Condition Lookup

Disseminated Intravascular Coagulation (DIC)

Specialty: Hematology

Category: Coagulation, Hemostasis, and Disorders

Symptoms:
bleeding from multiple sites (e.g., gums, nose, surgical sites); bruising; blood clots; shortness of breath; chest pain; confusion or altered mental status; petechiae or purpura (small red or purple spots); organ dysfunction

Root Cause:
Abnormal activation of the coagulation cascade leads to widespread clot formation and consumption of clotting factors, resulting in bleeding and thrombosis.

How it's Diagnosed: videos
Diagnosed through blood tests including elevated D-dimer, prolonged PT and aPTT, decreased platelet count, and low fibrinogen levels.

Treatment:
Addressing the underlying cause, supportive care, and replacement of clotting factors.

Medications:
Anticoagulants

Prevalence: How common the health condition is within a specific population.
Commonly seen in critically ill patients; exact prevalence depends on the underlying condition (e.g., sepsis, trauma).

Risk Factors: Factors or behaviors that increase the likelihood of developing the condition.
Sepsis, trauma, malignancy, obstetric complications, and severe infections.

Prognosis: The expected outcome or course of the condition over time.
Prognosis depends on the underlying cause; untreated DIC can lead to multi-organ failure and death.

Complications: Additional problems or conditions that may arise as a result of the original condition.
Organ failure, severe hemorrhage, and death.

Renal Vein Thrombosis

Specialty: Hematology

Category: Coagulation, Hemostasis, and Disorders

Symptoms:
flank pain; hematuria (blood in urine); proteinuria; enlarged kidney on imaging; nausea or vomiting; reduced urine output

Root Cause:
The formation of a blood clot in the renal vein, which obstructs blood outflow from the kidney, often associated with nephrotic syndrome, dehydration, or hypercoagulable states.

How it's Diagnosed: videos
Imaging studies such as Doppler ultrasound, CT angiography, or MR angiography, along with laboratory tests to assess renal function and coagulation status.

Treatment:
Anticoagulation therapy (e.g., LMWH or DOACs), treatment of underlying conditions like nephrotic syndrome, and, in severe cases, thrombectomy or thrombolysis.

Medications:
Anticoagulants such as LMWH, warfarin , or DOACs (e.g., rivaroxaban , apixaban ). These are classified as anticoagulants.

Prevalence: How common the health condition is within a specific population.
Rare, with higher incidence in individuals with nephrotic syndrome, severe dehydration, or hypercoagulable conditions.

Risk Factors: Factors or behaviors that increase the likelihood of developing the condition.
Nephrotic syndrome, dehydration, malignancy, trauma, oral contraceptive use, and inherited thrombophilias.

Prognosis: The expected outcome or course of the condition over time.
Favorable with timely diagnosis and treatment; chronic renal damage or loss of kidney function can occur in delayed or untreated cases.

Complications: Additional problems or conditions that may arise as a result of the original condition.
Kidney damage or failure, pulmonary embolism, chronic kidney disease, and recurrent thrombosis.

Acquired Hemophilia

Specialty: Hematology

Category: Coagulation, Hemostasis, and Disorders

Symptoms:
spontaneous bleeding; severe bruising; prolonged bleeding after injury or surgery; muscle or joint pain due to bleeding; internal organ bleeding; hematuria (blood in urine); gastrointestinal bleeding

Root Cause:
Autoimmune production of inhibitors (antibodies) against factor VIII, impairing normal blood clotting.

How it's Diagnosed: videos
Diagnosed through blood tests such as prolonged activated partial thromboplastin time (aPTT), mixing studies (to differentiate inhibitors from clotting factor deficiencies), and specific inhibitor assays to confirm factor VIII inhibitor presence.

Treatment:
Treatment involves controlling bleeding episodes, suppressing the immune system to reduce inhibitor levels, and replacing clotting factor VIII.

Medications:
Bypassing agents

Prevalence: How common the health condition is within a specific population.
Rare, with an incidence of 1.5 cases per million people annually; more common in the elderly or postpartum women.

Risk Factors: Factors or behaviors that increase the likelihood of developing the condition.
Autoimmune diseases, malignancies, postpartum state, certain medications, and no apparent cause (idiopathic).

Prognosis: The expected outcome or course of the condition over time.
Prognosis depends on timely diagnosis and treatment; bleeding episodes can be life-threatening, but remission is possible with appropriate therapy.

Complications: Additional problems or conditions that may arise as a result of the original condition.
Life-threatening hemorrhage, severe anemia, organ damage from bleeding, and complications from immunosuppressive therapy (e.g., infections).

Alpha2-Plasmin Inhibitor Deficiency

Specialty: Hematology

Category: Coagulation, Hemostasis, and Disorders

Symptoms:
excessive bleeding after injury or surgery; spontaneous bleeding; menorrhagia in women; hemorrhage into joints and muscles; easy bruising

Root Cause:
A deficiency in alpha2-plasmin inhibitor (a protein that regulates fibrinolysis), leading to uncontrolled breakdown of blood clots.

How it's Diagnosed: videos
Diagnosed through prolonged clot lysis time, low levels of alpha2-plasmin inhibitor in blood, and genetic testing.

Treatment:
Management includes antifibrinolytic agents to prevent excessive clot breakdown and supportive care during bleeding episodes.

Medications:
Antifibrinolytics

Prevalence: How common the health condition is within a specific population.
Extremely rare; exact prevalence is unknown, but it is a rare inherited disorder.

Risk Factors: Factors or behaviors that increase the likelihood of developing the condition.
Genetic mutations in the SERPINF2 gene (inherited in an autosomal recessive manner).

Prognosis: The expected outcome or course of the condition over time.
Lifelong management is required; patients can live a normal life with appropriate treatment, but severe bleeding episodes may be life-threatening.

Complications: Additional problems or conditions that may arise as a result of the original condition.
Life-threatening hemorrhages, chronic joint damage due to recurrent bleeding, and potential over-treatment leading to thrombosis.

Antithrombin Deficiency

Specialty: Hematology

Category: Coagulation, Hemostasis, and Disorders

Symptoms:
recurrent venous thromboembolism (vte); deep vein thrombosis (dvt); pulmonary embolism (pe); swelling and pain in affected limbs; rarely asymptomatic until an event occurs

Root Cause:
Low levels or reduced function of antithrombin, a natural anticoagulant, leading to increased risk of blood clots.

How it's Diagnosed: videos
Diagnosed through blood tests measuring antithrombin activity and antigen levels. Genetic testing may confirm hereditary cases.

Treatment:
Preventative anticoagulation therapy and antithrombin concentrates during high-risk situations like surgery or childbirth.

Medications:
Anticoagulants

Prevalence: How common the health condition is within a specific population.
Affects approximately 1 in 2,000–5,000 people; hereditary antithrombin deficiency is rare.

