Marchiafava-Bignami disease T2-weighted sagittal image in Marchiafava-Bignami disease demonstrating a small, well-defined, and hyperdense lesion in the genu of the corpus callosum (arrowed)

T2-weighted sagittal image in Marchiafava-Bignami disease demonstrating a small, well-defined, and hyperdense lesion in the genu of the corpus callosum (arrowed)

Hereditary hemorrhagic telangiectasia the dilation of small vessels and capillaries resulting from a genetic factor, with a tendency to bleed. Lesions may occur on the tongue as small, raised, red to bluish-red elevations.

the dilation of small vessels and capillaries resulting from a genetic factor, with a tendency to bleed. Lesions may occur on the tongue as small, raised, red to bluish-red elevations.

Osler Weber Rendu syndrome Osler Weber Rendu syndrome (also known as hereditary hemorrhagic telangiectasia). Note the multiple 1-2 mm, discrete, red macular and papular telangiectases on the lower lip and tongue. Reproduced with permission from: Fitzpatrick, TB, Johnson, RA, Wolff, K, Suurmond, D. Color Atlas & Synopsis of Clinical Dermatology, 4th ed, McGraw Hill Medical Publishing, New York 2001. Copyright © 2001 McGraw-Hill.

Osler Weber Rendu syndrome (also known as hereditary hemorrhagic telangiectasia). Note the multiple 1-2 mm, discrete, red macular and papular telangiectases on the lower lip and tongue. Reproduced with permission from: Fitzpatrick, TB, Johnson, RA, Wolff, K, Suurmond, D. Color Atlas & Synopsis of Clinical Dermatology, 4th ed, McGraw Hill Medical Publishing, New York 2001. Copyright © 2001 McGraw-Hill.

telangiectases on the lower lip and tongue. Reproduced with permission from: Fitzpatrick, TB, Johnson, RA, Wolff, K, Suurmond, D. Color Atlas & Synopsis of Clinical Dermatology, 4th ed, McGraw Hill Medical Publishing, New York 2001. Copyright © 2001 McGraw-Hill. Osler Weber Rendu syndrome Osler Weber Rendu syndrome (also known as hereditary hemorrhagic telangiectasia). Note the multiple 1-2 mm, discrete, red macular and papular telangiectases on the lower lip and tongue. Reproduced with permission from: Fitzpatrick, TB, Johnson, RA, Wolff, K, Suurmond, D. Color Atlas & Synopsis of Clinical Dermatology, 4th ed, McGraw Hill Medical Publishing, New York 2001. Copyright © 2001 McGraw-Hill. Osler Weber Rendu syndrome Telengiectasia on dorsum of tongue

Telengiectasia on dorsum of tongue

Osler Weber Rendu syndrome Telengiectasia on lip

Telengiectasia on lip

Ankylosing Spondylitis AP and lateral view of the lumbosacral spine demonstrate flowing osteophytes with bony bridges between the margins of adjacent vertebral bodies seen laterally at all the visualized levels

AP and lateral view of the lumbosacral spine demonstrate flowing osteophytes with bony bridges between the margins of adjacent vertebral bodies seen laterally at all the visualized levels

Erythema Multiforme (Stevens-Johnson Syndrome) Erythema multiforme lesions are often referred to as target lesions because of the concentric rings the lesions produce. The "target" appearance is well demonstrated in this photograph

Erythema multiforme lesions are often referred to as target lesions because of the concentric rings the lesions produce. The "target" appearance is well demonstrated in this photograph

Erythema Multiforme (Stevens-Johnson Syndrome)

Erythema Multiforme (Stevens-Johnson Syndrome)

Erythema Multiforme (Stevens-Johnson Syndrome)

Erythema Multiforme (Stevens-Johnson Syndrome)

Erythema Multiforme (Stevens-Johnson Syndrome)

Erythema marginatum This is an evanescent, erythematous, non-pruritic rash with pale centers and rounded or serpiginous margins. Lesions occur mainly on the trunk and proximal extremities and may be induced by application of heat

This is an evanescent, erythematous, non-pruritic rash with pale centers and rounded or serpiginous margins. Lesions occur mainly on the trunk and proximal extremities and may be induced by application of heat

Erythema marginatum This is an evanescent, erythematous, non-pruritic rash with pale centers and rounded or serpiginous margins. Lesions occur mainly on the trunk and proximal extremities and may be induced by application of heat

This is an evanescent, erythematous, non-pruritic rash with pale centers and rounded or serpiginous margins. Lesions occur mainly on the trunk and proximal extremities and may be induced by application of heat

Erythema marginatum

Dermatitis, herpetiformis This picture shows the forearm of a person with a chronic inflammatory disease known as dermatitis herpetiformis. It produces red, raised (papular), small or large blisters (vesicles or bullae) that burn and itch intensely. Dermatitis herpetiformis develops suddenly, lasts for weeks to months, and may be associated with digestive diseases (such as Celiac disease)

This picture shows the forearm of a person with a chronic inflammatory disease known as dermatitis herpetiformis. It produces red, raised (papular), small or large blisters (vesicles or bullae) that burn and itch intensely. Dermatitis herpetiformis develops suddenly, lasts for weeks to months, and may be associated with digestive diseases (such as Celiac disease)

This picture shows a chronic inflammatory disease (dermatitis herpetiformis) that produces red (erythematous), raised (papular), small or large blisters (vesicles or bullae) that burn and itch intensely. Dermatitis herpetiformis develops suddenly, lasts for weeks to months, and may be associated with digestive diseases (such as Celiac disease).

primary amyloidosis Facial involvement with amyloidosis. She has extensive nodules associated with purpura involving the eyelids and the naso-labial folds

Facial involvement with amyloidosis. She has extensive nodules associated with purpura involving the eyelids and the naso-labial folds

primary amyloidosis

primary amyloidosis Macroglossia, which can be subtle

Macroglossia, which can be subtle

Pemphigoid gestationis History PG typically manifests during late pregnancy, with an abrupt onset of extremely pruritic urticarial papules and blisters on the abdomen and trunk. Unrelenting pruritus often interferes with daily activities. Lesions may appear any time during pregnancy, but they most commonly develop during the second and third trimesters. Symptoms may abate at the end of pregnancy; however, dramatic flares can occur at or immediately after delivery. PG usually resolves spontaneously within weeks to months after delivery and possibly quicker with breastfeeding. The persistence of disease activity for years postpartum has been reported. PG may recur with the resumption of menses, use of oral contraception, and subsequent pregnancies. The 1999 cohort study by Jenkins et al 2 showed no association between change in partner and development of PG in subsequent pregnancies. Physical The initial clinical manifestations are erythematous urticarial patches and plaques, which are typically periumbilical. These lesions progress to tense vesicles and blisters (see Media File 1 and Media File 4 ). Some patients may present with urticarial plaques and may never develop blisters (see Media File 2 ). These hivelike plaques differ from true urticaria because of their relatively fixed nature. The rash spreads peripherally, often sparing the face, palms, and soles. Mucosal lesions occur in less than 20% of cases. Patients may have secondary infections at blister sites. Causes PG is a pregnancy-associated autoimmune disease. The autoantibodies are deposited in the skin and detectable in the circulation, and they are predominantly specific for the hemidesmosomal protein BPAG2. Circulating antibodies and T cells are directed against an immunodominant epitope. This epitope, located in the extracellular region of BPAG2 near the membrane, is called the MCW-1 domain. This region of BPAG2 is also an immunodominant epitope in a closely related autoimmune blistering disease, BP. The trigger for autoantibody production is still poorly understood. As described in Pathophysiology , autoantibodies to amniotic basement membrane (paternal major histocompatibility class II antigens) may cross-react with BPAG2 antigen in the skin, leading to the immune response. PG has also been described to occur in association with trophoblastic tumors, such as hydatifo

