This increases vascular resistance in fetoplacental vascular bed eventually leading to reduction in metabolically active mass of placenta like a vicious cycle. Fetal effects
Placental insufficiency can affect the fetus, causing fetal distress. Placental insufficiency may cause oligohydramnios, preeclampsia, miscarriage or stillbirth. Placental insufficiency is most frequent cause of asymmetric IUGR. Fetal metabolic changes
Metabolic changes occurring in uteroplacental insufficiency:

Fetal hormonal changes
Decrease in overall thyroid function is correlated with fetal hypoxemia. Serum glucagon, adrenaline, noradrenaline levels increase, eventually causing peripheral glycogenolysis and mobilization of fetal hepatic glycogen stores. Fetal hematologic changes
Fetal hypoxemia triggers erythropoietin release. This stimulates RBC production from medullary and extramedullary sites and eventually results in polycythemia. Oxygen carrying capacity of blood is thus increased. Prolonged tissue hypoxemia may cause early release of erythrocytes from maturation sites and thus count of nucleated RBCs in blood increases. These factors, increase in blood viscosity, decrease in cell membrane fluidity and platelet aggregation are important precursors in accelerating placental vascular occlusion. Fetal immunological changes
There is decrease in immunoglobulin, absolute B-cell counts  and total WBC count. T-helper and cytotoxic T-cells are suppressed in proportion of degree of acidemia. These conditions lead to higher infection susceptibility of infant after delivery. Fetal cardiovascular changes
There is decrease in magnitude of umbilical venous volume flow. In response to this, the proportion of umbilical venous blood diverted to fetal heart increases. This eventually leads to elevation of pulmonary vascular resistance and increased right ventricular afterload. This fetal cerebral redistribution
of blood flow is an early response to placental insufficiency.
Friedreichs ataxia (FRDA or FA) is an autosomal-recessive genetic disease that causes difficulty walking, a loss of sensation in the arms and legs, and impaired speech that worsens over time. Symptoms generally start between 5 and 20 years of age. Many develop hypertrophic cardiomyopathy and require a mobility aid such as a cane, walker, or wheelchair in their teens. As the disease progresses, some affected people lose their sight and hearing. Other complications may include scoliosis and diabetes mellitus. The condition is caused by mutations in the FXN gene on chromosome 9, which makes a protein called frataxin. In FRDA, cells produce less frataxin. Degeneration of nerve tissue in the spinal cord causes the ataxia; particularly affected are the sensory neurons essential for directing muscle movement of the arms and legs through connections with the cerebellum. The spinal cord becomes thinner, and nerve cells lose some myelin sheath. No effective treatment is known, but several therapies are in trials. FRDA shortens life expectancy due to heart disease, but some people can live into their 60s or older. FRDA affects one in 50,000 people in the United States and is the most common inherited ataxia. Rates are highest in people of Western European descent. The condition is named after German physician Nikolaus Friedreich, who first described it in the 1860s. Symptoms
Symptoms typically start between the ages of 5 and 15, but in late-onset FRDA, they may occur after age 25 years.