Risk Factors: Factors or behaviors that increase the likelihood of developing the condition.
Family history, surgery, prolonged immobility, pregnancy, oral contraceptives, and malignancies.

Prognosis: The expected outcome or course of the condition over time.
With anticoagulation therapy, most thrombotic events can be prevented or managed. Lifelong anticoagulation may be needed for some patients.

Complications: Additional problems or conditions that may arise as a result of the original condition.
Recurring thrombotic events, post-thrombotic syndrome, and bleeding complications from anticoagulant therapy.

Arsine Poisoning

Specialty: Hematology

Category: Coagulation, Hemostasis, and Disorders

Symptoms:
dark red urine (hemoglobinuria); jaundice; fatigue; shortness of breath; nausea and vomiting; abdominal pain; weakness

Root Cause:
Hemolysis (destruction of red blood cells) caused by exposure to arsine gas, a highly toxic compound.

How it's Diagnosed: videos
Diagnosed through history of exposure, symptoms, and laboratory findings of hemolysis (elevated lactate dehydrogenase, low haptoglobin, and hemoglobinuria).

Treatment:
Remove the patient from exposure, supportive care, and blood transfusions for severe hemolysis.

Medications:
Chelating agents

Prevalence: How common the health condition is within a specific population.
Extremely rare; typically occurs in industrial settings with accidental exposure to arsine gas.

Risk Factors: Factors or behaviors that increase the likelihood of developing the condition.
Working in industries handling arsenic compounds, such as semiconductor manufacturing or metallurgical processes.

Prognosis: The expected outcome or course of the condition over time.
Recovery is possible with prompt treatment, but severe cases may lead to kidney failure or death.

Complications: Additional problems or conditions that may arise as a result of the original condition.
Acute kidney injury, severe anemia, multi-organ failure, and death if untreated.

Dysfibrinogenemia

Specialty: Hematology

Category: Coagulation, Hemostasis, and Disorders

Symptoms:
mild to severe bleeding; recurrent miscarriages; excessive bruising; thrombosis in some cases; delayed wound healing

Root Cause:
Mutations in the fibrinogen gene leading to abnormal fibrinogen structure or function, impairing clot formation or promoting thrombosis.

How it's Diagnosed: videos
Diagnosed through abnormal clotting tests (prolonged PT, aPTT, and thrombin time), low functional fibrinogen, and genetic testing.

Treatment:
Management depends on symptoms, with replacement therapy for bleeding and anticoagulation for thrombosis.

Medications:
Fibrinogen concentrate

Prevalence: How common the health condition is within a specific population.
Very rare; typically hereditary with an autosomal dominant inheritance.

Risk Factors: Factors or behaviors that increase the likelihood of developing the condition.
Family history of dysfibrinogenemia or related mutations.

Prognosis: The expected outcome or course of the condition over time.
Highly variable; mild cases are asymptomatic, while severe cases may involve life-threatening bleeding or thrombosis.

Complications: Additional problems or conditions that may arise as a result of the original condition.
Life-threatening hemorrhage or recurrent thrombotic events.

Esophageal Hematoma

Specialty: Hematology

Category: Coagulation, Hemostasis, and Disorders

Symptoms:
chest pain; difficulty swallowing (dysphagia); vomiting blood (hematemesis); black or tarry stools (melena); upper abdominal pain

Root Cause:
Hemorrhage within the esophageal wall, often due to trauma, anticoagulation therapy, or underlying coagulopathy.

How it's Diagnosed: videos
Diagnosed via endoscopy, CT scan, or MRI revealing hematoma in the esophageal wall.

Treatment:
Supportive care, stopping anticoagulants, and occasionally endoscopic intervention or surgery.

Medications:
Reversal agents

Prevalence: How common the health condition is within a specific population.
Rare; occurs more often in patients on anticoagulation therapy or with trauma to the esophagus.

Risk Factors: Factors or behaviors that increase the likelihood of developing the condition.
Anticoagulant use, trauma, esophageal varices, or coagulopathies.

Prognosis: The expected outcome or course of the condition over time.
Generally favorable with prompt treatment; complications may arise if diagnosis or management is delayed.

Complications: Additional problems or conditions that may arise as a result of the original condition.
Severe bleeding, esophageal rupture, or mediastinitis.

Factor II Deficiency

Specialty: Hematology

Category: Coagulation, Hemostasis, and Disorders

Symptoms:
prolonged bleeding after injury or surgery; easy bruising; nosebleeds (epistaxis); gastrointestinal bleeding; menorrhagia in women; joint or muscle bleeding in severe cases

Root Cause:
Deficiency of prothrombin (factor II), a crucial protein in the coagulation cascade, leading to impaired blood clot formation.

How it's Diagnosed: videos
Diagnosed through prolonged PT and aPTT, low factor II activity on specific coagulation assays, and genetic testing for inherited forms.

Treatment:
Replacement therapy with prothrombin complex concentrates or fresh frozen plasma during bleeding episodes.

Medications:
Prothrombin complex concentrates (PCC)

Prevalence: How common the health condition is within a specific population.
Extremely rare; estimated at 1 in 2 million for inherited forms.

Risk Factors: Factors or behaviors that increase the likelihood of developing the condition.
Inherited mutations in the F2 gene or acquired vitamin K deficiency due to malabsorption, liver disease, or anticoagulants.

Prognosis: The expected outcome or course of the condition over time.
Generally good with appropriate treatment; severe cases may require lifelong management.

Complications: Additional problems or conditions that may arise as a result of the original condition.
Severe bleeding episodes, chronic joint damage from hemarthrosis, and complications from treatment (e.g., thromboembolism).

Factor V Deficiency

Specialty: Hematology

Category: Coagulation, Hemostasis, and Disorders

Symptoms:
nosebleeds (epistaxis); easy bruising; prolonged bleeding after injury or surgery; heavy menstrual bleeding; spontaneous bleeding in severe cases

Root Cause:
Deficiency of factor V, a protein essential for thrombin generation, causing impaired clot formation.

How it's Diagnosed: videos
Prolonged PT and aPTT, reduced factor V activity on specific assays, and normal fibrinogen levels.

Treatment:
Fresh frozen plasma or platelet transfusions during bleeding episodes.

Medications:
Fresh frozen plasma (FFP)

Prevalence: How common the health condition is within a specific population.
Rare; estimated at 1 in 1 million people.

Risk Factors: Factors or behaviors that increase the likelihood of developing the condition.
Inherited mutations in the F5 gene or acquired conditions like liver disease.

Prognosis: The expected outcome or course of the condition over time.
Good with appropriate management; spontaneous bleeding is rare in mild to moderate cases.

Complications: Additional problems or conditions that may arise as a result of the original condition.
Severe bleeding episodes, particularly in surgical or trauma settings.

