Another example is antiphospholipid syndrome, an autoimmune, hypercoagulable state. Causes other than coagulation
Bleeding diathesis may also be caused by impaired wound healing (as in scurvy), or by thinning of the skin, such as in Cushings syndrome. Genetic
Some people lack genes that typically produce the protein coagulation factors that allow normal clotting. Various types of hemophilia and von Willebrand disease are the major genetic disorders associated with coagulopathy. Rare examples are Bernard–Soulier syndrome, Wiskott–Aldrich syndrome and Glanzmanns thrombasthenia. Gene therapy treatments may be a solution as they involve in the insertion of normal genes to replace defective genes causing for the genetic disorder. Gene therapy is a source of active research that hold promise for the future. Diagnosis
Comparing coagulation tests
Treatments
Consult a hematologist and have a regular blood check ups. Have an early diagnostic test for any blood disorders or blood diseases including hemophilia, hemorrhage, and sickle-cell anemia. Prothrombin time and partial thromboplastin time blood tests are useful to investigate the reason behind the excessive bleeding. The PT evaluates coagulation factors I, II, V, VII and X, while the PTT evaluates coagulation factors I, II, V, VIII, IX, X, XI and XII. The analysis of both tests thus helps to diagnose certain disorders.Blood transfusion involves the transfer of plasma containing all the necessary coagulating factors (fibrinogen, prothrombin, thromboplastin) to help restore them and to improve the immune defense of the patient after excessive blood loss.
Sensenbrenner syndrome (OMIM #218330) is a rare (less than 20 cases reported by 2010) multisystem disease first described by Judith A. Sensenbrenner in 1975. It is inherited in an autosomal recessive fashion, and a number of genes appear to be responsible. Three genes responsible have been identified: intraflagellar transport (IFT)122 (WDR10), IFT43—a subunit of the IFT complex A machinery of primary cilia, and WDR35 (IFT121: TULP4)It is also known as Sensenbrenner–Dorst–Owens syndrome, Levin syndrome I and cranioectodermal dysplasia (CED)

Presentation
These are pleomorphic and include
dolichocephaly (with or without sagittal suture synostosis)
microcephaly
pre- and postnatal growth retardation
brachydactyly
narrow thorax
rhizomelic dwarfism
epicanthal folds
hypodontia and/or microdontia
sparse, slow-growing, hyperpigmented, fine hair
nail dysplasia
hypohydrosis
chronic kidney failure
heart defects
liver fibrosis
visual deficits
photophobia
hypoplasia of the posterior corpus callosum
aberrant calcium homeostasisElectroretinography shows gross abnormalities. Two fetuses of 19 and 23 weeks gestation have also been reported. They showed acromesomelic shortening, craniofacial characteristics with absence of craniosynostosis, small kidneys with tubular and glomerular microscopic cysts, persistent ductal plate with portal fibrosis in the liver, small adrenals, an enlarged cisterna magna and a posterior fossa cyst. Cause
The gene IFT122 is located on the long arm of chromosome 3 (3q21-3q24). The gene lies on the Watson (plus) strand and is 80,047 bases in length. The encoded protein has 1241 amino acids and a predicted weight of 141.825 kiloDaltons (kDa). It is a member of the WD repeat protein family.WDR35 is also a member of the WD repeat protein family.