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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
what affects the rate and degree of sickling in sickle cell disease?
- interaction of HbS with other Hb - mean cell Hb concentration - intracellular pH - transit time through vasculature
26
what are clinical features of sickle cell disease?
- reticulocytosis - hyperbilirubinemia - vaso-occlusive crisis -> pain - chest pain - priapism - stroke - blindness - organ damage - altered splenic fn -> increased infection risk
27
what is reticulocytosis?
increased immature RBC
28
what is thalassemia syndrome?
- due to inherited mutation - decreases synthesis of either alpha or beta globin chain on Hb - have ineffective erythropoiesis and extravascular hemolysis - microcytic and hypochromic
29
why do hemolytic anemias protect against malaria?
- malaria requires RBC to grow/ multiply | - because hemolytic anemias destroy RBC it protects against malaria
30
what is haptoglobin
- binds free Hb in blood | - free Hb in blood is toxic
31
pathogenesis of thalessemia
- 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
why does iron overload occur in thalassemia
- 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
clinical symptoms of thalassemia
- severity based on genetic defect - sx begin 6-9 mo after birth - anisocytosis- variable in size - extramedullary metaopoiesis - hepatosplenomegaly
34
what is the cure for thalassemia?
- bone marrow transplant | - can administer blood transfusions but is not a cure and pt will still have iron overload
35
what is the cause of death in thalassemia?
- cardiac disease from iron overload | - secondary hemochromatosis
36
what are the anemias due to decreased RBC production?
- vit B12 deficiency - folate deficiency - iron deficiency - anemia of chronic disease - aplastic anemia
37
what is a common cause of vit V12 deficiency?
pernicious anemia
38
what is pernicious anemia?
- autoimmune destruction of intrinsic factors required for absorption of vit B12 from food
39
why is vit B12 important?
- 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
where do we get most of our vit B12?
- through the diet | - B12 very rich in animal products
41
what is the fate of B12 after ingestion?
- 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
where is pepsin produced?
in stomach by chief cells
43
where is the intrinsic factor for B12 produced?
in the stomach by parietal cells
44
what are the clinical features of vit B12 deficiency?
- spastic paresis - sensory ataxia - all other complications can be reversed with folate supplementation
45
what are some causes of vit B12 deficiency?
- achlorhydria - gastrectomy - ileal resection - some tapeworms - malabsorption syndromes - increased requirements like pregnancy
46
when does folate deficiency commonly occur?
- inadequate intake - malabsorption syndromes - increased demand - folate antagonists
47
anemias of folate deficiency
- similar to B12 | - folate acts as one carbon acceptor which is important for methylation reactions
48
iron deficiency anemia
- most common nutritional disorder in the world - results in reduced Hb synthesis - sx related to reduced Hb
49
who is more likely to develop iron deficiency anemia?
- toddlers (breast milk is iron poor) - adolescent girls - women of childbearing age
50
where is the total body iron found?
- functional iron | - storage iron
51
where is our functional iron found?
- hemoglobin - myoglobin - enzymes
52
were is our storage iron found?
- ferritin * | - hemosiderin
53
what is transferrin?
- helps with iron transportation into cells | - synthesized in the liver
54
what is heme iron?
- found in animal sources | - readily absorbed in gut
55
what is nonheme iron?
- comes from plant sources - must be reduced before it can be absorbed - uses DMT1 transporters
56
what is the fate of iron after it is absorbed?
- stored as mucosal ferritin | - go to the blood
57
what is ferroportin?
- transports Fe2+
58
what is hepcidin?
- inhibits ferroportin | - will cause iron to stay in mucosal ferritin stores or to be excreted
59
what are the causes of iron deficiency anemia?
- dietary lack - increased requirement - impaired absorption - chronic blood loss
60
pathogenesis of iron deficiency anemia
- hypochromic microcytic anemia | - sx appear when iron stores are depleted and serum iron is low
61
why are many chronic diseases associated with anemia?
- 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
what are the categories of anemia of chronic disease?
- chronic microbial infections - chronic immune disorders - neoplasms
63
what is aplastic anemia?
- happens due to bone marrow suppression - chronic hematopoietic failure -> pancytopenia - usually idopathic - chemotherapy drugs are another common cause
64
what is pancytopenia?
- all cells synthesized by bone marrow are reduced - anemia - neutropenia - thrombocytopenia
65
what are the intrinsic causes of aplastic anemia?
- problem with stem cells | - causes reduced proliferative and differentiative properties
66
what are the extrinsic causes of aplastic anemia?
- immune mediated suppression of marrow progenitors | - genetically altered stem cells have abnormal antigens which are recognized by T cells
67
what are the hallmark characteristics of aplastic anemia?
- reticulocytopenia | - no splenomegaly
68
what is polycythemia
- abnormally high RBC - can be due to an increased Hb level which causes increased RBC production - either relative or absolute polycythemia
69
relative polycythemia
- 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
absolute polycythemia
- primary- mutation in stem cells that causes them to produce too many RBC - secondary- respond to increased levels of erythrpoietin
71
polycythemia vera
- mutation in RBC progenitor | - makes it to multiply irrespective of levels of erythrpoietin
72
what is thrombocytopenia
- reduction in platelet count | - increases the risk of bleeding
73
causes of thrombocytopenia
- decreased platelet production - decreased platelet survival - sequestration - dilution
74
chronic immune thrombocytopenia purpura (ITP)
- caused by autoantibody destruction of platelets - usually idiopathic - markedly improved by splenectomy
75
clinical features of ITP
- 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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