Factor VII Deficiency

Specialty: Hematology

Category: Coagulation, Hemostasis, and Disorders

Symptoms:
prolonged bleeding after injury or surgery; nosebleeds (epistaxis); easy bruising; gastrointestinal bleeding; intracranial hemorrhage in severe cases

Root Cause:
Deficiency of factor VII, a protein essential for initiating blood coagulation via the extrinsic pathway.

How it's Diagnosed: videos
Prolonged PT, normal aPTT, and reduced factor VII activity on specific assays.

Treatment:
Replacement therapy with recombinant activated factor VII or fresh frozen plasma.

Medications:
Recombinant activated factor VII (rFVIIa)

Prevalence: How common the health condition is within a specific population.
Rare; estimated at 1 in 500,000 people.

Risk Factors: Factors or behaviors that increase the likelihood of developing the condition.
Inherited mutations in the F7 gene or acquired vitamin K deficiency.

Prognosis: The expected outcome or course of the condition over time.
Variable; severe cases require frequent replacement therapy, while mild cases may remain asymptomatic.

Complications: Additional problems or conditions that may arise as a result of the original condition.
Severe bleeding, intracranial hemorrhage, and thromboembolic events from treatment.

Factor X Deficiency

Specialty: Hematology

Category: Coagulation, Hemostasis, and Disorders

Symptoms:
easy bruising; nosebleeds (epistaxis); gastrointestinal bleeding; hemarthrosis (joint bleeding); prolonged bleeding after injury or surgery

Root Cause:
Deficiency of factor X, a protein essential for the activation of thrombin and clot stabilization.

How it's Diagnosed: videos
Prolonged PT and aPTT, reduced factor X activity on specific coagulation assays.

Treatment:
Replacement therapy with prothrombin complex concentrates or fresh frozen plasma during bleeding episodes.

Medications:
Prothrombin complex concentrates (PCC)

Prevalence: How common the health condition is within a specific population.
Rare; estimated at 1 in 1 million people.

Risk Factors: Factors or behaviors that increase the likelihood of developing the condition.
Inherited mutations in the F10 gene or acquired vitamin K deficiency due to malnutrition or liver disease.

Prognosis: The expected outcome or course of the condition over time.
Good with appropriate treatment; severe cases may require lifelong management.

Complications: Additional problems or conditions that may arise as a result of the original condition.
Severe bleeding episodes, particularly in surgical or trauma settings.

Factor XI Deficiency

Specialty: Hematology

Category: Coagulation, Hemostasis, and Disorders

Symptoms:
prolonged bleeding after injury or surgery; nosebleeds (epistaxis); easy bruising; menorrhagia in women; bleeding into joints or muscles (rare); spontaneous bleeding (rare)

Root Cause:
Reduced levels or function of factor XI, a clotting protein involved in the intrinsic pathway of coagulation.

How it's Diagnosed: videos
Diagnosed through prolonged aPTT, normal PT, and low factor XI activity levels. Genetic testing may confirm hereditary cases.

Treatment:
Antifibrinolytics for minor bleeding, factor XI replacement for severe cases, and careful perioperative planning.

Medications:
Antifibrinolytics

Prevalence: How common the health condition is within a specific population.
Common in Ashkenazi Jewish populations, affecting 1 in 450; globally, rare with variable prevalence.

Risk Factors: Factors or behaviors that increase the likelihood of developing the condition.
Inherited mutations in the F11 gene; typically autosomal recessive but can be heterozygous with milder symptoms.

Prognosis: The expected outcome or course of the condition over time.
Good with proper management; spontaneous bleeding is rare.

Complications: Additional problems or conditions that may arise as a result of the original condition.
Severe bleeding during surgery or trauma; thromboembolic risks with replacement therapy.

Factor XIII Deficiency

Specialty: Hematology

Category: Coagulation, Hemostasis, and Disorders

Symptoms:
prolonged bleeding after injury or surgery; umbilical stump bleeding in neonates; intracranial hemorrhage; spontaneous abortion in women; poor wound healing; soft tissue hematomas

Root Cause:
Deficiency of factor XIII, a protein responsible for cross-linking fibrin and stabilizing blood clots.

How it's Diagnosed: videos
Diagnosed through normal PT and aPTT but abnormal clot solubility test; factor XIII activity assay confirms the diagnosis.

Treatment:
Regular prophylactic replacement therapy with factor XIII concentrate and acute management during bleeding episodes.

Medications:
Factor XIII concentrate

Prevalence: How common the health condition is within a specific population.
Extremely rare, affecting 1 in 1–5 million people worldwide.

Risk Factors: Factors or behaviors that increase the likelihood of developing the condition.
Autosomal recessive inheritance with mutations in F13A1 or F13B genes.

Prognosis: The expected outcome or course of the condition over time.
Lifelong replacement therapy significantly improves outcomes; untreated cases risk life-threatening bleeding.

Complications: Additional problems or conditions that may arise as a result of the original condition.
Intracranial hemorrhage, recurrent pregnancy loss, and delayed wound healing.

Glanzmann Thrombasthenia

Specialty: Hematology

Category: Coagulation, Hemostasis, and Disorders

Symptoms:
prolonged bleeding after injury or surgery; easy bruising; spontaneous nosebleeds (epistaxis); menorrhagia (heavy menstrual bleeding) in females; gingival bleeding

Root Cause:
A rare genetic disorder caused by mutations in the genes coding for glycoprotein IIb/IIIa complex on platelets, leading to impaired platelet aggregation.

How it's Diagnosed: videos
Diagnosed using platelet function assays, flow cytometry to evaluate glycoprotein IIb/IIIa, genetic testing, and bleeding history.

Treatment:
Management focuses on controlling bleeding episodes and preventing complications. Platelet transfusions are the mainstay treatment during acute bleeding episodes or surgery. Recombinant factor VIIa is used in refractory cases. Hematopoietic stem cell transplantation (HSCT) is curative in severe cases.

Medications:
No daily medication is used for prevention. Recombinant factor VIIa (class

Prevalence: How common the health condition is within a specific population.
Extremely rare; estimated prevalence is 1 in 1 million individuals worldwide. It is more common in populations with higher rates of consanguinity.

Risk Factors: Factors or behaviors that increase the likelihood of developing the condition.
Genetic inheritance, with an autosomal recessive pattern; family history of the disorder.

Prognosis: The expected outcome or course of the condition over time.
The prognosis varies depending on the severity of bleeding episodes. With appropriate management, most individuals can lead normal lives, but severe cases may require advanced treatments like HSCT.

Complications: Additional problems or conditions that may arise as a result of the original condition.
Severe hemorrhages, particularly intracranial or gastrointestinal; anemia due to chronic bleeding; complications from frequent transfusions, such as alloimmunization or iron overload.

