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First Aid > Hematology and Oncology - Pathology (2) > Flashcards

Hematology and Oncology - Pathology (2) Flashcards

1
Q

Coagulation disorders

  • PT
  • PTT
A
  • PT
    • Tests function of common and extrinsic pathway (factors I, II, V, VII, and X).
    • Defect –> increased PT.
  • PTT
    • Tests function of common and intrinsic pathway (all factors except VII and XIII).
    • Defect –>Ž increased PTT.
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2
Q

Hemophilia A or B

  • Type of disorder
  • PT
  • PTT
  • Mechanism and comments
  • Treatment
A
  • Type of disorder
    • Coagulation disorder
  • PT
    • No effect
  • PTT
    • Increased
  • Mechanism and comments
    • Intrinsic pathway coagulation defect.
      • A: deficiency of factor VIII –>Ž increased PTT.
      • B: deficiency of factor IX –>Ž increased PTT.
    • Macrohemorrhage in hemophilia
      • Hemarthroses (bleeding into joints), easy bruising, increased PTT.
  • Treatment
    • Recombinant factor VIII (in hemophilia A).
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3
Q

Vitamin K deficiency

  • Type of disorder
  • PT
  • PTT
  • Mechanism and comments
A
  • Type of disorder
    • Coagulation disorder
  • PT
    • Increased
  • PTT
    • Increased
  • Mechanism and comments
    • General coagulation defect.
    • Bleeding time normal.
    • Decreased synthesis of factors II, VII, IX, X, protein C, protein S.
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4
Q

Platelet disorders

A
  • Defects in platelet plug formation –>Ž increased bleeding time (BT).
  • Platelet abnormalities –>Ž microhemorrhage:
    • Petechiae
    • Mucous membrane bleeding
    • Purpura
    • Increased bleeding time
    • Possible decreased platelet count (PC)
    • Epistaxis
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5
Q

Bernard-Soulier syndrome

  • Type of disorder
  • PC
  • BT
  • Mechanism
A
  • Type of disorder
    • Platelet disorder
  • PC
    • Decreased
  • BT
    • Increased
  • Mechanism
    • Defect in platelet plug formation.
    • Decreased GpIb –>Ž defect in platelet-to-vWF adhesion.
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6
Q

Glanzmann thrombasthenia

  • Type of disorder
  • PC
  • BT
  • Mechanism
  • Labs
A
  • Type of disorder
    • Platelet disorder
  • PC
    • No effect
  • BT
    • Increased
  • Mechanism
    • Defect in platelet plug formation.
    • Decreased GpIIb/IIIa Ž–> defect in platelet-to-platelet aggregation.
  • Labs
    • Blood smear shows no platelet clumping.
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7
Q

Immune thrombocytopenia

  • Type of disorder
  • PC
  • BT
  • Mechanism
  • Labs
A
  • Type of disorder
    • Platelet disorder
  • PC
    • Decreased
  • BT
    • Increased
  • Mechanism
    • Defect: anti-GpIIb/IIIa antibodies –>Ž splenic macrophage consumption of platelet/antibody complex.
      • May be triggered by viral illness.
    • Decreased platelet survival.
  • Labs
    • Increased megakaryocytes on bone marrow biopsy.
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8
Q

Thrombotic thrombocytopenic purpura

  • Type of disorder
  • PC
  • BT
  • Mechanism
  • Pathogenesis
  • Labs
  • Symptoms
  • Treatment
A
  • Type of disorder
    • Platelet disorder
  • PC
    • Decreased
  • BT
    • Increased
  • Mechanism
    • Inhibition or deficiency of ADAMTS 13 (vWF metalloprotease) –>Ž decreased degradation of vWF multimers.
  • Pathogenesis
    • Increased large vWF multimers –>Ž increased platelet adhesion –> increased platelet aggregation and thrombosis.
    • Decreased platelet survival
  • Labs
    • Schistocytes, increased LDH.
  • Symptoms
    • Pentad of neurologic and renal symptoms, fever, thrombocytopenia, and microangiopathic hemolytic anemia.
  • Treatment
    • Exchange transfusion and steroids.
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9
Q

