Iron Deficiency and Vitamin B12 Deficiency Anemia Flashcards
Definition of anemia
-decrease in concentration of hemoglobin per unit volume of blood, often accompanied by a decrease of the concentration of erythrocytes per unit volume of blood.
Classification of Anemia
-By course- Acute and Chronic
-By origin- hereditary and acquired
-By Pathogenesis-posthemorrhagic, hemolytic, dyserythropoietic(IDA, Vit B12 deficiency , a plastic)
-By ability to regenerate- normo, hypo, hyperegenerative
-by colour index- normo, hypo, hyper chronic
-By type of hemopoiesis-normoblastic, megaloblastic
-By size of RBC- normo, micro, macrocytic
- By shape of RBCs-normocytic, spherocytic,sickle cell
-By severity
Mild -Hb >90g/l, Moderate -Hb 70-90g/l, severe Hb -less than 70
Hemolytic can be divided into 2 -hereditary or acquired
Hereditary- spherocytic anemia, G-6- PDH, thalassemia
Acquired-autoimmune,poisoning with hemolytic,medicinal poison + bacterial toxin
Etiology of Iron deficiency anemia(IDA)
1.Due to excessive loss of iron in Chronic blood loss due to
Esophageal gastric diseases
- reflux gastritis
- peptic ulcer colitis
- erosion
Intestinal disease
- diverticulosis
- Chrohns disease
- meckels diverticulum
Uterine disease
- menorrhagia
- myoma
- endometriosis
- hemorrhage
- diathesis
Nasal-hemorrhages ,diathesis
Renal
- hemorrhagic
- nephritis
- urolithiasis
- tumors
Iatrogenic
- blood donation
- private fences
- Due to impaired iron absorption
- enteritis
- malabsorption syndrome (absorption is maximum in GIT, maximum part in duodenum and in upper part of jejunum ). Malabsorption is observed in diseases of small intestine.
- operational interventions - Due to increased demand for iron
- pregnancy
- lactation
- prepubertal and pubertal periods
- treatment of macrocytic anemia vit IN12 - Due to alimentary insufficiency -daily intake of iron must not be less than 15-20mg
- malnutrition
- anorexia of various origins
- vegetarianism - drug associated- glucocorticoids, salicylates, NSAIDs, Ppis
- Genetic-iron refractory iron deficiency anemia
- Iron restricted erythropoietic- treatment with ESA(erythropoietin stimulating agent) , anemia of chronic diseases like chronic kidney disease
- Due to low HCL
Iron depot and iron metabolism in the body
Iron is stored mostly in the liver as ferritin or hemosiderin
Erythrocytes 2000-2500mg, plasma 4mg, stocks 800-1000mg,myoglobin and enzymes (cytochromes,catalase,peroxidase)-300mg,absorption =loss1-2mg per day, recycling in physiological hemolysis 20mg a day, for hemoglobin synthesis with erythropoiesis 20mg/day
For metabolism,
The iron from the GIT reacts with protoporphyrin 9 pigment through ferrochelatase which converts iron and protoporphyrin into Heme.
Heme is essential for Hb formation
With decrease of iron, there is decrease heme formation which will lead to decrease Hb( dysfunctional Hb)
Hb is the one which takes up cell volume in RBCs if there is decrease Hb the cell will be smaller. It is determined by blood test(mean corpuscular volume)
MCV= hematocrit x10
———————. X 100= 90 femtilitres
Total RBC in litre
MCV <90 fl = macrocytic
Clinical picture of IDA
- low energy levels
- symptoms of hypoxia(weakness, easy fatigue,dyspnea, palpitations, dizziness , headache)
- symptoms of sideropenia(dryness and fragility of hair, deformation of nails(koilonchyia),appearance of non- healing tissues on skin, atrophy of lingual pappillae, atrophy of GIT, pica- a desire to eat non-food materials- clay, sand, coal, chalk, ice)
- pale conjunctiva, mucosa or skin
- difficulties in memory and concentration
- decreased appetite, appearance of disturbances in taste and smell
- bed wetting
Clinical signs of IDA
IDA is characterised by decrease in synthesis of Hb and decrease concentration of RBCs
- decrease of Hb below 120g/l with decreased or normal RBCs
- decease of colour index -hypochromic
- increase of reticulocytes( up to 2-3%), normo or hyperegenarative anemia
- decrease in size of RBCs -microcytosis(55,7 - 70 micrometers cubed)
- increase iron binding capacity of serum
In labs
- CBC- decrease hematocrit depending on severity of anemia, leukopenia(sometimes), hypochromic microcytosis, reticulocytes are normal, increase ESR, increase thrombocytes(post hemorrhagic)
- Biochemical- decrease serum iron (norm 12,5-30,4 micromoles per litre),serum transferrin , transferrin saturation TSAT, serum ferritin level- below 12micrograms per decilitre.
