A urachal diverticulum (also vesicourachal diverticulum) is a congenital disorder caused by the partial persistence of the allantois. The allantois, which later becomes the urachus, connects an embryos bladder to the yolk sac. Normally, the urachus closes off to become the median umbilical ligament; however, if it does not seal close to the bladder, a blind pouch connected to the bladder remains. This is usually asymptomatic but can lead to recurrent urinary tract infections. If the urachus is wholly patent, urine can drain from the bladder to an opening by the umbilicus, a condition known as urachal fistula. == References ==
Thrombotic microangiopathy (TMA) is a pathology that results in thrombosis in capillaries and arterioles, due to an endothelial injury. It may be seen in association with thrombocytopenia, anemia, purpura and kidney failure. The classic TMAs are hemolytic uremic syndrome and thrombotic thrombocytopenic purpura. Other conditions with TMA include atypical hemolytic uremic syndrome, disseminated intravascular coagulation, scleroderma renal crisis, malignant hypertension,
antiphospholipid antibody syndrome, and drug toxicities, e.g. calcineurin inhibitor toxicity. Signs and symptoms
The clinical presentation of TMA, although dependent on the type, typically includes: fever, microangiopathic hemolytic anemia (see schistocytes in a blood smear), kidney failure, thrombocytopenia and neurological manifestations. Generally, renal complications are particularly predominant with Shiga-toxin-associated hemolytic uremic syndrome (STx-HUS) and atypical HUS, whereas neurologic complications are more likely with TTP. Individuals with milder forms of TTP may have recurrent symptomatic episodes, including seizures and vision loss. With more threatening cases of TMA, and also as the condition progresses without treatment, multi-organ failure or injury is also possible, as the hyaline thrombi can spread to and affect the brain, kidneys, heart, liver, and other major organs. Cause
The specific cause is dependent of the type of TMA that is presented, but the two main pathways that lead to TMA are external triggers of vascular injury, such as viruses, bacterial Shiga toxins or endotoxins, antibodies, and drugs; and congenital predisposing conditions, including decreased levels of tissue factors necessary for the coagulation cascade.