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HEMA 1 > Ferrokinetics > Flashcards

Ferrokinetics Flashcards

1
Q

movement of iron through the body

A

ferrokinetics

  • “ferro” = “iron”
  • “kinetic” = “movement”
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2
Q

the most abundant trace element in the body

A

Iron (Fe)

- present in very small amounts but enough as requirement for normal growth

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3
Q

function of iron in the blood

A 
Oxygen transporter (present in:)
- hemoglobin = iron could bind oxygen & transport it throughout the body through the blood
  • myoglobin = carry oxygen throughout the muscle cells
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4
Q

total Fe content in the blood

A

3-5 g (adults)

- 1mL blood = 1mg Fe

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5
Q

RBC turnover

A
  • 120 days
  • lifespan of RBCs
  • when they die, Fe is released to & “recycled” to make new RBCs
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6
Q

Fe requirement for erythropoiesis

A

20-25mg daily

- 95% comes from recycled iron

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7
Q

how is Fe “recycled”?

A
  • disintegrated from the heme after cell lysis

death of RBCs –> cells burst (lysis) –> Hgb is released –> Hgb is catabolized –> Fe is released –> Fe is stored

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8
Q

iron absorption

A
  • the body tries to absorb free Fe(3+) roaming around the body
  • first absorbed in the stomach –> regulated by intestines (duodenum, jejunum)
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9
Q

Fe3+

A
  • ferric state of iron
  • mobilized form
  • state of free iron
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10
Q

T/F:

5% of iron is newly absorbed to balance minimal iron loss due to fecal/urinary excretion

A

TRUE

  • not all excreted Fe from dead RBCs are being absorbed or stored
  • some are excreted in sweat, urine, stool
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11
Q

what happens to the remaining Fe not absorbed?

A

stored (temporarily) in other organs

  • liver
  • spleen
  • bone marrow
  • myoglobin
  • coenzyme of cytochrome electron transport
  • respiratory enzymes

*remaining free Fe = 1/3 of total Fe content

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12
Q

iron to be absorbed needs to be in ___________ state

A

Ferrous (Fe2+)

  • converts Fe3+ to Fe2+:
      • reductase enzymes
      • acidic pH of the stomach
      • reduction
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13
Q

iron transport & storage

A
  • Fe3+ –> converted to ferritin
  • “ferritin” = stored form of Fe attached to apoferritin
  • Fe should travel from 1 place to another
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14
Q

Iron-binding protein

A

Apoferritin

  • strengthens the binding capacity of Fe
  • intensifier of the storing capacity (Fe) especially in the liver, spleen, BM cells
  • helps Fe3+ compounds be converted to ferritin

*ferritin + apoferritin = 10-20% stored Fe

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15
Q

why is the stored Fe more than those being absorbed?

A

more Fe needs to be reserved in case of sudden drops

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16
Q

form of iron without apoferritin

A

Hemosiderin

  • usu. present in low amounts
  • created because of excessive bleeding in the body
  • presence is not bad BUT ITS EFFECT is harmful
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17
Q

effect of hemosiderin

A
  • hemorrhage/bleeding abnormality –> WBCs (part. macrophage) ingest RBCs –> Fe is stored in WBCs –> WBCs are used up –> immunity is decreased –> risk of infection is increased
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18
Q

why will macrophages store Fe?

A

They act as storage if the body cannot absorb or store any more Fe
- excessive amount of free Fe causes cytotoxicity

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19
Q

regulation of Fe absorption occurs

A

Duodenum, jejunum

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20
Q

T/F:

absorption of excessive amounts of Fe may occur

A

FALSE

  • it NEVER happens
  • excessive (free) Fe happens when there is a disease that affects the whole absorption process
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21
Q

what happens after Fe absorption?

