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Platelets are produced from _______ in the bone marrow.
Platelets are produced from megakaryocytes in the bone marrow.
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The key function of platelets is to rapidly form _______ in response to vascular injury.
The key function of platelets is to rapidly form mechanical plugs in response to vascular injury.
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Hemostasis is the process that prevents and stops _______.
Hemostasis is the process that prevents and stops bleeding.
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Primary hemostasis involves platelets and vessel wall integrity, while _______ involves the coagulation cascade.
Primary hemostasis involves platelets and vessel wall integrity, while secondary hemostasis involves the coagulation cascade.
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Platelet adhesion occurs when platelets adhere to exposed _______.
Platelet adhesion occurs when platelets adhere to exposed subendothelial collagen.
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In primary hemostasis, bleeding from a _______ suggests a structural lesion.
In primary hemostasis, bleeding from a single site suggests a structural lesion.
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Multiple site bleeding suggests _______.
Multiple site bleeding suggests coagulopathy.
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Immediate bleeding indicates a _______.
Immediate bleeding indicates a primary hemostasis disorder.
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Delayed bleeding is indicative of a _______.
Delayed bleeding is indicative of a secondary hemostasis disorder.
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Petechiae, which are pin point bleeding in skin or mucosa, suggest a _______ issue.
Petechiae, which are pin point bleeding in skin or mucosa, suggest a primary hemostasis issue.
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Hematoma and hemarthrosis, which involve large blood in soft tissues or joints, are seen in _______ disorders.
Hematoma and hemarthrosis, which involve large blood in soft tissues or joints, are seen in secondary hemostasis disorders.
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Mucosal bleeding and bruising are often associated with _______.
Mucosal bleeding and bruising are often associated with primary hemostasis.
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Immune Thrombocytopenia (ITP) can be classified as _______ (no other cause) or _______ (due to drugs, systemic disorders).
Immune Thrombocytopenia (ITP) can be classified as primary (no other cause) or secondary (due to drugs, systemic disorders).
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The autoantibodies in ITP target platelet glycoproteins such as _______ or _______.
The autoantibodies in ITP target platelet glycoproteins such as GP IIb/IIIa or Ib/IX.
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Acute ITP is mostly seen in _______ and is often post-viral or post-vaccine.
Acute ITP is mostly seen in children and is often post-viral or post-vaccine.
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Chronic ITP is more common in _______ aged 20–40 with no viral history.
Chronic ITP is more common in women aged 20–40 with no viral history.
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Clinical features of acute ITP include sudden onset, _______, and mucocutaneous bleeding.
Clinical features of acute ITP include sudden onset, petechiae, and mucocutaneous bleeding.
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Treatment for chronic ITP may include _______ or _______.
Treatment for chronic ITP may include splenectomy or immunosuppressants.
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Heparin-Induced Thrombocytopenia (HIT) can be classified into _______ (nonimmune) and _______ (immune-mediated).
Heparin-Induced Thrombocytopenia (HIT) can be classified into Type I (nonimmune) and Type II (immune-mediated).
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Type II HIT occurs _______ days after exposure to heparin and can be life-threatening.
Type II HIT occurs 4–10 days after exposure to heparin and can be life-threatening.
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Clinical features of HIT include thromboembolism such as _______ and _______.
Clinical features of HIT include thromboembolism such as DVT and MI.
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Thrombotic Thrombocytopenic Purpura (TTP) is caused by deficiency of _______.
Thrombotic Thrombocytopenic Purpura (TTP) is caused by deficiency of ADAMTS13.
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TTP may be triggered by infections like _______ or _______.
TTP may be triggered by infections like E. coli O157:H7 or Shigella.
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The pathogenesis of TTP involves accumulation of large _______ multimers due to ADAMTS13 deficiency.
The pathogenesis of TTP involves accumulation of large vWF multimers due to ADAMTS13 deficiency.
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Deficiency of _______ leads to accumulation of large _______.
Deficiency of ADAMTS13 leads to accumulation of large vWF multimers.
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The clinical features of TTP include a pentad of: - _______ - _______ - _______ - _______ - _______.
The clinical features of TTP include a pentad of: - microangiopathic hemolytic anemia - thrombocytopenia - neurologic symptoms - fever - renal disease.
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Neurologic symptoms in TTP may include: - _______ - _______ - _______.
Neurologic symptoms in TTP may include: - seizures - aphasia - hemiplegia.
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Laboratory findings in TTP include: - WBC: _______ - Hemoglobin: _______ - Platelets: _______.
Laboratory findings in TTP include: - WBC: normal/slightly elevated - Hemoglobin: 8–9 g/dL - Platelets: 20–50 x 10³/mm³.
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The treatment for TTP is a medical emergency that includes _______ which removes antibodies and _______.
The treatment for TTP is a medical emergency that includes plasma exchange which removes antibodies and vWF multimers.
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Hemolytic Uremic Syndrome (HUS) is the most common cause of acute kidney injury in children and is often associated with _______.
Hemolytic Uremic Syndrome (HUS) is the most common cause of acute kidney injury in children and is often associated with bacterial gastroenteritis.
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Atypical HUS is linked to mutations in the _______ and has a poor prognosis.
Atypical HUS is linked to mutations in the complement pathway and has a poor prognosis.
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The primary event in the pathogenesis of HUS is _______.
The primary event in the pathogenesis of HUS is endothelial damage.
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Clinical features of HUS include: - _______ - _______ - _______.
Clinical features of HUS include: - bloody diarrhea - fever - acute renal failure.
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Differential diagnosis for TTP includes: - _______: Prolonged PT/aPTT, elevated D-dimer - _______: Rash, arthralgia, no diarrhea.