Hemolytic-Uremic Syndrome

Specialty: Hematology

Category: Coagulation, Hemostasis, and Disorders

Symptoms:
pale or yellowed skin (jaundice); fatigue; irritability; reduced urination; swelling (edema), particularly in the face, hands, or feet; diarrhea (often bloody); high blood pressure; confusion or seizures in severe cases

Root Cause:
HUS is characterized by the triad of hemolytic anemia, thrombocytopenia, and acute kidney injury, commonly triggered by shiga toxin-producing Escherichia coli (STEC) infections or other causes like complement dysregulation (atypical HUS).

How it's Diagnosed: videos
Diagnosis is based on laboratory findings including hemolytic anemia (schistocytes on blood smear), low platelet count, elevated creatinine, and stool culture or PCR to detect STEC. Complement studies are performed for atypical HUS.

Treatment:
Supportive care, including fluid management, electrolyte correction, and blood transfusions as needed. Dialysis may be required for acute kidney injury. For atypical HUS, eculizumab (a monoclonal antibody targeting complement C5) is used.

Medications:
In STEC-HUS, no specific medication targets the infection, but supportive care is critical. In atypical HUS, eculizumab (class

Prevalence: How common the health condition is within a specific population.
STEC-HUS is more common in children under 5 years, with approximately 1-2 cases per 100,000 annually in developed countries. Atypical HUS is extremely rare, with an estimated incidence of 2 cases per 1 million individuals annually.

Risk Factors: Factors or behaviors that increase the likelihood of developing the condition.
Exposure to contaminated food or water (for STEC-HUS), genetic predisposition (for atypical HUS), and certain infections or medications.

Prognosis: The expected outcome or course of the condition over time.
The prognosis for STEC-HUS in children is favorable with appropriate supportive care, though some may develop long-term kidney damage. Atypical HUS has a more variable prognosis, heavily reliant on timely treatment with eculizumab.

Complications: Additional problems or conditions that may arise as a result of the original condition.
Chronic kidney disease, hypertension, seizures, or neurological complications; in atypical HUS, recurrent episodes can lead to significant morbidity.

Hemophilia A (Factor VIII Deficiency)

Specialty: Hematology

Category: Coagulation, Hemostasis, and Disorders

Symptoms:
prolonged bleeding after injuries or surgeries; spontaneous bleeding into joints (hemarthrosis); muscle hematomas; easy bruising; nosebleeds (epistaxis); blood in urine (hematuria); intracranial hemorrhage in severe cases

Root Cause:
Caused by a deficiency or dysfunction of clotting factor VIII due to mutations in the F8 gene. This results in impaired clot formation and prolonged bleeding.

How it's Diagnosed: videos
Diagnosed through clotting studies (prolonged activated partial thromboplastin time), low factor VIII activity levels, and genetic testing to confirm mutations in the F8 gene.

Treatment:
Treatment involves replacing deficient factor VIII using recombinant factor VIII concentrates or plasma-derived factor VIII. Prophylactic treatment is used to prevent bleeding episodes in severe cases. Emerging gene therapy offers potential long-term solutions.

Medications:
Recombinant factor VIII (class

Prevalence: How common the health condition is within a specific population.
Affects approximately 1 in 5,000 male births worldwide. Females can be carriers, rarely exhibiting mild symptoms.

Risk Factors: Factors or behaviors that increase the likelihood of developing the condition.
Family history of hemophilia A, X-linked inheritance pattern.

Prognosis: The expected outcome or course of the condition over time.
With appropriate treatment, individuals can lead near-normal lives, though severe cases may require lifelong prophylactic therapy.

Complications: Additional problems or conditions that may arise as a result of the original condition.
Chronic joint damage from recurrent hemarthrosis (arthropathy), inhibitors against factor VIII complicating treatment, severe hemorrhages, or infections from blood product transfusions (historically).

Hemophilia B (Factor IX Deficiency)

Specialty: Hematology

Category: Coagulation, Hemostasis, and Disorders

Symptoms:
prolonged bleeding after injuries or surgeries; spontaneous joint bleeds (hemarthrosis); muscle hematomas; easy bruising; nosebleeds (epistaxis); blood in urine (hematuria); intracranial hemorrhage in severe cases

Root Cause:
Caused by a deficiency or dysfunction of clotting factor IX due to mutations in the F9 gene. This results in impaired clot formation and prolonged bleeding.

How it's Diagnosed: videos
Diagnosed through clotting studies (prolonged activated partial thromboplastin time), low factor IX activity levels, and genetic testing to confirm mutations in the F9 gene.

Treatment:
Treatment involves replacing deficient factor IX using recombinant factor IX concentrates or plasma-derived factor IX. Prophylaxis is used to prevent bleeding in severe cases. Gene therapy is an emerging long-term treatment option.

Medications:
Recombinant factor IX (class

Prevalence: How common the health condition is within a specific population.
Affects approximately 1 in 25,000 male births worldwide. Females can be carriers but rarely exhibit symptoms.

Risk Factors: Factors or behaviors that increase the likelihood of developing the condition.
Family history of hemophilia B, X-linked inheritance pattern.

Prognosis: The expected outcome or course of the condition over time.
With appropriate treatment, individuals can lead near-normal lives. Long-acting factor IX products have improved management for severe cases.

Complications: Additional problems or conditions that may arise as a result of the original condition.
Chronic joint damage from recurrent hemarthrosis (arthropathy), development of inhibitors against factor IX, severe hemorrhages, or infections from blood product transfusions (historically).

Heparin-Induced Thrombocytopenia

Specialty: Hematology

Category: Coagulation, Hemostasis, and Disorders

Symptoms:
sudden drop in platelet count after heparin exposure; new or worsening thrombosis (deep vein thrombosis or pulmonary embolism); skin necrosis at the heparin injection site; discoloration or pain in extremities; stroke symptoms in severe cases

Root Cause:
Caused by an immune-mediated reaction where antibodies form against platelet factor 4 (PF4)-heparin complexes, activating platelets and leading to thrombocytopenia and a hypercoagulable state.

How it's Diagnosed: videos
Suspected based on a significant drop in platelets (50% or more) 5–14 days after starting heparin. Confirmed by HIT antibody testing (e.g., ELISA for PF4-heparin antibodies) and functional assays like the serotonin release assay (SRA).

Treatment:
Immediate discontinuation of all heparin products. Transition to a non-heparin anticoagulant such as argatroban or bivalirudin until platelet count recovers. Warfarin is initiated later for long-term anticoagulation, if needed.

Medications:
Direct thrombin inhibitors like argatroban and bivalirudin (class

Prevalence: How common the health condition is within a specific population.
Occurs in approximately 0.1–5% of patients exposed to heparin, with higher rates in patients receiving unfractionated heparin compared to low-molecular-weight heparin.

Risk Factors: Factors or behaviors that increase the likelihood of developing the condition.
Use of unfractionated heparin, recent surgery (especially cardiac or orthopedic), prolonged heparin exposure, female sex, and older age.