von Willebrand disease

  • Type of disorder
  • PC
  • BT
  • PT
  • PTT
  • Mechanism
  • Diagnosis
  • Treatment
A
  • Type of disorder
    • Mixed platelet and coagulation disorder
  • PC
    • No effect
  • BT
    • Increased
  • PT
    • No effect
  • PTT
    • No effect or increased
  • Mechanism
    • Intrinsic pathway coagulation defect
      • Decreased vWF –>Ž normal or increased PTT
      • Depends on severity;
      • vWF acts to carry/protect factor VIII
    • Defect in platelet plug formation
      • Decreased vWF –>Ž defect in platelet-to-vWF adhesion.
    • Mild but most common inherited bleeding disorder.
    • Autosomal dominant.
  • Diagnosis
    • Diagnosed in most cases by ristocetin cofactor assay
    • Decreased agglutination is diagnostic
  • Treatment
    • DDAVP, which releases vWF stored in endothelium.
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10
Q

DIC

  • Type of disorder
  • PC
  • BT
  • PT
  • PTT
  • Mechanism
  • Causes
  • Labs
A
  • Type of disorder
    • Mixed platelet and coagulation disorder
  • PC
    • Decreased
  • BT
    • Increased
  • PT
    • Increased
  • PTT
    • Increased
  • Mechanism
    • Widespread activation of clotting leads to a deficiency in clotting factors, which creates a bleeding state.
  • Causes
    • Sepsis (gram-negative), Trauma, Obstetric complications, acute Pancreatitis, Malignancy, Nephrotic syndrome, Transfusion
    • STOP Making New Thrombi
  • Labs
    • Schistocytes, increased fibrin split products (d-dimers), decreased fibrinogen, decreased factors V and VIII.
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11
Q

Hereditary thrombosis syndromes leading to hypercoagulability

  • Factor V Leiden
  • Prothrombin gene mutation
  • Antithrombin deficiency
  • Protein C or S deficiency
A
  • Factor V Leiden
    • Production of mutant factor V that is resistant to degradation by activated protein C.
    • Most common cause of inherited hypercoagulability in whites.
  • Prothrombin gene mutation
    • Mutation in 3′ untranslated region –>Ž increased production of prothrombin –> increased plasma levels and venous clots.
  • Antithrombin deficiency
    • Inherited deficiency of antithrombin: has no direct effect on the PT, PTT, or thrombin time but diminishes the increase in PTT following heparin administration.
    • Can also be acquired: renal failure/nephrotic syndrome –>Ž antithrombin loss in urine –>Ž increased factors II and X.
  • Protein C or S deficiency
    • Decreased ability to inactivate factors V and VIII. 
    • Increased risk of thrombotic skin necrosis with hemorrhage following administration of warfarin.
    • Skin and subcutaneous tissue necrosis after warfarin administration –>Ž think protein C deficiency.
    • “Protein C Cancels Coagulation.”
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12
Q

Blood transfusion therapy

  • Blood transfusion risks
  • For each
    • Dosage effect
    • Clinical use
  • Packed RBCs
  • Platelets
  • Fresh frozen plasma
  • Cryoprecipitate
A
  • Blood transfusion risks
    • Infection transmission (low)
    • Transfusion reactions
    • Iron overload
    • Hypocalcemia (citrate is a calcium chelator)
    • Hyperkalemia (RBCs may lyse in old blood units).
  • Packed RBCs 
    • Dosage effect: Increases Hb and O2 carrying capacity
    • Clinical use: Acute blood loss, severe anemia
  • Platelets 
    • Dosage effect: Increases platelet count (increase ~5000/mm3/unit)
    • Clinical use: Stop significant bleeding (thrombocytopenia, qualitative platelet defects)
  • Fresh frozen plasma 
    • Dosage effect: Increases coagulation factor levels
    • Clinical use: DIC, cirrhosis, warfarin overdose, exchange transfusion in TTP/HUS
  • Cryoprecipitate
    • Dosage effect: Contains fibrinogen, factor VIII, factor XIII, vWF, and fibronectin
    • Clinical use: Treat coagulation factor deficiencies involving fibrinogen and factor VIII
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13
Q

Leukemia vs. lymphoma

  • Leukemia
  • Lymphoma
A
  • Leukemia
    • Lymphoid or myeloid neoplasms with widespread involvement of bone marrow.
    • Tumor cells are usually found in peripheral blood.
  • Lymphoma
    • Discrete tumor masses arising from lymph nodes.
    • Presentations often blur definitions.
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14
Q

