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Heme > Iron, Folate, B12 metab > Flashcards

Iron, Folate, B12 metab Flashcards

1
Q

What are the enzymes produced by the stomach, what is their function?

A
  • Parietal cells produce:
  • -intrinsic factor (B12 intestinal absorption)
  • -secrete HCL (releases iron from heme)
  • Chief Cells aka peptic cells
  • -convert pepsinogen to pepsin
  • -digest proteins
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2
Q

Doudenum function

A
  • bile and pancreatic juices enter the duodenum.

- absorbs major of iron.

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3
Q

Jejunum function

A
  • specialized for absorption

- absorbed nutrients are transported to the liver via hepatic portal vein.

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4
Q

Ileum function

A

-absorbs Vit B12 and bile salts

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5
Q

Liver function

A
  • metabolic and regulatory roles:
  • -produces hepcidin
  • -produces bile (fat emulsifier)
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6
Q

What is the master regulator of iron absorption? Where is this synthesized?

A

Hepcidin, Liver

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7
Q

Function of Gallbladder

A

-store bile

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8
Q

Pancreas function

A
  • produces enzymes: protease (proteins) and lipase (fats)
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9
Q

Where is the abundance of iron in the body held?

A
  • MOST (2.5g of 5g) in Hgb

- remainder in FERRITIN complexes in ALL CELLS.

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10
Q

What state is most iron taken into the body? what state is required fro the absorption of Fe into the blood?

A

Fe3+

Fe2+

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11
Q

How much Iron consumption is recommended for males and females?

A

M- 10mg/day

F- 18mg/day

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12
Q

Functions of Iron

A
  • Oxygen Carrier (hgb)
  • Oxygen storage (Myoglobin in muscle)
  • energy production (cytochromes, kreb cycle enzymes)
  • other: liver detoxification
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13
Q

How is iron transported in the blood?

A

via :

  • Red blood cells as Hgb which cannot be exchanged
  • Plasma bound to transferrin(made in liver), carries iron between body locations. ex between gut, liver, bone marrow, mfs.
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14
Q

Transferrin:

  • where is this synthesized?
  • how many iron molecules can bind?
  • what % of the total serum Fe is bound to transferrin?
  • What % of transferrin is bound to Fe?
  • When is transferrin binding capacity increased and decreased?
A
  • liver
  • 2 molecules
  • 95%
  • 30%

-transferrin production is increased in iron deficiency
and decreased in iron overload.

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15
Q

What is measured in the blood as a marker of iron status?

A

Transferrin

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16
Q

What does Serum iron blood test measure?

A

-all serum iron (not in red blood cells)

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17
Q

What is ferritin used for?

A

used to store iron in the liver and nearly all other cells.

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18
Q

Types of Iron Loss

  • physiological
  • pathological
A

Physiological:

  • cell loss: gut, desquamation of epithelial cells
  • menstruation
  • pregnancy, lactation

Pathological

  • bleeding
  • gut, menorrhagia, surgery, gross hematuria
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19
Q

Iron loss, is this a regulated process?

A

-it is an unregulated process, no mechanism to up or down regulate iron LOSS from the body.

You can modify the intake but you cannot modify the output, this output is constant thus, homeostasis is regulated by adjusting iron intake.

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20
Q

Describe the process of iron re-use.

A
  • old cells broken down into mfs in spleen & other organs, iron transported to liver and other storage sites. Red blood cells recover iron from these storage sites.
  • routine metabolism doesn’t lose iron, its captured and recycled.
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21
Q

What are the three mechanisms to conserve iron in pathological situations?

A
  • free hgb bind haptoglobins–> taken up by liver
  • free heme binds hemopexin–> taken up by liver
  • heme passing through kindeys–> kidney reabsorbed.
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22
Q

Iron absorption

  • how much is absorbed each day? Lost?
  • where does absorption take place and in what form is iron absorbed?
  • What happens to excess dietary iron?
A
  • 1-2mg/day, lost the same amount.
  • duodenum, taken up as ionic iron or heme iron
  • only 10% is absorbed, rest is either not absorbed or kept in enterocytes and shed into the gut.
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23
Q

When is iron absorption increased and decreased?

A

Increased:

  • low dietary iron
  • low body iron stores*
  • increased red cell production*
  • low hgb*
  • low blood O2 content*
  • = leads to decreased hepcidin production.

