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The focus is on integrated cases and differential diagnoses, along with practical clinical correlations. This book uses unique mnemonic sentences that explain the disease and offers a deeper "second level understanding" that includes cardinal feature and hallmarks of the condition. It also includes useful algorithms and procedures that make day-to-day things easier for medical professionals. These tools are an effective way to memorize the facts that people usually forget.

Skip to Main Content. Buy on Amazon. Eliminate test-day anxiety with over 2, exam-like questions in Step 1 Qbank. The inclusion criteria are microan- giopathic hemolytic anemia and thrombocytopenia, with or without renal failure or neurologic abnormalities. Pathology includes widespread formation of platelet thrombi with fibrin hyaline thrombi leading to intravascular hemolysis throm- botic microangiopathy.

Lab studies typically show decreased platelet count and prolonged bleeding time but normal prothrombin time and partial thromboplastin time. Peripheral blood smear shows thrombocytopenia, schistocytes, and reticulocytosis. Treatment is plasma exchange. Hemolytic uremic syndrome HUS is a form of thrombotic microangiopathy due to endothelial cell damage. It occurs mostly in children, typically after a gastroenteritis typically due to Shiga toxin-producing E.

Typical HUS presents with abdominal pain, diarrhea an atypical variant is diar- rhea-negative , microangiopathic hemolytic anemia, thrombocytopenia, and renal failure. Renal involvement is seen more commonly than in TTP. The kidney shows fibrin thrombi in the glomeruli. Renal glomerular endothelial cells are targeted by the bacterial toxin.

Glomerular scarring may ensue. Treatment is supportive fluid management, dialysis, erythrocyte transfusions ; plasma exchange is only used for atypical cases. The majority of the clotting factors are produced by the liver. Note The factors are proenzymes that must be converted to the active form.

Some con- versions occur on a phospholipid surface, and some conversions require calcium. A longer time means blood takes longer to clot. Clinically, hemophilia A predominately affects males. Symptoms vary depending on the degree of deficiency. Laboratory studies typically show normal platelet count and normal bleeding time, normal PT and prolonged PTT. Treatment is factor VIII concentrate. Hemophilia B Christmas disease is an X-linked recessive condition resulting from a deficiency of factor IX that is clinically identical to hemophilia A. Treatment is recombinant factor IX.

Note Von Willebrand disease is an autosomal dominant bleeding disorder characterized Von Willebrand disease is the most by a deficiency or qualitative defect in von Willebrand factor. Clinical features include spon- taneous bleeding from mucous membranes, prolonged bleeding from wounds, and menorrhagia in young females.

Hemarthrosis is uncommon. Lab studies show normal platelet count, a prolonged bleeding time, normal PT, and often prolonged PTT. Abnormal platelet response to ristocetin adhesion defect is an important diagnostic test. Treatment for mild classic cases type I is desmo- pressin an antidiuretic hormone analog , which releases vWF from Weibel-Palade bodies of endothelial cells.

Disseminated intravascular coagulation DIC is always secondary to another dis- order. Causes are diverse. Treat the underlying disorder. Massive tissue Endothelial Sepsis destruction injury Release of tissue factor Platelet Widespread aggregation microvascular thrombosis Activation of Microangiopathic Vascular plasmin Consumption of hemolytic anemia occlusion clotting factors and platelets Fibrinolysis Proteolysis of Ischemic tissue clotting factors damage Fibrin split products Bleeding Inhibition of thrombin, platelet aggregation, and fibrin polymerization Figure Outcomes of thrombosis include vascular occlusion and infarctions; embolism; thrombolysis; and organization and recanalization.

EMBOLISM An embolism is any intravascular mass that has been carried down the bloodstream from its site of origin, resulting in the occlusion of a vessel. Doppler ultrasound of the leg veins can be used to detect a DVT. Most cases are clinically silent and resolve. Symp- toms include shortness of breath, hemoptysis, pleuritic chest pain, and pleural effu- sion.

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On gross examination there is typically a hemorrhagic wedge-shaped infarct. The infarction heals by regeneration or scar formation. Common sites of infarction include heart, brain, lungs, intestines, kidneys. Infarcts have multiple causes. On gross examination infarctions typically have a wedge shape, with the apex of the wedge tending to point to the occlusion. Microscopic pathology of infarction can show either coagulative necrosis most organs or liquifactive necrosis brain.


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    • The cel- lular injury is initially reversible; if the hypoxia persists, the cellular injury becomes irreversible, leading to the death of cells and the patient. Stages of Shock The stages of shock are arbitrarily defined as follows. Compensation is characterized by increased sympathetic tone, release of catecholamines, and activation of the renin-angiotensin system.

    Causes include increased hydrostatic pressure, increased interstitial sodium, hypoalbuminemia and decreased colloid pressure, lymphatic obstruction, and increased endothelial permeability. Vascular wall injury triggers transient vasoconstriction, facilitation of platelet adhesion, and activation of both the extrinsic and intrinsic clotting pathways.

    Formation of a platelet thrombus occurs when platelets adhere to von Willebrand factor attached to subendothelial collagen, undergo shape change and degranulation, and then aggregate with additional platelets. Causes of qualitative platelet defects include von Willebrand disease, Bernard-Soulier syndrome, Glanzmann thrombasthenia, aspirin, and uremia.

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    In TTP, there is widespread formation of platelet thrombi with fibrin but without activation of the coagulation system. Hemolytic uremic syndrome can clinically resemble TTP and is triggered by E. The extrinsic coagulation pathway is activated by the release of tissue factor, and is tested with the prothrombin time PT , which also tests the common coagulation pathway. Clinically, hemophilia B closely resembles hemophilia A but is due to deficiency of factor IX.


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    Acquired coagulopathies can be due to vitamin K deficiency and liver disease. Von Willebrand is an inherited bleeding disorder characterized by a deficiency or qualitative defect in von Willebrand factor, which facilitates formation of platelet clots. Thrombi can lead to a spectrum of outcomes, including vascular occlusion and infarction, embolism, thrombolysis, and organization and recanalization. Embolism is used for any intravascular mass solid, liquid, or gas that has been carried downstream from its site of origin, resulting in occlusion of a vessel.

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    Most emboli are thromboemboli, but many other materials have also formed emboli. Pulmonary emboli are a common form of emboli that are often clinically silent but can cause infarction or sudden death. Most pulmonary emboli arise from deep vein thromboses. Systemic arterial emboli usually arise in the heart and may cause infarction in a variety of sites, depending upon where they lodge.

    Most infarcts result from thrombotic occlusion of an artery. Anemic infarcts occur in organs with a single blood supply, whereas hemorrhagic infarcts occur in organs with a dual blood supply or secondary to venous occlusion. After infarction, ischemia leads to coagulative necrosis, which leads to inflammation, which leads to granulation tissue, which leads to fibrous scar. Major forms of shock include cardiogenic shock, hypovolemic shock, septic shock, neurogenic shock, and anaphylactic shock. Down syndrome is the most com- Note mon of the chromosomal disorders.

    This results in an extremely Clinical findings can include intellectual disability; mongoloid facial features flat large chromosome and a tiny one, which face, low-bridged nose, and epicanthal folds ; Brushfield spots speckled appearance is typically lost. Endocardial cushion defect, if present, leads to the forma- tion of an atrioventricular canal a common connection between all 4 chambers of Note the heart. Prenatal tests include maternal serum tests, ultrasonography, amniocentesis, and chorionic villus sampling.