USMLE STEP 1 NOTES PDF

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USMLE Platinum Notes Step 1 and USMLE Platinum Notes Step 2 CK are the latest editions of these preparatory guides for the United States Medical Licensing Examination. The first book, Step 1, is divided into seven chapters incorporating revision materials for anatomy, physiology. With the second edition of First Aid Q&A for the USMLE Step 1, we continue. Page 1 USMLE Step 2 CK Lecture Notes Psychiatry and Epidemiology & Ethics. USMLE Step1 Uworld Notes pdf webtiekittcenve.cf


Usmle Step 1 Notes Pdf

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This books (USMLE Step 1 Lecture Notes 7-Book Set (USMLE Prep) [PDF] ) Made by Kaplan Medical About Books none To Download. USMLE Step 1 Lecture Notes Anatomy by Kaplan Medical - Kaplan Medical's USMLE Step 1 Lecture Notes Anatomy offers in-depth review with a. USMLE Step 1 Lecture notes 7-book set (Kaplan test prep 1st edition pdf) is an essential book if you are preparing for the United States Medical Licencing.

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About The Author. Kaplan Medical. Product Details. Kaplan Publishing December Length: Resources and Downloads. Anatomy eBook Get a FREE e-book by joining our mailing list today! More books from this author: See more by Kaplan Medical. Mela- nomas on males have increased frequency on the upper back; females have increased frequency on the back and legs.

Several types of melanomas occur: Note the size, irregular borders, and variegated color. Melanoma The prognosis of melanomas is determined by TNM staging; T status is based on the depth of invasion Breslow thickness measured histologically in millimeters.

Local disease is treated with wide surgical excision and sometimes sentinel node biopsy. Systemic disease is treated with chemotherapy or immunotherapy. Metas- tases may occur after years of dormancy. On rare occasions it is associated with internal malignancy stomach and other gastrointes- tinal malignancies. Seborrheic keratoses are benign squamoproliferative neoplasms that are very com- mon in middle-aged and elderly individuals; they may occur on the trunk, head, neck, and the extremities.

They are usually left untreated, but may be removed if they become irritated or for cosmetic purposes. The most common form is psoriasis vulgaris. Common sites of involvement include the knees, elbows, and scalp; the classic skin lesion is a well- demarcated erythematous plaque with a silvery scale.

Removal of scale results in pinpoint bleeding Auspitz sign. Nail beds show pitting and discoloration. Psoriasis may be associated with arthritis, enteropathy, and myopathy. Pemphigus vulgaris is the most common form. The pathogenesis involves the production of autoantibodies directed against a part of the keratinocyte desmosome called desmoglein 3, with resulting loss of intercellu- lar adhesion acantholysis and blister formation.

Pemphigus causes mucosal lesions and easily ruptured, flaccid blisters. Oral involvement is common. Immunofluorescence shows a net-like pattern of IgG staining between the epidermal keratinocytes that create bullae.

Bullous pemphigoid is a relatively common autoimmune disorder of older individu- als characterized by subepidermal blister formation with tense bullae that do not rupture easily. Immunofluorescence shows linear deposits of IgG at the dermal- epidermal junction. Dermatitis herpetiformis is a rare immune disorder that is often associated with celiac sprue; it is characterized by subepidermal blister formation with itchy, grouped vesicles and occasional bullae on the extensor surfaces.

Production of IgA antibodies directed against gliadin and other antigens deposit in the tips of the dermal papillae and result in subepidermal blister formation. Routine microscopy shows microabscesses at the tips of the dermal papillae that can lead to eventual subepidermal separation results in blister formation; immunofluorescence shows granular IgA deposits at the tips of the dermal papillae.

Dermatitis herpetiformis often responds to a gluten-free diet. Porphyria cutanea tarda is an acquired and familial disorder of heme synthesis. Patients experience upper extremity blistering secondary to sun exposure and minor trauma. Microscopically, there are subepidermal blisters with minimal inflamma- tion. Dermal vessels are thickened.

Direct immunofluorescence shows deposition of immunoglobulins and complement at the epidermal basement membrane and around dermal vessels. Intraepidermal and Subepidermal Blisters Ichthyosis vulgaris is a common inherited autosomal dominant skin disorder characterized by a thickened stratum corneum with absent stratum granulosum.

