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Review / Wrong Answers > DIT review - Heme 3 > Flashcards

DIT review - Heme 3 Flashcards

1
Q

What does HELLP syndrome stand for?

A
  • Stands for:
    • H - Hemolysis (anemia)
    • EL - Elevated Liver enzymes (RUQ pain, jaundice)
    • LP - Low Platelets (bruising bleeding)
  • Preeclampsia + thrombotic microangiopathy
    • Hemolysis = thrombi causing schistocytes
    • Liver enzymes = lack of RBCs leads to infarction of liver tissue
    • Platelets = all used up in thrombi
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2
Q

Describe the steps of platelet plug formation (trigger, adhesions, activation, aggregation)

A
  • (1) Endothelial damage - transient vasoconstriction
    • Via neural stimulation reflex and endothelin (released from damaged cell)
  • (2) Platelet adhesion
    • Won Willebrand factor (vWF) binds to exposed subendothelial collagen
      • vWF from Weibel-Palade bodies of endothelial cells and a-granules of platelets
    • Platelets bind vWF via GPIb receptor and undergo conformational change
  • (3) Platelet activation/degranulation
    • Platelets shape change causes degranulation with release of:
      • ADP – promotes exposure of GPIIb/IIIa receptor on platelet surface
      • TXA2 – synthesized by platelet COX and promotes vasoconstriction and aggregation
      • Ca2+ – needed to activate the coagulation cascade
      • Fibrinogen
  • (4) Platelet aggregation
    • Platelets link to each other via GP2b3a, using fibrinogen as a linking molecule
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3
Q

MOA of Aspirin

A
  • Inhibits the COX, thus halting the synthesis of TXA2
    • ASA acts by covalently attaching an acetyl group to COX (both COX-1 and COX-2) enzyme, causing IRREVERSIBLE inhibition (lasts for the life-time of the platelet until new ones are produced in about 1 week)
  • Inhibition of TXA2 leads to inhibition of platelet aggregation
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4
Q

What are the names of the ADP receptor inhibitors

A
  • Clopidogrel, Ticagrelor, Prasugrel, Ticlopidine
  • Sketchy - hot dog grill
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5
Q

MOA of ADP receptor antagonists

A

Inhibiting ADP receptors = decreased expression of GP2b3a = decreased platelet aggregation

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6
Q

What are the names of the GP2b3a antagonists

A
  • Abciximab - ABC sports caster
  • Eptifibatide - tied game
  • Tirofiban - tied game
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7
Q

What are the names of phosphodiesterase inhibitors

A

Sketchy: “Don’t PHOSTER DISINTEREST” sign

Drugs:

  • Dipyridamole - two pyramids as top of tent
  • Cilostazol - lost the ball
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8
Q

MOA of phosphodiesterase inhibitors

A
  • Inhibition of phosphodiesterase leads to increases cAMP within the platelet which will activate protein kinase A, and impairing platelet function and aggregation
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9
Q

MOA of GP2b3a antagonists

A

Block GP2b3a, so it cannot bind fibrinogen = decreased platelet aggregation

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10
Q

What is the most common inherited bleeding disorder

A

von Willebrand disease

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11
Q

What will be the lab findings in von Willebrand disease (BT, PT, PTT)

A
  • Increased bleeding time – decreased platelet adhesion
  • Increased PTT – vWF normally stabilizes Factor VIII
  • Normal PT
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12
Q

Treatment of von Willebrand disease

A
  • Desmopressin – increases vWF release from Weibel-Palade bodies of endothelial cells
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13
Q

Describe the pathogenesis behind DIC

A
  • Widespread activation of clotting
  • This consumes all platelets and coagulation factors, resulting in bleeding
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14
Q

Findings in DIC

A
  • Increased bleeding time – low platelets
  • Increased PT and PTT
  • Low fibrinogen – being used up
  • High D-dimer (fibrin split products)
  • Schistocytes
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15
Q

Causes of DIC

A
  • STOP Making New Thrombi
    • Sepsis
    • Trauma
    • Obstetric complications
    • Acute Pancreatitis
    • Malignancy
    • Nephrotic syndrome
    • Transfusion
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16
Q
A
17
Q

