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HemOnc > Blood Cell Disorders--Vo > Flashcards

Blood Cell Disorders--Vo Flashcards

1
Q

a reduction in one+ of the major RBC measures

A

Anemia (RBC count (rarely used), Hct, Hgb) (most common hematologic disorder

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2
Q

“normal” Hct/Hgb levels influenced by (5)

A

PREGNANCY (37/12), sex, ^ altitude, hydration status, and age

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3
Q

damage to cells seen on blood smear (3), all schizocytes

A
  1. bite cells
  2. helmet cells
  3. triangle cells
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4
Q

RBCs w/ nuclear remnants, usually cleared out by spleen, but sign of cells leaving bone marrow while incompletely mature–possibly pointing to ________ ________

A

Howel Jolly bodies,

spleen absence

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5
Q

Acnthocytes:
Spur cells indicate:
Burr cells indicate:

A
  1. liver disease

2. renal failure

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6
Q

reticulocytes mature to RBC over ____ days

A

four

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7
Q

normal reticulocyte release:

acute anemia reticulocyte released:

A
  1. w/ 1 day left to mature

2. X 2-3 production released early

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8
Q

*reticulocyte count expressed in

A

% of total RBCs – 1-2% of Hct normally
Corrected:
% retics measured X Pt Hct/ normal Hct

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9
Q

retic index tells you

A

how the bone marrow is responding to the anemia.

absolute (corrected) reticulocytes count : # of days til mature

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10
Q

Reticulocyte index:
1 =
>2 =
<2 =

A
  1. normal
  2. adequate marrow response
  3. hypoproliferative marrow
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11
Q

Iron %’s (3)

A
  1. 65% in hemoglobin in RBCs
  2. 4% in myoglobin
  3. 30% stored as ferritin or hemosiderin in spleen, marrow, and liver
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12
Q

Transferrin =

A

iron + apotransferrrin

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13
Q

measurement of total available spaces for Fe to bind (total empty spaces remaining in the apotransferrin molecule)

A

Total Iron Binding Capacity

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14
Q

The Iron Panel (3)

A
  1. Serum Iron
  2. Total Iron Binding Capacity
  3. Ferritin (total stored iron)
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15
Q

test to detect antibodies that are already bound to the surface of red blood cells

A

Direct Comb’s test

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16
Q

test that looks for unbound circulating antibodies in serum against the RBCs

A

Indirect Comb’s test

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17
Q

Test that separates hemoglobin species according to aa composition (globin subunits)

A

Electrophoresis

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18
Q

Microcytic anemia MCV

A

<80

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19
Q

Cx’s of Microcytic anemias (5)

A
  1. *Fe deficiency anemia
  2. Anemia of Chronic Dz’s / Inflammatory Dz’s
  3. Thalassemia
  4. Sideroblastic anemia
  5. Lead Poisoning
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20
Q

Loss of RBC membrane size and/or structural integrity may lead to

A

Spherocytes

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21
Q

causes of spherocytes (2)

A
  1. hereditary spherocytosis

2. autoimmune hemolytic anemia

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22
Q

irregular adherence of RBCs cx from elevated plasma Globulins called ________ _________ seen in:

A

Rouleaux Formations,

Multiple myeloma

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23
Q

Lot’s of blue means…

A

lots of new

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24
Q

Normocytic anemias MCV

A

80-100 – Many cx’s slide 46

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25
Q

Macrocytic anemia MCV:

causes (3)

A

> 100,

  1. Vit B12 deficiency
  2. Folic acid deficiency
  3. Myelodysplastic disorders
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26
Q

Thalassemia

A

a blood disorder passed down through families (inherited) in which the body makes an abnormal form of hemoglobin, the protein in red blood cells that carries oxygen. The disorder results in excessive destruction of red blood cells, which leads to anemia

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27
Q

most common cause of anemia worldwide

A

iron deficiency anemia (a complication not a dx)

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28
Q

Cx’s of iron deficiency anemia (5) (slide 49)

A
  1. Chronic blood loss
  2. malnutrition
  3. malabsorption
  4. increased demand
  5. Fe+ sequestration (by liver or spleen)
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29
Q

Early Iron deficiency anemia (5)

A
  1. only iron stores low
  2. low ferritin
  3. serum Fe normal
  4. TIBC rises
  5. normal MCV
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30
Q

Stages of Iron deficiency (3)

A
  1. Early
  2. Iron deficient erythropoiesis
  3. iron deficiency anemia
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31
Q

esophageal webs aka

A

Plummer-Vinson Syndrome

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32
Q

Tx for Iron deficiency anemia (3)

A
  1. tx underlying cause
  2. Iron replacement (Fe Sulfate – DI PPI’s–need acidic environment)
  3. Repeat CBC in 2-3 months
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33
Q

Other iron formulations (3)

