis in G6PD def is referring to oxidizing agents, causing an increase in peroxide, which destroys the RBC; the same drugs that produce hemolysis in G6PD def are sulfa and nitryl drugs.

These drugs also produce methemoglobin. Therefore, potential complication of that therapy is methemoglobinemia. Curves: left and right shifts Want a right shifted curve — want Hb with a decreased affinity for O2, so it can release O2 to tissues. Problems related to problems related to oxidative pathway a. Most imp: cytochrome oxidase last enzyme before it transfers the electrons to O2. Uncoupling — ability for inner mito membrane to synthesize ATP. Inner mito membrane is permeable to protons.

Examples: dinitrylphenol chemical for preserving wood , alcohol, salicylates. Uncoupling agents causes protons to go right through the membrane; therefore you are draining all the protons, and very little ATP being made.

These are all the causes of tissue hypoxia ischemia, Hb related, cyto oxidase block, uncoupling agents. Absolute key things! What happens when there is: a. Decreased of ATP as a result of tissue hypoxia 1. Why do we have to use anaerobic glycolysis with tissue hypoxia? Mitochondria are the one that makes ATP; however, with anaerobic glycolysis, you make 2 ATP without going into the mitochondria. Mitochondrial system is totally shut down no O2 at the end of the electron transport system — can only get 2 ATP with anaerobic glycolysis.

Good news — get 2 ATP Bad news — build up of lactic acid in the cell and outside the cell increased anion-gap metabolic acidosis with tissue hypoxia due to lactic acidosis from anaerobic glycolysis. Therefore, buildup of lactic acid within the cell will lead to Coagulation necrosis. With no ATP, Na into the cell and it brings H20, which leads to cellular swelling which is reversible. Cell without O2 leads to irreversible changes.

With decrease in ATP, Ca has easy access into the cell. Within the cell, it activates many enzymes ie phospholipases in the cell membranes, enzymes in the nucleus, leading to nuclear pyknosis so the chromatin disappears , into goes into the mito and destroys it.

Therefore, with irreversible changes, Ca has a major role. Of the two that get damaged mito and cell membrane , cell membrane is damaged a lot worse, resulting in bad things from the outside to get into the cell. Types of Free Radicals: 1. Oxygen: We are breathing O2, and O2 can give free radicals. Water in tissues converted to hydroxyl free radicals, leading to mutations in tissues.

Audio file 2: Cell Injury 2 3. Cytochrome P in liver metabolizes drugs, and can change drugs into free radicals. Drugs are often changed in the liver to the active metabolite — ie phenytoin. Where in the liver does acetaminophen toxicity manifest itself? Treatment: n-acetylcysteine; how? Well, the free radicals can be neutralized.

Superoxide free radicals can be neutralized with supraoxide dismutase SOD. Main function is to neutralize free radicals esp drug free radicals, and free radicals derived from peroxide. Glutathione gets used up in neutralizing the acetaminophen free radicals. Therefore, when give n-acetylcysteine aka mucamist ; you are replenishing glutathione, therefore giving substrate to make more glutathione, so you can keep up with neutralizing acetaminophen free radicals.

Carbon tetrachloride: CCl4 can be converted to a free radical in the liver CCl3 in the liver, and a free radical can be formed out of that seen in dry cleaning industry.

Aspirin is knocking off the vasodilator PGE2, which is made in the afferent arteriole. Therefore AG II a vasoconstrictor is left in charge of renal blood flow at the efferent arteriole. Apoptosis Programmed cell death. Normal functions: 1 embryo — small bowel got lumens from apoptosis. MIF is a signal working with apoptosis, via caspasases. They destroy everything, then wrap everything in apoptotic bodies to be destroyed, and lipofuscin is left over.

Hepatitis — councilman body looks like eosinophilic cell without apoptosis of apoptosis individual cell death with inflammation around it. Just needs a signal hormone or chemical which activate the caspases, and no inflammation is around it.