Onset is in childhood. Patients have hyperkeratotic, dry skin on the trunk and extensor surfaces of limb areas. Xerosis is a common cause of pruritus and dry skin in the elderly that is due to decreased skin lipids. Cancer patients receiving epidermal growth factor receptor inhibitor are susceptible.

Treatment is with emollients. Eczema is a group of related inflammatory skin diseases characterized by pruritus and epidermal spongiosis edema. Defects in the keratinocyte barrier are due to mutations in the filaggrin gene FLG. There is dermal edema and inflammation. Verrucae warts are caused by human papillomavirus.

Verruca vulgaris is the most common type. Cutaneous lupus erythematosus may be acute facial butterfly rash , subacute pho- tosensitive rash on anterior chest, upper back and upper extremities , or chronic dis- coid plaques, usually above the neck.

Direct immunofluorescence shows deposition of immunoglobulin and complement at the dermal-epidermal junction. Serologies for autoantibodies and clinical correlation help establish the diagnosis. The most severe form is Stevens-Johnson syndrome, which has extensive involvement of skin and mucous membranes.

It is clinically diagnosed, self-limiting and possibly a viral exanthem.

Granuloma annulare is a chronic inflammatory disorder that causes papules and plaques. Palisaded granulomas are present microscopically. The pathogenesis is immunologic, but most cases occur in healthy patients. Erythema nodosum causes raised, erythematous, painful nodules of subcutaneous adipose tissue, typically on the anterior shins, which can be associated with granu- lomatous diseases and streptococcal infection.

Epidermoid cyst is a common benign skin cyst lined with stratified squamous epi- thelium and filled with keratin debris. Risk factors include chronic sun exposure ultraviolet UVB ; fair complexion; chronic skin ulcers or sinus tracts; long-term exposure to hydrocarbons, arsenic, burns, and radiation; immunosuppression; and xeroderma pigmentosum.

Microscopic examina- tion shows nests of atypical keratinocytes that invade the dermis, oftentimes formation of keratin pearls, and intercellular bridges desmosomes between tumor cells. Squamous cell carcinoma of the skin rarely metastasizes and complete excision is usually curative. Risk factors include chronic sun exposure, fair complexion, immunosuppression, and xeroderma pigmentosum.

BCC occurs on sun-exposed, hair-bearing areas face , and may form pearly pap- ules; nodules with heaped-up, translucent borders, telangiectasia, or ulcers rodent ulcer.

Microscopically, BCCs show invasive nests of basaloid cells with a palisading growth pattern. Muta- tions affecting the Hedgehog pathway are seen in sporadic and familial cases. In general melanomas cause asymmetric, irregular, large- diameter macules, papules, or nodules with variegated color, found most often on the upper back of men and the back and legs of women. Abnormal shape is called poikilocytosis poikilo means various.

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Elliptocytes may be seen in hereditary elliptocytosis. Spherocytes result from decreased erythrocyte membrane, and they may be seen in hereditary spherocytosis and in autoimmune hemolytic anemia. Target cells result from increased erythrocyte membrane, and they may be seen in hemoglobinopathies, thalassemia, and liver disease. Acanthocytes have irregular spicules on their surfaces; numerous acanthocytes can be seen in abetalipoprotein- emia.

Echinocytes burr cells have smooth undulations on their surface; they may be seen in uremia or more commonly as an artifact. Schistocytes are erythrocyte fragments helmet cells are a type of schistocyte ; they can be seen in microangiopathic hemolytic anemias or traumatic hemolysis. Teardrop cells dacrocytes may be seen in thalassemia and myelofibrosis.

Sickle cells drepanocytes are seen in sickle cell anemia. Rouleaux are characteristic of multiple myeloma. Red Cell Inclusions Basophilic stippling results from cytoplasmic remnants of RNA; it may indicate reticulocytosis or lead poisoning. Howell-Jolly bodies are remnants of nuclear chro- matin that may occur in severe anemias or patients without spleens. Pappenheimer bodies are composed of iron, and they may be found in the peripheral blood follow- ing splenectomy.

