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White lesion on cheek

This is a cutaneous calculus, or subepidermal calcified nodule, a lesion caused by the accumulation of calcium in the upper dermis. They have a cream white colour, are usually solitary, often appear filiform, and most commonly occur in children on the head and neck, especially the ear. It is thought that they usually arise in a pre-existing skin lesion, possibly a viral wart. They are usually not associated with disorders of calcium metabolism. They respond well to curettage or shave excision, and usually do not recur.

This 75-year-old woman has developed a painful haemorrhagic lesion in the last 2 days on her lateral calf. She has coronary artery disease and atrial fibrillation.

This is coumarin necrosis. It most frequently occurs shortly after the introduction of a coumarin anticoagulant (eg, warfarin). Natural anticoagulants reduce in concentration before natural pro-coagulants, so that there is the potential for a short period of relative thrombophilia and this can result in dermal vessel thrombosis andsubsequent skin necrosis. Dermal vessel thrombosis and skin necrosis has been reported in persons with protein S and C deficiency. It is occasionally seen later during anticoagulant treatment particularly if there has been erratic warfarin control. It can be managed by initiation of heparin, withdrawal of warfarin, and then the use of a new oral anticoagulant which directly inhibits either thrombin or factor Xa. Established necrosis may require devitalised tissue debridement.

This 83-year-old lady has had recurrent attacks of bruise-like lesions on the eyelids. They are sometimes provoked by bouts of coughing.

Purpura can be seen affecting the upper and lower lids of both eyes. It is quite common for lid purpura to be precipitated after bouts of coughing. In the absence of any clotting or platelet problems, systemic amyloidosis should be considered. The presence of amyloid in the upper dermis disrupts the integrity of the support around small blood vessels making them susceptible to rupturing, and this accounts for the physical signs. Amyloid deposits under the flexor retinaculum of the wrists has produced carpal tunnel syndrome which is quite common in systemic amyloid. Systemic AL amyloid is usually associated with a plasma cell dyscrasia, so serum electrophoresis, estimation of immunoglobulins, and detection of Bence Jones proteins should be undertaken. Skin biopsies from affected skin may show amorphous upper dermal accumulation of amyloid protein.

Nasopharynx, mucormycosis (zygomycosis), H and E stain, microscopic.

Nasopharyngea mucormycosis, with soft tissue infiltrated by broad, non-septate hyphae of Mucor, are seen best with a routine H and E stain, as shown here. Ketoacidosis predisposes to this complication.This is a feared complication of diabetes mellitus type I. Diabetic ketoacidosis helps to potentiate the growth of Mucor. The site of involvement is typically the nasopharyngeal region, but the infection can spread to involve soft tissues and bone of the face, orbit, skull, and brain.

Gangrenous necrosis and ulceration, lower extremity, gross.

Gangrenous necrosis and ulceration involving the lower extremity is shown here. Diabetics have accelerated atherosclerosis that can be extensive to involve peripheral vasculature and predispose to this complication.Persons with diabetes mellitus, either type I or type II, have early and accelerated atherosclerosis. The most serious complications of this are atherosclerotic heart disease, cerebrovascular disease, and renal disease. The most common cause of death with diabetes mellitus is myocardial infarction. Peripheral vascular disease is a particular problem with diabetes mellitus and is made worse through the development of diabetic neuropathy, leading to propensity for injury.

Foot with previous healed transmetatarsal amputation and recent ulcer, gross.

A diabetic foot with a previous healed transmetatarsal amputation demonstrates an ulcer in the region of the ankle.Persons with diabetes mellitus, either type I or type II, have early and accelerated atherosclerosis. The most serious complications of this are atherosclerotic heart disease, cerebrovascular disease, and renal disease. The most common cause of death with diabetes mellitus is myocardial infarction. Peripheral vascular disease is a particular problem with diabetes mellitus and is made worse through the development of diabetic neuropathy, leading to propensity for injury.

Aortic atherosclerosis demonstrated in three aortas, gross.

Aortic atherosclerosis is demonstrated in three aortas, from minimal at the bottom to severe at the top. Diabetics tend to have more advanced, extensive atherosclerosis.Persons with diabetes mellitus, either type I or type II, have early and accelerated atherosclerosis. The most serious complications of this are atherosclerotic heart disease, cerebrovascular disease, and renal disease. The most common cause of death with diabetes mellitus is myocardial infarction. Peripheral vascular disease is a particular problem with diabetes mellitus and is made worse through the development of diabetic neuropathy, leading to propensity for injury.

Interventricular septum, recent myocardial infarction, gross.

The interventricular septum has been sectioned to reveal a large recent myocardial infarction (about 4 to 7 days old) with a tan-yellow necrotic center surrounded by a zone of hyperemia, gross. About half of persons with diabetes mellitus will die from a myocardial infarction as a consequence of coronary atherosclerosis.Persons with diabetes mellitus, either type I or type II, have early and accelerated atherosclerosis. The most serious complications of this are atherosclerotic heart disease, cerebrovascular disease, and renal disease. The most common cause of death with diabetes mellitus is myocardial infarction. Peripheral vascular disease is a particular problem with diabetes mellitus and is made worse through the development of diabetic neuropathy, leading to propensity for injury.

Left anterior descending coronary artery, recent thrombus, microscopic.

The anterior interventricular (left anterior descending) coronary artery that courses over the anterior surface of the heart shown here is opened to demonstrate a recent red-black thrombus filling the lumen in a patient with diabetes mellitus.Persons with diabetes mellitus, either type I or type II, have early and accelerated atherosclerosis. The most serious complications of this are atherosclerotic heart disease, cerebrovascular disease, and renal disease. The most common cause of death with diabetes mellitus is myocardial infarction. Peripheral vascular disease is a particular problem with diabetes mellitus and is made worse through the development of diabetic neuropathy, leading to propensity for injury.

Left anterior descending coronary artery, advanced atherosclerosis, gross.

The anterior interventricular (left anterior descending) coronary artery sectioned along its length to reveal narrowing of the lumen, most pronounced in the proximal portion at the left, from advanced atherosclerosis in a diabetic.Persons with diabetes mellitus, either type I or type II, have early and accelerated atherosclerosis. The most serious complications of this are atherosclerotic heart disease, cerebrovascular disease, and renal disease. The most common cause of death with diabetes mellitus is myocardial infarction. Peripheral vascular disease is a particular problem with diabetes mellitus and is made worse through the development of diabetic neuropathy, leading to propensity for injury.

Cataract of the crystalline lens, gross.

Cataracts of the crystalline lens with opacification, as shown here, are more frequent in persons with diabetes mellitus.The eyes can be affected in several ways by diabetes mellitus. Diabetic retinopathy is one of the leading causes for irreversible blindness in the United States. This retinopathy can occur with either type I or type II diabetes mellitus, usually a decade or so after the onset of diabetes. Most persons with type I diabetes and many of those with type II diabetes develop some background (non-proliferative ) retinopathy. Proliferative retinopathy is more ominous and is more likely to occur when diabetes mellitus is poorly controlled. In severe retinopathy, neovascularization may lead to adhesions (synechiae) between iris and cornea or iris and lens. Neovascularization of the iris leads to secondary glaucoma with blindness. Cataracts are more common in diabetics. This predilection for development of cataracts is felt to result from hyperglycemia leading to accumulation of sorbitol that results in osmotic damage to the crystalline lens.

Glaucoma with excavation of the optic cup, microscopic.

Glaucoma with excavation of the optic cup is shown here microscopically. Diabetics are more prone to develop this complication.The eyes can be affected in several ways by diabetes mellitus. Diabetic retinopathy is one of the leading causes for irreversible blindness in the United States. This retinopathy can occur with either type I or type II diabetes mellitus, usually a decade or so after the onset of diabetes. Most persons with type I diabetes and many of those with type II diabetes develop some background (non-proliferative ) retinopathy. Proliferative retinopathy is more ominous and is more likely to occur when diabetes mellitus is poorly controlled. In severe retinopathy, neovascularization may lead to adhesions (synechiae) between iris and cornea or iris and lens. Neovascularization of the iris leads to secondary glaucoma with blindness. Cataracts are more common in diabetics. This predilection for development of cataracts is felt to result from hyperglycemia leading to accumulation of sorbitol that results in osmotic damage to the crystalline lens.

Glaucoma, cupping of the optic disk on funduscopic examination.

Glaucoma with marked cupping of the optic disk is seen on funduscopic examination. The incidence of glaucoma is higher in the diabetic population.The eyes can be affected in several ways by diabetes mellitus. Diabetic retinopathy is one of the leading causes for irreversible blindness in the United States. This retinopathy can occur with either type I or type II diabetes mellitus, usually a decade or so after the onset of diabetes. Most persons with type I diabetes and many of those with type II diabetes develop some background (non-proliferative ) retinopathy. Proliferative retinopathy is more ominous and is more likely to occur when diabetes mellitus is poorly controlled. In severe retinopathy, neovascularization may lead to adhesions (synechiae) between iris and cornea or iris and lens. Neovascularization of the iris leads to secondary glaucoma with blindness. Cataracts are more common in diabetics. This predilection for development of cataracts is felt to result from hyperglycemia leading to accumulation of sorbitol that results in osmotic damage to the crystalline lens.

Proliferative diabetic retinopathy on funduscopic examination.

Proliferative diabetic retinopathy on funduscopic examination is shown here. This is a particularly serious complication in diabetics that can lead to blindness.The eyes can be affected in several ways by diabetes mellitus. Diabetic retinopathy is one of the leading causes for irreversible blindness in the United States. This retinopathy can occur with either type I or type II diabetes mellitus, usually a decade or so after the onset of diabetes. Most persons with type I diabetes and many of those with type II diabetes develop some background (non-proliferative ) retinopathy. Proliferative retinopathy is more ominous and is more likely to occur when diabetes mellitus is poorly controlled. In severe retinopathy, neovascularization may lead to adhesions (synechiae) between iris and cornea or iris and lens. Neovascularization of the iris leads to secondary glaucoma with blindness. Cataracts are more common in diabetics. This predilection for development of cataracts is felt to result from hyperglycemia leading to accumulation of sorbitol that results in osmotic damage to the crystalline lens.

Diabetic retinopathy on funduscopic examination.