History

PG typically manifests during late pregnancy, with an abrupt onset of extremely pruritic urticarial papules and blisters on the abdomen and trunk. Unrelenting pruritus often interferes with daily activities.

Lesions may appear any time during pregnancy, but they most commonly develop during the second and third trimesters.

Symptoms may abate at the end of pregnancy; however, dramatic flares can occur at or immediately after delivery. PG usually resolves spontaneously within weeks to months after delivery and possibly quicker with breastfeeding. The persistence of disease activity for years postpartum has been reported.

PG may recur with the resumption of menses, use of oral contraception, and subsequent pregnancies. The 1999 cohort study by Jenkins et al 2 showed no association between change in partner and development of PG in subsequent pregnancies.

Physical

The initial clinical manifestations are erythematous urticarial patches and plaques, which are typically periumbilical.

These lesions progress to tense vesicles and blisters (see Media File 1 and Media File 4 ).

Some patients may present with urticarial plaques and may never develop blisters (see Media File 2 ). These hivelike plaques differ from true urticaria because of their relatively fixed nature.

The rash spreads peripherally, often sparing the face, palms, and soles. Mucosal lesions occur in less than 20% of cases.

Patients may have secondary infections at blister sites.

Causes

PG is a pregnancy-associated autoimmune disease.

The autoantibodies are deposited in the skin and detectable in the circulation, and they are predominantly specific for the hemidesmosomal protein BPAG2.

Circulating antibodies and T cells are directed against an immunodominant epitope.

This epitope, located in the extracellular region of BPAG2 near the membrane, is called the MCW-1 domain.

This region of BPAG2 is also an immunodominant epitope in a closely related autoimmune blistering disease, BP.

The trigger for autoantibody production is still poorly understood. As described in Pathophysiology , autoantibodies to amniotic basement membrane (paternal major histocompatibility class II antigens) may cross-react with BPAG2 antigen in the skin, leading to the immune response.

PG has also been described to occur in association with trophoblastic tumors, such as hydatifo

Bullous pemphigoid, Bullous pemphigoid is a blistering skin condition that most often affects the elderly. This is a close-up picture of the typical blisters. Large blisters, like these, are called bullae

Bullous pemphigoid is a blistering skin condition that most often affects the elderly. This is a close-up picture of the typical blisters. Large blisters, like these, are called bullae

alkaptonuria, ochronosis X-ray lower lumbo-sacral spine and sacro-iliac joints showing normal sacro-iliac joints and calcification of intervertebral discs

X-ray lower lumbo-sacral spine and sacro-iliac joints showing normal sacro-iliac joints and calcification of intervertebral discs

alkaptonuria, ochronosis grossly calcified intervertebal discs

grossly calcified intervertebal discs

alkaptonuria, ochronosis early ankylosis of spine

early ankylosis of spine

alkaptonuria, ochronosis bluish spots on his sclera

bluish spots on his sclera

alkaptonuria, ochronosis Bluish discoloration os ear cartillage

Bluish discoloration os ear cartillage

hypertrophic osteoarthropathy Note diffuse periosteal new bone formation of the distal radius and ulna. The metcarpals are also affected

Note diffuse periosteal new bone formation of the distal radius and ulna. The metcarpals are also affected

Reiter's syndrome(Keratoderma blennorrhagica)

Chronic myeloid leukaemia blast transformation: myeloid, with increased basophil precursors; peripheral blood.

Chronic myeloid leukaemia blast transformation: myeloid, with increased basophil precursors; peripheral blood.

BM of CML in chronic phase Hypercellularity. The megakaryocytes maybe decreased in size but generally increased in number. M/E ratio was much increased, generally > 5:1 The majority of the cells are neutrophils, metamyelocytes, and myelocytes. The basophil count is almost invariably increased, The eosinophils may also be increased. Monocytosis may be observed. While collagen fibrosis in the marrow is unusual at presentation, significant degrees of reticulin stain-measured fibrosis are noted in about half of the patients

Hypercellularity. The megakaryocytes maybe decreased in size but generally increased in number. M/E ratio was much increased, generally > 5:1 The majority of the cells are neutrophils, metamyelocytes, and myelocytes. The basophil count is almost invariably increased, The eosinophils may also be increased. Monocytosis may be observed. While collagen fibrosis in the marrow is unusual at presentation, significant degrees of reticulin stain-measured fibrosis are noted in about half of the patients

Reiter’s syndrome(anterior uveitis)

Reiter’s syndrome(arthritis) "An Xray of the same Patient is Shown, Demonstrating Erosive Arthritis of the 2nd MCP Joint : a Patient with a reite’s syndrome

"An Xray of the same Patient is Shown, Demonstrating Erosive Arthritis of the 2nd MCP Joint : a Patient with a reite’s syndrome

TTP The picture below is a microscopic view of blood cells from a patient with TTP. Notice that there are no platelets. There should be 10 to 20 platelets in this picture, just like in the picture of normal blood cells . Notice the broken shapes of the red blood cells. Compare these cells to the normal red blood cells . This is the result of blood trying to flow through partially obstructed blood vessels. This picture is an important part of the diagnosis of TTP-HUS .

The picture below is a microscopic view of blood cells from a patient with TTP. Notice that there are no platelets. There should be 10 to 20 platelets in this picture, just like in the picture of normal blood cells . Notice the broken shapes of the red blood cells. Compare these cells to the normal red blood cells . This is the result of blood trying to flow through partially obstructed blood vessels. This picture is an important part of the diagnosis of TTP-HUS .

TTP SYMPTOMS

Malaria, falciparum Malaria. Plasmodium falciparum. Blood film. Several red cells contain trophozoites (ring forms). The arrows point to a ring form and double-dot ring form.

Malaria. Plasmodium falciparum. Blood film. Several red cells contain trophozoites (ring forms). The arrows point to a ring form and double-dot ring form.

