Heme/onc Flashcards

1
Q

Definition of anemia

A

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

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2
Q

Hx components of iron deficiency anemia

A
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
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3
Q

PE of iron deficiency anemia

A
There may be no PE findings
Acute (blood loss)
-Tachycardia
-Orthostatic changes
-Heart murmur
-Extreme pallor (severe)
Chronic- more often asymptomatic
-Pallor
-Fatigue
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4
Q

Lab and workup for iron deficiency anemia

A

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

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5
Q

Tx of iron deficiency anemia- general principles

A

Can usually be managed by PCP, however, if not improving or requires IV iron therapy, a hematology consult may be necessary.

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6
Q

Meds for iron deficiency anemia

A

Start with oral iron 325 mg TID after meals

-Ferrous gluconate is generally more easily tolerated

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7
Q

Side effects of iron

A

Dark stools
GI upset
Constipation

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8
Q

Pts’ response to iron

A

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

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9
Q

F/u of iron deficiency anemia

A

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

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10
Q

IV meds for iron deficiency anemia

A

Ferllecit or InFed is given as loading dose weekly to build iron stores. Once anemia is corrected, may treat with maintenance dose

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11
Q

How should symptomatic anemia be treated?

A

With blood transfusion
Females with heavy menstrual periods should be referred to GYN for exam and possible hormonal manipulation to decrease frequency and flow

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12
Q

Hx of anemia of chronic dz

A
Any medical hx including:
Kidney dz
CA
Chronic infection
Inflammatory dz (such as lupus)
Hepatic dz
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13
Q

Lab and workup for anemia of chronic dz

A

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

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14
Q

How to diagnose anemia of chronic dz

A

A dx of exclusion, which means that other causes of anemia have been excluded

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15
Q

Tx of anemia of chronic dz

A

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

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16
Q

Hx of vit B12 deficiency

A

Important to ask about diet in hx. If pt is vegan/vegetarian

Previous surgeries? Gastrectomy or ileal resection?

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17
Q

S/sx of vit B12 deficiency

A
Glossitis
Anorexia/diarrhea
Paresthesias
Gait disturbances
Decreased position and vibratory sensation
AMS (in late presentation)
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18
Q

Lab and workup for vit B12 deficiency

A

CBC: hgb decreased; however, this is macrocytic anemia, therefore, the MCV is >100
Vit B12 decreased
If pernicious anemia, + intrinsic factor antibodies

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19
Q

Tx of vit B12 deficiency

A

Vit B12 injections
1,000 mcg weekly x4 and then monthly
Can generally be managed by PCP

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20
Q

DDx of anemia with low MCV

A
Iron deficiency anemia
Thalassemic disorders
Anemia of chronic dz
Sideroblastic anemia
Copper deficiency, zinc poisoning
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21
Q

DDx of anemia with nl MCV

A
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
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22
Q

DDx of anemia with high MCV

A
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
23
Q

Hx of thrombophilias

A

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)

24
Q

What is the most common thrombophilia?

A

Factor V Leiden

25
Q

What are other types of hereditary thrombophilias?

A

Prothrombin gene mutation
MTHFR
PAI

26
Q

Inheritance pattern of Factor V Leiden

A

Autosomal dominance

May be heterozygous or homozygous

27
Q

Dx of Factor V Leiden

A

APC resistance test
Factor V Leiden genetic testing
-When a mutation is identified, we encourage pts to have family members tested

28
Q

Tx of Factor V Leiden

A

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

29
Q

Hx of thrombocytopenia

A
FHx?
Hx of liver dz?
Pregnancy?
Alcohol consumption?
Meds?
-Heparin? Sulfonamides? Thiazides? Cimetidine?
Recent illness?
30
Q

PE of thrombocytopenia

A

Petechiae (< 3 mm)
Purpura (0.3-1.0 cm)
Ecchymoses (>1.0 cm)
Generalized hemorrhage

31
Q

What is the hallmark of thrombocytopenia?

A

Mucocutaneous bleeding

32
Q

Hallmark numbers of thrombocytopenia

A

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

33
Q

Acute ITP- who does it most commonly occur in?

A

Children, usually preceding a viral URI

34
Q

Acute ITP

A

Self-limited, autoimmune IgG disorder

Antibodies are formed against the platelet membrane

35
Q

Characteristics of acute ITP

A

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

36
Q

Chronic ITP

A

Develops at any age
More common in women
Usually coexists with another autoimmune disease.
Pts develop petechiae on the skin and mucous membranes

37
Q

Lab findings of acute ITP

A

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

38
Q

Lab findings of chronic ITP

A

CBC will only reveal platelet count, not as significantly decreased to 25,000-75,000

39
Q

Tx of acute ITP

A

Usually resolves spontaneously. Rarely requires prednisone or splenectomy

40
Q

Tx of chronic ITP

A

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

41
Q

Characteristics of thrombotic thrombocytopenic purpura

A
Severe thrombocytopenia
With:
Purpura
Petechiae
Pallor
Abd pain
Microangiopathic hemolytic anemia
Fever
CNS abnormalities (HA, aphasia, and AMS)
Renal failure
42
Q

Who usually gets TTP?

A

Usually seen in ages 20-50

43
Q

Causes of TTP

A
Sometimes unknown
Associated with:
Chemo drugs
Possibly shigella toxin
Pregnancy can increase risk
44
Q

Lab evaluation of TTP

A

CBC will reveal anemia, red cell fragments on peripheral smear (schistocytes) and thrombocytopenia
ADAMTS 13 is decreased
Indirect bilirubin is elevated

45
Q

PE of TTP

A

Febrile
Skin: petechiae, purpura, jaundice
Neuro: AMS
Abd: splenomegaly

46
Q

Effects of TTP

A
Blood vessel blockage
-Hemolytic anemia (RBC degradation)
Neuro/cardio problems
Thrombocytopenia: leads to purpura
Kidney failure
47
Q

Tx of TTP

A

This is a hematological emergency, so early consultation with hematology is imperative
Corticosteroids
Aggressive plasmapheresis
Avoid transfusion unless catastrophic bleeding, such as intracranial hemorrhage

48
Q

Median age of onset of AML

A

60

49
Q

RFs for AML

A

Chemical exposures:
-Benzene, previous chemo
Radiation

50
Q

S/sx of AML

A
Pallor
Fatigue
Joint pain
Fever
Wt loss
SOB
Persistent and frequent infections
Gingival bleeding
51
Q

PE of AML

A

Petechiae
Pallor
Gingival edema (d/t leukemic infiltration)
Chloroma (mass of leukemic cells outside of the bone marrow)

52
Q

Lab evaluation of AML

A

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

53
Q

Tx of AML

A

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