Diabetic retinopathy is shown here on funduscopic examination.The eyes can be affected in several ways by diabetes mellitus. Diabetic retinopathy is one of the leading causes for irreversible blindness in the United States. This retinopathy can occur with either type I or type II diabetes mellitus, usually a decade or so after the onset of diabetes. Most persons with type I diabetes and many of those with type II diabetes develop some background (non-proliferative ) retinopathy. Proliferative retinopathy is more ominous and is more likely to occur when diabetes mellitus is poorly controlled. In severe retinopathy, neovascularization may lead to adhesions (synechiae) between iris and cornea or iris and lens. Neovascularization of the iris leads to secondary glaucoma with blindness. Cataracts are more common in diabetics. This predilection for development of cataracts is felt to result from hyperglycemia leading to accumulation of sorbitol that results in osmotic damage to the crystalline lens.

Normal appearance, retina on funduscopic examination.

This is the normal appearance of the retina on funduscopic examination.The eyes can be affected in several ways by diabetes mellitus. Diabetic retinopathy is one of the leading causes for irreversible blindness in the United States. This retinopathy can occur with either type I or type II diabetes mellitus, usually a decade or so after the onset of diabetes. Most persons with type I diabetes and many of those with type II diabetes develop some background (non-proliferative ) retinopathy. Proliferative retinopathy is more ominous and is more likely to occur when diabetes mellitus is poorly controlled. In severe retinopathy, neovascularization may lead to adhesions (synechiae) between iris and cornea or iris and lens. Neovascularization of the iris leads to secondary glaucoma with blindness. Cataracts are more common in diabetics. This predilection for development of cataracts is felt to result from hyperglycemia leading to accumulation of sorbitol that results in osmotic damage to the crystalline lens.

Renal pelvis, infection with Candida albicans, PAS stain, microscopic.

The urinary tract can be involved by an ascending urinary tract infection. Diabetics are more prone to develop infections in general. Here are seen budding cells with pseudohyphae with Candida albicans on PAS stain in the renal pelvis.There are a variety of complications involving the kidney. Both nodular and diffuse glomerulosclerosis can lead to chronic renal failure. Diabetics are prone to infections, particularly pyelonephritis. Both bacterial and fungal infections can occur.

Kidney, acute pyelonephritis, microscopic.

An acute pyelonephritis shown involving the medulla of the kidney. Note the numerous neutrophils.There are a variety of complications involving the kidney. Both nodular and diffuse glomerulosclerosis can lead to chronic renal failure. Diabetics are prone to infections, particularly pyelonephritis. Both bacterial and fungal infections can occur.

Renal glomerulus, nodular glomerulosclerosis, hyaline arteriolosclerosis, PAS stain, microscopic.

A renal glomerulus with nodular glomerulosclerosis, along with hyaline arteriolosclerosis in the small arteriole to the lower right of the glomerulus, is shown here with PAS stain.There are a variety of complications involving the kidney. Both nodular and diffuse glomerulosclerosis can lead to chronic renal failure. Diabetics are prone to infections, particularly pyelonephritis. Both bacterial and fungal infections can occur.

Renal glomerulus, nodular glomerulosclerosis, microscopic.

A renal glomerulus demonstrate nodular glomerulosclerosis with diabetes mellitus. This lesion is quite characteristic for diabetes mellitus. A diffuse glomerulosclerosis may also be seen.There are a variety of complications involving the kidney. Both nodular and diffuse glomerulosclerosis can lead to chronic renal failure. Diabetics are prone to infections, particularly pyelonephritis. Both bacterial and fungal infections can occur.

Islet of Langerhans, deposition of amyloid, microscopic.

An islet of Langerhans demonstrates amorphous pink deposition of amyloid in a patient with type II diabetes mellitus.The pathogenesis of diabetes mellitus type I involves destruction of the islets of Langerhans. This occurs probably as a consequence of a genetic susceptibility, followed by the onset of autoimmune destruction triggered by some environmental factor such as a viral infection. Heavy lymphocytic infiltrates appear in and around islets. The number and size of islets are eventually reduced, leading to decreased insulin production and glucose intolerance. Insulin is a hormone required for glucose uptake into adipose tissue and muscle. When glucose uptake is impaired, the blood glucose rises, and alternate biochemical pathways are upregulated, including use of fatty acids as a fuel.In diabetes mellitus type II, the islets of Langerhans are normal in number or somewhat reduced. There can be increased resistance of cells to glucose uptake, impaired release of insulin, and other dysregulated metabolic pathways. The most common risk factor is increased amounts of adipose tissue. Fibrosis and deposition of amylin polypeptide within islets are most characteristic of the chronic states of type II diabetes.

Islet of Langerhans, insulitis, microscopic.

An islet of Langerhans demonstrates insulitis with lymphocytic infiltrates in a patient developing type I diabetes mellitus. This lesion precedes clinical onset of diabetes mellitus and is rarely observed.The pathogenesis of diabetes mellitus type I involves destruction of the islets of Langerhans. This occurs probably as a consequence of a genetic susceptibility, followed by the onset of autoimmune destruction triggered by some environmental factor such as a viral infection. Heavy lymphocytic infiltrates appear in and around islets. The number and size of islets are eventually reduced, leading to decreased insulin production and glucose intolerance. Insulin is a hormone required for glucose uptake into adipose tissue and muscle. When glucose uptake is impaired, the blood glucose rises, and alternate biochemical pathways are upregulated, including use of fatty acids as a fuel.In diabetes mellitus type II, the islets of Langerhans are normal in number or somewhat reduced. There can be increased resistance of cells to glucose uptake, impaired release of insulin, and other dysregulated metabolic pathways. The most common risk factor is increased amounts of adipose tissue. Fibrosis and deposition of amylin polypeptide within islets are most characteristic of the chronic states of type II diabetes.

Normal islets of Langerhans, with immunohistochemical stains (right, insulin and left, glucagon), microscopic.

Normal islets of Langerhans, on the right with immunohistochemical staining for insulin to identify beta cells and on the left with immunohistochemical staining for glucagon to identify alpha cells, are shown here.The pathogenesis of diabetes mellitus type I involves destruction of the islets of Langerhans. This occurs probably as a consequence of a genetic susceptibility, followed by the onset of autoimmune destruction triggered by some environmental factor such as a viral infection. Heavy lymphocytic infiltrates appear in and around islets. The number and size of islets are eventually reduced, leading to decreased insulin production and glucose intolerance. Insulin is a hormone required for glucose uptake into adipose tissue and muscle. When glucose uptake is impaired, the blood glucose rises, and alternate biochemical pathways are upregulated, including use of fatty acids as a fuel.In diabetes mellitus type II, the islets of Langerhans are normal in number or somewhat reduced. There can be increased resistance of cells to glucose uptake, impaired release of insulin, and other dysregulated metabolic pathways. The most common risk factor is increased amounts of adipose tissue. Fibrosis and deposition of amylin polypeptide within islets are most characteristic of the chronic states of type II diabetes.

Gynecomastia, gross.

The use of anabolic-androgenic steroids (AAS) has increased substantially over the past 4 decades. These drugs are used mainly for their effect of increasing muscle mass for the desired goal of increasing athletic performance and enhancing physical appearance. However, such drugs do not increase the level of skill in performance and cardiovascular function--the major enhancers to most sports-related activities. (Sjöqvist et al, 2008) (Thirumalai and Anawalt, 2023). Both oral and injectable compounds are used, more often the latter. Users may cycle on and off usage to avoid complications, but prolonged usage brings many adverse effects. In men these include: testicular atrophy, decreased testosterone production, gynecomastia, decreased sex drive, infertility, baldness, hypertension, heart disease, and tendon injuries. In women, the adverse effects reported include: decreased breast size, fluid retention, hypertension, and sleep disorders. Physical changes such as testicular atrophy and gynecomastia in men, or breast atrophy in women, are often not reversible even after stopping the drugs. Adolescents taking AAS may have diminished bone growth and shorter stature. AAS may produce cholestatic jaundice; they reduce the level of HDL cholesterol to promote atherogenesis and heart disease. (Sjöqvist et al, 2008) (Thirumalai and Anawalt, 2023). The major psychiatric effects of AAS use include changes in mood, worse with greater usage. While using the drugs increased aggression and mania can occur. Off the drugs depression occurs. The combination resembles bipolar disorder, a disabling mental health disorder. Such adverse effects could significantly impact athletic performance negatively and decrease sexual function. In short, AAS can prevent the very things that they are supposed to enhance. (Thirumalai and Anawalt, 2023). The most serious complication of AAS use is an increased risk for heart disease and sudden death. Anabolic steroids decrease HDL cholesterol and increase cardiac size. Myocardial fibrosis can occur, similar to cardiomyopathy. Hypertension induced by AAS further increases heart size. These effects may persist even after use of AAS has been stopped, increasing the risk for morbidity and mortality. Anabolic steroids have been shown to enhance the coronary artery response to catecholamines released during periods of stress, and this may play a role in the sudden cardiac deaths reported with their use. Contraction band necrosis, indicative of ischemia, has been observed in such deaths. (Fineschi et al, 2001). The use of growth hormone (GH), insulin-like growth factor-1 (IGF-1), and insulin at high, non-physiologic amounts, as anabolic hormonal substances has no significant effect upon increasing muscle mass. Instead, such compounds over time lead to disease states: acromegaly with disfiguring soft tissue changes, diabetes mellitus, hypertension, heart disease, and nerve damage. (García-Arnés and García-Casares, 2023). Improper methods of injection with lack of sterile technique increase the risk for transmissible infections, including viral hepatitis B, viral hepatitis C, and human immunodeficiency virus (HIV). (Thirumalai and Anawalt, 2023)

Testicular atrophy, microscopic.