Reactions

  • Leukemoid reaction
  • CML
A
  • Leukemoid reaction
    • Acute inflammatory response to infection. 
    • Increased WBC count with increased neutrophils and neutrophil precursors such as band cells (left shift)
    • Increased leukocyte ALP.
  • CML
    • Also increased WBC count with left shift
    • Decreased leukocyte ALP).
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15
Q

Hodgkin vs. non‑Hodgkin lymphoma

  • Location
  • Characteristics
  • Age
  • Associations
  • Constitutional sign / symptoms
A
  • Location
    • H: Localized, single group of nodes
      • Extranodal rare
      • Contiguous spread (stage is strongest predictor of prognosis).
      • Prognosis is much better than with non-Hodgkin lymphoma.
    • NH: Multiple, peripheral nodes
      • Extranodal involvement common
      • Noncontiguous spread
  • Characteristics
    • H: Characterized by Reed-Sternberg cells
    • NH: Majority involve B cells (except those of lymphoblastic T-cell origin)
  • Age
    • H: Bimodal distribution
      • Young adulthood and > 55 years
      • More common in men except for nodular sclerosing type
    • NH: Peak incidence for certain subtypes at 20–40 years old
  • Associations
    • H: 50% of cases associated with EBV
    • NH: May be associated with HIV and immunosuppression
  • Constitutional sign / symptoms
    • H: Constitutional (“B”) signs/symptoms—low-grade fever, night sweats, weight loss
    • NH: Fewer constitutional signs/symptoms
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16
Q

Reed-Sternberg cells

  • Characteristics
  • Prognosis
A
  • Characteristics
    • 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.
      • 2 owl eyes × 15 = 30.
    • Nodular sclerosing form most common (affects women and men equally).
    • Necessary but not sufficient for a diagnosis of Hodgkin disease.
  • Better prognosis with strong stromal or lymphocytic reaction against RS cells.
    • Lymphocyte-rich form has best prognosis.
    • Lymphocyte mixed or depleted forms have poor prognosis.
17
Q

Burkitt lymphoma

  • Type of condition
  • Occurs in…
  • Genetics
  • Comments
A
  • Type of condition
    • Non-Hodgkin lymphoma: neoplasm of mature B cells
  • Occurs in…
    • Adolescents or young adults
  • Genetics
    • t(8;14)—translocation of c-myc (8) and heavy-chain Ig (14)
  • Comments
    • “Starry sky” appearance [A], sheets of lymphocytes with interspersed macrophages (arrows).
    • Associated with EBV.
    • Jaw lesion [B] in endemic form in Africa; pelvis or abdomen in sporadic form.
18
Q

Diffuse large B-cell lymphoma

  • Type of condition
  • Occurs in…
  • Genetics
  • Comments
A
  • Type of condition
    • Non-Hodgkin lymphoma: neoplasm of mature B cells
  • Occurs in…
    • Usually older adults, but 20% in children
  • Genetics
    • t(14;18)
  • Comments
    • Most common type of non-Hodgkin lymphoma in adults.
19
Q

Mantle cell lymphoma

  • Type of condition
  • Occurs in…
  • Genetics
  • Comments
A
  • Type of condition
    • Non-Hodgkin lymphoma: neoplasm of mature B cells
  • Occurs in…
    • Older males
  • Genetics
    • t(11;14)—translocation of cyclin D1 (11) and heavy-chain Ig (14)
  • Comments
    • CD5+.
20
Q

Follicular lymphoma

  • Type of condition
  • Occurs in…
  • Genetics
  • Comments
A
  • Type of condition
    • Non-Hodgkin lymphoma: neoplasm of mature B cells
  • Occurs in…
    • Adults
  • Genetics
    • t(14;18)—translocation of heavy-chain Ig (14) and bcl-2 (18)
  • Comments
    • Indolent course; bcl-2 inhibits apoptosis.
    • Presents with painless “waxing and waning” lymphadenopathy.
21
Q

Adult T-cell lymphoma

  • Type of condition
  • Occurs in…
  • Genetics
  • Comments
A
  • Type of condition
    • Non-Hodgkin lymphoma: neoplasm of mature T cells
  • Occurs in…
    • Adults
  • Genetics
    • Caused by HTLV-1 (associated with IV drug abuse)
  • Comments
    • Adults present with cutaneous lesions
      • Especially affects populations in Japan, West Africa, and the Caribbean.
    • Lytic bone lesions, hypercalcemia.
22
Q

