General Pathology IllustrationsDr. Cooperstein :General Pathology IllustrationsDr. Cooperstein


Causes of Disease:The case of cancer :Causes of Disease:The case of cancer


Pathophysiology:A causal explanation :Pathophysiology:A causal explanation Structural changes Disturbed function Structure ? function Questions for the doctor Diagnosis: what disease Prognosis: what will happen Treatment Cause of the disease


The cell and its organelles :The cell and its organelles


Plasmalemma :Plasmalemma Structural envelope Selects macromolecules leaving and entering Maintains ionic concentration difference inside and outside


Acetylcholine receptor :Acetylcholine receptor


The mitochondrion: Power plant of the cell :The mitochondrion: Power plant of the cell


Ribosome :Ribosome


Ribosome structure :Ribosome structure


The Lysosome:Cellular Recycling :The Lysosome:Cellular Recycling


Nuclear pore and ER :Nuclear pore and ER The nuclear envelope has two membranes, each with the typical unit membrane structure. They enclose a flattened sac and are connected at the nuclear pore sites. The outermost membrane is continuous with the rough endoplasmic reticulum (ER) and has ribosomes attached.


Nuclear changes :Nuclear changes Pyknosis: Shrinking and darkening of the nucleus Karyolysis: Fading (dissolving) of the nucleus Karyorrhexis: Fragmentation of the nucleus


Pyknosis: irreversible :Pyknosis: irreversible It is difficult to define a "point of no return" but once changes to the nucleus take place (i.e. pyknosis, karyorrhexis and karyolysis) and cell membranes are disrupted the cell is on the path to irreversible injury and death.


Pyk-nosis . . . :Pyk-nosis . . .


Reversible and irreversible cellular changes :Reversible and irreversible cellular changes


Hydropic swelling :Hydropic swelling


Ischemia :Ischemia


Goiter, endemic :Goiter, endemic


Myeloid, lymphoid tissue :Myeloid, lymphoid tissue


Myositis Ossificans :Myositis Ossificans aberrant reparative process causing benign heterotopic (extraskeletal) ossification in soft tissue


Squamous Metaplasia of Bladder :Squamous Metaplasia of Bladder Etiology The etiology of squamous metaplasia is dependent upon the underlying pathologic process, i.e, bladder calculi, extrophy of the bladder, schistosomiasis. Probably normal in women. Pathogenesis The normal transitional epithelium will undergo squamous metaplasia as an adaptive change to chronic irritation, such as from bladder calculi. Epidemiology The epidemiology is dependent on the underlying disease process. Squamous metaplasia is found in a large percentage of women with no abnormalities. General Gross Description There is no striking gross changes to the epithelial lining of the bladder. There may be a perception that the epithelial lining is paler and thicker than normal. General Microscopic Description The normal transitional epithelium of the bladder is replaced by stratified squamous epithelium. Clinical Correlation Squamous metaplasia may occur in situations of chronic irritation such as bladder calculi, extrophy of the bladder and schistosomiasis. References Cotran RS, Kumar V, Robbins SL: Robbins Pathologic Basis of Disease. 5th ed. Philadelphia, W.B. Saunders, 1994, pp. 48


Hypothyroidism:Clinical Features :Hypothyroidism:Clinical Features Rubin and Farber, p 1111