Malaria, vivax Malaria. Plasmodium vivax. Blood film. Trophozoites (ring forms) and female gametocyte.

Malaria. Plasmodium vivax. Blood film. Trophozoites (ring forms) and female gametocyte.

Adult T-Cell Leukemia-Lymphoma (HTLV-1) Adult T-cell leukemia-lymphoma (HTLV-1). Blood films. White cell concentrate. Leukemic lymphocytes with folded or clefted nuclei. Cells have condensed nuclear chromatin with inconspicuous nucleoli, usually.

Adult T-cell leukemia-lymphoma (HTLV-1). Blood films. White cell concentrate. Leukemic lymphocytes with folded or clefted nuclei. Cells have condensed nuclear chromatin with inconspicuous nucleoli, usually.

HEREDITARY HEMORRHAGIC TELENGIECTASIA Findings: Multiple hyperenhancing lesions in the liver consistent with AVM's. � Splenic artery and Right renal artyer aneurysm.

Findings: Multiple hyperenhancing lesions in the liver consistent with AVM's. � Splenic artery and Right renal artyer aneurysm.

Discoid Lupus

Discoid Lupus

Livedo reticularis This is a close-up view of livedo reticularis on a person's legs. Livedo is a descriptive term used to describe the red, non-blanchable (doesn't turn white when pressed) network-pattern (reticulated) in the skin caused by plugging of the blood vessels. This condition has many causes

This is a close-up view of livedo reticularis on a person's legs. Livedo is a descriptive term used to describe the red, non-blanchable (doesn't turn white when pressed) network-pattern (reticulated) in the skin caused by plugging of the blood vessels. This condition has many causes

Livedo reticularis

Livedo reticularis

Chronic Lymphocytic Leukemia and Autoimmune Hemolytic Anemia Chronic lymphocytic leukemia and autoimmune hemolytic anemia. ( A ) Blood film. Increased small lymphocytes. Small spherocytic red cells and macrocytes (presumptive reticulocytes) reflect the concomitant immune hemolytic anemia. Red cell density on the film also reflects very severe anemia

Chronic lymphocytic leukemia and autoimmune hemolytic anemia. ( A ) Blood film. Increased small lymphocytes. Small spherocytic red cells and macrocytes (presumptive reticulocytes) reflect the concomitant immune hemolytic anemia. Red cell density on the film also reflects very severe anemia

Autoimmune Hemolytic Anemia, Warm Antibody Type autoimmune hemolytic anemia; macrocytic erythrocyte; spherocytosis; warm antibody autoimmune hemolytic anemia. Autoimmune hemolytic anemia, warm antibody type. Blood film. Intense spherocytosis and polychromatophilic macrocytes (reticulocytosis ).

autoimmune hemolytic anemia; macrocytic erythrocyte; spherocytosis; warm antibody autoimmune hemolytic anemia.

Autoimmune hemolytic anemia, warm antibody type. Blood film. Intense spherocytosis and polychromatophilic macrocytes (reticulocytosis ).

Chronic Lymphocytic Leukemia

Chronic Lymphocytic Leukemia

Acute anterior uveitis Photophobia is typical in these patients as the pupil’s constriction in the response to light causes pain. The redness is maximum near the limbus (ciliary injection) and the pupil is irregular where it is stuck to the front of the lens. Acute anterior uveitis should be managed with atropine to keep the pupil dilated. Topical steroids may be useful in severe cases.

Photophobia is typical in these patients as the pupil’s constriction in the response to light causes pain. The redness is maximum near the limbus (ciliary injection) and the pupil is irregular where it is stuck to the front of the lens. Acute anterior uveitis should be managed with atropine to keep the pupil dilated. Topical steroids may be useful in severe cases.

ANTERIOR UVEITIS

Diffuse Idiopathic Skeletal Hyperostosis (DISH) There is flowing ossification (black arrows)that spans more than four contiguous vertebral bodies while the disc height is maintained andthe flowing ossification is separated from the anterior aspect of the vertebral body (blue arrows).

There is flowing ossification (black arrows)that spans more than four contiguous vertebral bodies while the disc height is maintained andthe flowing ossification is separated from the anterior aspect of the vertebral body (blue arrows).

OSTEONECROSIS Tomogram of the right hip showing a segmental zone of sclerosis (arrows) in the superior portion of the femoral head, consistent with osteonecrosis (O).

Tomogram of the right hip showing a segmental zone of sclerosis (arrows) in the superior portion of the femoral head, consistent with osteonecrosis (O).

OSTEONECROSIS AP radiograph of the hip in a patient with osteonecrosis. Note the lucent crescent sign (white arrow) and the discontinuity where the subchondral bone has collapsed (black arrowhead). Also note a core decompression channel drilled up through the femoral neck (black arrows). AP radiograph of the hip in a patient with osteonecrosis. Note the lucent crescent sign (white arrow) and the discontinuity where the subchondral bone has collapsed (black arrowhead). Also note a core decompression channel drilled up through the femoral neck (black arrows).

AP radiograph of the hip in a patient with osteonecrosis. Note the lucent crescent sign (white arrow) and the discontinuity where the subchondral bone has collapsed (black arrowhead). Also note a core decompression channel drilled up through the femoral neck (black arrows). AP radiograph of the hip in a patient with osteonecrosis. Note the lucent crescent sign (white arrow) and the discontinuity where the subchondral bone has collapsed (black arrowhead). Also note a core decompression channel drilled up through the femoral neck (black arrows).

OSTEONECROSIS AP radiograph of the hip in a patient with osteonecrosis. Note the lucent crescent sign (white arrow) and the discontinuity where the subchondral bone has collapsed (black arrowhead). Also note a core decompression channel drilled up through the femoral neck (black arrows). AP radiograph of the hip in a patient with osteonecrosis. Note the lucent crescent sign (white arrow) and the discontinuity where the subchondral bone has collapsed (black arrowhead). Also note a core decompression channel drilled up through the femoral neck (black arrows).

AP radiograph of the hip in a patient with osteonecrosis. Note the lucent crescent sign (white arrow) and the discontinuity where the subchondral bone has collapsed (black arrowhead). Also note a core decompression channel drilled up through the femoral neck (black arrows). AP radiograph of the hip in a patient with osteonecrosis. Note the lucent crescent sign (white arrow) and the discontinuity where the subchondral bone has collapsed (black arrowhead). Also note a core decompression channel drilled up through the femoral neck (black arrows).

Gardner's syndrome Gardner syndrome in an 80-year-old man. Panorex radiograph demonstrates multiple osteomas (arrows) throughout the mandible. Note the osteoma within the right maxilla (arrowhead).

Gardner syndrome in an 80-year-old man. Panorex radiograph demonstrates multiple osteomas (arrows) throughout the mandible. Note the osteoma within the right maxilla (arrowhead).