Apoptosis of neurons — loss brain mass and brain atrophy, and leads to ischemia. Red cytoplasm, and pynotic nucleas. Atherosclerotic plaque. Therefore, apoptosis is involved in embryo, pathology, and knocking off cancer cells. Types of necrosis — manifestations of tissue damage. Coagulation Necrosis: Results often from a sudden cutoff of blood supply to an organ i.

In ischemia, there is no oxygen therefore lactic acid builds up, and leads to coagulation necrosis. Gross manifestation of coagulation necrosis is infarction. Under microscope, looks like cardiac muscle but there are no striations, no nuclei, bright red, no inflammatory infiltrate, all due to lactic acid that has denatured and destroyed all the enzymes cannot be broken down — neutrophils need to come in from the outside to breakdown.

Pale vs hemorrhagic infarctions: look at consistency of tissue. Pathogenesis of MI: coronary thrombosis overlying the atheromatous plaque, leading to ischemia, and lumen is blocked due to thrombosis.

Example: hemorrhagic infarction of small bowel due to indirect hernia. MCC of bowel infarction is adhesions from previous surgery. Example: In the Lung — hemorrhagic infarction, wedge shaped, went to pleural surface, therefore have effusion and exudates; neutrophils in it; have pleuritic chest pain knife-like pain on inspiration. Pulmonary embolus leads to hemorrhagic infarction. Liquefactive Necrosis: Exception to rule of Coagulation necrosis seen with infarctions: brain. MC site of infarction from carotid artery — why we listen for a bruit hearing for a noise that is going thru a vessel that has a narrow lumen — place with thrombus develops over atherosclerotic plaque and leads to stroke ; leads to transient ischemic attacks is little atherosclerotic plaques going to little vessels of the brain, producing motor and sensory abnormalities, that go away in 24 hrs.

Therefore, infarction of the brain basically liquefies it has no struct , and you see a cyst space — liquefactive necrosis. Therefore, exception to the rule of infarctions not being coagulative necrosis is the brain and it undergoes liquefactive necrosis no struc, therefore leaves a hole.

Cerebral abscess and old atherosclerotic stroke -both are liquefactive necrosis. Therefore, liquefactive necrosis usually applies to acute inflammation, related to neutrophils damaging the tissue. Exception to the rule: liquefactive necrosis related to infarct not an inflammatory condition, it just liquefies slide shows liquefactive necrosis due to infection in the brain. So, if you infarct the brain, or have an infection, or have an abscess it is the same process — liquefactive necrosis.

Why are they in clusters? Coagulase, which leads to abscesses with staph aur. Coagulase converts fibrinogen into fibrin, so it localizes the infection, fibrin strands get out, resulting in an abscess.

From point of view of necrosis, neutrophils are involved, therefore it is liquefactive necrosis. MCC of bronchopneumonia. Example: pt with fever, night sweats, wt loss — M tb, which has granulomatous caseous necrosis.

Caseous cheesy consistency Necrosis: — either have mycobacterial infection any infections, including atypicals, or systemic fungal infection ; these are the ONLY things that will produce caseation in a granuloma. Fat Necrosis: 1. A type of enzymatic FAT necrosis therefore necrosis related to enzymes. Example: A pt with pain constently penetrating into the back, show x-ray of RUQ.

Dx is pancreatitis and esp seen in alcoholics. Histo slide on enzymatic fat necrosis — bluish discoloration, which is calcification a type of dystrophic calcification-calcification of damaged tissue. What enzyme would be elevated? What type of necrosis? Another example: Enzymatic fat necrosis. Underlying cause? Alcohol produces a thick secretion that will lead to activation of enzymes; which leads to pancreatitis. Therefore, whenever you see blue discoloration and atherosclerotic plaque in a pancreas, it will be calcium.

Diff btwn that and calcification in breast cancer is that it is painFUL. Traumatic fat tissue usually occurs in breast tissue or other adipose tissue E. Pathogenesis of immune complex: damage of type III HPY an immune complex is an Ag-Ab circulating in the circulation; it deposits wherever circulation takes it — ie glomerulus, small vessel, wherever.