Mycosis fungoides / Sézary syndrome

  • Type of condition
  • Occurs in…
  • Comments
A
  • Type of condition
    • Non-Hodgkin lymphoma: neoplasm of mature T cells
  • Occurs in…
    • Adults
  • Comments
    • Adults present with cutaneous patches [C] / plaques/tumors with potential to spread to lymph nodes and viscera.
    • Circulating malignant cells seen in Sézary syndrome.
    • Indolent, CD4+.
23
Q

Multiple myeloma

  • Definition
  • Associated with:
A
  • Definition
    • Monoclonal plasma cell (“fried egg” appearance) cancer that arises in the marrow and produces large amounts of IgG (55%) or IgA (25%).
    • Most common 1° tumor arising within bone in the elderly (> 40–50 years old).
    • Numerous plasma cells with “clock face” chromatin and intracytoplasmic inclusions containing immunoglobulin [B].
  • Associated with:
    • Increased susceptibility to infection
    • Primary amyloidosis (AL)
    • Punched-out lytic bone lesions on x-ray [A]
    • ƒƒM spike on serum protein electrophoresis
    • Ig light chains in urine (Bence Jones protein)
    • Rouleaux formation (RBCs stacked like poker chips in blood smear)
  • Think CRRAABBB MMeat:
    • hyperCalcemia
    • Renal insufficienc
    • Rouleaux formation
    • Anemia
    • primary Amyloidosis
    • Bone lytic lesions
    • Back pain
    • Bence Jones protein
    • Monoclonal M protein spike
24
Q

Related to multiple myeloma

  • Waldenström macroglobulinemia Ž
  • Monoclonal gammopathy of undetermined significance (MGUS)
A
  • Waldenström macroglobulinemia Ž
    • M spike = IgM
    • –> hyperviscosity symptoms
    • No lytic bone lesions.
  • Monoclonal gammopathy of undetermined significance (MGUS)
    • Monoclonal expansion of plasma cells with serum monoclonal protein < 3g/dL (“M spike”) and bone marrow with < 10% monoclonal plasma cells.
    • Asymptomatic precursor to multiple myeloma.
    • Patients with MGUS develop multiple myeloma at a rate of 1–2% per year.
25
Q

Myelodysplastic syndromes

  • Definition
  • Pseudo–Pelger-Huet anomaly
A
  • Definition
    • Stem cell disorders involving ineffective hematopoiesis –>Ž defects in cell maturation of all non-lymphoid lineages.
    • Caused by de novo mutations or environmental exposure (e.g., radiation, benzene, chemotherapy).
    • Risk of transformation to AML.
  • Pseudo–Pelger-Huet anomaly
    • Neutrophils with bilobed nuclei (two nuclear masses connected with a thin filament of chromatin) typically seen after chemotherapy.
26
Q

Leukemias

A
  • Unregulated growth of leukocytes in bone marrow
    • –>Ž increased or decreased number of circulating leukocytes in blood and marrow failure Ž
    • –> anemia (decreased RBCs), infections (decreased mature WBCs), and hemorrhage (decreased platelets)
  • Leukemic cell infiltrates in liver, spleen, and lymph nodes are possible.
27
Q

Acute lymphoblastic leukemia/lymphoma (ALL)

  • Type of condition
  • Age
  • Characteristics
A
  • Type of condition
    • Leukemia: lymphoid neoplasm
  • Age
    • < 15 years
  • Characteristics
    • T-cell ALL can present as mediastinal mass (leukemic infiltration of the thymus).
    • Associated with Down syndrome.
    • Peripheral blood and bone marrow have really really increased lymphoblasts [A].
    • TdT+ (marker of pre-T and pre-B cells), CD10+ (pre-B cells only).
    • Most responsive to therapy.
    • May spread to CNS and testes.
    • t(12;21) –>Ž better prognosis.
28
Q

Small lymphocytic lymphoma (SLL)/ chronic lymphocytic leukemia (CLL)

