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Block 1 Week 2 > Introduction to Anemia > Flashcards

Introduction to Anemia Flashcards

1
Q

definition of anemia

A

-reduction of hemoglobin concentration
-is a symptom of disease, not entire disease
-

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2
Q

what does hemoglobin do?

A

-(Hb) in red blood cells, carries O2 from lungs to diff tissues

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3
Q

two different causes of anemia?

A

1) bone marrow working too hard (sickle cell; cells not survive marrow works harder to balance it)
2) bone marrow not working hard enough (in iron deficney, not enough materials to make RBC so bone marrow decreases production)

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4
Q

stages of RBC production?

A

1) stem cells
2) progenitors
3) early precursors
4) reticulocytes
5) mature RBC
6) RBC destruction/turn over

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5
Q

stem cells

A
  • when activated produce many different differentiated cell including RBC
  • make progenitors
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6
Q

progenitors

A

cells have been determined to go forward a certain direction, are committed to be one cell type

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7
Q

early precursors

A

-cells already committed to a lineage; begin to develop morphological characteristics of the lineage (RBC develop hb)

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8
Q

reticulocytes

A
  • last stage of RBC maturation
  • are in blood circulation
  • survive ~24hr, then become mature RBC (survive ~121 days)
  • make up 1% of bone marrow
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9
Q

what does it mean if we have 10% reticulocytes in bone marrow?

A
  • bone marrow is overworked, have an increased demand for RBC
  • potentially anemia
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10
Q

mature RBC destruction/turnover?

A

-break down after 121 days

& replaced by new cells

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11
Q

bone marrow composition?

A
  • usually 50% fat and 50% RBC
  • if 90% fat, indicates aplastic anemia (not making enough blood)
  • has variety of diff cell types to perform range of functions
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12
Q

aplastic anemia

A

-when bone marrow doesn’t produce enough blood cells

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13
Q

erythropoiesis mean?

A

-production of red blood cells

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14
Q

requirements for normal erythropoiesis?

A

1) healthy bone marrow env
2) DNA Synthesis (B12& Folic Acid)
3) Heme synthesis
4) global synthesis
5) erythropoietin
6) other cytokines

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15
Q

hemoglobin structure synthesis?

A
  • made form protein
  • 4 polypeptides (globin); 2 alpha, 2 beta chains
  • 4 heme with iron (non protein) bind one O2 each
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16
Q

erythropoietin?

A
  • hormone produced in kidneys
  • stimulates bone marrow cells to mature into RBC
  • is why kidney failure leads to anemia
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17
Q

causes of anemia?

A

1) bone marrow disorders
2) B12 or Folic acid deficiency
3) chemo
4) iron deficiency
5) protein malnutrition
6) chronic kidney failure
7) chronic blood loss
8) global gene abnormalities effecting protein structure of Hb

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18
Q

hemolytic anemia

A

when RBC are destroyed & removed from bloodstream before normal lifespan is over
-bone marrow can’t make RBC fast enough to replace the lost ones

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19
Q

how classify anemia (x2)?

A

1) RBC size: microcytic, normocytic, macrocytic

2) by mechanism: decreased/increased production, blood loss

20
Q

microcytic anemia?

A
  • small RBC

- typically due to low iron

21
Q

macrocytic anemia?

A
  • large RBC
  • blood with an insufficient concentration of hemoglobin
  • due to B12 & folic acid deficiency
22
Q

steps to diagnose anemia?

A

1) history
2) physical exam
3) CBC & reticulocyte count
4) peripheral smear
5) Hb electrophoresis
6) chemistry & other labs
7) bone marrow biopsy

23
Q

erythrocytes?

A

-are RBC

24
Q

-normal hemoglobin? how can one person w/ 9hb be totally fine & other be winded & exhausted?

A
  • 13-15g
  • if born w/ 9hb; body adapts to it and feel fine
  • other has acute anemia; a sudden bleeding ulcer and suddenly hit hb 9 & feel exhausted
  • need to ask about periods & any bleeding when diagnosing
25
Q

Why see jaundice in anemia?