Describe the cause of Immune thrombocytopenia (ITP)

A
  • IgG autoantibodies to GP2b3a
  • Antibodies produced by plasma cells of spleen and antibody-bound platelets consumed by macrophages of spleen
18
Q

Findings of immune thrombocytopenia

A
  • Decreased platelet count
  • Increased megakaryocytes on bone marrow biopsy
19
Q

Treatment of immune thrombocytopenia

A
  • Steroids and IVIG (autoimmune treatment)
  • Splenectomy
20
Q

Describe the defect in thrombotic thrombocytopenic purpura (TTP)

A
  • Platelets used up in pathologic formation of microthrombi in small vessels
  • Due to decreased ADAMTS13, enzyme that normally cleaves vWF for degradation
    • No vWF degradation = abnormal platelet adhesion = microthrombi
21
Q

Describe the findings in TTP

A
  • Pentad of findings
    • Thrombocytopenia = platelets being used up
    • Microangiopathic hemolytic anemia = RBCs sheared by microthrombi
    • Renal insufficiency (thrombi involve vessels of the kidney)
    • Neurological symptoms (confusion, HA, seizures, coma) – thrombi involve vessels of CNS
    • Fever
22
Q

Describe the defect in hemolytic uremic syndrome (HUS)

A
  • Platelets used up in pathologic formation of microthrombi in small vessels
  • Commonly caused by Shiga toxin-producing E. Coli O157:H7 (STEC)
    • Accompanied with diarrhea
23
Q

Findings in HUS

A
  • Findings (triad):
    • Microangiopathic hemolytic anemia
    • Renal insufficiency (thrombi involve vessels of the kidney)
    • Thrombocytopenia
24
Q

Describe the defect in Bernard-Soulier syndrome

A
  • Defect of glycoprotein 1b
  • Platelet can’t bind to vWF on collagen = defect of platelet plug formation
25
Q

Findings in Bernard Soulier

A
  • Platelet count is only slightly low – moderate thrombocytopenia
  • Large platelets
26
Q

Describe the defect in Glanzmann thrombasthenia

A
  • Genetic GP2b3a deficiency
  • Defect in platelet aggregation
27
Q

Describe the finding in Glanzmann thrombasthenia

A

Platelet count is normal (they aren’t being destroyed, just can’t aggregate)

28
Q

What is the difference between Leukemia and Lymphoma

A
  • Leukemia:
    • Malignancy within bone marrow or peripheral blood
  • Lymphoma:
    • Malignancy within lymph nodes
29
Q

Describe the basic difference between Hodgkin and Non-Hodgkin lymphoma

A

Hodgkin - Rare neoplastic cells (Reed-Sternberg cells) which secrete cytokine that draw in inflammatory cells, leading to a mass

Non-Hodgkin - Whole mass composed of malignant cells

30
Q

Describe Reed-Sternberg cells and their surface markers

A
  • Large cells with multiple/bi-lobed nuclei with clearing around the nuclei (“owl-eye”)
  • RS cells are CD15+ and CD30+
    • THINK: 2 owl eyes x 15 = 30
31
Q

Which lymphoma is found in a single group of lymph nodes and rarely extranodal vs. multiple lymph node and extranodal involvment

A
  • Hodgkin
    • Found in a single group of lymph nodes
    • Extranodal involvement is rare
  • Non-Hodgkin
    • Can be in multiple different lymph nodes
    • Often extranodal (GI tract, thyroid, CNS)
32
Q

Which lymphoma is associated with B-symptoms

A

Hodgkin - Due to cytokine released by RS cells

33
Q

Describe age distribution of Hodgkin vs. Non-hodgkin lymphoma

A

Hodgkin - bimodal distribution (peak at 20 and 65 y/o)

NHL - variable age range

34
Q

Describe the disease associated with Hodgkin and NHL

A

Hodgkin - EBV

NHL - HIV and autoimmune

35
Q

What is the most common type of Hodgkin lymphoma

A

Nodular sclerosing type

36
Q

What type of Hodgkin lymphoma has the best prognosis

A

Lymphocyte-predominant

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