A
  1. Gluconate
  2. Fumarate (time-release)
  3. Parental (veno-toxic)
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34
Q

iron absorbed in

A

proximal small intestine–thus in pt’s w/ gastric bypass give IV or higher doses of Iron

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35
Q

Anemia of Chronic/ Inflammatory Dz def

A

Anemia occuring as a complication of:

  1. chronic infxn–bac endocarditis, lung abscess
  2. inflammation–arthritis
  3. Cancer–Hodgkin dz, carcinomas
  4. Liver Dz–cirrhosis
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36
Q

inherited disorders involving gene deletions or point mutations resulting in a defect in the structure, function, or production of Hgb

A

Hemoglobinopathies–leads to anemia or even hemolysis

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37
Q

Hemoglobinopatheis (6)

A
  1. Thalassemia (alpha & beta) MOST COMMON
  2. Sickle cell
  3. Hgb C dz
  4. Hgb D dz
  5. Hgb E dz
  6. Hereditary spherocytosis
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38
Q

decreased production of 1,2,3,4 alpha-chain genes

A

Alpha Thalassemia (southeast asia or china)

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39
Q

(4) types of alpha thalassemia

A
  1. silent carrier or alpha thalassemia-2 (aa,a-)
  2. Alph thalassemia-1 (a-,a-) (aa,–)
  3. Hemoglobin H Dz (a-,–)
  4. Hydrops Fetalis (hemoglobin Barts) (–,–) stillborn
40
Q

Alpha Thalassemia Traits (5)

A
  1. mild anemia
  2. MCV LOW
  3. HYPOCHROMIC MICROCYTES
  4. TARGET CELLS
  5. you will see a PROPORTIONALdecrease in all type of hemoglobin
41
Q

if spleen is removed vaccinate for

A

encapsulated organisms

42
Q

Tx for Alpha Thalassemia

A

No tx necessary–genetic counseling

43
Q

Alpha thalassemia has 4 genetic possibilities BUT 2 possible clinical presentations.

A

(xx,x-) asymptomatic

(–,–) stillborn

44
Q

Beta thalassemia

A

gene deletions and point mutations result in reduced or absent beta synthesis

45
Q

beta thalassemia seen in

A
  • persons of greek and mediterranean decent

- chinese, black, asians less common

46
Q

hemoglobin ratios in beta thalassemia

A

increase in the % of Hgb A2 and F compared to hemoglobin A

47
Q

(3) types of Beta Thalassemia

A
  1. trait/ minor (B+,B)(B0,B) MCV 55-75
  2. Intermedia (B+,B+)(B0,B+) 2 mutations but milder
  3. Major (B0,B+)(B0,B0) (Cooley’s Anemia) severe anemia
48
Q

Blood smear is “crazy weird”

A

Beta Thalassemia

49
Q

basophile stippling =

A

lead poisoning

50
Q

those anemieas which result from an ^ in the rate of red cell destruction

A

hemolytic anemias

51
Q

normal adult marrow is able to produce RBCs at _________ X the normal rate

A

6-8X

52
Q

(2) types of hemolytic anemias

A
  1. intrinsic cx

2. extrinsic cx

53
Q

G6PD deficiency most common in

A

Mediterranean and Chinese populations (may see neonatal jaundice)

54
Q

Hct decrease faster than 3%/week indicates (2)

A
  1. blood loss

2. hemolysis– <3%/week = not hemolysis

55
Q

Stand-out Sickle cell Dz symptoms (6)

A
  1. jaundice
  2. pigment gallstones
  3. splenomegaly (early on)
  4. ulcers over lower leg
  5. non healing ulcers on lower legs
  6. RETINOPATHY
56
Q

dactylitis seen in

A

Sickle cell Dz

57
Q

Splenic infarction causes infxn by

A

encapsulated organisms (N. meningitidis, Strep, Hemophilus, Klebsiella)

58
Q

Pt w/ salmonella osteomyelitis think

A

Sickle Cell!

59
Q

“old school” method of Dx sickle cell

A

sickle-Dex test

60
Q
  • Tx mainstay of sickle cell
A

HYDROXYUREA (suppress WBCs, cytotoxic) +

O2, hydration, pain management

61
Q

Parvovirus B19 w/ sickle cell trait think

A

Aplastic crisis (transient arrest in erythropoiesis w/ marked decrease in reticulocytes) r/o w/ retics

62
Q

Most common hemolytic anemia in North Europeans

A

Hereditary Spherocytosis (auto dom)

63
Q

hereditary spherocytosis cx from

A

defect in the membrane protein responsible for the cytoskeletal structure and stability. Decreased SA:V

64
Q

Spherocytes are

A

unable to pass through spleen and are destroyed

65
Q

Hereditary spherocytosis clinical features (4)

