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Patho 1 > Chap 14- Red Blood Cells > Flashcards

Chap 14- Red Blood Cells Flashcards

1
Q

anemia

A
  • reduction in mass of RBC below normal
  • reduces the oxygen carrying capacity of RBC
  • leads to hypoxia
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2
Q

how do you diagnose anemia?

A
  • decreased hematocrit

- decreased Hb concentration

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3
Q

what is hematocrit?

A

percentage of RBC in the blood

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4
Q

useful red cell indices

A
  • mean cell volume
  • mean cell Hb
  • mean cell Hb concentration
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5
Q

what is the difference between mean cell Hb and mean cell Hb concentration?

A
  • mean cell Hb is the weight of Hb per RBC

- Mean cell Hb concentration tells you the concentration of Hb for given volume of packed RBC and isnt measured directly

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6
Q

mechanisms of anemia

A
  • acute blood loss
  • chronic blood loss
  • hemolysis
  • genetics
  • nutritional deficiencies
  • erythropoietin deficiencies
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7
Q

why are some symptoms of anemia?

A
  • weakness, malaise, fatiguability
  • dyspnea on mild exertion
  • fatty change in liver, myocardium and kidney
  • cardiac failure
  • CNS -> HA, worsened vision, faintness
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8
Q

what are there fatty changes seen in anemia?

A
  • hypoxia activates hypoxia inducible factors (HIF)

- HIF activates lipogenesis

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9
Q

what are the ranges of blood loss?

A
  • <15% no sx
  • 15-30% is moderate blood loss, compensatory mechanisms activated
  • 30-40% severe bood loss
  • above 40% slim chance of survival
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10
Q

how does the body compensate for blood loss?

A
  • moves water from interstitial fluid to intravascular space
  • causes hemodilution and reduced hematocrit
  • reduced O2 supply stimulates erythropoietin synthesis
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11
Q

How does the body compensate for massive blood loss?

A
  • NE/E released
  • mobilizes granulocytes from intravascular marginal pools
  • results in leukocytosis
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12
Q

what are the characteristics that hemolytic anemias share?

A
  • shorted red cell life
  • elevated erythropoietin levels and increased erythropoiesis
  • accumulation of Hb degradation products
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13
Q

what is the normal life span of a RBC?

A

120 days

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14
Q

what are the clinical features of extravascular hemolysis?

A
  • anemia
  • splenomegaly
  • jaundice
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15
Q

why does jaundice occur?

A
  • RBCs are destroyed and split into heme and globin
  • heme is split into iron and bilirubin
  • bilirubin transported to liver with albumin normally
  • plasma levels of unconjugated bilirubin increase -> jaundice
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16
Q

what are the clinical features of intravascular hemolysis?

A
  • anemia
  • hemoglobinemia
  • hemoglobinuria
  • hemosiderinuria
  • jaundice
  • *NO splenomegaly
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17
Q

what is hereditary spherocytosis?

A
  • genetic defect where RBC are spherical in shape
  • due to membrane defect
  • easily undergo hemolysis
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18
Q

pathogenesis of hereditary spherocytosis

A
  • mutation in proteins spectrin and ankyrin
  • normally the proteins maintain membrane integrity
  • causes reduced stability of lipid bilayer
  • loss of membrane fragments as RBC age
  • more likely to be trapped and destroyed
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19
Q

clinical features of hereditary spherocytosis

A
  • increased sensitivity to lysis
  • increased average Hb concentration
  • anemia
  • splenomegaly
  • jaundice
  • aplastic crisis with parvovirus infection
  • gallstones from hyperbilirubinemia
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20
Q

what is an aplastic crisis?

A

period of time where there are too many spherocytes

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21
Q

what is glucose-6 phosphate dehydrogenase deficiency?

A
  • deficiency in G6PD enzyme which is involved in glucose oxidation
  • produces NADPH which is a precursor for nucleotide synthesis
  • NADHP is also important antioxidant
  • results in cells that are more sensitive to oxidative stress
  • can cause intra and extravascular hemolysis
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22
Q

what are the causes of G6PD deficiency?

A
  • infections
  • drugs- antimalarials and sulfoamides
  • fava beans
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23
Q

what are the hemolytic anemias?