Gardner's syndrome Skull radiograph demonstrates multiple osteomas of the skull and mandible.

Skull radiograph demonstrates multiple osteomas of the skull and mandible.

achalasia The oesophagus is dilated, with a fluid level and tapers down smoothly below to a bird's beak appearance.

The oesophagus is dilated, with a fluid level and tapers down smoothly below to a bird's beak appearance.

achalasia Thorax x-ray revealed a para-cardiac double shade with hydro-aerial level and a mediastinum enlarged by esophageal dilatation.

Thorax x-ray revealed a para-cardiac double shade with hydro-aerial level and a mediastinum enlarged by esophageal dilatation.

Phayngeal pouch Clinical presentation: 53 year old female from the West-Indies with a history of left sided chest pain that was thought to be hiatus hernia. There is a largewide-mouthed diverticulum on the left side of the pharynx. It fills and empties promptly on swallowing. The half-shadowing in the upper part is swallowed air.

Clinical presentation: 53 year old female from the West-Indies with a history of left sided chest pain that was thought to be hiatus hernia.

There is a largewide-mouthed diverticulum on the left side of the pharynx. It fills and empties promptly on swallowing. The half-shadowing in the upper part is swallowed air.

Whipple's Disease Histology of the duodenal biopsy showing clubbed epithelial villi with inflammatory infiltrate including numerous foamy macrophages (haemtoxylin-eosin stain, magnification × 250)

Histology of the duodenal biopsy showing clubbed epithelial villi with inflammatory infiltrate including numerous foamy macrophages (haemtoxylin-eosin stain, magnification × 250)

pyoderma gangrenosum Ulcerative lesion of pyoderma gangrenosum measuring 6.0 x 4.0 cm on the right medial shin of a 34-year-old woman with psoriasis and psoriatic arthritis. The erythema on the patient's foot was psoriasis.

Ulcerative lesion of pyoderma gangrenosum measuring 6.0 x 4.0 cm on the right medial shin of a 34-year-old woman with psoriasis and psoriatic arthritis. The erythema on the patient's foot was psoriasis.

pyoderma gangrenosum Same lesion close up. Notice overhanging purplish border, necrotic center, and surrounding rim of erythema. This lesion was initially treated with antibiotics as either an infected brown recluse spider bite or an infected venous stasis ulcer.

Same lesion close up. Notice overhanging purplish border, necrotic center, and surrounding rim of erythema. This lesion was initially treated with antibiotics as either an infected brown recluse spider bite or an infected venous stasis ulcer.

Dermatitis herpetiformis This picture shows the forearm of a person with a chronic inflammatory disease known as dermatitis herpetiformis. It produces red, raised (papular), small or large blisters (vesicles or bullae) that burn and itch intensely. Dermatitis herpetiformis develops suddenly, lasts for weeks to months, and may be associated with digestive diseases (such as Celiac disease).

This picture shows the forearm of a person with a chronic inflammatory disease known as dermatitis herpetiformis. It produces red, raised (papular), small or large blisters (vesicles or bullae) that burn and itch intensely. Dermatitis herpetiformis develops suddenly, lasts for weeks to months, and may be associated with digestive diseases (such as Celiac disease).

dermatitis herpetiformis This picture shows a chronic inflammatory disease (dermatitis herpetiformis) that produces red (erythematous), raised (papular), small or large blisters (vesicles or bullae) that burn and itch intensely. Dermatitis herpetiformis develops suddenly, lasts for weeks to months, and may be associated with digestive diseases (such as Celiac disease).

This picture shows a chronic inflammatory disease (dermatitis herpetiformis) that produces red (erythematous), raised (papular), small or large blisters (vesicles or bullae) that burn and itch intensely. Dermatitis herpetiformis develops suddenly, lasts for weeks to months, and may be associated with digestive diseases (such as Celiac disease).

dermatitis herpetiformis his picture shows the fingers of a person with a chronic inflammatory disease known as dermatitis herpetiformis. It produces red, raised (papular), small or large blisters (vesicles or bullae) that burn and itch intensely. Dermatitis herpetiformis develops suddenly, lasts for weeks to months, and may be associated with digestive diseases (such as Celiac disease).

his picture shows the fingers of a person with a chronic inflammatory disease known as dermatitis herpetiformis. It produces red, raised (papular), small or large blisters (vesicles or bullae) that burn and itch intensely. Dermatitis herpetiformis develops suddenly, lasts for weeks to months, and may be associated with digestive diseases (such as Celiac disease).

Hivan hiv associated nephropathy

Goodpasture's Syndrom Crescent formation in glomerulonephritis associated with Goodpasture's Syndrom

Crescent formation in glomerulonephritis associated with Goodpasture's Syndrom

Good pasture syndrome AP Chest x-ray, diffuse bilateral alveolar infiltrate

AP Chest x-ray, diffuse bilateral alveolar infiltrate

Good pasture syndrome Immunoflorescence image of linear distribution of IgG on glomerular basement membrane

Immunoflorescence image of linear distribution of IgG on glomerular basement membrane

Goodpasture syndrome Diffuse bilateral predominately alveolar densities with a mild interstitial component

Diffuse bilateral predominately alveolar densities with a mild interstitial component

Good pasture syndrome Lung tissue biopsy consistent with acute lung injury characterized by interstitial and intra-alveolar organization, intra-alveolar fibrin deposition, squamous metaplasia of bronchiolar epithelium and rare fibrin thrombi associated with hemorrhage.

Lung tissue biopsy consistent with acute lung injury characterized by interstitial and intra-alveolar organization, intra-alveolar fibrin deposition, squamous metaplasia of bronchiolar epithelium and rare fibrin thrombi associated with hemorrhage.

Goodpasture's syndrome . (A) Computed tomographic (CT) image at the level of the aortic arch shows centrilobular ground-glass opacities throughout the upper lobes due to diffuse pulmonary hemorrhage. (B) CT image at the level of the right main pulmonary artery shows ground-glass opacities in the lower lobes. The patient was a 35-year-old woman.

. (A) Computed tomographic (CT) image at the level of the aortic arch shows centrilobular ground-glass opacities throughout the upper lobes due to diffuse pulmonary hemorrhage. (B) CT image at the level of the right main pulmonary artery shows ground-glass opacities in the lower lobes. The patient was a 35-year-old woman.

Behçet's disease . Computed tomographic image at the level of the superior pulmonary veins demonstrates circumferential nonocclusive thrombus within an aneurysm of the right interlobar artery (arrows). The patient was a 48-year-old man.

. Computed tomographic image at the level of the superior pulmonary veins demonstrates circumferential nonocclusive thrombus within an aneurysm of the right interlobar artery (arrows). The patient was a 48-year-old man.

