Ferrokinetics Flashcards
1
Q
movement of iron through the body
A
ferrokinetics
- “ferro” = “iron”
- “kinetic” = “movement”
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
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
4
Q
total Fe content in the blood
A
3-5 g (adults)
- 1mL blood = 1mg Fe
5
Q
RBC turnover
A
- 120 days
- lifespan of RBCs
- when they die, Fe is released to & “recycled” to make new RBCs
6
Q
Fe requirement for erythropoiesis
A
20-25mg daily
- 95% comes from recycled iron
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
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)
9
Q
Fe3+
A
- ferric state of iron
- mobilized form
- state of free iron
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
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
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
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
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
15
Q
why is the stored Fe more than those being absorbed?
A
more Fe needs to be reserved in case of sudden drops
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
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
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
19
Q
regulation of Fe absorption occurs
A
Duodenum, jejunum
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
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
22
Q
transferrin
A
- plasma beta-globulin
- iron transport protein
- enhances the storing capacity of iron into the cells
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)
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
25
when the new RBCs are in the blood, iron will be utilized for survival until they die through _____________
bursting/lysis
- 120 days
- recycling process of Fe begins
26
the rest of the iron not used by the bone marrow & RBCs are ____________
Stored in the liver
- main storage site (bec. readily available)
- stored to avoid cytotoxicity
27
cycle of iron transport & storage
intestine (absorption) --> blood (with transferrin) --> bone marrow (make RBCs) --> liver (unused Fe) --> blood (until RBC lysis) --> released Fe --> intestine (absorption)
28
factors that affect Fe metabolism
- abnormal loss of Fe
- hemosiderinuria
- pathologic blood loss
29
most common cause of abnormal loss of iron
Hemorrhage
| - loss of circulating RBCs
30
hemosiderinuria
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
the top suspect of Fe loss in males
Pathologic blood loss
| - results in iron deficiency (males)
32
storage forms of iron
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
sideroblast
nucleated RBC (nRBC) containing iron
34
siderocyte
- mature RBC containing unbound Fe AROUND it (Fe should be inside the RBC)
- does not normally exist outside the bone marrow
35
term referring to the unbound Fe around the siderocyte
Pappenheimer bodies
- can cause cytotoxicity if not controlled/absorbed
*PappenheIRON bodies
36
sources of iron
a. heme iron pool
| b. non-heme iron
37
heme iron pool
- stored in hemoglobin/myoglobin& absorbed directly by intestinal mucosal cells
- includes recycled iron
38
dietary iron
Non-heme iron
- from vegetables, eggs
- in a ferric hydroxide form; harder to be absorbed
39
aid in non-heme Fe absorption by breaking down ferric hydroxide to ferric & OH-
- vitamin A
- vitamin C
- meat (contains proteins, amino acids)
- fish
- poultry
40
when ferric ion reaches the stomach, _________________ will maintain the ferrous form for it to be absorbed
Vitamin C
Amino acid
Sugar
- ferrous-iron complex is formed
41
substances that decrease iron absorption
- oxalates
- phytates
- phosphates
- tannins
- antacids
- antibiotics
42
sources of tannins
large amount of beans, coffee, tea
43
effect of antacids, antibiotics
reduce the acidity of stomach thereby reducing the conversion of Fe3+ --> Fe2+
44
♀
female
45
♂
male
46
lab parameter which is a direct indication of the amount of storage Fe
Serum ferritin
- normal values:
- - ♂ = 20-300ng/mL
- - ♀ = 10-20ng/mL
47
serum ferritin of an individual with iron deficiency anemia (IDA)
<10ng/mL
48
why do males have higher serum ferritin?
they have more stored iron because they have more blood
49
average iron daily requirement for ♀
>1.2mg/day
| - due to frequent blood loss (menstruation, lactation, pregnancy)
50
average iron daily requirement for ♂
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
T/F:
| children do not need high amounts of iron
FALSE
- they need high amounts (higher than average adult males) because of rapid growth
- iron should be present all along during development
52
causes of iron deficiency
a. major defects in Fe metabolism
| b. IDA
53
major defects in iron metabolism may be due to the following:
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
injury in intestines
- after GIT operation
- chronic malabsorption state
- - ineffective absorption in digestive system
- severe chronic diarrhea
- - iron is excreted in stool
55
low transferrin levels may be due to:
- long-standing infections
- inflammation
- collagen diseases
- malignancies (rel. to inflammation)
56
most common cause of anemia worldwide
IDA
- blood does not contain enough Fe to survive or to oxygenate the whole body
- "iron-deficient"
57
manifestations of severe IDA
- fatigue
- headache
- - low O2 (body) --> low O2 (brain)
- pallor/paleness
- pica
- sore tongue/mouth
- thinning/spooning of fingernails
- - fingernails are thin & bending upwards
58
Pica
- distorted appetite
| - craving for weird substances eg. ice, laundry starch, earth, clay
59
causes of iron overload
a. increased absorption
b. increased RBC production
c. inadequate erythropoiesis
60
conditions with increased iron absorption
a. primary hemochromatosis
| b. hemosiderosis
61
a hereditary condition where the body absorbs too much Fe
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
treatment for PCH
- removal of excess Fe
- - bleeding the patient 500mL/week (or 2x/week) for 2-3 years
- treat the damaged organ
- - usu. liver, spleen
63
hemosiderosis
- high Fe primarily in mononuclear phagocytes
| - increased hemosiderin in the body
64
how does increased RBC production cause iron overload?
early lysis of RBCs --> more Fe is released --> Fe overload
65
causes of inadequate erythropoiesis
a. thalassemia
| b. sideroblastic anemia
66
anemia that is genetic
Thalassemia
- causes the body to have less Hgb than normal
- quantitative defect of hemoglobin production
- RBCs appear like a target butt
67
sideroblastic anemia
- 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
effect of ineffective/defective erythropoiesis
anemia --> BM hyperplasia --> release of premature RBCs
