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Hematology > Iron, B12, and Folate Metabolism > Flashcards

Iron, B12, and Folate Metabolism Flashcards

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1
Q

Mouth

A 
Ingests
Begins mechanical breakdown
Initiates propulsion (swallowing)
Buccal Phase 
Start Chemical Breakdown
Salivary amylase
Lingual lipase
R Protein (Binds to B12)
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2
Q

Esophagus

A

Continuation of the buccal phase
Tongue presses against hard palate
Peristalsis moves bolus of food

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3
Q

Stomach

A 
Fundus
Body (midportion)
Antrum
Enzymes produced
Parietal cells produce
Intrinsic factor (B12 intestinal absorption)
Secrete gastric acid (HCL)
Chief Cells (peptic cells)
Pepsinogen to Pepsin
Digestion of proteins
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4
Q

Duodenum

A

Bile from the liver

Pancreatic juice

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5
Q

Jejunum

A

Specialized for absorption
Nutrients once absorbed are
transported to the liver via
hepatic portal vein

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6
Q

Ileum

A

Absorbs Vitamin B12
Bile Salts that have not been
previously absorbed

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7
Q

Liver

Metabolic and regulatory roles

A

Produces Hepcidin
Master regulator of iron
Produces Bile
Fat emulsifier

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8
Q

Large Intestine

Digestion

A

Some remaining food residues are
digested by enteric bacteria which
produce Vitamin K & some Vit B

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9
Q

Large Intestine

Absorption

A

B12 absorbed in Ileum
Most remaining water, electrolytes
and vitamins produced by bacteria

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10
Q

Iron

A 
Element (Fe)
Molecular weight 56
Abundance
Absorption
Iron is in plus 3 state Fe3+
To be absorbed, must be in plus 2 state
With Vitamin C becomes Fe2+ (plus 2 state)
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11
Q

Iron

A 
No metabolic pathway to get rid of iron
Loss through bleeding, menstrual periods 
An essential element
Males 10mg per day recommended
Females 18mg per day recommended
We absorb about 1mg per day (10%)
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12
Q

Iron functions

A 
Oxygen carriers
hemoglobin
Oxygen storage
Myoglobin
Energy production
Cytochromes (oxidative phosphorylation)
Krebs cycle enzymes
Other
Liver detoxification
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13
Q

Iron Toxicity

A 
Iron can damage tissues
Hemochromatosis (iron overload)
Can take years to build up
Hemosiderin (extra iron in ferritin)  deposits in:
Liver (cirrhosis)
Pancreas (diabetes)
Joints (arthritis)
Skin (dermatitis)
Iron excess possibly related to cancers, cardiac toxicity and other factors
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14
Q

Iron Toxicity

A 
Symptoms (same symptoms as iron deficiency)
Being tired all the time
Lethargic
Lack of menstrual period
Blood tests for Iron:
Serum Iron
TIBC= Total Iron Binding Capacity
Transferrin saturation
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15
Q

Iron Distribution

A 
35 – 45 mg / kg iron in adult male body
Total approx 4 g 
Red cell mass as hemoglobin - 50%
Muscles as myoglobin – 7%
Storage as ferritin - 30%
Bone marrow (7%)
Reticulo-endothelial cells (7%)
Liver (25%)
Other Heme proteins - 5%
Cytochromes, myoglobin, others
In Serum - 0.1%
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16
Q

Iron Transport in Blood Red cells

A

As hemoglobin

Cannot be exchanged

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17
Q

Iron Transport in Blood Plasma

A

Bound to Transferrin which is made in the liver
Carries iron between body locations
eg between gut, liver, bone marrow, macrophages
Iron taken up into cells by transferrin rece

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18
Q

Transferrin

A

Synthesised in the liver.
Each molecule binds can bind two Fe3+ molecules (oxidized)
Contains 95% of serum Fe.
Usually about 30% saturated with Fe.
Production decreased in iron overload.
Production increased in iron deficiency.
Measured in blood as a marker of iron status.

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19
Q

Transferrin Receptors

A

Collects iron from transferrin for uptake into cells
Recognizes and binds transferrin
Receptor + transferrin endocytosed
Iron released into cell via Iron transporter (DMT1)
Receptor + transferrin return to cell surface
Transferrin released

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20
Q

Soluble Transferrin Receptors

A 
Truncated form of cell surface receptors
Found in the circulation
High levels with iron deficiency
Low levels with iron overload
Possible role in diagnosis of iron deficiency compared in setting of inflammation
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21
Q

Serum Iron

A

serum contains about 0.1% of iorn. 95% is bound to transferrin.

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22
Q

Iron Storage - Ferritin

A

Iron store in the liver and nearly all other cells.
Outer shell: apoferritin, consists of 22 protein subunits
Iron-phosphate-hydroxide core.
20% iron by
Small fraction found in circulation