Prognosis: The expected outcome or course of the condition over time.
With prompt diagnosis and treatment, most patients recover without long-term complications. Delayed diagnosis or untreated HIT can lead to life-threatening thrombosis or organ damage.

Complications: Additional problems or conditions that may arise as a result of the original condition.
Life-threatening venous or arterial thrombosis (e.g., pulmonary embolism, myocardial infarction, stroke), limb ischemia, organ infarction, and, in severe cases, death.

Hereditary and Acquired Hypercoagulability

Specialty: Hematology

Category: Coagulation, Hemostasis, and Disorders

Symptoms:
recurrent deep vein thrombosis (dvt); pulmonary embolism; unexplained stroke or transient ischemic attack; pregnancy complications (e.g., recurrent miscarriages); pain or swelling in limbs due to thrombosis; post-thrombotic syndrome

Root Cause:
Hypercoagulability can result from inherited genetic mutations (e.g., Factor V Leiden, prothrombin gene mutation, protein C or S deficiency) or acquired conditions (e.g., antiphospholipid syndrome, malignancy, prolonged immobility). These lead to an increased tendency to form abnormal blood clots.

How it's Diagnosed: videos
Blood tests for inherited thrombophilia (e.g., genetic testing for Factor V Leiden or prothrombin mutation, protein C/S/antithrombin levels) and acquired causes (e.g., antiphospholipid antibodies). Imaging studies (e.g., ultrasound, CT angiography) are used to detect clots.

Treatment:
Treatment focuses on preventing and managing thrombotic events. Anticoagulation with warfarin, direct oral anticoagulants (DOACs), or low-molecular-weight heparin (LMWH) is the mainstay. Duration of treatment depends on risk factors and the cause of hypercoagulability.

Medications:
Anticoagulants - Warfarin (vitamin K antagonist). Direct Oral Anticoagulants (DOACs) - Apixaban , Rivaroxaban , Edoxaban , or Dabigatran . Heparins - Unfractionated heparin (UFH) or low-molecular-weight heparin (LMWH, e.g., enoxaparin ). Antiplatelet Agents (for specific conditions) - Aspirin or Clopidogrel . Thrombolytics (for acute, severe thrombosis) - Alteplase or other tissue plasminogen activators (tPA). Targeted Therapies - Protein C concentrates or fresh frozen plasma in protein C/S deficiency, Danazol or antifibrinolytics in hereditary angioedema-related hypercoagulability.

Prevalence: How common the health condition is within a specific population.
Inherited thrombophilias affect up to 10% of the general population (e.g., Factor V Leiden in 5% of individuals of European descent). Acquired hypercoagulability is more variable, depending on underlying conditions like malignancy or antiphospholipid syndrome.

Risk Factors: Factors or behaviors that increase the likelihood of developing the condition.
Family history of thrombophilia, immobility (e.g., post-surgery or long travel), obesity, pregnancy, use of oral contraceptives or hormone replacement therapy, cancer, and autoimmune conditions.

Prognosis: The expected outcome or course of the condition over time.
Prognosis depends on the underlying cause and management. With appropriate anticoagulation, most patients avoid recurrent thrombosis.

Complications: Additional problems or conditions that may arise as a result of the original condition.
Recurrent thromboembolic events (DVT, pulmonary embolism), chronic post-thrombotic syndrome, organ damage (e.g., from arterial clots), and complications of anticoagulation therapy (e.g., bleeding).

Immune Thrombocytopenia (ITP)

Specialty: Hematology

Category: Coagulation, Hemostasis, and Disorders

Symptoms:
easy or excessive bruising; petechiae (small red or purple spots on the skin); prolonged bleeding from cuts; spontaneous nosebleeds (epistaxis); bleeding gums; heavy menstrual periods; blood in urine or stool in severe cases

Root Cause:
An autoimmune disorder where antibodies target and destroy platelets, leading to thrombocytopenia and an increased risk of bleeding. The exact trigger is often unknown but may follow infections or be associated with other autoimmune conditions.

How it's Diagnosed: videos
Diagnosis is based on low platelet count (less than 100,000/micro L) in the absence of other causes of thrombocytopenia, often confirmed with bone marrow examination (to exclude other conditions) and peripheral blood smear.

Treatment:
Treatment depends on platelet count and bleeding severity. First-line therapies include corticosteroids and intravenous immunoglobulin (IVIG). In refractory cases, splenectomy or second-line therapies like rituximab or thrombopoietin receptor agonists are used.

Medications:
First-Line Treatments - Corticosteroids (e.g., prednisone , dexamethasone ) to suppress the immune response, Intravenous immunoglobulin (IVIG) to temporarily increase platelet count, Anti-D immunoglobulin for Rh-positive patients. Second-Line Treatments - Rituximab (anti-CD20 monoclonal antibody) to reduce antibody production, Thrombopoietin receptor agonists (e.g., romiplostim , eltrombopag ) to stimulate platelet production. Other Options - Immunosuppressive agents (e.g., azathioprine , mycophenolate mofetil), Fostamatinib (a spleen tyrosine kinase inhibitor).

Prevalence: How common the health condition is within a specific population.
Estimated prevalence is 2–5 per 100,000 individuals annually, with higher rates in children and older adults. Chronic ITP is more common in adults, particularly females.

Risk Factors: Factors or behaviors that increase the likelihood of developing the condition.
Viral infections (e.g., Epstein-Barr virus, hepatitis C), autoimmune diseases (e.g., lupus), recent vaccinations, certain medications, and older age.

Prognosis: The expected outcome or course of the condition over time.
Many children with ITP recover spontaneously, while adults may experience a chronic course. With appropriate management, severe complications are rare.

Complications: Additional problems or conditions that may arise as a result of the original condition.
Severe bleeding (e.g., intracranial hemorrhage), complications from long-term corticosteroid use (e.g., osteoporosis, diabetes), and infections following splenectomy.

Immune Thrombocytopenia (ITP) in Emergency Medicine

Specialty: Hematology

Category: Coagulation, Hemostasis, and Disorders

Symptoms:
severe or sudden-onset bruising; extensive petechiae; spontaneous mucosal bleeding (e.g., nosebleeds, gum bleeding); blood in urine or stool; prolonged or excessive menstrual bleeding; life-threatening hemorrhage (e.g., intracranial or gastrointestinal) in rare cases

Root Cause:
Autoimmune destruction of platelets, often exacerbated by stress, infections, or trauma, leading to critically low platelet levels and a risk of severe bleeding.

How it's Diagnosed: videos
Emergency diagnosis focuses on platelet count, coagulation studies (to rule out other bleeding disorders), and clinical history. A peripheral blood smear helps exclude pseudothrombocytopenia or other hematological disorders.

