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HMS Homeostasis I > Nutritional Anemias > Flashcards

Nutritional Anemias Flashcards

1
Q

Transferrin receptor

A

enables the uptake of iron-bound transferrin from the plasma through the transferrin cycle

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2
Q

Ferritin

A

provides a bioavailable intracellular storage depot for iron, protecting the cell from toxicity

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3
Q

Hepcidin

A

a circulating hormone that controls both the absorption of dietary iron from the gut and release of recycled iron from macrophages

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4
Q

ferrireductase

A

Reduces ferric iron (Fe3+) to its ferrous form (Fe2+). Present at the villous tips of duodenal enterocytes, allowing iron to enter the cell through a luminal transmembrane channel, the divalent metal transporter DMT1.

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5
Q

Ferroportin

A

The only known cellular iron exporter, localized within the plasma membrane on the abluminal or basolateral side of the enterocyte

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6
Q

Export of iron from duodenal enterocytes is blocked by . . .

A

Export of iron from duodenal enterocytes is blocked by hepcidin, a small polypeptide hormone that is produced by hepatocytes and secreted into the plasma.

Hepcidin carries out this critical negative regulatory function by binding to ferroportin, triggering its internalization and subsequent degradation.

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7
Q

The expression of hepcidin in hepatocytes

A

Tightly regulated at the transcriptional level, in part by iron, allowing the body to adjust iron uptake from the gut according to iron stores.

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8
Q

The body’s iron stores and utilization

A
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9
Q

Enterocyte iron regulation

A
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10
Q

heme oxygenase

A

Enzyme in intestinal epithelium that degrades dietary hemoglobin or myoglobin, resulting in the release of iron that is either stored as ferritin or exits from the cell via ferroportin

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11
Q

Why is there rarely ever free serum iron?

A

The plasma protein transferrin binds ferric iron at two sites with extraordinarily high affinity. As a result, the concentration of free iron in the plasma is too low to be easily measured. Thus transferrin effectively protects tissues and cells from the toxicity of “free” iron during its transport in the plasma

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12
Q

Iron-dependent regulation of the rate of translation of ferritin and transferrin

A

When the intracellular iron level is low, iron regulatory proteins (IRPs) bind to a consensus stem loop iron regulatory element in the respective mRNAs, resulting in suppression of ferritin translation and enhancement of transferrin receptor mRNA levels.

When the intracellular iron level is high, the IRPs do not bind to the stem loops. The translation of ferritin is unimpeded and transferrin receptor mRNA is degraded

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13
Q

Transferrin receptor affinity

A

Transferrin molecules loaded with two iron atoms (Fe-transferrin) have much greater affinity for the receptor than do those with either a single atom or none

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14
Q

plasma Fe-transferrin uptake

A
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15
Q

Heme biosynthesis occurs. . .

A

. . . in the mitochondrion

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16
Q

__% of transferrin-bound iron is utilized in erythropoiesis.

A

90% of transferrin-bound iron is utilized in erythropoiesis.

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17
Q

___ upregulate the expression and secretion of hepcidin from hepatocytes, blocking not only iron uptake by enterocytes, but also the efflux of iron from macrophages.

A

Inflammatory cytokines such as interleukin-6 (IL-6) upregulate the expression and secretion of hepcidin from hepatocytes, blocking not only iron uptake by enterocytes, but also the efflux of iron from macrophages. Thus, if inflammation is sustained, anemia often results

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18
Q

With its increasing accumulation, some cellular ferritin becomes denatured and is converted to ___.

A

With its increasing accumulation, some cellular ferritin becomes denatured and is converted to hemosiderin, from which iron is less readily mobilized.

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19
Q

TIBC

A

Total iron binding capacity

The amount of iron that the transferrin in serum can hold.

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20
Q

Serum ferritin under different conditions

A
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21
Q

Serum Fe to TIBC

A

provides an index of the fractional iron saturation of transferrin.

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22
Q

Fractional transferrin saturation in patients with chronic inflammation

A

Patients with inflammatory disorders have both low serum iron levels and low levels of total transferrin. Accordingly, fractional transferrin saturation is often normal.

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23
Q

Serum ferritin levels are generally ___ in iron deficiency and ___ in patients with iron overload.