It activates the complement system the alt system , which produces C5a, which is chemotactic to neutrophils. Rhematic fever vegetations off the mitral valve — have fibrin like fibrinoid necrosis materials necrosis of immunologic dz. Liver: Triad area: portal vein, hepatic artery, bile duct. Other examples of sinusoid organs are BM and spleen. GBM is fenestrated, have little tiny pores within the cells, for filtration. Portal vein blood and hepatic artery blood go through sinusoids, and eventually taken up by central vein, which becomes the hepatic vein.

The hepatic vein dumps into the inf vena cava, which goes to the right side of the heart. Therefore, there is a communication between right heart and liver. Right HF blood fills behind failed heart , therefore the liver becomes congested with blood, leading to nutmeg liver aka congestive hepatomegaly.

Blockage of hepatic vein leads to budd chiari and liver becomes congested. Which part of liver is most susceptible to injury normally? Zone 2 is where yellow fever will hit midzone necrosis due to ides egypti. Fatty change is around zone 3 part around central vein.

Therefore, when asking about acetaminophen toxicity, which part is most susceptible? Alcohol related liver damage: a MCC fatty change: alcohol. NADH is part of the metabolism of alcohol, therefore, for biochemical rxns: What causes pyruvate to form lactate in anaerobic glycolysis?

However, you have lactate and not pyruvate therefore alcoholics will have fasting hypoglycemia. Why does it produce fatty change? In glycolysis, around rxn 4, get intermediates dihydroxyacetone phoshphate NADH rxn and is forced to become glycerol 3-phosphate. Big time board question! With glycerol 3 phosphate shuttle, get ATP. In liver, the lipid fraction if VLDL endogenous TG is synthesized in the liver from glycerol 3 phosphate derived from glycolysis.

Audio file 3: Inflammation 1 2. Kwashiorker — kid with fatty change. In kwashiorkor, there is decreased protein intake; they have adequate number of calories, but its all carbs. Lipid and water do not mix; therefore it is necessary to put proteins around the lipid to dissolve it in water.

Therefore, the protuberant abdomen in these pts is there for two reasons: 1 decreased protein intake which decreases oncotic pressure, leading to ascites.

In this case, there is a lack of protein to put around the VLDL and export it out of the liver. Ferritin is a soluble form of Fe, while hemosiderin is an insoluble form of Fe storage, and is stored in macrophages and BM.

Stain it with Prussian blue. Types of calcification: dystrophic and metastatic A. Dystrophic calcification: means abnormal calcification. The damaged tissue gets calcified. Example: Seen in enzymatic fat necrosis chalky white areas on x-ray are a result of dystrophic calcification. I do not believe that listening to them early in your first or second year of med school is helpful. They are not a great review for your school tests because they are only an overview.

Also, when you begin to make your study plan for Step 1 you are not going to have 40 hours to sit and listen to lectures. Frankly, you will fall asleep and get nothing out of it. I found that listening when I exercised every day was a fantastic way to use them. That way I didn't feel guilty about taking an hour to exercise which, by the way, is the best thing you can do when you are studying 10 hours every day and I surely learned more from Goljan than I would have from Eminem and Coldplay.

In fact, I know that just listening in the car and while running picked me up a good number of questions on Step 1. I still remember, word for word, one question that I absolutely would not have known if not for Goljan's lectures. I have heard that there are 'new' Goljan audio lectures since I took Step 1.

I can not verify this, and I search using my usual websites only found the same audio files that I used 3 years ago. If anyone knows more about this, please leave a comment. The debate usually comes down to Dr. Goljan's book tends to have more images, a more modern layout, and does not rely solely on text to teach pathology while the BRS book is a no-nonsense text book which attempts to teach the most important points of pathology quickly.

So, the choice depends on how you learn. While the issues at the heart of that debate will have to wait for a different post, we can all agree that BOTH books are very good. Links to the newest additions of both books on amazon. In fact, some students believe it added double digit points to their board score.

