Wondershare EdrawMind
EdrawMindBlood system-iron deficiency anemia
MindMap Gallery Blood system-iron deficiency anemia
- 22
Blood system-iron deficiency anemia
Blood system - a mind map of iron deficiency anemia, which summarizes the knowledge of epidemiology, iron metabolism, etiology and pathogenesis, clinical manifestations, laboratory tests, diagnosis and differential diagnosis, and treatment. Let's take a look at it together.
Edited at 2023-04-13 19:52:37- bacteria
This is a mind map about bacteria, and its main contents include: overview, morphology, types, structure, reproduction, distribution, application, and expansion. The summary is comprehensive and meticulous, suitable as review materials.
- Plant asexual reproduction
This is a mind map about plant asexual reproduction, and its main contents include: concept, spore reproduction, vegetative reproduction, tissue culture, and buds. The summary is comprehensive and meticulous, suitable as review materials.
- Reproductive development of animals
This is a mind map about the reproductive development of animals, and its main contents include: insects, frogs, birds, sexual reproduction, and asexual reproduction. The summary is comprehensive and meticulous, suitable as review materials.
Blood system-iron deficiency anemia
- bacteria
This is a mind map about bacteria, and its main contents include: overview, morphology, types, structure, reproduction, distribution, application, and expansion. The summary is comprehensive and meticulous, suitable as review materials.
- Plant asexual reproduction
This is a mind map about plant asexual reproduction, and its main contents include: concept, spore reproduction, vegetative reproduction, tissue culture, and buds. The summary is comprehensive and meticulous, suitable as review materials.
- Reproductive development of animals
This is a mind map about the reproductive development of animals, and its main contents include: insects, frogs, birds, sexual reproduction, and asexual reproduction. The summary is comprehensive and meticulous, suitable as review materials.
- Recommended to you
- Outline
Blood system-iron deficiency anemia
【concept】
1) Hemoglobin composition
heme
protoporphyrin
Iron (Fe2)
globin
2) Iron deficiency stage
A Iron deficiency period (ID): iron stores in the body are depleted
B Iron-deficient erythropoietic phase (IDE): iron deficiency in red blood cells
C Iron deficiency anemia (IDA): It is the final stage of iron deficiency (including ID, IDE, IDA) and manifests as microcytic hypochromic anemia.
3) Manifestation: Decreased bone marrow iron storage (serum ferritin) - low serum iron - anemia
【Epidemiology】
1) IDA is the most common anemia
【Iron metabolism】
I Iron metabolism
II Distribution of iron
1) Functional state iron
a Hemoglobin iron (accounts for 67% of iron in the body)
b Myoglobin iron (15% of iron in the body)
c transferrin iron
d Lactoferrin
e Iron bound by enzymes and cofactors
2) Store iron
a Ferritin
b Iron-containing heme
III Sources of Iron
1) Red blood cells destroyed by aging (main source)
2) Normal people consume 1 to 1.5 mg of iron from food every day, and pregnant and lactating women consume 2 to 4 mg of iron.
IV iron absorption
Mainly located in the duodenum and upper jejunum
V Factors affecting iron absorption
1) Animal foods have high iron absorption rates, while plant foods have low iron absorption rates.
2) Vitamin C and other reducing agents reduce high iron to ferrous iron; protein decomposition products can promote iron into a dissolved state, both of which can promote iron absorption.
3) Gastrointestinal function (pH, etc.), body iron storage capacity, bone marrow hematopoietic status and certain drugs (such as vitamin C) will affect iron absorption
VI Transport of Iron
1) In plasma: ferrous iron is oxidized to ferric iron by ceruloplasmin, combined with transferrin, and transported to various tissues
2) In red blood cells: Iron is separated from transferrin, reduced to ferrous iron, and combined with protoporphyrin and globin on the mitochondria to form hemoglobin.
VII Recycling and excretion of iron
1) Reuse: The heme iron after the destruction of red blood cells is used to produce heme for new red blood cells.