The use of anabolic-androgenic steroids (AAS) has increased substantially over the past 4 decades. These drugs are used mainly for their effect of increasing muscle mass for the desired goal of increasing athletic performance and enhancing physical appearance. However, such drugs do not increase the level of skill in performance and cardiovascular function--the major enhancers to most sports-related activities. (Sjöqvist et al, 2008) (Thirumalai and Anawalt, 2023). Both oral and injectable compounds are used, more often the latter. Users may cycle on and off usage to avoid complications, but prolonged usage brings many adverse effects. In men these include: testicular atrophy, decreased testosterone production, gynecomastia, decreased sex drive, infertility, baldness, hypertension, heart disease, and tendon injuries. In women, the adverse effects reported include: decreased breast size, fluid retention, hypertension, and sleep disorders. Physical changes such as testicular atrophy and gynecomastia in men, or breast atrophy in women, are often not reversible even after stopping the drugs. Adolescents taking AAS may have diminished bone growth and shorter stature. AAS may produce cholestatic jaundice; they reduce the level of HDL cholesterol to promote atherogenesis and heart disease. (Sjöqvist et al, 2008) (Thirumalai and Anawalt, 2023). The major psychiatric effects of AAS use include changes in mood, worse with greater usage. While using the drugs increased aggression and mania can occur. Off the drugs depression occurs. The combination resembles bipolar disorder, a disabling mental health disorder. Such adverse effects could significantly impact athletic performance negatively and decrease sexual function. In short, AAS can prevent the very things that they are supposed to enhance. (Thirumalai and Anawalt, 2023). The most serious complication of AAS use is an increased risk for heart disease and sudden death. Anabolic steroids decrease HDL cholesterol and increase cardiac size. Myocardial fibrosis can occur, similar to cardiomyopathy. Hypertension induced by AAS further increases heart size. These effects may persist even after use of AAS has been stopped, increasing the risk for morbidity and mortality. Anabolic steroids have been shown to enhance the coronary artery response to catecholamines released during periods of stress, and this may play a role in the sudden cardiac deaths reported with their use. Contraction band necrosis, indicative of ischemia, has been observed in such deaths. (Fineschi et al, 2001). The use of growth hormone (GH), insulin-like growth factor-1 (IGF-1), and insulin at high, non-physiologic amounts, as anabolic hormonal substances has no significant effect upon increasing muscle mass. Instead, such compounds over time lead to disease states: acromegaly with disfiguring soft tissue changes, diabetes mellitus, hypertension, heart disease, and nerve damage. (García-Arnés and García-Casares, 2023). Improper methods of injection with lack of sterile technique increase the risk for transmissible infections, including viral hepatitis B, viral hepatitis C, and human immunodeficiency virus (HIV). (Thirumalai and Anawalt, 2023)

Testicular atrophy, gross.

The use of anabolic-androgenic steroids (AAS) has increased substantially over the past 4 decades. These drugs are used mainly for their effect of increasing muscle mass for the desired goal of increasing athletic performance and enhancing physical appearance. However, such drugs do not increase the level of skill in performance and cardiovascular function--the major enhancers to most sports-related activities. (Sjöqvist et al, 2008) (Thirumalai and Anawalt, 2023). Both oral and injectable compounds are used, more often the latter. Users may cycle on and off usage to avoid complications, but prolonged usage brings many adverse effects. In men these include: testicular atrophy, decreased testosterone production, gynecomastia, decreased sex drive, infertility, baldness, hypertension, heart disease, and tendon injuries. In women, the adverse effects reported include: decreased breast size, fluid retention, hypertension, and sleep disorders. Physical changes such as testicular atrophy and gynecomastia in men, or breast atrophy in women, are often not reversible even after stopping the drugs. Adolescents taking AAS may have diminished bone growth and shorter stature. AAS may produce cholestatic jaundice; they reduce the level of HDL cholesterol to promote atherogenesis and heart disease. (Sjöqvist et al, 2008) (Thirumalai and Anawalt, 2023). The major psychiatric effects of AAS use include changes in mood, worse with greater usage. While using the drugs increased aggression and mania can occur. Off the drugs depression occurs. The combination resembles bipolar disorder, a disabling mental health disorder. Such adverse effects could significantly impact athletic performance negatively and decrease sexual function. In short, AAS can prevent the very things that they are supposed to enhance. (Thirumalai and Anawalt, 2023). The most serious complication of AAS use is an increased risk for heart disease and sudden death. Anabolic steroids decrease HDL cholesterol and increase cardiac size. Myocardial fibrosis can occur, similar to cardiomyopathy. Hypertension induced by AAS further increases heart size. These effects may persist even after use of AAS has been stopped, increasing the risk for morbidity and mortality. Anabolic steroids have been shown to enhance the coronary artery response to catecholamines released during periods of stress, and this may play a role in the sudden cardiac deaths reported with their use. Contraction band necrosis, indicative of ischemia, has been observed in such deaths. (Fineschi et al, 2001). The use of growth hormone (GH), insulin-like growth factor-1 (IGF-1), and insulin at high, non-physiologic amounts, as anabolic hormonal substances has no significant effect upon increasing muscle mass. Instead, such compounds over time lead to disease states: acromegaly with disfiguring soft tissue changes, diabetes mellitus, hypertension, heart disease, and nerve damage. (García-Arnés and García-Casares, 2023). Improper methods of injection with lack of sterile technique increase the risk for transmissible infections, including viral hepatitis B, viral hepatitis C, and human immunodeficiency virus (HIV). (Thirumalai and Anawalt, 2023)

Heart with myocardial contraction band necrosis, trichrome stain, microscopic.

The use of anabolic-androgenic steroids (AAS) has increased substantially over the past 4 decades. These drugs are used mainly for their effect of increasing muscle mass for the desired goal of increasing athletic performance and enhancing physical appearance. However, such drugs do not increase the level of skill in performance and cardiovascular function--the major enhancers to most sports-related activities. (Sjöqvist et al, 2008) (Thirumalai and Anawalt, 2023). Both oral and injectable compounds are used, more often the latter. Users may cycle on and off usage to avoid complications, but prolonged usage brings many adverse effects. In men these include: testicular atrophy, decreased testosterone production, gynecomastia, decreased sex drive, infertility, baldness, hypertension, heart disease, and tendon injuries. In women, the adverse effects reported include: decreased breast size, fluid retention, hypertension, and sleep disorders. Physical changes such as testicular atrophy and gynecomastia in men, or breast atrophy in women, are often not reversible even after stopping the drugs. Adolescents taking AAS may have diminished bone growth and shorter stature. AAS may produce cholestatic jaundice; they reduce the level of HDL cholesterol to promote atherogenesis and heart disease. (Sjöqvist et al, 2008) (Thirumalai and Anawalt, 2023). The major psychiatric effects of AAS use include changes in mood, worse with greater usage. While using the drugs increased aggression and mania can occur. Off the drugs depression occurs. The combination resembles bipolar disorder, a disabling mental health disorder. Such adverse effects could significantly impact athletic performance negatively and decrease sexual function. In short, AAS can prevent the very things that they are supposed to enhance. (Thirumalai and Anawalt, 2023). The most serious complication of AAS use is an increased risk for heart disease and sudden death. Anabolic steroids decrease HDL cholesterol and increase cardiac size. Myocardial fibrosis can occur, similar to cardiomyopathy. Hypertension induced by AAS further increases heart size. These effects may persist even after use of AAS has been stopped, increasing the risk for morbidity and mortality. Anabolic steroids have been shown to enhance the coronary artery response to catecholamines released during periods of stress, and this may play a role in the sudden cardiac deaths reported with their use. Contraction band necrosis, indicative of ischemia, has been observed in such deaths. (Fineschi et al, 2001). The use of growth hormone (GH), insulin-like growth factor-1 (IGF-1), and insulin at high, non-physiologic amounts, as anabolic hormonal substances has no significant effect upon increasing muscle mass. Instead, such compounds over time lead to disease states: acromegaly with disfiguring soft tissue changes, diabetes mellitus, hypertension, heart disease, and nerve damage. (García-Arnés and García-Casares, 2023). Improper methods of injection with lack of sterile technique increase the risk for transmissible infections, including viral hepatitis B, viral hepatitis C, and human immunodeficiency virus (HIV). (Thirumalai and Anawalt, 2023)

Heart with hypertrophy, gross.

The use of anabolic-androgenic steroids (AAS) has increased substantially over the past 4 decades. These drugs are used mainly for their effect of increasing muscle mass for the desired goal of increasing athletic performance and enhancing physical appearance. However, such drugs do not increase the level of skill in performance and cardiovascular function--the major enhancers to most sports-related activities. (Sjöqvist et al, 2008) (Thirumalai and Anawalt, 2023). Both oral and injectable compounds are used, more often the latter. Users may cycle on and off usage to avoid complications, but prolonged usage brings many adverse effects. In men these include: testicular atrophy, decreased testosterone production, gynecomastia, decreased sex drive, infertility, baldness, hypertension, heart disease, and tendon injuries. In women, the adverse effects reported include: decreased breast size, fluid retention, hypertension, and sleep disorders. Physical changes such as testicular atrophy and gynecomastia in men, or breast atrophy in women, are often not reversible even after stopping the drugs. Adolescents taking AAS may have diminished bone growth and shorter stature. AAS may produce cholestatic jaundice; they reduce the level of HDL cholesterol to promote atherogenesis and heart disease. (Sjöqvist et al, 2008) (Thirumalai and Anawalt, 2023). The major psychiatric effects of AAS use include changes in mood, worse with greater usage. While using the drugs increased aggression and mania can occur. Off the drugs depression occurs. The combination resembles bipolar disorder, a disabling mental health disorder. Such adverse effects could significantly impact athletic performance negatively and decrease sexual function. In short, AAS can prevent the very things that they are supposed to enhance. (Thirumalai and Anawalt, 2023). The most serious complication of AAS use is an increased risk for heart disease and sudden death. Anabolic steroids decrease HDL cholesterol and increase cardiac size. Myocardial fibrosis can occur, similar to cardiomyopathy. Hypertension induced by AAS further increases heart size. These effects may persist even after use of AAS has been stopped, increasing the risk for morbidity and mortality. Anabolic steroids have been shown to enhance the coronary artery response to catecholamines released during periods of stress, and this may play a role in the sudden cardiac deaths reported with their use. Contraction band necrosis, indicative of ischemia, has been observed in such deaths. (Fineschi et al, 2001). The use of growth hormone (GH), insulin-like growth factor-1 (IGF-1), and insulin at high, non-physiologic amounts, as anabolic hormonal substances has no significant effect upon increasing muscle mass. Instead, such compounds over time lead to disease states: acromegaly with disfiguring soft tissue changes, diabetes mellitus, hypertension, heart disease, and nerve damage. (García-Arnés and García-Casares, 2023). Improper methods of injection with lack of sterile technique increase the risk for transmissible infections, including viral hepatitis B, viral hepatitis C, and human immunodeficiency virus (HIV). (Thirumalai and Anawalt, 2023)

Heart with ischemic changes, microscopic.

