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Hematology Flashcards

1
Q

What is the most common cause of acute Idiopathic Thrombocytopenia in kids?

A

Idiopathic Thrombocytopenia Purpura (ITP

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2
Q

How do you treat ITP?

A
  • Kids: self limiting
  • Adults: coats platelets with antibodies and spleen gets rid of them
    • Steroids (2/3 of pts respond)
    • IVIG (expensive)
    • Platelets-Destroyed by Ab so use in critical pts only
    • Splenectomy
    • New drugs: Rhogam-destroys macrophage activity; Rituximab-monoclonal ab that destroys B cells
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3
Q

What is the Pentad for Thrombocytic Thrombocytopenic Purpura (TTP)? What are the most common sxs?

A
  • F.A.T. R.N
  • Fever, anemia, Thrombocytopenia
  • acute Renal failure, Neurological sxs

C.A.T=CNS sxs, Anemia, Thrombocytopenia

So if a pt has thrombocytoneia and microangiopathic hemolytic anemia==>start thinking TTP!

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4
Q

What is the Pathophysiology of TTP?

A
  • Endothelial injury–>exposes vWF
  • vWF=a big long chain to which PLTs like to adhere
  • An enzyme (ADAMTS-13) likes to cleave these platelets; but in TTP this enzyme is absent
  • local clot is formed–>Narrowed blood vessel
  • Platelets cannot get through without getting squashed–>hemolytic anemia
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5
Q

What are the major sxs of TTP?

A
  • sxs wax and wane (different from HUS)
  • gross hematuria (may be only clue to hemolytic anemia)
  • CNS sxs: Aphasia, hemiparesis, coma
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6
Q

How do you treat TTP?

A
  • Give FFP first
  • Plasma exchange therapy to remove antibodies
  • immunosuppressant therapy
  • Splenectomy
  • IVIG

DO NOT GIVE PLATELETS!! They will KILL the pt with TTP!!

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7
Q

What triad is seen with HUS?

A
  • Hemolytic anemia
  • Thrombocytopenia
  • Acute renal failure
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8
Q

What are the sxs of HUS?

A
  • Constant sxs (diff from TTP)
  • 95% have diarrhea (Ecoli, shiga like toxin)
  • baceria ingested–>3 days—>non-bloody diarrhea–>2 days—>Pain and bloody diarrhea!
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9
Q

How do you diagnose HUS?

A
  • Send for STOOL and URINE culture for Shiga Toxin
    • sending blood culture will NOT help you
  • Lab findings: Schistocytes (remenants of destroyed RBCs), normal Fibrin/Fibrinogen, Increased Bili and LDH, Negative direct coombs, thrombocytopenia
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10
Q

How do you treat HUS?

A
  • Supportive, admit for IVF
  • blood transfusion for Hgb <6
  • Resist giving platelets
  • Antibiotics CAN WORSEN the situation
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11
Q

How do you define Heparin induced thrombocytopenia (HIT)? what are the two types?

A
  • Defined as platelets <150K or >50% drop from basline
  • Type 1: Hours to days after receiving heparin
  • Type II: 4-14 days after receiving heparin–>most common
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12
Q

What are the clinical manifestations of HIT?

A
  • venous thrombosis; The only thrombocytopenia that presents with clots!
  • Skin lesions: skin necrosis, erythematous plaques
  • DIC (10%)
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13
Q

How do you treat HIT?

A
  • Stop Heparin!
  • Change to direct thrombin inhibitor
    • Lepirudin, Argatroban, Bivalirudin
  • NO Platelets or Coumadin
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14
Q

What is the pathophysiology of DIC? causes?

A
  • Endothelial damage leads to release of systemic cytokines
  • Widespread micro-vascular thrombosis
  • Anti-coagulation pathways become impaired
  • Clotting factors and platelets are then consumed rapidly–Sucks up all of your platelets!

Secondary to trauma, sepsis, malignancy, OB emergencies, pancreatitis, liver failure, snake bites, durgs, transplant rejections

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15
Q

How do you diagnose DIC?

A
  • Platelet count-usually less than 50 K
  • Increased D-dimer
  • PT- >6
  • Fibrinogen less than 1.0 g/L
    • Only thrombocytopenia with abnormal fibrin/fibrinogen levels
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16
Q

What types of Thrombocytopenia present with Hemolytic anemia?

A

TTP and HUS

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17
Q

What type of thrombocytopenia presents with a high PT/INR?