Decreased:

  • systemic inflamm
  • leads to increased hepcidin production
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24
Q

What proteins regulate hepcidin regulation?

A

HFE and hemojuvelin

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25
Q

What is the function of Hepcidin?

A
  • inactivates ferroportin (transports iron inside to outside), thereby stopping iron from getting out of the gut cells.
  • leads to decreased gut iron absorption.

the only way iron is lost is in the stool when gut cells shed.

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26
Q

How is iron released from cells?

A
  • ferroportin on the cell surfaces (gut, liver, and mf) releases the iron. The iron must be oxidized from 2+ to 3+ by hephestin(gut) and ceruloplasmin(other cells) in order to bind to transferrin in the blood.
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27
Q

Possible causes of iron, folate and B12 deficiency

A
  • reduced intake
  • increased loss
  • increased demands
28
Q

Can iron deficiency be a diagnosis?

A

-no! its a symptom of some other disease.

29
Q

Laboratory Changes in Iron deficiency

A
  • low iron (poor specificty)
  • low ferritin (excellent specificity)
  • elevated transferrin (TIBC)
  • Low transferrin saturation
  • hypochromia, microcytosis
  • anemia
30
Q

What is transferrin?

A

iron binding blood plasma glycoprotein. Controls the level of free iron in the blood. It binds iron reversibly and transports it to different locations in the body.

31
Q

Stages of iron deficiency

A
  1. reduced iron stores
  2. iron deficient erythropoiesis
  3. iron deficient anemia
32
Q

What is hemochromatosis?

A

-iron overload/toxicity, this may take years to build up

33
Q

What is hemosiderin?

A

-extra iron in ferritin that deposits in the liver (cirrhosis), pancreas (diabetes), joints (arthritis), skin(dermatitis)

34
Q

Iron toxicity may be related to what ?

A

definately cardiac toxicity and possibly related to cancers.

35
Q

Why is hemochromatosis evolved?

A
  • body deprived of iron, it stores up extra iron
  • survival of infections
  • w/o iron bacteria do not grow as fast.

-genetic, C282Y, recessive

36
Q

THe absence of iron is known as ______.?

Too much iron is known as________?

A
  • anemia/decreased hgb

- hemochromatosis

37
Q

Can iron be deadly to the human body?

A

YESSSS. too much or too little is deadly.

38
Q

Sx of Hemochromatosis

A
  • fatigue
  • anthralgia
  • loss of libido
  • skin bronzing*
  • abnormalities of liver
  • weakness
  • lethargy
  • cardiomyopathy*
  • hyperferritinemia
  • DM
  • impotence
  • ekg abnormalities
39
Q

Can serum levels of ferritin alone indicate hemochromatosis?

A

NO! serum levels of ferritin also rise during inflamm.

40
Q

vitamin B12

  • aka
  • what is its role?
A

-cobalamin

Role:
-normal functioning of brain and nervous system

  • formation of blood
  • cellular metabolism, especially DNA synthesis and regulation.
41
Q

Why do you need to consume folates (folic acid) and Vit B12?

A

insufficient intake of folic acid and vitamin B12 can increase the conversion of methionine to homocysteine, leading to high levels of inflammation. This may increase risk for cardiovascular disease.

42
Q

How much B12 is required each day?

What is an important distinction between Vit B12 and folate deficiencies?

A
  • 5ug

- B12 has neurological sx and folate does not, otherwise their sx are the same.

43
Q

Diseases that result from Vit B12 deficiency?

A
  • megaloblatic anemia: RBC are larger than normal and hypersegmented neutrophils, results from folic acid or vit b12 deficiency
  • one type is pernicious anemia
  • neurologic disorders: secondary to deficiency of methionine in nerves, parathesias
  • **Tx: with both B12 and folate TOGETHER.

-Homocysteinuria: kyphosis, lens adaptation, atherosclerosis (»>MI)

44
Q

Describe the process of B12 absorption and storage.

A

Absorption:
Phase 1: gastric phase; intrinsic factor binds B12

Phase 2: intestinal phase:
intrinsic factor-B12 complex is absorbed in the ileum.

Storage:
stored in blood and liver. Involves TCI II and III (trans-cobalamines)

45
Q

Mechanisms of B12 Deficiency

A

-Poor diet (vegan, little to no meat)

Impaired absorption of B12

  • lack of Intrinsic factor in stomach
  • gastric surgery
  • surgical removal of ileum
  • crohns disease, IBS, ulceritive colitis
  • bacterial overgrowth in ileum
  • pancreatic insufficiency (chronic pancreatitis)
  • metformin (diabetic med)
  • autoimmune disorders
  • ETOH
46
Q

What is the cause of Pernicious anemia?