2) Excretion: It can be excreted with the feces through the exfoliated cells of the intestinal mucosa, and a small amount can be excreted through urine, sweat, and milk.
VIII Iron Storage
It is stored in the monocyte-macrophage system in the liver, spleen, bone marrow and other organs in the form of ferritin and hemosiderin.
[Cause and pathogenesis]
(1) Cause of disease
I Increased iron requirements and insufficient iron intake
1) Infants, young children and teenagers
2) Pregnancy and lactation
II Iron malabsorption
1) After subtotal gastrectomy, gastric acid secretion is insufficient and food quickly enters the jejunum, bypassing the main absorption site of iron (duodenum)
2) Long-term unexplained diarrhea, chronic enteritis, Crohn's disease, intestinal parasites, etc.
III Excessive iron loss
1) Chronic gastrointestinal blood loss: hemorrhoids, gastroduodenal ulcers, etc.
2) Menorrhagia: intrauterine IUD placement, uterine fibroids, etc.
3) Hemoptysis and alveolar hemorrhage: pulmonary hemosiderosis, tuberculosis, lung cancer, etc.
4) Hemoglobinuria: PNH
5) Others: chronic renal failure, hemodialysis, multiple blood donations, etc.
(2) Pathogenesis
I Effect of iron deficiency on iron metabolism
II Effects of Iron Deficiency on Hematopoietic System
III Effects of iron deficiency on tissue and cell metabolism
[Clinical manifestations]
I Manifestations of primary disease caused by iron deficiency
1) Dark stools, bloody stools or abdominal discomfort caused by peptic ulcers, tumors or hemorrhoids
2) Abdominal pain or changes in stool properties caused by intestinal parasitic infection
3) Weight loss in neoplastic diseases
4) Hemoglobinuria with intravascular hemolysis
II manifestations of anemia
1) Common symptoms include fatigue, easy tiredness, dizziness, dizziness, tinnitus, etc.
2) Paleness and increased heart rate
III manifestations of tissue iron deficiency
1) Abnormal mental behavior, such as irritability, irritability, pica, etc.
2) Decreased physical strength and endurance
3) Susceptible to infection
4) Children’s growth retardation and mental retardation
5) Stomatitis, glossitis, dysphagia, etc.
6) Dry and falling hair
7) Dry and wrinkled skin
8) Finger (toe) nails become flat, even concave and spoon-shaped (spoon-shaped nails)
【Laboratory examination】
I blood picture
1) Microcytic hypochromic anemia: MCV<80fl, MCH<27pg, MCHC<32%
2) The red blood cells are small in size and the central light-stained area is expanded in the blood film.
II bone marrow image
1) Active or obviously active proliferation
2) Mainly hyperplasia of the erythroid system, with no obvious abnormalities in the granulocyte and megakaryocytic systems
3) Young red blood cells show the phenomenon of “old nuclei and young plasma”
4) After iron staining, extracellular iron and sideroblasts decrease or disappear.
III Iron metabolism
1) Serum iron (SI) <8.95 μmol/L, total iron binding capacity (TIBC) increases, transferrin saturation (TS) decreases, and serum soluble transferrin receptor (sTfR) increases
2) Serum ferritin (SF) <12μg/L
3) Decreased iron levels inside and outside cells
IV Porphyrin metabolism in red blood cells
V Serum transferrin receptor assay
1) sTfR measurement is the best indicator of iron deficiency erythropoiesis
2) sTfR>26.5nmol/L (2.25μg/ml) can diagnose iron deficiency
【Diagnosis and Differential Diagnosis】
(1) Diagnosis
I ID
1) Serum ferritin <12μg/L
2) Bone marrow iron staining shows that the small bone marrow granules that can stain iron disappear and the sideroblasts are less than 15%.