A

Serum ferritin levels are generally low in iron deficiency and elevated in patients with iron overload.

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24
Q

Interpretation of serum ferritin may be confounded in these two commonly encountered clinical settings:

A
  1. Inflammation, regardless of cause, increases ferritin synthesis by hepatocytes
  2. Liver disease may result in leakage of ferritin into the plasma.
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25
Q

In patients with iron deficiency and concurrent inflammation or liver disease. . .

A

. . . serum ferritin levels may be normal or even elevated

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26
Q

Prussian blue

A

Dye that specifically stains iron. Way to assess iron stores in various tissues.

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27
Q

Serum transferrin receptor

A

A small fraction of transferrin receptor is released from maturing erythroid precursors and enters the plasma, where it can be measured. Because a very large proportion of the body’s transferrin receptor is expressed on erythroid cells, the level of serum transferrin receptor is a good surrogate for erythropoietic activity.

Thus, serum levels are low in patients with marrow aplasia and elevated in patients with ineffective erythropoiesis and erythroid hyperplasia, for example in the setting of hemolysis.

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28
Q

Common etiologies of iron deficiency

A
  • Insufficient intake
  • Menstrual bleeding
  • GI bleeding
  • Pregnancy
  • Parasite infection
  • Malabsorption
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29
Q

Infants whose diets consist primarily of ___ often become iron deficient.

A

Infants whose diets consist primarily of cow’s milk often become iron deficient.

30
Q

Celiac disease-associated anemia

A

Gluten-sensitive enteropathy causes poor absorption of iron in the duodenum.

31
Q

Efficiency of iron absorption is enhanced by ___.

A

Efficiency of iron absorption is enhanced by low gastric pH.

So, those with autoimmune gastritis, gastric achlorhydria, and H. pylori are at increased risk of becoming iron deficient

32
Q

Iron-refractory iron deficiency anemia

A

Mutations in the gene matripase-2, which lead to robust overexpression of hepcidin and the blockade of duodenal iron absorption.

33
Q

___ may be a behavioral symptom of iron deficiency anemia, but not other anemias.

A

Pica may be a behavioral symptom of iron deficiency anemia, but not other anemias.

34
Q

What is going on in this patient?

A

Koilonychia or ‘spoon nail’

Symptom of chronic iron deficiency anemia.

35
Q

Plummer-Vinson syndrome

A

Syndrome of chronic iron deficiency:

  • Koilonychia
  • fissures at the angles of the mouth
  • thin membrane web in the esophagus that can cause dysphagia
  • Sometimes pica
36
Q

Incipient or latent iron deficiency

A

Characterized by normal hemoglobin, hematocrit, red cell indices, and serum iron level and the absence of iron stores in the bone marrow.

As the deficiency becomes more severe/prolonged, the mean cell volume (MCV) falls, followed by a decrease in hematocrit and hemoglobin concentrations. Serum ferritin and iron levels fall, whereas total iron binding capacity (transferrin) rises, resulting in decreased transferrin saturation.

Final stages are microcytosis accompanied by hypochromia.

37
Q

Iron deficiency anemia blood smear

A
  • microcytosis
  • increased central pallor
  • aberrantly shaped red cells (‘pencil’ forms)
  • anisocytosis (abnormally wide range in red cell volume)
38
Q

Anisocytosis

A

abnormally wide range in red cell volume

39
Q

Treatment of iron deficiency anemia

A

Oral administration of iron salts, particularly ferrous sulfate. However, many patients have difficulty tolerating oral iron owing to gastrointestinal symptoms such as heartburn and constipation. IV iron is also safe and effective.

1 week post administration via either method, body responds with a burst of reticulocytes. Hematocrit and volume return to normal levels in a few weeks.