Link to Amazon. The format that is available on the internet is not ideal, but I do think that these notes can be very useful. The document is a very rapid review of the pathology associations that are most common and most important to Steps 1 and 2. It is long pages and very dense no pictures, small font size, all pages are full of text but it highlights very efficiently the high points of pathology for the USMLE.

Again, you can search the internet for "Goljan High Yield" and you will be inundated with places to download the file. Alternatively, I will attempt to keep my copy on my website until someone tells me that it is illegal, which I do not believe it can be as this, too, is not available for purchase anywhere else. Click the link below to download the pdf.

Goljan High Yield Pathology Notes. Tags: Step 1 , Step 2 , books , goljan. August 13, at pm UTC -4 Link to this comment. Brain: Fat embolism Note the pinpoint areas of hemorrhage throughout the brain. The patient sustained multiple fractures of the pelvis and femoral bones from a car accident. Microglobules of marrow fat and fat in the surrounding tissue enter the injured vessels and embolize throughout the body. Symptoms of dyspnea usually develop with days owing to plugged pulmonary capillaries.

In the cerebral vessels, the microglobules of fat block the capillary lumens causing rupture of the vessels. Skin: Bee sting with acute inflammation Note the central raised area corresponding to the tumor of acute inflammation. It is due to histamine release by tissue mast cells. Histamine increases vessel permeability leading to an accumulation of protein rich fluid exudate in the interstitial tissue. The redness corresponds to the rubor of acute inflammation and is due to histamine-dependent arteriolar vasodilatation.

The calor heat of acute inflammation is also due to histamine-dependent arteriolar vasodilatation. Pain dolor in acute inflammation is due to bradykinin and PGE2.

A bee sting is an example of a type I hypersensitivity reaction. Acute inflammation-stasis This slide shows a small venule filled with neutrophils and red blood cells. There are also red blood cells outside of the blood vessel which represents diapedesis. This process of vasodilatation and increased vascular permeability, due to histamine, facilitates the adhesion of the neutrophils to endothelial cells.

This process is secondary to stasis of the blood flow and increased concentrations of plasma proteins which coat the red cells and cause them to stick together. Rouleau causes an increase in the erythrocyte sedimentation rate. Red blood cells-margination and pavementing This blood vessel against represents stasis of blood flow with accumulation of red blood cells.

Notice that some of the neutrophils are lined up. Neutrophils in acute inflammation This is an area in the tissue where acute inflammatory cells are accumulating. Chemotactic substances e. C5a, C3a, LTB4 draw these cells into an area of damage so they can undergo the process of phagocytosis. Peripheral blood smear-neutrophil This slide shows a segmented neutrophil polymorphonuclear leukocyte. Normal cells should have lobes in the nucleus. Neutrophils are the primary cell of acute inflammation.

Band neutrophil This peripheral blood smear shows a band neutrophil which is the precursor cell to the segmented neutrophil. If the stimulus for storage pool neutrophil release continues beyond a few days, the post-mitotic pool will become depleted the production of acute phase reactants causes release of the post-mitotic pool of neutrophils.

The mitotic pool will then increase production in an attempt to meet the demand for neutrophils. Monocytes This slide shows two examples of monocytes in peripheral blood. Once monocytes become macrophages, they lose the 02 dependent MPO system.

The nucleus is at the bottom of the slide. The dark granules represent lysosomes. Recall that macrophages used to be circulating monocytes. Monocytes and macrophages are the primary cells of chronic inflammation.

The chromatin in the nucleus is deeply condensed and lumpy. Electron microscopy of a small lymphocyte Note the condensed chromatin of the nucleus surrounded by a thin rim of cytoplasm. The remaining lymphocytes are B cells. Peripheral blood: eosinophil and basophil Cell number 1 is an eosinophil. Note that the red granules are the same color as the RBCs.

Granules do not cover the nucleus. Eosinophilia is associated with type I hypersensitivity reactions- e. Cell number 2 is a basophil. Note that the granules are darker than the RBCs and they cover the nucleus. Electron microscopy of an eosinophil Note the rod-shaped crystals in the granules. When eosinophils degenerate, the crystals may coalesce to form Charcot-Leyden crystals, a characteristic finding in the sputum of asthmatics.