Dysplasia :Dysplasia


Breast cancer and diet :Breast cancer and diet


Etiology of Tissue injury :Etiology of Tissue injury


Creatine phosphokinase isoenzymes :Creatine phosphokinase isoenzymes CPK isoenzymes are performed when the total CPK level is elevated. Isoenzyme testing can help differentiate the source of the damaged tissue. CPK is an enzyme found predominantly in the heart, brain, and skeletal muscle. CPK is composed of 3 isoenzymes that differ slightly in structure: CPK-1 (also called CPK-BB) is concentrated in the brain and lungs CPK-2 (also called CPK-MB) is found mostly in the heart CPK-3 (also called CPK-MM) is found mostly in skeletal muscle Because the CPK-1 isoenzyme is predominately found in the brain and lungs, injury to either of these organs (for example, stroke or lung injury due to a pulmonary embolism) are associated with elevated levels of this isoenzyme. CPK-2 levels rise 3 - 6 hours after a heart attack . If there is no further damage to the heart muscle, the level peaks at 12 - 24 hours and returns to normal 12 - 48 hours after tissue death. CPK-2 levels do not usually rise with chest pain caused by angina , pulmonary embolism (blood clot in the lung), or congestive heart failure . The CPK-3 isoenzyme is normally responsible for almost all CPK enzyme activity in healthy people. When this particular isoenzyme is elevated, it usually indicates injury or stress to skeletal muscle.


DNA repair enzymesdelivered via liposomes :DNA repair enzymesdelivered via liposomes


Nutrients robbed . . . :Nutrients robbed . . .


Ionizing radiation :Ionizing radiation


X-ray heretic Gofman :X-ray heretic Gofman


Gofman’s on-line book :Gofman’s on-line book By reasonable standards of proof, the safe-dose hypothesis is not merely implausible -- it is disproven. Disproof of any safe dose or dose-rate invalidates suggestions that, whenever an analyst calculates a number of radiation-induced cancers to be caused by very low-dose exposure, the cancers are just "hypothetical," "speculative," "theoretical," "non-existent," or "imaginary." It is true, of course, that radiation-induced cancers in a population from very low doses will rarely if ever be detectable epidemiologically, because of the signal-to-noise ratio (see Chapter 21). But it does not follow (from the lack of direct observation) that the cancers are therefore unreal, hypothetical, speculative, theoretical, non-existent, or imaginary. No rational person will deny that one of the most commonplace (and important) functions of science is to let people know what is really happening when direct observation is impossible. We conclude with a warning: Disproof of any safe dose or dose-rate means that fatal cancers from minimal doses and dose-rates of ionizing radiation are not imaginary. They are really occurring in exposed populations. Proposals, to declare that they need not be considered, have health implications extending far beyond the radiation issue, as pointed out in Chapter 24, Part 10 and Chapter 25, Part 5. Radiation-Induced Cancer From Low-Dose Exposure John W. Gofman, M.D., Ph.D. 1990. http://www.ratical.org/radiation/CNR/RIC/contentsF.html


Health effects of chiropractic x-ray :Health effects of chiropractic x-ray


Beta-carotene, potential problem :Beta-carotene, potential problem When beta-carotene is consumed in amounts found naturally in foods, or when consumed in oral supplement doses of 15mg/day or less in people with good general health, when used orally and appropriately. Beta-carotene is likely safe in children, when used orally in amounts commonly found in foods. Beta-carotene is likely safe in pregnant and lactating women, when used orally and appropriately in amounts commonly found in foods. Carcinogenic : Beta-carotene in doses of 20mg daily for 5-8 years has been associated with an increased risk of lung and prostate cancer and increased total mortality in people who smoke cigarettes, and in people with a history of high-level asbestos exposure. Smokers and people with a history of asbestos exposure should not use beta-carotene supplements. These adverse effects do not seem to occur in people who eat foods high in beta-carotene content. Cardiovascular : In people who smoke, beta-carotene 20 to 30mg daily may increase cardiovascular mortality by 12% to 26%. In men who smoke and have had a prior myocardial infarction (MI), the risk of fatal coronary heart disease increases by as much as 43% with beta-carotene 20mg daily. There is some evidence that beta-carotene in combination with selenium, vitamin C and vitamin E might lower high-density lipoprotein 2 (HDL2) cholesterol levels. HDL levels are protective so this is considered to be a negative effect.