A
  • hereditary spherocytosis

- G6PD deficiency

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24
Q

what are the anemias due to Hb abnormalities?

A
  • sickle cell anemia

- thalassemia

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25
Q

what affects the rate and degree of sickling in sickle cell disease?

A
  • interaction of HbS with other Hb
  • mean cell Hb concentration
  • intracellular pH
  • transit time through vasculature
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26
Q

what are clinical features of sickle cell disease?

A
  • reticulocytosis
  • hyperbilirubinemia
  • vaso-occlusive crisis -> pain
  • chest pain
  • priapism
  • stroke
  • blindness
  • organ damage
  • altered splenic fn -> increased infection risk
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27
Q

what is reticulocytosis?

A

increased immature RBC

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28
Q

what is thalassemia syndrome?

A
  • due to inherited mutation
  • decreases synthesis of either alpha or beta globin chain on Hb
  • have ineffective erythropoiesis and extravascular hemolysis
  • microcytic and hypochromic
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29
Q

why do hemolytic anemias protect against malaria?

A
  • malaria requires RBC to grow/ multiply

- because hemolytic anemias destroy RBC it protects against malaria

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30
Q

what is haptoglobin

A
  • binds free Hb in blood

- free Hb in blood is toxic

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31
Q

pathogenesis of thalessemia

A
  • cells die in bone marrow
  • leads to ineffective erythropoiesis -> severe anemia
  • RBC synthesis occurs outside of bone marrow
  • compensatory increase in erythropoietin and bone marrow expansion
  • iron overload
32
Q

why does iron overload occur in thalassemia

A
  • due to ineffective erythropoiesis
  • hepsidin goes down and causes too much iron to be absorbed in body
  • hepsidin is normally a negative feed back
33
Q

clinical symptoms of thalassemia

A
  • severity based on genetic defect
  • sx begin 6-9 mo after birth
  • anisocytosis- variable in size
  • extramedullary metaopoiesis
  • hepatosplenomegaly
34
Q

what is the cure for thalassemia?

A
  • bone marrow transplant

- can administer blood transfusions but is not a cure and pt will still have iron overload

35
Q

what is the cause of death in thalassemia?

A
  • cardiac disease from iron overload

- secondary hemochromatosis

36
Q

what are the anemias due to decreased RBC production?

A
  • vit B12 deficiency
  • folate deficiency
  • iron deficiency
  • anemia of chronic disease
  • aplastic anemia
37
Q

what is a common cause of vit V12 deficiency?

A

pernicious anemia

38
Q

what is pernicious anemia?

A
  • autoimmune destruction of intrinsic factors required for absorption of vit B12 from food
39
Q

why is vit B12 important?

A
  • required for DNA synthesis
  • without B12 absorption dont have proper DNA synthesis
  • cells must complete S phase for DNA synthesis
  • B12 deficiency results in cells that cannot divide properly so have an increased size (megaloblasts)
40
Q

where do we get most of our vit B12?

A
  • through the diet

- B12 very rich in animal products

41
Q

what is the fate of B12 after ingestion?

A
  • in stomach removed from protein binding partner by pepsin
  • B12 binds to haptocorin in stomach to protect it
  • leaves stomach
  • pancreas secretes proteases that removes haptocorin
  • B12 binds to intrinsic factor to be absorbed by small intestine
  • transcobalamin II helps transport B12 to liver and other cells
42
Q

where is pepsin produced?

A

in stomach by chief cells

43
Q

where is the intrinsic factor for B12 produced?

A

in the stomach by parietal cells

44
Q

what are the clinical features of vit B12 deficiency?

A
  • spastic paresis
  • sensory ataxia
  • all other complications can be reversed with folate supplementation
45
Q

what are some causes of vit B12 deficiency?

A
  • achlorhydria
  • gastrectomy
  • ileal resection
  • some tapeworms
  • malabsorption syndromes
  • increased requirements like pregnancy
46
Q

when does folate deficiency commonly occur?