Churg-Strauss Syndrome . (A) Posteroanterior chest radiograph shows small bilateral lower lobe consolidation, linear opacities, and small pleural effusions. (B) Computed tomographic image at the level of the carina demonstrates smooth thickening of the interlobular septa (arrows). The patient was a 69-year-old woman with no clinical or echocardiographic evidence of left heart failure. The septal thickening was due to pulmonary involvement.

. (A) Posteroanterior chest radiograph shows small bilateral lower lobe consolidation, linear opacities, and small pleural effusions. (B) Computed tomographic image at the level of the carina demonstrates smooth thickening of the interlobular septa (arrows). The patient was a 69-year-old woman with no clinical or echocardiographic evidence of left heart failure. The septal thickening was due to pulmonary involvement.

Takayasu's arteritis . Computed tomographic image obtained following intravenous administration of contrast demonstrates thickening and enhancement of the wall of the aorta at the level of the aortic arch (arrows). The patient was a 32-year-old woman.

. Computed tomographic image obtained following intravenous administration of contrast demonstrates thickening and enhancement of the wall of the aorta at the level of the aortic arch (arrows). The patient was a 32-year-old woman.

von Hippel-Lindau disease Angiomatosis retinae (von Hippel-Lindau disease)

Angiomatosis retinae (von Hippel-Lindau disease)

von Hippel-Lindau disease HBs of the CNS Figure 1 MRI scan of two small solid cerebellar HBs (arrows) in a 52-year-old VHL patient. Figure 2 MRI scan of a typical cystic cerebellar HB in a 39-year-old non-VHL patient. Figure 3 Two solid brain stem HBs and a cystic HB in the cervical spine in a 32-year-old VHL patient. Figure 4 An HB in cervical spine in a 21-year-old VHL patient: MRI with contrast (a), superselective angiography before (b) and after (c) preoperative embolization. Figure 5 Two small spinal HBs in the thoracic region (a and b) in the same patient as in Figure 4, three years later. Figure 6 A large solid recurrent HB 11 years after the primary total removal in a 66-year-old non-VHL patient.

HBs of the CNS

Figure 1

MRI scan of two small solid cerebellar HBs (arrows) in a 52-year-old VHL patient.

Figure 2

MRI scan of a typical cystic cerebellar HB in a 39-year-old non-VHL patient.

Figure 3

Two solid brain stem HBs and a cystic HB in the cervical spine in a 32-year-old VHL patient.

Figure 4

An HB in cervical spine in a 21-year-old VHL patient: MRI with contrast (a), superselective angiography before (b) and after (c) preoperative embolization.

Figure 5

Two small spinal HBs in the thoracic region (a and b) in the same patient as in Figure 4, three years later.

Figure 6

A large solid recurrent HB 11 years after the primary total removal in a 66-year-old non-VHL patient.

von Hippel-Lindau disease HBs of the retina Figure 8 A typical mature HB with a draining arteriole and venule in a 40-year-old non-VHL patient: ophthalmoscopic view (a), and FA (b) before treatment; ophthalmoscopic view (c) and FA (d) at two months after cryocoagulation, showing narrowing of the feeders. Ophthalmoscopic view (e) at six months, showing shrinkage of the HB. Figure 9 A large HB with draining vessels and lipid exudates in a 65-year-old VHL patient. Figure 10 A juxtapapillary HB in a 25-year-old suspect VHL patient. Figure 11 Local exudative and tractional retinal detachment caused by an HB in a 26-year-old non-VHL patient.

HBs of the retina

Figure 8

A typical mature HB with a draining arteriole and venule in a 40-year-old non-VHL patient: ophthalmoscopic view (a), and FA (b) before treatment; ophthalmoscopic view (c) and FA (d) at two months after cryocoagulation, showing narrowing of the feeders. Ophthalmoscopic view (e) at six months, showing shrinkage of the HB.

Figure 9

A large HB with draining vessels and lipid exudates in a 65-year-old VHL patient.

Figure 10

A juxtapapillary HB in a 25-year-old suspect VHL patient.

Figure 11

Local exudative and tractional retinal detachment caused by an HB in a 26-year-old non-VHL patient.

Copyright © 2007 by the American Roentgen Ray Society Herwick, S. et al. Am. J. Roentgenol. 2006;187:W472-W480 --52-year-old man with von Hippel-Lindau disease and pancreatic mass diagnosed as serous cystadenoma on basis of findings at previous fine-needle aspiration

Diabetic nephropathy Glomeruli with Kimmelstiel-Wilson nodules. The smallest nodules can be more cellular and the greatest nodules tend to be acellular in the centre and surrounded by more cellular zones. Capillaries are seen around these nodules, sometimes adopting an aspect in garland (like in the three nodules indicated with arrows); in some cases we see microaneurisms around nodules. Notice the variability of size of the nodules

Glomeruli with Kimmelstiel-Wilson nodules. The smallest nodules can be more cellular and the greatest nodules tend to be acellular in the centre and surrounded by more cellular zones. Capillaries are seen around these nodules, sometimes adopting an aspect in garland (like in the three nodules indicated with arrows); in some cases we see microaneurisms around nodules. Notice the variability of size of the nodules

Diabetic nephropathy Kimmelstiel-Wilson Nodules highlight with PAS stain; glomerular nodules in amiloidosis and light chain deposits disease have a more weak stain with PAS (PAS, X400).

Kimmelstiel-Wilson Nodules highlight with PAS stain; glomerular nodules in amiloidosis and light chain deposits disease have a more weak stain with PAS (PAS, X400).

Henoch-Schönlein purpura Lower extremity rash. Rash characteristically involves the buttocks and lower extremities. Purpuric areas coalesce and become confluent with adjacent lesions.

Lower extremity rash. Rash characteristically involves the buttocks and lower extremities. Purpuric areas coalesce and become confluent with adjacent lesions.

Henoch-Schönlein purpura Henoch-Schönlein purpura. Henoch-Schöenlein purpura in WAS. A : Cutaneous purpura; B : Urine sediment red blood cell cast; C : Acute glomerular inflammation and crescent formation; D : Details of basal membrane (arrowheads), mesangial proliferation (thin arrows), and IgA deposits (asterisks).

Henoch-Schönlein purpura. Henoch-Schöenlein purpura in WAS. A : Cutaneous purpura; B : Urine sediment red blood cell cast; C : Acute glomerular inflammation and crescent formation; D : Details of basal membrane (arrowheads), mesangial proliferation (thin arrows), and IgA deposits (asterisks).