Current epidemiological evidence regarding the health effects of low-dose ionizing radiation. Implications for radiation protection, public health and forensic medicine (2004) :Current epidemiological evidence regarding the health effects of low-dose ionizing radiation. Implications for radiation protection, public health and forensic medicine (2004) The health effects of low-dose ionizing radiation have been widely studied, but remain uncertain. Up-to-date knowledge about epidemiologic evidence for potential human health effects of low dose ionizing radiation is important for revising national radiation protection legislation. This review, conducted by a multidisciplinary research team of the Italian Institute of Social Medicine, evaluates epidemiologic studies published since July 2003. After careful selection, a total of 302 studies were reviewed. Greater emphasis was given to papers that analyzed data using standardized incidence and mortality ratios and to studies regarding occupational exposures in all workers, healthcare workers and aircrew members. Nevertheless, studies regarding A-bomb survivors of Hiroshima/Nagasaki, Chernobyl cleanup workers, patients exposed for medical reasons, and workers in nuclear plants were also included. Given the limitations of epidemiological studies and excluding the cosmic rays context, which requires further research, the authors conclude that harmful effects from exposures to ionizing radiation at doses lower than 100 mSv cannot be ruled out. Nevertheless, if any harmful health effects do exist, they are certainly very small. The implications for radiation protection, public health and forensic medicine are discussed.


Intracellular accumulations :Intracellular accumulations


Fatty change, pancreas and heart :Fatty change, pancreas and heart The normal pancreas in younger and thinner patients is less hyperechoic than the fat around the superior mesenteric artery and more hyperechoic than the left lobe of the liver. With advancing age and/or increasing body weight, the acinar tissue progressively atrophies and is replaced by fatty tissue. This causes the pancreas to increase uniformly in echogenicity. The appearance of a fatty pancreas can be seen in a number of conditions: (1) elderly, (2) obese, (3) diabetes mellitus, (4) Cushing's disease, (5) lipomatosis, and (6) after steroid administration. Fatty Heart. — This is a condition in which there is a deposit of fat between the sac which contains the heart and the heart muscle. The trouble is directly associated with obesity, and is dietetic in origin, being attributable to over-indulgence in food and drink. Shortness of breath on exertion and a feeling of distress or oppression in the region of the heart are its most marked symptoms.


Necrosis :Necrosis Liquefaction Necrosis: Watery breakup of cells; usually caused by bacterial enzymes or some body reaction to microbial infection. Coagulation Necrosis: "Coagulation" of cells in which tissue details remain; usually caused by sudden loss of blood supply. Caseous Necrosis: Accumulation of a "cheesy" material in an area of tissue injury; usually caused by infection with the organism of tuberculosis (Mycobacterium tuberculosis). Gummatous Necrosis: Accumulation of a "gummy" material in an area of tissue injury; usually caused by infection with the organism of syphilis (Treponema palladium). Fat Necrosis: Death of adipose cells (fat deposits) usually caused by release of fat-splitting enzymes into the tissues. Gangrenous Necrosis: Death of cells in an extremity (e.g., toe) caused by ischemia and (sometimes) superimposed bacterial infection.


Fatty necrosis, pancreas :Fatty necrosis, pancreas Pancreatic Fat NecrosisThis is a gross photograph of a remnant of canine pancreas (*) which has experienced repeated bouts of acute pancreatitis. After each bout, pancreatic lipases are released which, in turn, digest mesenteric adipose tissue. This produces necrosis of fat cells, release of free fatty acids and a further inflammatory response (Arrow). The process will continue until the pancreas is destroyed or until the damage to the abdomen is so great as to cause death. http://www.vet.ohio-state.edu/docs/vetbio550.01/necrosis/fatnec.html


Acute pancreatitis andenzymatic destruction :Acute pancreatitis andenzymatic destruction Discrete white areas of fat necrosis are present in the pancreatic parenchyma. The destruction of the pancreas, in this case of acute pancreatitis, is not extensive Discrete, white areas of fat necrosis are present in the omentum of this patient with severe, pancreatitis (acute hemorrhagic pancreatitis). http://zappa.ultrakohl.com/medstud/PicGal/actpan2.htm