Ring sideroblasts have iron trapped abnormally in mitochondria, forming a ring around nucleus; they can be seen in sideroblastic anemia. Heinz bod- ies result from denatured hemoglobin; they can be seen with glucosephosphate dehydrogenase deficiency.

Signs Patients with anemia have normal of anemia include palpitations, dizziness, angina, pallor of skin and nails, weakness, SaO2 and PaO2, but they have reduced claudication, fatigue, and lethargy. Reticulocytes do not have a nucleus; note that any erythrocyte with a nucleus nRBC in peripheral blood is abnormal. Reticulocyte maturation to a mature erythrocyte takes about 1 day.

The reticulocyte count is the percentage of red immature cells present in peripheral blood normal 0.

The division by 2 is because shift cells take twice as long as reticulo- cytes to mature 2 days versus 1 day. Laboratory terms used with respect to the Classification of anemia can be based on color: Classification of anemia can also be based on size MCV. Anemias The pathogenesis of anemia varies with the underlying disease. Blood loss can cause anemia. Hemolytic anemias are also important, and include hereditary spherocyto- sis, glucosephosphate dehydrogenase deficiency, sickle cell disease, hemoglobin C disease, thalassemia, and paroxysmal nocturnal hemoglobinuria.

Immunohe- molytic anemias, which are hemolytic anemias with an immune component to the pathology, include autoimmune hemolytic anemia AIHA , cold AIHA, incompat- ible blood transfusions, and hemolytic disease of the newborn. Anemias of dimin- ished erythropoiesis include megaloblastic anemia B12 and folate deficiencies , iron deficiency anemia, anemia of chronic disease, aplastic anemia, myelophthisic anemia, and sideroblastic anemia.

Functionally available iron is normally found in hemoglobin, myoglobin, and enzymes catalase and cytochromes. Additionally, ferritin is the physiological storage form plasma ferritin is normally close to the total body Fe , and hemosiderin Prussian blue positive is iron precipitated in tissues in the form of degraded ferritin mixed with lysosomal debris.

Iron is transported in the blood stream by transferrin. Transferrin saturation is reported as a percentage; it represents the ratio of the serum iron to the total iron- binding capacity, multiplied by Dietary deficiency of iron is seen in elderly populations, children, and the poor.

Increased demand for iron is seen in children and pregnant women. Iron deficiency can also be due to chronic blood loss due to gynecologic menstrual bleeding or gastrointestinal causes in the United States, think carcinoma; in the rest of the world, think hookworm.

The sequence of events during iron deficiency is as follows: Laboratory studies show increased serum ferritin with decreased total iron binding capacity. Increased IL-6 increases plasma hepcidin, which is a negative regulator of iron uptake in the small intestine and of iron release from macrophages.

Thalassemia syndromes are quantitative, not qualitative, abnormalities of hemo- globin. It is hypothesized that the thalassemia genes have been selectively preserved in the human genome because the thalassemias provide a protective advantage to carriers exposed to diseases such as malaria.

Composition of hemoglobins: Individuals with the silent carrier state are completely asymptomatic and all lab tests are normal. Patients are normal at birth, and symp- toms develop at about 6 months as hemoglobin F levels decline. Severe hemo- lytic anemia results from decreased erythrocyte life span. This severe anemia causes multiple problems: Sideroblastic anemia is a disorder in which the body has adequate iron stores, but is unable to incorporate the iron into hemoglobin.

It is associated with ring sideroblasts accumulated iron in mitochondria of erythroblasts in bone marrow. Sideroblastic anemia may be either pyridoxine vitamin B6 responsive or pyridoxine unrespon- sive; the latter is a form of myelodysplastic syndrome refractory anemia with ring sideroblasts.

The peripheral blood may show a dimorphic erythrocyte population. Acute blood loss may cause shock or death. If the patient sur- vives, the resulting hemodilution caused by shift of water from the interstitium will lower the hematocrit.

There will be a marked reticulocytosis in 5—7 days. Chronic blood loss, such as from the gastrointestinal tract or from the gynecologic system, may result in iron deficiency anemia. Hemolytic anemias. The hemoglobin may be oxidized to methemoglobin, which causes methemoglo- binemia and methemoglobinuria.