- Endoscopy
- ECG
- bone marrow puncture
- colonoscopy
- routine urine analysis
- US to rule out stones, cancer,uterus problems
- gynaecological examination
- Chest X-ray
- Bronchoscopy
Treatment of IDA
- it’s not possible to get enough iron from food only
- no need for blood transfusion without vital indications, the indication isn’t level of Hb but hemodynamics , readings below 50-40g//
We give
1.iron preparations without additional vitamin like glucose
Hb level should increase by 10g in one month by oral administration if not parenteral way of administration
Oral meds-Ferronlex 10mg, sorbifex durulex(vit C)- tablets 100mg, tardiferon (mucoprotease) tablets 80mg, fenuls(vit c, nicotinamide vit group B)- capsules 45mg, ferrogradumet( plastic matric- degree D)- tab 105, aktiferrin
Parenteral way I.v is better e.g ferrinject, iron dextran, iron sucrase, rapid injection of iron
Vitamin B12 deficiency anemia, etiology
- Disruption of gastric secretion of the intrinsic factor of gastromucoprotein
- atrophic autoimmune gastritis with the production of antibodies to parietal cells and gastromucoprotein
- total gastrectomy
- congenital disorder of gastromucoprotein secretion
- stomach cancer
- polyposis of stomach
- toxic effect of high doses of alcohol on the gastric mucosa - Impaired absorption of Vitamin B12 in the small intestine
- resection of a section of illeum (more than 60cm)
- malabsorption syndrome of various origins (enzymatic enteropathy , celiac disease, enteritis, Crohn’s disease,intestinal amyloidosis)
- small intestine cancer
- chronic pancreatitis with impaired trypsin secretion - Competitive consumption of Vitamin B12
- multiple pregnancies
- chronic hemolytic anemia
- thyrotoxicosis - impaired intake of Vitamin B12 from food (in vegetarians)
- decreased reserves of Vit B12 (cirrhosis of the liver)
- impaired transport of Vitamin B12(antibodies to transcobalamin 2)
Pathogenesis of Vitamin B12 deficiency anemia
Vit B12 is obtained from food
The main cause of the disease is autoimmune condition. The parietal cells secrete a glycoprotein called intrinsic factor.
B12 naturally binds with intrinsic factor. In some individuals autoantibodies are produced these autoantibodies bind with intrinsic factor and block B12 resulting in decreased absorption.
In result less B12 will be in the bloodstream.
B12 is also required for RBC DNA maturation and condensation
If the DNA doesn’t mature and condense the RBCs will be huge.
We do MCV>90 f.e (macrocytosis/ macrocytic)
These RBCs can’t deliver oxygen because DNA isn’t mature well m they will be so big that they may get stuck in capillaries and undergo hemolysis.
Pathogenesis of clinical manifestations in Vit B12 deficiency anemia
Vit B12 functions in 2 coenzymes
- methylcobalamin
- 5- deoxadenosylcobalamin
Changes in hematopoiesis and epithelial cells are associated with impaired thymidine formation and therefore impaired cell division. The Pathogenesis of neurological disorders is associated with impaired metabolism of fatty acids, the accumulation of methylmalonic and propionic acids, toxic to the nervous tissue.
Clinical picture of Vit B12 deficiency anemia
It mostly develops in the elderly, often with a history of gastritis with low acidity, but it can also occur in young people
- pale icteric skin
- sclera subicteric
- Hunters glossitis (burning tongue)
- funicular myelosis
- signs of jaundice
Lab instrumental diagnosis of Vit B12 deficiency anemia
CBC- hyperchromic,megaloblastic, reticulocytic crisis after treating for 5 days
- jolly bodies
-leukopenia, thrombocytopenia
Bone marrow function investigation-megaloblastic type of hemopoiesis, macrocytosis, erythrocytes anisocytosis, basophilic puncture
Decreased leukocytes and platelets
Hyper segmentation of neutrophils, moderate indirect hyperbilirubinemia
Serum iron levels are normal or elavated prior to treatment
Treatment of Vit B12 deficiency anemia
Treatment is carried out by parenteral administration intramuscular of Vit B12 till Hb becomes normal then give once a month at the dose of 500mcg for the whole life.
After 5-7days from the start of treatment, patients develop a reticulocytes crisis
Blood transfusions are used in rare cases for health reasons in the presence of symptoms of decompansation of cardiovascular activity, development of anemic coma
Normalisation of Hb levels occurs after 3-4weeks from the start of treatment
Subsequently the patient is transferred to a permanent mantainance therapy with 500 mcg of vitamin B12 once a month.