Pancreatitis: major causes :Pancreatitis: major causes The major causes are long-standing alcohol consumption or biliary stone disease. The most common cause of acute pancreatitis in developed countries is alcohol abuse. On the cellular level, ethanol leads to intracellular accumulation of digestive enzymes and their premature activation and release. On the ductal level, ethanol increases the permeability of ductules, which allow enzymes to reach the parenchyma, resulting in pancreatic damage. Ethanol increases the protein content of the pancreatic juice and decreases bicarbonate levels and trypsin inhibitor concentrations. This leads to the formation of protein plugs that block the pancreatic outflow and obstruction. Another major cause of acute pancreatitis is biliary stone disease (cholelithiasis and choledocholithiasis). A biliary stone may lodge in the pancreatic duct or ampulla of Vater and obstruct the pancreatic duct, leading to extravasation of enzymes into the parenchyma.


Wet and dry gangrene :Wet and dry gangrene


Dry gangrene(as in diabetes m.) :Dry gangrene(as in diabetes m.)


Tissue storage disorders :Tissue storage disorders


Fatty liver :Fatty liver


Ethanol and cirrhosis of the liver :Ethanol and cirrhosis of the liver


HDL vs LDL :HDL vs LDL HDL (High density lipoprotein) Carries cholesterol in blood from cells to liver Liver cells have HDL receptors Endocytose HDL Excrete to bile HDL removes cholesterol from body LDL carries cholesterol to cells Cholesterol forms plaques in blood vessels Clogs arteries Causes heart attacks


Hepatitis B :Hepatitis B Prognosis: Hepatitis B Outcome in adults and children over age 5 years Recovery: 90% Chronic Active Hepatitis: 10% Fulminant Hepatitis: <1% (high mortality) Outcome in children under age 5 years Chronic infection: 30-90% Worse prognosis if Hepatitis D also present Cirrhosis higher risk Hepatocellular Carcinoma higher risk Prognosis: Hepatitis A Over 85% of people with hepatitis A recover within 3 months, and over 99% of people recover by 6 months. The fatality rate is estimated at 0.1%, usually among the elderly and patients with chronic liver disease. Hepatitis A virus does not become a chronic infection. Prognosis: Hepatitis C Hepatitis C is one of the most common causes of chronic liver disease in the U.S. today. At least 80% of patients with acute hepatitis C ultimately develop chronic liver infection, and 20% to 30% develop cirrhosis. Between 1% and 5% of patients may develop liver cancer. Hepatitis C is now the number 1 cause for liver transplantation in the U.S.


Eggs have gotten a bad rap! :Eggs have gotten a bad rap!


Animal and plant sterols :Animal and plant sterols There is growing evidence that plant sterols/ stanols help in lowering total and low density lipoprotein (LDL) cholesterol levels and that this effect is additive to that achieved by dietary fatty acid manipulation. Cholesterol is the sterol of mammalian cells. ß-Sitosterol is the most common sterol in plants; it differs from cholesterol by having an ethyl group attached at C-24. Hydrogenation of the 5,6 double bond of ß-sitosterol converts it into sitostanol.5 Campesterol and campestanol carry a methyl instead of ethyl group at C-24.


Soy and LDL cholesterol: Then and now :Soy and LDL cholesterol: Then and now THEN: The Soy Health Claim In October 1999, FDA approved a health claim that can be used on labels of soy-based foods to tout their heart-healthy benefits. The agency reviewed research from 27 studies that showed soy protein's value in lowering levels of total cholesterol and low-density lipoprotein (LDL, or "bad" cholesterol). Food marketers can now use the following claim, or a reasonable variation, on their products: "Diets low in saturated fat and cholesterol that include 25 grams of soy protein a day may reduce the risk of heart disease. One serving of (name of food) provides __ grams of soy protein." To qualify for the claim foods must contain per serving: 6.25 grams of soy protein, low fat (less than 3 grams), low saturated fat (less than 1 gram), low cholesterol (less than 20 milligrams), sodium value of less than 480 milligrams for individual foods, less than 720 milligrams if considered a main dish, and less than 960 milligrams if considered a meal. NOW: Lowering cholesterol properties of soy disproved by study Posted on : Tue, 24 Jan 2006 00:02:00 GMT | Author : Ryan Jones According to the findings of a committee of the American Heart Association, benefits of soy-based food in lowering cholesterol have been overstated. Twenty two studies carried out on soy products analyzed by the committee revealed that they had very few benefits for the heart. Researchers go on to add that soy when taken in large amounts only shows slight decline in low-density lipoproteins (LDL), also known as bad cholesterol, and none whatsoever on HDL, known as good cholesterol. Science giveth and science taketh away . . .