Treatment:
Immediate treatment for severe bleeding includes intravenous immunoglobulin (IVIG), corticosteroids, platelet transfusions (in life-threatening bleeding), and antifibrinolytics. Emergency splenectomy is considered in refractory cases.

Medications:
High-Dose Corticosteroids - Intravenous methylprednisolone or oral dexamethasone for quick immune suppression. Intravenous Immunoglobulin (IVIG) - Administered to rapidly boost platelet counts in critical situations. Platelet Transfusion - Used in cases of severe bleeding, but only as a temporary measure. Emergent Splenectomy - Rarely performed in emergencies but considered in refractory, life-threatening cases.

Prevalence: How common the health condition is within a specific population.
Acute ITP in emergency settings is uncommon but can occur during severe disease exacerbations or in undiagnosed individuals.

Risk Factors: Factors or behaviors that increase the likelihood of developing the condition.
Viral infections, autoimmune conditions, recent surgery, certain medications, or trauma can precipitate acute ITP episodes.

Prognosis: The expected outcome or course of the condition over time.
Prompt intervention in emergency settings can stabilize patients and prevent severe complications. Long-term management depends on the chronicity and response to therapy.

Complications: Additional problems or conditions that may arise as a result of the original condition.
Life-threatening bleeding, particularly intracranial hemorrhage; complications from transfusions (e.g., alloimmunization); and adverse effects of emergency treatments like corticosteroids or IVIG.

Immune Thrombocytopenia (ITP) and Pregnancy

Specialty: Hematology

Category: Coagulation, Hemostasis, and Disorders

Symptoms:
low platelet count detected during routine pregnancy testing; easy bruising; petechiae (small red or purple spots on the skin); bleeding gums; prolonged bleeding from minor injuries; in rare cases, severe bleeding or postpartum hemorrhage

Root Cause:
Autoimmune-mediated destruction of platelets during pregnancy, with potential exacerbation due to physiological changes in platelet count during gestation. It poses risks to both maternal and neonatal health, as maternal antibodies can cross the placenta.

How it's Diagnosed: videos
Diagnosed by exclusion, based on low platelet count (less than 100,000/micro L) without other causes of thrombocytopenia. History and peripheral blood smear help rule out gestational thrombocytopenia or preeclampsia-associated thrombocytopenia.

Treatment:
Treatment is focused on managing bleeding risks. Corticosteroids or intravenous immunoglobulin (IVIG) are first-line therapies. Platelet transfusions are reserved for severe cases or imminent delivery. Delivery planning includes minimizing bleeding risks.

Medications:
First-Line Treatments - Corticosteroids (e.g., prednisone ): Used in the lowest effective dose to avoid long-term fetal exposure. Intravenous Immunoglobulin (IVIG) - Often preferred due to its safety and lack of significant side effects on the fetus. Second-Line Options (if first-line treatments fail) - Azathioprine - Considered safe during pregnancy for refractory cases. Thrombopoietin Receptor Agonists (e.g., eltrombopag , romiplostim ) - Generally avoided due to limited safety data in pregnancy. Avoided Medications - Rituximab and other immunosuppressive agents: Typically avoided due to potential risks to the fetus. Fostamatinib - Contraindicated during pregnancy.

Prevalence: How common the health condition is within a specific population.
ITP complicates 1–5 in 10,000 pregnancies. Gestational thrombocytopenia is more common but usually mild and resolves postpartum.

Risk Factors: Factors or behaviors that increase the likelihood of developing the condition.
Pre-existing ITP, autoimmune disorders, and certain infections.

Prognosis: The expected outcome or course of the condition over time.
Most pregnancies progress uneventfully with appropriate management. Neonates may experience transient thrombocytopenia but typically recover without intervention.

Complications: Additional problems or conditions that may arise as a result of the original condition.
Maternal complications include postpartum hemorrhage and severe thrombocytopenia during delivery. Neonatal complications include thrombocytopenia due to transplacental transfer of maternal antibodies, increasing the risk of intracranial hemorrhage.

Internal Jugular Vein Thrombosis (IJVT)

Specialty: Hematology

Category: Coagulation, Hemostasis, and Disorders

Symptoms:
neck pain or tenderness; swelling along the neck; difficulty swallowing (dysphagia); visible neck vein distention; headache; fever if associated with infection; pulmonary symptoms in cases of embolism

Root Cause:
Formation of a blood clot in the internal jugular vein, often secondary to trauma, central venous catheterization, malignancy, infection, or hypercoagulable states. This can impair venous drainage and lead to complications like pulmonary embolism or septic thrombophlebitis.

How it's Diagnosed: videos
Ultrasound with Doppler imaging is the primary diagnostic tool. CT or MRI venography can be used for further assessment. Blood tests for D-dimer and hypercoagulable states may aid diagnosis.

Treatment:
Anticoagulation therapy with low-molecular-weight heparin (LMWH) or direct oral anticoagulants (DOACs) is the cornerstone of treatment. Antibiotics are added if infection is suspected. In rare cases, surgical intervention (thrombectomy) is needed.

Medications:
Anticoagulation Therapy - Low-Molecular-Weight Heparin (LMWH) (e.g., enoxaparin ) or unfractionated heparin (UFH) initially, Transition to oral anticoagulants like warfarin or Direct Oral Anticoagulants (DOACs) (e.g., rivaroxaban , apixaban ) for maintenance therapy. Antibiotics (if IJVT is associated with infection) - Broad-spectrum antibiotics are used, particularly if Lemierre’s syndrome (IJVT associated with Fusobacterium necrophorum) is suspected. Thrombolysis or Surgical Intervention - Considered in severe cases with extensive thrombosis or complications like pulmonary embolism.

Prevalence: How common the health condition is within a specific population.
Rare, with an estimated incidence of 0.2–1 per 100,000 people annually. It is more common in hospitalized patients with risk factors like central venous catheters or cancer.

Risk Factors: Factors or behaviors that increase the likelihood of developing the condition.
Central venous catheterization, head and neck infections (e.g., Lemierre’s syndrome), malignancy, trauma, hypercoagulable disorders, and intravenous drug use.

Prognosis: The expected outcome or course of the condition over time.
Generally favorable with prompt treatment, although delayed diagnosis can lead to serious complications like pulmonary embolism or septicemia.

Complications: Additional problems or conditions that may arise as a result of the original condition.
Pulmonary embolism, septic thrombophlebitis (Lemierre's syndrome), venous congestion, and, in rare cases, death.

Miscarriages Caused by Blood Coagulation Protein or Platelet Deficits

Specialty: Hematology

Category: Coagulation, Hemostasis, and Disorders

Symptoms:
recurrent pregnancy loss (two or more consecutive miscarriages); fetal growth restriction; unexplained stillbirth; placental abruption in severe cases; evidence of thrombosis in other areas

Root Cause:
Miscarriages can result from hypercoagulable states (e.g., antiphospholipid syndrome), inherited thrombophilias (e.g., Factor V Leiden mutation), or platelet dysfunctions. These conditions impair placental circulation, leading to pregnancy loss.