Bone: acute osteomyelitis suppurative inflammation Note the yellow area in the metaphysis of the femur. This represents an area of acute suppurative inflammation liquefactive necrosis due to hematogenous spread of Staphylococcus aureus, the MCC of acute osteomyelitis in children. Neutrophils will lyse the bone and produce a radiolucent area that is visible on x-ray after one week. Face: erysipelas due to group A streptococcus Streptococcus pyogenes,. Cellulitis is commonly seen in streptococcal infections owing to the production of hyaluronidase, which breaks down GAGs and allows the infection to spread through subcutaneous tissue.

Pseudomembranous inflammation This slide is from a case of diphtheria. Note the gray membrane in the upper airway oropharynx. This membrane pseudomembrane is composed of neutrophils, necrotic tissue, and fibrinous exudate.

It is characteristic of diphtheria. The causative organism is Corynebacterium diphtheriae, a gram positive rod. The organism produces an exotoxin which damages the myocardium and peripheral nerves. Another type of pseudomembrane formation is pseumembranous colitis which is caused by use of antibiotics such as ampicillin.

Colon: pseudomembranous colitis due to Clostridium difficile pseudomembranous inflammation Note the gray-yellow pseudomembrane covering the entire mucosal surface.

Damage is due to a toxin produced by C. Similar to diphtheria, the toxin produces necrosis of the mucosa and submucosa without actual invasion by the bacteria. A toxin assay of stool is the best method for diagnosing the disease. Ampicillin is the MC drug causing pseudomembranous colitis and does so by destroying colonic bacteria that normally keep C. Granulomatous inflammation This is another example of a granuloma. Note the presence of multinucleated giant cells. Also note that lymphocytes predominate in the areas surrounding the granuloma.

Note that the nuclei are arranged at the periphery of the cell. These cells are prominent in areas of granulomatous inflammation but are not required for a diagnosis. Heart: Fibrinous pericarditis. Note the shaggy exudate surfacing the pericardium. In this case, it is a sterile acute inflammatory reaction due to acute rheumatic fever.

Increased vessel permeability causes protein includes fibrinogen to leak out of the vessels and congeal on the surface. Patients develop an audible friction rub due to the parietal pericardium separating away from the visceral pericardium covered with the exudate during different phases of the cardiac cycle. Other causes of fibrinous pericarditis include SLE, a transmural myocardial infarction, and coxsackie virus pericarditis MCC.

Adrenal adenoma This is an adrenal adenoma which is a benign tumor arising from the adrenal cortex. Notice how well-demarcated it is. There is absence of hemorrhage and necrosis. It also has the color of adrenal cortex. Tubular adenoma This is a microscopic section of a neoplastic polyp arising from the colon mucosa. The polyp is pedunculated and is composed of colonic glands which have lost many of the normal goblet cells.

This is called an adenomatous change. Squamous cell carcinoma This is a cluster of malignant squamous cells. These malignant cells are still able to undergo some degree of differentiation as shown by the pink area of keratinization.

Adenocarcinoma This is a slide showing malignant gland formation. The nests of malignant cells are producing gland lumina. The clear areas on the left represent mucin production by the tumor cells. Each side of the papillary process is lined by several layers of transitional cells.

This tumor is graded by the number of cell layers stratification present. Lipoma The yellow mass with the muscle is a benign tumor arising from mature adipose tissue. The tumor is well-circumscribed. Leiomyoma of stomach This is a gross photograph of a benign tumor of smooth muscle origin in the stomach.

These tumors may present with bleeding. Embryonal rhabdomyosarcoma This slide shows a striated malignant tumor cell strap cell. It arises in the vagina in girls and in the urethra of boys. It is desmin positive. Cystic teratoma dermoid cyst This is a benign teratoma arising from all three germ cell layers. It is typically composed of ectodermally derived hair and sebaceous secretions. These tumors frequently make tooth structures. The tumors arise in gonads or as midline lesions. In children, they are found in the sacrococcygeal area.

