Hamato plus Onko

Question 1

CML Treatment ?

50j, hepatomegalie, undeveloped cells in blood

Answer 1

Imatinib

Question 2

Heparin-induced ________________ (HIT)—development of ___ antibodies _____ heparin bound to platelet factor __ (____).

_______-heparin-PF4 complex _________ platelets → thrombosis and thrombocytopenia.

Answer 2

Heparin-induced thrombocytopenia (HIT)—development of IgG antibodies against heparin bound to platelet factor 4 (PF4).

Antibody-heparin-PF4 complex activates platelets Ž-> thrombosis and thrombocytopenia.

Question 3

PAM is horny (Horner). What it is ?

Answer 3

PAM is horny (Horner).

Ptosis (superior tarsal muscle), anhidrosis, and miosis (rhyming).

Question 4

\_\_\_\_\_\_ pathway coagulation defect, Defect in \_\_\_\_\_ plug formation: ↓ \_\_\_ → ↓ defect in platelet-to-vWF \_\_\_\_\_\_\_\_.
Autosomal \_\_\_\_\_\_. Mild but \_\_\_\_\_\_ common
inherited bleeding disorder. Diagnosed
in most cases by \_\_\_\_\_\_\_-cofactor assay
( _ agglutination is diagnostic).

Answer 4

Intrinsic pathway coagulation defect, Defect in platelet plug formation: ↓ vWF → ↓ defect in platelet-to-vWF adhesion.
Autosomal dominant. Mild but most common
inherited bleeding disorder. Diagnosed
in most cases by ristocetin-cofactor assay
(↓ agglutination is diagnostic).

Question 5

von Willebrand disease, Treatment: d________, which releases vWF stored in endothelium.
! aPTT may also be normal in von Willebrand disease. !
Wichtige Nebenwirkung: Hypo______

Answer 5

Treatment: desmopressin, which releases vWF stored in endothelium.
! aPTT may also be normal in von Willebrand disease. !
Wichtige Nebenwirkung: Hyponatriämie

Question 6

Platelet disorders
_____ in platelet ____ formation → _ bleeding time (__).
Platelet abnormalities → __________: mucous membrane ______ , epi______ , pet______,
pur____, ↑ bleeding time, possibly _______ platelet count (PC).

Answer 6

Platelet disorders
Defects in platelet plug formation → ↑ bleeding time (BT).
Platelet abnormalities → microhemorrhage: mucous membrane bleeding, epistaxis, petechiae,
purpura, ↑ bleeding time, possibly decreased platelet count (PC).

Question 7

Be____-So___ syndrome
Defect in platelet plug formation. ____ platelets.
_ GpI_ → defect in platelet-to-___ adhesion.
__ agglutination on _______ cofactor assay.

Answer 7

Bernard-Soulier syndrome
Defect in platelet plug formation. Large platelets.
↓ GpIb → defect in platelet-to-vWF adhesion.
No agglutination on ristocetin cofactor assay.

Question 8

G___mann _________nia
Defect in platelet ____ formation.
↓ Gp__/III_ → defect in platelet-to-_____ aggregation.
Labs: blood smear shows __ platelet ______.
yes , ________ with ristocetin cofactor assay.

Answer 8

Glanzmann thrombasthenia
Defect in platelet plug formation.
↓ GpIIb/IIIa → defect in platelet-to-platelet aggregation.
Labs: blood smear shows no platelet clumping.
Agglutination with ristocetin cofactor assay.

Question 9

Disseminated intravascular coagulation (DIC), life threatining.
Widespread activation of clotting → ________ in clotting factors → ________ state !. which causes ?

(STOP Making New Thrombi).

Answer 9

Widespread activation of clotting → deficiency in clotting factors → bleeding state.
Causes: Sepsis (gram-negative), Trauma,
Obstetric complications, acute Pancreatitis,
Malignancy, Nephrotic syndrome,
Transfusion

Question 10

DIC (Diss. intravascular coag.)

Labs: _______, ↑ fibrin split products (_-dimers), ↓ fibr____, ↓ factors _ and __.

Answer 10

DIC

Labs: schistocytes, ↑ fibrin split products (d-dimers), ↓ fibrinogen, ↓ factors V and VIII.

Question 11

DIC is a ___, life-________ condition that prevents blood from clotting normally. The blood-clots ______ blood flow and can _______ blood from reaching bodily organs. This increased clotting can use-___ the blood’s platelets and ______-factors.
_____ platelets and clotting factors available result in → ________ bleeding.

Answer 11

DIC is a rare, life-threatening condition that prevents blood from clotting normally. The blood-clots reduce blood flow and can block blood from reaching bodily organs. This increased clotting can use-up the blood’s platelets and clotting-factors.
Fewer platelets and clotting factors available result in → excessive bleeding.

Question 12

____-Sternberg cells
Distinctive tumor ___ cell seen in ______ disease; binucleate or __lobed with the _ halves as mirror images (“owl eyes” A ). RS cells are CD__+ and CD__+ _-cell origin. Necessary but __ ______ for a diagnosis of Hodgkin disease.
Merke → 2 owl eyes × 15 = 30 :)

Answer 12

Reed-Sternberg cells
Distinctive tumor giant cell seen in Hodgkin disease; binucleate or bilobed with the 2 halves as mirror images (“owl eyes” A ). RS cells are CD15+ and CD30+ B-cell origin. Necessary but not sufficient for a diagnosis of Hodgkin disease.
Merke → 2 owl eyes × 15 = 30 :)

Question 13

Hodgkin
______, _____ group of nodes; extranodal ___; _________ spread (____ is strongest ______ of prognosis). Prognosis is much _____ than with ___-Hodgkin lymphoma.
__modal distribution: ______ adulthood, and
> __ years; more common in ___ except for
______ scl____ type.

Answer 13

Hodgkin
Localized, single group of nodes; extranodal rare; contiguous spread (stage is strongest predictor of prognosis). Prognosis is much better than with non-Hodgkin lymphoma.
Bimodal distribution: young adulthood, and
> 55 years; more common in men except for
nodular sclerosing type.

Question 14

Hodgkin
No_____ sclerosing-form _____ common (affects women and men ____). Lymphocyte-____ form has ___ prognosis. Lymphocyte _____ or dep____-forms (verbraucht) have _____ prognosis.
Strongly associated with ___ ?

Answer 14

Hodgkin
Nodular sclerosing form most common (affects women and men equally). Lymphocyte-rich form has best prognosis. Lymphocyte mixed or depleted forms have worse prognosis.
Strongly associated with EBV