However, whether these microbes exist or are clinically important is highly controversial and is the subject of active research. Functions
Nutrition and gas exchange
The placenta intermediates the transfer of nutrients between mother and fetus. The perfusion of the intervillous spaces of the placenta with maternal blood allows the transfer of nutrients and oxygen from the mother to the fetus and the transfer of waste products and carbon dioxide back from the fetus to the maternal blood. Nutrient transfer to the fetus can occur via both active and passive transport. Placental nutrient metabolism was found to play a key role in limiting the transfer of some nutrients. Adverse pregnancy situations, such as those involving maternal diabetes or obesity, can increase or decrease levels of nutrient transporters in the placenta potentially resulting in overgrowth or restricted growth of the fetus. Excretion
Waste products excreted from the fetus such as urea, uric acid, and creatinine are transferred to the maternal blood by diffusion across the placenta. Immunity
The placenta functions as a selective barrier between maternal and fetal cells, preventing maternal blood, proteins and microbes (including bacteria and most viruses) from crossing the maternal-fetal barrier. Deterioration in placental functioning, referred to as placental insufficiency, may be related to mother-to-child transmission of some infectious diseases. A very small number of viruses including rubella virus, Zika virus and cytomegalovirus (CMV) can travel across the placental barrier, generally taking advantage of conditions at certain gestational periods as the placenta develops.
Dressler syndrome is a secondary form of pericarditis that occurs in the setting of injury to the heart or the pericardium (the outer lining of the heart). It consists of fever, pleuritic pain, pericarditis and/or a pericardial effusion. Dressler syndrome is also known as postmyocardial infarction syndrome and the term is sometimes used to refer to post-pericardiotomy pericarditis. It was first characterized by William Dressler at Maimonides Medical Center in 1956.It should not be confused with the Dresslers syndrome of haemoglobinuria named for Lucas Dressler, who characterized it in 1854. Presentation
Dressler syndrome was historically a phenomenon complicating about 7% of myocardial infarctions, but in the era of percutaneous coronary intervention, it is very uncommon. The disease consists of a persistent low-grade fever, chest pain (usually pleuritic), pericarditis (usually evidenced by a pericardial friction rub, chest pain worsening when recumbent, and diffuse ST elevation with PR segment depression), and/or a pericardial effusion. The symptoms tend to occur 2–3 weeks after myocardial infarction but can also be delayed a few months. It tends to subside in a few days, and very rarely leads to pericardial tamponade. Elevated ESR is an objective but nonspecific laboratory finding. Causes
It is believed to result from an autoimmune inflammatory reaction to myocardial neo-antigens formed as a result of the MI. A similar pericarditis can be associated with any pericardiotomy or trauma to the pericardium or heart surgery which is called postcardiotomy syndrome.