Neo They arise from the same germ cell layer but there are two distinct types of histologic patterns within the tumor. These tumors. This is a classic pattern seen in malignant lymphomas involving this area. The tumor arises from solid lymphoid tissue. Acute lymphocytic leukemia This is a peripheral blood smear showing a cluster of immature appearing lymphocytes lymphoblasts. This tumor is the most common leukemia of children with the peak age being 4. Chronic lymphocytic leukemia This is the most common leukemia in elderly patients.

Notice the mature appearing B lymphocytes in the peripheral blood smear. These B cells are long-lived and nonfunctional and infiltrate the bone marrow, blood, lymph nodes, and other tissues.

Acute myeloblastic leukemia Note the eosinophilic rod-shaped structures in the cytoplasm of the neoplastic cells. There are 8 classes of AML, each with unique features. Acute promyelocytic leukemia is associated with a t 15;17 translocation and disseminated intravascular coagulopathy is common. Bronchial hamartoma This is a non-neoplastic lesion composed of tissues normally found in the organ where the hamartoma arises.

The tissues in the hamartoma are typically disorganized in their arrangement. Peutz-Jeghers This is a syndrome associated with mucocutaneous pigmentation and hamartomatous polyps of the GI tract.

Microscopically, they show increased numbers of goblet cells. Choristoma heterotropic pancreas This is a section of duodenum showing an aggregate of pancreatic tissue in the wall. The pancreatic tissue is normal in appearance but in an abnormal location. This is a non-neoplastic process. Hemangioma This is a benign neoplasm arising from endothelial cells of blood vessels. Hemangioma This is the microscopic appearance of a hemangioma showing dilated blood vessels filled with red blood cells and lined by benign endothelial cells.

Malignant cells This slide shows several features of malignancy. Other cells show hyperchromatic nuclei or large and irregular nuclei and nucleoli all of which are features of malignancy. Retinoblastoma This is a retinoblastoma. This malignant tumor is associated with inactivation of the Rb tumor suppressor gene. Kaposi sarcoma Multiple vascular lesions are noted. This tumor is associated with HIV and arises from endothelial cells.

Xeroderma pigmentosum This autosomal recessive disorder involves a defect in DNA repair enzymes in the skin. The patients are susceptible to skin cancers such as melanomas, basal and squamous cell carcinomas of the skin associated with UVB light damage.

Squamous cell carcinoma of skin This neoplasm is associated with UVB light damage and immunosuppression. It is found on sun-exposed areas, particularly the face. Clear cell carcinoma of the vagina Diethylstilbestrol exposure. This is a malignant neoplasm occurring in the vagina of the daughters of DES exposed mothers. The DES causes persistence of Mullerian tissues in the vagina which gives rise to vaginal adenosis which is the precursor lesion for clear cell adenocarcinoma.

This tumor occurs in young females. Asbestos ferrunginous bodies bodies These dumbbell shaped particles are found in the lungs of patients exposed to asbestos. Pleural fibrous plaques and malignant mesotheliomas are associated with exposure to asbestos. Pleural mesothelioma This neoplasm arises from mesothelial cells of the pleura and peritoneum. It encases the lung-producing compressive atelectasis.

Prior asbestos exposure is the major risk factor. Metastasis Each of the organ systems featured on the slides represent favored sites for metastasis. The bone is a common site for metastasis from prostate, lung, and thyroid cancers. CNS is a common site of metastasis from small cell carcinomas of lung and breast cancers.

Liver is a common site of metastasis from lung and colon tumors. Metastasis The lung is a common site of metastasis from colon and other visceral neoplasms. Lymphangitic spread This slide shows a lymphatic vessel containing nests of malignant adenocarcinoma cells. Omental seeding This section of omental fat shows light tan tumor masses which are adherent to the omentum.

