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pathophysiology > ch21: alterations of hematologic function > Flashcards

ch21: alterations of hematologic function Flashcards

1
Q

anemia

A

low on RBCs, antimitotic chemo

  • decrease in # of circulating RBCs
  • decrease in quality/quantity of Hgb
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2
Q

what is the main result of anemia

A

tissue hypoxia

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3
Q

hypoxemia

A

O2 deprivation in the blood

  • altered production of RBCs
  • blood loss
  • increased destruction of RBCs
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4
Q

-cytic

A

alteration in cell size

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5
Q

normocytic

A

blood cells all normally sized, just might not have enough

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6
Q

macrocytic

A

blood cells largely sized

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7
Q

microcytic

A

blood cells small in size

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8
Q

-chromic

A

alteration in Hgb concentration

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9
Q

normochromic

A

normal amount of Hgb

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10
Q

hypochromic

A

Hgb amounts are too little

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11
Q

hyperchromic

A

Hgb amounts are too much

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12
Q

anisocytosis

A

all RBCs are diff shapes

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13
Q

poikilocytosis

A

all red blood cells are diff shapes

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14
Q

macrocytic-normochromic anemias

A

large cells, but normal Hgb amount

  • pernicious anemia
  • folate deficiency anemia
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15
Q

pernicious anemia

A

deficiency of absorption of vitamin b12

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16
Q

what is the purpose of vitamin b12

A

needed for RBC production

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17
Q

what is intrinsic factor and where is it made?

A

made in stomach to help absorption of b12

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18
Q

folate deficiency anemia

A

decreased folic acid

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19
Q

what is the purpose of folic acid

A

for DNA synthesis

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20
Q

t/f: b and c vitamin are water soluble which means you can excrete them through urine

A

true

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21
Q

microcytic-hypochromic anemias

A

small cells, too little Hgb amounts

  • iron deficiency anemia
  • sideroblastic anemia
  • thalassemias
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22
Q

iron deficiency anemia

  • signs
  • treatment
A

too little iron

signs: corners of mouth broken, dark circles around eyes
treatment: iron supplements

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23
Q

sideroblastic anemia

A

metabolic disorder; ineffective utilization of iron during erythropoiesis –> iron accumulation

“iron stuffed mitochondria”

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24
Q

thalassemias

A

similar to sickle cell anemia; both are mutations in hemoglobin that lead to malformed hemoglobin (but thalassemia does NOT malformed cell)

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25
Q

what is the most common type of thalassemia

A

beta thalassemia: mutation in beta subunits of hemoglobin that leads to small hgb and iron deficiency

26
Q

what is the difference between sickle cell anemia and thalassemia?

A

thalassemia: mutated hgb but not malformed cell

sickle cell: mutated hgb with malformed cell

27
Q

normocytic-normochromic anemias

A

normal cell size, normal Hgb number

  • aplastic anemia
  • hemolytic anemia
  • hemolytic disease of the newborn (HDN)
  • posthemorrhagic anemia
  • anemia of chronic inflammation
  • sickle cell anemia
28
Q

aplastic anemia

- treat?

A

cells might look normal but don’t have enough due to problem at bone marrow
- treat by diet (palliative measures)

29
Q

hemolytic anemia

- hereditary vs acquired

A

something is causing lysis of RBCs

  • heredity: due to genetics
  • acquired: infectious disease
30
Q

hemolytic disease of the newborn (HDN)

- what should the mom get injected with to prevent this?

A

Rh negative mom has antibodies that can attack Rh positive baby
- mother needs to be injected with RHOGAM

31
Q

what is RHOGAM

A

shot of Rh factor - sticks to Rh positive antibodies so they don’t cross the placenta

32
Q

posthemmorhagic anemia

A

lost a lot of blood = low on RBCs

33
Q

anemia of chronic inflammation

A

cytokines down regulate processes that synthesizes all bone marrow cells

34
Q

sickle cell anemia

A

RBCs abnormally shaped due to a mutated hemoglobin protein

- resistance to malaria

35
Q

myeloproliferative RBC disorders

A
  • polycythemia
  • polycythemia vera
  • iron overload
36
Q

polycythemia

A

too many RBCs –> many problems and dysfunctions

37
Q

relative polycythemia

A

appear to have a high [ ] of RBCs when you really don’t (dehydration)

38
Q

absolute polycythemia

A

where number of RBCs are truly elevated

39
Q

primary absolute polycythemia

A

problem in bone marrow leads to too many RBCs (polycythemia vera)

40
Q

secondary absolute polycythemia

A

Hyperactivity with Erythropoietin (EPO) → hormone produced that triggers RBC production; made by kidney

41
Q

where is erythropoietin produced

A

in the kidney

42
Q

polycythemia vera

A

increased # of RBCs due to a bone marrow problem –> results to thick and sticky blood

43
Q

clinical manifestations of polycythemia vera?

A
  1. ischemia/infarction of tissue
  2. petechial rash
  3. JAK2 mutation
44
Q

iron overload

A

too much iron in diet, but can also be a disease condition

45
Q

hereditary hemochromatosis

A

too much iron (can’t process iron properly) but through GENETICS and not DIET

46
Q

t/f: blood drawn for pt with hereditary hemochromatosis can still be used

A

false

47
Q

leukopenia

A 
WBC deficiency
(granulocytopenia [eosinopenia, basophenia], pancytopenia, lymphocytopenia)
48
Q

leukocytosis

A

overabundance of WBCs

granulocytosis, eosinophilia, basophilia

49
Q

what is the leukemoid reaction

A

“shift to the left” during leukocytosis; RESEMBLES leukemia but NOT due to a malignant condition of the bone marrow

can just be a response to infectious disease

50
Q

when do you see eosinophilia

A

parasitic infections

51
Q

yes/no: can you see tumors during dysfunctions of the blood?

A

no

52
Q

leukemia

A

producing too many blood cells; MALIGNANT disorder of blood and bone marrow

53
Q

what is the hallmark sign of leukemia

A

increased WBC proliferation (that aren’t made right)

54
Q

leukemia usually results in _______ (describe it)

A

pancytopenia: corresponding decrease in other cells (too much WBC, not much RBC or platelets)

55
Q

acute lymphocytic leukemia (ALL)

A

rapidly developing abnormally high number of malformed lymphocytes

56
Q

acute myelogenous leukemia (AML)

A

rapidly developing abnormally high overabundance of cells of myeloid lineage

57
Q

chronic lymphocytic leukemia (CLL)

A

gradual developing abnormally high number of malformed lymphocytes

58
Q

chroni myelogenous leukemia (CML)

A

gradual developing abnormally high overabundance of cells of myeloid lineage

59
Q

what happens to chromosomes during CML?

A

philadelphia translocation: eciprocal translocation over across a couple of chromosomes (almost always seen in ppl with CML)

-Segments of chromosome 9 and 22 switching places with each other
Not good for cells (don’t want crossovers between diff)

60
Q

lymphadenopathy

A

dysfunction of the lymphatic system

pathophysiology (16 decks)

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