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Hematology > Iron, B12, and Folate Metabolism > Flashcards

Iron, B12, and Folate Metabolism Flashcards

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
Q

Iron re-use

A

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
Q

Iron Scavenging

A

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
Q

Iron Loss

A

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
Q

Iron Absorption

A 
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
Q

Iron absorption regulation Increased

A 
Low dietary iron
Low body iron stores 
Increased red cell production
Low haemoglobin
Low blood oxygen content
30
Q

Iron absorption regulation Decreased

A

Systemic inflammation

31
Q

Hepcidin

A 
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
Q

The liver and iron metabolism

A

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
Q

Iron Release from cells

A

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
Q

Iron Deficiency

A 
Low iron (poor specificity)
Low ferritin (excellent specificity)
Elevated Transferrin (TIBC)
Low transferrin saturation
Hypochromia, microcytosis
Anemia
35
Q

Iron Deficiency Stages

A

Reduced iron stores
Iron deficient erythropoiesis
Iron deficient anemia

36
Q

Vitamin B12 (Cobalamin) Key Role

A

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
Q

Vitamin B12 (Cobalamin)

A

Water-soluble vitamin
Plays a role in recycling of folates
B12 plays a role in methionine synthesis

38
Q

Vitamin B12 Present in liver in three forms

A

Methylcobalamin, adenosylcobalamin, and hydroxycobalamin

39
Q

Vitamin B12 deficiency

A

Megaloblastic anemia:

40
Q

Megaloblastic anemia:

A

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
Q

Vitamin B12 deficiency Neurologic disorder:

A

probably secondary deficiency of methionine deprivation in the nerves.
Parathesias

42
Q

Vitamin B12 deficiency Homocysteinuria

A

Kyphosis (hunchback of Notre Dame)
Lens adaptation
Atherosclerosis (leads to MI)

43
Q

Absorption of Vitamin B12 2 pahses

A

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
Q

Mechanisms of B12 deficiency Diet

A

Comes from meat

A vegan diet (no B12 in all plants)

45
Q

Mechanisms of B12 deficiency Impaired absorption of B12

A 
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
Q

Vitamin B12 deficiency most commonly seen

A

Pernicious anemia

47
Q

Pernicious anemia

A

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
Q

Folate (Folic Acid)

A

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
Q

Folate deficiency

A 
Hyperhomocysteiemia, a risk factor for cardiovascular diseases
Megaloblastic anemia (which results from a deficiency of vitamin B12 and folic acid)
50
Q

Causes of folate deficiency

A

Inadequate intake
Impaired absorption
Impaired metabolism
Increased demand (e.g., pregnancy and lactation)

51
Q

Causes of folate deficiency

A

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
Q

Microcytes

A

Drastically smaller RBC (less than 7 microns) indicative of iron deficiency

53
Q

Macrocytes

A

Larger (>8.5 microns in diameter) indicative of megaloblastic anemias and aplastic anemias

54
Q

Polychromasia

A

Young RBC’s seen in severe anemia.

55
Q

Basophilic stippling

A

Pernicious anemia, seen in alcoholics and lead poisoning

56
Q

Helmet cells (schistocyte

A

Fragment of cell. Indicative of hemolytic anemia or acute leukemia.

57
Q

Burr Cells

A

Hemolytic anemias, iron deficiency or acute blood loss

58
Q

Hypochromasia

A

Cells have decreased hgb content has increased central pallor indicative iron deficiency anemia.

59
Q

Sickle Cells

A

Crescent shaped indicative of sickle cell anemia.

60
Q

Spherocytes

A

hemolytic anemia

61
Q

Target cells

A

Chronic liver disease

Hematology (4 decks)

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