Tumors associated with this type of seeding include mucinous cystadenocarcinomas of the ovary, and tumors of the GI tract. Vascular invasion-follicle carcinoma of the thyroid This tumor has the propensity to invade blood vessels and undergo hematogenous dissemination which is shown on the slide. Osteoblastic metastasis Certain neoplasms have a tendency to metastasize to bone and if so, produce stimulation of the osteoblasts with new bone formation. The bone alkaline phosphatase will be elevated in the serum.

Tumors associated with osteoblastic metastasis include prostate, thyroid, breast, and carcinoid. Osteolytic metastasis Tumors which metastasize to bone and cause bone breakdown include breast and lung.

Pathologic fractures are a risk. Lung radiographics showing cancer The top radiograph shows a peripheral density in the right lung which represents a primary adenocarcinoma of the lung.

Well-differentiated squamous cell carcinoma This slide shows two nests of welldifferentiated squamous cells low grade demonstrating features of normal squamous cells. Well-differentiated adenocarcinoma This slide shows a well-differentiated adenocarcinoma with well formed glands and distinct lumens. Hypertrophic osteo-arthropathy This is a paraneoplastic syndrome characterized by clubbing of the fingers, toes and periosteal elevation of the distal parts of the long bones. It is associated with lung cancer.

Acanthosis nigricans A paraneoplastic syndrome of hyperpigmentation of the axilla associated with an underlying gastric carcinoma. A phenotypic marker. Associated with underlying GI cancer. Marantic endocarditis Endocarditis associated with sterile vegetations that are thought to be due to a hypercoagulable state.

The normal squamous esophageal mucosa is replaced by gastric glandular mucosa. It is a precursor lesion for adenocarcinoma of the esophagus. These cells show atypical features with pleomorphism and hyperchromatic nuclei. Three mitotic figures are noted.

Squamous cell carcinoma of the larynx Note the fungating mass on the lateral border of the larynx with central ulceration. These tumors are associated with smoking and chronic alcohol use. The first symptom is hoarseness. Two radiographs with cancers The x-ray on the left shows a large upper lobe peripheral lesions of the left lung.

This is most likely an adenocarcinoma. The x-ray on the right shows a central density in the right lung which is most likely a squamous cell carcinoma. Squamous cell carcinoma of the lung This slide shows an airway that is opened.

The mucosa appears rough and there is an infiltrating mass involving the wall of the bronchi before and after the branching. This is most likely a squamous cell carcinoma. Squamous cell cardinoma-lungcytology These three photographs of cytologies show malignant squamous cells.

The cells in one slide are in a nest. The nuclei are hyperchromatic, irregular, and have prominent nucleoli. Small cell carcinoma of lung The slide on the left is a sputum cytology showing small dark staining cells. They mold around each other. There is almost no cytoplasm visible. The slide on the right is from the tumor in the lung. Notice the hyperchromatic cells which appear to be swarming around the blood vessels.

This tumor has the highest association with smoking and the worse prognosis. It is more common in men. Squamous cell carcinoma of lung. The upper lobe which appears dark demonstrates atelectasis from complete obstruction of the airway lumen by the cancer. Another lobe shows markedly dilated airways representing bronchiectasis with mucous plugs. This associated with incomplete obstruction of a proximal airway. The other lobe shows consolidation consistent with either golden pneumonia endogenous lipid pneumonia or a bacterial pneumonia secondary to incomplete obstruction.

Superior vena cava syndrome This patient shows obstruction of the venous supply from the head and neck with distention of the neck veins. This is due to a neoplasm infiltrating the mediastinum and obstruction of the superior vena cava. Leukoplakia and invasive cancer The slide on the right shows white patches consistent with leukoplakia, a premalignant change of the oral mucosa and tongue associated with either smokeless tobacco use or chronic irritation.

Squamous cell carcinoma of lower lip This patient has an ulcerated lesion of the left lower lip which is most likely a squamous cell carcinoma.

The associations are pipe smoking and sun exposure. This tumor typically arises in the middle third of the esophagus and infiltrates the wall. The most common symptom is dysphagia, first for solids and then both liquids and solids. Squamous cell carcinoma of esophagus This tumor has invaded the walls of local structures around the esophagus and infiltrates the wall. The most common symptom is dyphagia, first for solids and then both liquids and solids.