Methampetamine is a stimulant drug with inotropic effects upon the cardiovascular system. Methamphetamine is metabolized to amphetamine, which is also a stimulant. Methamphetamine and amphetamine have similar effects to cocaine on the cardiovascular system. The heart may have such stress placed upon it that there are ischemic changes to the myocardial fibers. Chronic use leads to hypertrophy, interstitial fibrosis and microvascular disease. The myocardial effects are made worse by concomitant ethanol use. 

Abruptio placenta with large recent blood clot compressing the parenchyma, gross.

Cocaine can exert a variety of effects. The major acute effects producing pathologic conditions result from the increased circulating catecholamine levels with cocaine use. These increased catecholamines can produce vasoconstriction. The lesions can include acute hemorrhages and infarction in the brain. Cerebral infarction can occur within 3 hours of cocaine use even in young persons. Subarachnoid haemorrhage is often associated with rupture of a berry aneurysm. Intraparenchymal haemorrhage can occur in the basal ganglia and thalamus. (Milroy and Parai, 2011). Ischemic changes in the heart from small artery narrowing and sclerosis lead to contraction band necrosis of the myocardium and possible sudden death. With chronic usage, the myocardium develops interstitial fibrosis, and the heart becomes enlarged. Atheroma formation in artereis as well as arterial dissection can occur. (Milroy and Parai, 2011) Combining cocaine use with ethanol use can compound the myocardial damage. (Awtry and Philippides, 2010). Pregnant mothers who use cocaine can affect their fetuses from abnormalities of placental function leading to low birth weight babies or an increased risk for placental abruption. Maternal cocaine use increases the risk for spontaneous abortion. (Kuczkowski, 2007). Persons with cocaine intoxication (not necessarily related to the drug level) may develop a state of iatrogenic psychosis (cocaine psychosis) with "excited delerium" in which they are markedly agitated and combative and develop hyperthermia, often of a severe degree (to 106 F). Organ damage can accompany this state of excited delerium and may include rhabdomyolysis of muscle, hepatotoxicity, and renal failure. Disseminated intravascular coagulation (DIC), hypotension, and sudden death are additional complications. (Devlin and Henry, 2008)

Heart with peripheral coronary artery sclerosis, microscopic.

Cocaine can exert a variety of effects. The major acute effects producing pathologic conditions result from the increased circulating catecholamine levels with cocaine use. These increased catecholamines can produce vasoconstriction. The lesions can include acute hemorrhages and infarction in the brain. Cerebral infarction can occur within 3 hours of cocaine use even in young persons. Subarachnoid haemorrhage is often associated with rupture of a berry aneurysm. Intraparenchymal haemorrhage can occur in the basal ganglia and thalamus. (Milroy and Parai, 2011). Ischemic changes in the heart from small artery narrowing and sclerosis lead to contraction band necrosis of the myocardium and possible sudden death. With chronic usage, the myocardium develops interstitial fibrosis, and the heart becomes enlarged. Atheroma formation in artereis as well as arterial dissection can occur. (Milroy and Parai, 2011) Combining cocaine use with ethanol use can compound the myocardial damage. (Awtry and Philippides, 2010). Pregnant mothers who use cocaine can affect their fetuses from abnormalities of placental function leading to low birth weight babies or an increased risk for placental abruption. Maternal cocaine use increases the risk for spontaneous abortion. (Kuczkowski, 2007). Persons with cocaine intoxication (not necessarily related to the drug level) may develop a state of iatrogenic psychosis (cocaine psychosis) with "excited delerium" in which they are markedly agitated and combative and develop hyperthermia, often of a severe degree (to 106 F). Organ damage can accompany this state of excited delerium and may include rhabdomyolysis of muscle, hepatotoxicity, and renal failure. Disseminated intravascular coagulation (DIC), hypotension, and sudden death are additional complications. (Devlin and Henry, 2008)

Heart with myocardial contraction band necrosis, microscopic.

Cocaine can exert a variety of effects. The major acute effects producing pathologic conditions result from the increased circulating catecholamine levels with cocaine use. These increased catecholamines can produce vasoconstriction. The lesions can include acute hemorrhages and infarction in the brain. Cerebral infarction can occur within 3 hours of cocaine use even in young persons. Subarachnoid haemorrhage is often associated with rupture of a berry aneurysm. Intraparenchymal haemorrhage can occur in the basal ganglia and thalamus. (Milroy and Parai, 2011). Ischemic changes in the heart from small artery narrowing and sclerosis lead to contraction band necrosis of the myocardium and possible sudden death. With chronic usage, the myocardium develops interstitial fibrosis, and the heart becomes enlarged. Atheroma formation in artereis as well as arterial dissection can occur. (Milroy and Parai, 2011) Combining cocaine use with ethanol use can compound the myocardial damage. (Awtry and Philippides, 2010). Pregnant mothers who use cocaine can affect their fetuses from abnormalities of placental function leading to low birth weight babies or an increased risk for placental abruption. Maternal cocaine use increases the risk for spontaneous abortion. (Kuczkowski, 2007). Persons with cocaine intoxication (not necessarily related to the drug level) may develop a state of iatrogenic psychosis (cocaine psychosis) with "excited delerium" in which they are markedly agitated and combative and develop hyperthermia, often of a severe degree (to 106 F). Organ damage can accompany this state of excited delerium and may include rhabdomyolysis of muscle, hepatotoxicity, and renal failure. Disseminated intravascular coagulation (DIC), hypotension, and sudden death are additional complications. (Devlin and Henry, 2008)

Cerebral infarction, gross.

Cocaine can exert a variety of effects. The major acute effects producing pathologic conditions result from the increased circulating catecholamine levels with cocaine use. These increased catecholamines can produce vasoconstriction. The lesions can include acute hemorrhages and infarction in the brain. Cerebral infarction can occur within 3 hours of cocaine use even in young persons. Subarachnoid haemorrhage is often associated with rupture of a berry aneurysm. Intraparenchymal haemorrhage can occur in the basal ganglia and thalamus. (Milroy and Parai, 2011). Ischemic changes in the heart from small artery narrowing and sclerosis lead to contraction band necrosis of the myocardium and possible sudden death. With chronic usage, the myocardium develops interstitial fibrosis, and the heart becomes enlarged. Atheroma formation in artereis as well as arterial dissection can occur. (Milroy and Parai, 2011) Combining cocaine use with ethanol use can compound the myocardial damage. (Awtry and Philippides, 2010). Pregnant mothers who use cocaine can affect their fetuses from abnormalities of placental function leading to low birth weight babies or an increased risk for placental abruption. Maternal cocaine use increases the risk for spontaneous abortion. (Kuczkowski, 2007). Persons with cocaine intoxication (not necessarily related to the drug level) may develop a state of iatrogenic psychosis (cocaine psychosis) with "excited delerium" in which they are markedly agitated and combative and develop hyperthermia, often of a severe degree (to 106 F). Organ damage can accompany this state of excited delerium and may include rhabdomyolysis of muscle, hepatotoxicity, and renal failure. Disseminated intravascular coagulation (DIC), hypotension, and sudden death are additional complications. (Devlin and Henry, 2008)

Massive intracerebral hemorrhage associated with cocaine use, gross.

Cocaine can exert a variety of effects. The major acute effects producing pathologic conditions result from the increased circulating catecholamine levels with cocaine use. These increased catecholamines can produce vasoconstriction. The lesions can include acute hemorrhages and infarction in the brain. Cerebral infarction can occur within 3 hours of cocaine use even in young persons. Subarachnoid haemorrhage is often associated with rupture of a berry aneurysm. Intraparenchymal haemorrhage can occur in the basal ganglia and thalamus. (Milroy and Parai, 2011). Ischemic changes in the heart from small artery narrowing and sclerosis lead to contraction band necrosis of the myocardium and possible sudden death. With chronic usage, the myocardium develops interstitial fibrosis, and the heart becomes enlarged. Atheroma formation in artereis as well as arterial dissection can occur. (Milroy and Parai, 2011) Combining cocaine use with ethanol use can compound the myocardial damage. (Awtry and Philippides, 2010). Pregnant mothers who use cocaine can affect their fetuses from abnormalities of placental function leading to low birth weight babies or an increased risk for placental abruption. Maternal cocaine use increases the risk for spontaneous abortion. (Kuczkowski, 2007). Persons with cocaine intoxication (not necessarily related to the drug level) may develop a state of iatrogenic psychosis (cocaine psychosis) with "excited delerium" in which they are markedly agitated and combative and develop hyperthermia, often of a severe degree (to 106 F). Organ damage can accompany this state of excited delerium and may include rhabdomyolysis of muscle, hepatotoxicity, and renal failure. Disseminated intravascular coagulation (DIC), hypotension, and sudden death are additional complications. (Devlin and Henry, 2008)

Talc granulomatosis of the lungs, polarized light, microscopic.

Many drugs can be injected intravenously. The drugs themselves may have the major effect of impairment of mental function, but the route of administration can have serious complications. Injection of drugs with needles that are not sterile leads to the potential for a wide variety of infections. Such infections include: human immunodeficiency virus (the causative agent for AIDS), viral hepatitis (particularly hepatitis B and C), and bacterial infections. (Marks et al, 2022). Persons with a history of intravenous drug abuse also are more likely to have tuberculosis of the lungs. The drug heroin can produce a nephropathy in the kidney that resembles focal segmental glomerulosclerosis. In addition, a "talc granulomatosis" can occur because many injected drugs have been adulterated with an inert substance (such as talcum powder) to "cut" or dilute the amount of drug. (Milroy and Parai, 2011)

Talc granulomatosis of the liver, gross.