How it's Diagnosed: videos
Diagnosis involves testing for antiphospholipid antibodies (lupus anticoagulant, anticardiolipin, and anti-beta-2 glycoprotein I antibodies), thrombophilia workup (e.g., genetic testing for Factor V Leiden or prothrombin mutation), and platelet function tests.

Treatment:
Treatment is tailored to the underlying cause. Low-dose aspirin and low-molecular-weight heparin (LMWH) are commonly used to improve placental circulation. For platelet dysfunction, treatments may include intravenous immunoglobulin (IVIG) or corticosteroids.

Medications:
Low-dose aspirin , low-molecular-weight heparin (e.g., enoxaparin ), and sometimes intravenous immunoglobulin (IVIG) or corticosteroids for immune-related platelet deficits.

Prevalence: How common the health condition is within a specific population.
Recurrent pregnancy loss affects approximately 1–2% of couples. Thrombophilic causes account for a significant proportion of these cases, particularly in women with a history of clotting disorders.

Risk Factors: Factors or behaviors that increase the likelihood of developing the condition.
History of thrombosis, known thrombophilic mutations, antiphospholipid syndrome, autoimmune diseases (e.g., lupus), obesity, advanced maternal age, and previous pregnancy complications.

Prognosis: The expected outcome or course of the condition over time.
With appropriate treatment, many women with thrombophilia or platelet deficits can achieve successful pregnancies. Early and multidisciplinary management improves outcomes.

Complications: Additional problems or conditions that may arise as a result of the original condition.
Placental insufficiency, preeclampsia, fetal growth restriction, and recurrent pregnancy loss.

Nonplatelet Hemostatic Disorders

Specialty: Hematology

Category: Coagulation, Hemostasis, and Disorders

Symptoms:
prolonged bleeding from injuries or surgery; spontaneous bleeding in soft tissues or muscles; joint bleeding (hemarthrosis); easy bruising; nosebleeds (epistaxis); excessive menstrual bleeding in females

Root Cause:
Disorders involving clotting factor deficiencies or dysfunctions, such as hemophilia A (Factor VIII deficiency), hemophilia B (Factor IX deficiency), or von Willebrand disease, which impair the body's ability to form stable clots.

How it's Diagnosed: videos
Diagnosed using coagulation studies like prolonged activated partial thromboplastin time (aPTT), factor assays to identify specific clotting factor deficiencies, and tests for von Willebrand factor levels and function.

Treatment:
Treatment depends on the specific condition and involves replacement of deficient factors using recombinant or plasma-derived concentrates. For von Willebrand disease, desmopressin or von Willebrand factor concentrates are used.

Medications:
Desmopressin (DDAVP) for mild hemophilia A or von Willebrand disease, factor replacement therapy (e.g., factor VIII, IX, or recombinant products), antifibrinolytics (e.g., tranexamic acid), and in specific cases, fibrinogen concentrates or prothrombin complex concentrates (PCCs).

Prevalence: How common the health condition is within a specific population.
Varies widely; hemophilia A affects approximately 1 in 5,000 males, hemophilia B affects 1 in 25,000 males, and von Willebrand disease affects about 1% of the population, though many cases are mild and undiagnosed.

Risk Factors: Factors or behaviors that increase the likelihood of developing the condition.
Genetic mutations, family history of bleeding disorders, and in rare cases, acquired deficiencies due to autoimmune conditions or liver disease.

Prognosis: The expected outcome or course of the condition over time.
With proper diagnosis and management, most individuals can live normal lives, though severe forms may require lifelong treatment and monitoring.

Complications: Additional problems or conditions that may arise as a result of the original condition.
Severe bleeding episodes, chronic joint damage (in hemophilia), and complications from transfusions or factor concentrates, such as inhibitors or infections (historically).

Paradoxical Embolism

Specialty: Hematology

Category: Coagulation, Hemostasis, and Disorders

Symptoms:
sudden onset of stroke symptoms (e.g., weakness, slurred speech, facial droop); transient ischemic attacks (tias); unexplained peripheral embolism (e.g., limb ischemia); pulmonary symptoms if associated with venous thromboembolism; possible migraine with aura in some cases

Root Cause:
Occurs when a venous thrombus bypasses the pulmonary circulation and enters the arterial system, typically through a right-to-left shunt like a patent foramen ovale (PFO) or atrial septal defect (ASD). This allows clots to bypass the lungs' filtering mechanism.

How it's Diagnosed: videos
Diagnosis involves imaging studies like transesophageal echocardiography (TEE) with bubble study to identify a right-to-left shunt, along with Doppler ultrasound to detect venous thrombi. MRI or CT scans assess embolic events in the brain or other organs.

Treatment:
Acute treatment includes thrombolysis or thrombectomy for embolic events. Long-term management focuses on anticoagulation (e.g., warfarin or direct oral anticoagulants) or closure of the shunt (e.g., percutaneous PFO closure) to prevent recurrence.

Medications:
Anticoagulants (e.g., warfarin , rivaroxaban , or apixaban ) to prevent further clot formation and, in certain cases, antiplatelet agents (e.g., aspirin ) or thrombolytics for acute embolic events, with closure of the atrial septal defect or patent foramen ovale considered in recurrent cases.

Prevalence: How common the health condition is within a specific population.
PFOs are present in about 25–30% of the general population, though not all cause paradoxical embolism. The condition is rare but more common in younger patients presenting with cryptogenic stroke.

Risk Factors: Factors or behaviors that increase the likelihood of developing the condition.
Deep vein thrombosis, prolonged immobility, hypercoagulable disorders, presence of a right-to-left shunt (e.g., PFO, ASD), and genetic thrombophilias.

Prognosis: The expected outcome or course of the condition over time.
With appropriate treatment, the risk of recurrence is low. Closure of PFO or long-term anticoagulation significantly reduces the chance of future embolic events.

Complications: Additional problems or conditions that may arise as a result of the original condition.
Recurrent strokes, transient ischemic attacks (TIAs), peripheral arterial embolism, and complications from anticoagulant therapy (e.g., bleeding).

Platelet Disorders

Specialty: Hematology

Category: Coagulation, Hemostasis, and Disorders

Symptoms:
prolonged bleeding from minor cuts; easy bruising; petechiae (small red or purple spots on the skin); frequent nosebleeds (epistaxis); gum bleeding; heavy menstrual bleeding (menorrhagia); spontaneous bleeding in severe cases

Root Cause:
Platelet disorders can involve quantitative abnormalities (thrombocytopenia or thrombocytosis) or qualitative defects in platelet function. They impair the body's ability to form stable clots, increasing the risk of bleeding.

