Anemia Flashcards

1
Q

What is the formation of hemoglobin

A

succinyl coA and glycine form Pyrroles -> 4 pyrroles form protoporphyrin IX -> Addition of iron forms Heme -> Addition of globin polypeptide completes a subunit -> **4 subunits usually 2 alpha, 2 beta in adults combine to form hemoglobin

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2
Q

Define anemia

A

Abnormally low number of circulating red blood cells or level of hemoglobin, or both, resulting in diminished oxygen-carrying capacity; a sign NOT a disease

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3
Q

What is the manifestations of Reduced O2 Carrying Capacity

A

1] Impaired oxygen transport, 2] Reduced red cell indices/Hgb, 3] Signs and symptoms of disease causing anemia

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4
Q

What is the red cell indices

A

indicators of red cell health and function, done w Hgb…this is a special test

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5
Q

What are the typical causes of anemia?

A

1] red cell loss (hemolysis/hemorrhage), 2] deficient erythropoiesis, 3] deficient hemoglobin production

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6
Q

What is an example of deficient erythropoiesis

A

*CKD, bc lack of EPO and red cell production. Too few cells.

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7
Q

What is an example of Low hemoglobin and red count.

A

GI bleed, fecal occult blood. hemophilia, GIB, women of reproductive age who bleed

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8
Q

If hemoglobin is abnormal what can that indicate?

A

there is a production issue. eg) Fe deficiency, B12, folate deficiency

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9
Q

What is Hereditary spherocytosis

A

round red cells are round instead of biconcave –> get trapped more often causing hemolysis

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10
Q

What are the effects of hypoxia

A

1] Fatigue, 2] Weakness, 3] Dyspnea, 4] Angina, 5] HA (morning), faintness, dim vision (tunnel or less acuity)

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11
Q

Why does angina occur due to hypoxia

A

body response to low oxygen, incr HR, resp drive, metabolic demand (including on the cardiac muscle), murmurs and angina may show up.

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12
Q

What is the manifestation of blood redistribution when oxygen starved

A

force blood into the core to support vital organs results in Pallor of skin, mucus membranes, conjunctiva, nails

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13
Q

What is blood loss

A

Can be Acute or chronic, Fluid enter compartment, dilutes blood, Hgb/Hct fall with normal cell morphology

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14
Q

What is acute blood loss

A

think hypovolemic/shock due to bleeding

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15
Q

What is chronic blood loss

A

Chronic loss leads to iron deficiency anemia over time, no volume depletion (microcytic anemia), the slower the blood loss the more you can tolerate it, their hemoglobins will go very low. GIB HgB of 4 compared to trauma pt with HgB of 10.

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16
Q

What is Hemolytic anemia

A

1] Usually normocytic/normochromic, 2] Increased reticulocyte count, 3] Possible jaundice

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17
Q

What is the pathophysiology of hemolytic anemia

A

loss of red cells results in the body pushing more of the reticulocytes into the bloodstream faster

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18
Q

What is Hereditary spherocytosis

A

Autosomal dominant transmission that results in Deficiency of red cell membrane proteins (spectrin, ankyrin). Red cell loses surface area throughout lifespan. Characteristic shape lost, spheres remain, Spherical shape leads to destruction = shorter lifespan/faster turnover =anemia

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19
Q

What are the signs of Hereditary spherocytosis

A

jaundice, splenomegaly, bilirubin stones

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20
Q

What is aplastic crisis

A

Aplastic crisis when red cell production disrupted as by virus or metabolic crisis and the bone marrow shuts down

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21
Q

What is the treatment of Hereditary spherocytosis

A

Tx with splenectomy, bc this is where the cells are getting degraded to frequently, so if you take out the spleen, the cells will last longer.

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22
Q

What is Sickle Cell Anemia

A

transmitted by recessive pattern results in Point mutation in beta chain of hemoglobin, abnormal substitution. 40% sickling with heterozygotic trait; 80-95% sickling in homozygote

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23
Q

What causes the sickling?

A

Low oxygen tension, can be brought on by Cold, Stress, Exertion, Infection, Hypoxia, Dehydration, Acidosis

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24
Q

What are the 2 results of sickle cell anemia?

A

chronic hemolytic anemia, blood vessel occlusion

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25
Q

What is thalassemia A

A

result of deletion of alpha subunit on Chromosome 16. In severe disease Hgb H formed.

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26
Q

What is thalassemia B

A

usually caused by point mutations in β subunit. Relative increases in *Hgb A2 and F. Excess alpha chains unstable and precipitate causing cell damage. Prevalent in Mediterranean ppl.

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27
Q

How do you determine the type of thalassemia

A

DX-hemoglobin electrophoresis, where the run the hemoglobin out on a gel. By the distance that the proteins travel, you can tell which form of HgB you carry. Higher than normal Hgb H = alpha thalassemia

28
Q

How does thalassemia causes anemia

A

anemic bc higher turnover of red cells and less oxygen carrying capacity.

29
Q

List the Disorders of red cell production

A

1] Decreased bone marrow activity, 2] Metabolic deficiency

30
Q

How are Disorders of red cell production is assessed

A

assessed w/CBC. Is it a pan cytopenia? global cell production (white cells are down too) or is it just red cells?

31
Q

What is the most common type of anemia worldwide?