Addison’s disease: The hand :Addison’s disease: The hand In their experience with 108 cases of Addison’s disease, Rowntree and Snell noted that asthenia, weight loss, gastrointestinal symptoms (anorexia, nausea, vomiting, and abdominal pain), and hypotension were almost always part of the syndrome. Hyperpigmentation was present in most cases and was described in such terms as “a suntan which does not wear off ... tinged somewhat with blue or gray . . . dirty in appearance.” The exposed portions of the body (hands, face, neck, and arms), points of pressure and friction, nipples, freckles, recently formed scars, genitalia, and creases of the palms often showed exaggerated pigmentation. Brown, blue, or gray spots on the lips and buccal mucous membranes were common. (Cecil’s)


Occupational Lung Disease :Occupational Lung Disease Pneumoconioses are caused by dust that gets into the lungs. Hypersensitivity diseases such as asthma are caused by the lungs' overreaction to airborne pollutants. Asbestosis: This disorder is caused by breathing dust from asbestos, the fireproofing and insulating product often used in the past to wrap water pipes and line furnaces and air conditioning ducts. During its heyday, asbestos was also compressed into floor tiles and was even woven into movie theater curtains, hot pads, and ironing board covers. Asbestos dust can cause inflammation and widespread scarring in the lungs. Berylliosis: This is a lung inflammation caused by inhaling dust or fumes that contain beryllium, a substance widely used in the aerospace industry and employed in the manufacture of fluorescent bulbs. Black Lung: Also known as coal workers' pneumoconiosis (CWP), this disease is found exclusively in coal miners. Caused by inhaling coal dust, it is marked by scarring in the lungs. Byssinosis: The hallmark of this condition is a temporary narrowing of the airways after inhaling particles of cotton, flax, or hemp. The disorder is found almost exclusively in those who work with unprocessed cotton. Occupational asthma: The intermittent breathing problems that mark this disorder can be brought on by a wide variety of substances, including paint, hair bleach and dye, foam and packaging materials that emit chemical dusts or vapors, animal hair and dander, organic dust from milled or ground food (such as flour and coffee), dust from textiles, and metals such as chromium and nickel. Western red cedar is also known to cause occupational asthma. Occupational lung cancer: Although cigarette smoking is the primary cause of lung cancer, some cases can be attributed to various workplace air pollutants, including arsenic, coal tar, petroleum, and radium. Silicosis: This oldest of occupational lung disorders is brought on by inhaling grains of silica (quartz) in mines, foundries, and factories. The particles cause gradual scarring in the lungs that, after many years, may end in emphysema. Industrial bronchitis: Bronchitis (inflammation of the passages in the lungs) has a host of causes, including respiratory infections and persistent exposure to irritants such as dusts, gases, vapors, cigarette smoke, and even general air pollution. Because there can be many causes of bronchitis, both inside and outside the workplace, it is often difficult to say whether the problem has its origin in the workplace. http://www.healthsquare.com/mc/fgmc9013.htm


Shaver’s Disease :Shaver’s Disease Inhalation of finely divided aluminum and aluminum oxide powder has been reported as a cause of pulmonary fibrosis and lung damage. This effect, know as Shaver’s Disease, is complicated by the presence in the inhaled air of silica and oxides of iron. May also be implicated in Alzheimer’s disease.