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23
Q

Iron Loss Physiological

A

Cell loss: gut, desquamation
Menstruation (1mg/day)
Pregnancy, lactation

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24
Q

Iron Loss Pathological

A

Bleeding

Gut, menorrhagia, surgery, gross hematuria

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25
Iron re-use
Old cells broken down in macrophages in spleen and other organs Iron transported to liver and other storage sites Red cell iron recovered from old red cells
26
Iron Scavenging
Breakdown of red cells in the circulation Free hemoglobin binds haptoglobins -> taken up by liver Free heme binds hemopexin -> taken up by liver Heme passing through kidney reabsorbed Three mechanisms to conserve iron in pathological situations
27
Iron Loss
An unregulated process No mechanisms to up- or down-regulate iron loss from the body Over-intake cannot be matched by increased loss Under intake cannot be matched by decreased loss Thus iron homeostasis is regulated by adjusting iron intake
28
Iron Absorption
``` 1 – 2 mg iron are absorbed each day (in iron balance 1 – 2 mg iron leaves the body each day) Occurs in the duodenum Taken up as ionic iron or heme iron Only 10% of dietary iron absorbed Dietary iron usually in excess ```
29
Iron absorption regulation Increased
``` Low dietary iron Low body iron stores Increased red cell production Low haemoglobin Low blood oxygen content ```
30
Iron absorption regulation Decreased
Systemic inflammation
31
Hepcidin
``` Antimicrobial activity Hepatic bacteriocidal protein Master iron regulatory hormone Inactivates ferroportin Stops iron getting out of gut cells Iron lost in stool when gut cells shed Leads to decreased gut iron absorptio ```
32
The liver and iron metabolism
Hepcidin production by the liver controls gut iron absorption and therefore body iron stores HFE (detects the amount of iron in the body) and hemojuvelin involved in hepcidin regulation
33
Iron Release from cells
Ferroportin present on cell surface to release iron Found on gut cells, liver cells and macrophages Requires cofactor to oxidize iron to allow for binding to transferrin Hephestin in gut Ceruloplasmin in other cells
34
Iron Deficiency
``` Low iron (poor specificity) Low ferritin (excellent specificity) Elevated Transferrin (TIBC) Low transferrin saturation Hypochromia, microcytosis Anemia ```
35
Iron Deficiency Stages
Reduced iron stores Iron deficient erythropoiesis Iron deficient anemia
36
Vitamin B12 (Cobalamin) Key Role
Normal functioning of the brain and nervous system Formation of blood Normally involved in the metabolism of every cell of the human body especially affecting DNA synthesis and regulation
37
Vitamin B12 (Cobalamin)
Water-soluble vitamin Plays a role in recycling of folates B12 plays a role in methionine synthesis
38
Vitamin B12 Present in liver in three forms
Methylcobalamin, adenosylcobalamin, and hydroxycobalamin
39
Vitamin B12 deficiency
Megaloblastic anemia:
40
Megaloblastic anemia:
Blood disorder characterized by anemia, with red blood cells that are larger than normal. This condition usually results from a deficiency of folic acid or of vitamin B-12. Hypersegmented neutrophils on CBC
41
Vitamin B12 deficiency Neurologic disorder:
probably secondary deficiency of methionine deprivation in the nerves. Parathesias
42
Vitamin B12 deficiency Homocysteinuria
Kyphosis (hunchback of Notre Dame) Lens adaptation Atherosclerosis (leads to MI)
43
Absorption of Vitamin B12 2 pahses
The gastric phase IF (Intrinsic factor) binds to B12 The intestinal phase IF-B12 complex is absorbed in the ileum through specific llieal receptors.
44
Mechanisms of B12 deficiency Diet
Comes from meat | A vegan diet (no B12 in all plants)
45
Mechanisms of B12 deficiency Impaired absorption of B12
``` Lack of IF in the stomach Gastric surgery Surgical removal of the ileum Crohns disease, IBS, Ulcerative Colitis Bacterial overgrowth in ileum Pancreatic insufficiency (chronic pancreatitis) Metformin (Common diabetic oral medication) Autoimmune disorders eg Graves or Lupus ETOH abuse ```
46
Vitamin B12 deficiency most commonly seen
Pernicious anemia
47
Pernicious anemia
a form of megaloblastic anemia; Basic underlying abnormality is an atrophic gastric mucosa Failure to secrete normal gastric secretions INCLUDING intrinsic factor Parietal cells of gastric glands secrete intrinsic factor (a glycoprotein) which is ESSENTIAL for absorption of B-12
48
Folate (Folic Acid)
Vitamin B9 Folate (the anion form of folic acid) Need a good balance between folate & B12 Participates in a single carbon transfer (e.g., synthesis of choline, serine, glycine, methionine, nucleic acids)
49
Folate deficiency
``` Hyperhomocysteiemia, a risk factor for cardiovascular diseases Megaloblastic anemia (which results from a deficiency of vitamin B12 and folic acid) ```
50
Causes of folate deficiency
Inadequate intake Impaired absorption Impaired metabolism Increased demand (e.g., pregnancy and lactation)
51
Causes of folate deficiency
Omeprazole (PPI used for gerd) Reduces iron absorption if taken at same time OTC H2 Blockers (Tagamet, Ranitidine) Reduces absorption of iron, folate &B12
52
Microcytes
Drastically smaller RBC (less than 7 microns) indicative of iron deficiency
53
Macrocytes
Larger (>8.5 microns in diameter) indicative of megaloblastic anemias and aplastic anemias
54
Polychromasia
Young RBC’s seen in severe anemia.
55
Basophilic stippling
Pernicious anemia, seen in alcoholics and lead poisoning
56
Helmet cells (schistocyte
Fragment of cell. Indicative of hemolytic anemia or acute leukemia.
57
Burr Cells
Hemolytic anemias, iron deficiency or acute blood loss
58
Hypochromasia
Cells have decreased hgb content has increased central pallor indicative iron deficiency anemia.
59
Sickle Cells
Crescent shaped indicative of sickle cell anemia.
60
Spherocytes
hemolytic anemia
61
Target cells
Chronic liver disease

Hematology (4 decks)

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