Markedly decreased because they have been used up hemoglobin-binding proteins in the blood, such as haptoglobin and hemopexin, are characteristic. No splenomegaly is seen. EV hemolyis causes increased bilirubin and decreased haptoglobin, but not to the degree seen with intravascular hemolysis. In EV hemolysis, there is an absence of hemoglobinemia, hemoglobinuria, and methemoglobin formation.

This biochemical change then makes a criti- been replaced by valine. Homozygous SS genome causes clinical disease sickle cell anemia. There are several factors affecting formation of irreversibly sickled red blood cells.

Clinical features include increased erythrocyte destruction which causes a severe hemolytic anemia, accompanied by erythroid hyperplasia in the bone marrow and increased bilirubin leading to jaundice and gallstone pigment formation. Capillary thrombi result from sickle cells blocking small vessels and may cause vaso-occlusive painful crises; hand-foot syndrome swelling in children; and autosplenectomy, which is seen in older children and adults.

Howell-Jolly bodies will appear in periph- eral blood after autosplenectomy, and the lack of a functional spleen predisposes to increased incidence of infections encapsulated organisms , increased incidence of Salmonella osteomyelitis leg pain , leg ulcers, and risk of aplastic crisis especially with parvovirus B19 infection. Emergencies that may occur include priapism and acute chest syndrome.

For testing, hemoglobin electrophoresis is used to diagnose the disease, though Bridge to Biochemistry genetic testing can be performed on amniotic fluid for prenatal diagnosis. Newborn G6PD is the rate-limiting enzyme in the screening is now mandatory in the United States and is commonly performed via hexose-monophosphate shunt HMP. Hemoglobin C disease occurs when a single nucleotide change in a codon causes Glutathione protects RBCs by breaking lysine basic to replace normal glutamic acid acidic at the beta 6 position.

Hemo- down hydrogen peroxide. Glucosephosphate dehydrogenase deficiency G6PD is a genetic disorder affect- ing the hexose monophosphate shunt pathway. It results in decreased levels of the antioxidant glutathione GSH , leaving erythrocytes sensitive to injury by oxidant stresses leading to hemolysis.

In some variants, G6PD is not due to decreased synthe- sis but rather to defective protein folding, resulting in a protein having a decreased half-life. The condition has X-linked inheritance. The hemolysis is intermittent even if the offending drug is continued because only older erythrocytes have decreased levels of glucosephosphate dehy- drogenase. Spherocytes are not flexible and are removed in the spleen by macrophages i. This causes multiple problems, including splenomegaly with a mild to moderate hemolytic anemia, increased bilirubin and increased risk for jaundice and pigment gallstones secondary to chronic hemolysis, and increased risk for acute red-cell aplasia due to parvovirus B19 infection.

Treatment is splenectomy and folic acid. Use which tends to induce splenomegaly as the spleen responds to the perceived need the osmotic fragility test HS and direct for increased phagocytosis. Coombs test AIHA to tell them apart. The Coombs test is negative in hereditary The etiology varies; most cases are idiopathic, but some cases are related to auto- spherocytosis. The peripheral blood smear typically shows microspherocytes, and laboratory con- firmation can be obtained by demonstrating a positive direct Coombs test direct antiglobulin test [DAT].

Paroxysmal nocturnal hemoglobinuria PNH is a hemolytic anemia caused by an acquired somatic mutation of a gene PIGA that encodes an anchor for proteins CD55 and CD59 in the cell membrane, causing complement-mediated lysis in red cells, white cells, and platelets. The condition causes episodes paroxysms of hemolysis at night.

Clinical Correlate Acidosis in vivo occurs during sleep breathing slowly retains CO2 and exercise Increased levels of 2,3-bisphosphoglycerate lactic acidosis , and the acidosis in turn causes activation of complement. Venous thrombosis may ensue. Pyruvate kinase deficiency is the most common enzyme deficiency in the glycolytic pathway and involves the enzyme that normally converts phosphoenolpyruvate to pyruvate.

Deficiency leads to decreased ATP with resulting damage to the erythro- cyte membrane. Clinically, there is a hemolytic anemia with jaundice from birth. Hereditary elliptocytosis is a mild, hereditary, hemolytic anemia caused by a defect in spectrin. Aplastic anemia is the term used when marrow failure causes a pancytopenia of the blood.

