Heme/onc Flashcards
Definition of anemia
Hgb <12 g/dL in females
Hgb <14 g/dL in males
Decrease in the oxygen carrying capacity of blood
Underproduction of nl erythrocytes
Loss or destruction of circulating erythocytes
A condition, not a dz. Must ID underlying cause
Hx components of iron deficiency anemia
Prior GI surgeries? Blood loss from GI tract, either BRB or melena -Ask pt to quantify if possible -How much blood loss? Female pts- blood loss -Are they menstruating? -If so, quantify the amount of flow on a daily basis and the duration of the cycle Hematuria -Ask pts to quantify if possible -Microscopic: seen on UA -Gross or macroscopic hematuria
PE of iron deficiency anemia
There may be no PE findings Acute (blood loss) -Tachycardia -Orthostatic changes -Heart murmur -Extreme pallor (severe) Chronic- more often asymptomatic -Pallor -Fatigue
Lab and workup for iron deficiency anemia
CBC and iron panel
-CBC will show a decreased hgb, and MCV of <80, MCH of <27 and an MCHC of <32
-Microcytic, hypochromic anemia
Iron panel
-Ferritin and serum iron will be decreased, TIBC will be increased
Tx of iron deficiency anemia- general principles
Can usually be managed by PCP, however, if not improving or requires IV iron therapy, a hematology consult may be necessary.
Meds for iron deficiency anemia
Start with oral iron 325 mg TID after meals
-Ferrous gluconate is generally more easily tolerated
Side effects of iron
Dark stools
GI upset
Constipation
Pts’ response to iron
Some pts will not be able to absorb oral iron d/t poor absorption, esp elderly or with a hx of gastric bypass
These pts will require IV iron
F/u of iron deficiency anemia
Recheck H/H, Fe, ferritin 6-8 wks after starting oral iron.
If there is no improvement or minimal improvement, pts may need to be treated with IV iron
IV meds for iron deficiency anemia
Ferllecit or InFed is given as loading dose weekly to build iron stores. Once anemia is corrected, may treat with maintenance dose
How should symptomatic anemia be treated?
With blood transfusion
Females with heavy menstrual periods should be referred to GYN for exam and possible hormonal manipulation to decrease frequency and flow
Hx of anemia of chronic dz
Any medical hx including: Kidney dz CA Chronic infection Inflammatory dz (such as lupus) Hepatic dz
Lab and workup for anemia of chronic dz
CBC: MCV may be nl or microcytic
Serum iron: nl
Ferritin: may be elevated because ferritin is an acute phase reactant
Some pts may have an undiagnosed chronic dz, so check TSH, RF, ANA, hepatitis serologies
CMP: Creatinine will be elevated in CKD, and AST/ALT may be elevated in liver dz
How to diagnose anemia of chronic dz
A dx of exclusion, which means that other causes of anemia have been excluded
Tx of anemia of chronic dz
Tx of choice is erythropoietin injections
Hgb must be <11.0 in order to receive EPO injections
Procrit 20,000 u SQ given weekly or monthly in order to stimulate the production of RBCs
Hx of vit B12 deficiency
Important to ask about diet in hx. If pt is vegan/vegetarian
Previous surgeries? Gastrectomy or ileal resection?
S/sx of vit B12 deficiency
Glossitis Anorexia/diarrhea Paresthesias Gait disturbances Decreased position and vibratory sensation AMS (in late presentation)
Lab and workup for vit B12 deficiency
CBC: hgb decreased; however, this is macrocytic anemia, therefore, the MCV is >100
Vit B12 decreased
If pernicious anemia, + intrinsic factor antibodies
Tx of vit B12 deficiency
Vit B12 injections
1,000 mcg weekly x4 and then monthly
Can generally be managed by PCP
DDx of anemia with low MCV
Iron deficiency anemia Thalassemic disorders Anemia of chronic dz Sideroblastic anemia Copper deficiency, zinc poisoning
DDx of anemia with nl MCV
Acute blood loss Iron deficiency anemia (early) Anemia of chronic dz Bone marrow suppression -Bone marrow invasion -Acquired pure red blood cell aplasia -Aplastic anemia Chronic renal insufficiency Endocrine dysfunction -Hypothyroidism -Hypopituitarism
DDx of anemia with high MCV
Ethanol abuse Folic acid deficiency Vit B12 deficiency Myelodysplastic syndrome Acute myeloid leukemias Reticulocytosis -Hemolytic anemia -Response to blood loss -Response to appropriate hematinic Drug-induced anemia Liver dz
Hx of thrombophilias
Thrombosis at a young age (age <50 yrs)
FHx of thrombosis
Recurrent thrombosis
Thrombosis in an unusual site (hepatic, mesenteric, or cerebral)
Pregnancies complicated by frequent miscarriage
Idiopathic thrombosis (no known predisposing factors)
What is the most common thrombophilia?