Many drugs can be injected intravenously. The drugs themselves may have the major effect of impairment of mental function, but the route of administration can have serious complications. Injection of drugs with needles that are not sterile leads to the potential for a wide variety of infections. Such infections include: human immunodeficiency virus (the causative agent for AIDS), viral hepatitis (particularly hepatitis B and C), and bacterial infections. (Marks et al, 2022). Persons with a history of intravenous drug abuse also are more likely to have tuberculosis of the lungs. The drug heroin can produce a nephropathy in the kidney that resembles focal segmental glomerulosclerosis. In addition, a "talc granulomatosis" can occur because many injected drugs have been adulterated with an inert substance (such as talcum powder) to "cut" or dilute the amount of drug. (Milroy and Parai, 2011)

Glomerulus of kidney demonstrating focal scarring with heroin nephropathy, microscopic.

Many drugs can be injected intravenously. The drugs themselves may have the major effect of impairment of mental function, but the route of administration can have serious complications. Injection of drugs with needles that are not sterile leads to the potential for a wide variety of infections. Such infections include: human immunodeficiency virus (the causative agent for AIDS), viral hepatitis (particularly hepatitis B and C), and bacterial infections. (Marks et al, 2022). Persons with a history of intravenous drug abuse also are more likely to have tuberculosis of the lungs. The drug heroin can produce a nephropathy in the kidney that resembles focal segmental glomerulosclerosis. In addition, a "talc granulomatosis" can occur because many injected drugs have been adulterated with an inert substance (such as talcum powder) to "cut" or dilute the amount of drug. (Milroy and Parai, 2011)

Mycobacterium tuberculosis, lung, cavitary disease, gross.

Mycobacterium tuberculosis infection of the lung has resulted in upper lung field granulomatous and cavitary disease.Many drugs can be injected intravenously. The drugs themselves may have the major effect of impairment of mental function, but the route of administration can have serious complications. Injection of drugs with needles that are not sterile leads to the potential for a wide variety of infections. Such infections include: human immunodeficiency virus (the causative agent for AIDS), viral hepatitis (particularly hepatitis B and C), and bacterial infections. (Marks et al, 2022). Persons with a history of intravenous drug abuse also are more likely to have tuberculosis of the lungs. The drug heroin can produce a nephropathy in the kidney that resembles focal segmental glomerulosclerosis. In addition, a "talc granulomatosis" can occur because many injected drugs have been adulterated with an inert substance (such as talcum powder) to "cut" or dilute the amount of drug. (Milroy and Parai, 2011)

Macronodular cirrhosis of the liver, gross.

Many drugs can be injected intravenously. The drugs themselves may have the major effect of impairment of mental function, but the route of administration can have serious complications. Injection of drugs with needles that are not sterile leads to the potential for a wide variety of infections. Such infections include: human immunodeficiency virus (the causative agent for AIDS), viral hepatitis (particularly hepatitis B and C), and bacterial infections. (Marks et al, 2022). Persons with a history of intravenous drug abuse also are more likely to have tuberculosis of the lungs. The drug heroin can produce a nephropathy in the kidney that resembles focal segmental glomerulosclerosis. In addition, a "talc granulomatosis" can occur because many injected drugs have been adulterated with an inert substance (such as talcum powder) to "cut" or dilute the amount of drug. (Milroy and Parai, 2011)

Viral hepatitis of the liver, microscopic.

Many drugs can be injected intravenously. The drugs themselves may have the major effect of impairment of mental function, but the route of administration can have serious complications. Injection of drugs with needles that are not sterile leads to the potential for a wide variety of infections. Such infections include: human immunodeficiency virus (the causative agent for AIDS), viral hepatitis (particularly hepatitis B and C), and bacterial infections. (Marks et al, 2022). Persons with a history of intravenous drug abuse also are more likely to have tuberculosis of the lungs. The drug heroin can produce a nephropathy in the kidney that resembles focal segmental glomerulosclerosis. In addition, a "talc granulomatosis" can occur because many injected drugs have been adulterated with an inert substance (such as talcum powder) to "cut" or dilute the amount of drug. (Milroy and Parai, 2011)

Viral hepatitis of the liver, gross.

Many drugs can be injected intravenously. The drugs themselves may have the major effect of impairment of mental function, but the route of administration can have serious complications. Injection of drugs with needles that are not sterile leads to the potential for a wide variety of infections. Such infections include: human immunodeficiency virus (the causative agent for AIDS), viral hepatitis (particularly hepatitis B and C), and bacterial infections. (Marks et al, 2022). Persons with a history of intravenous drug abuse also are more likely to have tuberculosis of the lungs. The drug heroin can produce a nephropathy in the kidney that resembles focal segmental glomerulosclerosis. In addition, a "talc granulomatosis" can occur because many injected drugs have been adulterated with an inert substance (such as talcum powder) to "cut" or dilute the amount of drug. (Milroy and Parai, 2011)

Surface of the brain with acute meningitis, gross.

Many drugs can be injected intravenously. The drugs themselves may have the major effect of impairment of mental function, but the route of administration can have serious complications. Injection of drugs with needles that are not sterile leads to the potential for a wide variety of infections. Such infections include: human immunodeficiency virus (the causative agent for AIDS), viral hepatitis (particularly hepatitis B and C), and bacterial infections. (Marks et al, 2022). Persons with a history of intravenous drug abuse also are more likely to have tuberculosis of the lungs. The drug heroin can produce a nephropathy in the kidney that resembles focal segmental glomerulosclerosis. In addition, a "talc granulomatosis" can occur because many injected drugs have been adulterated with an inert substance (such as talcum powder) to "cut" or dilute the amount of drug. (Milroy and Parai, 2011)

Normal aortic valve compared with infective endocarditis, gross.

Many drugs can be injected intravenously. The drugs themselves may have the major effect of impairment of mental function, but the route of administration can have serious complications. Injection of drugs with needles that are not sterile leads to the potential for a wide variety of infections. Such infections include: human immunodeficiency virus (the causative agent for AIDS), viral hepatitis (particularly hepatitis B and C), and bacterial infections. (Marks et al, 2022). Persons with a history of intravenous drug abuse also are more likely to have tuberculosis of the lungs. The drug heroin can produce a nephropathy in the kidney that resembles focal segmental glomerulosclerosis. In addition, a "talc granulomatosis" can occur because many injected drugs have been adulterated with an inert substance (such as talcum powder) to "cut" or dilute the amount of drug. (Milroy and Parai, 2011)

Wernicke's disease, hemorrhages in the mammillary bodies, gross.

The abuse of alcohol (ethanol) contributes to many deaths per year worldwide. It can also be a cause for drug overdose leading to death from ingestion of a large amount of alcohol, and second only to opioid overdose in number of drug-related deaths. Almost 1 in 5 visits to an emergency department involve prior use of alcohol. (https://www.niaaa.nih.gov/alcohols-effects-health/alcohol-topics/alcohol-facts-and-statistics/alcohol-related-emergencies-and-deaths-united-states). Chronic alcohol abuse leads to liver disease that can be manifested initially as fatty change (steatosis). Excessive alcohol ingestion over many years can lead to micronodular cirrhosis. A cirrhotic liver leads to portal hypertension and the complication of bleeding esophageal varices with massive, life-threatening gastrointestinal hemorrhage. There is also an increased risk for hepatocellular carcinoma arising in a cirrhotic liver. Acute excessive alcohol consumption can lead to alcoholic hepatitis. Laboratory testing of a blood specimen for evidence of ethanol ingestion includes phosphatidylethanol for recent (within 2 weeks) and carbohydrate-deficient transferrin for chronic use. (Patel and Flamm, 2023). In the brain, alcohol use disorder predisposing to poor dietary intake lacking nutrients can lead to thiamine deficiency with neurotoxicity and development of Wernicke–Korsakoff syndrome (WKS), with components of Wernicke encephalopathy and Korsakoff’s psychosis, with higher mental function affected by confusion and confabulation. Acute Wernicke encephalopathy is a potentially reversible condition characterized by confusion, oculomotor disturbances, and ataxia. Continued alcohol abuse leads to permanent brain damage. (Nutt et al, 2021). Abrupt cessation of alcohol ingestion in persons who are chronic alcohol abusers predisposes to alcohol withdrawal Symptoms, and signs within 8 to 24 hours include transient visual, auditory or tactile hallucinations. There can be progression to withdrawal-related seizures which, if not treated may progress to life-threatening delirium tremens. (Day and Daly, 2022). Alcohol use during pregnancy can lead to fetal alcohol spectrum disorders, also termed the fetal alcohol syndrome (FAS). The risk increases with the time and amount of exposure, but there is no completely safe level of maternal alcohol consumption. This syndrome is estimated to occur in 1 in 100 live births, but the actual incidence is probably higher. Whenever a pregnant woman stops drinking, she reduces the risk of having a baby with FAS. Damage to the fetus from FAS cannot be reversed. Later in development, affected children have increased behavioral problems and learning disabilities. There are no specific, distinctive morphologic findings, so it is challenging to diagnose. The most common deformity with FAS is moderate to severe growth retardation. The three most distinctive features are a thin upper lip, smooth philtrum, and short palpebral fissures. (Popova et al, 2023). Additional FAS anomalies include microcephaly, long and narrow forehead, hypotelorism, maxillary and mandibular hypoplasia, narrow palpebal fissures, thin elongated philtrum and vermillion border of the upper lip, temporomandibular joint disorders, and dental malocclusion. Ocular problems include microphthalmia, coloboma, nystagmus, strabismus, and ptosis. The physical anomalies tend to become less apparent as the child ages. (Mukherjee et al, 2006)

Esophageal varices, gross.

