These muscles can also classified by innervation, muscles supplied by the anterior subdivision of the plexus and those supplied by the posterior subdivision. The leg muscles acting on the foot are called the extrinsic foot muscles whilst the foot muscles located in the foot are called intrinsic.Dorsiflexion (extension) and plantar flexion occur around the transverse axis running through the ankle joint from the tip of the medial malleolus to the tip of the lateral malleolus. Pronation (eversion) and supination (inversion) occur along the oblique axis of the ankle joint. Extrinsic
Three of the anterior muscles are extensors. From its origin on the lateral surface of the tibia and the interosseus membrane, the three-sided belly of the tibialis anterior extends down below the superior and inferior extensor retinacula to its insertion on the plantar side of the medial cuneiform bone and the first metatarsal bone. In the non-weight-bearing leg, the anterior tibialis dorsal flexes the foot and lifts the medial edge of the foot. In the weight-bearing leg, it pulls the leg towards the foot. The extensor digitorum longus has a wide origin stretching from the lateral condyle of the tibia down along the anterior side of the fibula, and the interosseus membrane. At the ankle, the tendon divides into four that stretch across the foot to the dorsal aponeuroses of the last phalanges of the four lateral toes. In the non-weight-bearing leg, the muscle extends the digits and dorsiflexes the foot, and in the weight-bearing leg acts similar to the tibialis anterior.
Either of these pathways will result in decreased endothelial thromboresistance, leukocyte adhesion to damaged endothelium, complement consumption, enhanced vascular shear stress, and abnormal vWF fragmentation. The central and primary event in this progression is injury to the endothelial cells, which reduces the production of prostaglandin and prostacyclin, ultimately resulting in the loss of physiological thromboresistance, or high thrombus formation rate in blood vessels. Leukocyte adhesion to the damaged endothelial wall and abnormal von Willebrand factor (or vWF) release can also contribute to the increase in thrombus formation. More recently, researchers have attributed both TTP and HUS to targeted agents, such as targeted cancer therapies, immunotoxins, and anti-VEGF therapy.Bacterial toxins are the primary cause of one category of thrombotic microangiopathy known as HUS or hemolytic uremic syndrome. HUS can be divided into two main categories: Shiga-toxin-associated HUS (STx-HUS), which normally presents with diarrhea, and atypical HUS. The Shiga-toxin inhibits the binding of eEF-1-dependent binding of aminoacyl tRNA to the 60S subunit of the ribosome, thus inhibiting protein synthesis. The cytotoxicity from the lack of protein damages glomerular endothelial cells by creating voids in the endothelial wall and detaching the basement membrane of the endothelial layer, activating the coagulation cascade. Atypical HUS may be caused by an infection or diarrheal illness or it may be genetically transmitted. This category of TMA encompasses all forms that do not have obvious etiologies. Mutations in three of the proteins in the complement cascade have been identified in patients with atypical HUS.