Acute onset of hematuria and proteinuria associated with multiorgan involvement of the heart, liver, pancreas, kidneys, and skin in a patient with Henoch–Schönlein purpura CT scan of the abdomen and biopsy of skin and kidney. ( a ) Computer tomography scan of the abdomen shows significant thickening and edema of jejunum (arrow) (60 60 mm (300 300 DPI)). ( b ) The skin biopsy shows leukocytoclastic vasculitis. The dermal small vessels display endothelial cell swelling (arrowhead) and are infiltrated and surrounded by neutrophils, many of which show fragmentation of nuclei (karyorrhexis) (arrows) (hematoxylin–eosin (H&E), original magnification 600). ( c ) A glomerulus shows compression of the tuft by a segmental cellular crescent (arrow) admixed with fibrin (arrowhead). The underlying tuft exhibits mild segmental mesangial hypercellularity (H&E, original magnification 600). ( d ) On immunofluorescence, there is intense positivity for IgA in a global mesangial distribution (original magnification 400).

CT scan of the abdomen and biopsy of skin and kidney. ( a ) Computer tomography scan of the abdomen shows significant thickening and edema of jejunum (arrow) (60 60 mm (300 300 DPI)). ( b ) The skin biopsy shows leukocytoclastic vasculitis. The dermal small vessels display endothelial cell swelling (arrowhead) and are infiltrated and surrounded by neutrophils, many of which show fragmentation of nuclei (karyorrhexis) (arrows) (hematoxylin–eosin (H&E), original magnification 600). ( c ) A glomerulus shows compression of the tuft by a segmental cellular crescent (arrow) admixed with fibrin (arrowhead). The underlying tuft exhibits mild segmental mesangial hypercellularity (H&E, original magnification 600). ( d ) On immunofluorescence, there is intense positivity for IgA in a global mesangial distribution (original magnification 400).

Henoch-Shonlein purpura Anterior ischaemic optic neuropathy secondary to Henoch–Schönlein Purpura

Anterior ischaemic optic neuropathy secondary to Henoch–Schönlein Purpura

Wegener's granulomatosis

Aries PM et al. (2006) A case of destructive Wegener’s granulomatosis complicated by cytomegalovirus infection Nat Clin Pract Rheumatol 2: 511 – 515 doi:10.1038/ ncprheum0269 Figure 1 Wegener's granulomatosis with ear, nose and throat involvement and palatal destruction

Wegener's granulomatosis Wegener's granulomatosis with ear, nose and throat involvement and palatal destruction

Wegener's granulomatosis with ear, nose and throat involvement and palatal destruction

Wegener's granulomatosis (a) Right-upper-lid oedema at presentation, and (b) resolution of oedema following treatment.

(a) Right-upper-lid oedema at presentation, and (b) resolution of oedema following treatment.

Wegener's granulomatosis Active peripheral ulcerative keratitis (PUK), showing corneal thinning, at the edge of the corneal patch graft (arrow).

Active peripheral ulcerative keratitis (PUK), showing corneal thinning, at the edge of the corneal patch graft (arrow).

Horner's syndrome as manifestation of Wegener's granulomatosis (A) right-sided Horner's syndrome and sixth nerve palsy (fixating with left eye); collapsed nasal bridge (printed with patient's permission). (B, C) CT and MRI showing retroclival mass lesion extending to the right cavernous sinus. (D) Follow-up MRI after treatment showing diminishing of the lesion in the cavernous sinus.

(A) right-sided Horner's syndrome and sixth nerve palsy (fixating with left eye); collapsed nasal bridge (printed with patient's permission). (B, C) CT and MRI showing retroclival mass lesion extending to the right cavernous sinus. (D) Follow-up MRI after treatment showing diminishing of the lesion in the cavernous sinus.

Wegener's granulomatosis Wegener's granulomatosis. (A) Computed tomographic (CT) scan at the level of the upper lobes shows bilateral noncavitating nodules (arrows) in the apical regions of both lungs and a cavitating nodule in the left apex. (B) CT scan at the level of main stem bronchi shows multiple cavitating and noncavitating nodules mainly in the subpleural and peribronchovascular regions. The patient was a 50-year-old man

Wegener's granulomatosis. (A) Computed tomographic (CT) scan at the level of the upper lobes shows bilateral noncavitating nodules (arrows) in the apical regions of both lungs and a cavitating nodule in the left apex. (B) CT scan at the level of main stem bronchi shows multiple cavitating and noncavitating nodules mainly in the subpleural and peribronchovascular regions. The patient was a 50-year-old man

Wegener's granulomatosis Computed tomographic scan image at the level of the right main pulmonary artery shows poorly defined bilateral ground glass opacities and a cavitating nodule (arrow) in the right middle lobe. The ground-glass opacities were due to diffuse pulmonary hemorrhage. The patient was a 53-year-old man.

Computed tomographic scan image at the level of the right main pulmonary artery shows poorly defined bilateral ground glass opacities and a cavitating nodule (arrow) in the right middle lobe. The ground-glass opacities were due to diffuse pulmonary hemorrhage. The patient was a 53-year-old man.

Wegener's granulomatosis Chest radiograph and CT scans demonstrate bilateral nodules and masses, most prominent at the bases

Chest radiograph and CT scans demonstrate bilateral nodules and masses, most prominent at the bases

Hemolytic-uremic syndrome . Blood film. Frequent echinocytes and occasional poikiloechinocytes with both distorted cell shape and more regular blunted projections (arrows). Paucity of platelets characteristic (thrombocytopenia). One megathrombocyte noted in center of field.

. Blood film. Frequent echinocytes and occasional poikiloechinocytes with both distorted cell shape and more regular blunted projections (arrows). Paucity of platelets characteristic (thrombocytopenia). One megathrombocyte noted in center of field.

HUS Schistocytes are fragmented red blood cells, and indicate mechanical damage causing hemolysis. The commonest cause is probably the presence of a mechanical heart valve, particularly when dysfunctional. Hemolytic Uremic Syndrome, Thrombotic Thrombocytopenic Purpura, and Disseminated Intravascular Coagulation are other causes.

Schistocytes are fragmented red blood cells, and indicate mechanical damage causing hemolysis. The commonest cause is probably the presence of a mechanical heart valve, particularly when dysfunctional. Hemolytic Uremic Syndrome, Thrombotic Thrombocytopenic Purpura, and Disseminated Intravascular Coagulation are other causes.

NORMAL RETINA

RP

RETINITIS PIGMENTOSA RP is a retinal degeneration, often hereditary, which affects the photoreceptors (rods and cones) which are the light sensing receptors. Usually, but not always, the rod receptors are affected first causing progressive decrease vision during dark hours, that is ‘night blindness’. There is also loss of peripheral vision leading to tunnel vision. As research into the genetics evolve we are learning more about RP as a spectrum of a number of related retinal degenerations some of which are associated with other disabilities like hearing loss. Most cases of RP are chronic and progress very slowly over decades.

RP is a retinal degeneration, often hereditary, which affects the photoreceptors (rods and cones) which are the light sensing receptors. Usually, but not always, the rod receptors are affected first causing progressive decrease vision during dark hours, that is ‘night blindness’. There is also loss of peripheral vision leading to tunnel vision. As research into the genetics evolve we are learning more about RP as a spectrum of a number of related retinal degenerations some of which are associated with other disabilities like hearing loss. Most cases of RP are chronic and progress very slowly over decades.