The abuse of alcohol (ethanol) contributes to many deaths per year worldwide. It can also be a cause for drug overdose leading to death from ingestion of a large amount of alcohol, and second only to opioid overdose in number of drug-related deaths. Almost 1 in 5 visits to an emergency department involve prior use of alcohol. (https://www.niaaa.nih.gov/alcohols-effects-health/alcohol-topics/alcohol-facts-and-statistics/alcohol-related-emergencies-and-deaths-united-states). Chronic alcohol abuse leads to liver disease that can be manifested initially as fatty change (steatosis). Excessive alcohol ingestion over many years can lead to micronodular cirrhosis. A cirrhotic liver leads to portal hypertension and the complication of bleeding esophageal varices with massive, life-threatening gastrointestinal hemorrhage. There is also an increased risk for hepatocellular carcinoma arising in a cirrhotic liver. Acute excessive alcohol consumption can lead to alcoholic hepatitis. Laboratory testing of a blood specimen for evidence of ethanol ingestion includes phosphatidylethanol for recent (within 2 weeks) and carbohydrate-deficient transferrin for chronic use. (Patel and Flamm, 2023). In the brain, alcohol use disorder predisposing to poor dietary intake lacking nutrients can lead to thiamine deficiency with neurotoxicity and development of Wernicke–Korsakoff syndrome (WKS), with components of Wernicke encephalopathy and Korsakoff’s psychosis, with higher mental function affected by confusion and confabulation. Acute Wernicke encephalopathy is a potentially reversible condition characterized by confusion, oculomotor disturbances, and ataxia. Continued alcohol abuse leads to permanent brain damage. (Nutt et al, 2021). Abrupt cessation of alcohol ingestion in persons who are chronic alcohol abusers predisposes to alcohol withdrawal Symptoms, and signs within 8 to 24 hours include transient visual, auditory or tactile hallucinations. There can be progression to withdrawal-related seizures which, if not treated may progress to life-threatening delirium tremens. (Day and Daly, 2022). Alcohol use during pregnancy can lead to fetal alcohol spectrum disorders, also termed the fetal alcohol syndrome (FAS). The risk increases with the time and amount of exposure, but there is no completely safe level of maternal alcohol consumption. This syndrome is estimated to occur in 1 in 100 live births, but the actual incidence is probably higher. Whenever a pregnant woman stops drinking, she reduces the risk of having a baby with FAS. Damage to the fetus from FAS cannot be reversed. Later in development, affected children have increased behavioral problems and learning disabilities. There are no specific, distinctive morphologic findings, so it is challenging to diagnose. The most common deformity with FAS is moderate to severe growth retardation. The three most distinctive features are a thin upper lip, smooth philtrum, and short palpebral fissures. (Popova et al, 2023). Additional FAS anomalies include microcephaly, long and narrow forehead, hypotelorism, maxillary and mandibular hypoplasia, narrow palpebal fissures, thin elongated philtrum and vermillion border of the upper lip, temporomandibular joint disorders, and dental malocclusion. Ocular problems include microphthalmia, coloboma, nystagmus, strabismus, and ptosis. The physical anomalies tend to become less apparent as the child ages. (Mukherjee et al, 2006)

Hepatocellular carcinoma, liver with micronodular cirrhosis, gross.

The abuse of alcohol (ethanol) contributes to many deaths per year worldwide. It can also be a cause for drug overdose leading to death from ingestion of a large amount of alcohol, and second only to opioid overdose in number of drug-related deaths. Almost 1 in 5 visits to an emergency department involve prior use of alcohol. (https://www.niaaa.nih.gov/alcohols-effects-health/alcohol-topics/alcohol-facts-and-statistics/alcohol-related-emergencies-and-deaths-united-states). Chronic alcohol abuse leads to liver disease that can be manifested initially as fatty change (steatosis). Excessive alcohol ingestion over many years can lead to micronodular cirrhosis. A cirrhotic liver leads to portal hypertension and the complication of bleeding esophageal varices with massive, life-threatening gastrointestinal hemorrhage. There is also an increased risk for hepatocellular carcinoma arising in a cirrhotic liver. Acute excessive alcohol consumption can lead to alcoholic hepatitis. Laboratory testing of a blood specimen for evidence of ethanol ingestion includes phosphatidylethanol for recent (within 2 weeks) and carbohydrate-deficient transferrin for chronic use. (Patel and Flamm, 2023). In the brain, alcohol use disorder predisposing to poor dietary intake lacking nutrients can lead to thiamine deficiency with neurotoxicity and development of Wernicke–Korsakoff syndrome (WKS), with components of Wernicke encephalopathy and Korsakoff’s psychosis, with higher mental function affected by confusion and confabulation. Acute Wernicke encephalopathy is a potentially reversible condition characterized by confusion, oculomotor disturbances, and ataxia. Continued alcohol abuse leads to permanent brain damage. (Nutt et al, 2021). Abrupt cessation of alcohol ingestion in persons who are chronic alcohol abusers predisposes to alcohol withdrawal Symptoms, and signs within 8 to 24 hours include transient visual, auditory or tactile hallucinations. There can be progression to withdrawal-related seizures which, if not treated may progress to life-threatening delirium tremens. (Day and Daly, 2022). Alcohol use during pregnancy can lead to fetal alcohol spectrum disorders, also termed the fetal alcohol syndrome (FAS). The risk increases with the time and amount of exposure, but there is no completely safe level of maternal alcohol consumption. This syndrome is estimated to occur in 1 in 100 live births, but the actual incidence is probably higher. Whenever a pregnant woman stops drinking, she reduces the risk of having a baby with FAS. Damage to the fetus from FAS cannot be reversed. Later in development, affected children have increased behavioral problems and learning disabilities. There are no specific, distinctive morphologic findings, so it is challenging to diagnose. The most common deformity with FAS is moderate to severe growth retardation. The three most distinctive features are a thin upper lip, smooth philtrum, and short palpebral fissures. (Popova et al, 2023). Additional FAS anomalies include microcephaly, long and narrow forehead, hypotelorism, maxillary and mandibular hypoplasia, narrow palpebal fissures, thin elongated philtrum and vermillion border of the upper lip, temporomandibular joint disorders, and dental malocclusion. Ocular problems include microphthalmia, coloboma, nystagmus, strabismus, and ptosis. The physical anomalies tend to become less apparent as the child ages. (Mukherjee et al, 2006)

Micronodular cirrhosis of liver, microscopic.

The abuse of alcohol (ethanol) contributes to many deaths per year worldwide. It can also be a cause for drug overdose leading to death from ingestion of a large amount of alcohol, and second only to opioid overdose in number of drug-related deaths. Almost 1 in 5 visits to an emergency department involve prior use of alcohol. (https://www.niaaa.nih.gov/alcohols-effects-health/alcohol-topics/alcohol-facts-and-statistics/alcohol-related-emergencies-and-deaths-united-states). Chronic alcohol abuse leads to liver disease that can be manifested initially as fatty change (steatosis). Excessive alcohol ingestion over many years can lead to micronodular cirrhosis. A cirrhotic liver leads to portal hypertension and the complication of bleeding esophageal varices with massive, life-threatening gastrointestinal hemorrhage. There is also an increased risk for hepatocellular carcinoma arising in a cirrhotic liver. Acute excessive alcohol consumption can lead to alcoholic hepatitis. Laboratory testing of a blood specimen for evidence of ethanol ingestion includes phosphatidylethanol for recent (within 2 weeks) and carbohydrate-deficient transferrin for chronic use. (Patel and Flamm, 2023). In the brain, alcohol use disorder predisposing to poor dietary intake lacking nutrients can lead to thiamine deficiency with neurotoxicity and development of Wernicke–Korsakoff syndrome (WKS), with components of Wernicke encephalopathy and Korsakoff’s psychosis, with higher mental function affected by confusion and confabulation. Acute Wernicke encephalopathy is a potentially reversible condition characterized by confusion, oculomotor disturbances, and ataxia. Continued alcohol abuse leads to permanent brain damage. (Nutt et al, 2021). Abrupt cessation of alcohol ingestion in persons who are chronic alcohol abusers predisposes to alcohol withdrawal Symptoms, and signs within 8 to 24 hours include transient visual, auditory or tactile hallucinations. There can be progression to withdrawal-related seizures which, if not treated may progress to life-threatening delirium tremens. (Day and Daly, 2022). Alcohol use during pregnancy can lead to fetal alcohol spectrum disorders, also termed the fetal alcohol syndrome (FAS). The risk increases with the time and amount of exposure, but there is no completely safe level of maternal alcohol consumption. This syndrome is estimated to occur in 1 in 100 live births, but the actual incidence is probably higher. Whenever a pregnant woman stops drinking, she reduces the risk of having a baby with FAS. Damage to the fetus from FAS cannot be reversed. Later in development, affected children have increased behavioral problems and learning disabilities. There are no specific, distinctive morphologic findings, so it is challenging to diagnose. The most common deformity with FAS is moderate to severe growth retardation. The three most distinctive features are a thin upper lip, smooth philtrum, and short palpebral fissures. (Popova et al, 2023). Additional FAS anomalies include microcephaly, long and narrow forehead, hypotelorism, maxillary and mandibular hypoplasia, narrow palpebal fissures, thin elongated philtrum and vermillion border of the upper lip, temporomandibular joint disorders, and dental malocclusion. Ocular problems include microphthalmia, coloboma, nystagmus, strabismus, and ptosis. The physical anomalies tend to become less apparent as the child ages. (Mukherjee et al, 2006)

Micronodular cirrhosis of liver, gross.