3) Hemoglobin and serum iron and other indicators are still normal
II IDE
1) Serum ferritin <12μg/L
2) Bone marrow iron staining shows that the small bone marrow granules that can stain iron disappear and the sideroblasts are less than 15%.
3) Transferrin saturation (TS) <15%
4) FEP (free protoporphyrin)/Hb>4.5μg/gHb
5) Hemoglobin is still normal
IDA
1) Serum ferritin <12μg/L
2) Bone marrow iron staining shows that the small bone marrow granules that can stain iron disappear and the sideroblasts are less than 15%.
3) Transferrin saturation <15%
4) FEP (free protoporphyrin)/Hb>4.5μg/gHb
5) Microcytic hypochromic anemia: male Hb<120g/L, female Hb<110g/L, pregnant woman Hb<100g/L; MCV<80fl, MCH<27pg, MCHC<32%
IV etiology diagnosis
1) IDA is only a clinical manifestation. Only when the cause is clear can IDA be cured.
2) For IDA caused by gastrointestinal malignant tumors accompanied by chronic blood loss or cancer of the residual stomach after gastric cancer surgery, fecal occult blood should be checked multiple times, and gastrointestinal X-rays or endoscopy should be performed if necessary.
3) Women with menorrhagia should be checked for gynecological diseases
(2) Differential diagnosis
Differentiate from microcytic anemia
I sideroblastic anemia
1) Red blood cell iron utilization disorder anemia caused by hereditary or unknown reasons
2) Increased serum ferritin concentration, increased bone marrow hemosiderin granules, increased sideroblasts, and the appearance of ring sideroblasts
SI, TIBC, and TS all increased
3) Abnormal chromosome karyotype
II globinogenic anemia/thalassemia
1) There is a family history and hemolysis
2) A large number of target-shaped red blood cells can be seen in the blood film
3) Abnormal quantity of globin peptide chain synthesis: increased HbF and HbA2
4) Serum ferritin, bone marrow stainable iron, serum iron and iron saturation are not low and often increase
SF, SI, and TS can increase
III anemia of chronic disease
1) Abnormal iron metabolism anemia caused by chronic inflammation, infection or tumors
2) Increased iron storage (serum ferritin and bone marrow granular hemosiderin)
3) Decreased serum iron, serum iron saturation, and total iron binding capacity
SI, TS, and TIBC all decreased
IV transferrin deficiency
1) Caused by autosomal recessive inheritance (congenital) or secondary to severe liver disease or tumors (acquired)
2) Manifested as microcytic hypochromic anemia
3) Serum iron, total iron binding capacity, serum ferritin and bone marrow hemosiderin were all significantly reduced.
SI, TIBC, and SF all decreased
【treat】
Treatment principles: eradicate the cause and replenish iron stores
(1) General treatment
1) Encourage to eat more iron-rich foods or iron-fortified foods with higher absorption rates such as meat
2) Infants and young children should add complementary foods in time
3) Women during menstruation, especially during pregnancy, may consider preventive iron supplementation
4) Identify the cause and treat the primary disease
(2) Drug treatment
I Oral Iron
Safe and convenient, it is the preferred method
1) Classification
Inorganic iron: ferrous sulfate
Organic iron: iron dextran
2) Taking it after meals has little gastrointestinal reaction and is easy to tolerate
3) Eating cereals, milk, tea, etc. will inhibit the absorption of iron; fish, meat, and vitamin C can enhance the absorption of iron.
II Iron injection (intramuscular injection)
1) Iron dextran is the most commonly used injectable iron
(3) Judgment of therapeutic effect
1) The effective performance of oral iron medication is firstly an increase in reticulocytes (Ret) in peripheral blood, with the peak occurring 5 to 10 days after starting to take the medication.
2) Ret concentration increases after 2 weeks and usually returns to normal in about 2 months
3) Iron therapy should be continued for at least 4 to 6 months after hemoglobin returns to normal, and should be discontinued when ferritin returns to normal.
【prevention】
【Prognosis】