A

*iron deficiency anemia due to dietary deficiency or bleeding

32
Q

what will a deficiency in iron causes

A

decreased heme production, results in small RBC with low hemoglobin content there it is a microcytic hypochromic anemia also anisocytosis = they do not look the same, poikilocytosis = abnormal morphologic

33
Q

What is the issue with iron deficiency anemia?

A

Membrane may become friable and predispose to hemolysis

34
Q

What is what the MCV indicates

A

If MCV is lower than normal = microcytic (small red cells), MCV high = macrocytic (big red cells), MCV normal = normocytic

35
Q

What is reason that iron deficiency is considered hypochromic

A

*Hemoglobin is responsible for coloring the blood red. In lab terms, it’s a chromogen creates color. if Hgb is low there is less color

36
Q

Compare hemolytic anemia and iron deficiency anemia

A

Hemolytic anemia is normocytic and normochromic, they have anemia bc they’re breaking down red cells faster. In IDA cells are microcytic and Hypochromic,

37
Q

What is the pathophysiology of megaloblastic anemia

A

impaired nucleic acid synthesis results in Enlarged RBC and deficient nuclear maturation

38
Q

What is the most common cause of megaloblastic anemia

A

B12 or folate deficiency

39
Q

What is why B12 and folate results in megaloblastic anemia

A

B12 & folate are cofactors in DNA synthesis. Stem cells producing daughter cells, you need 2 things: mitosis & meiosis are processes of nuclear division. So if your nuclear division is slow bc you don’t have enough cofactor to turnover DNA as fast, and cytoplasm is allowed to keep going at a normal pace (bc that process is not impaired) == bigger cells in the end.

40
Q

What is absorption and storage of vitamin B12

A

Bound to intrinsic factor made in stomach, Absorbed at terminal ileum; Stored in liver (sufficient for 3 years without intake)

41
Q

What is use of vitamin B12

A

Necessary cofactor for methionine and succinyl co-A production in 2 pathways- DNA proteins

42
Q

What is absorption and storage of folate

A

Pteroylmonoglutamic acid (reduced to tetrahydrofolate)

43
Q

What is use of vitamin folate

A

Also a cofactor in conversion of homocysteine to methionine and conversion of deoxyuridylate to thymidylate (DNA synthesis)

44
Q

What should suspect with a macrocytic CBC?

A

B12 and folate levels

45
Q

What is the pathogenesis of Aplastic anemia (bone marrow depression)

A

Fatty replacement of bone marrow - loss of all 3 stem cell lines, Remaining cells normal

46
Q

What is the manifestation of aplastic anemia

A

Petechiae and bruising from loss of platelets, and infections from WBC loss

47
Q

What is the cause of aplastic anemia

A

Often caused by exposures (radiation, chemicals, Felbamate & tegretol [AED])

48
Q

What is the treatment of aplastic anemia

A

May require BMT (bone marrow transplant)

49
Q

What is anemia of chronic inflammation

A

Common result of chronic illnesses -AIDS, RA, SLE, Hodgkin’s, Similar to IDA (microcytic/hypochromic)

50
Q

What is the pathophysiology behind anemia of chronic inflammation

A

Theory focuses on macrophage and lymphocyte role in sequestering iron, destroying red cells, chemical suppression of EPO response, inhibited precursor cells, reduced Fe transport

51
Q

How is anemia due to chronic renal failure is different?

A

normocytic/normochromic

52
Q

What is the rule of 3s

A

Hgb should be roughly 3x the red count, Hct should be roughly 3x the Hgb; if wildly off, re-run CBC, there’s a problem.

53
Q

What is the Hct

A

take whole blood spin it down, get a red cell pellet –> Hct is proportion size of the red cell pellet to the whole thing, percentage

54
Q

What is the RDW

A

High mean variability in size indicates production of new cells red cell distribution width. Tells you if pt is working hard to pump out excess red cells. Reference range = 11-14.5;

55
Q

What is PLT

A

platelets, ability to clotting

56
Q

What is MCV

A

mean corpuscular volume, 80-100 = “normocytic”

57
Q

What is MCHC

A

mean corpuscular hgb content, 32-36% reference range (calculation [(hgbx100)/Hct]; Low = hypochromic; High = hyperchromic

58
Q

What is the normal values of HgB

A

14-18 men; 12-16 women

59
Q

What is ferritin

A

Ferritin is the iron’s form of storage, low ferritin can indicate iron deficiency, while increase ferritin could mean anemia of chronic disease

60
Q

What is transferrin

A

Binds free iron to reduce the oxidative damage associated with free iron and to transfer it

61
Q

What is total iron binding capacity

A

an indirect way to measure transferrin levels

62
Q

What lab values indicate iron deficiency anemia`

A

INC transferrin, INC TIBC, DEC ferritin, DEC serum Fe

63
Q

What lab values indicate anemia of chronic disease

A

DEC transferrin, DEC TIBC, iINC ferritin, DEC serum Fe

64
Q

What test can demonstrate pernicious anemia?

A

intrinsic factor made in the gut

65
Q

What is the hallmark of thalassemia

A

MCV that is low out of proportion to presentation

66
Q

What happens when you give a pt w normal Fe, Fe supplements?

A

Terrible GI side effects.