The various types of vWD present with varying degrees of bleeding tendency, usually in the form of easy bruising, nosebleeds, and bleeding gums. Women may experience heavy menstrual periods and blood loss during childbirth.

Severe internal bleeding and bleeding into joints are uncommon in all but the most severe type, vWD type 3.

Type 2 vWD (15-30% of cases) is a qualitative defect and the bleeding tendency can vary between individuals. Four subtypes exist: 2A, 2B, 2M, and 2N. These subtypes depend on the presence and behavior of the underlying multimers.

In terms of the symptoms of Hemophilia A there are internal or external bleeding episodes. Individuals with more severe haemophilia suffer more severe and more frequent bleeding, while others with mild haemophilia typically suffer more minor symptoms except after surgery or serious trauma. Moderate haemophiliacs have variable symptoms which manifest along a spectrum between severe and mild forms.

Prolonged bleeding from a venepuncture or heelprick is another common early sign of haemophilia, these signs may lead to blood tests which indicates haemophilia. In other people, especially those with moderate or mild haemophilia any trauma will lead to the first serious "bleed". Haemophilia leads to a severely increased risk of prolonged bleeding from common injuries, or in severe cases bleeding may be spontaneous and without obvious cause. Bleeding may occur anywhere in the body, superficial bleeding such as those caused by abrasions, or shallow lacerations may be prolonged and the scab may easily be broken up due to the lack of fibrin, which may cause re-bleeding. While superficial bleeding is troublesome, some of the more serious sites of bleeding are:

- Joints

- Muscles

- Digestive tract

- Brain

Muscle and joint haemorrhages - or haemarthrosis - are indicative of haemophilia, while digestive tract and cerebral haemorrhages are also germane to other coagulation disorders.Though typically not life-threatening, joint bleeding is one of the most serious symptoms of haemophilia. Repeated bleeds into a joint capsule can cause permanent joint damage and disfigurement resulting in chronic arthritis and disability. Joint damage is not a result of blood in the capsule but rather the healing process. When blood in the joint is broken down by enzymes in the body, the bone in that area is also degraded, this exerts a lot of pain upon the person afflicted with the disease.

The presentation of hemophilia B is consistent with easy bruising, urinary tract bleed and nosebleeds. Additionally, the affected individual may experience bleeding into their joints.

Individuals with congenital hypfibringenemia often lack any symptoms are detected by routine lab testing of fibrinogen or when tested for it because close relatives have symptomatic hypofibrinogenmeia. Indeed, studies indicate that, among family members with the identical congenital hypofibrinogenemia mutation, some never exhibit symptoms and those that are symptomatic develop symptoms only as adults.

Many cases of congenital dysfibrinogenemia are asymptomatic. Since manifestations of the disorder generally occur in early adulthood or middle-age, younger individuals with a gene mutation causing it may not have had time to develop symptoms while previously asymptomatic individuals of advanced age with such a mutation are unlikely to develop symptoms. Bleeding episodes in most cases of this disorder are mild and commonly involve easy bruising and menorrhagia. Less common manifestations of bleeding may be severe or even life-threatening; these include excessive bleeding after tooth extraction, surgery, vaginal birth, and miscarriage. Rarely, these individuals may suffer hemarthrosis or cerebral hemorrhage. In one study of 37 individuals >50 years old afflicted with this disorder, 19% had a history of thrombosis. Thrombotic complications occur in both arteries and veins and include transient ischemic attack, ischemic stroke, myocardial infarction, retinal artery thrombosis, peripheral artery thrombosis, and deep vein thrombosis. In one series of 33 individuals with a history of thrombosis due to congenital dysfibrinogenemia, five developed chronic pulmonary hypertension due to ongoing pulmonary embolism probably stemming form deep vein thrombosis. About 26% of individuals with the disorder suffer both bleeding and thrombosis complications.

Individuals with this disorder are usually less symptomatic than patients with other fibrinogen disorders because their fibrinogen levels are generally sufficient to prevent spontaneous bleeding. Those with particularly low blood fibrinogen levels (<0.5 gram/liter) may develop serious bleeding spontaneously and many with the disorder do so following trauma or surgery. Depending on their fibrinogen levels, women with the disorder may also bleed excessively during delivery and the postpartum period; in rare cases, they may have an increased risk of suffering miscarriages. Individuals with the disorder also suffer thrombotic events which may include blockage of large arteries in relatively young patients who have high levels of cardiovascular risk factors. The thrombi which form in these individuals are unstable, tend to embolize, and may therefore lead to thromboembolic events such as pulmonary embolism. Both bleeding and thrombotic events can occur at separate times or even concurrently in the same individual with the disorder.