The abuse of alcohol (ethanol) contributes to many deaths per year worldwide. It can also be a cause for drug overdose leading to death from ingestion of a large amount of alcohol, and second only to opioid overdose in number of drug-related deaths. Almost 1 in 5 visits to an emergency department involve prior use of alcohol. (https://www.niaaa.nih.gov/alcohols-effects-health/alcohol-topics/alcohol-facts-and-statistics/alcohol-related-emergencies-and-deaths-united-states). Chronic alcohol abuse leads to liver disease that can be manifested initially as fatty change (steatosis). Excessive alcohol ingestion over many years can lead to micronodular cirrhosis. A cirrhotic liver leads to portal hypertension and the complication of bleeding esophageal varices with massive, life-threatening gastrointestinal hemorrhage. There is also an increased risk for hepatocellular carcinoma arising in a cirrhotic liver. Acute excessive alcohol consumption can lead to alcoholic hepatitis. Laboratory testing of a blood specimen for evidence of ethanol ingestion includes phosphatidylethanol for recent (within 2 weeks) and carbohydrate-deficient transferrin for chronic use. (Patel and Flamm, 2023). In the brain, alcohol use disorder predisposing to poor dietary intake lacking nutrients can lead to thiamine deficiency with neurotoxicity and development of Wernicke–Korsakoff syndrome (WKS), with components of Wernicke encephalopathy and Korsakoff’s psychosis, with higher mental function affected by confusion and confabulation. Acute Wernicke encephalopathy is a potentially reversible condition characterized by confusion, oculomotor disturbances, and ataxia. Continued alcohol abuse leads to permanent brain damage. (Nutt et al, 2021). Abrupt cessation of alcohol ingestion in persons who are chronic alcohol abusers predisposes to alcohol withdrawal Symptoms, and signs within 8 to 24 hours include transient visual, auditory or tactile hallucinations. There can be progression to withdrawal-related seizures which, if not treated may progress to life-threatening delirium tremens. (Day and Daly, 2022). Alcohol use during pregnancy can lead to fetal alcohol spectrum disorders, also termed the fetal alcohol syndrome (FAS). The risk increases with the time and amount of exposure, but there is no completely safe level of maternal alcohol consumption. This syndrome is estimated to occur in 1 in 100 live births, but the actual incidence is probably higher. Whenever a pregnant woman stops drinking, she reduces the risk of having a baby with FAS. Damage to the fetus from FAS cannot be reversed. Later in development, affected children have increased behavioral problems and learning disabilities. There are no specific, distinctive morphologic findings, so it is challenging to diagnose. The most common deformity with FAS is moderate to severe growth retardation. The three most distinctive features are a thin upper lip, smooth philtrum, and short palpebral fissures. (Popova et al, 2023). Additional FAS anomalies include microcephaly, long and narrow forehead, hypotelorism, maxillary and mandibular hypoplasia, narrow palpebal fissures, thin elongated philtrum and vermillion border of the upper lip, temporomandibular joint disorders, and dental malocclusion. Ocular problems include microphthalmia, coloboma, nystagmus, strabismus, and ptosis. The physical anomalies tend to become less apparent as the child ages. (Mukherjee et al, 2006)

Fatty change of liver, microscopic.

The abuse of alcohol (ethanol) contributes to many deaths per year worldwide. It can also be a cause for drug overdose leading to death from ingestion of a large amount of alcohol, and second only to opioid overdose in number of drug-related deaths. Almost 1 in 5 visits to an emergency department involve prior use of alcohol. (https://www.niaaa.nih.gov/alcohols-effects-health/alcohol-topics/alcohol-facts-and-statistics/alcohol-related-emergencies-and-deaths-united-states). Chronic alcohol abuse leads to liver disease that can be manifested initially as fatty change (steatosis). Excessive alcohol ingestion over many years can lead to micronodular cirrhosis. A cirrhotic liver leads to portal hypertension and the complication of bleeding esophageal varices with massive, life-threatening gastrointestinal hemorrhage. There is also an increased risk for hepatocellular carcinoma arising in a cirrhotic liver. Acute excessive alcohol consumption can lead to alcoholic hepatitis. Laboratory testing of a blood specimen for evidence of ethanol ingestion includes phosphatidylethanol for recent (within 2 weeks) and carbohydrate-deficient transferrin for chronic use. (Patel and Flamm, 2023). In the brain, alcohol use disorder predisposing to poor dietary intake lacking nutrients can lead to thiamine deficiency with neurotoxicity and development of Wernicke–Korsakoff syndrome (WKS), with components of Wernicke encephalopathy and Korsakoff’s psychosis, with higher mental function affected by confusion and confabulation. Acute Wernicke encephalopathy is a potentially reversible condition characterized by confusion, oculomotor disturbances, and ataxia. Continued alcohol abuse leads to permanent brain damage. (Nutt et al, 2021). Abrupt cessation of alcohol ingestion in persons who are chronic alcohol abusers predisposes to alcohol withdrawal Symptoms, and signs within 8 to 24 hours include transient visual, auditory or tactile hallucinations. There can be progression to withdrawal-related seizures which, if not treated may progress to life-threatening delirium tremens. (Day and Daly, 2022). Alcohol use during pregnancy can lead to fetal alcohol spectrum disorders, also termed the fetal alcohol syndrome (FAS). The risk increases with the time and amount of exposure, but there is no completely safe level of maternal alcohol consumption. This syndrome is estimated to occur in 1 in 100 live births, but the actual incidence is probably higher. Whenever a pregnant woman stops drinking, she reduces the risk of having a baby with FAS. Damage to the fetus from FAS cannot be reversed. Later in development, affected children have increased behavioral problems and learning disabilities. There are no specific, distinctive morphologic findings, so it is challenging to diagnose. The most common deformity with FAS is moderate to severe growth retardation. The three most distinctive features are a thin upper lip, smooth philtrum, and short palpebral fissures. (Popova et al, 2023). Additional FAS anomalies include microcephaly, long and narrow forehead, hypotelorism, maxillary and mandibular hypoplasia, narrow palpebal fissures, thin elongated philtrum and vermillion border of the upper lip, temporomandibular joint disorders, and dental malocclusion. Ocular problems include microphthalmia, coloboma, nystagmus, strabismus, and ptosis. The physical anomalies tend to become less apparent as the child ages. (Mukherjee et al, 2006)

Normal liver, gross.

The abuse of alcohol (ethanol) contributes to many deaths per year worldwide. It can also be a cause for drug overdose leading to death from ingestion of a large amount of alcohol, and second only to opioid overdose in number of drug-related deaths. Almost 1 in 5 visits to an emergency department involve prior use of alcohol. (https://www.niaaa.nih.gov/alcohols-effects-health/alcohol-topics/alcohol-facts-and-statistics/alcohol-related-emergencies-and-deaths-united-states). Chronic alcohol abuse leads to liver disease that can be manifested initially as fatty change (steatosis). Excessive alcohol ingestion over many years can lead to micronodular cirrhosis. A cirrhotic liver leads to portal hypertension and the complication of bleeding esophageal varices with massive, life-threatening gastrointestinal hemorrhage. There is also an increased risk for hepatocellular carcinoma arising in a cirrhotic liver. Acute excessive alcohol consumption can lead to alcoholic hepatitis. Laboratory testing of a blood specimen for evidence of ethanol ingestion includes phosphatidylethanol for recent (within 2 weeks) and carbohydrate-deficient transferrin for chronic use. (Patel and Flamm, 2023). In the brain, alcohol use disorder predisposing to poor dietary intake lacking nutrients can lead to thiamine deficiency with neurotoxicity and development of Wernicke–Korsakoff syndrome (WKS), with components of Wernicke encephalopathy and Korsakoff’s psychosis, with higher mental function affected by confusion and confabulation. Acute Wernicke encephalopathy is a potentially reversible condition characterized by confusion, oculomotor disturbances, and ataxia. Continued alcohol abuse leads to permanent brain damage. (Nutt et al, 2021). Abrupt cessation of alcohol ingestion in persons who are chronic alcohol abusers predisposes to alcohol withdrawal Symptoms, and signs within 8 to 24 hours include transient visual, auditory or tactile hallucinations. There can be progression to withdrawal-related seizures which, if not treated may progress to life-threatening delirium tremens. (Day and Daly, 2022). Alcohol use during pregnancy can lead to fetal alcohol spectrum disorders, also termed the fetal alcohol syndrome (FAS). The risk increases with the time and amount of exposure, but there is no completely safe level of maternal alcohol consumption. This syndrome is estimated to occur in 1 in 100 live births, but the actual incidence is probably higher. Whenever a pregnant woman stops drinking, she reduces the risk of having a baby with FAS. Damage to the fetus from FAS cannot be reversed. Later in development, affected children have increased behavioral problems and learning disabilities. There are no specific, distinctive morphologic findings, so it is challenging to diagnose. The most common deformity with FAS is moderate to severe growth retardation. The three most distinctive features are a thin upper lip, smooth philtrum, and short palpebral fissures. (Popova et al, 2023). Additional FAS anomalies include microcephaly, long and narrow forehead, hypotelorism, maxillary and mandibular hypoplasia, narrow palpebal fissures, thin elongated philtrum and vermillion border of the upper lip, temporomandibular joint disorders, and dental malocclusion. Ocular problems include microphthalmia, coloboma, nystagmus, strabismus, and ptosis. The physical anomalies tend to become less apparent as the child ages. (Mukherjee et al, 2006)

Hyaline membrane disease in the lung of a premature neonate, microscopic.

Smoking tobacco leads to the greatest number of problems of any drug in use in the world today. Smoking contributes to more than 7 million deaths each year worldwide. These deaths are mainly the result of increased numbers of lung cancers as well as increased numbers of cases of atherosclerotic heart disease and emphysema of the lung. Smoking increases the risk for cancers of the bladder, pancreas, kidney, and cervix. There is an increased risk for gastritis and gastric ulceration in persons who smoke. Cataracts of the crystalline lens of the eye occur with increased frequency in smokers. (GBD, 2017). Women who are pregnant and who smoke put their fetuses at increased risk for spontaneous abortion, ectopic pregnancy, placental abruption, placenta praevia, premature labor, and preterm birth, stillbirth,low birth weight, and small for gestational age (SGA) compared to women who do not smoke during pregnancy. Prenatal maternal smoking is also associated with risk of sudden unexplained death in infancy. (Gould et al, 2020)

Acute gastric ulcerations, gross.

Smoking tobacco leads to the greatest number of problems of any drug in use in the world today. Smoking contributes to more than 7 million deaths each year worldwide. These deaths are mainly the result of increased numbers of lung cancers as well as increased numbers of cases of atherosclerotic heart disease and emphysema of the lung. Smoking increases the risk for cancers of the bladder, pancreas, kidney, and cervix. There is an increased risk for gastritis and gastric ulceration in persons who smoke. Cataracts of the crystalline lens of the eye occur with increased frequency in smokers. (GBD, 2017). Women who are pregnant and who smoke put their fetuses at increased risk for spontaneous abortion, ectopic pregnancy, placental abruption, placenta praevia, premature labor, and preterm birth, stillbirth,low birth weight, and small for gestational age (SGA) compared to women who do not smoke during pregnancy. Prenatal maternal smoking is also associated with risk of sudden unexplained death in infancy. (Gould et al, 2020)

Pelvis of kidney, urothelial carcinoma, gross.