Factor V Leiden
What are other types of hereditary thrombophilias?
Prothrombin gene mutation
MTHFR
PAI
Inheritance pattern of Factor V Leiden
Autosomal dominance
May be heterozygous or homozygous
Dx of Factor V Leiden
APC resistance test
Factor V Leiden genetic testing
-When a mutation is identified, we encourage pts to have family members tested
Tx of Factor V Leiden
Refer to hematology
If a thrombotic even present: Lovenox 1 mg/kg SQ q12h x 7 days with concurrent Coumadin therapy
Coumadin therapy will be needed for at least 6 mos. If another clot occurs, the pt will require lifelong therapy
Hx of thrombocytopenia
FHx? Hx of liver dz? Pregnancy? Alcohol consumption? Meds? -Heparin? Sulfonamides? Thiazides? Cimetidine? Recent illness?
PE of thrombocytopenia
Petechiae (< 3 mm)
Purpura (0.3-1.0 cm)
Ecchymoses (>1.0 cm)
Generalized hemorrhage
What is the hallmark of thrombocytopenia?
Mucocutaneous bleeding
Hallmark numbers of thrombocytopenia
Platelet count < 150K/mm cubed
>80,000/mm cubed- withstand all but most extreme hemostatic challenges (sx, major trauma)
<20,000/mm cubed- spontaneous bleeding
Acute ITP- who does it most commonly occur in?
Children, usually preceding a viral URI
Acute ITP
Self-limited, autoimmune IgG disorder
Antibodies are formed against the platelet membrane
Characteristics of acute ITP
Characterized by an abrupt onset of petechiae, purpura, and hemorrhagic bullae on the skin and mucutaneous membranes
No splenomegaly.
-If splenomegaly and pos thrombocytopenia, look for another underlying cause
Chronic ITP
Develops at any age
More common in women
Usually coexists with another autoimmune disease.
Pts develop petechiae on the skin and mucous membranes
Lab findings of acute ITP
CBC will reveal a platelet count, which is significantly decreased to usually 10,000-20,000
May also see lymphocytosis
Coagulation studies will be nl
Lab findings of chronic ITP
CBC will only reveal platelet count, not as significantly decreased to 25,000-75,000
Tx of acute ITP
Usually resolves spontaneously. Rarely requires prednisone or splenectomy
Tx of chronic ITP
Rarely resolves, and most of the time requires high-dose prednisone.
If no response to prednisone, pts require IVIG.
If pt is still not responding, then splenectomy may be warranted
Characteristics of thrombotic thrombocytopenic purpura
Severe thrombocytopenia With: Purpura Petechiae Pallor Abd pain Microangiopathic hemolytic anemia Fever CNS abnormalities (HA, aphasia, and AMS) Renal failure
Who usually gets TTP?
Usually seen in ages 20-50
Causes of TTP
Sometimes unknown Associated with: Chemo drugs Possibly shigella toxin Pregnancy can increase risk
Lab evaluation of TTP
CBC will reveal anemia, red cell fragments on peripheral smear (schistocytes) and thrombocytopenia
ADAMTS 13 is decreased
Indirect bilirubin is elevated
PE of TTP
Febrile
Skin: petechiae, purpura, jaundice
Neuro: AMS
Abd: splenomegaly
Effects of TTP
Blood vessel blockage -Hemolytic anemia (RBC degradation) Neuro/cardio problems Thrombocytopenia: leads to purpura Kidney failure
Tx of TTP
This is a hematological emergency, so early consultation with hematology is imperative
Corticosteroids
Aggressive plasmapheresis
Avoid transfusion unless catastrophic bleeding, such as intracranial hemorrhage
Median age of onset of AML
60
RFs for AML
Chemical exposures:
-Benzene, previous chemo
Radiation
S/sx of AML
Pallor Fatigue Joint pain Fever Wt loss SOB Persistent and frequent infections Gingival bleeding
PE of AML
Petechiae
Pallor
Gingival edema (d/t leukemic infiltration)
Chloroma (mass of leukemic cells outside of the bone marrow)
Lab evaluation of AML
CBC may reveal: leukocytosis or leukopenia, anemia, thrombocytopenia
Auer rods present in peripheral smear
Uric acid elevated
Cytogenetic studies reveal different chromosomal abnormalities
Definitive dx is done by bone marrow bx
-Reveals pos leukemic blast cells
Tx of AML
Induction (remission inducing chemo) followed by consolidation (destroys the remainder of leukemic cells)
-Cytarabine and idarubicin are generally used
Uric acid levels may become elevated d/t cell breakdown, so allopurinol is taken daily