A
  • atrophy in gastric mucosa

- failure to secrete normal gastric secretions (IF, so no aborption of B12)

47
Q

Common names for folates

A

folic acid

B9

48
Q

What is a disease resulting from folate deficiency?

A
  • hyperhomocysteinemia–risk for CVD

- megaloblastic anemia (vit B12 and B9 deficiency)

49
Q

Medication Causes of Folate Deficiency

A
  • omeprazole (GERD): reduces iron absorption

- OTC H2 blockers (Ranitidine) : reduces absorption of iron, B9 and B12

50
Q

Describe its structure: Microcytes, indicative of what disease?

A

-drastically smaller than RBC (

51
Q

Describe its structure: Macrocytes, indicative of what disease?

A

larger (>8.5 microns)

-megaloblastic and aplastic anemia

52
Q

Describe its structure: Polychromasia

A

young red blood cells seen in severe anemia

53
Q

Describe its structure: Hypochromasia indicative of what disease?

A

cells have decreased hgb content, increase central pallor

-iron deficiency anemia

54
Q

Describe its structure: Target cells, indicative of what disease?

A
  • bulls eye

- liver disease, hgb SC, thalassemia, Fe deficiency*, asplenia

55
Q

Describe its structure: Elliptocytes/Ovalcytes, indicative of what disease?

A

elongated RBC
E- long axis >/=2xshort axis
O- long axis

56
Q

Describe its structure: Dacrocyte, indicative of what disease?

A
  • tear drop

- thalassemia, myelofibrosis, megaloblastic anemia*

57
Q

Describe its structure: Sphereocyte, indicative of what disease?

A
  • sphericla, loss of membrane

- hereditary spherocytosis, immune hemolytic anemia

58
Q

Describe its structure: Schistocytes, indicative of what disease?

A
  • helmet cells, fragmented d/t traumatic membrane disruption

- microangiopathic hemolytic anemia, vasculitis, glomerulonephritis, prosthetic heart valve

59
Q

Describe its structure: Acanthocyte, indicative of what disease?

A
  • spur cell, irregularly distributed thorn-like projections d/t abnormal membrane lipids
  • severe liver disease(Spur cell anemia), starvation/anorexia, post splenectomy
60
Q

Describe its structure: Howell-Jolly Bodies , indicative of what disease?

A
  • small nuclear remnant of nucleus

- post splenectomy, hyposplenism, neonates, megaloblastic anemia*

61
Q

Describe its structure: Basophilic stippling indicative of what disease?

A
  • deep blue granulations indicating ribosome aggregation

- thalassemia, heavy metal poisoning, megaloblastic anema*, ETOH

62
Q

Describe its structure: Rouleaux, indicative of what disease?

A
  • stacks of coins d/t increased plasma conc. of high molecular weight proteins.
  • pregnancyy, inflamm conditions, polyclonal immunoglobulins, multiple myeloma
63
Q

Describe its structure: Sickle cell, indicative of what disease?

A
  • sickle shape d/t polymerization of HbS (hgb sickle cell)

- HbSC, HbSS (types of sickle cell)

64
Q

Describe its structure: Echinocytes, indicative of what disease?

A
  • “burr cells”, regularly spaced small spiny projections.

- uremia, HUS, burns, cardiopulmonary bypass, post transfusion, storage artifact

65
Q

RBC inclusion, Describe its structure: Heinz Body , indicative of what disease?

A
  • denatured and precipitated hgb, polyps growing off of them,
  • G6PD deficiency post exposure to oxidants, thalassemia, unstable Hgb
66
Q

RBC inclusions, Describe its structure: Sideroblast, indicative of what disease?

A
  • RBC w/ iron containing granules in cytoplasm, blue spots on outside rim of RBC
  • heriditary, idiopathic, drugs, hypothyroidism, sideroblastic anemia
67
Q

RBC inclusions, Describe its structure: Nucleus, indicative of what disease?

A
  • have nucleus, present in erythroblasts (immature RBC)

- hyperplastic erythropoesis seen in hypoxia, hemolytic anemia, extramedullary hematopoiesis

Heme (13 decks)

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