A
  • inadequate intake
  • malabsorption syndromes
  • increased demand
  • folate antagonists
47
Q

anemias of folate deficiency

A
  • similar to B12

- folate acts as one carbon acceptor which is important for methylation reactions

48
Q

iron deficiency anemia

A
  • most common nutritional disorder in the world
  • results in reduced Hb synthesis
  • sx related to reduced Hb
49
Q

who is more likely to develop iron deficiency anemia?

A
  • toddlers (breast milk is iron poor)
  • adolescent girls
  • women of childbearing age
50
Q

where is the total body iron found?

A
  • functional iron

- storage iron

51
Q

where is our functional iron found?

A
  • hemoglobin
  • myoglobin
  • enzymes
52
Q

were is our storage iron found?

A
  • ferritin *

- hemosiderin

53
Q

what is transferrin?

A
  • helps with iron transportation into cells

- synthesized in the liver

54
Q

what is heme iron?

A
  • found in animal sources

- readily absorbed in gut

55
Q

what is nonheme iron?

A
  • comes from plant sources
  • must be reduced before it can be absorbed
  • uses DMT1 transporters
56
Q

what is the fate of iron after it is absorbed?

A
  • stored as mucosal ferritin

- go to the blood

57
Q

what is ferroportin?

A
  • transports Fe2+
58
Q

what is hepcidin?

A
  • inhibits ferroportin

- will cause iron to stay in mucosal ferritin stores or to be excreted

59
Q

what are the causes of iron deficiency anemia?

A
  • dietary lack
  • increased requirement
  • impaired absorption
  • chronic blood loss
60
Q

pathogenesis of iron deficiency anemia

A
  • hypochromic microcytic anemia

- sx appear when iron stores are depleted and serum iron is low

61
Q

why are many chronic diseases associated with anemia?

A
  • a lot of chronic diseases are associated with inflammation
  • IL-6 is secreted which causes secretion of hepcidin
  • hepcidin reduces iron reabsorption and stops iron release by macrophages
  • too much iron is stored that cannot be utilized
  • also have reduced proliferation of erythroid progenators
62
Q

what are the categories of anemia of chronic disease?

A
  • chronic microbial infections
  • chronic immune disorders
  • neoplasms
63
Q

what is aplastic anemia?

A
  • happens due to bone marrow suppression
  • chronic hematopoietic failure -> pancytopenia
  • usually idopathic
  • chemotherapy drugs are another common cause
64
Q

what is pancytopenia?

A
  • all cells synthesized by bone marrow are reduced
  • anemia
  • neutropenia
  • thrombocytopenia
65
Q

what are the intrinsic causes of aplastic anemia?

A
  • problem with stem cells

- causes reduced proliferative and differentiative properties

66
Q

what are the extrinsic causes of aplastic anemia?

A
  • immune mediated suppression of marrow progenitors

- genetically altered stem cells have abnormal antigens which are recognized by T cells

67
Q

what are the hallmark characteristics of aplastic anemia?

A
  • reticulocytopenia

- no splenomegaly

68
Q

what is polycythemia

A
  • abnormally high RBC
  • can be due to an increased Hb level which causes increased RBC production
  • either relative or absolute polycythemia
69
Q

relative polycythemia

A
  • due to changes in blood volume
  • lose too much fluid so there is a relatively high amount of RBC
  • due to dehydration or excessive diuretic use
70
Q

absolute polycythemia

A
  • primary- mutation in stem cells that causes them to produce too many RBC
  • secondary- respond to increased levels of erythrpoietin
71
Q

polycythemia vera

A
  • mutation in RBC progenitor

- makes it to multiply irrespective of levels of erythrpoietin

72
Q

what is thrombocytopenia

A
  • reduction in platelet count

- increases the risk of bleeding

73
Q

causes of thrombocytopenia

A
  • decreased platelet production
  • decreased platelet survival
  • sequestration
  • dilution
74
Q

chronic immune thrombocytopenia purpura (ITP)

A
  • caused by autoantibody destruction of platelets
  • usually idiopathic
  • markedly improved by splenectomy
75
Q

clinical features of ITP

A
  • women <40 y/o
  • bleeding in skin and mucosa
  • easy bruising, nose bleeds, bleeding from gums
  • hemorrhages into soft tissues with minor trauma
  • melena- blood in stool
  • hematuria
  • excessive menstrual flow

Patho 1 (12 decks)

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