  • Type of condition
  • Age
  • Characteristics
A
  • Type of condition
    • Leukemia: lymphoid neoplasm
  • Age
    • > 60 years
  • Characteristics
    • CD20+, CD5+ B-cell neoplasm.
    • Often asymptomatic, progresses slowly
    • Smudge cells [B] in peripheral blood smear
    • Autoimmune hemolytic anemia.
    • SLL same as CLL except CLL has increased peripheral blood lymphocytosis or bone marrow involvement.
29
Q

Hairy cell leukemia

  • Type of condition
  • Age
  • Characteristics
  • Treatment
A
  • Type of condition
    • Leukemia: lymphoid neoplasm
  • Age
    • Adults.
  • Characteristics
    • Mature B-cell tumor in the elderly.
    • Cells have filamentous, hair-like projections [C] .
    • Stains TRAP (tartrate-resistant acid phosphatase (+)).
    • TRAP stain largely replaced with flow cytometry.
    • Causes marrow fibrosis –>Ž dry tap on aspiration.
  • Treatment
    • Cladribine (2-CDA), an adenosine analog (inhibits adenosine deaminase).
30
Q

Acute myelogenous leukemia (AML)

  • Type of condition
  • Age
  • Characteristics
  • Risk factors
A
  • Type of condition
    • Leukemia: myeloid neoplasm
  • Age
    • Median onset 65 years
  • Characteristics
    • Auer rods [D]
    • Peroxidase (+) cytoplasmic inclusions seen mostly in M3 AML
    • Really really increased circulating myeloblasts on peripheral smear
    • t(15;17) –>Ž M3 AML subtype responds to all-trans retinoic acid (vitamin A), inducing differentiation of myeloblasts
    • DIC is a common presentation in M3 AML and can be induced by chemotherapy due to release of Auer rods.
  • Risk factors
    • Prior exposure to alkylating chemotherapy, radiation, myeloproliferative disorders, Down syndrome.
31
Q

Chronic myelogenous leukemia (CML)

  • Type of condition
  • Age
  • Characteristics
  • Treatment
A
  • Type of condition
    • Leukemia: myeloid neoplasm
  • Age
    • Peak incidence 45–85 years, median age at diagnosis 64 years
  • Characteristics
    • Defined by the Philadelphia chromosome (t[9;22], bcr-abl)
    • Myeloid stem cell proliferation
    • Presents with increased neutrophils, metamyelocytes, basophils [E], splenomegaly
    • May accelerate and transform to AML or ALL (“blast crisis”).
    • Very low leukocyte alkaline phosphatase (LAP) as a result of low activity in mature granulocytes (vs. leukemoid reaction, in which LAP is increased).
  • Treatment
    • Responds to imatinib (a small-molecule inhibitor of the bcr-abl tyrosine kinase).
32
Q

Disorders associated with these chromosomal translocations

  • t(9;22)
  • t(8;14)
  • t(11;14)
  • t(14;18)
  • t(15;17)
A
  • t(9;22) (Philadelphia chromosome)
    • CML (bcr-abl hybrid)
    • Philadelphia CreaML cheese.
  • t(8;14)
    • Burkitt lymphoma (c-myc activation)
  • t(11;14)
    • Mantle cell lymphoma (cyclin D1 activation)
  • t(14;18)
    • Follicular lymphomas (bcl-2 activation)
    • Diffuse large B-cell lymphoma
  • t(15;17)
    • M3 type of AML (responsive to all-trans retinoic acid)
33
Q

Langerhans cell histiocytosis

  • Definition
  • Presentation
A
  • Definition
    • Proliferative disorders of dendritic (Langerhans) cells from monocyte lineage.
    • Cells are functionally immature and do not efficiently stimulate primary T lymphocytes via antigen presentation.
    • Cells express S-100 (mesodermal origin) and CD1a.
  • Presentation
    • Presents in a child as lytic bone lesions [A] and skin rash or as recurrent otitis media with a mass involving the mastoid bone.
    • Birbeck granules (“tennis rackets” on EM) are characteristic [B].
34
Q

Chronic myeloproliferative disorders

  • Definition
  • Disorders
A
  • Definition
    • The myeloproliferative disorders represent an often-overlapping spectrum
    • JAK2 is involved in hematopoietic growth factor signaling.
    • Mutations are implicated in myeloproliferative disorders other than CML.
  • Disorders
    • Polycythemia vera
    • Essential thrombocytosis
    • Myelofibrosis
    • CML
35
Q