In terms of the signs/symptoms of haemophilia C, unlike individuals with Haemophilia A and B, people affected by it are not ones to bleed spontaneously. In these cases, haemorrhages tend to happen after a major surgery or injury. However, people affected with haemophilia C might experience symptoms closely related to those of other forms of haemophilia such as the following:

Haemophilia A (or hemophilia A) is a genetic deficiency in clotting factor VIII, which causes increased bleeding and usually affects males. In the majority of cases it is inherited as an X-linked recessive trait, though there are cases which arise from spontaneous mutations.

Factor VIII medication may be used to treat and prevent bleeding in people with haemophilia A.

The dysfibrinogenemias consist of three types of fibrinogen disorders in which a critical blood clotting factor, fibrinogen, circulates at normal levels but is dysfunctional. Congenital dysfibrinogenemia is an inherited disorder in which one of the parental genes produces an abnormal fibrinogen. This fibrinogen interferes with normal blood clotting and/or lyses of blood clots. The condition therefore may cause pathological bleeding and/or thrombosis. Acquired dysfibrinogenemia is a non-hereditary disorder in which fibrinogen is dysfunctional due to the presence of liver disease, autoimmune disease, a plasma cell dyscrasias, or certain cancers. It is associated primarily with pathological bleeding. Hereditary fibrinogen Aα-Chain amyloidosis is a sub-category of congenital dysfibrinogenemia in which the dysfunctional fibrinogen does not cause bleeding or thrombosis but rather gradually accumulates in, and disrupts the function of, the kidney.

Congenital dysfibrinogenmia is the commonest of these three disorders. Some 100 different genetic mutations occurring in more than 400 families have been found to cause it. All of these mutations as well as those causing hereditary fibrinogen Aα-Chain amyloidosis exhibit partial penetrance, i.e. only some family members with one of these mutant genes develop dysfibrinogenemia-related symptoms. While both of these congenital disorders as well as acquired dysfibrinogenemia are considered very rare, it is estimated that ~0.8% of individuals with venous thrombosis have either a congenital or acquired dysfibrinogenemia. Hence, the dysfibrinogenemia disorders may be highly under-diagnosed conditions due to isolated thrombotic events that are not appreciated as reflecting an underlying fibrinogen disorder.

Congenital dysfibrinogenemia is distinguished from a similar inherited disorder, congenital hypodysfibrinogenemia. Both disorders involve the circulation of dysfunctional fibrinogen but in congenital hypodysfibrinogenemia plasma fibrinogen levels are low while in congenital dysfibrinogenemia they are normal. Furthermore, the two disorders involve different gene mutations and inheritance patterns as well as somewhat different symptoms.

Haemophilia C (also known as plasma thromboplastin antecedent (PTA) deficiency or Rosenthal syndrome) is a mild form of haemophilia affecting both sexes, due to factor XI deficiency. However, it predominantly occurs in Jewish people of Ashkenazi descent. It is the fourth most common coagulation disorder after von Willebrand's disease and haemophilia A and B. In the United States, it is thought to affect 1 in 100,000 of the adult population, making it 10% as common as haemophilia A.

Haemophilia B (or hemophilia B) is a blood clotting disorder caused by a mutation of the factor IX gene, leading to a deficiency of factor IX. It is the second-most common form of haemophilia, rarer than haemophilia A. Haemophilia B was first recognized as a different kind of haemophilia in 1952. It is sometimes called Christmas disease, named after Stephen Christmas, the first patient described with this disease. In addition, the first report of its identification was published in the Christmas edition of the "British Medical Journal".

While it is indicated that people with FXII deficiency are generally asymptomatic, studies in women with recurrent miscarriages suggest an association with FXII deficiency.

The condition is of importance in the differential diagnosis to other bleeding disorders, specifically the hemophilias: hemophilia A with a deficiency in factor VIII or antihemophilic globulin, hemophilia B with a deficiency in factor IX (Christmas disease), and hemophilia C with a deficiency in factor XI. Other rare forms of bleeding disorders are also in the differential diagnosis.