Retinitis pigmentosa <> <>

Retinitis pigmentosa http://www.blindness.org/content.asp?id=45

AGE RELATED MACULAR DEGENERATION AMD is the leading cause of new cases of blindness in patients over 60 years of age. It is a degenerative disease of the macula which is the central part of the retina and affects the central vision. There are two forms of macular degeneration: Dry AMD, or nonexudative AMD, where yellow white deposits called drusen accumulate in the deep macula with or without atrophy or ‘balding’ of the layers of the retina/macula. This leads to interference in the function of the photoreceptors responsible for processing of light coming into the eye which in turn causes decrease in vision. This dry AMD can progress to a more severe Wet AMD or exudative type of macular degeneration where abnormal choroidal vessels leak fluid, or rupture and bleed causing severe and often permanent central visual loss.

AMD is the leading cause of new cases of blindness in patients over 60 years of age. It is a degenerative disease of the macula which is the central part of the retina and affects the central vision. There are two forms of macular degeneration: Dry AMD, or nonexudative AMD, where yellow white deposits called drusen accumulate in the deep macula with or without atrophy or ‘balding’ of the layers of the retina/macula. This leads to interference in the function of the photoreceptors responsible for processing of light coming into the eye which in turn causes decrease in vision. This dry AMD can progress to a more severe Wet AMD or exudative type of macular degeneration where abnormal choroidal vessels leak fluid, or rupture and bleed causing severe and often permanent central visual loss.

BRANCH RETINAL VEIN OCCLUSION BRVO is a retinal vascular disease most often related to hypertension, elevated lipids/triglyceride/cholesterol, diabetes, carotid artery disease, cardiac disease, or hematologic (blood) disorders. In BRVO there is an occlusion of a branch retinal vein by a compressing, sclerotic retinal artery. This often leads to hemorrhage (bleeding), edema (swelling), or ischemia (poor circulation) of the retina and macula with resultant visual loss.

BRVO is a retinal vascular disease most often related to hypertension, elevated lipids/triglyceride/cholesterol, diabetes, carotid artery disease, cardiac disease, or hematologic (blood) disorders. In BRVO there is an occlusion of a branch retinal vein by a compressing, sclerotic retinal artery. This often leads to hemorrhage (bleeding), edema (swelling), or ischemia (poor circulation) of the retina and macula with resultant visual loss.

CRVO CRVO is also a retinal vascular disease but involves occlusion of the main central retinal vein. Vascular, hematologic, and cardiac disease may predispose individuals to develop CRVO which leads to leakage of blood and fluid into the retina. In many cases the resultant poor circulation (ischemia) can lead to abnormal blood vessel formation in the iris (rubeosis) with painful increases in eye pressure (neovascular glaucoma).

CRVO is also a retinal vascular disease but involves occlusion of the main central retinal vein. Vascular, hematologic, and cardiac disease may predispose individuals to develop CRVO which leads to leakage of blood and fluid into the retina. In many cases the resultant poor circulation (ischemia) can lead to abnormal blood vessel formation in the iris (rubeosis) with painful increases in eye pressure (neovascular glaucoma).

RETINAL HEMORRHAGE Bleeding or hemorrhage in the retina occurs when the blood vessels in the retina leak or rupture. Common causes include: diabetes, high blood pressure, blood disorders, cardiovascular problems, trauma, or aging.

Bleeding or hemorrhage in the retina occurs when the blood vessels in the retina leak or rupture. Common causes include: diabetes, high blood pressure, blood disorders, cardiovascular problems, trauma, or aging.

Macular Edema Swelling in the macula (edema) results from fluid build up and thickening within the layers of retinal tissue. Tiny blood vessels which surround the macula are usually responsible for the leakage. Many disorders including diabetes, vein occlusions, uveitis (inflammation), and cataract surgery can cause macular edema. Depending on the cause there are different treatments which may include eye drops, steroid injections, laser treatment, or if vitreoretinal tractional is present vitreous surger

Swelling in the macula (edema) results from fluid build up and thickening within the layers of retinal tissue. Tiny blood vessels which surround the macula are usually responsible for the leakage. Many disorders including diabetes, vein occlusions, uveitis (inflammation), and cataract surgery can cause macular edema. Depending on the cause there are different treatments which may include eye drops, steroid injections, laser treatment, or if vitreoretinal tractional is present vitreous surger

AR

AD

XLR

coal workers pneumoconiosis This picture shows complicated coal workers pneumoconiosis. There are diffuse, massive light areas that run together in the upper and middle parts of both lungs. These are superimposed on a background of small and poorly distinguishable light areas that are diffuse and located in both lungs. Diseases which may explain these X-ray findings include, but are not limited to: complicated coal workers pneumoconiosis (CWP), silico-tuberculosis, and metastatic lung cancer.

This picture shows complicated coal workers pneumoconiosis. There are diffuse, massive light areas that run together in the upper and middle parts of both lungs. These are superimposed on a background of small and poorly distinguishable light areas that are diffuse and located in both lungs. Diseases which may explain these X-ray findings include, but are not limited to: complicated coal workers pneumoconiosis (CWP), silico-tuberculosis, and metastatic lung cancer.

coal workers pneumoconiosis This picture shows complicated coal workers pneumoconiosis. There are diffuse, massive light areas that run together in the upper and middle parts of both lungs. These are superimposed on a background of small and poorly distinguishable light areas that are diffuse and located in both lungs. Diseases which may explain these X-ray findings include, but are not limited to: complicated coal workers pneumoconiosis (CWP), silico-tuberculosis, and metastatic lung cancer

This picture shows complicated coal workers pneumoconiosis. There are diffuse, massive light areas that run together in the upper and middle parts of both lungs. These are superimposed on a background of small and poorly distinguishable light areas that are diffuse and located in both lungs. Diseases which may explain these X-ray findings include, but are not limited to: complicated coal workers pneumoconiosis (CWP), silico-tuberculosis, and metastatic lung cancer

Silicosis The first PA film demonstrates miliary small well defined nodles

The first PA film demonstrates miliary small well defined nodles

Silicosis This chest radiograph demonstrates so many silicotic nodules that they have become confluent areas of silicotic nodules that have resulted in severe restrictive lung disease

This chest radiograph demonstrates so many silicotic nodules that they have become confluent areas of silicotic nodules that have resulted in severe restrictive lung disease

Rheumatoid lung Rheumatoid nodules in the lung. Chest radiograph demonstrates discrete rheumatoid nodules in both right and left lower lobes

Rheumatoid nodules in the lung. Chest radiograph demonstrates discrete rheumatoid nodules in both right and left lower lobes

Rheumatoid lung necrobiotic rheumatoid nodules in the right lung and pneumothorax of the left; thorax drain ‘in situ

necrobiotic rheumatoid nodules in the right lung and pneumothorax of the left; thorax drain ‘in situ

Rheumatoid lung subpleural necrobiotic nodule in the left lung and pneumothorax; thorax drain ‘in situ

subpleural necrobiotic nodule in the left lung and pneumothorax; thorax drain ‘in situ

Electrical alternans This EKG is characterized by low voltage and electrical alternans. The QRS axis alternates between beats. In this example it is best seen in the chest leads where the QRS points in different directions!

