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  • Опубликовано: 24 дек 2024

Комментарии • 25

  • @AM-cc3pw
    @AM-cc3pw 8 часов назад +1

    1- Anemia + schistocytes in bl smear + thrombocytopenia points towards MAHA
    Normal FDPs exclude DIC
    Fever and CNS symptoms favors the diagnosis of TTP over HUS
    2- digital gangrene and DVT occurs due to hypercoaguble state
    Decrease level of ADAMTS13 which breakdown large multimres of vWF leads to large sticky vWF cause PLTs to clump leading to thrombus formation
    3- while bleeding symptoms occur approximately in 20% of cases , in our cases PLTs number not severely reduced so there is no bleeding or petichae
    4 - explained above

  • @_kamaleldeen9451
    @_kamaleldeen9451 7 часов назад

    1 -The diagnosis is most probably (TTP) as there is MAHA and neurological abnormalities Renal impairment
    2- gangrene and DVT due to micro thrombosis
    3- no bleeding as platelet count not significantly reduced (not below 50k)
    4- the pathogenesis of disease is there is a deficiency in ADAM TS13 which is responsible for degradation of VWF polymers into small monomers ready for degradation

  • @mohamed.123Ragab
    @mohamed.123Ragab 15 часов назад +1

    1/lupus vasculitis
    2/inflammatory mediators , procagulants
    3/as autoimmune disese cause micro angiopathic hemolytic anemia (MAHA)
    4/lupus vasculitis causes psychogenic manifestions and induce inflammation causes stroke and dvt and autoimmune reaction causes MAHA and affect kidney

  • @albaraaelnemer3468
    @albaraaelnemer3468 11 часов назад

    Q1/
    SLE associated with Anti phospholipid syndrome
    Q2/
    Hypercoagulable state may involve veins and arteries causes DVT and Digital gangrene respectively.
    Q3/
    Because the platelets count is still above 100,000/cmm
    Q4/
    Autoimmune mechanism due to Antiphosphplipid antibodies (lupus anticoagulant, anticardiolipin and anti beta 2 glycoprotein I)
    والله أعلم

  • @مصطفيوليد-ب2و
    @مصطفيوليد-ب2و 9 часов назад

    Q1/primary antiphospholipid syndrome
    Q2/due to multiple thromboembolic evets that result from inactivation of natural anticoagulants as protein C&S and activation of coagulation facrors
    Q3/ due to prothrombotic effect of antiphospholipid ABs
    Also presense of FDPs whithin normal range exclude DIC
    Q4/formation of ABs as lupus anticoagulant and anti cardiolipin againest cell membrane phospholipid forming complexes result in inactivation of natural anticoagulants and activation of coagulation factors

  • @obaidaqwasmi
    @obaidaqwasmi 14 часов назад +1

    Number 1 : Antiphospholipid antibody syndrome
    Number 2: its a hypercoagulable state that involve BOTH veins and arteries
    Number 3 : its a procoagulant state , also the bleeding usually occur when the platelets are with a lower number than 100 K
    Number 4 : formation of procoagulatory antiphospholipids antibodies which lead to activation of platelets

  • @mariamahmed-kg7wr
    @mariamahmed-kg7wr 2 часа назад

    TTP
    Anti phospholipid syndrome secondary to SLE
    Thormboctopenia
    TTP ( mental confusion . Hemolytic anemia with presence of many fragemented RBCS . Renal
    impairment . Most probably secondary to SLE . Subcide . DVT . Digital gangrane ( small vessel vasculitis ) secondary to Systemic Lupus

  • @alhassanali3442
    @alhassanali3442 10 часов назад

    Q1 / Disseminated intravascular coagulation
    Q2 / because of immobilization because she had stroke before 2 weeks .
    Q3/ Because the disease in the early stage.
    Q4 / I don't remember and not sure for these answers , Thank you

  • @hamodysaied3642
    @hamodysaied3642 14 часов назад

    1) SLE ( lupus Nephritis and vasculitis)
    Due to ( sex female , autoimmune hemolytic anemia , hypercoagulable state , mild thrombocytopenia...)
    2) Due to thrombosis and vascultits
    3) Due to ( hypercoagulability predominance , mild decrease in platelets, normal clotting factor )
    4) Autoimmune mechanism ( genetic predisposition HLA DR2 and 3) + environmental factors
    Hormonal ( estrogen may have a role ) , autoantibody ( ANA and anti smith)

  • @sarrahsamaha9358
    @sarrahsamaha9358 7 часов назад

    Question number one answer:
    Thrombotic thrombocytopenic purpura (TTP)
    Question number two answer:
    due to platelet aggregation forming microthrombi that occludes blood vessels and due to hypercoagulability
    Question number three answer:
    •TTP primarily affecting platelet dysfunction
    •Intact coagulation profile Unlike (DIC) PT and PPT are typically normal in (TTP)
    •Platelet count not significantly low
    Question number four answer:
    ADAMTS13 inhibition leading to excessive vWF hence platelet aggregation

  • @emadalshathmay9349
    @emadalshathmay9349 13 часов назад

    1 -Diagnosis is (TTP) based on neurological signs, fever, digital gangrene, DVT, thrombocytopenia, and renal dysfunction.
    2-Digital Gangrene & DVT caused by microvascular thrombosis and hypercoagulable state in TTP,
    Reflects excessive platelet aggregation and microthrombi formation.
    3- Because of low platalets are consumed in microthrombi formation rather than causing bleeding and Thrombosis predominates over hemorrhage.
    4- Pathogenesis is accumulation of large von Wilebrand factor multimers and excessive platelet aggregation and microthrombi formation which lead to
    RBC destruction, platelet consumption, and renal dysfunction.