Smoking tobacco leads to the greatest number of problems of any drug in use in the world today. Smoking contributes to more than 7 million deaths each year worldwide. These deaths are mainly the result of increased numbers of lung cancers as well as increased numbers of cases of atherosclerotic heart disease and emphysema of the lung. Smoking increases the risk for cancers of the bladder, pancreas, kidney, and cervix. There is an increased risk for gastritis and gastric ulceration in persons who smoke. Cataracts of the crystalline lens of the eye occur with increased frequency in smokers. (GBD, 2017). Women who are pregnant and who smoke put their fetuses at increased risk for spontaneous abortion, ectopic pregnancy, placental abruption, placenta praevia, premature labor, and preterm birth, stillbirth,low birth weight, and small for gestational age (SGA) compared to women who do not smoke during pregnancy. Prenatal maternal smoking is also associated with risk of sudden unexplained death in infancy. (Gould et al, 2020)

Composite photograph with a narrowed coronary artery at the left and a markedly narrowed coronary artery at the right, microscopic.

Smoking tobacco leads to the greatest number of problems of any drug in use in the world today. Smoking contributes to more than 7 million deaths each year worldwide. These deaths are mainly the result of increased numbers of lung cancers as well as increased numbers of cases of atherosclerotic heart disease and emphysema of the lung. Smoking increases the risk for cancers of the bladder, pancreas, kidney, and cervix. There is an increased risk for gastritis and gastric ulceration in persons who smoke. Cataracts of the crystalline lens of the eye occur with increased frequency in smokers. (GBD, 2017). Women who are pregnant and who smoke put their fetuses at increased risk for spontaneous abortion, ectopic pregnancy, placental abruption, placenta praevia, premature labor, and preterm birth, stillbirth,low birth weight, and small for gestational age (SGA) compared to women who do not smoke during pregnancy. Prenatal maternal smoking is also associated with risk of sudden unexplained death in infancy. (Gould et al, 2020)

Emphysema, representing a modern version of "The Masque of the Red Death" in Edgar Allen Poe's short story.

Smoking tobacco leads to the greatest number of problems of any drug in use in the world today. Smoking contributes to more than 7 million deaths each year worldwide. These deaths are mainly the result of increased numbers of lung cancers as well as increased numbers of cases of atherosclerotic heart disease and emphysema of the lung. Smoking increases the risk for cancers of the bladder, pancreas, kidney, and cervix. There is an increased risk for gastritis and gastric ulceration in persons who smoke. Cataracts of the crystalline lens of the eye occur with increased frequency in smokers. (GBD, 2017). Women who are pregnant and who smoke put their fetuses at increased risk for spontaneous abortion, ectopic pregnancy, placental abruption, placenta praevia, premature labor, and preterm birth, stillbirth,low birth weight, and small for gestational age (SGA) compared to women who do not smoke during pregnancy. Prenatal maternal smoking is also associated with risk of sudden unexplained death in infancy. (Gould et al, 2020)

Emphysema, centrilobular type, gross.

Emphysema, of the centrilobular type, with numerous enlarged air spaces as a result of the loss of lung tissue from smoking is demonstrated here grossly.Smoking tobacco leads to the greatest number of problems of any drug in use in the world today. Smoking contributes to more than 7 million deaths each year worldwide. These deaths are mainly the result of increased numbers of lung cancers as well as increased numbers of cases of atherosclerotic heart disease and emphysema of the lung. Smoking increases the risk for cancers of the bladder, pancreas, kidney, and cervix. There is an increased risk for gastritis and gastric ulceration in persons who smoke. Cataracts of the crystalline lens of the eye occur with increased frequency in smokers. (GBD, 2017). Women who are pregnant and who smoke put their fetuses at increased risk for spontaneous abortion, ectopic pregnancy, placental abruption, placenta praevia, premature labor, and preterm birth, stillbirth,low birth weight, and small for gestational age (SGA) compared to women who do not smoke during pregnancy. Prenatal maternal smoking is also associated with risk of sudden unexplained death in infancy. (Gould et al, 2020)

Squamous cell carcinoma of lung, gross.

A large squamous cell carcinoma of the lung in a smoker is shown here. The incidence of both squamous cell carcinomas and small cell anaplastic carcinomas of lung is far greater in smokers than non-smokers.Smoking tobacco leads to the greatest number of problems of any drug in use in the world today. Smoking contributes to more than 7 million deaths each year worldwide. These deaths are mainly the result of increased numbers of lung cancers as well as increased numbers of cases of atherosclerotic heart disease and emphysema of the lung. Smoking increases the risk for cancers of the bladder, pancreas, kidney, and cervix. There is an increased risk for gastritis and gastric ulceration in persons who smoke. Cataracts of the crystalline lens of the eye occur with increased frequency in smokers. (GBD, 2017). Women who are pregnant and who smoke put their fetuses at increased risk for spontaneous abortion, ectopic pregnancy, placental abruption, placenta praevia, premature labor, and preterm birth, stillbirth,low birth weight, and small for gestational age (SGA) compared to women who do not smoke during pregnancy. Prenatal maternal smoking is also associated with risk of sudden unexplained death in infancy. (Gould et al, 2020)

Small cell anaplastic (oat cell) carcinoma of lung, gross.

Small cell anaplastic (oat cell) carcinoma of the lung appears here in a smoker. Smokers who stop will diminish their risk for lung cancer, even after just a couple of years.Smoking tobacco leads to the greatest number of problems of any drug in use in the world today. Smoking contributes to more than 7 million deaths each year worldwide. These deaths are mainly the result of increased numbers of lung cancers as well as increased numbers of cases of atherosclerotic heart disease and emphysema of the lung. Smoking increases the risk for cancers of the bladder, pancreas, kidney, and cervix. There is an increased risk for gastritis and gastric ulceration in persons who smoke. Cataracts of the crystalline lens of the eye occur with increased frequency in smokers. (GBD, 2017). Women who are pregnant and who smoke put their fetuses at increased risk for spontaneous abortion, ectopic pregnancy, placental abruption, placenta praevia, premature labor, and preterm birth, stillbirth,low birth weight, and small for gestational age (SGA) compared to women who do not smoke during pregnancy. Prenatal maternal smoking is also associated with risk of sudden unexplained death in infancy. (Gould et al, 2020)

Normal lung, gross.

The normal gross appearance of a lung in cross section is shown here for comparison.Smoking tobacco leads to the greatest number of problems of any drug in use in the world today. Smoking contributes to more than 7 million deaths each year worldwide. These deaths are mainly the result of increased numbers of lung cancers as well as increased numbers of cases of atherosclerotic heart disease and emphysema of the lung. Smoking increases the risk for cancers of the bladder, pancreas, kidney, and cervix. There is an increased risk for gastritis and gastric ulceration in persons who smoke. Cataracts of the crystalline lens of the eye occur with increased frequency in smokers. (GBD, 2017). Women who are pregnant and who smoke put their fetuses at increased risk for spontaneous abortion, ectopic pregnancy, placental abruption, placenta praevia, premature labor, and preterm birth, stillbirth,low birth weight, and small for gestational age (SGA) compared to women who do not smoke during pregnancy. Prenatal maternal smoking is also associated with risk of sudden unexplained death in infancy. (Gould et al, 2020)

Exit gunshot wound, gross

Here is a slit-like exit wound. Note that there is no powder or soot visible.

Entrance-exit wound, close proximity from low angle of bullet entrance, gross

Displayed here is an entrance at the left and an exit at the right. This particular bullet struck at an angle to produce the ovoid entrance. Exit wounds vary considerably in size and shape because the bullet can be deformed in its transit through the body. There may be no exit wound at all if the bullet's energy is absorbed by the tissues. Some bullets (such a a "hollowpoint") are designed to deform so that all their energy will be converted to tissue damage and not exit.

Intermediate range gunshot wound, gross

This is an intermediate range gunshot entrance wound in which there is powder "tattooing" around the entrance site.

Intermediate range gunshot wound, gross

Powder tattooing is seen in this intermediate range gunshot wound. The actual entrance site is somewhat irregular, because the bullet can tumble in flight.

Gunshot entrance wound with GSR, microsopic

Histologic examination of the entrance wound site on the skin demonstrates black gunshot residue and coagulative necrosis.

Blood spatter on hand, gross

With a contact or very close range gunshot wound, it is possible to have blood spatter as well as sooting on the hand of the person firing the weapon.

Contact range gunshot wound, gross

This is a contact range gunshot entrance wound with grey-black discoloration from the burned powder.

Contact range gunshot wound, gross

The abrasion ring, and a very clear muzzle imprint, are seen in this contact range gunshot wound.

Contact range gunshot wound, gross

An abrasion ring, formed when the force of the gases entering below the skin blow the skin surface back against the muzzle of the gun, is seen here in this contact range gunshot wound to the right temple.

Contact range gunshot wound, gross

This is an contact gunshot entrance wound. Since the barrel contacts the skin, the gases released by the fired round go into the subcutaneous tissue and cause the star-shaped laceration. Note also the grey-black discoloration from the soot, as well as the faint abrasion ring.

Sooting of hand, gross

Soot is seen on the hand of a suicide victim, giving an indication that he was holding the weapon when it was fired.

what kind of image is this?

cta - ct angiography

is this a t1 weighted image?

no

what type of imaging modality is used to acquire the image?

us - ultrasound

is this a noncontrast mri?

no

what type of image modality is this?

xr - plain film

with what modality is this image taken?

xr - plain film

what was this image taken with?

xr - plain film

is this a contrast or noncontrast ct?

noncontrast

was the ct scan taken with contrast?

yes

what is the mr weighting in this image?

t2

what type of imaging modality is shown?

ct w/contrast (iv)

what type of imaging does this represent?

xr - plain film

is this a ct scan?

yes

is this an mri image?

no

was gi contrast given to the patient?

no

was gi contrast given to the patient?

no

what was this image taken with?

xr - plain film

is this a ct scan?

no

what imaging modality was used to take this image?

mr - flair

what modality was used to take this image?

mammograph

is this an mri image?

no

is this a contrast or noncontrast mri?

noncontrast

is this a ct scan?

yes

what imaging modality was used to take this image?

ct with iv contrast

is this a ct scan?

yes

what type of image modality is this?

xr - plain film

what type of image modality is seen?

mammograph

was gi contrast given to the patient?

no

what imaging modality was used to take this image?

mr - flair

what type of imaging is this?

us - ultrasound