A
  • DIC
18
Q

Which types of thrombocytopenia can be treated with platelets?

A

ITP and DIC only

19
Q

Which type of thrombocytopenias commonly present with clots?

A

HIT only

20
Q

Which type of leukemia is most common in children?

A

Acute lymphocytic leukemia (ALL)

21
Q

What do you see on labs with ALL? How do you treat?

A

Pancytopenia and blasts

Tx: Chemotherapy–good prognosis

22
Q

Which type of leukemia has Auer rods?

A

Acute Myelogenous leukemia

23
Q

What is the hallmark of acute leukemia?

A

Pancytopenia with circulating blasts

24
Q

What type of leukemia presents in older adults (>65 y/o)? What are its clinical findings?

A
  • Chronic Lymphocytic leukemia
  • isolated lymphocytosis, really high WBCs!, Smudge cells
  • clonal malignancy of mature B cells
25
Q

What are the unigue characteristics of Chronic Myelogenous leukemia (CML)?

A

Splenomegaly, Wt loss, anemia, thrombocytosis, Philadelphia chromosome, BCR-ABL gene

Transforms to acute leukemia (may be stable for many years and then transform to a blast crisis)

26
Q

Hodgkins vs Non-hodgkins lymphomas

A
  • Hodgkins: Cervical/supraclavicular/mediastinal PAINLESS LAD; Reed sternberg cells seen on LN bx; Good prognosis, Tx: ABVD )adriamycin, bleomycin, Vinblastine, and dacarbazine)
  • NON-hodgkins:
  • diffuse painless LAD, Poor prognosis, Not as responsive to chemo as Hodgkins.
27
Q

What is the triad for Multiple Myeloma?

A

Anema, ARF, and Hypercalcemia

28
Q

What are the common findings of Multiple Myeloma? how is it tx?

A
  • bone destruction and pathological fractures (Punched out skull lesions)
  • Bone pain (2 to tumors growing in the marrow)
  • Rouleaux formation of RBC–>Stacked up RBCs
  • hyperviscosity syndrome
  • SPEP-Monoclonal spike
  • Tx: Thalidomide (flipper limb deformity in fetus of pg woman), dexamethasone, doxorubicin
29
Q

What classically causes Aplastic anemia?

A

Benzene

(idiopathic bone marrow failure, causes pancytopenia)

30
Q

What is G6PD deficiency and what drugs should they avoid?

A
  • X-linked recessive disorder causing a chronic hemolytic state; Common in AA males
  • Avoid oxidative drugs: Dapsone, Primaquine, Sulfonamides (bactrim)
31
Q

What hematologic disorders cause Hemolytic anemia?

A

G6PD deficiency, Sickle cell dz, TTP, HUS, DIC, cancer, and vasculitis

32
Q

What is Thalassemia syndromes? What common lab finding do you find?

A
  • Hereditary anemias in which alpha or beta globulin synthesis is reduced
  • Results in defective hemoglobinization of RBCs (can’t get enough hemoglobin into cells)
  • Lab finding: Microcystosis out of proportion to anemia (VERY LOW MCV with only mildly low Hgb)
33
Q

What is the most common hemophilia?

A

Type A–Factor 8 deficiency

34
Q

What type of hemophilia is known as the christmas dz? and what clotting factor deficiency?

A

Type B–Factor 9 deficiency

35
Q

What is the hallmark of hemophilia?

A

Hemarthrosis (nontraumatic bleeding in a joint) causing significant PAIN

36
Q

What is the most common bleeding disorder?

A

Von Willibrand disease

37
Q

What does Von Willebrand Factor (vWF) do?

A

Allows for platelet adhesion to collagen; Protects factor 8

38
Q

What is Von Willebrand dz? sxs? What lab findings would you see?

A
  • Quantitative or qualitative Defect in vWF (either decreased vWF, nonfunctional vWF, or lack of vWF)
  • sxs: Both primary hemostasis (mucous bleeds and tooth bleeds) and secondary (joint bleeds and CNS bleeds)
  • Labs: Normal platelets (bc not a platelet problem)
  • Prolonged bleeding time
  • Decreased VWF activity
39
Q

What kind of anemia will you see with Lead exposure? how is it diagnosed?

A

Sideroblastic Anemia

Dx: Basophilic stippling, Prussian blue staining of bone marrow; ringed sideroblasts, increased/normal serum iron

40
Q
A

PANCE-Flashcards (11 decks)

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