A

Fe goes to the circulation

  • ferritin binds with transferrin
      • Fe should not be roaming around the body on its own
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22
Q

transferrin

A
  • plasma beta-globulin
  • iron transport protein
  • enhances the storing capacity of iron into the cells
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23
Q

next stop of Fe (after the intestines)

A

Bone Marrow

  • for Hgb synthesis –> make new RBCs
  • transferrin injects Fe into the developing RBC membrane
  • Fe will then be incorporated in the heme area of the cell (w/in mitochondria)
  • new RBCs then go to the circulation (once enough Fe is used)
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24
Q

importance of “injecting” Fe into the RBCs by transferrin

A
  • so that RBC can create Hgb for it to be able to carry oxygen
  • Fe serves as the life of the RBC & aids in oxygen transport
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25
Q

when the new RBCs are in the blood, iron will be utilized for survival until they die through _____________

A

bursting/lysis

  • 120 days
  • recycling process of Fe begins
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26
Q

the rest of the iron not used by the bone marrow & RBCs are ____________

A

Stored in the liver

  • main storage site (bec. readily available)
  • stored to avoid cytotoxicity
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27
Q

cycle of iron transport & storage

A

intestine (absorption) –> blood (with transferrin) –> bone marrow (make RBCs) –> liver (unused Fe) –> blood (until RBC lysis) –> released Fe –> intestine (absorption)

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28
Q

factors that affect Fe metabolism

A
  • abnormal loss of Fe
  • hemosiderinuria
  • pathologic blood loss
29
Q

most common cause of abnormal loss of iron

A

Hemorrhage

- loss of circulating RBCs

30
Q

hemosiderinuria

A

Hemosiderin in urine

  • the most uncommon cause of Fe loss
  • not normal; hemosiderin should be absorbed by the kidneys
  • may mean that RBCs are abruptly dying before 120 days –> excess free Fe –> excreted to maintain balance
31
Q

the top suspect of Fe loss in males

A

Pathologic blood loss

- results in iron deficiency (males)

32
Q

storage forms of iron

A

a. ferritin
- normal storage form in storage sites

b. hemosiderin
- excess Fe to be absorbed as ferritin
- eaten by macrophage (storage)
- - stored in pseudo-crystalline form in the lysosomal membrane

33
Q

sideroblast

A

nucleated RBC (nRBC) containing iron

34
Q

siderocyte

A
  • mature RBC containing unbound Fe AROUND it (Fe should be inside the RBC)
  • does not normally exist outside the bone marrow
35
Q

term referring to the unbound Fe around the siderocyte

A

Pappenheimer bodies
- can cause cytotoxicity if not controlled/absorbed

*PappenheIRON bodies

36
Q

sources of iron

A

a. heme iron pool

b. non-heme iron

37
Q

heme iron pool

A
  • stored in hemoglobin/myoglobin& absorbed directly by intestinal mucosal cells
  • includes recycled iron
38
Q

dietary iron

A

Non-heme iron

  • from vegetables, eggs
  • in a ferric hydroxide form; harder to be absorbed
39
Q

aid in non-heme Fe absorption by breaking down ferric hydroxide to ferric & OH-

A
  • vitamin A
  • vitamin C
  • meat (contains proteins, amino acids)
  • fish
  • poultry
40
Q

when ferric ion reaches the stomach, _________________ will maintain the ferrous form for it to be absorbed

A

Vitamin C
Amino acid
Sugar
- ferrous-iron complex is formed

41
Q

substances that decrease iron absorption

A
  • oxalates
  • phytates
  • phosphates
  • tannins
  • antacids
  • antibiotics
42
Q

sources of tannins

A

large amount of beans, coffee, tea

43
Q

effect of antacids, antibiotics

A

reduce the acidity of stomach thereby reducing the conversion of Fe3+ –> Fe2+

44
Q

♀

A

female

45
Q

♂

A

male

46
Q

lab parameter which is a direct indication of the amount of storage Fe

A

Serum ferritin

  • normal values:
      • ♂ = 20-300ng/mL
      • ♀ = 10-20ng/mL
47
Q

serum ferritin of an individual with iron deficiency anemia (IDA)

A

<10ng/mL

48
Q

why do males have higher serum ferritin?