How it's Diagnosed: videos
Diagnosis is based on platelet count, peripheral blood smear, and specialized platelet function tests (e.g., platelet aggregation studies, flow cytometry). Genetic testing may identify inherited disorders like Glanzmann thrombasthenia.

Treatment:
Treatment depends on the specific disorder. Thrombocytopenia may require corticosteroids, intravenous immunoglobulin (IVIG), or platelet transfusions. Platelet function disorders are managed with antifibrinolytics, recombinant factor VIIa, or desmopressin.

Medications:
Medications to treat platelet disorders depend on the condition and include desmopressin (DDAVP) for platelet function defects, antifibrinolytics (e.g., tranexamic acid) for bleeding control, corticosteroids, intravenous immunoglobulin (IVIG), or thrombopoietin receptor agonists (e.g., eltrombopag , romiplostim ) for immune thrombocytopenia, and platelet transfusions for severe thrombocytopenia or dysfunction.

Prevalence: How common the health condition is within a specific population.
The prevalence varies depending on the disorder. For example, immune thrombocytopenia (ITP) affects 2–5 per 100,000 individuals annually, while inherited disorders like Bernard-Soulier syndrome are extremely rare.

Risk Factors: Factors or behaviors that increase the likelihood of developing the condition.
Genetic predisposition (inherited disorders), autoimmune conditions, certain medications (e.g., chemotherapy, heparin), infections, and bone marrow suppression.

Prognosis: The expected outcome or course of the condition over time.
Prognosis depends on the specific condition. With appropriate treatment, many platelet disorders can be managed effectively, although severe inherited conditions may require lifelong care.

Complications: Additional problems or conditions that may arise as a result of the original condition.
Severe bleeding episodes, intracranial hemorrhage, chronic anemia from frequent blood loss, and complications from platelet transfusions, such as alloimmunization or infections.

Protein C Deficiency

Specialty: Hematology

Category: Coagulation, Hemostasis, and Disorders

Symptoms:
deep vein thrombosis (dvt); pulmonary embolism; unusual blood clots in veins; swelling and pain in affected areas; skin necrosis (especially when using warfarin)

Root Cause:
A genetic or acquired deficiency in protein C, which is a vitamin K-dependent anticoagulant protein essential for regulating blood clotting and preventing excessive clot formation.

How it's Diagnosed: videos
Blood tests to measure protein C activity and levels, genetic testing for inherited mutations, and evaluation of clotting history.

Treatment:
Anticoagulation therapy (e.g., low-molecular-weight heparin or direct oral anticoagulants), avoidance of risk factors for thrombosis, and long-term prophylactic anticoagulation in severe cases.

Medications:
Anticoagulants such as warfarin , low-molecular-weight heparin (LMWH), and direct oral anticoagulants (DOACs) like apixaban or rivaroxaban . These medications belong to the "anticoagulant" drug class.

Prevalence: How common the health condition is within a specific population.
Estimated to occur in 1 in 200 to 1 in 500 individuals, with a higher prevalence in individuals with a personal or family history of thrombosis.

Risk Factors: Factors or behaviors that increase the likelihood of developing the condition.
Family history of Protein C Deficiency, pregnancy, oral contraceptive use, surgery, immobility, cancer, and advanced age.

Prognosis: The expected outcome or course of the condition over time.
Generally manageable with appropriate anticoagulation therapy, but the risk of recurrent clots is high without treatment. Severe deficiency can lead to life-threatening complications, especially in newborns.

Complications: Additional problems or conditions that may arise as a result of the original condition.
Recurrent venous thromboembolism (VTE), neonatal purpura fulminans in severe cases, warfarin-induced skin necrosis, and organ damage from thrombosis.

Protein S Deficiency

Specialty: Hematology

Category: Coagulation, Hemostasis, and Disorders

Symptoms:
deep vein thrombosis (dvt); pulmonary embolism; unusual thrombosis in veins or arteries; swelling, redness, and pain in affected areas; possible stroke symptoms in arterial clots

Root Cause:
A deficiency in protein S, a vitamin K-dependent glycoprotein that functions as a cofactor for protein C to regulate blood clot formation.

How it's Diagnosed: videos
Blood tests to measure free and total protein S levels, protein S activity tests, genetic testing for inherited mutations, and clinical history of thrombosis.

Treatment:
Anticoagulation therapy (e.g., warfarin, LMWH, or DOACs), lifestyle modifications to reduce clotting risk, and long-term anticoagulation in severe cases.

Medications:
Warfarin (a vitamin K antagonist), LMWH, and DOACs such as dabigatran , apixaban , or rivaroxaban . These medications are classified as anticoagulants.

Prevalence: How common the health condition is within a specific population.
Approximately 1 in 500 individuals, with increased frequency in those with a personal or family history of thrombotic events.

Risk Factors: Factors or behaviors that increase the likelihood of developing the condition.
Family history of Protein S Deficiency, pregnancy, oral contraceptive use, prolonged immobility, surgery, and malignancy.

Prognosis: The expected outcome or course of the condition over time.
Manageable with anticoagulant therapy; however, untreated cases carry a significant risk of recurrent thrombotic events. Severe deficiency can result in neonatal purpura fulminans or other life-threatening thrombotic complications.

Complications: Additional problems or conditions that may arise as a result of the original condition.
Recurrent venous thromboembolism, arterial thrombotic events, warfarin-induced skin necrosis, and long-term damage to affected tissues and organs.

Secondary Thrombocytosis

Specialty: Hematology

Category: Coagulation, Hemostasis, and Disorders

Symptoms:
elevated platelet count on blood tests; headaches; dizziness; chest pain; numbness or tingling in the extremities; bleeding or clotting tendencies (rare)

Root Cause:
Increased platelet production as a reactive response to another condition, such as inflammation, infection, iron deficiency, or cancer.

How it's Diagnosed: videos
Blood tests (complete blood count with differential, peripheral smear), inflammatory markers (CRP, ESR), and evaluation of underlying causes.

Treatment:
Management of the underlying condition; platelet-lowering treatment is typically not necessary unless symptomatic or very high counts.

Medications:
Platelet-lowering medications like hydroxyurea (a myelosuppressive agent) may be used in rare cases. Inflammation or infection might be treated with anti-inflammatory drugs or antibiotics. Iron deficiency is corrected with iron supplements.

Prevalence: How common the health condition is within a specific population.
Common in certain populations with chronic inflammation, infection, or malignancies; prevalence depends on the underlying condition.

Risk Factors: Factors or behaviors that increase the likelihood of developing the condition.
Chronic infections, inflammation, iron deficiency, splenectomy, and malignancies.

Prognosis: The expected outcome or course of the condition over time.
Good if the underlying cause is identified and treated; platelet levels typically normalize with resolution of the primary condition.

Complications: Additional problems or conditions that may arise as a result of the original condition.
Rare, but may include thrombosis or bleeding in cases of extreme platelet elevation.