This EKG is characterized by low voltage and electrical alternans. The QRS axis alternates between beats. In this example it is best seen in the chest leads where the QRS points in different directions!

Brudzinski’s sign

Accelerated Idioventricular Rhythm This EKG shows a slow wide complex tachycardia with intermittent narrow complex beats. The 5 th and 10 th beats are sinus rhythm and close examination of these beats will give you a clue to the cause of the wide complex rhythm. In Leads II and III you can appreciate ST elevation indicating an acute current of injury due to a myocardial infarction. The wide complex beats therefore represent an Accelerated Idioventricular Rhythm or AIVR which is usually seen following reperfusion after an acute infarct. Accelerated Idioventricular Rhythms are ectopic ventricular rhythms at rates between 40 bpm and 100 to 120 bpm. The ventricular origin of this rhythm can be demonstrated by the usual EKG criteria which include AV dissociation, fusion, and capture complexes. In this EKG the 4 th beat represents a fusion complex and the 5 th beath represents a capture beat proving that these beats are ventricular in origin. The incidence of Accelerated Idioventricular Rhythms following acute MI is reported to be between 8 and 36 percent. This rhythm can also be seen in patients with primarily myocardial disease, hypertensive, rheumatic, and congenital heart disease. It can also be caused by digoxin

This EKG shows a slow wide complex tachycardia with intermittent narrow complex beats. The 5 th and 10 th beats are sinus rhythm and close examination of these beats will give you a clue to the cause of the wide complex rhythm. In Leads II and III you can appreciate ST elevation indicating an acute current of injury due to a myocardial infarction. The wide complex beats therefore represent an Accelerated Idioventricular Rhythm or AIVR which is usually seen following reperfusion after an acute infarct.

Accelerated Idioventricular Rhythms are ectopic ventricular rhythms at rates between 40 bpm and 100 to 120 bpm. The ventricular origin of this rhythm can be demonstrated by the usual EKG criteria which include AV dissociation, fusion, and capture complexes. In this EKG the 4 th beat represents a fusion complex and the 5 th beath represents a capture beat proving that these beats are ventricular in origin. The incidence of Accelerated Idioventricular Rhythms following acute MI is reported to be between 8 and 36 percent. This rhythm can also be seen in patients with primarily myocardial disease, hypertensive, rheumatic, and congenital heart disease. It can also be caused by digoxin

Torsades de pointes

torsades de pointes This ECG is a classic example of torsades de pointes, which is French for &quot;twisting of the points.&quot; Torsades is a form of ventricular tachycardia that can most often be due to medications. The QRS complexes during this rhythm tend to show a series of &quot;points up&quot; followed by &quot;points down&quot; often with a narrow waist between. Recognition and reporting of this arrhythmia in association with terfenadine, astemizole (Hismanal), cisapride (Propulsid), grepafloxacin (Raxar), and mibefradil (Posicor) ultimately led to the removal of these medications from the market .

This ECG is a classic example of torsades de pointes, which is French for &quot;twisting of the points.&quot; Torsades is a form of ventricular tachycardia that can most often be due to medications. The QRS complexes during this rhythm tend to show a series of &quot;points up&quot; followed by &quot;points down&quot; often with a narrow waist between. Recognition and reporting of this arrhythmia in association with terfenadine, astemizole (Hismanal), cisapride (Propulsid), grepafloxacin (Raxar), and mibefradil (Posicor) ultimately led to the removal of these medications from the market .

Facies mitralis Facies mitralis is associated with prominent livid colour of the cheeks and acral cyanosis in the face (mitral stenosis)

Facies mitralis is associated with prominent livid colour of the cheeks and acral cyanosis in the face (mitral stenosis)

Malar fllush It is commonly seen in children with high fever, polycythaemia and severe mitral stenosis. Malar fllush with high fever is often seen in typhoid, pneumonia and pyelonephritis.

It is commonly seen in children with high fever, polycythaemia and severe mitral stenosis. Malar fllush with high fever is often seen in typhoid, pneumonia and pyelonephritis.

RV hypertrophy

Right ventricular hypertrophy (RVH) Note the qR pattern in the right precordial leads. This suggests right ventricular pressures greater than left ventricular pressures. The persistent S waves in lateral precordial leads and the right axis deviation are other findings in RVH.

Note the qR pattern in the right precordial leads. This suggests right ventricular pressures greater than left ventricular pressures. The persistent S waves in lateral precordial leads and the right axis deviation are other findings in RVH.

Right Ventricular Myocardial Infarction This EKG shows an Acute Inferior Myocardial Infarction which is often associated with a Right Ventricular Myocardial Infarction . If there is ST elevation in V1 and V2, the RV infarction should be considered.

This EKG shows an Acute Inferior Myocardial Infarction which is often associated with a Right Ventricular Myocardial Infarction . If there is ST elevation in V1 and V2, the RV infarction should be considered.

Acute right ventricular infarction Acute right ventricular infarction with acute inferior wall infarction. Note the ST elevation in the right precordial leads, as well as in leads II, III, and aVF, with reciprocal change in I and aVL. ST elevation in lead III, greater than in lead II, and right precordial ST elevation are consistent with proximal to middle occlusion of the right coronary artery. The combination of ST elevation in conventional lead V 1 (lead V 2 R here) and ST depression in lead V 2 (lead V 1 R here) has also been reported with acute right ventricular ischemia or infarction.

Acute right ventricular infarction with acute inferior wall infarction. Note the ST elevation in the right precordial leads, as well as in leads II, III, and aVF, with reciprocal change in I and aVL. ST elevation in lead III, greater than in lead II, and right precordial ST elevation are consistent with proximal to middle occlusion of the right coronary artery. The combination of ST elevation in conventional lead V 1 (lead V 2 R here) and ST depression in lead V 2 (lead V 1 R here) has also been reported with acute right ventricular ischemia or infarction.

Acute posterior myocardial infarction

Acute posterior myocardial infarction Acute posterior myocardial infarction (hyperacute) the mirror image of acute injury in leads V1 - 3 (fully evolved) tall R wave, tall upright T wave in leads V1 -3 usually associated with inferior and/or lateral wall MI

Acute posterior myocardial infarction

(hyperacute) the mirror image of acute injury in leads V1 - 3

(fully evolved) tall R wave, tall upright T wave in leads V1 -3

usually associated with inferior and/or lateral wall MI