A

they have more stored iron because they have more blood

49
Q

average iron daily requirement for ♀

A

> 1.2mg/day

- due to frequent blood loss (menstruation, lactation, pregnancy)

50
Q

average iron daily requirement for ♂

A
  1. 2 +/- 0.3mg/day
    - only need small amounts because they have more blood
    - they do not experience having low amounts of Hgb or IDA
51
Q

T/F:

children do not need high amounts of iron

A

FALSE

  • they need high amounts (higher than average adult males) because of rapid growth
  • iron should be present all along during development
52
Q

causes of iron deficiency

A

a. major defects in Fe metabolism

b. IDA

53
Q

major defects in iron metabolism may be due to the following:

A

a. inappropriate oral intake
- foods low in Fe affects recycling process

b. insufficient/defective absorption
- due to injury of intestines

c. inefficient transport, storage, and/or utilization
- because of low transferrin levels

d. abnormal loss of Fe
- (including) in peptic ulcer, hemorrhoids, esophageal varices

54
Q

injury in intestines

A
  • after GIT operation
  • chronic malabsorption state
      • ineffective absorption in digestive system
  • severe chronic diarrhea
      • iron is excreted in stool
55
Q

low transferrin levels may be due to:

A
  • long-standing infections
  • inflammation
  • collagen diseases
  • malignancies (rel. to inflammation)
56
Q

most common cause of anemia worldwide

A

IDA

  • blood does not contain enough Fe to survive or to oxygenate the whole body
  • “iron-deficient”
57
Q

manifestations of severe IDA

A
  • fatigue
  • headache
      • low O2 (body) –> low O2 (brain)
  • pallor/paleness
  • pica
  • sore tongue/mouth
  • thinning/spooning of fingernails
      • fingernails are thin & bending upwards
58
Q

Pica

A
  • distorted appetite

- craving for weird substances eg. ice, laundry starch, earth, clay

59
Q

causes of iron overload

A

a. increased absorption
b. increased RBC production
c. inadequate erythropoiesis

60
Q

conditions with increased iron absorption

A

a. primary hemochromatosis

b. hemosiderosis

61
Q

a hereditary condition where the body absorbs too much Fe

A

Primary hemochromatosis (PCH)

  • high iron stores (increased serum ferritin)
  • there is substantial deposit outside the phagocytes –> low immunity
      • macrophage cannot ingest any more RBCs
      • excess RBCs hemolyze –> Fe released in circulation
62
Q

treatment for PCH

A
  • removal of excess Fe
      • bleeding the patient 500mL/week (or 2x/week) for 2-3 years
  • treat the damaged organ
      • usu. liver, spleen
63
Q

hemosiderosis

A
  • high Fe primarily in mononuclear phagocytes

- increased hemosiderin in the body

64
Q

how does increased RBC production cause iron overload?

A

early lysis of RBCs –> more Fe is released –> Fe overload

65
Q

causes of inadequate erythropoiesis

A

a. thalassemia

b. sideroblastic anemia

66
Q

anemia that is genetic

A

Thalassemia

  • causes the body to have less Hgb than normal
  • quantitative defect of hemoglobin production
  • RBCs appear like a target butt
67
Q

sideroblastic anemia

A
  • early release of nRBCs from the BM
  • Fe is not utilized well
      • BM was not able to incorporate Fe in the nRBCs
      • unused Fe are excreted and/or free to roam around
  • the body recognizes decreased RBCs –> BM hyperplasia (hyperactive) to compensate for blood loss
68
Q

effect of ineffective/defective erythropoiesis

A

anemia –> BM hyperplasia –> release of premature RBCs

HEMA 1 (12 decks)

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