Idiopathic causes for aplastic anemia are most commonly seen; when the etiology is known, the aplastic anemia may be due to medications alkylating agents, chloramphenicol , chemical agents benzene, insecticides , infection EBV, CMV, parvovirus, hepatitis , or whole body radiation therapeutic or nuclear exposure. The erythrocytes are the haptocorrin.

Autohemolysis of the affected megaloblasts in bone marrow ineffective erythropoiesis will cause increased bilirubin and increased lac- 3. Unlike folate deficiency, vitamin B12 deficiency can also cause the central nervous system effects of subacute combined degeneration of the spinal cord, char- acterized by demyelination of the posterior and lateral columns of the spinal cord; the posterior sensory tract damage causes loss of vibratory and position sense, while the lateral cord damage involves dorsal spinocerebellar tracts arm and leg dystaxia and corticospinal tracts spastic paralysis.

Treatment is intramuscular vitamin B12, which will cause increased reticulocytes in about 5 days. Megaloblastic anemia due to folate deficiency can be caused by multiple processes: Lab tests show low serum folate levels and increased serum homo- cysteine. Treatment is folate replacement. See discussion of myeloproliferative disorders in chapter Secondary polycythemia refers to increased red cell mass due to compromised abil- ity of blood to supply oxygen to tissues.

Causes include chronic obstructive pulmo- nary disease and cyanotic congenital heart disease. Erythropoietin levels can be appropriately high. Secondary polycythemia may also be caused by inappropriately high erythropoietin levels, with renal cell carcinoma excreting erythropoietin being the typical cause. Relative polycythemia refers to an increased red cell count secondary to decreased plasma volume typically due to dehydration.

Red cell mass, erythropoietin, and blood oxygen content are normal. Anemias can be classified based on size and red cell color. They can also be classified based on pathogenesis. Chronic cases may develop superimposed iron deficiency anemia.

Hemoglobin C disease is also related to a single nucleotide change in a globin gene but produces milder disease than sickle cell anemia.

Hereditary elliptocytosis causes mild anemia. Important causes include vitamin B12 deficiency and folate deficiency. Relative polycythemia is the term used for increased hematocrit in the absence of increased red cell mass and is usually due to decreased plasma volume as in dehydration.

There are many systems used to categorize them. The system below is based largely on the size of the vessels involved. Microscopically, there is vessel wall thickening and disease is often categorized with the variable inflammation from a mononuclear adventitial infiltrate to medial necrosis vasculitides, but the main lesion is with granulomas. The disease, which presents are not always involved. The vertebral and ophthalmic arteries and aorta are often with severe distal extremity pain and involved.

The typical presentation evolves from nonspecific symptoms headache ulceration, is seen most often in young to more severe symptoms blindness. Microscopically, there are inner media granu- male cigarette smokers. Pharmacologic lomas in classic cases. Treatment is steroids and anti-TNF therapy. Medium Vessel Vasculitides Kawasaki disease presents with mucocutaneous symptoms and cervical lymph node enlargement in children.

Involvement of the coronary arteries leads to cardiovascu- lar sequelae, which can be circumvented with immunoglobulin therapy. Microscopi- cally, there is transmural vascular inflammation.

It has an association with hepatitis B virus. The clinical course is one of episodic nonspecific symptoms low-grade fever. Pulmonary involve- ment is rare; renal artery involvement can be fatal. Immunosuppressive therapy can achieve remission in most cases. Granulomatosis with polyangiitis typically occurs in middle-aged men; it is charac- terized by granulomas of the lung and upper respiratory tract, glomerulonephritis, and a necrotizing granulomatous vasculitis.

Eosinophilic granulomatosis with polyangiitis is associated with asthma, extravas- cular granulomas respiratory tract , and a systemic vasculitis that features eosino- phils; eosinophil counts may be extremely high in peripheral blood. There may be increased IgG4 levels.