  • @yahyasamady2308
    @yahyasamady2308 15 часов назад

    1- Thrombosis + low plateletes + anemia (schistocytes) + high creatinine + CNS affection = Thrombotic thrombocytopenic purpra (TTP) .
    2- Digital gangrene and DVT is due to thrmobus formation.
    3- There is no bleeding because the plateletes count is above 100,000 (platelets count above 100,000 = asymptomatic thrombocytopenia), "the low plateletes count is due to consumption of platelets in thrombus formation".
    4- The pathogenesis of TTP : mutation in ADAMS 13 >> accumulation of large vwf molecules in endothelium >> thrombus formation.

  • @Azmy-pz2ql
    @Azmy-pz2ql 15 часов назад

    Waiting...

  • @ornoodles
    @ornoodles 15 часов назад

    Female with Triad of thrombocytopenia ( decreased platelets) + microangiopathic hemolytic anemia + Acute kidney injury ( high Cr) could be TTP or HUS
    but presence of (stroke and hallucinations) neurologic symptoms + fever marks the diagnosis of TTP
    normal PT and PTT >> coagulation pathway is not involved
    Inhibition of ADAMTS13 level >> uncleaved vWF multimers >> platelet trapping & activation >> microthrombi formation and prothrombotic state.
    As there is not widespread activation of the clotting factors and FDP is normal unlike DIC >> no consumption of clotting factors >> no bleeding
    intact platelet function
    Treatment with plasma exchange + corticosteroids + rituximab + caplasizumab

  • @AdelMostafa-y7u
    @AdelMostafa-y7u 14 часов назад

    Most probably diagnosis is Acquired thrombotic thrombocytopenic purpra due to presence of (thrombocytopenia + microangiopathic hemolytic anemia ) , neurological manifestations, fever and kidney affection.
    It is classic pentad for TTP.
    Causes of gangrene and DVT
    Due to formation of microthrombi mainly by platlets
    Causes of absence of bleeding
    Due to mild thrombocytopenia
    Pathogensis
    May be inherited or acquired but in this case it is acquired
    Inhibitors of ADAMTS13 enzyme which results in presence of VWF Multimers ( more active )
    VWF multimers induce platelet microthrombi formation which cause consumption of platelets ( thrombocytopenia ), fragmented RBCs ( shistocytes ), which are the major criteria for diagnosis
    Also fever, AKI, and neurological manifestation could be present to microthrombi and ischemia which cause multi organ damage.

  • @tamerahmed6555
    @tamerahmed6555 15 часов назад +2

    TTP
    Hypercoagulability Microthrombi formation
    Platelets count above 100,000
    Inhibition or deficiency of ADAMTS13

  • @rashadomara1628
    @rashadomara1628 14 часов назад

    anti phospholibid syndrome 2 hypercogulable state with paradoxical plateletes def 3platelt more than 100000 4 form of anti phospholipid anti body

  • @ABNAltyeb
    @ABNAltyeb 15 часов назад

    TTP
    Hypercoagulability microthrombi formation
    Characterized microangiopathic hemolytic anemia and fever
    and thrombocytopenia >100000
    appear in mild renal problems creatinine 1.9
    and neurological dysfunction
    Deficiency of ADAMTS13
    Caused by failure to cleave vWF
    explain the absence of bleeding because Instead, they can cause damage to organs and tissues by blocking blood

  • @AdelMostafa-y7u
    @AdelMostafa-y7u 14 часов назад

    Most probably diagnosis is Acquired thrombotic thrombocytopenic purpra due to presence of (thrombocytopenia + microangiopathic hemolytic anemia ) , neurological manifestations, fever and kidney affection.
    It is classic pentad for TTP.
    Causes of gangrene and DVT
    Due to formation of microthrombi mainly by platlets
    Causes of absence of bleeding
    Due to mild thrombocytopenia
    Pathogensis
    May be inherited or acquired but in this case it is acquired
    Inhibitors of ADAMTS13 enzyme which results in presence of VWF Multimers ( more active )
    VWF multimers induce platelet microthrombi formation which cause consumption of platelets ( thrombocytopenia ), fragmented RBCs ( shistocytes ), which are the major criteria for diagnosis
    Also fever, AKI, and neurological manifestation could be present to microthrombi and ischemia which cause multi organ damage.