Iron deficiency Flashcards

0
Q

Is heme iron or elemental iron absorbed more efficiently?

A

-heme iron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

Where is iron absorbed?

A

-duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe the absorption of elemental iron.

A
  • Mostly in form of Fe3+ and must be reduced to Fe2+
  • DMT1 transport Fe2+ at the apical side
  • iron can be stored in intestinal cells as ferritin
  • or can be exported as Fe2+ by FPN1 (ferroportin) on basolateral side
  • Fe2+ is oxidized to Fe3+ to bind to transferrin (Tf) to circulate in the body
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is responsible for a majority of the iron available for erythropoiesis?

A
  • macrophage recycling: macrophages in spleen engulf old or damaged RBCs and release Heme from Hb. Heme oxygenase releases iron from heme
  • iron recovered from heme may be stored as ferritin or exported to plasma by FPN1 where it is oxidized to +3, binds Tf, and is available for erythropoeisis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Deficiency of ________ rapidly limits erythropoiesis.

A

-Fe2-Tf

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe the process of incorporating iron into Hb.

A
  • incorporated into erythroblasts in BM
  • diferric transferrin binds transferrin receptor on erythroblast surface. It is engulfed via cathrin-coated pit, endosome at low pH dissociated Fe from receptor (which is recycled). Fe is stored as ferritin or added to heme, then joined to a2B2 to form Hb
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the main iron regulatory protein in the body and what does it do?

A
  • Hepcidin: 25 AA made mainly in the liver
  • negative regulator of cellular iron export by binding and degrading ferroportin in enterocytes and macrophages; downregulated FPN1
  • iron is trapped in enterocytes and macrophages
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Who is at highest risk for iron deficiency anemia?

A

-infants, young children, women, elderly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

2 general categories and 5 subcategories of causes of iron deficiency

A
  1. Inadequate supply: nutritional, malabsorption

2. Increased demand: blood loss, rapid growth, pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Name some things that can increase or decrease absorption of iron.

A
  • increase: heme iron and vitamin C (facilitates ferrireduction)
  • decrease: plant iron, tannins (tea, coffee), fiber, Ca2+, disrupted mucosa, achlorhydria
  • *remember, take iron with OJ, not coffee
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Blood losses to be aware of that can lead to iron deficiency

A
  • Gastrointestinal (especially in adults!!): colon cancer, ulcers, gastritis (H. pylori, NSAIDs), hookworm, Meckel’s Diverticuli, hemorrhoids, vascular malformations
  • menstrual: menorrhagia
  • child birth
  • trauma
  • chronic hemoglobinuria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Signs and symptoms of iron deficiency

A

-pallor, weakness, fatigue, headache, irritability, angular stomatitis, pagophagia (chew ice, eat dirt), beeturia, blue sclera, koilonychia (brittle nails)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Lab evaluations for Iron Deficiency: hematological and biochemical markers.

A
  • Hematologic: decreased Hb, decreased RBC, microcytic, increase RDW, decrease retic, often but not always have increase in platelets
  • Biochem: dec. ferritin, dec. serum iron, dec. transferrin saturation, increase TIBC, increase serum transferrin R, increase free erythrocyte protoporphyrin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Rx of iron deficiency

A
  1. correct iron deficiency: give oral iron sulfate, slow release iron, parenteral iron, RBC transfusion is rarely needed
  2. identify and correct underlying cause of iron deficiency anemia
    - prevention is preferable
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe the body’s response to iron therapy.

A
  • retic count rises in 3-4 days, and peaks in 5-10 days

- following retic increase, Hb rises

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Non-hematologic effects of iron deficiency

A
  • GI issues: gastritis, mucosal atrophy, achlorhydria, malabsorption
  • development and behavior changes
  • impaired immunity
  • dec. work/exercise performance
  • developmental defects
16
Q

What is the most common anemia is hospitalized and chronically ill?

A

-anemia of chronic inflammation/disease

17
Q

Common conditions associated with anemia of chronic disease/inflammation.

A
  • chronic infection
  • connective tissue disorders (lupus)
  • cancer/lymphoma
  • major trauma
  • ulcerative colitis, regional enteritis
18
Q

Anemia of chronic disease is associated with symptoms of iron deplete and iron replete. What is thought to account for this?

A

-abnormal systemic iron distribution due to a relative hepcidin excess

19
Q

Pathogenesis of ACD/AI

A
  • inflammation stimulates IL-6 production
  • IL6 promotes expression of hepatic hepcidin
  • iron recycling becomes inefficient and iron is retains in macrophages
  • increase ferritin, decrease transferrin saturation
  • Erythropoiesis becomes iron restricted since this Fe is trapped in macrophages; inflammatory cytokines also directly suppress erythropoiesis, too. If inflammatory signal is sufficiently protracted, anemia ensures. May eventually turn into IDF due to blocked iron absorption
20
Q

Rx of ACI/ACD

A
  • treat underlying disease
  • EPO, IV iron
  • future rx may be hepcidin antagonist
21
Q

One huge difference and key lab evaluation to dissociate iron deficiency anemia from ACI/ACD is what?

A

-serum ferritin: decreased in IDA and normal or increased in ACI since ACI involved hepcidin excess which will trap iron in macrophages and enterocytes