ANCA is present in cases with glomerulonephritis. The sequential phases are allergic, followed by eosinophilic and vasculitic. Cardiac involvement may be fatal. Steroids are therapeutic. Microscopic findings depend upon the organ biopsied: Purpuric leg lesions show a leukocytoclastic vasculitis; the glomerulo- nephritis tends not to show eosinophilic infiltrates; the extravascular pulmonary granulomas contain eosinophils.

Other small vessel vasculitides include variable vessel vasculitides, e. The pathogenesis may involve CNS and intravascular factors. Secondary Raynaud phenomenon is caused by arterial insufficiency secondary to an underlying disease such as scleroderma CREST.

It is asymp- that results in arterial wall thickening tomatic, but may be detected by x-ray. Particularly likely to be affected are the aorta and a number of important muscular arteries coronary, carotid, cerebral, renal, iliac, and popliteal arteries. Risk factors for atherosclerosis are as follows: They cause chronic ischemia. Vulnerable atheromatous plaques are at risk for rupture, thrombosis or embolization due to their composition thin fibrous cap, large lipid core, dense inflammation.

Clinical complications of atherosclerosis are protean; these complications include ischemic heart disease myocardial infarctions ; cerebrovascular accidents CVA ; atheroemboli transient ischemic attacks [TIAs] and renal infarcts ; aneurysm for- mation; peripheral vascular disease; and mesenteric artery occlusion.

African Ameri- cans tend to be more seriously affected than Caucasians, and the risk increases with age. Mild to moderate elevations in blood pressure cause end-organ damage by damag- ing arterioles with hyaline arteriolosclerosis.

Late manifestations of hypertension include concentric left ventricular hypertrophy; congestive heart failure; accelerated atherosclerosis; myocardial infarction; aneurysm formation, rupture, and dissection; intracerebral hemorrhage; and chronic renal failure. Funduscopic examination may demonstrate retinal hemorrhages, exudates, and papilledema. See chapter 15 for a discussion of renal pathology. Malignant hypertension is a medical emergency; if untreated, most patients will die within 2 years from renal failure, intracerebral hemorrhage, or chronic heart failure.

Complications include thrombus formation, thromboembolism, and compression of nearby structures. Rupture or dissection may cause sudden death. Location of Aneurysms Atherosclerotic aneurysms are due to weakening of the media secondary to ather- oma formation, and typically occur in the abdominal aorta below the renal arteries.

They are associated with hypertension. Syphilitic aneurysms involve the ascending aorta in tertiary syphilis late stage. Syphilitic luetic aortitis causes an obliterative endarteritis of the vasa vasorum, leading to ischemia and smooth-muscle atrophy of the aortic media. Syphilitic aneu- rysms may dilate the aortic valve ring, causing aortic insufficiency.

Aortic dissecting aneurysm occurs when blood from the vessel lumen enters an inti- mal tear and dissects through the layers of the media. The etiology usually involves degeneration cystic medial degeneration of the tunica media. Aortic dissecting aneurysm presents with severe tearing pain. The dissecting aneurysm may compress and obstruct the aortic branches e. Hypertension and Marfan syndrome are predisposing factors. Microaneurysms are small aneurysms commonly seen in hypertension and diabetes.

Mycotic aneurysms are aneurysms usually due to bacterial or fungal infections. Arteriovenous AV fistulas are a direct communication between a vein and an artery without an intervening capillary bed.

They may be congenital or acquired e. Potential complications include shunting of blood which may lead to high-output heart failure and risk of rupture and hemorrhage.

It is often asymptom- atic and is consequently a commonly missed diagnosis. When symptomatic, it can produce unilateral leg swelling with warmth, erythema, and positive Homan sign increased resistance to passive dorsiflexion of the ankle by the examiner.

The major complication is pulmonary embolus. Varicose veins are dilated, tortuous veins caused by increased intraluminal pressure. A variety of veins can be affected.

Venous insufficiency is more common in women than men, and the incidence increases with age. Lower extremities demonstrate edema, hyperpigmentation and ulceration due to venous hypertension and incompetent valves. Vascular ectasias: They are the most Port wine stains are large, flat, vascular common tumor in infants appearing on the skin, mucous membranes, or internal malformations that are closely related to organs.