Differential diagnosis for TTP includes: - DIC: Prolonged PT/aPTT, elevated D-dimer - Systemic vasculitis: Rash, arthralgia, no diarrhea.
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Systemic vasculitis symptoms include _______, _______, and _______.
Systemic vasculitis symptoms include rash, arthralgia, and no diarrhea.
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Supportive care for treatment includes _______, _______, and _______.
Supportive care for treatment includes platelet transfusions, dialysis, and fluid/electrolyte management.
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Plasma exchange is used for treating _______.
Plasma exchange is used for treating atypical HUS.
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TTP and HUS comparison shows that peak incidence for TTP is at _______ years, while HUS is common in _______.
TTP and HUS comparison shows that peak incidence for TTP is at 40 years, while HUS is common in childhood.
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In terms of gender, TTP is more common in _______, while HUS affects _______.
In terms of gender, TTP is more common in females, while HUS affects both genders equally.
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Epidemic occurrence is common in _______ but not in _______.
Epidemic occurrence is common in HUS but not in TTP.
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Re-occurrence is _______ in TTP and _______ in HUS.
Re-occurrence is common in TTP and rare in HUS.
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HUS is linked to _______, while TTP has _______ links.
HUS is linked to E. coli 0157:H7, while TTP has occasional links.
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Renal failure is _______ in TTP but _______ in HUS.
Renal failure is uncommon in TTP but common in HUS.
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Thrombocytopenia in TTP is _______, while in HUS it is _______.
Thrombocytopenia in TTP is severe, while in HUS it is moderate to severe.
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Organ involvement in TTP is _______, while in HUS it is limited to the _______.
Organ involvement in TTP is multiple, while in HUS it is limited to the kidney.
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Xem thẻ ở đây, hoặc sign up to study with spaced repetition.
Platelets are produced from megakaryocytes in the bone marrow.
The key function of platelets is to rapidly form mechanical plugs in response to vascular injury.
Hemostasis is the process that prevents and stops bleeding.
Primary hemostasis involves platelets and vessel wall integrity, while secondary hemostasis involves the coagulation cascade.
Platelet adhesion occurs when platelets adhere to exposed subendothelial collagen.
In primary hemostasis, bleeding from a single site suggests a structural lesion.
Multiple site bleeding suggests coagulopathy.
Immediate bleeding indicates a primary hemostasis disorder.
Delayed bleeding is indicative of a secondary hemostasis disorder.
Petechiae, which are pin point bleeding in skin or mucosa, suggest a primary hemostasis issue.
Hematoma and hemarthrosis, which involve large blood in soft tissues or joints, are seen in secondary hemostasis disorders.
Mucosal bleeding and bruising are often associated with primary hemostasis.
Immune Thrombocytopenia (ITP) can be classified as primary (no other cause) or secondary (due to drugs, systemic disorders).
The autoantibodies in ITP target platelet glycoproteins such as GP IIb/IIIa or Ib/IX.
Acute ITP is mostly seen in children and is often post-viral or post-vaccine.
Chronic ITP is more common in women aged 20–40 with no viral history.
Clinical features of acute ITP include sudden onset, petechiae, and mucocutaneous bleeding.
Treatment for chronic ITP may include splenectomy or immunosuppressants.
Heparin-Induced Thrombocytopenia (HIT) can be classified into Type I (nonimmune) and Type II (immune-mediated).
Type II HIT occurs 4–10 days after exposure to heparin and can be life-threatening.
Clinical features of HIT include thromboembolism such as DVT and MI.
Thrombotic Thrombocytopenic Purpura (TTP) is caused by deficiency of ADAMTS13.
TTP may be triggered by infections like E. coli O157:H7 or Shigella.
The pathogenesis of TTP involves accumulation of large vWF multimers due to ADAMTS13 deficiency.
Deficiency of ADAMTS13 leads to accumulation of large vWF multimers.
The clinical features of TTP include a pentad of: - microangiopathic hemolytic anemia - thrombocytopenia - neurologic symptoms - fever - renal disease.
Neurologic symptoms in TTP may include: - seizures - aphasia - hemiplegia.
Laboratory findings in TTP include: - WBC: normal/slightly elevated - Hemoglobin: 8–9 g/dL - Platelets: 20–50 x 10³/mm³.
The treatment for TTP is a medical emergency that includes plasma exchange which removes antibodies and vWF multimers.
Hemolytic Uremic Syndrome (HUS) is the most common cause of acute kidney injury in children and is often associated with bacterial gastroenteritis.
Atypical HUS is linked to mutations in the complement pathway and has a poor prognosis.
The primary event in the pathogenesis of HUS is endothelial damage.
Clinical features of HUS include: - bloody diarrhea - fever - acute renal failure.
Differential diagnosis for TTP includes: - DIC: Prolonged PT/aPTT, elevated D-dimer - Systemic vasculitis: Rash, arthralgia, no diarrhea.
Systemic vasculitis symptoms include rash, arthralgia, and no diarrhea.
Supportive care for treatment includes platelet transfusions, dialysis, and fluid/electrolyte management.
Plasma exchange is used for treating atypical HUS.
TTP and HUS comparison shows that peak incidence for TTP is at 40 years, while HUS is common in childhood.
In terms of gender, TTP is more common in females, while HUS affects both genders equally.
Epidemic occurrence is common in HUS but not in TTP.
Re-occurrence is common in TTP and rare in HUS.
HUS is linked to E. coli 0157:H7, while TTP has occasional links.
Renal failure is uncommon in TTP but common in HUS.
Thrombocytopenia in TTP is severe, while in HUS it is moderate to severe.
Organ involvement in TTP is multiple, while in HUS it is limited to the kidney.
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