There is concern that individuals with FXII deficiency are more prone to thrombophilic disease, however, this is at variance with a long term study from Switzerland.

Factor XII deficiency (also Hageman factor deficiency) is a deficiency in the production of factor XII (FXII), a plasma glycoprotein and clotting factor that participates in the coagulation cascade and activates factor XI. FXII appears to be not essential for blood clotting, as individuals with this condition are usually asymptomatic and form blood clots in vivo. FXII deficiency tends to be identified during presurgical laboratory screening for bleeding disorders.

The condition can be inherited or acquired.

While there are several possible causes, they generally result in excessive bleeding and a lack of clotting.

In medicine (hematology), bleeding diathesis (h(a)emorrhagic diathesis) is an unusual susceptibility to bleed (hemorrhage) mostly due to hypocoagulability, in turn caused by a coagulopathy (a defect in the system of coagulation). Several types are distinguished, ranging from mild to lethal. Also, bleeding diathesis can be caused by thinning of the skin or impaired wound healing.

Coagulopathy may cause uncontrolled internal or external bleeding. Left untreated, uncontrolled bleeding may cause damage to joints, muscles, or internal organs and may be life-threatening. People should seek immediate medical care for serious symptoms, including heavy external bleeding, blood in the urine or stool, double vision, severe head or neck pain, repeated vomiting, difficulty walking, convulsions, or seizures. They should seek prompt medical care if they experience mild but unstoppable external bleeding or joint swelling and stiffness.

Coagulopathy (also called a bleeding disorder) is a condition in which the blood’s ability to coagulate (form clots) is impaired. This condition can cause a tendency toward prolonged or excessive bleeding (bleeding diathesis), which may occur spontaneously or following an injury or medical and dental procedures. Of note, coagulopathies are sometimes erroneously referred to as "clotting disorders"; a clotting disorder is a predisposition to clot formation (thrombus), also known as a hypercoagulable state or thrombophilia.

Telangiectasia (small vascular malformations) may occur in the skin and mucosal linings of the nose and gastrointestinal tract. The most common problem is nosebleeds (epistaxis), which happen frequently from childhood and affect about 90–95% of people with HHT. Lesions on the skin and in the mouth bleed less often but may be considered cosmetically displeasing; they affect about 80%. The skin lesions characteristically occur on the lips, the nose and the fingers, and on the skin of the face in sun-exposed areas. They appear suddenly, with the number increasing over time.

About 20% are affected by symptomatic digestive tract lesions, although a higher percentage have lesions that do not cause symptoms. These lesions may bleed intermittently, which is rarely significant enough to be noticed (in the form of bloody vomiting or black stool), but can eventually lead to depletion of iron in the body, resulting in iron-deficiency anemia.

Kasabach–Merritt syndrome (KMS), also known as Hemangioma with thrombocytopenia is a rare disease, usually of infants, in which a vascular tumor leads to decreased platelet counts and sometimes other bleeding problems, which can be life-threatening. It is also known as hemangioma thrombocytopenia syndrome. It is named after Haig Haigouni Kasabach and Katharine Krom Merritt, the two pediatricians who first described the condition in 1940.

Arteriovenous malformations (AVMs, larger vascular malformations) occur in larger organs, predominantly the lungs (50%), liver (30–70%) and the brain (cerebral AVMs, 10%), with a very small proportion (<1%) having AVMs in the spinal cord.

Vascular malformations in the lungs may cause a number of problems. The lungs normally "filter out" bacteria and blood clots from the bloodstream; AVMs bypass the capillary network of the lungs and allow these to migrate to the brain, where bacteria may cause a brain abscess and blood clots may lead to stroke. HHT is the most common cause of lung AVMs: out of all people found to have lung AVMs, 70–80% are due to HHT. Bleeding from lung AVMs is relatively unusual, but may cause hemoptysis (coughing up blood) or hemothorax (blood accumulating in the chest cavity). Large vascular malformations in the lung allow oxygen-depleted blood from the right ventricle to bypass the alveoli, meaning that this blood does not have an opportunity to absorb fresh oxygen. This may lead to breathlessness. Large AVMs may lead to platypnea, difficulty in breathing that is more marked when sitting up compared to lying down; this probably reflects changes in blood flow associated with positioning. Very large AVMs cause a marked inability to absorb oxygen, which may be noted by cyanosis (bluish discoloration of the lips and skin), clubbing of the fingernails (often encountered in chronically low oxygen levels), and a humming noise over the affected part of the lung detectable by stethoscope.