The major types are capillary and cavernous hemangiomas. Hemangiomas hemangiomas and are often seen on the may spontaneously regress. Hemangioma Hemangioblastomas are associated with von Hippel-Lindau disease, which may cause multiple hemangioblastomas involving the cerebellum, brain stem, spinal cord, and retina, as well as renal cell carcinoma.

Glomus tumors glomangioma are benign, small, painful tumors of the glomus body that usually occur under fingernails. Kaposi sarcoma is a malignant tumor of endothelial cells associated with Kaposi-sar- coma—associated virus HHV8. The condition causes multiple red-purple patches, plaques, or nodules that may remain confined to the skin or may disseminate. Microscopically, there is a proliferation of spindle-shaped endothelial cells with slit-like vascular spaces and extravasated erythrocytes.

Common sites of involvement include skin, GI tract, lymph nodes, and lungs. This form of Kaposi sarcoma is responsive to chemotherapy and interferon-alpha, and only rarely causes death. Angiosarcoma hemangiosarcoma is a malignant vascular tumor with a high mor- tality that most commonly occurs in skin, breast, liver, and soft tissues.

Liver angio- sarcomas are associated with vinyl chloride, arsenic, and thorotrast. The symptoms vary with the organ involved.

Headache, facial pain, and visual disturbances occur. Untreated temporal arteritis may cause blindness. It may produce blindness or loss of pulse in the upper extremities. Clinical complications of atherosclerosis include ischemic heart disease, cerebrovascular accidents, atheroemboli, aneurysm formation, peripheral vascular disease, and mesenteric artery occlusion.

Hypertension is a common, initially silent disease that may eventually produce cardiac disease, accelerated atherosclerosis, aneurysm formation, and renal and CNS damage.

Malignant hypertension is defined as markedly elevated pressures e. Untreated patients often die within 2 years from renal failure, intracerebral hemorrhage, or chronic heart failure. Complications include thrombus formation, compression of adjacent structures, and rupture with risk of sudden death. Common sites include the superficial veins of the lower extremities, esophageal varices, and hemorrhoids.

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It is most often seen in middle- age men and postmenopausal women. Angina pectoris is due to transient cardiac ischemia without cell death resulting in substernal chest pain.

Chest pain is brought on by increased cardiac demand exertional or emotional , and is relieved by rest or nitroglyc- erin vasodilation. Electrocardiogram shows ST segment depression suben- docardial ischemia. Electrocardiogram shows transient ST segment elevation transmural ischemia. This form of angina has a high risk for myocardial infarction. Myocardial infarction MI occurs when a localized area of cardiac muscle undergoes coagulative necrosis due to ischemia.

It is the most common cause of death in the United States. Other causes include decreased circulatory volume, decreased oxygenation, decreased oxygen-carrying capacity, or increased cardiac workload, due to systemic hypertension, for instance. Arterial Supply to the Heart Infarctions are classified as transmural, subendocardial, or microscopic.

It is associated with regional vascular occlusion by thrombus. It is associated with hypoperfu- sion due to shock. ECG changes are not noted. This type of infarction occurs in a setting of coronary artery disease with a decrease in oxygen delivery or an increase in demand. The microscopic and gross changes represent a spectrum that is preceded by biochemical changes going from aerobic metabolism to anaerobic metabolism within minutes.

The time intervals are variable and depend on the size of the infarct, as well as other factors. Cardiac rupture most commonly occurs 3—7 days after MI, and has effects that vary with the site of rupture: The mechanism is typically a fatal cardiac arrhythmia usually ventricular Auscultation of a friction rub is characteristic of pericarditis. Pericarditis fibrillation. It is characterized by left ventricular dilation due to accumulated ischemic antigens.

It is the final com- often quantified in terms of the number mon pathway for many cardiac diseases and has an increasing incidence in the of pillows the patient needs in order to United States.

Complications include both forward failure decreased organ per- sleep comfortably e. The heart has increased heart weight and shows left ventricular hypertrophy and dilatation. The lungs are heavy and edematous.

Left heart failure presents with dyspnea, orthopnea, paroxysmal nocturnal dyspnea, rales, and S3 gallop. Complications include passive pulmonary congestion and edema, activation of the renin-angiotensin-aldosterone system leading to secondary hyperaldosteronism, and cardiogenic shock.