40
Q

Menorrhagia

A

Menstrual periods with abnormally heavy blood loss

41
Q

Reasons an individual might have substantial “hemorrhagic” iron loss

A
  • Menorrhagia
  • Frequent blood donations
  • Occult blood in stool
42
Q

Typical diagnostic inquiry for iron deficiency anemia

A
  1. Thorough history to ascertain possibility of blood loss or poor nutrition.
  2. Fecal occult blood test
  3. If no satisfactory answer has been found in the history, also include radiologic/endoscopic evaluation of the gastrointestinal tract, particularly in males and post-menopausal women
43
Q

Clinical picture of iron deficiency vs iron overload

A
44
Q

Target organs vulnerable to damage in iron overload

A

heart, liver, and endocrine cells, particularly hormone-producing cells in the pituitary, pancreatic islets, and gonads

45
Q

Hereditary hemochromatosis

A

Inherited disorders of iron overload are caused by defects involving hepcidin or its receptor, ferroportin. Most commonly a mutation in HFE, an MHC analog that participates in the upregulation of hepcidin transcription. In those affected, the signs and symptoms are not apparent until middle age or later.

Unfettered iron absorption from the gut and egress from macrophages.

can have increased skin pigmentation and complain of fatigue and arthralgia

46
Q

Enterocyte iron regulation diagram

A
47
Q

Macrophage iron regulation diagram

A
48
Q

How does anemia feed back into the regulation of iron absorption?

A

If you are anemic, less oxygen will be delivered to the liver. If less oxygen is delivered to the liver, hepcidin transcription decreases. If hepcidin transcription decreases, more iron is taken up.

49
Q

Regulation of hepcidin transcription

A
50
Q

Signs and symptoms of iron deficiency

A

Signs: pallor, angular stomatitis, glossitis, spoon nails, Plummer-Vinson esophageal webs (rare)

Symptoms: Malaise, decreased work performance, fatigue, dyspnea on exertion, pica

51
Q

Notes on Anemia of Inflammation

A
  • Very common anemia in hospital patients
  • Most chronic inflammatory conditions: rheumatoid arthritis, IBD, chronic infections, malignancy
  • Rarely severe enough to require transfusion
52
Q

Clinical picture for anemia of inflammation

A
53
Q

___ accounts for the iron abnormalities in the anemia of chronic disease/inflammation

A

A relative hepcidin excess accounts for the iron abnormalities in the anemia of chronic disease/inflammation

54
Q

___ can confound the MCV measure.

A

Reticulocytosis can confound the MCV measure.

Since reticulocytes tend to be larger than mature erythrocytes on average.

55
Q

As a rule of thumb, non-megaloblatic macrocytic anemias have an MCV ____.

A

As a rule of thumb, non-megaloblatic macrocytic anemias have an MCV < 105

56
Q

Biochemistry of folate and b12 in DNA synthesis

A
57
Q

Markers specific to B12 deficiency

A

Elevated methylmalonic acid. Builds up because methylmalonyl-CoA mutase cannot operate without cobalamine.

58
Q

Markers of both B12 and folate deficiency

A

Homocysteine buildup

59
Q

Normoblastic vs megaloblastic bone marrow

A
60
Q

If there are so many erythroid precursors in megaloblastic anemia, why are no erythrocytes being generated?

A

An apoptosis program is initiated once they are at reticulocyte-form and their contents are spilled out into the bone marrow.

This means that there will be high LDH and bilirubin levels, which may cause scleral icterus and clinical jaundice.

61
Q

Symptoms unique to B12 deficiency

A

Neurologic and related to the demyelination process of B12 deficiency.

  • Numbness/tingling
  • Abnormal gait
  • Loss of proprioception
  • Fine motor deficit
  • Degeneration of the posterior columns of the spinal cord
62
Q

B12 absorption

A
63
Q

Folate absorption

A
64
Q

How might one acquire a B12 or folate deficiency?

A
65
Q

B12 deficiencies will sometimes present only as ___.

A

B12 deficiencies will sometimes present only as neurologic symptoms

66
Q

Patients with B12 deficiency that are misdiagnosed with folate deficiency and given folate will . . .

A

. . . improve hematologically. However, this will have no effect on the demyelination and neurologic symptoms.

67
Q

If erythrocytes are normocytic, but patient is very anemic and RDW is uncharacteristically huge, what is likely going on?

A

Combined iron deficiency anemia and B12/folate deficiency

68
Q

In normal individuals, what is the major source of iron bound to serum transferrin used for erythropoiesis?

A

Breakdown of senescent red blood cells by reticuloendothelial macrophages.

69
Q

How is the mean corpuscular volume calculated?

A

Hematocrit / RBC count

70
Q

Hepcidin regulation

A

HMS Homeostasis I (62 decks)

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