Linitis plastica adenocarcinoma of the stomach signet ring carcinoma This tumor invades the wall of the stomach producing a desmoplastic response. The stomach becomes hard like a leather bottle. This tumor presents late in its course and has a tendency to metastasize to the ovaries. The tumor is a metastatic gastric carcinoma which has spread to the ovaries. Carcinoid tumor of the appendix This is the most common location of an asymptomatic carcinoid tumor.

The tumor arises in the tail of the appendix from resident neuroendocrine cells APUD cells. It is usually an incidental finding in this location. The arrows point to dark staining cytoplasmic organelles which are features of neuroendocrine tumors. Familial polyposis This autosomal dominant condition is associated with multiple tubular adenomas and tubulovillous tumors in the colon.

There is an association with the APC tumor suppressor gene. Tubular adenoma There are four slide demonstrating a tubular adenoma.

The slide on the upper left is a endoscopic view of the pedunculated tumor. A barium outlines the polyp. The last two slides show the pedunculated polyp. There is a slight risk of malignant transformation with tubular adenomas. Villous adenoma This is a microscopic section of a villous adenoma. Note the long stalk-like papillary projections of the tumor. These tumors are typically sessile and have a high incidence of malignant transformation.

Adenocarcinoma of colon This tumor is a fungating mass with central necrosis which arises from colonic mucosa. Obstructive lesions occur in the descending colon. Adenocarcinoma of the colon This lesion is growing as a polypoid mass into the lumen of the ascending colon. Right sided colonic masses typically present with anemia and bleeding. Hepatocellular carcinoma This tumor arises from hepatocytes.

Conditions which predispose to this tumor include post-necrotic post-infectious cirrhosis, pigment cirrhosis hemosiderosis , alcoholic cirrhosis, aflatoxins, and thorotrast. Metastasis to the liver This liver shows numerous nodules, some having an umbilicated center, which are metastatic tumors.

The metastasis is most likely from lung, breast, or GI tract. CT of liver with metastasis The CT shows radiolucent areas in the liver consistent with metastatic nodules. Cholelithiasis and carcinoma of gallbladder This slide shows a gallbladder that is thin and fibrotic.

One portion of the gallbladder wall shows a tan mass of tumor which infiltrates the attached tissues. Gallbladder cancer may arise in a setting of chronic cholecystitis and cholelithiasis. This lesion will likely produce obstructive jaundice. A marker for the tumor is CA Renal cell carcinoma This tumor arises from proximal tubular cells in the kidney and is typically in the upper pole of the kidney.

It will be very vascular. The tumor presents with hematuria, flank mass, flank pain, or with paraneoplastic hormone production. The tumor tends to invade the renal vein and spread to the lungs with cannon-ball metastasis. It has tissues from two germ cell layers. Patients present with a flank mass and hypertension. This slide shows a papillary tumor by cytoscopy. It is arising from the transitional mucosa of the bladder and usually presents with hematuria. Carcinoma of prostate This is an adenocarcinoma arising in the posterior lobe of the prostate.

Prostate chips These are fragments of prostate tissue removed by the TURP procedure transurethral prostatic resection. Each piece of tissue will be examined microscopically after they are weighed collectively.

Leiomyosarcoma This is the most common sarcoma of the female genital tract, although rare. It usually arises de novo. It is bulky and hemorrhagic. Microscopic grading is based on the numbers of mitoses counted per high powered field. Papillary serous cystadenocarcinoma of ovary This is the most common malignant ovarian tumor and has a high incidence of bilaterality.

The tumor is derived from the surface epithelium of the ovary and the cells of the tumor resemble fallopian tube lining cells. The most solid areas of the tumor are associated with a higher grade of tumor. Thanks for your cooperation. Please enter your comment! Please enter your name here. You have entered an incorrect email address! Leave this field empty. If you still feel your copyrights have been violated, then you may contact us immediately: Contact us: admin cmecde.

All Rights Reserved.