Right heart failure presents with JVD, hepatosplenomegaly, dependent intrinsic lung disease: It is common in congenital bicuspid aortic valves. It can lead to concen- tric left ventricular hypertrophy LVH and congestive heart failure with increased risk of sudden death. The calcifications are on the outflow side of the cusps.

Treat- ment is aortic valve replacement. The condi- tion affects individuals with Marfan syndrome. Patients are asymptomatic and a mid-systolic click can be heard on auscultation.

Complications include infectious endocarditis and septic emboli, rupture of chordae tendineae with resulting mitral insufficiency, and rarely sudden death. In genetically susceptible individuals, the infection results in production of antibodies that cross-react with cardiac antigens type II hypersensitivity reaction. Rheumatic fever affects children ages 5—15 years , and there is a decreasing incidence in the United States.

Symptoms occur 2—3 weeks after a pharyngeal infection; laboratory studies show elevated anti- streptolysin O ASO titers. The Jones criteria are illustrated below. Diagnosis of rheumatic fever requires 2 major OR 1 major and 2 minor criteria, plus a preceding group A strep infection. The myocardium can develop myocarditis, whose most distinctive Endocarditis involving the tricuspid valve feature is the Aschoff body, in which fibrinoid necrosis is surrounded by is highly suggestive of IV drug use or macrophages Anitschkow cells , lymphocytes, and plasma cells.

Fibrinous central line bacteremia. Endocarditis may be a prominent feature that typically involves mitral and aortic valves forming fibrin vegetations along the lines of closure and may also cause left atrial endocardial thickening MacCallum plaques.

Risk factors include rheumatic heart disease, mitral valve prolapse, bicuspid aortic valve, degenerative calcific aor- tic stenosis, congenital heart disease, artificial valves, indwelling catheters, dental procedures, immunosuppression, and intravenous drug use.

Acute endocarditis pro- duces large destructive vegetations fibrin, platelets, bacteria, and neutrophils. Diagnosis is by serial blood cultures. Complica- tions include septic emboli, valve damage resulting in insufficiency and congestive heart failure, myocardial abscess, and dehiscence of an artificial heart valve.

The major complications are embolism and secondary occult colorectal tumors. Colonoscopy should be performed in all patients with S. Clinically, the patient may be asymptomatic or may suffer from acute heart failure or even dilated cardiomyopathy. Coarctation of the aorta is a segmental narrowing of the aorta. It is usu- ally associated with a patent ductus arteriosus PDA , which supplies blood to aorta distal to the narrowing, and right ventricular hypertrophy secondary to the need for the right ventricle to supply the aorta through the patent ductus arteriosus.

It presents in infancy with congestive heart failure that is accom- panied by weak pulses and cyanosis in the lower extremities; the prognosis is poor without surgical correction. It can present in a child or an adult with hyper- tension in the upper extremities, and hypotension and weak pulses in the lower extremities. Some collateral circulation may be supplied via the internal mammary and intercostal arteries; the effects of this collateral circulation may be visible on chest x-ray with notching of the ribs due to bone remodeling as a consequence of increased blood flow through the intercostal arteries.

Complications can include congestive heart failure the heart is trying too hard , intracerebral hemorrhage the blood pressure in the carotid arteries is too high , and dissecting aortic aneurysm the blood pressure in the aortic route is too high. Clinical findings include cyanosis, shortness of breath, digital clubbing, and polycythemia.The histologic hallmark of GVHD is apoptosis. NBME 19 wrong answers. Microscopically, benign lentigos show linear melanocytic hyperplasia.

Kaplan Medical. USMLE Step 1 Lecture Notes 2018: 7-Book Set

Increased demand for iron is seen in children and pregnant women. Tissue repair involves 5 overlapping processes: Patients are normal at birth, and symp- toms develop at about 6 months as hemoglobin F levels decline. Electron microscopy shows distended lysosomes with whorled membranes; the diagnosis can also be established with enzyme assays and DNA probes. Functionally available iron is normally found in hemoglobin, myoglobin, and enzymes catalase and cytochromes. Laboratory studies show increased serum ferritin with decreased total iron binding capacity.

GLORIA from Greensboro
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