Polycythemia vera

  • Type of disorder
  • Definition
  • RBCs (increased/decreased)
  • WBCs (increased/decreased)
  • Platelets (increased/decreased)
  • Philadelphia chromosome (+/-)
  • JAK2 mutations(+/-)
A
  • Type of disorder
    • Chronic myeloproliferative disorder
  • Definition
    • Hematocrit > 55%, somatic (non-hereditary) mutation in JAK2 gene.
    • 2° polycythemia is via natural or artificial increases in EPO levels.
  • Presentation
    • Often presents as intense itching after hot shower.
    • Rare but classic symptom is erythromelalgia (severe, burning pain and reddish or bluish coloration) due to episodic blood clots in vessels of the extremities [A].
  • RBCs
    • Increased
  • WBCs
    • Increased
  • Platelets
    • Increased
  • Philadelphia chromosome
    • (-)
  • JAK2 mutations
    • (+)
36
Q

Essential thrombocytosis

  • Type of disorder
  • Definition
  • RBCs (increased/decreased)
  • WBCs (increased/decreased)
  • Platelets (increased/decreased)
  • Philadelphia chromosome (+/-)
  • JAK2 mutations(+/-)
A
  • Type of disorder
    • Chronic myeloproliferative disorder
  • Definition
    • Similar to polycythemia vera, but specific for overproduction of abnormal platelets –>Ž bleeding, thrombosis.
    • Bone marrow contains enlarged megakaryocytes [B].
  • RBCs
    • No effect
  • WBCs
    • No effect
  • Platelets
    • Increased
  • Philadelphia chromosome
    • (-)
  • JAK2 mutations
    • (+) (30-50%)
37
Q

Myelofibrosis

  • Type of disorder
  • Definition
  • RBCs (increased/decreased)
  • WBCs (increased/decreased)
  • Platelets (increased/decreased)
  • Philadelphia chromosome (+/-)
  • JAK2 mutations(+/-)
A
  • Type of disorder
    • Chronic myeloproliferative disorder
  • Definition
    • Fibrotic obliteration of bone marrow [C].
    • Teardrop RBCs and immature forms of the myeloid line.
      • “Bone marrow is crying because it’s fibrosed.”
  • RBCs
    • Decreased
  • WBCs
    • Variable
  • Platelets
    • Variable
  • Philadelphia chromosome
    • (-)
  • JAK2 mutations
    • (+) (30-50%)
38
Q

CML

  • Type of disorder
  • Definition
  • Treatment
  • RBCs (increased/decreased)
  • WBCs (increased/decreased)
  • Platelets (increased/decreased)
  • Philadelphia chromosome (+/-)
  • JAK2 mutations(+/-)
A
  • Type of disorder
    • Chronic myeloproliferative disorder
  • Definition
    • bcr-abl transformation leads to increased cell division and inhibition of apoptosis.
  • Treatment
    • Imatinib (Gleevec).
  • RBCs
    • Decreased
  • WBCs
    • Increased
  • Platelets
    • Increased
  • Philadelphia chromosome
    • (+)
  • JAK2 mutations
    • (-)
39
Q

Polycythemia

  • For each
    • Plasma volume (increased/decreased)
    • RBC mass (increased/decreased)
    • O2 saturation (increased/decreased)
    • EPO levels (increased/decreased)
    • Associations
  • Relative
  • Appropriate absolute
  • Inappropriate absolute
  • Polycythemia vera
A
  • Relative
    • Plasma volume: Decreased
    • RBC mass: No effect
    • O2 saturation: No effect
    • EPO levels: No effect
    • Associations: decreased plasma volume (dehydration, burns).
  • Appropriate absolute
    • Plasma volume: No effect
    • RBC mass: Increased
    • O2 saturation: Decreased
    • EPO levels: Increased
    • Associations: Lung disease, congenital heart disease, high altitude.
  • Inappropriate absolute
    • Plasma volume: No effect
    • RBC mass: Increased
    • O2 saturation: No effect
    • EPO levels: Increased
    • Associations: Renal cell carcinoma, Wilms tumor, cyst, hepatocellular carcinoma, hydronephrosis.
      • Due to ectopic EPO.
  • Polycythemia vera
    • Plasma volume: Increased
    • RBC mass: Really increased
    • O2 saturation: No effect
    • EPO levels: Decreased
    • Associations: Due to negative feedback.

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