The symptoms produced by AVMs in the liver depend on the type of abnormal connection that they form between blood vessels. If the connection is between arteries and veins, a large amount of blood bypasses the body's organs, for which the heart compensates by increasing the cardiac output. Eventually congestive cardiac failure develops ("high-output cardiac failure"), with breathlessness and leg swelling among other problems. If the AVM creates a connection between the portal vein and the blood vessels of the liver, the result may be portal hypertension (increased portal vein pressure), in which collateral blood vessels form in the esophagus (esophageal varices), which may bleed violently; furthermore, the increased pressure may give rise to fluid accumulation in the abdominal cavity (ascites). If the flow in the AVM is in the other direction, portal venous blood flows directly into the veins rather than running through the liver; this may lead to hepatic encephalopathy (confusion due to portal waste products irritating the brain). Rarely, the bile ducts are deprived of blood, leading to severe cholangitis (inflammation of the bile ducts). Liver AVMs are detectable in over 70% of people with HHT, but only 10% experience problems as a result.

In the brain, AVMs occasionally exert pressure, leading to headaches. They may also increase the risk of seizures, as would any abnormal tissue in the brain. Finally, hemorrhage from an AVM may lead to intracerebral hemorrhage (bleeding into the brain), which causes any of the symptoms of stroke such as weakness in part of the body or difficulty speaking. If the bleeding occurs into the subarachnoid space (subarachnoid hemorrhage), there is usually a severe, sudden headache and decreased level of consciousness and often weakness in part of the body.

KMS is usually caused by a hemangioendothelioma or other vascular tumor, often present at birth. Although these tumors are relatively common, it is rare for them to cause KMS.

When these tumors are large or are growing rapidly, sometimes they can trap platelets, causing severe thrombocytopenia. The combination of vascular tumor and consumptive thrombocytopenia defines KMS. Tumors can be found in the trunk, upper and lower extremities, retroperitoneum, and in the cervical and facial areas.

This consumptive coagulopathy also uses up clotting factors, such as fibrinogen which may worsen bleeding. The coagulopathy can progress to disseminated intravascular coagulation and even death.

Hemolytic anemia secondary to microangiopathic destruction (physical damage) of the RBCs can be expressed as mild, moderate, or severe.

Hematomas can be subdivided by size. By definition, ecchymoses are 1 centimeter in size or larger, and are therefore larger than petechiae ( less than 2 millimeters in diameter) or purpura (2 millimeters to 1 centimeter in diameter). Ecchymoses also have a more diffuse border than other purpura.

People with visible marks generally feel fine (physically) and can act normally, but when it is mentioned, they may become withdrawn and self-conscious. Some children may have low self-esteem due to the condition.

CMTC is an uncommon, sporadic congenital vascular malformation characterized by a generalized or localized reticulated cutaneous vascular network.

Cutaneous lesions described in patients with CMTC include nevus flammeus, hemangioma, nevus anemicus, café-au-lait spots, melanocytic nevus, aplasia cutis and acral cyanosis.

It has a marbled bluish to deep-purple appearance. The dark skin lesions often show a palpable loss of dermal substance. The reticulated mottling frequently appears more prominent in a cold environment (physiologic cutis marmorata), but tends not to disappear with warming. Hence, the erythema may be worsened by cooling, physical activity, or crying.

CMTC frequently involves the extremities, with the lower extremities involved most commonly, followed by the upper extremities, and then the trunk and face. The lower extremities often show atrophy and seldom show hypertrophy resulting in limb circumference discrepancy.

When located on the trunk, the lesions of CMTC tend to show mosaic distribution in streaks with a sharp midline demarcation seen across the abdomen. The lesions are primarily localized, but can be segmental or generalized, often unilateral in appearance. Diffuse involvement of the skin is usually not observed.

Although its course is variable, the majority of lesions in mild cases fade by adolescence. Ulceration and secondary infection are complications in severe cases and can be fatal if present in the neonatal period.

The morphologic features of mild and moderate HDV include:

- Perivascular inflammatory cells,

- +/-Vascular thrombosis,

- Smooth muscle hypertrophy, and

- Endothelial hyperplasia.

Severe HDV is characterized by:

- Atherosis - foamy macrophages within vascular wall, and

- Fibrinoid necrosis of vessel wall (amorphous eosinophilic vessel wall).