A
  1. jaundice
  2. splenomegaly
  3. gallstones (pigmented from ^ bilirubin)
  4. Scleral icterus
66
Q

the only anemia where MCHC is increased

A

Hereditary Spherocytosis

67
Q

Tx for Hereditary spherocytosis (3)

A
  1. folate
  2. splenectomy
  3. possible cholecystectomy
68
Q

G6PD deficiency seen in

A

males of African or Mediterranean descent (X-linked)

69
Q

The G6PD enzyme is critical to

A

the metabolism w/in cells and protects the cells from oxidative stresses–>hemolysis of RBCs

70
Q

G6PD deficiency blood smear

A

Heinz bodies (oxydized Hgb)

71
Q

Most common form of acquired hemolytic anemia (besides malaria)

A

Autoimmune hemolytic anemia AIHA

72
Q

Warm AIHA mediated by

A

IgG –37C–RBC destruction in spleen (EXTRAVASCULAR)–ACUTE ANEMIA, SPLENOMEGALY (distinguishing)

73
Q

Cold AIHA mediated by

A

IgM–<37C–RBC destruction in blood vessels (INTRAVASCULAR)–DECREASED HAPTOGLOBIN (distinguishing)

74
Q

Warm AIHA Tx (5)

A
  1. Glucocorticosteroids (rapid taper)
  2. Chemo
  3. IV Ig
  4. Splenectomy
  5. support RBC production (folate)
75
Q

for AIHA Comb’s test will be positive in

A

Cold and Warm AIHA–history and physical most important dx factor

76
Q

Megaloblastic anemias (2) Roughly the same presentation except:

A
  1. Folate deficiency (NO NEURO SYMP’s)
  2. Vit B12 deficiency (NEURO SYMPTOMS, hyperseg neuts)
    (Defective DNA synth –>disordered RBC maturation–>cytoplasmic RNA acummulation–>larger RBC’s
77
Q

*Megaloblastic WBCs on smear

A

Neutrophils w/ 5+ lobes

78
Q

Neuro effects of vit B12 deficiency

A

Myelin breakdown –> neurological symptoms

79
Q

Vit B12 absorbed in

A

terminal ileum

80
Q

Cx of Vit B12 deficiency (rare)

A
  1. gastrectomy
  2. nutritional (vegan, alcoholism)
  3. Terminal ileal resection
  4. CROHN’S DZ
  5. Competing organisms (worm, bac)
  6. Medications (PPI’s, METFORMIN)
81
Q

autoimmune disorder disallowing against INTRINSIC FACTOR–> Can’t absorb B12

A

Pernicious Anemia

82
Q

HIGH METHYLMALONIC ACID w/ megablastic anemia

A

B12 deficiency

83
Q

Schilling test for

A

B12 deficiency (radioactive labeled B12, ABX, determines if bac causing low B12)

84
Q

Dx of pernicious anemia (3)

A
  1. EGD (visualize gastritis changes)
  2. Bx
  3. measure anti-parietal cell antibodis
85
Q

B12 storage:

Folate storage:

A
  • 2-3 years

- 3 months

86
Q

syndrome of chronic primary hematopoietic failure and attendant pancytopenia (low RBCs, WBCs, and platelets)

A

Aplastic Anemia (1000 cases in US/yr– 15-30yo’s and >60 yo’s)

87
Q

etiologies of aplastic anemia (5)

A
  1. inherited
  2. Idopathic
  3. Medications (Chemo)
  4. Viral (B12, Hep, CMV, HIV)
  5. Radiation exposure
88
Q

bone marrow failure consequences (aplastic anemia)

A
  1. anemia
  2. neutorpenia (recurrent infxn)
  3. thrombocytopenia
89
Q

if Cafe au lait spots and short stature w/ aplastic anemia think

A

Fanconi’s anemia (genetic)

90
Q

Only Tx for Aplastic Anemia

A

bone marrow transplant

91
Q

A myeloproliferative disorder of the hematopoietic progenitor cells in which there is overproduction of phenotypically normal red cells, granulocytes, and pltatelets

A

Polycythemia Vera (mostly RBC line effected)

92
Q

Dx of polycythemia vera (3)

A
  1. PRURITUS (aguagenic)
  2. hepatosplenomegaly
  3. Neuro (headache, dizziness, tinnitus, fatigue)
93
Q

DDx polycythemia vera (2)

A
  1. CML (PHILADELPHIA CHROMOSOME)

2. secondary polycythemia (Hyposemia)

94
Q

Polycythemia vera Labs (4)

A
  1. Hct >50%
  2. platelets >400K
  3. WBC >12K
  4. high B12
95
Q

Tx for polycythemia vera ()

A
  1. prevent thrombosis from hyperviscosity
  2. Myelosuppretion (damage bone marrow to decrease overproduction)
  3. ANAGRELIDE (decrease platelet count)

HemOnc (7 decks)

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