A

-because heme breaks down to billirueben, if have excess hemoglobin means excess heme means breakdown will affect the liver & billirueben amount in your body

26
Q

-CBC results?

A

-if CBC shows low RBC and WBC, platelets means effecting all cells in bone marrow means BONE MARROW disease; anemia just effects RBC

27
Q

high reticulocytes mean?

A

-short RBC cycle, bone marrow being overproduced (hemolytic anemia)

28
Q

two parts of hemoglobin synthesis?

A

1) heme synthesis (iron + protoporphyrin)

2) globin chain synthesis (alpha & beta)

29
Q

all components of RBC?

A

1) alpha chain
2) beta chain
3) iron
4) heme group
5) reversibly bound O2

30
Q

hemoglobinopathies? two ways it can happen?

A

disorders due to abnormal globin chain synthesis

1) decrease synthesis of the normal chain (thalassemia)
2) AA substitution resulting in abnormal chain (sickle cell)

31
Q

genetic mutations in hemoglobinopathies?

A

1) Point mutations–> AA substitution
2) point mutations–> defective splicing
3) point mutations–> premature termination codon
4) frame shift mutation
5) deletion of whole gene

32
Q

hemoglobin electrophorus qualitative & quantitative capabilities?

A
  • qualitative: IDs diff types of hemoglobin

- quantitative: IDs percentages of diff types of hemoglobin

33
Q

normal human adult elesctophoresis results?

A
  • HbA= 95%
    HbA2= <3.5%
    HbF =<1%
    HbS (sickle)= 0%

diff in adult vs children

34
Q

thalassemia and what looks like?

A
  • type of anemia varying severity “anemia of the sea”
  • fucks up spleen
  • jaundice& gall stones
  • bone marrow expansion & bone deformity
  • inadequate O2 delivery, growth retardation
  • iron overload (cirrhosis)
35
Q

thalassemia types & mechanism of anemia?

A
  • types: alpha, beta, others
  • mechanism:
    1) inadequate hemoglobin (globin chain) production (less RBC)
    2) unbalanced accumulation of globin sub-units (make too much alpha subunit, less Beta subunit
36
Q

bone marrow expansion & bone deformity in thalassemia?

A
  • enlargement of facial bones since bone marrow over working to produce more RBC
37
Q

how prevent bone marrow expansion & bone deformity in thalassemia?

A

need to treat at early age w/ hyper fusion (10g) to suppress bone marrow impulse to expand & prevent facial deformities

38
Q

what is normal MCV?

A

80-98

39
Q

if normal reticulocytes, decreased Hb, decreased iron…what does that suggest?

A
  • not iron deficiency since iron def. is seen as DECREASED RBC production (reticulocytes= baby RBCs)
  • is thalassemia because this causes overproduction of RBC by bone marrow therefore causing increased reticulocytes
40
Q

thalassemia major?

A
  • when kid gets 2 mutant genes for Beta Hb
  • Cooley’s anemia
  • chronic fatigue, defomritities if not treated soon
41
Q

treatment of thalassemia major?

A

1) early diagnosis (so prevent bone deformities)
2) folic acid
3) hypertransfusion
4) iron chelation
5) stem cell transplant

42
Q

complications of thalassemia major treatment?

A

1) iron overload
- transfusions cause extra RBC, when break down hard to recycle all components, so end up w/ excess iron
2) hepatitis C (from blood transfusion b4 knew how to screen for it )
3) line infections

43
Q

sickle cell anemia clinical picture?

A
  • chronic hemolytic anemia (not enough RBC)
  • splenic crisis
  • acute painful crisis
  • acute chest syndrome (hypoxic chest pain, life threatening)
  • neurological damage: if sickled cels block arteries can get stroke
44
Q

sickle cell anemia treatment?

A

1) stem cell transplant

2) induction of fetal Hb (hydroxyurea therapy)

45
Q

hydroxyurea therapy

A

the induction of fetal Hb into patients w/ sickle cell anemia
-fetal Hb shown to resist sickling of RBC

Block 1 Week 2 (9 decks)

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