Gout :Gout The uric acid level in the blood goes up in persons with gout. Alcohol is not recommended for persons with an elevated uric acid because it causes your body to lose water and may increase the uric acid levels in the blood. In general, foods that cause gout are high in fat, which is why dietary recommendations for people with this kind of arthritis advise that less than 30% of their calories come from fat. Proteins with large concentrations of purines include meat and dairy products. Fish, like mackerel, sardines, oysters, mussels, and scallops, should be avoided, as well as red and white meat like poultry, pork, and beef. Sweetmeats, or organ meat, like kidney, heart, or liver, are especially bad for those suffering from gout. Even foods related to meat, like chicken or beef broth, caviar, and bouillon might produce high levels of uric acid. Other foods that cause gout are dairy and vegetables, because they have lots of purines as well. High-fat dairy, like whole milk, ice cream, butter, and cheese, must be avoided in favor of low-fat dairy, or soy replacements. Spinach, mushrooms, cauliflower, peas, and asparagus have been shown to be rich in purines. In an unrelated food category, lentil beans and yeast increase one's chance of gout flaring up. For this reason, even beer and alcohol, because they are derived from yeast and grains, can increase the discomfort of gout.


Amyloidosis :Amyloidosis Amyloidosis refers to the extracellular deposition of a protein called amyloid. This protein deposition can affect multiple organs. In this picture, we see how amyloidosis can affect the skin as nodular deposits on the fingers. Amyloidosis can cause a patchy, bruised appearance to the skin. Bruises of the skin around the eyes are referred to as the characteristic "pinched purpura". Three major types of amyloid and several less common forms have been defined biochemically: (1) AL: an N-terminal sequence that is homologous to a portion of the variable region of an immunoglobulin light chain, occurs in primary amyloidosis and with multiple myelom; (2) AA: unique N-terminal sequence of a nonimmunoglobulin protein called AA protein; (3) associated with familial amyloid polyneuropathy, a transthyretin (prealbumin) molecule that has a single amino acid substitution.


Aging and free radicals :Aging and free radicals


Progeria and Werner’sSyndrome :Progeria and Werner’sSyndrome The cause of progeria (HGPS) is unknown. It is an autosomal recessive disease, meaning that an individual carrying a mutation in a single gene does not show any symptoms. When two individuals with the mutant gene have a child, that child has a 1 in 4 chance of inheriting two copies of the mutation and therefore having the disease. The autosomal recessive gene mutation causing Werner syndrome, on the other hand, has been identified (National Library of Medicine), and cloned. The Werner syndrome protein (WRN) codes for an enzyme in the family of enzymes called helicases. These enzymes are responsible for unwinding the double strand of DNA in each cell as the DNA is to be duplicated for cell division. Each strand of DNA has its own helicase associated with it. Although the mechanism by which a defect in this enzyme would cause Werner syndrome is not known, it's normal counterpart may be responsible for DNA repair, and thus preventing cancer and cell defects. http://www.seps.org/cvoracle/faq/progeria.html


Splenic notch :Splenic notch As the spleen enlarges, its motion with respiration diminishes. With a large mass in the left upper quadrant, the notch on the medial border at the splenic hilum is sometimes helpful to identify the mass as the spleen.


Pulsus alternans: sign of failing ventricle :Pulsus alternans: sign of failing ventricle Pulsus alternans or mechanical alternans is a term used to describe the phenomenon of alternate strong and weak ventricular contractions in the presence of an unaltered heart rate and QRS complex.


Renal cell carcinoma :Renal cell carcinoma Carcinoma, Renal Cell Important It is possible that the main title of the report Carcinoma, Renal Cell is not the name you expected. Please check the synonyms listing to find the alternate name(s) and disorder subdivision(s) covered by this report. Synonyms Grawitz Tumor Hypernephroma Nephrocarcinoma RCC Renal Adenocarcinoma